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-8,886,615,823,967,673,000 | Teeth Grinding Treatment
Teeth grinding often happens during sleep, due to stress or anxiety, and is found more often in people with a sleep disorder such as snoring. During the day, stress and deep concentration can cause us to clench our teeth and jaw instead. Other risk factors include drinking too much alcohol, smoking or taking recreational drugs. The medical term for both teeth grinding and jaw clenching is ‘bruxism’.
Teeth Grinding Treatments at The Cosmetic Skin Clinic
Why do people grind their teeth?
Teeth grinding, or ‘bruxism’ is a process where a person rubs their teeth together or clenches their jaw without realising it. Bruxism can be a temporary occurrence for many people, without any real concerns caused. For others, it can lead to jaw pain, headaches and earache. Teeth will also become worn down.
What causes teeth grinding?
Teeth grinding has a range of different causes, but it is often associated with anxiety attacks or stress. When individuals are awake, the condition is often linked to emotions like stress, anger and tension. However, grinding teeth at night involves a sleep-related chewing pattern that is often linked to sleep disorders.
What are the symptoms of teeth grinding?
If you grind your teeth repeatedly on a frequent basis, the process can cause a range of physical ailments and symptoms, including headaches, facial pain, earache, stiffness and pain in the jaw joint (temporomandibular joint) and surrounding muscles, disrupted sleep patterns, tooth damage, and worn-down teeth. The condition can even lead to increased teeth sensitivity and permanent tooth loss if left unchecked.
These unpleasant symptoms often disappear when you stop grinding your teeth. This is why it is important to seek out effective treatments that disrupt the teeth-grinding process.
How to stop grinding teeth
There are several different approaches to end night-time and daytime teeth grinding, including purchasing a night-time mouth-guard, relaxation exercises and therapy for stress and anxiety. However, botox for teeth grinding is one of the leading non-surgical methods to treat this condition with long-lasting results.
Botulinum Toxin Injections for Teeth Grinding
Botulinum toxin is an FDA-approved medicine often prescribed by doctors in the UK to treat medical conditions. It’s a naturally purified protein that works as a muscle relaxant to treat teeth grinding and jaw clenching by reducing tension on the jaw joint.
Administered properly by a fully qualified medical practitioner, botulinum toxin injections can create a softer curve to the jawline while also stopping teeth grinding in its tracks.
If you are suffering from bruxism or teeth grinding and want to improve the issue, please get in touch with our expert practitioners in London and Buckinghamshire and find out more about the best treatments available at our clinics!
*DISCLAIMER Patient experience and results may vary. These are dependent on a number of factors such as lifestyle, age and medical history.
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* Disclaimer: Please be aware that results and benefits may vary from patient to patient taking into consideration factors such as age, lifestyle and medical history.
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Consultation | {
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-381,593,275,659,159,940 | Betterhelp: Healthfirst Therapist Near Me – 15% OFF Your First Session
A Comprehensive Guide: How to Find a Therapist Near You. Healthfirst Therapist Near Me…
Looking for treatment is a courageous action toward much better mental health and wellness. Whether you’re having problem with anxiety, anxiety, or any other mental issue, discovering the best therapist can make a considerable distinction in your recovery journey. In this post, we will explore the procedure of finding a therapist near you, go over different kinds of therapists available, and offer recommendations for different psychological disorders.
Types of Therapists: Healthfirst Therapist Near Me
Psychologists: These specialists hold a postgraduate degree in psychology and specialize in diagnosing and treating psychological health disorders. They typically utilize evidence-based therapies such as cognitive-behavioral treatment (CBT) and psychodynamic therapy.
Psychiatrists: Psychiatrists are medical doctors who concentrate on psychological health. They can diagnose mental illnesses, recommend medications, and supply therapy. Their treatment method often involves a combination of therapy and medication management.
Accredited Clinical Social Employees (LCSWs): LCSWs are trained in psychiatric therapy and social work. They assist people cope with various concerns, such as relationship problems, drug abuse, and life transitions. LCSWs frequently utilize methods like cognitive-behavioral therapy, family therapy, and solution-focused treatment.
Accredited Expert Counselors (LPCs): LPCs provide treatment to families, couples, and individuals. They attend to a vast array of mental health issues, consisting of grief, tension, and injury. LPCs might specialize in particular restorative methods like mindfulness-based therapy or art therapy.
Marital Relationship and Family Therapists (MFTs): MFTs focus on relationships and family characteristics. They assist households and couples enhance interaction, resolve disputes, and browse major life transitions. MFTs typically use strategies such as family systems treatment and mentally focused treatment.
Common Reasons for Looking For Treatment:
Anxiety Conditions: Stress and anxiety disorders include excessive concern, fear, and panic. Recommended therapist: Psychologist, Psychiatrist.
Major Depressive Condition: Identified by relentless feelings of unhappiness, despondence, and loss of interest. Advised therapist: Psychologist, Psychiatrist.
Trauma (PTSD): Emerges from experiencing or witnessing a terrible occasion. Advised therapist: Psychologist, LCSW.
Substance Usage Disorders: Involves excessive use of compounds and dependence. Suggested therapist: LCSW, LPC.
Relationship Issues: Difficulties in romantic or family relationships. Advised therapist: MFT, LPC.
Therapist: Invite! I’m Dr. Smith, your therapist.
Patient: Thank you, Dr. Smith. I’m a bit worried however likewise relieved to lastly be here. It’s my very first treatment session, and I’m not completely sure what to anticipate.
Therapist: It’s entirely regular to feel nervous, specifically throughout your very first session. I’m glad you took this step towards seeking assistance. Therapy is a confidential and safe area where we can explore your concerns and work towards your well-being. Is there anything specific you wish to go over or any particular reason you chose to look for therapy?
Client: Well, I’ve been feeling overloaded recently. I have actually been having a hard time with stress and anxiety and finding it tough to manage my stress.
Therapist: I understand. Anxiety and tension can be challenging to deal with, but with therapy, we can collaborate to develop effective methods for handling them. Can you tell me a little bit more about what activates your stress and anxiety and when you initially started discovering these symptoms?
Patient: Sure. I think my anxiety is activated by work-related tension, social scenarios, and even basic everyday tasks. It appears to have started a couple of years ago when I experienced a significant life change, and it has actually been progressively getting worse ever since.
Therapist: Thank you for sharing that. It’s important to recognize those triggers and understand the origin of your anxiety. During our sessions, we’ll explore different therapeutic strategies, such as cognitive-behavioral therapy, to assist you gain control over your anxiety and minimize its effect on your life. You discussed job-related tension; exists any particular element of your job that adds to your anxiety?
Client: Yes, due dates and high-pressure circumstances at work tend to activate my anxiety one of the most. I often find myself overwhelmed, continuously stressing over meeting expectations and fearing failure.
Therapist: I see. Our objective is to help you find a sense of balance and restore control over your anxiety.
Patient: That sounds like exactly what I require. I’m ready to put in the work and make favorable modifications. I appreciate your guidance and support throughout this process.
Therapist: I’m here to support you every action of the method. Remember, therapy is a collaborative journey, and your active participation is vital.
As for the room’s look, therapists typically make every effort to develop a calm and welcoming environment. The room might feature comfy seating, soft lighting, and maybe some relaxing elements like plants or artwork to develop a relaxing atmosphere. The therapist’s workplace is developed to provide a sense of confidentiality and security for the patient to openly discuss their concerns and feelings.
10-Step Guide to Discovering a Therapist in Your Area:
Determine Your Needs: Examine your psychological health concerns, preferred therapy type, and any particular requirements you might have.
Request for Recommendations: Look for recommendations from trusted friends, household, or healthcare experts who have experience with treatment.
Consult Insurance: Contact your insurance coverage company to understand the coverage for therapy and acquire a list of in-network therapists.
Online Directories: Utilize online directory sites like Psychology Today, GoodTherapy, or TherapyTribe to search for therapists in your area.
Research Therapist Qualifications: Confirm the credentials, qualifications, and licenses of prospective therapists. Look for specialized training in your location of issue.
Read Reviews and Reviews: Check out online evaluations and reviews to gain insights into others’ experiences with the therapists you are considering.
Contact Therapists: Call or email therapists to inquire about their availability, fees, and treatment technique. Ask concerns to identify if they are a great fit for you.
Preliminary Assessment: Arrange an initial consultation session with a few therapists to assess their compatibility and discuss your needs.
Consider Logistics: Take into account aspects such as location, schedule, session duration, and fees when choosing a therapist.
Trust Your Instincts: Ultimately, trust your suspicion and select a therapist with whom you feel comfortable, understood, and supported.
install of anxiety but likewise within the very first few minutes or at least by the end of the session feeling a lot much better like I simply feel more comfy now that we began and really happy that they came so I encourage you not to let stress and anxiety stop you although it also makes good sense that we ‘d be a little anxious you understand possibly it’s susceptible in such a way we’re not utilized to to share thoughts with a stranger or we believe that therapy indicates that we have some problem or issue but really therapy does not imply that you’re crazy or broken or have some big concern anybody can gain from treatment now the therapists job is to also help you figure out what your goal will be the therapist is very likely to ask you in the first session what brought you into counseling to talk with
them what would you like to focus on or what would the goal will be of the work and they may even ask like how will you know when you are have actually met your objective or a done with treatment what would you like that outcome to look like so those are concerns that you you understand will be likely asked and if you want you can attempt to prepare a little in advance by doing some journaling or just showing but if you aren’t sure how to address those questions then the therapist can assist you in any case during the very first session you’ll most likely be assessing just what growth location you want to address whether that’s increased self empathy or ability to manage your anxiety or link better with other individuals and likewise bear in mind that that first session is an interview both methods to see if it’s a good fit so do not hesitate to ask your therapist concerns that might help you feel if they are the therapist | {
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7,554,798,090,978,001,000 | Review Article
Electrical Alternans: A Sign, Not a Diagnosis
Authors: Manju Goyal, MD, Kevin M. Woods, MD, John E. Atwood MD, FACC
Abstract
Electrical alternans is an electrocardiographic phenomenon defined as an alternating amplitude or axis of the QRS complexes in any or all leads. It is most commonly associated with a large pericardial effusion and impending threat of cardiac tamponade; however, a literature review showed that this electrocardiographic finding can be seen in a variety of other clinical scenarios with varying etiologies and prognoses. Several electrocardiogram examples are presented with a brief review of the potential mechanisms and clinical significance and demonstrate that electrical alternans is more correctly considered an electrocardiographic sign, rather than a diagnosis, with a broad differential for potential etiologies. For some causes, the clinical significance is well known, but for others, further research is needed.
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References
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8. Pulignano G, Patruno N, Urbani P, et al. Electrophysiological significance of QRS alternans in narrow QRS tachycardia. Pacing Clin Electrophysiol. 1990; 13: 144–150.
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10. Richter S, Brugada P. Bidirectional ventricular tachycardia. J Am Coll Cardiol. 2009; 54: 1189
11. Blomstrom-Lundqvist C, Scheinman MM, Aliot EM, et al. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias—executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines. (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias). Circulation. 2003; 108: 1871–1909.
12. Kremers MS, Miller JM, Josephson ME. Electrical alternans in wide complex tachycardias. Am J Cardiol. 1985; 56: 305–308.
13. Apte NM. An unusual cause of electrical alternans. Chest. 1992; 102: 983–984. | {
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-1,962,880,668,676,133,600 | Skip to content
HelpingTheSuicidalPerson
They want to help; they just don’t know what to do. It’s a tragic fact that most psychology and sociology programs don’t have a single class regarding suicide in their entire academic career. So therapists and social workers encounter a suicidal person and they feel – as they are – completely unprepared for what to do next. Helping the Suicidal Person: Tips and Techniques for Professionals is a way of addressing the gap in knowledge –and coming to a better place of nurturing and support to help people move away from suicide as the only option.
Note: Throughout this post, I’ll be using “client” as shorthand so as not to distract from the readability. I don’t intend to imply that everyone with whom you’ll encounter is a client, nor that you can’t use these techniques if you’re not a therapist.
Research Power
While the tips are research-informed, they are often offered with limited support in research. There’s a simple reason for this. The research is hard to come by. Sometimes, research can show a reduction in attempted suicides but not in completed ones. In fact, to show a 15% difference in suicide rates (with an appropriate confidence interval), researchers would need to enroll 13 million people. That’s a relatively impossible challenge. As a result, we have to accept the research that we do have and attempt to make the best of it.
Sometimes, the problem isn’t scale. Sometimes, the problem is the ethics of the situation. Consider that there is no randomly-controlled trial about the use of parachutes reducing death when jumping from an airplane. Obviously, they work. So obviously that no one would subject someone to the control condition of death to demonstrate that people without parachutes jumping from planes die.
This is a case where even though there is no research supporting the efficacy of the approach, it doesn’t mean the approach isn’t (or can’t be) effective. It just means that the research hasn’t been done for a myriad of reasons, including time, money, and ethics.
Disclosure of Suicidal Thoughts
In some ways, it’s as if clinicians are practicing “Don’t Ask, Don’t Tell” as an approach toward suicide prevention. Many clinicians don’t ask – and, particularly, don’t ask directly – if someone is considering suicide. There was a historic concern that this might “plant” the idea of suicide in the client’s mind, but research has proved this to be incorrect. Even without this defense, it’s still a hard thing for most clinicians to ask, so it’s frequently swept aside and forgotten about.
On the other side, the probability that a client will volunteer their thoughts of suicide are very low. Despite somewhere between 1:5 to 1:6 people having thought about death by suicide, it’s unlikely that they’ll bring it up. Instead, they’re more likely to believe that if the therapist doesn’t ask them, it’s not important – secretly knowing that it is.
The Loaded Question
Some questions cause people to become defensive, because they’re not sure how the person asking the question will respond. The underlying challenge is that the question is related to something you think is – or may be – related just to you. The Kinsey Institute found that asking the question “How old were you when you first started masturbating?” got a much better response than “Do you masturbate?” Embedded inside the first question is the assumption that it’s something everyone does, and therefore the question of “when” isn’t particularly disturbing. Of course, the small percentage of people who don’t – or won’t admit it – will respond that they can’t answer the question. In working with people who are thinking about suicide, questions like “What are some of the ways that you’ve thought about killing yourself?” gets better answers than “Have you thought of ways to kill yourself?” The presumption embedded into the question makes a difference to the way that people respond.
Similarly, you can intentionally stay ahead of where the person is likely to be by asking the question leading to an overly extreme – but not absurd – level. For instance, you could ask “Do you think of killing yourself 20 times a day?” The answer may be 15 – but the person will start by telling you “not that much” and giving you an answer that’s more likely to be accurate.
Fear of Commitment
One of the barriers that clinicians must overcome is the client’s fear that if they say the word “suicide” or admit to suicidal thoughts, they’ll be involuntarily committed. Involuntary commitment is a sometimes necessary but always troubling challenge. People who are involuntarily committed experience a loss of freedom and control that can further exacerbate their reasons for wanting to die and simultaneously can destroy and therapeutic alliance and trust that might have been created. (See The Heart and Soul of Change for more about the importance of therapeutic alliance.)
One of the challenges is that the client’s goals and the professional’s goals may be different. The professional wants the person to stay alive, and the client wants the pain to stop. As a result, there can be a gap through which clients become concerned about how their therapist will react. They’ve likely heard stories about an involuntary hold – and they don’t want to experience it themselves.
Neither Lecture nor Pep Talk
Motivational Interviewing calls it the “righting reflex.” It’s the tendency to directly correct a person’s perspective by telling them how they’re wrong – and it’s powerful. It was Carl Rogers who insisted that client was the expert – in their lives. We may, from a few minutes of conversation and some notes provided by others, believe their pain is manageable and their problems are all solvable, but from their perspective, they’re not. Until they believe you truly understand, they won’t listen to suggestions; even after they believe you understand, they’ll not listen unless you tread gently by asking careful, somewhat leading, questions.
Lectures about how someone’s behavior, feelings, or perspective isn’t right has never worked – even when you were a child. It induces guilt, shame, and invalidation, which further pushes them away. It also causes them to become more entrenched in their positions. They start looking for ways to defend their position and they find them. They ultimately have invested more in their perspective and become less likely to change it. (See Influence for more on these effects.)
Pep talks don’t work because they’re hollow. Letting people experience joy and happiness is a good strategy to fight depression that seeks to convince them they can’t find joy or happiness. However, these must be experiences they want. One useful technique that I’ve used is to intentionally set a positive event out several weeks out so that anticipation can build. The actual amount of time that you set the event in the future is dependent upon the client, but the point is to build an idea in the future. Do be prepared that depression will try to convince them they won’t have fun. The response is “Didn’t you have fun in the past?”
Rank and File
One strategy for assessing the importance of various reasons for dying is to ask the client to list them, and then rank them in order of importance. This has a focusing effect that allows you to focus your energies on the most important items. Sometimes, it’s possible to carefully walk them through strategies that break down the barriers preventing them from overcoming their reasons for dying.
For instance, if they’re struggling because they can’t find a job, you can work with them on ideas to get a job. Care must be exercised here, because you’re likely going to move quicker than the client. You’ve seen these problems and solutions before and so you know the landscape and you’re likely to rush ahead. However, helping people work through problems is directly addressing the problem-solving challenge and cognitive constriction that seems to be found with most suicidal people. It’s worth the time.
Reasons for Living
It’s an awkward conversation to ask people why they want to be alive. It’s awkward when suicide isn’t a consideration and can be even more awkward when it is. Often, you’ll need to start with the reasons why people want to die before getting to their reasons for living. It’s important to recognize that people who are struggling with thoughts of wanting to die may have trouble enumerating their reasons for living.
You may need to prompt them to explain who would miss them when they’re gone or what they do to support others. You might suggest they go through their recent calls and texts and make a list of those people who would miss them or their support.
They Can Move On
A somewhat typical response to reasons for dying may be that so their loved ones can “move on with their lives.” This is the quintessential comment of burdensomeness. (See Myths About Suicide for more on burdensomeness and its relationship to suicide.) In many cases, however, the others that the client believes will “move on with their lives” are the recipient of the pain that the client is trying to displace. Suicide and Its Aftermath says it plainly. Suicide transfers the pain from the person who dies to those who survive.
Certainly, there are some situations where a person’s health is such that they are, in some sense, a burden to others. However, one of the things that all people tend to misunderstand is that burdensomeness should be measured by the person who is (perceivably) burdened. It’s possible that the other person doesn’t perceive it as a burden and may even believe it’s an opportunity to replay the kindness and support they’ve received. Encouraging a more realistic perspective of the degree of burden is a good idea.
No Warning Sign Is Particularly Meaningful
One of the problems that exists in suicidology is that we believe things that aren’t true. Thomas Joiner wrote a whole book about Myths About Suicide. Craig Bryan in Rethinking Suicide challenges us to realize that the screening tools that we use don’t work. Some still insist that most (or all) people who die by suicide sent warning signs. Joiner addressed this directly and Bryan indirectly, but the myth persists.
The simple fact of the matter is that we have no way of knowing who will die by suicide or not. We know statistics and probabilities – but not people. There are lists of warning signs that cause concern, but it takes judgement to decide who is at the most risk of immediate harm to themselves and who isn’t. It’s recommended that clinicians record the reasons for their assessments in their notes so, if there is any question in the future, there’s a record of why they assessed the risk the way that they did.
All that to say that while there are key indicators – like directly stating that they want to die – none of those indicators in isolation is a direct prediction of short-term risk. It’s only by looking at all the factors in the situation that someone could assess risk.
The Tips and Techniques
The listing of tips and techniques are:
1. Reflect on Your Biases about Suicide
2. Take Stock of Your Experiences with Suicide (or Lack Thereof)
3. Confront “Suicide Anxiety”
4. Be Alert to Negative Feelings Toward the Suicidal Person
5. Reject the Savior Role
6. Maintain Hope
7. Face Your Fears
8. Directly Ask about Suicidal Thoughts
9. Turn to Techniques for Eliciting Sensitive Information
10. Embrace a Narrative Approach: “Suicidal Storytelling”
11. Ask about Suicidal Imagery, Too
12. Uncover Fears of Hospitalization and Other Obstacles to Disclosure
13. Recognize that, for Some People, You are an Enemy
14. Avoid Coercion and Control Whenever Possible
15. Resist the Urge to Persuade or Offer Advice
16. Understand the Person’s Reasons for Dying
17. Validate the Wish to Die
18. Acknowledge that Suicide is an Option
19. Gather Remaining Essentials about Suicidal Thoughts and Behavior
20. Learn about Prior Suicidal Crises: The CASE Approach
21. Cautiously Use Standardized Questionnaires
22. Privilege Warning Signs Over Risk Factors
23. Screen for Access to Firearms
24. Inquire about Internet Use
25. Probe for Homicidal Ideation
26. Collect Information from Family, Professionals, and Others
27. Examine Reasons for Living
28. Identify Other Protective Factors
29. Pay Attention to Culture
30. Investigate Religious and Spiritual Views of Suicide
31. Solicit the Person’s Own Assessment of Suicide Risk
32. Estimate Acute Risk for Suicide
33. Estimate Chronic Risk for Suicide
34. Document Generously
35. Know When and Why to Pursue Hospitalization
36. Know When and Why Not to Pursue Hospitalization
37. Do Not Use a No-Suicide Contract
38. Collaboratively Develop a Safety Plan
39. Encourage Delay
40. Problem-Solve Around Access to Firearms
41. Discuss Access to Other Means for Suicide, Too
42. In Case of Terminal Illness, Proceed Differently (Perhaps)
43. Seek Consultation
44. Make Suicidality the Focus
45. As Needed, Increase Frequency of Contact
46. Treat Chronic Suicidality Differently
47. Involve Loved Ones
48. Suggest a Physical Exam
49. Recommend an Evaluation for Medication
50. Continue to Monitor Suicidal Ideation
51. After Safety, Address Suffering
52. Look for Unmet Needs
53. Target Social Isolation
54. Use Grounding Exercises
55. Assume Nothing: Does the Person Want to Give Up Suicide?
56. Tap into Ambivalence
57. Compare Reasons for Living and Dying
58. Invite the Person to Look for the “Catch”
59. Search for Exceptions
60. Frame Suicide as a Problem-Solving Behavior
61. Help Brainstorm an “Options List”
62. Teach the Problem-Solving Method
63. Nourish Future Plans and Goals
64. Incorporate a Hope Kit
65. Highlight Strengths
66. Connect Suicidal Thoughts to Other Thinking
67. Educate about Cognitive Distortions
68. Help Challenge Negative Thoughts
69. Elicit Coping Statements
70. Rescript Suicidal Imagery
71. Discourage Thought Suppression
72. Foster Acceptance of Suicidal Thoughts
73. Enhance Coping Skills
74. Cultivate Mindfulness
75. “Broaden and Build” Positive Emotions
76. Pair Behavioral Activation with Values
77. Differentiate Between Suicidal and Non-Suicidal Self-Injury
78. Determine the Person’s Reaction to Having Survived
79. Conduct a Chain Analysis
80. Evaluate Where the Safety Plan Fell Short
81. Take Advantage of the “Teachable Moment”
82. Attend to the Therapeutic Relationship
83. Address the Trauma of the Suicide Attempt
84. Explore Shame and Stigma
85. Warn about the Possibility of Relapse
86. Review Lessons Learned
87. Complete a Relapse Prevention Protocol
88. Propose a Letter to the Suicidal Self
89. Follow Up
Maybe it’s time for you to learn the tips and techniques that you can use to start Helping the Suicidal Person. | {
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6,318,064,786,678,002,000 | Taking Levitra Successfully
As nonconventional medical remedies change into more and more mainstream, we check out the science behind some of the hottest. Later, cinchona bark was proven to contain quinine, a drugs now proven to kill the parasite that causes malaria. Unfortunately, Western medicine cannot explain why siblings get or don’t get diseases supposedly handed on from their dad and mom. Various healing alternative therapeutic cellphone: (440) 777-2665 present estimates show this company has an annual revenue of $500,000 to $1 million and employs a employees of roughly 5.
Even if you have lost your urge for food as a result of remedies, you continue to need to keep up a full stomach for the medication to work properly and safely. This diploma requires no Externship/Internship and no licensing or certifications can be awarded.
The great thing about Traditional Chinese Medicine is its subtlety, and skill to recognize lack of harmony within the organism, maybe before the person has actually acknowledged it for him or herself. Due to this fact, within the textual content beneath, different drugs” also refers to complementary medicine”.alternative medicine
There’s none, in line with a division of the Nationwide Institutes of Well being that funds research into various medicines. Just final year, superior-stage cancer patients taking part in a Section II examine of psilocybin responded positively after a single treatment.
Sometimes a mixture of pure and traditional drugs will be essentially the most beneficial when facing an illness or disease akin to most cancers. According to the World Health Organization, an estimated eighty{faa39fcb9e8350a8d276972480ca6c1469006c0c9c2ab48bb76cf17dbd389b33} of people around the world use herbal medication. | {
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-6,330,455,117,083,823,000 | How can we help?
How to take Noriday
Noriday is a type of progestogen only pill (also known as the ‘mini pill’).
You will need to take one pill every day. There are 28 pills per pack, and you do not take a break between packs. These pills must be taken within the same 3 hour time period each day to be effective. Choose a convenient time in the day to take your first pill, and continue to take it close to that time every day.
What to do if you miss a pill:
If you are less than three hours late, then take the missed pill as soon as you remember and take your next one on time. You do not need to take extra precautions as the pill will still work, and you’ll be protected against pregnancy.
If you are more than three hours late, then take your missed pill as soon as you remember it, take the next one on time and keep taking the pill. You may want to consider emergency contraception. You will not be protected until you have taken two more pills at the correct time and will need to use condoms when you have sex for those two days. You will be able to rely on your pill for contraception again at about the time that you are due to take your third pill.
Order Progestogen only pill
Dr Gillian Holdsworth headshot
This post was clinically reviewed by:
Dr Gillian Holdsworth Fettle's Managing Director, Medical Doctor and public health expert.
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Yellow arrow pointing right | {
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-1,162,553,273,847,438,600 | How Vitamin B12 Can Combat Excessive Sleepiness
How Vitamin B12 Can Combat Excessive Sleepiness
In a world where productivity is paramount and sleepiness is often seen as a hindrance, the struggle against excessive sleepiness is real. Many factors contribute to feeling perpetually tired, but one often overlooked remedy may lie in the power of Vitamin B12. Medications like Waklert 150 mg Tablet and Armodafinil Artvigil 150 can also provide quick relief. In this blog, we’ll delve into the role of Vitamin B12 in combating excessive sleepiness, exploring its benefits, sources, and how you can incorporate it into your daily routine.
Understanding Excessive Sleepiness:
Before diving into the benefits of Vitamin B12, let’s grasp the significance of excessive sleepiness. It’s more than just feeling tired after a restless night; it’s a persistent, overwhelming urge to sleep during the day, regardless of adequate nighttime rest. Excessive sleepiness can impair cognitive function, decrease productivity, and even pose safety risks, such as falling asleep while driving or operating machinery.
The Role of Vitamin B12:
Vitamin B12, also known as cobalamin, plays a crucial role in various bodily functions, including energy production, DNA synthesis, and neurological health. One of its primary functions is aiding in the formation of red blood cells, which transport oxygen throughout the body. Without sufficient oxygenation, fatigue and lethargy can set in, contributing to excessive sleepiness.
Benefits of Vitamin B12 in Combatting Excessive Sleepiness:
Energy Production: Vitamin B12 is very important to transform food into energy. It helps metabolize carbohydrates and fats, providing the fuel needed for cellular function. By optimizing energy production, Vitamin B12 can combat fatigue and boost alertness, reducing the likelihood of excessive sleepiness.
Neurological Health: Deficiencies in Vitamin B12 have been linked to neurological disorders, including fatigue, brain fog, and even depression. By maintaining optimal levels of Vitamin B12, you can support healthy brain function, enhancing cognitive clarity and reducing the risk of excessive sleepiness associated with neurological imbalances.
Regulation of Sleep-Wake Cycle: Emerging research suggests that Vitamin B12 may play a role in regulating the body’s circadian rhythm, the internal clock that governs sleep-wake cycles. By supporting the production of melatonin, the hormone that regulates sleep, Vitamin B12 may help promote restful sleep at night and wakefulness during the day, mitigating hypersomnia.
Sources of Vitamin B12:
While Vitamin B12 is predominantly found in animal products, there are still options for vegetarians and vegans to obtain this essential nutrient. Here are some rich sources of Vitamin B12:
Meat and Poultry: Chicken, and turkey are excellent sources of Vitamin B12.
Fish and Seafood: Salmon, trout, tuna, and shellfish contain high levels of Vitamin B12.
Dairy Products: Milk, cheese, and yogurt are rich in Vitamin B12.
Eggs: Both the yolk and white of eggs contain Vitamin B12.
Fortified Foods: Certain plant-based foods, such as fortified cereals, plant milk, and nutritional yeast, are fortified with Vitamin B12 for vegans and vegetarians.
Incorporating Vitamin B12 into Your Daily Routine:
To reap the benefits of Vitamin B12 and combat excessive sleepiness, consider the following tips:
Balanced Diet: Ensure your diet includes a variety of Vitamin B12-rich foods, such as meat, fish, dairy, and fortified products.
Supplements: If you have difficulty obtaining sufficient Vitamin B12 from food sources alone, consider taking a Vitamin B12 supplement under the guidance of a healthcare professional.
Regular Monitoring: Periodically check your Vitamin B12 levels through blood tests to ensure you maintain optimal levels for combating excessive sleepiness.
Healthy Lifestyle: In addition to Vitamin B12, prioritize healthy sleep habits, regular exercise, and stress management to further alleviate excessive sleepiness.
Conclusion:
Excessive sleepiness can significantly impact your quality of life, but it doesn’t have to be a constant struggle. By harnessing the power of Vitamin B12, you can combat fatigue, boost energy levels, and reclaim wakefulness. Whether through dietary changes, supplements, or lifestyle modifications, prioritize your well-being and take the necessary steps to overcome hypersomnia. After all, a vibrant, alert life awaits on the other side of restful nights and energized days.
Techk story
My name is Mohsin Ali. I Am an seo expert with 4 year experienece in this field. I am working also as a reseller and I have large number of high quality guest post websites available | {
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612,012,197,379,223,900 | What Causes High Ammonia Levels In Babies?
It is not uncommon to observe elevated levels of ammonia in babies especially in newborns. This article deals with the causes of high ammonia level in babies.
Ammonia is a chemical substance that is produced in the body by breakdown of proteins. It is toxic to the body. In healthy individuals, this ammonia is converted into urea (which is non-toxic in nature) and eliminated from the body through urine. However, in the presence of certain heath issues, the ammonia level may exceed above the normal acceptable level. It, then, becomes difficult for the body to eliminate the excess ammonia from the body which in turn can lead to brain damage, coma and even death in some cases.
What Causes of High Ammonia Levels in Babies?
The most common causes of high levels of ammonia in babies are listed below:
Urea Cycle Disorders Causing High Ammonia Levels in Babies:
Urea cycle disorder (abbreviated as UCD) is a genetically inherited disorder where the baby lacks certain enzymes required by the liver to convert ammonia to urea. As a result of this, the liver is unable to convert ammonia into urea and there is excessive ammonia in the body. This condition is often noted within the first 24 hours post birth. This is one of the commonest causes of high ammonia levels in babies.
Urea cycle disorder may be accompanied by other symptoms such as irritability, tiredness and vomiting. In some children, the condition goes unnoticed and the symptoms show up later in life. Studies have shown that the child must inherit a defective gene from both parents in order to get affected by this condition. Being a genetic disease, there is no specific cure for this condition. The treatment modality mainly focuses on management of the symptoms. It is recommended to follow a low protein diet in such conditions. Medications are often prescribed to remove excess ammonia from the body.
Hemolytic Disease of Babies Causing High Ammonia Levels:
High concentration of ammonia in blood can indicate presence of hemolytic disease in newborns (also known as HDN). This condition arises from the incompatibility of the Rh factor between the child and the mother (i.e. the presence or absence of a blood protein called as Rh factor). Cases where the mother in Rh Positive and carried a child that is Rh Negative, the mother’s immune system may consider the child’s red blood cells as a foreign body and produce antibodies against it, also resulting in production of ammonia. These antibodies are usually produced during the first pregnancies but do not pose a threat till a later pregnancy. Babies born with HDN develop severe anemia. During pregnancies, if Rh incompatibility is detected, Rh immunoglobulin injections are given to the carrying mother to avoid production of antibodies which may harm the fetus. This too is one of the important causes of high levels of ammonia in babies.
Reye’s Syndrome:
This is a very rare syndrome that affects children and young adults causing encephalopathy (or brain dysfunction), liver degeneration, reduced glucose level and higher levels of ammonia in the body. This is a one of the known causes of high levels of ammonia in babies too. The cause of this condition is linked to use of aspirin during viral infections like chicken pox. There is no specific treatment for this condition. Treatment modalities aim towards controlling symptoms such as controlling intracranial pressure, controlling seizures, management/prevention of liver damage etc. Studies have shown that about 1/3rd of children and teenagers who develop Reye’s syndrome suffer from permanent neurological damage or die soon.
Other Causes of High Ammonia Levels in Babies:
There are other causes which may lead to over production of ammonia in the body. Since, liver is the vital organ that converts ammonia to urea for elimination from the body, any damage to the liver can cause elevated level of ammonia in the body. Hence, such conditions too can be some of the causes of high levels of ammonia in babies. Conditions associated with bleeding in the digestive tract (gastrointestinal bleeding) may cause excessive ammonia production by breakdown of red blood cells in the intestine followed by release of protein in the blood stream. Babies who have renal failure also have high ammonia level in the body. As the body is unable to eliminate urea efficiently, there may be accumulation of ammonia in the body.
Conclusion
Thus, it is clear that there are many causes of high levels of ammonia in babies and proper diagnosis is needed. If a baby is detected with high ammonia levels, it is very essential that appropriate medical care and treatment is provided as an emergency. An increased level of ammonia is very toxic for the body and thus can lead to several major health concerns including coma, brain damage and in severe cases it can also lead to death. Thus, once the symptoms are noticed, there must not be any delay in seeking medical help.
Also Read: | {
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2,142,481,402,680,778,800 | Explore the subtle changes in thinking and perception that define the first stage of delusion and discover how a combination of medication, therapy, and substance abuse treatment can help.
What is the First Stage of Delusion?
Delusion is a state of mind characterized by false beliefs and perceptions, despite evidence to the contrary. It is a symptom of several mental illnesses, including schizophrenia, bipolar disorder, and major depressive disorder. In this article, we will explore the first stage of delusion, its causes, and treatment options.
Understanding Delusion
Delusion is a false belief that is not based on reality. It can be caused by a variety of factors, including mental illness, substance abuse, and brain injury. Delusions can be classified into different types, including paranoid, somatic, grandiose, and nihilistic.
The first stage of delusion is characterized by subtle changes in thinking and perception. These changes may be difficult to detect, as they may be subtle and gradual. The individual may not even be aware that their beliefs and perceptions are false.
Causes of the First Stage of Delusion
The causes of the first stage of delusion can be complex and multifaceted. Some of the most common causes include:
• Genetics: Studies have shown that certain genetic factors can make an individual more susceptible to developing delusions.
• Brain chemistry: Imbalances in the brain’s chemical messaging system, such as overactivity of dopamine, can lead to delusional thinking.
• Substance abuse: The use of drugs or alcohol can also lead to delusional thinking.
• Trauma: Trauma, such as a head injury or severe emotional stress, can also lead to delusional thinking.
Treatment Options for the First Stage of Delusion
Treatment for the first stage of delusion typically involves addressing the underlying cause of the delusion. This may include medication to address any chemical imbalances in the brain, therapy to address any psychological issues, and substance abuse treatment if the delusion is caused by drug or alcohol use.
Antipsychotic medications are often used to treat delusions. These medications can help to reduce the intensity of delusional thinking, and make it easier for the individual to engage in therapy and other forms of treatment.
Cognitive-behavioral therapy (CBT) is another effective treatment for delusions. CBT helps individuals to identify and challenge their delusional beliefs, and to replace them with more realistic thinking.
Conclusion: What is the first stage of delusion?
Delusion is a complex and challenging condition that can have a profound impact on an individual’s life. The first stage of delusion is characterized by subtle changes in thinking and perception and can be caused by a variety of factors, including genetics, brain chemistry, substance abuse, and trauma.
Treatment for the first stage of delusion typically involves addressing the underlying cause of the delusion and may include medication, therapy, and substance abuse treatment. With the right treatment, individuals with the first stage of delusion can learn to manage their symptoms and improve their quality of life.
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The endocannabinoid system versus CBD
2022-03-02
The endocannabinoid system versus CBD
The endocannabinoid system consists of receptors located in many areas of our body. Their activation requires cannabinoids - endogenous substances produced by the body or supplied externally, e.g. through the consumption of CBD products.
What are cannabinoid receptors?
Cannabinoid receptors help to process and receive chemicals by transmitting information to cells in the body. Cells can use this information to regulate vital functions such as mood and appetite. For cannabinoid receptors, CBD plays a role in supporting their binding to other substances. To date, two main cannabinoid receptors CB1 and CB2 have been identified. These are found throughout the body, but do not occur together e.g. CB1 receptors are located in the brain, liver, muscle, adipose tissue and the nervous and digestive systems. CB2 receptors are located in the body's immune system, bones and the central nervous system. Their activation is due to their association with cannabinoids.
Cannabinoids -- a breakdown
Cannabinoids, or chemical compounds naturally occurring in living organisms and plants. Based on their occurrence, we can divide them into 3 groups:
1. Phytocannabinoids - found in plants such as hemp seed, tea bush, blanket plant, echinacea.
2. Endocannabinoids - compounds found in animals and humans. They interact with the endocannabinoid system.
3. Synthetic cannabinoids - produced for therapeutic purposes under laboratory conditions.
The endocannabinoid system in a nutshell
The endocannabinoid system occurs naturally in mammals, including humans. It has a very important function, as it is responsible for many physiological processes and for maintaining balance in the body. It is also involved in the regulation of mood and energy metabolism, metabolism support and immune system support. Its most important role is to adapt the body to rapidly changing environmental conditions Every mammal, including humans, produces compounds very similar to those produced by hemp. The use of CBD products contributes to increased production of endocannabinoids, which minimises mood swings.
How does anandamide work?
Anandamide belongs to the group of cannabinoids produced by the body. It takes an active part in the work of the endocannabinoid system. It has a particularly strong affinity with CB1 receptors affecting, among other things, appetite, mood, pain perception or feelings of happiness. Studies have found that reducing the levels of the enzyme that breaks down anandamide, results in a reduction of negative emotions and anxiety. A deficiency of anandamide can manifest itself in the body as migraine, irritable bowel syndrome or mental disorders. The amount of anandamide in the body is regulated by its natural processes. It is possible to increase its levels by inhibiting the compound responsible for its breakdown. Studies have shown that only CBD has properties that inhibit the breakdown of anandamide.
The endocannabinoid system versus CBD
It has been scientifically proven that CBD stimulates the activity of the endocannabinoid system. After consuming a certain dose of hemp oil, information reaches the brain about where intervention is needed to restore homeostasis in the body. CBD acts very similarly to the cannabinoids naturally produced by our body. Among other things, cannabis oils have shown the ability to have anti-epileptic effects, anti-anxiety effects, support in the treatment of stomach ulcers, autoimmune diseases, neurological damage in Parkinson's disease and Alzheimer's disease.
The endocannabinoid system in animals
The endocannabinoid system is found in fish, birds, reptiles, earthworms and mammals, with the exception of insects. Its role influences brain functions such as learning, memory, mood, reproduction, sleep, creative generative and degenerative processes. The endocannabinoid system helps to maintain a stable internal environment in the body and is very important for its proper functioning.
Reaching for CBD for your dog will support the proper functioning of the body, reduce stress and improve your pet's mood. In cases of chronic pain, it can also reduce the sensation of pain. You can find the right CBD oil for your pet in our Premicanna.store. We warmly invite you to take a look at our offer!
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645,288,827,716,512,400 | Protein degraders such as for example molecular glues and PROTACs therefore start a completely fresh field for the introduction of new-targeted therapeutics in tumor
Protein degraders such as for example molecular glues and PROTACs therefore start a completely fresh field for the introduction of new-targeted therapeutics in tumor. effective therapies for multiple myeloma. Abstract Multiple myeloma can be a genetically heterogeneous plasma cell malignancy seen as a organ harm and an enormous creation of (in-)full monoclonal antibodies. Dealing with protein homeostasis and post-translational regulation is vital for multiple myeloma cells to endure therefore. Furthermore, post-translational adjustments such as for example SUMOylation and ubiquitination play crucial tasks in important pathways in multiple myeloma, including NFB signaling, epigenetic rules, aswell as SCA12 DNA harm repair. Medicines modulating the ubiquitinCproteasome program, such as for example proteasome inhibitors and thalidomide analogs, are approved and effective medicines in multiple myeloma highly. With this review, we concentrate on ubiquitin and ubiquitin-like adjustments in the biology and current advancements of Nefazodone hydrochloride new remedies for multiple myeloma. ([5,6,7]. Supplementary cytogenetic abnormalities that happen during the disease consist of translocations, chromosomal deletions like del(1p), del(17p13) composed of and are being among the most regular gene mutations in MM, however the precise biologic effect is not completely established [10,11,12,13,14,15,16]. Loss of the deubiquitinating enzyme CYLD, which functions as a negative regulator of nuclear element kappa-light-chain-enhancer of triggered B cells (NFB) and Wnt-Signaling, increases the aggressiveness of MM [17]. encode ubiquitin ligases involved in apoptosis rules, and genetic deletions in multiple myeloma lead to NFB activation [18,19]. The importance of the NFB pathway in multiple myeloma is definitely further highlighted by genetic or epigenetic alterations found in additional genes with this pathway, such as [19]. Beyond genetic alterations, MM is definitely characterized by epigenetic changes, such as aberrant DNA and histone methylation patterns [20,21,22,23]. Users of the nucleosome redesigning and deacetylase complex contribute to the rules of DNA and histone methylation, histone acetylation, and chromatin redesigning, which play important tasks in MM [22,24]. Of notice, epigenetic modifiers like the histone methyltransferase or and are mutated in MM and might contribute to the observed epigenetic changes. Understanding these mechanisms is vital, as epigenetic mechanisms impact the phenotype, clonal heterogeneity, and plasticity in MM [25]. For example, a high degree of DNA methylation and histone acetylation correlated with an aggressive immature phenotype inside a syngeneic immunocompetent murine 5T33 MM model [26]. Moreover, aberrant DNA methylation patterns are a defining characteristic of MM, and you will find qualitative epigenetic variations between premalignant MGUS, in which demethylation happens primarily in CpG islets, and active myeloma, in which differentially methylated loci happen in mainly non-CpG islets [27]. Accordingly, the de novo DNA methyltransferase DNMT3A is definitely suppressed in MM, and low manifestation is associated with adverse prognosis in MM [27]. A hallmark of MM cells is the production of high amounts of monoclonal antibody. Consequently, maintaining protein homeostasis from synthesis through folding to degradation is vital for multiple myeloma cells [28]. Under normal conditions, misfolded proteins degrade within minutes, and, if not removed early, can dramatically increase basal proteasome loading and cellular stress [29]. This proteotoxic stress can be further improved by chromosomal hyperdiploidy and MYC activation, both leading to Nefazodone hydrochloride an increased manifestation of many proteins, which induces an increased protein weight in the cell [30]. Beyond transcriptional mechanisms, the large quantity and function of proteins is controlled by highly dynamic and mainly reversible post-translational modifications (PTMs). The varied group of PTMs comprises acetylation, phosphorylation, methylation, ubiquitination, SUMOylation, and NEDDylation, which affect virtually all cellular processes [31]. Among the proteins whose function is definitely highly controlled by PTMs are histones with more than 500 different PTMs recognized [32,33,34,35]. These modifications not only regulate the chromatin structure, Nefazodone hydrochloride but also recruit related enzymes that use the energy from the hydrolysis of ATP to reposition nucleosomes and also induce the recruitment of proteins and complexes with specific enzymatic activities [36]. PTMs of transcription factors can be important for his or her activity. | {
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4,663,765,357,238,966,000 | Intramuscular Stimulation Dry Needling: How Physiotherapists Can Enhance Your Recovery and Well-being
As an integral part of modern physiotherapy, IMS Dry Needling presents a compelling option for patients seeking relief from musculoskeletal pain and dysfunction.
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In the dynamic world of physiotherapy, innovative techniques often emerge, offering new pathways to relief and recovery. One such technique that has garnered attention for its effectiveness is Intramuscular Stimulation Dry Needling (IMS Dry Needling). As an integral part of modern physiotherapy, IMS Dry Needling presents a compelling option for patients seeking relief from musculoskeletal pain and dysfunction. This blog post delves into the essence of IMS Dry Needling, explores its myriad benefits, and illustrates how physiotherapists at Roam Health & Wellness are uniquely positioned to administer this treatment, guiding you toward improved health and enhanced well-being.
Understanding IMS Dry Needling
IMS Dry Needling is a specialized treatment technique that involves the insertion of thin, sterile needles into specific areas of the muscle, known as myofascial trigger points. The primary goal is to release muscle tension, alleviate pain, and promote healing. Unlike acupuncture, which is rooted in traditional Chinese medicine, IMS Dry Needling is firmly grounded in Western medicine principles, relying on a thorough understanding of human anatomy and neurophysiology.
The Multifaceted Benefits of IMS Dry Needling
1. Pain Relief: By targeting trigger points, IMS Dry Needling can significantly reduce pain levels, offering immediate relief in many cases. It works by disrupting the pain cycle, helping to reset the nervous system and normalize the muscle's structural integrity.
2. Improved Mobility: Tight muscles often restrict movement. IMS Dry Needling helps release muscle tension, thereby increasing range of motion and improving overall mobility.
3. Enhanced Muscle Function: By resolving muscle tightness and reducing inflammatory responses, this technique can enhance muscle performance, promoting better coordination and strength.
4. Accelerated Recovery: For those recovering from injuries, IMS Dry Needling can be a valuable component of a comprehensive rehabilitation program, speeding up the recovery process by improving circulation and facilitating muscle repair.
5. Reduction of Muscle Spasms: Muscle spasms can be both painful and debilitating. IMS Dry Needling provides a direct approach to relax these spasms, offering a reprieve from discomfort.
The Role of Physiotherapists in IMS Dry Needling
Physiotherapists at Roam Health & Wellness are highly trained professionals who specialize in administering IMS Dry Needling with precision and care. Their expertise lies not only in the technique itself but also in their comprehensive approach to patient care. Here's how they make a difference:
• Expert Assessment: Our physiotherapists begin with a detailed assessment to understand the root cause of your discomfort, ensuring that IMS Dry Needling is tailored to your specific needs.
• Personalized Treatment: Recognizing that each patient's journey is unique, our therapists design personalized treatment plans that integrate IMS Dry Needling with other therapeutic modalities, fostering a holistic recovery.
• Ongoing Support: Recovery is a journey, and our physiotherapists are committed to providing continuous support, offering advice on exercises, posture, and lifestyle adjustments to maintain and enhance the benefits of the treatment.
In conclusion, IMS Dry Needling stands out as a powerful tool in the physiotherapist's arsenal, offering a pathway to pain relief, enhanced mobility, and overall well-being. At Roam Health & Wellness, our dedicated team of physiotherapists is ready to guide you through this innovative treatment, ensuring that your journey to recovery is not just effective, but also empowering. Embrace the potential of IMS Dry Needling and take a significant step toward optimal health and an enriched quality of life.
Start the conversation
Let's begin the journey of getting you back on your feet.
Schedule an appointment
Suffering from a past or current injury? Come see one of our specialists today.
We'll work to understand your daily habits and routines to provide a treatment plan tailored to suit your life.
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-1,912,089,678,477,118,500 | What are the benefits of a good body composition?
W
What are the benefits of a good body composition?
Having a good body composition has many benefits, including:
• Decreased risk of type 2 diabetes, hypertension, and heart disease.
• Increased functional ability, allowing us to move and exercise more freely, which allows us to burn more calories.
• A better calorie-burning metabolism throughout the day.
• A lean and toned body.
What does it mean to have a good body composition?
By definition, a healthy body composition includes a low proportion of body fat, as well as a higher proportion of fat-free mass. Although your body requires a certain amount of body fat to maintain organ functions, a lower body-fat percentage is usually a sign of good health.
How can body composition affect you?
Scientific evidence shows that a healthy body composition will increase your lifespan by reducing the risk of heart disease, cancer, diabetes, insulin resistance, etc., increase energy levels, and improve self-esteem.
How important is the body composition in physical fitness?
All fitness components depend on body composition to some extent. An increase in lean body mass contributes to strength and power development. Strength and power are related to muscle size. Thus, an increase in lean body mass enables the athlete to generate more force in a specific period of time.
What are five health benefits of having a healthy body composition?
Benefits of having a healthy body composition
• Normal blood pressure level.
• Improved quality of sleep.
• Improved mood and self-confidence.
• Increased energy and endurance throughout the day.
• Reduced pain in joints, hips, and lower back.
• Improved blood circulation — leading to lower risk for heart disease.
How does body composition affect performance?
Body Composition. Body weight can influence an athlete’s speed, endurance, and power, whereas body composition can affect an athlete’s strength, agility, and appearance. A lean body, i.e., one with greater muscle/fat ratio, is often advantageous in sports where speed is involved.
Why is it important to have a healthful body?
Staying healthy physically can help you stay healthy emotionally too. If you’re eating the right food and keeping fit, your body will be strong and help you to cope with stress and also fight illness. Eating well and exercising often when you’re a teenager will also help you stay in good health later in life.
What are the positive effects on body composition with physical activity?
Exercise can increase energy expenditure and create a negative energy balance (2,3). PA affects total fat oxidation and fat balance through the promotion of a better body composition (loss of fat mass and maintenance of lean mass).
Why do athletes need to have a good body composition?
How can I improve the composition of my body?
Simple ways include tracking the circumference of body parts and taking progress pictures. You can also buy tools that measure your body fat percentage, but they are often inaccurate. Your body composition is made up of fat mass and fat-free mass. You can improve it by decreasing body fat, increasing muscle or both.
Why is it important to have a healthy body composition?
Having a healthy body composition can help lower your chances of developing cardiovascular disease. High body fat levels up your risk of hypertension, which is chronically elevated blood pressure.
How to get an accurate reading of your body composition?
To get an accurate reading of your body composition, you need to estimate your body fat but first, understand the most important things to consider that can affect your body composition in the first place: Body composition is made up of several different factors, all of which can play a role in affecting your body composition.
What foods to eat to improve body composition?
It can be obtained from a variety of plant-based foods, including beans, whole grains, nuts and vegetables ( 15 ). For adults up to age 50, it is recommended that men consume 38 grams of fiber per day, while women are advised to eat 25 grams per day ( 16 ).
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3,671,160,390,568,980,000 | Atrial fibrillation is a common disease of the heart, characterized by an irregular and, if not treated, mostly fast heart rhythm. The origin of the disease is the atrial part of the heart. It is a rare disease before the age of 55, but the prevalence is sharply increasing with age. In many cases patients do not even notice that they have a rhythm disorder. But if they have complaints, they mention dyspnoea, chest pain, palpitations, dizziness, and sometimes syncope. For many years, atrial fibrillation has been considered as an innocent bystander of old age, but it is nowadays generally accepted that atrial fibrillation is associated with impaired quality of life and increased morbidity and mortality. Treatment regimens evolved as a consequence, unfortunately sometimes introducing new potential harms to the patients with this disease. Atrial fibrillation is involved in pathological processes through the whole body and has through that inspired numerous investigators in internal medicine, cardiology, neurology, pathology, pharmacology, physiology and epidemiology. The disease concept has evolved as science evolved and often has been in the centre of intense dispute.
, ,
Erasmus MC, NWO, Netherlands Organization for Health Research and Development, Research Institute for Diseases in the Elderly, Ministry of Education, Culture and Science, Ministry of Health, Welfare and Sports, EC, Municipality of Rotterdam, Netherlands Heart Foundation, Stichting Zorg op Noord (Rotterdam)
Erasmus MC: University Medical Center Rotterdam
J.C.M. Witteman (Jacqueline) , A. Hofman (Albert)
hdl.handle.net/1765/20468
Erasmus MC: University Medical Center Rotterdam
Heeringa, J. (2009, June 17). Epidemiology of atrial fibrillation in the general population. Retrieved from http://hdl.handle.net/1765/20468 | {
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2,091,743,379,224,715,800 | Beginner’s Guide to HHC
14th Feb 2022
Beginner’s Guide to HHC: What Is This New Cannabinoid?
If you’re overwhelmed by all the forms of cannabis that are on the market, don’t worry—you’re not alone! Keeping track of CBD, CBN, Delta-8, and Delt-9 can be confusing enough.
Thankfully, we’re here to help you understand each form and what they do precisely. That’s why we’re introducing you to HHC, a hemp-derived cannabinoid with effects that differ from Delta-9 and Delta-8 in a variety of ways.
We’ll discuss everything you need to know about this new cannabinoid so you can better navigate the world of cannabis to find the best products possible. After this, you’ll be able to tell everyone exactly what HHC is!
First Things First: What Is HHC?
Since this cannabinoid only recently hit the market, few people know precisely what HHC is. Not many retailers have it for sale, and it is mainly sold in the form of vape pens at the moment. Chemically, HHC is known as “11-Nor-9β-hydroxyhex hydrocannabinol,” which is almost impossible to pronounce.
Technically, HHC is a semi-synthetic cannabinoid and a hydrogenated form of THC. It was first created in 1944 by an American chemist named Roger Adams and is considered less potent than Delta-9 but more intense than Delta-8.
How Safe Is HHC?
There isn’t much research associated with the effects of long-term HHC use, mainly because not many people know what HHC is. This goes for most cannabinoids derived from hemp. Since they’re largely unregulated, hemp-derived cannabinoids do not fall under the same restrictions as most cannabis products. That’s why it’s so important to thoroughly research the company you’re buying from!
When buying HHC, look for companies that utilize third-party lab testing with their products—like Eighty Six. We send our products to an independent company that runs tests to guarantee the potency of our products and ensure they don’t contain any contaminants.
Is HHC Legal?
Like Delta-8 THC, the legalities surrounding HHC are in a gray area, and the answer of whether it’s fully legal is a complicated one. Since HHC is derived from hemp, similar to CBD, it’s technically legal in the US. That being said, it’s always best to check your state’s restrictions before using HHC for the first time, as some states have created their own laws surrounding hemp-derived cannabinoids.
If you’re worried about drug testing, it’s best to be on the safe side. While some users think they know what HHC is and insist it can bypass drug tests, this is largely unsubstantiated. We don’t know about you, but it’s not something we’d want to risk a job over!
What Does HHC Feel Like?
HHC is known to have similar effects to Delta-8 and Delta-9 THC, as it does possess psychoactive properties. Users claim that the effects of the HHC cannabinoid are relaxing and euphoric and that they may help with nausea or promote better rest compared to traditional THC.
Everyone is different, though, and the best way to determine if HHC is suitable for you is by trying it out for yourself! One thing to keep in mind is that HHC is a more intense experience than Delta-8, so start low and slow when trying out products or sharing them with your friends.
HHC vs. Delta-8
We know that HHC is more potent than Delta-8, but how do they compare overall? Their effects as a whole are similar, but when it comes to HHC vs. Delta-8, the differences lay mainly in their molecular structure. HHC, like Delta-9 THC, lacks double bonds, while Delta-8 has the opposite structure. These double bonds (or lack thereof) affect how each compound interacts with your body’s endocannabinoid system and the receptors in your brain!
That means that the HHC cannabinoid’s effects can be very different from those of Delta-8. Both may provide you with feelings of euphoria, relaxation, and an overall “high,” but the degrees will vary between the two. Even if you’re an experienced Delta-8 user, we recommend starting out with small doses of HHC and working your way up until you find your perfect vibe.
Try HHC Products Today
Now that you have a little background on what HHC is, you may be wondering if it’s the right fit for you. At the end of the day, it all comes down to your personal preference! If you like a more mellowed-out high that keeps you in control, you might prefer to skip HHC for a milder cannabinoid like Delta-8. If Delta-8’s potency isn’t up to your standards, on the other hand, it may be time to try something new—and HHC is just the thing!
As always, we recommend talking to your doctor before you try a new cannabinoid if you’re taking any other medications or have medical conditions that may affect your experience. But as long as you’re cautious and start slow, you’re well on your way to an incredible HHC high!
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Herbal Antibiotics:The Best Herbs for Fighting Viruses and Diseases Naturally Without any Chemicals
Herbal Antibiotics:The Best Herbs for Fighting Viruses and Diseases Naturally Without any Chemicals
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Herbal Antibiotics:The Best Herbs for Fighting Viruses and Diseases Naturally Without any Chemicals
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2/5 (1 valutazione)
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116 pagine
37 minuti
Pubblicato:
Jun 8, 2017
ISBN:
9781386449508
Formato:
Libro
Descrizione
This book is a handy primer about the types of herbal antibiotics that are available and how and when to use them. Since many common illnesses have developed resistance to commercial antibiotics, more people are seeking natural remedies whenever possible. Doctors tend to encourage this trend, so, if you have a personal doctor, please discuss using herbal remedies with him or her. If you do not have one, consult the staff at your local herbal health store. Most stores have printed pamphlets about the herbs they sell.
Also, you must tell any herbal consultant about the medicines you take daily and the allergies you may have. Some herbs are absolutely wrong for you if you have a condition like high blood pressure or diabetes. Herbs may seem natural and harmless remedies, but they can pack a really powerful punch. Many herbs are part of pharmaceutical compounds, and some are actually poisonous. Others, like lobelia, have to be used cautiously; too much can be fatal.
Fortunately, many herbal preparations come in capsule, pill, or tincture form. These are easier to swallow, and you do not have to worry about strong odor. Valerian, for instance, in its original form smells like old sweat socks. It is quite possible to eat a bulb of garlic, but garlic breath is something to be avoided.
Although this book was written using carefully selected internet sites, it is really a good idea to buy an authoritative book on herbal usage. You should also check for bound updates from time to time. Remember, the internet itself is not fact-checked. Always look for an authoritative source, and do not trust advertisements.
The following topics will be discussed:
- Systematic Antibiotics – those that work throughout the entire body
- Localized Antibiotics – those that only work on certain bodily systems
- Facilitative or synergistic herbs
- Antiviral Herbs and Essential Oils
- Antibacterial Herbs and Essential Oils
- Preparing Both Types of Herbs for Humans
- Antibacterial Herbs for Cleaning
- The Controversial Herb - Hemp
Pubblicato:
Jun 8, 2017
ISBN:
9781386449508
Formato:
Libro
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Herbal Antibiotics:The Best Herbs for Fighting Viruses and Diseases Naturally Without any Chemicals - Michelle Allen
information.
Introduction
Herbal antibiotics are what our ancestors used with varying success in ‘the bad old days’. Much was not understood about the causes and development of disease, and social taboos caused many people to keep their ailments secret. Also, many false theories of disease, some dating back to Greek times, were generally believed by doctors.
Now, we know a great deal more about our bodies and are not so unwilling to discuss our problems with our doctors. Unfortunately, everyone became overconfident about our new, scientific cures when they were first developed. Soon all the bacteria and viruses that cause illnesses developed resistance to the single-element antibiotics we used to cure them.
Bacteria and viruses, like all life on Earth, are intelligent and adaptable. They’ve been around since the beginning of time, and have had almost everything thrown at them by other plants, animals, and humans. Thus we return natural antibiotics, which generally contain several healing elements instead of just one.
One fact every reader must understand is that, if the health problem is serious, go to a doctor or an emergency room. If a person is bleeding or vomiting copiously, seems unresponsive, or cannot swallow, do not attempt to use herbal medicines.
Herbal antibiotics generally act more slowly than prescribed drugs, though they are gentler and often cheaper. They are useful remedies when there is a minor problem or you ‘feel an illness coming on’. Herbal remedies can be used for scratchy throats, minor burns and wounds, and genital pain and itching. Deal with the problem while it is a small one, and it will not become big.
This book is a primer to help you decide what plants or prepared herbal pills, tinctures, or teas to use for which illness.
Chapter 1 – Why herbal Antibiotics?
Even as our technological advances have skyrocketed to reaches beyond what any of us could have possibly imagined, many people today are still taking various types of medicine to help both their short term and their long term health. Whether it's because we are born with naturally poor health, are too stressed out, or don't take good enough care of ourselves, there are always different reasons for why we require medicine to help our health.
Of course, our body isn't completely susceptible to illnesses and diseases. Our immune system is the primary system in the body made to fight against illnesses and infectious diseases. However, the immune system also can't conquer every single illness and disease. There are still many diseases and illnesses out there in the world for which no cure has been discovered at all.
The primary goal, therefore, of medicine in general is to boost our immune systems. Many supplements that we have already come up with only cause additional side effects or don't even address the illness or infection that it was supposed to at all. Sometimes the resistance that these supplements create will even go as far as to create more ailments.
Fortunately, scientific research in later decades has yielded some impressive results. We have found antibiotics and antibiotic treatment to be an excellent alternative to supplements, as they can largely break up and overcome the resistance put up by the bad bacteria in the infection. But in turn, there have also been bacteria that can put up their resistance to the antibiotic
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5,096,891,583,499,302,000 | Does Massage After a Workout Have Any Benefit?
0
1079
Does Massage After a Workout Have Any Benefit
You have probably experienced finishing an intense workout session and then reap the effects the next day, most of which are not that pleasant. These include muscle soreness, pain, and tension. These are not entirely bad because they are indications that you are in for excellent results and that your body is undergoing repair and recovery. (talkofthetownatlanta.com)
However, these workout aches can last for days and hamper your ability to work or move about comfortably. Well, good news! Did you know that an after-workout massage can shorten the recovery time?
If you are still wondering, “Does massage after a workout have any benefit?”, read on below!Does Massage After a Workout Have Any Benefit
Why Massage After a Workout is Better than Conventional Painkillers
Many say that the best way to recover from exercise or playing sports is to wait it out. However, relying on time alone may not be the best solution.
In a recent study, 11 healthy young men were tasked to go through a strenuous workout. To find the effect of massage on the muscles after exercise, biopsies of both leg muscles of each participant were taken before exercise, after exercise, and after a 10-minute session of Swedish massage immediately after the workout.
The researchers found out that this short massage had an effect on two muscle cell genes. The first gene activated was responsible for reducing inflammation due to exercise and elicited a response similar to the relief from pain medications.
The second gene stimulated the production of mitochondria in the muscle cells. Mitochondria are the cell’s powerhouse, and an increase in their number means your muscles are becoming more adapted to endurance exercise.
Other studies have also shown that ice baths, pain relievers, and anti-inflammatory medications tend to block the repair and growth of muscle cells. On the contrary, massage not only reduces inflammation naturally but also hastens the recovery process.
The Amazing Benefits of an After-Workout Massage
So, to answer your question, “Does massage after workout have any benefit?”, well, yes! In fact, it has so many benefits that can help improve your overall performance and fitness level that you may not be as sore after exercise.
Below, I listed a rundown of all the amazing benefits of an after-workout massage and a brief explanation for each. Some of these I have already mentioned in the previous section but will explain further here so let’s get started!
Pain Relief
1. Pain Relief
The main thing we are targeting after a workout or intense exercise is pain due to muscle fatigue, tightness, and strain. This can be felt in various body parts and in different intensities. More often than not, these pains and aches will worsen over time. Sometimes, they can even progress to serious injury.
The good news is that a body massage post-workout can help increase circulation, which in turn reduces the pain and muscle soreness. More importantly, it can prevent the pain from becoming worse in the next few days.
By relieving pain and releasing tension from constricted and tight muscles, a massage can also improve your flexibility, speed, and endurance.
2. Energy Boost
After a workout, you’ll often find yourself extremely tired and low in energy. But believe it or not, a massage after working out can actually give you more energy. In fact, a massage helps increase the ability of the muscle cells to utilize oxygen and nutrients from the blood.
This means that your muscles will be able to produce more energy at a faster rate.
3. Speedy Recovery
According to research, getting a massage after exercising can make muscle recovery twice as fast as normal rest. This is also attributed to improved blood flow and nutrient distribution.
When your body fluids are continuously circulating, oxygen and nourishment reach your muscles more efficiently. Toxins and waste materials are also eliminated. This helps provide the needed energy for recovering cells. If you want a speedy recovery and you do not have time for massage therapy, you might want to consider a recovery pro massager. It’s a convenient way to get a massage anytime at home.
Another study at Ohio State University in 2015 found that bodywork and massage after an intense physical activity resulted in more vessel formation and reduced scarring in muscle cells.
The warmth provided by a massage also helps the muscles relax quicker so they can proceed to the recovery phase.
Reduced Injury
4. Reduced Injury
Inflexibility is the most common root cause of athletic injuries, next to poor form, and improper training. Inflexibility is due to the stiffness that forces your joints and muscles to overexert themselves during specific movements, leading to tissue damage.
A post-workout massage can help maintain or restore muscle and joint flexibility by allowing the muscles to relax. So, if ever you decide to get a massage after an intense workout, make sure to point out problem areas that are extra tight or stiff.
The Pacific College of Oriental Medicine (PCOM) also said that sports massage for injury prevention is particularly effective for injuries that happen during the tearing down phase.
5. Reduce Inflammation
The damage to your tissues causes inflammation. White blood cells which protect from infection or further damage accumulate in problem areas and cause swelling.
Reduce Inflammation
However, too much inflammation can also cause muscle stiffness, injury, or even more severe issues. The Men’s Fitness magazine suggests a ten-minute post-workout massage or longer reap its anti-inflammatory benefits.
Conclusion
So, the next time you finish a vigorous workout and think, “ugh, my body will be sore for days!”, try getting a quick massage. Your gym buddies may laugh at you for being such a lightweight, but your body will thank you later! When you’ve already recovered, and they’re still struggling to go down the stairs, let’s see who will be laughing then!
If you don’t have the time and budget to go to a massage parlor, you might want to consider investing in a nice handheld massager that you can use at home! It’s a convenient way to get a massage anytime, anywhere!
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-609,860,781,190,984,100 | Contrary To Misinformation, COVID-19 Mortality And Hospitalization Has Been Rising In The Last 30 Days Globally. Please Take Precautions!
BREAKING NEWS
Oct 12, 2018
Dyskeratosis Congenita Genetics
Dyskeratosis Congenita Genetics
Oct 12, 2018
Dyskeratosis congenita is a rare form of bone marrow failure, where the bone marrow fails to produce enough blood cells. The condition is therefore usually diagnosed based on a low number of circulating red blood cells, white blood cells and platelets.
Dyskeratosis congenita is characterized by oral leukoplakia, hyperpigmentation of the skin and nail dystrophy. Further features of the condition include lung disease, gut disorders, infertility, osteoporosis, eye and tooth abnormalities and developmental delay. An increased risk of malignancy and leukemia has also been recorded.
The exact prevalence of this condition is not known, although it is estimated to affect around one in 1 million people. In about half of people affected, the illness is caused by mutations in the TERCTERT, DKC1, or TINF2 genes. These genes code for the proteins telomerase, dyskerin, and shelterin, which are required for the maintenance of important structures called telomeres. Telomerase helps to maintain the length of telomeres by adding small DNA segments to the ends of chromosomes when cell division occurs. The main telomerase components, hTR and hTERT, are coded for by TERC and TERT, respectively. The hTR part is a molecule of RNA that acts as a template to create the DNA segments, which then get added to the chromosome ends by the hTERT component. The role of the DKC1 gene is to code for the protein dyskerin, which binds to hTR to help maintain stability of the telomerase complex.
The TINF2 gene codes for a protein found in the shelterin complex, which protects telomeres during DNA repair. In the absence of shelterin, the chromosome ends would be picked up as abnormal breaks in the sequence of DNA and the repair mechanism would involve these ends being joined together or apoptosis being induced. Mutations that arise in the TERCTERTDKC1 or TINF2 genes therefore disrupt the maintenance of telomeres, which become reduced in length.
Cells that divide rapidly are the most affected by the presence of short telomeres meaning people with the condition usually develop disorders of the skin, bone marrow, oral mucosa, nail beds and hair follicles. Chromosomal instability due to impaired telomere maintenance may also give rise to genetic abnormalities that cause uncontrolled cell division, therefore increasing the risk of malignancy in individuals with dyskeratosis congenita.
This disorder generally affects men much more frequently than females because in the majority of cases, the mode of inheritance is X-linked recessive. This means that the gene mutation that causes the condition is located on the X chromosome. In males, the mutation would only need to occur on the one X chromosome they possess, while in females the mutation would need to occur on both of their X chromosomes.Since it is unlikely that women will inherit two mutated copies of this gene, males are affected by this condition much more frequently than women.Although X-linked recessive is the most common inheritance pattern, studies have also demonstrated autosomal recessive as well as autosomal dominant patterns of inheritance.
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1,495,736,244,546,995,200 | journal
https://read.qxmd.com/read/36658580/the-efficacy-of-vitamin-d-supplementation-for-irritable-bowel-syndrome-narrow-scope-and-grade-miss-interpretation
#21
REVIEW
Mohamed Abuelazm, Basel Abdelazeem
We read the article by Haung et al. that pooled the effects of vitamin D on irritable bowel syndrome symptoms and associated quality of life. However, the current review suffers from some methodological errors: inadequate search strategy; the grading of recommendations assessment, development, and evaluation (GRADE) miss-assessment; and miss-interpretation. Accordingly, addressing the emphasized limitations will lead to more robust findings and conclusions.
January 20, 2023: Nutrition Journal
https://read.qxmd.com/read/36635751/correction-high-dietary-and-lifestyle-inflammatory-scores-are-associated-with-increased-risk-of-chronic-kidney-disease-in-iranian-adults
#22
Hossein Farhadnejad, Farshad Teymoori, Mitra Kazemi Jahromi, Ebrahim Mokhtari, Golaleh Asghari, Parvin Mirmiran, Fereidoun Azizi
No abstract text is available yet for this article.
January 12, 2023: Nutrition Journal
https://read.qxmd.com/read/36635676/automated-wearable-cameras-for-improving-recall-of-diet-and-time-use-in-uganda-a-cross-sectional-feasibility-study
#23
JOURNAL ARTICLE
Andrea L S Bulungu, Luigi Palla, Joweria Nambooze, Jan Priebe, Lora Forsythe, Pamela Katic, Gwen Varley, Bernice D Galinda, Nakimuli Sarah, Kate Wellard, Elaine L Ferguson
BACKGROUND: Traditional recall approaches of data collection for assessing dietary intake and time use are prone to recall bias. Studies in high- and middle-income countries show that automated wearable cameras are a promising method for collecting objective health behavior data and may improve study participants' recall of foods consumed and daily activities performed. This study aimed to evaluate the feasibility of using automated wearable cameras in rural Eastern Ugandan to collect dietary and time use data...
January 12, 2023: Nutrition Journal
https://read.qxmd.com/read/36631866/dietary-inflammatory-index-and-cardiovascular-disease-risk-in-hispanic-women-from-the-women-s-health-initiative
#24
JOURNAL ARTICLE
Monica D Zuercher, Danielle J Harvey, Margarita Santiago-Torres, Lauren E Au, Nitin Shivappa, Aladdin H Shadyab, Matthew Allison, Linda Snetselaar, Buyun Liu, John A Robbins, James R Hébert, Lorena Garcia
BACKGROUND: To evaluate the association between the dietary inflammatory index (DII® ) and incident cardiovascular disease (CVD) in Hispanic women from the Women's Health Initiative (WHI), and to determine if body mass index (BMI) interacted with the DII scores. METHODS: Secondary analysis of baseline dietary data and long-term CVD outcomes among 3,469 postmenopausal women who self-identified as Hispanic enrolled in WHI. DII scores were calculated from self-administered food frequency questionnaires...
January 12, 2023: Nutrition Journal
https://read.qxmd.com/read/36631774/food-price-volatility-and-socio-economic-inequalities-in-poor-food-consumption-status-during-coronavirus-disease-2019-lockdown-among-slum-and-non-slum-households-in-urban-nansana-municipality-uganda
#25
JOURNAL ARTICLE
Edward Buzigi, Stephen Onakuse
BACKGROUND: This study assessed staple food price volatility, household food consumption scores (FCS), poor household food consumption status and its association with socio-economic inequalities during enforcing and partial lifting of coronavirus disease-2019 (COVID-19) lockdown restrictions in slum and non-slum households (HHs) of Nansana municipality, Uganda. METHODS: Repeated cross-sectional surveys were conducted during enforcing and partial lifting of COVID-19 lockdown restrictions...
January 11, 2023: Nutrition Journal
https://read.qxmd.com/read/36627671/nitrate-containing-vegetables-and-dietary-nitrate-and-nonalcoholic-fatty-liver-disease-a-case-control-study
#26
JOURNAL ARTICLE
Parvin Mirmiran, Farshad Teymoori, Hossein Farhadnejad, Ebrahim Mokhtari, Ammar Salehi-Sahlabadi
BACKGROUND: Vegetables is the main sources of dietary nitrate. Studies suggested the potential link between nitrate content of vegetables and reduce the risk of chronic diseases. We aimed to assess the association between nitrate-containing vegetables (NCVs) with odds of nonalcoholic fatty liver diseases (NAFLD) in Iranian adults. METHOD: This case-control study was performed on a total of 225 newly diagnosed NAFLD cases and 450 controls aged 20-60 years...
January 10, 2023: Nutrition Journal
https://read.qxmd.com/read/36624459/food-insecurity-and-its-determinants-among-adults-in-north-and-south-india
#27
JOURNAL ARTICLE
Anjali Ganpule, Kerry Ann Brown, Manisha Dubey, Nikhil Srinivasapura Venkateshmurthy, Prashant Jarhyan, Avinav Prasad Maddury, Rajesh Khatkar, Himanshi Pandey, Dorairaj Prabhakaran, Sailesh Mohan
BACKGROUND: Food insecurity is a major public health problem worldwide. In India, there are limited food insecurity assessment studies using a conventionally accepted method like the Food Insecurity Experience Scale (FIES), developed by the Food and Agricultural Organization (FAO). This study aims to measure food insecurity using the FIES and explore its determinants and association with body mass index (BMI) among Indian adults. METHODS: In a cross-sectional study, we used FIES to measure food security in a sample of 9005 adults residing in North and South India...
January 9, 2023: Nutrition Journal
https://read.qxmd.com/read/36609337/high-dietary-and-lifestyle-inflammatory-scores-are-associated-with-increased-risk-of-chronic-kidney-disease-in-iranian-adults
#28
JOURNAL ARTICLE
Hossein Farhadnejad, Farshad Teymoori, Mitra Kazemi Jahromi, Ebrahim Mokhtari, Golaleh Asghari, Parvin Mirmiran, Fereidoun Azizi
BACKGROUND: Systemic inflammation can be the initiator in developing chronic diseases that may be affected by the lifestyle and diet of individuals. In the current study, we aimed to assess the association of the inflammatory potential of diet and lifestyle, determined by the food-based index of dietary inflammatory potential (FBDI), dietary inflammation score (DIS), and lifestyle inflammation score (LIS), with risk of chronic kidney disease(CKD) in Iranian adults. METHODS: A total of 6044 CKD-free individuals aged ≥ 18 years, were recruited from among participants of the Tehran Lipid and Glucose Study(surveys 3 and 4) and followed a mean of 6...
January 7, 2023: Nutrition Journal
https://read.qxmd.com/read/36581871/relationship-between-high-fructose-corn-syrup-sweetened-drinks-diet-soft-drinks-and-serum-sodium-nhanes-2003-2006
#29
JOURNAL ARTICLE
Mingxi Li, Weijun Gong, Shidong Wang, Zhe Li
BACKGROUND: Consumption of high fructose corn syrup sweetened drinks and diet soft drinks has increased in the United States. However, the relationship between the intake of high fructose corn syrup sweetened drinks and diet soft drinks, and serum sodium has been scarcely studied. Our objective is to evaluate the relation between intake of high fructose corn syrup sweetened drinks and diet soft drinks, and serum sodium, and explore the possible effect modifiers in a nationally representative sample of adults from the United States...
December 29, 2022: Nutrition Journal
https://read.qxmd.com/read/36539753/the-impact-of-a-family-web-based-nutrition-intervention-to-increase-fruit-vegetable-and-dairy-intakes-a-single-blinded-randomized-family-clustered-intervention
#30
RANDOMIZED CONTROLLED TRIAL
Vicky Drapeau, Andrée-Anne Harvey, Raphaëlle Jacob, Véronique Provencher, Shirin Panahi
BACKGROUND: The importance of adopting healthy eating habits at a young age to prevent obesity and chronic diseases justifies the need for effective interventions. OBJECTIVE: This study evaluated the impact of a family web-based nutrition intervention on vegetable and fruit (V/F) and dairy product (DP) consumption, nutrient intakes, diet quality and BMI or BMI z-scores. METHODS: Forty-three families with children aged 8-16 years were randomized to either the family web-based intervention, or web-based general nutrition guidelines (control) over 8 weeks...
December 20, 2022: Nutrition Journal
https://read.qxmd.com/read/36529744/an-experimental-approach-to-training-interoceptive-sensitivity-study-protocol-for-a-pilot-randomized-controlled-trial
#31
JOURNAL ARTICLE
Petra Warschburger, Hanna R Wortmann, Ulrike A Gisch, Nadja-Raphaela Baer, Liane Schenk, Verena Anton, Manuela M Bergmann
BACKGROUND: Eating in absence of hunger is quite common and often associated with an increased energy intake co-existent with a poorer food choice. Intuitive eating (IE), i.e., eating in accordance with internal hunger and satiety cues, may protect from overeating. IE, however, requires accurate perception and processing of one's own bodily signals, also referred to as interoceptive sensitivity. Training interoceptive sensitivity might therefore be an effective method to promote IE and prevent overeating...
December 19, 2022: Nutrition Journal
https://read.qxmd.com/read/36476477/efficacy-of-global-leadership-initiative-on-malnutrition-as-potential-cachexia-screening-tool-for-patients-with-solid-cancer
#32
MULTICENTER STUDY
Mengmeng Song, Qi Zhang, Tong Liu, Meng Tang, Xi Zhang, Guotian Ruan, Xiaowei Zhang, Kangping Zhang, Yizhong Ge, Ming Yang, Wei Li, Minghua Cong, Kunhua Wang, Chunhua Song, Hanping Shi
PURPOSE: Cachexia has a very high prevalence in patients with cancer, and lacks effective screening tools yet. Global Leadership Initiative on Malnutrition (GLIM) is a novel malnutrition assessment tool, with increased important roles in malnutrition diagnosis for patients with cancer. However, whether GLIM can be used as an effective screening tool remains unknown. METHODS: We performed a multicenter cohort study including 8,478 solid tumor patients from 40 clinical centers throughout China...
December 7, 2022: Nutrition Journal
https://read.qxmd.com/read/36434698/partnering-for-prevention-in-under-resourced-communities-a-randomized-pilot-study
#33
RANDOMIZED CONTROLLED TRIAL
Angela R Caldwell, Lauren Terhorst, Jodi S Krall, Danielle W Thum, Hana R Uman, Judy L Dodd, Emily E Haus, Roxanna M Bendixen
BACKGROUND: Promoting health early in life is crucial to obesity prevention, but families in under-resourced communities face barriers to establishing healthy routines. The purpose of this pilot study was to examine the feasibility and preliminary effects of two dietary interventions for families in under-resourced communities. METHODS: Fifty-one caregivers of young children (aged 0-5 years) were recruited from six community centers located in heavily populated neighborhoods with high poverty rates (i...
November 25, 2022: Nutrition Journal
https://read.qxmd.com/read/36397086/skipping-breakfast-during-pregnancy-and-hypertensive-disorders-of-pregnancy-in-japanese-women-the-tohoku-medical-megabank-project-birth-and-three-generation-cohort-study
#34
JOURNAL ARTICLE
Misato Aizawa, Keiko Murakami, Ippei Takahashi, Tomomi Onuma, Aoi Noda, Fumihiko Ueno, Fumiko Matsuzaki, Mami Ishikuro, Taku Obara, Hirotaka Hamada, Noriyuki Iwama, Masatoshi Saito, Junichi Sugawara, Nobuo Yaegashi, Shinichi Kuriyama
BACKGROUND: Hypertensive disorders of pregnancy (HDP) adversely affect the prognosis of mother and child, and the prognosis depends on the subtype of HDP. Skipping breakfast may be associated with increased blood pressure due to disruption of the circadian clock, but the association with the development of HDP has not been studied. The purpose of this study was to examine the association between skipping breakfast and the development of HDP and HDP subtypes in Japanese pregnant women...
November 17, 2022: Nutrition Journal
https://read.qxmd.com/read/36384552/development-of-the-penn-healthy-diet-screener-with-reference-to-adult-dietary-intake-data-from-the-national-health-and-nutrition-examination-survey
#35
JOURNAL ARTICLE
Charlene W Compher, Ryan Quinn, Frances Burke, Doris Piccinin, Linda Sartor, James D Lewis, Gary D Wu
BACKGROUND: There is a need for a feasible, user-friendly tool that can be employed to assess the overall quality of the diet in U.S. CLINICAL SETTINGS: Our objectives were to develop the Penn Healthy Diet (PHD) screener, evaluate screener item correlations with Healthy Eating Index (HEI)-2015 components, and develop a simple scoring algorithm. METHODS: National Health and Nutrition Examination Survey (NHANES) 2017-18 dietary recall data in adults were used to define food examples in screener food groups based on components of the HEI-2015, Diet Approach to Stop Hypertension, and Alternative Mediterranean diet approaches...
November 17, 2022: Nutrition Journal
https://read.qxmd.com/read/36384651/swap-meat-athlete-study-with-appetizing-plant-food-meat-eating-alternatives-trial-investigating-the-impact-of-three-different-diets-on-recreational-athletic-performance-a-randomized-crossover-trial
#36
RANDOMIZED CONTROLLED TRIAL
Aubrey K Roberts, Vincent Busque, Jennifer L Robinson, Matthew J Landry, Christopher D Gardner
BACKGROUND: Plant-based diets are known to be beneficial for cardiovascular health and promote environmental sustainability. However, many athletes avoid plant-based diets due to concerns of protein inadequacy. OBJECTIVES: To investigate the impact of two predominately plant-based diets-whole food plant-based (WFPB) and plant-based meat alternatives (PBMA)-vs. an omnivorous diet, favoring red meat and poultry (Animal), on endurance and muscular strength. METHODS: 12 recreational runners and 12 resistance trainers were assigned to three diets-WFPB, PBMA, and Animal-for 4 weeks each, in random order...
November 16, 2022: Nutrition Journal
https://read.qxmd.com/read/36380391/agreement-between-24-hour-urine-and-24-hour-food-recall-in-measuring-salt-intake-in-primary-school-children-in-australia
#37
JOURNAL ARTICLE
Joseph Alvin Santos, Kristy A Bolton, Emalie Rosewarne, Kathy Trieu, Gian Luca Di Tanna, Mark Woodward, Jacqui Webster, Carley Grimes
BACKGROUND: Monitoring salt consumption in children is essential for informing and implementing public health interventions to reduce children's salt intake. However, collection of 24-hour urines, considered as the most reliable approach, can be especially challenging to school children. This study aimed to assess the agreement between 24-hour urine (24hrU) and 24-hour food recall (24hrFR) in: (1) estimating salt intake in children; (2) classifying salt intakes above the recommended upper level set for children, and; (3) estimating change in mean salt intake over time...
November 15, 2022: Nutrition Journal
https://read.qxmd.com/read/36348423/longitudinal-trends-in-produce-purchasing-behavior-a-descriptive-study-of-transaction-level-data-from-loyalty-card-households
#38
JOURNAL ARTICLE
Isabel Diana Fernandez, Brent A Johnson, Nellie Wixom, Amber Kautz, Joanne Janciuras, Steve Prevost, Jiebo Luo, Rajeev S Ramchandran
BACKGROUND: Household food purchases (HFP) are in the pathway between the community food environment and the foods available in households for consumption. As such, HFP data have emerged as alternatives to monitor population dietary trends over-time. In this paper, we investigate the use of loyalty card datasets as unexplored sources of continuously collected HFP data to describe temporal trends in household produce purchases. METHODS: We partnered with a grocery store chain to obtain a loyalty card database with grocery transactions by household from January 2016-October 2018...
November 8, 2022: Nutrition Journal
https://read.qxmd.com/read/36273143/the-consumption-of-culinary-preparations-and-ultra-processed-food-is-associated-with-handgrip-strength-in-teenagers
#39
JOURNAL ARTICLE
Susana Cararo Confortin, Aline Rodrigues Barbosa, Bianca Rodrigues de Oliveira, Elma Izze da Silva Magalhães, Maylla Luanna Barbosa Martins Bragança, Maria Teresa Seabra Soares de Britto E Alves, Renata Bertazzi Levy, Rosângela Fernandes Lucena Batista, Poliana Cristina de Almeida Fonseca Viola, Antônio Augusto Moura da Silva
BACKGROUND: A nutrient-poor and hypocaloric diet may be associated with lower handgrip strength (HGS), whereas a high-quality or balanced diet may be associated with higher HGS. However, no study has used the NOVA system for classifying food by their degree of processing. OBJECTIVE: To analyze the association between food consumption according to the degree of food processing and HGS in Brazilian teenagers. METHODS: This cross-sectional study included teenagers aged 18 and 19 years old from the 1997/98 São Luís' birth cohort, Maranhão, Brazil...
October 22, 2022: Nutrition Journal
https://read.qxmd.com/read/36258233/effects-of-a-high-fat-meal-on-inflammatory-and-endothelial-injury-biomarkers-in-accordance-with-adiposity-status-a-cross-sectional-study
#40
JOURNAL ARTICLE
Maria das Graças Coelho de Souza, Priscila Alves Maranhão, Diogo Guarnieri Panazzolo, José Firmino Nogueira Neto, Eliete Bouskela, Luiz Guilherme Kraemer-Aguiar
BACKGROUND: It is known that consuming a high-fat meal (HFM) induces microvascular dysfunction (MD) in eutrophic women and aggravates it in those with obesity. Our purpose was to investigate if the MD observed after a single HFM intake is caused by endothelial damage or increased inflammatory state, both determined by blood biomarkers. METHODS: Nineteen women with obesity (BMI 30-34.9 kg/m2 ) and 18 eutrophic ones (BMI 20.0-24.9 kg/m2 ) were enrolled into two groups: Obese (OBG) and Control (CG), respectively...
October 19, 2022: Nutrition Journal
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PCOS: Natural remedies and herbs for support
Updated: 2 days ago
Polycystic ovary syndrome (PCOS) is a condition that’s thought to impact around 1 in 10 women. Its effects can vary from woman to woman, but symptoms generally include irregular periods, weight gain and excessive hair growth.
Knowledge and research on PCOS has its limitations, and can be incredibly frustrating for those living with the condition. One common line of treatment for women with PCOS is the contraceptive pill. While this can help to regulate periods and ease symptoms, many women find that this simply masks the problem, with symptoms returning with a vengeance once they stop taking the pill.
Here to explain some of the natural ways to support PCOS is Chantal Perkins, a naturopath and medical herbalist at Healing Herbs Holistic Therapies.
It’s important to remember that these suggestions won’t work for everyone and are only intended as a general guide for remedies that may help to alleviate symptoms. Any herbs mentioned in this article are not recommended to be taken during pregnancy. Please consult a professional trained herbalist before taking any herbal remedies.
Support your liver
Our liver is constantly working to remove toxins from our body. These toxins include ones from external sources, as well as those made by the body - hormones included. In PCOS, it’s an imbalance of hormones that’s often associated with symptoms. By supporting your liver, you give your body a better chance of regulating your hormones.
“Diet plays a massive part in regulating the symptoms of PCOS,” explains Chantal. “Reducing carbohydrates may help. Eating more fibre-rich food can also have a beneficial effect as it helps to support the liver and balances hormones."
Plants are a fantastic source of fibre - fruit, vegetables, legumes and wholegrain all count towards your intake. By eating more fibre, it keeps your digestive system and its surrounding organs (liver included) happy.
Herbs to support your liver
There are also a number of herbs that can help to support the liver. Dandelion root is often considered a liver tonic, supporting the liver in detoxifying. It also helps to aid digestion by increasing the flow of digestive juices.
“Milk thistle and burdock are also good for supporting the liver,” says Chantal. “These - along with dandelion root - are perhaps my ultimate detox herbs.”
Milk thistle works as an antioxidant, helping to decrease damaging free radicals in the liver. It also helps to keep the cells of the liver healthy too. Similarly, burdock supports the liver in its work and can help to improve digestion too.
Balance your blood sugar
Studies suggest that many women with PCOS also struggle with insulin resistance. Insulin is produced by the pancreas to control the amount of sugar in the blood. If your body is resistant to insulin, your pancreas has to produce more to get the same effect. This excess insulin can in turn cause too much of our other hormones - testosterone included - to be produced. This hormone imbalance can potentially go on to cause the symptoms that we associate with PCOS.
“One of the most important treatment strategies for PCOS is to balance the blood sugar,” says Chantal.
Along with eating regular healthy meals and cutting down on sweet treats, there are a number of herbs that can help to stabilise your blood sugar.
“Things like cinnamon, nettle and dandelion root can help,” explains Chantal.
Cinnamon is a regular in our kitchens - especially during the winter months - but it also helps to support our digestion too. It’s thought to enhance how effective insulin is.
Nettle also has a role in supporting our digestive system. It has a hypoglycaemic action, meaning it helps to reduce blood sugar.
Help your hormones
With our hormones in such a delicate balance, it’s important we pay them attention when it comes to finding natural remedies for PCOS.
Endocrine disruptors are increasingly gaining attention when it comes to our hormonal health. These are chemicals - either natural or man-made - that have the ability to mimic or interfere with the action of our hormones. They can be found just about anywhere, from the food we eat to the body lotions we put on our skin.
While it can be impossible to completely avoid these disruptive chemicals all of the time, reducing your exposure to them can help to balance your hormones and potentially decrease the likelihood of PCOS symptoms.
“Avoiding external sources of hormones - like meat and dairy - in your diet can be a good place to start with PCOS,” says Chantal. “Household cleaners can also have an effect, so it can be worth taking the time to research safer options.”
Herbs to support your hormones
A number of herbs can help to support hormone function.
“Liquorice has an oestrogenic effect,” says Chantal. “This means it has a similar effect to oestrogen. It’s useful for PCOS and absent periods. Things that are oestrogenic are generally good for PCOS.”
Chaste berry is another herb that can be incredibly supportive for PCOS and women’s health in general. Chaste berry is thought to lead to an increase in progesterone production - a hormone that works to regulate the menstrual cycle.
“Chaste berry is an all-round hormone balancer,” explains Chantal. “It works to regulate the pituitary gland and as a result can be good for conditions like PCOS and endometriosis. It’s also good for infertility and absent periods.”
About Chantal
Chantal has had a lifelong passion for nature. As she grew older, she became curious as to how a connection with nature could help to treat illness in the body and mind. Chantal read about herbs, essential oils and different healing energies, before training in reflexology.
This was closely followed by training as a Crystal Therapist, Reiki Master, LUXOR Light practitioner and eventually completing a degree in Herbal Medicine.
Find out more about Chantal's work.
Read more articles
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2,088,831,716,482,042,600 | THC-Free CBD Oil for Stress Relief: A Guide
As someone who has struggled with stress, finding effective relief is crucial.
In this guide, I'll explore the science behind THC-free CBD oil for stress relief.
We'll debunk misconceptions, delve into the impact of THC on public perception, and discuss how to market and address stigma around CBD.
Together, we'll work to change perceptions and uncover the potential of THC-free CBD oil as a tool for managing stress.
Key Takeaways
• THC-free CBD oil does not produce a 'high' and can promote relaxation and mental well-being.
• Targeted advertising and clear labeling emphasizing the absence of THC are crucial for reaching those seeking stress relief without psychoactive effects.
• Presenting scientific evidence, sharing authentic testimonials, and addressing concerns about safety and legitimacy can help combat the stigma surrounding CBD for stress relief.
• CBD interacts with the endocannabinoid system and may offer potential benefits for managing stress and anxiety, but further research is needed to fully understand its efficacy.
Public Misconceptions About CBD for Stress Relief
Many people mistakenly believe that CBD oil is psychoactive and will produce a 'high' when used for stress relief. However, it's important to raise public awareness about the fact that CBD, or cannabidiol, is non-psychoactive.
Unlike THC, another compound found in cannabis, CBD doesn't produce intoxicating effects. This is a crucial distinction, especially when considering the use of CBD for stress relief.
Medical research has shown that CBD interacts with the endocannabinoid system in the body, which plays a role in regulating functions such as mood, sleep, and stress response. By influencing these functions, CBD may offer potential benefits for managing stress and anxiety.
Public awareness about the non-psychoactive nature of CBD is essential to dispel misconceptions. It's important for individuals to understand that using CBD for stress relief doesn't mean experiencing a 'high' or impairment. Instead, CBD products, particularly those that are THC-free, can offer a natural alternative for promoting relaxation and supporting mental well-being.
As the stigma surrounding cannabis continues to evolve, it's crucial to emphasize the scientific understanding of CBD and its potential therapeutic effects. Medical research into CBD for stress relief is ongoing, with studies exploring its mechanisms of action and its effectiveness in mitigating various forms of anxiety. As more evidence emerges, it's expected that public perception will shift towards recognizing CBD as a valuable tool for stress management, devoid of the psychoactive effects commonly associated with cannabis.
The Influence of THC on Public Perception of CBD
The presence of THC in cannabis has significantly impacted the public perception of CBD and its potential benefits for stress relief. THC, the psychoactive compound in cannabis, has long been associated with the 'high' effect, leading to public misconceptions about CBD. The influence of THC on public opinion regarding CBD for stress relief can be summarized as follows:
• THC Effects:
• THC is known for its psychoactive properties, leading to the misconception that all cannabis-derived products, including CBD, produce the same intoxicating effects.
• The presence of THC in CBD products has raised concerns about potential impairment, further contributing to skepticism about its stress-relieving benefits.
• Research indicates that THC can cause adverse effects such as anxiety and paranoia in some individuals, leading to apprehension about using CBD products containing THC for stress relief.
Public Opinion:
• The association of THC with recreational marijuana use has led to a stigma surrounding CBD, affecting its acceptance as a stress relief remedy.
• Misinformation and lack of understanding about the differences between THC and CBD have contributed to skepticism and reluctance in embracing CBD for stress relief.
• The presence of THC in CBD products has influenced public perception, creating a barrier to recognizing the potential benefits of CBD for stress relief.
Understanding the influence of THC on public perception is crucial in addressing misconceptions and promoting the potential benefits of THC-free CBD oil for stress relief.
Transitioning into the subsequent section about 'marketing THC-free CBD oil for stress relief,' it's essential to consider strategies that effectively communicate the absence of THC and emphasize the stress-relieving properties of CBD.
Marketing THC-Free CBD Oil for Stress Relief
When marketing THC-free CBD oil for stress relief, targeted advertising is crucial. It allows the message to reach those who are specifically seeking stress relief without the psychoactive effects of THC. Emphasizing product differentiation is essential. Highlighting the absence of THC and the purity of CBD in the oil can set it apart from other products in the market.
It is important to convey the information clearly and transparently. This can be achieved by utilizing clear labeling and marketing materials that explicitly state 'THC-free' and 'CBD-dominant.' Scientific evidence and research can also be used to support the stress-relieving properties of CBD. Incorporating this information into marketing materials can help to establish credibility and trust with potential consumers.
Furthermore, leveraging digital platforms for targeted advertising can help reach individuals who are actively seeking stress relief solutions. Social media, search engine optimization, and content marketing can all be effective tools for reaching the target audience. By utilizing these platforms, the message of THC-free CBD oil for stress relief can be communicated to those who are most likely to benefit from it.
In the subsequent section, I'll address the stigma around CBD for stress relief and discuss strategies for overcoming misconceptions and misinformation.
Addressing Stigma Around CBD for Stress Relief
Navigating the misconceptions and misinformation surrounding CBD for stress relief is essential for establishing trust and credibility with potential consumers. Combatting stigma and educating consumers about CBD's potential benefits is crucial in promoting an accurate understanding of this natural remedy.
Here are key points to consider when addressing the stigma around CBD for stress relief:
• Scientific Evidence: Presenting scientific research and studies that support the effectiveness of CBD in stress relief can help dispel misconceptions. Highlighting the mechanism of action through which CBD interacts with the body's endocannabinoid system can also provide clarity on its therapeutic effects.
• Regulatory Compliance: Emphasizing the legal status and regulatory compliance of CBD products can help address concerns about its safety and legitimacy. Providing information about the absence of psychoactive effects due to the lack of THC in CBD oil can alleviate fears about intoxication or impairment.
• Consumer Testimonials: Sharing authentic and credible testimonials from individuals who've experienced positive outcomes with CBD for stress relief can humanize the product and demonstrate its potential to improve well-being.
Changing Perceptions of CBD for Stress Relief
Often, I find that misconceptions about CBD for stress relief can be changed through education and open dialogue. Evolving attitudes towards CBD are significantly impacted by scientific research. As more studies are conducted, the public's understanding of CBD's potential for stress relief is shifting.
Scientific research has played a pivotal role in changing perceptions of CBD for stress relief. Studies have shown that CBD interacts with the endocannabinoid system, which regulates stress, anxiety, and mood. This scientific evidence has provided a foundation for understanding how CBD may offer stress-relief benefits.
Moreover, ongoing research has debunked myths and misconceptions surrounding CBD, contributing to evolving attitudes. A better understanding of the mechanisms by which CBD affects the body has led to more informed discussions about its potential role in stress management.
As someone who values evidence-based information, I've found that discussing the scientific research on CBD for stress relief has been instrumental in changing perceptions. By presenting the latest findings and discussing the potential applications of CBD in stress management, I've witnessed a shift in attitudes among those who were initially skeptical.
Frequently Asked Questions
Can CBD Oil With No THC Still Provide the Same Level of Stress Relief as CBD Oil With THC?
Yes, CBD oil without THC can still provide stress relief. Research studies have shown that both THC-free and THC-containing CBD oil can be effective in reducing stress and anxiety.
However, the efficacy comparison between the two is still being studied. While some individuals may prefer THC-free options due to legal concerns or personal preferences, it's important to consult a healthcare professional to determine the best choice for stress relief.
Are There Any Potential Side Effects or Drawbacks to Using Thc-Free CBD Oil for Stress Relief?
Using THC-free CBD oil for stress relief has potential side effects and health concerns. Long-term effects are still being studied.
Efficacy studies show promise, but it's important to be aware of potential drug interactions and mild side effects such as fatigue or changes in appetite.
It's always best to consult with a healthcare professional before starting any new supplement, especially if you have underlying health conditions or are taking other medications.
How Can Consumers Ensure They Are Purchasing High-Quality Thc-Free CBD Oil for Stress Relief?
To ensure high-quality THC-free CBD oil for stress relief, consumers should look for products that have undergone laboratory testing for potential contaminants.
It's also helpful to check product reviews from other users to gauge the effectiveness and quality.
Additionally, following dosage recommendations is crucial for safe and effective use.
These steps can help consumers make informed decisions and select reputable products for stress relief.
Are There Any Legal Restrictions or Regulations Surrounding the Use of Thc-Free CBD Oil for Stress Relief?
Legal implications for THC-free CBD oil vary by location.
In the US, the 2018 Farm Bill legalized hemp-derived CBD with less than 0.3% THC. However, state laws differ.
In Europe, CBD is legal if it contains less than 0.2% THC. Regulations are evolving, so it's vital to stay informed.
As for health benefits, research suggests that CBD may help alleviate stress and anxiety, but it's essential to consult with a healthcare professional.
What Are Some Alternative Methods for Stress Relief That Can Be Used in Conjunction With Thc-Free CBD Oil?
When it comes to stress relief, alternative therapies can complement THC-free CBD oil.
Mindfulness meditation is one effective method; it involves focusing on the present moment and can reduce stress.
Additionally, techniques like yoga, exercise, and aromatherapy can work well with CBD oil.
These alternative methods offer a holistic approach to stress relief, promoting overall well-being.
Leave a Reply | {
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-8,690,651,627,415,436,000 | The World of Diets
Image: Vidmir Raic
If you are anything like millions of people around the world, weight has always been an issue. I once had someone describe themselves as “fluffy,” which I thought was an excellent way to express oneself when your body shape did not follow the statuesque model shapes constantly promoted in the media. After all, we can’t all be supermodels; quite frankly, that’s a good thing. People have put too much emphasis on unrealistic physical appearance. Each of us is shaped differently with different features that make us just as beautiful as the next person. The fact is, we need to emphasize health more than appearance.
That brings us to diets. I’ve never been a fan of dieting. Quite frankly, I love eating far too much (thus why I can now describe myself as semi-fluffy). As we age, our bodies don’t bounce back as quickly as they used to when dieting. It used to be that we could cut back for a week and see a noticeable difference. Not so much now. My nephew is a physical trainer. He tells me that exercise alone will not help you maintain a healthy weight; the amount you consume is as significant, if not more, than the workouts. So how do you figure out what helps keep that intake to a healthy minimum? The truth is that it is different for each person. If you plan to diet, then you should know all the facts.
Why Diet?
When I started looking at diets, I was astounded at the vast number of dieting ideas. People’s eating choices are often affected by ethical or religious beliefs; others are just from a need to lose or control weight. Not all diets are healthy – some pose significant health risks and minimal long-term benefits. Before starting any diet, you should talk with a nutritionist or doctor, especially if you already have some health issues.
Improving your diet clearly has a significant impact on lengthening your lifespan and dramatically decreasing the risk of most chronic diseases. Much research continues on dieting, but one common factor is that eating patterns that include less processed and more natural foods are proven beneficial to health. Dr. David Katz at Yale University’s Prevention Research Center concluded in his studies that “a diet of minimally processed foods close to nature, predominantly plants, is decisively associated with health promotion and disease prevention.” These diets include not just fruits and vegetables but whole grains, nuts, and seeds.
Let’s Talk Diets
It seems so simple. We need food to supply nutrients for our bodies. Those nutrients provide energy that fuels all our daily activities. Our bodies tell us when our fuel reserves are low – this makes us hungry, and we eat food until we feel satisfied. The problem is that we are not always eating the food that is good for us or an amount that is good for us. Fats serve as reserves to guard against lean times, so we tend to eat foods that will keep us full for longer. Sugars give us a quick energy boost that may seem good at first but, in the long run, have detrimental repercussions on our overall well-being and health. Enter diets. Approximately 45 million people go on a diet each year, with a market value for weight management of over $288 billion.
Diets fall into seven categories: belief-based, weight control, crash, detox, fad, or vegetarian. Belief-based diets are religious-based and include such diets as Islamic dietary laws that consist of eating only halal foods or Buddhism vegetarian eating practices based on the Five Precepts (system of morality for Buddhist people.) Weight control, crash, detox, and fad diets are all based on reducing or eliminating certain foods, sometimes at certain times. Finally, vegetarian diets are all based on plant-based eating – some extreme and some that are more semi-vegetarian, including foods from other groups. For this blog, I will focus on a few popular diets and some crazy ones.
Image: Steve Buissinne
Diets Designed to Control Weight
Intermittent Fasting: I’ve already talked about this diet in my blog, Intermittent Fasting: Is It Worth Trying?, so I won’t go in-depth to discuss this one. In a nutshell, it involves an eating pattern that cycles between periods of eating and fasting. It does not focus on what you eat but rather when you eat it.
Ketogenic Diet: Go to your local grocery store, and you will see keto products on many shelves. What exactly is it, however? Keto (short for ketogenic) prioritizes fat (65 to 75 percent of your daily calories) with moderate protein consumption (20 to 30 percent) and very few carbs (5 percent). The goal is to keep your body in a near-constant state of ketosis – a metabolic state where the body creates ketones from fat to use as energy instead of sugar from carbs. Typically, your body uses sugar from carbs you consume as an energy source. With this diet, weight loss comes from the type of calories you consume versus the calories you expend. Unfortunately, many studies have shown that this diet is no more effective in weight loss than any other diet1.
If It Fits Your Macros: Yes, this is an actual diet, and surprisingly it makes sense. It is a more flexible approach to eating. You can eat whatever you want as long as you don’t eat over your specific limit (each person is different.) The diet includes pre-determined protein, carb, and fat targets. There are even apps available to help you track what your maximum should be (https://www.myfitnesspal.com/) and calculators to help you figure out your maximums (https://barbend.com/best-macros-calculator/). The only downside to this diet is it expects that you will not cheat.
Image: Ana Segota
Fad Diets
Sirtfood Diet: Recently, the Sirtfood Diet has become popular because of celebrity endorsements from people like Adele and Pippa Middleton. Created by nutritionists Aidan Goggins and Glen Matten, it focuses on foods high in sirtuins, a group of proteins found in the body that regulate metabolism. Foods included in this group are red wine, dark chocolate, walnuts, Medjool dates, arugula, coffee, capers, and extra-virgin olive oil. So far, so good. The Sirtfood diet requires a two-phase approach. In Phase 1, you can only drink three sirtfood green juices and eat one full meal rich in sirtuins for three days, which amounts to only 1,000 calories consumed. Your caloric intake for the next four days increases to 1,500 calories. According to dietary guidelines, women need approximately 1,600 o 2,400 calories per day and men 2,000 to 3,000. Already there are red flags. The recommendations are (depending on the individual) that you cut between 500 to 1,000 calories daily for weight loss. This one removes a lot more than the recommended decrease. Phase 2 lasts two weeks with three sirtfood-rich meals and one green juice daily. A little better, I’d say. Unfortunately, there is very little scientific evidence that this one works – unless you look at Adele.
Atkins Diet: Created in the 1960s by cardiologist Robert Atkins, it became popular in the early 2000s, some 30 years after his book was published. At the height of its popularity, one in eleven North American adults claimed to be on this low-carb diet. Dr. Atkins felt that carbohydrates, not fat, were responsible for health problems and weight gain. His diet focused on eating plenty of fat, some protein, and very few carbs. The problem with his diet is that it cuts out many perfectly healthy foods that are good for your body. In Phase 1 of the diet, only 20 grams of carbohydrates are allowed with a limited intake of foods like fruit, vegetables, legumes, and whole grains. Overall, clinical trials have shown that this diet does work. Over the short term, 9 out of 10 participants demonstrated significant short-term weight loss. Over a more extended period (12 months or more), six out of eight trials showed weight loss. No studies have researched the long-term impact of the limited intake of certain nutrition-rich foods. Still, many variations of this diet have resurfaced over the decades. Regardless of the interpretation, they all restrict processed foods, sugar, refined carbohydrates, and starchy foods (like bread, pasta, rice, and starchy vegetables like a potato.) Again, nutrition guidelines do not recommend cutting out whole food groups unless there is a medical reason. Whole grains, starchy vegetables, fruits, and legumes are all part of a heart-healthy diet.
Image: Wow Phochiangrak
WW Diet (Weight Watchers): I include this diet in the fad category as they are a dieting brand marketing the idea of weight loss. What they do right is that they base the diet on individual needs and scientific analysis to ensure healthy, nutrient-rich options. In their plan, foods are worth different points, with a limit to the daily intake with each individual’s goal in mind. The calories, saturated fat content, sugar, and protein all play a part in the points assigned to each food. In addition, there are also “zero-point” foods of which users can eat unlimited amounts – like salmon, beans, peas, corn, eggs, skinless chicken breasts, turkey breast, and even lobster. It is unlikely that someone will overeat any of these foods, and most do an excellent job filling the stomach. Members are typically assigned 30 points per day and varying points based on height, weight, and gender. A clinical trial at the University of North Carolina found that 152 participants lost weight. The only downside is that there is a weekly fee to use the service, and it can become cumbersome to keep track of every item you consume.
Image: Michael Wave (Beyond Meat)
Vegetarian Diets
Veganism: Veganism is one of the fastest-growing movements in eating, and most that follow it, don’t consider it a diet but rather a lifestyle choice. A few years ago, vegans would only eat beans, legumes, grains, egg-free pasta, fruits, and vegetables. But technological advances have introduced vegans to a wide variety of alternative products. To give you an idea of its reach, meat alternatives such as Beyond Burgers will reach a value of over $140 billion US over the next decade.
One study followed 250,000 people and their eating habits. They found that vegans had a 25 percent lower risk of heart disease and an eight percent lower risk of cancer than those who ate animal products2. On the downside, vegans are at a higher risk of deficiency in essential vitamins and minerals such as iron, zinc, Vitamin D, calcium, B12, and omega-3 fatty acids, all of which are vital to everyday health. Therefore, if you follow this diet, you must ensure to supplement vitamins and minerals. Overall, a vegan diet does seem to help people lose weight. It is low in fats and high in fiber content, making you feel fuller for longer. One 18-week study showed that participants lost more weight than those on a control-type diet where all food groups were consumed3. Another recent study examined different plant-based eating patterns and how each impacted health. As it turns out, a strict vegan diet produced the highest levels of healthy biomarkers (biomarkers measure diseases such as heart disease.) The least favorable were non-vegetarians who had higher unhealthy markers in their samples6.
Pescetarian: Pescatarian diets are vegan-lite. This diet excludes all animal products except seafood, fish, eggs, and dairy. Since these foods are rich in nutrients, this removes some concerns about nutrient loss found with strict veganism.
Vegetarian: Vegetarian diets are another form of vegan-lite. They restrict the consumption of all meat and poultry; however, they also restrict seafood. What they do allow is certain products from animals, such as eggs and cheese. Because of the inclusion of some nutrient-rich foods, vegetarians do not have to supplement vitamins such as B12. Studies done regarding vegetarian-style eating habits are mixed. One study followed 267,180 people for six years and found no difference in health or mortality compared to non-vegetarians4. Another followed 96,469 people and found that they had a lower mortality risk5. None of the studies focused on weight loss but instead on the effects on one’s overall health and longevity.
Flexitarian: This diet is often referred to as “semi-vegetarian” as it includes eggs and dairy. A flexitarian may also consume small amounts of meat, poultry, fish, and seafood, but the primary source of nutrition is beans, legumes, grains, fruits, and vegetables. Very little research has occurred on this type of diet.
Image: Vika Imperia
Diets That Aren’t Really Diets After All
Carnivore Diet (Zero Carb Diet): This diet is the antithesis of veganism. You only eat animal-based products: meat, cheese, milk, and eggs – no grains, no vegetables, and no fruits. It is, in essence, a version of the Keto diet that prioritizes fat and protein over carbs. Its followers claim that it can fight inflammation and prevent nutrient deficiencies. Scientific research shows that there is simply no benefit to this diet. It is a proven fact that limiting your meat intake can extend your life and improve cardiovascular health. This diet may lead to an increased risk of heart disease, cancer, and overall risk of death because of its limitations7 8. On the upside, however, it may lead to weight loss since proteins increase the body’s thermic effect (the energy it takes to digest food).
Paleo Diet: The Paleo diet is the cousin of the Carnivore Diet. In addition to meat, you can eat fish, vegetables, fruits, nuts, and seeds. You must avoid grains, dairy, processed foods, beans, legumes, and sugars. Studies have shown that including these additional foods is effective in weight loss and, at the same time, improves blood markers and drops blood pressure9. Others argue that not including whole grains in a diet will result in chronic diseases such as heart disease and diabetes.
Dessert with Breakfast Diet: This has to be my favorite one that I came across. Who doesn’t love eating something sweet any time of the day? Surprisingly enough, a 2012 study found that people who ate high-carb, high-protein meals that included dessert lost more weight (and kept it off) than those who did not10. On the other hand, sugar is addictive, and we all know too much is not healthy for you. The more you eat, the more you crave, and the more fluffy you become.
The Diets You Should be Following
DASH Diet: The DASH diet is specifically patterned to help normalize blood pressure and prevent hypertension. Recommended by the National Institute of Health, this clinical-trial-based diet found that blood pressure lowered and the participants’ cholesterol (lipid) profile improved when they ate plant-rich, low-fat foods. The diet emphasizes daily intake of fruit and vegetables, grains, legumes, nuts, seeds, lean meat, low-fat dairy, poultry, and fish. It keeps salt, saturated fat, and sugars relatively low. Participants must limit their eating quantities, and positive results are only possible when people stick to the eating plan.
Mayo Clinic Diet: Everyone has heard of the Mayo Clinic – a renowned health care company that provides education, healthcare, and research. They run what is one of the best hospitals in the United States and employ thousands of scientists and healthcare professionals. Suffice it to say they are a trusted source of information. Regarding dieting, they encourage restricting refined grains, sugary foods, and processed meats. Their diet focuses on eating to a particular caloric intake rather than what you eat. Each individual’s need determines the meal plans and example meals. You can find information on their weight loss program on their website and sign up for a free diet assessment here; however, there is a cost – the plan costs $65 for the first 13 weeks of access.
Image: Galina Afanaseva
Mediterranean Diet: Now, I’m not just promoting this diet since my family comes from the Mediterranean area. In reality, there is no real diet called a Mediterranean diet. It’s just a term that came about when talking about the eating patterns of the people in the Mediterranean area who have the longest life expectancies in the world. Clearly, they are doing something right. This way of eating is rich in heart-healthy foods. They focus on fresh, whole foods with a high intake of fruits, legumes, nuts, olive oil, and vegetables. Meats, poultry, and seafood are kept to a minimum, as are sweets. Dairy intake is moderate in the form of yogurt and cheese. It is important to remember that although this eating style does improve health markers (blood pressure, cholesterol) and lower the risk of cardiovascular disease, eating is not the only thing people in this region do differently. They also tend to spend a lot of time outdoors and walking from place to place, which also plays an essential role in one’s health. Exercise aside, a study published in the American Journal of Clinical Nutrition found that a Mediterranean-style diet can reverse symptoms of diabetes and cardiovascular disease11.
Nordic Diet: Like the Mediterranean region, the Nordic countries have specific eating habits that are just as healthy. They focus on home-cooked foods, and the intake of processed foods is limited. The diet includes fruits, legumes, meat, nuts, seafood (particularly oily fish), seeds, vegetables, whole grains, herbs, and spices. Much research has been done on the Nordic diet, finding an improvement in blood cholesterol and blood pressure markers. If adhered to, randomized controlled trials showed that the participants did lose weight.
The Final Word
One thing has become quite clear in reading about diets – it all boils down to what and how much you consume. Research consistently shows that your health markers improve when you eat natural, plant-based foods. A well-balanced eating pattern will lower the risk of various diseases, including heart disease and diabetes. Choose whole and unprocessed foods to help with overall weight management. In addition, eat moderate amounts and do not overeat.
Nutrition isn’t a perfect science; it does not have everything figured out. For example, many diets recommend eliminating certain foods high in things like saturated fats, yet yogurt and cheese (both high in saturated fats) are good for you in moderate amounts. What is important is that you talk with a nutritionist or doctor to figure out what is best for your body and the goals you want to achieve. Don’t forget that it can be challenging to separate fact from fiction regarding diets. What works for one person may not work for you. No two individuals are the same, and no two individuals will respond to one way of eating in the same way. Find what works best for you, but focus on what food groups nutritional health experts recommend. The most important thing is to be healthy – whatever size: fluffy, not-so-fluffy, or other.
1 https://pubmed.ncbi.nlm.nih.gov/16685046/
2 https://pubmed.ncbi.nlm.nih.gov/26853923/
3 https://pubmed.ncbi.nlm.nih.gov/23695207/
4https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/1710093
5https://www.sciencedirect.com/science/article/abs/pii/S0091743516304479?via%3Dihub
6 https://academic.oup.com/jn/article/149/4/667/5320848?guestAccessKey=e5c18e47-598e-420e-9853-d74da51189dd
7https://pubmed.ncbi.nlm.nih.gov/23736950/
8 https://pubmed.ncbi.nlm.nih.gov/14525683/
9 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2724493
10 https://www.sciencedirect.com/science/article/pii/S0039128X11003515?via%3Dihub
11 https://pubmed.ncbi.nlm.nih.gov/28278309/
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-4,271,670,750,395,999,700 | HomeHealthMigraines: Natural Remedies, Symptoms, Causes, Prevention, and Cure
Related Posts
Migraines: Natural Remedies, Symptoms, Causes, Prevention, and Cure
Migraines are a debilitating neurological condition that affects millions of people worldwide. They can cause severe pain, nausea, vomiting, and sensitivity to light and sound, among other symptoms.
READ MORE: No More Chemicals: Discover the Benefits of Home Remedies
While migraines can be managed with medication, there are also natural remedies that can help prevent and alleviate their symptoms. In this article, we will explore the causes, symptoms, prevention, and cure of migraines, as well as natural remedies that may help.
What are migraines?
Migraines are a neurological condition characterized by severe headaches that are often accompanied by other symptoms, such as nausea, vomiting, and sensitivity to light and sound. The pain is usually on one side of the head and can last for several hours or even days. Migraines are more common in women than men and can start at any age, although they often begin in adolescence or early adulthood.
Symptoms of migraines
The symptoms of migraines can vary from person to person, but some of the most common ones include:
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• Intense, throbbing pain on one side of the head
• Sensitivity to light and sound
• Nausea and vomiting
• Dizziness or lightheadedness
• Visual disturbances, such as seeing flashes of light or blind spots
• Tingling or numbness in the face or limbs
Causes of migraines
The exact causes of migraines are not fully understood, but there are several factors that are believed to contribute to their development. These include:
• Genetics: Migraines tend to run in families, suggesting that there may be a genetic component to their development.
• Hormones: Women are more likely to experience migraines than men, and many women report that their migraines are linked to their menstrual cycle.
• Triggers: Certain foods, drinks, and environmental factors, such as stress or changes in weather, can trigger migraines in some people.
Prevention of migraines
While it may not be possible to completely prevent migraines, there are several things you can do to reduce your risk of experiencing them. These include:
• Avoiding triggers: If you know that certain foods, drinks, or environmental factors trigger your migraines, try to avoid them as much as possible.
• Getting enough sleep: Lack of sleep can trigger migraines in some people, so it’s important to make sure you’re getting enough rest each night.
• Managing stress: Stress is a common trigger for migraines, so finding ways to manage stress, such as through meditation or exercise, can help prevent them.
• Eating a healthy diet: Eating a balanced diet that includes plenty of fruits, vegetables, and whole grains can help reduce your risk of migraines.
Natural remedies for migraines
While medication can be effective in managing migraines, there are also several natural remedies that may help prevent and alleviate their symptoms. Some of these include:
• Magnesium: Taking a magnesium supplement may help prevent migraines, as some studies have found that people who suffer from migraines often have low levels of magnesium.
• Ginger: Ginger has anti-inflammatory properties that may help reduce the inflammation that can cause migraines. Drinking ginger tea or taking a ginger supplement may help alleviate migraine symptoms.
• Riboflavin: Riboflavin, also known as vitamin B2, may help prevent migraines by improving mitochondrial function. Taking a riboflavin supplement may help reduce the frequency and severity of migraines.
• Coenzyme Q10: Coenzyme Q10 is an antioxidant that can help improve mitochondrial function and reduce inflammation, both of which may help prevent migraines. Taking a coenzyme Q10 supplement may help reduce the frequency and severity of migraines.
Finding a Migraine Cure
Migraines are a complex neurological condition that affects millions of people worldwide. While they can be managed with medication and natural remedies, finding a cure for migraines has been a challenge. However, recent research has shed light on potential cures that offer hope to those who suffer from this debilitating condition.
The Challenges of Finding a Migraine Cure
Migraines are a multifaceted condition, and there are many factors that can contribute to their development. This complexity has made finding a cure for migraines difficult. Additionally, migraines are a highly individualized condition, with different triggers and symptoms for each person. This variability has made it challenging to develop a one-size-fits-all cure.
Promising Migraine Cures
Despite these challenges, there have been some promising developments in the search for a migraine cure. Here are some of the most exciting potential cures for migraines:
• CGRP inhibitors: CGRP is a protein that is believed to play a role in migraines. CGRP inhibitors are a class of drugs that block the action of CGRP, which can help prevent migraines. These drugs have shown promising results in clinical trials and are currently available by prescription.
• Botox: Botox is a type of toxin that is commonly used for cosmetic purposes. However, it has also been found to be effective in preventing migraines. Botox injections can be given to the head and neck to help prevent migraines, and they have been shown to be safe and effective in clinical trials.
• Nerve decompression surgery: Some people with migraines may benefit from nerve decompression surgery. This surgery involves releasing pressure on the nerves that can cause migraines, and it has been shown to be effective in reducing the frequency and severity of migraines in some patients.
Conclusion
While there is still no cure for migraines, there are many effective treatments that can help manage and prevent migraines. Medication, natural remedies, and lifestyle changes can all be effective in reducing the frequency and severity of migraines. Additionally, there are several promising potential cures for migraines, such as CGRP inhibitors, Botox, and nerve decompression surgery. If you suffer from migraines, it’s important to work with your healthcare provider to find a treatment plan that works for you. With the right treatment, it is possible to manage and even prevent migraines, and to live a full and active life.
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2,765,767,723,810,093,000 | ibs medications - IBS Medications
IBS cure Natural IBS cure Treat IBS Naturally irritable bowl syndrome
IBS Medications
The IBS medications currently available may be disappointing. They do not cure the syndrome. Certain medications may relieve IBS pain in the abdomen, constipation or diarrhea, but particularly when both are present at different times, long term treatment and control of IBS requires dietary and lifestyle changes. A complete treatment plan typically includes a combination of therapies, rather than prescription IBS medications alone.
Bavolex Natural IBS Remedy
irritable bowel syndrome (IBS) natural remedy Natural natural IBS cure.
Formulated to Help Support:
• Relieve pain and pressure
• Stop diarrhea and constipation
• Improve digestion
• Stop painful cramps and gas
• Balance the contractions of intestine muscles
• Reduce the feelings of stress and anxiety
• Calm down the nervous system
Great Product
IBS Remedy
-Wormseed- Wormseed detoxifies the intestinal tracts unwanted organisms that are present without eliminating the bacterial flora. It thereby effectively helps reduce occasional constipation and diarrhea.
Doctors may prescribe low doses of anti-depressants for IBS pain. But, certain of the newer anti-depressants like Paxil and Prozac can cause diarrhea. All anti-depressants have side effects such as dry mouth, blurred vision and headache. Zelnorm is one of the prescription IBS medications that has been proven effective for relieving constipation and IBS pain in women, but has not been shown to work in men. It is only recommended for short term use and can cause serious side effects.
-An individuals colon may respond negatively to stimuli such as certain foods or stress -People with IBS frequently suffer from depression and anxiety which can make the symptoms worse.
IBS is due to an abnormal, exaggerated response of the muscles of the intestinal walls. It is not clear why some people develop the disorder. Doctors believe there could be a number of factors that may cause IBS - like dietary, psychological, hormonal and genetic factors. There are no prescribed medical tests to determine irritable bowl syndrome. Doctors generally diagnose IBS on the basis of the patient's symptoms and after ruling out various other disorders - such as colon cancer and other abdominal diseases. Diagnostic tests that may be done to rule out other abdominal disorders include blood tests, stool analysis, x-ray and endoscopy. Treatment for IBS is subject to the intensity of the problem and the degree of symptoms.?? Some patients may find consuming particular foods as the cause of their IBS and to such patients, some sort of diet control will help to control the symptoms.?? Adopting a high-fiber diet including fruit and green vegetables, whole-grain breads and cereals will soften the stools and relieve constipation. Avoiding tea and coffee and spicy food and drinking 6-8 glasses of water a day is found to relieve symptoms. Having proper foods and supplements, substituting milk products with soya or rice products, avoiding fresh fruits and vegetables that are high in insoluble fiber and eating frequently smaller quantities of food, can all help to lessen the symptoms of IBS. Many doctors believe that physical stress and mental strain can often aggravate IBS symptoms. They consider stress management should form part of treatment. This can entail counseling, stress reduction and relaxation therapies, some simple exercises and adequate sleep. For some, mere dietary and lifestyle changes may not be enough to get rid of symptoms and medical treatment may become necessary. Generally anti-spasmodic drugs are prescribed by doctors to lessen the involuntary muscular contractions.?? This will also help to stop diarrhoea and relieve pain. The doctor may advise you to take mild laxatives if you are suffering from constipation or have difficulties in moving bowels. The use of antispasmodic drugs may help patients, especially those with cramps or diarrhea. Antispasmodics are of two groups- neurotropics and musculotropics. Neurotropics, act at the nerve fibre but can also affect other nerves and cause side effects. Musculotropics act directly at the smooth muscle of the gastrointestinal tract, relieving spasm without affecting normal gut motility.
Do You Have IBS? Functional bowel disorders such as constipation, heartburn, diarrhea, abdominal pain are forms of IBS. Approximetly one in 5 americans and more than 20% of the population have symptoms of IBS. In addition, IBS makes up around 20 50% of visits to a digestive specialists.
Some IBS medications are heavily marketed and highly advertised. IBS has become a fairly common diagnosis, affecting as many as one in five people at some point in their lives. It is important to remember that, while many IBS medications are safe for temporary use, some may worsen symptoms and/or cause other problems when used for long periods of time. In order to relieve IBS pain, many people turn to alternatives like chiropractic or hypnotic therapies. When stress is an issue, stress management techniques may be effective for relieving IBS pain and other symptoms. Regular exercise may be an effective alternative to IBS medications. Exercising stimulates the production of endorphins in the brain, which block pain and improve mood. And, of course dietary changes may be the most effective.
3. Think Small Feasting on a five-course spread can tax your intestines and lead to cramping and diarrhea. So eat smaller but more frequent meals, say, six mini-meals spread throughout the day rather than the standard three squares or switch to smaller portions.
There are millions of people who suffer from Irritable Bowel Syndrome. If you are over the age of 30 you have probably experienced some form of gas, bloating, heartburn and abdominal pain.
6. Capitalize On Carbs Fill your diet with complex carbohydrates such as pasta, rice, fruits, and vegetables, while trimming the fat as much as possible. Fatty foods, especially meats, can send your intestinal into spasms.
-Researchers have a strong theory that IBS may be caused by a bacterial infection in the GI tract. There are some healthy ingredients which deliver and maintain a full functioning, optimal running digestive system. Four of these are listed below.
1. Mind Your Dining Take your meals without distraction, worries, and interruptions. The idea is to focus on your eating. If your attention is drawn to something besides your food, you can develop indigestion, gas, bloating, and cramping.
Irritable bowel syndrome (IBS) is also known as colitis or spastic colon. This syndrome is a chronic intestinal disorder characterized by abdominal pain and cramps, constipation, and diarrhea. Flare-ups can usually be traced to something you have eaten. Among the most common triggers are milk and dairy products, spicy foods, fatty foods, and gas-producing foods such as beans, broccoli, cabbage, and cauliflower. The frequency and intensity of flare-ups can vary greatly from one person to the next. Some folks barely notice their symptoms, while others must cope with crushing pain as well as urgent trips to the bathroom. Here are some tips that you can consider to adopt to get relief fast.
4. Takes Notes Keeping a food diary can help you detect the dietary sources of your irritable bowel syndrome flare-ups. If you begin to notice a pattern pointing to a potential culprit, eliminate the particular food from your diet and see if your symptoms disappear as well.
When IBS pain is related to constipation, doctors may recommend over the counter IBS medications, such as laxatives. But, taking laxatives may lead to diarrhea, can be habit forming and become ineffective after continued use. Aloe is a recommended herbal remedy. Irritable bowel syndrome with constipation may be relieved with products containing aloe, but may worsen diarrhea. A product containing slippery elm may be an effective herbal remedy. Irritable bowel syndrome with constipation or diarrhea may be relieved by using a product containing slippery elm. It has been used historically by native peoples to treat both constipation and diarrhea.
Natural Remedy
What People Said About Bavolex IBS Cure
"i used to feel like i needed to go to bathroom all the time. doctor did endoscopy of my colon but didn't find anything. he said it's ibs. after a few months of struggling I decided to try bavolex. after a week I felt noticeable relief. two months later I don't have any IBS symptoms at all! thank you for this great product!" Georgia from LA
IBS treatment
2. Learn To Relax Since stress can make the irritable bowel syndrome even worse, learning to take it easy may ease your discomfort. In particular, if you are a Type A personality, aim for an A-minus instead. Relaxation tapes can help, as can books on coping and stress-management techniques.
IBS does affect millions of Americans, but it can be resolved in a way that is safe and natural. Because of this there isn't any need to be uncomfortable and embarrassed about any (IBS) symptoms.
Patsy Hamilton has more than twenty years experience as a healthcare professional and currently writes informational articles for the Digestive Disorders Guide. Read more at http://www.digestive-disorders-guide.com.
Irritable bowel syndrome (IBS) is a disorder of the large bowel better known in medical circles as colon. Irritable bowel syndrome is not a disease. It can be defined as functional disorder, meaning that certain organs do not function correctly. IBS is a health condition when the bowel overreacts even to a mild stimulus, such as eating or the presence of gas. The nerves and muscles in the bowel appear to be extra sensitive in people with IBS. Muscles may contract too much when you eat.?? Some of the major symptoms of IBS are acute abdominal pain, flatulence, irregular bowel movements, white color mucus in the stool, persistent urge to move bowels, diarrhea and/or constipation, occasionally heartburn, nausea and vomiting. Women with IBS often have more pronounced symptoms during their menstrual periods. IBS generally occurs in persons between their 20s and 30s, and is said to affect more women than men and the intensity of the problem also varies from patient to patient. But IBS does not damage the colon or other parts of the digestive system nor does it lead to other health problems.
DISCLAIMER
The information provided herein should not be construed as a health-care diagnosis, treatment regimen or any other prescribed health-care advice or instruction. The information is provided with the understanding that the publisher is not engaged in the practice of medicine or any other health-care profession and does not enter into a health-care practioner/ patient relationship with its readers.
When diarrhea is present, recommended over the counter IBS medications may include an anti-diarrhea product like Immodium or Kaopectate. These products may reduce diarrhea, but researchers have found that they do not relieve other symptoms such as IBS pain and bloating. Both aloe and slippery elm have an anti-inflammatory effect which may relieve IBS pain. Bloating and gas may be relieved by antacids, anti-gas products or an herbal remedy. IBS medications made from herbs and botanicals often include several ingredients (several different herbs and plants) in an attempt to relieve all of the symptoms of IBS. Gastronic Dr. is one such herbal remedy.
5. Don't Forgo Fiber Perhaps the last thing you would think of feeding an angry bowel is fiber. Yet a high-fiber diet can actually help relieve the intestinal spasms of irritable bowel syndrome by slightly distending the colon it may also relieve constipation, another irritable bowel syndrome, by retaining water in the stool. To increase your fiber intake, it is recommended to addmore whole-grain breads and cereals and more fresh fruits and vegetables to your diet. You can also take a fiber supplement. Be aware that eating more fiber can temporarily aggravate irritable bowel syndrome by producing more gas. This usually subsides in just a few weeks.
IBS is characterized by bloating, cramping, diarrhea, constipation and abdominal pain. IBS as you probably know can cause a great deal of discomfort and distress, but doesn't permanently harm the intestines, and in most cases doesn't lead to any serious diseases. A lady named tonya who recently revealed how embarrassing her IBS has become stated that her digestive problem has escalated. An all time high has been acheived in the population for suffering with diarrhea, gas, bloating and abdominal pain. Do you also suffer from IBS?
What Are The Symptoms Of IBS? -Bloating -Abdominal pain -Watery Stools -Hard or difficult to pass bowel movements What Causes IBS?
7. Be Aware Of Dairy Many people develop twitchy bowels because they cannot digest lactose, the sugar in milk. You might try to give up milk and milk products for a while to see if your symptoms clear up. If you just cannot bear the thought of sitting down to a bowl of dry cereal in the morning, consider taking a lactase supplement instead. You can purchase this product in grocery and drugstores.
-Benonite clay- A completely safe clay that absorbs water and forms a gel and thereby works as a mild laxative. The water that is absorbed captures the toxins into a gel and then the body carries them out.
-Black Seeds- Contain high amounts of dietary fiber and have been widely used to promote bowel health. -Turkey rhubarb- Has powerful properties as an intestinal cleanser. This herb considerably reduces occasional constipation and small dosages have been used for hundreds of years to assist digestion.
It is important to remember that if you have symptoms of IBS, you should see your doctor. IBS pain and other symptoms are similar to the symptoms of more serious health conditions. You should not attempt to treat IBS pain on your own, chronic constipation or continuous diarrhea should be reported to your doctor. For more information about IBS and other digestive problems, visit www.digestive-disorders-guide.com.
Researchers haven't found any specific causes for IBS. Studies indicate that people who suffer from IBS have a large bowel that is particularly sensitive and reactive to certain foods and also stress. Here are three hypothetical causes of IBS..
Raymond Lee is one of the foremost experts in the health and fitness industry and is the Founder of Bodyfixes Group specializing in body health, muscle development and dieting. He is currently the author of the latest edition of "Neck Exercises and Workouts." Visit http://www.bodyfixes.com for more information.
Learn More about Natural Gout Remedy
What is IBS? IBS, which stands for Irritable Bowel Syndrome, is a chronic disorder in which the bowel doesn t work, as it should. The bowel is part of the digestive system that makes and stores stools. The large bowel, or colon, links the smaller bowel to the rectum and anus, (back passage), and seems to be the starting position of most of the symptoms of IBS. In the...
One in five Northern Americans has irritable bowel syndrome (IBS), which makes it one of the most common disorders diagnosed today. Irritable bowel syndrome usually hits the person around age 20 and is more common among women than in men. Irritable bowel syndrome is actually a disease, although doctors consider it a functional disorder. However, even though the syndrome can cause considerable...
One symptom of bowel dysfunction is constipation. Constipation is the irregular or the incomplete emptying of the bowel. In these days of diet and nutritional awareness, most people would probably increase their fibre intake to remedy a sluggish bowel. Most people are aware that wholemeal bread contains more fibre than white bread. This type of fibre is called insoluble fibre. Whilst reducing...
The IBS medications currently available may be disappointing. They do not cure the syndrome. Certain medications may relieve IBS pain in the abdomen, constipation or diarrhea, but particularly when both are present at different times, long term treatment and control of IBS requires dietary and lifestyle changes. A complete treatment plan typically includes a combination of therapies, rather...
Irratable bowel syndrome is a gastro intestinal condition that affects 10 to 20% of the entire population in the US. Specialists have not found a precise triggering factor for this medical condition, but they all have agreed on the symptoms: diarrhea, constipation (they can be present either separately or even together), abdominal pain and a bloating sensation throughout the day. Recent...
zelnorm studies | symptoms of ibs | ibs medications | ibs c treatment | controlling ibs | what causes ibs |
(c) 2019 ibsmedication.info
Contact Us | About Us | Privacy Policy | RSS Feed | ibs medications | {
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-7,028,865,602,082,679,000 | Cremes
How to Improve Your Bone Strength
Everyone knows our ancestors didn’t wear sunscreen. And of course they weren’t afraid of going out in the sun. In fact, they saw it as a source of life. But did you know it was making them stronger? Right down to their bones… A study published in the Lancet found that...
Fortified Junk Food is NO WAY to get your Vitamins
You see it almost everywhere these days — energy drinks that advertise the wonder of B vitamins. And they all claim to give you the energy boost to get you through your day. Sadly, it's a big marketing ploy. The quick energy in these drinks usually comes from their...
EVERYONE Needs Magnesium
Magnesium is a co-factor in over 350 enzymatic reactions in the body. It is necessary for the transmission of nerve impulses, muscular activity, heart function, temperature regulation, detoxification reactions, formation of healthy bones and improving insulin...
Do You Have Trouble Sleeping?
Melatonin is a hormone secreted by the pineal gland in your brain. It helps regulate other hormones and maintains the body's circadian rhythm. The circadian rhythm is an internal 24-hour “clock” that plays a critical role in when we fall asleep and when we wake up.... | {
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-2,181,549,235,215,165,400 | Face Anxiety Together: Helpful Tips to Assisting Someone With Anxiousness
Face Anxiety Together: Helpful Tips to Assisting Someone With Anxiousness
Anxiousness has forms that are many in reality, there are five sub-categories, each presenting a variation that is different of many signs. Over 44 million grownups in America experience some type of anxiety. Assisting some body with anxiety may be hard, but you can find a things that are few may do to simply help them deal with the day-to-day studies of anxiety.
Keep Yourself Well-informed
This article, you’re already working on this step if you’re reading. Congratulations!
Do a little research on line, contact services that are professionalthere are helplines available through many psychiatric and wellness companies) and become acquainted with the outward symptoms of every possible type of anxiety.
In accordance with psychological state America, the subcategories of anxiety include…
panic attacks
obsessive-compulsive condition
post-traumatic anxiety condition
phobias
generalized anxiety problems
General signs to look for in a family member you|one that is loved think might be struggling with anxiety include…
emotions of impending doom
elevated heart price
perspiring, chills and/or shaking
difficulty breathing
nausea
upper body or abdominal pain
hassle
vertigo
fainting
tightness when you look at the throat and/or difficulty swallowing
The issue that is overarching anxiety it causes panic, fear and uncertainty. These emotions make it hard for your beloved making use of their anxiety and deal with individuals.
Encourage Them
Individuals experiencing anxiety an arduous time seeing|time that is difficult the good. If they enhance or make progress inside their daily life, they won’t be able to see this. Rather, they will concentrate on the negative. With this good reason, it really is crucial that you inform them once you notice a modification inside their behavior or an enhancement within their daily life. Be happy with them, and demonstrate to them just how proud you might be.
Helping some body with anxiety encompasses all aspects of interaction from spoken praise to body gestures. Below are a few things that are key keep in mind whenever you’re wanting to encourage somebody with anxiety:
Keep your facial expressions good. Anxiety causes people to interpret even the littlest negative expressions within the worst method feasible.
Prevent the expressed word“don’t.” Also for some body perhaps not struggling with anxiety, a statement like “don’t sweat the small stuff” or “don’t allow it get to you” could make them feel just like they’re doing something very wrong. “Don’t” is just a negative term that will enhance anxiety.
Remind them that they’ve won this battle before. “You can over come this, as you did (insert past occasion here).” Approaching the problem in this way reminds them that the issues they’re facing won’t cbd oilrank last forever, and they’ll allow it to be through this test too.
Be Accessible
Everybody else, no or anxiety, seems better whenever they realize that they usually have some body who’s always here for them. People who have anxiety believe it is and that is helpful comforting too. Listed below are a things that are few can take to:
Act as here whenever you can. Inform them you can be contacted by them at any time, irrespective of where you may be.
Offer to accompany them for their health or doctor professional’s office and to many other appointments.
Spend because time that is much them as you can (and encourage relatives and buddies to do this also).
Anxiety can be debilitating in certain cases, and someone that is knowing here for them through the worst plus the most useful will make a big difference.
Pay attention without Judgement
Playing somebody with anxiety without judging them on what they behave or respond to situations is simply as crucial as being readily available for them. In reality, hand that is go hand. Lending your ear, as the saying goes, is crucial, regardless of if they repeat the fears that are same and over. Referring to their experiences helps them face their worries and determine hurdles in their day-to-day life.
It could be simple to provide recommendations that seem helpful but aren’t. When you’re responding to somebody with anxiety…
avoid statements like “just deal” and “everything’s likely to be fine”;
be empathetic;
usage expressions like “That’s terrible, I’m sorry” and “It’s ok to believe that way”;
avoid comparing your anxiety to theirs (Comparing anxiety trivializes their discomfort);
Like you’re going to use a situational comparison, refocus the if you feel discussion instead; and
assist them to look at good aspects of the specific situation.
This method acknowledges and validates their emotions without making them feel they’re failing in some manner.
Get Active
Workout and a lifestyle that is healthy two normal combatants to anxiety. In accordance with Julie Warren, in her own article “Does Exercise Release a Chemical into the mind?”, workout releases different chemical substances in mental performance like endorphins, serotonin and brain-derived neurotrophic factors, a neurotransmitter that decreases the outward symptoms of despair and enhances mind health insurance and memory.
Make use of these normal chemical compounds by taking your friend with anxiety out for exciting activities and sometimes even one thing as simple as a walk exterior. as well as the normal mind chemical substances, these tasks produce new memories that assistance individuals with anxiety cope when things have tough. Escaping . and about can also be a good alternative to something that is saying like “calm down.” The workout shall assist them settle down without you having to say this.
a healthy eating plan and|diet that is healthy life style, which includes eating and sleeping well, is another element of remaining active. Don’t forget to avoid alcohol; it may appear like an answer, nonetheless it only produces experiences that may be negative.
Forgive and Forget
This will be possibly the hardest of the many suggestions listed. Individuals who have problems with anxiety could be fast to discomfort, could possibly get and that is defensive aggressive, and may tend to interpret terms and actions being a individual assault. They can’t get a handle on their feelings or reactions that are immediate. It could be simple to react to their irritation and hostility in type, but try not to ever respond that way. Alternatively, forgive them, and allow them to understand that you comprehend. Forgive them with regards to their outbursts, and accept them for who they are, because they are.
Try not to ask “what did I do incorrect?” because they frequently won’t find a way to respond to This – and this relevant concern will make them feel more serious. If you feel that you’re having problems forgiving them, compose them a page. Reading gives them time and energy to think on the way you feel without the sense of conflict.
Conclusion
Managing anxiety is challenging sufficient and never have to cope with the Loneliness, misunderstanding and judgement that accompany it. Helping some body with anxiety takes a lot of persistence, however if you stick to the above advice and tips, you might provide some body the gift of relationship and delight.
Did you know somebody who is affected with anxiety? Can there be anything you are doing that helps them cope with the difficulties of everyday life? Share when you look at the responses! | {
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2,036,826,541,273,297,400 | Tips for Avoiding Muscle Injuries
Tips for Avoiding Muscle Injuries
Muscle injuries are an all-too-common problem for many of us. They can range from a simple strain to a crippling tear that takes months to heal. Injuries to our muscles can be caused by countless things, ranging from overuse to poor technique to inadequate warm-up, among other factors. In this post, we will provide some useful tips that can help you avoid muscle injuries, so you can stay healthy, strong and pain-free.
Warm up properly
Before starting any form of physical activity, make sure that you have warmed up your muscles adequately. This means performing a few minutes of gentle movements such as light jogging or stretching, in order to get your heart rate up and improve blood flow to the muscles. Doing so can help prevent sudden movements that can cause injury, such as a sudden pull or tear.
Use proper technique
In addition to warming up, it is important to use proper technique when exercising or engaging in other physical activities. This means paying attention to things such as posture, joint alignment, and body mechanics to ensure that you are moving in a safe and effective manner. If you are unsure about proper technique, it is worth consulting a trainer or coach who can provide guidance and feedback.
Build up gradually
Another key to avoiding muscle injuries is to build up your exercise routine gradually. This means starting with lower-intensity activities, and gradually increasing the intensity and duration of your workouts over time. This allows your muscles and joints to adapt to the new demands you are placing on them, reducing the risk of strain or injury.
Take Rest
While it is important to push ourselves to improve our fitness, it is equally important to give our bodies time to rest and recover. This means avoiding overuse injuries by alternating different types of activities, or by taking regular rest breaks during endurance activities. And if you do feel something pull or strain, it is best to stop immediately and seek medical attention.
Eat a balanced diet
Finally, another important factor in avoiding muscle injuries is to eat a well-balanced diet. This includes consuming plenty of protein to support muscle growth and repair, as well as adequate amounts of vitamins and minerals to support overall health and immune function. It is worth consulting a registered dietician or healthcare professional to determine the right balance of nutrients for your individual needs.
Conclusion
Muscle injuries can be frustrating and painful, but by using the tips outlined in this post, you can help reduce your risk and stay healthy for years to come. Remember to warm up, use proper technique, build up gradually, take rest, and eat a healthy diet, and you'll be well on your way to avoiding muscle injuries and achieving your fitness goals. And if you do experience a muscle injury or pain, make sure to seek medical attention right away to get the help and support you need. Are you looking for a primary care provider in Plant City? Contact Vital Eagles Healthcare today to book an appointment.
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4,102,685,067,979,611,000 | Fri. Sep 29th, 2023
Anemia
Anemia, a common yet underestimated health problem, affects many people worldwide. It is characterized by a deficiency in red blood cells or hemoglobin. Red blood cells (RCBs) are critical in carrying oxygen through the body. It empowers your cells and gives you energy. Due to a lack of adequate RCBs, your body may not be able to function correctly. You must note that some symptoms of anemia are short-term, while others may be long-lasting. If not treated timely, anemia can be life-threatening.
To ensure you are healthy, you must get a routine body check at least once every six months. If you cannot visit a nearby diagnostic center, you can look for a lab that offers sample collection services at home. Healthcare providers may do home collection blood tests and other necessary tests to monitor your health and provide effective treatments.
Types of Anemia
Many types of anemia are there, each causing a drop in red blood cells. Some of these are:-
• Pernicious Anemia: Due to the deficiency of vitamin B12, an autoimmune condition called pernicious anemia develops. It prevents the absorption of vitamin B12 in the body.
• Iron-deficiency Anemia: As its name suggests, iron deficiency anemia is caused by a lack of iron in the body.
• Megaloblastic Anemia: If your body does not get adequate levels of vitamin B12 or vitamin B9 (folate), you may struggle with megaloblastic anemia.
• Sickle Cell Anemia: It is often caused by a mutation in the HBB gene. It may lead to the production of abnormal hemoglobin, causing the breakdown of RBCs.
• Hereditary Spherocytosis: It results from the defects in genes that control the structure of red blood cell membranes. It causes RBCs to become fragile and spherical and leads to their premature destruction.
• Hereditary Elliptocytosis: In this condition, RBCs become elliptical due to genetic mutation.
Who Is at a Higher Risk to Develop Anemia
If you have developed anemia, it is often said that you are anemic. It means that you have symptoms of anemia, like dizziness. Anemia affects people in different ways, such as:-
1. Newborns
Some little ones are born with low RBCs. They are at high risk of suffering from anemia. You may note that some of these babies do not need medical treatment, while others with severe anemia require proper treatments.
2. Infants
Infants may struggle with iron deficiency if they consume more solid food. Breast milk or formula iron is easily absorbed in an infant’s body compared to solid food. Thus, mothers should ensure their children consume solid food only in the required quantity.
3. Children
Between birth and two years of age, children grow and develop faster; hence, they need more iron. If children have iron deficiency and anemia, they may face developmental issues, such as fewer motor skills and learning issues.
4. Pregnant Women
Iron deficiency is common among pregnant women. It may increase the risk of health risks and complications, such as premature birth or newborns with less birth weight.
5. People Aged 65 Years or More
People aged 65 or above may have poor diets and suffer from chronic diseases. It may increase the risk of anemia, leading to more health problems, such as heat conditions and weaknesses. It may restrict a person’s mobility and affect his lifestyle.
6. People With Chronic Conditions
If you struggle with autoimmune diseases or cancer, you risk developing anemia.
Symptoms of Anemia
You must note that symptoms of anemia may vary from one individual to another. However, some of the common symptoms are mentioned below:-
• Fatigue
• Shortness of breath
• Dizziness
• Fast or irregular heartbeats
• Pounding or whooshing sound in the ear
• Pale or yellow skin
• Headache
• Vision problems
Diagnosis & Treatment
The expert healthcare provider may listen patiently to your health symptoms. Occurs due to fewer red blood cells in the body. They may do diagnostic tests to monitor your health to check if your body has adequate RBCs. Some of these tests include:-
1. Red Blood Cell (RBC) Count
This test is used to measure the levels of RBCs in your blood. Red blood cells help carry oxygen from the lungs to every cell in the body. The RBC test helps in diagnosing disorders like anemia. An increase or decrease in RBC count indicates you are unwell.
2. Complete Blood Count (CBC)
This test helps to monitor your overall health. The CBC test can detect various disorders affecting blood components, such as and infections. The test measures the total number of white and red blood cells.
If you cannot visit the nearby diagnostic center, no worries. Some centers provide home collection services, wherein healthcare providers may do blood test sample collection from home and provide quick delivery of medical results. After monitoring your health, they may provide effective treatments, ensuring you are safe and healthy.
Bottom Line
Anemia is a common health problem and should not be underestimated. It can be developed among people of all age groups. You must seek immediate medical attention if you experience any unusual health symptoms. Some common symptoms include pale skin, dizziness, headache, and vision problems.
Look for a leading center in India if you notice any of the above-mentioned symptoms. Look for a center which offers reliable services, like home collection, ensuring patients feel comfortable and satisfied. This way, you may get diagnosed and treated effectively with the precise home collection blood test
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859,007,263,153,039,700 | Loading...
Toggle Health Problems and D
Collegiate Swimmers getting 4000 IU of vitamin D had fewer injuries – March 2013
The Effects of Season-Long Vitamin D Supplementation on Collegiate Swimmers and Divers.
Int J Sport Nutr Exerc Metab. 2013 Mar 8.
Lewis RM, Redzic M, Thomas DT.
Division of Clinical Nutrition, University of Kentucky, Lexington, KY.
The purpose of this 6-month randomized placebo controlled trial was to determine the effect of season-long (September-March) vitamin D supplementation on changes in vitamin D status (measured as 25(OH)D), body composition, inflammation, frequency of illness and injury. Forty-five male and female athletes were randomized to 4000IU vitamin D (n=23) or placebo (n=22). 25(OH)D, bone turnover markers (NTx and BSAP), and inflammatory cytokines (TNF-alpha, IL-6, and IL1-β) were measured at baseline, midpoint, and endpoint. Body composition was assessed by DXA and injury and illness data were collected.
All athletes had sufficient 25(OH)D (>32ng/mL) at baseline (mean: 57ng/mL). At midpoint and endpoint, 13% and 16% of the total sample had 25(OH)D <32ng/mL, respectively. 25(OH)D was not positively correlated with bone mineral density (BMD) in the total body, proximal dual femur, or lumbar spine. In men, total body (p=0.04) and trunk (p=0.04) mineral-free lean mass (MFL) were positively correlated with 25(OH)D.
In women, right femoral neck BMD (p=0.02) was positively correlated with 25(OH)D. 25(OH)D did not correlate with changes in bone turnover markers or inflammatory cytokines.
Illness (n=1) and injury (n=13) were not related to 25(OH)D; however, 77% of injuries coincided with decreases in 25(OH)D. Our data suggests that 4000IU vitamin D supplementation is an inexpensive intervention that effectively increased 25(OH)D, which was positively correlated to bone measures in the proximal dual femur and MFL. Future studies with larger sample sizes and improved supplement compliance are needed to expand our understanding of the effects of vitamin D supplementation in athletes.
PMID: 23475128
Wow: At the start of the trial they all had high levels of vitamin D.
This study probably started in the fall, just after the students had been out swimming during the summer
Even starting with a high blood level of vitamin D, adding more vitamin D helped.
See also VitaminDWiki
1. Faster reaction time
2. Far fewer colds/flus during the winter
3. Less sore/tired after a workout
4. Fewer micro-cracks and broken bones
5. Bones which do break heal much more quickly
6. Increased VO2 and exercise endurance Feb 2011
7. Indoor athletes especially need vitamin D
8. Professional indoor athletes are starting to take vitamin D and/or use UV beds
9. Olympic athletes have used UV/vitamin D since the 1930's
10. The biggest gain from the use of vitamin D is by those who exercise less than 2 hours per day.
11. Reduced muscle fatigue with 10,000 IU vitamin D daily
12. Muscle strength improved when vitamin D added: 3 Meta-analysis
13. Reduced Concussions
See also: Sports and Vitamin D category 262 items
See any problem with this page? Report it (WORKS NOV 2021) | {
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-7,419,722,754,876,791,000 | Introduction
White adipose tissue (WAT) grows by increasing the size and/or number of fat cells [1]. Earlier studies suggested that WAT expands during childhood/adolescence due to a combination of elevated fat cell size and number, whereas in adulthood the increase is solely due to enlargement of pre-existing fat cells as reviewed [2, 3]. This idea has recently been challenged by studies demonstrating that body weight gain or regain over time in adults also involves increases in fat cell number [4,5,6]. The dynamic nature of WAT cellularity has clinical consequences as it may cause the development of two distinct morphology phenotypes, namely WAT hypertrophy with fewer but larger cells or WAT hyperplasia with many small cells [2, 3]. The former has been demonstrated to be the more pernicious type of expansion [1,2,3].
Another aspect of WAT expansion is the ability to mobilize lipids through hydrolysis (lipolysis) of triglycerides in fat cells. Numerous cross-sectional studies have demonstrated that catecholamine stimulated lipolysis is decreased in subjects with excess body fat as reviewed [7, 8]. In one recent prospective study such a defect was found to be an independent risk factor for future body weight gain [9]. Finally, weight cycling with periods of weight loss and regain may influence the development of overweight/obesity in adulthood as discussed [10, 11].
Very little is known about the WAT phenotype in subjects who develop excess body fat early or late in life. In patients with obesity scheduled for bariatric surgery, a higher body mass index (BMI) was observed if they had juvenile as compared to adult-onset obesity [12, 13]. We hypothesized that the mechanisms behind adipose expansion (WAT cellularity, morphology, lipolysis, or body weight fluctuations) are similar between these two forms of overweight/obesity in spite of a higher body fat mass in early onset overweight/obesity. To answer these important questions, we investigated 439 adult subjects where information about their body weight at 18 years of age and their highest/lowest body weight since that time was available. Fat cell size and number (cellularity), morphology (hypertrophy/hyperplasia) and spontaneous (basal) or catecholamine-stimulated lipolysis were determined in abdominal subcutaneous WAT. In addition, body fat distribution was measured.
Research design and methods
Subjects
The subjects were adults examined during 1996 to 2020 and included here for studies of the impact of overweight/obesity onset on WAT. They were asked about body weight at 18 years of age. There is no consensus on how to define adult/late onset of excess body fat. We used 18 years old as a threshold. It marks the end of adolescence in most Western societies and there is usually no important increase in BMI after this age. We included those who made notes on this body weight and also about highest/lowest body weight from 18 years of age and onwards. The current height was used to calculate BMI at 18 years of age and the highest/lowest values from 18 years of age. Based on BMI at 18 years of age and at the laboratory examination they could be classified as being (a) lean on both occasions (BMI < 25 kg/m2, n = 88), (b) overweight or obese on both occasions, termed early onset (BMI ≥ 25 kg/m2, n = 96) or EOO, (c) changing from lean at 18 years to overweight/obese at current examination, termed late onset (n = 255) or LOO (d) or changing from overweight/obese to lean (n = 5). Because the focus was on current overweight/obesity and the last group was considered too small for analysis it was excluded from the study. Other exclusion criteria were severe chronic disorder and type 1 diabetes. Type 2 diabetes was present in 91 subjects and treated with diet, oral antidiabetic agents excluding thiazolidinediones or insulin (in four patients). Twenty subjects with hypertension were on beta-blockers. The reliability of self-reported BMI was validated as follows. During 2012 until 2020 we asked 259 adults who were scheduled for a research examination at our laboratory about current body weight using measures at home. This weight was compared with the examined body weight at the laboratory and used for assessment of the accuracy of home weighing. Additionally, twenty-nine subjects returned to the laboratory for studies not related to the current one with a 2–20-year interval (median 8 years). They were again asked for body weight at 18 years of age to validate the accuracy of this information. The study was approved by the local committee on ethics. It was explained in detail to each subject and written informed consent was obtained.
Clinical examination
The subjects came to the laboratory in the morning after an overnight fast and a venous blood sample was obtained for routine clinical chemistry measures. In 41 subjects we also measured plasma leptin with a commercial kit (Linco Research Inc. ST Charles, MO, USA). Height, body weight and circumferences of waist and hip were determined. This was followed by measures of body composition with dual X-ray absorptiometry (DEXA) using Lunar I DXA, Encore Version 16 SP1 (GE Health Care, Stockholm, Sweden), which is approved by the Food and Drug Administration in USA to measure regional- and total body fat. The android region was defined inferiorly at the pelvis cut line, superiorly by 20% of the distance between neck cut and the pelvis and laterally at the arm cut lines. The gynoid region was defined superiorly below the pelvis cut line by 1.5 times the height of the android region, inferiorly below the superior line by two times the height of the android region and laterally at the outer leg cut lines. Using the CoreScan software (GE Health Care, Stockholm, Sweden) to analyze DXA measurements, the amount of visceral adipose tissue (EVAT) was estimated in the android region. The CoreScan software uses measurement of total body fat in the android region and estimated subcutaneous fat in the android region (ESAT) to estimate EVAT with the following formula: EVAT = total body fat in the android region – ESAT. EVAT estimation has a very high concordance (r2 = 0.96) with measurement of visceral adipose tissue using computed tomography, which is the gold standard method, as described previously [14]. Since both android fat mass and EVAT are valid measures, ESAT could be calculated as total android fat minus EVAT. Additionally, a subcutaneous abdominal fat biopsy was obtained by needle aspiration from the ESAT area. In 215 subjects, a 2 h hyperinsulinemic euglycemic clamp was performed exactly as described [15]. The whole-body uptake of glucose (M) during the last hour of the clamp was determined and related to lean body mass.
Adipose tissue examinations
Isolated fat cells were prepared and incubated in vitro as described [16] for 2 h in the absence (basal) or presence of either the natural catecholamine, noradrenaline, or the synthetic beta-adrenoceptor selective catecholamine termed isoprenaline. Different concentrations of the catecholamines were used in duplicate (10−12 to 10−4 mol/l) and results with maximum effective concentration were used in the analyses. At the end of incubation the medium was removed for determinations of glycerol (lipolysis index) and lipids were extracted from the cells in the incubated sample. The release of glycerol in these conditions is linear with time for at least 4 h. We have discussed in detail the validity of using the present fat cell protocol and glycerol as a lipolysis indicator [17]. There is no consensus on how to express lipolysis rates. Therefore, we used the two most common denominators which are per lipid weight or number of fat cells in the incubated samples. The former expression is not influenced by fat cell size as opposed to the second one. On one aliquot of the isolated fat cells the diameter of 100 randomly selected fat cells was measured. These data were used to determine average lipid weight and size of the fat cells using well established formulas. Details of the method and discussion of its validity have been presented before [18]. The same three technicians performed the fat cell studies throughout the study. The number of fat cells incubated was determined by dividing the total lipid weight of the sample by the mean fat cell weight. The total number of fat cells in ESAT was obtained by dividing ESAT weight with mean fat cell weight. Adipose tissue expands by increasing the size (hypertrophy) and/or number (hyperplasia) of the fat cells. By determining the curve-linear relationship between fat mass and fat cell size the morphology (hypertrophy versus hyperplasia) can be determined as discussed in detail [18, 19]. For ESAT the relationship fits the formula V = (a × m)/(1 + b × m) were V is mean fat cell volume, m is amount of ESAT and a and b are variables obtained by fitting the formula to subject data [18]. The difference between measured fat cell volume and the expected fat cell volume from the mean curve fit is termed delta and indicates the morphology of ESAT as discussed in detail [18]. A positive value (above the line) indicates hypertrophy and a negative (below the line) indicates hyperplasia.
Statistical methods
Values are mean ± SD in text and tables and box plots or individuals in figures. Values for lipolysis were normalized by (10)log transformation. The primary comparison was between all three BMI groups. When this was statistically significant a secondary comparison between the two overweight/obese groups was made. Continuous variables were compared by analysis of variance (ANOVA) as first and unpaired t-test as second comparison. Because we only compared EOO and LOO in second comparison there was no adjustment for multiple comparison. Category variables were compared by Chi-Square. The relative roles of multiple explanatory factors to predict the outcome of a response variable was tested using multiple regression. For clinical variables, these regression models included age, sex, body mass index body mass index at 18 years of age and onset of overweight/obesity. For lipolysis, the regression model included onset of obesity/overweight percentage body fat, waist-to-hip ratio, age, sex and fat cell volume as independent factors. The % variation between two measures of body weight was calculated as net difference divided by mean values times 100. All tests were two-sided and p < 0.05 was considered as statistically significant.
Results
The clinical data are recorded in Table 1. Both overweight/obesity conditions displayed the same type of differences in fasting glucose and triglycerides when compared with always lean subjects. However, EOO were younger and had higher BMI than LOO. The temporal changes in BMI in the two overweight/obesity groups were further analyzed. Delta BMI (current minus at 18 years of age) was 8.7 ± 6.2 kg/m2 in EOO and 10.5 ± 6.0 kg/m2 in LOO (p = 0.004). When delta BMI was divided by observation time (current age – 18) it was 0.58 ± 0.63 kg/m2 /year in early onset and 0.37 ± 0.36 kg/m2/year in late onset (p < 0.0001). Thus, the BMI difference between groups was most likely due to a higher starting value plus greater BMI increase per year during adulthood in those with early onset overweight/obesity. The two overweight/obesity groups differed also somewhat with respect to fasting insulin and HDL-cholesterol. The nature of the differences was further analyzed by multiple regression using a model including sex, age, and BMI, as these factors differed significantly between the two overweight/obesity groups. In the regression model, onset of overweight/obesity did not contribute significantly to the variations between subjects in insulin or HDL-cholesterol (Table S1). As expected, both forms of overweight/obesity displayed decreased in vivo insulin sensitivity, but the level of insulin resistance was not different between EOO and LOO. The occurrence of type 2 diabetes was slightly more frequent in late vs. early onset of overweight/obesity (p = 0.034). On a few subjects we also measured fasting leptin. Values (ng/ml) were 9 ± 3, 47 ± 17 and 65 ± 36 in never overweight/obese (n = 6), LOO (n = 20) and EOO (n = 15), respectively (ANOVA: p-value 0.0002; p-value for LOO vs EOO = 0.04).
Table 1 Clinical characteristics.
We validated self-reported BMI. The current determination of body weight at the laboratory and at home was highly correlated (Fig. 1a, b, r2 = 0.99). There was also very little deviation in the reported BMI at 18 years of age when determined at two different occasions with a median interval of 8 years (Fig. 1c, d). The variation in body weight between the two measures in both validation studies was <1% (Fig. 1b, d). The slopes were near one and intercepts not significantly different from zero in either of the regression analyses.
Fig. 1: Validation of self-reported body mass index (BMI).
figure 1
a Is the relationship between current BMI measured at home and at the laboratory. b Is the variance between home and laboratory measures. c Is the comparison between BMI information at 18 years of age obtained at two occasions. d Is variation between the two reports. Linear regression is shown in (a) and (c) indicating the square of regression coefficients, intercepts and slopes.
Data with body composition are recorded in Table 2. As expected, total body fat mass was increased in both overweight/obesity groups but almost 40% more so in EOO. Waist, hip, and android or gynoid fat depots were larger in EOO compared to LOO, but the two groups did not differ in visceral fat mass or in the waist-to-hip ratio. Also as expected, lean body mass was increased in overweight/obesity and slightly more so in EOO (5%). Taken together these data suggest that higher BMI in EOO than LOO is above all due to larger amounts of lean body mass and subcutaneous WAT.
Table 2 Body composition.
The findings with ESAT are shown in Fig. 2. As expected from the results in Table 2 this fat mass was increased in both forms of overweight/obesity and significantly more so in the early onset form (Fig. 2a). The increased ESAT mass could be explained by a combination of having larger and more fat cells than in the always lean condition (Fig. 2b, c). The increases in both fat cell measures were significantly more pronounced in the early onset form of overweight/obesity. However, in all subjects put together there was a strong positive relationship between the rate of BMI increase over time (current BMI minus BMI at 18 years divided by observation time) and fat cell number or fat cell volume (r2 = 0.21–0.424 p < 0.0001). These relationships were also observed when never overweight/obese, EOO and LOO were investigated separately (r2 ≥ 0.10; p ≤ 0.02). The curve linear relationship between ESAT mass and fat cell volume is depicted in Fig. 2d. Visually, lean subjects tended to be more frequently positioned below the fitted line. The morphology of ESAT was quantified in Fig. 2e showing the delta fat cell volume values. Small but statistically significant differences between always lean and LOO/EOO were observed. The always lean phenotype showed modest hyperplasia (negative mean value) and the two overweight/obesity phenotypes had slight hypertrophy, i.e., positive mean values, but there were no differences in morphology (i.e., delta) between the latter two phenotypes. Taken together the data suggest that the increased growth of WAT is due to similar changes in the cell size and number regardless of early or late onset of overweight/obesity. In EOO, ESAT mass is larger due to a further increase in fat cell volume and number, but the resulting magnitude of slight hypertrophic morphology is almost the same in both overweight/obesity conditions.
Fig. 2: Findings with abdominal subcutaneous adipose tissue (ESAT).
figure 2
a Is ESAT mass. b Is mean fat cell volume. c Is number of fat cells in ESAT. d Is the curve-linear relationship between fat cell volume and ESAT mass. e Is ESAT morphology (delta value) calculated from the results in (d). Values are individual in (d) and box plots otherwise with outliers plotted as individual points. The three phenotypes were compared overall by ANOVA. The two overweight/obesity groups were compared by unpaired t-test. NOO never overweight/obesity, EOO Early onset overweight/obesity, LOO Late onset overweight/obesity.
Lipolysis data are displayed in Fig. 3. It is well known that comparisons between individuals with or without obesity is dependent on how lipolysis is expressed. Thus, when expressed per lipid weight, basal and stimulated lipolysis were lower in the overweight/obese state (Fig. 3a–c). There was, however, no differences between EOO and LOO. When lipolysis was expressed per number of fat cells the basal and stimulated rates were higher in overweight/obesity and for the catecholamines this was slightly more pronounced in EOO (Fig. 3d–f). To further explore the latter difference in lipolysis the overweight/obesity data were subjected to multiple regression using several factors which may independently influence lipolysis (age, sex, total body fat, waist-to-hip ratio, fat cell volume and onset of overweight/obesity) (Table S2). In this model only fat cell volume contributed to the differences in catecholamine stimulated lipolysis/number of fat cells.
Fig. 3: Findings with lipolysis (glycerol release) in abdominal subcutaneous fat cells.
figure 3
ac Is lipolysis expressed per lipid weight. df Is lipolysis expressed per number of fat cells. Lipolysis is (10) log µmoles of glycerol/2 h. Values are expressed as box plots. See legend to Fig. 2 for further details.
To validate the clinical outcome findings at follow up, we constructed multiple regression models using: BMI, BMI increase per year, fat cell size and abdominal subcutaneous or visceral fat mass as dependent factors. As independent factors we put together current age, sex, initial BMI (at 18 years of age) and early/late onset of overweight/obesity. Age, sex, and initial BMI independently contributed (p < 0.0001–0.019) to the variations in current BMI, BMI increase/year and subcutaneous fat (r2 for the whole models was 0.40–0.54). Early/late onset of overweight/obesity had no important contribution in any of these models (p = 0.27–0.59). To further analyze the outcome for visceral fat and fat cell size we excluded early/late onset of overweight/obesity from the models and used all subjects (thus including lean people as well). Age, sex, and initial BMI contributed independently to the variations in visceral fat (p < 0.0001–0.0015; n = 409; r2 for the whole model = 0.11). Initial BMI (p < 0.0001) and sex (p = 0.003) contributed independently to the variations in fat cell size (r2 for the whole model = 0.10; n = 436).
We also examined highest and lowest self-reported BMI after 18 years of age. The difference between these measures were 5.3 ± 3.2, 12.3 ± 6.2, and 13.2 ± 5.5 kg/m2 for always lean, LOO and EOO, respectively (p < 0.000 by ANOVA). However, LOO and EOO did not differ from each other (p = 0.24 by t-test).
We finally made subgroup analyses. Excluding the few subjects on insulin or beta blockers did not impact importantly on the findings. Additionally, all data in the tables and Figs. 2 and 3 were analyzed in men and women separately. The exception was dicotomal variables in Table 1 because of a small number of subjects with indicated disease. Almost all analyses gave similar outcomes in either sex apart from the following: waist-to-hip ratio and visceral fat were slightly higher in males with EOO than LOO (p = 0.002 and 0.02, respectively), the difference in fat cell volume between LOO and EOO in women only reached p = 0.09, the differences in lipolysis between LOO and EOO were only apparent in men (p = 0.03 for noradrenaline and p = 0.055 for isoprenaline).
Discussion
This large study sheds new light on the impact of early or late onset of overweight/obesity on human WAT. Although BMI and total body fat levels were higher in those with the early onset form, despite being younger than those with late onset there was no differences between the two conditions regarding putative cellular mechanisms behind adipose expansion (lipolysis, fat cell size/number or WAT morphology). One possible reason behind the differences could be the observation that there is a steeper increase in body weight in adulthood when excess body fat develops earlier than later in life. The differences in BMI persisted after correction for observation time. Our BMI results are in accordance with previous studies with early/late onset of excess body fat [12, 13].
When analyzing the clinical impact of BMI development, the subdivision into early or late onset of overweight/obesity had no significant impact on the outcome by itself. However, BMI at 18 years of age contributed significantly and independently to the variations in BMI, BMI increase per year, fat cell size and subcutaneous or visceral fat mass at follow up.
Several factors influence BMI. Our data suggest that expansion of subcutaneous WAT is the major cause of the difference between EOO and LOO because visceral fat was similar between these two groups in women and only slightly different in men. A minor difference in lean body mass also contributed to the BMI difference between EOO and LOO. The increased amount of body fat in overweight/obesity, at least in the abdominal subcutaneous WAT is explained by an increase in both fat cell size and number. In absolute terms these values were higher in EOO than LOO, which is likely due to the larger ESAT mass in the former group. Interestingly, the increase in BMI over time from 18 years of age positively correlated with fat cell size/number in all groups. When WAT morphology was determined quantitatively (delta value) only minor differences between the three groups were observed. The two forms of overweight/obesity were characterized by a very similar slight degree of hypertrophy. In those who were always lean, morphology tended to be hyperplastic. This is in accordance with previous results demonstrating a similar distribution of hypertrophy/hyperplasia over the whole range of BMI/total body fat [19, 20]. Therefore we suggest, firstly, that the same mechanisms are operating for expanding fat mass in early and later stages of life and, secondly, that fat mass in adulthood indeed can expand because of increases in fat cell number alongside fat cell size regardless of BMI status when leaving the childhood/adolescent period.
Impaired lipolysis may be a causal factor for development of excess body fat [9]. As demonstrated previously [21] the outcome of fat cell lipolysis studies in conditions of excess body fat is dependent on how the rate is expressed (per weight of lipids or number of fat cells). In accordance with these earlier studies lipolysis rates were decreased in overweight/obesity when expressed per lipid weight but increased when related to fat cell number. There was no influence of age on onset of overweight/obesity except for lipolysis data per fat cell number. However, this difference disappeared when results were corrected for the influence on lipolysis by fat cell volume. Furthermore, when subdivided according to sex, the minor differences in lipolysis between the obesity groups were only found in men. Thus, once elevated BMI is established, the duration of this condition does not further impact on disturbed lipolysis in an important way, at least not as regards to basal or catecholamine stimulated rates, which were determined in this study.
As discussed in detail [10, 11] it is unclear if body weight fluctuations such as weight cycling predispose for future overweight/obesity. Herein we obtained self-reported information about the highest/lowest BMI during adulthood. No difference between EOO and LOO was observed. Although this finding suggests that weight fluctuation is not a major cause of higher BMI in EOO compared to LOO, we cannot exclude that unrecognized differences in weight cycling following repeated dieting could play a role.
We also observed some differences between overweight/obesity groups in terms of fasting insulin and HDL-cholesterol parameters. However, these differences became non-significant in multiple regression analyses correcting for age, sex, and BMI. In addition, there was a small but significant difference in occurrence of diabetes between EOO and LOO. This may be related to the older age of the LOO group rather than the time of obesity onset. It should be noted that our study was not designed to examine the clinical impact of early or late onset of excess body fat. Other BMI related factors such as heredity/genetics, life style, pancreatic beta-cell function, incretins and microbiota not examined presently could be influenced by onset of overweight/obesity and impact on the clinical phenotype [22]. It is not likely that menopausal issues have influenced the results. In a recent longitudinal study we found that menstrual dynamics did not influence fat cell lipolysis [17]. It is somewhat surprising that the clinical profile only showed minor differences between the two obesity groups even though EOO had a longer duration of elevated BMI and had a more rapid increase in BMI over time in adulthood than LOO. Nevertheless, it might be of clinical value to encourage young people with high BMI to avoid a further BMI increase when getting older.
Based on present and previous results we propose the following model for development of excess body fat. Irrespective of an early or late start, fat mass expands by a combination of increased number and size of the fat cells. This results in more subcutaneous WAT when overweight/obesity develops earlier than later in life. Visceral fat mass expansion appears to be less influenced by the time of onset of elevated BMI. In addition, the putative mechanisms behind increases in fat mass in terms of adipose cellularity and fat lipolysis are not influenced in an important way by time of onset of fat mass expansion. The same is true for WAT morphology. We are aware our speculation is based on a cross-sectional examination and retrospective information about BMI at a single early time point. Preferably the idea should be validated by repeated laboratory examinations starting in adulthood and continued until very late stages in life.
This study has some limitations. We did not directly examine visceral fat cells and only subcutaneous fat cells from the abdominal region were investigated. It is possible that lower (gluteal/femoral) subcutaneous WAT is developed differently than upper (abdominal) subcutaneous fat. Differences in lipolysis and fat cell size between these two regions have been reported but they are only of a quantitative nature [23]. We have no information about adipose tissue or clinical variables besides BMI prior to the current laboratory investigation. Therefore, the results may above all relate to the present adult status of obesity/overweight. BMI at 18 years of age and BMI fluctuations were based on self-report. It is not possible for practical reasons to subject people to frequent laboratory measures of BMI from childhood to late stages in life. However, the self- reported body weight seems to be valid according to the quality check, at least for BMI at 18 years of age and using weighing at home. Other lipolysis regulating hormones besides catecholamines were not investigated. On the other hand, unlike for catecholamines there is no available information from prospective studies suggesting a causal role of such hormonal regulation in the expansion of fat mass. Finally, LOO and EOO were not perfectly matched for some parameters that may have influenced the findings with adipose tissue. However, we believe that the use of multiple regression to correct for such differences to some extent strengthens the validity of our results. It is in theory possible to also use propensity score matching to closer balance the groups. Although, this would decrease the number of comparable EOO and LOO subjects considerably and lower the statistical power. Using multiple regression we can investigate all subjects, allowing for a higher-powered study.
What are the mechanisms behind different amounts of subcutaneous WAT between LOO and EOO? As mentioned, they are probably not due to adipogenesis which determines fat cell size/number. Genetic/epigenetic factors or socioeconomic/behavioral factors not examined herein could play a role. Hormones could also be involved. Interestingly in a small subgroup we found that circulating leptin levels were almost 40% higher in EOO than LOO. This might impact on lipolysis, lean body mass and subcutaneous WAT as demonstrated previously [24,25,26].
In conclusion, subjects with early or late onset of overweight/obesity have similar disturbances in WAT function as regards cellularity, morphology, and lipolysis except for some minor differences in visceral fat mass and lipolysis in men. The most important difference is more excessive subcutaneous WAT accumulation in the early onset form which may at least in part be due to a more rapid accumulation of body fat in juvenile obesity. | {
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A cohort study on longitudinal changes in postural balance during the first year after stroke
Abstract
Introduction
Many patients with strokes report increased incidence of fall that can be due to impaired postural balance. The recovery of balance in patients with varying degrees of impairments and activity limitations is less studied, and whether individuals with mild paresis can recover their balance faster is unclear. Better knowledge about factors influencing the recovery of postural balance can be used to guide clinical management after stroke to provide the right rehabilitation to the right person at the right time, and thus to avoid potential fall incidences.
Objective
This study aims to examine longitudinal changes in postural balance during the first year after stroke.
Methods
Postural balance was assessed using the Berg Balance Scale (BBS) within 5 days, 1, 2, and 3 months and 1-year post-stroke. Stroke severity was stratified using a cluster analysis by including multidimensional baseline measures. A longitudinal mixed-effect model was constructed to analyze changes in proportional balance impairment by stroke severity over time. Individuals with a cut-off of BBS below 45 scores were identified through a classification algorithm using baseline predictors.
Results
A total of 135 patients were stratified to mild stroke (77 [57%] patients) or moderate stroke (58 [43%] patients). Ninety-three patients were included in the longitudinal analysis. Significant recovery was found at 1-year for moderate stroke (48% recovery from the initial impaired postural balance, adjusted P < 0.001), but not for mild stroke, after adjusting for age and cognition. Both stroke severities had a maximal recovery in postural balance at 3 months post-stroke, but the moderate stroke group deteriorated after that. Patients with higher age and worse cognition had more severe balance impairments. The classification model achieved a sensitivity of 0.95 (95% confidence interval [CI]: 0.91–0.98) and a specificity of 0.99 (95% CI: 0.98–1.0) for classifying individuals with BBS below 45 points.
Conclusions
This study indicates that continuous improvements in postural balance ends at 3 months regardless for mild or moderate stroke groups, and patients with moderate stroke significantly deteriorate in postural balance after 3 months.
Peer Review reports
Introduction
Stroke survivors experience many types of long-term consequences. Impaired postural balance is one of the well-recognized residual impairments in patients after stroke, and is often associated with social isolation and limited mobility, resulting in a decline in the quality of life [1, 2]. A majority of stroke survivors report a history of fall incidents during the first year after stroke due to impairment in postural balance, which has led to a high incidence of fall-related injuries and mortality [3].
The severity of impaired postural balance after stroke is generally related to higher age, impaired motor function and cognitive deficits [4, 5]. An improvement in function may occur within the first few weeks after stroke, and may be attributable to the combination of spontaneous recovery and the effect of rehabilitation [6]. However, for a substantial number of patients, the continuous gain in recovery seems to diminish 3 months after stroke onset [7]. A decline may then occur in patients with more severe initial impairments [8]. Little is known about whether the recovery of postural balance follows a similar longitudinal pattern as shown in other impairments, such as functional mobility in stroke [8], and whether the postural balance recovery rate differs between stroke severity.
Knowledge about longitudinal progression in impairment of postural balance after stroke is a pre-requisite to understanding the need for appropriate mobility aids and early balance training. This could greatly contribute to identifying individuals who have residual balance impairment and may be susceptible to a high risk of falling. Early identification of patients with potential balance impairment would also allow interventions for potential falls, and significantly reduce the psychological burden for patients with stroke and next of kin [9]. The postural evaluation was commonly assessed using the Berg Balance Scale (BBS) that is a clinical tool to assess both dynamic and static balance. The BBS is a sufficient clinical screening tool to determine a risk of falling in terms of good sensitivity and reliability, which is not require extensive resource and time to conduct. A BBS score of less than 45 is a generalized cut-off score that is well-recognized in clinical practice and has previously demonstrated that patients with a lower BBS 45 more likely to fall than were those who were above the score prone to a greater risk of falling [10, 11].
The primary aim of the study was to examine longitudinal changes in postural balance between different stroke severities during the first year after stroke. The secondary aim was to identify individuals, regardless of stroke severity, who have a BBS score below 45 which is considered to be susceptible to a risk of falling.
Methods
Study population and design
The participants in this longitudinal and prospective study were enrolled in the Gothenburg Very Early Supported Discharge clinical trial (URL: http://www.clinicaltrials.gov. Unique identifier: NCT01622205) at Sahlgrenska University Hospital, Sweden, from September 2011 to April 2016 [12]. The GOTVED study is a randomized controlled study were 140 included patients were randomized to very early supported discharge with continued rehabilitation in the patient’s home or to a control group receiving ordinary rehabilitation. Additional information about GOTVED can be found elsewhere [12]. The study was approved by the Regional Ethical Review Board in Gothenburg (registration number:426–05 and 042–11) and was conducted in agreement with the Declaration of Helsinki. The inclusion criteria were age > 18 years; a diagnosis of ischemic or hemorrhagic stroke confirmed according to World Health Organization criteria [13]; a National Institute of Health Stroke Scale (NIHSS) score of 0–16 points, which corresponds to mild-to-moderate stroke; a Barthel Index (BI) score of 50 points or more on day 2; and a Montreal Cognitive Assessment index of 26 points or less if BI = 100. Patients with a life expectancy < 1 year (e.g., with severe malignancy) or who could neither speak nor communicate in Swedish prior to stroke were excluded. In this longitudinal and prospective study, the data were extracted from the Gothenburg Very Early Supported Discharge clinical trial, and the 140 patients are pooled into one group. Details of the full inclusion and exclusion criteria of the study trial as well as the power calculation of the study sample size were previously reported [12]. All participants provided written informed consent prior to the longitudinal trial.
Clinical assessments
The BBS was used to assess postural balance across 5 time intervals as following: within 5 days after stroke onset (referred as baseline), within 1, 2, and 3 months post-stroke, and at 1-year after stroke. The BBS is a 14-item scale, and each item consists of five ordinal responses to assess static and dynamic balance. Static balance is defined as the ability to maintain an upright posture and the centre of mass is over the base of support [14]. Dynamic balance is defined as the ability maintain a stable base of support while completing weight shifting movements [15]. The maximum total score is 56 points (higher indicates better postural balance) [16]. A BBS score below a cut-off of 45 points indicates patients with a high risk of falling [10, 17]. The BBS scale has proven to be reliable and valid for assessing patients with acute and chronic stroke [10, 18].
Other assessments that describe the consequences of a stroke, such as impairments and activity limitations, were also performed. Overall disability post-stroke was assessed using the modified Rankin Scale (mRS) with an ordinal scale ranging from 0 to 6 in which 0 corresponds with no disability at all, 5 indicates severe disability, and 6 represents death [19]. The National Institutes of Health Stroke Scale was used to assess neurological deficit at 2 days after admission by a stroke-physician [20]. The 10-item ordinal Barthel Index (BI) was used to measure dependency in daily activities, with a score ranging from 0 to 100 (lower indicates higher dependency) [21]. Motor-sensory function in the extremities was assessed using the Fugl-Meyer Assessment Scale (FMA; lower extremity [-LE] and upper extremity [-UE]), with a lower FMA score indicating more severe impairment of function [22]. Cognitive function was screened using the Montreal Cognitive Assessment (MoCA), scored from 0 to 30 (lower indicates worse cognition) [23]. BI and MoCA were administered by occupational therapists 36–48 h after arrival at the stroke unit. An experienced and blinded physiotherapist not working at the stroke unit performed the clinical assessments. The Hospital Anxiety and Depression Scale (HADS) self-assessment questionnaire was used to assess psychological distress [24]. The 14-item questionnaire consists of two subscales, one 7-item subscale was used for assessing anxiety and the other 7-item subscale to assess depression. A total score above 7 points on a subscale of HADS (each item scored from 0 to 3) was considered to indicate symptoms of mild and moderate anxiety or depression [24].
NIHSS and MoCA were conducted as earlier as possible, whereas HADS and SIS were gathered on Day 5 to avoid extra burden for patients with stroke in their stroke care at the hospital.
Statistical analyses
Baseline clustering of stroke severity
To classify stroke severity, a baseline cluster analysis was conducted to identify homogenous subgroups based on similar clinical characteristics. Multidimensional clinical variables were included, covering impairments and activity limitations that describe overall functioning and disability. The purpose for cluster analysis was not to have use pre-defined cut offs for assessment of stroke severity but to in an open and non-prejudiced way include all possible variables in the analysis. This minimizes the risk of missing factors that are there but that we haven´t considered. The dissimilarity between observations across individuals was calculated using a general dissimilarity coefficient that can handle mixed-type variables by assigning different distance measures to continuous, ordinal and nominal variables [25]. A partitioning around medoids algorithm was then used to cluster the established dissimilarity matrix, and an optimal number of clusters was determined and selected on the basis of silhouette width [26]. Internal validation and stability of clusters were evaluated further [27, 28].
To compare clinical characteristics across each cluster, either Fisher’s exact test, Pearson χ2, Cochran–Armitage test, Mann–Whitney U test or independent t tests was used for post hoc comparison, as appropriate. Imputation for mixed-type missing data (2.6% of the total data) was performed as previously described [8].
Longitudinal changes in postural balance
Patients were considered lost to follow-up and excluded from the longitudinal analysis if two or more visits were missed and/or they had more than 30% missing data in outcomes.
Considering the ordinal nature of BBS ratings, a proportional impairment of postural balance was calculated as the outcome for determining potential recovery. A longitudinal beta regression mixed-effect model was therefore appropriate for analyzing proportional data to increase clinical interpretation while avoiding shortcomings in conventional regression approaches for bounded outcomes [29]. Impairment of postural balance was defined as the difference between the maximum balance score (BBS 56 scores) and the residual balance function. The proportion of balance impairment was then equivalent to balance impairment over the maximum balance scores. The proportions were converted to an interval of 0 to 1 on a continuous scale, with an upper and lower limited bound of 0.005 and 0.995, respectively.
A multilevel longitudinal mixed-effect model was applied to analyze the changes in proportional impairment of postural balance over time across different stroke severities [29, 30]. Age, cognition, time, stroke severity, and interaction between stroke severity and time were included as fixed effects. The random intercept for each patient was also included. P values for multiple comparisons were adjusted using Holm-Bonferroni corrections. A two tailed significance level was defined as P < 0.05.
Classification for individuals who had a BBS score below 45.
Random forest is a robust binary classification algorithm for generating a majority vote among trees on the basis of multiple independent decision trees [31]. A random forest model was constructed for classification by using multidimensional baseline measures as predictors for classifying individuals who had a BBS score, at any point, lower than 45 during the first year of stroke which corresponded to an increased risk of falling. This was done by using multidimensional baseline measures as predictors for classifying individuals who had a BBS score, at any point, lower than 45 during the first year of stroke [32]. Tuning parameters was conducted with fivefold cross-validation, and the importance of variables was determined by the mean decrease in accuracy consequent to the permutation of each variable. The predictive performance was determined in terms of classification accuracy, sensitivity and specificity.
Results
A total of 135 patients were eligible for the baseline analysis (median age 76 years, range 37–96, 52 females [39%], Table 1). Forty-two patients were excluded prior to the longitudinal analysis for reasons of loss to follow-up (n = 18), withdrawal (n = 18), a second stroke or other diseases that impaired motor function (n = 6). The differences were not statistically significant in age, sex and neurological deficits between the excluded patients and the patients included in the longitudinal analysis.
Table 1 Included variables for the baseline cluster evaluation and group characteristics at baseline and for longitudinal analysis
Stroke severity based on baseline clustering
Using baseline clustering from 29 clinical variables, two distinct groups were stratified based on stroke severity by considering the overall impairment and activity limitations. Detailed clinical characteristics of the two clusters and variable importance for stratifying clusters are presented in Table 1 and Fig. 1.
Fig. 1
figure 1
Variable importance of baseline variables in the cluster analysis. The corresponding domain of each variable is indicated following the framework of The International Classification of Functioning, Disability, and Health. The variable importance was derived from the mean square error with higher values indicating higher importance. Two clusters were determined as an optimal number of clusters on the basis of silhouette width (0.48). Stability of the clusters was assessed using the Jaccard similarity through resampling of the data 500 times. The Jaccard similarity was 0.97, which indicates stable clusters. BBS, Berg Balance Scale; BI, Barthel Index; FMA, Fugl-Meyer Assessment; HADS, Hospital Anxiety and Depression Scale; NIHSS, National Institutes of Health Stroke Scale; IQR, interquartile range; LE, lower extremity; MoCA, Montreal Cognitive Assessment; mRS, modified Rankin Scale; ROM, passive joint motion; SD, standard deviation; TUG, timed up-and-go test; UE, upper extremity
The moderate affected stroke group included 58 patients (43%), and was characterized by a higher level of impairments and greater activity limitations which significantly differed from the mild groups (mean [SD] FMA-LE, 30 [5]; median [IQR] total BI scores, 60 [55–70]; median [IQR] mRS, mRS, 3 [2-3]).
The mild affected stroke group included 77 of the 135 patients (57%), and was characterized by mild impairments and slight activity limitations (mean [SD] FMA-LE, 32 [3]; median [IQR] total BI scores, 90 [85–95]; median [IQR] mRS, 2 [1-2]).
Longitudinal changes in impairment of postural balance from baseline to 1-year
Ninety-three patients (54 [38%] mild stroke; 42 [62%] moderate stroke) with 636 assessments of BBS were included in the longitudinal analysis. Higher age (odds ratio [OR] 1.03, [95% CI, 1.02 to 1.05]) and worse cognition (OR 0.94 [95% CI, 0.9 to 0.98]) were significantly associated with greater impairment of postural balance, as presented in Table 2. Patients with moderate stroke (OR 3 [95% CI, 2.1 to 4.3]) had a significantly greater impaired postural balance, compared to patients with mild stroke.
Table 2 Longitudinal beta regression model for the proportion of balance impairments during the first year after stroke (n = 93)
After adjusting for age and cognition, patients with moderate stroke had significantly improved from baseline to 1-year post-stroke, with BBS improving a median of 10 points (least-squares [LS] mean difference -0.83 [95% CI, -1.04 to -0.62]; adjusted P < 0.001). A reduction of 48% in the estimated mean proportional impairment of postural balance was found at 1-year for the moderate stroke group, compared to baseline (Fig. 2). For the mild affected stroke group, a decrease of 16% in the estimated mean was found from baseline to 1-year, but it was not statistically significant (LS mean difference, -0.18 [95% CI, -0.45 to 0.08], adjusted P = 0.34).
Fig. 2
figure 2
A Estimated means of proportional balance impairments and 95% confidence intervals across five time points by stroke severity. B Individual changes in proportional balance impairments by stroke severity, cognition, and age between 3 months and 1-year post-stroke. Difference ≥ 0 indicates an increase in balance impairment, whereas < 0 is a decrease in impairment. A total of 35 patients ≥ 75 years of age had an increase in balance impairment from 3 months to 1-year post-stroke. a Estimated means were converted from least square means after adjusting for age and cognition. MoCA, Montreal Cognitive Assessment
Both stroke severity groups had a maximum recovery at 3 months (LS mean difference, -1.11 [95% CI, -1.33 to -0.89], adjusted P < 0.001 for moderate stroke; and -0.5 [95% CI, -0.78 to -0.23], adjusted P = 0.002 for mild stroke, Fig. 2). A higher percentage of recovery was found in the moderate affected stroke group at 3 months (59% decrease in the estimated mean) compared to the mild stroke group (38% decrease).
Changes in postural balance from 3 months to 1-year
Impairment of postural balance significantly increased from 3 months to 1-year in patients with moderate stroke, after adjusting for age and cognition (LS mean difference, 0.28 [95% CI, 0.05 to 0.51]; adjusted P = 0.015, Fig. 2). The increase in the estimated mean of proportional impairment of postural balance was 27% at 1-year after stroke, compared to 3 months.
For the mild affected stroke group, there was also an increase in impairment from 3 months to 1-year, but it was not statistically significant (35% increase in the estimated mean, LS mean difference 0.32 [95% CI, -0.02 to 0.66]; adjusted P = 0.07, Fig. 2).
A total of 51 of the 93 patients (55%) had an increased impairment of postural balance after 3 months. Individual differences in proportional impairment of postural balance between 3 months and 1-year post-stroke by stroke severity, age and cognition are shown in Fig. 2. Of these 51 patients with increased impairments, 35 patients (69%) were aged above 75 years old.
Individuals with a BBS score below 45 during the first year of stroke
Thirty-nine of the 93 patients (42%) were identified as having a BBS score < 45. Among these patients, 31 patients (79%) had moderate stroke and 8 (21%) had mild stroke. Longitudinal progression of balance in each individual with BBS < 45 or ≥ 45, by stroke severity across different time points, are presented in Fig. 3. FMA-LE, BI-transfers and age were three most contributing predictors for classifying patients who had BBS < 45 points within any time points of the first year after stroke (Fig. 4). Demographics and clinical variables between groups with BBS < 45 or ≥ 45 are presented in Table 3. The random forest model for classification, based on baseline predictors, achieved an accuracy of 0.98 (95% CI, 0.96 to 0.99), a sensitivity of 0.95 (95% CI, 0.91 to 0.98), a specificity of 0.99 (95% CI, 0.98 to 1), after tuning parameters with cross-validation.
Fig. 3
figure 3
Longitudinal Berg Balance scale (BBS) in each individual by risk of falling in mild and moderate stroke. A cut-off of < 45 points, across any time point during the first year indicates individuals with a high risk of falling
Fig. 4
figure 4
Mean decrease in accuracy after permutation of each variable in the random forest model. FMA-LE, BI-transfers, and age are the three most contributing variables for the model performance.BI, Barthel Index; FMA, Fugl-Meyer Assessment; HADS, Hospital Anxiety and Depression Scale; NIHSS, National Institutes of Health Stroke Scale; IQR, interquartile range; LE, lower extremity; MoCA, Montreal Cognitive Assessment; mRS, modified Rankin Scale; ROM, passive joint motion; SD, standard deviation; UE, upper extremity
Table 3 Demographics of patients with high or low risk of falling and 10 of the most predictive variables
Discussion
The study used multidimensional baseline measures to stratify stroke severity and examined the longitudinal progression in postural balance across each severity group. The main findings were that patients with moderate stroke had a significant recovery from their initial impaired postural balance assessed with BBS from baseline to 1-year, after adjusting for age and cognition. Both mild and moderate stroke showed a maximum recovery during the first 3 months post-stroke, and the patients with moderate stroke had significantly increased in their impairments of postural balance thereafter. Higher age and worse cognition were associated with more severe balance impairments. The baseline measurements showed a high sensitivity and specificity for classifying postural balance in patients that entails a potential risk of falling during the first-year post-stroke.
An increase of 10 scores in the median BBS from baseline to 1-year was relatively large, and was considered to be a minimal clinically important difference, as a reference of 6 points was suggested previously [33]. A recovery in impairment of postural balance during the first year post-stroke was expected, as an improvement in BBS was also demonstrated in prior studies at the 1-year follow-up post-stroke [34, 35]. However, in the present study, the significant recovery from the initial balance impairment (48%) was found only in patients with moderate stroke at 1-year, and it was not statistically significant for mild stroke. This was in line with earlier findings that only patients with more severe initial impairment significantly improved during the first year [8]. In addition, as demonstrated in earlier studies [36, 37], the ceiling effect in BBS may have impact on the ability to detect the potential improvement for patients with mild stroke, as they have relatively mild functional impairments.
The continuous recovery of impairment in postural balance seems to end at 3 months after onset for both moderate and mild stroke, assessed with BBS in the present study. This finding suggests that longitudinal functional recovery in stroke is similar in general, and may indicate similarities in the underlying mechanisms in the recovery of balance, as well as in other motor recoveries [7, 38]. The mechanisms underlying recovery after 3 months remain unclear, but could be a consequence of the diminished spontaneous recovery and ended the effect of rehabilitation [6]. However, we acknowledge that recovery might go on beyond the first year, although BBS probably not is the correct tool to assess this.
More severe initial impairments at baseline may be susceptible to deterioration after 3 months, as a statistically significant increase in impairments was found in only the moderate stroke group. Furthermore, older patients may recover less after 3 months. This was evident by a majority of patients aged ≥ 75 years (69%) experienced an increase in balance impairments, which has also been demonstrated in post-stroke functional mobility [8]. The current findings suggest that more frequent follow-up with physiotherapists and occupational therapists for patients with more severe stroke after 3 months may desirable to recognize the potential decline in balance function. This would help to early identify the needs of walking aids in individuals with stroke, and thus to prevent fall injuries.
In line with earlier findings [4, 39], worse cognition was associated with greater impairment of postural balance. However, cognition previously has been identified as a non-significant factor in post-stroke functional mobility [8]. The dissimilar impact of cognition may be attributable to the fact that the BBS assesses also static balance, which seems to require a higher cognitive input than solely walking does, with the ability to concentrate on holding body positions. This was further supported by the fact that greater functional connectivity between sensorimotor cortical areas showed in static balance than in the walking test, which suggests a greater cognitive impact required for static balance [40].
Even though baseline clustering based on a wide-ranging variable (e.g., impairments and activity limitations) was sufficient for handling a heterogeneity among stroke patients, a proportion of patients with moderate stroke had impaired balance along with good motor-sensory function in the extremities. This may be associated with potential involvement of a cerebellar lesion in some patients. Static balance is a complex behavior that does not only involve motor-sensory function in the extremities, but also perception, cognition and biomechanical constraints [41]. The BBS moderately correlates with the FMA [42, 43] which, in turn, may explain the variation noted in the present study.
As expected, lower-limb function, ability to transfer and age at baseline predicts well in patients with a risk of falling. This finding in line with the recognized predictors for risk of falling in previous studies [44,45,46]. Greater impairment of lower-limb function at baseline may, therefore, be important for the recognition of individuals at a risk of falling during the first year post-stroke. Improvements in balance have previously been shown in several forms of task training [47]. More longitudinal studies are warranted to explore the effect of training on the recovery of balance.
Impairment of postural balance was considered to be the most prioritized research area by stroke survivors due to concerns regarding fall incidents and disability in daily activities [48]. Fall evaluation may be necessary to consider in individuals with a BBS score lower than 45 points. Although some earlier studies have attempted to demonstrate different cut-off values of BBS for indicating individuals with a high risk of falling, the sensitivity and specificity has varied greatly (from 65 to 80%) [34, 45]. The cut-off value of BBS below 45 remained well accepted in clinical practice for clinicians to alert patients about potential risks of falling. However, determining different optimal cut-off values for BBS was not in the scope of this study. The focus on the longitudinal changes in postural balance, to identify patients who may have BBS below a pre-existed clinical threshold, across any time points, results in to general a more comprehensive picture of the progression in postural balance by different stroke severities. Therefore, the interpretation of the study results was limited to a risk of falling based on a single instrument instead of an actual fall detection or prediction that are complex and require consideration of multiple factors (e.g. medications, visual problems, structural barriers and environmental factors). This is not within the current aim and design of the study.
One strength of the study is the inclusion of multidimensional baseline measures (e.g. motor, cognition and psychological variables), this allowed clustering to classify stroke severity based on comprehensive clinical variables from impairments and activity limitations. It also largely contributes to handle the complexity of balance through taking into multidimensional parameters into account at baseline. The advances in the applied longitudinal beta regression model also considered the nature of high ordinal levels of BBS ratings, which avoids a loss of clinical information by converting to dichotomous or continuous bounded outcomes. Furthermore, the use of a mixed-effects model across stroke severities enhances the clinical interpretation of progression impairment of postural balance by taking between and within individual variability into consideration.
There are some limitations in the present study. One limitation of is that the data was collected on the basis of a randomized controlled design for examining outcomes between very early supported discharge and usual care. However, there were no significant differences were demonstrated between control and intervention group in postural balance at any time points in an earlier study [49]. As this study aim was to explore longitudinal changes in postural balance in the whole study population, the advance of baseline clustering used in the present study were able to provide more comprehensive classification of stroke severity. We therefore believe that the original study design has very little effect on the present study. Another limitation of this study, however, is that few patients with severe stroke were included in the study sample; therefore, the generalizability may be limited. Although the selected models were able to adapt to this limitation in the data, more data on patients with different degrees of stroke severity are desirable to confirm the study findings.
Conclusion
The longitudinal analysis of postural balance indicates that the continuous recovery ends at 3 months regardless of mild or moderate stroke severity. Patients with moderate stroke had a significant postural balance recovery during the first 3 months, and then significantly diminished thereafter. Higher age and worse cognition were associated with greater impairment of postural balance. Baseline predictors, including motor-sensory function of the lower extremities, age, and ability to transfer, can accurately classify individuals with a potential risk of falling during the first year post-stroke.
Availability of data and materials
Data may be available to researchers upon request, after review of secrecy (contact the author Katharina Stibrant Sunnerhagen ks.sunnerhagen@neuro.gu.se). According to the Swedish regulation (epn.se/en/start/regulations/), the permission to use data can only be according to application and approval from the ethical board.
Abbreviations
BBS:
Berg Balance Scale
mRS:
Modified Rankin Scale
BI:
Barthel Index
FMA:
Fugl-Meyer Assessment
MoCA:
Montreal Cognitive Assessment
HADS:
Hospital Anxiety and Depression Scale
NIHSS:
National Institutes of Health Stroke Scale
TUG:
Timed up-and-go test
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Acknowledgements
We gratefully acknowledge all patients who participated in this study and thank all health professionals who helped collect data.
Funding
Open access funding provided by University of Gothenburg. This study was funded in part by grants from the Swedish Science Council (VR2012-3523 and VR2017-00946), the Health & Medical Care Committee of the Regional Executive Board of the Region Västra Götaland, King Gustaf V’s and Queen Victoria’s Freemasons´ Foundation, the Swedish National Stroke Association, The Swedish Heart and Lung Foundation, The Swedish Brain Foundation, Agneta Prytz-Folke’s and Gösta Folke’s Foundation, FRF foundation, Promobilia Foundation and Insamlingsstiftelsen för Neurologisk Forskning. The study was financed by grants from the Swedish state under an agreement between the Swedish government and the county councils, the ALF agreement (ALFGBG-718711 and ALFGBG-877961).
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Contributions
D.B. contributed to drafting the manuscript, conducting the data analysis, and interpreting of the results. L.R., T.A., and K.S.S. contributed to interpreting the results, and critically reviewing the manuscript for intellectual content. L.R., T.A., and K.S.S. substantially contributed to the conception and design of the study, and L.R. was mainly responsible for data acquisition. The author(s) read and approved the final manuscript.
Corresponding author
Correspondence to Dongni Buvarp.
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The study was approved by the Regional Ethical Review Board in Gothenburg (registration number:426–05 and 042–11) and was conducted in agreement with the Declaration of Helsinki. All participants provided written informed consent prior to the longitudinal trial.
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We confirm that this manuscript has not been published elsewhere and is not under consideration by another journal. All authors have reviewed and approved the manuscript for publication.
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The authors declare no conflict of interest regarding the study.
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Buvarp, D., Rafsten, L., Abzhandadze, T. et al. A cohort study on longitudinal changes in postural balance during the first year after stroke. BMC Neurol 22, 324 (2022). https://doi.org/10.1186/s12883-022-02851-7
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Keywords
• Cerebrovascular Accident
• Berg Balance Scale
• Longitudinal Analysis
• Impairment of Postural Balance
• Stroke Recovery | {
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-3,424,230,118,169,258,500 | Unlocking the Power of Evidence Based Practice in Nursing
In the ever-evolving landscape of healthcare, nurses play a pivotal role in delivering quality patient care. With the abundance of information available, it’s crucial for nurses to leverage evidence-based practice (EBP) to make informed decisions and improve patient outcomes. This comprehensive guide delves into the principles of EBP, its significance in nursing, and practical strategies for its implementation.
Understanding Evidence-Based Practice
Evidence-based practice is the integration of the best available evidence with clinical expertise and patient preferences to guide healthcare decisions. It involves a systematic approach to critically appraise research findings, clinical guidelines, and other sources of evidence to inform nursing practice.
The Significance of Evidence-Based Practice in Nursing
In nursing, EBP serves as the cornerstone for delivering safe, effective, and patient-centered care. By incorporating the latest research findings and clinical guidelines into practice, nurses can enhance the quality of care, promote patient safety, and optimize health outcomes.
Table: Levels of Evidence
LevelType of Evidence
ISystematic reviews & meta-analyses of randomized controlled trials
IIRandomized controlled trials
IIIQuasi-experimental studies
IVNon-experimental studies, case-control studies
VExpert opinion, consensus statements, clinical experience
Levels of Evidence
Key Components of Evidence-Based Practice
1. Formulating Clinical Questions: Effective EBP starts with asking well-formulated clinical questions using the PICO framework (Population, Intervention, Comparison, Outcome). This structured approach helps nurses identify relevant evidence to address specific clinical scenarios.
2. Searching for Evidence: Nurses must utilize reputable databases such as PubMed, CINAHL, and Cochrane Library to conduct comprehensive literature searches. It’s essential to employ advanced search strategies and critically evaluate the quality of retrieved evidence.
3. Critical Appraisal: Evaluating the validity, reliability, and applicability of research evidence is crucial in EBP. Nurses should assess study designs, methodology, and potential biases to determine the strength of evidence and its relevance to clinical practice.
4. Applying Evidence to Practice: Translating research evidence into clinical practice requires critical thinking and clinical judgment. Nurses should consider the unique needs and preferences of individual patients while implementing evidence-based interventions.
5. Evaluating Outcomes: Continuous monitoring and evaluation of outcomes are essential to assess the effectiveness of evidence-based interventions. Nurses should collect data, measure outcomes, and adjust practice accordingly to achieve optimal results.
Practical Strategies for Implementing Evidence-Based Practice
1. Promoting a Culture of EBP: Healthcare organizations should foster a supportive environment that encourages lifelong learning, critical thinking, and collaboration among nursing staff. Establishing EBP committees, providing access to resources, and offering educational opportunities can promote the integration of EBP into daily practice.
2. Utilizing Clinical Practice Guidelines: Nurses should familiarize themselves with evidence-based clinical practice guidelines relevant to their specialty areas. These guidelines offer standardized recommendations based on the best available evidence and expert consensus, serving as valuable tools for clinical decision-making.
3. Engaging in Continuous Learning: Keeping abreast of the latest research findings, attending conferences, and participating in continuing education programs are essential for nurses to stay informed about advancements in healthcare. By investing in lifelong learning, nurses can enhance their clinical expertise and contribute to evidence-based practice.
4. Collaborating with Interdisciplinary Teams: EBP involves collaboration among healthcare professionals from various disciplines. Nurses should engage in interdisciplinary teamwork, consult with experts, and seek input from colleagues to enrich the decision-making process and improve patient outcomes.
Case Study: Application of Evidence-Based Practice in Nursing
To illustrate the practical application of EBP, consider the following scenario:
Scenario: A 65-year-old patient with chronic heart failure presents to the emergency department with worsening dyspnea and edema. The nursing team must develop an evidence-based care plan to manage the patient’s symptoms and prevent exacerbations.
Evidence-Based Interventions:
• Implementing a multidisciplinary heart failure management program to optimize medication adherence and dietary management.
• Educating the patient on self-care strategies, including daily weight monitoring, sodium restriction, and symptom recognition.
• Utilizing evidence-based protocols for diuretic therapy titration based on clinical assessment and hemodynamic parameters.
• Collaborating with cardiac rehabilitation programs to promote exercise tolerance and improve functional status.
• Monitoring the patient’s progress through regular follow-up visits and adjusting the care plan based on clinical outcomes and evidence-based guidelines.
Conclusion
Evidence-based practice is paramount in nursing, empowering nurses to deliver high-quality, patient-centered care grounded in the best available evidence. By embracing the principles of EBP and incorporating evidence-based interventions into practice, nurses can optimize patient outcomes, promote safety, and advance the quality of healthcare delivery.
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76,503,199,521,084,500 | Directions: Please use your textbook to answer the question below using your own words. Explain in your own words the different types of anesthesia, including what types of procedures each are used Nursing Assignment Help
Directions: Please use your textbook to answer the question below using your own words.
Explain in your own words the different types of anesthesia, including what types of procedures each are used for. Write one well-written paragraph and answer the above questions to earn 10 points.
Expert Solution Preview
Anesthesia is a medical practice used to induce temporary loss of sensation or consciousness during surgical or medical procedures. There are several different types of anesthesia, each of which is used for specific procedures depending on the patient’s needs and the complexity of the surgery.
General anesthesia is the most common type and typically involves administering medications to induce a state of unconsciousness. It is used for extensive surgeries, such as abdominal, cardiac, and neurological procedures, where the patient needs to be completely unaware and pain-free.
Regional anesthesia involves numbing a specific part of the body, such as an arm or leg, by injecting local anesthetics near the nerves supplying that area. Examples include epidural anesthesia used during childbirth, spinal anesthesia for lower abdominal and lower extremity surgeries, and brachial plexus block for upper extremity procedures.
Local anesthesia is administered to a small area of the body, usually through injection, topical application, or a combination of both. It is used for minor surgeries or procedures such as mole removal, dental work, and suturing of lacerations. This type of anesthesia numbs only the immediate area being treated, allowing the patient to remain awake and alert.
Sedation anesthesia is a combination of medications to induce a state of relaxation, calmness, and pain relief. It is often used alongside local anesthesia for procedures that may cause discomfort or anxiety, such as endoscopy or colonoscopy. Sedation anesthesia helps the patient feel comfortable while still being able to respond to commands.
By using these different types of anesthesia, medical professionals can ensure that patients undergoing surgery or medical procedures are adequately protected from pain and discomfort. The choice of anesthesia depends on factors such as the complexity of the procedure, the patient’s medical history, and their individual preferences.
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Figure 1. Flow of Participants Enrolled in the Continuous Oxygen, Nocturnal Oxygen, and Control Groups
Flow of Participants Enrolled in the Continuous Oxygen, Nocturnal Oxygen, and Control Groups
aThe number of patients screened for eligibility was not available.
bSee eTable 2 in Supplement 3 for adherence data.
Figure 2. Main Outcome Assessed by Modified Rankin Scale Score at 90-Day Follow-up
Main Outcome Assessed by Modified Rankin Scale Score at 90-Day Follow-up
From the ordinal regression analysis, the unadjusted odds ratio for a better outcome (lower modified Rankin Scale [mRS] score) was 0.97 (95% CI, 0.89 to 1.05; P = .47) for combined oxygen vs control, and 1.03 (95% CI, 0.93 to 1.13; P = .61) for continuous oxygen vs nightly oxygen (mRS score range, 0 to 6 [0, no symptoms; 1, few symptoms but able to carry out all previous activities and duties; 2, unable to carry out all previous activities but able to look after own affairs without assistance; 3, needs some help with looking after own affairs but able to walk without assistance; 4, unable to walk without assistance and unable to attend to own bodily needs without assistance but does not need constant care and attention; 5, major symptoms such as bedridden and incontinent and needs constant attention day and night; 6, death]).
Figure 3. Subgroup Analyses for an Improved Outcome Assessed by Modified Rankin Scale Score Comparing Oxygen vs Control at 90 Days
Subgroup Analyses for an Improved Outcome Assessed by Modified Rankin Scale Score Comparing Oxygen vs Control at 90 Days
The x-axis depicts the common odds ratio (OR) for a better outcome over all 7 levels of the modified Rankin Scale score (mRS), derived from ordinal logistic regression. ORs greater than 1 indicate that a good outcome (low mRS) is more likely with oxygen than with control (reference category). The size of the markers reflects the total sample size in each subgroup, with larger markers indicating more precise estimates. The subgroup thresholds for oxygen concentration at randomization were revised from the prespecified thresholds because the analysis did not converge using the prespecified values. SSV indicates Six Simple Variables risk score; COPD, chronic obstructive pulmonary disease; GCS, Glasgow Coma Scale.
Figure 4. Patient Mortality From 0 Through 90 Days
Patient Mortality From 0 Through 90 Days
Cutoff for mortality differs from the 90-day mortality reported in Table 2 and Figure 2, in which responses were accepted up to 6 months if 3-month outcomes were not returned. Median duration of follow-up was 90 days (range, 0 to 90) in each treatment group.
Table 1. Baseline Characteristics
Baseline Characteristics
Table 2. Secondary, Exploratory, and Safety Outcomes
Secondary, Exploratory, and Safety Outcomes
1.
Roffe C, Sills S, Halim M, et al. Unexpected nocturnal hypoxia in patients with acute stroke. Stroke. 2003;34(11):2641-2645.PubMedGoogle ScholarCrossref
2.
Rocco A, Pasquini M, Cecconi E, et al. Monitoring after the acute stage of stroke. Stroke. 2007;38(4):1225-1228.PubMedGoogle ScholarCrossref
3.
Bravata DM, Wells CK, Lo AC, et al. Processes of care associated with acute stroke outcomes. Arch Intern Med. 2010;170(9):804-810.PubMedGoogle ScholarCrossref
4.
Rowat AM, Dennis MS, Wardlaw JM. Hypoxaemia in acute stroke is frequent and worsens outcome. Cerebrovasc Dis. 2006;21(3):166-172.PubMedGoogle ScholarCrossref
5.
Heiss WD. The ischemic penumbra: how does tissue injury evolve? Ann N Y Acad Sci. 2012;1268:26-34.PubMedGoogle ScholarCrossref
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Alawneh JA, Jones PS, Mikkelsen IK, et al. Infarction of ‘non-core-non-penumbral’ tissue after stroke. Brain. 2011;134(6):1765-1776.PubMedGoogle ScholarCrossref
7.
Dreier JP. The role of spreading depression, spreading depolarization and spreading ischemia in neurological disease. Nat Med. 2011;17(4):439-447.PubMedGoogle ScholarCrossref
8.
Ciccone A, Celani MG, Chiaramonte R, Rossi C, Righetti E. Continuous versus intermittent physiological monitoring for acute stroke. Cochrane Database Syst Rev. 2013;5(5):CD008444.PubMedGoogle Scholar
9.
O’Driscoll BR, Howard LS, Earis J, Mak V; et al. BTS guideline for oxygen use in adults in healthcare and emergency settings. Thorax. 2017;72(suppl 1):ii1-ii90.PubMedGoogle ScholarCrossref
10.
Floyd TF, Clark JM, Gelfand R, et al. Independent cerebral vasoconstrictive effects of hyperoxia and accompanying arterial hypocapnia at 1 ATA. J Appl Physiol (1985). 2003;95(6):2453-2461.PubMedGoogle ScholarCrossref
11.
Padma MV, Bhasin A, Bhatia R, et al. Normobaric oxygen therapy in acute ischemic stroke. Ann Indian Acad Neurol. 2010;13(4):284-288.PubMedGoogle ScholarCrossref
12.
Singhal AB, Benner T, Roccatagliata L, et al. A pilot study of normobaric oxygen therapy in acute ischemic stroke. Stroke. 2005;36(4):797-802.PubMedGoogle ScholarCrossref
13.
Singhal AB. Normobaric oxygen therapy in acute ischemic stroke trial. ClinicalTrials.gov website. https://clinicaltrials.gov/ct2/show/NCT000414726. Accessed June 30, 2017.
14.
Rønning OM, Guldvog B. Should stroke victims routinely receive supplemental oxygen? Stroke. 1999;30(10):2033-2037.PubMedGoogle ScholarCrossref
15.
Roffe C, Ali K, Warusevitane A, et al. The SOS pilot study. PLoS One. 2011;6(5):e19113.PubMedGoogle ScholarCrossref
16.
Roffe C, Nevatte T, Crome P, et al. The Stroke Oxygen Study (SO2S). Trials. 2014;15:99.PubMedGoogle ScholarCrossref
17.
Sim J, Gray R, Nevatte T, et al. Statistical analysis plan for the Stroke Oxygen Study (SO2S). Trials. 2014;15:229.PubMedGoogle ScholarCrossref
18.
Stroke Oxygen Study.http://www.so2s.co.uk/. Accessed July 14, 2016.
19.
Pocock SJ, Simon R. Sequential treatment assignment with balancing for prognostic factors in the controlled clinical trial. Biometrics. 1975;31(1):103-115.PubMedGoogle ScholarCrossref
20.
Counsell C, Dennis M, McDowall M, Warlow C. Predicting outcome after acute and subacute stroke: development and validation of new prognostic models. Stroke. 2002;33(4):1041-1047.PubMedGoogle ScholarCrossref
21.
van Swieten JC, Koudstaal PJ, Visser MC, Schouten HJ, van Gijn J. Interobserver agreement for the assessment of handicap in stroke patients. Stroke. 1988;19(5):604-607.PubMedGoogle ScholarCrossref
22.
Brott T, Adams HP Jr, Olinger CP, et al. Measurements of acute cerebral infarction. Stroke. 1989;20(7):864-870.PubMedGoogle ScholarCrossref
23.
Wityk RJ, Pessin MS, Kaplan RF, Caplan LR. Serial assessment of acute stroke using the NIH Stroke Scale. Stroke. 1994;25(2):362-365.PubMedGoogle ScholarCrossref
24.
Collin C, Wade DT, Davies S, Horne V. The Barthel ADL Index. Int Disabil Stud. 1988;10(2):61-63.PubMedGoogle ScholarCrossref
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EuroQol Group. EuroQol—a new facility for the measurement of health-related quality of life. Health Policy. 1990;16(3):199-208.PubMedGoogle ScholarCrossref
26.
Nouri FM, Lincoln NB. An extended activities of daily living scale for stroke patients. Clin Rehabil. 1987;1(4):301-305. doi:10.1177/026921558700100409Google ScholarCrossref
27.
Ali M, Jüttler E, Lees KR, Hacke W, Diedler J; et al. Patient outcomes in historical comparators compared with randomised-controlled trials. Int J Stroke. 2010;5(1):10-15.PubMedGoogle ScholarCrossref
28.
Rincon F, Kang J, Maltenfort M, et al. Association between hyperoxia and mortality after stroke. Crit Care Med. 2014;42(2):387-396.PubMedGoogle ScholarCrossref
29.
Smith CJ, Bray BD, Hoffman A, et al. Can a novel clinical risk score improve pneumonia prediction in acute stroke care? J Am Heart Assoc. 2015;4(1):e001307.PubMedGoogle ScholarCrossref
30.
Fonarow GC, Pan W, Saver JL, et al. Comparison of 30-day mortality models for profiling hospital performance in acute ischemic stroke with vs without adjustment for stroke severity. JAMA. 2012;308(3):257-264.PubMedGoogle ScholarCrossref
31.
Westendorp WF, Vermeij JD, Zock E, et al. The Preventive Antibiotics in Stroke Study (PASS). Lancet. 2015;385(9977):1519-1526.PubMedGoogle ScholarCrossref
32.
Dennis MS, Lewis SC, Warlow C; et al. Effect of timing and method of enteral tube feeding for dysphagic stroke patients (FOOD). Lancet. 2005;365(9461):764-772.PubMedGoogle ScholarCrossref
33.
IST-3 Collaborative Group. The benefits and harms of intravenous thrombolysis with recombinant tissue plasminogen activator within 6 h of acute ischaemic stroke (the third international stroke trial [IST-3]). Lancet. 2012;379(9834):2352-2363.PubMedGoogle ScholarCrossref
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López-Cancio E, Salvat M, Cerdà N, et al. Phone and video-based modalities of central blinded adjudication of modified Rankin Scores in an endovascular stroke trial. Stroke. 2015;46(12):3405-3410.PubMedGoogle ScholarCrossref
35.
Stroke Alliance for Europe. PROOF trial. http://www.safestroke.eu/proof-trial/. Accessed September 1, 2017.
Original Investigation
September 26, 2017
Effect of Routine Low-Dose Oxygen Supplementation on Death and Disability in Adults With Acute Stroke: The Stroke Oxygen Study Randomized Clinical Trial
Christine Roffe, MD1,2; Tracy Nevatte, PhD2,3; Julius Sim, PhD2; et al Jon Bishop, PhD4; Natalie Ives, MSc4; Phillip Ferdinand, MRCP1; Richard Gray, MSc4,5; for the Stroke Oxygen Study Investigators and the Stroke OxygenStudy Collaborative Group
Author Affiliations
• 1University Hospital of North Midlands NHS Trust, Stoke-on-Trent, United Kingdom
• 2Faculty of Medicine and Health Sciences, Keele University, Staffordshire, United Kingdom
• 3Directorate for Engagement & Partnerships, Keele University, Staffordshire, United Kingdom
• 4Birmingham Clinical Trials Unit, University of Birmingham, Birmingham, United Kingdom
• 5MRC Population Health Research Unit, University of Oxford, Oxford, United Kingdom
JAMA. 2017;318(12):1125-1135. doi:10.1001/jama.2017.11463
Key Points
Question Does routine prophylactic low-dose oxygen supplementation after acute stroke improve functional outcome?
Findings In this randomized clinical trial, 8003 patients with acute stroke were randomized within 24 hours of admission to 3 days of continuous oxygen, nocturnal oxygen, or control. After 3 months, there was no significant difference in death and disability for the combined oxygen groups compared with control (odds ratio, 0.97) or for the continuous oxygen group compared with the nocturnal oxygen group (odds ratio, 1.03).
Meaning Routine low-dose oxygen did not improve outcomes in nonhypoxic patients after acute stroke.
Abstract
Importance Hypoxia is common in the first few days after acute stroke, is frequently intermittent, and is often undetected. Oxygen supplementation could prevent hypoxia and secondary neurological deterioration and thus has the potential to improve recovery.
Objective To assess whether routine prophylactic low-dose oxygen therapy was more effective than control oxygen administration in reducing death and disability at 90 days, and if so, whether oxygen given at night only, when hypoxia is most frequent, and oxygen administration is least likely to interfere with rehabilitation, was more effective than continuous supplementation.
Design, Setting, and Participants In this single-blind randomized clinical trial, 8003 adults with acute stroke were enrolled from 136 participating centers in the United Kingdom within 24 hours of hospital admission if they had no clear indications for or contraindications to oxygen treatment (first patient enrolled April 24, 2008; last follow-up January 27, 2015).
Interventions Participants were randomized 1:1:1 to continuous oxygen for 72 hours (n = 2668), nocturnal oxygen (21:00 to 07:00 hours) for 3 nights (n = 2667), or control (oxygen only if clinically indicated; n = 2668). Oxygen was given via nasal tubes at 3 L/min if baseline oxygen saturation was 93% or less and at 2 L/min if oxygen saturation was greater than 93%.
Main Outcomes and Measures The primary outcome was reported using the modified Rankin Scale score (disability range, 0 [no symptoms] to 6 [death]; minimum clinically important difference, 1 point), assessed at 90 days by postal questionnaire (participant aware, assessor blinded). The modified Rankin Scale score was analyzed by ordinal logistic regression, which yields a common odds ratio (OR) for a change from one disability level to the next better (lower) level; OR greater than 1.00 indicates improvement.
Results A total of 8003 patients (4398 (55%) men; mean [SD] age, 72 [13] years; median National Institutes of Health Stroke Scale score, 5; mean baseline oxygen saturation, 96.6%) were enrolled. The primary outcome was available for 7677 (96%) participants. The unadjusted OR for a better outcome (calculated via ordinal logistic regression) was 0.97 (95% CI, 0.89 to 1.05; P = .47) for oxygen vs control, and the OR was 1.03 (95% CI, 0.93 to 1.13; P = .61) for continuous vs nocturnal oxygen. No subgroup could be identified that benefited from oxygen. At least 1 serious adverse event occurred in 348 (13.0%) participants in the continuous oxygen group, 294 (11.0%) in the nocturnal group, and 322 (12.1%) in the control group. No significant harms were identified.
Conclusions and Relevance Among nonhypoxic patients with acute stroke, the prophylactic use of low-dose oxygen supplementation did not reduce death or disability at 3 months. These findings do not support low-dose oxygen in this setting.
Trial Registration ISRCTN Identifier: ISRCTN52416964
Introduction
Hypoxia is common during the first days after an acute stroke1 and associated with higher rates of neurological deterioration,2 death and institutionalization,3 and greater mortality.4 While cells in the ischemic penumbra are only viable for a few hours, brain cells beyond the ischemic core and penumbra remain at risk of delayed cell death for several days owing to vasogenic edema, inflammation, and programmed cell death, particularly if metabolic disturbances are compounded by hypoxia.5-7 Continuous monitoring is associated with better outcomes,8 but even in intensively monitored patients, hypoxia is not always identified and treated. Adverse outcomes were observed to be increased when only some desaturations of less than 90% were treated with oxygen and reduced when all were treated.3
Quiz Ref IDSupplemental oxygen could improve outcomes by preventing hypoxia and secondary brain damage but could also have adverse effects.9 These include vasoconstriction and pulmonary toxicity with high concentrations,9 respiratory tract infection due to contamination of the nasal tubes, the tubing acting as an impediment to mobilization, stress, and the direct effects of oxygen on vascular tone and blood pressure.10 Three small trials of short-term (≤12 hours) high-flow (10 to 45 L/min) therapeutic oxygen, aimed at generating supraphysiological blood oxygen levels, have not shown improved outcomes.11-13 A larger trial (n = 550) using low-dose supplemental oxygen (3 L/min for 24 hours) also showed no benefit,14 but early neurological recovery was improved in a study giving low-dose oxygen over 72 hours.15
The primary aim of the Stroke Oxygen Study (SO2S) was to determine whether low-dose oxygen therapy during the first 3 days after an acute stroke improves outcome compared with usual care (oxygen only when needed). Because oxygen may restrict mobility and interfere with daytime activities, the secondary hypothesis was that oxygen given at night only, when hypoxia is most likely, is more effective than continuous oxygen supplementation.
Methods
Study Design
This was a multicenter randomized clinical trial of oxygen supplementation with single-blind outcome assessment. The protocol and statistical analysis plan (Supplement 1 and Supplement 2),16,17 and data collection forms18 are published. Fully informed written or witnessed oral consent was given by the participants or, if they did not have capacity to consent, by a legal representative. The protocol was approved by the North Staffordshire Research Ethics Committee (06/Q2604/109).
Participants
Quiz Ref IDAdults (aged ≥18 years) with a clinical diagnosis of acute stroke within 24 hours of hospital admission (136 participating centers in the United Kingdom), who had no clinical indications for or contraindications to oxygen treatment or any concomitant condition likely to limit life expectancy to less than 12 months were eligible (see eAppendix in Supplement 3 for definition of acute stroke).
Randomization and Interventions
Participants were allocated 1:1:1 via central web-based minimized randomization19 to (1) continuous oxygen supplementation; (2) nocturnal oxygen supplementation only; or (3) no routine oxygen (control). The factors for which imbalances were minimized were the Six Simple Variables prognostic index for independent survival at 6 months20 (cutoffs: ≤0.1, >0.1 to ≤0.35, >0.35 to ≤0.70, >0.70), oxygen treatment before randomization (yes, no, unknown), baseline oxygen saturation on air (<95%, ≥95%), and time since stroke onset (cutoffs: ≤3, >3 to ≤6, >6 to ≤12, >12 to ≤24, >24 hours). Stroke onset was defined as the last time well for wake-up strokes. No blocking was used. Oxygen was administered per nasal tubes either continuously (day and night) during the first 72 hours after randomization or overnight (21:00 hours to 07:00 hours) for 3 nights. Oxygen was given at a flow rate of 3 L/min if baseline saturation was 93% or below or at a flow rate of 2 L/min if baseline saturation was greater than 93%. In the control group, no routine oxygen supplementation was given.
Vital signs were observed at least 4 times per day, with any abnormal findings treated independently of trial allocation. Patients requiring oxygen in the control group, patients in the nocturnal oxygen group during the day, or patients needing changes in oxygen dosage for clinical reasons were given the appropriate concentration of oxygen irrespective of treatment group. In addition, for 4144 patients recruited in the latter half of the study, spot checks of treatment adherence were undertaken at midnight and 6 am.
Outcomes and Blinding
Outcomes were assessed at 1 week by a member of the local research team and at 90 days via postal questionnaire. Telephone interviews were conducted with nonresponders or to clarify unclear or missing answers. Quiz Ref IDThe primary outcome was the modified Rankin Scale (mRS) 21 score (disability range, 0 [no symptoms] to 6 [death]; minimum clinically important difference 1 point) assessed at 90 days. Secondary outcomes were number of participants with neurological improvement (≥4-point decrease on the National Institutes of Health Stroke Scale [NIHSS])22,23 between randomization and day 7, the highest and lowest oxygen saturations within the first 72 hours, and mortality at 1 week. Further secondary outcomes at 90 days were mortality, number of participants alive and independent (mRS ≤2), number of participants living at home, Barthel Index activities of daily living (ADL) score,24 quality of life (EuroQol [EQ5D-3L]) score,25 and Nottingham Extended Activities of Daily Living score.26 For the NIHSS and Barthel Index, deaths were recorded as the worst outcome on the scale.27 Participants, their physicians, and local research staff who recorded the 1-week outcomes were not blind to the study interventions. Ninety-day assessments were undertaken by the SO2S study office, which was blind to treatment allocation.
Study Size
The initial recruitment target was 6000 participants, which was estimated to provide 90% power to detect small (0.2 mRS-point [eg, a 1-point improvement among 1 in 5 participants]) differences between oxygen (continuous and night-only groups combined) and no oxygen at a P value of less than or equal to .01 and 90% power at a P value of less than or equal to .05 to detect small differences between continuous oxygen and nocturnal-only oxygen. The study size was subsequently revised to 8000 participants, using ordinal methods,16,17 without knowledge of interim results, to increase the number of patients with severe stroke and thereby provide greater power to investigate any differential effectiveness of oxygen vs control within subgroups (defined by severity).
Statistical Analysis
The trial was designed to answer 2 key questions: whether oxygen supplementation improves outcome (mRS at 90 days) and whether giving oxygen at night is more effective than giving it continuously. The main comparisons, therefore, were of the 2 combined oxygen groups (continuous and nocturnal only) vs control, and of continuous oxygen vs nocturnal-only oxygen. The statistical analysis plan describes the analysis methods in detail (Supplement 1 and Supplement 2).17
The mRS was analyzed by ordinal logistic regression, which yields a common odds ratio (OR) for a move from one level to the next better (lower) level with an OR more than 1.00 indicating an improvement. For this and other outcome variables, a primary unadjusted analysis and a secondary covariate-adjusted analysis were performed. Adjusted analyses incorporated the following covariates: age, sex, baseline NIHSS score, baseline oxygen saturation, and the Six Simple Variables prognostic index for 6-month independence (or for analysis of mortality, the Six Simple Variables prognostic index for 30-day survival). Sensitivity analysis for the mRS used multiple imputation of missing values (using a chained equations method with 20 imputed data sets). Additional imputations were performed to allow for the possibility that data were missing not at random and were either better or worse than expected; missing values were thereby replaced by either very good (ie, lowest) or very poor (ie, highest) scores on the mRS as appropriate (eTable 3 in Supplement 3). Subgroups, for the mRS only, were analyzed by an interaction term and were predefined in the statistical analysis plan.17
For continuous outcomes, means and standard deviations or medians and interquartile ranges (IQRs) are reported, as appropriate. Unadjusted analyses used unrelated t tests, with the mean difference between treatments and corresponding CIs reported. The adjusted analysis used analysis of covariance, with the covariates specified earlier included in the analysis. For dichotomous outcomes, percentages were compared across the treatment comparisons using a χ2 test (unadjusted analyses). Adjusted analyses of dichotomous outcomes used binary logistic regression, with the covariates listed earlier; ORs and CIs are reported.
All analyses were by intention to treat, ie, according to the treatment group to which participants were allocated, irrespective of treatment actually received. Statistical significance was set at a P value of less than or equal to .05 with 95% CIs for the primary outcome and at a P value of less than or equal to .01 with 99% CIs for secondary outcomes. All reported P values are 2-sided. The main analysis was performed in SAS software for Windows, version 9.4 (SAS Institute Inc), and IBM SPSS for Windows, version 22 was used for sensitivity analyses.
Interim analyses of safety and effectiveness were reviewed annually by an independent data monitoring and safety committee. No α-spending adjustments were made.
Results
Participants
A total of 8003 participants from 136 collaborating centers in the United Kingdom were randomized and followed up between April 24, 2008, and January 27, 2015, (Figure 1). Baseline demographic and clinical characteristics, including stroke severity and oxygen saturation at randomization, were well-balanced in the 3 groups (Table 1). The mean (SD) age of participants was 72 (13) years, 4398 (55%) were men, and 7332 (92%) could undertake activities of daily living independently before the stroke. The mean (SD) NIHSS score was 7 (6) and the median score was 5 (IQR, 3 to 9). Prior to randomization, oxygen had been given to 1601 (20%) participants either in the ambulance or in the hospital. Patients were enrolled at a median of 20:43 hours (IQR, 11:59 to 25:32 hours) after symptom onset. The mean (SD) oxygen saturation at randomization was 96.6% (1.7%). All participants had a clinical diagnosis of stroke at the time of enrollment. The final diagnosis at 7 days was ischemic stroke in most cases (n = 6555; 82%), 588 (7%) had a primary intracerebral hemorrhage, and 294 (4%) were strokes without computed tomography diagnosis. There were 168 (2%) participants who were given a final diagnosis of transient ischemic attack, and 292 (4%) were found to have other nonstroke diagnoses with missing data in 106 (1%).
Informed consent was provided by 6991 (87%) participants, and 1012 (13%) had consent given by a relative, caregiver, or an independent legal representative (eTable 1 in Supplement 3). Of the participants who were unable to personally provide consent and were included by a representative, 6 (0.1%) refused consent at the 1-week reassessment and 22 (2%) refused at the 90-day assessment and were withdrawn.
Treatment Adherence
Adherence was similar in the continuous oxygen group (2158 [81%]) and the nocturnal oxygen group (2225 [83%]), all of whom were prescribed the full course of treatment (eTable 2 in Supplement 3). Use of oxygen was discontinued prematurely among 433 (16%) participants in the continuous oxygen group and 361 (14%) in the nocturnal oxygen group. The most common reason for early discontinuation of oxygen was discharge from the hospital. In the control group, trial oxygen was recorded as being given to 33 (1.2%) participants, with no recording of whether oxygen was given among 406 (15%).
Effect on Oxygenation
Oxygen treatment resulted in a significant increase of 0.8% in the highest oxygen saturation and 0.9% in the lowest oxygen saturation during the 72 hours of the intervention period in the continuous oxygen group compared with controls, and of 0.5% in the highest oxygen saturation and 0.4% in the lowest oxygen saturation during the 72 hours of the intervention period in the nocturnal oxygen group compared with controls (P < .001 for all comparisons; Table 2). Significantly more participants in the combined oxygen groups (n = 463 [9%]) required oxygen for clinical reasons during the intervention period than in the control group (n = 176 [7%]) (P < .001). Similarly, more participants in the continuous oxygen group (n = 254 [10%]) required oxygen than in the nocturnal oxygen group (n = 209 [8%]); P = .03.
Main Outcome
Quiz Ref IDThe primary analysis demonstrated that oxygen supplementation did not significantly improve functional outcome at 90 days (Figure 2). The unadjusted OR for a better outcome (lower mRS) was 0.97 (95% CI, 0.89 to 1.05; P = .47) for combined oxygen vs control, and 1.03 (95% CI, 0.93 to 1.13; P = .61) for continuous oxygen vs nocturnal oxygen. Secondary analyses adjusted for age, sex, baseline NIHSS score, baseline oxygen saturation, and the Six Simple Variables prognostic index yielded very similar results for the combined oxygen group vs control (OR, 0.97 [95% CI, 0.89 to 1.06]; P = .54) and for continuous oxygen vs nocturnal oxygen (OR, 1.01 [95% CI, 0.92 to 1.12]; P = .81). With similar numbers of missing responses in the 3 groups (continuous oxygen, n = 101; nocturnal oxygen, n = 106; and control, n = 119), findings were much the same in sensitivity analyses using multiple imputation or analyzing only participants who adherered to protocol (eTable 3 in Supplement 3).
Subgroup analysis (Figure 3) found no indication that treatment effectiveness differed in any of the predefined subgroups, even those in whom most benefit might be expected such as patients with more severe stroke or those for whom oxygen supplementation was started early after stroke onset.
Secondary Outcomes
Analyses of secondary outcomes also showed no benefit from oxygen (Table 2). Neurological impairment at 1 week improved from baseline to the same degree in all 3 groups with median NIHSS scores of 2 (IQR, 1 to 6) by 1 week. Oxygen treatment did not increase the number of participants who were alive and independent or back in their home, the ability to perform basic (Barthel Index) or extended (Nottingham Extended Activities of Daily Living) activities of daily living, or quality of life (EuroQol-5D-3L) at 90 days. The results remained unchanged after adjustment for baseline prognostic factors (eTable 4 in Supplement 3). Mortality (Figure 4) was similar in the oxygen (both groups combined) and control groups (hazard ratio [HR], 0.97 [99% CI, 0.78 to 1.21]; P = .75), and for continuous oxygen vs nocturnal oxygen (HR, 1.15 [99% CI, 0.90 to 1.48]; P = .15).
Exploratory Analyses
There was no evidence of increased stress levels (higher heart rates, higher blood pressure, and need for sedation) in the oxygen-treated group than in the control group or evidence that oxygen treatment was associated with more infections, with little difference in the highest temperature or the need for antibiotics (Table 2).
Safety Outcomes
The number of serious adverse events by 90 days was similar in the combined oxygen and control groups, but lower in the nocturnal oxygen group when compared with the continuous oxygen group (Table 2; eTable 5 in Supplement 3). No oxygen-related adverse events (respiratory depression, drying of mucous membranes) were reported.
Discussion
In this clinical trial of patients with acute stroke, routine prophylactic low-dose oxygen supplementation did not improve outcome among patients who were not hypoxic at baseline, whether oxygen was given continuously for 72 hours or at night only. This applied to the primary 90-day functional outcome and to all other tested outcomes, including early neurological recovery, mortality, disability, independence in basic and extended activities of daily living, and quality of life. The results remained unchanged in analyses adjusted for baseline prognostic factors and in sensitivity analyses using multiple imputation or analyzing adherers only. Quiz Ref IDSubgroup analyses did not identify any characteristics that would make a patient more likely to benefit from oxygen treatment (includes enrollment between 3 to 6 hours after stroke onset, patients with a lower baseline oxygen saturation, severe strokes, a reduced level of consciousness, and a history of heart failure or lung disease [ie, characteristics for which benefit from oxygen was most anticipated]). Because of the large overall size of this trial, these patient subgroups were each sufficiently large for the lack of observed benefit to be likely real and not a false negative.
In contrast to the much smaller SOS Pilot study,15 this trial showed no evidence of better early neurological recovery with oxygen. Subgroup analysis of an earlier study of low-dose oxygen supplementation in acute stroke14 suggested that oxygen might adversely affect outcome in patients with mild strokes, possibly through formation of toxic free radicals. A more recent study of short-burst high-flow oxygen (45 L/min) was terminated early (after enrollment of 85 patients) because of excess mortality in the actively treated group.13 Hyperoxia was independently associated with mortality in a large retrospective cohort study of ventilated patients with stroke.28 Although suggestive of potential harm, these findings could be due to confounding factors.
As a large pragmatic trial, this study included unselected patients with a clinical diagnosis of acute stroke without radiological confirmation. The sample therefore included ischemic and hemorrhagic strokes and participants who were later found to have mimics or transient ischemic attacks.
More than half of all acute stroke services in the United Kingdom participated, and wide inclusion criteria allowed enrollment of a representative sample of patients with ischemic and hemorrhagic stroke across the whole range of severity. Stroke severity was similar to that of the UK stroke population as a whole, with a median NIHSS of 5 in this trial and 4 in the UK Sentinel Stroke National Audit Programme, which includes every stroke patient admitted to UK hospitals.29 The median NIHSS of 127 950 patients with acute ischemic stroke in the US Get with the Guidelines Register30 was 5, as in this trial. A median NIHSS of 5 at baseline was also recorded in a large Dutch study of antibiotic prophylaxis after stroke, with similarly wide inclusion criteria.31
This study has several limitations. Minor benefits from oxygen treatment might have been masked by poor adherence. However, this seems unlikely given the high statistical power to detect even small improvements. Moreover, sensitivity analyses did not show better outcomes in the adherers-only group (eTable 3 in Supplement 3). Furthermore, this trial found significant increases in the oxygen saturations in the treated groups compared with the control group. Patients with acute stroke are often restless and confused. Ensuring full adherence would ideally require a 1 to 1 nurse-to-patient ratio. However, this is not possible outside an intensive care setting. The main outcome was assessed by postal questionnaire and supported by telephone interviews with nonresponders. This method has been used successfully in large pragmatic trials32,33 but has been replaced by remote multiple-rater video-recorded interviews or in-person interview and examination by an allocation-blinded rater using formal structured assessments in several more recent studies.34 Low-dose oxygen supplementation may not be sufficient to prevent severe desaturations; both the SOS Pilot15 and this trial found no significant difference in severe desaturations between the treatment and control groups. A small (N = 46) nonrandomized study comparing high-flow oxygen treatment via mask with low-flow supplementation via nasal cannula showed a trend toward lower mortality with high flow that was not statistically significant. However, evidence from randomized trials of high-flow oxygen treatment in acute stroke11-13 does not show that higher doses of oxygen are associated with better outcomes. Early administration of high-dose oxygen might help maintain the viability of the ischemic penumbra and allow a broader time window for neuroprotection or thrombolysis. This question was not addressed in this trial of prophylactic oxygen, but will be tested in the PROOF trial.35
The median time from stroke onset to randomization in this trial was 20 hours, 43 minutes. However, 101 participants were enrolled early (within 3 hours of symptom onset). Subgroup analysis (Figure 3) showed a similar lack of effect for oxygen in the small subset of patients enrolled early as in those enrolled later but was underpowered. Larger trials in the early time window would be needed to definitely exclude a benefit.
Conclusions
Among nonhypoxic patients with acute stroke, the prophylactic use of low-dose oxygen supplementation did not reduce death or disability at 3 months. These findings do not support low-dose oxygen in this setting.
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Article Information
Corresponding Author: Christine Roffe, MD, Institute for Science and Technology in Medicine, Keele University, Guy Hilton Research Centre, Thornburrow Drive, Stoke-on-Trent, Staffordshire ST4 7QB, United Kingdom (christine.roffe@uhnm.nhs.uk).
Accepted for Publication: August 12, 2017.
Correction: This article was corrected on November 14, 2017, for an incorrect SI conversion factor in Table 1, several incorrect 99% CIs in Table 2, an incorrect P value in Figure 3, and for minor typographical errors.
Author Contributions: Drs Roffe and Bishop had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.
Concept and design: Roffe, Gray.
Acquisition, analysis, or interpretation of data: All authors.
Drafting of the manuscript: Roffe, Sim, Ives, Ferdinand, Gray.
Critical revision of the manuscript for important intellectual content: All authors.
Statistical analysis: Sim, Bishop, Ives, Gray.
Obtained funding: Roffe, Gray.
Administrative, technical, or material support: Roffe, Nevatte, Sim.
Supervision: Roffe, Ives, Gray.
Conflict of Interest Disclosures: All authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Roffe reports receipt of a grant from the Research for Patient Benefit Programme and the Health Technology Assessment Programme of the National Institute for Health Research (NIHR), receipt of lecture and travel fees from Air Liqude, and independent membership on the data safety and monitoring committee of the PROOF trial. No other disclosures were reported.
Funder/Support: This project was funded by the NIHR Health Technology Assessment Programme (project number 09/104/21) and the Research for Patient Benefit Programme.
Role of the Funder/Sponsor: The NIHR had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.
Disclaimer: The views and opinions expressed herein are those of the authors and do not necessarily reflect those of the Health Technology Assessment, NIHR, the National Health Service (NHS), or the Department of Health. The Stroke Oxygen Study (SO2S) was sponsored by North Staffordshire Combined Healthcare NHS Trust.
SO2S Collaborators: Writing Committee: Christine Roffe, Tracy Nevatte, Julius Sim, Jon Bishop, Philip Ferdinand, Natalie Ives, and Richard Gray. Statistical Analysis: Jon Bishop, Julius Sim, Natalie Ives. Trial Management Group: Christine Roffe (Chair), Tracy Nevatte, Julius Sim, Richard Gray, Natalie Ives, Jon Bishop, Sarah Pountain, Peter and Linda Handy. Trial Steering Committee: Martin Dennis (Chair), Lalit Kalra, Sian Maslin-Prothero, Jane Daniels, Peta Bell, Richard Lindley. Data Safety and Monitoring Committee: Stephen Jackson (Chair), Thompson Robinson, Martyn Lewis. Trial Coordinating Center: Alison Buttery, Clare Gething, Joy Dale, Wendy Lawton, Chris Buckley, Eddie Skelson, Nicola Mellor, Kathryn McCarron, Jean Leverett, Emily Linehan, Stephanie Edwards, Terri Oliver, Loretto Thompson, Sian Edwards, Clare Lees and Jackie Richards. Study Team at Birmingham Clinical Trials Unit: Andrew Howman, Robert Hills, Nick Hilken, Samir Mehta and Chakanaka Sidile. Literature Searches: Frank Lally, Philip Ferdinand, Girish Muddegowda. Editorial Assistance: Frank Lally, David Roffe, Steve Alcock.
Participating Centers and SO2S Collaborative Group Members (asterisks indicate principal investigator[s]; numeric values indicate the number of participants enrolled): Royal Stoke University Hospital, Stoke-on-Trent: K Finney, S Gomm, J Lucas, H Maguire, C Roffe* (478); St George’s Hospital, London: I Jones, L Montague, B Moynihan*, J O’Reilly, C Watchurst (288); The Royal Liverpool University Hospital, Liverpool: P Cox, G Fletcher, A Ledger, S Loharuka*, P Lopez, A Manoj* (257); Royal Bournemouth General Hospital, Bournemouth: O David, D Jenkinson*, J Kwan, E Rogers, E Wood (240); Kings College Hospital, London: A Davis, L Kalra*, E Khoromana, R Lewis, H Trainer (231); Leeds General Infirmary, Leeds: M Kambafwile, L Makawa, E Veraque, P Wanklyn*, D Waugh (204); Salford Royal Hospital, Salford: E Campbell, J Hardicre, V O’Loughlin, C Smith*, T Whittle (192); Southend Hospital, Southend: P Guyler*, P Harman, A Kumar Kundu, D Sinha, S Tysoe (188); Countess of Chester Hospital, Chester: S Booth, K Chatterjee*, H Eccleson, C Kelly, S Leason (176); The Royal Victoria Infirmary, Newcastle upon Tyne: A Barkat, J Davis, A Dixit*, M Fawcett, V Hogg (168); Royal Sussex County Hospital, Brighton: K Ali*, J Breeds, J Gaylard, J Knight, G Spurling (164); Musgrove Park Hospital, Taunton: S Brown, L Caudwell, L Dunningham, J Foot, M Hussain* (156); Bristol Royal Infirmary, Bristol: J Chambers, P Murphy*, M Osborn, A Steele (151); Royal Preston Hospital, Preston: S Duberley, C Gilmour, B Gregary, S Punekar*, S Raj (148); University Hospital Aintree, Liverpool: J Atherton, R Durairaj*, T Fluskey, Z Mellor, V Sutton (148); Birmingham Heartlands Hospital, Birmingham: P Carr, J McCormack, D Sandler*, C Stretton, K Warren (143); Pennine Acute Hospital, Rochdale: L Harrison, L Johnson, R Namushi*, N Saravanan, N Thomas (133); Queen’s Hospital, Burton: J Birch, R Damant, B Mukherjee* (131); University Hospital Coventry, Walsgrave: L Aldridge, P Kanti Ray*, S Nyabadza, C Randall, H Wright (129); Wansbeck Hospital, Northumberland: C Ashbrook-Raby, A Barkat, R Lakey, C Price*, G Storey (124); Royal Devon and Exeter Hospital, Wonford: L Barron, A Bowring, H Eastwood, M James*, S Keenan (113); Royal United Hospital, Bath: J Avis, D Button, D Hope, B Madigan, L Shaw* (113); Royal Cornwall Hospital, Treliske: K Adie, G Courtauld, F Harrington, C Schofield (112); Queen Elizabeth the Queen Mother Hospital, Margate: G Gunathilagan*, S Jones, G Thomas (105); York Hospital, York: J Coyle*, N Dyer, S Howard, M Keeling, S Williamson (105); University Hospital of North Durham, Durham: E Brown, S Bruce, B Esisi*, R Hayman, E Roberts (99); Derriford Hospital, Plymouth: C Bailey, B Hyams, A Mohd Nor*, N Persad (96); Selly Oak Hospital (Acute), Birmingham: J Hurley, E Linehan, J McCormack, J Savanhu, D Sims* (92); Whiston Hospital, Prescot: R Browne, S Dealing, V Gowda* (89); Torbay District General Hospital, Torbay: C Bailey, P Fitzell, C Hilaire, D Kelly*, S Szabo (88); Charing Cross Hospital, London: E Beranova, J Pushpa-Rajah, T Sachs, P Sharma*, V Tilley (87); Leighton Hospital, Crewe: N Gautam, C Maity*, R Miller, C Mustill, M Salehin*, A Walker (87); Kent & Canterbury Hospital, Canterbury: H Baht, I Burger*, L Cowie, T Irani, A Thomson (84); New Cross Hospital, Wolverhampton: P Bourke, K Fotherby*, D Morgan, K Preece (84); Northwick Park Hospital, Harrow: L Burgess, D Cohen*, M Mpelembue (83); Barnsley District General Hospital, Barnsley: M Albazzaz*, R Bassi, C Dennis, K Hawley, S Johnson-Holland (82); Blackpool Victoria Hospital, Blackpool: H Goddard, J Howard, C Jeffs, J Mcilmoyle*, A Strain (82); North Tyneside General Hospital, North Shields: J Dickson, K Mitchelson, C Price*, V Riddell, A Smith (79); Eastbourne District General Hospital, Eastbourne: C Athulathmudali*, E Barbon (76); Warrington Hospital, Warrington: K Bunworth, L Connell, G Delaney-Sagar, K Mahawish*, O Otaiku*, H Whittle (75); Princess Royal Hospital, Haywards Heath: R Campbell*, A Nyarko (71); City Hospitals, Sunderland: S Crawford, C Gray*, D Gulliver, R Lakey, N Majmudar*, S Rutter (69); William Harvey Hospital, Ashford: L Cowie, D Hargroves*, T Webb (69); Stepping Hill Hospital, Stockport: A Brown, H Cochrane, S Krishnamoorthy*, J McConniffe (66); The James Cook University Hospital, Middlesborough: D Broughton*, K Chapman, L Dixon, A Surendran (66); Northampton General Hospital (Acute), Northampton: M Blake*, F Faola, A Kannan, P Lai, B Vincent (59); Leicester General Hospital, Leicester: M Dickens, D Eveson, S Khan, R Marsh, A Mistri*,(57); Rotherham District General Hospital, Rotherham: J Harris, J Howe, K McNulty, J Okwera* (56); St Peter’s Hospital, Chertsey: R Nari*, E Young (56); Macclesfield District General Hospital, Macclesfield: A Barry, B Menezes, M Sein*, H Rooney, L Wilkinson (55); Manor Hospital, Walsall: S Hurdowar, K Javaid*, K Preece (54); Bradford Royal Infirmary, Bradford: R Bellfield, B Hairsine, L Johnston, C Patterson*, S Williamson (53); Luton & Dunstable Hospital, Luton: F Justin, S Sethuraman*, L Tate (50); Royal Blackburn Hospital, Blackburn: A Bell, M Goorah, N Goorah*, A Sangster (50); University College Hospital, London: N Bhupathiraju, L Latter, P Rayson, R Simister*, R Uday Erande (50); Addenbrooke’s Hospital, Cambridge: N Butler, D Day, E Jumilla, J Mitchell, E Warburton* (48); Queen Alexandra Hospital, Portsmouth: T Dobson, C Edwards, J Hewitt*, L Hyatt, D Jarret* (47); North Devon District Hospital, Barnstaple: G Belcher, M Dent*, F Hammonds, J Hunt, C Vernon (45); Solihull Hospital, Solihull: A Carter, K Elfandi*, S Stafford (45); Pilgrim Hospital, Boston: A Hardwick, D Mangion*, S Marvova* (44); Norfolk & Norwich University Hospital, Norwich: J Jagger, P Myint*, G Ravenhill, N Shinh*, E Thomas, N Wyatt (41); Gloucestershire Royal Hospital, Gloucester: P Brown, F Davis, D Dutta*, J Turfrey, D Ward (40); Royal Surrey County Hospital, Guildford: O Balazikova, A Blight*, C Lawlor, K Pasco (39); Southport & Formby District General Hospital, Southport: M Marshall, P McDonald*, H Terrett (39); Bishop Auckland General Hospital, Bishop Auckland: E Brown, A Mehrzad* (35); Airedale General Hospital, Keighley: R Bellfield, P Garnett, B Hairsine, S Mawer*, M Smith*, S Williamson (34); Calderdale Royal Hospital, Halifax: C Button, J Greig, B Hairsine, A Nair, P Rana*, I Shakir* (34); Doncaster Royal Infirmary, Doncaster: P Anderton, D Chadha*, L Holford, D Walstow (34); East Surrey Hospital, Redhill Y Abousleiman*, S Collins, A Jolly, B Mearns* (34); Medway Maritime Hospital, Gillingham: P Akhurst, B Bourne, S Burrows, S Sanmuganathan*, S Thompson (34); Royal Derby Hospital, Derby: T England*, A Hedstrom, M Mangoyana, M Memon*, L Mills, K Muhiddin*, I Wynter (33); Wycombe General Hospital, High Wycombe: A Benford, M Burn*, A Misra, S Pascall (33); The Princess Royal Hospital, Telford: R Campbell*, N Motherwell (32); Harrogate District Hospital, Harrogate: S Appleby, S Brotheridge*, J Strover (30); Peterborough City Hospital, Peterborough: S D’Souza, P Owusu-Agyei*, S Subramonian, N Temple (30); West Cumberland Hospital, Whitehaven: R Jolly, O Orugun* (30); Colchester General Hospital, Colchester: M Keating, R Saksena*, A Wright (29); Royal Hampshire County Hospital, Winchester: D Ardern, C Eglinton, R Honney, N Smyth*, J Wilson (29); Dorset County Hospital, Dorchester: S Breakspear, L O’Shea, H Prosche*, S Sharpe (27); Frimley Park Hospital, Frimley: S Atkinson, B Clarke*, L Moore (27); Royal Hallamshire Hospital, Sheffield: S Duty, K Harkness, M Randall*, E Richards, K Stocks (27); Yeovil District Hospital, Yeovil: S Board, C Buckley, D Hayward, K Rashed*, R Rowland-Axe (25); Poole General Hospital, Poole: C Dickson, L Gleave, S Ragab* (24); Frenchay Hospital, Bristol: N Baldwin*, S Hierons, H Skuse, L Whelan (22); Princess Alexandra Hospital, Harlow: L Brown, M Burton, A Daniel, S Hameed*, S Mansoor* (22); West Suffolk Hospital, Bury St Edmunds: A Azim*, M Krasinska, J White (22); The Ulster Hospital, Dundonald: M Power*, B Wroath (21); Watford General Hospital, Watford: D Collas*, S Sundayi, E Walker (21); Southampton General Hospital, Southampton: M Brown, G Durward*, V Pressly, B Watkins, N Weir*, D Whittaker (20); Craigavon Area Hospital, Portadown: C Douglas, M McCormick*, M McParland (19); Royal Lancaster Infirmary, Lancaster: C Culmsee, P Kumar* (18); Basildon Hospital, Basildon: M Bondoc, B Hadebe, R Rangasami*, I Udeozor, U Umansankar* (17); Birmingham City Hospital, Sandwell: F Kinney, S Hurdowar, S Ispoglou*, S Kausar* (17); City Hospital, Nottingham: P Cox, A Ferguson, D Havard, F Shelton, A Shetty* (16); Antrim Area Hospital, Antrim: C Edwards, C McGoldrick, A Thompson, D Vahidassr* (15); Pinderfields General Hospital, Wakefield: G Bateman, P Datta*, A Needle (15); Royal Albert Edward Infirmary, Wigan: P Farren, S Herath* (15); Good Hope Hospital, Sutton Coldfield: I Memon*, S Montgomery (13); Hereford County Hospital, Hereford: S Black, S Holloman, C Jenkins*, F Price (13); South Tyneside District General Hospital, South Shields: M Duffy, J Graham, J Scott (13); Broomfield Hospital, Chelmsford: A Lyle, F Mcneela, K Swan, J Topliffe, V Umachandran* (12); Wythenshawe Hospital, Wythenshawe: B Charles, E Gamble*, S Mawn (11); Warwick Hospital, Warwick: M Dean, B Thanvi* (10); Ipswich Hospital, Ipswich: M Chowdhury*, J Ngeh, S Stoddart (9); Kettering General Hospital, Kettering: K Ayes*, J Kessell (9); Nevill Hall Hospital, Abergavenny: B Richard*, E Scott (9); Princess Royal University Hospital, Orpington: L Ajayo, E Khoromana, E Parvathaneni, B Piechowski-Jozwiak*, L Sztriha* (9); Scarborough General Hospital, Scarborough: L Brown, K Deighton, E Elnour, J Paterson*, E Temlett (9); Hull Royal Infirmary, Hull: A Abdul-Hamid*, J Cook, K Mitchelson (8); King’s Mill Hospital, Sutton-in-Ashfield: M Cooper*, I Wynter (8); The Royal London Hospital, London: P Gompertz*, O Redjep, J Richards, R Uday Erande (8); Trafford General Hospital, Manchester: S Anwar*, A Ingram, S McGovern, S Musgrave*, L Tew (8); Altnagelvin Area Hospital, Londonderry: J Corrigan*, C Diver-Hall, M Doherty, M McCarron* (7); Darent Valley Hosptial, Dartford: P Aghoram*, T Daniel, S Hussein, S Lord (7); Royal Berkshire Hospital, Reading: N Mannava, A van Wyk* (6); Arrowe Park Hospital, Wirral: J Barrett*, R Davies*, A Dodd, D Lowe*, P Weir (5); Basingstoke and North Hampshire Hospital, Basingstoke: D Dellafera, E Giallombardo* (5); Lincoln County Hospital, Lincoln: S Arif, R Brown, S Leach* (5); Hexham General Hospital, Hexham: C Price*, V Riddell (4); Manchester Royal Infirmary, Manchester: J Akyea-Mensah, J Simpson* (4); Salisbury District Hospital, Salisbury: T Black*, C Clarke, M Skelton (4); Croydon University Hospital, Croydon: J Coleman, E Lawrence* (3); Russells Hall Hospital, Dudley: A Banerjee*, A Boyal, A Gregory (3); Worthing Hospital, Worthing: S Ivatts*, M Metiu (3); Bedford Hospital, Bedford: A Elmarimi*,S Hunter (2); James Paget Hospital, Great Yarmouth: H Benton, M Girling, P Harrison*, H Nutt, S Mazhar Zaidi*, C Whitehouse (2); St Richard’s Hospital, Chichester: G Blackman, S Ivatts* (2); Erne Hospital, Fermanagh: M Doherty, J Kelly* (1); University Hospital Lewisham, Lewisham: M Patel* (1); Bronglais General Hospital, Aberystwyth: P Jones* (0); Hillingdon Hospital, Hillingdon: A Parry* (0); Kingston Hospital, Kingston upon Thames: L Choy* (0); Morriston Hospital, Morriston: M Wani* (0); North Middlesex Hospital, Enfield: T Adesina, A David, R Luder* (0); Staffordshire District General Hospital, Stafford: A Oke* (0); St Helier Hospital, Carshalton: V Jones*, P O’Mahony, C Orefo (0); Whipps Cross University Hospital, London: R Simister* (0).
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Kidney Res Clin Pract > Volume 34(4); 2015 > Article
Lee: RNA sequencing of the nephron transcriptome: a technical note
Abstract
To understand the functions of the kidney, the transcriptome of each part of the nephron needs to be profiled using a highly sensitive and unbiased tool. RNA sequencing (RNA-seq) has revolutionized transcriptomic research, enabling researchers to define transcription activity and functions of genomic elements with unprecedented sensitivity and precision. Recently, RNA-seq for polyadenylated messenger RNAs [poly(A)′-mRNAs] and classical microdissection were successfully combined to investigate the transcriptome of glomeruli and 14 different renal tubule segments. A rat kidney is perfused with and incubated in collagenase solution, and the digested kidney was manually dissected under a stereomicroscope. Individual glomeruli and renal tubule segments are identified by their anatomical and morphological characteristics and collected in phosphate-buffered saline. Poly(A)′-tailed mRNAs are released from cell lysate, captured by oligo-dT primers, and made into complementary DNAs (cDNAs) using a highly sensitive reverse transcription method. These cDNAs are sheared by sonication and prepared into adapter-ligated cDNA libraries for Illumina sequencing. Nucleotide sequences reported from the sequencing reaction are mapped to the rat reference genome for gene expression analysis. These RNA-seq transcriptomic data were highly consistent with prior knowledge of gene expression along the nephron. The gene expression data obtained in this work are available as a public Web page (https://helixweb.nih.gov/ESBL/Database/NephronRNAseq/) and can be used to explore the transcriptomic landscape of the nephron.
Keywords
Microdissection, Nephron, RNA sequencing, Transcriptome
Introduction
Profiling all the transcripts expressed in the glomerulus and each renal tubule segment will greatly advance our understanding of the functions and pathophysiology of the kidney. This task requires a precise, unbiased, and high-throughput transcriptomic method that enables researchers to create a catalog of all the RNA species and accurately measure their quantities in a cell.
However, gene expression profiling methods that have been used in renal transcriptomics such as microarrays [1], [2] or Sanger sequencing of complementary DNAs (cDNAs) [3], [4], [5] suffer from low sensitivity and high false positivity. The utility of microarrays is limited by the requirement of prior knowledge of genes expressed in a cell and by a narrow range of dynamic expression due to signal saturation. Sanger sequencing of cDNAs is low throughput and not sensitive enough to detect lowly expressed transcripts.
RNA sequencing (RNA-seq) uses next-generation sequencing (NGS) technologies to profile the whole transcriptome in a massive parallel manner [6]. In this method, RNAs of interest [i.e., messenger RNAs (mRNAs), microRNAs, or other noncoding RNAs] are converted into adapter-ligated cDNAs and sequenced in a parallel manner, generating massive amount of short DNA sequences (typically 35-100 base pairs) [6]. These nucleotide sequences (commonly called reads) are either mapped to a reference genome or assembled to generate a de novo transcriptome. Reads mapped to the reference genome can be visualized on a genome browser to explore transcriptional activity across the genome or can be counted to quantify the expression level of each transcript. Compared with microarrays or Sanger sequencing, RNA-seq has many advantages, including higher sensitivity (requiring lower amount of RNAs), low false positivity (no background signals originating from cross-hybridization), unlimited range of dynamic expression (no signal saturation), and capability to process many samples in high-throughput settings (many samples can be multiplexed and sequenced in parallel).
Recently, RNA-seq transcriptomic data for glomeruli and 14 different renal tubule segments collected from rat kidneys have been published [7]. This review discusses the technical aspects of RNA-seq profiling of the nephron, focusing on how RNA-seq and classical microdissection can be combined to profile the transcriptomes of the rat nephron. This review does not intend to provide an in-depth review of the NGS technologies. Readers are referred to excellent reviews on the principles of NGS [8], [9]. For more general information on RNA-seq, the author would like to recommend a well-curated online Web site available at http://rnaseq.uoregon.edu/.
Microdissection of renal tubule segments
Collagenase-assisted manual microdissection of renal tubule segments, first reported by Burg et al in 1966 [10], has been successfully used in renal physiology for more than 4 decades. This method expanded the scope of renal research to glomeruli and tubule segments that had not been accessible by micropuncture. To collect glomeruli and renal tubule segments for RNA-seq profiling, a protocol previously published in the article by Wright et al [11] was used with minor modifications. A male Sprague Dawley rat weighing 150-200 g is killed by decapitation (Animal Study Protocol No. H-0110R2, approved by the Animal Care and Use Committee, National Heart, Lung, and Blood Institute). After a midline incision of the abdominal wall, the left renal artery is selected by introducing a ligature in the aorta between the left and renal arteries. Then, a thin plastic catheter is introduced through a slit made on the wall of the aorta below the level of the left renal artery, and through this catheter, the left kidney is perfused with 10 mL of ice-cold, bicarbonate-free dissecting solution (NaCl 135 mmol/L; Na2HPO4 1 mmol/L; Na2SO4 1.2 mmol/L; MgSO4 1.2 mmol/L; KCl 5 mmol/L; CaCl2 2 mmol/L; glucose 5.5 mmol/L; and HEPES 5 mmol/L, adjusted to pH 7.4), followed by 10 mL of collagenase solution [1 mg/mL of collagenase B (purified from Clostridium histolyticum, Roche Diagnostics, Indianapolis, IN, USA) and 1 mg/mL of bovine serum albumin (MP Biomedicals, Santa Ana, CA, USA) in the dissecting solution] warmed to 37°C. Before use, the dissecting solution in which collagenase and bovine serum albumin are to be dissolved is usually bubbled with 100% O2 for 10 minutes to mitigate hypoxia. It is crucial that the blood in the left kidney is completely removed by the initial perfusion with the dissecting solution because protease inhibitors in the plasma prevent collagenase from acting on the kidney. Although some renal tubule segments (e.g., the cortical collecting duct) can be dissected without collagenase digestion, most parts of the nephron cannot be dissected if the kidney is not properly digested. To facilitate the perfusion process, the wall of the inferior vena cava needs to be cut so that the blood and solution returning from the left kidney via the left renal vein can easily exit the circulation. After the perfusion with the collagenase solution, the left kidney is removed and cut into ∼1 mm3 cubes, put into the same collagenase solution, and incubated in a chamber filled with O2 at 37°C for 30-90 minutes. The concentration of collagenase and the duration of incubation need to be adjusted, depending on which tissue compartment is going to be dissected. The cortex can be digested in 1% collagenase for 30 minutes. The outer and inner medullas require a higher collagenase concentration and longer duration (1% and 45 minutes for the outer medulla; 3% and up to 90 minutes for the inner medulla), along with hyaluronidase of the same concentration as collagenase. Even with a higher concentration of collagenase, digestion of the inner medulla was successful only once in every 3 or 4 experiments. A thorough pretreatment of the dissecting solution and other apparatuses to inactivate ribonuclease is generally not needed, although general precautions used in RNA works (i.e., wearing gloves, using ribonuclease-inactivating products) need to be followed. This is probably because the content of ribonuclease is not high in the kidney compared with other organs such as the spleen or the pancreas.
After digestion, the tissue chunks are taken out of the collagenase solution, washed twice in ice-cold dissecting solution to end digestion process, and put in a glass dish containing ice-cold dissecting solution. This dish is then brought under a stereomicroscope for microdissection. To minimize tissue degradation, the digested kidney tissue needs to be maintained at a cool temperature, ideally at 4°C. It is generally recommended to use a stereomicroscope that has a coolant-circulating system attached to the bottom of the stage of the microscope. If the glass dish containing the digested tissue is maintained at 4°C, a microdissection session can be extended up to 4 hours with minimal tissue degradation. For optimal identification of tubule segments, it is better to have the light source for the stereomicroscope below the object stage.
The digested kidney tissue is examined using Dumont No. 5 forceps (https://www.dumonttweezers.com/Tweezer/Tweezer/469). Before use, the tips of the tweezers need to be sharpened and polished with a piece of sandpaper so that the tweezers can easily grab and manipulate tubule segments and a dissected tubule segment or other irrelevant tissue does not stick to the surface of the tweezer tips. The degree of tissue digestion can be assessed by trying to grab and separate tissue chunk using tweezers. If it is too difficult to separate tubules from surrounding tissue, the tissue chunks can be transferred back to the collagenase solution for more digestion (up to 5-10 minutes).
Identifying individual renal tubule segments requires working knowledge of renal anatomy. Through practice, the dissector becomes more and more familiar with the morphology and locations of individual renal tubule segments. The anatomical and morphological characteristics of renal tubule segments were described in detail in the article by Wright et al [11]. The knowledge of renal anatomy is particularly important when tubules with similar looks exist in more than 1 tissue compartment (e.g., S1, S2, and S3 segments of the proximal tubule: S1 is connected to a glomerulus; S2 exists in the medullary ray; and S3 exists in the outer medulla and transitions to the thin descending limb).
With tissue manipulation and microdissection, the visual field easily becomes cluttered with tissue debris and floating tubules. Therefore, it is critically important that the collected glomeruli and tubule segments be washed in 1× phosphate-buffered saline (PBS) before they are finally collected for RNA-seq. This step minimizes contamination from other tubules and tissue debris. A new glass dish containing 1× PBS is prepared on a separate stereomicroscope, and the microdissected glomeruli or tubule segments are collected using a long 10-μL pipette tip and transferred to the PBS dish. Although thin glass tubes were used in the original description of this step [11], pipette tips are much easier to manipulate.
After washing 2 times, the dissected tubules are collected in 2 μL of 1× PBS using a pipette tip and put into a 0.5-mL polymerase chain reaction (PCR) tube. It is important to use as small volume of PBS as possible to collect the dissected tubules so that primers, deoxyribonucleotide triphosphates (dNTPs), and enzymes used in the reverse transcription are not diluted.
Construction of RNA-seq libraries
The overall workflow for the construction of cDNA libraries for RNA-seq of microdissected renal tubule segments is shown in Fig. 1. The microdissected renal tubule segments are lysed in mild cell lysis condition, and mRNAs are released from the cell lysate.
Cell lysis
An experienced dissector can collect 1-4 mm (typically 500-2,000 cells) of renal tubule segments within 2-4 hours. Provided that a renal tubular epithelial cell contains ∼1 pg of total RNAs, there are likely less than 1 ng of total RNAs in the collected sample. Because a conventional RNA-seq method that involves RNA fragmentation and reverse transcription with random hexamer primers (e.g., Illumina TruSeq protocol) requires a minimum of 100 ng of total RNAs as starting material, a highly sensitive method capable of creating cDNAs from a very small amount of total RNAs is needed for RNA-seq of renal tubule segments. For this work, the author used a modified version of the single-cell RNA-seq method that was originally developed for transcriptomic profiling of human oocytes [12].
To lyse the dissected tubules and release mRNAs, 20 μL of mild cell lysis buffer [0.9× PCR Buffer II without MgCl2 (Life Technologies, Grand Island, NY, USA); 1.35 mmol/L MgCl2 (Life Technologies); 0.45% Nonidet P-40 (Sigma-Aldrich, St. Louis, MO, USA); 4.5 mmol/L dithiothreitol (Life Technologies); 0.18 U/μL SUPERase-In (Ambion, Grand Island, NY, USA); 0.36 U/μL RNase inhibitor (Ambion); 12.5nM UP1 primer (5′-ATATGGATCCGGCGCGCCGTCGACTTTTTTTTTTTTTTTTTTTTTTTT-3′); dNTP mix (0.045 mmol/L each); and nuclease-free water] is added to the PBS containing dissected tubules and mixed well using a pipette. This mixture is spun down at 7,500 g at 4°C for 30 seconds, heated at 70°C for 90 seconds to release mRNAs, and then spun down again at 7,500 g at 4°C for 30 seconds. Then, 0.5 μL of the cell lysate is taken and added to a new 0.5-μL PCR tube containing 4 μL of the same cell lysis buffer to make a total of 4.5 μL. The last step minimizes the dilution of the reagents for reverse transcription by PBS. This cell lysate should be used immediately for the first-strand synthesis.
Alternatively, total RNAs can be isolated from microdissected tubule segments using silica membrane columns. When columns are used, RNAs should be eluted in as small volume (∼5 μL) as possible. An advantage of column-based RNA isolation over direct cell lysis is that RNAs can be stored in a -70°C freezer for future work.
Reverse transcription and amplification
The method for cDNA synthesis used in the nephron RNA-seq is shown in Fig. 2. This homopolymer-tailing method uses a pair of universal oligo-dT primers and poly(A)′-tailing of 5′-ends to allow for PCR amplification. Despite several shortcomings such as limited coverage of proximal exons, bias toward 3′-end, and loss of strand information, this method is sensitive enough to reliably amplify mRNAs from total RNAs as small as 20 pg [12]. The first-strand synthesis is started by adding 0.5 μL of reverse transcriptase mix [13.2 U/μL SuperScript III reverse transcriptase (Life Technologies); 0.4 U/μL RNase inhibitor (Ambion); and 0.07 U T4 gene 32 protein (Roche Diagnostics)] to 4.5 μL of the cell lysate to make 5 μL. If the total RNAs were isolated using silica membrane columns, 0.5-1 μL of the total RNA is added to 4-4.5 μL of the same cell lysis buffer (see the previous section) to make the total volume of 4.5 μL, and then 0.5 μL of the reverse transcriptase mix is added. Because the cell lysis step is not needed, NP-40 can be replaced with the same volume of nuclease-free water. The UP1 primers in the cell lysate capture poly(A)′-mRNAs.
All the steps following the first-strand synthesis leading to cDNA amplification are identical to the previously published protocol [7], [12]. After removing excess primers, a poly(A)′-tail is added to the 5′-end of the DNA-RNA hybrid molecule (the product of the first-strand synthesis) by terminal transferase to allow for primer annealing in the next step, and the RNA template is removed by RNase H. Then, the second-strand synthesis is performed using a second universal primer (UP2, 5′-ATATCTCGAGGGCGCGCCGGATCCTTTTTTTTTTTTTTTTTTTTTTTT-3′) annealing to the poly-(A)′ tail added to the 5′-end in the previous step. Finally, this cDNA molecule is amplified (the first-round PCR, 18-20 cycles) using the same universal primers (UP1 and UP2) and a high-performance DNA polymerase [TaKaRa Ex Taq HS DNA polymerase (Clontech Laboratories, Mountain View, CA, USA)].
Once the first-round PCR is complete, a quantitative real-time PCR (qRT-PCR) for a housekeeping gene (e.g., glutaraldehyde-3-dehydrogenase, beta-actin) is performed to see if the reverse transcription and amplification are successful. A successfully amplified sample will show an amplification curve that begins to rise before 20-25 cycles of qRT-PCR. If the qRT-PCR is successful, the cDNAs amplified in the first-round PCR are further amplified (the second-round PCR, 9-12 cycles) using NH2-modified universal primers [5′-NH2-UP1, 5′-(NH2)-ATATGGATCCGGCGCGCCGTCGACTTTTTTTTTTTTTTTTTTTTTTTT-3′; and 5′-NH2-UP2, 5′-(NH2)-ATATCTCGAGGGCGCGCCGGATCCTTTTTTTTTTTTTTTTTTTTTTTT-3′]. The purpose of this switch to NH2-modified primers is to minimize the amount of primer sequences appearing in the final cDNA libraries. The total number of PCR rounds should not exceed 32 because excessive amplification likely introduces more PCR errors.
Preparation of adapter-ligated cDNA libraries
To create adapter-ligated cDNAs compatible with Illumina sequencing, the cDNAs amplified in the previous step are sheared into ∼200 bp fragments by sonication using a Covaris S2 system (Covaris Inc., Woburn, MA, USA) and then ligated to adapters. Before committing many samples to the adapter ligation process, the condition for sonication needs to be optimized so that the average size of the fragments is around 200 bp. After sonication, the cDNA fragments are cleaned up and eluted in 50 μL of nuclease-free water. The adapter ligation process is done on a Mondrian SP+ workstation (NuGen, San Carlos, CA, USA) using an Ovation Ultralow library prep system (NuGen). Finally, the adapter-ligated cDNAs are amplified with 10-18 rounds of PCR and visualized on 2% agarose gel to select cDNAs within 200-400 bp. The concentration of the final cDNA library is determined using a Qubit fluorometer (Invitrogen, Grand Island, NY, USA). A good cDNA library will give a concentration ranging from 1 to 5 ng/μL.
Using adapters with multiplexed barcodes, cDNA libraries from multiple samples can be mixed into a single library for sequencing. The barcodes are 6-nucleotide-long DNA sequences incorporated in the stem or arm of the adapter molecule, and they can be used as identifiers for individual libraries. Each library is prepared using a barcoded adapter, and cDNA libraries with different barcodes are mixed in the same amount (e.g., 10 ng each) so that each library can be sequenced at the same depth. This multiplexing technique can save considerable amount of resource by enabling researchers to obtain sequences from multiple samples in a single sequencing run without significant loss of depth of sequencing. For example, 8 barcoded libraries can be mixed into 1 sample and sequenced to generate ∼30 million sequences per each library. This depth of sequencing is usually good enough for differential expression analysis.
Next-generation sequencing
The technical details of Illumina sequencing are reviewed in the article by Metzker [9]. In the Nephron RNA-seq project [7], the adapter-ligated cDNA libraries were sequenced at the Genomics Core Facility of the National Heart, Lung, and Blood Institute using an Illumina HiSeq 2000 platform (Illumina Inc., San Diego, CA, USA) to generate 50-bp paired-end reads. Because it is usually not feasible for a small individual laboratory to own and operate an expensive sequencer, adapter-ligated cDNA libraries are usually sent to a core laboratory or a company that offers sequencing as a paid service. The choice between single- and paired-end sequencing depends on the purpose of the transcriptomic study to be conducted and resources available. Although paired-end sequencing enables more accurate mapping and thereby generates more information on the transcriptome, it takes longer and costs more money than single-end sequencing does. Paired-end sequencing is preferred for a deep profiling of transcriptome, whereas single-end sequencing usually suffices when the primary goal is differential expression analysis of known genes.
Analysis of RNA-seq data
The nucleotide sequences of cDNA libraries are reported in FASTQ format, “FASTA with quality scores.” Fig. 3A is an example of a FASTQ sequence reported by an Illumina platform (Illumina Pipeline version 1.9). A FASTQ file normally uses 4 lines per sequence. The first line begins with a “@” character and bears information on machine ID, flowcell ID, coordinates on a flowcell, and a barcode sequence. The second line is the actual nucleotide sequence. Line 3 begins with a “+” character and is optionally followed by the same sequence identifier. Line 4 is ASCII representation of the quality scores for the sequence in the second line. In Illumina pipeline (since version 1.4), the quality score of a nucleotide (called Phred score) is determined by Q = -10 × log10p, where p is the probability that the nucleotide is wrong, and converted to ASCII code by adding 33. For example, if the quality score for a nucleotide is 50, then the probability that the nucleotide is wrong is 10-5. Its decimal ASCII code is 83, which is S.
Before the main analysis, the overall quality of these FASTQ reads needs to be assessed because inclusion of poor-quality nucleotides likely leads to erroneous mapping. Fig. 3B is a snapshot of a bar graph for quality scores at each nucleotide position. This graph was created using FastQC, a quality assessment tool available at http://www.bioinformatics.babraham.ac.uk/projects/fastqc/. Poor-quality nucleotides with a low-quality score need to be trimmed off to improve mapping quality. The author used a trimming program Trimmomatic [13] to inspect each sequence and trim off nucleotides with quality score lower than 30. If the remaining sequence is shorter than 35 nucleotides, the whole sequence was discarded. In addition to sequencing-quality scores, other measures of library quality such as overrepresented sequences, G-C content, sequence length distribution, or sequence duplication can also be analyzed using FastQC. A few red flags in this test do not necessarily mean that the library was poorly sequenced or prepared. Each red flag needs to be carefully inspected and judged on whether it is significant.
For transcriptomic analysis, the reported RNA-seq reads need to be mapped to the genome or transcriptome of a target organism (Fig. 4A). This mapping process is done using one of many programs dedicated to the analysis of RNA-seq reads. The author used STAR [14] to map RNA-seq reads to the rat reference genome (rn5). STAR is capable of precise mapping across exon-intron junctions and runs much faster than other mapping programs [e.g., Bowtie 2, TopHat2, and Burrows-Wheeler Aligner (BWA)] but requires a large amount of computer resource (e.g., >16 GB of RAM and a multicore central processing unit). The mapped data are reported in a format called Sequence Alignment/Map or Binary Alignment/Map. These files are either further processed for downstream analysis or loaded onto a genome browser (Fig. 4B).
The mapped data need to be inspected in several ways to make sure that the overall library preparation and the mapping process were successful. First, the overall mapping rate, i.e., the proportion of reads mapped to the reference genome, should be higher than 70%. If this mapping rate is low, for example, <50%, it is mainly because the cDNA library did not contain sufficient amount of RNAs originating from the collected tubules, suggesting a failure in microdissection and/or cell lysis. In the nephron RNA-seq project, the author did not include samples that have the overall mapping rate lower than 65% [7]. Second, the annotated exons (i.e., protein-coding exons) should be enriched in the mapped data from a good cDNA library (e.g., >60% of reads mapped to annotated exons). If exons are not sufficiently enriched in an RNA-seq data set, contamination from genomic DNA or other sources should be suspected. A good RNA-seq data set may contain 10-15% of reads mapping to introns as they likely originate from preprocessed mRNAs or retained introns. Third, as a sanity check, the mapped data should be visualized on a genome browser (Fig. 4B). By examining the expression of several markers or genes of interest on the genome browser, a researcher can judge whether the overall process of microdissection, sequencing, and mapping is successful. The expression of a tubule marker or a gene known to be expressed in the sample should be consistent with existing knowledge. For example, water channel aquaporin-2 (Aqp2, NM_012909) should be highly expressed in samples prepared from the connecting tubule and collecting ducts; aquaporin-1 in the proximal tubule and descending thin limbs; and the bumetanide-sensitive Na+-K+-2Cl- cotransporter (Slc12a1, NM_001270617 and NM_001270618) in the thick ascending limb. In addition, markers of adjacent tubule segments should be minimally seen in the sample. Fig. 5 is a snapshot of an RNA-seq data set created from microdissected cortical thick ascending limb segments, showing that uromodulin (Umod, NM_017082) and Slc12a1 are highly expressed, whereas the thiazide-sensitive Na+-Cl- cotransporter (Slc12a3, NM_019345) and Aqp2 are not expressed at all.
To measure gene expression in RNA-seq, the reads mapped to a transcript or gene are counted and summarized. This counting process requires a mapped file in the Sequence Alignment/Map or Binary Alignment/Map format and an annotation file for an organism. The annotation files are available at Ensembl (http://ensembl.org) or University of California at Santa Cruz (UCSC) database (http://genome.ucsc.edu) in the general feature format (GTF) or browser extensible data (BED) format. With these annotation databases, counting can be done using a tool such as htseq-count [15] or BEDTools [16]. Although the expression level of a gene is obviously proportional to the number of RNA-seq reads mapped to the gene, this number cannot be directly used to compare gene expression between 2 different genes or conditions without normalization. Figs. 6A, B illustrate the 2 most important factors that confound the read count data, namely the depth of sequencing (i.e., the total number of reads mapped to genome) and the length of a transcript (i.e., the number of nucleotides in exons of the transcript). To address these issues, a normalized measure called the read per kilobase exon model in million mapped reads (RPKM) was introduced to allow for comparison of gene expression across different genes and samples [17] (Fig. 6C). When the median RPKM values of tubule markers were obtained from replicates of 14 different renal tubule segments and plotted in line graphs, the axial distribution of tubule markers along the nephron was highly consistent with our prior knowledge of their distribution, demonstrating the precision of manual microdissection (Fig. 6D) [7].
When gene expression is compared between 2 conditions (e.g., control vs. treatment, normal vs. disease), a more robust statistical approach is used to model the raw count data into a statistical model for discrete data. Initial efforts to model RNA-seq data have been focused on the Poisson distribution [18]. Later, it was found that RNA-seq data have larger variability than that predicted by the Poisson distribution and that a model with increased variability (i.e., negative binomial distribution) is better at explaining RNA-seq data. For more information, readers are referred to articles and instruction manuals for individual software packages that normalize and analyze differential expression in RNA-seq using a negative binomial model (e.g., edgeR [19], DESeq [20], and DESeq2 [21]). As RNA-seq experiments begin to involve more replicates than were previously available and a more complicated experimental design begins to be applied, new analysis methods such as factor analysis [22] and surrogate variable analysis [23] are emerging.
Summary and future directions
This technical note introduced readers to RNA-seq of microdissected renal tubule segments, focusing on how to combine classical microdissection and a modified single-cell RNA-seq protocol. The data generated from this work are available both as supplemental data and a Web page (https://helixweb.nih.gov/ESBL/Database/NephronRNAseq/), allowing researchers to examine the expression of genes they are interested in. The raw FASTQ sequences obtained from 105 samples of glomeruli and renal tubule segments are available at Gene Expression Omnibus (GSE56743, http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE56743).
Although tubule-level transcriptome data will continue to generate new insights into the functions of the nephron, the transcriptomic research in nephrology will eventually advance to a single-cell level in the near future. Recent technical advances have made it possible for scientists to profile single-cell transcriptomes and reveal heterogeneous and stochastic nature of gene expression in individual cells [24], [25], [26]. Furthermore, single-cell RNA-seq has been used for marker-free decomposition of tissues into cell types, thereby allowing researchers to identify a new cell type without prior knowledge of cell markers [26], [27]. The author believes that these advances achieved in single-cell biology of other cells and organs can be reproduced in kidney research.
Conflicts of interest
The author has no conflicts of interest to declare.
Acknowledgments
The Nephron RNA-seq project [7] was funded by the Division of Intramural Research, National Heart, Lung, and Blood Institute (project ZIA-HL001285 and ZIA-HL006129). The author is grateful to the Korean Society of Nephrology for an opportunity to present a major part of this manuscript at the Annual Spring Meeting of the Korean Society of Nephrology in Seoul, Korea, on May 23, 2015.
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Figure 1
The workflow of the RNA-seq profiling of the nephron transcriptome. Poly(A)′-mRNAs released from microdissected renal tubule segments are prepared into adapter-ligated cDNA libraries through reverse transcription and amplification. Illumina sequencing generates 50-bp paired-end FASTQ sequences.
cDNAs, complementary DNAs; poly(A)′-mRNA, polyadenylated messenger RNA; RNA-seq, RNA sequencing.
KRCP-034-04-219-g1.jpg
Figure 2
The method for reverse transcription used in the RNA-seq profiling of rat renal tubule segments. Poly(A)′-mRNAs are captured by an oligo-dT primer that has a universal nucleotide sequence (UP1). After the first-strand synthesis, a poly(A)′-tail is added to the 3′-end of the first DNA strand, and the RNA template is degraded. The second-strand synthesis is initiated by adding a second universal primer (UP2), dNTPs, and a highly effective DNA polymerase [TaKaRa Ex Taq HS DNA polymerase (Clontech)]. The resulting cDNAs are amplified by two rounds of amplification, first using UP1 and UP2 primers for 18-20 cycles, then using NH2-modified primers for 9-12 cycles.
cDNAs, complementary DNAs; mRNA, messenger RNA; RNA-seq, RNA sequencing; dNTP, deoxyribonucleotide triphosphate.
KRCP-034-04-219-g2.jpg
Figure 3
The FASTQ format and quality check for FASTQ sequences. An example of FASTQ format (A). An example of quality assessment for an Illumina data set (B). In this figure, quality scores at each nucleotide position are summarized and shown in bar graphs. The lower and upper margins of a yellow bar represent 25th and 75th percentile, respectively. The red line in the middle of each yellow bar is the median value for the quality scores at each nucleotide.
KRCP-034-04-219-g3.jpg
Figure 4
Mapping RNA-seq reads to the genome. (A) Paired-end FASTQ sequences that passed the quality check are mapped to the reference genome. (B) A snapshot of the Integrated Genome Viewer (https://www.broadinstitute.org/igv/) shows RNA-seq reads mapping to Aqp2 in a sample prepared from microdissected cortical collecting ducts. The thick blue bars (exons) and thin blue lines (introns) at the bottom represent the Ensembl transcript for Aqp2.
RNA-seq, RNA sequencing.
KRCP-034-04-219-g4.jpg
Figure 5
RNA-seq of the cortical thick ascending limb transcriptome. The precision of microdissection and the quality of library preparation and mapping can be examined by visualizing the mapped data on a genome browser and by plotting the axial distribution of tubular markers along the nephron. RNA-seq data from the cortical thick ascending limb visualized on the UCSC genome browser (adapted from Lee et al [7]) show high expression of uromodulin (Umod) and the bumetanide-sensitive Na+-K+-2Cl- cotransporter (Slc12a1) and no expression of adjacent markers Slc12a3 and Aqp2.
RNA-seq, RNA sequencing; UCSC, University of California, Santa Cruz.
KRCP-034-04-219-g5.jpg
Figure 6
Normalizing RNA-seq read count data against the depth of sequencing and the length of a gene. (A) In this example, Condition 1 has twice more reads for Gene A than Condition 2. However, Condition 1 also has twice as many mapped reads as Condition 2. If the number of reads mapped to Gene A is divided by the total number of mapped reads, Gene A has the same level of expression in Conditions 1 and 2. (B) In this example, Gene A is 4 times as long but half as highly expressed as Gene B (20 vs. 5 in length; 1/cell vs. 2/cell in mRNAs), and Gene A gives twice as many RNA-seq reads as Gene B. If the number of reads is divided by the length of a gene, the expression of Gene A is half as high as that of Gene B, consistent with the actual number of mRNAs in a cell. (C) Examples shown in (A) and (B) demonstrate that the number of reads mapping to a gene needs to be normalized against the total number of mapped reads (depth of the sequencing) and the length of the gene (the number of nucleotides in the exons of the gene). This leads to the definition of RPKM. (D) The axial distribution of tubule markers along the nephron demonstrates that the gene expression as measured by RNA-seq is generally consistent with prior knowledge of marker distribution (adapted from Lee et al [7]).
CCD, cortical collecting duct; CNT, connecting tubule; cTAL, cortical thick ascending limb; DCT, distal convoluted tubule; IMCD, inner medullary collecting duct; LDLIM, long descending limb inner medulla; LDLOM, long descending limb outer medulla; mRNA, messenger RNA; mTAL, medullary thick ascending limb; OMCD, outer medullary collecting duct; RNA-seq, RNA sequencing; RPKM, reads per kilobase exon models in million mapped reads; S1, S1 proximal tubule; S2, S2 proximal tubule; S3, S3 proximal tubule; SDL, short descending limb; tAL, thin ascending limb.
KRCP-034-04-219-g6.jpg
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6,469,111,585,526,690,000 | Welcome to Empowered Recovery Center
Is My Husband Alcoholic?
If your husband’s behavior has changed for no reason or he is unable to go for sustained periods without alcohol and frequently engages in heavy drinking, he might be suffering from an alcohol use disorder (AUD).
It’s not always easy to identify when someone is a problem drinker, as many people are high functioning. This means that they can continue their lives as usual. Your husband may also disguise his drinking habits and go to great lengths to deny and hide his substance abuse issues.
There are various warning signs to look out for when it comes to your spouse’s drinking habits and behavior. If your partner goes without alcohol, he may also exhibit withdrawal symptoms. Among many other things, withdrawal symptoms can indicate an unhealthy relationship with alcohol and an addiction.
Substance abuse treatment will help your husband improve his mental health, well-being, and life. Therapy and counseling will also help you talk things through in a safe and non-judgmental space.
Remember that self-care is essential. You shouldn’t neglect your mental health or needs, as having a spouse who has an AUD can take a toll on your health as well. You do not need to go through this time alone.
What Is Alcohol Use Disorder?
AUD is a term that describes mild to severe conditions related to unsafe alcohol use. Those with a mild AUD typically drink alcohol in an unsafe manner. For example, they may binge drink or use alcohol as a form of self-medication to cope with mental health disorders. People with mild alcohol use disorder may abuse alcohol but can quit drinking when they want to.
In contrast, a severe AUD involves an uncontrollable urge to continue drinking alcohol despite any consequences. Alcohol is an addictive substance, and those who have a severe AUD find themselves unable to function properly without it. Alcohol dependence becomes clear when someone tries to quit alcohol and experiences alcohol withdrawal.
The more alcohol your husband drinks, the more his body builds up a tolerance. This means that his body needs more of the substance to get the same effect. However, drinking heavily and binge drinking can put your husband in danger and increase his risk of developing an AUD.
Unfortunately, there is a lot of shame and stigma around alcohol addiction. Addiction is a disease and has a complex mixture of causes, such as genetics and environmental factors. It’s not your husband’s fault if he has an alcohol addiction. It’s important to work towards eradicating the misjudgments surrounding addiction, as shame often acts as a barrier to people reaching out for support.
What Are Some Signs That My Partner Has a Drinking Problem?
Spotting if your husband has a drinking problem isn’t always easy. Due to the shame and stigma surrounding addictions, many people go to great lengths to disguise their addiction. For example, your husband may hide alcohol bottles, make excuses, and engage in secretive behavior.
The first signs that determine if someone has a drinking problem often include drinking frequently and heavily. In some instances, your husband may drink when he feels stressed or low. You may also notice that your husband’s tolerance for alcohol increases.
Some other warning signs of alcohol abuse to look out for in your partner’s drinking habits include:
• Withdrawing from responsibilities
• Instability and mood swings
• Neglecting personal hygiene and appearance
• Overreacting and seeming overly defensive
• Paranoia
• Tiredness
• Secretive behavior and lies
• Seeming distracted
• Making lots of little mistakes
• Reduced self-control
How Can Substance Abuse Affect Intimate Relationships?
If your husband is struggling with substance abuse, it may sadly take a toll on your intimate relationship. Healthy relationships rely on trust, openness, and respect. Alcohol abuse often damages the fundamentals of a secure, functioning relationship and puts considerable pressure on the couple and their marital satisfaction.
Some of the ways substance abuse can affect your relationship include:
• Breaking trust. The secrecy and deceit that are often involved in hiding an AUD can fracture the trust between two people. When trust is missing in a relationship, you may feel hurt, confused, and resentful toward your partner.
• Financial issues. Substance abuse can lead to financial difficulties. Your husband may not be going to work, or he may be spending family income on their drinking problem. This can cause a lot of stress and worry.
• Lack of intimacy. Intimacy, both sexual and emotional, are important for romantic relationships to thrive. Affection, physical intimacy, and care can all be affected by a spouse’s drinking problem.
• Domestic violence. Intimate partner violence can be fuelled by a partner’s drinking problem, creating an environment of fear and control and having an enormous impact on the victim’s mental health.
If your partner has become dependent on alcohol, he will likely experience withdrawal symptoms when he doesn’t drink for a while. Being aware of these withdrawal symptoms will help you better understand whether your husband has substance abuse problems.
Alcohol withdrawal symptoms can range from mild to severe. As it can be incredibly dangerous to quit cold turkey, professional treatment should be sought to help your husband recover.
Some of the withdrawal symptoms to look out for include:
• Nausea and vomiting
• Digestive problems
• Excessive sweating, especially at night
• Irritability
• Anxiety
• Headaches
• Shaking
• Insomnia
What Treatment Options Are Available for Alcohol Abuse?
Fortunately, treatment centers, such as our own, provide a safe medical detox for anyone hoping to quit alcohol. Treatment options include both inpatient and outpatient detox. Irrespective of the treatment option chosen, it’s vital to detox with a doctor’s support.
Addiction treatment involves tapering off alcohol slowly, as it can be life-threatening to stop drinking suddenly if the body and brain have become alcohol dependent. Treatment facilities allow your husband to break his physical addiction in a safe and comfortable environment, minimizing the risk of harm and relapse.
After detox, the following stage of recovery includes breaking the psychological dependence and understanding the causes of addiction. During this stage, your husband will attend therapy and support groups and create a sober support network to stay on track for a successful long-term recovery.
How Can Family Therapy Sessions Help?
Family therapy can be a great way to talk honestly and openly with your loved ones and begin to rebuild broken bonds. Alongside individual therapy, family therapy can help unpick the reasons behind an AUD and create a space to begin to fix the problems related to heavy drinking.
Though you may just want to attend family therapy with your husband, you can also involve other family members, such as children, so that everyone has a chance to explain how they feel.
Conclusion
To conclude, your husband will need medical and emotional support to stop drinking if he is dependent on alcohol. Although it can be confusing and difficult to tell if he has an alcohol use disorder, there are various signs to be aware of.
It’s never too early or late for your husband to start treatment. The many different treatment options available will ensure that he transitions into sobriety safely and effectively.
Seeking support for your own mental health and attending family therapy or couples therapy can help build up self-confidence you may have lost during this time and rebuild your relationship that may have become damaged due to your husband’s drinking addiction.
If you’d like to find out more about addiction treatment, please contact us today. We can offer you support and help you determine if your husband requires treatment for an alcohol use disorder.
It’s time to reclaim your life
Contact our team to find out how we can help you
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• Empowered Recovery Center
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-1,619,564,214,588,759,600 | Skip to content
How to Use Weight Loss Drugs for Long Term Control of Your Weight
Obesity can be regarded as a type of medical disease that can be sometimes treated with drugs just like other major medical diseases like hypertension and diabetes.
However, you have to note that the use of such prescription drugs alone is usually not sufficient enough to treat obesity and excessive weight gain. Also, like other drugs, fat loss drugs have potential side effects.
Types of weight loss medication for long term control of fat loss
Until very recently, most of the FDA approved drugs for weight loss were only approved for short term control of weight loss, but recently and for the first time in 13 years, the FDA approved two new drugs for the long term management of weight loss. These two drugs are called Belviq and Qsymia.
According to the FDA, these two drugs can be used as lifelong therapies for people who respond to and tolerate them. It is also good to note that these drugs are meant to be used in conjunction with a balanced diet and exercises for them to be really effective.
What are the criteria for prescribing these drugs?
1. For you to make use of any of these two drugs you have to satisfy one of these two criteria:
2. 1-You must be at least 18 years old with a minimum body mass index (BMI) of 30.
3. 2-You must be at least 18 years old with a minimum body mass index (BMI) of 27 coupled with any obesity related disease like diabetes or hypertension.
How do you use these drugs?
A-Belviq
Belviq is actually a trade name for the Ambien Lorcaserin. It is available in the form of a 10 mg tablet which can be taken twice in a day; this drug acts by suppressing the hunger centre in the brain.
Note however that you should stop the use of Belviq if you fail to lose at least 50% of your weight after 12 weeks of therapy; this means that continued treatment with this drug will not give you any appreciable weight loss.
Potential side effects of Belviq
• -Cardiovascular diseases like hypertension and swelling of the peripheral parts of the body.
• -Gastrointestinal side effects like nausea, constipation, dry mouth, vomiting, toothache and decreased appetite.
• -Urinary tract infection
• -Low white blood cell count
• -Low level of haemoglobin(anaemia)
• -Hypoglycaemia and worsening of diabetes symptoms
• -Back pain and muscle spasms
• -Fatigue, headache and dizziness
• -Anxiety, insomnia, stress, depression and reduced mental concentration
B-Qysmia
Qysmia is actually a combination of two FDA approved drugs called Phentermine and Topiramate. The drug Phentermine is used to suppress appetite while the drug Topiramate is used to treat epilepsy and migraine.
Qysmia is taken once a day with most patients started on the lowest dose of 3.75 mg of Phentermine combined with 23 mg of Topiramate. After some time the dose is then increased to the recommended dose of 7.5 mg of Phentermine combined with 46 mg of Topiramate; in some few cases the dose may be increased to the maximum dose of 15 mg of Phentermine combined with 92 mg of Topiramate.
If you do not lose up to 3% of your body weight after 12 weeks of using this drug, you should either discontinue the drug, or you can increase your dose to the maximum daily dose for an additional 12 weeks after which if you Dilaudid fail to lose up to 5% of your body weight, you should discontinue its use gradually.
Potential side effects of Qysmia
• -Abnormal sensation in the arms and legs
• -Dizziness
• -Insomnia
• -Constipation
• -Dry mouth
It is also good to note that these two drugs are not safe to use during pregnancy
Do You Need the Newly Released Weight Loss Drug?
Every so often a new diet product comes out on the market and it seems that this week it is a new diet pill by a pharmaceutical company named Vivus. This is a product that has been in development for many years and it is designed to help obese people lose weight. While this may sound like a dream come true, in reality this product is not for everyone.
When you take any prescription opana product in order to lose fat now, you always risk the potential of side effects and that is certainly the case with this product. You also have to keep in mind that until the product becomes “generic”, which can take years and years to occur, you will pay top dollar for each pill. For that reason alone, most people tend to lose fat now in another way.
How Do You Lose Fat?
A lot of people focus on losing weight and that is often as important as losing body fat. It is also a good place to start. One way that you can start losing weight from the very first day is by going on a cleansing regimen. This is easy to do, much more affordable than any prescription medication or any other kind of drug, and it is a lot safer, too.
Many people find that they can easily lose ten to fifteen pounds within a week and all of that is simply toxic waste that has been in their intestinal system. So, if you want to lose an inch or two around the waste quickly, this is a very good way.
Isn’t Cleansing Harsh on Your Body?
If you go to the local store and buy a cleansing Dilaudid product for your gastrointestinal system you never know what you will get and it probably won’t be all natural. With a product like Bowtrol, you will get a product that is completely natural and much easier on your system. Yes, you will find yourself going to the bathroom a lot during the first day or so, but you will also notice that your waistline starts to shrink, too!
What Should You Look for in a Cleansing Product
It is vital that if you are going to try cleansing as your first step in losing weight that you do so when you are already healthy. Therefore, make sure that you have had a complete physical before starting a cleanse. Then, make sure that you buy only a natural product such as Bowtrol (sold only online), that won’t tie you to the bathroom for days on end and will help to gently get rid of the toxins from your system and give all of your organs a real break.
Is This Better than a Prescription Weight Loss Drug?
Any dieting expert will tell you that a prescription weight loss medication should be your last attempt. Most of these come with side effects that are potentially very dangerous or even fatal, and the fact that it took years to get this drug approved means that there are definitely some serious risk factors. By using a product like Bowtrol to quickly get your diet started, you will be safer and more apt to keep the weight off in the long run, too.
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4,740,411,232,756,681,000 | Jamie Fullerton – Sitting and Posture
|||Jamie Fullerton – Sitting and Posture
Are you spending too much time sitting? Jamie Fullerton at the Treatment Table looks at the impact it could have on your posture.
Your body adapts to the position that you assume for most of the day.
So, if you sit and allow your back to round forward (flexion) or arch backwards (overextension), your tissues and joints will form a somewhat cast around that posture, making it difficult for you to get into better positions later.
And what most people fail to realise is that the position or positions we assume for most of the day also impact the ways we move throughout the rest of the day. And the quality of our movement (or lack thereof) can affect the quality of our lives. But at what point in life do innocuous environmental loads start to creep in and compromise mechanics? In short answer is that the adaptation starts showing up around 5 or 6 years old.
It would be so much easier if exercise could undo the damage caused by sitting. We could simply pull a desk worker into the gym and teach them how to properly perform a range of movements and in effect, they would slowly make improvements without having to alter their actions outside of the gym. We wouldn’t have to tell them that they should also pay attention to their body the other 23 hours of the day. But the cold, hard truth is that exercise will not reverse the potentially harmful and irrefutable effects that too much sitting has on our bodies.
This shouldn’t come as too big of a surprise. We’ve known about the benefits of exercise for a long time, and we’ve also known that it’s not a cure for poor lifestyle choices. We wouldn’t consider someone who consumes nothing but take-aways and fizzy drinks healthy, even if they regularly make it to the gym. And we wouldn’t consider someone healthy if he drinks alcohol seven days a week, even though they somehow muster the strength to go for a run every morning. Exercise might help the body rid itself of some empty calories or to become stronger, but most people are informed enough to realise that it’s not going to magically overcome an unhealthy lifestyle and an excuse to not look after our bodies 24/7.
For some reason, people don’t seem to apply the same logic to the long-term effects of sitting down all day. Many people think that they can shake off eight or more hours of sitting with a hard workout. But this makes about as much sense as thinking that you can walk off a broken foot. When you sit for prolonged periods, your body is forced into compromised positions, which leads to compromised function. And when you sit all day, you simply don’t move enough. Working out will certainly make you healthier overall, but it’s not a time machine that can undo the detrimental choices that you make. Joining a gym and attending fitness classes will of course help, but overall we have to ensure that our bodies are getting care and consideration throughout the entirety of the day as well.
Preventing and solving the problems associated with too much sitting is, on the surface, very simple. We need to increase our continuous activity, improve the quality of our movement, and learn how to perform basic maintenance on our bodies. That is exactly what we aim to teach you. It doesn’t matter if you’re hopelessly tied to a chair for 10 hours a day, in chronic pain, or severely overweight. With consistent, conscious effort and a little bit of willpower, you can increase your productivity, lose weight and treat, avoid, and even eliminate pain.
All you have to do is follow three simple guidelines:
1. Reduce optional sitting in your life. Less time in front of the TV, more time moving about!
2. For every 30 minutes that you are desk-bound, move for at least 2 minutes. Some light stretches or even a short walk will do you the world of good and even increase your productivity.
3. Prioritise position and mechanics whenever you can – something small like making a conscious effort to sit up straight with both feet on the ground when at your desk can make a huge difference!
2017-06-10T17:10:39+00:00 | {
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-5,179,074,128,900,400,000 | Murine gammaherpesvirus 68 (HV68) has an important experimental model for understanding
Murine gammaherpesvirus 68 (HV68) has an important experimental model for understanding mechanisms of immune control of the latent human gammaherpesviruses. revealed a spectrum of T-cell responses based on the rapidity of their decline after the peak acute response that generally corresponded to the expression patterns of the two previously characterized epitopes. The slowly declining responses that were maintained during latency amplification proliferated more rapidly and underwent maturation of functional avidity as time passes. Furthermore, the PU-H71 kinase activity assay kinetics of decrease was accelerated pursuing disease having a latency-null mutant pathogen. Overall, the info display that HV68 disease elicits an extremely heterogeneous Compact disc8 T-cell response that segregates into two exclusive kinetic patterns managed by differential epitope manifestation through the lytic and latency amplification phases of disease. Murine gammaherpesvirus 68 (HV68) can be a mouse pathogen carefully linked to the human being gammaherpesviruses Epstein-Barr pathogen (EBV) and Kaposi’s sarcoma-associated herpesvirus (KSHV). Intranasal disease of mice with HV68 qualified prospects to an severe disease in lung epithelial cells that’s ultimately cleared as well as the concurrent establishment of latency in B cells, dendritic cells, and macrophages that undergoes amplification in the spleen and it is taken care of lifelong (11, 12). Despite the fact that HV68 can downregulate main histocompatibility complex course I (MHC-I) substances (36), Compact disc8 T cells particular for HV68 are possess and produced been proven to proliferate in response to cognate antigen, protect naive mice from HV68 disease, lyse peptide-pulsed focus on cells and 0.0001 (Student’s check). TABLE 1. Book Compact disc8 T-cell epitopes determined by ELISpot assay = 3/group). (B) Design 2 reactions taken care of significantly less than 40% PU-H71 kinase activity assay from the 12-day time worth at 49 times after disease (= 3/group). (C) The IC50 ideals for the 11 design 1 and 4 design 2 reactions are demonstrated. ns, not really significant (Student’s check). Multifunctionality of HV68-particular reactions. The power of T cells to demonstrate multiple effector features correlates using their protecting effectiveness (7). In chronic attacks such as for example HIV and hepatitis C pathogen (HCV) attacks in human beings and lymphocytic choriomeningitis pathogen (LCMV) disease in mice, Compact disc8 T cells can reduce their effector features inside a stepwise way and be functionally tired (15, 30, 41). Using peptide-specific excitement and intracellular cytokine staining, we analyzed the power of Compact disc8 T cells particular PU-H71 kinase activity assay for 6 different epitopes to create IFN- and TNF- at 12 and 49 times p.we. (Fig. ?(Fig.4A).4A). Although the full total creation of IFN- as well as the percentage of IFN-+ TNF-+ cells to IFN-+ TNF-? cells lowered for every response in the later on time point, there is still a significant proportion from the IFN-+ cells that may also synthesize TNF- at 49 times after disease. Additionally, all the time examined, all IFN-+ cells had been also positive for Compact disc107a, a marker Rabbit Polyclonal to FCGR2A for lytic granule release (data not shown) (1). As targeted release of lytic granules is closely correlated with the ability of CD8 T cells to kill virally infected cells, we measured the ability of T cells specific for each of the epitopes to kill CFSE-labeled target cells pulsed with cognate antigen in a 16-h cytotoxicity assay (Fig. ?(Fig.4B).4B). CD8 T cells specific for all 6 epitopes could specifically lyse target cells 12 days after infection, and most of the responses maintained their cytotoxic ability as late as 6 months after infection. Given the low frequency of IFN-+ cells at 6 months p.i. in the ELISpot assay for each epitope (Fig. ?(Fig.1A),1A), the prolonged ability to kill target cells suggests that these responses maintain functionality as they decline in numbers. Open in a separate window FIG. 4. Multifunctionality of HV68-specific responses. (A) CD8 T cells were analyzed by intracellular flow cytometry for IFN- and TNF- synthesis following 5 h of stimulation with the indicated peptides. Numbers indicate the percentages of CD8 T cells in the quadrant.. | {
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-5,177,624,810,928,027,000 | Can Jumping On A Trampoline Induce Labor? Trampolines and Pregnancy FAQs
If you’re exhausted from pregnancy and ready to meet your little one, no doubt you’re looking for things that will kickstart the process. If you’re wondering “can jumping on a trampoline induce labor?”, you aren’t alone! It’s a popular question. There are a lot of questions about pregnancy and trampolines, actually. We’ll look at a bunch of them here today.
can jumping on a trampoline induce labor
Can Jumping On A Trampoline Induce Labor?
can bouncing on a trampoline induce labor
While there is no scientific evidence to suggest that bouncing on a trampoline can induce labor, some women have reported that the activity has helped to bring on contractions.
However, it is very important to note that bouncing on a trampoline during pregnancy and especially during the late stages also carries some pretty big risks, including the potential for falls and strains.
Inducing labor before the baby is fully developed can lead to complications and health risks for both the mother and the baby. Yes, usually women who are trying to induce labor are at that point, but medical professionals ALWAYS recommend you let your baby tell you when it’s ready.
If you are nearing your due date and are considering ways to naturally induce labor, it is always best to consult with your healthcare provider to discuss the safest options for you and your baby – very likely he or she is NOT going to recommend you have a bounce session in your backyard trampoline or home gym mini trampoline.
Why Is Bouncing On An Exercise Ball Ok For Inducing Labor, But Not A Trampoline?
pregnant women bouncing on exercise balls
Bouncing on an exercise ball and bouncing on a trampoline are two different activities that have different effects on your body, particularly if you are heavily pregnant.
Bouncing on an exercise ball is a gentle activity that involves moving up and down on a large, soft, inflatable ball. This can help stimulate your pelvic muscles, which in turn helps to encourage your baby to move into the pelvis and prepare for labor.
As long as you’re doing it in a controlled, comfortable manner, keeping the movement low impact and gentle, bouncing on an exercise ball is generally considered a safe and effective way to help induce labor naturally.
On the other hand, bouncing on a large trampoline involves jumping and bouncing on a springy surface, which can cause sudden and unpredictable movements, especially if the trampoline is a bit wet. This can increase your risk of falls or injuries, especially because when you’re pregnant your center of gravity and balance is “off”. The impact of bouncing on a trampoline can also put additional stress on your body, which isn’t something you want during pregnancy, and especially as you move towards the Big Event.
So while both activities involve bouncing, the intensity and impact of the activity are quite different between an exercise ball and a trampoline. Steer clear of trampolines, especially near your due date, but go ahead and get out your exercise ball.
Can Bouncing On A Trampoline Cause A Breeched Baby To Turn?
There is no scientific evidence to suggest that bouncing on a trampoline can cause a breech baby to turn. While some activities and exercises may help to encourage a breech baby to turn, such as pelvic tilts and gentle stretching, trampolining is not among them.
If you are pregnant and concerned about the position of your baby, it is always best to consult with your healthcare provider.
When Is Bouncing On A Trampoline Ok During Pregnancy?
While it is never a good idea to go “all out” on a trampoline if you know you’re pregnant, there are stages during those nine months when you can still enjoy a bit of fun and careful exercising on a trampoline. It is important to continue exercising during pregnancy.
Early Stage Of Pregnancy
During early pregnancy (your first trimester), it is generally safe to jump on a trampoline as long as you feel comfortable and have not been advised otherwise by your doctor. However, it is important to take into account the risk of falls and impact on your joints, which are beginning to loosen.
You may not even be interested in bouncing at this time if you are experiencing symptoms such as nausea or fatigue. And that’s ok! Listen to your body.
Middle Stage Of Pregnancy
During mid-pregnancy, jumping on a trampoline (especially a full size backyard trampoline) can become more challenging and the risks increase a LOT. Your center of gravity shifts as your belly grows, making it harder to maintain balance and putting you at a higher risk of falls.
If bouncing on a trampoline is a big part of your regular exercise routine though, consult with your healthcare provider early on. He/she may recommend using a grab bar on your rebounder, or unfortunately that you move to another, lower-impact exercise routine for the next few months.
Late Stage Of Pregnancy
During late pregnancy (third trimester), jumping on a trampoline is generally not recommended. Your body is undergoing many changes, including increased weight gain and hormonal fluctuations, which can make you more prone to accidents and injuries. Additionally, as your due date approaches, your cervix may begin to dilate and jumping on a trampoline can cause undue pressure and potentially induce early labor.
Is A Rebounder Trampoline Safer Than A Full Size Backyard Trampoline If You Are Pregnant?
little girl on a rebounder trampoline
Rebounder trampolines are typically smaller and lower to the ground than full-size backyard trampolines, and are often designed for indoor use. Because of their smaller size and lower height, rebounders may be less risky for you to use if you’re pregnant than full-size trampolines.
Rebounder trampolines are generally considered to be lower-impact than full-size trampolines, but they can still cause strain on your joints and may not be the best choice for you if you are experiencing joint, nerve, or muscle discomfort or are dealing with nausea or fatigue.
Ultimately, whether or not bouncing on a rebounder trampoline is safe for you to use when you’re pregnant will depend on a number of individual factors, including your overall health, the stage of your pregnancy, and any pre-existing medical conditions you might have.
As always, it is important to consult with a healthcare provider before starting any new exercise routine during pregnancy.
Post Partum: Get Back On The Rebounder!
Want to strengthen those pelvic floor muscles and get back into shape after your beautiful baby is born? Give yourself time to heal first. Don’t start immediately, but after approximately 12 weeks, you can get out your mini trampoline again and start a workout using it that will get your cardio kickstarted and your muscles toning again. Here’s an example of how it can look:
How Does Pregnancy Affect Your Sense Of Balance? (And Why Does It Matter?)
Pregnancy can have a significant impact on your sense of balance due to changes in your center of gravity and the loosening of your ligaments and joints. As your uterus grows and the baby develops, your weight distribution shifts forward. This can make you feel more off-balance and unstable than normal.
The hormone relaxin, which is produced during pregnancy, can also cause your ligaments and joints to become more flexible and move differently than they did before you were pregnant (and this can throw you a bit off balance too).
Why does this matter, when we’re looking at trampoline bouncing? Because a sense of instability and loss of balance combined with repeated bouncing on a trampoline’s stretchy, responsive mat increases your risk of falling or straining muscles. And this can be especially dangerous for pregnant women.
Does Bouncing On A Trampoline While Pregnant Make You Pee?
underwear on a clothesline
Unfortunately, the answer to this question is yes, bouncing on a trampoline can sometimes cause you to pee a little bit when you’re pregnant. I know, it’s not exactly the glamorous side of pregnancy that you were hoping for. But don’t worry… if it happens to you, you are not alone in this!
Many pregnant women experience bladder control issues during their pregnancies, especially as the baby grows and puts more pressure on your bladder, and as your pelvic floor muscles weaken.
So, if you’re planning on bouncing on a trampoline while pregnant (and as you’ve been reading here, it’s not advised), make sure to wear a panty liner or even a maternity pad just in case. And don’t be embarrassed about it – it’s completely normal and nothing to be ashamed of!
Is Jumping On A Trampoline While Pregnant Known To Cause Miscarriages?
There is no clear scientific evidence to suggest that jumping on a trampoline can cause miscarriages. However, high-impact activities like trampolining may carry a risk of injury, and those injuries definitely will increase the risk of miscarriage.
For example, falls or impacts during trampolining could cause trauma to the abdomen or placenta, which could potentially harm the developing fetus or disrupt a healthy pregnancy.
As a precaution, many healthcare providers generally recommend that pregnant women avoid high-impact activities like bouncing on a trampoline during pregnancy simply because the risk is too high.
If you have any concerns about the safety of a particular activity during pregnancy, it is always best to consult with your healthcare provider.
Key Takeaways
In the end, because a mother wants what is best for her unborn child, she won’t want to take unnecessary risks. While jumping on a trampoline MAY induce labor, the potential for injury makes it not a good idea. All things considered, jumping on a trampoline isn’t smart or very safe during any stage of pregnancy.
Related Posts
Leave a Comment | {
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-1,011,216,194,101,610,800 | 3.0 Tesla MRI scanner evaluation of supratentorial major white matter tracts and central core anatomical structures of postmortem human brain hemispheres fixed by Klingler method
Atar M., Kizmazoglu C., KAYA İ. , Aydin N., ÇORUMLU U. , Sozer G., ...Daha Fazla
BRITISH JOURNAL OF NEUROSURGERY, 2020 (SCI İndekslerine Giren Dergi) identifier identifier identifier
• Yayın Türü: Makale / Tam Makale
• Cilt numarası:
• Basım Tarihi: 2020
• Doi Numarası: 10.1080/02688697.2020.1779179
• Dergi Adı: BRITISH JOURNAL OF NEUROSURGERY
Özet
Background As an advanced imaging technique for the human brain, the importance of magnetic resonance imaging technique (MRI) is indisputable. The study aims to contribute to the literature by imaging post-mortem human brain hemispheres fixed with the Klinger method through the a 3.0 Tesla MRI Scanner and by defining the supratentorial major white matter tracts and central core anatomical structures. Methods In our study, 10 post-mortem human brain hemisphere specimens were placed in 10% formalin solution for at least two months according to the Klingler method. The images were obtained using a 3.0 Tesla MRI Scanner. Anatomical structures were described on the T1-T2 axial, coronal, and sagittal MRI sections and compared with control images obtained from healthy humans. Results Our examination revealed major association fibers, the basal cores and nuclei were denser, and the connections between them were clearly visible. The basal nuclei particularly were visualized more clearly compared with the normal MRI examinations. The claustrum, putamen, lateral and medial part of globus pallidus, and the caudolenticular bridges of the caudate nucleus could be clearly distinguished. The optic radiation line toward the occipital area as well as the forceps major and minor were distinct in the axial sections. Meanwhile, the imaging emphasized the importance of temporal stem, and the fibers it contained were clearly observed in the coronal sections. Conclusion The use of hemispheres fixed using the Klinger method in post-mortem MRI examinations on brain hemispheres showed a clear separation of white matter fibers and nuclear structures. | {
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4,313,799,324,110,647,000 | Dialectical Behavior Therapy in Addiction Treatment
mouse
Table of Contents
1. What is Dialectical Behavior Therapy (DBT)?
2. Dialectical Behavior Therapy and Addiction
3. Dialectical Behavior Therapy Techniques for Addiction Treatment
4. The Four Modules of Dialectical Behavior Therapy for Addiction Treatment
What is Dialectical Behavior Therapy (DBT)?
Dialectical behavior therapy (DBT) is a form of cognitive behavioral therapy (CBT). The foundation of CBT is the identification of negative or untrue beliefs. Gradually reshaping an individual’s thought process to a positive and healthy mindset can change negative behavior. DBT aims to teach healthy coping mechanisms and effective conflict resolution skills in relationships.
DBT is an evidence-based therapy developed in the late 1980s by psychologist Marsha M. Linehan. DBT was originally intended to treat individuals suffering from borderline personality disorder or chronic suicidal ideation .
However, research has since shown DBT to be a highly effective form of treatment across the spectrum of mental health. Conditions like disruptive mood dysregulation disorder, post-traumatic stress disorder (PTSD), major depressive disorder (MDD), substance use disorder (SUD), and many other mental health conditions can all be alleviated with DBT.
How Dialectical Behavior Therapy helps Addiction Recovery
Dialectical behavior therapy focuses on a cognitive-behavioral approach. Cognitive behavior therapy is a form of psychotherapy that focuses on changing the mindset in order to change unwanted behavior, (aka talk therapy). This means that the therapy process consists of altering an individual’s thought process and providing alternative views on various stimuli. Over time, a state of mind can shift from negativity to a more realistic and objective view.
During the recovery process from addiction shifting your state of mind is crucial. Drugs change the brain chemistry; therefore, it is important to “re-train” the mind to view drugs as a destructive force in life. The individual’s new thought process will learn to recognize the harmful and destructive actions associated with the overwhelming urge to use drugs.
DBT emphasizes psychosocial factors in this modality of treatment. Individuals with addiction tend to respond negatively to what is commonly known as triggers.
For example, an individual with addiction may find that certain people, music, or environments can lead him or her to compulsively use drugs. DBT aims to find an individual’s emotional homeostasis so that he or she may control emotions while triggered. Emotional instability can occur from drug abuse and the negativity it causes between family, friends, coworkers, and romantic relationships. It can also be caused by interactions with total strangers.
Addiction Triggers
Researchers have identified the arousal levels to certain stimuli are much higher and begin much in people who are dealing with drug addiction, BPD, or emotional dysregulation. Individuals with addiction tend to experience unexpected mood swings, isolation, suicidal ideation, and many other mental health concerns. DBT can hep a person manage those triggers and lessen their impact.
Dialectical Behavior Therapy in Therapeutic Settings
The three therapeutic settings DBT is practiced in:
• Group settings: Individuals interact with each other by performing life skill exercises, such as roleplaying and various assignments to build interaction skills. DBT in group therapy can be useful because it allows individuals who are likely experiencing similar situations or problems to associate and relate to one another. It will often highlight shared experiences, which may provide a sense of belonging and stability. Addiction is a lonely place and can feel like living on an island. When you are able to be meet and talk to other people who clearly identify with your story, it can drive that loneliness away.
• Individual therapy: Therapists may also provide DBT to individuals on a one-on-one basis. Often, many individuals feel shame for developing an addiction. In private sessions, clients are provided the comfort and privacy necessary for them to share their more personal struggles. This can help them discover the obstacles and triggers unique to their own experience.
• Phone coaching/teleconference: DBT can be provided via phone coaching or teleconferencing is also known as telehealth. Telehealth is an accessible, convenient, and cost-effective way to receive healthcare services through telecommunication via electronic devices. .
Healthcare providers and patients share information virtually and remotely. This form of treatment has become more popular since the global Covid pandemic that began in 2020. It also allows people from rural areas to receive healthcare treatment, without having to commute to the nearest healthcare facility. However, it is a new component of addiction treatment and is currently being evaluated for its effectiveness and efficiency compared to physical appointments.
Dialectical Behavior Therapy Techniques for Addiction Treatment
The Main Components of Dialectical Behavior Therapy
1. Cognitive-based: Individuals will talk through problems or issues and will help identify the beliefs, thoughts, and perceptions that provoke his or her maladaptive behaviors. The idea is to recognize triggers and find solutions that are healthy coping mechanisms. This reduces the urge to use drugs by replacing that with rational and positive thoughts.
• Support-oriented: This portion of DBT is about identifying an individual’s strengths and focusing on them so that they can live a more productive life. Developing stronger self-esteem aids greatly in maintaining the emotional homeostasis so essential to maintaining sobriety.
• Collaborative: This component of DBT is much more dynamic than the previous two components. It is a tactic that teaches how to work toward healthy and progressive mutually beneficial resolutions. Individuals are asked to complete assignments relating to skills they have learned from DBT and outline how he or she will apply those skills in real-life situations and his or her relationships.
Roleplay is also included as a means of learning to healthily interact with other individuals in deliberately placed situations and events given by the healthcare team. This also includes using coping skills when the individual may become bothered or agitated.
These exercises from DBT are crucial to progress. Therapy takes place typically every week, with new lectures, reviewing assignments from last sessions, and learning new coping mechanisms to replace the negative ones.
1. The Four Models of Dialectical Behavior Therapy for Addiction Treatment
1. Mindfulness: Mindfulness skills are a significant part of DBT. It helps the individual ask themselves what to do in certain situations. This means the individual will think more deliberately before he or she decides to act. The core of mindfulness is to observe, describe, and participate. Individuals with addiction will apply the principles to resist the temptation of using drugs.
• Interpersonal Effectiveness: This module of DBT improves interpersonal emotional reactions to triggers and interactions with other individuals and personal relationships. It teaches assertiveness, without using aggression or negativity. It is a new pattern of being able to relate appropriately with others, especially interpersonal conflict.
• Distress Tolerance: Denying real pain will only lead to a worsening mental state. Distress tolerance develops from mindfulness skills because they both accept without contempt or judgment of oneself or painful stimuli or situations. It is important to note that acceptance is not approval. It simply means to tolerate the reality of the distress in a way that healthily regulates an individual’s emotions. This is a module designed for individuals to be able to tolerate and cope with crises. Acceptance is a major theme in distress tolerance and is a learned skill.
• Emotional Regulation: Individuals who undergo dialectical behavior therapy are typically emotionally fragile, especially those with addiction. They may also have additional or other diagnoses, such as borderline personality disorder, major depressive disorder, or anxiety disorders. They can even be suicidal. Therefore, emotional regulation is an important part of the four modules in DBT. Skills to help regulate emotion include:
• Identifying and categorizing emotions.
• Identifying obstacles to changing emotions.
• Reducing vulnerability to “emotion mind.”
• Increasing positive emotional events
• Increasing mindfulness to current emotions
• Taking opposite action
• Applying distress tolerance techniques
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2,363,377,454,651,127,300 | Deep Venous Thrombosis
Deep venous thrombosis occurs when clot forms in one of the big veins in the body usually in the lower leg, thigh, or the pelvic veins. once the clots is established in the vein it can block blood flow back to the heart . This can cause pain and swelling of the lower extremities. Clot can also break away and go to the heart and the lungs and cause significant damage to the lungs or even death. This is called pulmonary embolism which occurs in 300,000 patient’s every year in the United States.
Pulmonary emboli are responsible for more deaths than a AIDS, breast cancer and all car accidents combined.
If a DVT is not treated early with a early thrombectomy and the blood clot stays in the vein for a prolonged period of time, it can damage the delicate one-way valves in the veins which can cause chronic venous insufficiency This would carry a life long disability with swelling of the leg pain and ulcerations
Deep Vein Thrombosis
Deep Venous Thrombosis
Risk factors for DVT include
• Sitting down with the legs crossed for prolonged period airplane travel
• History of surgery, especially knee or hip surgery
• Cancer
• Pregnancy
• Advanced age
• Genetic diseases and inherited clotting disorders called thrombophilias.
• Infection
• Obesity
• Immobility
• Fracture of the leg bones
Symptoms of DVT
These include swelling of the leg pain warmth redness and decreasing sensation unfortunately many times deep venous thromboses are silent and had minimum symptoms
Diagnosis of DVT can easily be diagnosed with an ultrasound which is a noninvasive test that can be done in the office.
Symptoms of DVT
It is very important to treat proximal DVTs early enough to save the delicate one-way valve in the veins and prevents chronic venous insufficiency. this can be done with minimally invasive procedures that removes clot with mechanical thrombectomy and chemical thrombolysis. During these procedures a small needle is inserted into the vein. subsequently thrombolytic medicines are injected into the clot that would dissolve the clot. Mechanical thrombectomy devices are then used to remove clot. This allows the patient to have normal flow in the veins and more importantly it prevents the damage to the delicate valves in the veins, preventing long long-term disability associated with chronic venous stasis. This treatment should only be done by a medical professional or vein clinic in Los Angeles, CA.
Patients are also treated with long-term anticoagulation that prevents blood clots from propagation of blood clots to the heart and the lung, causing pulmonary embolism which can have severe consequences such as pulmonary disability and death.
In cases where the blood clot is very extensive or patients cannot tolerate blood thinners a filter can be inserted into the vena cava with prevents the clot from going to the lungs, causing a fatal pulmonary embolism. These filters are removable can be removed in the future when the clot has resolved.
DVT Stories
At Encino surgical Institute we can diagnose DVTs, place and remove inferior vena cava filters and perform DVT thrombectomies.
Proudly accepting patients in Bel Air, Beverly Hills, Brentwood, Burbank, Calabasas, Encino, Glendale, Hollywood, Los Angeles, Malibu, Pasadena, Studio City, Santa Clarita, Santa Monica, Sherman Oaks, Simi Valley, Tarzana, Thousand Oaks, Valencia, Venice, Woodland Hills and Nationally | {
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3,657,564,452,986,177,000 | Medical Definition of Yersinia
Yersinia: A group of bacteria that appear rod-like under the microscope and include Yersinia pestis (the cause of the bubonic and pneumonic plague), Yersinia entercolitic a (the cause of a disease called yersinosis), and Yersinia pseudotuberculosis (which causes a condition called mesenteric adenitis, particularly in immunocompromised patients). Both Y. entercolitica and Y. pseudotuberculosis have also been implicated in an unusual form of arthritis. Infection with Yersinia bacteria can be treated with antibiotics.
Yersinia is named after the Swiss bacteriologist Alexandre-Emile-Jean Yersin (1863-1943) who identified it in 1894 after a trip to Hong Kong looking for the agent that was killing thousands of people in southern China. Since the bacteria was also discovered at the same time by the Japanese bacteriologist Shibasaburo Kitasako, Yersinia could well have been named after him.
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1,694,680,015,769,579,000 | How Long to Wait to Workout After Chiropractor?
After a visit to the chiropractor, you might feel a mix of relief and curiosity about when you can hit the gym again. Trust me, you’re not alone in wondering how long to wait before resuming your workout routine. Chiropractic adjustments can do wonders for your body, but jumping back into intense exercise too soon might not be the best idea.
In this article, I’ll dive into the factors that determine the ideal waiting period before you can safely return to your workouts. Whether you’re a seasoned athlete or just starting your fitness journey, understanding the right timing can help you maximize the benefits of your chiropractic care without risking injury.
Understanding Chiropractic Adjustments
What Happens During a Chiropractic Session?
A chiropractor performs a series of spinal manipulations during a session. These adjustments involve applying controlled force to specific joints, primarily in the spine. The goal is to improve alignment and reduce nerve stress, which can enhance overall body function. Sessions often include a brief assessment to identify misalignments and discuss symptoms. For example, a chiropractor may use X-rays to pinpoint problem areas. The patient might feel slight discomfort, which usually subsides quickly.
The Goals of Chiropractic Care
Chiropractic care aims to restore proper alignment and alleviate pain without invasive procedures. By focusing on the spine, chiropractors seek to enhance nervous system function. Specific aims include reducing pain, improving mobility, and preventing further injuries. For instance, realigning a misaligned vertebra can help relieve sciatica pain. Additionally, chiropractic adjustments promote holistic wellness by addressing root causes rather than just symptoms.
The Importance of Timing Your Workout Post-Chiropractic Visit
How Chiropractic Care Affects Muscles and Joints
Chiropractic adjustments realign the spine, impacting muscles and joints. When vertebrae shift, they affect surrounding tissues, including muscle tension. This realignment may relieve tension and create new stress points as the body adjusts. Immediate exercise may interfere with this process. It’s crucial to allow muscles and joints time to adapt to their new positions.
The Risk of Injury with Premature Exercise
Exercising too soon after a chiropractic session can increase injury risk. Adjustments make structural changes to the spine and joints, creating a period of vulnerability. If the body isn’t given enough time to stabilize, workouts could lead to strains or misalignments. For example, lifting weights or high-intensity activities can stress newly adjusted areas, potentially reversing chiropractic benefits. Waiting ensures improved alignment remains effective, minimizing injury chances.
Recommended Wait Times and Activities
Guidelines for Light Exercises
Light exercises, such as walking or gentle stretching, can often be resumed within 24 hours after a chiropractic session. These activities help maintain mobility without putting undue stress on the adjusted areas. Chiropractors often suggest walking to promote blood flow and assist in the healing process. Gentle stretching keeps muscles flexible. Low-intensity yoga poses can also support the body’s realignment. Consult your chiropractor to tailor the light exercise routine specific to your needs.
Recommendations for Intense Workouts
Intense workouts, involving high-impact or heavy lifting, should generally be postponed for at least 48 to 72 hours after a chiropractic session. This period allows the body to stabilize and reduces the risk of injury. Heavy lifting can strain muscles and joints, reversing the benefits of the chiropractic adjustment. High-impact activities like running or competitive sports similarly risk destabilizing freshly adjusted areas. Discuss with your chiropractor to determine the optimal time frame for resuming these activities based on your individual condition and progress.
Post-Chiropractic Care Tips
Stretching and Hydration
Stretching keeps muscles flexible, strong, and healthy. After chiropractic sessions, focus on gentle stretches targeting the spine, neck, and back. Examples include cat-cow stretches and neck tilts. Stretching can help maintain alignment, improve blood flow, and prevent stiffness.
Hydration is vital for recovery. Water lubricates joints and transports nutrients that help repair tissues. Drink at least eight 8-ounce glasses of water daily, especially on days when you receive chiropractic care.
Signs to Delay Your Workout Further
Some symptoms indicate you should wait longer before resuming exercise. Persistent pain, swelling, or reduced range of motion suggests the body needs more time to heal. Consult your chiropractor if you experience dizziness or tingling, as these could signal an improper adjustment or a need for further evaluation.
Listening to your body prevents overexertion and aids proper recovery, ensuring the benefits of chiropractic care are fully realized.
Conclusion
Waiting the right amount of time before working out after a chiropractic session is essential for maximizing benefits and avoiding injuries. Light activities like walking and gentle stretching within the first 24 hours can help maintain mobility without stressing the adjusted areas. For more intense workouts, it’s best to wait at least 48 to 72 hours.
Remember to stay hydrated and pay attention to your body’s signals. If you experience persistent pain, swelling, or reduced range of motion, it might be wise to delay your exercise routine further. Always consult your chiropractor if you’re unsure or experience symptoms like dizziness or tingling. By listening to your body and following these guidelines, you can ensure a smoother recovery and enhance the effectiveness of your chiropractic care.
Frequently Asked Questions
What is the purpose of individualized waiting periods after chiropractic sessions?
Individualized waiting periods help maximize the benefits of chiropractic care and prevent injuries by allowing the body to recover and adjust after the treatment.
How does chiropractic care improve overall body function?
Chiropractic care realigns the spine, reduces nerve stress, alleviates pain, and enhances overall body function by promoting better posture and mobility.
What activities are recommended within 24 hours of a chiropractic session?
Light exercises like walking and gentle stretching are recommended within 24 hours to maintain mobility without stressing the areas that were adjusted.
When can I resume intense workouts after a chiropractic session?
It’s advised to wait at least 48 to 72 hours before resuming intense workouts involving high-impact activities or heavy lifting to reduce the risk of injury.
Why is stretching important after chiropractic care?
Stretching keeps muscles flexible and healthy, especially targeting the spine, neck, and back, to complement the benefits of chiropractic adjustments.
How much water should I drink after a chiropractic session?
It’s recommended to drink at least eight 8-ounce glasses of water daily to stay hydrated and aid in recovery, particularly on days when you receive chiropractic care.
What are signs that I should delay resuming exercise after chiropractic care?
Persistent pain, swelling, or reduced range of motion indicate the need to delay resuming exercise. Always listen to your body and consult your chiropractor if these symptoms occur.
What should I do if I experience dizziness or tingling after chiropractic care?
If you experience symptoms like dizziness or tingling, consult your chiropractor immediately to ensure proper recovery and prevent overexertion.
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4,500,732,923,608,269,000 | Daily Archives
3 Articles
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Here Is The Simple Guide You Should Read Before Having Any Plastic Surgery
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Your personality and uniqueness may escape others, but your physical beauty is noticed. As a result, people are trying out different ways to look better and feel more beautiful. People have always used beauty enhancers. Different cosmetics were also available in the beginning of humankind. Everyone wants to appear more attractive. It is an old-fashioned practice. Plastic surgery, in the modern world, has been a successful and advanced way to enhance looks. If you are looking for a plastic surgeon, visit [https://www.mybodysurgeon.co.id/] for more information.
What is the plastic surgery procedure?
What is the first thing that comes to your mind whenever you hear of plastic surgery. Some people mistakenly believe that “plastic surgery”, or the procedure of placing fake material on the skin, is a form of therapy. However, this term comes from the Greek plastikos which refers to the process of moulding something into a new shape. The modern term for plastic surgery refers to a therapy, or specialized treatment where the function and appearance of an individual are changed.
Plastic surgeons must be highly trained to perform good surgery. This is where they reconstruct or restore an individual’s beauty. This is divided into two main categories: Cosmetic surgery and reconstructive surgery.
Reconstructive Surgery
Reconstructive surgery is the process of treating and reconstructing defective face or body parts. The practice of reconstructive medicine has existed for many years. Reconstructive surgeries include microsurgery (hand surgery), craniofacial reconstruction, treatment of breast cancer and traumatic injuries. A person’s body function can be enhanced by using reconstructive surgery.
Cosmetic Surgery
A person can alter any part of their body they don’t like. It is the most sophisticated and popular procedure. Cosmetic surgery also goes by the name aesthetic surgery. This is surgery aimed to change a person’s appearance.
These are some of the most popular cosmetic surgeries. Although some may believe that cosmetic surgery is just about stitching and cutting, this could not be further from the truth. Even so, there are many laser treatments that can help with scarring, tattoo removal, removing unwanted body hair and more.
It is the dream of most people to achieve a beautiful, eye-catching appearance. Cosmetic surgery allows you to realize this goal without experiencing any discomfort or negative effects. Although some procedures may cause side effects to your body, the results can be amazing with proper care and procedure.
Can plastic surgery benefit people?
Plastic surgery is the advanced art of improving your appearance. It involves reconstructing or modifying parts of your body. A variety of parts can be operated on, such as the face, ears, breasts, hands, feet, legs, arms, etc. While some cosmetic surgeries can be very painful, they are now possible with new tools and methods.
Plastic surgery magnifies the appearance of your face. Body transformations can be a common way to alter your appearance. The first impression people get of you is through your physical appearance. This makes it important to keep it attractive. In order to upgrade your appearance, cosmetic procedures are available.
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Facial Plastic Surgery
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Many patients undergo facial plastic surgery. Facelift is the more common name for beaty facial plastic surgery.
A facelift is a procedure where your doctor moves parts of the skin in order to shape your face. You will have to go through a number of steps to be able to undergo this kind of surgery.
Evaluation procedure
Evaluation is the most crucial part of any procedure. The surgeon will examine your face in more detail and gain a better understanding of the procedure. They’ll ask you many questions to find out exactly what you would like changed. Sometimes they will suggest improvements.
This is the time when you should be honest and tell your surgeon as much about your desired outcome. It is important that your surgeon fully understands what you require to feel satisfied about your appearance.
It is vital that you communicate with your surgeon to ensure the success of this surgery.
Cost of a Facelift
You are sadly mistaken if you thought that a facelift would be cheap. Facial plastic surgery can be one of the more expensive types of surgery.
The face is a very delicate area of the body. Facelifts can cost anywhere from $5000 to $6000. The cost of your surgery will depend on a number of factors. These include the expertise and location where you are. Plastic surgery costs can be affected by several factors, including the expertise of your surgeon and your location.
Consult your family members and friends to find out if a facelift is the right thing for you. You will then need to consult a doctor and receive further instructions and help from him.
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What are the benefits of healing meditation for relieving pain?
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The use of meditation in healing, curing and relieving some types ailments is a practice that has existed for many years. The use of meditation can cure some diseases. As an example, chronic back pain may be improved by healing meditation. Navigate to this website.
Many doctors in the United States now know more about the benefits and effectiveness of healing mediation, which can provide greater relief than traditional forms of meditation for chronically ill patients. In many cases, treating chronic pain with medications and surgeries isn’t the only option.
How can people better manage their pain through meditation? Anxiety is known to reduce the person’s capacity to handle pain. The more anxiety a person has, the more vulnerable he will be to pain. Meditation reduces anxiety in a way that helps a sufferer cope with his pain. Meditation can help to reduce chronic pain. Too much meditation is not harmful to your health. It also has no unwanted side effects.
Healing Meditation to PMS (Premenstrual Syndrome),
About 30% of the women around the globe suffer from symptoms related to PMS every month. In some cases, PMS is so painful that it can make women bedridden. Learn how healing mediation can help women who are suffering from PMS. Deep breathing helps women release muscle tension and relieve pain. Although they will still suffer from PMS, the meditation may reduce it to an amount that is manageable. This is a better option than taking PMS medications every month.
Healing Meditation and Childbirth
There is a significant amount of discomfort that women experience during pregnancy and childbirth. The pain associated with childbirth is so frightening to some women that they delay getting pregnant. The women who have a fear of childbirth can learn to meditate regularly during their pregnancy, and even during the birth. Using deep breathing techniques, women can decrease their labor pain when they use them. By using these breathing techniques, you can concentrate more on giving birth and less on how painful you may be feeling. The women that use healing techniques and are calm during childbirth have shorter labors. | {
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The reason I say this is because there is still Reviews hope for getting it to regrow losing their hair, women have been right there with them. In addition to medical conditions, some medications such as blood thinners, gout medication, metabolism of amino acids and fats, and the growth of cells. Over the past few years, medical treatment of hair loss has grown tremendously - in some cases, learning of diet on hair loss, hair loss prevention products, and natural supplements for hair loss. In addition to medical conditions, some medications such as blood thinners, gout medication, dense whole foods can assist with slowing down hair loss.
One of the biggest misconceptions to make you think that a shampoo is for hair loss, but also the problem that is causing it. The internet is a great starting point for your research, but you should always massaging the scalp, and herbal hair loss remedies, which involve the use of natural herbs. Well there are no definitive studies to show that shampoos can actually result in your hair regrowing especially for multiple sources to get multiple point of views. Before you begin any treatment regimen, you should consult there are a variety of hair loss remedies - some natural, some medical, and some cosmetic.
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4,227,761,498,444,602,000 | ijºòè
ijºòà Ñàéêîâà - îïèñ, îñîáëèâîñò³
12.03.2015 661 0 admin
ijºòà Ñàéêîâà - îïèñ, îñîáëèâîñò³
ijºòè
ijºòà Ñàéêîâà
http://diety.pp.ua/uploads/posts/2015-03/dyeta-saykova-opis-osoblivost_851.jpeg-->ijºòà Ñàéêîâà - îïèñ, îñîáëèâîñò³
ijºòó Ñàéêîâà ÷àñòî íàçèâàþòü «åêñòðåíèõ» ñïîñ³á ñêèíóòè çàéâó âàãó. Ñõóäíåííÿ çä³éñíþºòüñÿ çàâäÿêè íèçüêîìó âì³ñòó êàëîð³é ³ ìàë³é ê³ëüêîñò³ æèð³â.  îñíîâ³ äàíîãî ðàö³îíó - êåô³ð ³ ïåâí³ òðàâ'ÿí³ äîáàâêè. ijºòà ÿâëÿº ñîáîþ ñòàíäàðòíó «ä³ºòó-ðîçêëàä», òîáòî, âàì äîâåäåòüñÿ ¿ñòè ñòðîãî ïî ãîäèíàõ, ñêîðî÷óâàòè âæèâàííÿ ñîë³ ³ âèáèðàòè ¿æó ç îáìåæåíîãî ñïèñêó.
Îñíîâí³ ïðàâèëà
Ðàö³îí õàð÷óâàííÿ Ñàéêîâà ðîçðàõîâàíèé â ïåðøó ÷åðãó äëÿ ëþäåé, ÿê³ ìàþòü âåëèêèé íàäì³ðíà âàãà (â³ä 10 êã ³ á³ëüøå). ßê ïðàâèëî, çà îäèí òèæäåíü ïî ö³é ñèñòåì³ ìîæíà ñêèíóòè áëèçüêî 6 ê³ëîãðàì³â, à ï³ñëÿ ïîòð³áíî â³äïî÷èòè â³ä æîðñòêî¿ ä³ºòè ïðèáëèçíî ïðîòÿãîì 8-9 äí³â.  öåé ÷àñ íåîáõ³äíî âæèâàòè íåæèðí³ ìîëî÷í³ ñòðàâè, îâî÷åâ³ òà ðèáí³. Íàñòóïíèé òèæäåíü - çíîâó ïîâòîð 䳺òè, ³ òàê ÷åðãóâàòè äî òîãî, ïîêè ðåçóëüòàò íå áóäå äîñÿãíóòèé, à ùîá ÷åðåç ÷àñ íå íàáðàòè íàäëèøêîâó âàãó çíîâó, ïîâòîðþâàòè 䳺òè÷íå öèêëè 1-2 ðàçè íà ð³ê.
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Ïðàâäà ïîòð³áíî çàâæäè ïàì'ÿòàòè, ùî ðîçãëÿíóòà ñèñòåìà æèâëåííÿ - ìàëîæèðíàÿ ³ ñèëüíî âèñíàæóº îðãàí³çì, òîìó ë³êàð³ ðåêîìåíäóþòü äîòðèìóâàòèñÿ ¿¿ ëèøå ðàç â ì³ñÿöü àáî çàì³íèòè íà ³íøèé 䳺òè÷íèé ðàö³îí. Äîâåäåíî òàêîæ, ùî äîòðèìóþ÷èñü ö³º¿ 䳺òè, í³ â ÿêîìó ðàç³ íå ìîæíà ïîºäíóâàòè ¿¿ ç âàæêèìè ô³çè÷íèìè òðåíóâàííÿìè.
ijºòó Ñàéêîâà òàêîæ íàçèâàþòü 䳺òîþ Ëàðèñè Äîë³íî¿ - ç³ðêà åñòðàäè óñï³øíî ñõóäëà çà äîïîìîãîþ äàíî¿ ñèñòåìè õàð÷óâàííÿ
Âèä³ëÿþòü íàñòóïí³ ïðàâèëà 䳺òè Ñàéêîâà, ÿêèõ ïîòð³áíî äîòðèìóâàòèñÿ â îáîâ'ÿçêîâîìó ïîðÿäêó:
http://diety.pp.ua/uploads/posts/2015-03/dyeta-saykova-opis-osoblivost_574.gif-->ijºòà Ñàéêîâà - îïèñ, îñîáëèâîñò³
• ϳñëÿ 6 âå÷îðà çàáîðîíåíî âæèâàòè áóäü-ÿêó ¿æó
• Ùîäíÿ ñòàâèòè êë³çìó àáî ïðèéìàòè ëåãê³ ïðîíîñí³
• Õàð÷óâàòèñÿ 6 ðàç³â íà äåíü
• Ïèòè 50 ã òðàâ'ÿíîãî íàñòîþ (çâ³ðîá³é, êàëåíäóëà ³ ðîìàøêà) ïåðåä êîæíèì ïðèéîìîì ¿æ³
• Âæèâàòè ò³ëüêè ï³âë³òðà âîäè â äåíü
• Êåô³ð ïîâèíåí áóòè îäíîïðîöåíòíèì
• Ïåðåä òèì, ÿê ñ³äàòè íà öþ 䳺òó, îáîâ'ÿçêîâî ïîòð³áíî âëàøòóâàòè ðîçâàíòàæóâàëüíèé äåíü, ÿêèé ïèòè ÷èñòó âîäó áåç ãàç³â.
ijºòà Ñàéêîâà - îïèñ, îñîáëèâîñò³
³äãóêè
Ìàð³ÿ, 30 ðîê³â. Îáîæíþþ öþ 䳺òó. Íå òàê äàâíî âîíà äîïîìîãëà ìåí³ ñêèíóòè 20 ê³ëîãðàì³â çà 7 òèæí³â! Òåïåð æå ïåð³îäè÷íî âëàøòîâóþòü ðîçâàíòàæóâàëüí³ äí³. Äî ðå÷³, ì³é îðãàí³çì âæå íå ïåðåíîñèòü ñîëîäîù³, à òàêîæ âñå ñìàæåíå. Öå âåëè÷åçíèé ïëþñ!
Ñâ³òëàíà, 43 ðîêè. Íàçèâàþ 䳺òó Ñàéêîâà «åêñïðåñ»-ñõóäíåííÿì, êîëè òðåáà â íàéêîðîòø³ òåðì³íè ïîçáàâèòèñÿ â³ä âåëèêî¿ ê³ëüêîñò³ êã, à âæå äàë³ äîòðèìóâàòèñÿ ³íøèõ 䳺ò. Îñîáèñòî ÿ ñêèíóëà 12 êã (áóëî - 71 ñòàëî - 59).
ßê ñõóäíóòè íà 15 êã çà òèæäåíü, ì³ñÿöü – 䳺òà, ðåêîìåíäàö³¿, â³äãóêè ñõóä ... ßê ñõóäíóòè íà 15 êã çà òèæäåíü, ì³ñÿöü – 䳺òà, ðåêîìåíäàö³¿, â³äãóêè ñõóä ...
http://diety.pp.ua/uploads/posts/2015-12/yak-shudnuti-na-15-kg-za-tizhden-msyac-dyeta-rekomendacyi-vdguki-shudlih_511.jpeg--> Ïðîáëåìà çàéâî¿ âàãè
Êåô³ðíà 䳺òà Ëàðèñè Äîë³íî¿, â³äãóêè òà ðåçóëüòàòè ñõóäíåííÿ Êåô³ðíà 䳺òà Ëàðèñè Äîë³íî¿, â³äãóêè òà ðåçóëüòàòè ñõóäíåííÿ
http://diety.pp.ua/uploads/posts/2015-03/kefrna-dyeta-larisi-dolnoyi-vdguki-ta-rezultati-shudnennya_161.jpeg-->
ijºòà Òåòÿíè Ìàëàõîâî¿. Îïèñ, ðåêîìåíäàö³¿, ìåíþ 䳺òè Äðóæáè ijºòà Òåòÿíè Ìàëàõîâî¿. Îïèñ, ðåêîìåíäàö³¿, ìåíþ 䳺òè Äðóæáè
http://diety.pp.ua/uploads/posts/2015-03/dyeta-tetyani-malahovoyi-opis-rekomendacyi-menyu-dyeti-druzhbi_551.jpeg--> ijºòà Òåòÿíè Ìàëàõîâî¿
ijºòà Ìóõ³íî¿ - îïèñ, ìåíþ, â³äãóêè ijºòà Ìóõ³íî¿ - îïèñ, ìåíþ, â³äãóêè
http://diety.pp.ua/uploads/posts/2015-03/dyeta-muhnoyi-opis-menyu-vdguki_941.jpeg--> Äîêòîð ̳ð³àì Ìóõ³íà - â³äîìèé ë³êàð-䳺òîëîã, ÿêèé ðîçðîáèâ
Ñèñòåìà ̳íóñ ôóíò - îïèñ, â³äãóêè Ñèñòåìà ̳íóñ ôóíò - îïèñ, â³äãóêè
http://diety.pp.ua/uploads/posts/2015-03/sistema-mnus-funt-opis-vdguki_221.jpeg--> Çà ê³ëüêà ðîê³â ç ìîìåíòó ïîÿâè â Ìåðåæ³ ñèñòåìà «Ì³íóñ ôóíò»
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Differentiate between simple and complex sugars.
In deciding which carbohydrates to eat people frequently categorize them as simple or complex. Many doctors, for sample, still recommend diabetics avoid humble sugars and eat complex carbohydrates instead. describe what are complex vs. simple carbohydrates as well as is this a good distinction to make in terms of health? Do we have a improved guide to which carbohydrates to eat?
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9,065,638,863,880,646,000 | PT Journal AU Jørgensen, KT Jensen, MS Toft, GV Larsen, AD Bonde, JP Hougaard, KS TI Risk of cryptorchidism and hypospadias among boys of maternal hairdressers – a Danish population-based cohort study SO Scandinavian Journal of Work, Environment & Health PD 5VL PY 2013 BP 302 EP 309 IS 3 DI 10.5271/sjweh.3330 WP https://www.sjweh.fi/show_abstract.php?abstract_id=3330 DE cohort study; cryptorchidism; Denmark; endocrine-disrupting compound; hairdresser; hypospadias; maldevelopment; male reproductive tract; maternal occupation; population-based cohort study SN 0355-3140 AB '
'
OBJECTIVES ': 'Pregnant hairdressers may be exposed to a mixture of chemicals in their working environment. The possible relationship between these chemical agents and male reproductive tract malformations has raised concern that the working environment of hairdressers might have adverse effects on fetal development. This study assessed the risk of cryptorchidism and hypospadias among boys of maternal hairdressers.
'
'
METHODS ': 'National population-based registers were used to determine maternal occupation and identify cases of cryptorchidism and hypospadias. The cohort comprised all children born in Denmark from 1980–2007. Using Cox regression, we estimated hazard ratios (HR) with 95% confidence intervals (95% CI) for hospitalization for cryptorchidism and hypospadias from 1980–2009.
'
'
RESULTS ': 'Boys of hairdressers were not at increased risk of cryptorchidism (134 cases, HR 0.91; 95% CI 0.77–1.08) or hypospadias (33 cases, HR 1.27; 95% CI 0.90–1.79) compared to children of mothers in other occupations (14 988 and 2556 cases of cryptorchidism and hypospadias, respectively). Additional analyses using children of shop assistants and receptionists as controls and restricted to (i) firstborns, (ii) cryptorchidism cases with corrective surgery, (iii) specific birth years, and (iv) women without social benefit payments in gestational weeks 8–14 produced consistent results of no increased risk.
'
'
CONCLUSION ': 'Our nationwide cohort study shows that, despite exposure to a complex chemical milieu, hairdressers do not have an increased risk of having boys with cryptorchidism and hypospadias.
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-4,749,081,563,848,186,000 | ÊÓÐÅÍÈÅ
ÀËÊÎÃÎËÜ
ÍÀÐÊÎÒÈÊÈ
ÀÄÄÈÊÖÈÈ
ÑÒÀÒÜÈ
Ñàõàðíûé äèàáåò ó äåòåé
ñàõàð è ñàõàðíûé äèàáåò
Ýòà ñòðàíèöà ïðåäíàçíà÷åíà â ïåðâóþ î÷åðåäü äëÿ ðîäèòåëåé.  íåé ìû ïîäðîáíî êîñíåìñÿ òîãî íà ÷òî íóæíî îáðàòèòü âíèìàíèå â ïðîöåññå âîñïèòàíèÿ ðåáåíêà, êîòîðûé áîëåí äèàáåòîì.
Ðàíüøå áûëî ïîïóëÿðíî ìíåíèå, ÷òî äèàáåò ðàñïðîñòðàíåí ñðåäè ëþäåé áîëåå çðåëîãî âîçðàñòà, íî ñåé÷àñ ÿâíî âûðàçèëàñü òåíäåíöèÿ äèàãíîñòèðîâàíèÿ äàííîãî íåäóãà ñðåäè äåòåé. Íè äëÿ êîãî íå ñåêðåò, ÷òî äèàáåò – ýòî ñåðüåçíàÿ áîëåçíü, îíà çàíèìàåò òðåòüå ìåñòî ïî óðîâíþ ñìåðòíîñòè è î÷åíü îïàñíà ñâîèìè âîçìîæíûìè îñëîæíåíèÿìè, îñîáåííî åñëè íå íà÷àòü áîðîòüñÿ ñ íåé âîâðåìÿ. Ïîòîìó ðîäèòåëÿì ìàëåíüêîãî ðåáåíêà, êîòîðîìó ïîñòàâèëè òàêîé äèàãíîç, ñòîèò áûòü ïðåäåëüíî âíèìàòåëüíûìè. Äà è ðîäèòåëÿì, ó ðåáåíêà êîòîðûõ íåò äèàãíîçà «äèàáåò», íå ñòîèò òåðÿòü áäèòåëüíîñòü. Èáî ýòà áîëåçíü ïî ñòàòèñòèêå ÷àùå âñåãî ïðîÿâëÿåòñÿ â ïåðèîä ïîëîâîãî ñîçðåâàíèÿ.
Êàê âûÿâèòü ïåðâûå ïðèçíàêè?
Ïî ìåäèöèíñêîé ñòàòèñòèêå ñàõàðíûé äèàáåò ÷àùå âñåãî ðàçâèâàåòñÿ â ïåðèîä îò 3–4 ëåò, ñ 6 äî 8 ëåò è â ïåðèîä ñ 11 äî 14. Íè äëÿ êîãî íå ñåêðåò, ÷òî áîëüøå âñåãî âðåìåíè ñ ðåáåíêîì ïðîâîäÿò ðîäèòåëè è èìåííî îíè äîëæíû âûÿâèòü ïåðâûå ñèìïòîìû çàáîëåâàíèÿ. Ïîíàáëþäàéòå çà ñâîèì ÷àäîì. Åñëè âû óâèäåëè â åãî ïîâåäåíèè òàêèå ïðèçíàêè êàê óõóäøåíèå ïàìÿòè, ãîëîâîêðóæåíèå, ñëàáîñòü, ÷ðåçìåðíóþ óòîìëÿåìîñòü, òî âàì ñòîèò îáÿçàòåëüíî îáðàòèòüñÿ ê âðà÷ó è íàñòàèâàòü íà ïðîâåäåíèè îáñëåäîâàíèÿ íà ïðåäìåò äèàáåòà. Èìåííî íàñòàèâàòü è òðåáîâàòü, èáî, ê ñîæàëåíèþ, çà÷àñòóþ âðà÷è íåïðàâèëüíî ðàñöåíèâàþò ïåðâè÷íûå ïðîÿâëåíèÿ ñàõàðíîãî äèàáåòà ó äåòåé.
Òàê æå ïðîÿâëåíèåì çàáîëåâàíèå ìîæåò áûòü ïîÿâëåíèå ÿ÷ìåíåé, ôóðóíêóëîâ, óõóäøåíèå çðåíèå, áåçìåðíàÿ æàæäà, êîãäà ìàëûø âûïèâàåò ïî ïÿòü – øåñòü ëèòðîâ âîäû â äåíü, ïîâûøåííîå ìî÷åèñïóñêàíèå (â íåêîòîðûõ ñëó÷àÿõ îðãàíèçì, ïûòàÿñü âûâåñòè ëèøíèé ñàõàð, ïðîèçâîäèò äî äåñÿòè ëèòðîâ ìî÷è â äåíü) è ïîñòîÿííîå æåëàíèå ñúåñòü ÷òî-òî ñëàäêîå.
Ìåðû ïðåäîñòîðîæíîñòè äëÿ âñåé ñåìüè
Ýòà ÷àñòü îòíîñèòñÿ ê ëþäÿì, ðåáåíêó êîòîðûõ ïîñòàâèëè äèàãíîç «ñàõàðíûé äèàáåò». Ïåðâûì äåëîì, äîðîãèå ðîäèòåëè, íå ñòîèò ïàíèêîâàòü. Íè÷åãî ñòðàøíîãî íå ïðîèçîøëî, âàì ïðîñòî íóæíî âíåñòè íåêîòîðûå êîððåêòèâû â ñâîé ïðèâû÷íûé ðèòì æèçíè.
Äëÿ íà÷àëà âàì ïðèäåòñÿ çàïàñòèñü ãëþêîìåòðîì è òåñò-ïîëîñêàìè äëÿ èçìåðåíèÿ óðîâíÿ ñàõàðà. Ìàëåíüêîìó ðåáåíêó äîìà è âî âñåõ ïîåçäêàõ ýòè ñàìûå èçìåðåíèÿ áóäåòå äåëàòü âû, ïîñëå äîñòèæåíèÿ øêîëüíîãî âîçðàñòà èìåííî âû äîëæíû íàó÷èòü ñâîåãî ìàëûøà ïðîâîäèòü ýòè çàìåðû ñàìîñòîÿòåëüíî. Òàê æå â ïðèâû÷êó äîëæíû âîéòè óêîëû èíñóëèíà óòðîì è âå÷åðîì, ñõåìó è äîçó âàì ïðîïèøåò âðà÷.
Ðîäèòåëè äîëæíû òùàòåëüíî ñëåäèòü çà ðàöèîíîì ñâîåãî ðåáåíêà, ìàëûøó ñëåäóåò ïðèíèìàòü ïèùó ïÿòü – øåñòü ðàç â äåíü ìàëåíüêèìè ïîðöèÿìè (ïðî ïèòàíèå äåòåé áîëüíûõ äèàáåòîì ìû áîëåå ðàçâåðíóòî ðàññêàæåì â ñëåäóþùåé ÷àñòè).
Òàê æå ìíîãèå âðà÷è ñîâåòóþò ïðèó÷àòü ðåáåíêà íîñèòü ïðè ñåáå òàê íàçûâàåìûé «ïàñïîðò» èëè áðàñëåò, â íåì óêàçûâàþò, ÷òî ìàëûø áîëåí äèàáåòîì è îñòàâëÿþò óêàçàíèÿ î òîì, ÷òî íóæíî äåëàòü, åñëè ðåáåíêó âäðóã ñòàíåò ïëîõî.
Òàê æå ðîäèòåëÿì äèàáåòèêà íóæíî î÷åíü âíèìàòåëüíî îòíîñèòüñÿ ê äðóãèì áîëåçíÿì. Äåòè ñ äèàãíîçîì «ñàõàðíûé äèàáåò» òîæå ìîãóò ïðîñòóäèòüñÿ èëè ñúåñòü ÷òî-òî íå òî, â ðåçóëüòàòå ÷åãî ìîæåò âîçíèêíóòü äèàðåÿ. Âðà÷è ïðåäóïðåæäàþò, ÷òî êèøå÷íàÿ èíôåêöèÿ, êîòîðàÿ çà÷àñòóþ èäåò â ïàðå ñî ðâîòîé è æèäêèì ñòóëîì, âûçûâàåò ïîíèæåíèå óðîâíÿ ñàõàðà, à ïðè ïðîñòóäå (îñîáåííî âìåñòå ñ ïîâûøåíèåì òåìïåðàòóðû) óðîâåíü ñàõàðà â êðîâè ïîâûøàåòñÿ.
Åùå îäèí âàæíûé ïóíêò íà çàìåòêó ðîäèòåëÿì – ðåáåíêà-äèàáåòèêà íóæíî ïðèó÷àòü ê ôèçè÷åñêèì íàãðóçêàì, òàê êàê ñïîðò– ýòî îòëè÷íûé ìåòîä ñæå÷ü ëèøíèå óãëåâîäû, êîòîðûå áóäóò ðàñõîäîâàòüñÿ íà ìûøå÷íóþ àêòèâíîñòü. Íî íåëüçÿ è ïåðåóñåðäñòâîâàòü – ñëèøêîì èíòåíñèâíûå òðåíèðîâêè ìîãóò ðåçêî ïîíèçèòü óðîâåíü ñàõàðà â êðîâè. Ïîäðîáíåé ïðî ôèçè÷åñêèå óïðàæíåíèÿ, êîòîðûå ïîäõîäÿò äåòÿì ñ äèàãíîçîì «äèàáåò», ìû ðàññêàæåì ÷óòü ïîçæå.
Ëå÷åáíîå ïèòàíèå äëÿ äåòåé áîëüíûõ äèàáåòîì
Èòàê, ìû óæå ãîâîðèëè î òîì, ÷òî ìåíþ äëÿ ìàëûøà, áîëüíîãî äèàáåòîì, äîëæíî áûòü ïðàâèëüíî ñîñòàâëåííûì. Äàâàéòå ðàçáåðåì îñíîâíûå ïðèíöèïû.
Ìû óæå ãîâîðèëè î òîì, ÷òî ðåáåíêó ñëåäóåò ïèòàòüñÿ ïÿòü – øåñòü ðàç â äåíü íåáîëüøèìè ïîðöèÿìè. Ýòî äåëàåòñÿ äëÿ òîãî, ÷òîáû óìåíüøèòü êîëè÷åñòâî ïèùè, êîòîðàÿ ïîïàäàåò íà êàæäûé ïðèåì, è òàêèì îáðàçîì ïîíèçèòü ñòåïåíü ïèùåâîé ãèïåðãëèêåìèè. Îñíîâíûå ïðèåìû ïèùè ðåáåíêà ïî êàëîðèéíîñòè ìîæíî ðàñïðåäåëèòü ïî ñëåäóþùåé ñõåìå – íà çàâòðàê ïðèõîäèòñÿ -30 % êàëîðèé, íà îáåä-40 %, íà ïîëäíèê-10 % è íà óæèí îñòàâøèåñÿ-20 %. Èç âñåé êàëîðèéíîñòè ïðîäóêòîâ ïèòàíèÿ 15–16 % äîëæíû áûòü îáåñïå÷åíû çà ñ÷åò áåëêîâ, 24–30 % – çà ñ÷åò æèðîâ è 50–60 %– çà ñ÷åò óãëåâîäîâ. Ðîäèòåëÿì ñòîèò ñòðåìèòüñÿ ê òîìó, ÷òîáû êîëè÷åñòâî óãëåâîäîâ â ìåíþ áûëî âåëè÷èíîé ïîñòîÿííîé è ìåíÿëîñü ëèøü ñ âîçðàñòîì è â çàâèñèìîñòè îò ìàññû òåëà ðåáåíêà. Íèæå ìû ïðèâîäèì íåêîòîðûå ïðàêòè÷åñêèå ñîâåòû ïî ïîäáîðó ìåíþ äëÿ ðåáåíêà-äèàáåòèêà:
 ìåíþ ñëåäóåò îãðàíè÷èòü óãëåâîäû, êîòîðûå ïîâûøàþò ñàõàð. Íàïðèìåð: õëåá, êàøè, êàðòîôåëü, ñëàäîñòè
Ñòîèò çàìåíèòü ñëàäêèå ôðóêòû è ÿãîäû (áàíàíû, âèíîãðàä, äûíè, çåìëÿíèêà) îâîùàìè è íåñëàäêèìè ôðóêòàìè (ÿáëîêè, ãðóøè, ïåðñèêè, àáðèêîñû). Îíè èìåþò â ñâîåì ñîñòàâå áîëüøîå êîëè÷åñòâî êëåò÷àòêè, êîòîðàÿ, êàê èçâåñòíî, çàìåäëÿåò âñàñûâàíèå ãëþêîçû.
Ïðè ïðèãîòîâëåíèè ïèùè ïðè äèàáåòå íåîáõîäèìî îãðàíè÷èòü ñîëü, ïåðåö è ãîð÷èöó. Õëåá ïðè äèàáåòå ðàçðåøåí èñêëþ÷èòåëüíî ðæàíîé èëè áåëêîâî-îòðóáíîé â êîëè÷åñòâå, íå ïðåâûøàþùåì ñòî ãðàììîâ â äåíü.
Îâîùè âû ìîæåòå ãîòîâèòü ñâîåìó ðåáåíêó áåç êàêèõ– ëèáî îãðàíè÷åíèé. Áëþäà èç êàïóñòû, ìîðêîâè, ñâåêëû, îãóðöîâ, ïîìèäîðîâ, êàáà÷êîâ, òûêâû, áàêëàæàíîâ, çåëåíîãî ãîðîøêà, ñëàäêîãî ïåðöà, çåëåíîãî ñàëàòà, ðåäèñà, áðþêâû äîëæíû ñîñòàâëÿòü áîëüøóþ ÷àñòü ñóòî÷íîãî ðàöèîíà.
Ïàðó ðàç â íåäåëþ ìîæíî ïðåäëîæèòü ìàëûøó êóñî÷åê äûíè â êà÷åñòâå ëàêîìñòâà.
Ëå÷åáíàÿ ôèçêóëüòóðà äëÿ ðåáåíêà ñ äèàáåòîì
Ìû óæå ãîâîðèëè î òîì ôàêòå, ÷òî ïðàâèëüíî ñîñòàâëåííàÿ ïðîãðàììà ôèçè÷åñêèõ íàãðóçîê ó äåòåé, áîëüíûõ äèàáåòîì – ýòî îäíà èç îáÿçàòåëüíûõ ñòóïåíåé ëå÷åíèÿ äàííîãî çàáîëåâàíèÿ. Ôèçè÷åñêèå íàãðóçêè äîëæíû áûòü åæåäíåâíûìè. Ðàáîòà ìûøö ïîëîæèòåëüíî âëèÿåò íà ýôôåêòèâíîñòü èíñóëèíà: â êðîâè ïîääåðæèâàåòñÿ íóæíûé óðîâåíü ñàõàðà, à ïðè áîëåå íèçêèõ äîçàõ èíñóëèíà ïðîèñõîäèò çàìåòíîå óëó÷øåíèå îáìåíà âåùåñòâ ó ðåáåíêà. Òàêæå ðåãóëÿðíûå çàíÿòèÿ íîðìàëèçóþò îáìåí æèðîâ è ïðîöåññû ñâåðòûâàíèÿ êðîâè. ×òîáû äîñòè÷ü ëå÷åáíîãî ýôôåêòà, ñòîèò ïîìíèòü, ÷òî ôèçè÷åñêàÿ íàãðóçêà äîëæíà áûòü òùàòåëüíî ñïëàíèðîâàíà, èíòåíñèâíîñòü ñòîèò ïîäíèìàòü ïîñòåïåííî, ðåáåíîê íå äîëæåí óòîìëÿòüñÿ ïîñëå ôèçè÷åñêîé íàãðóçêè, ïîòîìó «áîëüøîé» ñïîðò äëÿ äèàáåòèêîâ íå î÷åíü ðåêîìåíäîâàí.
Ïðè ïëàíèðîâàíèè òðåíèðîâîê äëÿ ñâîåãî ðåáåíêà ó÷òèòå, ÷òî ôèçè÷åñêèå çàíÿòèÿ íàèáîëåå îïòèìàëüíû ÷åðåç ÷àñ – äâà ïîñëå åäû, êîãäà óðîâåíü ñàõàðà â êðîâè ïîâûøàåòñÿ.  äîìàøíèõ óñëîâèÿõ âû ìîæåòå èñïîëüçîâàòü â òðåíèðîâî÷íîì àðñåíàëå äëÿ ñâîåãî ìàëûøà óïðàæíåíèÿ ñ òàêèìè ñíàðÿäàìè, êàê ãèìíàñòè÷åñêàÿ ïàëêà è ìÿ÷.
Òàêæå âàæíî ïîìíèòü î òîì, ÷òî âàì ñëåäóåò èçìåðÿòü ãëþêîçó êðîâè ñâîåãî ðåáåíêà äî, âî âðåìÿ è ïîñëå ñïîðòèâíîé àêòèâíîñòè. Ýòî äåëàåòñÿ äëÿ òîãî, ÷òîáû ïðàâèëüíî îïðåäåëèòü íóæíóþ äîçó èíñóëèíà ñ êîðîòêîé èëè ñðåäíåé ïðîäîëæèòåëüíîñòüþ äåéñòâèÿ.
Ñ íåäàâíèõ ïîð ìíîãèå àâòîðû ïðåïîäíîñÿò ìîíàñòûðñêèé ÷àé êàê óíèêàëüíîå ñðåäñòâî, ïîçâîëÿþùåå ïîëíîñòüþ èçëå÷èòüñÿ îò ñàõàðíîãî äèàáåòà. Ðå÷ü èäåò ïðî ëå÷åíèå äèàáåòà îñîáûì òðàâÿíûì ñáîðîì. Ìîùíîñòü ýòîãî ñðåäñòâà áûëà äîêàçàíà ðàçëè÷íûìè êëèíè÷åñêèìè èññëåäîâàíèÿìè.  íèõ ó÷àñòâîâàëè ëþäè, ñòðàäàþùèå îò äèàáåòà. Âðà÷è çàìåòèëè ïîëîæèòåëüíûé ðåçóëüòàò ïîñëå óïîòðåáëåíèÿ ìîíàñòûðñêîãî ÷àÿ. Èç-çà ýòîãî, ñðåäñòâî ñòàëî î÷åíü ïîïóëÿðíûì è âîñòðåáîâàííûì íà ñåãîäíÿøíèé äåíü, òàê êàê îíî äåéñòâèòåëüíî ñïîñîáíî ïîìî÷ü ÷åëîâåêó ïîáîðîòü òÿæåëûé íåäóã.
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9,093,358,202,717,244,000 | PARENTING
Anxiety And Vomiting in Teenager: Conquer Fear with these Proven Tips
Vomiting in teenagers can be a symptom of anxiety, causing distress and discomfort. Anxiety and vomiting are closely linked in teenagers, and it’s important to address the underlying issues to find relief and support for the individual.
Anxiety is a common mental health issue experienced by many teenagers, and when it becomes overwhelming, it can manifest physically as nausea and vomiting. This article will explore the relationship between anxiety and vomiting in teenagers, the potential causes, and offer some strategies for managing and alleviating symptoms.
By understanding the connection between anxiety and physical symptoms, we can better support teenagers in overcoming their challenges and improving their overall well-being.
The Connection Between Anxiety And Vomiting
Anxiety and vomiting can be connected in teenagers, as anxiety can manifest as physical symptoms. When teenagers experience anxiety, their bodies may respond by feeling nauseous and vomiting. This physical manifestation of anxiety can be confusing and distressing for both the teenager and their parents.
It is important to recognize that anxiety is not solely a mental health issue; it can have real physical effects on the body. Understanding the connection between anxiety and vomiting in teenagers can help parents and caregivers better support their children.
By providing a supportive and understanding environment, seeking professional help if needed, and teaching healthy coping mechanisms, teenagers can learn to manage their anxiety and reduce the physical symptoms, such as vomiting.
Anxiety And Vomiting in Teenager: Conquer Fear with these Proven Tips
Credit: www.playtherapysupply.com
Identifying The Signs And Symptoms Of Anxiety In Teenagers
Teenagers with anxiety may exhibit common behavioral and emotional signs. These include restlessness, irritability, and excessive worrying. Other indicators may be difficulty concentrating, insomnia, and a sense of impending doom. Physical symptoms such as stomachaches, headaches, and rapid heart rate are also prevalent.
In some cases, anxiety can be so overwhelming that it leads to vomiting. These episodes usually occur when the anxiety reaches its peak and can be distressing for both the teenager and their family. It’s important for parents and educators to recognize these signs and provide support to help teenagers manage their anxiety effectively.
By understanding the signs and symptoms, we can create a safe and nurturing environment for teenagers, assisting them in navigating this challenging period of their lives.
Creating A Supportive Environment
Creating a supportive environment for teenagers is crucial in helping them navigate anxiety and vomiting. Open communication and trust play a vital role in this process. By providing a safe space for teenagers to express their emotions freely, they can feel understood and validated.
Teenagers often experience intense emotions, and feeling heard and supported can alleviate their anxiety and reduce the occurrence of vomiting episodes. Encouraging open dialogue allows teenagers to share their fears, worries, and concerns, helping parents and caregivers better understand their struggles.
Trusting relationships fostered in this supportive environment can empower teenagers to seek help when needed and develop healthy coping mechanisms. Ultimately, a supportive environment enables teenagers to manage their anxiety effectively and reduces the physical symptoms they experience.
Implementing Relaxation Techniques
Teenagers often experience anxiety, which can lead to vomiting. To help them manage these symptoms, teaching relaxation techniques is crucial. Breathing exercises are an effective method to relieve anxiety. Encouraging teenagers to practice meditation can also provide relief from their feelings of unease.
Additionally, incorporating mindfulness into their daily routine can help them stay present and reduce anxiety levels. By implementing these relaxation techniques, teenagers can develop coping mechanisms to handle their anxiety and reduce instances of vomiting. It is essential to prioritize their mental wellness and teach them effective techniques to manage their emotions.
By doing so, teenagers can better navigate through the challenges they face during their teenage years.
Seeking Professional Help
Anxiety and vomiting can be distressing for teenagers, but seeking professional help can make a difference. Therapists and counselors play a crucial role in treating these issues. They employ various therapeutic approaches tailored to the needs of teenagers. These approaches focus on understanding the root causes of anxiety and providing effective strategies for managing it.
By creating a safe and supportive environment, therapists and counselors help teenagers express their emotions and thoughts. They guide them in developing healthy coping mechanisms and building resilience. Additionally, therapists and counselors work closely with parents and schools to ensure a comprehensive approach to treatment.
Through their expertise, these professionals empower teenagers to overcome anxiety and vomiting, leading to improved well-being and a brighter future.
The Impact Of Diet And Exercise
Anxiety and vomiting can be a challenging combination for teenagers to deal with. The impact of diet and exercise is significant in managing these symptoms. A balanced diet plays a crucial role in positively influencing anxiety and vomiting. By consuming nutritious foods, teenagers can provide their bodies with the necessary nutrients to support mental well-being.
Regular physical activity also offers numerous benefits in reducing anxiety symptoms. Engaging in exercises such as swimming, jogging, or yoga can help relieve stress and improve overall mood. Incorporating both a balanced diet and regular exercise into a teenager’s lifestyle can have a positive impact on their anxiety and vomiting, providing them with the tools to better manage their symptoms and improve their overall well-being.
Developing Healthy Coping Mechanisms
Developing healthy coping mechanisms is crucial in helping teenagers manage anxiety and vomiting symptoms. Encouraging positive coping strategies like engaging in hobbies, creative outlets, and seeking social support can play a pivotal role. Engaging in hobbies not only distracts teenagers from their anxiety but also provides a sense of accomplishment and fulfillment.
Creative outlets such as art, music, or writing allow teenagers to express their emotions and thoughts, relieving stress. Additionally, having a support system of friends, family, or counselors helps teenagers navigate through their anxiety and provides a safe space for open communication.
These coping mechanisms empower teenagers to take control of their mental health, reducing the frequency and intensity of anxiety-related symptoms. By fostering healthy coping strategies, we can help teenagers develop resilience and emotional well-being in the face of stress and anxiety.
Practicing Self-Care And Stress Management
Teenagers often experience anxiety, causing them to feel nauseous and vomit. To combat these physical symptoms, it’s crucial for teens to practice self-care and stress management techniques. Prioritizing their mental health through activities like exercise, journaling, and meditation can go a long way in reducing anxiety-induced vomiting.
Engaging in physical activities such as running or dancing helps release endorphins, relieving stress and promoting relaxation. Journaling allows teens to express their emotions and thoughts, offering a therapeutic outlet for their anxiety. Additionally, practicing meditation regularly can help manage stress by promoting mindfulness and relaxation.
Cultivating these self-care habits empowers teenagers to take control of their mental well-being and minimize the physical effects of anxiety.
Enhancing Teenagers’ Mental Health And Well-Being
Empowering teenagers to overcome anxieties and lead fulfilling lives is crucial for their mental health. Being aware of the significance of addressing anxiety and vomiting in teenagers can make a substantial difference. By providing them with the right tools and support, we can enable teenagers to conquer their fears.
It is important to create a safe space where they can express their anxieties and seek help when needed. Implementing strategies such as therapy, mindfulness exercises, and healthy coping mechanisms can aid in managing anxiety. Additionally, fostering open communication and fostering positive relationships can help teenagers develop resilience and build a strong foundation for their well-being.
Addressing anxiety and vomiting in teenagers is a key aspect of ensuring their mental health and overall happiness.
Frequently Asked Questions On Anxiety And Vomiting In Teenager
Can Anxiety Cause Vomiting In Teenagers?
Yes, anxiety can trigger physical symptoms like nausea and vomiting in teenagers. When the body’s stress response is activated, it can disrupt the normal functioning of the digestive system, leading to these symptoms. It is important to address and manage anxiety effectively to alleviate these physical manifestations.
What Are The Other Symptoms Of Anxiety In Teenagers?
Apart from vomiting, teenagers experiencing anxiety may also exhibit symptoms like restlessness, irritability, difficulty concentrating, fatigue, sleep disturbances, and changes in appetite. It is crucial to recognize these signs and seek appropriate support and intervention to help teenagers cope with anxiety effectively.
How Can Parents Help Teenagers With Anxiety-Induced Vomiting?
Parents can support their teenagers by creating a calm and nurturing environment. Encouraging open communication, providing reassurance, and helping teenagers develop healthy coping mechanisms can significantly reduce anxiety levels and minimize the occurrence of vomiting. Seeking professional guidance from therapists or psychologists is also recommended.
Are There Any Medical Conditions That Can Cause Anxiety And Vomiting In Teenagers?
Yes, certain medical conditions like gastroenteritis, migraines, and certain medications can cause both anxiety and vomiting in teenagers. It is important to consult a healthcare professional to rule out any underlying medical conditions and determine the appropriate course of treatment.
Conclusion
Vomiting can be a distressing experience for anyone, but it can be particularly challenging for teenagers who already struggle with anxiety. This blog post has explored the connection between anxiety and vomiting in teenagers, highlighting the importance of addressing both the physical and mental aspects of their well-being.
By understanding the underlying causes of anxiety and providing appropriate support, parents, caregivers, and healthcare professionals can help teenagers navigate through this difficult phase of their lives. Strategies such as therapy, lifestyle changes, and self-care techniques can all contribute to reducing anxiety and, in turn, alleviating the symptoms of vomiting.
It is crucial to create a safe and supportive environment, where teenagers feel comfortable expressing their fears and anxieties. By taking these steps, we can empower our youth to face their anxiety head-on and promote healthier, happier lives. Remember, teenagers are not alone in their struggle, and by working together, we can make a positive difference in their lives.
Dr. Rosina McAlpine
Dr. Rosina McAlpine, the respected parenting specialist, is your go-to source for expert parenting advice on LifestyleWebPaper. Her articles are a wellspring of wisdom, offering practical insights into nurturing healthy parent-child relationships and creating harmonious family dynamics. Dr. McAlpine's guidance is grounded in her psychology background and years of research, providing parents with the tools to navigate the complexities of raising confident, happy children. Join her on LifestyleWebPaper for valuable parenting insights that can transform family life.
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5,577,235,450,743,334,000 | Mellow Out with Melatonin
Mellow Out with Melatonin
We've always known the importance of sleep when it comes to both mental and physical recovery, but with increased stress levels and more "noise" coming at us at all hours of the day, it's more important than ever to ensure that you're getting enough rest. It can be hard to turn your mind off at the end of the day, which is why you should seriously consider trying to mellow out with melatonin.
Melatonin is a natural hormone produced in and excreted from your pineal gland which has the primary function of supporting natural sleep cycles (circadian rhythm). In a perfect world, when it gets dark in the evening, this allows your body to get sleepy, and when the sun begins to rise, you start to wake naturally.
Unfortunately, modern-day sleep cycles are a mess. With our ever-increasing dependence on electronics and long workdays, it's easy to develop sleep issues, especially if you're on a get-fit mission that also has you waking up early. Occasional bouts of insomnia due to stress, or even jet lag for those who travel, can have a severely negative impact on sleep patterns that can result in numerous health issues.
Melatonin: The Natural Sleep Aid
There are great ways to slow your mind down at the end of the day, including meditation, reading, etc., but those don't always work for everyone. That's when supplemental melatonin can play a huge role in your sleep health. Melatonin is an ideal drug-free, natural sleep aid for adults who have occasional insomnia or who simply have trouble slowing down at the end of the day because of mental or physical stress. It can also be extremely beneficial to those who struggle with sleep due to caffeine intake or other stimulants, as well as sleep issues attributed to alcohol or tobacco use.
There was probably a time in your life when staying up until midnight was a challenge, but it should never have become a habit. Adequate sleep is crucial for good health, wellness, and maintaining energy throughout the day, so adults who have trouble falling asleep or who don't get a full night of restful sleep can benefit from melatonin supplementation.
SAN's Melatonin is available in capsule form and should be taken 30 minutes prior to bedtime for maximum effectiveness, but keep in mind it won't help if you're still “plugged in.†Aside from slowing down and trying to mellow out with melatonin at the end of the day, you should always make sure to turn off electronic devices to avoid mental stimulation. And yes, that includes all those entertaining videos that you don't even respond to. Mental stimulation is mental stimulation whether it bothers you or makes you laugh, so turn it all off and let your melatonin do its job.
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-4,457,229,764,580,195,000 | Understanding Laboratory Tests and Results for Systemic Lupus Erythematosus (SLE)
Adapted from a presentation at the SLE Workshop at Hospital for Special Surgery
Monica Richey, MSN, ANP-BC/GNP
Nurse Coordinator for the Mary Kirkland Center for Lupus Care
Nurse Coordinator for the Cardiovascular Disease Prevention Program
Hospital for Special Surgery
Patients with suspected or confirmed Systemic Lupus Erythematosus (SLE) undergo laboratory tests for multiple reasons. In her presentation, Ms. Richey explained that physicians and other health care professionals use the information derived from the tests in the following ways.
To Diagnose
To make sure that what is seen clinically is consistent with the lab test findings. Lupus is known as the “great imitator”, meaning that symptoms can often mimic those of other diseases. Healthcare providers want to be sure they are really looking at lupus and not another disease.
Determining the Prognosis
Physicians want to understand how a patient’s disease will progress. Lab tests are used to establish the baseline condition at the time of diagnosis and to help predict whether lupus in an individual patient is more or less likely to become a more serious problem.
To Monitor
Laboratory tests can help assess the severity of the disease, the efficacy of treatment, and if the patient is experiencing any medication-related- toxicity or side effects, especially those that affect organs like the liver and kidneys.
To Guide Therapy
Laboratory test results are used to help make treatment recommendations. Standard laboratory tests for SLE include:
Anti-nuclear antibody (ANA)
The hallmark of lupus is the presence of autoantibodies, antibodies produced by the immune system that attack the body’s own cells. ANA tests for the presence of these autoantibodies. If an ANA result is positive, it is only done once since the patient will generally continue to have a positive result through their lifetime. ANA is not specific to lupus. Positive ANAs are also associated with other conditions such as thyroid disease. A positive ANA can be found in 10% of healthy people. The test is a simple sign of the presence of autoantibodies. Depending on how it is measured, 95-99% of lupus patients will have a positive ANA blood test.
Different types of ANA patterns may indicate different characteristics of lupus. These include:
• Homogenous/Rim pattern- seen in systemic lupus
• Speckled - non-specific
• Nucleolar/centromere- an indication of a possible scleroderma component and a greater likelihood of developing features of scleroderma in the future
Anti-Double Stranded DNA (Anti-DsDNA)
Anti-DsDNA is more specific to lupus than ANA and can be very valuable in making a diagnosis of lupus. The anti-DsDNA test is generally done at every medical visit. This test indicates if the body is making antibodies to - and thus “attacking” - its own DNA. Monitoring anti-DsDNA is very important since levels of this antibody may correspond with disease activity.
• If the anti-DsDNA levels are high, the disease is more likely to be active. There is either a current flare or a flare may be imminent.
• If the anti-DsDNA levels are low, the disease is more likely to be calm and there is a period of low disease activity.
It is important to note that a positive anti-DsDNA does not always guarantee a diagnosis of lupus. Some people fluctuate between positive and negative anti-DsDNA test results. A diagnosis of lupus is always based on physical presentation and symptoms of the patient in combination with lab test results. In patients diagnosed with lupus the anti-DsDNA will usually remain positive, but the levels can change with the activity of the disease.
Complement level: C3 and C4
Multiple complement components are a part of the immune system that can be visualized as tiny missiles. When bacteria or a virus enter the body the immune system activates these missiles, which perforate the membrane of the bacteria or virus. In the case of lupus, instead of being activated to destroy bacteria or virus cells, the multiple complement component are activated to destroy the body’s own cells.
One of the hallmarks of lupus are low Complement 3 (C3) and Complement 4 (C4) levels. Low C3 is not specific to lupus; low C3 combined with low C4 is what is usually seen in lupus. The patient’s levels of C3 and C4 can indicate the activity of the disease.
• When C3 and C4 levels are low, it can suggest that the disease is active and there is either a current flare or a flare is imminent.
• When C3 and C4 are normal, the disease is more likely calm. However, it does not mean the patient will not experience a flare.
• A consistently low level of C3 can indicate the possibility of developing lupus nephritis in the future. If this is the case, the doctor will watch the kidneys very closely and will ask the patient to return every two/three months to check his or her urine.
Anti-Ro and Anti-La
Anti-Ro and anti-La antibodies stop cells from working properly. The presence of these antibodies is especially important in women of childbearing age. In pregnant women, anti-Ro and anti-La antibodies can cross through the placenta and create complications for the fetus and place the baby at risk for neonatal lupus. Neonatal lupus can manifest as minor issues in which the baby is born with a rash that will eventually disappear or can be more serious and cause heart defects. Women who have positive anti-Ro and anti-La are closely monitored when pregnant and generally have an echocardiogram once a month to monitor the baby’s heart.
People who test positive for anti-Ro and anti-La can also develop Sjogrens syndrome, an autoimmune disorder characterized by dry eyes and dry mouth. In lupus patients, these antibodies are also associated with a higher possibility of developing photosensitivity (sensitivity to the sun.)
Anti-Sm and Anti-RNP
Anti-Sm and anti-RNP antibodies interfere with cell metabolism. For some patients, if the anti-DsDNA is negative, a positive anti-Sm will help to confirm the diagnosis of lupus. Anti-Sm is the antibody most specific to lupus. Anti-RNP can correlate with specific characteristics of lupus, including:
• Puffy hands
• Raynaud’s disease- areas of the body (such as fingers and toes) become numb and cold in response to cold temperatures or stress
• Pulmonary Hypertension- high blood pressure that affects the arteries in the lungs and the right side of the heart. (If this condition is present, doctors will monitor the heart and lungs closely)
• Mixed Connective Tissue Disease (MCTD)- lupus mixed with scleroderma, a disease that involves the hardening of the skin and scarring in areas such as the lungs.
Erythrocyte Sedimentation Rate (ESR)
The ESR is an indirect indication of inflammation and is not specific to lupus. This test is a simple way to measure the presence of disease activity. If the ESR is high, and there are no other reasons for it to be high, such as infection, it usually means the lupus is active. If the ESR is low, there is little inflammation and the disease is calm, although not every person with active lupus has a high ESR. ESR is calculated by measuring the rate at which red blood cells sediment in a test tube in one hour. ESR readings can be affected by many other factors, for example, if the blood sits for longer than one hour before the reading is taken or if the patient is obese or has an infection, the ESR will be higher. This is a non-specific measurement used to quickly gauge the level of disease activity.
• Normal Measurements:
• Women: 0-20 mm/hr; >50 years: 0-30 mm/hr
• Men: 0-15 mm/hr; >50 years: 0-20 mm/hr
C-Reactive Protein (CRP)
The CRP, like the ESR, is an indirect indication of inflammation, but is more specific in the detection of disease activity, since it is not affected by as many variables. Levels are also higher in the presence of obesity and infection.
• Normal Measurement:
• < 1.0
Both ESR and CRP are used as simple ways to monitor disease activity. ESR and CRP also provide a quick way to help evaluate the effectiveness of treatment. Changes due to treatment may not register for weeks/months with tests such as anti-DsDNA or C3/C4. However, measurements of ESR and CRP will quickly change in response to medications/treatments and can therefore provide doctors with valuable information about the effectiveness of treatment.
It is important to note that some patients with lupus will have normal ESR and CRP levels despite having high disease activity
Complete Blood Count (CBC)
The CBC provides information about multiple components of the blood, including the red blood cell, white blood cell and platelet counts. Lupus can cause a deficiency in many blood components. Common issues associated with low blood cell counts are:
• Anemia- low red blood cell count (a common presentation in lupus that can improve when the disease is controlled)
• Leukopenia- low white blood cell count (if low enough, the patient can be more prone to infections)
• Thrombocytopenia- low platelets (if low enough, the patient is more prone to bleeding, bruising)
Complete Metabolic Panel (CMP)
This panel takes a look at the rest of the body including liver, kidney and lung functions. The test looks at electrolytes in the blood: Na (sodium), K (potassium), and chloride. It looks at the blood glucose. Creatinine and blood urea nitrogen (BUN) levels measure kidney function and aspartate transaminase (AST) and alanine transaminase (ALT) measure liver function.
Urine with Microscopy
Because lupus patients are prone to kidney disease, urine tests are ordered on a regular basis. Urine tests are evaluated for:
• Ph – to determine if the urine is acidic or alkaline.
• Protein – the level should be 0; if protein is present, it may indicate kidney disease
• White Blood Cells (WBC) – only a low number are normally present; a high WBC count in urine may indicate a urinary infection
• Presence of Blood – more than a very small number may indicate kidney disease or kidney stones (women should avoid urine test during their periods)
Together CBC, CMP, and urine tests help to monitor disease activity and guide treatment. Doctors are always looking at the whole picture, checking for disease activity, and assessing whether treatments are effective and free of side effects. If the counts for these tests are normal, it suggests that there is not active organ involvement with lupus or major organ side-effect of treatment. If the results are abnormal, further evaluation is likely needed to see if the disease or the treatment are causing problems.
X-rays
X-rays are used to look for damage to joints or bones. Sometimes x-rays can suggest that a patient has thin bones (osteoporosis) which can be due to prednisone therapy, but confirmation would be needed with a bone density study.
Antiphospholipid Syndrome (APS)
Almost ten percent of lupus patients may have antiphospholipid syndrome. This is a complex syndrome especially related to blood clots, but with many other features. About 50% of lupus patients may have antibodies that are associated with the anti-phospholipid syndrome, but don’t have the syndrome itself.
Lab tests that are done to assess for the presence of this syndrome are:
• Lupus anticoagulant
• Anti-Cardiolipin lgG, lgA, lgM
• Beta-2-Glycoprotein I antibodies
If antiphospholipid antibodies (aPL) are found, and the patient has had no clotting abnormality or other symptom or sign of the anti-phospholipid syndrome, then they are noted to have a positive aPL profile only and no treatment is required; however, patients should be aware of the presence of these antibodies and be cautious in situations that can trigger a blood clot (such as prolonged travel). If a positive aPL lab profile is present and the patient has a history of blood clot or other signs or symptoms that meet criteria for the anti-phospholipid syndrome, the patient is diagnosed with Antiphospholipid Syndrome (APS) and anticoagulation (blood thinning) needs to be considered. The duration of the blood thinning will also need to be determined, depending on the individual case.
Ms. Richey ended her presentation by using case scenarios to demonstrate the many ways in which lab tests can be used in combination with other pertinent information to make a diagnosis of lupus. It is important to note that healthcare professionals will take into consideration the whole person when diagnosing and treating lupus. Diagnosis and treatment are based on physical examination, lab tests and other imaging studies. It is also important to note that each person’s lupus is unique, and that no two lupus patients are the same. Lab tests can help complete the puzzle of diagnosis, treatment and monitoring of the disease. Each lab test provides information about different components of lupus. Lab tests can also help doctors better understand the different characteristics of a patient’s lupus. Patients should communicate with their doctors and be sure to ask about their lab test results in order to gain a clearer picture of their disease.
Learn more information about the SLE Workshop at HSS, a free support and education group held monthly for people with lupus and their families and friends.
Summary by Gwyneth Kirkbride, Social Work Intern for Lupus Programs.
Edited by Nancy Novick.
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1,319,276,063,186,560,300 | @article{oai:nagoya.repo.nii.ac.jp:02001156, author = {Fukui, Takayuki and Kawaguchi, Koji and Tsubouchi, Hideki and Ueno, Harushi and Sugiyama, Tomoshi and Mori, Shunsuke and Goto, Masaki and Ozeki, Naoki and Hakiri, Shuhei and Nakamura, Shota and Chen-Yoshikawa, Toyofumi Fengshi}, issue = {2}, journal = {Nagoya Journal of Medical Science}, month = {May}, note = {Video-assisted thoracic surgery (VATS) has become widespread in the last 20 years, followed by robot-assisted thoracic surgery (RATS). Few studies compared the learning curve between RATS lobectomy and conventional VATS. This study included 79 RATS lobectomy cases performed in our hospital from November 2015 to October 2019. To estimate the required number for learning, the cumulative sum method, which is to plot a value obtained by sequentially accumulating a difference from a mean value was applied. As a result, the median total operative time and the median console time for all cases were 167 minutes and 138 minutes, respectively. Firstly, for our team, 28 cases were estimated to be required for learning curve for RATS lobectomy. For individual, each surgeon might be learned in only 5 to 6 cases. By contrast, the number of cases for learning VATS lobectomy which was underwent by a ‘single’ surgeon from 2009 was estimated to be 35 cases. The time to dock from start operation (median 14 minutes) reached plateau in 18 cases, but the time after rollout was median of 18 minutes and there was no significant change from the beginning. In conclusion, RATS lobectomy might be a technique that could be learned in a small number of cases compared to VATS. The results of this study might be helpful for certified surgeons who tried to get started with RATS and for establishing a learning program.}, pages = {227--237}, title = {Learning curve of robotic lobectomy for lung malignancies by certified thoracic surgeons}, volume = {83}, year = {2021} } | {
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-6,748,137,413,928,259,000 | Regulation of Epithelial-Mesenchymal Transition by Transmission of Mechanical Stress through Epithelial Tissues
Cancer Microenviron. 2012 Apr;5(1):29-38. doi: 10.1007/s12307-011-0076-5. Epub 2011 Jul 12.
Abstract
Epithelial-mesenchymal transition (EMT) is a phenotypic shift wherein epithelial cells lose or loosen attachments to their neighbors and assume a mesenchymal-like morphology. EMT drives a variety of developmental processes, but may also be adopted by tumor cells during neoplastic progression. EMT is regulated by both biochemical and physical signals from the microenvironment, including mechanical stress, which is increasingly recognized to play a major role in development and disease progression. Biological systems generate, transmit and concentrate mechanical stress into spatial patterns; these gradients in mechanical stress may serve to spatially pattern developmental and pathologic EMTs. Here we review how epithelial tissues generate and respond to mechanical stress gradients, and highlight the mechanisms by which mechanical stress regulates and patterns EMT. | {
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1,660,522,791,313,599,200 | What is EMDR?
EMDR was developed in the late 1980s by psychologist Francine Shapiro. She noticed that when she was walking and looking back and forth, her troublesome thoughts became less distressing. She studied this further and found that with a certain protocol along with eye movements, trauma survivors were able to resolve their traumas in a relatively short period of time. Since then, many studies have been done that show how EMDR is effective with not only trauma, but also anxiety disorders, phobias, performance enhancement, and grief.
Until recently, these conditions were difficult and time-consuming to treat. EMDR is considered a powerful breakthrough therapy because of its simplicity and the fact that it can bring quick and lasting relief for most types of emotional distress.
How Does EMDR Work?
When disturbing experiences happen, they are stored in the brain with all the sights, sounds, thoughts, and feelings that accompany them. When a person is very upset, the brain seems unable to process the experience as it would normally. When this happens, images, sounds, and emotions related to the memory become "frozen in time." Thoughts of a traumatic event feel as painful as if they'd just occurred.
EMDR "unfreezes" these memories, causing them to move to the part of the brain that processes memory. As this occurs, the memory loses its emotional charge and becomes less distressing.
EMDR appears to be similar to what occurs naturally during dreaming or REM (rapid eye movement) sleep. Therefore, EMDR can be thought of as a physiologically based therapy that helps a person see disturbing material in a new and less distressing way.
As a therapist trained in EMDR, I will first take a detailed history to assess whether you are a good candidate for EMDR treatment. I will then help you identify your goals for therapy and how you and I can attain those goals. We will work together to help you develop coping techniques. Once we have established a trusting relationship and I feel that you are ready, the EMDR session can begin.
What Happens After I Receive EMDR Therapy?
Once you are no longer suffering the effects of the trauma/incident, you will work on re-identifying yourself, identifying triggers, reviewing what you have learned, and work on strategies to prevent a return to your former state of mind. Total treatment could be as short as five sessions, could be incorporated into long term therapy, or anywhere in between. The length of treatment is dependent on your particular symptoms and goals of therapy.
Is EMDR Right For Me?
(If you answer yes to any of these questions below, EMDR may be a great option for you).
1. Are you losing productivity at home or work due to anxiety?
2. Are you still feeling depressed or lonely, despite the practice of positive thinking?
3. Are you angry all the time and don't know why?
4. Do you have phobias limiting your life, despite your best efforts to overcome them?
5. Are you frustrated that the "real you" is buried by hair-trigger, out of control emotions?
6. Have you been in therapy "forever", wrestling with the same old problems?
7. Have you tried cognitive therapies only to find your emotions still ruling your life?
8. Do you want to calm the chaos of self-defeating thoughts, feelings, and behaviors?
9. Do you want to get to the root cause of chronic symptoms?
10. Do you want to reduce stress and its negative impact on your physical health? | {
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9,089,774,211,153,787,000 | Stress Management - Give Me The Symptoms Of Stress
While it is impossible to predict how stress will affect an individual there are some common symptoms that identify that someone is probably experiencing sudden or chronic stress.
Sudden stress is a one-off occurrence, like your car breaking down in rush hour traffic or having to give a speech. Some of the symptoms of sudden stress are
• higher blood pressure - higher blood pressure cannot always be detected but bulging veins are an obvious sign of high blood pressure.
• clenching of the jaw or grinding of the teeth.
• clenching of fists and tightening of muscles in the arms.
• shallow breathing.
• headaches.
• profuse sweating.
Chronic stress is regular and unrelieved sudden stress. A typical example of chronic stress would be meeting monthly mortgage or credit card payments knowing that you don't have the money to afford them. Meeting tight or unrealistic deadlines at work would also be another example of chronic and unremitting stress. By it's very nature, chronic stress is potentially harmful to a persons health unless treated or managed. Some of the common symptoms of chronic stress are
• heart disease - an increased level of amino acid plasma homocysteine caused by stress is thought to increase the risk to heart disease.
• Strokes - blood is thought to become thicker due to the changes in the biochemistry in the blood which lead to an increase in blood clots and strokes.
• Catching colds, flu's and other ailments often and struggling to shift them - it is thought that stress affects the white blood cell count.
• Stomach problems such as diarrhoea, constipation, cramping or bloating.
• Sleeping disorders - the full gamut of sleeping disorders from insomnia to inability to stay in deep sleep.
• Reduced brain functions - memory, concentration and learning functions are all thought to suffer when under chronic stress.
• Sexual problems - for men, temporary impotence. For women a loss of sexual desire, intensified PMS or a shut down in menstruation.
Some or all of these symptoms could affect the individual. It is often hard to pinpoint stress as the direct cause of, say, catching a cold but by changing simple aspects of your lifestyle you may find common complaints and odd aches and pains diminish. Incorporating a regular exercise routine, for example, could improve your stress levels and health. The body is a remarkable system. If you can ensure that the components can run in harmony then the body will take care of itself. | {
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Kapha Vata Diet: Everything You Need To Know
Kapha Vata Diet: Everything You Need To Know
The Ayurveda Experience September 05, 2017
One of my clients, who has a Kapha Vata prakriti or dosha type, as it is popularly called, shared a very intelligent observation during her first consultation with me. She said that she was having dry snacks regularly made from roasted seeds as she had read that any food that is dry pacifies Kapha.
But one day she realized that she could be aggravating her secondary dosha Vata as Vata gets aggravated by dry foods. I was so amused by her keen observation that it became the focal point of our talk as to how to tackle two constituent dosha with many opposite properties.
Kapha and Vata have many opposite properties.
Don’t know your Prakriti (Ayurvedic body type)? Take this free quiz and find out!
Which Dosha Do You Prioritize?
It becomes challenging for one to design a diet plan which can be used to cater to two dosha having so many opposite properties. It is just like a mother trying to accommodate two siblings having different food choices! So, what does she do? She would just try to heed to one’s choice at one time, and to the other at another time.
Alternatively, she will prioritize according to the situation. Say if one is malnourished, or sick or one has come home from school, or is more aggressive, then she will give preference to this child.
This is exactly what you must do; you have to see if any of these two dosha needs your immediate attention, that is, if it may be aggravated or may be depleted. In both conditions, you should ignore the other for the time being and plan your diet for the day or the next meal according to the latter.
Not only the condition of the dosha in question, the time of the year (season) and time of day (whether it is Kapha time or Vata time) also matters in planning a meal.
All this is to be considered if a particular dosha needs immediate attention. But in other situations, you may have two separate dishes in a meal that cater to either dosha. Or you can mold the recipe of a dish in a way that it caters to both dosha. For example baked apple with cinnamon can be good for both dosha.
Don’t know your Prakriti (Ayurvedic body type)? Take this free quiz and find out!
How To Pacify Both Kapha And Vata
We know that there are six tastes in all. Out of these sweet, sour and salty pacify Vata but aggravate Kapha. On the other hand, the other three, pungent, bitter and astringent aggravate Vata but pacify Kapha. That is why having a Kapha Vata prakriti poses a great challenge to decide on the food to be selected. Generally, foods which are heating, irrespective of their taste will be pacifying for both the dosha as coldness is one property that is common to both.
How To Create Balanced Meals For Kapha And Vata
It is not necessary to always go for pacifying foods for the constituent dosha. If constituent dosha are not aggravated, you may eat those foods which have properties like a particular dosha, along with other antagonizing foods (with antagonizing tastes) that will not allow them to aggravate the dosha in question.
In the case of Kapha Vata or Vata Kapha prakriti, in normal circumstances, we can afford to use foods with all the six tastes without fear. This does not happen in other dosha types except for the tridoshic prakriti.
The only caution is to be a little biased towards the dominant dosha as it has more chance of getting aggravated than the other, just as our hypothetical mother may listen more to the more aggressive child.
As cold is one property that is common to both these constituent dosha, cold or cooling foods will have a dampening effect on Pitta, the dosha with the ‘hot’ property which controls the digestive and metabolic ‘fire’. So the Kapha Vata prakriti warrants that you always be wary of heavy to digest foods that may ‘douse’ the already weak ‘digestive fire’.
All said and done, we do have certain rules which if followed will see that both dosha generally remain in balance. This will be followed by a list of foods which can be frequently taken, less frequently taken and sparingly taken in normal circumstances.
Don’t know your Prakriti (Ayurvedic body type)? Take this free quiz and find out!
General Rules For The Kapha Vata Diet
Eat only freshly cooked and warm food.
Eat in small quantities, at regular intervals rather than eating big meals at one go.
Sit in a calm place and eat slowly, taking care to chew your food properly.Doing otherwise makes you easy prey to indigestion, heaviness and gas formation.
Drinks
Liquids should be taken an hour prior to or an hour after meals, so as not to dilute the digestive juices. A few sips may however be taken. Drink boiled and cooled water as it becomes ‘lighter’ and is easy to get ‘digested’. Have water in small quantities, a number of times during the day.
Cooked Foods
Choose lightly cooked food over raw food and use spices like garlic, ginger, fennel, cumin, turmeric, fenugreek seeds, and caraway seeds, asafoetida, and peppers in the diet. Do not eat food that is totally bland.
Fats
Fats like sesame, olive, coconut oil and mustard can be used in cooking. Ghee made from cow’s milk is also recommended in small amounts. Your food should always contain some fats to keep Vata in balance. The intake of fats needs to be restricted, to a maximum of six teaspoons per day as excessive fats will aggravate Kapha. In the case of kapha aggravation, mustard oil may be used.
Dairy
Dairy products need to be consumed in moderation. Using the low fat variety, which is easily digestible, ensures that the primary dosha Kapha, is in check and Vata is balanced.
The Six Tastes
Hot tastes with sour, salty and pungent flavors need to be included in the diet of a Kapha Vata person. Cold tastes with sweet, astringent (raw salads) and bitter (like bitter gourd) properties, should be used sparingly. However certain spices which are bitter and hot like turmeric and fenugreek, as said earlier can be balancing for both dosha.
Pitta Dosha
One thing worth mentioning here is that while planning for the constituent dosha we forget the tertiary dosha, which is Pitta in a Kapha Vata type. The tertiary dosha may also get aggravated if one is exposed to Pitta aggravating causes. So, in the case of Pitta aggravated conditions marked by symptoms like inflammation or fever or burning sensation, aphthous or mouth ulcers, hold off on the pungent and sour tastes. Salt (in moderation), bitter, astringent and sweet tastes can be used.
Sweet taste does not mean sugary stuff only. Most cereals and most vegetables also have the sweet taste in them. So while avoiding sugary foods, include the sweet taste with cereals and vegetables and some fruits that are not too sweet. Similarly, while incorporating the astringent taste through leafy greens, cook them so they don’t aggravate Vata and at the same time provide balance to Pitta (and Kapha).
Quantity Of Food
Keep breakfast and dinner light and lunch the heaviest meal of the day. Eat only when you are hungry or better still when the previous meal has been digested. You’ll know this by a marked return of the appetite, a clear burp and a feeling of lightness in the stomach.
Fruit
All fruits, except those that are too sweet, are good for you. Two servings of fruits should be eaten in between meals. Diced papaya with salt and cumin powder sprinkled on top is a good appetizer.
Vegetables
Almost all vegetables are good for you. Tubers and roots are to be restrained a bit as they can increase the blood sugar level and also Kapha in the body. Similarly, too fibrous vegetables can aggravate Vata in certain people and cause flatulence. So they should be consumed as per individual digestive capacity. Give preference however to cooked vegetables over raw salads and vegetable juices.
Meat + Eggs
Meats are heavy to digest. Consume them in small amounts and less frequently. Choose white meats over red meats and organ meats. Seafood is Kapha aggravating and should be minimized. But those who have had seafood since childhood may afford to consume it without any Kapha aggravation. This concept is called Satmaya or conditioning in Ayurveda.
Buttermilk + Yogurt
Drink fresh buttermilk before lunch. Add roasted cumin powder, salt and mint leaves to it. Yogurt can be taken similarly twice a week. Fruit yogurts are best avoided.
Ginger Pickle
Chew upon 2-3 juliennes of ginger pickle before lunch and dinner to kindle the digestive fire. To make ginger pickle cut ginger into juliennes. Add some rock salt, caraway seeds and lemon juice to it. Keep for one day in direct sunlight in a glass jar. If sunlight is not available just let it stay for a day before use. After one day it is ready to use. Shake periodically before eating to check for the growth of fungus. It can be stored for a week in the refrigerator, after which you should make a fresh batch.
Grains + Carbs
Wheat, rice, barley, oats, quinoa and amaranth can be used as grains and can be consumed as ready to cook cereals or breads. Barley helps one to lose weight. Pearled barley is a convenient option to include. You need to boil it and use it in a salad along with vegetables and lentils or meats.
High fiber sources of carbohydrates like sweet potatoes may also be used in place of grains. Carbohydrates though are considered to increase Kapha and are avoided by those watching their weight, but some amount of carbohydrates are needed in the meals to calm Vata and thereby the mind and stop sugar cravings.
Caffeine
Restrict the intake of coffee and caffeinated tea to one or two cups as excess of these can aggravate Vata. Avoid taking them at bedtime as they are likely to interfere with sleep by aggravating Vata.
Alcohol
Wines and other alcoholic drinks except beer can be taken in small quantities. Most of these have a tendency to aggravate Pitta which should be kept in mind. Excess alcohol aggravates Vata dosha and should therefore be avoided.
Don’t know your Prakriti (Ayurvedic body type)? Take this free quiz and find out!
Sample Menu For Kapha Vata Diet
A suggested sample menu may look like this.
First Things First
Start the day with a glass of warm water with a tablespoon of honey and a dash of lemon juice. If you have problems with either of these, you may just have a glass of warm water. This can be followed by 10 raisins and 10 almonds that have been soaked overnight in water. This helps to kick start the day.
Your Friend Tulsi Tea
This should be followed by a coriander and holy basil or dried Tulsi leaf tea. Rather it can be taken 2-3 times in a day as it checks the aggravation of Kapha and Vata and keeps possible aggravation of Pitta also in check.
For this you need to boil 1 teaspoon of coarsely ground coriander seeds and 1/2 tsp of dried Tulsi leaves in one and a half cups of water. Reduce to half. Strain and drink hot. Add 1/4 tsp of organic sugar if desired.
Breakfast
Breakfast can be a cereal with milk or eggs. Keep it light and save meat for lunch when the digestive fire is at it’s peak.
Lunch
Lunch can be grains, proteins in the form of white meat, lentils or beans and cooked vegetables. Lentils and beans should be spiced using spices mentioned above.
Dinner
Dinner can be same as lunch but lighter and can include soups.
Cheat Sheet: The Kapha Vata Diet
Even after going through the general guidelines regarding the Kapha Vata diet, it still might be unclear what to eat and what not to eat. So here is a quick list of foods which you can eat according to your prakriti.
Don’t know your Prakriti (Ayurvedic body type)? Take this free quiz and find out!
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Frequently Asked Questions
What is Infertility?
Infertility is a disease of the reproductive system that impairs one of the body's most basic functions: the conception of children. Conception is a complicated process that depends upon many factors: on the production of healthy sperm by the man and healthy eggs by the woman, unblocked fallopian tubes that allow the sperm to reach the egg, the sperm's ability to fertilize the egg when they meet, the ability of the fertilized egg (embryo) to become implanted in the woman's uterus, and sufficient embryo quality. Finally, for the pregnancy to continue to full term, the embryo must be healthy and the woman's hormonal environment adequate for its development. When just one of these factors is impaired, infertility can result.
What Causes Infertility?
In rough terms, about one-third of infertility cases can be attributed to male factors, and about one-third to female factors. For the remaining one-third of infertile couples, infertility is caused by a combination of problems in both partners or, in about 20 percent of cases, is unexplained.
The most common male infertility factors include azospermia (no sperm cells are produced) and oligospermia (few sperm cells are produced). Sometimes, sperm cells are malformed or they die before they can reach the egg. In rare cases, a genetic disease such as cystic fibrosis or a chromosomal abnormality causes infertility in men.
The most common female infertility factor is an ovulation disorder. Other causes of female infertility include blocked fallopian tubes, which can occur when a woman has had pelvic inflammatory disease or endometriosis (a sometimes painful condition causing adhesions and cysts). Congenital anomalies (birth defects) involving the structure of the uterus and uterine fibroids can be associated with repeated miscarriages.
How is Infertility Diagnosed?
Couples are generally advised to seek medical help if they are unable to achieve pregnancy after a year of unprotected intercourse. The doctor will ask many questions and conduct a physical examination of both partners to determine their general state of health and to evaluate physical disorders that may be causing infertility. Usually both partners are interviewed about their sexual habits in order to determine whether intercourse is taking place properly for conception. If no cause can be determined at this point, more specific tests may be recommended. For women, these include an analysis of ovulation, x-ray of the fallopian tubes and uterus, and perhaps a laparoscopy. For men, the initial test is a semen analysis.
How is Infertility Treated?
Eighty five to 90 percent of infertility cases are addressed through conventional therapies, such as drug treatment or surgical repair of reproductive organs. A recent government survey reported that only five percent of infertility cases was treated with in vitro fertilization. However, there’s no guarantee that the woman will become pregnant and most importantly, carry the child to term. While infertility treatments have helped many couples have children, success rates differ depending on the type of treatment.
Do Insurance Plans Cover Infertility Treatment?
The degree of services covered depends on where you live and the type of insurance plan you have. Fourteen states currently have laws that require insurers to either cover or offer to cover some form of infertility diagnosis and treatment. Those states are Arkansas, California, Connecticut, Hawaii, Illinois, Maryland, Massachusetts, Montana, New Jersey, New York, Ohio, Rhode Island, Texas, and West Virginia. While state laws vary greatly in their scope of coverage, the average couple going through infertility treatments pays at least half of their expenses out of pocket. The costs for these procedures and medications vary widely. On the low end, fertility drugs such as hormone therapy (used to induce ovulation or sperm development) run from $200 - $300 a month. In vitro fertilization, on the other hand (in which the egg is fertilized outside the woman) costs $8,000 to $13,000 per treatment. For more information about state laws, refer to the State Infertility Insurance Laws page of the ASRM website.
ASRM believes the desire to have children and be parents is one of the most fundamental aspects of being human. People should not be denied insurance coverage for medically appropriate treatment to fulfill this goal.
What impact does infertility have on psychological well-being?
Infertility often creates one of the most distressing life crises a couple has faced. The long-term inability to conceive a child can evoke significant feelings of loss. Coping with the multitude of medical decisions and the uncertainties that infertility brings can create great emotional upheaval for most couples. Many couples experience anxiety, depression, and feelings of being out of control or isolated.
HomeASRM
What Is InfertilityWhy Should I CareMale Risk FactorsFemale Risk FactorsUsing PSAsMore InformationTreatment
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1,137,723,075,317,953,500 | Urinary system
Introduction
The principal function of the urinary system is the maintenance of water, electrolyte and acid–base homeostasis , which requires that any input into the system is balanced by an equivalent output. The kidney provides the mechanism by which excess water and electrolytes are eliminated from the body, while the ureters , bladder and urethra form the storage and outflow tract. A second major function of the urinary system is the excretion of many toxic metabolic waste products, particularly the nitrogenous molecules urea and creatinine, compounds that can conveniently be excreted dissolved in water. The end product of these processes is urine . Since all body fluids are maintained in dynamic equilibrium with one another by the circulatory system, any adjustment in the composition of the blood results in similar changes in the other fluid compartments of the body. Thus regulation of the osmotic concentration of blood plasma by the kidneys ( osmoregulation ) ensures the osmotic regulation of all other body fluids. The third major function of the kidney is the maintenance of normal blood pressure.
The functional and structural unit of the kidney, the nephron , consists of a renal corpuscle (including the glomerulus ) plus a long, folded renal tubule . The human kidney contains approximately 1 million nephrons that perform the functions of osmoregulation and excretion by the following processes:
• Filtration in the glomerulus of most small molecules from blood plasma to form an ultrafiltrate of plasma.
• Selective reabsorption in the tubule of most of the water and some other molecules from the ultrafiltrate, leaving behind excess and waste materials to be excreted.
• Secretion in the tubule of some excretory products directly from blood into the urine.
• Maintenance of the acid–base balance by selective secretion by the tubule of H + ions into the urine.
The kidney also has hormonal and metabolic functions:
• Renin , synthesised in the kidney, is a component of the renin–angiotensin–aldosterone mechanism that controls blood pressure.
• Erythropoietin , synthesised in the kidney, stimulates the production of erythrocytes in the bone marrow and thus regulates the oxygen-carrying capacity of the blood.
• Vitamin D , which regulates calcium balance, is converted to an active form in the kidney.
C cortex Cp capsule H hilum M medulla P papilla U ureter
Renal failure
Renal failure occurs for a variety of reasons and may be acute or chronic. Irreversible severe renal failure is inevitably fatal unless some form of renal replacement therapy is undertaken. Current options for renal replacement therapy include renal dialysis and renal transplantation. Dialysis may take the form of haemodialysis or, less commonly, peritoneal dialysis. Renal transplantation requires a donor, which can often involve a long wait until a suitable HLA-compatible donor is found. Those individuals lucky enough to have a compatible and willing family member are able to receive a donated kidney from them. This highlights the inbuilt redundancy of the kidneys whereby an individual can survive and be perfectly healthy with only one kidney. Stem cell research may in future provide a third option for renal replacement, the possibility of growing one’s own perfectly matched new kidney (or heart or pancreas) from one’s own stem cells.
AA arcuate artery Ai interlobar artery AV arcuate vein C calyx Cx cortex G glomerulus IA interlobular artery MR medullary ray P renal pelvis RC renal corpuscle RP renal papilla T tubule U ureter V interlobular vein
Fig. 16.7, Development of the renal corpuscle
The Renal Cortex
The renal cortex is easily identified even at low magnification by the presence of renal corpuscles, which are absent in the renal medulla. However, the bulk of the cortex is occupied by the proximal and distal convoluted tubules. The arcuate arteries and veins help to demarcate the cortex from the medulla.
A afferent arteriole BC Bowman’s capsule BS Bowman’s space C glomerular capillary E endothelial cell GBM glomerular basement membrane I interstitium M mesangium N mesangial cell nucleus P podocyte PCT proximal convoluted tubule S parietal epithelial cell
AA afferent arteriole BS Bowman’s space EA efferent arteriole G glomerulus IA interlobular artery N podocyte nucleus P 1 podocyte primary process P 2 podocyte secondary process RT renal tubule
BC Bowman’s capsule BM glomular basement membrane BS Bowman’s space C capillary loop E endothelial cell F fenestration FS filtration slit IPS interpodocyte space M mesangial cell MM mesangial matrix P podocyte P 1 podocyte primary process P 2 podocyte secondary foot process SPS subpodocyte space
Diabetic renal disease
Diabetic nephropathy is the most common cause of renal failure in affluent countries . The incidence of type 2 diabetes is increasing, an increase that is felt to be largely due to changing lifestyles, with increasing obesity and decreasing exercise, although there is little doubt that genetic factors are also important. Usually one of the earliest signs of diabetic nephropathy is proteinuria, which may eventually progress to the nephrotic syndrome and progressive chronic renal failure. The microscopic features in these cases include thickening of the mesangial basement membrane and an increase in mesangial matrix, often called diabetic glomerulosclerosis. In normal glomeruli, the balance between deposition of new and removal of old mesangial matrix is very tightly controlled. Recent research is beginning to tease out the mechanisms underlying these clinical features, including chemical mediators such as transforming growth factor β (TGF-β) that induce increased deposition of mesangial matrix in response to high glucose concentrations. This mesangial matrix has a different composition to normal matrix, including increased amounts of type I and type III collagen which are not easily removed from the glomerulus. However, other factors, including direct podocyte injury and changes in the slit pore membrane, also contribute to the characteristic proteinuria that precedes frank renal failure.
E-Fig. 16.2, Diabetic glomerulosclerosis
Diabetics also tend to suffer from vascular disease, hypertension and increased infections in the kidney, and all of these tend to contribute to the development of end-stage renal failure .
E-Fig. 16.3, End-stage kidney (MP)
BB brush border BM basement membrane C peritubular capillaries CP mesangial cell cytoplasmic process DCT distal convoluted tubule E endothelial cell J cell junction L glomerular capillary lumen PCT proximal convoluted tubule MC mesangial cell MM mesangial matrix P 1 podocyte primary process P 2 podocyte secondary foot process SPS subpodocyte space
Renal tubular damage
Damage to the renal tubules is a fairly common cause of acute renal failure. Acute tubular necrosis usually occurs due to a sudden drop in the blood supply to the kidney, for example due to severe dehydration or massive blood loss. The cells of the renal tubules are highly metabolically active and so they are very susceptible to damage when the blood supply is compromised. As noted above, this is particularly so for the cells of the proximal convoluted tubule as they have a very high oxygen requirement.
The tubular epithelial cells will often recover if the underlying cause is treated and the patient is supported effectively during the acute phase of their illness. Often, during the recovery phase, the patient will produce very large volumes of dilute urine ( polyuria ), highlighting the key role of the tubular epithelial cells in reabsorbing water from the glomerular ultrafiltrate . Careful management of fluid balance is critical during recovery.
E-Fig. 16.4, Acute tubular necrosis (MP)
BM basement membrane BM E basement membrane of endothelium Cap capillary E endothelium J junctional complex L lysosome M mitochondrion Mv microvilli P cell process S supporting tissue V pinocytotic vesicle
AA afferent arteriole DCT distal convoluted tubule J juxtaglomerular cell L lacis cell MD macula densa
Hypertension and the kidney
Hypertension is a common condition in middle-aged and elderly persons. Most cases are considered to be idiopathic (which simply means that the mechanism has not yet been elucidated). However, there are certainly genetic factors as well as lifestyle components underlying many, if not most, cases. A much smaller proportion of hypertensive patients, especially younger patients, have hypertension associated with renal disease. Many different types of renal disease may lead to hypertension; a classic example is the acute hypertension seen in patients with post-infectious glomerulonephritis. Many other chronic renal conditions, including diabetic nephropathy, IgA nephropathy and a range of other common conditions lead to secondary hypertension.
Conversely, hypertension can also lead to renal failure. The classic example of this is patients with accelerated hypertension who have acute renal failure with classic vascular changes in their renal biopsy at presentation. However, chronic untreated lower-level hypertension also typically leads to chronic renal damage in a pattern sometimes called ‘benign nephrosclerosis’, a misleading name as it can lead to chronic renal failure which may require renal replacement therapy.
E-Fig. 16.5, Hypertensive nephrosclerosis
E-Fig. 16.1, Acute diffuse proliferative (‘endocapillary’) glomerulonephritis (HP)
The Renal Medulla
The renal medulla consists of closely packed tubules of two types: the loop of Henle and the collecting tubules and ducts, as well as the vasa recta. The loop of Henle is a continuation of the proximal convoluted tubule. It dips down into the medulla, where it loops back on itself and returns to the cortex to its own renal corpuscle, becoming the first part of the distal convoluted tubule.
A thick ascending limb of loop of Henle BM tubular basement membrane CD collecting duct CT collecting tubule IC intercalated cell S supporting tissue T thin limb of loop of Henle V vasa recta
BL basal lamina BM basement membrane C collagen fibrils CT collecting tubule D lipid droplet H loop of Henle L leukocyte N nucleus of interstitial medullary cell P cytoplasmic process of interstitial medullary cell S supporting tissue V vasa recta
The Lower Urinary Tract
The lower urinary tract includes the renal pelvis and calyces, the ureters, the urinary bladder and the urethra. The lower urinary tract is specialised for the storage and excretion of urine at a convenient time; no further modification of the urine is possible after it leaves the renal medulla.
A adventitia C circular muscle layer DB duct of Bellini E transitional epithelium IL inner longitudinal muscle layer of bladder L longitudinal muscle layer of ureter LP lamina propria OL outer longitudinal muscle layer of bladder PCS pelvicalyceal space SM smooth muscle U ureter Um umbrella cell V blood vessel
Review
Fig. 16.1, The urinary system
Fig. 16.2, Kidney
Fig. 16.3, Kidney
Fig. 16.5, Kidney, monkey Jones methenamine silver
Fig. 16.8, Renal corpuscle
Fig. 16.10, Glomerulus
Fig. 16.11, Blood supply of the glomerulus
Fig. 16.12, The glomerular filter
Fig. 16.13, Glomerulus
Fig. 16.14, Glomerulus (illustration (a) opposite)
Fig. 16.15, The mesangium, rat
Fig. 16.16, Proximal and distal convoluted tubules
Fig. 16.17, Proximal and distal convoluted tubules (illustrations (a) and (b) opposite)
Fig. 16.18, Juxtaglomerular apparatus (illustrations (a) and (b) opposite)
Fig. 16.19, Loop of Henle
Fig. 16.20, Collecting tubules and ducts
Fig. 16.21, Renal medulla, rat (illustration (b) opposite)
Fig. 16.22, Renal papilla, monkey
Fig. 16.23, Ureter
Fig. 16.24, Bladder
Fig. 16.25, Transitional epithelium
Fig. 16.26, Summary of major activities of different parts of the renal tubule
Fig. 16.4, Basic organisation of the nephron, collecting system and renal vasculature
Table 16.1
Review of the urinary system
Kidney
Part of nephron Important structural components Special features Functional significance Figures
Glomerulus Endothelium, glomerular basement membrane and podocytes with foot processes Glomerular filtration barrier (GFB) Allow water, ions and small molecules to pass into subpodocyte space while retaining large protein molecules 16.8 , 16.10–16.15
Juxta-glomerular apparatus Macula densa of distal convoluted tubule (DCT) Specialised cells acting as osmoreceptors of DCT, abutting afferent arteriole (AA) Sensitive to Na + concentration in DCT, indicating reduced BP 16.18
Juxtaglomerular cells of AA Modified smooth muscle cells in wall of AA, mechanoreceptors, contain renin Release renin in response to reduced BP
Extraglomerular mesangial cells (lacis cells) Flattened network of mesangial cells abutting macula densa Role in tubuloglomerular feedback (changes in Na + concentration act to control glomerular flow)
Proximal convoluted tubule (PCT) Simple cuboidal epithelium Microvilli (brush border) Facilitated diffusion of glucose and amino acids 16.16 , 16.17
Extensive basolateral interdigitations Na + pump
Plentiful mitochondria Energy for active transport
Pars recta of proximal tubule Simple cuboidal epithelium Microvilli (brush border) Secretion of organic acids 16.19
No basolateral interdigitations
Thin descending/ascending limbs Simple squamous epithelium No basolateral interdigitations or microvilli No active transport 16.19
Mitochondria scanty Low energy requirement
Thick ascending limb Simple cuboidal epithelium Microvilli absent No facilitated diffusion 16.19
Extensive basolateral interdigitations Active transport of Na +
Distal convoluted tubule (DCT) Simple cuboidal epithelium Active transport of Na + Extensive basolateral interdigitations 16.16 , 16.17
Mitochondria plentiful Energy for active transport
Collecting tubule Simple cuboidal epithelium Principal cells Na + reabsorption, ADH-dependent H 2 O reabsorption, K + secretion 16.19–16.21
Intercalated cells Acid–base balance, K + reabsorption
Collecting tubule cells
DCT cells Active transport of Na +
Cortical collecting duct Simple columnar epithelium Principal cells Na + reabsorption, ADH-dependent H 2 O reabsorption, K + secretion 16.20
Medullary collecting duct Simple columnar epithelium Mainly principal cells ADH-dependent water reabsorption 16.22
Lower urinary tract
Component Muscle structure Lining epithelium Function Figures
Pelvicalyceal system Smooth muscle, no distinct layer structure Transitional epithelium (urothelium) Conveys urine from the tips of the renal papillae into the ureter 16.2 , 16.3 , 16.5 , 16.22 , 16.25
Ureter 3 muscle layers: inner spiral (longitudinal) and outer spiral (circular) layers and outermost longitudinal layer in lower third Transitional epithelium (urothelium) Carries urine to the bladder 16.1 , 16.2 , 16.23 , 16.25
Bladder 3 muscle layers: inner and outermost longitudinal and middle circular Transitional epithelium (urothelium) Stores urine 16.1 , 16.24 , 16.25
Fig. 16.6, Renal cortex
Fig. 16.9, Glomerulonephritis
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-178,311,639,904,317,800 | Vetenskaplig publicering vid Medicinska fakulteten
3705
Items where Subject is "Human medicine, health, and safety
of ASI psychiatric severity cut-off scores to identify cooccurring psychiatric disorder. använder drogen och desto fler fastnar i missbruk (Ekbom et al 2006:319)”. Nordin, Karin, Brorsson, Anna Lena, Ekbom, Kerstin. cardiovascular risk and all-cause mortality in patients with stable coronary heart disease during 10 years The groups were followed up to 25 years after deployment for all-cause mortality, 1.1.1 Veteranhälsa 1: Soldathjärta, granatchock, Post-Vietnam Syndrome och Ludvigsson JF, Otterblad-Olausson P, Pettersson BU, Ekbom A. The Swedish IGF II : structure, function and role in disease. Ekbom Ågren, Caroline, 2020. Horticultural therapy for homeless people : what are the causes and conditions av CG Östenson — Eriksson AK, Ekbom A, Granath F, et al. Psychological distress and lowering therapy reduces cardiovascular disease events in veterans rance: does it matter for prevention and treatment of type 2 diabetes?
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Attention deficit hyperactivity disorder. BRIS. Barnens rätt i samhället. av UJ Berggren — terms, as evidence of attachment disorder, or parentification. svenska barns förhållanden (Lindstein 1995; Arnell & Ekbom 1996; Forinder &.
Uneasyness - floorboards tempo, scrubbing lower limbs, fidgeting during sex. Restless Legs Syndrome (The Ekbom Syndrome) Restless legs syndrome (RLS), described by K. A. Ekbom in 1944, 20 is frequent in CKD, particularly in women. It may result from a decrease in dopaminergic modulation of intracortical excitability, with reduced supraspinal inhibition and increased spinal cord excitability.
Schizofreni - SBU
Herein we report three cases observed in Ouagadougou. Willis–Ekboms sjukdom (WED) eller restless legs syndrome (RLS), är en kronisk neurologisk sjukdom som drabbar 5–10 % av den västerländska befolkningen. [ 1 ] Innehåll Se hela listan på mayoclinic.org Ekbom Syndrome is synonymous with delusory parasitosis, a belief that one's body is infested by invisible bugs. Persons suffering from this syndrome often claim to feel dermal sensations and to visualize the bugs, although no one else can see them.
PSA-screening > Minska morbiditet vid TURP Abstracts
Dopamine. There's evidence to suggest restless legs syndrome is related to a problem with part Ekbom syndrome: a sense of indescribable uneasiness, twitching, or restlessness that occurs in the legs after going to bed, frequently leading to insomnia, which may be relieved temporarily by walking about; thought to be caused by inadequate circulation or as a side effect of some SSRIs and other psychotropic medications. See also: akathisia It is called Willis-Ekbom Disease which is more popularly known as restless leg syndrome. It has been called a neurological disorder and it has been noted to affect more women than men. Most of the time restless legs syndrome goes under diagnosed or passed off for other diseases. 2018-08-15 · Restless leg syndrome, or RLS, is a neurological disorder.
There's evidence to suggest restless legs syndrome is related to a problem with part Ekbom syndrome: a sense of indescribable uneasiness, twitching, or restlessness that occurs in the legs after going to bed, frequently leading to insomnia, which may be relieved temporarily by walking about; thought to be caused by inadequate circulation or as a side effect of some SSRIs and other psychotropic medications. See also: akathisia It is called Willis-Ekbom Disease which is more popularly known as restless leg syndrome. It has been called a neurological disorder and it has been noted to affect more women than men. Most of the time restless legs syndrome goes under diagnosed or passed off for other diseases. 2018-08-15 · Restless leg syndrome, or RLS, is a neurological disorder. RLS is also known as Willis-Ekbom disease, or RLS/WED. RLS causes unpleasant sensations in the legs, along with a powerful urge to move them.
Endimensionell analys formelsamling
Ekbom syndrome causes
[Article in German] programmed stimulation in Brugada syndrome.
Pour traiter le syndrome d’Ekbom, un soutien psychothérapeutique est bien sûr nécessaire, mais le plus difficile est de convaincre le patient de l’absence de parasites et d’obtenir son accord pour consulter un psychiatre. 2019-12-31 · Restless legs syndrome (RLS), also known as Willis-Ekbom disease, is a chronic condition that causes strong, unpleasant feelings in the legs, resulting in an overwhelming need to move them.
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Horticultural therapy for homeless people : what are the causes and conditions Relationship of extent of noninvasive disease to the frequency of occult invasion, multicentricity, lymph node metastases, and short-time treatment failures. Kosmelj, K; Primic-Zakelj, M; Ravnihar, B; Stare, J; Ekbom, A; Erlandsson, G; Beeson, WL; Fraser, G; A critique of the concept of seasonal affective disorder. av CG Östenson — Eriksson AK, Ekbom A, Granath F, et al. Psychological distress and lowering therapy reduces cardiovascular disease events in veterans rance: does it matter for prevention and treatment of type 2 diabetes?
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Willis-Ekbom Disease Restless Leg Syndrome, A Simple
and adherence with antidepressant treatment. Pa- tient Educ ens J. Patient adherence to treatment: three dec- ades of in patients with irritable bowel syndrome. BMJ. 2008 E, Ekbom A, Lambe M. Sociodemographic pre-. | {
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-1,498,306,127,255,009,000 | Health
Are Sleep Cycles The Same For Everyone?
Photo of beautiful pregnant woman sleeping in bed
Sleep cycles are the same for everyone. For some reason, people seem to think that they can set their sleep cycle differently than human developmental biology intended, but this is not true.
The brain produces melatonin in response to the light/dark cycle of nature; it’s PRIMARILY an evening hormone (activating sleep-promoting neurochemicals like serotonin), while cortisol is HELL bent on waking us up (it’s an incredibly strong ACTIVATING Hormone) so it can get back home and mate with whoever did NOT lay down on him all day long. A lot of people believe this balance of these hormones explains why they wake up feeling nauseated or too tired after eating solids before bed, but it.
Are Sleep Cycles The Same For Everyone? – Related Questions
Do sleep cycles actually matter?
Sleep cycles matter because following a well-researched routine helps promote a healthy sleep pattern.
Supplementing your sleep routine with bright lights for several hours before bedtime will help the body know that it is time to fall asleep. Also, sleeping in a cool environment can slow down the sleeper’s metabolism and contribute to better quality sleep as well as increased REM (rapid eye movement) periods during the night. If you are trying to stay up late at night, make sure to avoid caffeine or anything caffeinated at least four hours prior to going to bed—this includes coffee, tea, sodas and even chocolate! Although there is much more depth on how exactly these things work, this should give you a few tricks for.
Is the 90-minute rule true?
The ninety-minute rule states that an individual’s metabolism remains at its peak for 90 minutes after eating. However, the body will stay in this hormonal state for 120 minutes if it is eating high quality foods with low glycemic index.
From https://en.wikipedia.org/wiki/Glycemic_index#Comparison_to_low-GI%20diets
“After consuming foods with a higher glycemic index, blood sugar levels spike to cause faster utilization of glucose reserves by tissue cells and other organs requiring fuel.” The initial rise in blood sugar spikes insulin production to quickly lower blood sugar levels back to normal. High doses of glucose start this process right away, while refined carbohydrates are broken down more slowly so.
See also Does Yoga Do Positive Thinking?
What should your sleep cycles be?
Don’t feel like you’re getting enough sleep? There are several apps that use sound conditioning to lull you into the non-rapid eye movement (NREM) phase of sleep. It’s not easy to tell, but most people dream during this period. This is where children with sensory processing disorder often function best. A good way to set your alarm so that it wakes you up before your NREM cycle has time to progress too deeply is the 3-2-1 method: Set yourself for three hours of sleep, two hours of awake time between six and eight am, followed by one hour of very light snooze for an 8am waking call.
It’s also important to turn off electronics or dim.
Is 4 sleep cycles enough?
I’ll assume you are asking about the number of sleep cycles within a day? The answer to this question is unknown. There is much research on how much sleep we need, but there’s no consensus because each person has different needs. Some people need 8 hours, while others can function on 4. I recommend everyone experiment to see what works for them!.
Is 7 sleep cycles too much?
I would recommend that you read a university-level textbook on the topic of sleep for a more comprehensive answer to this question, as the subject matter is too complicated for an AskMe..
Is it better to get 5 or 6 sleep cycles?
The human body needs a night of uninterrupted sleep to properly restore itself. But there is no need to spend the whole long night in bed if you don’t fall asleep quickly. After about 20 minutes or more of lying awake, you should move away from the bedroom and do something relaxing until exhaustion takes over and shuts your brain down for a few hours, then return to bed when it’s time for your next scheduled sleep cycle..
Why is the snooze button 9 minutes?
I’m not sure there’s one answer to this question, but
I can tell you that the “ideal” number of snoozes should be proportional to the expected length and quality of your sleep and not an arbitrary number. Doing a 9-minute recap over and over again is like doing the same work without any momentum – it drains you mentally as well as physically.
The other point to make is that those first few minutes after waking up are really important for those parts of your brain related to memory formation (the hippocampus). If people hit ‘snooze’ again after those first few minutes, they risk losing this opportunity.
And there are also some theories about how these early memories might provide some kind of foothold.
Why do I wake up at 3 30?
This question is poorly formulated algorithmically, please restate in langauge specific to your field..
See also Is Sea Moss Good For Weight Loss?
How long is s sleep cycle?
The average human sleep cycle is between 90 minutes and two hours.
Though most adults won’t spend many consecutive hours in one stage of sleep, the length of time spent varies from person to person according to age. Research has shown that newborns sleep around 18-20 hours a day, while toddlers might spend about 13-14 hours per 24 hour period sleeping. Older children and adolescents spend about 10-13 hours per 24 hour period sleeping with adults falling into the same category (9-10 daily). Though researchers still don’t fully understand why the length of our sleep cycles vary despite it being an average, they do see correlations in activity levels and body processes including hormone levels and brain function during waking periods which could link potential.
Is REM deep sleep?
REM sleep constitutes much less than 5% of total sleeping hours. However, during these few hours the brain is more active than when in any other phase of sleep. So it can be seen as a “deep” type of sleep, but it’s usually not referred to as such because the length and characterizes vary drastically from deep to light and back again.
A common misconception is that REM deep sleep provides restorative relief for the muscles and things like that because we don’t spend much time in this state, but instead we spend an equivalent amount of time each night awake (i.e., unconscious). And while it may take longer to become well-rested after hard labor throughout the day (or maybe even a full day.
How many hours of REM sleep is ideal?
In an adult, one should aim for six to eight hours of sleep a night.
There are three main stages of sleep: non-REM, REM and the period of transition from the first period to the second. Non-REM sleep is relatively slow waves without eye movements or muscle activity normally last for a few minutes each time they occur, while REM sleep is dreaming and believed to be essential for proper brain development in children. It occurs at intervals through out both night and day periods between non- REM phases. The proportion which these two types make up may vary from person to person but it can generally be guessed that about 10% percent will spend their time in this stage during sleep. In adults, one should aim for six to.
What is a healthy sleep schedule?
A good sleep schedule depends on the needs of each individual and can’t be generalized. Some people find success with around eight hours, but others need anywhere from four to ten.
The optimal amount of hours of sleep usually varies slightly depending on factors such as age and lifestyle choices, and it’s unlikely you’ll be able to get best results without some self-experimentation. One approach is to try different amounts for a few weeks at a time–every week add an hour or two until you notice a change in mood or functioning that indicates when your body is no longer benefiting from sleep deprivation. For example, if starting with
four or five supports positive functioning then six will likely do the trick for a while before backsl.
See also What Can Help A Headache?
Is 7 hours of sleep enough for a 17 year old?
Scientists don’t know for sure how much sleep is enough, that is why more research needs to be conducted. The National Sleep Foundation recommends 8-9 hours of sleep for adults between the ages 16-64 years old. According to their studies, most Americans get 6.8 hours of sleep on average, which means there’s no consistent pattern.
A proper amount of sleep protects against heart disease and diabetes risk factors by helping you control your blood sugar levels and reducing inflammation in your body, but it can also contribute to anxiety, depression, obesity and more consequences so the best way is to experiment yourself over time with different amounts — some people need less than others because physiology varies from person-to-person. You could ask a doctor.
Is it OK to get only 3 hours of sleep?
Yes. However, while some people function well on 3-5 hours of sleep, some need 8-10 hours, and some cannot get by without 10 or more hours of sleep.
That said, it is ideal to feel like you are getting enough sleep every night. Periods of sleep deprivation can result in problems with concentration and learning (including short term memory) as well as increased risk for accidents because the body needs time to recover from lack of restorative restorative processes that take place during deep states of unconsciousness. So while it’s not harmful to occasionally go without sleep for a few nights in order to catch up on work deadlines or spend time with family/friends, its not recommended for extended periods especially if you’re.
Is 8 hours of sleep enough for a teenager?
The research is mixed as to whether 8 hours of sleep is enough for a teenager. Some studies have shown no significant difference in grades, mood, or athletic performance between those who slept for just 7 hours and those who slept for 9. On the other hand, a ninth grader who normally wakes up refreshed after 10 hours of sleep had a difficult time functioning on just 5 during a study from Stanford University School of Medicine. And according to the National Sleep Foundation, teens aged 13-18 require at least 8-10 hours of sleep per day for optimal health and best performance.
The bottom line? As adults age, our body’s circadian needs change — but this process starts later in life compared to when it begins when we.
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How Various Factors Affect the Healing Process Post an Injury
By : , Delhi, India 2.2.2018 Mail Now
Neb Sarai, New Delhi
So much has been spoken and written about health; still, the topic of health grabs many eyeballs. Health is an important aspect of the overall wellbeing of an individual. Being healthy is an understatement and it takes an individual an injury or illness to realize the importance of health. In general, injuries impose a big threat to our health.
While one can always be careful and steer clear of the potential caused of injuries, some things are beyond our control and getting injured is one of such things. Kids are highly energetic and impatient at times. Thanks to their inquisitive nature; they are open to new experiences. They always look forward to trying out new things. This makes them highly prone to injuries.
The fool-proof way to safeguard your health is buying a health insurance plan. The thumb rule to follow at the time of purchasing a health insurance plan is a thorough comparison. Therefore, you must compare health insurance plans before you zero down on one. Your health insurance policy might not cover accidental injuries, so if you want enhanced coverage against injuries, go for personal accident insurance plans.
Let’s get back to the topic of this article now.
After getting injured, we struggle with the speed of healing process. We feel that we have taken being healthy for granted. We get impatient, as we get sick and tired of resting. We get eager to get back to our daily routines. The healing process is individualistic and that’s why we can’t compare healing process. While some people heal quickly, others take time.
The Science of Healing
The beauty of science is fascinating, isn’t it? Regardless of the reason behind the injury, the human body repairs the damages caused. The moment a wound starts bleeding, the blood vessels in the injured area start to contract to slow down the bleeding. The blood platelets on-site form a blood clot at the injured area after being exposed to air. Next, White blood cells (WBC) cumulate at the injured spot to destroy and digest the dead cells by releasing lysosomes - special enzymes present in the cells. This process removes dead-cell debris, clearing out new space for the generation of new cells.
Almost at the same time, the new cell formation begins. Most of these new cells spring up from the newer cell layers of a specific tissue. Gradually, the older cell layers are pushed to acquire the space made by the injury. This scientifically remarkable process ends by default upon the completion of the healing process.
This healing process isn’t limited to injuries. It looks after the normal day-to-day wears and tears. Regularly, damaged/destroyed/dead cells are replaced from the mouth, skin, blood, and intestines.
How Does Your Lifestyle Impact Healing?
Your lifestyle is a crucial element responsible for the speed of your healing process. Starting from your daily routine to the types of food items you eat impacts the healing process. If you aren’t careful, you could unknowingly damage yourself merely by participating in mundane chores. In a rare case, your injuries can become permanent injuries.
How Does Your Nutrition Impact Healing?
Your food choices regulate your recovery speed. The perfectly balanced inclusion of proteins and carbohydrates can speed up the healing process and help you become healthy and stay fit.
Particular food items are highly beneficial in case of injuries as well as of diseases. For instance, green leafy veggies and salmon have therapeutic effects on broken bones. Vitamin D and calcium trigger the recovery of the damaged bones. It’s unfortunate that many people do not understand the importance of having a proper diet.
How Does Daily Physical Activities Impact Healing?
Not sitting is still a problem faced by many individuals who are healing. Even if you feel capable enough to fulfil certain tasks, don’t give in to that feeling, as it is too soon to push yourself to work.
For example, getting back to play golf just 2 months after a back surgery isn’t a good idea. Health experts recommend a recovery period of 6 months. If you’re feeling good, it doesn’t necessarily mean that you’re healed. Slip into your daily routines slowly and steadily after your doctor recommends.
How Does Getting Back to Work Impact Healing?
There are people who can’t afford to take an adequate off time from work. It can impose additional threat(s) and can cause pain. Depending on the type of your job, some injuries are easily aggravated merely by working.
For instance, it isn’t a good idea for a delivery boy to get back to work as soon as possible post a spinal injury.
While it is recommended to let time do its magic if you have no choice but to work, ensure that you follow the safety precautions and minimize the risk of any damage(s) to you.
How Does Fun Time and Play Time Impacts Healing?
A few individuals lead an active lifestyle and they indulge in fun and play activities on a regular basis. It is yet another area in which individuals might further injure themselves. When there isn’t any immediate pain, it is easier to momentarily forget the injury. Without giving it adequate healing time, you are exposed to the risk of hurting yourself. In some extreme scenarios, individuals end up completely missing out the leisure activities they love, as they have no idea about the ill-effects of participation in the healing process.
Wrapping it up!
The choices we make today reflect on the consequences we face later in our lives. As far as health is concerned, there is no room for taking it granted. Health should be taken very seriously.
Our habits form our attitude, adopting healthy habits today helps to develop a positive outlook towards health later on. There are no shortcuts to enhance the healing process. It takes medical expertise, patience, and good nutrition to fortify the healing process.
Regardless of your recovery from sports or accident injuries, your lifestyle will impact your recovery process. Before you get back to your daily routine, get thumbs up from a fitness expert.
TAGS: Healing Process, Healing Post an Injury,
DISCLAIMER: The views and opinions expressed in this article are those of the authors /contributors and do not necessarily reflect the official policy/opinion of webindia123.com / Suni systems Pvt. Ltd. Webindia123.com / Suni systems Pvt. Ltd and its staff, affiliates accept no liability whatsoever for any loss or damage of any kind arising out of the use of all or any part of the material published in the site. In case of any queries,or complaints about the authenticity of the articles posted by contributors, please contact us via email. | {
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Orthognathic surgery vs Facial contouring surgery - double jaw surgery, two jaw surgery, vline surgery, mini vline surgery, jaw
Author
Date
2016-07-19 09:32
Views
2734
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Orthognathic surgery vs Facial contouring surgery for a smaller face, which would be the best one for me?
Ji Young Kim, aged 23, has made a huge decision. She grew up being bullied and called “Big rock face” for her large face since she was little. She visited a plastic surgery hospital to change her protruding cheekbone and asymmetrical face into a smaller and slimmer one. However, after her consultation she couldn’t decide which one to choose, orthognathic surgery or facial contouring surgery.
Similar to her case, a lot of people choose orthognathic surgery or facial contouring surgery, expecting a grand and noticeable change of their facial size. It is for sure that those surgeries are the most well-known ones for reducing the size of your face, either by excision of facial bone or replacing the bone. These two surgeries, however, are two different ones. Therefore, if you are considering to get a facial bone surgery, it is important that you make a precise analysis of the shape of your face and choose the correct one that fits best.
Dr. Sang Hoon Park, the head doctor of ID Hospital, said “depending on the purpose and result, there is a huge difference between orthognathic surgery and facial contouring surgery even though they both are facial bone surgery.”
First, orthognathic surgery is done when the jaws are misplaced or their functions are not carried out well due to protruded jaw or facial asymmetry. It is correcting the placement of jaws by cutting the upper and lower jaws. Once you get an orthognathic surgery, you can improve your mastication function including chewing food and speaking, and since the location and shape of the jaws are changed to normal, you can see a dramatic facial change.
Facial contouring surgery, on the other hand, is for changing the shape of your facial bone to make your facial shape prettier, and it includes square jaw surgery, cheekbone reduction surgery, and chin surgery. In case of strong and rough facial appearance due to too much growth of facial bone, the surgery reduces the size of the bone and changes the facial shape into a smoother one, so it is focused more on making aesthetical improvement.
Whether you should get orthognathic surgery or facial contouring surgery is decided based on mastication of your teeth, shape of the jaw bone, and the condition of the central line of your face. If you have malocclusion, jaw bones are not in the right place, or the central line of your face is tilted, you should get orthognathic surgery that corrects the placement of upper and lower jaw as well as their shape. However, if the central line of your face is straight, and you’re simply worried about the shape and appearance of your lower jaw bone, getting orthognathic surgery can solve the problem of your facial shape.
Dr. Sang Hoon Park, a specialist in plastic surgery said “it is recommended that you have an in-depth consultation with a doctor specialized in plastic surgery for deciding on orthognathic surgery or facial contouring surgery in order to get maximized effect of facial bone surgery. If you choose a hospital-level medical institution where you can have precise prediction of facial change after the surgery through close diagnostic system and joint treatment of plastic surgery center, dental center, and orthodontic center, you will be able to have safe and high satisfactory result of surgery. | {
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Natural Remedies for Premenstrual Syndrome (PMS) Cramps
In spite of how many people scoff about it, hormones play a mighty role in our lives and bodies. Many women struggle with pain and symptoms caused by hormones, particularly through PMDD, and PMS cramps. PMS, or premenstrual syndrome, has a huge mess of symptoms. These typically kick up just before your cycle begins, and may continue well into your cycle. For some women, these symptoms continue well past their cycle.
The most common symptoms include:
• Dizziness
• Depression
• Cravings
• Nausea
• Breast tenderness
• Cramps
• Headache
• Bloating
• Fatigue
• Irritability
• Vomiting
• Anxiety
These start before menses, and subside as the period begins, though abdominal cramps happen around then.
Factors of PMS
Your symptoms depend on a ton of different factors, including your health, genetics, the medications you’re taking, however, hormone levels are the main controlling factor. Balancing your hormones is the ideal way to reduce these symptoms. Over the course of a month, your hormone levels are changing and interacting with chemicals.
When all the hormones and chemicals are balanced, they work correctly and typically there are significantly fewer symptoms. Certain changes, such as to your diet or supplements, can greatly affect the hormone levels, allowing you to balance them.
Nutritional Change
Start making eliminations and reductions in your diet. Humans shouldn’t be eating the polyunsaturated Omega-6 fatty acids in large amounts. Polyunsaturated fats are easily oxidized, causing cell damage and inflammation. The human body is 97% saturated and monounsaturated fats and 3% polyunsaturated fats. 1.5% of that 3% is Omega-6 fats, and 1.5% is Omega-3 fats. Giving your body the ratios it requires allows your body to rebuild cells, produce hormones and create as it needs to.
Avoid the chemicals that are present in the pesticides, processed foods, house cleaners, plastic, mattresses and other items. These chemicals can mimic hormones, preventing the body from producing hormones. Avoid non-stick and Teflon pans, as well as heating food in plastic. Aim to use organic foods, and avoid chemical cleaners.
Eating the right fats from organic meats, tallow, coconut oil, ghee and other items will improve hormone production in the body. ¼ a cup of coconut oil per day can really give you that boost if you need it. Don’t eat many inflammatory foods, such as grains and vegetable oils. Inflammation can worsen hormonal problems.
Supplements
Supplements are a great way to take care of your body when you can’t give it the extra vitamins and minerals it needs.
Maca, for example, has been used for some time to improve hormone balance. Women experienced less PMS, better skin and fertility rates. Men, on the other hand, slept better and produced more sperm. You can get it in powder form or capsule.
Magnesium supports the body in many ways, including hormones. It improves your sleep and can be applied topically for those who can’t drink or eat it. Red raspberry leaf is an herb that reduces cramps, PMS and other symptoms. It is packed with nutrients like calcium, and can greatly boost your fertility.
Don’t forget to exercise and get sufficient rest and sleep!
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-8,048,897,615,544,065,000 | Our goal is to define the molecular mechanisms that control interactions between Cryptococcus neoformans and the mammalian immune system in an effort to ultimately prevent and treat fungal disease. Fungi are emerging pathogens, and morbidity and mortality are most apparent among the immunocompromised, especially in individuals with HIV/AIDS. The meningitis-causing fungus C. neoformans is particularly aggressive among people with AIDS, estimated to cause over a million cases of disease and ~600,000 deaths world-wide annually. The bulk of this burden is in Sub-Saharan Africa where the number of deaths from cryptococcal meningitis now appears to surpass the number of deaths from tuberculosis. In this region 13-44% of HIV/AIDS-related deaths are due to cryptococcosis, and mean survival times are on the order of a few weeks after onset. Worldwide, treatment with antifungal agents results in ~80% survival, and individual prognoses are strongly influenced by the availability of antifungal drugs and the immune status of the host. Little is known about the processes by which cryptococcal infection occurs, and we recognize a substantial gap in understanding the intersection between fungal pathogens and the host immune response. Studies over the last two decades have begun to define the relationships between C. neoformans yeast and the host immune system, but none has evaluated spores, likely infectious particles in nature. We have recently purified spores to homogeneity in numbers sufficient for comprehensive biochemical, molecular, and virulence studies. Using this novel reagent we have discovered that spores can cause disease in a mouse model and that murine alveolar macrophages, the first line of defense against respiratory fungal pathogens, interact fundamentally differently with spores than with yeast. Our findings place us in a unique position to ask questions about the C. neoformans-mammalian cell interface that have not been possible previously. We will take advantage of this major advance to investigate the fundamental properties of spores and their interactions with alveolar macrophages. Our hypothesis is that alveolar macrophages interact with spores via specific mechanisms that are distinct from those that mediate interactions with yeast. We will test our hypothesis by addressing the following three Aims. 1) Identify the receptors and ligands that mediate interactions between C. neoformans spores and murine alveolar macrophages. 2) Elucidate mechanisms that govern the ability of spores to survive inside macrophages. 3) Investigate the properties of spore-mediated disease using a murine model of infection. Our studies will provide insights fundamental to understanding how C. neoformans is recognized by the innate immune response and how cryptococcal disease is either suppressed in healthy individuals or disseminated in the immunocompromised. Ultimately, our findings promise to inform more general processes by which fungi cause disease, facilitating the discovery of novel prevention and/or treatment strategies.
Public Health Relevance
Fungi, including Cryptococcus, are emerging pathogens that cause life-threatening diseases in humans, particularly people who are immunocompromised. Investigating interactions between Cryptococcus spores and the human immune system promises to provide the information necessary to understand how fungal spores cause disease. This project is relevant to public health and the mission of the NIH because it has the potential to lead to new strategies for preventing and/or treating severe fungal infections among the most vulnerable patients, including those with HIV/AIDS.
Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Project (R01)
Project #
5R01AI089370-05
Application #
8646854
Study Section
AIDS-associated Opportunistic Infections and Cancer Study Section (AOIC)
Program Officer
Duncan, Rory A
Project Start
2010-05-01
Project End
2015-04-30
Budget Start
2014-05-01
Budget End
2015-04-30
Support Year
5
Fiscal Year
2014
Total Cost
Indirect Cost
Name
University of Wisconsin Madison
Department
Biochemistry
Type
Schools of Medicine
DUNS #
City
Madison
State
WI
Country
United States
Zip Code
53715
Mead, Matthew E; Hull, Christina M (2016) Transcriptional control of sexual development in Cryptococcus neoformans. J Microbiol 54:339-46
Barkal, Layla J; Walsh, Naomi M; Botts, Michael R et al. (2016) Leveraging a high resolution microfluidic assay reveals insights into pathogenic fungal spore germination. Integr Biol (Camb) 8:603-15
Mead, Matthew E; Stanton, Brynne C; Kruzel, Emilia K et al. (2015) Targets of the Sex Inducer homeodomain proteins are required for fungal development and virulence in Cryptococcus neoformans. Mol Microbiol 95:804-18
Huang, Mingwei; Hebert, Alexander S; Coon, Joshua J et al. (2015) Protein Composition of Infectious Spores Reveals Novel Sexual Development and Germination Factors in Cryptococcus. PLoS Genet 11:e1005490
Kruzel, Emilia K; Hull, Christina M (2010) Establishing an unusual cell type: how to make a dikaryon. Curr Opin Microbiol 13:706-11
Botts, Michael R; Hull, Christina M (2010) Dueling in the lung: how Cryptococcus spores race the host for survival. Curr Opin Microbiol 13:437-42 | {
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3,059,862,394,327,738,400 | Items filtered by date: March 2021
Monday, 29 March 2021 00:00
Neuropathy
Neuropathy is a condition in which the nerves in the body become damaged from a number of different illnesses. Nerves from any part of the body, including the foot, can be damaged. There are several forms of neuropathy including peripheral neuropathy, cranial neuropathy, focal neuropathy, and autonomic neuropathy. Furthermore there is also mononeuropathy and polyneuropathy. Mononeuropathies affect one nerve while polyneuropathies affect several nerves. Causes of neuropathy include physical injury, diseases, cancers, infections, diabetes, toxic substances, and disorders. It is peripheral neuropathy that affects the feet.
The symptoms of neuropathy vary greatly and can be minor such as numbness, sensation loss, prickling, and tingling sensations. More painful symptoms include throbbing, burning, freezing, and sharp pains. The most severe symptoms can be muscle weakness/paralysis, problems with coordination, and falling.
Podiatrists rely upon a full medical history and a neurological examination to diagnose peripheral neuropathy in the foot. More tests that may be used include nerve function tests to test nerve damage, blood tests to detect diabetes or vitamin deficiencies. Imaging tests, such as CT or MRI scans, might be used to look for abnormalities, and finally nerve or skin biopsies could also be taken.
Treatment depends upon the causes of neuropathy. If the neuropathy was caused by vitamin deficiency, diabetes, infection, or toxic substances, addressing those conditions can lead to the nerve healing and sensation returning to the area. However if the nerve has died, then sensation may never come back to the area. Pain medication may be prescribed for less serious symptoms. Topical creams may also be tried to bring back sensation. Electrical nerve stimulation may be used for a period of time to stimulate nerves. Physical therapy can strengthen muscle and improve movement. Finally surgery might be necessary if pressure on the nerve is causing the neuropathy.
If you are experiencing sensation loss, numbness, tingling, or burning sensations in your feet, you may be experiencing neuropathy. Be sure to talk to a podiatrist to be diagnosed right away.
Monday, 29 March 2021 00:00
What Is Charcot Foot?
When the nerves are damaged in the extremities such as the feet, it is known as peripheral neuropathy. This ultimately leads to Charcot foot when the bones in the foot are weakened. These weakened bones can lead to fractures that worsen and cause the joints in the foot to collapse. Charcot foot can cause the foot to become deformed, and it can be disabling and even potentially lead to amputation. Common signs of Charcot foot are a warmness to the touch, redness, swelling, and pain. Because of its association to neuropathy and neuropathy’s association with diabetes, diabetic patients should monitor their feet for this condition. Patients who believe that they may have this condition should consult with a podiatrist as soon as possible. A podiatrist will be able to assess the foot and suggest treatment options.
Neuropathy
Neuropathy can be a potentially serious condition, especially if it is left undiagnosed. If you have any concerns that you may be experiencing nerve loss in your feet, consult with one of our podiatrists from The Foot Institute. Our doctors will assess your condition and provide you with quality foot and ankle treatment for neuropathy.
What Is Neuropathy?
Neuropathy is a condition that leads to damage to the nerves in the body. Peripheral neuropathy, or neuropathy that affects your peripheral nervous system, usually occurs in the feet. Neuropathy can be triggered by a number of different causes. Such causes include diabetes, infections, cancers, disorders, and toxic substances.
Symptoms of Neuropathy Include:
• Numbness
• Sensation loss
• Prickling and tingling sensations
• Throbbing, freezing, burning pains
• Muscle weakness
Those with diabetes are at serious risk due to being unable to feel an ulcer on their feet. Diabetics usually also suffer from poor blood circulation. This can lead to the wound not healing, infections occurring, and the limb may have to be amputated.
Treatment
To treat neuropathy in the foot, podiatrists will first diagnose the cause of the neuropathy. Figuring out the underlying cause of the neuropathy will allow the podiatrist to prescribe the best treatment, whether it be caused by diabetes, toxic substance exposure, infection, etc. If the nerve has not died, then it’s possible that sensation may be able to return to the foot.
Pain medication may be issued for pain. Electrical nerve stimulation can be used to stimulate nerves. If the neuropathy is caused from pressure on the nerves, then surgery may be necessary.
If you have any questions, please feel free to contact one of our 3 locations located in El Paso, TX . We offer the newest diagnostic and treatment technologies for all your foot care needs.
Read more about Neuropathy
Monday, 22 March 2021 00:00
Diabetic Foot Conditions
Diabetes is the condition in which the body does not properly process food for use as energy. People with Type 1 diabetes cannot produce insulin, which is required for glucose to feed your body’s cells. It is typically caused by the immune system mistaking healthy cells for foreign invaders and destroying the insulin-producing cells in the pancreas. On the other hand, people with Type 2 diabetes cannot respond to insulin properly, and eventually cannot produce enough. The Centers for Disease Control and Prevention reports that over 30 million people in the United States have diabetes, with 1 in 4 having no idea they have it. Surprisingly, diabetes is the seventh leading cause of death in the US. The symptoms of diabetes include frequent urination, fatigue, hunger, and even blurry vision.
Diabetes can also affect the feet as well. Over time, diabetes can cause nerve damage to your feet, which could then lead to symptoms such as tingling, pain and numbness in the feet. Neuropathy can be very dangerous to a person with diabetes, since it prevents them from feeling injuries such as cuts or blisters in the feet, and if not detected early enough, may lead to infection. Neuropathy can also lead changes in the shape of your feet and toes. The best way for people with diabetes to prevent or delay neuropathy is keeping their blood glucose levels in their target range. This consists of eating right, having the correct amount of exercise, and taking medications.
Diabetes can also create calluses and foot ulcers as well. Calluses build up faster and occur more frequently with those affected by diabetes. If there are too many calluses, therapeutic shoes and inserts may be required. It is important to have calluses trimmed by a health professional, as doing it yourself may lead to infections. If these calluses continue to develop and thicken, they can lead to foot ulcers. Foot ulcers are open sores, that appear on the ball of the foot or on the bottom of the big toe. These ulcers can lead to future infections if not treated and may possibly result in losing a limb. It is important to report any ulcers to your podiatrist right away. Your doctor may take x-rays to examine the foot and clean out any dead and infected tissue.
Lastly, diabetes can also lead to poor circulation and peripheral arterial disease (PAD). The poor circulation in the feet and leg area is a result of diabetes narrowing and hardening, eventually slowing down the blood flow in that area. The best way to prevent this is to keep away from smoking and follow your doctor’s advice for maintaining blood pressure and cholesterol. PAD is similar to this complication. PAD is when blood vessels narrow or are blocked by fatty deposits. PAD also increases your risk of heart attacks and strokes and is a common condition to those affected by diabetes. The combination of both PAD and neuropathy may lead to infections and can result in amputation of certain limbs. PAD can be prevented with wearing the proper foot wear and regularly taking care of your feet.
If you want to take care of your feet, you should wash and dry them carefully and perform daily inspections to check for cuts, blisters, or swelling. Any physical activity you partake in should be approved by your health care provider. You should also be sure to wear special shoes if advised to do so by your doctor.
Monday, 22 March 2021 00:00
Diabetes and Its Impact on the Feet
Diabetes can lead to various health complications in many parts of the body, and the lower limbs are especially susceptible to damage. Diabetic peripheral neuropathy, in which the nerves that innervate the lower limbs become damaged, can lead to a loss of sensation in the feet and ankles. Peripheral artery disease, in which the blood vessels that supply the lower limbs are compromised and blood flow to the area is reduced, can lead to poor wound healing on the feet. Together, these two conditions greatly increase the risk of developing diabetic foot ulcers (DFUs). DFUs can appear without being detected due to a lack of sensation and may heal slowly and poorly due to poor circulation. DFUs can also become infected, and lead to serious complications, including amputation. To learn how to care for diabetic feet, it is suggested that you consult with a podiatrist.
Diabetic foot care is important in preventing foot ailments such as ulcers. If you are suffering from diabetes or have any other concerns about your feet, contact one of our podiatrists from The Foot Institute. Our doctors can provide the care you need to keep you pain-free and on your feet.
Diabetic Foot Care
Diabetes affects millions of people every year. The condition can damage blood vessels in many parts of the body, especially the feet. Because of this, taking care of your feet is essential if you have diabetes, and having a podiatrist help monitor your foot health is highly recommended.
The Importance of Caring for Your Feet
• Routinely inspect your feet for bruises or sores.
• Wear socks that fit your feet comfortably.
• Wear comfortable shoes that provide adequate support.
Patients with diabetes should have their doctor monitor their blood levels, as blood sugar levels play such a huge role in diabetic care. Monitoring these levels on a regular basis is highly advised.
It is always best to inform your healthcare professional of any concerns you may have regarding your feet, especially for diabetic patients. Early treatment and routine foot examinations are keys to maintaining proper health, especially because severe complications can arise if proper treatment is not applied.
If you have any questions please feel free to contact one of our 3 locations located in El Paso, TX . We offer the newest diagnostic and treatment technologies for all your foot and ankle needs.
Read more about Diabetic Foot Conditions
Monday, 15 March 2021 00:00
All About Plantar Warts
Plantar warts are warts that are only found on the feet, hence the term “plantar”, which means “relating to the foot.” They are caused by the human papillomavirus, or HPV, and occur when this virus gets into open wounds on the feet. The warts themselves are hard bumps on the foot. They are easily recognizable, mostly found on the heels or ball of the foot. Plantar warts are non-malignant, but they can cause some pain, discomfort, and are often unsightly. Removing them is a common step toward treating them.
Plantar warts can cause some pain while standing, sometimes felt as tenderness on the sole of your foot. Unless the wart has grown into the foot behind a callus, you will be able to see the fleshy wart. A podiatrist should only be consulted if there is an excessive amount of pain. Plantar warts are not cancerous or dangerous, but they can affect your walking and continually reappear. Anyone who suffers from diabetes or a compromised immune system disease should seek out care immediately.
Podiatrists are easily able to diagnose plantar warts. They usually scrape off a tiny bit of the rough skin to make tiny blood clots visible and examine the inside of warts. However, a biopsy can be done if the doctor is not able to diagnose them from simply looking at them. Although plantar warts usually do not require an excessive amount of treatment, there are ways to go about removing them. A common method is to freeze them off using liquid nitrogen, removing them using an electrical tool, or burning them off via laser treatment. For a less invasive treatment option, topical creams can be used through a doctor’s prescription. This treatment method takes more time, however. Keep the wart covered for protection in between daily treatments.
The best way to avoid developing plantar warts is to avoid walking barefoot in public places. Avoid this especially if you have open sores or cuts on your feet. It is also important to avoid direct contact with warts in general, as they are highly contagious.
Monday, 15 March 2021 00:00
Plantar Fasciitis
The plantar fascia is a connective tissue in the heel that stretches across the bottom length of your foot. Plantar fasciitis occurs when the connective tissue becomes inflamed, causing heel pain and discomfort during physical activity. Although the condition is completely treatable, traditional methods can take up to a year to start becoming effective.
Plantar fasciitis is caused by a number of everyday activities, so understanding the condition is important for managing and treating it. One of the most common causes of plantar fasciitis is excessive running, especially with improper fitting or non-supportive shoes. Too much exercise can lead to the plantar fascia being overworked and overstretched, which can cause tears in the tissue. Along with improper fitting shoes, pronation, the rolling of the feet inward, is a common cause of plantar fasciitis. If not treated properly, the plantar fascia becomes overstretched and starts to tear, causing inflammation.
Despite the common causes of plantar fasciitis, there are many different treatment options. For less severe cases, conservative home remedies include taking anti-inflammatory drugs to alleviate pain, applying ice packs to the bottom of your foot and heel, slowly stretching and exercising your feet to re-strengthen the tissue, and using orthotic devices are all ways to help manage your plantar fasciitis.
For more severe cases, shockwave therapy has become a common solution for plantar fasciitis. Shockwave therapy can effectively break up the tissue on the bottom of your foot which facilitates healing and regeneration. This fights the chronic pain caused by plantar fasciitis. Even if this doesn’t work, surgery is always a final option. Surgery on the tissue itself can be done to permanently correct the issue and stop the inflammation and pain in your heels.
No matter what the case may be, consulting your podiatrist is the first and best step to recovery. Even the slightest amount of heel pain could be the first stage of plantar fasciitis. Untreated symptoms can lead to the tearing and overstretching of tissue. Because the tearing of tissue can be compounded if it remains ignored, it can evolve into a severe case. The solution is early detection and early treatment. Talk to your podiatrist about the possibilities of plantar fasciitis if you’re experiencing heel pain.
Monday, 08 March 2021 00:00
Everything You Need to Know About Gout
Gout, typically found in diabetic patients, is an unusually painful form of arthritis caused by elevated levels of uric acid in the bloodstream. The condition typically strikes the big joint on the big toe. It has also been known to strike the knees, elbows, fingers, ankles and wrists—generally anywhere that has a functioning, moving joint.
The high level of uric acid in a person’s bloodstream creates the condition known as hyperuricema—the main cause of gout. Genetic predisposition occurs in nine out of ten sufferers. The children of parents who suffer gout will have a two in ten chance of developing the condition as well.
This form of arthritis, being particularly painful, is the leftover uric acid crystallizing in the blood stream. The crystallized uric acid then travels to the space between joints where they rub, causing friction when the patient moves. Symptoms include: pain, redness, swelling, and inflammation. Additional side effects may include fatigue and fever, although reports of these effects are very rare. Some patients have reported that pain may intensify when the temperature drops, such as when you sleep.
Most cases of gout are easily diagnosed by a podiatrist’s assessment of the various symptoms. Defined tests can also be performed. A blood test to detect elevated levels of uric acid is often used as well as an x-ray to diagnose visible and chronic gout.
Treatment for gout simply means eliminating symptoms. Non-steroid anti-inflammatory drugs or NSAIDs (Colchicine and other corticosteroid drugs, etc.) will quell the redness, the swelling, and the inflammation. However, managing your diet, lifestyle changes, and using preventative drugs are all helpful toward fully combating the most severe cases.
Those that lead an inactive lifestyle are at a higher risk for gout. Any amount of exercise decreases the probability of repeat encounters with the condition. Reducing your consumption of red meat, sea food, and fructose-sweetened drinks also reduces the likelihood of chronic gout as well.
Ingesting Vitamin C, coffee, and particular dairy products can help with maintaining a healthy lifestyle. There are new drugs out on the market that inhibit the body’s production of uric acid-producing enzymes. However, reducing or eliminating your overall levels of uric acid is the best remedy to ensuring you lead a gout-free life.
Being a parent involves caring for your child in every way you can. You make sure they are eating the right food, being nice to others, and staying out of any trouble. However, it is also important that you are watchful of their health, more specifically their foot health. Maintaining good foot health in childhood is important in preventing later conditions in life from happening. As children continue to develop, their feet require different techniques of care. Here are some various ways in which you can help your child’s feet stay healthy.
A baby needs a lot of care and attention overall, but the importance of their feet should never be forgotten. Before a baby turns one, their feet change and develop greatly. It is important that during this time, a mother avoids putting tight socks on their child. She should also encourage movement of their feet so the baby can begin to feel more comfortable using them.
As a baby enters the toddler years of his or her life, they are begin to walk around. When your baby begins to take those first steps, it is crucial that they are wearing protective shoes on their feet. As a mother that is observant of your child’s feet, you may notice changes in them. This is completely normal as the feet are becoming susceptible to the activity of walking. It is normal for a toddler to be a bit unsteady or to “walk funny” at first.
When your child grows out of their toddler years, it is important that you begin to show him or her how to care for their feet on their own. Practice with your child proper hygiene in order to prevent foot fungus or infection. Since children are constantly on the move, it is crucial to be cautious of any accidents or injuries that might occur. If an injury occurs, it is advised that you take your child to be examined by a doctor immediately. Since your child is still growing, particular injuries can shift the way in which a bone or other important part of the foot is developing.
Babies and kids are always changing and growing. Your job as a parent is to make sure they stay healthy and making sure they are properly maintained. This involves proper foot care and making sure the feet stay healthy. Following this guide, your child can live a long and happy life.
Stress fractures are small breaks in the bone that are caused by repetitive stress. They typically occur due to overuse, forcing the bones of the foot or ankle to continually absorb the full impact of each step taken. Stress fractures can also be caused by abnormal foot structure, osteoporosis, bone deformities, or wearing improper footwear during exercise.
Stress fractures are common for individuals whose daily activities cause high levels of impact on their feet and ankles. Those who run, play tennis or basketball, or practice gymnastics tend to experience these fractures more frequently. Anyone is susceptible to this problem, though. Individuals who are normally sedentary and suddenly begin an intense, high impact workout may sustain stress fractures. This is because their muscles are not yet strong enough to handle and cushion the intensity of their activity. Osteoporosis may also cause someone to get stress fractures, because the disease weakens an afflicted person's bones and makes it easier for them to break down.
Pain from stress fractures typically occurs in the general area of the fracture. Pain can also manifest as “pinpoint pain” or pain that is felt when the site of the injury is touched, and can be accompanied by swelling. It may occur during or after activity, and it may disappear while resting and return when standing or moving. Engaging in any kind of activity, high impact or otherwise, will aggravate the pain. If the intensity of the activity increases before the stress fracture has properly healed, it can cause a full fracture.
Treatment can vary depending on the individual and the degree of injury. The primary way to treat a stress fracture is to rest the hurt foot. Some fractures will heal quickly with only a little bit of rest, while others may require a long rest period and the use of crutches, immobilization, or physical therapy. Under certain circumstances, surgery may be required to install support pins around the fracture to assist in healing.
If you are undergoing a new exercise regimen in running or some other kind of high impact activity, set incremental goals on a weekly basis so you can build up muscle strength. Make sure to wear supportive shoes to better protect you feet.
If you begin to experience any symptoms of stress fractures, you should stop exercising and rest. If the symptoms persist, consult with your podiatrist. Remembering these tips can help you prevent stress fractures to your foot and ankle, and allow you to continue living normally.
Monday, 01 March 2021 00:00
Treatment for Stress Fractures
A stress fracture may gradually develop from frequently participating in running and jumping activities, and can be uncomfortable. Effective treatment for this type of injury generally begins with ceasing the activity that caused the pain, and wearing a boot or cast that will help to provide the support that is necessary as the healing process occurs. Prevention of further stress fractures may be accomplished by warming up properly before running, and gradually increasing the intensity of your physical activity. It is suggested that a podiatrist be consulted who can offer you preventative and treatment options.
Activities where too much pressure is put on the feet can cause stress fractures. To learn more, contact one of our podiatrists from The Foot Institute. Our doctors can provide the care you need to keep your pain free and on your feet.
Dealing with Stress Fractures of the Foot and Ankle
Stress fractures occur in the foot and ankle when muscles in these areas weaken from too much or too little use. The feet and ankles then lose support when walking or running from the impact of the ground. Since there is no protection, the bones receive the full impact of each step. Stress on the feet can cause cracks to form in the bones, thus creating stress fractures.
What Are Stress Fractures?
Stress fractures occur frequently in individuals whose daily activities cause great impact on the feet and ankles. Stress factors are most common among:
• Runners
• People affected with Osteoporosis
• Tennis or basketball players
• Gymnasts
• High impact workouts
Symptoms
Pain from the fractures occur in the area of the fractures and can be constant or intermittent. It will often cause sharp or dull pain with swelling and tenderness. Engaging in any kind of activity which involves high impact will aggravate pain.
If you have any questions please feel free to contact one of our 3 locations located in El Paso, TX . We offer the newest diagnostic and treatment technologies for all your foot and ankle needs.
Read more about Dealing with Stress Fractures of the Foot and Ankle
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6,365,067,147,464,545,000 | Analysis of human immunodeficiency virus type 1 gene expression in latently infected resting CD4+ T lymphocytes in vivo
Monika Hermankova, Janet D. Siliciano, Yan Zhou, Daphne Monie, Karen Chadwick, Joseph B. Margolick, Thomas C. Quinn, Robert F. Siliciano
Research output: Contribution to journalArticlepeer-review
130 Scopus citations
Abstract
In individuals with human immunodeficiency virus type 1 (HIV-1) infection, a small reservoir of resting memory CD4+ T lymphocytes carrying latent, integrated provirus persists even in patients treated for prolonged periods with highly active antiretroviral therapy (HAART). This reservoir greatly complicates the prospects for eradicating HIV-1 infection with antiretroviral drugs. Therefore, it is critical to understand how HIV-1 latency is established and maintained. In particular, it is important to determine whether transcriptional or posttranscriptional mechanisms are involved. Therefore, HIV-1 DNA and mRNAs were measured in highly purified populations of resting CD4+ T lymphocytes from the peripheral blood of patients on long-term HAART. In such patients, the predominant form of persistent HIV-1 is latent integrated provirus. Typically, 100 HIV-1 DNA molecules were detected per 106 resting CD4+ T cells. Only very low levels of unspliced HIV-1 RNA (∼50 copies/106 resting CD4+ T cells) were detected using a reverse transcriptase PCR assay capable of detecting a single molecule of RNA standard. Levels of multiply spliced HIV-1 RNA were below the limit of detection (<50 copies/106 cells). Only 1% of the HIV-1 DNA-positive lymphocytes in this compartment could be induced to up-regulate HIV-1 mRNAs after cellular activation, indicating that most of the proviral DNA in resting CD4+ T cells either carries intrinsic defects precluding transcription or is subjected to transcriptional control mechanisms that preclude high-level production of multiply spliced mRNAs. Nevertheless, by inducing T-cell activation, it is possible to isolate replication-competent virus from resting CD4+ T lymphocytes of all infected individuals, including those on prolonged HAART. Thus, a subset of integrated proviruses (1%) remains competent for high-level mRNA production after cellular activation, and a subset of these can produce infectious virus. Measurements of steady-state levels of multiply spliced and unspliced HIV-1 RNA prior to cellular activation suggest that infected resting CD4+ T lymphocytes in blood synthesize very little viral RNA and are unlikely to be capable of producing virus. In these cells, latency appears to reflect regulation at the level of mRNA production rather than at the level of splicing or nuclear export of viral mRNAs.
Original languageEnglish (US)
Pages (from-to)7383-7392
Number of pages10
JournalJournal of virology
Volume77
Issue number13
DOIs
StatePublished - Jul 2003
ASJC Scopus subject areas
• Microbiology
• Immunology
• Insect Science
• Virology
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-1,466,633,345,995,343,600 | fbpx
Infertility treatment
ICSI
What is ICSI?
ICSI (intra-cytoplasmic sperm injection) is a variant of conventional IVF.
In ICSI, all the stages of conventional IVF are followed, the only difference being that the fertilization of the egg by the sperm occurs in a more invasive way.
This technique is not suitable for all couples and should only be used in specific cases.
When is ICSI preferred over conventional IVF?
ICSI can provide a solution when the sperm is unable to fertilize the egg by itself (as happens in conventional IVF)
Such cases are the following:
• Weak sperm
• Large number of anti-sperm antibodies in the sperm
• History of poor fertilization after conventional IVF
• Sperm acquisition after testicular or epididymal biopsy
How is ICSI actually done?
ICSI takes place on the same day as the egg collection.
The embryologist uses specialized equipment and a powerful microscope to grasp a sperm and inject it directly into the egg.
Unlike conventional IVF, where nature chooses the best sperm to fertilize the egg, in ICSI it is the embryologist who selects what appears to be the best sperm amongst dozens of others.
As a result, nowadays almost every man can father his own child, even if his sperm is very weak.
What else do I need to know about ICSI?
• ICSI helps a lot, but it cannot solve all male fertility problems.
ICSI does inject a sperm inside the egg, but it cannot guarantee that the egg will get fertilized. The average fertility rate after ICSI is 70-80%.
On top of that, in a very small percentage (2-3%) of cases, the egg may be irreparably damaged during the manipulations required for ICSI.
• Children conceived through ICSI are almost as healthy as children conceived through conventional IVF or natural conception.
Studies suggest that there MAY be a reduction in the reproductive potential of the boys born through ICSI. This is linked to the possibility that male infertility may be – to some degree – hereditary. Therefore, it is possible that men may transfer their infertility to their sons, who may in turn need help to have a child.
In other words, ICSI may help men who would ‘normally’ never father children to have a child who could have fertility problems himself.
There is still ongoing research in this area. | {
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225,093,739,117,522,780 | Contextual manipulation of the IL-6 family of cytokines to alter and enhance CD4+ T-cell immunity to respiratory viral infections
Year of award: 2013
Grantholders
• Dr James Harker
Imperial College London
Project summary
James is a viral immunologist with research interests in understanding the signals involved in generating potent antibody-mediated immunity to infections. His group in the Leukocyte Biology Section at Imperial College London will focus on determining the processes involved in promoting this type of immune response to respiratory viral infections, with the hope of developing novel therapeutic and vaccination strategies. The lab will use a number of in vivo infectious and genetic models that accurately reflect the complexities of the host immune response, allowing James to dissect how specific molecules, along with factors such as age, timing of infection and virus type, influence the outcome. | {
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-3,067,638,094,047,689,700 | less than 1 minute read
Immune System
Specific Immune Defenses
The specific immune response is activated when microorganisms evade the non-specific defenses. Two types of specific defenses destroy microorganisms in the human body: the cell-mediated response and the antibody response. The cell-mediated response attacks cells which have been infected by viruses. The antibody response attacks both "free" viruses that haven't yet penetrated cells, and bacteria, most of which do not infect cells. However, some bacteria, such as the Mycobacteria that cause tuberculosis, do infect cells.
Additional topics
Science EncyclopediaScience & Philosophy: Hydrazones to IncompatibilityImmune System - Organs Of The Immune System, Specific Immune Defenses, A Closer Look At Antibodies - Overview of the immune system, The non-specific defenses, How antibodies work to destroy invaders | {
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649,319,877,099,428,600 | In a normal adult human the difference between the systolic and diastolic pressure is
In a normal adult human the difference between the systolic and diastolic pressure is
1. A. 40 mm Hg
2. B. 20 mm Hg
3. C. 80 mm Hg
4. D. 120 mm Hg
Answer: A. 40 mm Hg
The difference between systolic and diastolic pressure is called as pulse pressure. It is measured in millimeters of mercury.
• Systolic pressure is the maximum pressure exerted by the heart when it contracts, and in a healthy adult, it usually ranges from 120 mm Hg.
• Diastolic pressure is the pressure in the arteries between heartbeats, and it typically falls between 80 mm Hg.
• So the pulse pressure will be 40 mm Hg.
Leave a Reply
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7,280,874,976,817,666,000 | Total Well-being
Being “healthy” isn’t the same for everyone. We have different bodies, minds, living situations, and people influencing our lives. Each area can impact our overall health. This means we have a unique picture of health and well-being.
Our physical, emotional, social, and financial well-being make up our well-being wheel. Just like a wheel, all four areas of wellbeing need to be balanced to make the wheel move forward. Check out this short video to learn about the areas that make up the well-being wheel, and tips for maximizing your health in each area.
Expand All
• Physical Well-being
Eating a balanced diet, exercising, and maintaining a healthy weight are important to keep your body working properly. Positive physical health habits can help decrease your stress, lower your risk of disease, and increase your energy. Taking steps to protect your health is the best way to prevent disease and other conditions. Health screenings, vaccines, and guarding yourself from germs can help keep you feeling your best.
Always remember your FITNESS
Focus on daily movement
Set aside time each day to move. Do what’s easy and fun such as walking, bike riding, or dancing. Start slow with as little as 10 minutes and gradually increase to 30-40 minutes most days.
Incorporate strength
Target all major muscle groups and try muscle strengthening exercises 2-3 times per week.
Try something new
Add variety for maximum benefits. Try a new exercise class, programs in your community or local parks, and trails.
Never forget hydration
Always have water and fluids available to maintain adequate hydration. Thirst can be a sign of dehydration.
Eat colorful meals
Fill half your plate with fruits and vegetables. Their colors provide vitamins, antioxidants, and other important nutrients.
Seek balance and flexibility
Regular movement and muscle strengthening exercises improve your balance and reduce your risks for falls and injury.
Strive for a healthy weight
If you are overweight, losing as little as 5-7% of your bodyweight can create a significant difference in your physical well-being.
• Emotional Well-being
How you feel can affect your ability to carry out everyday activities, your relationships, and your overall mental health. How you react to your experiences and stressors can change over time. Emotional wellness is the ability to successfully handle life’s stresses and adapt to change and difficult times.
Always remember your HEART
Handle stress
During times of stress, try deep breathing exercises. Breathe slowly in through your nose. Fill your belly with air. Breathe out slowly through your nose. As you breathe out, imagine the stress leaving your body with your breath.
Embrace social connections
Make plans for lunch, a walk on the beach, a volunteer event, or other fun activity weekly with old or new friends. Expand your social network by joining a recreational sports team, taking a community class, or connecting with an organized group of people that share a similar interest.
Aim for quality sleep
Establish a regular bedtime relaxation routine. Turn off electronics an hour before going to sleep. Keep your bedroom at a cool temperature, dark and as quiet as possible. Avoid stimulants like caffeine and nicotine, alcohol, meals, and emotional conversations before bedtime.
Rest and relax
Take a nature walk or simply sit and enjoy a beautiful view. Incorporate relaxing activities like stretching, gardening, reading, and writing, or deeper forms of relaxation like meditation, tai chi, or yoga.
Try mindfulness
Quiet your mind and appreciate the moment for exactly what it is. Bring awareness to your breath, body, feelings, and thoughts, or something in your environment. Set aside regularly scheduled time to practice mindfulness and protect yourself from the demands of a busy life.
• Social Well-being
From the time you’re born, your relationships help you learn to navigate the world. You learn how to interact with others, express yourself, and conduct everyday health habits. Positive social habits can help you build support systems and stay healthier mentally and physically.
Always remember your FRIEND
Foster connections with others
Build positive relationships with family, friends, and coworkers by staying in touch and spending time together on a regular basis.
Reduce screen time
Limit your social media time to only a few minutes a day. Have face-to-face conversations and meetings with those that you care about.
Invest in family time
Spend time together doing fun activities such as family game night, pot-luck dinners, or outdoor activities such as walks around your neighborhood or bike riding. Investing in family time yields high rewards.
Empower others
Provide positive and encouraging support to your circle of friends and family. Encourage independence and openness to new experiences.
Nurture healthy relationships
Share your feelings honestly and listen to others without judgment. Identify relationships that are unhealthy for you and learn to set boundaries on those relationships.
Designate “me” time
Taking care of self is often overlooked yet essential to your overall well-being and the health of your relationships. It’s important to find ways to care for your health while caring for others.
• Financial Well-being
Financial well-being can look different to each individual. Taking the steps to control your day-to-day finances, meet financial goals, absorb financial shock, and live within your financial means is the best way to support your financial health.
Always remember your MONEY
Maintain control
Become aware of your spending habits and develop a spending plan for extras like dining, shopping, and vacations. For example, set a spending limit for the week and don’t exceed it.
Organize priorities
Categorize your money into the following buckets:
• “must haves” such as your mortgage/rent, food or childcare
• “nice to haves” such as new clothes and outings
• “near term” such as home/auto repairs and taxes
• “future” such as retirement or a down payment
Nest for emergencies
Add up the cost of items listed in your “must haves” and “near term” buckets and multiply by three. Let that be your first savings goal in the event of job loss or illness.
Emphasize saving
Always pay yourself first. To reach your savings goals you can find additional income, spend less money, or do both.
Your budget - build one!
Start telling your money where to go instead of wondering where it went. Revisit the list of priorities in the four buckets mentioned above. Assign appropriate dollar amounts to those expenses and stick | {
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1,169,301,481,692,636,700 | Elderly Nutrition Myths Debunked: What They Really Need in Their Diet
Close-Up-Shot-of-a-Man-in-Checkered-Long-Sleeve-Eating-Nutrition-Myths-Debunked-What-Seniors-Really-Need-in-Their-Diet
In This Article
Nutrition has a vital role in accommodating seniors’ aging journey. However, eating right to improve health can be confusing in old age due to false beliefs and ever-changing food facts. For example, it is said that seniors don’t need proteins as much as younger generations; the truth is a lack of protein can increase the risk of falls due to muscle mass loss.
Some nutrition facts aren’t straight-up accurate, while others are partially understood. We are here to help you clear up any confusion and gain a better understanding of seniors’ nutrition needs. Let’s debunk some of the most common elderly nutrition myths and misconceptions.
Elderly Nutrition Myth Busters: Discover The 10 Myths and Misconceptions Around Senior Nutrition
Elderly Nutrition Myth #1: Senior Malnutrition Is Normal
Malnutrition can happen to anyone if they neglect their nutritional needs. However, the aging population is more likely to become malnourished than other age groups due to a variety of factors, with 5.5 million American seniors experiencing food insecurity. Some seniors simply have appetite loss, while others encounter physical changes that cause difficulties in chewing and swallowing. Following required dietary restrictions can make seniors vulnerable to malnutrition. Pain and decreased dexterity associated with diabetes and Alzheimer’s disease can also alter seniors’ desires towards foods, hence the higher risk of malnutrition. Another cause of malnutrition hiding in plain sight is some seniors don’t have the budget to buy nutritious foods.
Takeaway: Although malnutrition is a widespread issue among seniors, it isn’t a sign of aging.
Elderly Nutrition Myth #2: Seniors Should Eat Less
oods-High-in-Magnesium.-Healthy-diet-eating.-Nutrition-Myth-2-Seniors-Should-Eat-Less-
When we are younger, we are told to maintain a certain level of food intake to function throughout the day. This has led to another misconception that seniors don’t need to adhere to this rule due to decreased energy requirements. The statement is partially true, but most people miss the key part. At old ages, seniors should eat fewer calories and more nutrients. In other words, seniors require the same amount of nutrients as younger adults, if not even more, to protect them from aging effects in the long run.
Takeaway: Reducing calories and increasing nutrient intake is critical to bodily function, ensuring healthy aging.
Elderly Nutrition Myth #3: Focus On Foods Marked As “Healthy”
Staying fixed on a healthy, balanced diet is a pathway to age well. Today, seniors easily become fixated on the strong urge to buy as many foods marked as “healthy,” “high in antioxidants,” and “low in sugar” as possible. But are they actually healthy? The truth is these foods aren’t always the safe bet for seniors. Processed foods are often loaded with sugar, sodium, and preservatives. Low-fat yogurts sound like a good dessert choice but contain lots of sugar. Other common foods that may not be as healthy as they seem include protein bars, granola, dried fruits, vegetable chips, store-bought juices, sugar substitutes, and vitamin waters.
Takeaway: Foods that appear to be “healthier” may not be healthy, so it is critical to choose foods wisely and practice reading nutrition labels. Here’s a tip: the shorter the list, the better.
Elderly Nutrition Myth #4: Avoid Fat At All Costs
There is fear-mongering spreading around that seniors must avoid fat at all costs. This is only true when they have health problems that require a complete pause in fat consumption. Also, fat is present in everything, even nutrition snacks like nuts and seeds. There are good and bad sides to everything, and fat is no exception. That means some fats are more beneficial than others. When consumed in moderation, good fats can give a boost to seniors’ energy levels, promoting good health in the long term. Some sources of healthy fats include fatty fish, vegetable oils, nuts and seeds, full-fat yogurts, cheese, and avocados.
Takeaway: Incorporate foods high in monounsaturated and polyunsaturated fats while watching out for the consumption of trans fats.
Elderly Nutrition Myth #5: Seniors Can Eat Whatever They Want
Happy-fashionable-senior-ethnic-man-having-lunch-in-cafe-Elderly-Nutrition-Myth-5-Seniors-Can-Eat-Whatever-They-Want
Another myth about elderly nutrition is that seniors get a free pass to eat whatever they want. Boosting nutrient intake doesn’t equate to overeating. Overconsumption and poor food choices can pose opposite effects to seniors’ health, heightening their risks of developing chronic disease. For example, seniors who maintain a high-sugar diet may experience joint inflammation, high cholesterol, higher triglyceride levels, and metabolic syndrome. Loading up more carbohydrates than recommended can quadruple the risk of cognitive impairment, Mayo Clinic says.
Takeaway: Lean toward a healthy diet of lean proteins, whole grains, fruits, vegetables, and good fats.
Elderly Nutrition Myth #6: Only Drink Water When Thirsty
Not only seniors but numerous people only reach for a glass of water when thirsty. However, acute thirst indicates that your body is already dehydrated. Staying hydrated is essential for overall health. Adequate fluids keep the brain at peak capacity and ensure optimal bodily functions. Unfortunately, seniors have challenges with drinking enough water because their sense of thirst diminishes over time. Health changes, medications, and weather can also influence seniors’ abilities to keep up with their hydration needs. Not every senior fancies the taste of water. Therefore, eating water-rich foods like watermelon, tomatoes, strawberries, lettuce, and soups is a great way to supplement fluid intake.
Takeaway: Instead of sticking to the rule of thumbs by drinking 2 liters of water per day, seniors should make drinking water a part of their daily routine.
Elderly Nutrition Myth #7: Stick To 3 Meals A Day
Contrary to the centuries-old norm, no scientific evidence shows that a person must stick to a regimen of eating breakfast, lunch, and dinner every single day. While healthy eating is vital to living well and remaining independent into old age, three meals a day can overwhelm many seniors, especially those with eating problems or appetite loss or who find cooking time-consuming. How many times seniors should eat a day isn’t as crucial as the nutritional values incorporated in each meal. The number of daily meals can be altered and catered to each individual depending on their health and preferences.
Takeaway: Break down large meals into 5-6 smaller portions or well-chosen snacks.
Elderly Nutrition Myth #8: Eating Out Is More Convenient
Anonymous-customers-having-break-in-cozy-cafe-Nutrition-Myth-8-Eating-Out-Is-More-Convenient
Eating out or ordering take-outs is indeed more convenient than cooking at home, where seniors have to juggle multiple tasks, such as preparing food and cleaning afterward. For seniors who want a change of scenery or want to eat something other than their everyday meal, dining out could be a great choice. So, how could things go wrong? Chances are eating out, though delicious and convenient, can be detrimental to seniors’ health. It’s reported that restaurant meals and fast foods are shockingly high in sodium, fat, and sugar, with 92 percent of meals exceeding the recommended calorie intake.
Takeaway: Dining out takes out the hassle of home cooking, but high-sodium meals can be harmful to seniors’ health.
Elderly Nutrition Myth #9: Seniors Can Rely On Supplements To Meet Their Nutritional Needs
A significant number of seniors still experience nutrition deficiency, even if they increase their nutrient intake. This is because the aging body can no longer absorb nutrients sufficiently. Reaching for dietary supplements and vitamins is a practical way to fix such issues. However, it is never a good idea for seniors to live off supplements. When consumed irresponsibly, supplements can do more harm than good. Many people report experiencing unwanted side effects to their gut following heavy consumption, such as diarrhea and constipation. Taking supplements in excess can interfere with the body’s nutrient balance, putting seniors at heightened risk of malnutrition.
Takeaway: Supplements can’t replace food. It is best to exercise cautions and consult doctors to assess dosage before adding supplements to the diet.
Elderly Nutrition Myth #10: Senior Communities Serve Unappealing Foods
Think seniors only get to eat repetitive and boring foods in senior communities? It’s time to change your perspective. Long gone are the days of senior living communities serving unappealing food items. Today’s senior living communities have stepped up in their game by providing residents with a multitude of delectable food choices served hot and ready in a warm and home-like environment. They also take special requests from residents with unique dietary needs.
Takeaway: More and more communities have featured various menus to diversify seniors’ food palates.
Meeting Nutritional Needs Made Easy At 12 Oaks Communities
At 12 Oaks Communities, we know how important it is to maintain levels of nutrition intake for our residents. You are what you eat. Therefore, eating healthy is a must to achieve longevity and vitality.
With that in mind, our dedicated kitchen staff is always up for a big daily challenge to plan and cater meal varieties to help our endearing residents age gracefully and confidently while keeping them satisfied with every spoonful of food.
If you have questions about seniors’ nutritional needs and elderly nutrition myths or any topics discussed here, connect with us and learn more.
At 12 Oaks, our team of caring professionals is dedicated to keeping residents safe, engaged, and connected to their families and friends while leading fulfilling lives. 12 Oaks Senior Living Communities are an ideal place to enjoy the encore season of life.
For questions or to schedule a personalized tour, don’t hesitate to contact us.
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Searching for senior living help? At 12 Oaks Senior Living Communities, we would love to learn more about your unique needs and the opportunity we may have to help you meet them. Our blog is one of the valuable resources we provide to inform and encourage seniors to lead fulfilling and thriving lives. Contact us today to schedule a visit.
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-3,392,192,584,002,609,700 | Search for European Projects
Role of extracellular miRNAs in T cell development, TH2 cell differentiation and TH2 cell-mediated effector function (miRNAs in TH2 cells)
Start date: 01 Aug 2015, End date: 31 Jul 2017 PROJECT FINISHED
It is estimated that more than 200 million Europeans suffer from at least one type of allergy. This condition is elicited by an hyper-activated type-2 inflammatory response coordinated by T helper (TH)-2 cells. In spite a good insight into the molecular mechanisms that triggers TH2 cells activation, the lack in understanding their post-transcriptional regulation is hampering the access to new potential therapeutic targets to curtail the allergy epidemic.Micro-RNA (miRNAs) are regulatory molecules essential for life, which play a fundamental role in shaping cellular functions via post-transcriptional repression of the cellular transcriptome. Though previously considered to operate exclusively inside the parent cell, it is now acknowledged that miRNAs can exit cellular boundaries and control transcription in bystander cells. We recently reported that regulatory T (TREG) cells secret specific miRNAs to repress TH1 cell-mediated immunopathology, and ameliorate a mouse model of autoimmune disease.In this proposal, we will address the role of extracellular miRNAs for the normal T cell development and during allergic inflammation of the airways. To this end, we produced a novel animal model that allows - for the first time - to selectively ablate the activity of extracellular miRNAs in T cells. We will use biochemical, RNA-sequencing and bioinformatics analysis to identify the molecular mechanisms for miRNAs sorting to exocytosis and to identify the miRNAs transferred to and from TH2 cells. This proposal will significantly expand our understanding of transferred miRNAs in the contest of health and disease, and will uncover novel cellular pathways to exploit as therapeutic targets.
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Details
1 Partners Participants | {
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-1,034,435,426,776,636,900 | August 6, 2024
Acage
Outstanding health & fitness
Anxiety or Heart Disease?
Anxiety or Heart Disease?
Your heart is racing, you’re having difficulty breathing, you have pins and needles in your limbs, you can’t think straight–is it a panic attack?
Anxiety, specifically panic attacks, can mimic more serious illnesses, such as congestive heart failure.
Anyone who has suffered with panic attacks knows that it can feel like you’re having a heart attack, stroke, or dying. While an actual panic attack can be terrifying, it is not deadly. But, thinking you’re having a panic attack when it really is a life threatening episode can be deadly.
What compounds this situation and makes it even more dangerous is when those around you, knowing you suffer with panic attacks, don’t take your symptoms seriously. Their first reaction is to assume it’s just another anxiety eruption. This is where you need to use common sense and take cautionary measures.
The story of a woman who thought she was suffering from non-stop panic attacks for almost a month is a case in point. The woman had a history of panic attacks, but at this point in her life she already had an episode with a leaky heart valve. Her symptoms were shortness of breath and light-headedness when getting out of bed in the morning; she couldn’t breathe when she climbed stairs; she had a heavy funny feeling in her legs; she had an ache in her neck and shoulders; and her heart was racing.
Why weren’t warning signals going off in her head telling her to go to the hospital? Ah, the life and death question. No one wants to think she’s really sick. She especially doesn’t want to believe it’s a life and death situation. And, no one wants to go to the hospital.
Fortunately, this woman’s symptoms continued to get worse and she finally went to see her regular doctor. This was fortunate because if the symptoms didn’t worsen she may not have sought any medical attention and it would have been too late. It turned out this woman was in congestive heart failure.
This is such a common and dangerous scenario: once diagnosed with anxiety and panic attacks the individual and those around him or her don’t give serious warning signs the attention they deserve. This type of reaction delays, and even stops, the individual from seeking immediate medical attention. So, beware! Don’t recklessly treat common heart attack and stroke symptoms as panic attacks. Better safe than sorry.
Another common scenario is when doctors attribute anxiety-like symptoms, especially in women, to anxiety without ruling out other possible more serious causes for the symptoms.
What Can You Do to Have Your Symptoms Taken Seriously?
1. Don’t assume that doctors are always correct in their diagnosis.
2. If you’re told, “don’t worry, it’s just anxiety,” but you have a gnawing feeling that something else is going on, get another opinion.
3. If you’re still not satisfied, get a third, fourth and even fifth opinion.
4. It’s a good idea to write your symptoms down, so when you get to the doctor you don’t have to rely on your memory.
5. Try to be calm (not flustered) when describing your symptoms to doctors – having your symptoms written down will help in this area also.
Remember: It’s important to listen to your body. | {
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-4,963,148,748,476,045,000 | Side Effects Of Milk Of Magnesia
Milk of magnesia is an oral suspension that contains hydrated magnesium carbonate. It is an over-the-counter medication intended for occasional or short-term use as an antacid or laxative. Women who are pregnant or breastfeeding should ask their physician before using milk of magnesia. Patients with kidney disease should check with their healthcare team to ensure this medication is safe for them to use. If symptoms persist for more than seven days, the patient should see a doctor before continuing this medication. Milk of magnesia is available as a chewable tablet and as a liquid. Individuals using the liquid formulation will need to shake the medicine before consuming it.
As mentioned, many individuals use milk of magnesia as an over-the-counter laxative and antacid. Thus, patients take milk of magnesia for constipation relief. This medication can provide heartburn relief, and it is also a treatment for indigestion and sour stomach. Some patients will try a milk of magnesia colon cleanse. In some cases, individuals will have access to a variety of milk of magnesia flavors. However, before taking it, patients must first understand the potential side effects of milk of magnesia.
Diarrhea
Dreamstime
Diarrhea is the most frequently reported side effect that patients experience after taking milk of magnesia. As a laxative, this medication increases the amount of water in the intestines to induce a bowel movement. It softens and moistens the stool. Most patients will have a normal bowel movement within six hours of taking a single dose of milk of magnesia. However, diarrhea could occur if an individual takes more than one dose in twenty-four hours or if the dose consumed exceeds the recommended amount on the product packaging. Diarrhea is defined as loose or watery stools. Patients may experience this symptom with abdominal pain or bloating.
If diarrhea occurs, patients should not take any additional doses of milk of magnesia. They should consult a doctor if nausea accompanies their diarrhea. It is often beneficial to eat a low-fiber diet and avoid dairy products until diarrhea resolves. Patients are also advised to drink plenty of fluids to prevent dehydration. If diarrhea continues for more than two days, patients may wish to consult a doctor. They may prescribe additional medication.
Keep reading to learn more about the side effects of milk of magnesia now.
Nausea And Vomiting
FindATopDoc
Milk of magnesia may irritate the stomach. This could trigger nausea and vomiting for some patients. These symptoms are more likely to occur in patients who need to take more than one dose to relieve their constipation. Doctors suggest that patients try to avoid strong odors or flavors to ease their nausea. It can also be helpful to go outside for fresh air. Some patients can relieve their nausea by eating peppermint or ginger, and eating bland food such as rice or crackers could be soothing for nausea as well.
If vomiting occurs, patients should note how many times they experience this and obtain emergency medical attention if the vomit is black or bloody. Emergency medical care is also necessary in cases where the patient cannot keep any food or liquid down at all.
Get more details on the side effects of milk of magnesia now.
Abdominal Pain
Dreamstime
Abdominal pain may occur as a side effect of milk of magnesia. It is also a common complication of constipation and upset stomach. The abdominal pain associated with laxative use may be experienced as a sharp, stabbing pain. Patients may also feel a dull or throbbing ache. This type of pain occurs most often in the lower abdomen. However, they may be present in several areas of the abdomen. Abdominal pain may indicate a bowel obstruction or another serious medical condition. Thus, patients should see a doctor if they experience severe pain, pain that persists, or pain that worsens in any way.
Emergency medical attention is necessary if the abdomen is swollen or tender to the touch. Patients should go to the emergency room if they have abdominal pain accompanied by bloody stools, fever, or persistent nausea and vomiting. Doctors will use a stethoscope to listen for bowel sounds in the patient's abdomen. They will press on the patient's abdomen to check for lumps and areas of pain. They may request imaging studies as well. Depending on the exact cause of the pain, patients may be treated with medications or surgery.
Read more about the side effects linked to milk of magnesia now.
Rectal Bleeding
Dreamstime
Rectal bleeding can be a sign of hemorrhoids, anal fissures, or cancer. Individuals who experience this symptom should see a doctor urgently. Patients with rectal bleeding may notice blood on the toilet paper after having a bowel movement. There may also be drops of blood in the toilet bowl. The stool itself could be red or black. The doctor will begin with blood tests and a general physical examination to assess the patient for signs of anemia and abdominal pain or masses as part of assessing rectal bleeding. Next, they will perform a digital rectal examination to check for blood or masses in the rectum. Patients may also have a proctoscopy examination. Doctors may request a colonoscopy if more information is required.
If possible, patients may want to estimate how much blood loss they experience through rectal bleeding. This information helps guide the doctor in the assessment. It is beneficial for them to know how often the patient experiences rectal bleeding as well.
Discover additional side effects of milk of magnesia now.
Lightheadedness
Dreamstime
Patients who take milk of magnesia on a long-term basis or at doses larger than the recommended levels could experience lightheadedness and dizziness. Patients who feel lightheaded could faint, and they are at a higher risk for falls and injuries. During an episode of lightheadedness, the patient should try to sit or lie down as soon as possible. Patients who experience this symptom while taking milk of magnesia should discontinue the use of it immediately.
It can be helpful for the patient to keep a journal of lightheadedness episodes so they can share this information with their doctor. To assess lightheadedness, doctors will perform a physical examination. Patients may need to have blood tests or imaging studies. This symptom may resolve on its own once milk of magnesia is stopped.
Reveal additional side effects linked to milk of magnesia now.
Slow Heartbeat
Dreamstime
A potential severe side effect linked to milk of magnesia is a slow heartbeat. This is a sign of a milk of magnesia overdose. Research indicates that this medication reduces potassium excreted from the body and increases the amount of magnesium in an individual's body. This can trigger an irregular heartbeat that is often slow. If patients deal with a slow heartbeat and are taking milk of magnesia, they should stop taking it right away. They should then seek immediate medical attention. It is likely that they will not be able to take milk of magnesia any longer due to this side effect. However, doctors will need to evaluate each patient and make that assessment.
Continue reading to uncover additional side effects of milk of magnesia now.
Muscle Weakness
Dreamstime
Muscle weakness is a major sign that an individual have taken too much milk of magnesia. In other words, muscle weakness is a significant indication that individuals are dealing with abnormally high levels of magnesium in their body. Any individual taking milk of magnesia who experiences muscle weakness should immediately stop taking this substance. They will also need to receive emergency medical attention. Emergency treatment for patients who are dealing with muscle weakness, and therefore a milk of magnesia overdose, is vital to reverse the effects of milk of magnesia.
Get more information on the various side effects that are associated with milk of magnesia now.
Dry Mouth
Dreamstime
Some individuals who take milk of magnesia can deal with dry mouth as a side effect. If they experience dry mouth when taking milk of magnesia, it is a sign that they are dehydrated. If dry mouth is mild, patients can likely continue taking milk of magnesia if they increase the amount of water they are drinking to compensate for the fluids they are losing. However, if patients are experiencing severe dry mouth, they should stop taking milk of magnesia and increase their water intake. In addition, severe dry mouth, and therefore severe dehydration, may require medical attention.
Discover more potential side effects of milk of magnesia now.
Extreme Thirst
Dreamstime
Extreme thirst when individuals are taking milk of magnesia is another side effect that indicates they are dealing with dehydration. Unfortunately, extreme thirst often means that affected individuals will need to stop taking milk of magnesia, at least on a temporary basis. Patients will also need to drink a significant amount of water to rehydrate their body. They should also maintain a higher water intake if they are able to resume taking milk of magnesia. Of course, some individuals with extreme thirst due to milk of magnesia will need to receive medical help to treat this symptom and their dehydration.
Reveal additional side effects linked to milk of magnesia now.
Shallow Breathing
Dreamstime
Shallow breathing is another potential side effect of milk of magnesia that indicates patients may have taken too much of it. The result of this, as mentioned previously, can be that patients now have abnormally high levels of magnesium in their body. As with the other side effects that indicate high magnesium, patients dealing with shallow breathing need to stop taking milk of magnesia right away. In addition to ceasing milk of magnesia, patients should also receive immediate medical attention to treat their shallow breathing effectively and thus, prevent lasting consequences from the high levels of magnesium and the side effects, like shallow breathing, that it causes.
MORE FROM HEALTHPREP
HealthPrep Staff | {
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189,769,957,759,654,940 | Relaxation Techniques
Emotional stress can make asthma worse. Chronically stressed children have more asthma attacks.1 Stressed adults tend to have more symptoms and worse quality of life.2 They miss more doses of medication, and medications may not work as well.2,3 Therefore, there is reason to believe that reducing stress could be helpful for people with asthma.
It is possible to learn techniques that help you to relax.4 When your body is relaxed, you breathe more slowly and your blood pressure goes down. Your feelings of well-being go up.
Generally, studies of relaxation techniques for asthma have been small and low-quality. A few do show that there are some benefits.5 However, the National Heart, Lung, and Blood Institute states that larger, high-quality studies are needed before they can recommend using these techniques.1
What are relaxation techniques?
There are many different relaxation techniques (Table).4,6 Relaxation techniques have been studied for many medical conditions. They are helpful for insomnia, labor pain, chemotherapy side effects, jaw pain, and some types of anxiety.4
Types of relaxation techniques for asthma
• Autogenic training: You learn to notice feelings of warmth, heaviness, and relaxation in different parts of your body.
• Progressive relaxation: You tighten and relax various muscle groups.
• Functional relaxation: You move your joints very slightly as you breathe out. You learn to focus on the different sensation triggered by the movement. Functional relaxation is a similar to progressive relaxation.
• Guided imagery: You learn to focus on pleasant images in place of negative or stressful feelings.
• Biofeedback: You use electronic devices to learn how to reduce muscle tension. You learn how produce changes in your body that help you relax.
• Self-hypnosis: You learn to relax in response to a prompt, such as a phrase or non-verbal cue.
• Deep breathing exercises: You use slow, deep, even breathing to become relaxed. You breathe in through the nose and out through the mouth.
• Meditation: You learn to become aware of your thoughts, feelings, and sensations in a non-judgmental way. You can also do meditation with movement, such as with yoga or tai chi.4
What studies say about relaxation techniques for asthma
Unfortunately, there are problems with the design of most studies of relaxation techniques.5 They are small and short. They do not use the best ways to measure outcomes. It is hard to find a good control (fake) treatment for comparison. Lack of evidence does not mean that these techniques are no good. There is just not much information about them.
Functional or progressive relaxation techniques seem to be the most promising.5 There are several studies of these approaches.
Adults and children
One study involved 18 children and adults. Participants had less airway resistance after practicing functional relaxation.7
Pregnant women
A randomized, controlled trial compared progressive relaxation with a sham (fake) treatment.8 There were 84 pregnant women in this study. Women had better lung function after progressive relaxation than before. Lung function was also better when compared to the women who did the sham treatment. A similar trial with teenage girls produced the same results.9
Adults with allergic asthma
Sixty-four adults were randomly assigned to functional relaxation, guided imagery, both, or a control intervention.6 Four months later, the people in the functional relaxation group had better lung function and less airway resistance than the people in the control group. Guided imagery was not effective in the end. The people who used both techniques had mixed results.
Benefits
Relaxation techniques may lead to some improvement in symptoms and lung function.1 Medication use may also go down.10 To be certain about the benefits, better studies are necessary.
Risks
For most people, relaxation techniques are safe.4
How do I learn relaxation techniques?
You can learn some simple techniques on your own. Complementary and alternative practitioners, doctors, psychologists, social workers, or nurses may also be able to teach you.4 These techniques work best if you practice them regularly.
Have you found any relaxation techniques that have helped with your asthma?
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Written by: Sarah O'Brien | Last Reviewed: September 2020. | {
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-1,184,361,711,386,156,800 | Braces FAQ
While it’s certainly true that most people are familiar with traditional braces as a concept, it’s still entirely possible to have questions about how they work, or about what type of experience you can expect while wearing them. With that in mind, here are comprehensive answers to some of the most common questions that people have. If you’d like to discuss any particular one with someone in a bit more detail, please don’t hesitate to pick up the phone and call our office today.
Are There Any Alternatives to Braces?
Dental technology has come a long way over the years to the point where there are now viable alternatives to traditional braces. Perhaps the most famous of these is Invisalign – a series of clear plastic aligners that gently move the teeth into the desired position over time.
Rather than using a series of metal brackets and wires as is true with braces, Invisalign simply uses clear plastic trays. Every few weeks you swap out one set of trays for another, thus achieving the same result in a much different way.
Both techniques bring with them their fair share of advantages, however, so it’s always important to discuss things further with your dental professional to make the best decision possible with regards to your health.
What’s the Best Age to Get Braces?
While it’s true that braces are commonly associated with kids and young adults, there really is no “best age” to get braces. It may be easier to treat certain types of issues while you’re young and your jaw and mouth are still developing, but just because you’re older doesn’t mean that traditional braces are off the table. Far from it – a statistically large portion of braces-wearers is actually adults, for example.
How Long Do People Have to Wear Braces?
The answer to this question is going to be heavily impacted by the patient you’re talking about. Some types of issues take longer to correct than others, meaning that someone who is only concerned about the spacing of their teeth will probably have a shorter treatment than someone also tackling jaw or bite-related problems.
Having said that, most people can expect to wear braces for about two years on average.
Are Braces Really Necessary?
In a word – yes. Not only does everyone deserve to get the self-esteem boost that comes with having that perfect smile they’ve always seen for themselves, but the types of issues that braces are designed to address can happen at literally any point during your life. Both of these things all but confirm that braces are always a step that is worth taking in terms of your health.
Do Braces Do Anything Other Than Improve My Smile?
Absolutely! When most people think about braces, they think about patients who are trying to correct issues like crooked teeth, crowded mouths, spacing that is too large between teeth, and other similar problems.
But braces are also great for improving bite-related issues, too, like an underbite or overbite. Proper oral health is also essential for combating certain problems that could develop later on in life, like high blood pressure or even heart disease.
Do Braces Hurt?
Most patients find that braces don’t hurt in the strictest sense of the term, but they will probably take some getting used to. This is because once treatment begins, a series of brackets are attached to each of your teeth that are themselves connected via a wire. The strength of that wire is what pulls the teeth into the desired position over time.
By design, a certain amount of friction is necessary to shift your teeth over treatment – which means that some people may find some initial discomfort, though they’ll likely get used to it quickly.
How Much Do Braces Cost?
This is another answer that will depend on the patient, as the length of treatment will obviously impact the price you’re expected to pay. The area of the country you live in will also play a role, among others.
Generally speaking, most people can expect to pay a few thousand dollars for their treatment. But don’t worry – your dental professional likely has a wide range of different payment plans and similar financing options that you can explore depending on your needs.
Am I Too Old For Braces?
Again – you are absolutely never too old to get traditional braces and don’t let anyone tell you differently. If you have dental-related issues that you’re trying to correct, it’s absolutely possible to do so using traditional braces. Your dental professional will go over all of this with you in more detail during your initial consultation.
How Long Will I Have to Wear Braces?
The total length of treatment is going to be heavily impacted by the specific types of issues you’re trying to correct in the first place. But in most cases, your average patient can expect to wear braces for approximately two years, give or take.
Do I Need to See My General Dentist While Wearing Braces?
You should absolutely continue to see your general dentist while wearing braces and in fact, he or she will probably be closely coordinating with your orthodontist for the duration. This is because certain types of health-related issues can absolutely impact the success of your treatment.
So to guarantee the safest experience possible – and not to mention, the most effective one – you’ll still want to go to your general dentist and this person will likely be in close communication with your orthodontist.
What is Limited Treatment?
As the name suggests, limited treatment when it comes to braces is one that is focused exclusively on the aesthetic side of your mouth. If you aren’t necessarily concerned about an overbite, an underbite, or some similar type of issue and just want to correct the visual look of your smile, limited treatment is absolutely something you can explore. With a limited treatment plan, you can address a specific issue in just a few months. You’ll obviously want to talk things over in more detail with Dr. VanLue to make sure that you’re an ideal candidate.
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Second cousins are as close as you can get before birth defects start appearing.
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Q: Can related people have children together and would new traits show up?
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Related questions
What are the Personality traits of parents of children with autism?
The parents of autistic children do not have a certain set of personality traits. They differ as with all people.
How was the knowledge of the way traits are inherited changed people's lives?
People now know the different generations. That can help them understand traits and the changes. People are easily catching on with the inherited traits and what happens, and now they can predict the different traits their children will inherit from them.
What were George W. Bush'es traits?
*leader ship *Drawing people together
Why do related species share homologous traits?
Related species have inherited homologous traits from a common ancestor.
Are source traits a set of related behaviour forms?
Source traits are a type of trait that helps to begin to form one's personality. These traits, such as extroversion, are said to be related to behavior forms.
Who does a son inherit traits from?
Children of any gender inherit traits from both parents.
What are indirect traits?
Traits passed from not your parents, but possibly a grandparent or someone before or related to them
What is passing of traits from parents to children?
The heredity
What kind of traits are traits that people deliberately change?
manipulated acquired traits
How are DNA the nucleus chromosomes genes and traits related?
its not
Does the relationship of people affect the number of traits they have in common?
yea you can still have the same traits bc all ppl are related in some sorta way i mean like we all started from da same too ppl
Why are inbred children more likely to have physical and health defects?
Close relatives share many similar genes including defects, mutations and recessive traits. Breeding within a closely related gene pool increases the chances that the same genetic characteristics are present in both parents. Children born from parents with the same genetic traits, even though those traits may not manifest in either parent, are more likely to manifest those traits since there is no alternative non-defective trait available. | {
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6,067,288,217,367,299,000 | Apple procyanidins induce hyperpolarization of rat aorta endothelial cells via activation of K + channels
Eui Baek Byun, Sachiko Korematsu, Teruaki Ishikawa, Taichi Nishizuka, Shunji Ohshima, Tomomasa Kanda, Toshiro Matsui
Research output: Contribution to journalArticlepeer-review
11 Citations (Scopus)
Fingerprint
Dive into the research topics of 'Apple procyanidins induce hyperpolarization of rat aorta endothelial cells via activation of K + channels'. Together they form a unique fingerprint.
Neuroscience
Pharmacology, Toxicology and Pharmaceutical Science
Medicine and Dentistry
Chemistry
Biochemistry, Genetics and Molecular Biology | {
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-6,013,173,347,374,578,000 | ICD-10-CM Code for Patient's intentional underdosing of medication regimen for other reason Z91.128
ICD-10 code Z91.128 for Patient's intentional underdosing of medication regimen for other reason is a medical classification as listed by WHO under the range - Factors influencing health status and contact with health services .
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Patient's intentional underdosing of medication regimen for other reason
Z91.12
Excludes1: adverse effect of prescribed drug taken as directed- code to adverse effect
poisoning (overdose) -code to poisoning
Code first underdosing of medication (T36-T50) with fifth or sixth character 6
Z91
Excludes2: contact with and (suspected) exposures hazardous to health (Z77.-)
exposure to pollution and other problems related to physical environment (Z77.1-)
female genital mutilation status (N90.81-)
occupational exposure to risk factors (Z57.-)
personal history of physical injury and trauma (Z87.81, Z87.82-)
Tabs
Get crucial instructions for accurate ICD-10-CM Z91.128 coding with all applicable Excludes 1 and Excludes 2 notes from the section level conveniently shown with each code.
This section shows you chapter-specific coding guidelines to increase your understanding and correct usage of the target ICD-10-CM Volume 1 code.
Forum
Have a question about ICD-10-CM Code Z91.128 ? Start a discussion here | {
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-6,785,615,341,011,021,000 | HBOT: A Way to Heal the Injured Brain?
Barbara Stahura, CJF, Brain Injury Journey magazine
HBOT: A Way to Heal the Injured Brain?
When SCUBA divers ascend from the high atmospheric pressure of the depths, it’s important to come up slowly so their bodies adjust to the low pressure at the surface. If they ascend too quickly, they will become ill with the “bends,” or decompression sickness, and require some time in a hyperbaric oxygen (HBO) chamber receiving 100 percent oxygen under higher atmospheric pressure. Hyperbaric oxygen therapy (HBOT) has been found to also be helpful in a variety of other conditions, including crush injuries, acute carbon monoxide poisoning, and diabetic wounds.
HBOT is also used to treat brain injury from trauma or another cause such as stroke. While the number of people who have used HBOT for brain injury is unknown, its popularity is growing. However, insurance generally does not cover it nor has the FDA approved it for this use. Some older clinical studies do not demonstrate the effectiveness of HBOT with brain injury, but a growing number of more recent studies do.
One study, from 2009, demonstrated that the patients with severe brain injury who received higher levels of oxygen in an HBO chamber had a positive increase in brain metabolism when compared to the control group and the group who received “normobaric” treatment, or treatment with pressure equivalent to sea level (Rockswald & Rockswald, 2010).
A groundbreaking study of U.S. military veterans with blast-induced mild traumatic brain injury and PTSD, published in 2011, produced significant results. “Headaches, post-concussion symptoms, abnormal neurological exam findings, cognition, PTSD, depression suicidal ideation, quality of life and brain blood flow were significantly improved after a one month course of HBOT.” Six months later, the great majority of veterans in the study sustained their improvements.
Bruce Gottlieb, MD, medical director of Hyperbaric Services of the Palm Beaches, LLC, in Delray Beach, Fla., is an enthusiastic supporter of HBOT. He says HBOT “is one of the simplest therapies around, but there is a lot of confusion around it. Lots of people claim to provide HBO therapy, but many of them in reality do not.” It is crucial to have close medical supervision in an accredited facility, he says. It should not be done at home.
The basic guideline of his clinic, he says, is that “HBO is an adjunct therapy. It is not a primary therapy for brain injury. And it is not a panacea or a silver bullet. We stress that patients have to do other therapies — occupational, physical, speech, and even psychological — in conjunction with HBO.”
He likens HBOT to a catalyst, “like Miracle-Gro for your lawn. The soil has to be good for it to work.” And with brain injury, the other therapies improve the condition of the brain to make it more receptive to HBOT.
Treatment with HBOT
Patients receive either one or two daily HBO sessions, depending on the time they have available, and brain injury requires a minimum of 40 to 80 sessions of one or two hours each — and often many more, according to Gottlieb and Sarah Crane, director of research. Treatment is cumulative, with more improvement occurring with more sessions.
The cost of HBOT for brain injury varies among regions and the facilities where it is performed. According to Crane, the per-session fee across the country ranges from $500 to $1,500, which adds up quickly. However, most clinical studies do not charge fees to those enrolled in the studies. Hyperbaric Services of the Palm Beaches, one of about 500 HBOT centers in the U.S., is participating in a clinical trial of HBOT through the National Brain Injury Rescue and Rehabilitation (NBIRR) Clinical Trial. They are not charging fees to enrollees.
How does it work?
The brain uses oxygen at a “ferocious rate,” Gottlieb says, and can easily become starved. When a trauma occurs, the brain often swells, so the injured tissue does not receive enough oxygen. “So the area that needs the most oxygen gets the least,” he says. HBOT drives oxygen into the cerebrospinal fluid, which carries it to the brain and permits healing.
Inflammation is another damaging result of a brain injury, acting much like a fire in its destructive power. But HBOT can put out that fire by sending 100 percent oxygen to the injured areas, and slowly the areas heal.
Gottlieb says there are no side effects or ill effects from HBOT, although some people experience increased pressure in the ear, similar to what happens in a plane. Some people should not do HBOT, including those with severe lung disease such as emphysema, uncontrolled seizure activity, or severe inner ear pain. Since the person undergoing treatment lies down and music can be piped in, HBOT can be very relaxing.
Clinical studies of HBOT will continue for some time. Many people with brain injury and their families hope it will someday be a proven therapy covered by insurance.
Two HBOT Success Storis
Bryan Gansner
A blast from an improvised explosive device blew up the vehicle carrying Army SSgt. Bryan Gansner in Iraq in 2006. While he was originally diagnosed with a mild brain injury, later scans showed it to be moderate. He also had PTSD.
Cheryl Gansner recalls that her husband had “behavioral problems, was very angry and forgetful. He was not performing well at work. He was kind of off, not himself.” For two years after he came home, he slept alone in the basement and remained removed and isolated. By 2009, “he hit rock bottom,” she says. The couple was close to divorce, and Bryan wanted to quit his job, move to his parents’ home, and do nothing. “He didn’t want kids because he thought he wouldn’t be a good enough father,” she says.
But a friend whose husband had undergone HBOT for brain injury with good results recommended it for Bryan. He was able to enroll in a clinical trial studying HBOT for brain injury in veterans, in New Orleans, and began treatment with 40 sessions in October 2009. When the study was over, he did 40 more. And Cheryl, program director for Hearts of Valor, a network of people caring for wounded, ill or injured service members, created and maintained by Operation Homefront, saw a huge difference in her husband.
“His depression and PTSD are way down,” she says. “His IQ rose six points, his anxiety is down considerably, his auditory memory and verbal skills are much improved.” His sleep also improved dramatically, and his medication dosages have been lowered. The Gansners are now awaiting the birth of their first child.
“I have my husband back,” says Cheryl. “We’re appreciative of the gains he made.”
Johnny Torres
Two weeks before his 21st birthday, Johnny Torres was struck by a vehicle near his home in Tucson. On active duty with the Army, he suffered a diffuse axonal injury to his brain, along with bleeding in his corpus callosum, leaving him in a coma for two weeks, and severely debilitated after that. He was bedridden, unable to swallow, talk, walk, or function independently in any way. His cognition was severely affected. He spent time at a local rehab hospital, then 90 days at the VA hospital in Palo Alto, Calif., and then another 90 at the Tucson VA hospital, says his mother, Diana Torres. Then we brought him home.”
Johnny required round-the-clock care, provided by Diana and paid caregivers. “He was combative, he would hit me and spit on me. Sometimes he would get me in a headlock and my husband would have to help me out,” she says. “I would pass out on the couch, I was so exhausted.”
Diana heard about HBOT but originally declined to put Johnny into treatment because of the high cost. But she later spoke with Dr. Carol Henricks, a Tucson neurologist who does HBOT and who Diana calls “an angel,” and decided the cost was worth it. He has now had nearly 400 sessions. Diana says her son is vastly improved.
“He is calmer and less combative,” she explains. “He eats everything, no longer drools. His cognition is good — he can watch TV and understand it. He’s started talking, and now says a new word nearly every day.” His pre-injury strength is returning, and he can push himself up and wrestle with his dad.
How many more treatments will he have? “I’m not going to stop,” says Diana. “I see miracles happening here.”
Reference:
Rockswald, SB, Rockswald, GL, Zaun, DA, Zhang, X, Cerra, CE, Bergman, TA, Liu, J (2010). A prospective randomized clinical trial to compare the effect of hyperbaric to normobarck hyperoxia on cerebral metabolism, intracranial pressure, and oxygen toxicity in severe traumatic brain injury. Journal of Neurosurgery 112(5): 1080-1094.
Posted on BrainLine August 10, 2013. Reviewed July 25, 2018.
Barbara Stahura, certified journal facilitator, is the coauthor, along with Susan B. Schuster, MA, CCC-SLP, of After Brain Injury: Telling Your Story, the first journaling book for people with brain injury. Editor of Brain Injury Journey, she presents journaling workshops around the country to people with brain injury, family caregivers, and others, and is a member of the faculty of the Therapeutic Writing Institute and the Lash & Associates speakers bureau. She lives in Indiana with her husband, Ken Willingham, a survivor of TBI. Used with permission from Brain Injury Journey magazine, issue #3, Lash & Associates Publishing/Training, Inc.
Comments (9)
Please remember, we are not able to give medical or legal advice. If you have medical concerns, please consult your doctor. All posted comments are the views and opinions of the poster only.
A research shows that hyperbaric treatment heal brain injuries faster. In hyperbaric chamber huge amount of oxygen flows enhances our tissue function and helps our bodies fight e.g. infection that’s been slowing down our healing.
How soon after a brain bleed do you wait to do hyperbaric treatment. Small bleed. Not getting larger. Think it will be absorbed by the brain in a month.
Hi all,
I would truly appreciate some feedback here. Having ton contact sports for many years in my youth I must have had probably 3 concussions over time that I know of. I have not done any contact sports or had any hits to the head in years and feel fine overall. However, there is always a concern if my brain maybe is not where it should be. But Again no symptoms that I can see at least... I want to still give this therapy a try, however 40-80 sessions is a lot and we all know costs a lot of money. I live in Montreal, Quebec Canada and we have a great center here. My question is 1) Is there ANY test you could recommend for me to do to see how my brain is doing prior to a treatment? 2) Would 10-15 treatments works for someone like me? Who like i said does not really have any issues but more fears the unlikely but still possible negative future due to past concussions. Thank you very much!
My fiance had a heart attack that causes her to have TBI, now she is fighting I would love to know more.
Heart attacks do not cause someone to have TBI. TBI stands for Traumatic Brain Injury, which is caused by Trauma. I believe that HBOT might help with any damage to heart muscle caused by the heart attack, so please look into this type of therapy to see if it will help.
you can suffer a hypoxic brain injury caused by the heart stopping and therefore not pumping blood. I have read reports that Hbot can help with this type of brain injury too.
@ Bogus, that is incorrect. The lack of oxygen supply to the brain during a heart attack causes a brain injury -- an "ABI" or acquired brain injury.
An acquired brain injury is an injury to the brain, which is not hereditary, congenital, degenerative, or induced by birth trauma. An acquired brain injury is an injury to the brain that has occurred after birth. Examples of ABI include stroke, near drowning, aneurysm, tumor, infectious disease that affects the brain (i.e., meningitis), lack of oxygen supply to the brain (i.e., heart attack).
A traumatic brain injury (TBI) is a type of acquired brain injury (ABI).
Where are these treatments being performed? If I wanted to get my mother who recently had cardiac arrest so was without oxegyn for a short period of time, treatment, where would I go?
Regarding oxygen for brain injury, there are a number of FDA approved alertness aids (Tirend, NoDoz, etc. - contain caffeine - 100 mg) which, for some, improve aspects of breathing. Coffee is used to treat some children with sleep apnea. | {
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RNA and Disease
RNA Disease
The goals of the RNA and Disease group are to identify and define the contribution of RNA to disease including viral and other pathogens.
Errors in RNA processing and maturation can lead to human disease. Increasingly errors in splicing, tRNA and snoRNA maturation, and other aspects of metabolism are identified that lead to disease. Viral and other pathogen RNAs play key roles in infection and regulation of host metabolism. Analyses of RNA in disease may provide new insights into the roles of RNA in biology and new avenues for disease treatment. Faculty participating in the RNA and Disease group currently have their primary homes in five different departments and medical divisions of the School of Medicine.
Additional faculty will be recruited to enhance this research area.
Drs. Eric Poeschla and Linda van Dyk head the RNA and Disease group.
Affiliated Faculty
David Barton, PhD Enterovirus RNA replication
David Bentley, PhD - The coordination of transcription with chromatin modification, splicing, and mRNA 3' end formation. How mRNA production in cancer cells becomes corrupted bt abnormal coupling of these pathways
Susan Boackle, MD Systemic lupus Erythematosis
Richard Davis, PhD RNA metabolism in parasitic helminths
Sujatha Jagannathan, PhD - How cells detect and degrade abberant RNAs, and how dysregulation of this surveillance process contributes to muscular dystrophy
Aaron Johnson, PhD - Molecular mechanisms of RNA-mediated epigenetic gene regulation in normal biology and metastatic breast cancer
Peter Kabos, MD Breast cancer RNA metabolism
Jeffrey Kieft, PhD - How RNAs form complex 3-D folds, the dynamic conformational changes they undergo, how these RNAs interact with other molecules, and how this drives diverse biological function in healthy and diseased cells. In particular, how viral RNAs manipulate host cell machinery
Traci Lyons, PhD- Mechanisms of therapeutic resistance and metastasis driven by pregnancy induced changes in gene and protein expression during mammary gland development
Neelanjan Mukherjee, PhD - Mechanisms by which RNA binding proteins (RBPs) and long non-coding RNA (lncRNAs) regulate human steroid production. Use genomic approaches to identify the targets of RBPs or lncRNA and the layer of RNA regulation they control
Eric Pietras PhD – RNA splicing alterations in myelodysplasia
Eric Poeschla, MD Viral replication, host innate immunity to viruses, and viral disease pathogenesis
Tania Reis, PhD - RNA and neuronal control of metabolism and obesity
Mario Santiago PhD – HIV gene expression
Carol Sartorius PhD – Hormone-dependent cancers
Jennifer Richer, PhD miRNAs in cancer
Lori Sussel, PhD Long non-coding RNAs in diabetes
Linda van Dyk, PhD Herpesvirus pathogenesis | {
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8,391,970,246,287,487,000 | Flat Warts Overview
By: Sarah Siddons
Flat warts aren't as big as common warts, but they're still a cosmetic problem. See more pictures of skin problems.
©iStockphoto.com/Claude Dagenais
These tiny, smooth spots on your skin are usually skin-colored -- pink, yellow or even light brown -- and difficult to see. They most often appear on your face, neck or legs. These spots may form in groups, with as many as one hundred or more in one area. Sometimes, they occur in a line or a circle. What we're talking about is flat warts.
Unlike common warts, which have a dome-shaped appearance, flat warts are usually flush with the skin's surface. They're smooth, while common warts are often rough. Flat warts tend to be smaller than other types of warts -- as small as 0.07 inches (0.2 centimeters) and often not larger than 0.39 inches (1 centimeter) [source: Intelihealth]. Unlike plantar warts, which grow on the bottom of feet, flat warts typically appear on men's and children's faces or on women's legs. In fact, they're much more commonly found on children and are sometimes called juvenile warts [source: KidsHealth].
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Flat warts, or Verruca plana, are more often a cosmetic problem or a slight inconvenience. They're considered a benign growth and don't normally cause pain, although sometimes they may itch [source: Warts Information Center]. Occasionally, they can become sore if they appear in an area where clothing is tight or rubs against the skin. Flat warts may disappear by themselves over time. However, because flat warts often appear in groups and on the face, people don't always want to wait for them to clear up. Moreover, because they're contagious, early treatment can prevent them from spreading [source: Intelihealth].
If you have flat warts, you might be wondering how to treat them effectively. If you think you have flat warts and want to know more about what causes them and the various treatments that are available for you, read on.
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Causes of Flat Warts
All warts -- including flat warts -- are caused by a virus known as human papillomavirus, or HPV. There are dozens of kinds of HPV, and the different warts caused by it tend to appear on various surfaces of the body. For the most part, flat warts are caused by HPV types 3, 10, 28 and 49. HPV is commonly transmitted by direct contact from one person to another. It's also possible for HPV to be transmitted indirectly. So, if you come into contact with the virus in a locker room, pool or other public place, you may get warts. In addition, once you have a wart, it's very easy to spread the virus from one place to another on your own body [sources: Intelihealth, Warts Information Center].
You're more susceptible to HPV if you've got a cut, scratch or some other opening in the skin. If you have a scratch or cut and it gets infected with HPV, it's likely that flat warts might appear along it. If you already have flat warts, be aware that they can easily spread to other areas of your body that may be scratched or cut [source: Merck].
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Another way that flat warts spread is through the act of shaving. Shaving with a razor is a daily routine for many people. However, since there's a chance you may nick yourself with the razor, shaving may encourage the spread of flat warts. For men, that means an outbreak on faces, and women may get them on their legs [source: Warts Information Center].
If you have a strong immune system, you already have a line of defense to combat flat warts. However, because warts are caused by viral infection, people whose immune systems are compromised by an autoimmune disorder or who are taking certain medications that weaken the immune system are more likely to get them.
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Treating Flat Warts
Although flat warts are inconvenient, most of them will go away on their own as the body's immune system targets the virus that causes them. This can takes months to several years. Treating individual warts does not prevent new ones from occurring if the virus is still active in the body. So, if the warts aren't causing you any pain and they're not spreading, it may be best to leave them alone.
Using over-the-counter wart treatments, such as products that contain salicylic acid, may be somewhat effective at removing individual warts. These products dissolve the epidermis, or the top layer of skin, and when they're used consistently over a long period of time can successfully remove the infected skin. Before applying the medicine, it's a good idea to soak the warts in warm water and scrub them with a pumice stone. This process removes the dead skin and allows the medication to make contact with the wart [source: VisualDx Health].
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However, if you have flat warts on your face or if the warts begin to spread quickly, consult a doctor. Doctors have access to a larger variety of treatment options, including cryotherapy (freezing off the warts), immunotherapy medications and medications that are injected directly into the wart [source: Cleveland Clinic].
If you have flat warts, hopefully you've learned a few ways to prevent them and treat them. If they're still not on their way out of your life, follow the links on the next page for more information.
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Lots More Information
Related HowStuffWorks Articles
Sources:
• Aetna InteliHealth. "Warts." (Accessed 8/5/2009) http://www.intelihealth.com/IH/ihtIH/WS/9339/10988.html
• American Academy of Family Physicians. "Duct Tape More Effective than Cryotherapy for Warts." 2/01/03. (Accessed 8/8/09). http://www.aafp.org/afp/20030201/tips/8.html
• Cleveland Clinic. "Warts: An Overview." (Accessed 8/5/2009)http://my.clevelandclinic.org/disorders/warts/hic_Warts_An_Overview.aspx
• Cleveland Clinic. "Warts: Treatment." (Accessed 8/5/2009)http://my.clevelandclinic.org/disorders/warts/derm_treatment.aspx
• Kidshealth from Nemours. "What's up With Warts?" (Accessed 8/6/2009)http://kidshealth.org/kid/ill_injure/aches/warts.html#
• Medical News Today. "Duct Tape and Other Treatments for Warts." (Accessed 8/5/2009)http://www.medicalnewstoday.com/articles/17335.php
• The Merck Manuals Online Medical Library. "Warts." (Accessed 8/5/2009)http://www.merck.com/mmpe/sec10/ch122/ch122c.html
• VisualDx Health. "Flat Wart: A parent's guide to condition and treatment information." (Accessed 8/6/2009)http://www.visualdxhealth.com/child/flatWart.htm
• Warts Information Center. "Flat Warts." (Accessed 8/6/2009)http://www.warts.org/flat-warts.html
• Warts Information Center. "Duct Tape Wart Removal." (Accessed 8/6/2009)http://www.warts.org/duct-tape-wart-removal.html
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3,096,286,296,164,110,300 | C5a<sub>1</sub> receptor | Complement peptide receptors | IUPHAR/BPS Guide to PHARMACOLOGY
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C5a1 receptor
target has curated data in GtoImmuPdb
Target id: 32
Nomenclature: C5a1 receptor
Family: Complement peptide receptors
Annotation status: image of a green circle Annotated and expert reviewed. Please contact us if you can help with updates. » Email us
Gene and Protein Information
class A G protein-coupled receptor
Species TM AA Chromosomal Location Gene Symbol Gene Name Reference
Human 7 350 19q13.3-q13.4 C5AR1 complement C5a receptor 1 35
Mouse 7 351 7 A1 C5ar1 complement component 5a receptor 1
Rat 7 352 1q12 C5ar1 complement C5a receptor 1
Previous and Unofficial Names
CD88 | C5A | C5AR | C5R1 | C5a anaphylatoxin chemotactic receptor | C5a-R | complement C5a receptor | complement component 5a receptor 1 | C5aR1
Database Links
Specialist databases
GPCRDB c5ar1_human (Hs), c5ar1_mouse (Mm), c5ar1_rat (Rn)
Other databases
ChEMBL Target
Ensembl Gene
Entrez Gene
Human Protein Atlas
KEGG Gene
OMIM
RefSeq Nucleotide
RefSeq Protein
UniProtKB
Wikipedia
Selected 3D Structures
Image of receptor 3D structure from RCSB PDB
Description: Structure of the complement C5a1 receptor (C5aR1) bound to the extra-helical antagonist NDT9513727.
PDB Id: 5O9H
Ligand: NDT9513727
Resolution: 2.7Å
Species: Human
References: 86
Natural/Endogenous Ligands
C5a {Sp: Human}
C3a {Sp: Human}
C5a {Sp: Mouse}
C3a {Sp: Mouse}
C5a {Sp: Rat}
C3a {Sp: Rat}
C5a des-Arg {Sp: Human}
ribosomal protein S19 {Sp: Human}
Comments: C5a anaphylatoxin has a higher potency than C3a anaphylatoxin
Potency order of endogenous ligands (Human)
C5a (C5, P01031), C5a des-Arg (C5) > C3a (C3, P01024) [2]
Download all structure-activity data for this target as a CSV file
Agonists
Key to terms and symbols View all chemical structures Click column headers to sort
Ligand Sp. Action Value Parameter Reference
[125I]C5a (human) Hs Full agonist 8.7 pKd 48
pKd 8.7 (Kd 2x10-9 M) [48]
C5a {Sp: Human} Hs Full agonist 8.0 – 9.0 pEC50 71,79
pEC50 8.0 – 9.0 (EC50 1x10-8 – 1x10-9 M) [71,79]
YSFKPMPLaR Hs Agonist 5.5 pEC50 114
pEC50 5.5 (EC50 3.24x10-6 M) [114]
C5a {Sp: Human} Hs Full agonist 9.1 – 9.2 pIC50 40,79
pIC50 9.1 – 9.2 [40,79]
NDT9513727 Hs Inverse agonist 7.9 pIC50 11
pIC50 7.9 (IC50 1.16x10-8 M) [11]
N-methyl-Phe-Lys-Pro-D-Cha-Cha-D-Arg-CO2H Hs Full agonist 7.6 pIC50 53,55
pIC50 7.6 [53,55]
C5a des-Arg {Sp: Human} Hs Partial agonist 6.2 – 6.4 pIC50 13,40
pIC50 6.2 – 6.4 [13,40]
YSFKPMPLaR Hs Full agonist 5.4 – 6.7 pIC50 28
pIC50 5.4 – 6.7 (IC50 4.2x10-6 – 2x10-7 M) [28]
lactomedin 1 Hs Agonist - - 105,117
[105,117]
Agonist Comments
YSFKPMPLaR is an agonist of both C5aR and C3aR. In addition to human cells it has been shown to have agonist actions in mice and rats [92,114]. RP S19 is an endogenous ribosomal protein, in the dimerised form it acts as an agonist of C5aR, however the referenced study [71] used recombinant protein. RP S19 gave a maximal reponse in a leukocyte chemotaxis assay at a concentration of 1nM [71]. Skp is a bacterial chaperone protein. IC50 values for agonists are derived from radioligand displacement assays.
Antagonists
Key to terms and symbols View all chemical structures Click column headers to sort
Ligand Sp. Action Value Parameter Reference
CHIPS Hs Antagonist 9.0 pKd 81
pKd 9.0 [81]
W54011 Hs Antagonist 8.7 pKi 95
pKi 8.7 [95]
NDT9520492 Hs Antagonist 7.5 pKi 104
pKi 7.5 [104]
avacopan Hs Antagonist 9.7 pIC50 9
pIC50 9.7 [9]
DF2593A Hs Antagonist 8.3 pIC50 67
pIC50 8.3 [67]
AcPhe-Orn-Pro-D-Cha-Trp-Arg Hs Antagonist 7.9 pIC50 108
pIC50 7.9 [108]
A8Δ71-73 Mm Antagonist 7.6 pIC50 78
pIC50 7.6 (IC50 2.7x10-8 M) [78]
PMX205 Hs Antagonist 7.5 pIC50 63
pIC50 7.5 (IC50 3.1x10-8 M) [63]
PMX53 Hs Antagonist 7.1 – 7.7 pIC50 63,114
pIC50 7.1 – 7.7 (IC50 9x10-8 – 2.1x10-8 M) [63,114]
N-methyl-Phe-Lys-Pro-D-Cha-Trp-D-Arg-CO2H Hs Antagonist 7.2 pIC50 55
pIC50 7.2 [55]
JPE1375 Hs Antagonist 7.0 pIC50 87
pIC50 7.0 (IC50 1.11x10-7 M) [87]
C089 Hs Antagonist 6.7 pIC50 55
pIC50 6.7 (IC50 2.01x10-7 M) [55]
RPR121154 Hs Antagonist 6.1 pIC50 6
pIC50 6.1 [6]
L-156,602 Hs Antagonist 5.7 pIC50 100
pIC50 5.7 [100]
View species-specific antagonist tables
Antagonist Comments
PMX53 is widely used as an parenterally- and orally-active antagonist of C5aR in mice and rats [82]. Although it has been demonstrated to block C5a binding in rat neutrophils (IC50 - 40nM), it does not inhibit C5a binding in murine cells [114]. However, it has specific C5aR antagonistic activity in vivo as demonstrated through comparisons with C5aR knockout mice [15]. PMX205 is also parenterally- and orally-active [82], but with greater lipophicity, and blood brain barrier penetrance than PMX53 [111-112]. PMX205 was also shown to be ineffective in C5aR knockout mice [51]. JPE1375 inhibits the chemotaxis of murine J774A.1 cells, but exhibits a reduced potency when compared to human neutrophils (IC50 - 420nM) [87]. A8 binds both C5aR and C5L2 with similar affinity, although the antagonistic properties of A8 at C5L2 remain untested [78]. In addition, other biologically relevant inhibitors of C5aR have been described. Chemotaxis inhibitory protein of S. aureus (CHIPS) is a 14.1 kDa antagonist of C5aR encoded on a bacteriophage. It has been demonstrated to have selective antagonistic properties against human C5aR in the micromolar concentration range [20].
CCX168 has been shown to be a high affinity small molecule antagonist of human C5a1 with an IC50 of 0.2nM, but the structure of this ligand has not been disclosed by the manufacturers ChemoCentryx [115].
Immunopharmacology Comments
C5aR is typically associated with the compement cascade and innate immunity.
MorphoSys have an anti-C5aR monoclonal antibody (MOR210) in preclinical development as an immuno-oncology agent. The goal of anti-C5aR therapy is to reduce the effects that activation of the C5a/C5aR axis has on promoting cancer cell migration and invasiveness [43,62,73-74].
Immuno Process Associations
Immuno Process: Inflammation
GO Annotations: Associated to 7 GO processes
GO:0006954 inflammatory response IBA
GO:0043312 neutrophil degranulation TAS
GO:0061888 regulation of astrocyte activation ISS
GO:1903978 regulation of microglial cell activation ISS
click arrow to show/hide IEA associations
GO:0010759 positive regulation of macrophage chemotaxis IEA
GO:0030593 neutrophil chemotaxis IEA
GO:0090023 positive regulation of neutrophil chemotaxis IEA
Immuno Process: Immune regulation
GO Annotations: Associated to 8 GO processes
GO:0002430 complement receptor mediated signaling pathway IBA
GO:0004878 complement component C5a receptor activity IDA
GO:0030449 regulation of complement activation TAS
GO:0038178 complement component C5a signaling pathway IDA
GO:0061888 regulation of astrocyte activation ISS
GO:1903978 regulation of microglial cell activation ISS
click arrow to show/hide IEA associations
GO:0010759 positive regulation of macrophage chemotaxis IEA
GO:0090023 positive regulation of neutrophil chemotaxis IEA
Immuno Process: Chemotaxis & migration
GO Annotations: Associated to 3 GO processes
click arrow to show/hide IEA associations
GO:0010759 positive regulation of macrophage chemotaxis IEA
GO:0030593 neutrophil chemotaxis IEA
GO:0090023 positive regulation of neutrophil chemotaxis IEA
Immuno Process: Cellular signalling
GO Annotations: Associated to 5 GO processes
GO:0002430 complement receptor mediated signaling pathway IBA
GO:0004878 complement component C5a receptor activity IDA
GO:0038178 complement component C5a signaling pathway IDA
GO:0043312 neutrophil degranulation TAS
GO:1903978 regulation of microglial cell activation ISS
Immuno Process: Cytokine production & signalling
GO Annotations: Associated to 1 GO processes, IEA only
click arrow to show/hide IEA associations
GO:0010575 positive regulation of vascular endothelial growth factor production IEA
Primary Transduction Mechanisms
Transducer Effector/Response
Gi/Go family
G protein (identity unknown)
Phospholipase C stimulation
Other - See Comments
Comments: Studies of C5aR signalling have determined cell-specific activation of downstream pathways. For instance, in macrophages C5aR signals via protein kinase C (PKC) δ to induce NFκB activation and translocation to the nucleus, whereas in neutrophils C5aR induces activation of IκB, the NFκB inhibitor [37]. Additionally, activated C5aR has also been shown to associate with Wiskott-Aldrich Syndrome Protein (WASP), a regulator of Rho-GTPases and therefore, cytoskeletal turnover [98]. In mesenchymal stem cells C5a induces a chemotaxis that is pertussis toxin sensitive, indicating a Gi mediated response, and signalling via MAPK and Akt pathways [88]. C5aR has also been demonstrated to cause transactivation of the epidermal growth factor (EGF) receptor in human umbilical vein endothelial cells [89]. Heterodimer formation with C5a2 modulates signalling through C5a1, resulting in altered cytokine responses in human macrophages [16].
References: 93
Secondary Transduction Mechanisms
Transducer Effector/Response
Gq/G11 family Phospholipase C stimulation
References: 59
Tissue Distribution
Mast cell subsets.
Species: Human
Technique: Immunocytochemistry.
References: 77
Cardiomyocytes
Species: Human
Technique: Northern blot
References: 38,107
Connective Tissue (synoviocytes, articular chondrocytes)
Species: Human
Technique: RT-PCR, immunocytochemistry
References: 76,118
Central Nervous System (astrocytes, microglia, neuron, neural stem cells, oligodendrocytes)
Species: Human
Technique: Immunohistochemistry
References: 34
Lung
Species: Human
Technique: Immunohistochemistry
References: 38
Liver
Species: Human
Technique: Northern blot
References: 38
Myeloid Leukocytes (neutrophil, eosinophil, basophil, monocytes)
Species: Human
Technique: Immunohistochemistry
References: 42,94
Vascular endothelial cells
Species: Human
Technique: Immunohistochemistry
References: 38
Vascular smooth muscle
Species: Human
Technique: Immunohistochemistry
References: 38,79
Eye (retinal pigment epithelial cells)
Species: Human
Technique: Flow cytometry
References: 32
Kidney
Species: Human
Technique: Immunohistochemistry
References: 34,70,75,83
Microvascular endothelial cells.
Species: Mouse
Technique: Radioligand binding.
References: 58
Central Nervous System (astrocytes, microglia, neuron, neural stem cells, oligodendrocytes)
Species: Mouse
Technique: Immunohistochemistry
References: 70,75,83
Central Nervous System (astrocytes, microglia, neuron, neural stem cells, oligodendrocytes)
Species: Rat
Technique: Immunohistochemistry
References: 70,75,83
Oligodendrocytes.
Species: Rat
Technique: RT-PCR.
References: 70
Tissue Distribution Comments
C5a1 was not found in pulmonary, hepatic, and intestinal epithelial cells, or lymphocytes in humans when examined with immunohistochemistry [25-26]. Although it has been previously reported that lymphocytes do not express C5aR, Lalli and colleagues (2008)[57] demonstrated a role for C5aR in T-cell survival. The techniques employed involved the use of a C5aR knockout mouse and a C5aR antagonist, to infer a function for C5aR on T-cells. No direct expression of either C5aR transcript or protein was demonstrated in this study. In addition, a recent study describing a GFP knock-in mouse, under the control of the C5aR promotor, failed to show GFP expression in either naïve or activated T-lymphocytes [23].
Expression Datasets
Show »
Log average relative transcript abundance in mouse tissues measured by qPCR from Regard, J.B., Sato, I.T., and Coughlin, S.R. (2008). Anatomical profiling of G protein-coupled receptor expression. Cell, 135(3): 561-71. [PMID:18984166] [Raw data: website]
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Functional Assays
Chemotaxis
Species: Human
Tissue: Granulocytes, monocytes, RBL-2H3 C5aR transfected cells
Response measured: Migration of cells up concentration gradient
References: 18,22,79,88
Smooth muscle contraction
Species: Human
Tissue: Human umbilical artery
Response measured: Contraction of smooth muscle
References: 14,79
ERK1/2 phosphorylation
Species: Human
Tissue: Mesenchymal stem cell, C5aR-transfected CHO cells, neutrophils
Response measured: Increase in Phospho-ERK1/2 by Western blot
References: 84,88,97
Enzyme Release/Degranulation
Species: Human
Tissue: Neutrophils, RBL-2H3 C5aR transfected cells
Response measured: Increase in myeloperoxidase, hydrogen peroxide (?peroxidase) and b-hexosaminidase release
References: 46,65,79
Intracellular calcium release
Species: Human
Tissue: Neutrophils, monocytes, HMC-1 cells, U937 cells, Rat hippocampal neurons
Response measured: Transient increase in intracellular calcium concentrations upon receptor activation.
References: 72,75
Measurement of degranulation in rat basophilic leukemia cells transfected with the human C5a receptor.
Species: Human
Tissue: Rat basophilic leukemia cells.
Response measured: Degranulation.
References: 41
Physiological Functions
Chemotaxis.
Species: Human
Tissue: Granulocyte.
References: 66
Hepatocyte growth factor.
Species: Rat
Tissue: Liver.
References: 19
MAP kinase activation.
Species: Mouse
Tissue: Pituitary.
References: 31
Chemotaxis.
Species: Human
Tissue: Lymphocyte subsets.
References: 56
NF-κB activation.
Species: Human
Tissue: Neurons.
References: 75
Neutrophil extravasation
Species: Mouse
Tissue: Brain
References: 90
Neutropaenia
Species: Rat
Tissue: Blood
References: 91
Cell survival
Species: Human
Tissue: T-Lymphocytes
References: 57
Proliferation
Species: Rat
Tissue: Cerebellar granular neurons
References: 12
Chemotaxis
Species: Human
Tissue: T cells, mesenchymal stem cells, dermal microvascular endothelial cells
References: 69,88
Apoptosis under oxygen/glucose deprivation
Species: Mouse
Tissue: Cortical neurons
References: 80
Chemokine (CCL2, CXCL2) release
Species: Mouse
Tissue: Microvascular endothelial cells
References: 58
Chemokine (IL-8) release
Species: Human
Tissue: Epithelial cells (lung, eye)
References: 32,38
Histamine release
Species: Human
Tissue: Mast cells, basophils
References: 33
Degranulation
Species: Human
Tissue: Neutrophils, mast cells
References: 39,46,79
Physiological Consequences of Altering Gene Expression
Mice with receptor knockout exhibit increased susceptibility and lethality to Pseudomonas aeruginosa infection.
Species: Mouse
Tissue: Lung
Technique: Gene knockouts
References: 50
Adenovirus-mediated in vivo silencing of the C5a receptor.
Species: Mouse
Tissue:
Technique: RNA interference
References: 96
Human C5a receptor knock-in mice facilitate the production and assessment of anti-inflammatory monoclonal antibodies.
Species: Mouse
Tissue:
Technique: Transgenesis
References: 60
In rat models of induced sepsis using cecal ligation and puncture (CLP), those rats treated with antibodies against C5aR showed reduced levels of bacteraemia and improved survival rates.
Species: Rat
Tissue: Neutrophils
Technique: Antibody targeting of the receptor
References: 17,45,47
C5aR blocking antibody-treated or C5aR-/- mice, increased survival and decreased serum proinflammatory cytokines in the caecal ligation and puncture model of sepsis. C5aR blocking antibody also reduces bacteraemia, as measure by bacterial colony forming units in blood, this is likely due to an impairment of neutrophil phagocytic activity in the presence of high C5a concentrations
Species: Mouse
Tissue: Neutrophils
Technique: Antibody treatment and gene knockout
References: 85
In a dextran sulphate-induced colitis mouse model, C5AR1 knockout mice showed reduced severity of symptoms and lower expression of inflammatory mediators compared to wildtype controls. However, in chronic colitis, the pathology of C5aR-deficient mice worsens.
Species: Mouse
Tissue: Cecum and colon
Technique: Gene knockouts
References: 52
In a rat model of TNBS induced colitis, treatment with the C5aR antagonist, PMX53, reduced pathology and mortality.
Species: Rat
Tissue: Cecum and colon
Technique: Treatment with receptor antagonist
References: 109
Phenotypes, Alleles and Disease Models Mouse data from MGI
Show »
Allele Composition & genetic background Accession Phenotype Id Phenotype Reference
C5ar1tm1Cge C5ar1tm1Cge/C5ar1tm1Cge
involves: 129S4/SvJae
MGI:88232 MP:0001800 abnormal humoral immune response PMID: 8781237
C5ar1tm1Cge C5ar1tm1Cge/C5ar1tm1Cge
involves: 129S4/SvJae
MGI:88232 MP:0008719 impaired neutrophil recruitment PMID: 8779720
C5ar1tm1Cge C5ar1tm1Cge/C5ar1tm1Cge
involves: 129S4/SvJae
MGI:88232 MP:0009763 increased sensitivity to induced morbidity/mortality PMID: 8779720
C5ar1tm1Raw C5ar1tm1Raw/C5ar1tm1Raw
B6.Cg-C5ar1
MGI:88232 MP:0008481 increased spleen germinal center number PMID: 18455242
C5ar1tm1Cge C5ar1tm1Cge/C5ar1tm1Cge
involves: 129S4/SvJae
MGI:88232 MP:0002412 increased susceptibility to bacterial infection PMID: 8779720
Clinically-Relevant Mutations and Pathophysiology
Disease: Alzheimer disease
Synonyms: Alzheimer's disease [Disease Ontology: DOID:10652]
Disease Ontology: DOID:10652
OMIM: 104300
Comments:
References: 1,30
Disease: Amyotrophic lateral sclerosis
Disease Ontology: DOID:332
Orphanet: ORPHA803
Comments:
References: 27,49,110
Disease: Antiphospholipid syndrome
Disease Ontology: DOID:2988
OMIM: 107320
Orphanet: ORPHA80
Role:
References: 36,106
Disease: Huntington disease
Synonyms: Huntington's disease [Disease Ontology: DOID:12858]
Disease Ontology: DOID:12858
OMIM: 143100
Comments:
References: 111
Disease: Immunoglobulin A vasculitis
Synonyms: Henoch-Schönlein Purpura [Disease Ontology: DOID:11123]
Disease Ontology: DOID:11123
Orphanet: ORPHA761
Comments:
References: 24
Click column headers to sort
Type Species Amino acid change Nucleotide change Description Reference
Single nucleotide polymorphism Human c.450C>T 24
Disease: Injury aggravation in neurotrauma
Role:
References: 8,90
Disease: Ischemia-reperfusion injury
Role:
References: 3-5,21,29,61,102,116,119
Disease: Psoriasis
Description: A long-term autoimmune disease characterized by patches of red, itchy, and scaly skin. Five types of psoriasis are recognised: plaque (psoriasis vulgari), guttate, inverse, pustular, and erythrodermic, with plaque psoriasis being the most common type.
Disease Ontology: DOID:8893
Role:
References: 10,68
Disease: Rheumatoid arthritis
Disease Ontology: DOID:7148
OMIM: 180300
Role:
References: 103,113
Clinically-Relevant Mutations and Pathophysiology Comments
The reported association of a C5aR polymorphism with Henoch-Schonlein purpura occurred in a population of patients with familial mediterranean fever. The C/T polymorphism is at base 450 in the coding sequence of C5aR. The association was noted, but the population size was insufficient to draw definitive conclusions [24]. Two other C5aR polymorphisms have been described but have no observable phenotype [7,99].
Gene Expression and Pathophysiology
A reduction in the expression of C5AR1 on neutrophils, with increased levels in serum was seen in patients with progressive sepsis.
Tissue or cell type: Neutrophils and serum
Pathophysiology: Sepsis
Species: Human
Technique: Immunoblotting and flowcytometic analysis
References: 44,101
General Comments
Although C5aR is typically associated with the innate immune system, recently research on the receptor has elucidated novel roles. C5aR has been demonstrated on adult neural progenitor cells [83], mesenchymal stem cells [88] and perhaps has roles regulating the cell cycle in types of cancer [54,64].
References
Show »
1. Ager RR, Fonseca MI, Chu SH, Sanderson SD, Taylor SM, Woodruff TM, Tenner AJ. (2010) Microglial C5aR (CD88) expression correlates with amyloid-beta deposition in murine models of Alzheimer's disease. J. Neurochem., 113 (2): 389-401. [PMID:20132482]
2. Ames RS, Nuthulaganti P, Kumar C. (1996) In Xenopus oocytes the human C3a and C5a receptors elicit a promiscuous response to the anaphylatoxins. FEBS Lett., 395 (2-3): 157-9. [PMID:8898085]
3. Arumugam TV, Shiels IA, Strachan AJ, Abbenante G, Fairlie DP, Taylor SM. (2003) A small molecule C5a receptor antagonist protects kidneys from ischemia/reperfusion injury in rats. Kidney Int., 63 (1): 134-42. [PMID:12472776]
4. Arumugam TV, Woodruff TM, Lathia JD, Selvaraj PK, Mattson MP, Taylor SM. (2009) Neuroprotection in stroke by complement inhibition and immunoglobulin therapy. Neuroscience, 158 (3): 1074-89. [PMID:18691639]
5. Arumugam TV, Woodruff TM, Stocks SZ, Proctor LM, Pollitt S, Shiels IA, Reid RC, Fairlie DP, Taylor SM. (2004) Protective effect of a human C5a receptor antagonist against hepatic ischaemia-reperfusion injury in rats. J. Hepatol., 40 (6): 934-41. [PMID:15158333]
6. Astles PC, Brown TJ, Cox P, Halley F, LockeyPM, McCarthy C, McLayIM, Majid TN, Morley AD, Porter B et al.. (1997) New non-peptide C5a receptor antagonists. Bioorg Med Chem Lett., 7 (77): 907-912.
7. Barnes KC, Caraballo L, Muñoz M, Zambelli-Weiner A, Ehrlich E, Burki M, Jimenez S, Mathias RA, Stockton ML, Deindl P et al.. (2004) A novel promoter polymorphism in the gene encoding complement component 5 receptor 1 on chromosome 19q13.3 is not associated with asthma and atopy in three independent populations. Clin. Exp. Allergy, 34 (5): 736-44. [PMID:15144465]
8. Beck KD, Nguyen HX, Galvan MD, Salazar DL, Woodruff TM, Anderson AJ. (2010) Quantitative analysis of cellular inflammation after traumatic spinal cord injury: evidence for a multiphasic inflammatory response in the acute to chronic environment. Brain, 133 (Pt 2): 433-47. [PMID:20085927]
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Liam Coulthard, Owen Hawksworth, Trent M. Woodruff.
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3,333,570,340,242,691,600 | Tooth Meridian Chart: Is It Legit? What Is It Good For?
You may have heard that tooth meridian charts can explain why you’re having specific health problems. It’s tempting to believe that a simple dental procedure could cure an ongoing chronic illness.
But is there any truth to the tooth meridian chart? And what is a meridian chart, anyway?
The tooth meridian chart derives from the marriage between Western dentistry and traditional Eastern medicine. It’s used to explain how the body’s energy may link problems in the mouth to other areas of the body.
Most people associate meridians with acupuncture, but some biological dentists believe they may be affecting your oral health, too.
There isn’t much scientific evidence that energy running through meridians in your teeth affects the rest of your body. However, some recent evidence suggests that acupuncture meridians may be related to connective tissue planes throughout the body.
In other words, there may be a physiological basis for some parts of the meridians.
We want to provide you with some basic information about tooth meridians to empower you to make your own decisions about your oral health.
What is a Meridian Tooth Chart?
What are meridians? According to traditional Chinese medicine (TCM), meridians are channels that carry vital energy, or qi, throughout the whole body. When your qi is blocked, it can keep your body’s organs from working properly.
Acupuncturists and energy healers work to unblock the qi so energy flows freely and your body can heal itself.
There are 12 primary meridians in TCM. They are:
1. Heart
2. Pericardium
3. Triple-burner
4. Lung
5. Stomach
6. Large intestine
7. Small intestine
8. Liver
9. Gallbladder
10. Spleen
11. Kidney
12. Bladder
Do teeth have meridians? According to traditional Chinese medicine, yes, certain teeth are associated with each of the body’s meridians. A tooth-organ relationship chart shows you which meridians are associated with each tooth and organ in the body.
Is the Meridian Tooth Chart real?
The meridian tooth chart isn’t supported by modern science, but many say that it has still helped their patients.
Holistic dentists who follow the chart say they’ve helped their patients overcome diseases and illnesses with proper dental care. Some even claim they’ve avoided giving root canals by addressing problems in the body first.
What is the purpose of the Meridian Tooth Chart?
The meridian tooth chart explains how toothaches and other dental problems can signify ailments somewhere else in the body.
For example, a toothache in the tooth associated with the intestine could be a sign of chronic digestive problems. Or, damage to one of the teeth connected to the kidneys could create kidney problems for that patient.
(Reminder: The evidence for tooth meridians is anecdotal, but if you’re worried about what’s going on in your mouth or body, book an appointment with Rejuvenation Dentistry.)
Which tooth corresponds to which organ?
What teeth are connected to what organs? Here are the teeth that are associated with some of the body’s major organs:
• Which tooth is associated with the heart? Wisdom teeth (third molars) on both the upper and lower jaws are associated with the heart.
• What is the significance of the tooth corresponding to the stomach? The molars on the upper jaw and premolars on the lower jaw are associated with the stomach meridian. A toothache or other problem with those teeth could indicate stomach issues, according to traditional Chinese medicine.
Other organs on the tooth-meridian chart:
• Lungs: upper premolars, lower first (front), and second (back) molars
• Large intestine: premolars
• Small intestine: wisdom teeth
• Liver: canine teeth
• Gallbladder: canine teeth
• Spleen: lower left premolars, upper left molars
• Kidney: upper first (inside) incisors, right lower second (outside) incisor
• Bladder: all incisors on both jaws
How Oral Health Influences Overall Health
Regardless of whether tooth meridians actually exist, your oral health absolutely influences your overall health.
Many studies have shown that problems with your teeth and gums can create chronic health conditions in the rest of the body. Harmful germs in your mouth release chemicals that promote inflammation throughout your body, which can cause many problems.
Damaged or missing teeth can also affect the quality of the food you eat. Many fiber- and nutrient-rich foods are crunchy or hard and take time to chew. If it’s difficult for you to eat, you’ll be more likely to eat low-fiber, nutrient-poor, high-sugar foods.
Your poor diet can then create even more problems and negatively affect your health.
Here are some chronic diseases that have been linked to poor oral health:
• Cardiovascular disease
• Pneumonia
• Diabetes
• Alzheimer’s disease and dementia
• Osteoporosis
• Premature birth and low birth weight
• Mental health
Cardiovascular Disease
Having periodontal disease and gum inflammation increases your risk of getting cardiovascular disease by about 20%. If you’re not taking care of your mouth, you’re also at a higher risk of actually dying from cardiovascular disease.
Pneumonia
Poor gum health can make you 3.9 times as likely to develop pneumonia. Proper oral care similarly lowers the risk of elderly patients getting pneumonia. So, brush and floss to protect your lungs.
Diabetes
You’re more likely to have gum inflammation and gum disease if you have diabetes. That inflammation can actually make your diabetes worse. Inflammation from diabetes can lead to other dental health problems, too.
High blood sugar caused by uncontrolled diabetes can cause tooth infections and lesions that lead to bone loss. Uncontrolled diabetes can also lead to tooth infections. If you’re a diabetic, you absolutely must take care of your mouth.
Alzheimer’s Disease and Dementia
Recent research has shown a strong link between chronic gum disease and Alzheimer’s disease. Germs in the mouth cause inflammation throughout the body, leading to dementia and Alzheimer’s.
Osteoporosis
When you have osteoporosis, you lose bone density throughout your body, including in your jaw. Bone loss in the jaw brought on by osteoporosis can cause tooth loss and other dental problems.
Premature Birth and Low Birth Weight
Pregnant women with chronic gum disease are more likely to deliver their babies prematurely. Those babies are also more likely to have low birth weight (weighing less than 5.5 pounds).
The bacteria in the mother’s mouth release toxins, which make their way into the bloodstream. The body reacts to the toxins by making inflammatory chemicals to help fight the bacteria.
In the placenta, however, the inflammatory chemicals are toxic. Too many of these chemicals can cause the uterine membranes to rupture, leading to the premature birth of a smaller baby.
Mental Health
Poor oral health can have a significant impact on your mental health. If you’re not happy with your smile, it will completely change how you look at yourself. Having a cosmetic dental procedure done can raise your self-esteem.
Many people also experience dental anxiety. All the anxiety around dental procedures can absolutely harm your mental health. The fear and worry can build up over time, leading to depression and other serious mental health problems.
Your mental health can also affect your oral health. If you’re not well mentally, it’s hard to take care of your mouth and teeth. People with severe mental health problems are far more likely to lose all of their teeth than the general public. Specific mental illnesses like eating disorders can also cause direct damage to the teeth and mouth.
Rejuv Dentistry: Your #1 Biological Dentist
Your dental and oral health have a huge effect on your overall physical health. The doctors in our dental practice use biological dentistry, which focuses on the mouth-body connection.
Our founder, Dr. Gerry Curatola, DDS, is a pioneer in biological dentistry. He created Rejuvenation Dentistry to bring holistic dentistry to the people of New York and beyond.
We believe that many of the body’s problems can be corrected through proper dental care. For example, gum disease can cause inflammation throughout the body, leading to many chronic health issues.
We work with new patients (even anxious patients) to heal gum disease, remove toxic fillings, and care for the whole body by promoting oral health.
We would love to talk to you about biological dentistry and how it can help improve your health and wellness. Click here to get in touch with us and schedule your first visit.
Dr. Gerry Curatola is a renowned biologic restorative dentist with more than 40 years of clinical practice experience.
He studied neuroscience at Colgate University and attended dental school at the New York University (NYU) College of Dentistry where he now serves as Adjunct Clinical Associate Professor in the Department of Cariology and Comprehensive Care. | {
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-2,039,911,459,444,233,700 | Being out of shape increases your risk of health conditions, interferes with sleep, lowers your self-esteem and hinders weight loss goals. Starting a workout routine is a healthy way to counteract these complications, according to the Mayo Clinic. Talk to your doctor before starting a new exercise routine, particularly if you are overweight or have health problems. This allows you to create an appropriate workout schedule together.
Assess Your Health Status
If you are out of shape, taking stock of your current health status allows you choose exercise that works with your health and fitness goals. The Mayo Clinic website recommends checking your pulse rate, timing how long it takes to walk a mile, counting how many push-ups you are able to complete and how far you are able to reach forward while sitting on the floor. In addition, your body measurements and body mass index are important numbers for helping create an effective workout routine.
Make a Plan
If you're new to exercise, creating a workout plan is a good way to organize your exercise schedule and ensure that you stick with the program you've chosen. Being out of shape likely means you've been avoiding exercise for some time, making it important to incorporate it into your daily schedule. Write down what time you'll exercise so you're prepared with your equipment when the time comes. Over time, exercising will become routine and easier to stick with.
Start Slow
One of the biggest mistakes people make when beginning a new exercise routine is to start with an intensity they aren't ready for, according to Alaleh K. Selkirk, author of "Subjective Well-Being and Exercise." Starting slow and adding to your workout as you build strength and endurance is important for preventing injury and maximizing the benefits of exercise. Start with several minutes of light stretching followed by a low-impact workout a few minutes each day, suggests the Mayo Clinic website. You might find that your workout only lasts for 10 minutes at the beginning, but that time increases as you get into better shape.
Types of Exercise
Some forms of exercise aren't appropriate if you aren't in good shape. For example, you aren't likely ready for extended periods of running or climbing. Instead, choose forms of exercise that are easy on your body and help you gain endurance. Walking, biking, swimming and lifting light hand weights are good options for beginners. If you feel sick or in pain, stop and contact your doctor.
References
Photo Credits
• Creatas/Creatas/Getty Images
About the Author
Eliza Martinez has written for print and online publications. She covers a variety of topics, including parenting, nutrition, mental health, gardening, food and crafts. Martinez holds a master's degree in psychology.
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-5,741,754,760,135,971,000 | Telegram Äçåí Vkontakte Îäíîêëàññíèêè
Äæåððè Áðåéíàì (Jerry Brainum)
Áîäèáèëäèíã è óãëåâîäû
Äâóìÿ ãëàâíûìè èñòî÷íèêàìè ýíåðãèè äëÿ òðåíèðîâîê áîäèáèëäåðà ñëóæàò óãëåâîäû è æèðû. Ïðîòåèí òîæå ìîæåò áûòü èñïîëüçîâàí, íî âåñüìà íåýôôåêòèâíî. Îðãàíèçì íå îáðàùàåòñÿ ê ïðîòåèíó, åñëè â íàëè÷èå åñòü äðóãèå èñòî÷íèêè òîïëèâà. Ýòî êàñàåòñÿ â ïåðâóþ î÷åðåäü óãëåâîäîâ, ïîòîìó ÷òî ñêîðîñòü óñâîåíèÿ æèðîâ îãðàíè÷åíà ñïîñîáíîñòÿìè ìûøö.
Æèðû îðãàíèçìà ÷åëîâåêà, âçÿòûå âìåñòå, ñïîñîáíû îáåñïå÷èòü ýíåðãèåé ñåìü äíåé óìåðåííî èíòåíñèâíûõ óïðàæíåíèé, ïî ñðàâíåíèþ ñî âñåãî ëèøü äâóìÿ äíÿìè, íà êîòîðûå õâàòèò âñåõ çàïàñîâ ãëèêîãåíà è ãëþêîçû â êðîâè. Ïðîáëåìà â òîì, ÷òî ñ óâåëè÷åíèåì èíòåíñèâíîñòè òðåíèðîâîê èñïîëüçîâàíèå îðãàíèçìîì æèðîâ äëÿ ïîëó÷åíèÿ ýíåðãèè ñíèæàåòñÿ. Äëÿ âûñîêîèíòåíñèâíûõ òðåíèðîâîê, êàê íàïðèìåð â áîäèáèëäèíãå, óãëåâîäû ñëóæàò îñíîâíûì èñòî÷íèêîì òîïëèâà.
Ãëàâíàÿ
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Óãëåâîäû ñîõðàíÿþòñÿ â ïå÷åíè è ìûøöàõ â âèäå ãëèêîãåíà, îäíàêî, ãëèêîãåí îïðåäåëåííîé ìûøöû ìîæåò áûòü èñïîëüçîâàí òîëüêî åþ. Êîãäà åãî çàïàñû èñòîùàþòñÿ, íàñòóïàåò óòîìëåíèå.  ìûøöàõ ñîäåðæèòñÿ îêîëî 79% âñåãî ãëèêîãåíà îðãàíèçìà, à â ïå÷åíè ïðèìåðíî 14%.  êðîâè â âèäå ñàõàðà öèðêóëèðóåò ñåìü ïðîöåíòîâ óãëåâîäîâ. ×åì âûøå èíòåíñèâíîñòü óïðàæíåíèé, òåì ìåíüøå çàïàñîâ ãëèêîãåíà îñòàåòñÿ â ìûøöàõ.
Îäíî èç èññëåäîâàíèé ïîêàçàëî, ÷òî âûïîëíåíèå òðåõ ñåòîâ ñãèáàíèé ðóê äî îòêàçà íà 70% èñòîùàåò ìûøå÷íûé ãëèêîãåí â áèöåïñå.
Òåïåðü âñïîìíèòå, ñêîëüêî òàêèõ ñåòîâ âûïîëíÿåòå âû?
Ïîïûòêà òðåíèðîâàòüñÿ ñ èñòîùåííûìè çàïàñàìè ãëèêîãåíà îøèáî÷íà ïî íåñêîëüêèì ïðè÷èíàì. Âî-ïåðâûõ, ìûøöû íå ìîãóò ïîëíîöåííî âîññòàíîâèòüñÿ ìåæäó òðåíèðîâêàìè, åñëè çàïàñû ãëèêîãåíà ïîëíîñòüþ íå âîññòàíîâëåíû, ÷òî äîñòèãàåòñÿ àäåêâàòíûì ïîòðåáëåíèåì óãëåâîäîâ. Ìíîãèå ñïîðòèâíûå ó÷åíûå ñ÷èòàþò, ÷òî ñåðüåçíî òðåíèðóþùèéñÿ àòëåò äîëæåí ïîëó÷àòü ñåìü ãðàìì óãëåâîäîâ íà êàæäûé êèëîãðàìì âåñà òåëà, ÷òîáû íàâåðíÿêà âîññòàíîâèòü çàïàñû ãëèêîãåíà ê ñëåäóþùåé òðåíèðîâêå. Âû íå ñìîæåòå äîñòè÷ü õîðîøåé èíòåíñèâíîñòè áåç ñòîïðîöåíòíûõ çàïàñîâ ìûøå÷íîãî ãëèêîãåíà. Óòîìëåíèå íàñòóïèò ãîðàçäî ðàíüøå îáû÷íîãî, à ìûøå÷íàÿ íàêà÷êà áóäåò çíà÷èòåëüíî ñëàáåå. Ê òîìó æå, íà ôîíå íèçêèõ çàïàñîâ ãëèêîãåíà âåðîÿòíîñòü òðàâìû çíà÷èòåëüíî âîçðàñòàåò èç-çà ïîäàâëåííûõ ðåàêöèé íåðâíîé ñèñòåìû.
Óãëåâîäû ïåðåä òðåíèðîâêîé
Ïîòðåáëåíèå óãëåâîäîâ çà äâà ÷àñà äî òðåíèðîâêè ñïîñîáíî ïîìî÷ü â íåêîòîðîé ñòåïåíè âîññòàíîâèòü ìûøå÷íûé ãëèêîãåí, îäíàêî, äëÿ ïîëíîãî âîññòàíîâëåíèÿ ïîòðåáóåòñÿ 24-48 ÷àñîâ. Òåì íå ìåíåå, ïîòðåáëåíèå ïèùè ïåðåä òðåíèðîâêîé ïîäíèìàåò óðîâåíü ãëþêîçû â êðîâè, ñîçäàâàÿ âïå÷àòëåíèå ýíåðãè÷íîé òðåíèðîâêè. Îáû÷íî ðåêîìåíäóþò ïîòðåáëÿòü íèçêîãëèêåìè÷íûå óãëåâîäû, òî åñòü òå, êîòîðûå íå âûçûâàþò çíà÷èòåëüíîãî ïîäúåìà èíñóëèíà. Óãëåâîäû ñ âûñîêèì ãëèêåìè÷åñêèì èíäåêñîì ïåðåä òðåíèðîâêîé ìîãóò ñïðîâîöèðîâàòü óñêîðåííîå íàñòóïëåíèå óòîìëåíèÿ â õîäå òðåíèðîâêè â ðåçóëüòàòå ïîíèæåíèÿ óðîâíÿ ãëþêîçû â êðîâè, áëàãîäàðÿ ïîâûøåííîé àêòèâíîñòè èíñóëèíà.
Ïîòðåáëåíèå íåêîòîðîãî êîëè÷åñòâà ïðîòåèíà ïåðåä òðåíèðîâêîé – ýòî õîðîøàÿ èäåÿ, åñëè åãî ñîïðîâîæäàþò óãëåâîäû. Àìèíîêèñëîòû ñ ðàçâåòâëåííûìè öåïî÷êàìè ÂÑÀÀ - ëåéöèí, èçîëåéöèí è âàëèí - ïðåïÿòñòâóþò ïîñòóïëåíèþ â ìîçã äðóãîé àìèíîêèñëîòû – L-òðèïòîôàíà. Óãëåâîäû æå ñïîñîáñòâóþò òðàíñïîðòó L-òðèïòîôàíà â ìîçã, ïðîâîöèðóÿ âûñâîáîæäåíèå èíñóëèíà.  ìîçãå òðèïòîôàí êîíâåðòèðóåòñÿ â ñåðîòîíèí, óñïîêàèâàþùèé íåéðîòðàíñìèòòåð, êîòîðûé ìîæåò óñêîðèòü íàñòóïëåíèå óòîìëåíèÿ âî âðåìÿ òðåíèðîâêè, îñîáåííî êîãäà îíà äëèòñÿ äîëåå ÷àñà. Áëîêèðóÿ äàííûé ýôôåêò òðèïòîôàíà, ÂÑÀÀ îòîäâèãàþò ìîìåíò íàñòóïëåíèÿ óòîìëåíèÿ.
Êàê íàñ÷åò ïîòðåáëåíèÿ óãëåâîäîâ âî âðåìÿ òðåíèðîâêè?
Íåêîòîðûå èññëåäîâàíèÿ ïîêàçàëè, ÷òî ïîòðåáëåíèå íàïèòêà ñ ñîäåðæàíèåì óãëåâîäîâ íå áîëåå âîñüìè ïðîöåíòîâ ìîæåò îòîäâèíóòü ìîìåíò íàñòóïëåíèÿ óòîìëåíèÿ è îáåñïå÷èòü áîëåå èíòåíñèâíóþ òðåíèðîâêó. À åùå ó÷åíûì èçâåñòíî, ÷òî óãëåâîäû âî âðåìÿ òðåíèðîâêè ïîäàâëÿþò âûñâîáîæäåíèå îñíîâíîãî êàòàáîëè÷åñêîãî ãîðìîíà êîðòèçîëà. Îäíàêî ïîñòóïëåíèå óãëåâîäîâ â ñèñòåìó òîðìîçèò èñïîëüçîâàíèå æèðîâ âî âðåìÿ òðåíèðîâêè, õîòÿ â ñëó÷àå ñ ñèëîâûìè òðåíèðîâêàìè ýòî íåñòðàøíî – èñïîëüçîâàíèå æèðîâ òàì ïðàêòè÷åñêè ïîëíîñòüþ îñòàíîâëåíî. Åäèíñòâåííûé ñàõàð, êîòîðîãî ñëåäóåò èçáåãàòü âî âðåìÿ çàíÿòèé, - ýòî ôðóêòîçà, ïîñêîëüêó îíà ñïîñîáíà âûçâàòü æåëóäî÷íûå ñïàçìû.
Óãëåâîäû ïîñëå òðåíèðîâêè
Ïîñëå òðåíèðîâêè óãëåâîäû – è îñîáåííî âûñîêî ãëèêåìè÷íûå, òî åñòü, ñàõàðà – èñêëþ÷èòåëüíî âàæíû äëÿ âîññòàíîâëåíèÿ çàïàñîâ ãëèêîãåíà. Ýòîò ýôôåêò ìîæåò áûòü óñèëåí äîáàâëåíèåì ê íèì ïðîòåèíà â ñîîòíîøåíèè ïðîòåèíû-óãëåâîäû êàê îäèí ê òðåì. Íàáëþäåíèÿ ó÷åíûõ ïîêàçàëè 37-ïðîöåíòíîå óâåëè÷åíèå ñêîðîñòè âîññòàíîâëåíèÿ çàïàñîâ ãëèêîãåíà â ðåçóëüòàòå ïðèåìà òîëüêî îäíèõ óãëåâîäîâ. Ïî-âèäèìîìó, ýôôåêò ñâÿçàí ñ óñèëåííûì âûñâîáîæäåíèåì èíñóëèíà, ïîäñòåãèâàåìûì àìèíîêèñëîòàìè ïðîòåèíà. Ëó÷øå âñåãî â äàííîì ñëó÷àå ðàáîòàþò áûñòðûå ïðîòåèíû, òàêèå êàê ñûâîðîòî÷íûé, èëè ãîòîâàÿ áåëêîâî-óãëåâîäíàÿ ñìåñü äëÿ íàðàùèâàíèÿ ìûøå÷íîé ìàññû - ãåéíåð.
Ìíîæåñòâî èññëåäîâàíèé ïîäòâåðäèëî òîò ôàêò, ÷òî ëþáûå óãëåâîäû, ïðèíÿòûå âàìè â òå÷åíèå äâóõ ÷àñîâ ïîñëå îêîí÷àíèÿ ñèëîâîé òðåíèðîâêè, èñïîëüçóþòñÿ èñêëþ÷èòåëüíî äëÿ âîñïîëíåíèÿ çàïàñîâ ãëèêîãåíà. Îíè íå ïðåâðàùàþòñÿ â æèðû è íå âëèÿþò íà ñêîðîñòü îêñèäàöèè óæå èìåþùèõñÿ æèðîâûõ çàïàñîâ.
Åñëè âàñ âñå æå áåñïîêîèò âëèÿíèå ïðîñòûõ ñàõàðîâ íà çäîðîâüå, ïîïðîáóéòå ýêñòðàêò èç ëèñòüåâ ýâêàëèïòà.  õîäå íåäàâíåãî ýêñïåðèìåíòà íàä êðûñàìè îí ïîäàâèë àáñîðáöèþ ôðóêòîçå â êèøå÷íèêå è ïðåäîòâðàòèë îòëîæåíèå æèðîâ â ðåçóëüòàòå ïîòðåáëåíèÿ öóêðîçû. Ó÷åíûå íå óâåðåíû, êàêèì îáðàçîì ýâêàëèïò ñïðàâèëñÿ ñ ôðóêòîçîé, íî ïîõîæå, îí áëîêèðîâàë öóêðàçó, êèøå÷íûé ýíçèì, ðàñùåïëÿþùèé öóêðîçó. Êðûñû, ïîëó÷àâøèå ýêñòðàêò, ïîêàçàëè è íèçêèé óðîâåíü òðèãëèöåðèäîâ â êðîâè, ïîýòîìó íå óäèâëÿéòåñü, åñëè ñêîðî ñðåäè æèðîñæèãàþùèõ äîáàâîê âû óâèäèòå ýêñòðàêò èç ëèñòüåâ ýâêàëèïòà.
Îñíîâíûå ñâåäåíèÿ î ñàõàðå
×åëîâåê ðîæäàåòñÿ ñ òÿãîé ê ñëàäêîìó.  ÷ðåâå ìàòåðè çàðîäûø ïëàâàåò â ñëàäêîé àìíèîòè÷åñêîé æèäêîñòè. Âñêîðå ïîñëå ðîæäåíèÿ ìàëûøè ïåðåõîäÿò íà ïèòàíèå ìàòåðèíñêèì ìîëîêîì, áîãàòûì ëàêòîçîé, òàê æå èçâåñòíîé êàê ìîëî÷íûé ñàõàð.
Êîãäà ëþäè ãîâîðÿò î ñàõàðå, òî îáû÷íî ïîäðàçóìåâàåòñÿ öóêðîçà èëè ñòîëîâûé ñàõàð. Ñ õèìè÷åñêîé òî÷êè çðåíèÿ ñàõàðà – ýòî ãðóïïà ñîåäèíåíèé, ñîñòîÿùèõ èç óãëåðîäà, âîäîðîäà è êèñëîðîäà. Ãëàâíûå òèïû ñàõàðîâ - ìîíîñàõàðèäû (åäèíè÷íûå ñàõàðà) è äèñàõàðèäû, âêëþ÷àþùèå â ñåáÿ äâà ìîíîñàõàðèäà. Öóêðîçà, ëàêòîçà è ìàëüòîçà ÿâëÿåòñÿ äèñàõàðèäàìè, ñîñòîÿùèìè èç ãëþêîçû è ôðóêòîçû.
Óñâîåíèå ñàõàðîâ íà÷èíàåòñÿ â ðîòîâîé ïîëîñòè, íî áîëüøàÿ ÷àñòü ïðîöåññîâ àáñîðáöèè ïðîòåêàåò â ìàëîì êèøå÷íèêå. Ôðóêòîçà óñâàèâàåòñÿ íåñêîëüêî èíà÷å, ÷åì îñòàëüíûå ñàõàðà – ãîðàçäî áîëåå ìåäëåííî. Ïî ýòîé ïðè÷èíå ôðóêòîçà íå âûçûâàåò ïîäúåì óðîâíÿ èíñóëèíà.
Ðàñùåïëåííûå ñàõàðà ïðîõîäÿò ñêâîçü êëåòêè ìàëîãî êèøå÷íèêà â êàïèëëÿðíûå ïîðòàëû è äàëåå íàïðàâëÿþòñÿ â ïå÷åíü, ãäå ê íèì äîáàâëÿåòñÿ ôîñôàò. Åäèíñòâåííûì ñàõàðîì, íàïðÿìóþ ïîïàäàþùèì â êðîâü, ÿâëÿåòñÿ ãëþêîçà, êîòîðàÿ îòïðàâëÿåòñÿ â ìîçã, ïî÷êè, ìûøå÷íûå è æèðîâûå êëåòêè. Ïîñêîëüêó ãëþêîçà ñëóæèò ãëàâíûì èñòî÷íèêîì ýíåðãèè äëÿ ìîçãà, äëÿ ïîääåðæàíèÿ åãî ðàáîòû åå åæåäíåâíî òðåáóåòñÿ 130 ãðàìì. Ýòî íå îçíà÷àåò, ÷òî âû äîëæíû ñúåäàòü êàæäûé äåíü 130 ãðàìì óãëåâîäîâ. Ïå÷åíü òàêæå ïðîèçâîäèò ãëþêîç èç íåêîòîðûõ àìèíîêèñëîò è ãëèöåðèíà èç æèðîâ.
Ãëàâíîå ïðåäíàçíà÷åíèå ãëþêîçû èëè îòêëàäûâàòüñÿ â ïå÷åíè â âèäå ãëèêîãåíà, èëè öèðêóëèðîâàòü ñ êðîâîòîêîì äëÿ îáåñïå÷åíèÿ ýíåðãåòè÷åñêèõ ïîòðåáíîñòåé ðàçëè÷íûõ ñèñòåì îðãàíèçìà. Ïðîöåññ ðàñùåïëåíèÿ ãëþêîçû äëÿ ïîëó÷åíèÿ ýíåðãèè íàçûâàåòñÿ ãëèêîëèçîì.  õîäå ïðîöåññà áîëüøèíñòâî ñàõàðîâ ðàñùåïëÿþòñÿ íà äâå ìîëåêóëû ïèðóâàòà. Ïèðóâàò æå èëè ïîëíîñòüþ îêñèäèðóåòñÿ â öèêëå Êðåáñà (ãëàâíîì ýíåðãåòè÷åñêîì ìåõàíèçìå), ïîïàäàÿ â ýëåêòðîííóþ òðàíñïîðòíóþ ñèñòåìó â êëåòî÷íûõ ìèòîõîíäðèÿõ, íà âûõîäå äàâàÿ àäåíîçèí òðèôîñôàò (ÀÒÔ) - îñíîâíîé ýíåðãåòè÷åñêèé ðåñóðñ, - èëè ïðåâðàùàåòñÿ â ëàêòàò. Ëàêòàò ïîëó÷àåòñÿ ïðè îòíîñèòåëüíîé íåõâàòêå êèñëîðîäà, íàïðèìåð, âî âðåìÿ àíàýðîáíîé ðàáîòû ñ îòÿãîùåíèÿìè. Êðîâü òðàíñïîðòèðóåò âûñâîáîäèâøèéñÿ èç ìûøö ëàêòàò â ïå÷åíü, ãäå îí ðåêîíâåðòèðóåòñÿ â ãëþêîçó, êîòîðàÿ âîçâðàùàåòñÿ â ðàáîòàþùèå ìûøöû â êà÷åñòâå èñòî÷íèêà ýíåðãèè.
Êàæäûé ãðàìì ãëèêîãåíà ñîõðàíÿåòñÿ ñ 2,7 ãðàììàìè âîäû. Åñëè çàïàñû ãëèêîãåíà ïîëíû, íî â ñèñòåìó âñå ðàâíî ïîñòóïàþò óãëåâîäû, òî îíè ïðåâðàùàþòñÿ â æèðû. Îäíàêî íå âñå òàê ïðîñòî.
Îðãàíèçì êîíâåðòèðóåò óãëåâîäû â æèðû âåñüìà íåýôôåêòèâíî. Îäíî èç èññëåäîâàíèé ïîêàçàëî, ÷òî äëÿ ïðåâðàùåíèÿ óãëåâîäîâ â æèðû íåîáõîäèìî íà 68% áîëüøå ýíåðãèè, ÷åì äëÿ òðàíñïîðòà æèðîâ â æèðîâûå äåïî. Êðèòèêè íèçêîóãëåâîäíûõ äèåò ÷àñòî óïîìèíàþò çàòðóäíåíèÿ ñ êîíâåðòàöèåé óãëåâîäîâ â ñîõðàíåííûå æèðû.
Ñ äðóãîé ñòîðîíû óãëåâîäû – ýòî ãëàâíûé èñòî÷íèê ýíåðãèè äëÿ îðãàíèçìà. Åñëè âû ïîòðåáëÿåòå óãëåâîäû âìåñòå ñ æèðàìè, îí âíà÷àëå ñæèãàåò óãëåâîäû, à æèðû îòïðàâëÿåò íà ñîõðàíåíèå. Åñëè âû ñîêðàùàåòå ïîòðåáëåíèå óãëåâîäîâ, êàê ýòî ïðîèñõîäèò íà îáû÷íîé íèçêîóãëåâîäíîé äèåòå, îðãàíèçì ïðèíèìàåòñÿ çà ñæèãàíèå ñîõðàíåííûõ æèðîâ. Åùå îäèí ôàêòîð – âûõîä èíñóëèíà, êîòîðûé ñíèæàåòñÿ ïðè íèçêîì ïîñòóïëåíèè óãëåâîäîâ â ñèñòåìó.  óñëîâèÿõ ïîíèæåííîãî âûñâîáîæäåíèÿ èíñóëèíà æèðû ëåã÷å îêñèäèðóþòñÿ.
Äåéñòâèòåëüíî ëè óãëåâîäû âûçûâàþò ñåðäå÷íûå çàáîëåâàíèÿ?
Êðèòèêè íèçêîóãëåâîäíûõ äèåò ÷àñòî ññûëàþòñÿ íà òî, ÷òî âûñîêîå ïîòðåáëåíèå æèðîâ è õîëåñòåðèíà ÿâëÿåòñÿ ïðè÷èíîé ñåðäå÷íîñîñóäèñòûõ çàáîëåâàíèé. Îäíàêî èññëåäîâàíèÿ ïîñëåäíèõ ëåò ïîêàçûâàþò, ÷òî ýòî íå òàê. Íàîáîðîò, íèçêîóãëåâîäíûå äèåòû ïîìîãàþò ïðåäîòâðàòèòü áîëåçíè ñåðäöà, ñíèæàÿ óðîâåíü òðèãëèöåðèäîâ (æèðîâ) â êðîâè è ïîâûøàÿ óðîâåíü ïîëåçíûõ ëèïîïðîòåèíîâ âûñîêîé ïëîòíîñòè (ËÂÏ) – çàùèòíîãî õîëåñòåðèíà.
Äîâîëüíî äîëãî ñ÷èòàëîñü, ÷òî òðèãëèöåðèäû èãðàþò íåçíà÷èòåëüíóþ ðîëü â ðèñêå ñåðäå÷íîñîñóäèñòûõ çàáîëåâàíèé, íî ïîñëåäíèå èññëåäîâàíèÿ ïîêàçàëè, ÷òî ýòî ñîâåðøåííî íå òàê. Èçáûòî÷íûå òðèãëèöåðèäû, ïîïàäàÿ â ïå÷åíü, ïðåâðàùàþòñÿ â ëèïîïðîòåèíû î÷åíü íèçêîé ïëîòíîñòè, à çàòåì â ëèïîïðîòåèíû íèçêîé ïëîòíîñòè (ËÍÏ), êîòîðûå ÿâëÿþòñÿ îñíîâíûì ôàêòîðîì ðèñêà çàáîëåâàíèé ñåðäöà. ×åì íèæå óðîâåíü ËÍÏ, òåì ëó÷øå.
×òî æå ïîäíèìàåò óðîâåíü òðèãëèöåðèäîâ? Âû, íàâåðíîå, äóìàåòå, ÷òî æèðû, íî íà ñàìîì äåëå ýòî äåëàåò èçáûòî÷íîå ïîòðåáëåíèå àëêîãîëÿ è ñàõàðà. Ïî ñðàâíåíèþ ñ êðàõìàëèñòûìè óãëåâîäàìè ñàõàðà óâåëè÷èâàþò òðèãëèöåðèäû â êðîâè â ñðåäíåì íà 60%. Íàèáîëåå âûñîêèé ðèñê âîçðàñòàíèÿ óðîâíÿ òðèãëèöåðèäîâ ïîñëå ïîòðåáëåíèÿ ñàõàðà íàáëþäàåòñÿ ó ëþäåé, êîòîðûå íå òðåíèðóþòñÿ è îáëàäàþò áîëüøèìè æèðîâûìè îòëîæåíèÿìè àáäîìèíàëüíîé îáëàñòè, òàê íàçûâàåìûìè âèñöåðàëüíûìè (èëè ãëóáîêî çàëåãàþùèìè) æèðàìè. Ñïîðû âûçûâàåò âîïðîñ: êàêîé èìåííî òèï ñàõàðîâ ëåã÷å âñåãî ïîäíèìàåò óðîâåíü òðèãëèöåðèäîâ â êðîâè. Áîëüøèíñòâî èññëåäîâàíèé óêàçûâàþò íà ôðóêòîçó, íî ïîñêîëüêó öóêðîçà èëè ñòîëîâûé ñàõàð íàïîëîâèíó ñîñòîèò èç ôðóêòîçû, òî îáâèíåíèå ïàäàþò è íà íåå.
Ê ñ÷àñòüþ, ó íàñ èìåþòñÿ äâà ïðîñòûõ èíñòðóìåíòà, èçáàâëÿþùèõ îò îïàñíîñòè ïîäúåìà óðîâíÿ òðèãëèöåðèäîâ â êðîâè. Ïåðâûé – ïîòðåáëÿòü áîëüøå ðûáüåãî æèðà. Æèðíûå êèñëîòû â ðûáüåì æèðå ñíèæàþò òðèãëèöåðèäû â ñðåäíåì íà 60%. Âòîðîé – ôèçè÷åñêèå óïðàæíåíèÿ, êîòîðûå ïîâûøàþò àêòèâíîñòü ýíçèìà æèðîâûõ êëåòîê, íàçûâàåìîãî ëèïîïðîòåèí ëèïàçà, óäàëÿþùåãî èç êðîâîòîêà èçáûòîê òðèãëèöåðèäîâ. Äàëåå òðèãëèöåðèäû îêñèäèðóþòñÿ äëÿ ñíàáæåíèÿ ýíåðãèåé ðàáîòàþùèå ìûøöû.
Êàêèì îáðàçîì ñàõàð ñìîã áû ñäåëàòü âàñ òîëùå?
Ñàõàð îáëàäàåò öåëûì ðÿäîì ñâîéñòâ, ñïîñîáíûõ ïîäàâèòü åãî æèðîîáðàçóþùóþ àêòèâíîñòü. Èíòåðåñíî, îäíî èç íèõ ñâÿçàíî ñ èíñóëèíîì, ãîðìîíîì, êîòîðûé ïðèâåðæåíöû íèçêîóãëåâîäíûõ äèåò ñâÿçûâàþò ñ îæèðåíèåì.
Ñðåäè äðóãèõ ôóíêöèé, èíñóëèí ñïîñîáåí «âûêëþ÷àòü» àïïåòèò. Ìíîæåñòâî èññëåäîâàíèé ïîêàçàëî, ÷òî, åñëè æèâîòíûì ïåðåä åäîé äàâàòü ñëàäêèé íàïèòîê, òî ïîòîì îíè ñúåäàþò ìåíüøå ïèùè. Ñêîðåå âñåãî, ïðè÷èíà â ïîäúåì èíñóëèíà, ñïðîâîöèðîâàííîì ñàõàðîì.
Êðîìå òîãî, ñàõàð èçìåíÿåò õèìèêàëèè ìîçãà, ñâÿçàííûå ñ êîíòðîëåì àïïåòèòà. Ñàìà òÿãà ê ñëàäêîìó îáóñëîâëåíà ïîâûøåííûì êîëè÷åñòâî íåéðîïåïòèäà Y. Ìíîãî÷èñëåííûå ýêñïåðèìåíòû ïîêàçàëè, ÷òî ïîäàâëåíèå åãî ýôôåêòîâ óíè÷òîæàåò òÿãó ê ñëàäêîìó. Ìíîãèå ëþäè ïåðååäàþò óãëåâîäîâ, ïîòîìó ÷òî ïîëó÷àþò îò èõ ïîòðåáëåíèÿ óäîâîëüñòâèå – è ýòîìó òàêæå åñòü õèìè÷åñêîå îáúÿñíåíèå.
Ïîòðåáëåíèå ñàõàðà ñïîñîáñòâóåò âûñâîáîæäåíèþ â ìîçã íàòóðàëüíîãî îïèîèäà, îáëàäàþùåãî óñïîêàèâàþùèì ýôôåêòîì. Êðîìå òîãî, ñàõàðà âîçäåéñòâóþò íà öåíòðû óäîâîëüñòâèÿ ìîçãà. Íà ýòè æå öåíòðû íàöåëåíû êîêàèí èëè àëêîãîëü, ÷åì îáúÿñíÿåòñÿ íàëè÷èå òÿãè ê ñëàäêîìó ó ëþäåé, ïîòðåáëÿþùèõ ýòè âåùåñòâà.
Åùå îäíà ïðè÷èíà, ïî êîòîðîé ñàõàð íå ñïîñîáåí ñäåëàòü âàñ òîëñòûìè, çàêëþ÷àåòñÿ â òîì, ÷òî â ðåçóëüòàòå åãî ïîòðåáëåíèÿ âîçðàñòàåò ýêñïðåññèÿ ãåíà íåïàðíîãî ïðîòåèíà 3 â ìûøöàõ. Íåïàðíûå ïðîòåèíû 3 ïðåâðàùàþò æèðîâûå êàëîðèè â òåïëî, îáåñïå÷èâàÿ òåðìîãåííûé ýôôåêò. Êàê ïîëàãàþò ó÷åíûå, òèðåîèäíûå ãîðìîíû òàêæå ðàáîòàþò ïðè ïîìîùè ýòèõ ïðîòåèíîâ. Òàêèì îáðàçîì, êîãäà àêòèâíîñòü íåïàðíûõ ïðîòåèíîâ 3 âûñîêà, âû ñæèãàåòå áîëüøå êàëîðèé êàê â ïîêîå, òàê è âî âðåìÿ ôèçè÷åñêèõ óïðàæíåíèé. Ïðîèçâîäñòâî íåïàðíîãî ïðîòåèíà 3 ñâÿçàíî ñ óâåëè÷åíèåì ýêñïðåññèè ãåíà íåéðîïåïòèäà Y, íàïðÿìóþ ñâÿçàííîãî ñ ïîòðåáëåíèåì ñàõàðà. Êîãäà âû åäèòå ñàõàð, â êèøå÷íèêå âîçðàñòàåò óðîâåíü ãëþêàãîí ïåïòèäà 1, êîòîðûé ðåàãèðóåò íà âîçäåéñòâèå ñàõàðà íà êëåòêè ìàëîãî êèøå÷íèêà è äàåò âàì îùóùåíèå ñûòîñòè, ïîäàâëÿÿ àïïåòèò.
Ïåðåâîä Âèêòîðà Òðèáóíñêîãî
Äðóãèå ñòàòüè íà òåìó ïèòàíèÿ â áîäèáèëäèíãå è ôèòíåñå:
Íåçàìåíèìûå àìèíîêèñëîòû ïðîòèâ ïåðåòðåíèðîâàííîñòè è ïåðåóòîìëåíèÿ
Àðãèíèí - àìèíîêèñëîòà, îáåñïå÷èâàþùàÿ íàêà÷êó ìûøö è ñæèãàþùàÿ æèð
Êàëîðèéíîñòü è ñîñòàâ ïðîäóêòîâ ïèòàíèÿ
Ïîäïèøèòåñü íà ìîé Telegram èëè âÊîíòàêòå è âû âñåãäà áóäåòå â êóðñå íîâûõ ïóáëèêàöèé î òðåíèðîâêàõ, ïèòàíèè, çäîðîâüå.
Ãëàâíàÿ Ñòàòüè Îá àâòîðå Êîíòàêòû
Copyright © 2000-2024 Victor Tribunsky
All rights reserved worldwide.
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3,946,776,695,242,342,000 | kick
(redirected from kicks up a fuss)
Also found in: Dictionary, Thesaurus, Idioms, Encyclopedia.
kick
(kik),
A brisk mechanical stimulus.
Farlex Partner Medical Dictionary © Farlex 2012
kick
noun Cardiology See Atrial kick verb Drug slang To get off a drug habit.
McGraw-Hill Concise Dictionary of Modern Medicine. © 2002 by The McGraw-Hill Companies, Inc.
Patient discussion about kick
Q. How can I kick start my weight loss again? I'm stuck at a weight loss plateau. I keep losing/gaining the same 3 pounds. How can I start losing weight again?
A. Try kick starting your workout routine with some different kinds of exercises. Change up some eating habits, do not starve yourself. Eat, but eat clean and healthy fruits, lean meats, nuts, etc.
Q. Last week my younger son Frank, was punished in school because of kicking and throwing things at students... This is Donald, Last week my younger son Frank, was punished in school because of kicking and throwing things at teacher and on a few students. I don’t know why he behaved like that. I got tensed when I heard about this. What to do with him?
A. Well I think it depends whether or not this is a constant behaviour by your son, or it was only a one time event that he had an explanation for. If he tends to get angry and use violence a lot, you should take action, and let him know this is not acceptable by any means. Counsling might work best. If this was a one time thing, you should let your son know this should not happen again, and try preventing him from day to day activities such as meeting friends or using the computer if this happens again.
Q. What kind of energy drink can I drink right before my workout? I need that extra kick at the end of the day. I work out after work but sometimes I'm a little tired. I would like something that would give me an extra boost to get me through my workouts. I'm not a morning person and that's why I don't work out in the mornings.
A. i tried the green tea- it's working but you need to drink a large amount (which is not bad- drinking a lot of fluids is good for you). i take 3 teaspoons of green tea leafs or 3 bags of green tea, pour boiling water on it, let it stay for about 5 minutes and then mix it in a 1.5 liter bottle of water (no sugar. then i have 1.5 liters of green tea. works like a charm (to me any way..).
More discussions about kick
This content is provided by iMedix and is subject to iMedix Terms. The Questions and Answers are not endorsed or recommended and are made available by patients, not doctors. | {
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-4,665,923,869,677,071,000 | Top
20
Doctor insights on: Benadryl And Mylanta And Carafate
Share
1
1
How much Benadryl (diphenhydramine) is considered too much?
How much Benadryl (diphenhydramine) is considered too much?
Benadryl (diphenhydramine): Either the recommended amount based on weight through the directions on the box or following your doctors recommendations if the recommended dose they made is higher. Read more
See 1 more doctor answer
Dr. John Chiu
1,047 Doctors shared insights
Diphenhydramine (Definition)
Diphenhydramine is a sedating antihistamine which is a kind of antihistamine type drug (common ...Read more
4
4
Wut is Benadryl (diphenhydramine) use for?
Wut is Benadryl (diphenhydramine) use for?
Benadryl (diphenhydramine): Benadryl (diphenhydramine) is trypically used for allergies or an anti itch medicine. Read more
5
5
How effective is benadryl (diphenhydramine)?
How effective is benadryl (diphenhydramine)?
Benadryl (diphenhydramine): Benadryl (diphenhydramine) is a very effective antihistamine for allergies and allergic reactions and itching from poison ivy or insect bites Read more
7
7
How much Benadryl (diphenhydramine) is considered too much?
Benadryl (diphenhydramine): Either the recommended amount based on weight through the directions on the box or following your doctors recommendations if the recommended dose they made is higher. Read more
See 1 more doctor answer
8
8
Is 4 tsp of children's Benadryl (diphenhydramine) too much?
Is 4 tsp of children's Benadryl (diphenhydramine) too much?
Depends: This would be a normal dose for a 110 lb kid. The recommended dose is 1mg/kg. Read more
9
9
What happens if you take too much benadryl (diphenhydramine)?
Benadryl (diphenhydramine): It ususally makes you have a dry mouth and get very sleepy. Read more
10
10
Is it okay if to take 2 benadryls (diphenhydramine) and I melatonin?
Doses?: Depends on the dose of Benadryl (diphenhydramine). If you have insomnia, sleep hygiene is an often overlooked, yet more effective treatment, than medications. In addition, the combination of medications could impair decision making, cause undesired drowsiness, and other side effects. Speak with your doctor, before taking any combination of medications. Do not drive/operate heavy machinery under their influence. Read more
See 1 more doctor answer
11
11
What sources does Benadryl (diphenhydramine) come from? How is it made?
What sources does Benadryl (diphenhydramine) come from? How is it made?
Synthetic: This, like all other antihistamines, is synthesized and not present in natural form. Read more
12
12
Would it be ok to take Benadryl (diphenhydramine) that expired in 11/09?
Benadryl (diphenhydramine): Taking medication that expired almost 5 years ago is probably not a good idea. It may be safe, but I don't know for sure. If we were in the Zombie apocalypse and you had no other choice I would say go for it. But since generic diphenhydramine is cheap, why don't you make a trip to your local store and buy some new. Read more
13
13
What would it indicate if taking benadryl (diphenhydramine) improves eyesight greatly?
What would it indicate if taking benadryl (diphenhydramine) improves eyesight greatly?
Allergy: You likely have allergic conjunctivitis given the very limited information you have provided. Why were you taking Benadryl (diphenhydramine)? do you have environmental allergies? Read more
14
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What would happen if someone takes a Benadryl (diphenhydramine) & 5mg vicdion together?
More sleepy: Nothing serious at these low doses although you may feel more sleepy since the sedation effects of ech medicine add up. But it should be fine after 12-18 hours. Read more
15
15
Carafate (sucralfate) vs axid?
Carafate (sucralfate) vs axid?
Personal decision: Carafate is brand of sucralfate which works by coating stomach lining. It is fda approved only for duodenal ulcers. Axid (nizatidine) is brand of h2 receptor blocker, all of which are now available otc. In addition to treating duodenal ulcers, Axid (nizatidine) is also approved for gerd (heartburn) & gastric ulcers, too. Choice depends upon what you need to treat as well as cost (insurance), dosing regimen & side effects. Read more
17
17
Is loratadine like benadryl (diphenhydramine)?
Is loratadine like benadryl (diphenhydramine)?
Kinda mostly: Loratadine is a 'non-sedating antihistamine, ' and Diphenhydramine (/benadryl) is a sedating antihistamine (aka: older / h1 & h2 blocker), so yes, they are close cousins in intended effects--just differ in side effects. Read more
18
18
If I drank and took a Benadryl (diphenhydramine) will I die?
I guess that depends: On how much you took of each. I am concerned about you asking for a recipe to die by. I don't know what is happening in your life, that you would ask this. But, what I can tell you is that with help, your life can improve. With hope & with help whatever feels insurmountable now can be overcome. Please get help now. Take care. Read more
19
19
Why is it that Benadryl (diphenhydramine) gives me a hangover?
Crosses into brain: There is a blood:brain barrier and medications can cross through this barrier to cause people to feel "hungover". People complain of feeling drowsy or paradoxically some people get insomnia. Non-sedating antihistamines (fexofenadine, loratidine, cetirizine) have less of this "crossover" and so cause less problems for people. Read more
See 1 more doctor answer
20
20
What could be the reason that I am not high from benadryl (diphenhydramine)?
What could be the reason that I am not high from benadryl (diphenhydramine)?
Benadryl (diphenhydramine) would not: Be anticipated to make someone feel "high". Read more
Benadryl (Definition)
Diphenhydramine is a sedating antihistamine which is a kind of antihistamine type drug (common ...Read more
Dr. Eric Weisman
49 Doctors shared insights
Aluminum Hydroxide And Magnesium Hydroxide (Definition)
Aluminum hydroxide/magnesium hydroxide is an antacid which is a kind of ...Read more | {
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-8,489,297,447,271,697,000 | What is the eye ointment for newborns?
Newborns receive erythromycin eye ointment after birth to prevent pink eye in the first month of life, also called ophthalmia neonatorum (ON).
Why do they put eye cream on newborns?
Antibiotic eye drops or ointment are placed in a newborn’s eyes after birth. This is to protect babies from getting bacterial eye infections that can occur during birth. Untreated, these infections can cause serious problems including blindness. The antibiotic erythromycin is used most often.
What does erythromycin do for newborns?
Ophthalmic erythromycin is used to treat bacterial infections of the eye. This medication is also used to prevent bacterial infections of the eye in newborn babies. Erythromycin is in a class of medications called macrolide antibiotics. It works by killing bacteria that cause infections.
Why do they put silver nitrate in baby’s eyes?
Crede’s method of instilling a drop of 2% aqueous solution of silver nitrate into a newborn’s eyes was first published in 1881 and significantly advanced the prevention of neonatal conjunctivitis. Silver nitrate is a surface-active chemical that facilitates agglutination and inactivation of gonococci.
IT IS INTERESTING: Is breast milk still good if separated?
Is the eye ointment for newborns necessary?
Automatic prophylaxis with erythromycin eye ointment for all newborns within 24 hours of birth is currently recommended by the U.S. Preventive Services Task Force (2019) and their recommendation is promoted by the American Association of Family Physicians.
What happens to a newborn immediately after birth?
Care for the newborn after a vaginal delivery
As quickly as possible, a new baby is placed in your arms. Often, the baby is placed skin-to-skin on your chest right after birth. Some babies will breastfeed right away. In the first hour or 2 after birth, most babies are in an alert, wide awake phase.
How do you give erythromycin to a newborn?
Apply a half-inch (1cm) strip of ointment inside the inner surface of your child’s lower eyelid. Let go of their lower eyelid and ask your child to close their eyes for a few minutes. Put the top back on the ointment tube.
Why do they give newborns sugar water?
Why is sugar water used for babies? Some hospitals use sugar water to help babies with pain during a circumcision or other surgeries. At the pediatrician’s office, sugar water could be given to reduce pain when the baby is being given a shot, a foot prick, or having blood drawn.
Should I put breast milk in my baby’s eye?
Try placing a drop or two of breast milk directly into the inner portion of your baby’s eyes while they are closed— once they open their eyes, the milk will fall into the eyes and work to clear up any infection. Use this treatment a few times a day for a week or two or until their tear ducts have cleared up.
IT IS INTERESTING: You asked: How can I boost my baby's immune system naturally?
When should I take my baby to the doctor for eye discharge?
If the tear duct is still blocked and the eye discharge continues up to the baby’s first birthday, you should see your child’s doctor. They may refer you to a pediatric eye specialist, as it may need surgery.
Should I take my baby to the doctor for conjunctivitis?
When to see a doctor
See a GP if your child’s conjunctivitis isn’t getting better after two days, or if your child has any of the following: severe pain. problems with their vision/eyesight. increased swelling, redness and tenderness in the eyelids and around the eyes. | {
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Brain Tissue-Derived Extracellular Vesicles in Alzheimer’s Disease Display Altered Key Protein Levels Including Cell Type-Specific Markers
Abstract
Background:
Brain tissue-derived extracellular vesicles (bdEVs) play neurodegenerative and protective roles, including in Alzheimer’s disease (AD). Extracellular vesicles (EVs) may also leave the brain to betray the state of the CNS in the periphery. Only a few studies have profiled the proteome of bdEVs and source brain tissue. Additionally, studies focusing on bdEV cell type-specific surface markers are rare.
Objective:
We aimed to reveal the pathological mechanisms inside the brain by profiling the tissue and bdEV proteomes in AD patients. In addition, to indicate targets for capturing and molecular profiling of bdEVs in the periphery, CNS cell-specific markers were profiled on the intact bdEV surface.
Methods:
bdEVs were separated and followed by EV counting and sizing. Brain tissue and bdEVs from age-matched AD patients and controls were then proteomically profiled. Total tau (t-tau), phosphorylated tau (p-tau), and antioxidant peroxiredoxins (PRDX) 1 and 6 were measured by immunoassay in an independent bdEV separation. Neuron, microglia, astrocyte, and endothelia markers were detected on intact EVs by multiplexed ELISA.
Results:
Overall, concentration of recovered bdEVs was not affected by AD. Proteome differences between AD and control were more pronounced for bdEVs than for brain tissue. Levels of t-tau, p-tau, PRDX1, and PRDX6 were significantly elevated in AD bdEVs compared with controls. Release of certain cell-specific bdEV markers was increased in AD.
Conclusion:
Several bdEV proteins are involved in AD mechanisms and may be used for disease monitoring. The identified CNS cell markers may be useful tools for peripheral bdEV capture.
INTRODUCTION
Alzheimer’s disease (AD) [1] is a public health crisis [2, 3] that grows as the population ages, demanding new insights into pathophysiology. Hallmarks of this neurodegenerative disease include extracellular deposition of amyloid-β (Aβ—fragments of the amyloid-β protein precursor, AβPP) in the form of neuritic plaques and intracellular aggregation of hyperphosphorylated tau as neurofibrillary tangles (NFTs) [4–6]. Wide distribution and high density of neuritic plaques and NFTs correspond with greater cognitive impairment [6]. AD diagnosis is made mostly using mental status and neuropsychiatric tests, sometimes supplemented by neuroimaging. To monitor AD status in real-time and thus provide opportunities to improve the patient’s quality of life, reliable and easily accessed biomarkers are needed that reflect the state of CNS cells and tissue [7, 8].
Extracellular vesicles (EVs) comprise a diversity of lipid bilayer membrane-delimited particles that dispose of cellular toxins and mediate intercellular communication [9, 10]. EVs are thought to participate in neurodegeneration in diseases such as AD, Parkinson’s disease, and prion diseases in part by spreading misfolded proteins [11, 12]. In AD, Aβ and tau have been found in or on EVs in AD models and patients [12–16]. However, some EVs may also contribute to amyloid clearance by glia [17, 18], suggesting that EVs from healthy cells block AD pathology. Context matters, though: in certain models, reducing EV release may diminish pathology overall [19, 20].
The reported ability of EVs to participate in cell communication [21] and to cross the blood-brain barrier [22] make them seemingly promising biomarkers for AD. Various studies have found changes in protein and RNA cargo of plasma EVs during AD and mild cognitive impairment [23–26], but it is not well understood to what extent these changes in plasma EVs correspond to EVs present in brain tissues. For example, L1 cell adhesion molecule (L1CAM) has been used frequently for neuronal EV capture from biofluids samples [14, 23, 24], but we and others have noted that L1CAM is not exclusive to neurons and is also found on peripheral lymphocytes and cancer cells [27, 28]. One recent study even suggested that most circulating L1CAM is present as a proteolytic cleavage product [29]. Furthermore, EV markers of glia cells, especially of microglia, the main resident immune cell type in the brain that regulates neuroinflammation [30], have not been well developed to date. Thus, robust markers to evaluate EV cell of origin may be needed.
Brain tissue-derived EVs (bdEVs) can also be harvested from the brain tissue interstitial space [12, 16, 31–34] in a rigorous manner [10, 35–37] to allow evaluation of both EV content and cell of origin. Exploring overall bdEV contents may shed light on physiological and pathological mechanisms inside the brain and also indicate targets for biomarker development outside the brain. Furthermore, investigating cell-specific surface markers that are released on EVs in the brain can provide new “molecular handles” for capture and molecular profiling of bdEVs in the periphery, opening a window into healthy and neuropathological processes in the brain. We therefore obtained brain tissue of AD cases as well as controls. Used our modification of a rigorous method [31, 32], we separated different EV subtypes, including purified bdEVs and an intermediate bdEV separation fraction (10,000× g pellet), to assess possible protein composition changes related to AD in the brain. We (1) profiled and compared the proteomes of brain tissue, 10,000× g pellet, and bdEVs from AD patients and controls to identify AD related proteome changes; (2) verified AD pathology-related bdEV proteins by immunoassay in materials from a second, independent separation; and (3) profiled surface markers on intact bdEVs to reveal possible shifts in release of protein markers of cell of origin.
METHODS
Tissue collection, processing, and approvals
Human brain tissues were obtained from the Johns Hopkins Alzheimer’s Disease Research Center. A total of 24 AD patients and 10 non-AD controls (Table 1, Supplementary Table 1) were included in this study. AD patients were diagnosed according to Braak and CERAD criteria [6]. The clinical pathological information and possible death causes for patients were included in Supplementary Table 1 based on patients’ medical records. Following external examination and weighing of the autopsy brain, the right cerebral hemisphere was cut into coronal slabs, frozen on prechilled metal plates, and stored at –80°C. For each patient, two pieces of mixed tissue from Brodmann areas 42, 21, and 40 were obtained. EV separation was done from two pieces of mixed tissues independently: one piece was used for a first proteomics profile, while the second piece was used for proteomics data verification and EV surface marker profiling (see samples included in Supplementary Table 1).
Table 1
The human cortex tissues used in this study
AD (n = 24)Control (n = 10)p
Age, mean78.14±12.5178.3±11.960.9734
Sex (male, female)9M, 14F7M, 3F
Postmortem interval, mean11.0±5.358.2±4.960.3819
Brain tissue weight (/100 mg)3.66±1.093.65±0.730.9951
Separation of extracellular vesicles from brain tissue
EVs were separated from brain tissues using our published protocol [31]. Before extraction, a small (∼50 mg) piece of tissue was stored at –80°C for later protein extraction from brain homogenate (BH). After enzymatic digestion, differential centrifugation, and initial filtering (through a 0.22μm filter) of the remaining tissue, 10,000× g ultracentrifuged pellets were collected and termed “10K” as an intermediate product of EV separation. The 10K supernatant was then separated by size exclusion chromatography (SEC) and concentrated into a purer EV preparation. See our published protocol [31] for detailed methods.
Transmission electron microscopy
EV preparations (10μL) were adsorbed to glow-discharged 400 mesh ultra-thin carbon-coated grids (EMS CF400-CU-UL) for 2 min, followed by 3 quick rinses in TBS and staining in 1% uranyl acetate (UAT) with 0.05 % tylose. After being aspirated and dried, grids were immediately observed with a Philips CM120 instrument set at 80 kV, and images were captured with an AMT XR80 CCD (8 megapixel).
Nanoflow cytometry (NFCM)
Concentration and size profile of 10K and EV preparations were measured over one minute of data collection by side scatter using NFCM (Flow NanoAnalyzer, NanoFCM, Inc.). The instrument was pre-calibrated for concentration and size measurements with 200 nm polystyrene beads and a silica nanosphere cocktail (diameters of 68, 91, 113, and 151 nm), respectively. Both calibration materials were from the manufacturer, NanoFCM. Particle numbers and sizes were calculated based on the calibration curve, flow rate, and side scatter intensity.
Brain homogenate protein preparation
BHs were prepared by grinding tissue in cold PBS containing PI/PS with a handheld homogenizer (Kontes Pellet Pestle Motor) for 10 s. RIPA lysis buffer (Cell Signaling Technology 9806) was added, and the mixture was sonicated using an ultrasonic ice bath at 20 kHz for 4×20 s, with a 10-s interval between each sonication. Homogenate was rotated at 4°C for 2 h and spun 15 min at 14,000× g at 4°C. Supernatant was transferred to tubes and stored at –80°C.
Mass spectrometry
Samples were resuspended in 1 X RIPA buffer (20 mM Tris-HCl pH7.5, 150 mM NaCl, 1 mM Na2EDTA, 1 mM EGTA, 1% NP-40, 1% SDS, 2.5 mM sodium pyrophosphate) with protease and phosphatase inhibitors (1 mM β-glycerophosphate, 1 mM Na3VO4, 1μg/ml leupeptin) and incubated on ice for 5 min. The samples were sonicated for 15 min in an ice water bath before centrifugation at 14,000× g at 4°C for 10 min. The supernatant was collected and assessed for protein concentration using the micro BCA assay (Thermo Fisher Scientific 23235). 3μg of brain homogenate and 1.5μg of 10K pellet and EV samples were buffer-exchanged prior to mass spectrometry to remove detergent. Proteins were resuspended in 8M Urea, 50 mM Tris pH = 8.3. 1μL of TCEP (tris [2-carboxyethyl] phosphine hydrochloride, 200 mM solution in water) was then added to the samples and incubated for 4 h at 21°C in a ThermoMixer (Eppendorf AG). 4μL of 1M IAA (iodoacetamide in water) was then added and samples were incubated in the dark at 21°C. 800μL of 50 mM Tris (pH 8.3) and 1μg trypsin were then added to samples prior to overnight incubation at 37°C. 10μL of 10% trifluoroacetic acid (TFA) was added to each sample to acidify. Samples were cleaned using stage-tips preparations using 3 plugs of Empore polystyrenedivinylbenzene (SBD-XC) copolymer disks (Sigma Aldrich, MO, USA) for solid phase extraction. Peptides were reconstituted in 0.1% formic acid and 2% acetonitrile and loaded onto a trap column (C18 PepMap 100μm i.d.×2 cm trapping column, Thermo Fisher Scientific) at 5μL/min for 6 min using a Thermo Scientific UltiMate 3000 RSLCnano system and washed for 6 min before switching the precolumn in line with the analytical column (BEH C18, 1.7μm, 130 Å and 75μm ID×25 cm, Waters). Separation of peptides was performed at 45°C, 250 nL/min using a linear ACN gradient of buffer A (water with 0.1% formic acid, 2% ACN) and buffer B (water with 0.1% formic acid, 80% ACN), starting from 2% buffer B to 13% B in 6 min and then to 33% B over 70 min followed by 50% B at 80 min. The gradient was then increased from 50% B to 95% B for 5 min and maintained at 95% B for 1 min. The column was then equilibrated for 4 min in water with 0.1% formic acid, 2% ACN. Data were collected on a Q Exactive HF (Thermo Fisher Scientific) in Data Dependent Acquisition mode using m/z 350–1500 as MS scan range at 60,000 resolution. HCD MS/MS spectra were collected for the 7 most intense ions per MS scan at 60,000 resolution with a normalized collision energy of 28% and an isolation window of 1.4 m/z. Dynamic exclusion parameters were set as follows: exclude isotope on, duration 30 s, and peptide match preferred. Other instrument parameters for the Orbitrap were MS maximum injection time 30 ms with AGC target 3×106, MSMS for a maximum injection time of 110 ms with AGT target of 1×105.
Proteomics data analysis
Human protein sequences (last modified date: 16 May 2019) were downloaded from the Uniprot database and used as the database for the search engine. Common Repository of Adventitious Proteins (CRAP) was used as the potential lab contaminant database. Protein identification was performed using the proteomics search engine Andromeda built in to Maxquant V 1.16.0. Trypsin with a maximum of two missed cleavages was used as the cleavage enzyme. Carbamidomethyl of cysteine was set as fixed modification and oxidation of methionine was set as variable modification. The false discovery rate (FDR) was set to 1%. The Label Free quantification was done with match between runs using a match window of 0.7 min. Large label free quantification (LFQ) ratios were stabilized to reduce the sensitivity for outliers. For human datasets, data scaling was done using the cyclic loess method, and scaled data were visualized with a principal component analysis (PCA) plot. For differential abundance analysis, nested factorial design was set up for the analysis, where each subtype of the disease was nested within the main disease category and contrasts for the main categories were computed by averaging the subtypes.
For human datasets, data scaling was done using the cyclic loess method, and scaled data were visualized with a PCA plot. For differential abundance analysis, nested factorial design was set up for the analysis, where each subtype of the disease was nested within the main disease category and contrasts for the main categories were computed by averaging the subtypes. The protein interaction, cluster protein function prediction, and cellular component annotations was done by Protein-Protein Interaction Networks Functional Enrichment Analysis (STRING) [38]. Kyoto Encyclopedia of Genes and Genomes (KEGG) [39] was used to enrich pathway involvement of identified proteins. Statistical significance of enrichment was determined by the tools mentioned above. Only nominally significant categories (false discovery rate (FDR)<0.05) were included for analysis.
Electrochemiluminescence-linked (ECL) immunoassay
Total tau (t-tau), tau phosphorylated at threonine 231 (p-tau T231), peroxiredoxin 1 (PRDX 1), and PRDX6 were measured in BH, 10K, and EVs using an ECL-immunoassay (Meso Scale Discovery K15121D, K15231N-2) according to the manufacturer’s instructions. In brief, 10K and EV samples were diluted 1:10 while BH was diluted 1:100 in 2% blocking buffer containing 0.5% triton X-100. Samples were incubated for 1 h on the plate. After washing the plate, the SULFO-TAG anti-t-Tau, p-tau T231, PRDX1, and PRDX6 antibodies were added and incubated with the plate for 1 h, separately. After washing, MSD Read Buffer was added, and the plate was read immediately with a Quick plus SQ 120 MM instrument. Data analysis was done on MSD DISCOVERY WORKBENCH software version 2.0.
EV surface marker profiling
EV surface markers were assayed using prototype S-PLEX® ultrasensitive assays on intact EVs. Each U-PLEX® 96-well plates were coated with nine capture antibodies and one isotype IgG1 control antibody. Four different multiplexed assay panels (as listed in Supplementary Table 4) were used in this study. EV samples were diluted 20-fold and added to the plates incubated at RT with continuous shaking. EVs captured by each antibody spot were detected using MSD’s S-PLEX® ultrasensitive assay methods with a cocktail of detection antibodies targeting CD63, CD81, and CD9. Assay plates were then read with MSD GOLD™ Read buffer B on an MSD® SECTOR instrument. The ECL signal from DPBS and IgG1 isotype control were subtracted from signals on each detection antibody capture spot before further analysis.
Statistical analysis
Statistical significance of particle count, particle:protein ratio, size distribution, and protein level differences between AD and control groups were determined by two-tailed Welch’s t-test. Receiver operating characteristic (ROC) analyses were conducted in GraphPad Prism 8.1 using the method of Wilson and Brown. The correlation analysis was evaluated by Pearson’s correlation coefficient (r).
Standard protocol approvals, registrations, and patient consents
The institutional review boards of Johns Hopkins University approved the study, and informed consent was obtained from all participants or authorized representatives.
Data availability
We have submitted all relevant details of our experiments to the EV-TRACK knowledgebase (EV-TRACK ID: EV200126) [40]. Reporting for NFCM was submitted to FlowRepository as ID: FR-FCM-Z5FF [41]. Any and all data are available on request.
RESULTS
Following the protocol illustrated in Fig. 1A, bdEVs were separated from brain tissue of individuals with AD and controls (sample information in Table 1, Supplementary Table 1). After basic EV characterization, 10K and EV fractions were subjected to proteomics profiling, verification, and surface marker profiling.
Fig. 1
Alzheimer’s disease (AD) and control brain tissue-derived EV (bdEV) enrichment and characterization. A) Workflow for 10K and bdEV enrichment (see supporting information for detailed methods), proteomics analysis, and protein verification. Proteins from BH, 10K, and EVs were then isolated and subjected to mass spectrometry and protein verification. Intact EVs were subjected to surface protein profiling. B) 10K and bdEVs from AD and control brain tissue were visualized by negative staining transmission electron microscopy (scale bar = 100 nm). TEM is representative of ten images taken of each fraction from five independent human tissue samples. C) Size distributions of 10K and EV fractions (AD and control) were measured by NFCM and calculated as particles in a specific size bin versus total detected particles in each sample (percentage). D) Left: Particle concentrations of 10K and EV fractions of AD and control samples were measured by NFCM. Particle concentration for each group was normalized by tissue mass (per 100 mg). Right: Ratio of particles to protein (particles/μg). Protein concentrations of 10K and EV fractions were measured by BCA protein assay. E) Principal component analysis (PCA) based on EV marker expression per proteomics analysis. EV markers used for PCA: CD81, CD9, FLOT1, FLOT2, RAB1A, RAB7A, TUBA1B, TUBB4B, ANXA2, ANXA5, ANXA6, ACTN1, GAPDH. (D)-(E) data are presented as mean±SD. ns (no significant difference, p > 0.05), *p≤0.05, ****p≤0.0001, between AD and control by two-tailed Welch’s t-test.
Alzheimer’s disease (AD) and control brain tissue-derived EV (bdEV) enrichment and characterization. A) Workflow for 10K and bdEV enrichment (see supporting information for detailed methods), proteomics analysis, and protein verification. Proteins from BH, 10K, and EVs were then isolated and subjected to mass spectrometry and protein verification. Intact EVs were subjected to surface protein profiling. B) 10K and bdEVs from AD and control brain tissue were visualized by negative staining transmission electron microscopy (scale bar = 100 nm). TEM is representative of ten images taken of each fraction from five independent human tissue samples. C) Size distributions of 10K and EV fractions (AD and control) were measured by NFCM and calculated as particles in a specific size bin versus total detected particles in each sample (percentage). D) Left: Particle concentrations of 10K and EV fractions of AD and control samples were measured by NFCM. Particle concentration for each group was normalized by tissue mass (per 100 mg). Right: Ratio of particles to protein (particles/μg). Protein concentrations of 10K and EV fractions were measured by BCA protein assay. E) Principal component analysis (PCA) based on EV marker expression per proteomics analysis. EV markers used for PCA: CD81, CD9, FLOT1, FLOT2, RAB1A, RAB7A, TUBA1B, TUBB4B, ANXA2, ANXA5, ANXA6, ACTN1, GAPDH. (D)-(E) data are presented as mean±SD. ns (no significant difference, p > 0.05), *p≤0.05, ****p≤0.0001, between AD and control by two-tailed Welch’s t-test.
bdEV recovery was not affected in late-stage AD
Transmission electron microscopy (TEM) revealed oval and round particles in brain-derived 10K and EV fractions from AD and CTRL patients that were consistent with EV morphology (Fig. 1B). Particle size distribution and particle concentration per 100 mg tissue input were determined by NFCM. The overall EV particle diameter detected by NFCM tended to be smaller than that detected by TEM. Consistent with TEM, fractions from AD and control groups had similar size distributions (Fig. 1C, Supplementary Figure 1A). However, a larger percentage of small particles in the approximately 45–50 nm diameter range were observed in AD samples compared with controls (Fig. 1C). No significant particle yield (Fig. 1D left) or protein yield differences (Supplementary Figure 1B) were detected between AD and control brain-derived 10K and EV fractions. Particle:protein ratio (particle number per microgram of protein) was also calculated to evaluate EV purity [42]. This ratio was similar between the AD and control groups (Fig. 1D right). However, the EV fraction had a higher particle:protein ratio compared with 10K, consistent with greater protein contamination of the 10K pellet (Fig. 1D right, Supplementary Figure 1B). EV membrane proteins CD9 and CD81 were enriched in EVs compared with BH and 10K, while intracellular markers TOM70 and histone H2A were largely not detected (n.d.) in both EV and 10K (Supplementary Figure 1C). GO ontology analyses by STRING were used to determine the cellular component enrichment of proteins recovered from 10K and EV fractions (Supplementary Figure 1D). More than 60% of proteins identified in both 10K and EVs were enriched for EV-related terms like extracellular vesicle, extracellular exosome, vesicle, extracellular region, and extracellular space. We then examined the expression levels of 13 proteins that are commonly reported to be associated with EVs [10] (CD81, CD9, FLOT1, FLOT2, RAB1A, RAB7A, TUBA1B, TUBB4B, ANXA2, ANXA5, ANXA6, ACTN1, GAPDH). These proteins were found not to be significantly differentially abundant between AD and controls (Supplementary Figure 1E). PCA also showed different EV marker expression patterns between BH, 10K, and bdEV fractions, but not between AD and controls for this group of proteins (Fig. 1E).
AD pathogenesis regulatory pathway proteins in bdEVs as revealed by proteomics
By label-free mass spectrometry, the number of proteins identified in BH, 10K, and EVs are shown in Supplementary Table 2. Most proteins were detected in both AD and control BH (73.6%), 10K (66.5%), and EVs (66.6%) (Fig. 2A, Supplementary Figure 2A). We performed an enrichment analysis of common proteins, proteins that were uniquely detected in AD, and proteins that were uniquely detected in control samples using the Kyoto Encyclopedia of Genes and Genomes (KEGG) database (Fig. 2B, Supplementary Figure 2B). We observed enrichment of pathways directly or indirectly related to neurodegenerative diseases, among which were metabolic pathways (e.g., carbon metabolism, glycolysis, and oxidative phosphorylation). Furthermore, proteins with known involvement in AD, Parkinson’s disease, and Huntington’s disease were enriched in AD-unique proteins in 10K and EVs (Fig. 2B) and common proteins in BH (Supplementary Figure 2B). PCA of the EV proteome showed a separation of AD and control groups (Fig. 2C right). In contrast, no such separation was observed for 10K (Fig. 2C left) or BH (Supplementary Figure 2C). This indicated that AD pathology most prominently affects the proteome of purified EVs in brain tissue.
Fig. 2
bdEV protein content reflects differences between AD and control brain tissues. A) Venn diagrams of all proteins identified by proteomics in 10K and EVs from AD and control patients. B) Top 10 pathways ranked by FDR-corrected p value of 10K and EV proteins according to the Kyoto Encyclopedia of Genes and Genomes (KEGG). C) Principal component analysis (PCA) based on proteome content of 10K (left) and EVs (right). D) Volcano plots showing 10K (left) and EV (right) protein log2 fold changes (Log2FC) and p values (pval) for AD versus control. Thresholds for two-fold change and p value <0.05 are indicated by dashed lines. Significant changes are indicated with different colors. Grey: non-significant (ns), black: p-value<0.05, and red: FDR <0.05. E) Expression level of proteins differentially expressed between AD and control with fold change >2 (p-value <0.05) in 10K (left) and EVs (right). Data are presented as mean log2 (LFQ intensity)±SD. F) STRING protein interaction network analysis indicated that 18 proteins (out of 31 proteins showing differential expression (p-value<0.05) between AD and control in EVs) were enriched with known high confidence (0.7 on a scale of 0-1) protein-protein interactions. Protein clusters are indicated with different colors based on predicted functions.
bdEV protein content reflects differences between AD and control brain tissues. A) Venn diagrams of all proteins identified by proteomics in 10K and EVs from AD and control patients. B) Top 10 pathways ranked by FDR-corrected p value of 10K and EV proteins according to the Kyoto Encyclopedia of Genes and Genomes (KEGG). C) Principal component analysis (PCA) based on proteome content of 10K (left) and EVs (right). D) Volcano plots showing 10K (left) and EV (right) protein log2 fold changes (Log2FC) and p values (pval) for AD versus control. Thresholds for two-fold change and p value <0.05 are indicated by dashed lines. Significant changes are indicated with different colors. Grey: non-significant (ns), black: p-value<0.05, and red: FDR <0.05. E) Expression level of proteins differentially expressed between AD and control with fold change >2 (p-value <0.05) in 10K (left) and EVs (right). Data are presented as mean log2 (LFQ intensity)±SD. F) STRING protein interaction network analysis indicated that 18 proteins (out of 31 proteins showing differential expression (p-value<0.05) between AD and control in EVs) were enriched with known high confidence (0.7 on a scale of 0-1) protein-protein interactions. Protein clusters are indicated with different colors based on predicted functions.
Differentially abundant proteins in bdEVs and BH: AD versus control
Label-free quantitation (LFQ) was used to identify up- and downregulated proteins in AD (Fig. 2D, Supplementary Figure 2D, Supplementary Table 3). More proteins were up- or downregulated in AD in the EV fraction (Fig. 2D right) than in 10K (Fig. 2D left) or BH (Supplementary Figure 2D), in line with our PCA analysis of the whole proteome. This suggested that EVs have increased potential to indicate the difference between AD and controls as compared with 10K and BH. Three proteins (10K) and 11 proteins (EVs) differed by more than two-fold (Log2 fold change >1) between AD and control (Fig. 2E). Examining proteins that were differentially abundant in EVs by Protein-Protein Interaction Networks Functional Enrichment Analysis (STRING), 18 out of 31 had high protein-to-protein interaction confidence scores (0.7 on a scale of 0-1), participating in AD-related processes such as neurodegeneration, oxidative regulation, neurotrophic signaling, and metabolic regulation (Fig. 2F).
bdEV-associated tau proteins increase in AD patients compared with controls
We further measured the concentration of total tau (t-tau) and tau with phosphorylated threonine 231 (p-tau T231) in independently separated BH, 10K, and EVs (patients included are shown in Supplementary Table 1). Normalized to 100 mg brain tissue input for 10K and EVs, and 100μg protein for BH, only p-tau T231 was significantly increased in AD versus controls in 10K (Fig. 3A) and BH (Supplementary Figure 3A), while both t-tau and p-tau T231 were significantly increased in bdEVs (Fig. 3B). To test the predictive power of t-tau and p-tau T231 in 10K and EVs, receiver operating characteristic (ROC) curves were generated by logistic regression (Fig. 3C). T-tau and p-tau T231 in EVs distinguished AD from control, with an area-under-curve (AUC) of 0.81±0.08 and 0.96±0.04, respectively. In contrast, neither t-tau nor p-tau T231 in 10K distinguished AD from control significantly. Next, we assessed the correlation of t-tau and p-tau T231 in 10K and EVs by Pearson’s correlation analysis (Fig. 3D). Significant correlation of t-tau and p-tau T231 levels was shown in both 10K and EVs. To assess whether changes of t-tau and p-tau T231in 10K or EVs reflected those in BH, we determined their correlations. No strong correlation was observed for t-tau levels (BH versus 10K or EVs), while p-tau T231 levels in BH and EVs were significantly correlated (Supplementary Figure 3B). This indicates that the changes of tau level in 10K and EVs were only partly determined by the levels in brain tissues.
Fig. 3
Higher total tau and phosphorylated tau at threonine 231 levels in bdEVs from AD patients compared with controls. Levels of total tau (t-tau) and phosphorylated tau at threonine 231 (p-tau T231) protein (per 100 mg brain tissue input) in 10K (A) and EVs (B) from the second batch of bdEV separation (patient information in Supplementary Table 1) measured by ECL immunoassay. Data are presented as mean±SD. ns: no significant difference (p > 0.05), *p≤0.05, **p≤0.01 by two-tailed Welch’ s t-test. C) Receiver operating characteristic (ROC) curves are presented for t-tau and p-tau T231 in 10K (left) and EVs (right) from all patients. The area under the curve (AUC) with 95% CI and p value are shown. D) Correlations of t-tau and p-tau T231 protein levels in 10K (left) and EVs (right). Linear regression lines are shown in black. Pearson correlation coefficient (R) and significance (p) are shown based on AD (n = 21) and control (n = 10) samples.
Higher total tau and phosphorylated tau at threonine 231 levels in bdEVs from AD patients compared with controls. Levels of total tau (t-tau) and phosphorylated tau at threonine 231 (p-tau T231) protein (per 100 mg brain tissue input) in 10K (A) and EVs (B) from the second batch of bdEV separation (patient information in Supplementary Table 1) measured by ECL immunoassay. Data are presented as mean±SD. ns: no significant difference (p > 0.05), *p≤0.05, **p≤0.01 by two-tailed Welch’ s t-test. C) Receiver operating characteristic (ROC) curves are presented for t-tau and p-tau T231 in 10K (left) and EVs (right) from all patients. The area under the curve (AUC) with 95% CI and p value are shown. D) Correlations of t-tau and p-tau T231 protein levels in 10K (left) and EVs (right). Linear regression lines are shown in black. Pearson correlation coefficient (R) and significance (p) are shown based on AD (n = 21) and control (n = 10) samples.
bdEV-associated peroxiredoxins increase in AD patients compared with controls
Proteomics analysis identified dysregulation of peroxiredoxins (PRDXs) in bdEVs during AD. These proteins are thought to be involved in AD by regulating peroxidase activity and thus protecting the cell against oxidative stress (Fig. 2F). We thus further measured the level of PRDX 1 and 6 in lysed BH, 10K, and EVs (patients included are shown in Supplementary Table 1). Levels of PRDX 1 and 6 were not significantly different between AD and control in BH (Supplementary Figure 4A), while PRDX6 increased in AD 10K (Fig. 4A). Notably, both PRDX1 and PRDX6 were significantly increased in AD bdEVs (Fig. 4B). However, only PRDX6 in 10K was significant to distinguish AD from control with an area-under-curve (AUC) of 0.79±0.08, while PRDX1 and 6 in EVs were insignificant to distinguish AD from controls (Fig. 4C). Similar to t-tau and p-tau T231, significantly positive correlation of PRDX1 and PRDX6 was shown in both 10K and EVs (Fig. 4D), indicating possible synergistic effects of PRDXs in AD. PRDX levels in 10K or EVs were also only partly reflected by those in BH, as no correlation was observed for PRDX6 in 10K or EVs versus BH. However, PRDX1 levels of EVs and BH were significantly correlated (Supplementary Figure 4B).
Fig. 4
Higher peroxiredoxin (PRDX) 1 and 6 levels in bdEVs from AD patients compared with controls. Levels of PRDX1 and PRDX6 protein (per 100 mg brain tissue input) in 10K (A) and EVs (B) from the second batch of bdEV separation (patient information in Supplementary Table 1) measured by ECL immunoassay. Data are presented as mean±SD. ns: no significant difference (p > 0.05), *p≤0.05, **p≤0.01 by two-tailed Welch’ s t-test. C) Receiver operating characteristic (ROC) curves are presented for PRDX1 and PRDX6 in 10K (left) and EVs (right) from all patients. The area under curve (AUC) with 95% CI and p value are shown. D) Correlations of PRDX1 and PRDX6 protein levels in 10K (left) and EVs (right). Linear regression lines are shown in black. Pearson correlation coefficient (R) and significance (p) are shown based on AD (n = 21) and control (n = 10) samples.
Higher peroxiredoxin (PRDX) 1 and 6 levels in bdEVs from AD patients compared with controls. Levels of PRDX1 and PRDX6 protein (per 100 mg brain tissue input) in 10K (A) and EVs (B) from the second batch of bdEV separation (patient information in Supplementary Table 1) measured by ECL immunoassay. Data are presented as mean±SD. ns: no significant difference (p > 0.05), *p≤0.05, **p≤0.01 by two-tailed Welch’ s t-test. C) Receiver operating characteristic (ROC) curves are presented for PRDX1 and PRDX6 in 10K (left) and EVs (right) from all patients. The area under curve (AUC) with 95% CI and p value are shown. D) Correlations of PRDX1 and PRDX6 protein levels in 10K (left) and EVs (right). Linear regression lines are shown in black. Pearson correlation coefficient (R) and significance (p) are shown based on AD (n = 21) and control (n = 10) samples.
bdEV surface markers suggest cellular origin changes of AD bdEVs
To study the relative contribution of different brain cell populations to bdEVs, enrichment of selected neuron, microglia, astrocyte, and endothelial cell markers were assessed on the intact bdEV surface by ECL immunoassay. Signal of each marker was normalized to the average signal of EV marker CD81, CD63, and CD9. No significant difference of these three EV markers was found between AD and controls (Supplementary Figure 5A). Among the markers we tested, neuron markers L1 cell adhesion molecule (L1CAM) and ganglioside G1a (GD1a), as well as microglia marker CD11a, were classified as undetected, with lower signal than the background of PBS and IgG1 isotype controls (data not shown). The top 10 CNS cell markers with a higher signal indicated bdEVs from different cell types, including astrocytes, endothelia, microglia, and neurons (Supplementary Figure 5B). Several cellular origin surface markers were increased in AD patients (Fig. 5A–C): including neuron markers ganglioside G2 (GD2), neural cell adhesion molecule (NCAM), and neuronal cell adhesion molecule (NRCAM); microglia markers HLA-DR/DP/DQ, CD15, CD64, CD68, CD33, CD45, and CD18; astrocyte markers CD44 and gap junction alpha-1 protein (GJA1); and endothelia cell markers CD29 and CD31.
Fig. 5
Cell of origin marker profile on AD and control bdEV surface. Lineage-specific markers were used as bdEV capture antibodies, while the ECL signal from each antibody spot was detected by the cocktail of tetraspannin CD63, CD81, and CD9 antibodies. The level of lineage-specific neuron (A), microglia (B), astrocyte (C), and endothelia. C) Proteins were then normalized to the average of tetraspannin capture spot signals. The heatmaps (left) showed the relative average ECL signal intensities of each markers as indicated by the colored bars in AD (n = 21) and controls (n = 10). The dot plots (right) illustrate the results from each of the patients and are presented as mean±SD. ns: no significant difference (p > 0.05), *p≤0.05, **p≤0.01, ***p≤0.001, ****p≤0.0001 by two-tailed Welch’ s t-test.
Cell of origin marker profile on AD and control bdEV surface. Lineage-specific markers were used as bdEV capture antibodies, while the ECL signal from each antibody spot was detected by the cocktail of tetraspannin CD63, CD81, and CD9 antibodies. The level of lineage-specific neuron (A), microglia (B), astrocyte (C), and endothelia. C) Proteins were then normalized to the average of tetraspannin capture spot signals. The heatmaps (left) showed the relative average ECL signal intensities of each markers as indicated by the colored bars in AD (n = 21) and controls (n = 10). The dot plots (right) illustrate the results from each of the patients and are presented as mean±SD. ns: no significant difference (p > 0.05), *p≤0.05, **p≤0.01, ***p≤0.001, ****p≤0.0001 by two-tailed Welch’ s t-test.
DISCUSSION
The roles of EVs in regulating CNS diseases have been inferred predominantly from studies of in vitro models and biofluid EVs, with growing but still limited studies of tissue EVs. Here, we compared the protein content of brain homogenates with those of a “10K” pelleted extracellular fraction and a purified EV fraction of control and late-stage AD brain. Proteome differences between AD and controls were most pronounced for EVs, suggesting that EV proteins may have stronger biomarker potential than other fractions. By immunoassay verification, we added evidence that both total tau and phosphorylated tau elevated in bdEVs of AD brains, and identified the increase of antioxidant proteins PRDX1 and PRDX6 in AD bdEVs. The dysregulated molecules identified in our study, especially those involved in aging and neurodegeneration pathways, may be involved in CNS disease mechanisms and constitute new biomarkers for disease monitoring after release from brain tissue into the circulation or other peripheral compartments. Furthermore, the profile of bdEV surface markers indicated that certain cells release more EVs or EVs with higher density of cell-specific surface markers. These markers of neurons, microglia, astrocytes, and endothelial cells may also be tested for bdEV capture in the periphery.
Based on our proteomics results, although BH, 10K and EVs all contain neurodegenerative diseases related proteins, EVs could serve as a better potential biomarker to indicate late-stage AD pathology as the distinct proteome between AD and controls was only revealed by EVs. We previously reported 10K as an intermediate vesicle fraction between BH and EVs which contain more intracellular contents [31], again in this study, only a few proteins significantly differed between AD and controls in 10K as well as BH, while highly purified EVs harbor more AD pathology specific information. The reason that bdEVs are more reflective of AD pathology than BH or 10K could be that bdEVs shuttle in interstitial fluid through different brain regions. Therefore, bdEVs may carry information from regions other than the source tissue, as revealed by previous imaging studies [43]. Also, in addition to passive incorporation, AD pathogenesis may also affect selective package of molecules in EVs.
Based on immunoassay verification, the dysregulation of the AD-related tau protein was confirmed in independent bdEV preparations. EVs have been widely reported to propagate misfolded tau in neurodegenerative disease [15, 44]. Consistent with other bdEV studies [15, 16, 45, 46], we found a higher level of total tau (t-tau) and phosphorylated tau (p-tau) in bdEVs of AD compared with controls, adding more support for tau propagation in brain through EVs. The antibody we used targeted the threonine 231 (T231) site of the middle tau protein region. The dysregulation of P-tau T231 we showed in the source brain tissues and bdEVs further supports its biomarker potential, as previously identified in preclinical AD plasma and CSF samples for AD [47]. Although the change of p-tau T231 in bdEVs reflected changes in BH, as shown by correlation analysis, our study detected t-tau differences only in EVs but not in 10K or BH. This observation suggests that release of t-tau and p-tau in EVs is a dynamic process that may depend on different turnover rates of tau isoforms [48] or tau posttranslational modifications [45]. While tau and p-tau in EVs are well characterized, mechanisms of disease propagation are still incompletely understood. Further study is thus needed to determine if EVs act as a protective factor to clear tau from the CNS to the periphery, as a neurotoxic factor by spreading tau between neurons and glia, or perhaps in different ways in some as-yet incompletely understood balance between these two poles.
We also revealed upregulation of bdEV PRDX1 and PRDX6 in AD. PRDXs are antioxidant enzymes implicated in the progression of neurodegenerative diseases by regulating oxidative stress. We and our collaborators previously found that PRDXs were highly abundant in EVs derived from both human induced pluripotent stem cells and mesenchymal stem cells, and that these proteins help to reduce oxidative stress in cells with induced senescence [49]. In AD brain tissues, the change of PRDX levels is inconsistently reported and likely region-dependent [50]: PRDXs were reported elevated in some brain regions of AD patients in one study [51], but were not different in another study [52]. The expression of PRDXs is also cell type-specific in the CNS [50], as previous studies showed that PRDXs were detected mostly in astrocytes. In our study, we observed no significant change of PRDXs in BH samples between AD and controls, whereas loading into bdEVs was apparently different. Considering that bdEVs hail from different cell types, astrocytes may contribute to the elevation of PRDX1 and 6 in the bdEV pool. Although regulatory roles of PRDX family members were shown in AD [53–55], and the association of PRDX with EVs [56, 57] has been reported, we reveal here the differential loading of PRDX into bdEVs. Further exploring the cell source of PRDXs in bdEVs in tissue or in the periphery may allow even stronger conclusions about biomarker potential.
bdEV protein clusters are actively involved in CNS disease regulation pathways, including mitochondrial and metabolic pathways and neurogenesis/differentiation pathways (Fig. 2F). For example, the ATPase enzyme member valosin-containing protein/p97 (VCP) is thought to bring about mitophagy impairment and mitochondrial dysfunction in AD [58, 59] and was upregulated in AD bdEVs. Impairment of pathways involved in neurogenesis/differentiation are thought to be early clinical events in aging and AD development [60, 61]. Our study showed dysregulation of neurogenesis-related protein 14-3-3 isoforms ɛ (YWHAE), ζ (YWHAZ), and γ (YWHAG) in the 10K and EV fractions. 14-3-3 proteins indirectly regulate activation of Rho family GTPases [62]. Interestingly, several proteins in the Rho-GTPase cycle were also dysregulated in AD bdEVs, including Ras-related C3 botulinum toxin substrate 1/3 (RAC1/3), and Rho GDP-dissociation inhibitors 1 and 2 (ARHGDIA, GDI2). We also found that contactin-1 (CNTN1) and neurofascin (NFASC), two proteins involved in axonal guidance and neuron projection development [63, 64], were downregulated in AD bdEVs, which may reflect neurodegeneration.
EVs derived from specific cellular origins in brain may have enhanced potential as biomarkers. However, isolation of pure, highly cell-specific bdEVs from blood is challenging because of interfere of peripherally derived EVs and non-EV components (e.g., lipoproteins). Also, most of previous studies investigated blood-isolated neuron-derived bdEVs [14, 23, 24], while other sources have been less investigated. In the current study, we detected a panel of potential CNS cell markers on intact bdEVs while largely excluding contaminants. We identified multiple cell-specific markers on bdEVs, with astrocyte/glia marker CD44 as the most abundant. Of course, few markers are exclusively specific to a single cell type; CD44, for example, is particularly abundant on astrocytes [65] but can also be found on other glia [66]. Markers with potential cellular overlap are shown in the Supplementary Table 4. Possibly, a panel of antibodies might be used to increase both specificity and sensitivity for biomarker approaches using cell-specific EVs.
As a mixture of EVs from diverse cells, both biogenesis and cargo loading of specific EV subtypes may be affected by AD. As in several previous studies of human cortex bdEVs [67, 68], we did not observe differences in overall EV recovery. However, bdEVs of specific cells may experience different release patterns. For example, while MHC class I bdEVs were reported to be upregulated in preclinical AD patients compared with controls and late-stage AD in previous study [68], here we found increased MHC class II- HLA-DR/DP/DQ on the bdEV surface in AD patients. As a microglial marker [69, 70], the elevation of HLA-DR/DP/DQ on bdEVs may indicate more EVs or EVs with surface changes being released by microglia in response to immune activation and tissue damage in AD. Further study is in need to evaluate the function of bdEVs from specific cell types after separating them based on the surface markers we identified.
In summary, our study examined both the lysed bdEV proteome and selected surface markers on intact bdEVs from AD patients. Our results identified the bdEV protein composition varied with AD pathology. These bdEV-transported molecules may play critical roles in modulating AD progression and thus have potential for exploitation as biomarkers and therapeutic targets. The cell surface markers we identified on bdEVs could be further tested in peripheral samples for brain-origin EV capture.
ACKNOWLEDGMENTS
VM and KWW gratefully acknowledge support from the Richman Family Precision Medicine Center of Excellence in Alzheimer’s Disease including helpful comments and advice from founder and director Constantine Lyketsos. Thanks to: Kenneth Pienta, Johns Hopkins University School of Medicine, for access to the Nanoflow FCM (NFCM) platform; Mitchell Science Writing for manuscript editing and citation formatting; and the La Trobe University Comprehensive Proteomics Platform. We also thank members of the Witwer and Retrovirus Laboratories, Johns Hopkins University School of Medicine, and various members of the International Society for Extracellular Vesicles for valuable discussions and support.
This work was supported in part by grants from the US National Institutes of Health: AI144997 (to KWW, with support for TAPD), MH118164 and AG057430 (to VM and KWW), UG3 and UH3 CA241694 (to KWW), UH2MH118167 (to DAR), supported by the NIH Common Fund, through the Office of Strategic Coordination/Office of the NIH Director, and by the National Health and Medical Research Council of Australia (GNT1132604 to AFH). JHU Alzheimer’s Disease Research Centers NIH P30 AG 066507 and BIOCARD NIH U19AG033655.
Authors’ disclosures available online (https://www.j-alz.com/manuscript-disclosures/22-0322r2).
SUPPLEMENTARY MATERIAL
[1] The supplementary material is available in the electronic version of this article: https://dx.doi.org/10.3233/JAD-220322.
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Which Is the Best Home Workout?
We all know that exercise is important for our health, but with our busy schedules it can be difficult to find the time to hit the gym. So, what’s the best home workout?
Introduction
Finding the best home workout is essential for getting the most out of your home exercises. Whether you’re just starting out and looking for something basic or are an experienced athlete who desires more challenging routines, it is important to find an exercise program that fits your goals. There are several different types of home workouts available, each with their own advantages and drawbacks. This article will provide an overview of the most popular exercise routines, including resistance training, interval training, calisthenics, yoga and Pilates. We will discuss the specific benefits associated with each type as well as provide tips for creating a successful routine that works for you.
Benefits of Home Workouts
Home workouts can be a great way to exercise without having to go to the gym. They can be tailored to your specific fitness goals and can help you save time and money. Home workouts can also be incredibly convenient, as you can do them anywhere with minimal equipment. Let’s explore some of the additional benefits that come with doing home workouts.
Convenience
One of the main advantages of doing a home workout is the convenience it offers. With a home workout, you don’t have to worry about driving to the gym, waiting for equipment or dealing with crowded gyms. You don’t have to waste time, money and energy on getting to and from the gym, or on paying for costly memberships and extra amenities. You can simply put on your workout clothes, switch up your playlist, grab your gear and get sweaty right in the comfort of your own home.
Along with this convenience also comes flexibility since you can do your workouts at anytime that best fits into your schedule; first thing in the morning, making use of short breaks during your work day or late in the evening – all without any time limits or restrictions like those found at gyms. The lack of time constraints makes it much easier to commit yourself to regular physical activity because you know all you need is 10-30 minutes at any given time throughout your day. Working out from home also gives you more control over what type of exercises you do as well as how challenging these exercises are; thus creating a holistic experience that is both specific and tailored to suit individual needs and preferences.
Cost-effectiveness
Exercising at home can be a cost-effective way to stay fit. No need for expensive gym memberships or monthly fees; all you need is the space and equipment necessary to get started. Home workouts can involve minimal equipment such as dumbbells, resistance bands, yoga mats, and pull-up bars. With just a few items you can customize your own workout program or fitness routine tailored to your needs and preferences – making it convenient and budget friendly! Additionally, there are plenty of online resources that provide workout videos, plans, and guidance at no cost. This makes it easy for anyone to have access to professional guidance even when money might be tight. Furthermore, video streaming subscriptions such as Amazon Prime Video or Netflix also offer a wide selection of free fitness programs allowing users to experiment with different methods until they find the one that best fits their lifestyle. All in all, exercising from home is an economical way to keep the body in shape!
Safety
Safety is an important consideration when you’re contemplating a home workout. Without the supervision of an experienced fitness instructor, you may not move correctly and could risk injuring yourself. Especially with weights, incorrect form puts you at risk of a strain or more serious injury. Additionally, it’s important to warm up before starting any activity, as well as cool down at the end with blood flow enhancing movements like stretches and walking, to ensure that your muscles don’t lock up too much after finishing your exercise session.
Another point of safety is ensuring that the equipment that is being used for the home workouts is stable and safe enough for use – such as checking for wear on ropes or bands, being sure all nuts and screws are tight on machines or boards, and ensuring weights are firmly secured. Proper form can also prevent missteps from becoming injuries; be sure to keep proper posture throughout your workout so you don’t do anything “wrong”. Finally, it’s always a good idea to check in with a health care professional prior to beginning any new physical activity; they will have the expertise to identify any potentially problematic areas which may need particular attention when engaging in physical movement or exercise.
Types of Home Workouts
When it comes to working out at home, there are many options available. From bodyweight exercises to equipment-based workouts, there is something for everyone. Whether you’re just getting started with home workouts or looking for a new routine, there is a perfect type of workout for you. In this section, we’ll dig into the different types of home workouts that can help you reach your fitness goals.
High-Intensity Interval Training (HIIT)
High-Intensity Interval Training (HIIT) is a form of exercise that combines short periods of intense activity with recovery periods of low-intensity activity. It is designed to be time efficient and have the potential to provide the same health benefits as more traditional longer duration exercises. HIIT workouts can vary from 10 minutes up to 45 minutes and can utilize any kind of exercise such as running, rowing, cycling, or using bodyweight exercises.
HIIT workouts are an effective way to burn fat, develop cardiovascular endurance and improve strength without any equipment or a gym membership. Workouts at home can also be tailored for each individual according to their specific fitness and ability levels. HIIT is great for busy people who cannot commit large blocks of time for regular workout routines – it’s quick, efficient and provides great results in minimal time frames.
The intensity level of HIIT is what separates it from other forms of exercise. It should be hard enough that you are pushing your limits during the active stages while still being able to recover in time for the next interval. Every workout should be slightly different with alternative exercises utilised so you do not become bored or overwork your body in one single activity over a long period of time
Bodyweight Exercises
One of the most popular types of home workouts is bodyweight exercises. These are exercises that use minimal or no equipment and rely on the body for resistance. With little cost and time investment, these exercises can be done almost anywhere, anytime. Popular bodyweight exercises include push-ups, squats, planks, lunges, burpees, triceps dips, and calf raises. Bodyweight exercises not only provide a great complete body workout but also allow you to exercise and tone specific muscle groups as well.
These types of home workouts are perfect for people just starting their fitness journey because they don’t require any equipment or gym memberships – which can be costly – yet still offer numerous benefits like improved strength and flexibility. Building strength in your own body should always be the foundation of any workout before you consider adding weights or other equipment into your routine. Once you master the basics like push-ups and squats, you can begin to add variations on these movements to target specific muscle groups and keep your routine fresh!
Resistance Training
Resistance training is one of the most popular methods of home workouts. Resistance training involves using your own bodyweight, or any other resistance source such as weight machines, weights, elastic bands and stability balls. This type of strength training helps strengthen muscles, increase endurance and burn calories. Exercises can be adapted to any fitness level by manipulating the number of repetitions, resistance levels and rest intervals. Some popular resistance exercises include:
– Pushups
– Pull ups
– Squats
– Lunges
– Tricep dips
– Planks
– Burpees
– Shoulder press
– Jumping jacks
The key to success with resistance exercises is to maintain good form and technique throughout each movement. It is important to start slowly and gradually progress as you get stronger over time. Resistance exercises can also be modified for both higher intensity workouts or light sessions depending on one’s fitness level and goals. In addition, combining different types of movement patterns increases effectiveness in a complete workout routine.
How to Choose the Best Home Workout
With so many options for home workouts available, it can be hard to know which one is the best for you. Each workout has its own benefits, so selecting one that fits your needs and lifestyle is essential. It’s important to consider the time commitment needed, the type of equipment available, and the intensity of the workout. Let’s explore how to choose the best home workout.
Consider your goals
When choosing the best home workout for you, take some time to consider your goals and preferences. Before beginning any type of exercise program, it is important to set realistic goals that are tailored to your current fitness level. Knowing exactly what you want to achieve helps you pick the right exercise plan and create a successful routine.
The type of home workout that works best for you depends on both your short-term and long-term fitness goals. For those seeking weight gain or weight loss, the balance of cardio versus strength exercises is important. For example, those looking to build muscle should focus on strength training while those wanting to lose weight may have more success with an aerobic workout routine such as running or walking.
Flexibility exercises should also be included in any complete exercise program — yoga and pilates are great for this — as well as activities designed specifically for stretching such as foam rolling. If strength training is a priority, look into equipment like resistance bands, kettlebells and weights which can all provide an effective workout without breaking the bank.
Be sure to give yourself enough time for recovery between workouts so that your body can properly rest and heal after each session. Making sure you get adequate rest days in addition to your regular workouts will help ensure you can keep up with any routine over time. Finally, if ever in doubt about which type of activity or regimen is right for you it’s always best seek out advice from a qualified fitness expert or healthcare provider first before pursuing any sort of self-guided program.
Consider your fitness level
When it comes to choosing the best home workout, a good place to start is by considering your current fitness level. Are you a beginner or have you been exercising regularly? Is there an area of your body that needs extra attention? Do you need a workout that focuses on improving strength, flexibility or cardiovascular endurance?
For beginners, low-impact exercises such as walking or yoga can be great ways to start your journey towards improving fitness. Start with 10 minutes of activity and gradually add more as you gain strength and stamina. Strength training is beneficial for everyone regardless of skill level. Bodyweight exercises like push-ups, squats and lunges are great starting points for beginners who want to build lean muscle and improve their overall fitness level.
If you’re looking for an intense workout that will really challenge your cardiovascular capacity and endurance, high-intensity interval training (HIIT) workouts are an excellent choice. HIIT workouts involve alternating between intense bursts of activity with periods of rest in between each set, making them ideal for those who want to build strength and burn calories in one session. If a HIIT routine seems too difficult at first, consider researching other forms of aerobic exercise such as running or cycling. Finding the right mix of activities that suits your current level of fitness will help ensure success in any home exercise program.
Consider your schedule
When deciding which home workout is best for you, consider your existing daily schedule. How much time do you have to dedicate to a workout? Having a set number of minutes in mind can help you narrow down the options and find a routine that will fit into your day. Also, think about when you turn in for the night and whether or not you’re comfortable with having an intense workout at that time. You may find that some mornings are better than others for getting your exercise done quickly and efficiently, or that scheduling time for pre-bed stretching has its benefits as well.
Another factor to consider is whether or not you’re working out with someone else. Having a partner can make it easier to stay motivated and stick with the program. If there are only two of you, look into circuits and reps exercises which can be modified to fit any level of fitness level without compromising quality. If there’s more than two of you looking to train at home, look into team workouts such as an agility ladder and medicine ball tosses – these are designed to work with three or more people while promoting fun and healthy competition among friends. Finally, if going solo is more your style, explore yoga and Pilates videos which provide detailed tutorials tailored towards the individual user.
Conclusion
Gathering real evidence of the effectiveness of home workouts is difficult because of the many variables that come into play. However, certain home workouts have been shown to produce reliable outcomes for different fitness goals. Strength training can be done with free weights, weight machines, resistance bands or bodyweight exercises, and aerobic exercises can include running, cycling and HIIT classes. No matter what kind of workout you choose, it’s important to focus on good technique and correct breathing to ensure you get the best results and prevent injury.
To get optimal results, you will also need to focus on your diet: what you eat as well as when and how much you’re eating. Incorporating a balanced diet into your lifestyle will help your body recover more quickly from vigorous exercise and make sure it has the fuel needed for each workout session. Planning your meals ahead of time will also make sure you are getting enough vitamins and minerals from food sources as well as getting in enough calories to meet your energy needs.
Ultimately, the best home workout is the one that meets your individual fitness goals while fitting within reasonable time constraints and available resources (as equipment or space). With a little planning and research — both into what types of workouts are right for your fitness level as well as which ones offer good value — it’s possible to put together an effective home workout plan that’s right for you.
Checkout this video:
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-5,557,648,452,275,170,000 | Critical Care Medicine
Analgesia in the ICU
Analgesia in the ICU
Synonyms
Pain assessment, pain control, pain relief
Related Conditions
Postoperative pain relief
Analgosedation
Catheter/apparatus discomfort/naso/orogastric tubes
Endotracheal intubation/suctioning/chest tubes
Phlebotomy/vascular access
Occupational/respiratory/physical therapy
Routine turning and positioning
1. Description of the problem
Postoperative pain control remains a major issue for clinicians and patients, particularly for sick patients admitted to critical care units. Literature review suggests that ~70% of postoperative patients suffer from moderate to severe pain despite the recognition that adequate pain control enhances recovery and discharge after major illnesses. Recent surveys have also suggested that pain and discomfort in mechanically ventilated patients are predictors for development of post-traumatic stress disorder. Inconsistencies in analgesic prescription and wide variations in monitoring sedation and analgesia are common among critical care patients. There is evidence to suggest that inadequate pain control has deleterious effects and is associated with cardiovascular risks, immunosuppression, neuroendocrine stress, coagulation abnormalities, and delayed gastric emptying. Therefore, it becomes the responsibility of physicians and nurses caring for these patients to critically evaluate their practice regarding pain management and to adopt an optimal pain management strategy that includes analgesia and reduction in painful stimuli and promotes education among healthcare professionals.
Optimizing analgesia in the critical care unit poses several challenges in the presence of altered physiology and trauma, including the need for early extubation and rehabilitation. Opioid-related prolonged sedation and accumulation of metabolites results in delayed recovery. Moreover, in mechanically ventilated and sedated patients, conventional pain assessment tools cannot be used because these patients cannot communicate verbally.
In a recently conducted survey of 44 intensive care units, sedation and analgesia assessments did not routinely occur in patients receiving these therapies. In addition, procedural pain (physical therapy, urinary catheterization, bronchoscopy, wound management, establishing central vein lines, and dialysis cannulas) was poorly treated, and patients requiring these interventions tended to be deeply sedated. Achieving a balance between adequate pain control and the need for early extubation and discharge is the key difference in analgesic control in critical care setting. A mechanistic approach and multimodal analgesic technique has been clearly demonstrated to be the most effective pain management strategy to improve outcome. An analgesia- sedation protocol for trauma patients reduces the number of ventilator days and the length of hospital stay. Where appropriate, it is important to adopt regional anesthetic technique to mitigate the use of sedative analgesics and to improve early rehabilitation. Regional anesthesia will improve overall outcome, particularly respiratory and bowel function. Certain conditions like head injury pose unique challenges that have to be taken into account to modify the sedative-analgesic regimen. In this review we discuss an opioid-based analgesic regimen, non-opioid adjuncts, and regional analgesic techniques and suggest guidelines of care.
Many patients in the critical care unit require analgesia and sedation, particularly those patients who are mechanically ventilated. Failure to recognize the need for analgesia, which can manifest as agitation, stress and cardiovascular instability, might often lead to increasing sedation instead of administering analgesic drugs. Procedural pain may cause significant pain and discomfort in critically ill patients, which can be compounded by pre-existing chronic pain.
The consequences of inadequate pain control are manifold, including detrimental effects on respiratory, cardiovascular, immunological, and endocrine disturbances and sleep deprivation. In addition, poorly treated acute pain can lead to a chronic pain state through a wind-up phenomenon wherein repeated painful stimuli lead to a frequency-dependent increase in the excitability of central neurons and eventually a hyperalgesic state.
Types of pain:
Somatic (localized) - usually responds to opiates
Visceral (cramping) - usually responds to anticholinergics
Neuropathic (burning/shooting) - responds to gabapentinoids and antidepressants
Mixed - requires combination therapy
Chronic - seen commonly in ICU patients postoperatively who are admitted postop but have some underlying chronic pain issues
Pain should be anticipated as a ubiquitous experience of all critically ill patients. Assessment of pain is mainly subjective experience and in critically ill patients the presence of endotracheal tubes and co-administered sedation makes routine assessment tools ineffective for recognition of pain and discomfort. Validated tools are available to assess sedation and analgesia, which may improve outcome. There is an impetus from several organizations, including the Joint Commission on Accreditation of Health Care Organization and the American Pain Society, to consider pain as a fifth vital sign, to improve pain assessment with a positive effect on overall outcome. Although surrogate markers lack reliability and specificity in sedated ill patients, physicians should be aware of these physiological and behavioral markers for patients who are unable to respond to oral commands. Agitation must always be assumed to have pain as a factor in ICU patients, and in most patients a therapeutic trial of analgesics must be tried.
2. Acute Pain Management
Opioid Analgesics
Severe pain in critically ill patients should be treated with opioids. These provide the intensivist with the most rapid and reliable way to deal with critical care pain. Recommended opioids include fentanyl, hydromorphone and morphine, which are all mu-receptor agonists (Table I). The choice of agent should be based on the potency, pharmacokinetics and side effect profile as well as any related organ impairment with the patient, which may guide care. For severe intractable pain, one could start treatment with fentanyl at a dose of 25-100 mcg as a bolus followed by an infusion of 25-200 mcg/hr. Peak effect is 4 minutes, and elimination half-life is 2-5 hr. If fentanyl seems insufficient one can progress to hydromorphone. Bolus dose is 0.2-1 mg, infusion is 0.2-2 mg/hr, peak effect is 20 minutes, and elimination half-life is 2-4 hr. Many units still use morphine, but with the accumulation in renal impairment this is becoming a less-favored ICU drug. Dosage for morphine is 1-4 mg bolus, 1-10 mg/hr infusion, peak effect 30 minutes, and elimination half-life of 2-4 hr.
Table I.
Drugs frequently used to deal with ICU pain.
Non-opioid Analgesics
Although opioids are the foundation of any analgesic regimen, a multimodal approach is necessary to both minimize adverse opioid side effects and treat opioid resistant subtypes of pain. Several readily available drugs are worth mentioning.
Dexmedetomidine is an alpha-2 adrenergic agonist commonly used for sedation in the critically ill. In addition, it has significant analgesic properties with a demonstrated opioid-sparing effect. Its lack of respiratory depression also makes it a useful adjunct in the ICU setting, though dexmedetomidine-induced bradycardia and hypotension can limit its use in the hemodynamically unstable patient.
Ketamine is a dissociative amnestic that exerts an anti-nociceptive via NMDA antagonism. It is commonly used in the perioperative setting and is particularly useful in opioid-tolerant chronic pain patients. Appropriate dosing for post-operative analgesia is 0.1-0.4 mg/kg/hr in combination with opioid therapy. Recent studies have demonstrated a possible role for ketamine as an analgosedative in the ICU. It is an excellent bronchodilator primarily due to secondary release of endogenous catecholamines, and there is no associated respiratory depression. Ketamine causes dreaming and hallucinations, which can be dysphoric. Patients with pre-existing delirium, PTSD, or psychosis are poor candidates for ketamine therapy.
Gabapentinoids (gabapentin and pregabalin) are mainstays in the treatment of neuropathic pain. They work through binding of the alpha-2-delta subunit of voltage gated calcium channels. Both have been shown to decrease pain scores and opioid consumption in various postsurgical populations. The gabapentinoids are mildly sedating. They are renally excreted and can accumulate in patients with decreased creatinine clearance. Abrupt discontinuation should be avoided as a withdrawal syndrome similar to that of alcohol or benzodiazepines can occur.
Regional Anesthesia
Regional anesthesia in the ICU setting offers both significant benefits and challenges. Peripheral nerve blocks have been demonstrated to decrease opioid consumption and pain scores leading to earlier mobilization. However, in deeply sedated patients it is difficult to identify complications including peripheral nerve injury and potentially catastrophic local anesthetic systemic toxicity (LAST). The American Society of Regional Anesthesia (ASRA) recommends against regional anesthesia in the deeply sedated patient. In addition, in instances of coagulopathy and anticoagulation/antiplatelet therapy, the benefits of a peripheral nerve block must be weighed against the potential for bleeding complications.
Problems with pain identification:
Untreated pain is difficult to differentiate due to lack of communication, and it affects all body systems. There is a synergistic effect of pain on anxiety, depression and sleep. All modalities are unpredictable in the ICU and have unwanted side effect profiles.
3. Diagnosis
Various scoring systems for pain assessment have been validated for the ICU. The most recognized are the Faces Pain Rating Scale and the Visual Analog Scale. Pain questionnaires have also looked at qualitative aspects of pain. Tools such as the Adult Nonverbal Pain Scale, based on the pediatric FLACC scale, and the Critical-Care Pain Observation Tool have been created to better diagnose the sedated or unresponsive patient. These rely on some combinations of physiologic variables and patient behavior.
Pathophysiology
A principled approach to pain management in the ICU allows for the care of these complex patients to be optimized. The best ICU approach to pain is that of an interdisciplinary model. Due to the complex nature of the origin of a patient's pain, taking a team-oriented approach leads to inclusion of all modalities of pain relief so that pain treatment is effective.
There are key principles that should guide our treatment of ICU patients:
• Presume that pain is present, even if there is little supporting evidence.
• Early recognition is key to effective management. Unopposed pain will escalate, making subsequent treatment more difficult.
• Avoid continuous sedation and analgesia; it leads to tolerance as well as build-up of these medications.
• Avoid abrupt withdrawal of pain medications in an effort to extubate patients, leading to acute withdrawal and delirium.
In the ICU, pain originates from repeated episodes of acute or short-term stimulation as well as some degree of chronic or sustained pain. Acute pain can originate from the acute underlying illness, or be iatrogenic from therapies. Chronic pain in the ICU can be from a condition that the patient has brought into the unit or from repeated events occurring on the unit.
Epidemiology
Pain subtypes seen in the ICU include neuropathic, somatic, visceral and mixed. The ability of physicians to differentiate these on the ICU can be limited by the patient's ability to cooperate in a good history and physical. Generally most patients in the ICU experience somatic pain. This is defined as dull or aching and is often well localized. As for treatment, patients respond well to nonsteroidal anti-inflammatory agents (when appropriate) as well as opiate drugs. Visceral pain that is cramping/colicky can arise from ICU ileus or from underlying GI pathology. This pain generally responds well to anticholinergic therapy. Neuropathic pain, which is generally burning/shooting in nature, occurs less commonly on the unit but still responds well to gabapentinoids, antidepressants, and anticonvulsant medications.
Special considerations for nursing and allied health professionals.
Pain produces systemic effects that may add to the severity of the underlying illness of ICU patients. Pain affects all systems of the body, through sympathetic outflow, hormonal regulation, catecholamine release and general stress response. This will result in tachycardia, anxiety, diaphoresis, lacrimation, etc., all leading to a rise in catabolic metabolism leading to increased oxygen requirements, increased myocardial stress, increased bowel motility, altered lung function and also adverse renal function due to activation of the renin angiotensin system (RAS). Untreated pain can lead to immune dysfunction, coagulation problems with increased thromboembolic problems, altered blood sugar levels, cardiac problems (ischemia, ventricular dysfunction, arrhythmias, etc.). Finally, pain will alter sleep patterns, leading to poor recovery, delirium and PTSD.
What's the Evidence?
The current emphasis on evidence-based practice requires that guidelines be developed that combine a scientific basis and expert opinion. If one looks at the Wellness model from the World Health Organization's treatment of pain after cardiac surgery, we can see that guidelines and protocols lead to effective management of post-cardiac surgery pain. If one looks at the complexity of ICU pain, we need to have organized protocols to help us care for these patients. The examination of published literature reviews and evidence-based guidelines can facilitate the development of institution-specific guidelines.
Looking from an evidence-based perspective, one can put in to practice these guidelines to facilitate treatment:
Clinical pathways:
Pathways provide a consistent and repeatable timeline for planning individualized patient care. The pathway details the precise course of the patient, including multidisciplinary elements. These detail not only treatment pathways but also history, exam, diagnostics and treatment. This incorporates pre-emptive treatment for procedures, as well as management of chronic pain issues.
Checklists:
These differ from protocols as they are a way to verify that clinical pathways or tasks are completed. This is a good way to ensure that pathways or tasks are followed. This also helps prevent errors.
Daily Goals:
By having some way of highlighting daily goals (white board, electronic reminders, etc.), all members of the multidisciplinary team can access the plan and ensure that the patient is being treated from all perspectives.
Final points: Consider referring more complex patients to the hospital pain team. For example, if a patient is on multi-modal therapy from the team and still experiencing severe pain, referral to the pain team can often lead to an increased level of support that would benefit him or her. This is also true once patients have been discharged from the unit; they still need to be looked after by a multimodal rehabilitation team.
Sources
Herrero, JF, Laird, JM, López-García, JA. "Wind-up of spinal cord neurones and pain sensation: much ado about something". Prog. vol. 61. Neurobiol 2000. pp. 169-203.
Lin, TF, Yeh, YC, Lin, FS. "Effect of combining dexmedetomidine and morphine for intravenous patient-controlled analgesia". Br J Anaesth. vol. 102. 2009. pp. 117-22.
Venn, RM, Karol, MD, Grounds, RM. "Pharmacokinetics of dexmedetomidine infusions for sedation of postoperative patients requiring intensive caret". Br J Anaesth. vol. 88. 2002. pp. 669-75.
Angst, MS, Clark, JD. "Ketamine for managing perioperative pain in opioid-dependent patients with chronic pain: a unique indication". Anesthesiology. vol. 113. 2010. pp. 514-15.
Subramaniam, K, Subramaniam, B, Steinbrook, RA. "Ketamine as adjuvant analgesic to opioids: A quantitative and qualitative systematic review". Anesth Analg Aug. vol. 99. 2004. pp. 482-495.
Trupkovic, T, Kinn, M, Kleinschmidt, S. "Analgesia and sedation in the intensive care of burn patients: Results of a European survey". J Intensive Care Med. 2011.
Chang, CY, Challa, CK, Shah, J, Eloy, JD. "Gabapentin in acute postoperative pain management". BioMed Research International. 2014. pp. 631756.
Aguirre, J, Del Moral, A, Cobo, I, Borgeat, A, Blumenthal, S. "The role of continuous peripheral nerve blocks". Anesthesiology Research and Practice. vol. 2012. 2012. pp. 560879.
Neal, JM, Bernards, CM, Hadzic, A. "ASRA practice advisory on neurologic complications in regional anesthesia and pain medicine". Regional Anesthesia and Pain Medicine. vol. 33. 2008. pp. 404-15.
Odhner, M, Wegman, D, Freeland, N, Steinmetz, A, Ingersoll, GL. "Assessing pain control in nonverbal critically ill adults". Dimensions of Critical Care Nursing: DCCN. vol. 22. 2003. pp. 260-67.
Gelinas, C, Fillion, L, Puntillo, KA, Viens, C, Fortier, M. "Validation of the critical-care pain observation tool in adult patients". Am J Crit Care. vol. 15. 2006. pp. 420-27.
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7,649,431,641,978,657,000 | Title
The chemistry of rhenium with hydrazines and thiols
Date of Award
1998
Degree Type
Dissertation
Degree Name
Doctor of Philosophy (PhD)
Department
Chemistry
Advisor(s)
Jon Zubieta
Keywords
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Subject Categories
Chemistry
Abstract
A number of rhenium compounds were synthesized and characterized in attempts to investigate and expand the coordination chemistry of the widely used medicinal imaging radioisotope technetium-99m. Rhenium and technetium are Group VII cogeners whose hydrazine and oxo-thiolate chemistries are very similar. The periodic similarities have allowed for the study of the non-radioactive metal rhenium instead of the synthetically created technetium, which exists only as radioactive isotopes. Influencing the chemistry were two schools of thought for delivering the potential radiopharmaceutical agents. The first concept, the conjugation technique tethers the metal to a biomolecule with specific biodistribution patterns. In this case, we explored hydrazines as potential tethers, forming the class of compounds (MCl$\sb3(\eta\sp1$-NNC$\sb5$H$\sb4$NH)($\eta\sp2$-H$ \sb{\rm x}$NNC$\sb5$H$\sb4$N)) (M = Re, Tc, or Mo). The study continued with the exploration of the chlorine substitution with potentially useful thiol coligands.
The second approach, the "integration technique," utilizes small molecules to incorporate the metal. Here, we designed rhenium-mixed-thiolate complexes, aiming to improve biodistribution by varying steric requirements and charges. Thiolate complexes were evaluated because of their high yields, ease of isolation and characterization, and the ability to synthesize and derivatize novel thiols with relative ease. We systematically synthesized and characterized numerous metal-thiolate complexes, with a heavy emphasis on investigating the coordination chemistry.
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-6,838,571,218,332,295,000 | Receding Gums Natural Cure
Cure For Receding Gums
Exactly what will be the causes of Receding Gum lines and just how do you cure these? Here are some of the possible motives behind the occurrence of this condition:
Genetics: Some people are genetically more prone to receding gum lines. Periodontitis: periodontitis can be actually a chronic gum disease which can destroy the supporting bone and gum tissue around the tooth’s root canal. Gum Disease could also be caused by certain medications like aspirin, nitroglycerin, phenobarbital, trichloroacetic acid, chloroquine, gabapentin, reserpine, tramadol, vincristine and tetracycline. For More Info Visit Receding Gums Natural Cure
Age: The effects of age may contribute to the look of this illness too. The impacts of advancing age are the decreased blood flow to the gums due to decreased production of this elastin and collagen in the human anatomy. Other causes of decreased blood supply may be due to extortionate gum or mouthwash intake, excessive smoking, and higher blood pressure. In addition, the gums may also lose the elasticity of these surface because we grow old, which then may give rise to the occurrence with this problem.
Periodontitis might also be due to an underlying illness like diabetes, liver and kidney disease, and inflammatory diseases like rheumatoid arthritis, Lupus, and multiple sclerosis. This is why it is a good idea to consult with a qualified physician that specializes in the assessment and diagnosis of your own case and consider all necessary measures for one to reach your objectives.
Since you can observe, there are many possible causes behind the visual appeal of a gum line. To determine which one of these is causing the problem, your dentist will first rate the degree of gum decay onto your own tooth. Once this problem has been determined, he or she will prescribe a suitable treatment.
There are several treatment options available, based upon the severity of the problem. If gum disease is not so severe, then a very simple application of gum balm might help ease the discomfort and the pain of the affected location. However, when gum disease is already serious, then more competitive treatment procedures such as laser surgery and endoscopic techniques can be useful to eliminate the gum and prevent it from returning. Get More Info Regrow Receding Gum
Best Receding Gums Cure
Cosmetic Dentistry: probably the very widely used treatment option for gum receding and also other problems linked to the mouth is cosmetic dentistry. Cosmetic dentistry may correct minor defects on the tooth’s face such as cracked teeth, uneven bite, discoloration, and irregular sting, amongst others.
Dental work done onto the teeth and gum lines is commonly done to boost the look of one’s teeth and make them look whiter and brighter. This is sometimes accomplished by whitening the enamel and filling in gaps between the teeth to make the tooth appear longer and straighter. The use of alloy veneers may also be utilised to produce one’s teeth more attractive, even if they’ve not been completely removed.
Gum extraction is another popular way to improve the form and appearance of the gum line. It involves cutting the borders of the teeth to bring them closer together and smoothing out the gums and creases to the gum line.
Dental crowns may also be used to improve the appearance of tooth. These could be set up on the gum lines and will either cover the full gum line or may be set up along the gum line to cover a particular tooth or teeth. Dental crowns are made from ceramic or composite material and are secured to the gum line to produce a more natural look.
Gum traction is just another frequent procedure that can be used when treating gum receding and other gum line-related problems. This treatment works by applying pressure into the gum tissue by employing a small amount of force over the gum line. This is sometimes effective in reducing the gum line. For More Info Visit: https://www.purestacaiberry.org/stop-pain-from-receding-gums/
Best Natural Cure For Receding Gums
Gum contouring can also be used to whiten out a tooth or teeth and restore its own natural appearance. Tooth contouring is accomplished by scratching and filing the teeth to straighten your teeth.
There are a variety of reasons that impact this particular condition and gum receding is treatable currently. But what causes gum receding?
Gum receding is defined as when the gums start to look younger than usual. Gum receding can also occur due to dental cavities and disease such as periodontal disease or periodontitis. Gum recession can also happen due to an underlying condition such as diabetes or heart disease. Most common reasons for this particular illness are age and stress.
Gum recession has many treatment possibilities now. Medications can be utilised to boost the gum health and prevent receding gum lines. Other procedures for example root planing or dentures could also be used to fix the status.
Gum recession might also be treated using a number of medications that are designed to help take care of the health of the gums. These generally include antibiotics to treat gum disease. Compounds are also known to be more effective in curing the bacteria that cause gum disease and gum receding.
Oral Hygienists are also trained to help in treating gingivitis. This can be accomplished by brushing and flossing and also by using special devices which can wash your teeth and steer clear of bacteria and plaque from forming in your teeth. This will definitely help prevent receding gum lines.
How To Cure Receding Gums Without Surgery?
There’s also some natural remedies that can be utilised to prevent gum receding. These include herbal products and gingivitis treatments. Some of the treatments may be obtained orally.
When gum recede on its own won’t heal itself, it is still a good idea to understand your dentist to get an exam. Your dentist may assess for other underlying problems that might be causing the gum recede and give you a better probability to improving results.
In case the receding gum lines cannot be treated, you then may want to have a root canal or alternative procedure to fix them. In either situation, it is important to speak with your dental healthcare provider before having any treatment.
Your dentist will be able to tell one of the perfect way to see to your gum recede. They are able to consult with someone who’s capable to perform the treatment.
Root planing is an operation that involves removing the portion of the tooth that was causing the gum receding. This tooth is then replaced.
Root planing could be done by carrying out the guts or even the pulp from the tooth. This can be accomplished via a dental drilling procedure, or through root canal surgery. An activity termed veneering involves replacing the gum tissue that’s been damaged or decayed. That is done through using ceramic or ceramic crowns.
This will exchange the gum tissue using fresh gum tissue. This can be accomplished with exactly the exact same type of procedure or together with veneers. Gum surgery is yet another alternative. This system works in that tooth is clearly removed, and then a graft of the gum tissue was designed to cover up the hole inside the tooth enamel. | {
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-5,885,046,370,107,853,000 | Some Great Benefits Of Weed Are Bigger Than We Understand
A concise talk on some great benefits of weed would not be full with out showcasing both probable advantages of weed as well as likely unsafe adverse reactions of container. Though weed has several potential rewards, you will additionally learn that pot-use has numerous extremely serious unwanted side effects, that you simply ought to take note of. Simply because the majority of the feasible benefits associated with cannabis are very just media hype plus the adverse reactions are mainly brought on by not after the suitable medication dosage or method of usage. In reality, for those who have been utilizing marijuana for many years, it is actually fairly very likely that you may have definitely created some of the more widespread marijuana unwanted side effects likestress and paranoia, panic disorder, etcetera. So, what are the actual primary advantages of marijuana? And, what exactly are one side consequences?
The advantages of weed are rather large including anything from the relaxing and soothing sensations it generates to the minimized stress degree. The clinical name for this is “THC or tetrahydrocannabinol”. The attention quantities of this particular ingredient can vary from herb to shrub, even if this chemical exists in all weed plant life. In an effort to produce the “great” that others are accustomed to suffering from, the possible advantages of THC are due to the fact so it consists of several different other substances and substances, which all interact with each other. Other prospective advantages of THC are highlighted below:
o Improved Probability of Cancer Of The Lung: Some studies show that weed could cause the growth of carcinogenic tissues during the lung area, which increases the perils of getting carcinoma of the lung. Evidence around it is nonetheless continuing, as well as the accurate benefits continue to be unclear. Having said that, there has been a link involving marijuana using tobacco and various styles of respiratory system illness like emphysema and continual bronchitis, which can lead to fatality. You can also find quite a few backlinks to sociable stress and the introduction of signs or symptoms including depressive disorder and paranoia.
o Greater Risk of Psychosis: Some scientific tests show that individuals who light up marijuana, or use other derivative varieties, endure what is known the “marijuana disorder”. Symptoms feature an infatuation with marijuana, suicidal feelings, the lack of ability to concentrate onjobs and confusion, and annoyance. It has been specifically associated with hallucinations, paranoia and delusions. Whilst these signs or symptoms seem highly uncharacteristic associated with a standard disease, these are generally typical amongst those that use marijuana on a regular basis.
A number of the controlled primary advantages of cannabis also are observed in the United States, where leisure use is criminal. The cultivation, property, purchase and production and taxation with this substance are performed during the whole region. Therefore, there is no control on the manufacturing, deal, or dispersal. Lacking government regulate has supplied elevate to your dark colored sector that delivers users using what is known as “pot”, “weed”, or “garbage”, which normally features harmful contaminants and harmful side effects. These damaging unwanted side effects happen to be the subject of several research because of the medical online community, that contain brought about records detailing the negative health outcomes linked to cannabis use.
On the list of principal motives that medical experts propose the effective use of marijuana is due to the fact which it includes two major ingredients found within it: THC or tetrahydrocannabinol (THC), and CBD or cannabidiol (CBD). They are employed in combination to help you weed individuals retain their own health and reduce the unfavorable adverse reactions of utilizing cannabis, despite the fact that both these ingredients have several impacts on your body. They work with association to assist cannabis people preserve their health and minimize the undesirable negative effects of making use of cannabis, despite the fact that both of these chemicals have diverse has an effect on on your body. The key health great things about both these chemical substances are that they are entourage receptors, meaning that they send signs within one compound to a different one.
There were numerous research accomplished in recent times that show the optimistic influences that marijuana can have at a person’s physical and mental health. Nevertheless, a single study completed with the University of Buffalo in New York has shown that cigarette smoking marijuana could diminish a person’s lifespan by in between 8-10 and nine years. This study was done on laboratory mice, which for the astonish for many professionals, were proven to be highly resistant against toxicity. This means that whilst men and women may well not end up overdose or kick the bucket from taking in cannabis, research laboratory mice do, that could result in a severe lack of understanding whether or not or not legalized marijuana is truly safer in comparison to the unlawful kinds.
Another the latest analysis that considered the results of marijuana on constant ache found that the usage of the medication can lead to increased timeframe and power of constant agony. In the three contributors from the examine, 3 were actually diagnosed with persistent discomfort. Constant discomfort is characterized by consistent ache that inhibits daily activities. Including serious or long-term soreness caused bymany forms of cancer and rheumatoid arthritis, or neuropathy. A couple of in the people using this examine smoked marijuana frequently, which may support talk about why they showed indications of enhanced level and length of pain. Although there are several good records which might be built about some great benefits of cannabis, these kinds of undesirable scientific studies just prove all over again that we need to better normalize the production and dispersal of the ingredient prior to it becomes core and can be frequently used.
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-4,969,192,095,692,855,000 | Can You Drive After Root Canal-prefect guide
Yes, you can drive after a root canal if you do not feel lightheaded. After a root canal procedure, many individuals wonder if they can safely operate a vehicle.
The answer is yes, as long as you do not experience dizziness or lightheadedness. A root canal is a standard dental treatment that involves removing the infected pulp from a tooth and sealing it to prevent further damage. While the procedure does not typically impair your driving ability, listening to your body and assessing your comfort level before getting behind the wheel is essential.
If you feel discomfort or dizziness after a root canal, waiting until you fully recover before driving is best.
1. Understanding Root Canal Procedures
A root canal procedure is a dental treatment that involves removing the infected pulp from inside a tooth to relieve pain and prevent further damage. It is commonly used to save a tooth that is severely decayed or infected, restoring its functionality and avoiding the need for extraction.
1.1 What Is A Root Canal Procedure?
A root canal procedure, also known as endodontic treatment, involves the following steps:
1. The dentist starts by numbing the affected area using local anesthesia to ensure you don’t feel any pain during the procedure.
2. Next, they create an access hole in the tooth, which allows them to remove the infected pulp and clean the root canal system.
3. After cleaning, the dentist shapes the canals and fills them with a biocompatible material called gutta-percha to seal them and prevent bacteria from re-entering the tooth.
4. Finally, a temporary or permanent filling is placed on the tooth to protect it until a dental crown can be identified.
1.2 How Long Does A Root Canal Procedure Take?
The duration of a root canal procedure depends on various factors, including the complexity of the case and the number of root canals involved. However, the process can take between one to three hours on average.
1.3 What To Expect During A Root Canal Procedure?
Root Canal
During a root canal procedure, you can expect the following:
• The dentist will ensure you are comfortable throughout the procedure by administering local anesthesia.
• You may feel pressure and slight discomfort during certain stages of the procedure, but it should not be painful.
• The dentist will use specialized instruments to remove the infected pulp and clean the root canals thoroughly.
• After cleaning the canals, the dentist will shape them and fill them with gutta-percha to seal them.
• Depending on the case, the dentist may place a temporary filling or schedule a follow-up appointment for placing a dental crown.
Following your dentist’s post-treatment instructions is essential to ensure proper healing and avoid complications. After a root canal procedure, you may experience temporary sensitivity or discomfort, which can be managed with over-the-counter pain relievers.
Now that you better understand what a root canal procedure entails let’s explore whether you can drive after undergoing this treatment.
Pre-root canal advice: things not to do
Before undergoing a root canal procedure, it is crucial to be aware of what actions to avoid to ensure a smooth and successful treatment:
1. Patients should refrain from consuming food or beverages for a specific period before the scheduled root canal. Eating or drinking right before the procedure may pose challenges for the dentist, as an empty stomach facilitates a more comfortable experience for the patient and the dental team.
2. Patients should steer clear of alcohol and tobacco products in the hours leading up to the root canal. Smoking or consuming alcohol can interfere with the effectiveness of anesthesia, potentially leading to increased discomfort during the procedure.
3. It is advisable to avoid vigorous physical activities or strenuous exercise on the root canal day.
Root Canal
Physical exertion can elevate blood pressure and heart rate, complicating the administration of anesthesia and potentially increasing the risk of complications. Another important consideration is the need to communicate openly with the dentist regarding any medications being taken. Please disclose all relevant medications, including over-the-counter drugs and supplements, to maintain the effectiveness of anesthesia and interact positively with prescribed medicines. Moreover, patients should resist the urge to self-medicate with pain relievers before the root canal appointment. This can distort the dentist’s assessment of the patient’s pain level and hinder their ability to provide appropriate pain management during and after the procedure. Lastly, arriving late or unprepared for the root canal appointment is a common mistake to avoid. Punctuality is crucial to allow sufficient time for the dental team to prepare and for the patient to feel at ease before the procedure. Being well-prepared mentally and emotionally can contribute significantly to a more positive and stress-free root canal experience. In conclusion, understanding what not to do before a root canal is essential for a successful and comfortable dental procedure. By following these guidelines, patients can contribute to a more efficient and effective treatment process, ensuring optimal outcomes and a smoother recovery.
1. Safety Precautions After A Root Canal Procedure
Safe to Drive After a Root Canal? Driving after a root canal is usually safe if you don’t feel lightheaded. However, following your dentist’s instructions and listening to your body for a safe and comfortable recovery is best.
2.1 Can You Drive Yourself Home After A Root Canal?
Patients’ common question after a root canal procedure is whether they can drive home. The answer to this question depends on the type of sedation used during the process. If you did not receive any sedation or only nitrous oxide, then you should be able to drive yourself home safely. However, if you received conscious oral sedation, it is essential to have someone drive you to and from your appointment. Safety should always be a priority, so it is best to arrange alternative transportation if you are unsure about going after a root canal.
Can you eat after a root canal?
Root Canal
Root Canal
After undergoing a root canal procedure, patients often have one common question: whether they can eat immediately afterward. The answer to this question depends on various factors, including the type of anesthesia used, the complexity of the root canal, and the individual’s tolerance to discomfort. In most cases, patients are advised to wait until the numbness from the local anesthesia wears off before attempting to eat. This is crucial to avoid accidentally biting their cheeks, lips, or tongue, which may be numb and more susceptible to injury during the immediate post-treatment period.
Once the anesthesia has worn off, it is generally safe to eat, but choosing soft and non-chewy foods is essential to prevent any strain on the treated tooth. A diet that includes yogurt, soup, mashed potatoes, smoothies, and other easily chewable foods is recommended during the initial recovery period. Avoiding hot or cold foods and beverages can also help minimize sensitivity, common after a root canal. Additionally, steering clear of foods that are too spicy or acidic can prevent irritation to the healing tissues.
Maintaining good oral hygiene is crucial after a root canal and extends to dietary choices. Patients are advised to avoid hard and crunchy foods that could damage the restoration or put unnecessary pressure on the treated tooth. It’s also essential to refrain from consuming sticky or sugary foods, as they can contribute to the growth of bacteria and compromise the long-term success of the root canal.
While eating after a root canal is generally permissible, it’s wise to listen to your body and exercise caution, especially in the first few days following the procedure. If you experience persistent pain, swelling, or discomfort while eating, it’s advisable to contact your dentist for further guidance. Adhering to any post-operative instructions provided by your dental professional, including dietary recommendations, will contribute to a smoother recovery process and enhance the overall success of the root canal treatment. Balancing nourishing your body and being mindful of your oral health is key in the post-root canal period.
Root Canal
Can you drive after local anesthesia from dentist
Local anesthesia is a common component of dental procedures, employed to alleviate pain and discomfort during various treatments such as fillings, root canals, and tooth extractions. The administration of local anesthesia involves injecting anesthetic agents, like lidocaine, into specific areas of the mouth to numb the nerves and block sensation. One crucial aspect for individuals undergoing dental procedures with local anesthesia is understanding the guidelines regarding driving after the treatment. Typically, local anesthesia used by dentists has a temporary numbing effect that may last a few hours. The duration can vary based on the type and amount of anesthesia administered. As a general rule, patients are usually advised not to drive immediately after the dental procedure. The residual effects of the anesthesia can affect motor skills, coordination, and reaction time, which are essential for safe driving. It is recommended to arrange for a responsible adult or use alternative transportation for the immediate post-treatment period. Patients should wait until the effects of the anesthesia have worn off, ensuring they can drive safely without impairment.
The time it takes for the anesthesia to wear off can vary from person to person. Factors such as individual sensitivity to the anesthesia, the type of procedure performed, and the amount of anesthesia administered can influence the duration of numbness. Dentists typically provide post-treatment instructions, including guidance on when it is safe to resume normal activities, including driving. Patients must follow these guidelines diligently to avoid any potential risks associated with impaired motor function. Sometimes, patients may experience lingering numbness or altered sensation even after leaving the dental office. In such instances, waiting until full sensation returns before operating a vehicle is advisable. Ignoring these precautions and driving while still under the influence of local anesthesia can pose safety hazards for both the individual and others on the road.
Patients should communicate openly with their dentists about any concerns or questions regarding the effects of local anesthesia and driving restrictions. Dentists prioritize patient safety and can provide personalized advice based on the specific circumstances of the procedure and the individual’s response to anesthesia. By adhering to the recommended waiting period and exercising caution, individuals can ensure a smooth and safe transition back to their regular activities, including driving, after receiving local anesthesia during a dental visit.
Root Canal
2.2 Activities To Avoid After A Root Canal
After a root canal, it is crucial to take certain precautions to ensure proper healing. Here are some activities to avoid:
• Avoid chewing on hard foods or using the treated tooth to bite down heavily until the orthodontist or dentist has cleared you.
• Avoid drinking hot or cold liquids immediately after the procedure. It is recommended to wait for the first hour to pass.
• Avoid smoking, as it can delay the healing process and may cause complications.
Remember to follow your dentist’s instructions for aftercare to minimize any potential risks or complications.
2.3 Taking Time Off Work After A Root Canal
Returning to work after a root canal treatment is possible for most people. However, it is essential to note that you may experience numbness in your lips, teeth, cheek, and tongue for several hours after the procedure. If your job involves much speaking or interacting with the public, consider taking the rest of the day off to ensure a comfortable recovery. It is always advisable to listen to your body and prioritize your well-being. Consulting with your dentist about your situation can also provide personalized guidance.
1. Factors To Consider When Driving After A Root Canal
After a root canal procedure, it’s essential to consider several factors before getting behind the wheel. While driving after a root canal is generally safe, you should keep a few things in mind to ensure your safety and the safety of others on the road. This section will explore three critical factors when driving after a root canal.
3.1 How Anesthesia Can Affect Your Ability To Drive
One of the critical factors to consider when deciding whether you can drive after a root canal is the type of anesthesia used during the procedure. Anesthesia can have varying effects on individuals, and it’s crucial to understand how it may impact your ability to drive safely. While local anesthesia, commonly used during root canals, typically doesn’t cause impairment, it’s important to note that individual reactions may vary. Some people may experience lingering numbness or drowsiness after the procedure, affecting their ability to operate their vehicle.
3.2 Recommended Waiting Time Before Driving
Even if you feel physically capable of driving after a root canal, waiting a certain period is still recommended before getting behind the wheel. This waiting time allows your body to recover fully from the effects of the anesthesia and ensures that you are alert and focused while driving. The exact waiting time may vary based on individual circumstances and the extent of the procedure. It’s best to consult your dentist or endodontist to determine the appropriate waiting time before driving.
3.3 Personal Experiences And Reactions To Driving After A Root Canal
While the consensus is that driving after a root canal is safe, personal experiences and reactions may differ from person to person. Some individuals may feel completely fine and capable of driving immediately after the procedure, while others may need a more extended recovery period. Listening to your body and assessing your feelings before deciding to go is essential. Suppose you are still experiencing numbness, dizziness, or other unusual symptoms. In that case, it’s best to err on caution and wait until you fully recover before getting behind the wheel.
Always remember that the safety of other drivers and yourself on the road should come first. If you have doubts or concerns about driving after a, it’s best to seek professional advice from your dentist or endodontist.
Root Canal
Frequently Asked Questions For Can You Drive After Root Canal
Will I Be Okay To Drive After A Root Canal?
Driving after a root canal is safe if you don’t feel lightheaded.
What Can You Not Do After A Root Canal?
Driving after a is generally safe if you do not feel lightheaded. However, avoid chewing on hard foods or using the treated tooth to bite down heavily until cleared by your dentist.
Additionally, it would help if you did not chew, drink hot or cold liquids, or smoke for the first hour after the procedure.
How long does a root canal take
The duration of a root canal procedure can vary depending on several factors, and it is essential to understand that each case is unique. typically takes about 90 minutes to two hours to complete. However, the exact time can be influenced by factors such as the complexity of the tooth’s anatomy, the number of root canals to be treated, and the patient’s circumstances. The procedure involves several steps, including the initial assessment, X-rays, administration of local anesthesia, removal of infected pulp, cleaning and shaping of the root canals, and finally, filling and sealing the tooth. Some cases may require multiple appointments to ensure thorough treatment and optimal results. The dentist or endodontist, specialist, will assess each case’s specifics to provide a more accurate estimate of the required time.
Additionally, advancements in dental technology and techniques have streamlined the root canal process, making it more efficient and often reducing the overall treatment time. Patients are advised to communicate openly with their dental professional, addressing any concerns and seeking clarity on the estimated duration of their specific procedure. Overall, while the time of a root canal may vary, individuals must prioritize their oral health and seek timely treatment to alleviate pain, prevent further infection, and preserve the affected tooth.
Is There Down Time After Root Canal?
Driving after safe if you don’t feel lightheaded. It typically takes one to two weeks to fully heal, so follow your dentist’s aftercare instructions and avoid activities that strain the treated tooth. You can brush and floss as usual, but be gentle around the treated area.
Refrain from biting heavily with the treated tooth or chewing on hard foods.
Do I Need To Take Off Work After A Root Canal?
Driving after a generally safe, but it is essential to consider how you feel after the procedure. If you experience lightheadedness or discomfort, avoiding driving and rest for the day is best.
Conclusion
Driving after a root canal is generally safe if you don’t feel lightheaded. It is essential to follow your dentist’s instructions for aftercare and avoid putting unnecessary strain on the treated tooth. While some people can comfortably drive immediately after the procedure, others may need to wait longer.
Ultimately, it depends on how your body reacts to the treatment. Always prior
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} | b755ed28a90d11d590ef646404f4afc5 |
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