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Study Expands Link Between Childhood Stress and Chronic MS Symptoms

The AHA! Team — Fri, 30 Aug 2024 08:46:29 +0000

Duke Health – DURHAM, N.C. – Childhood stress may predict pain, fatigue, and mental illness in adults with multiple sclerosis, according to a study led by a Duke Health researcher. The findings, appeared online in the journal PLOS ONE, support efforts to integrate trauma-informed care and screenings for stressors into clinical practice. Childhood stress and adversity has been linked to numerous adult health outcomes This could help providers better conceptualize patient backgrounds and potential disease trajectories to create personalized approaches to patient care. “Since the original Adverse Childhood Experiences (ACEs) study in the late 90’s, childhood stress and adversity has been linked to numerous adult health outcomes, including many of the leading causes of mortality in the U.S.,” said lead author Carri Polick, Ph.D., a clinical associate in the Duke University School of Nursing. “This is, in part, due to the physiological stress response and how it sets the tone for how people experience stress and cope over their lifetime.” Researchers analyzed data from 719 adults with MS who responded to an online self-report survey deployed by the National MS Society. Researchers analyzed data from 719 adults with MS Stressors were categorized into emotional stressors, physical stressors, and environmental stressors. They were then analyzed with hierarchical modeling to show accumulation while retaining insight into specific types of stressors. This study is unique in that it moves beyond stressors that are traditionally measured, such as abuse and neglect, to capture environmental factors such as housing instability, discrimination, and the impact of living in an unsafe neighborhood. This is also the first study to include nuanced stressor data like duration and severity of exposures within the context of clinical symptoms of MS. The study found childhood emotional and physical stressors were significantly associated with the presence and severity of both fatigue and pain in adulthood. Environmental, emotional, and physical stressors were significantly associated with mental health challenges including depression, anxiety, PTSD, and other psychiatric disorders. Environmental, emotional, and physical stressors were significantly associated with mental health challenges “From a preventative perspective, teasing out which stressors are potentially most impactful during childhood is important to help inform intervention and policy efforts to decrease the stress experience and promote healthy trajectories from childhood into adulthood,” Polick said. Additional authors of the study include Robert Ploutz-Snyder, Tiffany Braley, Cathleen Connell, and Sarah Stoddard. The study received funding support from the National Institutes of Health (T32NR016914). To read the original article click here.

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Diabetes Medications Can Increase Your Risk of Multiple Sclerosis

AHA Publisher — Wed, 07 Dec 2022 08:00:33 +0000

News Staff via NaturalHealth365 – Type 2 diabetes is a chronic disease that afflicts more than 37 million people in the US alone. Many people with diabetes have to rely on medications to keep their blood sugar under control. Unfortunately, these medications often carry risks of their own. A recent study from the University of Arizona Health Sciences shows that certain diabetes medications may be linked to a higher risk of multiple sclerosis (MS). Scientists Discover a Startling Link Between Anti-Hyperglycemic Medications and MS Type 2 diabetes is an endocrine disorder that typically develops later in life, although it can come on at any time. The condition occurs when your body doesn’t respond to insulin as it should. Insulin is an essential hormone produced by the pancreas that enables your cells to use glucose (sugar) for energy. When the body becomes resistant to insulin, the pancreas must make more insulin. But eventually, it can’t keep up. This can lead to elevated blood sugar levels and, ultimately, type 2 diabetes. So, to keep blood sugar in check, diabetic people often need to take anti-hyperglycemic medication. This includes insulin injections and some other medications. However, the new study suggests that anti-hyperglycemic drugs may put people over age 45 at greater risk of developing multiple sclerosis, especially women. Multiple sclerosis is an autoimmune disorder affecting the central nervous system that causes severe disabilities. Researchers sought to better understand the role between age, sex, and anti-hyperglycemic drugs on disease risk. MS Risk Is Not the Same for Everyone For the study, researchers evaluated a database of over 151 million people. They then looked closely at 5 million of these patients who had a type 2 diabetes diagnosis as well as MS. The data revealed that anti-hyperglycemic use in people over age 45 increased the risk of MS onset. In addition, this risk was significantly higher in women compared to men. Additionally, insulin exposure was linked to the highest increase in MS risk when compared to other anti-hyperglycemic therapies. Interestingly, multiple sclerosis risk was actually lower in people younger than 45 who used anti-hyperglycemic medications. Still, the association between insulin, anti-hyperglycemic drugs, and MS risk is striking. Not only that, but diabetes often starts after age 45 for most people – the time when they’re most vulnerable to the increased risk of MS. Can You Prevent Type 2 Diabetes? Anti-hyperglycemic drugs, such as insulin injections, are often viewed as “vital” by conventionally-trained physicians for the health and survival of those with diabetes. Yet, it’s clear that these drugs can also come with unwanted side effects and risks. Fortunately, diet and lifestyle changes can clearly help prevent diabetes. In addition, exercise such as strength training or aerobic activities like walking can be a great way to lower your risk of diabetes and other chronic diseases. It’s also a good idea to avoid processed foods, sugar and artificial sweeteners. Over time, diets high in junk food can cause many health problems, including diabetes. Staying active and eating a nutrient-rich, plant-based diet is the best way to go. Sources for this article include: Sciencedaily.com CDC.gov To read the original article click here.

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Study Shows Adequate Sunlight Exposure May Protect Against Autoimmune Disease

AHA Publisher — Mon, 23 May 2022 07:00:23 +0000

Patrick Tims via NaturalHealth365 – According to a recent study done at the University of California – San Francisco, exposure to the sun can protect youngsters and young adults against multiple sclerosis (MS) and other autoimmune diseases. The scientists found that exposure to the sun’s UV rays increases vitamin D and might help prevent autoimmune diseases. Though parents have certainly been warned about subjecting their little ones to too much sun, the truth is the sun has its benefits. Not to mention that slathering on commercial sunscreens with potentially harmful chemicals poses a danger, now there is even more reason to let kids, tweens, teens, and adults enjoy the sun without excessive worry. Sunlight May Reduce Risk of MS, Research Suggests MS, short for multiple sclerosis, might be less likely to develop in individuals subjected to sunlight in considerable amounts at a relatively young age. The study referenced above indicates an association between heightened exposure to ultraviolet light and a reduction in the chances of developing MS. However, it must also be noted that significant exposure to sunlight without protection has the potential to heighten the chances of skin cancer. The study pertained to slightly more than 330 individuals between the ages of 3 and 22. The study participants had MS for an average period of seven months. As revealed in the web-based issue of Neurology, the result of the study was officially made available to the public in December of 2021. Responses to study inquiries showed that about 20% spent less than half an hour outdoors one summer ago. Only 6% of those without MS spent less than half an hour outside during the summer. The study showed that those who averaged half an hour to a full hour outside had a 52% less risk for developing MS when compared to individuals who spent less than half an hour outdoors on summer days. Sun Exposure Is More Important Than Most Think The key takeaway from the study is that the sun has meaningful benefits. Exposure to sunlight enhances vitamin levels, stimulates the skin’s immune cells that help protect against MS, and possibly even alters the functionality of immune cells to help guard against autoimmune diseases and maintain optimum health. It is interesting to note that some MS patients show symptoms during their childhood though the disease usually doesn’t fully manifest until the adult years of 20 to 50. Here Is Why Geography Is Important in the Context of MS The researchers also pointed out that those involved in the study who live in Florida were more than 20% less likely to develop MS than those living in New York state. The reduced chance of developing MS is likely the result of the heightened sunlight intensity in Florida. The study also revealed that exposure to the sun provides benefits dependent on the dose. In other words, the more time that one spends exposed to the sun, the lower the risk is for MS and other autoimmune disorders. It is also interesting to note that the study reveals exposure to the sun’s rays in the initial year of life also played an important role in protecting against the development of MS. One final warning, if you’re concerned about MS, do everything you can to avoid the consumption of artificial sweeteners. Click here for more information about the dangers of artificial sweeteners. Sources for this article include: ScienceDaily.com

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NEW Study Reveals SURPRISING Cause of Multiple Sclerosis

AHA Publisher — Mon, 31 Jan 2022 08:00:27 +0000

Sara Middleton via NaturalHealth365 – According to the National Multiple Sclerosis Society, multiple sclerosis (MS) is a chronic inflammatory disease in which a person’s immune system mistakenly attacks their central nervous system, including the brain, spinal cord, and optic nerves. It can lead to a wide range of signs and symptoms, from numbness and weakness in the limbs to blurry vision to bowel and bladder problems. There are still so many unknowns about MS, which affects about 2.6 to 2.8 million people worldwide. But recent research from Harvard University points to an unexpected potential cause: the Epstein-Barr virus (EBV). New Harvard Study Sheds Light on Potential Cause of MS: A Common Herpes Virus Led by researchers at the Harvard T.H. Chan School of Public Health, a study recently found a “high prevalence of Epstein-Barr virus associated with multiple sclerosis.” Senior author Alberto Ascherio said in an article published by Harvard that the “hypothesis that EBV causes MS has been investigated by our group and others for several years, but this is the first study providing compelling evidence of causality.” The evidence came from an analysis of serum samples taken from 10 million U.S. soldiers over 20 years. Of this cohort, around 1,000 were diagnosed with MS during their period of service. After establishing the soldiers’ EBV status at the time of their first serum sample and tracking their medical histories, the Harvard researchers determined that the risk of MS was 32 times greater after infection with EBV. Interestingly, this increased risk of MS “was not increased after infection with other viruses.” What’s more, the authors found that the serum levels of a biomarker of nerve damage typical in MS patients increased only after EBV infection. Based on these findings, the authors conclude that their data indicate EBV is “the leading cause of MS.” Right now, there is no way to prevent or treat EBV infection, Ascherio says to Harvard, but suggests that specific drugs or vaccines against EBV may help “prevent or cure” MS. Never Heard of the Epstein-Barr Virus Before? Here Are Three Things to Know Epstein-Barr isn’t a virus we hear about very often in the media, even though it is pervasive. To help you understand more about this virus, here are three things you might not know about Epstein-Barr: Epstein-Barr virus (EBV) is a member of the herpes virus family that spreads easily, primarily via bodily fluids such as saliva, semen, and blood. A person can become infected with EBV by sharing food, drinks, utensils, and toothbrushes with someone who already has it. It really is extremely common. According to Science Daily, around 90 percent of all people will be infected with EBV at some point in their lifetime, but usually with no adverse effects. Most people who contract EBV will not go on to develop MS. Other diseases or illnesses already associated with EBV infection include infectious mononucleosis (“mono”) and certain types of cancer, including Hodgkin lymphoma. Signs and symptoms of an acute EBV infection, which usually occurs in childhood, are similar to those seen in other viral infections, including fever, fatigue, swollen lymph nodes, enlarged spleen and liver, and a skin rash. But while acute infections are often easy to recognize, chronic, low-grade infections are much more difficult to identify. If you suspect that EBV may be wreaking havoc in your body, seeking out an integrative physician may be your best bet, as they tend to be more familiar with how EBV infections work. They understand that after exposure, EBV lies dormant in your body, even after the initial symptoms subside. As long as your immune system is robust and you are healthy, your body’s specialized immune cells will keep the virus dormant. But when your immune system becomes compromised, EBV can come out of hiding and become reactivated. Keeping your immune function strong is a critical part of tackling EBV infections. So, make your health a top priority. After all, it’s a great foundation for a good life. Sources for this article include: MayoClinic.org Harvard.edu Science.org NationalMSsociety.org CDC.gov Cancerresearchuk.org Cell.com Sciencedaily.com NIH.gov

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The Answer to Parkinson’s and Alzheimer’s Is All in Your Eyes

AHA Publisher — Wed, 12 Jan 2022 08:00:46 +0000

Brian Blum via Israel21c – “Look into my eyes. What do you see?” the man says to his wife. “I see Parkinson’s, Alzheimer’s and MS,” she replies. Not the most romantic interchange. But imagine if gazing into someone’s eyes were the key to diagnosing neurological disorders, which are the world’s leading cause of disability and cost some $800 billion a year in direct treatment expenses. The correlations between “oculometrics” (the biometric measurement of the movement and condition of the eyes) and neurological conditions is a much-researched area of study, with over 750 papers published in journals such as The Lancet, Nature and Neurology. Developing a technology that can decode the data from the eyes has proven to be challenging, however. No one has successfully made strides toward commercializing an oculometric approach. Until now. In October 2021, Tel Aviv and Austin, Texas-based startup Neuralight launched out of stealth with a $5.5 million seed investment and a goal of digitizing and even automating neurological evaluation and care. You Can Only Improve What You Can Measure Neurological exams have traditionally relied on a subjective, manual assessment of symptoms. “The physician will ask 50 questions, like how hard is it to button your shirt? Or the doctor asks the patient to walk across the room so they can assess their gait,” explains Neuralight CEO Micah Breakstone. The lack of objective criteria has prevented pharmaceutical companies from developing effective drugs. Breakstone notes that for dementia, studies have shown that two physicians looking at the same patient on the same day could have a 35 percent variable in diagnosis. “We need a statistically significant result,” Breakstone says. Neuralight’s technology is not a cure or a treatment for neurological disease. Rather, the platform is meant mainly to accelerate pharmaceutical development, with an initial focus on Parkinson’s, Alzheimer’s and multiple sclerosis. The platform automatically extracts microscopic eye movement measurements that serve as “digital endpoints” for neurological disorders. A physician will record a short, five-minute video of a patient’s eyes. Neuralight’s imaging tools clean up the video, then artificial intelligence and machine learning get to work at deciphering what’s behind the eye movements. Once Neuralight has extracted ocular metrics on a patient, it plans to sell the data to pharma companies. As Breakstone tells ISRAEL21c, “You can’t improve what you don’t measure.” “Digital endpoints are the future of neurology,” adds Rivka Kreitman, the company’s chief innovation officer and the former head of global innovative research and development at Israeli pharmaceutical giant Teva. “This technology has been the missing piece pharma has needed to make drug development for neurological diseases effective and ultimately more successful.” Privacy Compliant In Breakstone’s ideal world, all the data extracted from videos by Neuralight would be processed on the Neuralight cloud, which he says is HIPAA compliant with all data de-identified (“We don’t need to see a patient’s face, only his or her eyes”). Some organizations do want to keep the data in-house for privacy reasons; in those cases, Neuralight brings its own server. Neuralight does not require eye-trackers, making the process simpler for patients because they don’t have to sit still for a relatively long period of time. Instead, a simple iPhone or even Zoom recording is fine. A Neuralight video recording takes 10 minutes vs. 40 minutes when working with an eye-tracker. Neuralight’s AI “amplifies and augments standard video resolution so you can glean from standard video signals what you could traditionally do only with professional lab equipment,” Breakstone explains. He likens the resolution to how satellites in space can make out the numbers on a car’s license plate using a similar kind of “super-resolution.” Neuralight analyzes close to 100 parameters, including blinking rate, how quickly the patient can fix on a specific object, and the speed of pupil dilation (the latter is highly correlated with Parkinson’s). Digital Biomarkers Breakstone cofounded Neuralight with CTO Edmund Benami after Breakstone sold his previous startup, Chorus.ai, to ZoomInfo for $575 million. “I could have retired, but that would have been a little empty,” he says. His grandfather suffered from Alzheimer’s, and that led Breakstone to want “to do something to make the world a better place, something I deeply believed in,” he tells ISRAEL21c. “Digital biomarkers are very much in vogue,” he says, and investors agreed. Initial funding for Neuralight came from VSC Ventures, Operator Partners, Clover Health CEO Vivek Garipalli and Noam Solomon, the CEO of Immunai. While most of the 19-person team is in Israel, where R&D is based, Breakstone relocated to Austin to build up the company’s connections in the United States. Neuralight has a working MVP (tech speak for “minimum viable product”) and Breakstone hopes to receive initial FDA clearance by the end of 2022 with the first commercial contracts signed in 2023. Clinical trials are due to kick off in the next few months. Neuralight is in conversations with three large pharma companies. Although neurotechnology is a booming industry, Breakstone says most of Neuralight’s competition “is doing things with devices, not with the eyes.” Boston-based Beacon Biosignals, for example, uses EEG data to create biomarkers for neurological disorders, which he says “will be harder to be adopted as a universal solution.” Fortunately for the billion people suffering from neurological disorders, Breakstone feels that Neuralight is “on an urgent mission. We are building a value-driven company.” For more on Neuralight, click here. To read the original article click here.

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Researchers Link “Genetic Signatures” of Bacteria in the Human Gut to Multiple Diseases

AHA Publisher — Thu, 20 May 2021 07:00:24 +0000

Harvard Medical School via News-Medical – We are truly never alone, not even within our own bodies. Human beings play host to trillions of bacteria, fungi, viruses, and other microorganisms that make up the human microbiome. In recent years, the mix of these resident bacteria, and the presence of specific bacterial species, has been linked to conditions ranging from obesity to multiple sclerosis. Now, going a step farther, researchers at Harvard Medical School and Joslin Diabetes Center have gone beyond microbial species. Analyzing the genetic makeup of bacteria in the human gut, the team has successfully linked groups of bacterial genes, or “genetic signatures,” to multiple diseases. The work brings scientists closer to developing tests that could predict disease risk or identify disease presence based on a sampling of the genetic makeup of a person’s microbiome. The findings, to be published May 18 in Nature Communications, link sets of bacterial genes to the presence of coronary artery disease, cirrhosis of the liver, inflammatory bowel disease, colon cancer, and type 2 diabetes. The analysis indicates that three of these conditions–coronary artery disease, inflammatory bowel disease, and liver cirrhosis–share many of the same bacterial genes. In other words, people whose guts harbor these bacterial genes seem more likely to have one or more of these three conditions. The work represents a significant advance in the current understanding of the relationship between microbes residing in the human gut and specific diseases, the team said. If confirmed through further research, the results could inform the design of tools that could gauge a person’s risk for a range of conditions based on analysis of a single fecal sample, they added. “This opens a window for the development of tests using cross-disease, gene-based indicators of patient health. We’ve identified genetic markers that we think could eventually lead to tests, or just one test, to identify associations with a number of medical conditions.” (Braden Tierney, Study First Author and Graduate Student, Biological and Biomedical Sciences Program, Harvard Medical School) The researchers caution that their study was not designed to elucidate exactly how and why these microbial genes may be linked to different diseases. Thus far, they said, it remains unclear whether these bacteria are involved in disease development or are mere bystanders in this process. The goal of the study was to determine whether groups of genes could reliably indicate the presence of different diseases. These newly identified microbial genetic signatures, however, could be studied further to determine what role, if any, the organisms play in disease development. “Our study underscores the value of data science to tease out complex interplay between microbes and humans,” said study senior author Chirag Patel, associate professor of biomedical informatics in the Blavatnik Institute at HMS. The researchers started out by collecting microbiome data from 13 groups of patients totaling more than 2,500 samples. Next, they analyzed the data to pinpoint linkages between seven diseases and millions of microbial species, microbial metabolic pathways, and microbial genes. By trying out a variety of modeling approaches–computing a total of 67 million different statistical models–they were able to observe what microbiome features consistently emerged as the strongest disease-associated candidates. Of all the various microbial characteristics–species, pathways, and genes–microbial genes had the greatest predictive power. In other words, the researchers said, groups of bacterial genes, or genetic signatures, rather than merely the presence of certain bacterial families, were linked most closely to the presence of a given condition. Some of the main observations included: Clusters of bacterial genes, or genetic signatures, rather than individual bacterial genes, appear implicated in various types of human disease. Coronary artery disease, inflammatory bowel disease, and liver cirrhosis have similar gut microbiome genetic signatures. Type 2 diabetes, by contrast, has a microbiome signature unlike any other phenotype tested. The analysis did not find a consistent link between the presence of the bacterial species Solobacterium moorei and colon cancer–an association previously reported in numerous studies. However, the researchers did identify particular genes from a S. moorei subspecies associated with colorectal cancer. This finding indicates that gene-level analysis can yield biomarkers of disease with greater precision and more specificity compared with current approaches. Patel said this result underscores the notion that it is not merely the presence of a given bacterial family that may portend risk, but rather the strains and gene signatures of the microbes that matter. The ability to identify interconnections with such precision will be critical for designing tests that can measure risk reliably, he added. Thus, in this specific example, a test intended to measure colon-cancer risk by merely detecting the presence of S. moorei in the gut may not be as reliable as a more refined test that measures bacterial genes to detect the presence of specific strains of S. moorei that are associated with colon cancer. Two conditions–ear inflammation and benign soft-tissue tumors called adenomas–showed weak associations with the gut microbiome, suggesting that microorganisms residing in the human gut are not likely to play a role in the development of these conditions, nor are they likely to be reliable indicators that these conditions are present. In a previous study, the HMS team used massive amounts of publicly available DNA-sequencing data from human oral and gut microbiomes to estimate the size of the universe of microbial genes in the human body. The analysis revealed that there may be more genes in the collective human microbiome than stars in the observable universe. Given the sheer number of microbial genes that reside within the human body, the new findings represent a major step forward in understanding the complexity of the interplay between human diseases and the human microbiome, the researchers said. “The ultimate goal of computational science is to generate hypotheses from a huge swath of data,” said Tierney. “Our work shows that this can be done and opens up so many new avenues for research and inquiry that we are only limited by the time, people, and resources needed to run those tests.” To read the original article click here.

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How Fasting Improves Mental & Brain Health

AHA Publisher — Wed, 20 Jan 2021 08:00:38 +0000

Dr. Will Cole via Dr. Caroline Leaf – The brain is no doubt one of our most important organs. Not only does it control our basic movements and bodily functions, it allows us to think, feel, and recall information. All of these things are vital to the human experience and when one of these functions goes awry, it can make life a lot more difficult and a lot less enjoyable. And sadly, brain problems are on the rise at a rapid pace. In fact, The National Institute of Mental Health estimates that close to 20% of American adults currently suffer from a diagnosable mental disorder. That doesn’t take into account the many people struggling through brain fog on a daily basis or those with autoimmune brain problems like dementia, autism, or multiple sclerosis. Something has to be done. As a functional medicine practitioner and the author of the new book Intuitive Fasting, I am always on the search for the most effective, natural way to optimize your health – including your brain. Intermittent fasting has some serious next-level health benefits that are backed up both scientifically and anecdotally. Here’s exactly what fasting can do for your brain health. Lowered Brain Inflammation Chronic inflammation plays such a role in brain health that an entire area of research known as “the cytokine model of cognitive function” is dedicated to studying how inflammation, specifically inflammation of the brain, is correlated with brain problems. Elevated inflammation levels increase the microRNA-155 molecule that ends up creating gaps in the blood brain barrier that let bacteria and other toxins slip through causing your brain’s immune system to work in overdrive to fight off these invaders. This ends up creating a cascade of inflammation to your brain in order to try to protect it. This inflammatory oxidative stress in the hypothalamus of the brain is the underlying cause of brain fog. Fasting has been shown to reduce the release of pro-inflammatory cells called monocytes, which when circulating at high levels – as a result of the eating habits humans have acquired over the last few centuries – can cause series tissue damage. Studies have shown that in periods of fasting, these cells go into a type of “sleep mode” and turn off. This means that fasting works essentially as an antidote to the high-sugar, processed food-filled standard American diet. Which brings me to my next point. Clean Brain Energy Intermittent fasting helps push your metabolism into a state of ketosis where your body utilizes fat, in the form of ketones for energy instead of sugar in the form of glucose. As fasting continues, deeper ketosis develops, you mobilize more stored fat to use as fuel, and ketones including beta-hydroxybutyrate (BHB), acetoacetate (AcAc), and acetone (BrAce) end up replacing glucose as the primary energy source for the central nervous system. BHB is particularly important to brain health because when BHB is produced, it activates the AMPK pathway, which is involved in regulating energy balance and inflammation, and inhibits the NLRP3 inflammasome an inflammatory protein that activates the inflammatory response and has been connected to various inflammatory and autoimmune diseases. This ketone acts as a more effective fuel source for your brain considering it gets transported straight to the brain and enters the mitochondria of brain cells where it is used to make energy. It’s suspected that the production of BHB is responsible for the increased focus and concentration – and the lack of brain fog – many ketogenic dieters report. BHB also acts as a signaling molecule in brain cells and can induce the expression of proteins. One such protein, brain-derived neurotrophic factor (BDNF), is known for promoting cellular resilience and synaptic plasticity. More specifically, BDNF works to support the survival of existing brain cells and encourages the growth of new, healthy ones. Lowered synaptic plasticity has been shown to contribute to a range of brain health, psychiatric, and neurodegenerative disorders, including Alzheimer’s disease, autism, schizophrenia. De-Stress Your Brain If there’s one thing we can all probably agree upon, it’s that we’re all chronically stressed. And, unfortunately, chronic stress does a number on our mind and body. In fact, studies have found that chronic stress can actually cause long-term changes in the structure and function of the brain that can contribute to mental health issues. Another study even found an association between chronic stress and an increased risk of insomnia and dementia. You see, chronic stress triggers a chain reaction in your brain’s hypothalamus, which then sends a message to your adrenal glands to release cortisol and adrenaline, which are two of your stress hormones. Unfortunately for us, cortisol release also causes our blood sugar to rise, which means it can contribute to chronic inflammation in a feedback loop: The more stressed you are, the worse your inflammation; and the worse your inflammation the more stressed you get. As you begin to quell inflammation, support autophagy (cellular renewal), stabilize blood sugar, balance the gut microbiome as well as increase BDNF and stem cells through flexible intermittent fasting, you’ll be able to see and feel the results of being less stressed and way more zen. But this is just the tip of the iceberg of what fasting can do for your health. If you want to take your brain health to the next-level and experience the overreaching benefits of fasting, pre-order my book Intuitive Fasting to receive access to my private online fasting group, shopping guide for the meal plan in the book and a sneak peek of the book right now. To read the original article click here. For more articles from Dr. Leaf click here.

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Study Reveals a Promising Method for Treating Multiple Sclerosis

AHA Publisher — Mon, 31 Aug 2020 07:00:04 +0000

University of Mainz via News-Medical Net – Researchers reveal a potential method for treating multiple sclerosis/Theophylline activates histone deacetylase, enabling the reconstruction of myelin sheaths. A research team led by neurobiologist Professor Claire Jacob has identified an important mechanism that can be used to control the restoration of myelin sheaths following traumatic injury and in degenerative diseases. With the insights gained, the researchers were able to regenerate damaged myelin sheaths in mice by treating them with the active substance theophylline, thereby restoring their nerve cell function. The groundbreaking findings are the result of research carried out at Johannes Gutenberg University Mainz (JGU) and the University of Fribourg in Switzerland. Neurons are composed of axons, i.e., long fiber-like extensions that transmit signals to other cells. Many of them are surrounded by a myelin sheath, a thick fatty layer that protects them and helps to transfer stimuli rapidly. Without myelin, the functional capacity of neurons – and therefore of the whole nervous system – is limited and neurons can easily degenerate. Multiple sclerosis (MS) is one of the diseases associated with myelin sheath degradation. MS patients suffer successive episodes of demyelination resulting in a progressive loss of function of their nervous system. Remyelination of the axons can prevent this. The Aim Is to Restore the Axons’ Protective Myelin Coating Intact myelin sheaths are a prerequisite for the healthy functioning of the peripheral and central nervous systems. If the peripheral nervous system (PNS) is damaged, in an accident involving injury to the arms or legs for example, the axons and their myelin sheaths can recover relatively well. “Regeneration of the PNS is quite efficient, although it could be improved,” said Professor Claire Jacob, pointing out that even young people do not experience complete regeneration. However, the central nervous system (CNS) is completely different in this regard as there is no efficient restoration of the axons and therefore of the myelin sheath after a lesion. This means that CNS injuries usually result in permanent paralysis – as in the case of MS when loss of myelin leads to axon degeneration. MS is the most common neurodegenerative disease of the CNS and is attributable to the degradation of the myelin sheath of neurons. The occurrence of successive lesions can cause permanent loss of function of the CNS if myelin sheath restoration is inefficient. The capacity of the body to remyelinate decreases dramatically with age. “In order to promote the restoration of myelin, we need to understand the process that controls the mechanism.” (Claire Jacob, Neurobiologist Professor, Johannes Gutenberg University Mainz) In the recent project, her research group investigated how remyelination occurs in both peripheral and central nervous systems of mice. “First, we wanted to understand the process that blocks remyelination. We subsequently studied how to counteract this blocking effect.” The neuroscientists identified a protein called eEF1A1 as a key factor in the process and found that eEF1A1 activated by acetylation prevents the remyelination process, but if eEF1A1 is deactivated by deacetylation, myelin sheaths can be rebuilt.The protein that deacetylates eEF1A1 is the enzyme called histone deacetylase 2 (HDAC2). Theophylline Promotes Myelin Reconstruction in Both Peripheral and Central Nervous Systems “Once we understood this process, we decided to try to control it by boosting the HDAC2 activity and its synthesis in cells,” said Jacob. This was achieved by using the active substance theophylline, which is also present in tea leaves and has long been used in the treatment of asthma. In a mouse model, the use of theophylline over a period of four days resulted in significant recovery. Restoration of myelin sheaths was particularly impressive in the PNS, where they recovered completely. Regeneration also improved in the CNS, as there was rapid and efficient rebuilding of myelin sheaths in both young and old mice. A low dose of the active substance was sufficient to trigger the improvements – a big plus with regard to the known side effects of theophylline, which occur at higher doses. “In summary, this study […] shows that theophylline, by activating HDAC2, promotes eEF1A1 deacetylation, increases […] remyelination speed and efficiency after lesion of the PNS and CNS, thus appearing as a very promising compound to test in future translational studies to accelerate and promote remyelination after traumatic lesions or in the context of demyelinating disorders,” write the authors in their paper published in Nature Communications. To read the original article click here.

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Cashew Shell Compound Appears to Mend Damaged Nerves

AHA Publisher — Wed, 19 Aug 2020 07:00:10 +0000

Vanderbilt University Medical Center via EurekAlert – In laboratory experiments, a chemical compound found in the shell of the cashew nut promotes the repair of myelin, a team from Vanderbilt University Medical Center reports today in the Proceedings of the National Academy of Sciences. Myelin is a protective sheath surrounding nerves. Damage to this covering — demyelination — is a hallmark of multiple sclerosis and related diseases of the central nervous system. “We see this as an exciting finding, suggesting a new avenue in the search for therapies to correct the ravages of MS and other demyelinating diseases,” said the paper’s senior author, Subramaniam Sriram, MBBS, William C. Weaver III Professor of Neurology and chief of the Division of Neuroimmunology. Previous work led by Sriram showed that a protein called interleukin 33, or IL-33, induced myelin formation. IL-33 is, among other things, an immune response regulator, and multiple sclerosis is an autoimmune disorder. The cashew shell compound is called anacardic acid. Sriram and team grew interested in it because it’s known to inhibit an enzyme involved in gene expression called histone acetyltransferase, or HAT, and the team had discovered that whatever inhibits HAT induces production of IL-33. The report includes a range of new findings that point to potential therapeutic use of anacardic acid for demyelinating diseases: In vitro, the addition of the compound to rat cells most responsible for myelination — oligodendrocyte precursor cells, or OPCs — spurred induction of IL-33 and rapidly increased the expression of myelin genes and proteins, including dose-dependent increases in myelin basic protein; In two animal models of demyelination, treatment with the compound increased the relative presence of IL-33-expressing OPCs and led to reduced paralysis; In an animal model of demyelination treated with the compound, dissection and electron microscopy showed dose-dependent increases in myelination. “These are striking results that clearly urge further study of anarcardic acid for demyelinating diseases,” Sriram said. To read the original article click here.

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