Autoimmunity
Episodes
Dr. Rhonda Patrick discusses her supplement stack, avoiding microplastics, creatine for brain health, and mRNA vaccine autoimmunity risks.
Dr. Dominic D'Agostino discusses how ketones affect exercise performance, reduce inflammation, and improve neurological health.
Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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Dr. Rhonda Patrick discusses her supplement stack, avoiding microplastics, creatine for brain health, and mRNA vaccine autoimmunity risks.
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Dr. Dominic D'Agostino discusses how ketones affect exercise performance, reduce inflammation, and improve neurological health.
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Rhonda Vitamin D Exercise Parkinson's Epigenetics Omega-3 Fasting Melatonin Vaccine Resveratrol Sauna Insulin COVID-19 Cardiovascular AutoimmunityDr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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In this clip, Dr. Eran Elinav discusses the importance of the early childhood period in shaping a healthy microbiome.
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Dr. Eran Elinav discusses the complex interactions between humans and their resident gut microbiomes.
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In this clip, Dr. Rhonda Patrick explains how allergens in the environment may shape the immune system during early life.
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In this clip, Dr. Rhonda Patrick discusses how a lack of sleep impacts the immune response.
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COVID-19 Vitamin D Nutrition Exercise Microbiome Sleep Vitamin C Omega-3 Inflammation Immune System Virus Micronutrients Vitamin E Vaccine Genetics Testosterone Estrogen Zinc Fiber AutoimmunityCOVID-19 Q&A Part 2: Rhonda Patrick, Ph.D. answers subscriber questions in a multi-part series.
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Dr. Patrick covers vitamin C's diverse aspects: bioavailability, immune function, viral protection, lung health, cancer impact, exercise effects, and more!
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COVID-19 Q&A Series Part 1: Rhonda Patrick, Ph.D. addresses subscriber questions in this multi-part series.
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Dr. Longo discusses his work that indicates that the fasting-mimicking diet holds promise for the treatment of autoimmune diseases, particularly multiple sclerosis.
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Fasting mimicking diet treatment for multiple sclerosis (remyelinating axons & halting autoimmunity) ClipDr. Valter Longo describes how the fasting-mimicking diet can be beneficial in the treatment of various diseases, including multiple sclerosis.
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Dr. Valter Longo on Resetting Autoimmunity and Rejuvenating Systems with Prolonged Fasting & the FMDFasting Cancer Obesity Aging Heart Disease Diabetes Insulin Resistance Inflammation Stem Cells Immune System Tissue Repair Autophagy Apoptosis Insulin AutoimmunityDr. Valter Longo discusses fasting as a means to treat or prevent age-related diseases such as cancer, Alzheimer’s disease, and others.
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Dr. Valter Longo discusses the role of fasting and the fasting-mimicking diet in longevity, cancer & multiple sclerosis.
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Nutrition Brain Diet Epigenetics Cholesterol Omega-3 Inflammation Micronutrients Multiple Sclerosis Mitochondria Vitamin K Antioxidant AutoimmunityDr. Terry Wahls discusses the nutrition protocol she used to reverse her secondary-progressive multiple sclerosis.
Topic Pages
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Autophagy
Autophagy constrains autoimmunity by eliminating damaged organelles, limiting cytosolic DNA sensing, and modulating MHC-II self-antigen presentation.
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Hydrolyzed collagen
Hydrolyzed collagen is enzymatically cleaved collagen producing low-molecular-weight peptides absorbed intestinally as bioactive di- and tri-peptides.
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Intestinal permeability
Zonulin-mediated tight junction disassembly heightens intestinal permeability, permitting non-self antigens to activate autoreactive lymphocytes and propagate autoimmunity.
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Thymic involution
Age-associated thymic involution impairs negative selection, permitting peripheral escape of autoreactive T cells, thereby fostering autoimmunity.
News & Publications
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Omega-3 fatty acids reduce inflammation and disease activity in rheumatoid arthritis and lupus—according to an umbrella review of 21 analyses. www.sciencedirect.com
Autoimmune diseases occur when the body mistakenly attacks its own tissues, driving chronic inflammation and tissue damage. However, evidence suggests that omega-3 fatty acids may benefit people with autoimmune diseases. A recent study found that omega-3s help reduce disease severity in rheumatoid arthritis and lupus but are less effective against other autoimmune disorders.
Researchers conducted an umbrella review to summarize findings from 21 systematic reviews and meta-analyses on the effects of omega-3s on autoimmune diseases. They also used Mendelian randomization—a method that leverages genetic data to identify causal relationships—to explore further whether omega-3s directly influence the risk of developing autoimmune diseases.
They found that omega-3s were associated with reduced inflammation and disease activity in people with rheumatoid arthritis and lupus. However, they found no clear evidence of omega-3s' effects on other autoimmune diseases, including multiple sclerosis, type 1 diabetes, or Crohn’s disease. The quality of evidence varied, with one high-quality study and several moderate or low-quality studies.
These findings suggest that omega-3 fatty acids benefit people with certain autoimmune disorders, but their effects vary across different conditions. Omega-3 fatty acids exert robust anti-inflammatory properties due to their formation of specialized pro-resolving molecules (SPMs), a broad class of metabolites that resolve inflammation. Learn more about SPMs in this clip featuring Dr. Bill Harris.
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Blocking activity of aryl hydrocarbon receptor in T Cells shuts off multiple sclerosis autoimmunity newsroom.uvahealth.com
Blocking a key regulator of autoimmunity reduces the inflammation associated with multiple sclerosis.
A protein found on the surface of some immune cells regulates autoimmunity in multiple sclerosis, a new study has found. Blocking the protein’s activity reduced the inflammation associated with the disease.
Researchers studied the role that the aryl hydrocarbon receptor – a protein found on specific immune cells called T cells – plays in autoimmunity in a mouse model of multiple sclerosis. They bred mice that lacked the aryl hydrocarbon receptor and examined the effects its absence had on T cell activity.
They found that the absence of the aryl hydrocarbon receptor altered the types and numbers of microbial metabolites produced in the animals' guts. Specifically, the microbes produced more bile acids and short-chain fatty acids – both of which exhibit robust anti-inflammatory properties.
Multiple sclerosis (MS) is a progressive autoimmune disorder that targets the central nervous system. A dominant feature of MS is inflammation of the nerves. T cells play an instrumental role in the inflammation and pathophysiology of MS.
These findings suggest that blocking the key regulator of inflammation in MS prevents the inflammation associated with the disease. Some evidence suggests that the fasting-mimicking diet reduces the number of autoimmune cells in people with multiple sclerosis. Learn more in this episode featuring Dr. Valter Longo.
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Estrogen may increase susceptibility to inflammatory disease by negatively affecting wound healing and protective lipid mediator circuits. (2012) www.sciencedaily.com
From the article:
To make this discovery, Gronert and colleagues administered a mild abrasion injury to the front of the eye of genetically similar male and female mice, and analyzed wound healing by image analysis. To test the role of estrogen, they gave male mice estrogen eye drops and/or drugs that activate specific estrogen receptors. Gene expression of essential enzymes was quantified for the formation of protective lipid signals, specific receptors that mediate their bioactivity, as well as estrogen receptors in mouse corneas and human/mouse epithelial cell cultures. The formation of protective lipid signals was analyzed by a mass-spectrometry based lipidomic method. They found that estrogen negatively affects a highly evolved protective lipid circuit, called “15-lipoxygenase-Lipoxin A4” that has recently emerged as an important protective pathway in many diseases. This pathway balances the activity of pro-inflammatory signals to promote wound healing and to keep inflammation within safe ranges.
“This study goes a long way to explaining gender differences in inflammation and its resolution,” said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal. “It’s long been known that women suffer more than men from chronic inflammatory diseases such as lupus or rheumatoid arthritis; this study suggests that estrogen itself is responsible for that difference and pinpoints the molecular pathways that estrogen affects. Molecules that promote the resolution of inflammation show promise as new treatments for autoimmune disease.”
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Estrogen may contribute to T cell–mediated autoimmune inflammation by promoting T cell activation and proliferation, mouse study suggests. ( 2018) www.sciencedaily.com
From the article:
Estrogen hormone shows its action on cells mostly through (ERα). Researchers from Turku generated mice with ERα protein specifically deleted in T cells.
“The eureka moment of our research is that in a mouse model of human inflammatory bowel disease, transfer of naive T helper cells from ERα [estrogen receptor alpha] deficient mice did not succumb to colitis, unlike transfer from their counterparts,” Docent Zhi Chen tells.
“Furthermore, using cutting-edge technique RNA sequencing approach combined with in vitro and in vivo experiments, we discovered that ERα regulates multiple aspects of T cell function, including T cell activation, proliferation and survival,” Chen adds.
Regulatory T cells are group of T cells that help in preventing autoimmune diseases. The researchers found that ERα influences the function and differentiation of regulatory T cells.
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Testosterone may protect men from stomach inflammation, mouse study suggests. (2021) www.sciencedaily.com
From the article:
In researching mice without either glucocorticoids or testosterone, Busada, his research partner John Cidlowski – a senior investigator with the National Institutes of Health – and their colleagues observed that males' stomach inflammation increased as much as the females' did.
What’s more, when he and his team gave testosterone to the female mice, their inflammation vanished.
“We were able to completely rescue them from their stomach inflammation,” Busada said. “We proved that androgens were the hormones giving male mice that double layer of protection from inflammation. In the females, the only anti-inflammatory hormone was glucocorticoids. In males, it could be either glucocorticoids or androgens. This study potentially explains why women have a much higher incidence of autoimmune and chronic inflammatory diseases.”
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Repeated head injury damage the blood-brain barrier and produce an autoimmune response that promotes neurological disease www.sciencedaily.com
From the article:
A new study suggests that brain injury from repeat blows to the head – observed among football players and soldiers – might not be a traumatic phenomenon, but an autoimmune phenomenon. It indicates that brain injury may be the result of an out-of-control immune response, much like multiple sclerosis. This is an entirely new way of thinking about how trauma could cause long term degeneration and opens the door to investigating a vaccine/drug to prevent head trauma.
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Researchers found that S100B, a well-accepted protein biomarker for traumatic brain injury, was present in varying degrees in the blood samples of the 67 football players after every game – even though none of them suffered a concussion. This demonstrates that even the most routine hits have some impact on the blood-brain barrier and possibly the brain itself, Bazarian said.
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Air pollution may promote the production of autoantibodies against tight-junctions and neural proteins: neuroinflammation in children in Mexico City www.sciencedaily.com
Exposure to air pollution promotes the production of autoantibodies against tight-junctions of the blood-brain barrier.
Separately, evidence has also shown that even very young children show evidence of amyloid-beta build up under these conditions.
From the article:
The study found when air particulate matter and their components such as metals are inhaled or swallowed, they pass through damaged barriers, including respiratory, gastrointestinal and the blood-brain barriers and can result in long-lasting harmful effects.
The results found that the children living in Mexico City had significantly higher serum and cerebrospinal fluid levels of autoantibodies against key tight-junction and neural proteins, as well as combustion-related metals.
“We asked why a clinically healthy kid is making autoantibodies against their own brain components,” Calderón-Garcidueñas said. “That is indicative of damage to barriers that keep antigens and neurotoxins away from the brain. Brain autoantibodies are one of the features in the brains of people who have neuroinflammatory diseases like multiple sclerosis.”
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Milk May Exacerbate Multiple Sclerosis Symptoms www.sciencedaily.com
Antibodies that destroy myelin in multiple sclerosis may cross-react with casein, a milk protein.
Multiple sclerosis (MS) is a neurodegenerative and autoimmune disease caused when the immune system attacks myelin proteins on nerves, mistaking them for proteins produced by pathogens. The cause of this immune confusion is complex but may involve exposure to proteins found in cow’s milk, which anecdotally worsen MS symptoms for some patients. New research supports this anecdotal evidence, finding that MS autoantibodies cross-react with casein, the principal protein in cow’s milk.
In order to create antibodies that react to new pathogens, B cells (a type of immune cells) use somatic hypermutation, a process during which they intentionally mutate regions of their DNA involved in antibody production. These rapid mutations are needed to increase antibody repertoire, the collection of an individual’s B cell receptor and antibody sequences; however, somatic hypermutation can result in the creation of autoantibodies, which bind to self-proteins produced by the body. While autoimmune B cells are usually destroyed shortly after creation, lingering autoimmune cells can proliferate and lead to diseases such as type 1 diabetes, rheumatoid arthritis, and MS. One reason autoantibodies persist is cross-reactivity with other proteins, such as those produced by pathogens or absorbed from the diet, especially in cases where gut leakiness increases the introduction of new proteins to the blood.
The investigators gave one group of mice an injection of casein with adjuvants, which are compounds added to vaccines to increase the body’s antibody response. To compare casein to other milk proteins, they also immunized one group of mice with alpha-lactalbumin and another with beta-lactoglobulin, both whey proteins, for a total of three mouse groups. Changes in behavior and nerve degeneration were observed at 13, 20, or 40 days after immunization. The researchers also collected blood samples from 39 patients with MS and 23 patients with other neurological diseases in order to test for cross-reactivity of autoantibodies with casein.
Mice immunized with casein exhibited a range of MS symptoms such as weakness and disorientation, while mice immunized with whey proteins did not. Immunization with casein led to a progressive increase in casein-reactive antibodies and deterioration of myelin in nerves of the lower spinal cord. The researchers found that casein-immunized mice produced autoantibodies that cross-react with myelin-associated glycoprotein (MAG), a protein produced by nerve cells called oligodendrocytes, which have a similar structure to casein. Finally, they found that 42 percent of participants with MS had casein-reactive antibodies compared to only 28 percent of participants with other neurological disorders.
While it is not clear from these results what role dairy consumption plays in the development of MS, the authors suggest that some patients with MS may benefit from restricting dairy in their diet.
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New research identifies critical differences between the two types of vitamin D, with vitamin D2 having a questionable impact on human health. www.sciencedaily.com
Vitamins D2 and D3 exert differing effects on the human immune system.
Scientists have identified five forms of vitamin D, but the two primary forms relevant to human health are ergocalciferol, commonly referred to as vitamin D2 (produced by invertebrates), and cholecalciferol (produced by mammals), commonly referred to as vitamin D3. Prescription vitamin D supplements in the United States typically provide D2, but over-the-counter dietary supplements and fortified foods typically provide D3. Considerable controversy exists regarding the bioequivalence of D2 and D3. Findings from a recent study suggest that D2 and D3 exert differing effects on the human immune system.
Vitamin D modulates both innate and adaptive immune responses via its interactions with immune cells, including antigen presenting cells, B cells, and T cells. Evidence suggests that people with vitamin D deficiency are at greater risk of viral infection and autoimmune disorders. This is in keeping with the widely held belief that a principal role of vitamin D is to restrain, or balance, immune system activity.
The study was part of a previous randomized placebo-controlled trial involving healthy white European and South Asian females who received 15 micrograms (600 IU) of vitamin D2 or D3 every day for 12 weeks during the winter months, when sun exposure was limited. Participants also consumed vitamin D-fortified foods (orange juice and tea biscuits) daily. The investigators used microarray analysis to measure changes in 97 of the participants' blood transcriptome (the full range of RNA molecules an organism produces) and weighed the changes against any influence of ethnic background.
They found that while the effects of both D2 and D3 showed some overlap, the two forms of the vitamin showed distinct differences in terms of changes to gene expression. In particular, D3 switched off the activity of genes involved in the regulation of the innate and adaptive immune systems. The investigators posited that these changes could make the immune system more tolerant and therefore less likely to promote autoimmunity. They also noted that vitamin D3 (and not D2) had a dramatic effect on genes involved in activation of interferon, which plays important roles in providing protection against pathogens and cancer. The investigators' analysis revealed that some of the variation in overall gene expression was likely due to ethnic differences among the participants.
These findings suggest that vitamins D2 and D3 exert differing effects on the human immune system, with D3s effects modulating tolerance and immunoreactivity. They also may have relevant implications for supplementation with vitamin D.
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Epstein-Barr virus is one of the most common human viruses in the world. It is the primary cause of mononucleosis (often called “mono”) – a highly infectious disease that affects mostly teenagers and young adults. Findings from a recent study suggest that Epstein-Barr infection increases a person’s risk for developing multiple sclerosis.
Multiple sclerosis is an autoimmune disorder characterized by the progressive destruction of myelin – the insulating sheath that surrounds nerves and facilitates neural transmission. The disease affects approximately 3 million people worldwide and is twice as likely to manifest in women than men. Symptoms of multiple sclerosis typically appear between the ages of 20 and 50 years.
The study investigators analyzed blood samples from more than 10 million active duty military personnel, collected during routine health exams over a period of 20 years. From this group, they identified 801 personnel who had been tested for Epstein-Barr virus and later developed multiple sclerosis while on active duty. The investigators looked for the presence of antibodies in the blood samples that signaled past Epstein-Barr infection, as well as a protein called neurofilament light chain, a marker of myelin degeneration.
They found that the average age at which personnel were diagnosed with Epstein-Barr infection was 20 years; multiple sclerosis onset typically occurred approximately ten years later. The risk of developing multiple sclerosis later in life was 32 times higher after having experienced Epstein-Barr infection during young adulthood. Levels of neurofilament light chain were higher among the military personnel who had experienced Epstein-Barr infection.
These findings suggest that Epstein-Barr virus is the causal factor in the development of multiple sclerosis and underscore the need for developing vaccines against the virus. Although there is no cure for multiple sclerosis, evidence suggests that the fasting-mimicking diet may be beneficial in treating the condition. Learn about the fasting-mimicking diet in this episode featuring Dr. Valter Longo.
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SARS-CoV-2 infection may cause autoimmune disease, especially in men. www.sciencedaily.com
SARS-CoV-2, the virus that causes COVID-19, elicits a wide range of effects on the human body, many of which are sex-specific. For example, males and females are equally likely to become infected with SARS-CoV-2, but men are more likely to experience worse outcomes and death, regardless of age. Findings from a recent study suggest that men are more likely than women to develop autoimmune activation after SARS-CoV-2 infection.
Autoimmune activation occurs when the body launches an immune response to its own tissue, driving autoimmune disease. Scientists don’t fully understand the causes of autoimmune activation, but evidence suggests that interactions between genetic and environmental factors play critical roles. Autoimmune diseases affect approximately 7 percent of people in the United States and are more common in women than in men. Examples include type 1 diabetes, Hashimoto’s thyroiditis, lupus, and multiple sclerosis.
The authors of the study recruited male and female health care workers who had been infected with SARS-CoV-2 and were either symptomatic or asymptomatic for COVID-19. They tested the participants' blood to identify the presence of autoantibodies – antibodies that are directed against the body’s own tissues. Then they measured the autoantibodies' reactivity to proteins linked to several common autoimmune disorders.
They found that males and females who had been infected with SARS-CoV-2 had autoantibodies in their blood that persisted up to six months post infection, regardless of disease severity. However, men were more likely to exhibit greater autoantibody reactivity, especially if they had experienced at least a mild infection.
These findings suggest that SARS-CoV-2 infection elicits an autoimmune response that may persist several months, potentially contributing to the phenomenon known as “long COVID.” Males appear to be more vulnerable to this autoimmune response than females. Learn more about the long-term complications associated with COVID-19 in this episode featuring Dr. Roger Seheult.
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Sunlight reduces the risk of developing early-onset multiple sclerosis. www.sciencedaily.com
Exposure to ultraviolet (UV) light is critical for maintaining many aspects of human health. For example, compounds present in the skin react to UV light, initiating the production of vitamin D, a steroid hormone that participates in many physiological processes. Similarly, photoreceptors in the eyes respond to UV exposure, modulating the regulation of circadian rhythms. Findings from a new study suggest that early life exposure to ultraviolet light reduces the risk of developing early-onset multiple sclerosis (MS).
Multiple sclerosis is an autoimmune disorder characterized by the progressive destruction of myelin – the insulating sheath that surrounds nerves and facilitates neural transmission. The disease affects approximately 3 million people worldwide and is twice as likely to manifest in women than men. Symptom onset typically occurs between the ages of 20 and 50 years, but as many as [5 percent of people with MS experience early onset](https://pubmed.ncbi.nlm.nih.gov/11205364/], with symptoms manifesting during childhood or young adulthood.
The study involved 322 children and young adults with MS (ages 3 to 22 years) and 534 healthy participants of similar ages and sexes. All the participants (or their parents) provided information about their medical history, place of residence, and sun exposure.
The authors found that among the participants who reported having spent fewer than 30 minutes outside per day during the previous summer, 19 percent had MS, while only 6 percent did not. When they accounted for other risks associated with MS, such as smoking or being female, they found that those who spent 30 to 60 minutes outside per day were 52 percent less likely to develop MS, compared to those who spent fewer than 30 minutes outside per day.
These findings suggest that early life UV exposure reduces the risk of developing MS. Although these findings were based on observational data and do not assign causality, the authors of the study pointed out that they align with results of other studies suggesting that low UV exposure is associated with other neurological diseases, including Parkinson’s disease, Alzheimer’s disease, and other forms of dementia. Although there is no cure for Parkinson’s disease, evidence suggests that the fasting-mimicking diet may be beneficial in treating the condition. Learn more about the fasting-mimicking diet in this episode featuring Dr. Valter Longo.
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Patients with obesity and COVID-19 produce mostly autoimmune SARS-CoV-2 antibodies, not neutralizing. pubmed.ncbi.nlm.nih.gov
Obesity is a strong independent risk factor for COVID-19, the disease caused by the SARS-CoV-2 virus. Previous research has shown that people with obesity generate fewer antibodies in response to viral infection or vaccination; however, whether antibody quality is also affected by obesity is unknown. Findings published in a new report show that the majority of the antibodies found in people with obesity are autoimmune and not able to neutralize the SAR-CoV-2 virus, putting individuals with obesity at greater risk of severe COVID-19.
Obesity increases the rate of inflammaging, the process of chronic low-grade inflammation that wears down the body’s tissues over time, putting people with obesity at greater risk of many diseases. Inflammaging increases the risk of autoimmunity by increasing the concentration of damaged cellular components in the blood, potentially triggering the immune system to generate antibodies against its own cells. Previous research has shown that many patients with severe COVID-19 generate autoimmune antibodies that increase the risk of long-term complications. Because people with obesity experience increased baseline inflammaging, they may be at greater risk of developing long-term autoimmune complications for COVID-19; however, no published studies have yet addressed this concern.
The investigators collected blood from 15 participants with a lean BMI (less than 25) and 15 participants with an obese BMI (greater than 30) who tested positive for SARS-CoV-2. The investigators also collected blood from 30 participants who had not had a SARS-CoV-2 infection and were matched for age, sex, and BMI. The researchers measured the concentration of neutralizing antibodies (meaning antibodies that bind to the SARS-CoV-2 spike protein and prevent viral entry into cells), non-neutralizing antibodies, and autoimmune antibodies.
Participants with obesity had fewer SARS-CoV-2 antibodies than participants with a lean BMI, confirming previous reports. While all 15 SARS-CoV-2-positive participants with a lean BMI had circulating neutralizing antibodies, only a few participants with obesity did. The researchers found that SARS-CoV-2 infection increased the concentration of autoimmune antibodies in all patients, but the concentration of autoimmune antibodies was always higher in participants with obesity. Finally, they found that participants with the highest concentration of autoimmune antibodies also had the highest levels of serum C-reactive protein, a marker of chronic inflammation, suggesting that inflammation is integral to developing autoimmunity.
These data confirm previous reports that obesity reduces the effectiveness of the immune response in COVID-19 patients and increases the risk of autoimmunity.
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Garlic alleviates symptoms of rheumatoid arthritis. pubmed.ncbi.nlm.nih.gov
Rheumatoid arthritis is an autoimmune disorder characterized by pain, swelling, and loss of function in the joints. The condition affects as many as 2 percent of people worldwide and is two to three times more common in women than in men. Findings from a new study demonstrate that garlic alleviates clinical symptoms and inflammatory markers associated with rheumatoid arthritis.
Garlic is a bulbous plant used in cooking and traditional medicine practices. It exerts antibacterial, anti-inflammatory, and antioxidant properties. The primary bioactive compound in garlic, allicin, is widely recognized for its capacity to lower blood pressure, prevent atherosclerosis, reduce serum cholesterol and triglycerides, inhibit platelet aggregation, and increase fibrinolytic activity (breaking down blood clots).
The randomized, double-blind, placebo-controlled trial involved 70 women (average age, 51 years) who had rheumatoid arthritis. Half of the women took 1,000 milligrams of garlic daily for eight weeks, and the other half took a placebo. The authors assessed the women’s clinical symptoms, fatigue, C-reactive protein (CRP) levels, tumor necrosis factor-alpha (TNF-alpha), and erythrocyte sedimentation rate (ESR) were determined.
At the end of the study, the women who took garlic showed marked improvements in their clinical symptoms, pain intensity, tender joint count, and fatigue, and their serum levels of CRP and TNF-alpha decreased. Their swollen joint count decreased as well, but not in the placebo group.
These findings demonstrate that garlic improves clinical symptoms and modulates inflammatory markers associated with rheumatoid arthritis and may be useful as an adjunct therapy in treating the condition.
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Maternal immune activation during pregnancy increases the severity of autism symptoms in children. www.eurekalert.org
Autism spectrum disorder (ASD) is a developmental condition characterized by impaired social interaction, behavioral problems, and poor communication. The disorder typically manifests in early childhood and is slightly more common among boys than girls. Roughly one in 54 people living in the United States has ASD. Findings from a new study suggest that maternal immune activation during pregnancy increases the severity of ASD in offspring.
Maternal immune activation due to autoimmune disorders, asthma, or allergies switches on the activity of inflammatory pathways and proinflammatory molecules. Many of these molecules can cross the blood–brain barrier and the placenta, potentially disrupting fetal development. Elevated levels of these proinflammatory molecules have been found at birth or during development in some people with ASD – a finding that has been linked with increased severity of symptoms.
The study involved 363 children who were enrolled in the Autism Phenome Project or the Girls with Autism Imaging of Neurodevelopment studies, along with their mothers. The authors of the study assessed children’s behavioral and emotional problems and reviewed the mothers' pregnancy histories.
They found that asthma was the most common immune condition among the mothers, but other conditions, including Hashimoto’s thyroiditis, rheumatoid arthritis, and psoriasis were reported as well. Roughly 20 percent of the mothers of male children with ASD had asthma. Maternal immune conditions were associated with increased behavioral and emotional problems but not cognitive function in both sexes.
These findings indicate that maternal immune conditions may influence the severity of ASD symptoms in offspring and the severity of these symptoms may vary between males and females. Although there is no cure for ASD, robust data demonstrate that sulforaphane, a bioactive compound derived from cruciferous vegetables, especially broccoli sprouts, may be beneficial in reducing many of the behavioral and emotions symptoms associated with the condition.
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Enzymes produced by common oral bacteria show promise for treating celiac disease. www.sciencedaily.com
Celiac disease is an autoimmune disorder characterized by an inflammatory response to eating gluten. An estimated 1 percent of people worldwide have celiac disease, but diagnosing the condition is difficult, often due to vague, seemingly minor, or even absent symptoms. Consequently, the epidemiology of celiac disease is best described by the “iceberg model.” That is, for every diagnosed case of celiac disease (the visible part of the iceberg), roughly five cases remain undiagnosed (the hidden part of the iceberg). Findings from a new study indicate that enzymes from Rothia bacteria may be useful in treating people who have celiac disease.
Gluten is a composite of two proteins found in wheat, barley, and rye. During normal digestion, enzymes break proteins down into groups of amino acids called peptides. Most peptides can be broken down further, taken up in the intestine, and then transported to the body’s tissues for use. However, gluten cannot be broken down by the digestive enzymes and can provoke an immune response in susceptible people, causing celiac disease.
Rothia bacteria are regular inhabitants of the mouth and respiratory tract. They rarely cause infections, except in some immunocompromised people. Rothia bacteria can break down the peptides in gluten that provoke the immune response.
The authors of the study extracted subtilisins, a type of enzyme found in the membrane of Rothia bacteria, and monitored the enzymes' activity. They also monitored the activity of food-grade subtilisins, enzymes used to make natto, a fermented soybean product. They found that both types of bacterial subtilisins effectively broke down the immunogenic peptides present in gluten, demonstrating that subtilisins from Rothia bacteria or other food-grade bacteria might be useful in treating celiac disease.
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Stressed mitochondria leak DNA fragments that induce inflammation. www.sciencemagazinedigital.org
Oxidative stress drives many disease processes. In mitochondria, in particular, it promotes the release of mitochondrial DNA into surrounding cytosol where it can trigger cellular responses involved in autoimmunity.
A critical aspect of mitochondrial DNA release is the formation of pores created by the oligomerization of specific proteins called voltage-dependent anion channels (VDACs), which are found in the outer mitochondrial membrane. A new study in a mouse model of lupus suggests that inhibition of VDAC oligomerization blocks mitochondrial DNA release, preventing subsequent immune responses.
These findings suggest that inhibition of VDAC oligomerization may be an alternative therapeutic approach for a wide range of diseases likely associated with mitochondrial DNA release, such as lupus and Parkinson’s disease.
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Long-term reduction in hyperglycemia in advanced type 1 diabetes: the value of induced aerobic glycolysis with BCG vaccinations www.nature.com
Mycobacterium are among the oldest co-evolutionary partners of humans. The attenuated Mycobacterium bovis Bacillus Calmette Guérin (BCG) strain has been administered globally for 100 years as a vaccine against tuberculosis. BCG also shows promise as treatment for numerous inflammatory and autoimmune diseases. Here, we report on a randomized 8-year long prospective examination of type 1 diabetic subjects with long-term disease who received two doses of the BCG vaccine. After year 3, BCG lowered hemoglobin A1c to near normal levels for the next 5 years. The BCG impact on blood sugars appeared to be driven by a novel systemic and blood sugar lowering mechanism in diabetes. We observe a systemic shift in glucose metabolism from oxidative phosphorylation to aerobic glycolysis, a state of high glucose utilization. Confirmation is gained by metabolomics, mRNAseq, and functional assays of cellular glucose uptake after BCG vaccinations. To prove BCG could induce a systemic change to promote accelerated glucose utilization and impact blood sugars, murine data demonstrated reduced blood sugars and aerobic induction in non-autoimmune mice made chemically diabetic. BCG via epigenetics also resets six central T-regulatory genes for genetic re-programming of tolerance. These findings set the stage for further testing of a known safe vaccine therapy for improved blood sugar control through changes in metabolism and durability with epigenetic changes even in advanced Type 1 diabetes.
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Hair Regeneration by Small Molecules That Activate Autophagy papers.ssrn.com
Hair plays important roles, ranging from the conservation of body heat to the preservation of psychological well-being. Hair loss or alopecia affects millions worldwide and can occur because of aging, hormonal dysfunction, autoimmunity, or as a side effect of cancer treatment. Methods that can be used to regrow hair are highly sought after, but lacking. Here we report that hair regeneration can be stimulated by small molecules that activate autophagy, including the longevity metabolites α-ketoglutarate and α-ketobutyrate, and the prescription drugs rapamycin and metformin which impinge on TOR and AMPK signaling.
Chai, Min and Jiang, Meisheng and Vergnes, Laurent and Fu, Xudong and de Barros, Stéphanie C. and Jiao, Jing and Herschman, Harvey R. and Crooks, Gay M. and Reue, Karen and Huang, Jing, Hair Regeneration by Small Molecules That Activate Autophagy (2018). Available at SSRN: https://ssrn.com/abstract=3188356 or http://dx.doi.org/10.2139/ssrn.3188356
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Intermittent fasting (every other day) increased gut bacteria diversity and reduced inflammation, demyelination, and axonal damage in multiple sclerosis (MS) animal model. A small pilot trial in humans with MS showed many similar changes to the gut microbiome and blood adipokines such as leptin. The effects of fasting on immune cells included a reduction of pro-inflammatory IL-17-producing T cells and increased numbers of T regulatory cells which prevent autoimmunity.
The small pilot trial in humans showed increased bacteria richness in species that have previously been shown to promote T regulatory cell accumulation in the colon.
Interestingly, this study did what is called a metagenomic analysis and found that the ketone pathway was enhanced in the gut microbiome by intermittent fasting. This is super interesting because bacteria in the gut normally produce short chain fatty acids and ketones from fermentable fiber but suggests that the gut microbiome regulates its own ketone body metabolism during fasting!
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People with multiple sclerosis increased beneficial gut bacteria & induced an anti-inflammatory immune response after supplementation with a probiotic www.ncbi.nlm.nih.gov
A pilot study finds people with multiple sclerosis (and healthy controls) increased several species of beneficial gut bacteria and induced an anti-inflammatory immune response after supplementation with a strong, high CFU probiotic for 3 months.
Multiple sclerosis patients also displayed a decrease in a type of immune cell called myeloid-derived dendritic cells which play a role in suppressing immune cells that prevent autoimmunity (called T-regulatory cells). Larger studies are needed to replicate these findings as well as investigate whether the probiotic supplementation has any effect on clinical symptoms.
To my knowledge, there are exactly three brands that have this type of formulation of high CFU probiotic that seems to have a strong and growing body of clinical, published evidence: • VSL#3 (the original formulation) • Visbiome (a newer brand used in this study that is supposed to be substantially similar) • Vivomixx (European branded Visbiome)
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A certain type of bacteria found in the small intestine can travel to other organs and initiate the production of auto-antibodies and inflammation. www.sciencedaily.com
A certain type of bacteria found in the small intestine (E. gallinarum) can travel to other organs and initiate the production of auto-antibodies and inflammation which both play a role in autoimmune disease.
A certain species called Enterococcus gallinarum, was found to spontaneously “translocate” outside of the gut to lymph nodes, the liver, and spleen in mice and was found in cultured liver cells of healthy people, and in livers of patients with autoimmune disease.
Most bacteria in the gut is in the large intestine near the colon and not small intestine. Typically, certain phyla and classes of bacteria that crop up on a low fiber diet and these bacteria possess flagella that allows move or “swim” up the intestines and penetrate the small intestine (where they are not supposed to be). This is often referred to as small intestine bacterial overgrowth.
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Fasting-like diet kills autoimmune cells & replaced them with healthy cells & improved symptoms in MS patients. www.sciencedaily.com
This fasting-like diet also promotes regeneration of the myelin in mice with multiple sclerosis. In human patients with multiple sclerosis, the fasting-like diet led to improvements in symptoms if followed by a Mediterranean diet or a ketogenic diet.
Here is the fasting-like diet that humans were given: Day 1 – pre-fasting followed by Day 2-8 – very low calorie diet. Day 1-prefasting consists of an 800 kcal (about 40% of normal caloric intake similar to mouse Day1 FMD) monodiet (fruit, rice, or potatoes) by preference of individuals. On the following day patients were recommended to use an oral laxative, Natrium Sulfuricum (20-40 g). FMD consisted of 100 ml vegetable broth or vegetable juice with 1tablespoon of linseed oil 3 times daily, plus additional calorie-free liquids. The daily calorie intake was predefined with 200 – 350 kcal (10-18% of normal caloric intake similar to mouse Day 2-3 FMD). Patients were advised to drink 2-3 L of unsweetened fluids each day (water, and herbal teas) and to use an enema if tolerated. After the 7-day fasting period solid foods were stepwise reintroduced for three days, starting with a steamed apple at day 8. After the fasting and refeeding period a normocaloric, plant-based Mediterranean diet was maintained until study end.