Category: Diseases, Syndromes and Conditions

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Investigating Vaping’s Impact on Gum Disease

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A series of new studies investigates how e-cigarettes alter oral health and may be contributing to gum disease. The latest, published in mBio, finds that e-cigarette users have a distinctive oral microbiome that is less healthy than nonsmokers but potentially healthier than cigarette smokers, and measures worsening gum disease over time.

“To our knowledge, this is the first longitudinal study of oral health and e-cigarette use. We are now beginning to understand how e-cigarettes and the chemicals they contain are changing the oral microbiome and disrupting the balance of bacteria,” said co-lead researcher Prof Deepak Saxena.

While cigarette smoking is known to increase gum disease risk, much less is known about the impact of e-cigarette use on oral health, especially in the long term.

The researchers studied the oral health of 84 adults from three groups: cigarette smokers, e-cigarette users, and people who have never smoked. Gum disease was assessed through two dental exams six months apart, during which plaque samples were taken to analyse the bacteria present.

Gum health changes
All participants had some gum disease at the start of the study, with cigarette smokers having the most severe disease, followed by e-cigarette users. After six months, the researchers observed that gum disease had worsened in some participants in each group, including several e-cigarette users.

Clinical attachment loss is a key indicator of gum disease, measured by gum ligament and tissue separating from a tooth’s surface, leading the gum to recede and form pockets. These pockets are bacterial breeding grounds and can lead to worsening gum disease. In a study of the same participants published in Frontiers in Oral Health, the research team found that clinical attachment loss was significantly worse only in the e-cigarette smokers after six months.

A unique microbiome
Analysis of the bacteria in plaque samples showed that e-cigarette users had a different oral microbiome than smokers and nonsmokers, in line with their earlier results.

While all groups shared roughly a fifth of the types of bacteria, the bacterial makeup for e-cigarette users had strikingly more in common with cigarette smokers than nonsmokers. Several types of bacteria, including Selenomonas, Leptotrichia, and Saccharibacteria, were abundant in both smokers and vapers compared to nonsmokers. Several other bacteria – including Fusobacterium and Bacteroidales, linked to gum disease – were particularly dominant in the mouths of e-cigarette users.

When plaque samples were gathered and analysed in the six-month follow-up, the researchers found greater diversity in bacteria for all groups studied, yet each group maintained its own distinct microbiome.

“Vaping appears to be driving unique patterns in bacteria and influencing the growth of some bacteria in a manner akin to cigarette smoking, but with its own profile and risks to oral health,” said Fangxi Xu, study co-first author.

An altered immune response
The researchers found that the distinct microbiome in e-cigarette users was correlated with clinical measures of gum disease and changes to the host immune environment. In particular, vaping was associated with different levels of cytokines. Certain cytokines are linked to an imbalance in oral bacteria and can worsen gum disease by making people prone to inflammation and infection.

TNFα, a cytokine that causes inflammation, was significantly elevated among e-cigarette users. In contrast, cytokines IL-4 and IL-1β were lower among e-cigarette users; because IL-4 tends to be reduced in people with gum disease and increases after treatment, it suggests that certain bacteria in the mouths of e-cigarette users are worsening inflammation.

The researchers concluded that the distinct oral microbiome of e-cigarette users elicits altered immune responses, which along with clinical markers for gum disease illustrate how vaping presents its own challenge to oral health.

“E-cigarette use is a relatively new human habit,” said Scott Thomas, study co-first author. “Unlike smoking, which has been studied extensively for decades, we know little about the health consequences of e-cigarette use and are just starting to understand how the unique microbiome promoted by vaping impacts oral health and disease.”

Source: New York University

Categories : Diseases, Syndromes and Conditions GeneticsTags :

A Life-changing Genetic Cure for Sickle Cell Patient

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Sickle cell disease occurs in people who inherit two copies of the sickle cell gene, one from each parent. This produces abnormal haemoglobin, called haemoglobin S. Credit: Darryl Leja, National Human Genome Research Institute, National Institutes of Health

Jimi Olaghere, who had suffered all his life from the chronic pain of sickle cell disease, recently received a genetic cure decades sooner than he would have believed possible.

Mr Olaghere is one of the first seven sickle cell patients who received a new gene-editing treatment going through its first clinic trials in the US. “It’s like being born again,” he said, adding that it has changed his life. “When I look back, it’s like, ‘Wow, I can’t believe I lived with that.'”

Mr Olaghere, 36 said: “You always have to be in a war mindset, knowing that your days are going to be filled with challenges.”

Sickle cell disease is caused by a mutated gene that results in abnormal haemoglobin, leading to blood cells becoming more rigid and taking on their characteristic sickle shape. These malformed cells often get stuck in blood vessels, giving rise to ischaemias and an increase in cardiovascular disease risk and organ damage. Mr Olaghere may need a hip replacement due to avascular necrosis.

The disease also causes chronic pain, which he likened to “shards of glass flowing through your veins or someone taking a hammer to your joints.”

Severe pain episodes known as crises are the hallmark of sickle cell disease. For years, Mr Olaghere was hospitalised on a monthly basis. Winters worsened the problem as the cold restricted surface blood vessels, increasing the risk of blockages. He moved to a warmer city, and became a tech entrepreneur as he didn’t think any employer would be sympathetic to going to the hospital so often.

His family urged him to participate in clinical trials or receive a bone marrow transplant. However, he thought it would take too much time and instead pinned his hopes on DNA editing “in the future, probably 20 to 50 years from now”.

But in 2019 he read about a new gene editing therapy and emailed the medical team right away. When he learned he was accepted, he said it was “the best Christmas present ever”. As the pandemic hit and flights were cancelled, he was still able to make the four-hour drive for treatment appointments.
In order to genetically edit his stem cells the stem cells were flushed out of his bone marrow and into the bloodstream for collection.

“You sit there for eight hours and this machine is literally just sucking all the blood out of you,” he said.

The process left him physically and mentally drained, and still needed  blood transfusions. Mr Olaghere had to go through this process, the most difficult of all for him, four times. 

The key to the treatment lies not in correcting the genetic defect that produces the cell but rather sidestepping it by getting the body to use an alternative: foetal haemoglobin 

Ordinarily, at around 40 weeks of pregnancy, a genetic switch called BCL11A is flipped and the body starts producing adult haemoglobin – which is the only form affected by sickle cell disease. 

“Our approach is to turn that switch off and increase the production of foetal haemoglobin again, basically turning the clock back,” explained Dr Haydar Frangoul, who treated Mr at the Sarah Cannon Research Institute.

Mr Olaghere’s stem cells were sent to Vertex Pharmaceuticals’ laboratories for genetic editing. By September 2020, the engineered cells were ready to be infused into his body. “It was the week of my birthday, actually. So it was almost like getting a new life,” he recalled.

The original faulty stem cells that remained in his body were killed off with chemotherapy, and then genetically engineered replacements were infused into his body to produce sickle-free blood.

“I remember waking up without any pain and feeling lost,” he said. “Because my life is so associated with pain, it’s just a part of who I am. It’s weird now that I don’t experience it any more.'”

Dr Frangoul said that the first seven patients’ results have been “nothing short of amazing” and represented a “functional cure” for their disease.
“What we are seeing is patients are going back to their normal life, none have required admission to hospital or doctor visits because of sickle cell related complications,” Dr Frangoul said.

So far, the genetic technique has been conducted on 45 patients with either sickle cell disease or beta thalassaemia. However, the data are still being gathered.

Source: BBC News

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In MS, Twin Study Reveals Disease-causing T Cells

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By studying the immune system of pairs of monozygotic twins to rule out genetics in cases of multiple sclerosis, researchers may have discovered a smoking gun: precursor cells of the disease-causing T cells.

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system CNS and the most common cause of neurological impairment in young adults. In MS, the patient’s own immune system attacks the CNS, resulting in cumulative neurological damage. The cause of MS still unclear but a variety of genetic risk factors and environmental influences have already been linked to the disease.

Genetics have already been found to be a necessary condition for developing multiple sclerosis. “Based on our study, we were able to show that about half of the composition of our immune system is determined by genetics,” said Florian Ingelfinger, a PhD candidate at the UZH Institute of Experimental Immunology. The study shows that these genetic influences, while always present in MS patients, are not on their own sufficient to trigger multiple sclerosis. In the study, 61 pairs of monozygotic twins where one twin is affected by MS whereas the co-twin is healthy were examined. From a genetic point of view, the twins were thus identical. “Although the healthy twins also had the maximum genetic risk for MS, they showed no clinical signs of the disease,” said Lisa Ann Gerdes.

With this cohort of twins, the researchers were  tease out environmental differences. “We are exploring the central question of how the immune system of two genetically identical individuals leads to significant inflammation and massive nerve damage in one case, and no damage at all in the other,” explained Professor Burkhard Becher, leader of the research team. Using identical twins let the researchers block out the genetic influence and focus on the immune system changes that were ultimately responsible for triggering MS in one twin.

The researchers harnessed state-of-the-art technologies to describe the immune profiles of the twin pairs in great detail. “We use a combination of mass cytometry and the latest methods in genetics paired with machine learning to not only identify characteristic proteins in the immune cells of the sick twin in each case, but also to decode the totality of all the genes that are switched on in these cells,” Florian Ingelfinger explained. 

“Surprisingly, we found the biggest differences in the immune profiles of MS affected twins to be in the cytokine receptors, ie the way immune cells communicate with one another. The cytokine network is like the language of the immune system,” said Ingelfinger. Increased sensitivity to certain cytokines leads to greater T cell activation in the bloodsteams of patients with multiple sclerosis. These T cells are more likely to migrate into the CNS and cause damage there. The identified cells were found to have the characteristics of recently activated cells, which were in the process of developing into fully functional T cells. “We may have discovered the cellular big bang of MS here – precursor cells that give rise to disease-causing T cells,” said Prof Becher.

“The findings of this study are particularly valuable in comparison to previous studies of MS which do not control for genetic predisposition,” said Prof Becher. “We are thus able to find out which part of the immune dysfunction in MS is influenced by genetic components and which by environmental factors. This is of fundamental importance in understanding the development of the disease.”

The study findings were reported in Nature.

Source: University of Zurich

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New Insights Into Atopic Dermatitis Yield Possible Therapy

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Atopic dermatitis (AD) is often thought of as an inflammatory disease that arises from a breakdown in the barrier function of the skin. Now a new study pinpoints a cascade of inflammatory signalling that precedes the appearance of skin ulcers, shedding light on the early stages of the condition and possible new drug targets.

The work, published in the journal Science Translational Medicine, was the result of a cross-school and cross-institutional collaboration among researchers.

“You have researchers in the dental school noticing a skin condition, broadening their work to the medical school and experts on computational systems biology,” said Professor Dana Graves, a co-corresponding author on the paper. “Without this interdisciplinary collaboration, that initial finding would not have gone anywhere.”

John Seykora, a co-corresponding author and professor of dermatology, agreed. “This shows one of the benefits of being part of a university with experts across fields,” he says. “Our dental school colleagues developed a mouse that manifested a particular skin phenotype, and the question was, What was this and did it resemble any disease we might know? And in the end it did, and it’s providing some novel insights into a very common skin condition in humans.”

The work began with an exploration of the role of inflammatory signalling in bone fracture healing in diabetes. A focus was on nuclear factor kappa-B (NF-kB), a master regulator of inflammatory responses. As part of that work, researchers developed a mouse model lacking an activator of NF-kB signalling, IKKB. The researchers noticed that these animals developed skin lesions as they became young adults.

“That was interesting to us because these ulcerations looked like an inflammatory event, but we had effectively turned off the activity of NF-kB, which should reduce inflammation,” said Prof Graves. “So this was a paradox.”

To better understand what was driving this response, they sought expertise in skin diseases from Prof Seykora. When they examined the mice, they noted several features quite similar to AD, “albeit the mouse version” said Prof Graves.

In particular, they noted skin thickening and an infiltration of certain types of white blood cells that are also seen in human AD. Delving deeper into how the loss of IKKB was driving these effects, the team performed single-celled RNA analysis combined with a new analysis method. The team learned that fibroblasts were the culprit, a major component of the skin’s dermis layer and typically thought to support the structural integrity of skin.

Though NF-kB typically promotes inflammation, here, decreased NF-kB activity was paradoxically leading to recruitment of immune cells and associated inflammation. Data from the team’s single-cell RNA analysis pointed to high activities of a protein transcription factor called CEBPB, as well as a signalling molecule, CCL11, “We worked out the mechanism in the mouse,” Prof Sekora said, “then showed that much of it applied in human tissue as well.”

When the researchers compared what they had seen in the mouse cells to skin samples from people with AD, they found similar patterns; CCL11 and CEBPB were both found at higher levels in the affected skin than in unaffected skin.

Testing a monoclonal antibody against CCL11 in mice tamped down the inflammatory response they had initially seen in animals lacking IKKB, suggesting that this could be a target to reduce AD-associated inflammation.

The researchers say the work also highlights a developing appreciation that fibroblasts play important roles in immune processes in the skin, indicating that they are important regulators of white blood cells.

AD  typically emerges in childhood, often manifesting along with asthma. Indeed, in the mice, too, the signalling abnormalities the researchers observed occurred in a period corresponding to the animals “childhood.” The group’s findings suggest that fibroblasts may be involved during this period in helping to establish appropriate immune signalling in the skin.

“We have viewed NF-kB as a factor that stimulates inflammation, but it could be that, during development, its activation might be important for maintaining homeostasis,” said Prof Graves.

The team’s next steps are to further explore NF-kB signalling in fibroblasts.

Source: University of Pennsylvania

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A Simple Technique to Reduce Light-headedness upon Standing Up

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Light-headedness upon standing up due to initial orthostatic hypotension (IOH) is a common but poorly understood condition. A new study offers two simple  techniques to effectively manage symptoms of IOH and improve quality of life by activating lower body muscle before or after standing. The research appears in Heart Rhythm.

IOH is a transient decrease in blood pressure and increase in heart rate. Syncope, light-headedness, dizziness, or loss of consciousness from IOH, affects up to 40% of the general population (all ages), while presyncope is probably even more common. However, the condition is under-studied and there are very few options currently available to patients with IOH and no pharmacological treatments. The most common recommendations have been to stand up slowly or sit up first before standing.

IOH symptoms often present during an active stand but not with a passive tilt-table test, suggesting that a muscle activation response plays an important role in the pathophysiology of IOH. This muscle activation response refers to the rapid and excessive vasodilation that occurs in response to the brief lower body muscle contraction required to stand due to local mechanisms. Additional factors involved in this response include the increase in heart rate, initially due to the muscle heart reflex and secondarily in response to the arterial baroreflex triggered by the drop in BP as well as the increase in peripheral resistance, which is also triggered by the arterial baroreflex.

This study investigated physical manoeuvres before or after standing and their efficacy in reducing the drop in blood pressure as well as the symptoms typically seen in IOH patients upon standing. Study participants included 24 young women with a history of IOH. Two participants had inadequate heart rate recordings and were excluded from the analysis. The interventions tested consisted of lower body muscle pre-activation (thighs) through repeated knee raises prior to standing (PREACT) and lower body muscle tensing (thighs and buttocks) through leg crossing and tensing immediately after standing (TENSE).

The 22 study participants completed three sit-to-stand manoeuvres including a stand with no intervention (control), and two interventions. Researchers found that both PREACT and TENSE effectively improve the blood pressure drop. This led to a reduction in symptoms upon standing. They found that the PREACT manoeuvre accomplished this by increasing cardiac output, while the TENSE manoeuvre did so by increasing stroke volume.

“Our study provides a novel and cost-free symptom management technique that patients with IOH can use to manage their symptoms,” noted first author Nasia A. Sheikh, MSc. “Since it is a physical manoeuvre, it simply requires the lower body limbs, which patients can utilise at any time and from anywhere to combat their symptoms.”

Source: Elsevier

Categories : Diet and Nutrition Diseases, Syndromes and ConditionsTags :

Selenium Could Help Reverse Cognitive Decline

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The trace metal selenium could help reverse the cognitive impact of stroke and boost learning and memory in ageing brains, according to a study published in Cell Metabolism.

Previous studies on the impact of exercise on the ageing brain found levels of a protein key to transporting selenium in the blood were elevated by physical activity.

Lead researcher Dr Tara Walker said: “We’ve known for the last 20 years that exercise can create new neurons in the brain, but we didn’t really understand how,” Dr Walker said.

The research team sought to find out whether dietary selenium supplements could replicate the effects of exercise.

“Our models showed that selenium supplementation could increase neuron generation and improve cognition in elderly mice,” Dr Walker said. “The levels of new neuron generation decrease rapidly in aged mice, as they do in humans. When selenium supplements were given to the mice, the production of neurons increased, reversing the cognitive deficits observed in ageing.”

Selenium is an essential trace metal which can play an important role in human health. It is absorbed from soil and water and is found in foods such as grains, meat and nuts, with the highest levels found in Brazil nuts. The researchers also investigated whether selenium would have an impact on post-stroke cognitive decline.

“Young mice are really good at the learning and memory tasks, but after a stroke, they could no longer perform these tasks,” Dr Walker said. “We found that learning and memory deficits of stroke affected mice returned to normal when they were given selenium supplements.”

Dr Walker said the results opened a new therapeutic avenue to boost cognitive function in people who were unable to exercise due to poor health or old age.

“However, selenium supplements shouldn’t be seen as a complete substitute for exercise, and too much can be bad for you,” she said. “A person who is getting a balanced diet of fruits, nuts, veggies and meat usually has good selenium levels. But in older people, particularly those with neurological conditions, selenium supplements could be beneficial.”

Source: University of Queensland

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Atopic Dermatitis Linked to Range of Comorbid Conditions

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A comprehensive review has uncovered “clear evidence” of associations between atopic dermatitis (AD) and a range of comorbid conditions, which has informed updated clinical guidelines for AD. 

An expert panel reported on the results of a wide-ranging review in the Journal of the American Academy of Dermatology.  They found evidence linking AD to certain allergic, atopic, and immune-mediated conditions, as well as mental health problems, bone diseases, and skin infections. There is some evidence which supports associations between AD and substance use, attention deficit-hyperactivity disorder (ADHD), and some elements of metabolic syndrome. Less compelling evidence suggests AD has links to some cardiovascular conditions. There is inconclusive evidence for associations between adult AD and autism spectrum disorders, myocardial infarction, stroke, and metabolic syndrome. 

“Atopic dermatitis is one of several atopic diseases, meaning that there are internal sensitivities that can help drive the disease in the organ of choice, including asthma, allergic rhinoconjunctivitis, and food allergies, among others,” Dawn M.R. Davis, MD, co-chair of the guideline panel, told MedPage Today. “We always knew there was an association between atopic dermatitis and the other atopic diseases, but we lacked the evidence. Fortunately, because we’re getting more attention and more research is being performed in these areas, we now have data to back up our suspicions regarding the associations between atopic dermatitis and other atopic diseases.”

“Thanks to research by our colleagues, we discovered several other comorbidities that we did not expect, including skin diseases like alopecia areata and urticaria, as well as mental health conditions, including depression, anxiety, and substance use,” she continued. “We also have some evidence of associations with metabolic conditions, such as disorders of bone metabolism, and cardiovascular diseases.”

This review was conducted in concert with updating the American Academy of Dermatology clinical guideline on AD. The quantity and depth of data also warranted a separate guideline component for recognition of comorbidities associated with AD. The main goal was to increase awareness of the associations.

“The goal of this guideline is to plant a seed in the mind of providers and to empower and validate patients, so they can have a customised, individualised, robust discussion about how their particular circumstances relate to any of the risk factors,” said Dr Davis.

Key findings and statements in the guideline include:

  • The association between AD and asthma is well established, but the “atopic march” explanation remains unproven
  • “Clear evidence” of an association between AD and food allergy, but estimated prevalence of food allergy in adults with AD remains low
  • Epidemiologic studies “consistently show” an association between AD and alopecia areata, but there are limited data on severity of alopecia or treatment response
  • Analysis of four studies showed that AD doubles the odds ratio of depression though reasons for this are unclear
  • A “potential association” between AD and substance use/abuse (limited evidence)
  • Accumulating evidence suggests small associations between AD and hypertension, peripheral and coronary artery disease, congestive heart failure, and acute clinical events
  • A “small association” suggested between adult AD with obesity and dyslipidemia; however, limited data have pointed to a possible inverse association with diabetes
  • Several studies have shown associations with increased risk of osteoporosis and fracture in adults with AD, possibly linked by systemic inflammation.

“To date, research on AD-associated comorbidities has focused on identifying potential associations in epidemiologic studies,” the guideline authors wrote. “There is currently no conclusive evidence demonstrating that screening for comorbid conditions associated with AD improves patient outcomes. For the evidence of AD associations to be put into action, research is required on whether screening or management of these comorbidities among adults with AD beyond what is recommended for the general population is beneficial.”

Besides the comorbidities document, other documents will be published over two years which will address topical therapy, systemic treatment and phototherapy, and paediatric AD.

Source: MedPage Today

Categories : Diseases, Syndromes and Conditions ImmunologyTags :

Meat, Gut Bacteria and Multiple Sclerosis

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Gut microbiome. Credit: Darryl Leja, NIH

There appears to be a link between eating meat, gut bacteria and multiple sclerosis, according to new research published in EBioMedicine. The study teased out subtle connections that could lead to a better understanding of the causes of the disease.

The autoimmune disease multiple sclerosis (MS) is more prevalent in specific regions, particularly the northern mid-latitudes, suggesting that geography is somehow linked to the disease, perhaps involving diet. However, the exact relationships between diet, immune response, and MS has been a mystery. What exactly triggers the body to attack the myelin sheaths in MS in the first place is unknown.

Growing evidence suggests that bacteria might play a role. Gut bacteria affect the immune system, and diet affects the gut. Researchers studied the gut microbiome, immune systems, diet, and blood metabolites in 25 MS patients and 24 healthy controls to look for any subtle but important correlations.

“We found a number of gut bacteria associated with MS and severity of disability of MS patients,” said Dr Yanjiao Zhou. “We also found increased autoimmune markers and signature metabolites in MS. But what is really interesting is how these systems connect with each other, and how diet is involved in these connections. Using multi-OMICS approaches, we try to close the loop and show the associations between multiple systems.”

Meat eating was the strongest link in their analysis, where higher meat consumption saw a decrease in the population of Bacteroides thetaiotaomicron, a bacteria associated with digesting carbohydrates from vegetables.

Higher meat consumption, seen in the MS patients, was also linked to an increase in T-helper 17 cells in the immune system, and an increase in S-adenosyl-L-methionine (SAM) in their blood.

Meat eating was not a predictor of MS. But the evidence suggested that, in MS, something causes gut bacteria to disassociate with the immune system, leading to heightened T-helper 17 cells and autoimmune attacks on the nervous system. And it tends to be associated with eating meat.

Future research aims to recruit more volunteers, including those with more severe MS. Eventually they hope to understand more of the cause-and-effect between diet, bacterial ecosystems in the gut, and immune response, and potentially help prevent or mitigate MS symptoms in people suffering from the disease.

Source: University of Connecticut

Categories : Diseases, Syndromes and Conditions Mental HealthTags :

In Chronic Disease, Psychiatric Comorbidity Doubles Mortality Risk

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The risk of all-cause mortality among patients with chronic, non-communicable diseases is more than doubled if they also have a psychiatric comorbidity, according to a new study published in PLOS Medicine.

Non-communicable diseases such as diabetes and heart disease are a global public health challenge accounting for an estimated 40 million excess deaths annually. Researchers drew on Swedish health data for 1 million patients born between 1932 and 1995 who had diagnoses of chronic lung disease, cardiovascular disease, and diabetes. More than a quarter of the people in the analysis also had a co-occurring psychiatric disorder during their lives.

Within 5 years of diagnosis, 7% of the people included in the study had died from any cause and 0.3% had died from suicide. Comorbid psychiatric disorders were associated with higher all-cause mortality (15.4% to 21.1%) when compared to those without such conditions (5.5% to 9.1%). When compared with an unaffected sibling to account for familial risk factors, patients with psychiatric comorbidity remained consistently associated with elevated rates of premature mortality and suicide (7.2–8.9 times higher). Different psychiatric diagnoses affected mortality risks; in those with comorbid substance use disorder it was 8.3–9.9 times compared to unaffected siblings, and by 5.3–7.4 times in those with comorbid depression.

“Improving assessment, treatment, and follow-up of people with comorbid psychiatric disorders may reduce the risk of mortality in people with chronic non-communicable diseases,” the authors concluded.

Source: EurekAlert!

Categories : Diseases, Syndromes and ConditionsTags :

Vitamin D Supplements Reduce Autoimmune Disease Risk

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A five year-long randomised, placebo-controlled study found that in older adults taking vitamin D supplements, alone or with omega-3 fatty acids, the risk of developing autoimmune disease was reduced.

Autoimmune diseases (AD) such as rheumatoid arthritis, polymyalgia rheumatica, autoimmune thyroid disease and psoriasis, are a leading cause of morbidity and mortality as people age. Few effective treatments are available for AD, but some research has hinted that supplements, including vitamin D and omega-3 fatty acids, could have beneficial effects.

In a new study published in the BMJ, investigators from Brigham and Women’s Hospital evaluated whether taking vitamin D and/or omega fatty acid supplements could affect rates of AD. The large-scale vitamin D and Omega-3 Trial (VITAL), a randomised study which followed participants for approximately five years. Taking vitamin D, or vitamin D and omega-3 fatty acids had a significantly lower rate of AD than placebo.

“It is exciting to have these new and positive results for non-toxic vitamins and supplements preventing potentially highly morbid diseases,” said senior author Karen Costenbader, MD, MPH. “This is the first direct evidence we have that daily supplementation may reduce AD incidence, and what looks like a more pronounced effect after two years of supplementation for vitamin D.”

“Now, when my patients, colleagues, or friends ask me which vitamins or supplements I’d recommend they take to reduce risk of autoimmune disease, I have new evidence-based recommendations for women aged 55 years and older and men 50 years and older,” said Dr Costenbader. “I suggest vitamin D 2000 IU a day and marine omega-3 fatty acids (fish oil), 1000 mg a day – the doses used in VITAL.”

VITAL included 25 871 participants, with men aged 50 and older and women aged 55 and older, conducted to investigate whether taking vitamin D3 and/or omega-3 supplements could reduce the risk for developing cancer, heart disease and stroke in people who do not have a prior history of these illnesses. Prior to the launch of VITAL, investigators determined that they would also look at rates of AD among participants, as part of an ancillary study.

Participants answered questionnaires about new diagnoses of diseases, including rheumatoid arthritis, polymyalgia rheumatica, autoimmune thyroid disease, psoriasis and inflammatory bowel disease, with space to write in all other new onset ADs. Medical records were reviewed to confirm reported diagnoses.

“Autoimmune diseases are common in older adults and negatively affect health and life expectancy. Until now, we have had no proven way of preventing them, and now, for the first time, we do,” said first author Jill Hahn, ScD, post-doctoral fellow at the Brigham.

Among patients randomised to vitamin D, 123 participants in the treatment group and 155 in the placebo group were diagnosed with confirmed AD (22 percent reduction). Among those in the fatty acid arm, confirmed AD occurred in 130 participants in the treatment group and 148 in the placebo group. Omega-3 fatty acids alone did not significantly lower incidence of AD, but there was some evidence of a decrease over long periods.

Source: EurekAlert!