Antioxidant treatment in acute ischemic stroke may delay the onset of Alzheimer's dementia
Clinical Muncipal Hospital (Romania), March 17, 2020
Currently we are facing a dementia epidemic, with estimations showing that by 2050 approximately 131 million people will be affected. Every 7 seconds a patient is diagnosed worldwide. Because the common forms of dementia occur in the elderly, delaying the onset or worsening of the cognitive impairment could translate into a significant reduction of the incidence of the disease. Estimations have shown that of the huge number of cases expected by 2050, roughly 23 million could be avoided if the onset of the disease could be delayed by 2 years. Despite the ambition to identify a disease modifying therapy or a cure for dementia by 2025 set by the G8 dementia summit in 2013, the findings so far are not very encouraging.
To date there is growing evidence of the association of vascular risk factors like hypertension, high cholesterol levels or diabetes mellitus with cognitive impairment and Alzheimer's disease. Unfortunately, simply managing these risk factors had little effect in reducing the incidence of dementia. These factors, however, strongly increase the risk of a patient to suffer an ischemic stroke and incident stroke approximately doubles the risk of dementia. From the study of Saver published in 2006 we know that "each hour in which treatment fails to occur the brain loses as many neurons as it does in 3.6 years of normal aging".
These neuronal losses occur through ischemic necrosis in the core of the infarction, but may be prolonged up to 2 weeks after the ischemic insult in the penumbral area surrounding the ischemic core through another type of cell loss, namely apoptosis. In initiating apoptosis oxidative species have a major role. Several authors have shown consistent increases in oxidative stress after an ischemic stroke. As the authors pointed out in a previous study, oxidative stress increases mainly after cardioembolic stroke, followed by lacunar stroke, with a less prolonged burst of generation of oxidative species following thrombotic stroke.
There is a considerable overlap between the oxidative stress-induced pathogenesis in ischemic stroke and Alzheimer's disease including mitochondrial dysfunction (the mitochondria being the main generators of energy in the cells), calcium overload of the cells, activation of different destructive enzymes by the excess intracellular calcium, aberrant gene transcription and expression, induction of autophagy (a process by which cells degrade their own cytoplasmic proteins and organelles) and activation of inflammatory responses.
Despite promising results of antioxidant molecules in animal models of ischemic stroke, human clinical trials were disappointing possibly due to late administration and incorrect selection of patients. However, in a study published in 2019, edaravone (an antioxidant molecule) given within 48 hours after endovascular revascularization in acute ischemic stroke was associated with greater functional independence at hospital discharge, lower in-hospital mortality and reduced intracranial hemorrhage after admission in a study which enrolled over 10,000 patients. More recently in a report presented at the International Stroke Conference 2020, nerinetide or NA1, a molecule which reduces endogenous nitric oxide (also an oxidative species) generated inside the cell during ischemia, improved the outcome of ischemic stroke patients who underwent endovascular thrombectomy. Unfortunately, NA1 interacted with alteplase, limiting its efficiency in patients who were also thrombolysed.
Antioxidants have been evaluated also in patients suffering from degenerative diseases, Alzheimer's disease included, with promising results in animal models but inconclusive results in clinical trials. Therapeutic strategies are hampered by the dual role of oxidative species in the organism. On one hand, increased ROS production contributes to age-related chronic conditions and on the other, oxidant species function as signaling molecules in pathways that are critical for cell survival. However, based on the compelling evidence of the implication of oxidative stress in AD pathogenesis and of the pivotal role of mitochondria, molecules acting as mitochondria-targeted antioxidants show promise in animal models of neurodegenerative diseases, improve mitochondrial function after coronary ischemia/reperfusion in rats, and some have already been developed into drugs used in clinical trials in type 2 diabetic patients.
In view of the implication of oxidative stress in the genesis of AD pathology, the authors hypothesize that with aging, in the presence of well-established vascular risk factors, and possibly with a genetic contribution, AD pathology develops slowly without clinically overt cognitive impairment. However, after a stroke there is a sudden burst in oxidative stress which accelerates the pathogenesis of dementia and leads to clinically obvious cognitive impairment. If this hypothesis would be proven the reason for reaching antioxidant treatment in acute ischemic stroke would be reinforced. Further studies in this direction with long follow-up periods would be needed. Nonetheless, in view of the high incidence and prevalence of the disease, the results could be rewarding.
Spinach supplements can enhance athletic performance
Freie University (Germany), March 17, 2020
Supplements that contain an anabolic compound from spinach should be in the list of prohibited substances in sports, according to a recent study. Researchers from Australia, Germany and Italy looked at the effects of ecdysterone, a naturally occurring plant steroid, in young men undergoing strength training and found that it can boost physical performance and increase muscle mass. This compound has been dubbed the “Russian secret” in the 1980s due to heavy suspicions that Russian athletes were using it as a performance-boosting supplement.
How anabolic agents work
Substances that fall under the category of anabolic steroidal agents or anabolic-androgenic steroids are either synthetic or naturally occurring variations of the male sex hormone, testosterone. Often referred to as simply steroids, these drugs are designed to treat hormonal issues, such as delayed puberty. Steroids are also used to address muscle loss brought about by serious conditions like AIDS or cancer.
However, steroids rose to notoriety when athletes and weight lifters began misusing them. The anabolic and androgenic properties of steroids allow them to promote not only male sex characteristics, but also anabolism, a bodily process that allows the growth of new cells. These activities result in enhanced athletic performance and increased muscle growth and strength.
Ecdysterone is the main compound in spinach extract and is classified as a phytosteroid. In plants, phytosteroids serve as structural components of cell membranes, as insect deterrents and as growth hormones. Many plant steroids, such as those derived from boswellia, fenugreek and licorice, are valued in traditional medicine for their anti-inflammatory activities and are used to treat conditions like lung diseases, allergic asthma and rheumatoid arthritis.
According to previous studies in animals, ecdysterone from spinach has many beneficial effects, most notably increasing the synthesis of protein in skeletal muscles. The compound has also proven itself to be more potent than anabolic agents currently banned in sports, such as the synthetic steroid metandienone. (Related: Pump up your body with the Popeye vegetable – spinach.)
Ecdysterone from spinach can boost athletic performance
Recent studies suggest that the anabolic effect of ecdysterone is influenced by its binding to estrogen receptors. But while multiple studies have investigated the effects of this plant steroid, those that involved humans are very rarely accessible.
For their study, which appeared in the journal Archives of Toxicology, the researchers recruited 46 young men to participate in an intervention study of strength training that lasted for 10 weeks. They gave the participants ecdysterone-contaning supplements and evaluated their effect on physical performance.
The researchers analyzed blood and urine samples for ecdysterone and biomarkers of performance enhancement, and screened for prohibited performance-enhancing substances to ensure the specificity of the measured effects. They also tested the supplements for anabolic steroid contamination before giving them to the participants.
The researchers reported that those who received ecdysterone showed significantly higher increases in muscle mass. They also observed the same increase in the number and growth of muscle cells (hypertrophy) in cell culture experiments.
With respect to athletic performance, the researchers found that ecdysterone enabled the participants to perform more one-repetition bench presses without increasing biomarkers for liver or kidney toxicity.
Based on these findings, the researchers concluded that ecdysterone from spinach can greatly enhance athletic performance, so its use as a supplement should be prohibited in sports. They propose that ecdysterone be classified under “other anabolic agents,” the use of which is banned in any competition.
Adding turmeric to green tea enhances its health benefits, study finds
Rajarshi Shahu College of Pharmacy (India), March 17, 2020
Today, numerous studies on the beneficial properties of green tea credit it with possessing a variety of antioxidant compounds. Among these compounds, epigallocatechin-3-gallate (EGCG) is the most abundant and extensively studied. EGCG is said to reduce inflammation, aid in weight loss and even support heart health by lowering blood cholesterol levels. However, the effectiveness of EGCG is hindered by its poor bioavailability.
In an attempt to increase its absorption in the intestines, researchers from Rajarshi Shahu College of Pharmacy and Research in India decided to combine it with another potent plant compound. Like EGCG, curcumin from turmeric has plenty of beneficial properties but poor bioavailability. Despite this, the researchers found that curcumin can enhance the absorption of EGCG by increasing intestinal permeability. They discussed this finding in detail in an article published in BMC Complementary and Alternative Medicine.
EGCG and curcumin: a potent combo against hypercholesterolemia
According to previous studies, EGCG from green tea is effective against high blood cholesterol or hypercholesterolemia. However, its low bioavailability decreases its potential, especially in promoting heart health.
To solve this problem, the researchers first extracted EGCG from green tea leaves and confirmed its presence using chromatography. They then confirmed the compatibility of the green tea extract (GTE) with curcumin.
Using everted goat intestine, the researchers tested the effect of GTE alone or in combination with curcumin on intestinal permeability. They reported that the GTE-curcumin mixture showed higher permeation than GTE alone.
When they treated rats fed a high-fat diet with GTE or the GTE-curcumin mixture, the researchers found that the mixture exerted a significant lipid-regulating effect. At the end of the treatment, the rats that received the mixture had lower cholesterol, triglyceride, HDL, LDL and VLDL levels than the rats given GTE alone.
Based on these findings, the researchers concluded that curcumin can enhance intestinal permeability and consequently the absorption of EGCG. Hence, EGCG-curcumin formulations can be a promising nutraceutical for the treatment of hyperlipidemia.
Vitamin D boosts chances of walking after hip fracture
Rutgers University, March 16, 2020
Senior citizens who are not vitamin D deficient have a better chance of walking after hip fracture surgery, according to a Rutgers-led study.
The findings in The American Journal of Clinical Nutrition suggest that vitamin D deficiency could limit mobility in older adults, said senior author Sue Shapses, a professor in the Department of Nutritional Sciences at the School of Environmental and Biological Sciences at Rutgers University-New Brunswick.
Shapses suggests that older adults take 800 international units (IU), equivalent to 20 micrograms, of vitamin D daily to prevent deficiency. Vitamin D is important for bone health, and people get it through some foods, exposure to the sun and vitamin pills.
"An important next step is learning how vitamin D affects mobility," said Shapses, who is also an adjunct professor in the Department of Medicine at Rutgers Robert Wood Johnson Medical School and director of the Center for Human Nutrition, Exercise and Metabolism at Rutgers' New Jersey Institute for Food, Nutrition, and Health. "For example, it is not clear if severe vitamin D deficiency is associated with direct effects on muscle, cognition and/or other organ systems."
A broken hip - among the most serious fall injuries - is hard to recover from, with many people unable to live on their own afterward. In the United States, more than 300,000 people 65 or older are hospitalized for hip fractures annually and falling causes more than 95 percent of these type of fractures. Women fall more frequently than men, experiencing three-quarters of hip fractures, and the number of fractures is likely to rise as the population ages, according to the U.S. Centers for Disease Control and Prevention.
Regaining mobility after a hip fracture is important for full recovery and to reduce the risk of death. But vitamin D deficiency is associated with reduced mobility after surgery to repair a hip fracture.
The multi-site study of patients 65 or older in the United States and Canada examined the influence of vitamin D levels in blood serum and nutrition on mobility. The study focused on death rate or inability to walk 10 feet (or across a room) without someone's help after surgery.
The findings showed that vitamin D levels greater than 12 nanograms per milliliter (12 parts per billion) in blood serum are associated with a higher rate of walking at 30 and 60 days after hip fracture surgery. While poor nutrition is associated with reduced mobility 30 days after surgery, that factor was not statistically significant. Still, in patients with high levels of parathyroid hormone, which leads to high levels of calcium in blood, mobility was reduced if their nutritional status was poor.
"This matters because vitamin D deficiency and malnutrition are common disorders in elderly patients with hip fractures and often occur together since both are complications of poor nutrition," Shapses said.
Previous studies have shown that taking 800 IU of vitamin D a day can prevent falling and fractures. A Rutgers-led study published last year indicated that high vitamin D intake (4,000 IU a day) compared with 600 IU a day may reduce reaction time, potentially boosting the risk of falling and fractures. The recommended dietary allowance for vitamin D is 600 IU daily for people from 1 to 70 years old and 800 for people over 70.
"These studies suggest that too much or too little vitamin D will affect mobility and falls in the elderly," Shapses said.
Inflammation in the brain linked to several forms of dementia
University of Cambridge, March 16, 2020
Inflammation in the brain may be more widely implicated in dementias than was previously thought, suggests new research from the University of Cambridge. The researchers say it offers hope for potential new treatments for several types of dementia.
Inflammation is usually the body's response to injury and stress - such as the redness and swelling that accompanies an injury or infection. However, inflammation in the brain - known as neuroinflammation - has been recognised and linked to many disorders including depression, psychosis and multiple sclerosis. It has also recently been linked to the risk of Alzheimer's disease.
In a study published today in the journal Brain, a team of researchers at the University of Cambridge set out to examine whether neuroinflammation also occurs in other forms of dementia, which would imply that it is common to many neurodegenerative diseases.
The team recruited 31 patients with three different types of frontotemporal dementia (FTD). FTD is a family of different conditions resulting from the build-up of several abnormal 'junk' proteins in the brain.
Patients underwent brain scans to detect inflammation and the junk proteins. Two Positron Emission Tomography (PET) scans each used an injection with a chemical 'dye', which lights up special molecules that reveal either the brain's inflammatory cells or the junk proteins.
In the first scan, the dye lit up the cells causing neuroinflammation. These indicate ongoing damage to the brain cells and their connections. In the second scan, the dye binds to the different types of 'junk' proteins found in FTD.
The researchers showed that across the brain, and in all three types of FTD, the more inflammation in each part of the brain, the more harmful build-up of the junk proteins there is. To prove the dyes were picking up the inflammation and harmful proteins, they went on to analyse under the microscope 12 brains donated after death to the Cambridge Brain Bank.
"We predicted the link between inflammation in the brain and the build-up of damaging proteins, but even we were surprised by how tightly these two problems mapped on to each other," said Dr Thomas Cope from the Department of Clinical Neurosciences at Cambridge.
Dr Richard Bevan Jones added, "There may be a vicious circle where cell damage triggers inflammation, which in turn leads to further cell damage."
The team stress that further research is needed to translate this knowledge of inflammation in dementia into testable treatments. But, this new study shows that neuroinflammation is a significant factor in more types of dementia than was previously thought.
"It is an important discovery that all three types of frontotemporal dementia have inflammation, linked to the build-up of harmful abnormal proteins in different parts of the brain. The illnesses are in other ways very different from each other, but we have found a role for inflammation in all of them," says Professor James Rowe from the Cambridge Centre for Frontotemporal Dementia.
"This, together with the fact that it is known to play a role in Alzheimer's, suggests that inflammation is part of many other neurodegenerative diseases, including Parkinson's disease and Huntington's disease. This offers hope that immune-based treatments might help slow or prevent these conditions."
Intestinal flora dysbiosis aggravates cognitive dysfunction associated with neuroinflammation in heart failure
Harbin Medical University (China), March 15, 2020
According to news reporting from Harbin, People’s Republic of China, by NewsRx journalists, research stated, “Cognitive dysfunction after heart failure (HF) is characterized by neuroinflammation, which plays an important role in the occurrence and development of cognitive dysfunction. Recent studies have shown that an intestinal flora imbalance may also trigger neuroinflammation in Alzheimer’s disease.”
The news correspondents obtained a quote from the research from the Fourth Affiliated Hospital of Harbin Medical University, “The present study was designed to reveal that intestinal flora dysbiosis caused by HF aggravates neuroinflammation-associated cognitive impairment. Adult male SD rats were fed daily for 2 weeks with probiotics or placebo until the day of surgery. HF was then triggered by 8 weeks of sustained coronary artery occlusion. 16S rDNA sequencing was used to confirm intestinal flora dysbiosis after HF and demonstrate that the changes paralleled intestinal pathology scores. The permeability of the blood-brain barrier was increased after HF, and such an increase in permeability may increase the levels of inflammatory cytokines caused by intestinal flora disorders. The changes in the intestinal flora caused by probiotics significantly reduced the level of neuroinflammation. In addition, probiotic administration considerably improved the impaired spatial memory in HF rats.”
According to the news reporters, the research concluded: “We conclude that intestinal flora dysbiosis plays a potential role in aggravating the impaired cognition associated with neuroinflammation and that these effects may be attenuated by probiotics.”
Cellular stress makes obese mothers have obese babies
French National Institute of Health and Medical Research, March 16, 2020
Maternal obesity increases the risk for obesity and metabolic perturbations in their offspring, but what are the mechanisms? In a new study published March 12 in the open-access journal PLOS Biology, Sebastien Bouret of the French National Institute of Health and Medical Research (INSERM) in Lille, France, and colleagues show that a key step in the process is the triggering of stress in a complex membrane system within all cells called the endoplasmic reticulum (ER). That stress leads to critical changes in the development of the hypothalamus, a part of the brain that controls hunger, satiety, and metabolic rate.
The ER constitutes the largest network of membranes within a cell, and plays a central role in the synthesis of proteins and many other biological processes. In response to cellular stress, the ER activates the so-called "unfolded protein response," whose normal function is to restore the cellular balance, but whose prolonged activation has been linked to obesity-induced insulin resistance and type 2 diabetes in adults. Because of this link, and because maternal obesity has also been linked to abnormal development of the hypothalamus, the authors asked whether ER stress might be tied directly to obesity-driven hypothalamic changes.
Working in mice, they began by showing that maternal obesity led to increased body weight in male offspring, with an increase in food intake, reduced oxygen consumption, and impaired glucose tolerance (female offspring were not affected, for reasons that remain to be explored). These changes were accompanied by ER stress in several tissues, including the arcuate nucleus of the hypothalamus, a key site for metabolic regulation. One known mechanism for that regulation is through signaling by the hormone leptin; leptin inhibits hunger, and maternal obesity is known to increase resistance to its effects.
The authors showed that all these changes could be mitigated by treating offspring with the naturally occurring bile acid tauroursodeoxycholic acid (TUDCA), which is known to promote refolding of proteins and alleviate ER stress. When the mice pups of obese mothers received TUDCA, neuronal development within their arcuate nucleus was normalized, leptin signaling was restored, and the alterations in body weight, glucose tolerance, and most other physiologic measures were reversed.
"Obesity is a complex phenomenon that likely has multiple drivers but the relative importance of maternal obesity-induced ER stress in promoting offspring obesity was not known," Bouret said. "The results from this study suggest it does play an important role by disrupting the development of brain pathways that control appetite" he adds. "Interestingly, TUDCA has been approved in the United States and Europe to treat specific liver and neurodegenerative disorders, raising the possibility that the clinical use of this ER stress-relieving drug could be expanded to treatment of childhood obesity, which now affects more than 40 million children worldwide."
Dietary anti-cancer compound may work by influence on cellular genetics
Oregon State University, March 15, 2020
Researchers have discovered one of the reasons why broccoli may be good for your health.
They found that sulforaphane, a dietary compound from broccoli that's known to help prevent prostate cancer, may work through its influence on long, non-coding RNAs. This is another step forward in a compelling new area of study on the underlying genetics of cancer development and progression.
The findings were published by researchers from Oregon State University in the Journal of Nutritional Biochemistry.
The research provides more evidence for how these lncRNAs, which were once thought to be a type of "junk DNA" of no particular value or function, may instead play a critical role in triggering cells to become malignant and spread.
Growing evidence shows that lncRNAs, which number in the thousands, have a major role in cell biology and development, often by controlling what genes are turned on, or "expressed" to carry out their genetic function. Scientists now believe that when these lncRNAs are dysregulated they can contribute to multiple disease processes, including cancer.
Unlike many chemotherapeutic drugs that affect healthy cells as well as malignant ones and can cause undesired side effects, the control of lncRNAs may offer a new way to specifically prevent or slow the progression of malignant cells.
"This could be a turning point in our understanding of how cancer may be triggered and spreads," said Emily Ho, the endowed director of the Moore Family Center for Whole Grain Foods, Nutrition and Preventive Health at OSU, a professor in the College of Public Health and Human Sciences and principal investigator with the Linus Pauling Institute.
"It's obviously of interest that this dietary compound, found at some of its highest levels in broccoli, can affect lncRNAs. This could open the door to a whole range of new dietary strategies, foods or drugs that might play a role in cancer suppression or therapeutic control."
In particular, this research showed that one lncRNA, called LINC01116, is upregulated in a human cell line of prostate cancer, but can be decreased by treatment with sulforaphane. The data "reinforce the idea that lncRNAs are an exciting new avenue for chemoprevention research, and chemicals derived from diet can alter their expression," the scientists wrote in their study.
"We showed that treatment with sulforaphane could normalize the levels of this lncRNA," said Laura Beaver, a research associate in the Linus Pauling Institute and College of Public Health and Human Sciences, and lead author on the study. "This may relate to more than just cancer prevention. It would be of significant value if we could develop methods to greatly slow the progress of cancer, help keep it from becoming invasive."
The impact of diet on lncRNA expression has been largely unknown until now, the researchers said. In this study, they identified a four-fold decrease in the ability of prostate cancer cells to form colonies when LINC01116 was disrupted.
Among men, prostate cancer is the second most frequently diagnosed cancer globally, and the second leading cause of cancer-related deaths in the United States. Worth noting, the researchers said, is that an increased consumption of cruciferous vegetables such as broccoli, which are high in sulforaphane, appears to be associated with a lower risk of developing prostate cancer.
That same lncRNA, they noted, is also overexpressed in studies of several other types of cancer, including brain, lung and colon cancer. Some other lncRNAs have been found at higher levels in breast, stomach, lung, prostate cancer and chronic lymphocytic leukemia.
In other research, a knockout of the gene that encodes one type of lncRNA in mice conferred some resistance to obesity caused by a high-fat diet.
"Taken together, this literature and our own study begin to paint a picture of the important and previously unappreciated role of lncRNAs in the body's response to diet," the researchers wrote in the study. "These discoveries illustrate that lncRNAs can play important roles in cancer development and may be useful targets for cancer prevention, detection and treatment."
Tyrosine, tryptophan fight “baby blues”
University of Toronto, March 16, 2020
THREE supplements, including blueberry juice, could help new mums beat postnatal depression, experts have suggested.
The “baby blues” is a precursor to full blown postnatal depression. One in 10 women will be affected by postnatal depression within a year of giving birth.
By reducing the risk of the “baby blues”, which typically hits around three days after birth, it’s possible to reduce the risk of more serious depression.
The kit included three supplements – tryptophan, tyrosine and blueberry extract.
They were carefully selected by scientists at Toronto’s Centre for Addiction and Mental Health.
All can compensate for a surge in the brain protein MAO-A, which happens in the early stages of postnatal depression.
The same pattern is seen people with clinical depression.
The protein breaks down three chemicals that help maintain mood – serotonin, norepinephrine and dopamine. When there are low levels of these three chemicals, it can lead to feelings of sadness. MAO-A levels peak five days after giving birth, the same time when it’s most likely a mum will succumb to postnatal depression.
Trytophan – which is found in high levels in turkey – and tyrosine – found in cheese, soybeans, and meat – help boost the three chemicals.
Dr Jeffrey Meyer, who lead the study, said: “Developing successful nutrition-based treatments, based on neurobiology, is rare in psychiatry.
The supplements – trytophan and tyrosine and blueberry extract – produced dramatic results, stopping the “baby blues”, a precursor to full blown postnatal depression
“We believe our approach also represents a promising new avenue for creating other new dietary supplements for medicinal use.”
Dr Meyer and his team also tested and found the levels of trytophan and tyrosine supplements – given in higher amounts than you could get normally in your diet – did not affect a mum’s breast milk.
His team gave 21 women the supplements and compared them to 20 new mums who took a placebo.
They took their supplements over three days, starting three days after giving birth. On day five, when postnatal depression typically peaks, the women underwent tests to measure their mood.
Dr Meyer’s team found the results were dramatic. Women not taking the supplements had a significant increase in depression scores. Those taking the three supplements, did not experience any depression.
Dr Meyer said: “We believe this is the first study to show such a strong, beneficial effect of an intervention in reducing the baby blues at a time when postpartum sadness peaks. “Postpartum blues are common and usually resolves 10 days after giving birth, but when they are intesnse, the risk of postpartum depression increases four-fold.” He added more research is now needed to trial the supplements in a larger group of new mums.
B vitamins protect epigenome from pollution effects
Columbia University, March 13 2020
A trail reported in the Proceedings of the National Academy of Sciences reveals a protective effect for supplementation with B vitamins on the human epigenome: the chemicals surrounding DNA that modify the genome and help determine the genes that are active in a cell. The trial’s results suggest that B vitamins could help protect the epigenome from the detrimental effects of air pollution.
"The molecular foundations of air pollution's health effects are not fully understood, and the lack of individual-level preventative options represented a critical knowledge gap," noted coauthor Andrea Baccarelli, MD, PhD, who is a professor and chair of Environmental Health Sciences at Columbia University’s Mailman School of Public Health. "Our study launches a line of research for developing preventive interventions to minimize the adverse effects of air pollution on potential mechanistic markers. Because of the central role of epigenetic modifications in mediating environmental effects, our findings could very possibly be extended to other toxicants and environmental diseases."
In a crossover trial, 10 adults were given a placebo for 2 weeks, followed by exposure to particle-free air; a placebo for 4 weeks, followed by exposure to fine particulate matter (PM2.5); and 2.5 milligrams (mg) folic acid, 50 mg vitamin B6 and 1 mg vitamin B12 daily for 4 weeks, followed by exposure to fine particulate matter. Epigenome changes in peripheral CD4+ T-helper cells were assessed at the end of each of the three experiments.
“This crossover intervention trial with controlled exposure experiments demonstrated that 2 hour exposure to concentrated ambient PM2.5 affects the dynamic epigenetic landscape in circulating CD4+ T helper cells among healthy adults,” the authors report. “We showed that these effects can be prevented with B-vitamin supplementation (i.e., folic acid and vitamins B6 and B12).”