Probiotics may help manage childhood obesity

September 7, 2020

Science Daily/European Society of Endocrinology

Probiotics may help children and adolescents with obesity lose weight when taken alongside a calorie-controlled diet, according to a study being presented at e-ECE 2020. The study found that obese children who were put on a calorie-restricted diet and given probiotics Bifidobacterium breve BR03 and Bifidobacterium breve B632, lost more weight and had improved insulin sensitivity compared with children on a diet only. These findings suggest that probiotic supplements and a calorie-controlled diet may help manage obesity in the younger population and reduce future health risks, such as heart disease and diabetes.

Obesity is a global health concern and can lead to a number of life-threatening conditions, such as diabetes and heart disease. Treatment and prevention is a serious public health challenge, especially in children and adolescents. Bifidobacteria are a group of probiotic bacteria that are part of the natural gut microbiome and help with preventing infection from other bacteria, such as E.coli, and digestion of carbohydrates and dietary fibre. During digestion, they release chemicals called short-chain fatty acids, which play an important role in gut health and controlling hunger. Low numbers of Bifodobacteria may impair digestion, affect food intake and energy expenditure, leading to body weight gain and obesity.

Previous studies suggested that probiotic supplementation with Bifidobacteria could help restore the composition of the gut microbiome, which may aid weight loss and could be a potential approach for obesity management. However, current research uses mixtures of different strains of probiotics and does not examine the effects of administering Bifidobacteria alone.

Dr Flavia Prodam and her team at the University of Piemonte Orientale, aimed to assess the impact of Bifidobacteria probiotic treatment in children and adolescents with obesity on a controlled diet, on weight loss and gut microbiota composition. 100 obese children and adolescents (6-18 years) were put on a calorie-controlled diet and randomly given either probiotics Bifidobacterium breve BR03 and Bifidobacterium breve B632, or a placebo for 8 weeks. Clinical, biochemical and stool sample analyses were carried out to determine the effect of probiotic supplementation on weight gain, gut microbiota and metabolism.

The results suggested that children who had taken probiotics had a reduction in waist circumference, BMI, insulin resistance and E.coli in their gut. These beneficial effects demonstrate the potential of probiotics in helping to treat obesity in children and adolescents, when undergoing dietary restrictions.

"Probiotic supplements are frequently given to people without proper evidence data. These findings start to give evidence of the efficacy and safety of two probiotic strains in treating obesity in a younger population," Dr Prodam comments.

The study suggests that supplementation with probiotics could modify the gut microbiome environment and beneficially affect metabolism, helping obese children or adolescents who are also undergoing a restricted diet to lose weight. However, larger studies over a longer period of time are needed to investigate this.

Dr Prodam explains, "The next step for our research is to identify patients that could benefit from this probiotic treatment, with a view to creating a more personalised weight-loss strategy. We also want to decipher more clearly the role of diet and probiotics on microbiome composition. This could help us to understand how the microbiota is different in young people with obesity."

https://www.sciencedaily.com/releases/2020/09/200907080342.htm

Why do arteries age? Study explores link to gut bacteria, diet

July 1, 2020

Science Daily/University of Colorado at Boulder

Eat a slab of steak and your resident gut bacteria get to work immediately to break it down. But new research shows that a metabolic byproduct, called TMAO, produced in the process can be harmful to the lining of arteries, making them age faster.

A compound produced in the gut when we eat red meat damages our arteries and may play a key role in boosting risk of heart disease as we get older, according to new University of Colorado Boulder research.

The study, published this month in the American Heart Association journal Hypertension, also suggests that people may be able to prevent or even reverse such age-related decline via dietary changes and targeted therapies, like novel nutritional supplements.

"Our work shows for the first time that not only is this compound directly impairing artery function, it may also help explain the damage to the cardiovascular system that naturally occurs with age," said first author Vienna Brunt, a postdoctoral researcher in the Department of Integrative Physiology.

Eat a slab of steak or a plate of scrambled eggs, and your resident gut bacteria get to work immediately to break it down. As they metabolize the amino acids L-carnitine and choline, they churn out a metabolic byproduct called trimethylamine, which the liver converts to trimethylamine-N-Oxide (TMAO) and sends coursing through your bloodstream.

Previous studies have shown that people with higher blood levels of TMAO are more than twice as likely to have a heart attack or stroke and tend to die earlier.

But to date, scientists haven't completely understood why.

Drawing on animal and human experiments, Brunt and her team set out to answer three questions: Does TMAO somehow damage our vascular system? If so, how? And could it be one reason why cardiovascular health gets worse -- even among people who exercise and don't smoke -- as we get older?

The researchers measured the blood and arterial health of 101 older adults and 22 young adults and found that TMAO levels significantly rise with age. (This falls in line with a previous study in mice, showing the gut microbiome -- or your collection of intestinal bacteria -- changes with age, breeding more bacteria that help produce TMAO).

Adults with higher blood levels of TMAO had significantly worse artery function, the new study found, and showed greater signs of oxidative stress, or tissue damage, in the lining of their blood vessels.

When the researchers fed TMAO directly to young mice, their blood vessels swiftly aged.

"Just putting it in their diet made them look like old mice," said Brunt. She noted that 12-month-old mice (the equivalent of humans about 35 years old) looked more like 27-month-old mice (age 80 in people) after eating TMAO for several months.

Preliminary data also show that mice with higher levels of TMAO exhibit decreases in learning and memory, suggesting the compound could also play a role in age-related cognitive decline.

On the flip side, old mice that ate a compound called dimethyl butanol, (found in trace amounts in olive oil, vinegar and red wine) saw their vascular dysfunction reverse. Scientists believe that this compound prevents the production of TMAO.

Brunt notes that everyone -- even a young vegan -- produces some TMAO. But over time, eating a lot of animal products may take a toll.

"The more red meat you eat, the more you are feeding those bacteria that produce it," she said.

Senior author Doug Seals, director of the Integrative Physiology of Aging Laboratory, said the study is an important breakthrough because it sheds light on why our arteries erode with age, even in the healthiest people.

"Aging is the single greatest risk factor for cardiovascular disease, primarily as a result of oxidative stress to our arteries," said Seals. "But what causes oxidative stress to develop in our arteries as we age? That has been the big unkown. This study identifies what could be a very important driver."

The research team is now further exploring compounds that might block production of TMAO to prevent age-related vascular decline.

For now, they said, a plant-based diet may also keep levels in check.

https://www.sciencedaily.com/releases/2020/07/200701100019.htm

Universal gut microbiome-derived signature predicts cirrhosis

June 30, 2020

Science Daily/University of California - San Diego

Researchers report that stool microbiomes of NAFLD patients are distinct enough to potentially be used to accurately predict which persons with NAFLD are at greatest risk for having cirrhosis.

Nonalcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease worldwide, affecting an estimated one-quarter of the global population. It is a progressive condition that, in worst cases, can lead to cirrhosis, liver cancer, liver failure and death.

In a new paper published online June 30, 2020 in Cell Metabolism, a team of scientists, led by researchers at University of California San Diego School of Medicine, report that stool microbiomes -- the collection of microorganisms found in fecal matter and in the gastrointestinal tract -- of NAFLD patients are distinct enough to potentially be used to accurately predict which persons with NAFLD are at greatest risk for having cirrhosis -- the late-stage, irreversible scarring of the liver that often requires eventual organ transplantation.

"The findings represent the possibility of creating an accurate, stool microbiome-based, non-invasive test to identify patients at greatest risk for cirrhosis," said senior author Rohit Loomba, MD, professor of medicine in the Division of Gastroenterology at UC San Diego School of Medicine and director of its NAFLD Research Center. "Such a diagnostic tool is urgently needed."

Loomba said a novel aspect of the study is the external validation of gut microbiome signatures of cirrhosis in participant cohorts from China and Italy. "This is one of the first studies to show such a robust external validation of a gut microbiome-based signature across ethnicities and geographically distinct cohorts.

The work builds upon previous published research in 2017 and 2019 by Loomba and colleagues.

A link between NAFLD and the gut microbiome is well-documented, but specifics were scant and it has not been clear that discrete metagenomics and metabolomics signatures might be used to detect and predict cirrhosis. In the latest study, researchers compared the stool microbiomes of 163 participants encompassing patients with NAFLD-cirrhosis, their first-degree relatives and control-patients without NAFLD.

Combining metagenomics signatures with participants' ages and serum albumin (an abundant blood protein produced in the liver) levels, the scientists were able to accurately distinguish cirrhosis in participants differing by cause of disease and geography.

The next step, said Loomba, is to establish causality of these gut microbial species or their metabolites in causing cirrhosis, and whether this test can be used and scaled up for clinical use.

https://www.sciencedaily.com/releases/2020/06/200630125126.htm

Gut microbiome influences ALS outcomes

Scientists identify gut-brain connection in ALS

May 13, 2020

Science Daily/Harvard University

Scientists have identified a new gut-brain connection in the neurodegenerative disease ALS. Researchers found that in mice with a common ALS genetic mutation, changing the gut microbiome using antibiotics or fecal transplants could prevent or improve disease symptoms. The findings provide a potential explanation for why only some individuals carrying the mutation develop ALS, and point to a possible therapeutic approach based on the microbiome.

Harvard University scientists have identified a new gut-brain connection in the neurodegenerative disease amyotrophic lateral sclerosis, or ALS. The researchers found that in mice with a common ALS genetic mutation, changing the gut microbiome using antibiotics or fecal transplants could prevent or improve disease symptoms.

Published in the journal Nature, the findings provide a potential explanation for why only some individuals carrying the mutation develop ALS. They also point to a possible therapeutic approach based on the microbiome.

"Our study focused on the most commonly mutated gene in patients with ALS. We made the remarkable discovery that the same mouse model -- with identical genetics -- had substantially different health outcomes at our different lab facilities," said Kevin Eggan, Harvard professor of stem cell and regenerative biology. "We traced the different outcomes to distinct gut microbial communities in these mice, and now have an intriguing hypothesis for why some individuals carrying this mutation develop ALS while others do not."

Different facilities, different outcomes

The researchers initially studied the ALS genetic mutation by developing a mouse model at their Harvard lab facility. The mice had an overactive immune response, including inflammation in the nervous system and the rest of the body, which led to a shortened lifespan.

In order to run more detailed experiments, the researchers also developed the mouse model in their lab facility at the Broad Institute, where Eggan is the director of stem cell biology at the Stanley Center for Psychiatric Research. Unexpectedly, although the mice had the same genetic mutation, their health outcomes were dramatically different.

"Many of the inflammatory characteristics that we observed consistently and repeatedly in our Harvard facility mice weren't present in the Broad facility mice. Even more strikingly, the Broad facility mice survived into old age," said Aaron Burberry, postdoctoral fellow in the Eggan lab and lead author of the study. "These observations sparked our endeavor to understand what about the two different environments could be contributing to these different outcomes."

Searching the gut microbiome

Looking for environmental differences between the mice, the researchers honed in on the gut microbiome. By using DNA sequencing to identify gut bacteria, the researchers found specific microbes that were present in the Harvard facility mice but absent in the Broad facility mice, even though the lab conditions were standardized between facilities.

"At this point, we reached out to the broader scientific community, because many different groups have studied the same genetic mouse model and observed different outcomes," Burberry said. "We collected microbiome samples from different labs and sequenced them. At institutions hundreds of miles apart, very similar gut microbes correlated with the extent of disease in these mice."

The researchers then tested ways to change the microbiome and improve outcomes for the Harvard facility mice. By treating the Harvard facility mice with antibiotics or fecal transplants from the Broad facility mice, the researchers successfully decreased inflammation.

Gut-brain connection

By investigating the connection between genetic and environmental factors in ALS, the researchers identified an important gut-brain connection. The gut microbiome could influence the severity of disease -- whether individuals with the genetic mutation develop ALS, the releated condition frontotemporal dementia, or no symptoms at all -- and could be a potential target for therapy.

"Our study provides new insights into the mechanisms underlying ALS, including how the most common ALS genetic mutation contributes to neural inflammation," Eggan said. "The gut-brain axis has been implicated in a range of neurological conditions, including Parkinson's disease and Alzheimer's disease. Our results add weight to the importance of this connection."

https://www.sciencedaily.com/releases/2020/05/200513111432.htm

Can poor air quality make you gain weight?

Study shows pollution harms gut bacteria, contributes to diabetes, obesity

March 12, 2020

Science Daily/University of Colorado at Boulder

Breathing dirty air takes a heavy toll on gut bacteria, boosting risk of obesity, diabetes, gastrointestinal disorders and other chronic illnesses, new University of Colorado Boulder research suggests.

The study, published online in the journal Environment International, is the first to link air pollution to changes in the structure and function of the human gut microbiome -- the collection of trillions of microorganisms residing within us.

The gaseous pollutant ozone, which helps make up Denver's infamous 'brown cloud' -- is particularly hazardous, the study found, with young adults exposed to higher levels of ozone showing less microbial diversity and more of certain species associated with obesity and disease.

"We know from previous research that air pollutants can have a whole host of adverse health effects," said senior author Tanya Alderete, an assistant professor of integrative physiology, pointing to studies linking smog with Type 2 diabetes, weight gain and inflammatory bowel diseases. "The takeaway from this paper is that some of those effects might be due to changes in the gut."

The study comes at a time when air quality in many U.S. cities is worsening after decades of improvement. In December, the Environmental Protection Agency downgraded the Denver metro and north Front Range regions to "serious non-attainment" status for failing to meet national ozone standards.

Regions of eight other states, including some in California, Texas, Illinois, Connecticut, Indiana, New Jersey, New York and Wisconsin, were also penalized for high ozone. Worldwide, according to research published this month, air pollution kills 8.8 million people annually -- more than smoking or war.

While much attention has been paid to respiratory health, Alderete's previous studies have shown pollution can also impair the body's ability to regulate blood sugar and influence risk for obesity. Other research has shown visits to emergency rooms for gastrointestinal problems spike on high pollution days, and youth with high exposure to traffic exhaust have greater risk of developing Crohn's disease.

To investigate just what might be going on inside the gut, Alderete's team used cutting-edge whole-genome sequencing to analyze fecal samples from 101 young adults in Southern California.

The researchers looked at data from air-monitoring stations near the subjects' addresses to calculate their previous-year exposure to ozone (which forms when emissions from vehicles are exposed to sunlight), particulate matter (hazardous particles suspended in the air), and nitrous oxide (a toxic byproduct of burning fossil fuel).

Of all the pollutants measured, ozone had the greatest impact on the gut by far, accounting for about 11% of the variation seen between study subjects -- more of an impact than gender, ethnicity or even diet. Those with higher exposure to ozone also had less variety of bacteria living in their gut.

"This is important since lower (bacteria) diversity has been linked with obesity and Type 2 diabetes," noted Alderete.

Subjects with higher exposure to ozone also had a greater abundance of a specific species called Bacteroides caecimuris. That's important, because some studies have associated high levels of Bacteroides with obesty.

In all, the researchers identified 128 bacterial species influenced by increased ozone exposure. Some may impact the release of insulin, the hormone responsible for ushering sugar into the muscles for energy. Other species can produce metabolites, including fatty acids, which help maintain gut barrier integrity and ward off inflammation.

"Ozone is likely changing the environment of your gut to favor some bacteria over others, and that can have health consequences," said Alderete.

The study was relatively small and has some limitations, including the fact that stool samples were taken only once.

Alderete is now moving ahead with a larger, more expansive study of young adults in the Denver area. Thanks to a new grant from the nonprofit Health Effects Institute, she's also exploring how prenatal or early-life exposure to air pollution impacts the formation of the gut microbiome in 240 infants.

She said she hopes her work will ultimately influence policymakers to consider moving parks, playgrounds and housing developments away from busy roads and high pollution areas, and invest more in meeting or exceeding air quality standards.

"A lot of work still needs to be done, but this adds to a growing body of literature showing that human exposure to air pollution can have lasting, harmful effects on human health."

https://www.sciencedaily.com/releases/2020/03/200312101033.htm

Mediterranean diet for one year promotes gut bacteria linked to 'healthy aging'

It may help curb advance of frailty and cognitive decline, suggest researchers

February 17, 2020

Science Daily/BMJ

Eating a Mediterranean diet for a year boosts the types of gut bacteria linked to 'healthy' ageing, while reducing those associated with harmful inflammation in older people, indicates a five-country study, published online in the journal Gut.

As ageing is associated with deteriorating bodily functions and increasing inflammation, both of which herald the onset of frailty, this diet might act on gut bacteria in such a way as to help curb the advance of physical frailty and cognitive decline in older age, suggest the researchers.

Previous research suggests that a poor/restrictive diet, which is common among older people, particularly those in long term residential care, reduces the range and types of bacteria (microbiome) found in the gut and helps to speed up the onset of frailty.

The researchers therefore wanted to see if a Mediterranean diet might maintain the microbiome in older people's guts, and promote the retention or even proliferation of bacteria associated with 'healthy' ageing.

They analysed the gut microbiome of 612 people aged 65 to 79, before and after 12 months of either eating their usual diet (n = 289) or a Mediterranean diet (n = 323), rich in fruits, vegetables, nuts, legumes, olive oil and fish and low in red meat and saturated fats, and specially tailored to older people (NU-AGE diet).

The participants, who were either frail (n=28), on the verge of frailty (n=151), or not frail (n=433) at the beginning of the study, lived in five different countries: France, Italy, Netherlands, Poland, and the UK.

Sticking to the Mediterranean diet for 12 months was associated with beneficial changes to the gut microbiome.

It was associated with stemming the loss of bacterial diversity; an increase in the types of bacteria previously associated with several indicators of reduced frailty, such as walking speed and hand grip strength, and improved brain function, such as memory; and with reduced production of potentially harmful inflammatory chemicals.

More detailed analysis revealed that the microbiome changes were associated with an increase in bacteria known to produce beneficial short chain fatty acids and a decrease in bacteria involved in producing particular bile acids, overproduction of which are linked to a heightened risk of bowel cancer, insulin resistance, fatty liver and cell damage.

What's more, the bacteria that proliferated in response to the Mediterranean diet acted as 'keystone' species, meaning they were critical for a stable 'gut ecosystem,' pushing out those microbes associated with indicators of frailty.

The changes were largely driven by an increase in dietary fibre and associated vitamins and minerals -- specifically, C, B6, B9, copper, potassium, iron, manganese, and magnesium.

The findings were independent of the person's age or weight (body mass index), both of which influence the make-up of the microbiome.

And while there were some differences in the make-up of a person's gut microbiome, depending on country of origin to start with, the response to the Mediterranean diet after 12 months was similar and consistent, irrespective of nationality.

The study findings can't establish a causative role for the microbiome in health, added to which some of the implications are inferred rather than directly measured, say the researchers.

"The interplay of diet, microbiome and host health is a complex phenomenon influenced by several factors," they emphasise.

"While the results of this study shed light on some of the rules of this three-way interplay, several factors such as age, body mass index, disease status and initial dietary patterns may play a key role in determining the extent of success of these interactions," they explain.

Older people may have dental problems and/or difficulty swallowing, so it may be impractical for them to eat a Mediterranean diet, they add. But the beneficial bacteria implicated in healthy ageing found in this study might yet prove useful therapeutic agents to ward off frailty, they suggest.

https://www.sciencedaily.com/releases/2020/02/200217192025.htm

Teens with obesity and PCOS have more 'unhealthy' bacteria

Gut microbiome may play a role in PCOS and its related metabolic complications

January 23, 2020

Science Daily/The Endocrine Society

Teens with obesity and polycystic ovary syndrome (PCOS) have more "unhealthy" gut bacteria suggesting the microbiome may play a role in the disorder, according to new research published in the Endocrine Society's Journal of Clinical Endocrinology & Metabolism.

PCOS is complicated endocrine disorder affecting 6 percent to 18 percent of women of reproductive age and work in adult women indicates that changes in bacteria be involved. The. The hormone disorder is characterized by elevated testosterone levels in the blood that cause acne, excess hair growth and irregular periods. Teens with PCOS often also struggle with obesity and have a higher risk for type 2 diabetes, infertility, and depression.

"We found that in adolescents with PCOS and obesity, the bacterial profile (microbiome) from stool has more "unhealthy" bacteria compared to teens without PCOS," said the study's corresponding author, Melanie Cree Green, M.D., Ph.D., of Children's Hospital Colorado in Aurora, Colo. "The unhealthy bacteria related to higher testosterone concentrations and markers of metabolic complications."

The researchers studied 58 teens with obesity and found that girls with PCOS have an altered gut microbiome compared to those without the condition. These girls had more "unhealthy" bacteria in their stool which was related to higher testosterone levels and other markers of metabolic syndrome, such as higher blood pressure, liver inflammation and plasma triglycerides

"The gut microbiome may play a role in PCOS and its related metabolic complications, and these changes can be found in teenagers who are early in the course of the condition," Green said.

https://www.sciencedaily.com/releases/2020/01/200123090342.htm

Diet's effect on gut bacteria could play role in reducing Alzheimer's risk

September 3, 2019

Science Daily/Wake Forest Baptist Medical Center

Could following a certain type of diet affect the gut microbiome -- the good and bad bacteria that live in the gastrointestinal tract -- in ways that decrease the risk of Alzheimer's disease?

According to researchers at Wake Forest School of Medicine, that is a fair possibility.

In a small pilot study, the researchers identified several distinct gut microbiome signatures -- the chemicals produced by bacteria -- in study participants with mild cognitive impairment (MCI) but not in their counterparts with normal cognition, and found that these bacterial signatures correlated with higher levels of markers of Alzheimer's disease in the cerebrospinal fluid of the participants with MCI.

Through cross-group dietary intervention, the study also showed that a modified Mediterranean-ketogenic diet produced changes in the gut microbiome and its metabolites that correlated with reduced levels of Alzheimer's markers in the members of both study groups.

The study appears in the current issue of EBioMedicine, a journal published by The Lancet.

"The relationship of the gut microbiome and diet to neurodegenerative diseases has recently received considerable attention, and this study suggests that Alzheimer's disease is associated with specific changes in gut bacteria and that a type of ketogenic Mediterranean diet can affect the microbiome in ways that could impact the development od dementia," said Hariom Yadav, Ph.D., assistant professor of molecular medicine at Wake Forest School of Medicine, who co-authored the study with Suzanne Craft, Ph.D., professor gerontology and geriatric medicine at the medical school and director of Wake Forest Baptist Health's Alzheimer's Disease Research Center.

The randomized, double-blind, single-site study involved 17 older adults, 11 with diagnosed MCI and six with normal cognition. These participants were randomly assigned to follow either the low-carbohydrate modified Mediterranean-ketogenic diet or a low-fat, higher carbohydrate diet for six weeks then, after a six-week "washout" period, to switch to the other diet. Gut microbiome, fecal short-chain fatty acids and markers of Alzheimer's, including amyloid and tau proteins, in cerebrospinal fluid were measured before and after each dieting period.

The study's limitations include the subject group's size, which also accounts for the lack of diversity in terms of gender, ethnicity and age.

"Our findings provide important information that future interventional and clinical studies can be based on," Yadav said. "Determining the specific role these gut microbiome signatures have in the progression of Alzheimer's disease could lead to novel nutritional and therapeutic approaches that would be effective against the disease."

https://www.sciencedaily.com/releases/2019/09/190903120514.htm

New study points to another possible correlation between sleep and overall good health

Your gut microbiome and quality sleep are interconnected

October 28, 2019

Science Daily/Nova Southeastern University

As if you didn't already have enough to worry about to keep you up at night, a new study indicates that poor sleep can negatively affect your gut microbiome, which can, in turn, lead to additional health issues.

Great.

That's at the heart -- or gut -- of the study just published in PLoS ONE that involved several researchers from Nova Southeastern University (NSU.) They wanted to see just how much of a connection there is between what is going on in our insides and how that may impact the quality of sleep we experience.

"Given the strong gut-brain bidirectional communication they likely influence each other," said Jaime Tartar, Ph.D., a professor and research director in NSU's College of Psychology who was part of the research team. "Based on previous reports, we think that poor sleep probably exerts a strong negative effect on gut health/microbiome diversity."

What you may be asking yourself right now is: "what in the world is a gut microbiome?" Simply put -- it's all the microorganisms (bacteria, viruses, protozoa and fungi) and their genetic material found in your gastrointestinal (GI) tract. And yes, we all have these in our GI tract, but not all at the same levels (diversity.) As it turns out, it's this diversity that could be the key.

For this study, subjects wore what Tartar called an "Apple Watch on steroids" to bed, which monitored all sorts of vitals. This way the researchers could determine just how well a night's sleep the subjects got, and then they tested the subjects' gut microbiome. What they found was those who slept well had a more diverse -- or "better" -- gut microbiome.

Tartar said that gut microbiome diversity, or lack thereof, is associated with other health issues, such as Parkinson's disease and autoimmune diseases, as well as psychological health (anxiety and depression.) The more diverse someone's gut microbiome is, the likelihood is they will have better overall health.

"We know that sleep is pretty much the 'Swiss Army Knife of health," Tartar said. "Getting a good night's sleep can lead to improved health, and a lack of sleep can have detrimental effects. We've all seen the reports that show not getting proper sleep can lead to short term (stress, psychosocial issues) and long-term (cardiovascular disease, cancer) health problems. We know that the deepest stages of sleep is when the brain 'takes out the trash' since the brain and gut communicate with each other. Quality sleep impacts so many other facets of human health."

Tartar's area of research focuses on the mechanisms and consequences of acute and chronic stress in humans and the impact of normal sleep and sleep deprivation on emotion processing and physiological functioning.

So what determines someone's gut microbiome? According to Robert Smith, Ph.D., an associate professor and research scientist at Nova Southeastern University (NSU) Halmos College of Natural Sciences and Oceanography, who is also a member of the research team, there are a couple of factors that come into play.

One is genetics -- some people are predisposed at a genetic level to have a more diverse gut microbiome than their friends and neighbors. Another factor is drugs -- certain medications, including antibiotics, can have an impact on the diversity of your gut microbiome. He also said that your diet plays a factor as well.

Smith said that their team, which included colleagues from Middle Tennessee State University, examined the association between sleep, the immune system and measures of cognition and emotion. He said understanding how these parts of human physiology work may lead to a better understanding of the "two-way communication" between the person and their gut microbiome, and could lead to novel sleep intervention strategies.

"The preliminary results are promising, but there's still more to learn," Smith said. "But eventually people may be able to take steps to manipulate their gut microbiome in order to help them get a good night's sleep."

https://www.sciencedaily.com/releases/2019/10/191028164311.htm

Gut microbes may affect the course of ALS

Researchers isolated a molecule that may be under-produced in the guts of patients

July 22, 2019

Science Daily/Weizmann Institute of Science

Researchers at the Weizmann Institute of Science have shown in mice that intestinal microbes, collectively termed the gut microbiome, may affect the course of amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease. As reported today in Nature, progression of an ALS-like disease was slowed after the mice received certain strains of gut microbes or substances known to be secreted by these microbes. Preliminary results suggest that the findings on the regulatory function of the microbiome may be applicable to human patients with ALS.

"Our long-standing scientific and medical goal is to elucidate the impact of the microbiome on human health and disease, with the brain being a fascinating new frontier," says Prof. Eran Elinav of the Immunology Department. His team performed the study together with that of Prof. Eran Segal of the Computer Science and Applied Mathematics Department. Segal elaborates: "Given increasing evidence that microbiome affects brain function and disease, we wanted to study its potential role in ALS." The study was led by postdoctoral fellows Drs. Eran Blacher and Stavros Bashiardes, and by staff scientist Dr. Hagit Shapiro, all in the Elinav lab. They collaborated with Dr. Daphna Rothschild, a postdoctoral fellow in Eran Segal's lab, and Dr. Marc Gotkine, Head of the Motor Neuron Disease Clinic at Hadassah Medical Center, as well as with other scientists from Weizmann and elsewhere.

The scientists started out demonstrating in a series of experiments that the symptoms of an ALS-like disease in transgenic mice worsened after these mice were given broad-spectrum antibiotics to wipe out a substantial portion of their microbiome. In addition, the scientists found that growing these ALS-prone mice in germ-free conditions (in which, by definition, mice carry no microbiome of their own), is exceedingly difficult, as these mice had a hard time surviving in the sterile environment. Together, these results hinted at a potential link between alterations in the microbiome and accelerated disease progression in mice that were genetically susceptible to ALS.

Next, using advanced computational methods, the scientists characterized the composition and function of the microbiome in the ALS-prone mice, comparing them to regular mice. They identified 11 microbial strains that became altered in ALS-prone mice as the disease progressed or even before the mice developed overt ALS symptoms. When the scientists isolated these microbial strains and gave them one by one -- in the form of probiotic-like supplements -- to ALS-prone mice following antibiotic treatment, some of these strains had a clear negative impact on the ALS-like disease. But one strain, Akkermansia muciniphila, significantly slowed disease progression in the mice and prolonged their survival.

To reveal the mechanism by which Akkermansia may be producing its effect, the scientists examined thousands of small molecules secreted by the gut microbes. They zeroed in on one molecule called nicotinamide (NAM): Its levels in the blood and in the cerebrospinal fluid of ALS-prone mice were reduced following antibiotic treatment and increased after these mice were supplemented with Akkermansia, which was able to secrete this molecule. To confirm that NAM was indeed a microbiome-secreted molecule that could hinder the course of ALS, the scientists continuously infused the ALS-prone mice with NAM. The clinical condition of these mice improved significantly. A detailed study of gene expression in their brains suggested that NAM improved the functioning of their motor neurons.

https://www.sciencedaily.com/releases/2019/07/190722111923.htm