Saturday, December 3, 2016

The Collapse of the Body's Ecosystem?


thescientist |  Many people with Parkinson’s disease have digestive symptoms like constipation years before they have neurological symptoms, and scientists have found differences in the gut microbiome compositions of patients with Parkinson’s disease and healthy controls. But whether and how gut microbes contribute to the pathology and symptoms of the disease has been an open question.

In a study published today (December 1) in Cell, a team led by Timothy Sampson and Sarkis Mazmanian of Caltech demonstrate that gut microbiota promote neuroinflammation and motor deficits in a mouse model of Parkinson’s disease. The researchers also identify a possible mechanism for the influence of intestinal microbes and on the development of the disease in mice.

“It’s a beautiful study,” Justin Sonnenburg of Stanford University School of Medicine, who did not participate in the work, told The Scientist. “It’s really a first in establishing that gut microbes can not only contribute, but appear to play a causal role in neurodegenerative disease in this mouse model,” he added.

Sampson, Mazmanian, and colleagues used transgenic mice that overexpress human α-synuclein, the protein that forms the insoluble aggregates that are a hallmark of Parkinson’s disease. These mice exhibit deficits in motor function and gut motility.

Transgenic animals raised germ-free or treated with antibiotics performed better at motor tasks and maintained fecal output, as compared to those with typical microbiota, the researchers reported. Mice without intestinal microbes or those receiving antibiotic treatment also developed fewer α-synuclein aggregates in their brains than did their counterparts with intestinal microbes. In other words, in transgenic mice without intestinal bacteria and in those treated with antibiotics, both Parkinson’s-like symptoms and brain pathology decreased.

Saturday, November 26, 2016

You Are What You Eat: Diet-Biota-Epigenetics


sciencenewsline |  You are what you eat, the old saying goes, but why is that so? Researchers have known for some time that diet affects the balance of microbes in our bodies, but how that translates into an effect on the host has not been understood. Now, research in mice is showing that microbes communicate with their hosts by sending out metabolites that act on histones--thus influencing gene transcription not only in the colon but also in tissues in other parts of the body. The findings publish November 23 in Molecular Cell.

"This is the first of what we hope is a long, fruitful set of studies to understand the connection between the microbiome in the gut and its influence on host health," says John Denu, a professor of biomolecular chemistry at the University of Wisconsin, Madison, and one of the study's senior authors. "We wanted to look at whether the gut microbiota affect epigenetic programming in a variety of different tissues in the host." These tissues were in the proximal colon, the liver, and fat tissue.

In the study, the researchers first compared germ-free mice with those that have active gut microbes and discovered that gut microbiota alter the host's epigenome in several tissues. Next, they compared mice that were fed a normal chow diet to mice fed a Western-type diet--one that was low in complex carbohydrates and fiber and high in fat and simple sugars. Consistent with previous studies from other researchers, they found that the gut microbiota of mice fed the normal chow diet differed from those fed the Western-type diet.

"When the host consumes a diet that's rich in complex plant polysaccharides (such as fiber), there's more food available for microbes in the gut, because unlike simple sugars, our human cells cannot use them," explains Federico Rey, an assistant professor of bacteriology at UW-Madison and the study's other senior author.

Why it's Easier to Change a Man's Religion



theatlantic |  In 2009, Danny Cahill won the eighth season of The Biggest Loser, a reality TV show in which contestants compete to lose the most weight. Over the program’s seven months, Cahill’s weight dropped from 430 pounds to just 191. But since then, he has regained 100. The same is true for most of the show’s contestants, several of whom are now heavier than they were before they took part.

Their story is all too common. Even when people successfully manage to lose weight, in the majority of cases, the vanished pounds return within a year—and often with reinforcements. For many people, weight loss isn’t just hard, it’s Sisyphean.

No one really understands the reasons behind this “weight cycling”, this so-called “yo-yo effect”. It seems to happen no matter your starting weight, or how much exercise you do. As my colleague Julie Beck noted earlier this year, the speed at which people lose weight might be important—but even that’s controversial. “There’s a lot of speculation but very little knowledge,” says Eran Elinav from the Weizmann Institute of Science in Israel.

Thursday, November 24, 2016

It is Easier to Change a Man's Religion than to Change his Diet



cnsnews |  Soft drinks were the top commodity bought by food stamp recipients shopping at outlets run by a single U.S. grocery retailer.

That is according to a new study released by the Food and Nutrition Service, the federal agency responsible for running the Supplemental Nutrition Assistance Program (SNAP), commonly known as the food stamp program.

By contrast, milk was the top commodity bought from the same retailer by customers not on food stamps.

In calendar year 2011, according to the study, food stamp recipients spent approximately $357,700,000 buying soft drinks from an enterprise the study reveals only as “a leading U.S. grocery retailer.”

That was more than they spent on any other “food” commodity—including milk ($253,700,000), ground beef ($201,000,000), “bag snacks” ($199,300,000) or “candy-packaged” ($96,200,000), which also ranked among the top purchases.

Sunday, November 20, 2016

Genetics of Aging


ibiology |  Why do some people age more quickly than others? This video describes pioneering research performed by the biologist Cynthia Kenyon, who hypothesized that genes could control the rate of aging. To figure out which genes regulate aging, scientists in Dr. Kenyon’s lab made mutations in the DNA of a tiny worm called C. elegans and looked to see which mutations caused the worms to live longer, healthier lives. Amazingly, modifying just one gene, called Daf-2, allowed the worms to live twice as long as normal. Daf-2 is a conserved gene found in flies, mice, and humans, so its activity may regulate aging in our species as well.

Wednesday, November 16, 2016

Aging is a Disease That Can Be Cured Within My Children's Lifetime


thescientist |  The concept of aging is undergoing a rapid transformation in medicine. The question has long been asked: Is aging a natural process that should be accepted as inevitable, or is it pathologic, a disease that should be prevented and treated? For the vast majority of medicine’s history, the former position was considered a self-evident truth. So futile was any attempt to resist the ravages of aging that the matter was relegated to works of fantasy and fiction. But today, the biomedical community is rethinking its answer to this question.

The controversy has been fanned, to a great extent, by one Aubrey de?Grey, a Cambridge University–trained computer scientist and a self-taught biologist and gerontologist. Over the past decade, de Grey has undertaken an energetic campaign to reframe aging as a pathologic process, one that merits the same level of attention as, say, cancer or diabetes. Although many of de Grey’s claims remain controversial—notably, that the first person who will live to 1,000 years old is already among us—I agree that we can and should pathologize aging. In fact, it seems we already have.

“Aging” is a term we use to describe the changes our bodies undergo over time. Colloquially, we tend to refer to early changes, say from infancy to early adulthood, as maturation or development and reserve “aging” for changes that occur thereafter. The early changes are generally considered good: stronger muscles, wiser minds, and so on. The later changes are far less popular: thinning skin and hair, weakening bones, and other forms of decline.

Thursday, October 20, 2016

Visceral Fat Not Only An Alien Invader, It's a HERITABLE Alien Invader!!!


biomedcentral |  Variation in the human fecal microbiota has previously been associated with body mass index (BMI). Although obesity is a global health burden, the accumulation of abdominal visceral fat is the specific cardio-metabolic disease risk factor. Here, we explore links between the fecal microbiota and abdominal adiposity using body composition as measured by dual-energy X-ray absorptiometry in a large sample of twins from the TwinsUK cohort, comparing fecal 16S rRNA diversity profiles with six adiposity measures.

Results
We profile six adiposity measures in 3666 twins and estimate their heritability, finding novel evidence for strong genetic effects underlying visceral fat and android/gynoid ratio. We confirm the association of lower diversity of the fecal microbiome with obesity and adiposity measures, and then compare the association between fecal microbial composition and the adiposity phenotypes in a discovery subsample of twins. We identify associations between the relative abundances of fecal microbial operational taxonomic units (OTUs) and abdominal adiposity measures. Most of these results involve visceral fat associations, with the strongest associations between visceral fat and Oscillospira members. Using BMI as a surrogate phenotype, we pursue replication in independent samples from three population-based cohorts including American Gut, Flemish Gut Flora Project and the extended TwinsUK cohort. Meta-analyses across the replication samples indicate that 8 OTUs replicate at a stringent threshold across all cohorts, while 49 OTUs achieve nominal significance in at least one replication sample. Heritability analysis of the adiposity-associated microbial OTUs prompted us to assess host genetic-microbe interactions at obesity-associated human candidate loci. We observe significant associations of adiposity-OTU abundances with host genetic variants in the FHIT, TDRG1 and ELAVL4 genes, suggesting a potential role for host genes to mediate the link between the fecal microbiome and obesity.
Conclusions
Our results provide novel insights into the role of the fecal microbiota in cardio-metabolic disease with clear potential for prevention and novel therapies.