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.

New Study Links Protein in Wheat to the Inflammation of Chronic Health Conditions


sciencenewsline |  Scientists have discovered that a protein in wheat triggers the inflammation of chronic health conditions, such as multiple sclerosis, asthma and rheumatoid arthritis, and also contributes towards the development of non-coeliac gluten sensitivity.

With past studies commonly focusing on gluten and its impact on digestive health, this new research, presented at UEG Week 2016, turns the spotlight onto a different family of proteins found in wheat called amylase-trypsin inhibitors (ATIs). The study shows that the consumption of ATIs can lead to the development of inflammation in tissues beyond the gut, including the lymph nodes, kidneys, spleen and brain. Evidence suggests that ATIs can worsen the symptoms of rheumatoid arthritis, multiple sclerosis, asthma, lupus and non-alcoholic fatty liver disease, as well as inflammatory bowel disease.

ATIs make up no more than 4% of wheat proteins, but can trigger powerful immune reactions in the gut that can spread to other tissues in the body. Lead researcher, Professor Detlef Schuppan from the Johannes Gutenberg University, Germany, explains, "As well as contributing to the development of bowel-related inflammatory conditions, we believe that ATIs can promote inflammation of other immune-related chronic conditions outside of the bowel. The type of gut inflammation seen in non-coeliac gluten sensitivity differs from that caused by coeliac disease, and we do not believe that this is triggered by gluten proteins. Instead, we demonstrated that ATIs from wheat, that are also contaminating commercial gluten, activate specific types of immune cells in the gut and other tissues, thereby potentially worsening the symptoms of pre-existing inflammatory illnesses".

Clinical studies are now due to commence to explore the role that ATIs play on chronic health conditions in more detail. "We are hoping that this research can lead us towards being able to recommend an ATI-free diet to help treat a variety of potentially serious immunological disorders" adds Professor Schuppan.

Wednesday, October 5, 2016

Obesity genes probably didn't evolve to help us survive famine


physorg |  Genes that helped our ancestors store fat in times of famine may have been useful, but whether they cursed future generations with a predisposition toward obesity is a little more controversial. This popular "thrifty gene hypothesis" has had its critics, but with a study published September 22 in Cell Metabolism, there is now evidence that nearly all the common obesity-related genes show no properties of traits that evolved because they provide an adaptive advantage.

"This is probably the hardest evidence so far against the thrifty gene hypothesis—our ambition here is for people to entertain a wider range of ideas about where the genetic basis of complex diseases, like obesity, comes from," says John Speakman, a biologist at the Chinese Academy of Sciences Institute of Genetics and Developmental Biology in Beijing, who co-authored the piece with Guanlin Wang, one of his PhD students at the Chinese Academy of Sciences. "The process of evolution is a lot more complex than just the spread of favorable traits by natural selection, and the thrifty gene is like an emblem of this older way of thinking about evolutionary aspects of medicine."

Thursday, September 1, 2016

fungal infections acquire drug-resistance


guardian |  “Fungi are everywhere,” said Prof Gordon Brown, head of the Aberdeen mycology centre.
“We breathe in more than 100 spores of aspergillus every day. Normally our immune systems mop them up but, when our disease defences are compromised – for example, during cancer treatments or after traumatic injuries – they lose the ability to fight back. 

“Fungi can spread through patients’ bodies and into their spines and brains. Patients who would otherwise survive treatments are dying every year from such infections.”

This point was also stressed by Prof Neil Gow, another Aberdeen researcher. “Essentially fatal fungal infections are diseases of the diseased,” he said. 

In addition, premature babies and patients with the inherited condition cystic fibrosis are also vulnerable. 

However, the problem is even worse in developing countries. In sub-Saharan nations, where millions are infected with HIV – which causes severe depletion of patients’ immune systems – infections with cryptococcus and pneumocystis fungi account for more than half a million deaths a year.

“The total global number of fungal deaths is about the same as the number of deaths from malaria but the amount that is spent on fungal infection research is only a fraction of the cash that goes on malaria research,” added Gow.

A vaccine that could protect against fungal disease has yet to be developed, while the rise of resistance to the class of medicines known as azole drugs is causing alarm among doctors.

Recent reports from the US and Europe indicate that resistance to azole drugs is increasing in both aspergillus and candida fungi. The widespread use of agricultural fungicides to protect crops and their use in some paints and coatings has been linked to the rise of this resistance.

gnotobiotic: the woes of a germ-free organism


guardian |  Peering inside one of these chambers, I met the eyes of one of the strangest animals on the planet. It looked like just a mouse, and that is precisely why it was so weird. It was just a mouse, and nothing more.

Almost every other animal on Earth, whether centipede or crocodile, flatworm or flamingo, hippo or human, is a teeming mass of bacteria and other microbes. Each of these miniature communities is known as a microbiome. Every human hosts a microbiome consisting of some 39 trillion microbes, roughly one for each of their own cells. Every ant in a colony is a colony itself. Every resident in a zoo is a zoo in its own right. Even the simplest of animals such as sponges, whose static bodies are never more than a few cells thick, are home to thriving microbiomes.

But not the mice in Gordon’s lab. They spend their entire lives separated from the outside world, and from microbes. Their isolators contain everything they need: drinking water, brown nuggets of chow, straw chips for bedding, and a white styrofoam hutch for mating in privacy. Gordon’s team irradiates all of these items to sterilise them before piling them into loading cylinders. They sterilise the cylinders by steaming them at a high temperature and pressure, before hooking them to portholes in the back of the isolators, using connecting sleeves that they also sterilise.

It is laborious work, but it ensures that the mice are born into a world without microbes, and grow up without microbial contact. The term for this is “gnotobiosis”, from the Greek for “known life”. We know exactly what lives in these animals – which is nothing. Unlike every other mouse on the planet, each of these rodents is a mouse and nothing more. An empty vessel. A silhouette, unfilled. An ecosystem of one.

Each isolator had a pair of black rubber gloves affixed to two portholes, through which the researchers could manipulate what was inside. The gloves were thick. When I stuck my hands in, I quickly started sweating.

I awkwardly picked up one of the mice. It sat snugly on my palm, white-furred and pink-eyed. It was a strange feeling: I was holding this animal but only via two black protrusions into its hermetically sealed world. It was sitting on me and yet completely separated from me. When I had shaken hands with Gordon earlier, we had exchanged microbes. When I stroked this mouse, we exchanged nothing.
The mouse seemed normal, but it was not. Growing up without microbes, its gut had not developed properly – it had less surface area for absorbing nutrients, its walls were leakier, it renewed itself at a slower pace, and the blood vessels that supplied it with nutrients were sparse. The rest of its body hadn’t fared much better. Compared with its normal microbe-laden peers, its bones were weaker, its immune system was compromised, and it probably behaved differently too. It was, as microbiologist Theodor Rosebury once wrote, “a miserable creature, seeming at nearly every point to require an artificial substitute for the germs [it] lacks”.

Wednesday, July 27, 2016

leaky-gut syndrome confirmed at columbia university...,


columbia |  A new study may explain why people who do not have celiac disease or wheat allergy nevertheless experience a variety of gastrointestinal and extra-intestinal symptoms after ingesting wheat and related cereals. The findings suggest that these individuals have a weakened intestinal barrier, which leads to a body-wide inflammatory immune response.

Findings from the study, which was led by researchers from Columbia University Medical Center (CUMC), were reported in the journal Gut.

“Our study shows that the symptoms reported by individuals with this condition are not imagined, as some people have suggested,” said study co-author Peter H. Green, MD, the Phyllis and Ivan Seidenberg Professor of Medicine at CUMC and director of the Celiac Disease Center. “It demonstrates that there is a biological basis for these symptoms in a significant number of these patients.”

Celiac disease is an autoimmune disorder in which the immune system mistakenly attacks the lining of the small intestine after someone who is genetically susceptible to the disorder ingests gluten from wheat, rye, or barley. This leads to a range of gastrointestinal symptoms, including abdominal pain, diarrhea, and bloating.

Researchers have struggled to determine why some people, who lack the characteristic blood, tissue, or genetic markers of celiac disease, experience celiac-like GI symptoms, as well as certain extra-intestinal symptoms, such as fatigue, cognitive difficulties, or mood disturbance, after ingesting foods that contain wheat, rye, or barley. One explanation for this condition, known as non-celiac gluten or wheat sensitivity (NCWS), is that exposure to the offending grains somehow triggers acute systemic immune activation, rather than a strictly localized intestinal immune response. Because there are no biomarkers for NCWS, accurate figures for its prevalence are not available, but it is estimated to affect about 1 percent of the population, or 3 million Americans, roughly the same prevalence as celiac disease.

Monday, July 25, 2016

the poop gap


westhunt |  There’s a new article out in Science tracing the splits in gut flora. It looks as if the gut bacteria in chimpanzees split with those in humans 5.3 million years: doesn’t quite match our genetic estimates based on Human/chimp autosomal DNA differences, but it’s in the ball park. They estimate the human-gorilla split at 15.6 million year ago, but that can’t be right: we know that gorillas split off just a bit before the human-chimp split. Perhaps gorilla diet changed drastically, and maybe they picked up new bacteria from some other species.

Different populations of modern humans apparently have pretty different microbiomes. The gut bacteria from people in Malawi appear to have diverged 1.7 million years ago from those in Europeans (people from Connecticut). That is surely too old to be a consequence of modern humans’ trek out of Africa: it looks as if AMH, after leaving Africa, picked up gut flora from archaic sapiens like Neanderthals and Denisovans and dwarves.

Microbiomes are trendy. We know that fecal transplants can cure C difficile (pseudomembranous colitis) lickety-split: they might help with Crohn’s disease and ulcerative colitis. Some researchers think the microbiome has something to do with the initiation of multiple sclerosis. Others suspect that it may play a role regulating how people think and feel – in particular, mood disorders. Autism has been mentioned. 

So.. Poop matters: it certainly can affect health, and it may influence brain function. People from sub-Saharan have divergent poop, or you could say that Eurasians do. Are there differences in brain function between sub-Saharan Africans and Eurasians? Sure: Africans do poorly on IQ tests and in academic subjects. They have significant higher rates of schizophrenia, higher murder rates, etc.
Maybe it’s the poop. It’s worth checking out. Perhaps the fault lies not in our stars, or our genes, but in our stool. 

Already, eager experimenters – paleos on stilts – are trying to dramatically modulate their internal flora.

Monday, July 18, 2016

immune system controls social interactions


medicalxpress |  In a startling discovery that raises fundamental questions about human behavior, researchers at the University of Virginia School of Medicine have determined that the immune system directly affects - and even controls - creatures' social behavior, such as their desire to interact with others. So could immune system problems contribute to an inability to have normal social interactions? The answer appears to be yes, and that finding could have great implications for neurological conditions such as autism-spectrum disorders and schizophrenia. 

"The brain and the adaptive immune system were thought to be isolated from each other, and any in the brain was perceived as sign of a pathology. And now, not only are we showing that they are closely interacting, but some of our behavior traits might have evolved because of our to pathogens," explained Jonathan Kipnis, PhD, chairman of UVA's Department of Neuroscience. "It's crazy, but maybe we are just multicellular battlefields for two ancient forces: pathogens and the immune system. Part of our personality may actually be dictated by the immune system."

Sunday, July 3, 2016

gut bacteria spotted eating brain chemicals for the first time


newscientist |  Bacteria have been discovered in our guts that depend on one of our brain chemicals for survival. These bacteria consume GABA, a molecule crucial for calming the brain, and the fact that they gobble it up could help explain why the gut microbiome seems to affect mood.

Philip Strandwitz and his colleagues at Northeastern University in Boston discovered that they could only grow a species of recently discovered gut bacteria, called KLE1738, if they provide it with GABA molecules. “Nothing made it grow, except GABA,” Strandwitz said while announcing his findings at the annual meeting of the American Society for Microbiology in Boston last month.

GABA acts by inhibiting signals from nerve cells, calming down the activity of the brain, so it’s surprising to learn that a gut bacterium needs it to grow and reproduce. Having abnormally low levels of GABA is linked to depression and mood disorders, and this finding adds to growing evidence that our gut bacteria may affect our brains.

Treating depression 
An experiment in 2011 showed that a different type of gut bacteria, called Lactobacillus rhamnosus, can dramatically alter GABA activity in the brains of mice, as well as influencing how they respond to stress. In this study, the researchers found that this effect vanished when they surgically removed the vagus nerve – which links the gut to the brain – suggesting it somehow plays a role in the influence gut bacteria can have on the brain.  Fist tap Big Don

Thursday, May 26, 2016

Royal Society calls for review of European GM ban



bbcnews |  In a statement, the Soil Association said it believed that the Royal Society guide was neither neutral nor unbiased as it claims.

"Everyone knows that there are at least some scientific controversies, and disagreements about evidence concerning GM crops. None of these are mentioned in the Royal Society document," the statement read.

"This may not be surprising, given that there are no scientists who have consistently expressed scepticism about the application of GM technology to agriculture listed among the authors.

"Scientific enquiry normally proceeds by open discussion of disagreements about evidence - the Royal Society's involvement in GM has been consistently one-sided, ignoring scientists with dissenting views, and overlooking facts which do not fit with the views of supporters of GM crops."

An analysis of 900 pieces of published research into GM technology by the US National Academy of Sciences concluded that GM food was safe to eat - though it did highlight some environmental concerns.

Prof Ramakrishnan said he recognised that the answers in the Royal Society guide would not end the controversy.

"But we hope that they will inform people about the science and allow those who might previously have felt excluded from the discussion to form a view," he said.

The Royal Society will hold a series of public panel discussion events (Growing tomorrow's dinner - should GM be on the table?) across the UK during the summer and autumn.

Thursday, May 19, 2016

Conflict of interest? Members of UN panel on glyphosate have Monsanto ties...,


RT | Two people on the UN panel that just ruled the herbicide glyphosate “unlikely” to cause cancer in humans have ties to groups that have accepted over $1 million from Monsanto and another industry group representing agrochemical giants. 

The people in question are Professor Alan Boobis, chairman of the UN panel investigating glyphosate – the active ingredient in Monsanto’s herbicide Roundup and other similar products – and Professor Angelo Moretto, the panel’s co-chair, the Guardian reported.

Boobis is the vice president of the International Life Science Institute (ILSI Europe). Moretto, meanwhile, is a board member of ILSI’s Health and Environmental Sciences Institute and of its Risk21 steering group. Notably, Boobis is a co-chair of Risk21.

ILSI Europe accepted a donation of $500,000 from Monsanto back in 2012, according to a document released by the US Right to Know campaign. The group also accepted donations from CropLife – which represents agriculture companies such as Monsanto, Dow, DuPont and Syngenta – totaling more than $528,000.

Tuesday, May 3, 2016

gotta get some o'that all-natural biocide into me before the first cigarette of a morning..,


RT |  The use of glyphosate in herbicides has increased by more than 250 times in the United States in the last 40 years, according to the New England Journal of Medicine. Long-term exposure to glyphosate has been linked to kidney and liver damage, as well as cellular and genetic diseases. 

Monsanto and defenders of glyphosate use called the World Health Organization's carcinogen classification too "dramatic" and have pointed to assurances that the chemical is, indeed, safe.

Last month, the European Parliament approved the seven-year re-authorization of glyphosate, though it recommended the chemical should be used only by professionals and not in public places.
In September, Monsanto was sued by two agricultural workers in the US who claimed Roundup had caused their cancers.

In February, the US Food and Drug Administration said it would begin to test some products – including milk, corn, eggs, and soybeans, among possible others in the future – for glyphosate.

In 2013, the EPA approved Monsanto's plea for use of increased levels of glyphosate, which was first created in 1970 by Monsanto. In 1974, the company began selling the chemical in Roundup, which has become a top bioicide for both farming, especially regarding genetically-engineered crops, and home and garden uses.

Saturday, April 16, 2016

worm infection counters inflammatory bowel disease by changing gut microbiome


sciencedaily |   Infection with worms counters inflammatory bowel diseases (IBD) by triggering immune responses that change the mix of bacteria, or microbiome, in the gut. This is according to a study published online April 14 in the journal Science.

The study results support the hygiene hypothesis which, in the case of IBD, argues that the absence of exposure to worms in too-clean modern living spaces has left some with oversensitive, gut-based immune systems vulnerable to inflammatory diseases. Gut worms have helped to train and balance immune systems throughout human evolution, but are now missing in developed nations, which, in turn, have the highest rates of Crohn's disease and ulcerative colitis.

In the newly published study, a team led by researchers from NYU Langone Medical Center found that mice infected with intestinal worms experienced as much as a thousand-fold decrease in Bacteroides -- a group of bacterial species linked by past studies to higher risk for IBD. At the same time, the number of Clostridia, a bacterial species known to counter inflammation, increased tenfold. The investigators argue that the immune response to the worms triggers the growth in Clostridia, which then either outcompete Bacteroides for nutrients or release toxins harmful to Bacteroides.

"Our findings are among the first to link parasites and bacteria to the origin of IBD, supporting the hygiene hypothesis," says study co-senior investigator and parasitologist P'ng Loke, PhD, an associate professor at NYU Langone. Loke says this model may also be applicable to other autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, and type 1 diabetes, in which processes meant to attack foreign invaders instead become oversensitive and react to the body's own cells.

Saturday, April 9, 2016

gum disease opens up the body to a host of infections


sciencenews |  For centuries, the mouth and the body have been disconnected — at least when it comes to health care. Through the Middle Ages and beyond, teeth fell under the care of barbers, who could shave a customer and pull a molar with equal skill. In the 1700s, French surgeon Pierre Fauchard published the Treatise on Teeth, establishing dentistry as its own science.

Across the channel in England, as physicians gained stature in the 19th century, surgeons and dentists engaged in a power struggle. In the modern United States, after medicine became linked to employer insurance and Medicare, the fissure between medicine and dentistry widened. Insurance coverage began at the throat.

So when Salomon Amar, a periodontal specialist at Boston University, began exploring links between oral bacteria and heart disease in animal studies in the late 1990s, reactions were lukewarm. “Many cardiologists thought we were a bit crazy,” he says. Skepticism still abounds, but the same molecular tools that have dramatically changed understanding of the gut microbiome are now allowing scientists to track and examine bacteria in the mouth. Advocates of a connection between the artery disease atherosclerosis and microbes are hoping to find convincing proof of their suspicions, while exploring links between ailing gums and other conditions, including cancer, arthritis, diabetes and even Alzheimer’s disease.

The work has profound implications for public health, given that more than 65 million American adults are thought to have periodontal disease, which occurs when bacterial overgrowth inflames the gums and can lead to erosion of gums and bone. If it turns out that periodontal decay drives other diseases, doctors would have a new, and relatively simple, means of prevention.

Wenche Borgnakke, a dental researcher at the University of Michigan in Ann Arbor, has been making this case for years, citing “solid evidence that periodontal treatment has an effect on systemic disease.” She points to a study published last year in the journal Medicine comparing patients on dialysis who received periodontal treatment with those who did not. Those getting treatment had an almost 30 percent lower risk of pneumonia and hospitalization from infections. Another study published earlier this year found that gum disease is associated with a roughly 10 percent higher mortality over 10 years among patients with kidney problems.

Sunday, March 20, 2016

can you catch alzheimers?


nature |  In the 25 years that John Collinge has studied neurology, he has seen hundreds of human brains. But the ones he was looking at under the microscope in January 2015 were like nothing he had seen before.

He and his team of pathologists were examining the autopsied brains of four people who had once received injections of growth hormone derived from human cadavers. It turned out that some of the preparations were contaminated with a misfolded protein — a prion — that causes a rare and deadly condition called Creutzfeldt–Jakob disease (CJD), and all four had died in their 40s or 50s as a result. But for Collinge, the reason that these brains looked extraordinary was not the damage wrought by prion disease; it was that they were scarred in another way. “It was very clear that something was there beyond what you'd expect,” he says. The brains were spotted with the whitish plaques typical of people with Alzheimer's disease. They looked, in other words, like young people with an old person's disease.
For Collinge, this led to a worrying conclusion: that the plaques might have been transmitted, alongside the prions, in the injections of growth hormone — the first evidence that Alzheimer's could be transmitted from one person to another. If true, that could have far-reaching implications: the possibility that 'seeds' of the amyloid-β protein involved in Alzheimer's could be transferred during other procedures in which fluid or tissues from one person are introduced into another, such as blood transfusions, organ transplants and other common medical procedures.

Collinge felt a duty to inform the public quickly. And that's what he did, publishing the study in Nature in September1, to headlines around the world. “Can you CATCH Alzheimer's?” asked Britain's Daily Mail, about the “potentially explosive new study”. Collinge has been careful to temper the alarm. “Our study does not mean that Alzheimer's is actually contagious,” he stresses. Carers won't catch it on the job, nor family members, however close. “But it raises concern that some medical procedures could be inadvertently transferring amyloid-β seeds.”

Tuesday, March 1, 2016

the new yorker and the scientist shamelessly presstitute for monsanto...,


thescientist |  There are many unknowns when it comes to tracing the march of Zika through Latin America and the effects it is having on those infected. As researchers get a handle on how Zika works and how it might be stopped, Zika conspiracy theories abound: depending on which fringe group you listen to, the disease is caused by vaccines, pesticides, Monsanto, or genetically modified (GM) mosquitos. None of these appear to be true, and The New Yorker set the record straight—particularly regarding the GM-mosquito-theory—last week (February 25). “This is a particularly dangerous misapprehension, because, for now, controlling mosquitoes may be the only way we can hope to control Zika,” wrote Michael Specter.

Friday, February 26, 2016

epigenetics control aging and cancer...,



northwestern | Epigenetic age is a new way to measure your biological age. When your biological (epigenetic) age is older than your chronological age, you are at increased risk for getting and dying of cancer, reports a new Northwestern Medicine study.

And the bigger the difference between the two ages, the higher your risk of dying of cancer.

“This could become a new early warning sign of cancer,” said senior author Dr. Lifang Hou, who led the study. “The discrepancy between the two ages appears to be a promising tool that could be used to develop an early detection blood test for cancer.”

Hou is chief of cancer epidemiology and prevention in preventive medicine at Northwestern University Feinberg School of Medicine and co-leader of the cancer prevention program at the Robert H. Lurie Comprehensive Cancer Center of Northwestern University.

“People who are healthy have a very small difference between their epigenetic/biological age and chronological age,” Hou said. “People who develop cancer have a large difference and people who die from cancer have a difference even larger than that. Our evidence showed a clear trend.”

A person’s epigenetic age is calculated based on an algorithm measuring 71 blood DNA methylation markers that could be modified by a person’s environment, including environmental chemicals, obesity, exercise and diet. This test is not commercially available but is currently being studied by academic researchers, including a team at Northwestern.

Monday, February 15, 2016

latin american doctors don't think zika is causing microencephaly...,

 
gmwatch |  report from the Argentine doctors’ organisation, Physicians in the Crop-Sprayed Towns,[1] challenges the theory that the Zika virus epidemic in Brazil is the cause of the increase in the birth defect microcephaly among newborns.  

The increase in this birth defect, in which the baby is born with an abnormally small head and often has brain damage, was quickly linked to the Zika virus by the Brazilian Ministry of Health. However, according to the Physicians in the Crop-Sprayed Towns, the Ministry failed to recognise that in the area where most sick people live, a chemical larvicide that produces malformations in mosquitoes was introduced into the drinking water supply in 2014. This poison, Pyriproxyfen, is used in a State-controlled programme aimed at eradicating disease-carrying mosquitoes. 

The Physicians added that the Pyriproxyfen is manufactured by Sumitomo Chemical, a Japanese "strategic partner" ofMonsanto. Pyriproxyfen is a growth inhibitor of mosquito larvae, which alters the development process from larva to pupa to adult, thus generating malformations in developing mosquitoes and killing or disabling them. It acts as an insect juvenile hormone or juvenoid, and has the effect of inhibiting the development of adult insect characteristics (for example, wings and mature external genitalia) and reproductive development. It is an endocrine disruptor and is teratogenic (causes birth defects), according to the Physicians.

The Physicians commented: “Malformations detected in thousands of children from pregnant women living in areas where the Brazilian state added Pyriproxyfen to drinking water are not a coincidence, even though the Ministry of Health places a direct blame on the Zika virus for this damage.”

They also noted that Zika has traditionally been held to be a relatively benign disease that has never before been associated with birth defects, even in areas where it infects 75% of the population.

astonishing levels of transatlantic presstitution obfuscating the cause of the pinhead epidemic

WaPo |  Brazil on Friday reported a nearly 50 percent jump in cases of dengue fever reported over a three-week period in January, a worrying finding because the disease is carried by the same mosquito that spreads the Zika virus.
“This is a very strong indication that the Zika cases are increasing and that the combat against the mosquito is not being efficient,” said Marcos Lago, an associate professor of infectious diseases and pediatrics at the State University of Rio de Janeiro.
Brazil has been panicked by thousands of suspected cases of the birth defect microcephaly, which the government has linked to an epidemic of the Zika virus that began last year.
“We will probably have a dengue epidemic,” Lago said. “And this dengue epidemic will be accompanied by a Zika epidemic.”

amazing the lengths gone to preserve plausible deniability for monsanto...,

guardian |  Mukwaya says he was astonished to hear of what was in Uganda a pretty harmless disease evolving into a potential global monster almost overnight on another continent. “I was very surprised by what has happened in Brazil,” he said. “Here it causes only a mild fever. I did not expect it to be that dangerous. It would be extraordinary if it really could spread from mosquito to human to human.”
He said had been bitten several times by mosquitoes carrying the Zika virus but, like most Ugandans, had no symptoms. “In Brazil,” he said, “the mosquito that can spread Zika is Aedes aegypti formosus. In Uganda, it is Aedes africanus. Both carry the same viruses, including dengue, yellow fever and chikungunya.
“What do we know about Aedes africanus? It bites mostly at altitudes of 18 to 24 metres, it lays 300 eggs at a time, it likes a temperature of 26C-27C, it prefers forest to open land, and, like other mosquitoes, it is attracted to alcohol. How the virus was transmitted to Latin America, and how it might develop or mutate, is just not known.”
Nor have there been any reported cases of birth defects in Uganda. “We do haveaegypti [mosquitoes] here, but I think we are protected. It does not regularly feed on man here, but on small animals like rodents, and cats and dogs. I believe we are safe. The mosquito carries both yellow fever and Zika, but it normally never bites humans and when it does it leads only to a short mild fever that many people do not even notice.”
Zika infection may be unknown in Uganda but the forest is a reservoir of disease. Despite this, it attracts its share of tourists and was once visited by the US president Jimmy Carter, who came to spot birds such as the rare crested crane. In the 65 years since the tower was built, UVRI researchers have isolated hundreds of arboviruses – diseases spread by insects and ticks.
“Most of them are potentially deadly,” says Mukwaya, who helped isolate the yellow fever virus in the 1970s and has had a mosquito sub-species named after him. “We do not know what else is in there. If you want to study little-known flora and fauna, you come to Uganda.”

Friday, February 12, 2016

shikimate inhibition by roundup (glyphosate)


mdpi |  Glyphosate, the active ingredient in Roundup®, is the most popular herbicide used worldwide. The industry asserts it is minimally toxic to humans, but here we argue otherwise. Residues are found in the main foods of the Western diet, comprised primarily of sugar, corn, soy and wheat. Glyphosate's inhibition of cytochrome P450 (CYP) enzymes is an overlooked component of its toxicity to mammals. CYP enzymes play crucial roles in biology, one of which is to detoxify xenobiotics. Thus, glyphosate enhances the damaging effects of other food borne chemical residues and environmental toxins. Negative impact on the body is insidious and manifests slowly over time as inflammation damages cellular systems throughout the body. Here, we show how interference with CYP enzymes acts synergistically with disruption of the biosynthesis of aromatic amino acids by gut bacteria, as well as impairment in serum sulfate transport. Consequences are most of the diseases and conditions associated with a Western diet, which include gastrointestinal disorders, obesity, diabetes, heart disease, depression, autism, infertility, cancer and Alzheimer’s disease. We explain the documented effects of glyphosate and its ability to induce disease, and we show that glyphosate is the “textbook example” of exogenous semiotic entropy: the disruption of homeostasis by environmental toxins.


the shikimate pathway

wikipedia |  The shikimate pathway (shikimic acid pathway) is a seven step metabolic route used by bacteria, fungi, algae, parasites and plants for the biosynthesis of aromatic amino acids (phenylalanine, tyrosine, andtryptophan). This pathway is not found in animals, hence the products of this pathway represent essential amino acids that must be obtained from the animal's diet. However, this pathway is found with microbes that live within animals in the gut microbiome.
The first enzyme involved is the shikimate kinase, an enzyme that catalyzes the ATP-dependent phosphorylation of shikimate to form shikimate 3-phosphate.[1] Shikimate 3-phosphate is then coupled withphosphoenol pyruvate to give 5-enolpyruvylshikimate-3-phosphate via the enzyme 5-enolpyruvylshikimate-3-phosphate (EPSP) synthase.