Scientists investigate possible connection between autism and vitamin D

http://www.environmentalhealthnews.org/ehs/news/2013/autism-and-vitamin-d

Vitamin D plays a pivotal role in a number of disorders. Now scientists are investigating whether the “sunshine vitamin” could be implicated in autism. With autism rates climbing and levels of vitamin D declining because of more sunscreen use and less time spent outdoors, scientists have begun to look into a possible link. A recent study in Saudi Arabia was the first to discover that children with autism had significantly lower levels of vitamin D in their bloodstreams than non-autistic children. “There is a growing body of literature linking vitamin D to various immune-related conditions, including allergy and autoimmunity,” said Laila Y. AL-Ayadhi, a professor of neurophysiology at King Saud University and one of the new study’s lead researchers. Yet many questions remain, and experts say none of the research so far has shown a convincing link. Vitamin D is one of many environmental factors, including air pollution and pesticides, that are eyed by researchers seeking to understand why autism rates have continued their uninterrupted climb over the past several decades.

By Brita Belli
Environmental Health News

Jan. 31, 2013

Vitamin D plays a pivotal role in a number of disorders. Now scientists are investigating whether the “sunshine vitamin” could be implicated in autism.

With autism rates climbing and levels of vitamin D declining because of more sunscreen use and less time spent outdoors, scientists have begun to look into a possible link. A recent study was the first to discover that children with autism had significantly lower levels of vitamin D in their bloodstreams than non-autistic children. Yet many questions remain, and experts say none of the research so far has shown a convincing link.

Vitamin D is one of many environmental factors eyed by researchers seeking to understand why autism rates have continued their uninterrupted climb over the past several decades. One in every 88 U.S. kids by the age of 8 has been diagnosed with an autism spectrum disorder, according to the Centers for Disease Control and Prevention.

Some of this increase is attributed to heightened awareness of the brain disorders, which are marked by social impairment, difficulty with communication and repetitive behaviors. Still, greater diagnosis alone cannot explain it, leading researchers to increasingly look for environmental answers.

In recent years, limited evidence has emerged that suggests a link between autism and pregnant women’s exposure to pesticides, air pollutants, phthalates and heavy metals like mercury. Now, in a Saudi Arabian study, a possible association between vitamin D and autism is gaining some traction.

Children with autism had lower levels of vitamin D than non-autistic kids, according to the study by researchers at King Saud University. And the lower the vitamin D levels, the higher the children’s scores on the Childhood Autism Rating Scale, which measures autism severity.

Fifty children with autism, ages 5 to 12, were recruited and matched with 30 children without autism. Forty percent of the autistic children were vitamin D deficient; none of the control children were.

The study also revealed another first-of-its-kind finding – 70 percent of the children with autism had elevated levels of antibodies that can disrupt the signaling of neurons in the brain. These antibodies could trigger an autoimmune response causing brain inflammation, and perhaps autistic traits, in genetically susceptible kids. And the study found that the less vitamin D a child had, the greater the level of the antibodies, and the more severe the autism symptoms.

“There is a growing body of literature linking vitamin D to various immune-related conditions, including allergy and autoimmunity,” said Laila Y. AL-Ayadhi, a professor of neurophysiology at King Saud University and one of the study’s lead researchers.

One study in 2009 found that autistic patients had significant levels of brain inflammation, indicating an autoimmune disorder – when the body’s immune system begins attacking healthy tissues, in this case, brain tissues. Vitamin D deficiency, in turn, has been identified as a possible environmental trigger for other autoimmune disorders, including multiple sclerosis and lupus.

Vitamin D deficiency in the study apparently was unrelated to sun exposure, which was about the same for the autistic and non-autistic kids. Instead, AL-Ayadhi said “the most probable explanation” for the children’s lowered vitamin D was “an abnormality in the liver,” where vitamin D is converted into its usable form, although that hypothesis was not fully explored.

The study has limitations, said Heather Volk, an assistant professor at the University of Southern California who studies gene-environment interactions in relation to autism. “While they can find differences of circulating vitamin D, it’s difficult to really say this is potentially a causal factor because we’re looking at things in one point in time in these individuals,” she said. “We don’t really know if [the lowered] vitamin D levels preceded the autism.”

“But,” she added, “it is important and interesting and the more environmental factors that can be modified that we manage to study for autism, the more insights that we start to get.”

"There is a growing body of literature linking vitamin D to various immune-related conditions." - Laila Y. AL-Ayadhi, King Saud University Vitamin D deficiency in mothers is thought to be a risk factor for autism, too, and has been supported by studies examining where children are born and during what season in relation to autism rates.

“Vitamin D performs a number of biological functions that are important for neurodevelopment, including promoting cell division and protecting against neurotoxins. A research goal now is to hone in on what the exact biological mechanisms are that may link maternal vitamin D insufficiency and atypical brain development,” said Andrew Whitehouse, head of the Developmental Disorders Research Group at the Telethon Institute for Child Health Research in Australia.

In rats, vitamin D deficiency during gestation has resulted in permanent changes in developing brains. Also, babies born with low vitamin D levels have twice the risk of developing schizophrenia, and deficiency in pregnant mothers has been associated with language impairment in children.

Results of autism studies, however, have been mixed. Whitehouse led a study of more than 900 pregnant women that measured Vitamin D at 18 weeks gestation; their children were later assessed for autism. It found no correlation between children’s scores on an autism rating scale and maternal vitamin D levels.

But research at the University of California, Davis found an increased risk for children with autism among 700 mothers who did not take prenatal vitamins during the three months before and the first month of pregnancy.

While that study did not specifically call out vitamin D as a suspect, UC Davis researcher Rebecca Schmidt is currently working on a similarly large study that will focus on the importance of maternal vitamin D intake on autism rates.

“This is the kind of study I think needs to be done where we go back and look at the vitamin D levels in the maternal blood during pregnancy and we follow these children up to see if they’ve developed autism,” Schmidt said.

Air pollution, studies show, could be acting as a double-edged sword: increasing inflammation and contributing to maternal vitamin D deficiency. Volk’s research has focused on a possible link between maternal air pollution exposure and autism, but she notes that her findings also could implicate vitamin D.

Her study, published in January, found that children with autism were more likely to live in homes that had the highest percent of traffic-related air pollution during their mothers’ pregnancy and the first year of life compared to control children. One explanation is that pollution may induce inflammation in the body that raises the risk of autism.

“Air pollution exposure can increase systemic inflammation in the body that really might be affecting the brain,” Volk said, adding that “vitamin D helps your body deal with inflammation. It helps turn on the body’s responses.”

Air pollution, studies show, could be acting as a double-edged sword: increasing inflammation and contributing to maternal vitamin D deficiency.

Of course pollution isn’t the only reason women are getting less sunlight, and less vitamin D. For decades, women have been avoiding the sun with the help of sunscreens and more time spent indoors. And those decades track with the rising incidence of autism disorders. A 2007 study of 400 pregnant women found that 42.1 percent of white women and 54.1 percent of black women were vitamin D insufficient even though 90 percent of these women took prenatal vitamins.

One study published last year found that children in states with the highest exposure to UVB rays in summer and fall had about half the autism rates of states with lower UVB exposures. The study was conducted by John Cannell of the Vitamin D Council and another researcher; both reported that they received funding from vitamin manufacturers.

Such studies linking sunshine exposure and autism remain highly speculative, Schmidt said. “There are a lot of things that could be explaining those types of associations besides vitamin D,” Schmidt said. “You have to be careful about making those kind of big links until there’s better data.”

For instance, experts originally suggested a link between sunshine and autism in relation to immigrants with autism, but now other factors are considered more likely. Somali immigrants moving to northern latitudes in Sweden and Minnesota had higher-than-average rates of autism than surrounding communities, according to government officials and the Minnesota Health Department. Vitamin D quickly became a suspect. But on closer examination, the theory didn’t hold. Instead, it was found that the stress of migrating may have been the more critical factor.

So is it worthwhile to begin preventive measures, such as five to 30 minutes of sun exposure a couple times a week? Schmidt says supplements alone are not enough.

"There are lots of things that could be explaining those types of associations besides vitamin D. You have to be careful about making those kind of big links until there's better data." - Rebecca Schmidt, UC Davis The levels in those supplements are so low compared to what you get from the sunlight that they may not be making as much of a difference as they need to,” she said.

In 2007, the Canadian Pediatric Society recommended a sharp increase in supplementation during pregnancy and breastfeeding, from 400 international units (IU) per day, which are typically found in prenatal vitamins, to 4,000 IU/day. The American College of Obstetricians and Gynecologists advises that 1,000-2,000 IUs of vitamin D during pregnancy can be considered safe for women with an identified vitamin D deficiency although they add that “most experts agree that supplemental vitamin D is safe in dosages up to 4,000 international units per day during pregnancy or lactation.”

“We don’t want to get people too concerned before we need to,” Schmidt said, “but it is something we can do something about.”

Brita Belli is the author of The Autism Puzzle: Connecting the Dots Between Environmental Toxins and Rising Autism Rates and the editor of E – The Environmental Magazine http://www.emagazine.com/.

 

 

Autism Linked to the Gut, Study Finds: The gut bacteria of autistic children is much different than that of typical children, according to a new study.

Autism Linked to the Gut, Study Finds

The gut bacteria of autistic children is much different than that of typical children, according to a new study

http://www.everydayhealth.com/autism/autism-may-start-in-the-gut-study-finds-3835.aspx?xid=aol_eh-digest_6_20130708_&aolcat=AHD&icid=maing-grid7|htmlws-main-bb|dl19|sec1_lnk3%26pLid%3D341246

By Amir Khan, Everyday Health Staff Writer

WEDNESDAY, July 3, 2013 — An autism breakthrough may be sitting in your gut, according to a new study published in the journal PLOS ONE. The gut bacteria of autistic children is vastly different than that of typical children, and researchers say that bringing their gut bacteria into line with that of a typical child could help doctors better treat autistic kids.

"One of the reasons we started addressing this topic is the fact that autistic children have a lot of GI problems that can last into adulthood," study author Rosa Krajmalnik-Brown, PhD, a researcher with Arizona State University, said in a statement. "Studies have shown that when we manage these problems, their behavior improves dramatically."

Researchers compared the gut bacteria of 20 autistic and 20 healthy children, and found that autistic children not only had far less gut bacteria, but also had much lower diversity. Prevotella, a bacteria thought to play a role in regulating the gut microbiome, was found in conspicuously low levels in the stomachs of the autistic children, according to the study. Researchers theorize that a lack of prevotella, coupled with lack of diversity in the gut, may be the root cause of the gastrointestinal problems that often affect autistic children.

"We believe that a diverse gut is a healthy gut," Dr. Krajmalnik-Brown said in the statement.

This lack of diversity could also lead to inflammation, says Robert Melillo, DC, a chiropractor and nutritionist and author of the book The Scientific Truth About Preventing, Diagnosing, and Treating Autism Spectrum Disorders — and What Parents Can Do Now. Fixing their gut bacteria could help reduce the inflammation throughout the body.

“People with autism have an overactive immune response, and they develop antibodies against too many foods, chemicals and even their own tissue,” Melillo said. “Identifying those substances and eliminating them from the child’s diet or reducing their exposure to these antigens reduces the inflammation and reduces many of the symptoms of autism.”

Can Fixing the Gut Treat Autism?

While the Arizona study was small, researchers said uncovering the link between gut bacteria and autism could pave the way for future treatments for the condition. Normalizing the gut bacteria of autistic kids, they added, could help treat not only their GI problems, but other problems as well.

“The findings from this study are stepping stones for better understanding of the crosstalk between gut microbiota and autism,” the researchers wrote in the study, “which may provide potential targets for diagnosis or treatment of neurological as well as GI symptoms in autistic children.”

However, Dr. Melillo said, normalizing gut bacteria would not be a miracle cure.

“It’s clear that the brain is the cause of most of the immune and gut issues in children with autism,” he said. “You cannot explain all of this the other way around where the gut can cause all of these issues and what we see in the brain.”

And while it is still unclear how to fix the brain in someone with autism, he said, it’s clear that the gut should not be the primary target for treating autism.

“Gut problems are very important and need to be part of the solution, but the gut problems are really brain problems that are manifesting in the gut,” he said. “To heal the gut we need to fix the brain.”

 

ARTICLE: Vitamin D Requirements for Nursing Mothers and Infants

Vitamin D requirements during lactation: high-dose maternal supplementation as therapy to prevent hypovitaminosis D for both the mother and the nursing infant

by Bruce W Hollis and Carol L Wagner
http://ajcn.nutrition.org/content/80/6/1752S.long

Abstract

Scientific data pertaining to vitamin D supplementation during lactation are scarce. The daily recommended intake for vitamin D during lactation has been arbitrarily set at 400 IU/d (10 μg/d). This recommendation is irrelevant with respect to maintaining the nutritional vitamin D status of mothers and nursing infants, especially among darkly pigmented individuals. Our objective was to examine the effect of high-dose maternal vitamin D2 supplementation on the nutritional vitamin D status of mothers and nursing infants.

Fully lactating women (n = 18) were enrolled at 1 mo after birth to 1 of 2 treatment arms, ie, 1600 IU vitamin D2 and 400 IU vitamin D3 (prenatal vitamin) or 3600 IU vitamin D2 and 400 IU vitamin D3, for a 3-mo study period.

High-dose (1600 or 3600 IU/d) vitamin D2 supplementation for a period of 3 mo safely increased circulating 25-hydroxyvitamin D [25(OH)D] concentrations for both groups.

The antirachitic activity of milk from mothers receiving 2000 IU/d vitamin D increased by 34.2 IU/L, on average, whereas the activity in the 4000 IU/d group increased by 94.2 IU/L. Nursing infant circulating 25(OH)D2 concentrations reflected maternal intake and the amount contained in the milk. With limited sun exposure, an intake of 400 IU/d vitamin D would not sustain circulating 25(OH)D concentrations and thus would supply only limited amounts of vitamin D to nursing infants in breast milk.

A maternal intake of 2000 IU/d vitamin D would elevate circulating 25(OH)D concentrations for both mothers and nursing infants, albeit with limited capacity, especially with respect to nursing infants.

A maternal intake of 4000 IU/d could achieve substantial progress toward improving both maternal and neonatal nutritional vitamin D status.

Read more about this study here.

 

New York Times Regarding The Latest Gut Research

New York Times regarding the latest gut research

http://www.nytimes.com/2013/05/19/magazine/say-hello-to-the-100-trillion-bacteria-that-make-up-your-microbiome.html?pagewanted=1&_r=0

By MICHAEL POLLAN

I can tell you the exact date that I began to think of myself in the first-person plural — as a superorganism, that is, rather than a plain old individual human being. It happened on March 7. That’s when I opened my e-mail to find a huge, processor-choking file of charts and raw data from a laboratory located at the BioFrontiers Institute at the University of Colorado, Boulder. As part of a new citizen-science initiative called the American Gut project, the lab sequenced my microbiome — that is, the genes not of “me,” exactly, but of the several hundred microbial species with whom I share this body. These bacteria, which number around 100 trillion, are living (and dying) right now on the surface of my skin, on my tongue and deep in the coils of my intestines, where the largest contingent of them will be found, a pound or two of microbes together forming a vast, largely uncharted interior wilderness that scientists are just beginning to map.
I clicked open a file called Taxa Tables, and a colorful bar chart popped up on my screen. Each bar represented a sample taken (with a swab) from my skin, mouth and feces. For purposes of comparison, these were juxtaposed with bars representing the microbiomes of about 100 “average” Americans previously sequenced.
Here were the names of the hundreds of bacterial species that call me home. In sheer numbers, these microbes and their genes dwarf us. It turns out that we are only 10 percent human: for every human cell that is intrinsic to our body, there are about 10 resident microbes — including commensals (generally harmless freeloaders) and mutualists (favor traders) and, in only a tiny number of cases, pathogens. To the extent that we are bearers of genetic information, more than 99 percent of it is microbial. And it appears increasingly likely that this “second genome,” as it is sometimes called, exerts an influence on our health as great and possibly even greater than the genes we inherit from our parents. But while your inherited genes are more or less fixed, it may be possible to reshape, even cultivate, your second genome.
Justin Sonnenburg, a microbiologist at Stanford, suggests that we would do well to begin regarding the human body as “an elaborate vessel optimized for the growth and spread of our microbial inhabitants.” This humbling new way of thinking about the self has large implications for human and microbial health, which turn out to be inextricably linked. Disorders in our internal ecosystem — a loss of diversity, say, or a proliferation of the “wrong” kind of microbes — may predispose us to obesity and a whole range of chronic diseases, as well as some infections. “Fecal transplants,” which involve installing a healthy person’s microbiota into a sick person’s gut, have been shown to effectively treat an antibiotic-resistant intestinal pathogen named C. difficile, which kills 14,000 Americans each year. (Researchers use the word “microbiota” to refer to all the microbes in a community and “microbiome” to refer to their collective genes.) We’ve known for a few years that obese mice transplanted with the intestinal community of lean mice lose weight and vice versa. (We don’t know why.) A similar experiment was performed recently on humans by researchers in the Netherlands: when the contents of a lean donor’s microbiota were transferred to the guts of male patients with metabolic syndrome, the researchers found striking improvements in the recipients’ sensitivity to insulin, an important marker for metabolic health. Somehow, the gut microbes were influencing the patients’ metabolisms.
Our resident microbes also appear to play a critical role in training and modulating our immune system, helping it to accurately distinguish between friend and foe and not go nuts on, well, nuts and all sorts of other potential allergens. Some researchers believe that the alarming increase in autoimmune diseases in the West may owe to a disruption in the ancient relationship between our bodies and their “old friends” — the microbial symbionts with whom we coevolved.
These claims sound extravagant, and in fact many microbiome researchers are careful not to make the mistake that scientists working on the human genome did a decade or so ago, when they promised they were on the trail of cures to many diseases. We’re still waiting. Yet whether any cures emerge from the exploration of the second genome, the implications of what has already been learned — for our sense of self, for our definition of health and for our attitude toward bacteria in general — are difficult to overstate. Human health should now “be thought of as a collective property of the human-associated microbiota,” as one group of researchers recently concluded in a landmark review article on microbial ecology — that is, as a function of the community, not the individual.
Such a paradigm shift comes not a moment too soon, because as a civilization, we’ve just spent the better part of a century doing our unwitting best to wreck the human-associated microbiota with a multifronted war on bacteria and a diet notably detrimental to its well-being. Researchers now speak of an impoverished “Westernized microbiome” and ask whether the time has come to embark on a project of “restoration ecology” — not in the rain forest or on the prairie but right here at home, in the human gut.
In March I traveled to Boulder to see the Illumina HiSeq 2000 sequencing machine that had shed its powerful light on my own microbiome and to meet the scientists and computer programmers who were making sense of my data. The lab is headed by Rob Knight, a rangy, crew-cut 36-year-old biologist who first came to the United States from his native New Zealand to study invasive species, a serious problem in his home country. Knight earned his Ph.D. in ecology and evolutionary biology from Princeton when he was 24 and then drifted from the study of visible species and communities to invisible ones. Along the way he discovered he had a knack for computational biology. Knight is regarded as a brilliant analyst of sequencing data, skilled at finding patterns in the flood of information produced by the machines that “batch sequence” all the DNA in a sample and then tease out the unique genetic signatures of each microbe. This talent explains why so many of the scientists exploring the microbiome today send their samples to be sequenced and analyzed by his lab; it is also why you will find Knight’s name on most of the important papers in the field.
Over the course of two days in Boulder, I enjoyed several meals with Knight and his colleagues, postdocs and graduate students, though I must say I was a little taken aback by the table talk. I don’t think I’ve ever heard so much discussion of human feces at dinner, but then one thing these scientists are up to is a radical revaluation of the contents of the human colon. I learned about Knight’s 16-month-old daughter, who has had most of the diapers to which she has contributed sampled and sequenced. Knight said at dinner that he sampled himself every day; his wife, Amanda Birmingham, who joined us one night, told me that she was happy to be down to once a week. “Of course I keep a couple of swabs in my bag at all times,” she said, rolling her eyes, “because you never know.”
A result of the family’s extensive self-study has been a series of papers examining family microbial dynamics. The data helped demonstrate that the microbial communities of couples sharing a house are similar, suggesting the importance of the environment in shaping an individual’s microbiome. Knight also found that the presence of a family dog tended to blend everyone’s skin communities, probably via licking and petting. One paper, titled “Moving Pictures of the Human Microbiome,” tracked the day-to-day shifts in the microbial composition of each body site. Knight produced animations showing how each community — gut, skin and mouth — hosted a fundamentally different cast of microbial characters that varied within a fairly narrow range over time.
Knight’s daily sampling of his daughter’s diapers (along with those of a colleague’s child) also traced the remarkable process by which a baby’s gut community, which in utero is sterile and more or less a blank slate, is colonized. This process begins shortly after birth, when a distinctive infant community of microbes assembles in the gut. Then, with the introduction of solid food and then weaning, the types of microbes gradually shift until, by age 3, the baby’s gut comes to resemble an adult community much like that of its parents.
The study of babies and their specialized diet has yielded key insights into how the colonization of the gut unfolds and why it matters so much to our health. One of the earliest clues to the complexity of the microbiome came from an unexpected corner: the effort to solve a mystery about milk. For years, nutrition scientists were confounded by the presence in human breast milk of certain complex carbohydrates, called oligosaccharides, which the human infant lacks the enzymes necessary to digest. Evolutionary theory argues that every component of mother’s milk should have some value to the developing baby or natural selection would have long ago discarded it as a waste of the mother’s precious resources.
It turns out the oligosaccharides are there to nourish not the baby but one particular gut bacterium called Bifidobacterium infantis, which is uniquely well-suited to break down and make use of the specific oligosaccharides present in mother’s milk. When all goes well, the bifidobacteria proliferate and dominate, helping to keep the infant healthy by crowding out less savory microbial characters before they can become established and, perhaps most important, by nurturing the integrity of the epithelium — the lining of the intestines, which plays a critical role in protecting us from infection and inflammation.
“Mother’s milk, being the only mammalian food shaped by natural selection, is the Rosetta stone for all food,” says Bruce German, a food scientist at the University of California, Davis, who researches milk. “And what it’s telling us is that when natural selection creates a food, it is concerned not just with feeding the child but the child’s gut bugs too.”
Where do these all-important bifidobacteria come from and what does it mean if, like me, you were never breast-fed? Mother’s milk is not, as once was thought, sterile: it is both a “prebiotic” — a food for microbes — and a “probiotic,” a population of beneficial microbes introduced into the body. Some of them may find their way from the mother’s colon to her milk ducts and from there into the baby’s gut with its first feeding. Because designers of infant formula did not, at least until recently, take account of these findings, including neither prebiotic oligosaccharides or probiotic bacteria in their formula, the guts of bottle-fed babies are not optimally colonized.
Most of the microbes that make up a baby’s gut community are acquired during birth — a microbially rich and messy process that exposes the baby to a whole suite of maternal microbes. Babies born by Caesarean, however, a comparatively sterile procedure, do not acquire their mother’s vaginal and intestinal microbes at birth. Their initial gut communities more closely resemble that of their mother’s (and father’s) skin, which is less than ideal and may account for higher rates of allergy, asthma and autoimmune problems in C-section babies: not having been seeded with the optimal assortment of microbes at birth, their immune systems may fail to develop properly.
You acquire most of the initial microbes in your gut community from your parents, but others are picked up from the environment. “The world is covered in a fine patina of feces,” as the Stanford microbiologist Stanley Falkow tells students. The new sequencing tools have confirmed his hunch: Did you know that house dust can contain significant amounts of fecal particles? Or that, whenever a toilet is flushed, some of its contents are aerosolized? Knight’s lab has sequenced the bacteria on toothbrushes. This news came during breakfast, so I didn’t ask for details, but got them anyway: “You want to keep your toothbrush a minimum of six feet away from a toilet,” one of Knight’s colleagues told me.
Some scientists in the field borrow the term “ecosystem services” from ecology to catalog all the things that the microbial community does for us as its host or habitat, and the services rendered are remarkably varied and impressive. “Invasion resistance” is one. Our resident microbes work to keep pathogens from gaining a toehold by occupying potential niches or otherwise rendering the environment inhospitable to foreigners. The robustness of an individual’s gut community might explain why some people fall victim to food poisoning while others can blithely eat the same meal with no ill effects.
Our gut bacteria also play a role in the manufacture of substances like neurotransmitters (including serotonin); enzymes and vitamins (notably Bs and K) and other essential nutrients (including important amino acid and short-chain fatty acids); and a suite of other signaling molecules that talk to, and influence, the immune and the metabolic systems. Some of these compounds may play a role in regulating our stress levels and even temperament: when gut microbes from easygoing, adventurous mice are transplanted into the guts of anxious and timid mice, they become more adventurous. The expression “thinking with your gut” may contain a larger kernel of truth than we thought.
The gut microbes are looking after their own interests, chief among them getting enough to eat and regulating the passage of food through their environment. The bacteria themselves appear to help manage these functions by producing signaling chemicals that regulate our appetite, satiety and digestion. Much of what we’re learning about the microbiome’s role in human metabolism has come from studying “gnotobiotic mice” — mice raised in labs like Jeffrey I. Gordon’s at Washington University, in St. Louis, to be microbially sterile, or germ-free. Recently, Gordon’s lab transplanted the gut microbes of Malawian children with kwashiorkor — an acute form of malnutrition — into germ-free mice. The lab found those mice with kwashiorkor who were fed the children’s typical diet could not readily metabolize nutrients, indicating that it may take more than calories to remedy malnutrition. Repairing a patient’s disordered metabolism may require reshaping the community of species in his or her gut.
Keeping the immune system productively engaged with microbes — exposed to lots of them in our bodies, our diet and our environment — is another important ecosystem service and one that might turn out to be critical to our health. “We used to think the immune system had this fairly straightforward job,” Michael Fischbach, a biochemist at the University of California, San Francisco, says. “All bacteria were clearly ‘nonself’ so simply had to be recognized and dealt with. But the job of the immune system now appears to be far more nuanced and complex. It has to learn to consider our mutualists” — e.g., resident bacteria — “as self too. In the future we won’t even call it the immune system, but the microbial interaction system.” The absence of constructive engagement between microbes and immune system (particularly during certain windows of development) could be behind the increase in autoimmune conditions in the West.
So why haven’t we evolved our own systems to perform these most critical functions of life? Why have we outsourced all this work to a bunch of microbes? One theory is that, because microbes evolve so much faster than we do (in some cases a new generation every 20 minutes), they can respond to changes in the environment — to threats as well as opportunities — with much greater speed and agility than “we” can. Exquisitely reactive and adaptive, bacteria can swap genes and pieces of DNA among themselves. This versatility is especially handy when a new toxin or food source appears in the environment. The microbiota can swiftly come up with precisely the right gene needed to fight it — or eat it. In one recent study, researchers found that a common gut microbe in Japanese people has acquired a gene from a marine bacterium that allows the Japanese to digest seaweed, something the rest of us can’t do as well.
This plasticity serves to extend our comparatively rigid genome, giving us access to a tremendous bag of biochemical tricks we did not need to evolve ourselves. “The bacteria in your gut are continually reading the environment and responding,” says Joel Kimmons, a nutrition scientist and epidemiologist at the Centers for Disease Control and Prevention in Atlanta. “They’re a microbial mirror of the changing world. And because they can evolve so quickly, they help our bodies respond to changes in our environment.”
A handful of microbiologists have begun sounding the alarm about our civilization’s unwitting destruction of the human microbiome and its consequences. Important microbial species may have already gone extinct, before we have had a chance to learn who they are or what they do. What we think of as an interior wilderness may in fact be nothing of the kind, having long ago been reshaped by unconscious human actions. Taking the ecological metaphor further, the “Westernized microbiome” most of us
Preliminary results indicate that a pristine microbiome — of people who have had little or no contact with Westerners — features much greater biodiversity, including a number of species never before sequenced, and, as mentioned, much higher levels of prevotella than is typically found in the Western gut. Dominguez-Bello says these vibrant, diverse and antibiotic-naïve microbiomes may play a role in Amerindians’ markedly lower rates of allergies, asthma, atopic disease and chronic conditions like Type 2 diabetes and cardiovascular disease.
One bacterium commonly found in the non-Western microbiome but nearly extinct in ours is a corkscrew-shaped inhabitant of the stomach by the name of Helicobacter pylori. Dominguez-Bello’s husband, Martin Blaser, a physician and microbiologist at N.Y.U., has been studying H. pylori since the mid-1980s and is convinced that it is an endangered species, the extinction of which we may someday rue. According to the “missing microbiota hypothesis,” we depend on microbes like H. pylori to regulate various metabolic and immune functions, and their disappearance is disordering those systems. The loss is cumulative: “Each generation is passing on fewer of these microbes,” Blaser told me, with the result that the Western microbiome is being progressively impoverished.
He calls H. pylori the “poster child” for the missing microbes and says medicine has actually been trying to exterminate it since 1983, when Australian scientists proposed that the microbe was responsible for peptic ulcers; it has since been implicated in stomach cancer as well. But H. pylori is a most complicated character, the entire spectrum of microbial good and evil rolled into one bug. Scientists learned that H. pylori also plays a role in regulating acid in the stomach. Presumably it does this to render its preferred habitat inhospitable to competitors, but the effect on its host can be salutary. People without H. pylori may not get peptic ulcers, but they frequently do suffer from acid reflux. Untreated, this can lead to Barrett’s esophagus and, eventually, a certain type of esophageal cancer, rates of which have soared in the West as H. pylori has gone missing.
When after a recent bout of acid reflux, my doctor ordered an endoscopy, I discovered that, like most Americans today, my stomach has no H. pylori. My gastroenterologist was pleased, but after talking to Blaser, the news seemed more equivocal, because H. pylori also does us a lot of good. The microbe engages with the immune system, quieting the inflammatory response in ways that serve its own interests — to be left in peace — as well as our own. This calming effect on the immune system may explain why populations that still harbor H. pylori are less prone to allergy and asthma. Blaser’s lab has also found evidence that H. pylori plays an important role in human metabolism by regulating levels of the appetite hormone ghrelin. “When the stomach is empty, it produces a lot of ghrelin, the chemical signal to the brain to eat,” Blaser says. “Then, when it has had enough, the stomach shuts down ghrelin production, and the host feels satiated.” He says the disappearance of H. pylori may be contributing to obesity by muting these signals.
But what about the diseases H. pylori is blamed for? Blaser says these tend to occur only late in life, and he makes the rather breathtaking suggestion that this microbe’s evolutionary role might be to help shuffle us off life’s stage once our childbearing years have passed. So important does Blaser regard this strange, paradoxical symbiont that he has proposed not one but two unconventional therapeutic interventions: inoculate children with H. pylori to give them the benefit of its services early in life, and then exterminate it with antibiotics at age 40, when it is liable to begin causing trouble.
These days Blaser is most concerned about the damage that antibiotics, even in tiny doses, are doing to the microbiome — and particularly to our immune system and weight. “Farmers have been performing a great experiment for more than 60 years,” Blaser says, “by giving subtherapeutic doses of antibiotics to their animals to make them gain weight.” Scientists aren’t sure exactly why this practice works, but the drugs may favor bacteria that are more efficient at harvesting energy from the diet. “Are we doing the same thing to our kids?” he asks. Children in the West receive, on average, between 10 and 20 courses of antibiotics before they turn 18. And those prescribed drugs aren’t the only antimicrobials finding their way to the microbiota; scientists have found antibiotic residues in meat, milk and surface water as well. Blaser is also concerned about the use of antimicrobial compounds in our diet and everyday lives — everything from chlorine washes for lettuce to hand sanitizers. “We’re using these chemicals precisely because they’re antimicrobial,” Blaser says. “And of course they do us some good. But we need to ask, what are they doing to our microbiota?” No one is questioning the value of antibiotics to civilization — they have helped us to conquer a great many infectious diseases and increased our life expectancy. But, as in any war, the war on bacteria appears to have had some unintended consequences.
One of the more striking results from the sequencing of my microbiome was the impact of a single course of antibiotics on my gut community. My dentist had put me on a course of Amoxicillin as a precaution before oral surgery. (Without prophylactic antibiotics, of course, surgery would be considerably more dangerous.) Within a week, my impressively non-Western “alpha diversity” — a measure of the microbial diversity in my gut — had plummeted and come to look very much like the American average. My (possibly) healthy levels of prevotella had also disappeared, to be replaced by a spike in bacteroides (much more common in the West) and an alarming bloom of proteobacteria, a phylum that includes a great many weedy and pathogenic characters, including E. coli and salmonella. What had appeared to be a pretty healthy, diversified gut was now raising expressions of concern among the microbiologists who looked at my data.
“Your E. coli bloom is creepy,” Ruth Ley, a Cornell University microbiologist who studies the microbiome’s role in obesity, told me. “If we put that sample in germ-free mice, I bet they’d get inflamed.” Great. Just when I was beginning to think of myself as a promising donor for a fecal transplant, now I had a gut that would make mice sick. I was relieved to learn that my gut community would eventually bounce back to something resembling its former state. Yet one recent study found that when subjects were given a second course of antibiotics, the recovery of their interior ecosystem was less complete than after the first.
Few of the scientists I interviewed had much doubt that the Western diet was altering our gut microbiome in troubling ways. Some, like Blaser, are concerned about the antimicrobials we’re ingesting with our meals; others with the sterility of processed food. Most agreed that the lack of fiber in the Western diet was deleterious to the microbiome, and still others voiced concerns about the additives in processed foods, few of which have ever been studied for their specific effects on the microbiota. According to a recent article in Nature by the Stanford microbiologist Justin Sonnenburg, “Consumption of hyperhygienic, mass-produced, highly processed and calorie-dense foods is testing how rapidly the microbiota of individuals in industrialized countries can adapt.” As our microbiome evolves to cope with the Western diet, Sonnenburg says he worries that various genes are becoming harder to find as the microbiome’s inherent biodiversity declines along with our everyday exposure to bacteria.
Catherine Lozupone in Boulder and Andrew Gewirtz, an immunologist at Georgia State University, directed my attention to the emulsifiers commonly used in many processed foods — ingredients with names like lecithin, Datem, CMC and polysorbate 80. Gewirtz’s lab has done studies in mice indicating that some of these detergentlike compounds may damage the mucosa — the protective lining of the gut wall — potentially leading to leakage and inflammation.
A growing number of medical researchers are coming around to the idea that the common denominator of many, if not most, of the chronic diseases from which we suffer today may be inflammation — a heightened and persistent immune response by the body to a real or perceived threat. Various markers for inflammation are common in people with metabolic syndrome, the complex of abnormalities that predisposes people to illnesses like cardiovascular disease, obesity, Type 2 diabetes and perhaps cancer. While health organizations differ on the exact definition of metabolic syndrome, a 2009 report from the Centers for Disease Control and Prevention found that 34 percent of American adults are afflicted with the condition. But is inflammation yet another symptom of metabolic syndrome, or is it perhaps the cause of it? And if it is the cause, what is its origin?
One theory is that the problem begins in the gut, with a disorder of the microbiota, specifically of the all-important epithelium that lines our digestive tract. This internal skin — the surface area of which is large enough to cover a tennis court — mediates our relationship to the world outside our bodies; more than 50 tons of food pass through it in a lifetime. The microbiota play a critical role in maintaining the health of the epithelium: some bacteria, like the bifidobacteria and Lactobacillus plantarum (common in fermented vegetables), seem to directly enhance its function. These and other gut bacteria also contribute to its welfare by feeding it. Unlike most tissues, which take their nourishment from the bloodstream, epithelial cells in the colon obtain much of theirs from the short-chain fatty acids that gut bacteria produce as a byproduct of their fermentation of plant fiber in the large intestine.
But if the epithelial barrier isn’t properly nourished, it can become more permeable, allowing it to be breached. Bacteria, endotoxins — which are the toxic byproducts of certain bacteria — and proteins can slip into the blood stream, thereby causing the body’s immune system to mount a response. This resulting low-grade inflammation, which affects the entire body, may lead over time to metabolic syndrome and a number of the chronic diseases that have been linked to it.
Evidence in support of this theory is beginning to accumulate, some of the most intriguing coming from the lab of Patrice Cani at the Université Catholique de Louvain in Brussels. When Cani fed a high-fat, “junk food” diet to mice, the community of microbes in their guts changed much as it does in humans on a fast-food diet. But Cani also found the junk-food diet made the animals’ gut barriers notably more permeable, allowing endotoxins to leak into the bloodstream. This produced a low-grade inflammation that eventually led to metabolic syndrome. Cani concludes that, at least in mice, “gut bacteria can initiate the inflammatory processes associated with obesity and insulin resistance” by increasing gut permeability.
These and other experiments suggest that inflammation in the gut may be the cause of metabolic syndrome, not its result, and that changes in the microbial community and lining of the gut wall may produce this inflammation. If Cani is correct — and there is now some evidence indicating that the same mechanism is at work in humans — then medical science may be on the trail of a Grand Unified Theory of Chronic Disease, at the very heart of which we will find the gut microbiome.
My first reaction to learning all this was to want to do something about it immediately, something to nurture the health of my microbiome. But most of the scientists I interviewed were reluctant to make practical recommendations; it’s too soon, they told me, we don’t know enough yet. Some of this hesitance reflects an understandable abundance of caution. The microbiome researchers don’t want to make the mistake of overpromising, as the genome researchers did. They are also concerned about feeding a gigantic bloom of prebiotic and probiotic quackery and rightly so: probiotics are already being hyped as the new panacea, even though it isn’t at all clear what these supposedly beneficial bacteria do for us or how they do what they do. There is some research suggesting that some probiotics may be effective in a number of ways: modulating the immune system; reducing allergic response; shortening the length and severity of colds in children; relieving diarrhea and irritable bowel symptoms; and improving the function of the epithelium. The problem is that, because the probiotic marketplace is largely unregulated, it’s impossible to know what, if anything, you’re getting when you buy a “probiotic” product. One study tested 14 commercial probiotics and found that only one contained the exact species stated on the label.
But some of the scientists’ reluctance to make recommendations surely flows from the institutional bias of science and medicine: that the future of microbiome management should remain firmly in the hands of science and medicine. Down this path — which holds real promise — lie improved probiotics and prebiotics, fecal transplants (with better names) and related therapies. Jeffrey Gordon, one of those scientists who peers far over the horizon, looks forward to a time when disorders of the microbiome will be treated with “synbiotics” — suites of targeted, next-generation probiotic microbes administered along with the appropriate prebiotic nutrients to nourish them. The fecal transplant will give way to something far more targeted: a purified and cultured assemblage of a dozen or so microbial species that, along with new therapeutic foods, will be introduced to the gut community to repair “lesions” — important missing species or functions. Yet, assuming it all works as advertised, such an approach will also allow Big Pharma and Big Food to stake out and colonize the human microbiome for profit.
When I asked Gordon about do-it-yourself microbiome management, he said he looked forward to a day “when people can cultivate this wonderful garden that is so influential in our health and well-being” — but that day awaits a lot more science. So he declined to offer any gardening tips or dietary advice. “We have to manage expectations,” he said.
Alas, I am impatient. So I gave up asking scientists for recommendations and began asking them instead how, in light of what they’ve learned about the microbiome, they have changed their own diets and lifestyles. Most of them have made changes. They were slower to take, or give their children, antibiotics. (I should emphasize that in no way is this an argument for the rejection of antibiotics when they are medically called for.) Some spoke of relaxing the sanitary regime in their homes, encouraging their children to play outside in the dirt and with animals — deliberately increasing their exposure to the great patina. Many researchers told me they had eliminated or cut back on processed foods, either because of its lack of fiber or out of concern about additives. In general they seemed to place less faith in probiotics (which few of them used) than in prebiotics — foods likely to encourage the growth of “good bacteria” already present. Several, including Justin Sonnenburg, said they had added fermented foods to their diet: yogurt, kimchi, sauerkraut. These foods can contain large numbers of probiotic bacteria, like L. plantarum and bifidobacteria, and while most probiotic bacteria don’t appear to take up permanent residence in the gut, there is evidence that they might leave their mark on the community, sometimes by changing the gene expression of the permanent residents — in effect turning on or off metabolic pathways within the cell — and sometimes by stimulating or calming the immune response.
What about increasing our exposure to bacteria? “There’s a case for dirtying up your diet,” Sonnenburg told me. Yet advising people not to thoroughly wash their produce is probably unwise in a world of pesticide residues. “I view it as a cost-benefit analysis,” Sonnenburg wrote in an e-mail. “Increased exposure to environmental microbes likely decreases chance of many Western diseases, but increases pathogen exposure. Certainly the costs go up as scary antibiotic-resistant bacteria become more prevalent.” So wash your hands in situations when pathogens or toxic chemicals are likely present, but maybe not after petting your dog. “In terms of food, I think eating fermented foods is the answer — as opposed to not washing food, unless it is from your garden,” he said.
With his wife, Erica, also a microbiologist, Sonnenburg tends a colony of gnotobiotic mice at Stanford, examining (among other things) the effects of the Western diet on their microbiota. (Removing fiber drives down diversity, but the effect is reversible.) He’s an amateur baker, and when I visited his lab, we talked about the benefits of baking with whole grains.
“Fiber is not a single nutrient,” Sonnenburg said, which is why fiber supplements are no magic bullet. “There are hundreds of different polysaccharides” — complex carbohydrates, including fiber — “in plants, and different microbes like to chomp on different ones.” To boost fiber, the food industry added lots of a polysaccharide called inulin to hundreds of products, but that’s just one kind (often derived from the chicory-plant root) and so may only favor a limited number of microbes. I was hearing instead an argument for a variety of whole grains and a diverse diet of plants and vegetables as well as fruits. “The safest way to increase your microbial biodiversity is to eat a variety of polysaccharides,” he said.
His comment chimed with something a gastroenterologist at the University of Pittsburgh told me. “The big problem with the Western diet,” Stephen O’Keefe said, “is that it doesn’t feed the gut, only the upper G I. All the food has been processed to be readily absorbed, leaving nothing for the lower G I. But it turns out that one of the keys to health is fermentation in the large intestine.” And the key to feeding the fermentation in the large intestine is giving it lots of plants with their various types of fiber, including resistant starch (found in bananas, oats, beans); soluble fiber (in onions and other root vegetables, nuts); and insoluble fiber (in whole grains, especially bran, and avocados).
With our diet of swiftly absorbed sugars and fats, we’re eating for one and depriving the trillion of the food they like best: complex carbohydrates and fermentable plant fibers. The byproduct of fermentation is the short-chain fatty acids that nourish the gut barrier and help prevent inflammation. And there are studies suggesting that simply adding plants to a fast-food diet will mitigate its inflammatory effect.
The outlines of a diet for the new superorganism were coming clear, and it didn’t require the ministrations of the food scientists at Nestlé or General Mills to design it. Big Food and Big Pharma probably do have a role to play, as will Jeffrey Gordon’s next-generation synbiotics, in repairing the microbiota of people who can’t or don’t care to simply change their diets. This is going to be big business. Yet the components of a microbiota-friendly diet are already on the supermarket shelves and in farmers’ markets.
Viewed from this perspective, the foods in the markets appear in a new light, and I began to see how you might begin to shop and cook with the microbiome in mind, the better to feed the fermentation in our guts. The less a food is processed, the more of it that gets safely through the gastrointestinal tract and into the eager clutches of the microbiota. Al dente pasta, for example, feeds the bugs better than soft pasta does; steel-cut oats better than rolled; raw or lightly cooked vegetables offer the bugs more to chomp on than overcooked, etc. This is at once a very old and a very new way of thinking about food: it suggests that all calories are not created equal and that the structure of a food and how it is prepared may matter as much as its nutrient composition.
It is a striking idea that one of the keys to good health may turn out to involve managing our internal fermentation. Having recently learned to manage several external fermentations — of bread and kimchi and beer — I know a little about the vagaries of that process. You depend on the microbes, and you do your best to align their interests with yours, mainly by feeding them the kinds of things they like to eat — good “substrate.” But absolute control of the process is too much to hope for. It’s a lot more like gardening than governing.
The successful gardener has always known you don’t need to master the science of the soil, which is yet another hotbed of microbial fermentation, in order to nourish and nurture it. You just need to know what it likes to eat — basically, organic matter — and how, in a general way, to align your interests with the interests of the microbes and the plants. The gardener also discovers that, when pathogens or pests appear, chemical interventions “work,” that is, solve the immediate problem, but at a cost to the long-term health of the soil and the whole garden. The drive for absolute control leads to unanticipated forms of disorder.
This, it seems to me, is pretty much where we stand today with respect to our microbiomes — our teeming, quasi-wilderness. We don’t know a lot, but we probably know enough to begin taking better care of it. We have a pretty good idea of what it likes to eat, and what strong chemicals do to it. We know all we need to know, in other words, to begin, with modesty, to tend the unruly garden within.

In health,
________________________________

Kari J. Kindem, CFHom, CEASE Practitioner, Classical Homeopath....Let Miracles Find You!

www.HomeopathyForWomen.org
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ARTICLE & FILM: Blockbuster documentary "$tatin Nation" reveals the great cholesterol cover-up

http://www.naturalnews.com/040233_Statin_Nation_cholesterol_drugs_movie_trailer.html

Blockbuster documentary '$tatin Nation' reveals the great cholesterol cover-up

Wednesday, May 08, 2013
by Mike Adams, the Health Ranger

Click here to watch the powerful preview trailer on Natural News.

Cholesterol drugs are based on the intentional misrepresentation of medical evidence

$tatin Nation is the first film to publicly question the Big Pharma narrative on statin drugs. It explores these three shocking facts that are now emerging in the medical literature:

1) People with high cholesterol tend to live longer

2) People with heart disease tend to have low levels of cholesterol

3) Cholesterol-lowering on a population level does not reduce the rate of heart disease

Huh? But your doctor told you exactly the opposite, right? That's because your doctor has been brainwashed or bribed by the drug companies that now generate $29 billion dollars a year from selling statin drugs.

Your doctor needs to see this film! Show him the trailer at:
http://programs.naturalnews.com/Statin_Nation__NN.htm

Meet filmmaker Justin Smith

Justin Smith, the creator of $tatin Nation, is also the author of $29 Billion Reasons to Lie About Cholesterol. He has a degree in engineering and was a competitive cyclist before turning to research and filmmaking.

Here's some Q&A with Justin Smith:

Why did you make this film?

I have made this film out of sheer frustration with the current situation. To date, most of the information that people receive about this subject is provided directly or indirectly by the pharmaceutical companies. This information is heavily biased, of course, toward increasing company profits, with a disregard for peoples' health.

In the film, you raise some important issues concerning statin medications. How would you like people to react to this?

My approach, with this film, is to provide people with information to make better informed decisions about their own health. Each person should make a personal decision about the issues raised. I hope that the film will prompt more people to ask their doctor important questions like: if I take this cholesterol medication, how much longer might I live? This question is important because most people will not receive any life extension from statins. While statins may, in some cases, slightly reduce the risk of heart problems, at the same time statins also increase the risk for other serious diseases. So, overall there is usually no net benefit.

There is some evidence that cholesterol medications can be beneficial for middle-aged men who have already had at least one heart attack. However, the benefit here has got nothing to do with cholesterol lowering. It relates to the positive effects that statins can have on inflammation and plaque stabilization. In this situation, there is some life extension, but it is difficult to say how much. The life extension even here may still only be a few days or weeks and this, of course, has to be balanced against the adverse effects of statins.

In addition, there is a well established connection between low cholesterol levels and a shorter life span. So, even if the statin was beneficial during middle-age, the adverse effects are likely to drastically outweigh any positive effects as the person reaches old age.

Was the film commissioned / How was the film funded?
I desperately wanted to make this film and I knew that getting it commissioned would be difficult and time consuming. Therefore. I invested some money myself and managed to raise money from crowd funding.

In addition, I managed to build a crew of people who are also passionate about this subject and would be willing to work on a deferred payment basis. The crew have all been willing to defer their payment until the film is released.

Originally, I planned to go through the traditional route (festivals and commissioning editors etc.) once the film was finished. However, I am concerned that this might take several months to a year, possibly longer, and I have a burning desire to expose this issue as soon as possible.

Personally, I feel that the timing is right to present this information to people. I hope to gain the interest of a major broadcaster in the UK, in the United States, or elsewhere but in the meantime I plan to release the film online via video on demand.

Do you think that people can freely consume cholesterol-rich foods?

Well, the idea that saturated fats and cholesterol simply clog-up the arteries has never been proven scientifically. It was just an idea.

In addition, there are many fascinating facts, such as the foods that contain cholesterol also contain large amounts of the nutrients that we know protect the heart. We have been told to avoid cholesterol-rich foods, but these foods often contain antioxidants and high levels of vitamins that keep our arteries healthy.

Click here for full access to $tation Nation from Natural News.

Learn more: http://www.naturalnews.com/040233_Statin_Nation_cholesterol_drugs_movie_trailer.html#ixzz2SjU1wXV3