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Old 08-19-2015, 02:19 PM   #381
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Here's an article discussing the study Joe posted:

Whole Health Source: More Thoughts on the Recent Low-fat vs. Low-carb Metabolic Ward Study

Mostly what's already been mentioned, plus 1 more:

- The reason the low-fat group lost more fat in the 6 day test is probably that the low-carb group was burning through their glycogen stores. A longer test may have shown different results. This reasoning is based on deduction from earlier studies.
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Old 10-16-2015, 12:35 AM   #382
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Scientists Have Developed a Pill to Help Gluten-Intolerant People -- Grub Street


Scientists Have Developed a Pill to Help Gluten-Intolerant People
By Clint Rainey

Canadian scientists are working on a pill that could help people who can't digest gluten. This might cause some panic for actual gluten-free people, half of whom do actually get sick, and half of whom just read Goop. ("I've only been gluten-free for a week, but I'm already really annoying," as that New Yorker cartoon quips.)

Hoon Sunwoo, a professor at the University of Alberta, says that he and his team have developed an antibody out of chicken yolks that prevents the absorption of the troublesome component of gluten known as gliadin. "This supplement binds with gluten in the stomach and help to neutralize it," Sunwoo explains, "therefore providing defense to the small intestine, limiting the damage gliadin causes."

Celiacs and gluten-senstives can swallow the pill a few minutes before eating, and researchers say it opens a one- to two-hour window where they can gorge on bread, pasta, and beer with impunity (side effects to their waistlines perhaps notwithstanding). Clinical trials are supposed to kick off within the year, and the pill could be for sale in Canada as soon as three years from now. Sunwoo tells Quartz that it's expected to be sold as a simple over-the-counter med, just like Tylenol.

[UPI, Quartz]
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Old 10-19-2015, 10:45 AM   #383
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Old 11-05-2015, 10:15 PM   #384
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Processed white bread promotes healthy gut biome:

New Study Suggests Some People Still Think White Bread Is Awesome


Booyah, whole wheat! In your face! Photo: Shutterstock


Entry-level plain white bread, with all its bleached flour, trouble-making gluten, and uncouth carbohydrates, really lost a lot of love from the good sandwich-making people of the United States during the last few years. It's been a victim of local food movements and fad diets, on a clear decline since 2010 when whole wheat surpassed white for the first time ever and everybody basically cheered. Sales are down again this year; 56 percent of shoppers say they want nothing at all to do with white bread; and hell, we even almost lost Wonder Bread when parent company Hostess foundered. But a new study conducted at the University of Oviedo in Spain says, essentially, maybe it's time to stop the hate.

A team of seven researchers looked at fibers and polyphenols found in white bread and oranges, respectively, with relation to production of intestinal microbiota, the vast bacterial colonies that do the heaviest lifting of your digestive process. "In terms of food consumption," researchers write, "probably the most novel finding of our study was the positive association between the intake of white bread and Lactobacillus levels." Specifically, people who ate more white bread had higher numbers of Lactobacilli, which is generally believed to be a good thing and runs contrary to the notion that a favored "prebiotic effect of cereals" comes from whole grain foods. In other words: Up yours, whole wheat.

While the authors of the paper, which appeared in the Journal of Agricultural and Food Chemistry last month, write that a number of other factors — everything from mastication to more variables of the other stuff that gets eaten with white bread, like good pickles and fatty brisket — need consideration in subsequent experiments, let's just call it peanut butter jelly time. "[O]ur results reveal that the consumption of refined grains, often undervalued in this regard, could beneficially modulate intestinal microbiota," the researchers write.
Article: New Study Suggests Some People Still Think White Bread Is Awesome -- Grub Street

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Old 11-08-2015, 09:10 PM   #385
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Effect of low-fat diet interventions versus other diet interventions on long-term weight change in adults: a systematic review and meta-analysis

Quote:
Summary

Background


The effectiveness of low-fat diets for long-term weight loss has been debated for decades, with many randomised controlled trials (RCTs) and recent reviews giving mixed results. We aimed to summarise the large body of evidence from RCTs to determine whether low-fat diets contribute to greater weight loss than participants' usual diet, low-carbohydrate diets, and other higher-fat dietary interventions.

Methods

We did a systematic review and random effects meta-analysis of RCTs comparing the long-term effect (≥1 year) of low-fat and higher-fat dietary interventions on weight loss by searching MEDLINE, Embase, Cochrane Central Register of Controlled Trials (CENTRAL), and Cochrane Database of Systematic Reviews to identify eligible trials published from database inception up until July 31, 2014. We excluded trials if one intervention group included a non-dietary weight loss component but the other did not, and trials of dietary supplements or meal replacement drink interventions. Data including the main outcome measure of mean difference in weight change between interventions, and whether interventions were intended to lead to weight loss, weight maintenance, or neither, were extracted from published reports. We estimated the pooled weighted mean difference (WMD) with a DerSimonian and Laird random effects method.

Findings

3517 citations were identified by the search and 53 studies met our inclusion criteria, including 68 128 participants (69 comparisons). In weight loss trials, low-carbohydrate interventions led to significantly greater weight loss than did low-fat interventions (18 comparisons; WMD 1·15 kg [95% CI 0·52 to 1·79]; I2=10%). Low-fat interventions did not lead to differences in weight change compared with other higher-fat weight loss interventions (19 comparisons; WMD 0·36 kg [−0·66 to 1·37; I2=82%), and led to a greater weight decrease only when compared with a usual diet (eight comparisons; −5·41 kg [−7·29 to −3·54]; I2=68%). Similarly, results of non-weight-loss trials and weight maintenance trials, for which no low-carbohydrate comparisons were made, showed that low-fat versus higher-fat interventions have a similar effect on weight loss, and that low-fat interventions led to greater weight loss only when compared with usual diet. In weight loss trials, higher-fat weight loss interventions led to significantly greater weight loss than low-fat interventions when groups differed by more than 5% of calories obtained from fat at follow-up (18 comparisons; WMD 1·04 kg [95% CI 0·06 to 2·03]; I2=78%), and when the difference in serum triglycerides between the two interventions at follow-up was at least 0·06 mmol/L (17 comparisons; 1·38 kg [0·50 to 2·25]; I2=62%).

Interpretation

These findings suggest that the long-term effect of low-fat diet intervention on bodyweight depends on the intensity of the intervention in the comparison group. When compared with dietary interventions of similar intensity, evidence from RCTs does not support low-fat diets over other dietary interventions for long-term weight loss.
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Old 11-18-2015, 08:35 PM   #387
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This is absolutely amazing research.

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Old 11-19-2015, 12:30 AM   #388
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Quote:
Originally Posted by sixshooter View Post
This is absolutely amazing research.
That was an extremely interesting and informative lecture. I'm not being the least bit sarcastic.

But it was more than a trifle abstract.

Serious question: how do I sterilize my innards and populate my gut with skinny-mouse biome? What factors determine, in the aforetomentioned identical-twin studies, which twin develops "obese" gut flora vs. "skinny" gut flora?

Or, how does one apply these findings?
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Old 11-19-2015, 04:25 PM   #389
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Get the skinniest person your age to vomit into your mouth. This doesn't count if their skinny is due to anorexia nervosa or marathoning.

..



No idea if it'll work, but please film it.
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Old 11-19-2015, 05:52 PM   #390
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Quote:
Originally Posted by y8s View Post
Get the skinniest person your age to vomit into your mouth.
If I understand the science correctly, I'd actually need for them to **** into my mouth.



To paraphrase XKCD, I'm assuming there's an easier way.


"I know it seems unpleasant, but of the two ways we typically transfer them, I promise this is the one you want."
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Old 11-19-2015, 07:11 PM   #391
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You might be right.

And you can wash it down with this guy's vomit:

Beer Gut: Man?s Belly Brews Own Beer | National Geographic (blogs)
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Old 11-19-2015, 08:01 PM   #392
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This is amazing research with huge implications.

I hope the islamic caliphate doesn't blow them up for being Jews before they can finish their research. /isis rant
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Old 11-19-2015, 08:43 PM   #393
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No no, you need them to **** in your anus. It might be easier to just do an alaskan pipeline.
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Old 11-19-2015, 08:48 PM   #394
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Fecal transplant therapy is about to get a lot less icky*.

$635 poop pills cure deadly gastrointestinal infection | Ars Technica




*Still pretty icky, but then if you can't eat without shitting your pants 30 minutes later, you're probably not so concerned with the ickiness of the treatment.
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Old 11-20-2015, 09:59 AM   #395
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Six's video led me down an interesting path of Googling. Specifically, there's a fair bit of work being done in both identification of the functions of various gut flora, as well as the transplantation of said critters not just for disease-prevention as MG notes, but also specifically to combat obesity.
How Gut Bacteria Help Make Us Fat and Thin
Intestinal bacteria may help determine whether we are lean or obese
By Claudia Wallis | Jun 1, 2014

For the 35 percent of American adults who do daily battle with obesity, the main causes of their condition are all too familiar: an unhealthy diet, a sedentary lifestyle and perhaps some unlucky genes. In recent years, however, researchers have become increasingly convinced that important hidden players literally lurk in human bowels: billions on billions of gut microbes.

Throughout our evolutionary history, the microscopic denizens of our intestines have helped us break down tough plant fibers in exchange for the privilege of living in such a nutritious broth. Yet their roles appear to extend beyond digestion. New evidence indicates that gut bacteria alter the way we store fat, how we balance levels of glucose in the blood, and how we respond to hormones that make us feel hungry or full. The wrong mix of microbes, it seems, can help set the stage for obesity and diabetes from the moment of birth.

Fortunately, researchers are beginning to understand the differences between the wrong mix and a healthy one, as well as the specific factors that shape those differences. They hope to learn how to cultivate this inner ecosystem in ways that could prevent—and possibly treat—obesity, which doctors define as having a particular ratio of height and weight, known as the body mass index, that is greater than 30. Imagine, for example, foods, baby formulas or supplements devised to promote virtuous microbes while suppressing the harmful types. “We need to think about designing foods from the inside out,” suggests Jeffrey Gordon of Washington University in St. Louis. Keeping our gut microbes happy could be the elusive secret to weight control.


An Inner Rain Forest

Researchers have long known that the human body is home to all manner of microorganisms, but only in the past decade or so have they come to realize that these microbes outnumber our own cells 10 to one. Rapid gene-sequencing techniques have revealed that the biggest and most diverse metropolises of “microbiota” reside in the large intestine and mouth, although impressive communities also flourish in the genital tract and on our skin.

Each of us begins to assemble a unique congregation of microbes the moment we pass through the birth canal, acquiring our mother's bacteria first and continuing to gather new members from the environment throughout life. By studying the genes of these various microbes—collectively referred to as the microbiome—investigators have identified many of the most common residents, although these can vary greatly from person to person and among different human populations. In recent years researchers have begun the transition from mere census taking to determining the kind of jobs these minute inhabitants fill in the human body and the effect they have on our overall health.

An early hint that gut microbes might play a role in obesity came from studies comparing intestinal bacteria in obese and lean individuals. In studies of twins who were both lean or both obese, researchers found that the gut community in lean people was like a rain forest brimming with many species but that the community in obese people was less diverse—more like a nutrient-overloaded pond where relatively few species dominate. Lean individuals, for example, tended to have a wider variety of Bacteroidetes, a large tribe of microbes that specialize in breaking down bulky plant starches and fibers into shorter molecules that the body can use as a source of energy.

Documenting such differences does not mean the discrepancies are responsible for obesity, however. To demonstrate cause and effect, Gordon and his colleagues conducted an elegant series of experiments with so-called humanized mice, published last September in Science. First, they raised genetically identical baby rodents in a germ-free environment so that their bodies would be free of any bacteria. Then they populated their guts with intestinal microbes collected from obese women and their lean twin sisters (three pairs of fraternal female twins and one set of identical twins were used in the studies). The mice ate the same diet in equal amounts, yet the animals that received bacteria from an obese twin grew heavier and had more body fat than mice with microbes from a thin twin. As expected, the fat mice also had a less diverse community of microbes in the gut.

Gordon's team then repeated the experiment with one small twist: after giving the baby mice microbes from their respective twins, they moved the animals into a shared cage. This time both groups remained lean. Studies showed that the mice carrying microbes from the obese human had picked up some of their lean roommates' gut bacteria—especially varieties of Bacteroidetes—probably by consuming their feces, a typical, if unappealing, mouse behavior. To further prove the point, the researchers transferred 54 varieties of bacteria from some lean mice to those with the obese-type community of germs and found that the animals that had been destined to become obese developed a healthy weight instead. Transferring just 39 strains did not do the trick. “Taken together, these experiments provide pretty compelling proof that there is a cause-and-effect relationship and that it was possible to prevent the development of obesity,” Gordon says.


Gordon theorizes that the gut community in obese mice has certain “job vacancies” for microbes that perform key roles in maintaining a healthy body weight and normal metabolism. His studies, as well as those by other researchers, offer enticing clues about what those roles might be. Compared with the thin mice, for example, Gordon's fat mice had higher levels in their blood and muscles of substances known as branched-chain amino acids and acylcarnitines. Both these chemicals are typically elevated in people with obesity and type 2 diabetes.

Another job vacancy associated with obesity might be one normally filled by a stomach bacterium called Helicobacter pylori. Research by Martin Blaser of New York University suggests that it helps to regulate appetite by modulating levels of ghrelin—a hunger-stimulating hormone. H. pylori was once abundant in the American digestive tract but is now rare, thanks to more hygienic living conditions and the use of antibiotics, says Blaser, author of a new book entitled Missing Microbes.

Diet is an important factor in shaping the gut ecosystem. A diet of highly processed foods, for example, has been linked to a less diverse gut community in people. Gordon's team demonstrated the complex interaction among food, microbes and body weight by feeding their humanized mice a specially prepared unhealthy chow that was high in fat and low in fruits, vegetables and fiber (as opposed to the usual high-fiber, low-fat mouse kibble). Given this “Western diet,” the mice with obese-type microbes proceeded to grow fat even when housed with lean cagemates. The unhealthy diet somehow prevented the virtuous bacteria from moving in and flourishing.

The interaction between diet and gut bacteria can predispose us to obesity from the day we are born, as can the mode by which we enter the world. Studies have shown that both formula-fed babies and infants delivered by cesarean section have a higher risk for obesity and diabetes than those who are breast-fed or delivered vaginally. Working together, Rob Knight of the University of Colorado Boulder and Maria Gloria Dominguez-Bello of N.Y.U. have found that as newborns traverse the birth canal, they swallow bacteria that will later help them digest milk. C-section babies skip this bacterial baptism. Babies raised on formula face a different disadvantage: they do not get substances in breast milk that nurture beneficial bacteria and limit colonization by harmful ones. According to a recent Canadian study, babies drinking formula have bacteria in their gut that are not seen in breast-fed babies until solid foods are introduced. Their presence before the gut and immune system are mature, says Dominguez-Bello, may be one reason these babies are more susceptible to allergies, asthma, eczema and celiac disease, as well as obesity.

A new appreciation for the impact of gut microbes on body weight has intensified concerns about the profligate use of antibiotics in children. Blaser has shown that when young mice are given low doses of antibiotics, similar to what farmers give livestock, they develop about 15 percent more body fat than mice that are not given such drugs. Antibiotics may annihilate some of the bacteria that help us maintain a healthy body weight. “Antibiotics are like a fire in the forest,” Dominguez-Bello says. “The baby is forming a forest. If you have a fire in a forest that is new, you get extinction.” When Laurie ***, a graduate student in Blaser's laboratory, combined a high-fat diet with the antibiotics, the mice became obese. “There's a synergy,” Blaser explains. He notes that antibiotic use varies greatly from state to state in the U.S., as does the prevalence of obesity, and intriguingly, the two maps line up—with both rates highest in parts of the South.


Beyond Probiotics

Many scientists who work on the microbiome think their research will inspire a new generation of tools to treat and prevent obesity. Still, researchers are quick to point out that this is a young field with far more questions than answers. “Data from human studies are a lot messier than the mouse data,” observes Claire Fraser of the University of Maryland, who is studying obesity and gut microbes in the Old Order Amish population. Even in a homogeneous population such as the Amish, she says, there is vast individual variation that makes it difficult to isolate the role of microbiota in a complex disease like obesity.

Even so, a number of scientists are actively developing potential treatments. Dominguez-Bello, for example, is conducting a clinical trial in Puerto Rico in which babies born by cesarean section are immediately swabbed with a gauze cloth laced with the mother's vaginal fluids and resident microbes. She will track the weight and overall health of the infants in her study, comparing them with C-section babies who did not receive the gauze treatment.

A group in Amsterdam, meanwhile, is investigating whether transferring feces from lean to overweight people will lead to weight loss. U.S. researchers tend to view such “fecal transplants” as imprecise and risky. A more promising approach, says Robert Karp, who oversees National Institutes of Health grants related to obesity and the microbiome, is to identify the precise strains of bacteria associated with leanness, determine their roles and develop treatments accordingly. Gordon has proposed enriching foods with beneficial bacteria and any nutrients needed to establish them in the gut—a science-based version of today's probiotic yogurts. No one in the field believes that probiotics alone will win the war on obesity, but it seems that, along with exercising and eating right, we need to enlist our inner microbial army.
How Gut Bacteria Help Make Us Fat and Thin - Scientific American
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Old 11-23-2015, 11:24 PM   #396
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Watch from 5:30-10:30 for information regarding Hitler's dietary habits, the color and consistency of his feces, his general health and medical problems, and how a little-known **** physician by the name of Theodor Morell used fecal bacteriotherapy (poop transplantation) to treat the Führer's digestive ailments.



I post this purely to shine light on the rather interesting fact that such diagnoses and treatments as are being hailed as "revolutionary" over the past few years were, in fact, known to German medicine (if, admittedly, on the fringes of then-credible science) in the 1930s.
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Old 11-24-2015, 11:16 AM   #397
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Old 11-24-2015, 12:23 PM   #398
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Gut flora appears to play a huge role in autoimmune disease:
Does the Gut Microbiome Play a Role in Autoimmune Disease?
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Old 11-24-2015, 12:53 PM   #399
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I liked this thread when it wasnt so shitty.
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Old 12-11-2015, 12:28 PM   #400
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A Protein In The Gut May Explain Why Some Can't Stomach Gluten
December 9, 20156:01 PM ET


Those who avoid gluten may not be food faddists after all. Researchers are finally homing in on markers for gluten sensitivity in the body.

If you've found that you are sensitive to gluten — the stretchy protein that makes wheat bread fluffy and pie crusts crisp – perhaps you've had to bear the brunt of the gluten-free backlash.

Some 47 percent of American consumers say the gluten-free diet is a fad, according to Mintel research. And that's partly because there's been scant proof of what causes non-celiac gluten sensitivity. As far as diagnosing it goes, there's nothing akin to the gold standard tests that help diagnose the one percent of the population that has celiac disease.

But those who shun gluten (and don't have celiac disease) may not be food faddists after all. Researchers are finally homing in on markers for gluten sensitivity in the body. A study from Giovanni Barbara and his team at the University of Bologna, Italy, suggests that gluten sensitive individuals may harbor high levels of a molecule called zonulin that is linked to inflammation.

Levels of zonulin in the blood have already shown to be high in celiacs. In Barbara's study, levels in gluten-sensitive individuals almost matched those of celiacs. Though the results are preliminary, they point in a hopeful direction for future tests to help diagnose this controversial condition.

About 6 percent of the global population may be sensitive to gluten, according to gastroenterologist Alessio Fasano of Massachusetts General Hospital in Boston. Symptoms can be similar to irritable bowel syndrome, with abdominal pain, bloating, alternating diarrhea or constipation. And there can be other symptoms, including "brain fog", headache, fatigue, joint and muscle pain.

Enter zonulin, stage left. Zonulin is an inflammatory protein first discovered by Fasano and his team in 2000. It helps regulate leakiness in the gut by opening and closing the spaces or "junctions" between cells in the lining of the digestive tract. Zonulin is triggered by harmful bacteria, and offers important protection to the body: If you accidentally eat a food contaminated with salmonella, you rely on zonulin to help trigger diarrhea and flush out the bugs.

Once the pathogen is gone, zonulin levels drop and the junctions close.

So what does it have to do with gluten? It turns out that gluten is a strong trigger of zonulin in some individuals. "No human being completely digests gluten," says Fasano. "And in a small percentage of us, that undigested gluten triggers the release of zonulin," leading to high levels of it.

To test the theory, Giovanni Barbara and a team of researchers at the University of Bologna measured blood levels of zonulin in four groups of individuals: those with celiac disease, those with irritable bowel syndrome marked by diarrhea, those with self-diagnosed gluten sensitivity and healthy volunteers. Both celiacs and gluten sensitives turned up with remarkably high levels of zonulin in their blood. Those with IBS had elevated levels but less than half of celiacs or gluten sensitive individuals. Healthy volunteers had negligible blood levels of zonulin.

The results were presented in October as an abstract at the 23rd United European Gastroenterology Week in Barcelona, Spain. "I was very surprised, but not only by the zonulin levels," says Barbara. "In our study, gluten-sensitive individuals who responded to a gluten-free diet had a genetic predisposition to celiac disease. They had no evidence of celiac, but they did have the vulnerable genes that put a person at risk of celiac."

Despite having found two potential biomarkers, Barbara cautions that it's far too soon to recommend any kind of clinical testing. "We need more research to determine the clinical usefulness of these markers .... Other laboratories need to reproduce our data, and we need to repeat our own experiment with gluten sensitive patients who have been identified by strict criteria in double blind studies." Barbara adds that his center only sees the most severe patients who been unsuccessful finding treatment elsewhere, which may have influenced the results.

Fasano, who was not involved in Barbara's study, says the discovery of zonulin is part of a larger evolving picture. "This molecule is extremely important in a lot of illness, from Type 1 diabetes to other autoimmune diseases. Many illnesses link back to loss of barrier function in the gut." Soon, a trial will begin to test whether it's possible to shut down zonulin production in the gut for a few hours.

"It would be really great," says Fasano, "if we had a safe medication that could keep this molecule at bay and offer help for celiac disease, gluten sensitivity, and perhaps other conditions."


A Protein In The Gut May Explain Why Some Can't Stomach Gluten : The Salt : NPR
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