Video: Gluten sensitivity may exist mostly in the mind

What’s really behind ‘gluten sensitivity’?

Video: Gluten sensitivity may exist mostly in the mind

The patients weren't crazy—Knut Lundin was sure of that. But their ailment was a mystery. They were convinced gluten was making them sick. Yet they didn't have celiac disease, an autoimmune reaction to that often-villainized tangle of proteins in wheat, barley, and rye. And they tested negative for a wheat allergy. They occupied a medical no man's land.

About a decade ago, gastroenterologists Lundin, based at the University of Oslo, came across more and more of those enigmatic cases. “I worked with celiac disease and gluten for so many years,” he says, “and then came this wave.

” Gluten-free choices began appearing on restaurant menus and creeping onto grocery store shelves. By 2014, in the United States alone, an estimated 3 million people without celiac disease had sworn off gluten.

It was easy to assume that people claiming to be “gluten sensitive” had just been roped into a food fad.

“Generally, the reaction of the gastroenterologist [was] to say, ‘You don't have celiac disease or wheat allergy. Goodbye,’” says Armin Alaedini, an immunologist at Columbia University. “A lot of people thought this is perhaps due to some other [food] sensitivity, or it's in people's heads.”

But a small community of researchers started searching for a link between wheat components and patients' symptoms—commonly abdominal pain, bloating, and diarrhea, and sometimes headaches, fatigue, rashes, and joint pain. That wheat really can make nonceliac patients sick is now widely accepted. But that's about as far as the agreement goes.

As data trickle in, entrenched camps have emerged. Some researchers are convinced that many patients have an immune reaction to gluten or another substance in wheat—a nebulous illness sometimes called nonceliac gluten sensitivity (NCGS).

Others believe most patients are actually reacting to an excess of poorly absorbed carbohydrates present in wheat and many other foods.

Those carbohydrates—called FODMAPs, for fermentable oligosaccharides, disaccharides, monosaccharides, and polyols—can cause bloating when they ferment in the gut.

If FODMAPs are the primary culprit, thousands of people may be on gluten-free diets with the support of their doctors and dietitians but without good reason.

Those competing theories were on display in a session on wheat sensitivity at a celiac disease symposium held at Columbia in March. In back-to-back talks, Lundin made the case for FODMAPs, and Alaedini for an immune reaction. But in an irony that underscores how muddled the field has become, both researchers started their quests believing something completely different.

Known wheat-related illnesses have clear mechanisms and markers. People with celiac disease are genetically predisposed to launch a self-destructive immune response when a component of gluten called gliadin penetrates their intestinal lining and sets off inflammatory cells in the tissue below.

People with a wheat allergy respond to wheat proteins by churning out a class of antibodies called immunoglobulin E that can set off vomiting, itching, and shortness of breath.

The puzzle, for both doctors and researchers, is patients who lack both the telltale antibodies and the visible damage to their intestines but who feel real relief when they cut out gluten-containing food.

Some doctors have begun to approve and even recommend a gluten-free diet.

“Ultimately, we're here not to do science, but to improve quality of life,” says Alessio Fasano, a pediatric gastroenterologist at Massachusetts General Hospital in Boston who has studied NCGS and written a book on living gluten-free. “If I have to throw bones on the ground and look at the moon to make somebody better, even if I don't understand what that means, I'll do it.”

many doctors, Lundin believed that (fad dieters and superstitious eaters aside) some patients have a real wheat-related ailment. His group helped dispel the notion that NCGS was purely psychosomatic.

They surveyed patients for unusual levels of psychological distress that might express itself as physical symptoms. But the surveys showed no differences between those patients and people with celiac disease, the team reported in 2012.

As Lundin bluntly puts it: “We know they are not crazy.”

Still, skeptics worried that the field had seized on gluten with shaky evidence that it was the culprit. After all, nobody eats gluten in isolation.

“If we did not know about the specific role of gluten in celiac disease, we would never have thought gluten was responsible for [NCGS],” says Stefano Guandalini, a pediatric gastroenterologist at the University of Chicago Medical Center in Illinois. “Why blame gluten?”

Defenders of NCGS generally acknowledge that other components of wheat might contribute to symptoms.

In 2012, a group of proteins in wheat, rye, and barley called amylase trypsin inhibitors emerged as a potential offender, for example, after a team led by biochemist Detlef Schuppan of Johannes Gutenberg University Mainz in Germany (then at Harvard Medical School in Boston) reported that those proteins can provoke immune cells.

Data from the National Health and Nutrition Examination Survey show the rising tide of gluten avoidance by people without celiac disease. Celiac diagnoses also rose, but probably not its actual prevalence.

But without biological markers to identify people with NCGS, researchers have relied on self-reported symptoms measured through a “gluten challenge”: Patients rate how they feel before and after cutting out gluten. Then doctors reintroduce gluten or a placebo—ideally disguised in indistinguishable pills or snacks—to see whether the symptoms tick back up.

Alaedini has recently hit on a more objective set of possible biological markers—much to his own surprise. “I entered this completely as a skeptic,” he says.

Over his career, he has gravitated toward studying spectrum disorders, in which diverse symptoms have yet to be united under a clear biological cause—and where public misinformation abounds.

His team published a study in 2013, for example, that debunked the popular suggestion that children with autism had high rates of Lyme disease. “I do studies [where] there is a void,” he says.

In NCGS, Alaedini saw another poorly defined spectrum disorder. He did accept that patients without celiac disease might somehow be sensitive to wheat, on the basis of several trials that measured symptoms after a blinded challenge.

But he was not convinced by previous studies claiming that NCGS patients were more ly than other people to have certain antibodies to gliadin.

Many of those studies lacked a healthy control group, he says, and relied on commercial antibody kits that gave murky and inconsistent readings.

In 2012, he contacted researchers at the University of Bologna in Italy to obtain blood samples from 80 patients their team had identified as gluten sensitive on the basis of a gluten challenge.

He wanted to test the samples for signs of a unique immune response—a set of signaling molecules different from those in the blood of healthy volunteers and celiac patients. He wasn't optimistic.

“I thought if we were going to see something, with a lot of spectrum conditions that I have looked at, we would see small differences.”

The results shocked him. Compared with both healthy people and those with celiac, these patients had significantly higher levels of a certain class of antibodies against gluten that suggest a short-lived, systemic immune response.

That didn't mean gluten itself was causing disease, but the finding hinted that the barrier of those patients' intestines might be defective, allowing partially digested gluten to get the gut and interact with immune cells in the blood. Other elements—such as immune response–provoking bacteria—also might be escaping.

Sure enough, the team found elevated levels of two proteins that indicate an inflammatory response to bacteria. And when 20 of the same patients spent 6 months on a gluten-free diet, their blood levels of those markers declined.

For Alaedini, the beginnings of a mechanism emerged: Some still-unidentified wheat component prompts the intestinal lining to become more permeable. (An imbalance in gut microbes might be a predisposing factor.) Components of bacteria then seem to sneak past immune cells in the underlying intestinal tissue and make their way to the bloodstream and liver, prompting inflammation.

“This is a real condition, and there can be objective, biological markers for it,” Alaedini says. “That study changed a lot of minds, including my own.”

The study also impressed Guandalini, a longtime skeptic about the role of gluten. It “opens the way to finally reach an identifiable marker for this condition,” he says.

Although consumers focus on gluten, other wheat components could be at the root of symptoms.

But others see the immune-response explanation as a red herring. To them, the primary villain is FODMAPs. The term, coined by gastroenterologist Peter Gibson at Monash University in Melbourne, Australia, and his team, encompasses a smorgasbord of common foods.

Onions and garlic; legumes; milk and yogurt; and fruits including apples, cherries, and mangoes are all high in FODMAPs. So is wheat: Carbs in wheat called fructans can account for as much as half of a person's FODMAP intake, dietitians in Gibson's group have estimated.

The team found that those compounds ferment in the gut to cause symptoms of irritable bowel syndrome, such as abdominal pain, bloating, and gas.

Gibson has long been skeptical of studies implicating gluten in such symptoms, arguing that those findings are hopelessly clouded by the nocebo effect, in which the mere expectation of swallowing the dreaded ingredient worsens symptoms.

His team found that most patients couldn't reliably distinguish pure gluten from a placebo in a blinded test.

He believes that many people feel better after eliminating wheat not because they have calmed some intricate immune reaction, but because they've reduced their intake of FODMAPs.

Lundin, who was firmly in the immune-reaction camp, didn't believe that FODMAPs could explain away all his patients. “I wanted to show that Peter was wrong,” he says.

During a 2-week sabbatical in the Monash lab, he found some quinoa-based snack bars designed to disguise the taste and texture of ingredients.

“I said, ‘We're going to take those muesli bars and we're going to do the perfect study.’”

His team recruited 59 people on self-instituted gluten-free diets and randomized them to receive one of three indistinguishable snack bars, containing isolated gluten, isolated FODMAP (fructan), or neither. After eating one type of bar daily for a week, they reported any symptoms. Then they waited for symptoms to resolve and started on a different bar until they had tested all three.

Before analyzing patient responses, Lundin was confident that gluten would cause the worst symptoms. But when the study's blind was lifted, only the FODMAP symptoms even cleared the bar for statistical significance. Twenty-four of the 59 patients had their highest symptom scores after a week of the fructan-laced bars.

Twenty-two responded most to the placebo, and just 13 to gluten, Lundin and his collaborators—who included Gibson—reported last November in the journal Gastroenterology. Lundin now believes FODMAPs explain the symptoms in most wheat-avoiding patients. “My main reason for doing that study was to find out a good method of finding gluten-sensitive individuals,” he says.

“And there were none. And that was quite amazing.”

At the Columbia meeting, Alaedini and Lundin went head to head in consecutive talks titled “It's the Wheat” and “It's FODMAPS.” Each has a list of criticisms of the other's study.

Alaedini contends that by recruiting broadly from the gluten-free population, instead of finding patients who reacted to wheat in a challenge, Lundin ly failed to include people with a true wheat sensitivity.

Very few of Lundin's subjects reported symptoms outside the intestines, such as rash or fatigue, that might point to a widespread immune condition, Alaedini says. And he notes that the increase in patients' symptoms in response to the FODMAP snacks was just barely statistically significant.

Lundin, meanwhile, points out that the patients in Alaedini's study didn't go through a blinded challenge to check whether the immune markers he identified really spiked in response to wheat or gluten. The markers may not be specific to people with a wheat sensitivity, Lundin says.

Despite the adversarial titles of their talks, the two researchers find a lot of common ground. Alaedini agrees that FODMAPs explain some of the wheat-avoidance phenomenon. And Lundin acknowledges that some small population may really have an immune reaction to gluten or another component of wheat, though he sees no good way to find them.

After the meeting, Elena Verdù, a gastroenterologist at McMaster University in Hamilton, Canada, puzzled over the polarization of the field. “I don't understand why there is this need to be so dogmatic about ‘it is this, it is not that,’” she says.

She worries that the scientific confusion breeds skepticism toward people who avoid gluten for medical reasons.

When she dines with celiac patients, she says, waiters sometimes meet requests for gluten-free food with smirks and questions. Meanwhile, the conflicting messages may send nonceliac patients down a food-avoidance rabbit hole.

“Patients are withdrawing gluten first, then lactose, and then FODMAPs—and then they are on a really, really poor diet,” she says.

But Verdù believes careful research will ultimately break through the superstitions.

She is president of the North American Society for the Study of Celiac Disease, which this year awarded its first grant to study nonceliac wheat sensitivity.

She's hopeful that the search for biomarkers those Alaedini has proposed will show that inside the monolith of gluten avoidance lurk multiple, nuanced conditions. “It will be difficult,” she says, “but we are getting closer.”

Source: https://www.sciencemag.org/news/2018/05/what-s-really-behind-gluten-sensitivity

Non-Celiac Gluten Sensitivity May Not Exist

Video: Gluten sensitivity may exist mostly in the mind

In 2011, Peter Gibson, a professor of gastroenterology at Monash University and director of the GI Unit at The Alfred Hospital in Melbourne, Australia, published a study that found gluten, a protein found in grains wheat, rye, and barley, to cause gastrointestinal distress in patients without celiac disease, an autoimmune disorder unequivocally triggered by gluten. Double-blinded, randomized, and placebo-controlled, the experiment was one of the strongest pieces of evidence to date that non-celiac gluten sensitivity (NCGS), more commonly known as gluten intolerance, is a genuine condition.

By extension, the study also lent credibility to the meteoric rise of the gluten-free diet. Surveys now show that 30% of Americans would to eat less gluten, and sales of gluten-free products are estimated to hit $15 billion by 2016 — that's a 50% jump over 2013's numbers!

But any meticulous scientist, Gibson wasn't satisfied with his first study. His research turned up no clues to what actually might be causing subjects' adverse reactions to gluten.

Moreover, there were many more variables to control! What if some hidden confounder was mucking up the results? He resolved to repeat the trial with a level of rigor lacking in most nutritional research. Subjects would be provided with every single meal for the duration of the trial.

Any and all potential dietary triggers for gastrointestinal symptoms would be removed, including lactose (from milk products), certain preservatives benzoates, propionate, sulfites, and nitrites, and fermentable, poorly absorbed short-chain carbohydrates, also known as FODMAPs.

And last, but not least, nine days worth of urine and fecal matter would be collected. With this new study, Gibson wasn't messing around.

37 subjects took part, all confirmed not to have celiac disease but whose gastrointestinal symptoms improved on a gluten-free diet, thus fulfilling the diagnostic criteria for non-celiac gluten sensitivity.

** They were first fed a diet low in FODMAPs for two weeks (baseline), then were given one of three diets for a week with either 16 grams per day of added gluten (high-gluten), 2 grams of gluten and 14 grams of whey protein isolate (low-gluten), or 16 grams of whey protein isolate (placebo).

Each subject shuffled through every single diet so that they could serve as their own controls, and none ever knew what specific diet he or she was eating. After the main experiment, a second was conducted to ensure that the whey protein placebo was suitable.

In this one, 22 of the original subjects shuffled through three different diets — 16 grams of added gluten, 16 grams of added whey protein isolate, or the baseline diet — for three days each.

Analyzing the data, Gibson found that each treatment diet, whether it included gluten or not, prompted subjects to report a worsening of gastrointestinal symptoms to similar degrees. Reported pain, bloating, nausea, and gas all increased over the baseline low-FODMAP diet.

Even in the second experiment, when the placebo diet was identical to the baseline diet, subjects reported a worsening of symptoms! The data clearly indicated that a nocebo effect, the same reaction that prompts some people to get sick from wind turbines and wireless internet, was at work here. Patients reported gastrointestinal distress without any apparent physical cause. Gluten wasn't the culprit; the cause was ly psychological. Participants expected the diets to make them sick, and so they did. The finding led Gibson to the opposite conclusion of his 2011 research:

“In contrast to our first study… we could find absolutely no specific response to gluten.”

Instead, as RCS reported last week, FODMAPS are a far more ly cause of the gastrointestinal problems attributed to gluten intolerance.

Jessica Biesiekierski, a gastroenterologist formerly at Monash University and now based the Translational Research Center for Gastrointestinal Disorders at the University of Leuven in Belgium,* and lead author of the study alongside Gibson, noted that when participants consumed the baseline low-FODMAP diet, almost all reported that their symptoms improved!

“Reduction of FODMAPs in their diets uniformly reduced gastrointestinal symptoms and fatigue in the run-in period, after which they were minimally symptomatic.”

Coincidentally, some of the largest dietary sources of FODMAPs — specifically bread products — are removed when adopting a gluten-free diet, which could explain why the millions of people worldwide who swear by gluten-free diets feel better after going gluten-free.

Indeed, the rise in non-celiac gluten sensitivity seems predominantly driven by consumers and commercial interests, not quality scientific research.

“On current evidence the existence of the entity of NCGS remains unsubstantiated,” Biesiekierski noted in a review published in December to the journal Current Allergy and Asthma Reports.

Consider this: no underlying cause for gluten intolerance has yet been discovered. Moreover, there are a host of triggers for gastrointestinal distress, many of which were not controlled for in previous studies.

Generally, non-celiac gluten sensitivity is assumed to be the culprit when celiac disease is ruled out.

But that is a “trap,” Biesiekierski says, one which could potentially lead to confirmation bias, thus blinding researchers, doctors, and patients to other possibilities.

Biesiekierski recognizes that gluten may very well be the stomach irritant we've been looking for. “There is definitely something going on,” she told RCS, “but true NCGS may only affect a very small number of people and may affect more extraintestinal symptoms than first thought. This will only be confirmed with an understanding of its mechanism.”

Currently, Biesiekierski is focused on maintaining an open mind and refining her experimental methods to determine whether or not non-celiac gluten sensitivity truly exists.

“We need to make sure that this research is as well controlled as possible and is reproducible,” Biesiekierski told RCS, subsequently adding the quintessential adage of proper science.

“Much, much more research is needed.”

Source: Biesiekierski JR, Peters SL, Newnham ED, Rosella O, Muir JG, Gibson PR. “No effects of gluten in patients with self-reported non-celiac gluten sensitivity after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates.” Gastroenterology. 2013 Aug;145(2):320-8.e1-3. doi: 10.1053/j.gastro.2013.04.051. Epub 2013 May 4.

Source:

Source: https://www.realclearscience.com/blog/2014/05/gluten_sensitivity_may_not_exist.html

Gluten Intolerance May Not Exist

Video: Gluten sensitivity may exist mostly in the mind

In 2011, Peter Gibson, a professor of gastroenterology at Monash University and director of the GI Unit at The Alfred Hospital in Melbourne, Australia, published a study that found gluten, a protein found in grains wheat, rye, and barley, to cause gastrointestinal distress in patients without celiac disease, an autoimmune disorder unequivocally triggered by gluten. Double-blinded, randomized, and placebo-controlled, the experiment was one of the strongest pieces of evidence to date that non-celiac gluten sensitivity (NCGS), more commonly known as gluten intolerance, is a genuine condition.

By extension, the study also lent credibility to the meteoric rise of the gluten-free diet. Surveys now show that 30% of Americans would to eat less gluten, and sales of gluten-free products are estimated to hit $15 billion by 2016 — that's a 50% jump over 2013's numbers!

But any meticulous scientist, Gibson wasn't satisfied with his first study. His research turned up no clues to what actually might be causing subjects' adverse reactions to gluten.

Moreover, there were many more variables to control! What if some hidden confounder was mucking up the results? He resolved to repeat the trial with a level of rigor lacking in most nutritional research. Subjects would be provided with every single meal for the duration of the trial.

Any and all potential dietary triggers for gastrointestinal symptoms would be removed, including lactose (from milk products), certain preservatives benzoates, propionate, sulfites, and nitrites, and fermentable, poorly absorbed short-chain carbohydrates, also known as FODMAPs.

And last, but not least, nine days worth of urine and fecal matter would be collected. With this new study, Gibson wasn't messing around.

Oat grains in their husks (Photo credit: Wikipedia)

37 subjects took part, all confirmed not to have celiac disease but whose gastrointestinal symptoms improved on a gluten-free diet, thus fulfilling the diagnostic criteria for non-celiac gluten sensitivity.

**  They were first fed a diet low in FODMAPs for two weeks (baseline), then were given one of three diets for a week with either 16 grams per day of added gluten (high-gluten), 2 grams of gluten and 14 grams of whey protein isolate (low-gluten), or 16 grams of whey protein isolate (placebo).

Each subject shuffled through every single diet so that they could serve as their own controls, and none ever knew what specific diet he or she was eating. After the main experiment, a second was conducted to ensure that the whey protein placebo was suitable.

In this one, 22 of the original subjects shuffled through three different diets — 16 grams of added gluten, 16 grams of added whey protein isolate, or the baseline diet — for three days each.

Analyzing the data, Gibson found that each treatment diet, whether it included gluten or not, prompted subjects to report a worsening of gastrointestinal symptoms to similar degrees. Reported pain, bloating, nausea, and gas all increased over the baseline low-FODMAP diet.

Even in the second experiment, when the placebo diet was identical to the baseline diet, subjects reported a worsening of symptoms! The data clearly indicated that a nocebo effect, the same reaction that prompts some people to get sick from wind turbines and wireless signals, was at work here. Patients reported gastrointestinal distress without any apparent physical cause. Gluten wasn't the culprit; the cause was ly psychological. Participants expected the diets to make them sick, and so they did. The finding led Gibson to the opposite conclusion of his 2011 research:

“In contrast to our first study… we could find absolutely no specific response to gluten.”

Instead, as RCS reported last week, FODMAPS are a far more ly cause of the gastrointestinal problems attributed to gluten intolerance.

Jessica Biesiekierski, a gastroenterologist formerly at Monash University and now based the Translational Research Center for Gastrointestinal Disorders at the University of Leuven in Belgium,* and lead author of the study alongside Gibson, noted that when participants consumed the baseline low-FODMAP diet, almost all reported that their symptoms improved!

“Reduction of FODMAPs in their diets uniformly reduced gastrointestinal symptoms and fatigue in the run-in period, after which they were minimally symptomatic.”

Coincidentally, some of the largest dietary sources of FODMAPs — specifically bread products — are removed when adopting a gluten-free diet, which could explain why the millions of people worldwide who swear by gluten-free diets feel better after going gluten-free.

Indeed, the rise in non-celiac gluten sensitivity seems predominantly driven by consumers and commercial interests, not quality scientific research.

“On current evidence the existence of the entity of NCGS remains unsubstantiated,” Biesiekierski noted in a review published in December to the journal Current Allergy and Asthma Reports.

Consider this: no underlying cause for gluten sensitivity has yet been discovered. Moreover, there are a host of triggers for gastrointestinal distress, many of which were not controlled for in previous studies.

Generally, non-celiac gluten sensitivity is assumed to be the culprit when celiac disease is ruled out.

But that is a “trap,” Biesiekierski says, one which could potentially lead to confirmation bias, thus blinding researchers, doctors, and patients to other possibilities.

Biesiekierski recognizes that gluten may very well be the stomach irritant we've been looking for. “There is definitely something going on,” she told RCS, “but true NCGS may only affect a very small number of people and may affect more extraintestinal symptoms than first thought. This will only be confirmed with an understanding of its mechanism.”

Currently, Biesiekierski is focused on maintaining an open mind and refining her experimental methods to determine whether or not non-celiac gluten sensitivity truly exists.

“We need to make sure that this research is as well controlled as possible and is reproducible,” Biesiekierski told RCS, subsequently adding the quintessential adage of proper science.

“Much, much more research is needed.”

This article was first published at RealClearScience.

Source: Biesiekierski JR, Peters SL, Newnham ED, Rosella O, Muir JG, Gibson PR. “No effects of gluten in patients with self-reported non-celiac gluten sensitivity after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates.” Gastroenterology. 2013 Aug;145(2):320-8.e1-3. doi: 10.1053/j.gastro.2013.04.051. Epub 2013 May 4.

Source:

Source: https://www.forbes.com/sites/rosspomeroy/2014/05/15/non-celiac-gluten-sensitivity-may-not-exist/

What if your gluten intolerance is all in your head?

Video: Gluten sensitivity may exist mostly in the mind

By Alan Levinovitz

Was Chinese restaurant syndrome the gluten intolerance of its day?

(Image: Martin Puddy/Getty)

While living in China from 2003 to 2005, I often served as the designated translator for fellow expatriates.

Whenever we ate out, this involved asking our server which menu items contained monosodium glutamate (MSG).

Invariably I was told that almost everything is made with weijing (“flavour essence”), including, on one occasion, the roast peanut appetiser my MSG-sensitive friends were snacking on as I made my enquiry.

After observing that no one reacted to the peanuts, I was inspired to conduct a simple (and admittedly unethical) experiment. One evening, instead of translating honestly, I told my companions at a large banquet that the kitchen had promised to avoid using MSG. Everyone thanked me and happily ate their meal, dish after poisoned dish.

An hour later? Two hours later? The next day? Nothing.

I repeated this experiment on multiple occasions, always with the same result. And yet foreigners living in China routinely complained of reactions to their food that included headaches, chest pain and shortness of breath. Was there something about my presence that conferred temporary resistance to MSG? Or could it be that MSG sensitivity was only in their heads?

Chinese restaurant syndrome

In April 1968, the New England Journal of Medicine published a letter by Robert Ho Man Kwok that described a strange set of symptoms: “Numbness at the back of the neck, gradually radiating to both arms and the back, general weakness and palpitation.” Stranger still was the fact that Kwok, himself a Chinese immigrant, typically noted the onset of these symptoms 20 minutes after eating at restaurants serving “Northern Chinese food”.

An editor at the journal titled Kwok’s letter “Chinese restaurant syndrome”, and thus began a minor epidemic. For countless sufferers, a mystery had been finally solved. “No MSG” signs sprang up across the US, and, eventually, the world. Study upon study confirmed the syndrome’s existence and speculated about the science underlying it.

But after reading some of these studies, even a layperson will start to get suspicious.

Take the editorial note that precedes Russell Asnes’s article “Chinese restaurant syndrome in an infant”: “The evidence that this infant had the Chinese Restaurant syndrome may be only circumstantial.

However, the description of the symptom is accurate as attested to by the Editor’s wife who suffers from the same malady. Incidentally, she remains a devotee of Chinese cuisine.”

Science, that sworn enemy of circumstantial evidence, marched on, and slowly but surely physiological explanations of Chinese restaurant syndrome began to lose credibility. Double-blinded studies failed to turn up evidence of a clinical condition.

MSG, many people noted, appears in everything from sushi to Doritos.

Journalists performed experiments similar to mine, their results echoing the consensus of professional scientists: in the overwhelming majority of cases, MSG sensitivity is a psychological phenomenon.

Despite this thorough debunking, a surprisingly large number of people – generally those who lived through the epidemic – still insist they are sensitive to MSG.

Google around and you’ll turn up scores of alarmist websites, which tend to combine outdated research with anecdotal, indignant rebuttals of the current scientific wisdom: “How dare you suggest my MSG sensitivity is only in my head? Why, just the other day I went out for Chinese and forgot to ask about MSG. After 45 minutes I couldn’t breathe and my heart was racing.”

Occasionally, as with vaccines and climate change denial, alarmism veers into paranoia, yielding accusations that a shadowy east Asian cabal is paying off scientists and journalists to regurgitate their propaganda. (Ajinomoto Corporation, I await your cheque!).

For a small minority, MSG sensitivity somehow became more than a medical condition, and challenging its physiological basis poses a threat to their very identity.

The harmfulness of MSG, a seemingly trivial assertion, took on the importance of a religious doctrine, a fundamental truth to be defended at any cost. But why?

Gluten rising

In 2007, my wife’s cake shop did not offer a gluten-free option. Six years later, hardly a month goes by without a request for a gluten-free tasting.

Thanks in part to celebrities such as Oprah Winfrey and Lady Gaga, nearly one-third of all consumers are now interested in gluten-free food, a multi-billion-dollar industry projected to exceed $10 billion by 2017.

(Even children’s play sand now comes with a gluten-free guarantee!)

This is very perplexing, given that only 1 per cent of the population has coeliac disease and only 0.5 per cent is allergic to wheat.

What could possibly be causing widespread reports of non-coeliac gluten intolerance, commonly blamed for a raft of symptoms including gas, bloating, diarrhoea, constipation, fatigue, goose bumps, dizziness, infertility, migraines, joint inflammation and even mood disorders?

Scientists are applying themselves to the riddle, and last February Slate‘s Darshak Sanghavi reported on an Italian study that confirmed the existence of gluten intolerance (“non-coeliac wheat sensitivity”) as a third, “distinct clinical condition”. In the study, one-third of patients who self-identified as gluten-intolerant did in fact experience symptom relief after adopting a gluten-free diet. Case closed, right? Pass the gluten-free pasta.

Not so fast. An important implication of the study is that two-thirds of people who think they are gluten intolerant really aren’t. In light of this, the even-handed Sanghavi suggested that “patients convinced they have gluten intolerance might do well to also accept that their self-diagnosis may be wrong”.

Predictably, the comment thread exploded with rebuttals: defensive anecdotes, doctrinal pronouncements about the evils of gluten and accusations of corporate malfeasance, all of which bear a striking resemblance in tone and content to the rhetoric of anti-MSG advocates. For many, the truth of physiological gluten intolerance has now acquired a quasi-religious status.

Allergic to evidence

No one s to be told they are mistaken about the foundation of their most dearly held beliefs. It offended the faithful when Karl Marx suggested that religions are psychological tools meant to placate the masses.

Suggesting that gluten intolerance might have a psychological basis threatens a similarly foundational belief, namely that we are rational beings, competent interpreters of reality immune to mass hysteria and self-deception.

Obviously this is not the case. For one, our memories are notoriously unreliable. You may remember getting headaches from Chinese food when in fact those memories were created when you read about Chinese restaurant syndrome in the news.

The same is true for memories of gluten intolerance. Don’t forget, certainty about your memories is not sufficient evidence of their truth: “Look, I know that for the last 20 years, every time I ate gluten it gave me terrible gas.

Under oath, eyewitnesses constantly forget crucial details and replace them with their own fabrications. They aren’t liars – they’re just human. One reason for this unreliability is that memory and perception are prone to confirmation bias. Once a bias is in place, we’ll selectively remember – and notice – whatever facts help confirm it.

Food historian Ian Mosby has explained the “success” of Chinese restaurant syndrome by connecting it to racialised discourse that drew on a vision of Chinese cooking as bizarre or extreme. In the case of gluten intolerance, it doesn’t take much to come up with a plausible confirmation bias. Only nine years ago, 1 in every 11 Americans was on a low-carb diet.

In a country terrified of weight gain and recently obsessed with the Atkins diet, gluten makes a great villain. It’s hard not to notice the theme of weight loss on gluten-free sites. Pasta, bread, cake, cookies, pretzels – they don’t just make you fat, they make you sick! (Added bonus: diets motivated by a medical condition are far more effective – ask any diabetic.

)

Nocebo nosh

Confirmation bias meets physiology in the placebo effect, a well-documented phenomenon in medical treatments ranging from sham drugs to sham acupuncture (where patients respond positively to sham needles) to sham knee surgery.

People’s desire to believe in a cure actually affects their symptoms. That’s why placebo-controlled, double-blinded studies are integral to medical research. Without them, we’d be in constant danger of ascribing physiological causality to treatments that are actually psychological.

Needless to say, placebo effects aren’t always beneficial. Strong belief can also render a harmless substance poisonous, which is exactly what happened with MSG. Scientists refer to this as the nocebo effect, and it means that careful studies are necessary to distinguish between poisons and poisonous beliefs.

None of this minimises the relief felt by those who undergo sham acupuncture, or the symptoms of those who think they are gluten intolerant. Pain is pain; chronic diarrhoea is chronic diarrhoea.

All it means is that pain relief might not be caused by the physical presence of an acupuncture needle, and diarrhoea might not be caused by the physical presence of gluten.

In these instances, the symptoms may be real, but their cause (and potential resolution) is all in our heads.

Mindful of suffering

It is here where the trouble begins. There’s something intensely disturbing about the notion that we can make ourselves sick. Belief, not physiology, becomes the causal agent, displacing MSG or gluten as the source of blame for someone’s suffering. This can make us feel vulnerable, stupid and weak, as though we have the choice to be better but lack the mental acuity to manage it.

Not only that, it’s hard not to feel a psychological explanation trivialises one’s condition – hence the expression “It’s only in your head.” But things that are in our heads aren’t fake or unimportant (OCD? anorexia?), and susceptibility to a nocebo effect isn’t a sign of weakness. Anyone can unknowingly invent a false memory or react to a substance that is actually benign.

Accepting a psychological explanation of gluten intolerance is especially difficult because food aversions often turn into a way of life. religion, avoiding gluten requires personal sacrifice.

Gluten intolerance creates communities, which, religious communities, share stories of suffering and redemption, and share meals made special by the presence of a food taboo.

It’s no wonder people take offence at the suggestion that gluten intolerance could be psychological – after all, who wants to have built their way of life on a “mere” trick of the mind?

Thinking that way is a mistake. Reductionist psychological explanations of religious beliefs can be offensive because they deny fundamental religious truths: “You believe in heaven to stave off your fear of death, not because it really exists.

” Legitimate psychological explanations of medical conditions, on the other hand, deny no such truths. The question of whether and to what extent MSG and gluten cause physiological reactions is scientific, not religious.

When one’s explanation of a medical condition becomes an unquestionable truth, the explanation is no longer scientific.

Many basic claims of nutrition science are unintuitive and sometimes don’t stand up to repeated research. (Salt? Cholesterol? Vitamins? Alcohol? Coffee?) At this point, scientists simply don’t have a good explanation for the mechanism and prevalence of gluten intolerance – hence the need for studies about whether it exists at all.

Maybe people have always been gluten intolerant and were going undiagnosed – as is true with coeliac disease. Maybe our guts haven’t evolved to process gluten – as some advocates of the Palaeolithic diet claim.

Maybe it’s Monsanto (conspiracy theorists rejoice!). Maybe gluten intolerance isn’t really caused by gluten, and we should actually be blaming a family of proteins in wheat called amylase trypsin inhibitors.

None of these explanations is “only” in our heads, which makes them feel more acceptable. But to deny the distinct possibility that gluten could be another MSG, at least for some people, is to deny what science has confirmed, again and again, about our nature as human beings.

So when some annoying friend implies that your gluten intolerance is psychological, go right ahead and be offended. But when science suggests it? Best to listen up, question your self-diagnosis, and remind yourself that nocebo effects are nothing to be ashamed of.

More on these topics:

  • psychology
  • brains
  • biology
  • food and drink
  • allergies

Source: https://www.newscientist.com/article/dn23851-what-if-your-gluten-intolerance-is-all-in-your-head/

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