What some people say is gluten sensitivity might actually not have to do with gluten at all, a new study published in scientific journal “The Lancet” found. The lead researcher of the study, University of Melbourne associate professor Jessica Biesiekierski, said in a statement these results overturn long-held assumptions about gluten sensitivity, which is reported by about 10% of adults worldwide.
“Contrary to popular belief, most people with [non-celiac gluten sensitivity] aren’t reacting to gluten,” she said.
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About 2 million people in the United States have celiac disease, which is a chronic digestive and immune disorder that damages the small intestine and is triggered by eating gluten, according to the National Institutes of Health. Biesiekierski and other researchers analyzed 58 studies about the symptom changes for people with gluten sensitivities who didn’t have celiac disease, as well as how these symptoms happened. They looked at the immune system, gut barrier, microbes in the gut and psychological explanations, Biesiekierski wrote in an article for The Conversation.
Across these studies, Biesiekierski said, gluten-specific reactions were “uncommon and, when they occurred, changes in symptoms were usually small.”
“Many participants who believed they were “gluten sensitive” reacted equally — or more strongly — to a placebo,” Biesiekierski wrote.
One of these trials studied how fermentable carbohydrates affected people who said they were sensitive to gluten. Those who ate a diet low in these carbs, such as certain fruits, vegetables, legumes and cereals, saw their symptoms improve, Biesiekierski said, even when they started eating gluten again. Another showed that fructans, which are a kind of fermentable carbohydrate in wheat, onion, garlic and other foods, caused more bloating and discomfort than actual gluten, Biesiekierski wrote.
“A consistent finding is how expecting to have symptoms profoundly shapes people’s symptoms,” she said. “In blinded trials, when people unknowingly ate gluten or placebo, symptom differences almost vanished. Some who expected gluten to make them unwell developed identical discomfort when exposed to a placebo. This nocebo effect — the negative counterpart of placebo — shows that belief and prior experience influence how the brain processes signals from the gut.”
This was supported by brain-imaging research. Expectation and emotion activate brain regions involved in pain and how people perceive threats, Biesiekierski explained, which can heighten sensitivity to “normal gut sensations.”
“What the evidence is telling us is that focusing attention on the gut, coupled with anxiety about symptoms or repeated negative experiences with food, has real effects,” Biesiekierski said. “This can sensitise how the gut interacts with the brain (known as the gut–brain axis) so normal digestive sensations are felt as pain or urgency.”
This doesn’t mean that people are imagining their symptoms, but rather that when one’s brain thinks a meal could cause harm, “gut sensory pathways amplify every cramp or sensation of discomfort,” which creates “genuine distress.”
“Symptoms are real, but the mechanism is often driven by expectation rather than gluten,” Biesiekierski said.
Based on these results, Biesiekierski is calling for public health messaging to “shift away from the narrative that gluten is inherently harmful, as research shows this often isn’t the case.”
When it comes to gluten sensitivity, researchers recommend that clinicians rule out celiac disease or wheat allergies first, and then optimize the quality of their overall diet. If symptoms persist, they say, clinicians could have their patients try a diet low in fermentable carbohydrates. Only then, researchers said, should a gluten-free trial be suggested.
“These findings additionally call for better diagnostic tools, more rigorous clinical pathways and research funding in this field, as well as improved public education and food labelling,” Biesiekierski said.
