A major scientific review is challenging one of the most widespread beliefs in nutrition: that gluten is the cause of symptoms for people who identify as gluten-sensitive. According to new findings published in The Lancet, those reactions may have more to do with the way the gut and brain communicate than with gluten itself.
Non-coeliac gluten sensitivity (NCGS) affects people who report symptoms like bloating, abdominal pain and fatigue after eating gluten but test negative for celiac disease (spelled “coeliac” outside the United States). The condition has grown increasingly common, yet researchers say the science behind it has been surprisingly unclear.
Lead author Jessica Biesiekierski, an associate professor at the University of Melbourne, said the new evidence challenges long-standing assumptions.
“Contrary to popular belief, most people with NCGS aren’t reacting to gluten,” she said.
The review brought together data from clinical trials across several countries. It found that true gluten-specific reactions were rare, and that most participants responded the same way whether they consumed gluten or a placebo. According to Biesiekierski, the symptoms often stemmed from other components of wheat or from fermentable carbohydrates known as FODMAPs.
“Our findings show that symptoms are more often triggered by fermentable carbohydrates, commonly known as FODMAPs, by other wheat components or by people’s expectations and prior experiences with food,” she said.
That link between expectations and symptoms is a growing area of research. In several trials, people with irritable bowel syndrome who believed they were sensitive to gluten reacted similarly to gluten, wheat and placebo foods. These patterns suggest that the gut–brain connection may play a central role in how symptoms develop.
“Across recent studies, people with IBS who believe they’re gluten-sensitive react similarly to gluten, wheat, and placebo. This suggests that how people anticipate and interpret gut sensations can strongly influence their symptoms,” Biesiekierski said.
Instead of viewing NCGS as a stand-alone reaction to gluten, the authors argue it fits more closely within the spectrum of gut–brain interaction disorders, which includes IBS. That shift could have meaningful implications for diagnosis and treatment.
Jason Tye-Din, a gastroenterologist and director of the Snow Centre for Immune Health in Melbourne, said the updated understanding can help clinicians provide more precise care.
“Distinguishing NCGS from related gut conditions is essential for clinicians to offer accurate diagnosis and individualized care, as well as treating underlying drivers,” he said.
The authors emphasized that treatment should extend beyond removing certain foods. Biesiekierski said effective care for NCGS involves addressing dietary triggers without overly restrictive eating patterns and supporting the emotional and cognitive elements that influence gut symptoms.
“We would like to see public health messaging shift away from the narrative that gluten is inherently harmful, as this research shows that this often isn’t the case,” she said.
The review also calls for better diagnostic tools, more consistent clinical pathways and clearer labeling to help people understand whether gluten-free products are necessary for them.
For the millions of people who avoid gluten because of uncomfortable symptoms, the findings may offer some clarity: the culprit might not be gluten itself but how the body and brain respond to certain foods and sensations. That distinction could open the door to more personalized and less restrictive approaches to managing gut discomfort.
The authors disclosed receiving research support from a mix of public, academic and industry sources. These include grants or funding relationships with the Rome Foundation, Yakult, NHMRC, Australian Eggs, PrecisionBiotics, Tillotts and several European public–private partnership programs such as TKI Agri & Food, Health Holland and Horizon 2020.