Newswise \u2014 CHAPEL HILL, N.C. (Aug. 20, 2026) \u2013 Spinach, almonds, and sweet potatoes are celebrated as some of the healthiest foods on the planet. But for the millions of Americans living with inflammatory bowel disease (IBD), a new study from the UNC School of Medicine suggests that these same foods may be quietly worsening gut inflammation through a compound most people have never heard of.<\/p>\n
Published August 13, 2026 in\u00a0Cellular and Molecular Gastroenterology and Hepatology\u00a0(CMGH),\u00a0the study<\/a>\u00a0was led by postdoctoral scholar Anna Salvador, PhD, RD, LDN, in the lab of\u00a0Shehzad Z. Sheikh<\/a>, MD, PhD, Professor of\u00a0Medicine\u00a0and Genetics. The team measured gene expression, stool oxalate content, and dietary intake in IBD patients and controls, and conducted complementary experiments in mouse models and cell culture systems to evaluate how dietary oxalate relates to mucosal inflammation in IBD.<\/p>\n The Gut\u2019s Oxalate Machinery Is Broken in IBD<\/p>\n Oxalate is a naturally occurring compound present in all plant foods.\u00a0Most dietary oxalate is eliminated in the stool, even in the healthy gut. However, the study found that\u00a0specialized\u00a0transporter\u00a0proteins responsible for the absorption of oxalate from the gut,\u00a0SLC26A2\u00a0and\u00a0SLC26A3\u00a0are consistently and significantly reduced in gut tissue from both ulcerative colitis and Crohn\u2019s disease patients, across affected tissues, and irrespective of inflammation status. The more inflamed the tissue, the lower the transporter expression drops.<\/p>\n When these transporters are impaired, dietary oxalate is not properly\u00a0absorbed\u00a0leaving more of it to accumulate in the intestinal environment, where the\u00a0study\u2019s\u00a0data suggest it amplifies the very inflammation that defines IBD.<\/p>\n A Dietary Paradox \u2014 and a Methodological First<\/p>\n Crohn\u2019s disease patients had significantly higher stool oxalate levels than non-IBD\u00a0controls\u00a0even though both groups\u00a0habitually\u00a0consume similar amounts of plant-based foods. This was confirmed using two independent dietary measures: a validated dietary questionnaire (Diet History Questionnaire III) and DNA metabarcoding, a molecular technique that\u00a0identifies\u00a0plant\u00a0species present in stool samples. This is the first time metabarcoding has been used to assess diet in an IBD population.<\/p>\n \u201cFor the first time, we\u00a0observed\u00a0that IBD patients and healthy controls were eating similar amounts of plant-based\u00a0foods\u00a0yet CD patients still had more oxalate in their stool,\u201d said Dr. Salvador. \u201cThat told us this isn\u2019t just about what patients eat. Something is fundamentally different about how their gut handles oxalate.\u201d<\/p>\n The finding points to a biological defect in oxalate\u00a0handling\u00a0not simply how much oxalate a patient consumes\u00a0as the key driver of elevated intestinal oxalate in IBD.<\/p>\n Mouse Models Reinforce the Human Signal<\/p>\n The human findings were reinforced in controlled animal experiments. Mice fed an oxalate-supplemented diet alongside a colitis-inducing agent were 60 percent less likely to survive than those not receiving dietary oxalate. In two independent,\u00a0genetically susceptible mouse models of spontaneous colitis, dietary oxalate accelerated disease onset and worsened severity. Critically, the oxalate transporter genes were already reduced at baseline in these susceptible models before dietary oxalate was\u00a0introduced\u00a0mirroring the pattern seen in human IBD patients. In cell culture experiments, oxalate exaggerated inflammatory responses in macrophages and dendritic cells, key players in intestinal immune defense.<\/p>\n A Potential Signal for Disease Trajectory<\/p>\n In an exploratory analysis, low expression of a third transporter\u00a0SLC26A6\u00a0was associated with\u00a0stricturing\u00a0Crohn\u2019s disease, the more aggressive, fibrous form of the disease in which the intestine scars and narrows.\u00a0Nearly 75 percent\u00a0of patients with low\u00a0SLC26A6\u00a0expression had\u00a0stricturing\u00a0disease, raising the possibility that oxalate transporter expression could serve as a molecular signal predicting clinical trajectory a precision medicine opportunity that\u00a0warrants\u00a0validation in larger cohorts.<\/p>\n \u201cDr. Salvador really conceptualized and drove this work from the beginning,\u201d said Dr. Sheikh. \u201cShe asked a question that hadn\u2019t been asked before: What if a specific dietary molecule is an active driver of gut inflammation in IBD, not just a bystander? The rigor she brought to answering it is what makes these findings so compelling.\u201d<\/p>\n Why It Matters for Patients\u00a0<\/p>\n The findings do not call for\u00a0eliminating\u00a0plant foods from the IBD diet. Rather, they suggest that for genetically susceptible individuals, even moderate oxalate intake may promote mucosal\u00a0inflammation\u00a0and that prior dietary studies in IBD may have been confounded by unmeasured differences in oxalate exposure or handling.\u00a0Importantly, it is possible to\u00a0maintain\u00a0a nutritionally complete, plant-based dietary pattern while reducing total oxalate intake.<\/p>\n The authors also point to the gut microbiome as a promising therapeutic target. Oxalate-degrading bacteria such as\u00a0Oxalobacter\u00a0formigenes\u00a0are depleted in IBD patients, and\u00a0microbiome-based strategies to\u00a0optimize\u00a0oxalate degradation may offer a more sustainable path than dietary restriction alone.<\/p>\n Prior to formal clinical recommendations\u00a0regarding\u00a0dietary oxalate intake, future research should focus on validation in larger, longitudinal patient cohorts that integrate stool oxalate measurements, rigorously captured dietary intake, molecular\u00a0profiling\u00a0and microbiome analyses.<\/p>\n \u201cFor patients living with Crohn\u2019s disease or ulcerative colitis, this research opens a genuinely new therapeutic angle one that connects the food on their plate to the inflammation in their gut,\u201d said Dr. Sheikh. \u201cDiet is one of the most powerful, modifiable levers we have in medicine, and this study gives us a molecular framework to start using it more precisely.\u201d<\/p>\n The study was supported by the Helmsley Charitable Trust, the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), the Chan Zuckerberg Initiative, Schmidt Sciences, the Burroughs\u00a0Wellcome\u00a0Fund, and\u00a0additional\u00a0National Institutes of Health sources. Co-authors span UNC-Chapel Hill, Texas A&M University and Duke University.\u00a0<\/p>\n","protected":false},"excerpt":{"rendered":"Newswise \u2014 CHAPEL HILL, N.C. 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