Spinach, almonds, and sweet potatoes are widely celebrated for their health benefits. However, recent research from UNC School of Medicine indicates that a naturally occurring compound in these foods may exacerbate intestinal inflammation in individuals with inflammatory bowel disease (IBD).
The study, published August 13, 2026, in Cellular and Molecular Gastroenterology and Hepatology (CMGH), was led by postdoctoral scholar Anna Salvador, PhD, RD, LDN, under the guidance of Shehzad Z. Sheikh, MD, PhD, Professor of Medicine and Genetics.
Researchers examined gene activity, oxalate levels in stool, and dietary patterns in people with IBD as well as those without the disease. They also conducted experiments in mice and cultured cells to explore how dietary oxalate might influence intestinal inflammation.
IBD May Disrupt the Gut’s Ability to Handle Oxalate
The compound in question, known as oxalate, occurs naturally in virtually all plant foods. Under normal digestion, most dietary oxalate is absorbed and passed through the body via the stool.
Two key transporter proteins—SLC26A2 and SLC26A3—that move oxalate out of the gut were found at lower concentrations in the intestinal tissue of patients with ulcerative colitis and Crohn’s disease. This reduction persisted across affected organs regardless of active inflammation status. Notably, the more inflamed the tissue, the lower the transporter expression tended to be.
When these transport systems are compromised, less dietary oxalate is cleared from the lumen, leaving elevated levels that the researchers believe can aggravate existing IBD‑associated inflammation.
Crohn’s Patients Had More Oxalate Despite Similar Diets
Strikingly, people with Crohn’s disease exhibited significantly higher stool oxalate concentrations compared with non‑IBD individuals, even when their plant‑based diets were otherwise comparable.
This discrepancy was identified through two complementary approaches: a validated Dietary History Questionnaire (III) and DNA metabarcoding—a molecular technique that profiles the plant species present in stool samples. According to Dr. Salvador, “the difference cannot be explained solely by intake.” Consequently, the authors infer that gut processing of oxalate differs markedly between the two groups.
The evidence points toward a physiological limitation rather than dietary excess driving increased oxalate accumulation.
Animal Experiments Strengthen the Link
The team also tested dietary oxalate in several animal models. Mice fed an oxalate‑supplemented diet alongside a colitis‑inducible agent were 60 % less likely to survive than those receiving the same supplement alone. In two genetically susceptible mouse models, oxalate accelerated the onset and severity of colitis, mirroring human observations where transporter genes were already reduced prior to intervention.
Cell‑culture work provided additional insight: oxalate amplified inflammatory responses in macrophages and dendritic cells—immune cells essential for gut barrier maintenance.
A Possible Marker of More Severe Crohn’s Disease
The investigators further examined whether oxalate‑related genes predict disease severity. They discovered that low expression of the SLC26A6 transporter correlated with stricturing Crohn’s disease, a more aggressive form characterized by intestinal narrowing due to fibrosis.
Approximately 75 % of patients exhibiting low SLC26A6 activity developed stricturing disease, suggesting potential utility of oxalate transporter levels as a biomarker for prognosis. Larger cohorts are needed to confirm these associations.
What the Findings Mean for People With IBD
These results imply that for genetically predisposed individuals, even modest dietary oxalate exposure may exacerbate gut inflammation. Rather than mandating complete elimination of plant foods, physicians should consider individual susceptibility when advising dietary choices.
Maintaining a nutrient‑complete plant‑based diet while moderating oxalate intake remains advisable. Emerging microbiome therapies offer hope; certain commensals, such as Oxalobacter formigenes, degrade oxalate and are less abundant in IBD patients, suggesting that targeted probiotic strategies could reduce oxalate burden beyond dietary restriction alone.
More Research Is Needed Before Diet Guidelines Change
The authors stress that current data are insufficient to formulate formal recommendations regarding oxalate intake for IBD patients. Future studies plan to track larger patient cohorts over time, integrating stool oxalate measurements, detailed diet records, molecular profiling, and microbiome analyses.
“This research opens a transformative therapeutic avenue that directly connects dietary intake to gut inflammation,” said Dr. Sheikh. “Precise modulation of oxalate consumption may become a cornerstone of personalized IBD management.”
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 Wellcome Fund, and additional National Institutes of Health sources. Co‑authors include institutions from UNC‑Chapel Hill, Texas A&M University, and Duke University.
