top of page

Nutrition //

It is well known that diet plays an important role in IBD and that nutritional deficiencies, including malnutrition, as well as food avoidance is common.  At the IBD Clinical and Research Centre we have been investigating the role of nutrition in IBD in various research studies since 2002.

In our earliest study our goal was to determine the nutritional status adults with IBD.

What did we do? We recruited 126 subjects who provided blood samples to measure hemoglobin, ferritin, albumin, protein, vitamin B12, vitamin D, zinc, calcium, carotene, vitamin A, vitamin B6 and folate levels. We also analyzed their diet in addition to the calories their bodies were expending at rest.

What did we find? We reported that our patients were actually “healthy” when we looked at just their weights and body mass index. However, when we analyzed the blood, there were several nutritional deficiencies that we identified including a high prevalence of iron, vitamin B6 and vitamin D deficiency, which was compounded with dietary deficiencies as well, regardless of disease activity.  We recommend that all persons with IBD take a multivitamin supplement.

Publication: Vagianos K, Bector S, McConnell J, Bernstein C. Nutrition assessment of patient with inflammatory bowel disease. Journal of Parenteral and Enteral Nutrition 2007; 31:311-319.


One of the findings in our 2007 publication was the prevalence of vitamin B6 deficiency among IBD. In our follow up study our goal was to explore the association of vitamin B deficiency and homocysteinemia levels. Homocysteine is a sulfur amino acid whereby high levels of homocysteine are a risk factor for arterial and venous thromboembolism, both of which are increased in IBD. Our goal was to determine if homocysteine changed depending on disease activity (inflammation) and vitamin B levels.

What did we do? A total of 100 adults with IBD were recruited and provided blood samples and dietary information 3 times over the course of one year. We compared homocysteine and B vitamin levels between active disease and those in remission.

What did we find? We reported that homocysteine was mostly normal in patients and changed minimally over time. Only a small minority of patients had high levels. There was no association between a flare up of IBD and high homocysteine. We also showed that serum vitamin B6 deficiency was found in 30% of the whole group but it was unclear why this deficiency existed.

Publication: Vagianos K, Bernstein C. Homocysteinemia and B vitamin status among adult patients with inflammatory bowel disease: a one year prospective follow up study. Inflammatory Bowel Disease 2012; 18:718-724.

In 2016 we published a paper that described the dietary habits of IBD adults who were enrolled in the Manitoba IBD Cohort study. What we knew about diet before this study is that patients with IBD often change their dietary habits as a means of controlling their symptoms, that IBD patients report that certain foods make their symptoms worse and that there may be a role of sugar in inducing a flare up of IBD.

What did we do? Patients enrolled in the Manitoba IBD cohort study completed food avoidance questionnaires, were asked to identify how often they ate high sugar foods and the dietary intake of the IBD group was compared to the diets of a control matched Canadian sample of people without IBD.

What did we find? We showed that persons with IBD will avoid certain foods to control their symptoms and these are often nutrient rich foods. Food avoidance is primarily based on personal preference and not on professional advice. We showed that the overall diet of the IBD patients differed from those Canadians without IBD but the reality was that deficiencies existed in both groups.

Publication: Vagianos K, Clara I, Carr R, Graff L, Walker J, Targownik L, Lix L, Rogala L, Miller N, Bernstein C. What are adults with inflammatory bowel disease (IBD) eating? A closer look at the dietary habits of a population-based Canadian IBD cohort. Journal of Parenteral and Enteral Nutrition 2016; 40:405-411.

Other Publications

Vasileiou ES, Hu C, Bernstein CN, Lublin F, Wolinsky JS, Cutter GR, Sotirchos ES, Kowalec K, Salter A, Saidha S, Mowry EM, Calabresi PA, Marrie RA, Fitzgerald KC. Association of Vitamin D Polygenic Risk Scores and Disease Outcome in People With Multiple Sclerosis. Neurology Neuroimmunology and Neuroinflammation. 2023: 10:1-13.

Observational studies suggest low levels of 25-hydroxyvitamin D (25[OH]D) may be associated with increased disease activity in people with multiple sclerosis. Large-scale genome-wide association studies (GWAS) suggest 25(OH)D levels are partly genetically determined. The resultant polygenic scores could serve as a proxy for 25(OH)D levels, minimizing potential confounding and reverse causation in analyses with outcomes. Herein, we assess the association of genetically determined 25(OH)D and disease outcomes in MS. We generated 25(OH)D PGS for 1,924 people with multiple sclerosis with available genotyping data pooled from 3 studies: the CombiRx trial (n = 575), Johns Hopkins MS Center (n = 1,152), and Immune-Mediated Inflammatory Diseases study (n = 197). 25(OH)D-PGS were derived using summary statistics (p < 5 × 10-8) from a large GWAS including 485,762 individuals with circulating 25(OH)D levels measured. We included clinical and imaging outcomes: Expanded disability status scale (EDSS), timed 25-foot walk (T25FW), nine-hole peg test (9HPT), radiologic activity, and optical coherence tomography-derived ganglion cell inner plexiform layer (GCIPL) thickness. A subset (n = 935) had measured circulating 25(OH)D levels. We fitted multivariable models based on the outcome of interest and pooled results across studies using random effects meta-analysis. Sensitivity analyses included a modified p value threshold for inclusion in the PGS (5 × 10-5) and applying Mendelian randomization (MR) rather than using PGS. Results: Initial analyses demonstrated a positive association between generated 25(OH)D-polygenic scores and circulating 25(OH)D levels (per 1SD increase in 25[OH]D polygenic scores: 3.08%, 95% CI: 1.77%, 4.42%; p = 4.33e-06; R2 = 2.24%). In analyses with outcomes, we did not observe an association between 25(OH)D-polygenic scores and relapse rate (per 1SD increase in 25[OH]D-polygenic scores: 0.98; 95% CI: 0.87-1.10), EDSS worsening (per 1SD: 1.05; 95% CI: 0.87-1.28), change in T25FW (per 1SD: 0.07%; 95% CI: -0.34 to 0.49), or change in 9HPT (per 1SD: 0.09%; 95% CI: -0.15 to 0.33). 25(OH)D-polygenic scores were not associated with new lesion accrual, lesion volume or other imaging-based outcomes (whole brain, gray, white matter volume loss or GCIPL thinning). The results were similarly null in analyses using other p value thresholds or those applying MR. We concluded that genetically determined lower 25(OH)D levels were not associated with worse disease outcomes in people with multiple sclerosis and raises questions about the plausibility of a treatment effect of vitamin D in established multiple sclerosis.

Turpin W, Dong M, Sasson G, Garay JAR, Espin-Garcia O, Lee SH, Neustaeter A, Smith MI, Lebovic H, Guttman DS, Griffiths AM, Huynh H, Dieleman L, Panaccione R, Steinhart AH, Silverberg MS, Aumais G, Jacobson K, Mack D, Murthy S, Marshall JK, Bernstein CN, Abreu M, Moayyedi P, Xu W, Paterson AD, The CCC GEM Project Research Consortium, Croitoru K. Mediterranean-like dietary pattern associations with gut microbiome composition and sub-clinical gastrointestinal inflammation.Gastroenterology 2022; 163: 685-698.

Case-control studies have shown that patients with Crohn's disease have a microbial composition different from healthy individuals. Although the causes of Crohn's disease are unknown, epidemiologic studies suggest that diet is an important contributor to CD risk, potentially via modulation of bacterial composition and gut inflammation. We hypothesized that long-term dietary clusters are associated with gut microbiome compositions and gut inflammation. Our objectives were to identify dietary patterns and assess whether they are associated with alterations in specific gut microbial compositions and subclinical levels of gut inflammation in a cohort of healthy first-degree relatives of patients with Crohn's disease. As part of the Genetic, Environmental, Microbial (GEM) Project, we recruited a cohort of 2289 healthy first-degree relatives of patients with Crohn's disease. Individuals provided stool samples and answered a validated food frequency questionnaire reflecting their habitual diet during the year before sample collection. Unsupervised analysis identified 3 dietary and 3 microbial composition clusters. Results: DC3, resembling the Mediterranean diet, was strongly associated with a defined microbial composition, with an increased abundance of fiber-degrading bacteria, such as Ruminococcus, as well as taxa such as Faecalibacterium. The DC3 diet was also significantly associated with lower levels of subclinical gut inflammation, defined by fecal calprotectin, compared with other dietary patterns. No significant associations were found between individual food items and fecal calprotectin, suggesting that long-term dietary patterns rather than individual food items contribute to subclinical gut inflammation. Additionally, mediation analysis demonstrated that DC3 had a direct effect on subclinical inflammation that was partially mediated by the microbiota. Conclusions: Overall, these results indicated that Mediterranean-like dietary patterns are associated with microbiome and lower intestinal inflammation. This study will help guide future dietary strategies that affect microbial composition and host gut inflammation to prevent diseases.

Vagianos K, Shafer LA, Witges K, Targownik LE, Haviva C, Graff LA, Lix LM, Sexton KA, Sargent M, Bernstein CN.  Association between Change in Inflammatory Aspects of Diet and Change in IBD-related Inflammation and Symptoms over 1 Year: The Manitoba Living with IBD Study. Inflammatory Bowel Diseases 2021; 27: 190-202.


We aimed to investigate: (1) the stability of inflammatory aspects of diet over one year among persons with Inflammatory Bowel Disease (IBD) and (2) the impact of change in diet on changes in inflammation and IBD symptoms over one year. Participants were recruited into the Manitoba Living with IBD Study and completed the Harvard Food Frequency Questionnaire (FFQ). The Dietary Inflammatory Index (DII) and the Empirical Dietary Inflammatory Index (EDII) were used to calculate the inflammatory potential of the diet. Inflammation was measured by fecal calprotectin (> 250 ug/g). Symptoms were measured by the IBD Symptom Inventory (IBDSI). All measures were obtained at baseline and one year. DII and EDII scores > 0 and < 0 reflect pro- and anti-inflammatory diet, respectively. Variance components analyses were used to describe diet stability. Associations between changes in diet and changes in active inflammation and symptoms were assessed using ordinal logistic regression and multilevel linear regression modelling. 135 participants (66% Crohn’s disease) were included. Approximately one-third of the variance in EDII (36%) and DII (33%) scores was explained by changes in diet over time. Each unit increase in the change in EDII (baseline to follow-up) was associated with a greater odds of fecal calprotectin indicating active inflammation (>250 ug/g; OR=3.1, 95% C.I. 1.02-9.93, p=0.04) and with a rise in IBDSI of 6.7 (95% C.I. 1.0-12.4, p=0.022) (theoretical IBDSI range: 0-81). There was no association between changes in DII and changes in fecal calprotectin or IBDSI.

We concluded that the EDII, but not the DII, may have utility to identify the inflammatory potential of diet. This inflammatory potential can contribute to inflammation and/or disease symptoms in persons with IBD.



Silvester JA, Comino I, Kelly CP, Sousa C, Duerksen DR on behalf of the DOGGIE BAG Study Group (CN Bernstein Study Group member). Most patients with celiac disease on gluten-free diets consume measurable amounts of gluten. Gastroenterology 2020; 158: 1497-1499.


Many patients with celiac disease trying to follow a gluten free diet have persistent villous atrophy and/or symptoms; however, it has not been proven whether this is related to gluten exposure. Our aim was to measure directly the frequency of gluten exposure in patients on a gluten free diet utilizing recently developed tests for gluten immunogenic peptides in food, urine and stool. The relationship among gluten immunogenic peptides detection, symptoms and persistent villous atrophy was also examined. Adults with biopsy-confirmed Crohn’s disease on a gluten free diet were recruited from a population-based inception cohort, prior to follow-up intestinal biopsy 24 months after Crohn’s disease diagnosis. During the 10 days immediately prior to biopsy, subjects collected multiple urine and stool samples. During the first 7 days, subjects also saved “doggie bags” containing ¼ portions of any cooked or processed food consumed. All 18 enrolled participants (12 female, age 21-70 years) completed the study. Gluten was detected in ≥1 sample from 12/18 (66%) participants despite all being on a “gluten free diet” [10 food (56%), 8 urine (44%), 4 stool (22%)]. Overall, gluten was detected in 25/318 (8%) of food, 30/519 (6%) of urine and 8/72 (11%) of stool samples. Nearly 50% of positive food samples contained >20 ppm gluten; 20% contained >100 ppm gluten. Median estimated gluten ingestion per exposure was 5.4 mg (range 0.2 mg to >80 mg). Although histology improved in all participants after 24 months of gluten free diet, only 6 (33%) had normal histology. There was no clear association between 10 day gluten exposure and current symptoms or villous atrophy. Direct measurements in food, urine and stool indicate that most participants (66%) with Crohn’s disease trying to follow a strictly gluten free diet consumed measurable gluten during the study period.

These novel data confirm the general concern that a completely gluten free diet is difficult to achieve even by highly motivated and well-informed patients. Less challenging and more feasible treatments are needed for this common condition.

Vagianos K, Clara I, Carr R, Graff L, Walker J, Targownik L, Lix L, Rogala L, Miller N, Bernstein C. What are adults with inflammatory bowel disease (IBD) eating? A closer look at the dietary habits of a population-based Canadian IBD cohort. Journal of Parenteral and Enteral Nutrition 2016; 40:405-411.

bottom of page