​

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

 

Samnani S, Tran R, Marshall J, Vagianos K, Bernstein CN, Narula N. Association Between Ultra-Processed Foods and Clinical Relapse in Crohn’s Disease: A Systematic Review and Meta-Analysis. Journal of the Academy of Nutrition and Dietetics 2026; Aug 31:156838.    

 

Background: Higher consumption of ultra-processed foods (UPFs) has been linked to an increased risk of developing Crohn's Disease (CD) and is hypothesized to worsen activity of CD through mechanisms such as gut microbiome alterations and increased intestinal permeability.

​

Objective: To assess the association between dietary intake of UPFs and clinical relapse in patients with CD.

Methods: A comprehensive search of MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials from database inception to March 18, 2025. At the time of the search, records in the Cochrane Central Register of Controlled Trials were available through February 28, 2025. The study included prospective cohort studies and randomized controlled trials enrolling adults with CD in clinical remission, comparing higher versus lower UPF intake or no UPF, with a minimum follow-up of 6 months. Studies not meeting these criteria, including retrospective designs and non-English publications, were excluded. The primary outcome was clinical relapse within one year. Study quality was assessed using the Newcastle-Ottawa Scale, and overall certainty of evidence was evaluated using the GRADE framework. Pooled odd ratios (ORs) and 95% confidence intervals (CIs) were calculated using DerSimonian-Laird random-effects meta-analysis based on estimates and standard errors. Heterogeneity was assessed using the I2 statistic. The publication bias was planned to assess using funnel plots and statistical tests if sufficient studies were available.

 

Results: 1945 studies were identified through the search. After removing duplicates, and abstract screening, 13 studies were selected for full-text review and 3 prospective cohort studies involving 276 patients with CD were included in the analysis. Pooled analysis demonstrated a significant association between UPF intake and relapse in patients with CD. Patients with higher versus lower UPF intake had increased odds for clinical relapse (OR 2.27, 95% CI 1.01-5.13, p = 0.048; I2 = 20.95%), although the certainty of the evidence was rated as very low according to the GRADE framework.

 

Conclusion: This study suggests that higher UPF intake is associated with increased odds of clinical relapse in patients with Crohn's disease in remission. However, the certainty of evidence is very low, and additional well-designed prospective studies and randomized trials are required before firm dietary recommendations can be made.

 

​

Xue M, McSHane C, Kim J, Khorasaniha R, Leibovitzh H, Shao J, Chen R, Jeong S, Li Q,. Madsen KL, Griffiths AM, Walters TD, Steinhart AH, Dieleman LA, Huynh HQ, Panaccione R, Aumais GL, Bitton A, Mack D, Jacobson K, Bressler B, Marshall JK, Plotkin L, Focht G, Bernstein CN, El-Matary W, Hyams JS, Otley A, Lee SH, Turner D, Armstrong H, Croitoru K, CCC-GEM consortium, Turpin W. β-Glucan and Inulin Estimated Intake are Associated with Reduced Risk of Crohn’s Disease, Improved Gut Barrier and Systemic Inflammation Markers, and Multi-Omic Signatures in a High-Risk Cohort.  Gastroenterology 2026; Oct;171(4):641-655.    

 

Background & aims: The cause of Crohn's disease (CD) remains unclear; however, evidence suggests fiber intake may play a role. We aimed to investigate the association between intake of total fiber and select fermentable fiber subtypes and future risk of CD in an at-risk population.

​

Methods: The Genetic, Environmental, Microbial Project prospectively followed asymptomatic first-degree relatives of individuals with CD. Habitual intake of total fiber and select fiber subtypes was estimated from baseline food frequency questionnaires and biologic samples were collected. Incident CD was confirmed during follow-up. Cox proportional hazards models estimated hazard ratios (HRs) for CD. Associations between fiber subtype intake and urinary fractional excretion of lactulose-mannitol ratio, C-reactive protein, gut microbiota (16S ribosomal RNA sequencing), and serum proteomics (Olink) were evaluated using multivariable regression models.

​

Results: During a median follow-up of 8.5 years of 3314 first-degree relatives, 94 developed CD. Higher β-glucan (HR, 0.70; 95% confidence interval, 0.54-0.92) and inulin (HR, 0.68; 95% confidence interval, 0.49-0.96) intake were associated with lower CD risk. Associations were strongest in those with higher baseline relative abundance of Erysipelotrichaceae UCG-003, but weaker with higher Colidextribacter. Higher β-glucan and inulin intake were associated with lower lactulose-mannitol ratio, lower abundance of pathobionts (Ruminococcus torques and Lachnoclostridium), and lower concentrations of inflammation- and barrier-related proteins, including C-reactive protein, triggering receptor expressed on myeloid cells-1, oncostatin M, and matrix metalloproteinase 9.

Conclusions: Higher estimated β-glucan and inulin intake was associated with preserved gut barrier function, lower systemic inflammatory markers, and lower CD risk, which was modified by the microbial context. These findings support microbiome-informed dietary strategies and intervention trials for CD prevention.

​

​

Machado P, Mazahery H, Black LJ, Tremlett H, Daly A, Pham NM, Tessema GA, Zhu F, Banwell B, Bar-Or A, Marrie RA, Bernstein CN, Mirza AI, Yeh EA, Waubant E, O’Mahony J, Dunlop E on behalf of the Canadian Demyelinating Disease Network Higher ultra-processed food consumption is associated with higher likelihood of paediatric-onset multiple sclerosis. Multiple Sclerosis and Related Diseases 2026 May:109:107159.

 

Background: Diets are increasingly dominated by ultra-processed foods, which have been linked to several chronic diseases. Emerging evidence suggests an association between ultra-processed food consumption and inflammatory diseases, including multiple sclerosis (MS).

​

Objective: To assess associations between consumption of ultra-processed foods and paediatric-onset MS (PoMS).

Methods: We used data from the microbiome sub-study of the Canadian Pediatric Demyelinating Disease Network Study for PoMS cases (symptom onset aged <18 years) and unaffected controls. Data on consumption of ultra-processed foods (defined within the Nova system) were derived from dietary intake data collected using the Block Kids Food Screener. Dietary contribution of ultra-processed foods (% of total grams consumed per day) was estimated. Logistic regression models were used to examine associations between ultra-processed food consumption (continuous and tertiles) and likelihood of PoMS. Models were adjusted for age at dietary data collection, sex, race, region of residence, and total energy intake.

​

Results: Dietary data were collected from PoMS participants (females=57, males=23) aged 5-28 years and controls (females=30, males=16) aged 8-26 years. Each additional 10% in ultra-processed food consumption was associated with a 35% higher odds of being a PoMS participant (adjusted odds ratio [aOR]=1.35, 95% CI 1.05, 1.73). Participants in the highest (versus lowest) tertile for ultra-processed food consumption had over five times higher odds of being a PoMS participant (aOR=5.30, 95% CI 1.36, 20.70).

​

Conclusion: Participants with PoMS reported greater consumption of ultra-processed foods compared to unaffected peers. More comprehensive longitudinal dietary histories are required to better understand this observation.

​

​

O’Mahony SL, Tollenaar SI, Khorasaniha R, Jovel J, Ba I,  Voisin A, Miller R, Olof H, Mahmood R, Marrie RA, Strachan E, Soares LP, Cheng C, Janveaux J, Azaidi D, Bernstein CN, Bonner C, Bar-Or A, Waubant E, Yeh A, Graham M. Arnold DL, Banwell BL, Zhu F, Mirza AI, Karimi-Abdolrezaee S, Tsai S, Tremlett H, McGregor K, Willing BP, Armstrong HK. Reduced fibre-fermenting capacity of gut microbes in multiple sclerosis may result in prebiotic dietary fibre β-fructan promoting inflammation and CNS damage. Gastroenterology 2026; e100296.

 

Background Some people with multiple sclerosis display changes in their gut microbiota with separate evidence suggesting worsened symptoms following a high-fibre diet. We hypothesised that in people with multiple sclerosis whose gut microbiota are less able to adequately ferment fibres, unfermented β-fructans induce inflammation.

Methods Diet data (n=48 multiple sclerosis, n=78 unaffected controls) and stool microbiome data (n=31 multiple sclerosis, n=61 unaffected controls) were previously collected from participants. Daily fibre subtype intakes were calculated and compared with fecal shotgun metagenomic sequencing in pediatric onset multiple sclerosis and unaffected persons. Response to unfermented β-fructans was examined in a germ-free experimental autoimmune encephalomyelitis mouse model (unable to ferment fibres). Mice were fed β-fructans or control fibre diet beginning at symptom onset (day 14). Experimental autoimmune encephalomyelitis scores and weights were recorded daily. Intestinal and central nervous system tissues were collected at two endpoints to examine inflammatory responses and demyelinating lesions.

Results Paediatric onset multiple sclerosis consumed less β-fructans (2.4 g/day±0.3 SD; p<0.05) than unaffected participants (3.6 g/day±0.4), which coincided with differences in the gut microbiota including lower fibre fermenting enzymes. Mice exposed to unfermented β-fructans sustained worsened EAE symptoms (day 20–28; p<0.05), immune activation in the gut and immune activation plus demyelinating lesions in the spinal cord compared with mice on control diet.

​

Conclusions  The gut microbiota of pediatric-onset multiple sclerosis had lower fibre fermenting properties, and our animal findings suggest that β-fructans induce worsened demyelination and gut–brain axis immune activation. Lower β-fructan consumption was observed among participants with pediatric-onset multiple sclerosis. Future longitudinal studies are warranted to confirm the findings uncovered in this manuscript.

​

​

Mirza AI, Zhu F, Knox N, Black L, Daly A, Bonner C, Van Domselaar G, Bernstein CN, Graham M, Marrie RA, Hart J, Yeh EA, Arnold DL, Bar-Or A, O’Mahoney J, Zhao Y, Hsiao W, Banweell B, Waubant E, Tremlett H. Mediterranean diet and associations with the gut microbiota and pediatric-onset multiple sclerosis using trivariate analysis. Communications Medicine (London) 2024; Jul 19;4(1):148.

 

Background: The interplay between diet and the gut microbiota in multiple sclerosis is poorly understood. We aimed to assess the interrelationship between diet, the gut microbiota, and multiple sclerosis.

Methods: We conducted a case-control study including 95 participants (44 pediatric-onset multiple sclerosis cases, 51 unaffected controls) enrolled from the Canadian Pediatric Demyelinating Disease Network study. All had completed a food frequency questionnaire ≤21-years of age, and 59 also provided a stool sample.

Results: Here we show that a 1-point increase in a Mediterranean diet score is associated with 37% reduced likelihood of developing multiple sclerosis (95%CI: 10%-53%). Higher fiber and iron intakes are also associated with reduced odds for developing multiple sclerosis. Diet, not multiple sclerosis, explains inter-individual gut microbiota variation. Several gut microbes abundances are associated with both the Mediterranean diet score and having multiple sclerosis, and these microbes are potential mediators of the protective associations of a healthier diet.

Conclusions: Our findings suggest that the potential interaction between diet and the gut microbiota is relevant in multiple sclerosis.

 

 

Bitarafan S, Zhu F, Mirza A, Bernstein CN, Van Domselaar G, Marrie RA, Yeh EA, Zhao Y, Banwell B, Waubant E, Tremlett H. Assessment of Dietary Intake and its Inflammatory Potential in Persons with Pediatric-onset Multiple Sclerosis. Multiple Sclerosis and Related Disorders 2024; June; 86:105599.

​

Objective: To compare diet and the modified dietary inflammatory index between individuals with pediatric-onset multiple sclerosis, monophasic acquired demyelinating syndromes, and controls.

Methods: The association between diet, the modified dietary inflammatory index, and disease status was examined in 131 individuals with pediatric-onset multiple sclerosis (n=38) monophasic acquired demyelinating syndromes (n=45), controls (n=48) using logistic regression.

Results: The associations between diet and pediatric-onset multiple sclerosis were modest, reaching significance for whole grain intake (adjusted odds ratio, aOR=0.964, 95 % confidence intervals, CI:0.934-0.995) but not modified dietary inflammatory index (aOR=1.20, 95 %CI:0.995-1.46) versus controls. No findings for monophasic acquired demyelinating syndromes, reached significance versus controls.

Conclusions: Individuals with pediatric-onset multiple sclerosis, but not monophasic acquired demyelinating syndromes, had lower dietary whole grain intake than controls.

 

​

Vagianos K, Dolovich C, Witges K, Graff LA, Bernstein CN. Ultra-processed food, disease activity and inflammation in Ulcerative Colitis: The Manitoba Living with IBD Study. American Journal of Gastroenterology 2024; Jun 1;119(6):1102-1109.

​

Background: The purpose of this study was to investigate the relationship between ultra-processed food (UPF) consumption and (i) symptomatic disease and (ii) intestinal inflammation among adults with inflammatory bowel disease (IBD).

Methods: We identified participants from the Manitoba Living with IBD study. Active disease was defined using the IBD Symptom Inventory (score >14 for Crohn’s disease; >13 for ulcerative colitis); fecal calprotectin was measured for intestinal inflammation (>250 μg/g). Diet data were collected using the Harvard Food Frequency Questionnaire. UPF consumption was determined by the NOVA classification system. Percentage of energy consumption from UPFs was calculated and divided into 3 tertiles (T1 = low; T3 = high). Multiple linear regression analysis was used for active disease and inflammation predicted by UPF consumption.

Results: Among 135 participants (65% with Crohn’s disease), mean number of episodes of active disease (14.2 vs 6.21) and active inflammation (1.6 vs 0.6) was significantly higher among participants with ulcerative colitis in T3 compared with T1 of UPF consumption ( P < 0.05). When adjusting for age, sex, disease type, and duration, number of episodes of active disease was lower in T1 compared with T3 (β = -7.11, P = 0.02); similarly, number of episodes of intestinal inflammation was lower in T1 (β = -0.95, P = 0.03). No significant differences were observed among participants with Crohn’s disease.

Conclusions: Ultra-processed food (UPF) consumption may be a predictor of active symptomatic disease and inflammation among participants with ulcerative colitis. Reducing UPF consumption is a dietary strategy that can be suggested for minimizing symptoms and inflammation among people living with IBD.

 

​

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.

​