Western and Carnivorous Dietary Patterns are Associated with Greater Likelihood of IBD Development in a Large Prospective Population-based Cohort.

OBJECTIVE: Nutrition plays a role in the development of Crohn's disease [CD] and ulcerative colitis [UC]. However, prospective data on nutrition and disease onset are limited. Here, we analysed dietary patterns and scores in relation to inflammatory bowel disease [IBD] development in a prospective population-based cohort. METHODS: We analysed 125 445 participants of whom 224 individuals developed de novo UC and 97 CD over a maximum 14-year follow-up period. Participants answered health-related [also prospectively] and dietary questionnaires [FFQ] at baseline. Principal component analysis [PCA] was conducted deriving a-posteriori dietary patterns. Hypotheses-based a-priori dietary scores were also calculated, including the protein score, Healthy Eating Index, LifeLines Diet Score [LLDS], and alternative Mediterranean Diet Score. Logistic regression models were performed between dietary patterns, scores, and IBD development. RESULTS: PCA identified five dietary patterns. A pattern characterised by high intake of snacks, prepared meals, non-alcoholic beverages, and sauces along with low vegetables and fruit consumption was associated with higher likelihood of CD development (odds ratio [OR]: 1.16, 95% confidence interval [CI]: 1.03-1.30, p = 0.013). A pattern comprising red meat, poultry, and processed meat, was associated with increased likelihood of UC development [OR: 1.11, 95% CI: 1.01-1.20, p = 0.023]. A high diet quality score [LLDS] was associated with decreased risk of CD [OR: 0.95, 95% CI: 0.92-0.99, p = 0.009]. CONCLUSIONS: A Western dietary pattern was associated with a greater likelihood of CD development and a carnivorous pattern with UC development, whereas a relatively high diet quality [LLDS] was protective for CD development. Our study strengthens the importance of evaluating dietary patterns to aid prevention of IBD in the general population.

Predicting (side) effects for patients with inflammatory bowel disease: The promise of pharmacogenetics.

Inflammatory bowel disease (IBD) is a chronic and heterogeneous intestinal inflammatory disorder. The medical management of IBD aims for long-lasting disease remission to prevent complications and disease progression. Early introduction of immunosuppression forms the mainstay of medical IBD management. Large inter-individual variability in drug responses, in terms of both efficacy and toxicity, leads to high rates of therapeutic failure in the management of IBD. Better patient stratification is needed to maximize patient benefit and minimize the harm caused by adverse events. Pre-treatment pharmacogenetic testing has the potential to optimize drug selection and dose, and to minimize harm caused by adverse drug reactions. In addition, optimizing the use of cheap conventional drugs, and avoiding expensive ineffective drugs, will lead to a significant reduction in costs. Genetic variation in both TPMT and NUDT15, genes involved in thiopurine metabolism, is associated to an increased risk of thiopurine-induced myelosuppression. Moreover, specific HLA haplotypes confer risk to thiopurine-induced pancreatitis and to immunogenicity to tumor necrosis factor-antagonists, respectively. Falling costs and increased availability of genetic tests allow for the incorporation of pre-treatment genetic tests into clinical IBD management guidelines. In this paper, we review clinically useful pharmacogenetic associations for individualized treatment of patients with IBD and discuss the path from identification of a predictive pharmacogenetic marker to implementation into IBD clinical care.

Development and validation of a web-based questionnaire to identify environmental risk factors for inflammatory bowel disease: the Groningen IBD Environmental Questionnaire (GIEQ).

BACKGROUND: In the complex etiology of inflammatory bowel disease (IBD), the exposome is a major contributor. Though many environmental exposures have been identified, quality of evidence varies greatly and overall evidence for the exposome is inconclusive. A universal, precise, and reproducible measurement tool is needed to study the exposome in IBD. METHODS: We built the web-based Groningen IBD Environmental Questionnaire (GIEQ), an extensive and structured questionnaire measuring potentially involved environmental exposures, consisting of 848 items, subdivided into 15 categories. For validation, 76 IBD patients completed the GIEQ twice (2-month interval). Cohen's kappa and correlation coefficients were used to compare both fills. Internal consistency was evaluated using Cronbach's alpha tests. Proportional bias was examined using Bland-Altman plots. RESULTS: In general, we obtained a mean kappa coefficient of 0.78 (standard deviation 0.17) for categorical questions and a mean intraclass correlation coefficient of 0.88 (0.15) for numeric questions. Cronbach's alpha ranged from 0.64 to 1.0 with a mean of 0.79 (0.14). Bland-Altman plots showed proportional bias only for current physical activity score. CONCLUSIONS: The GIEQ is a reliable measurement tool to study the exposome in IBD, enabling consistent measurement of an extended number of environmental factors and their interactions. Use of the GIEQ across IBD cohorts will lead to more standardized, generalizable, and comparable results. Also, the GIEQ can be used for calculation of an exposome risk score, applicable for secondary prevention by identifying high-risk patients as well as to analyze interactions between the exposome and other aspects of IBD etiology.