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G.W. Moran, Subrata Ghosh, Reply to Mendall, Inflammatory Bowel Diseases, Volume 20, Issue 5, 1 May 2014, Page E13, https://doi.org/10.1097/MIB.0000000000000012
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We thank Dr. Mendall for his comments1 about our study describing the increasing average weight of patients with Crohn's disease in clinical trials over the years and the significant correlation between this novel finding and disease activity.2 This was a hypothesis-generating study of the data published in connection with previous clinical trials.
The author states that fecal calprotectin is a useful surrogate marker for Crohn's disease risk and could thus be useful in future epidemiological studies. The role of fecal calprotectin in the association between obesity and Crohn's disease is a valid one. It was not possible to address this in our study of previous clinical trials of therapeutic agents. The associations ascribed to obesity, such as decreased physical activity3 and a high-fat diet,4 are ecological and do not impute causality with Crohn's disease. Adiposity in general may be proinflammatory as a result of multiple adipokine and cytokine effects.
We agree that obesity might have a causal effect in Crohn's disease and could possibly affect its clinical outcome.2 Even in the absence of adiposity, a high-fat diet might accelerate disease pathogenesis in Crohn's disease,5 and alteration of the microbiome and barrier function could underlie this association.
