Is Splenda, or Sucralose, Causally Linked to Inflammatory Bowel Disease?

Extract

To the Editor:

Rodriguez-Palacios et al.¹ concluded, on the basis of the microbiome and myeloperoxidase (MPO) observations in ileitis-prone (SAMP) mice, that “consumption of sucralose/maltodextrin-containing foods might exacerbate MPO intestinal reactivity only in individuals with a pro-inflammatory predisposition, such as CD [Crohn’s disease].” Chassaing and Gewirtz comment that this study’s findings “suggest that consumption of this synthetic sweetener may be a specific factor that contributes to the development of IBD [inflammatory bowel disease] in persons genetically prone to this disorder.”² Both statements require critical analysis for the sake of clinicians who treat, and patients who have, IBD. The tested material was 99% maltodextrin and 1% sucralose by weight. Maltodextrin is a natural derivative of starch. Sucralose is not a substrate for gut microflora, nor does it cause adverse gastrointestinal effects, even after chronic exposure to high doses.^{3, 4} The authors acknowledge that maltodextrin is a substrate for Gammaproteobacteria. The reported increase in Escherichia coli is consistent with this fact. It is also well known that gut microbiome populations are driven primarily by host diet. As noted by Chassaing and Gewirtz, maltodextrin is also “widely incorporated into many processed foods at levels that would result in greater exposure than that attained from consuming [the retail] Splenda [product tested].” There was, however, no test on maltodextrin alone, or on any other similarly fermentable carbohydrate in the study by Rodriguez-Palacios et al.; additionally, no data were presented to understand normal variability in the SAMP mouse microbiome with normal dietary fluctuations, so it is not appropriate to assume that the tested product is some sort of “smoking gun.” SAMP mice also produce little or no CCL21,⁵ which is important for normal immune response, and this could predispose the intestinal tissue to bacterial infiltration into the ileal lamina propria. There is also a lack of a dose response in MPO activity, the end point treated as a surrogate marker for inflammation, after a 10-fold increase in dose. Finally, no histological differences in actual disease severity were detected in treated vs control healthy or SAMP mice, consistent with the toxicological research.³ There are also serious problems with the methodology in the cited IBD/low-calorie sweetener correlations. In particular, the citation provides no information correlating sucralose intake to IBD, so no true correlation can be established. In all, the headlines and conclusions presented are not supported by the collective evidence relevant to the tested product.