Studies in the last decade reveal a remarkable increase in the incidence of pediatric inflammatory bowel disease (IBD). Abramson et al (1) determined that the annual incidence of Crohn disease in northern California increased from 2.2/100,000 in 1996 to 4.3 in 2006, and ulcerative colitis increased from 1.8 to 4.9 in the same period. Intriguingly, the pattern of increase is not the same among all developed countries. Wrobel et al (2) determined that the incidence of pediatric IBD in southern Alberta, Canada, had been 2.3 from 1983 to 1987, 2.5 from 1988 to 1992, 5.0 from 1993 to 1998, and 6.5 from 1999 to 2005, indicating a dramatic increase in the early 1990s. A study by Perminow et al (3) identified a sharp increase in pediatric IBD in south eastern Norway since 2005. The cause for these increases remains a mystery. Furthermore, if real, contemporary increases in pediatric IBD would argue against many popular recognized or suspected etiological factors, such as genes, smoking, nonsteroidal anti-inflammatory drugs, bugs (eg, Mycobacterium avium subsp paratuberculosis), vitamin D deficiency, or improved hygiene. It seems also unlikely to be explained by changes in immigration or diagnostic strategies.
About 10 years ago, a series of findings led me to suspect that saccharin may be an important causative factor for the emergence of and dramatic increase in IBD in the last century, through its inhibition of gut bacteria, impairing inactivation of digestive protease, which may compromise the mucus layer and gut epithelium (4). I have found further evidence suggesting that sucralose, a new artificial sweetener, may be also linked to IBD through a similar mechanism (5). Sucralose was first approved in Canada in 1991, followed by approval in many other countries such as the United States in 1998 and the European Union in 2004 (6). Interestingly, the observed increase in pediatric IBD in the different countries as described above occurred shortly after the approval of sucralose. Although both saccharin and sucralose were widely used sweeteners, the use of saccharin in food and drink products specified for children was greatly restricted, given concerns about the potential carcinogenicity in animals (7). Thus, the introduction, without restriction, of sucralose would have a potentially greater impact on children and, as I have argued, on the prevalence of pediatric IBD.
I strongly encourage further investigation of the role of food additives, particularly artificial sweeteners, in the etiology of IBD in children.
1. Abramson O, Durant M, Mow W, et al. Incidence, prevalence, and time trends of pediatric inflammatory bowel disease in northern California, 1996 to 2006. J Pediatr
2. Wrobel I, Butzner J, Nguyen N, et al. Epidemiology of pediatric IBD in a population-based cohort in southern Alberta, Canada (1983-2005). J Pediatr Gastroenterol Nutr
3. Perminow G, Brackmann S, Lyckander LG, et al. A characterization in childhood inflammatory bowel disease, a new population-based inception cohort from South-Eastern Norway, 2005-07, showing increased incidence in Crohn's disease. Scand J Gastroenterol
4. Qin XF. Impaired inactivation of digestive proteases by deconjugated bilirubin: the possible mechanism for inflammatory bowel disease. Med Hypotheses
5. Qin X. What caused the recent worldwide increase of inflammatory bowel disease: should sucralose be added as a suspect? Inflamm Bowel Dis
6. Davies E. Sweets for my sweet. Chem World
7. Hicks J. The pursuit of sweet: a history of saccharin. Chem Herit Mag