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Journal of Pediatric Gastroenterology & Nutrition:
doi: 10.1097/MPG.0b013e3182a504e8
Letters to the Editor

How to Explain the Discordant Change of Ulcerative Colitis and Crohn Disease in Adjacent or Even the Same Regions and Time Periods

Qin, Xiaofa

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Department of Surgery, UMDNJ-New Jersey Medical School, Newark

To the Editor:

I read with great interest the article by Malmborg et al (1) regarding the increase of ulcerative colitis (UC) but decrease in Crohn disease (CD) in children in northern Stockholm County during 2005–2007 after a previous decade-long continuous increase in CD and stability of UC. This article also discussed the discordances in the incidence, ratio, and temporal changes of UC versus CD in other Scandinavian and Western countries over time (2–5). It remains a big puzzle and seems overwhelmingly complex; however, in my opinion, it could be extremely simple. Most of these studies are in children, which may rule out many presently suspected factors such as smoking. Recently, I came up with a unified hypothesis for the etiology of inflammatory bowel disease (IBD) (6), suggesting that UC and CD may be just 2 manifestations of the same morbidity rather than 2 different diseases. Both UC and CD may be caused by the inhibition of gut bacteria by some dietary chemicals and the resultant overdigestion of the mucus layer and gut tissue by poorly inactivated proteases. Although I focus on saccharin and sucralose in my article (6), other dietary chemicals such as cyclamate and acesulfame K actually have similar inhibitory effects on gut bacteria as saccharin, thus may also be linked to IBD (7). According to the proposed hypothesis, certain extent inhibition of gut bacteria by a factor may cause UC, whereas a further inhibition by even the same factor may lead to a shift toward CD (6). Thus, the simultaneous increase in UC but decrease in CD in northern Stockholm as shown in the study by Malmborg et al may be caused by a decreased exposure of some causative factor such as a remarkable decrease in cyclamate consumption because of a change in European Union regulation in 2004 that reduced the maximum permitted level for cyclamate in soft drinks from 400 to 250 mg/L (8,9). Interestingly, in 2004, the European Union approved the marketing of sucralose, which is suspected to be linked to IBD (6). Cyclamate is heavily used in countries such as Denmark (8,9) and Sweden (10), with consumption far beyond the acceptable daily intake in some children, whereas the use of cyclamate in the neighboring Norway is near zero (11); however, a study conducted in 2007 found high concentrations of sucralose in the surface water near cities such as Oslo, Norway, but much lower concentrations in cities in Sweden and Denmark (12). The negligible use of cyclamate but heavy use of sucralose in Norway is in accordance with the remarkable increase in pediatric IBD in southeastern Norway during 2005–2007 (3). We can see that the differences in legislation and marketing in food additives makes it possible for big variations among different regions and over time. Thus, the peculiar pattern of changes may not be that mysterious and it may have actually reflected the innate similarity and connection between UC and CD, rather than the differences between them.

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REFERENCES

1. Malmborg P, Grahnquist L, Lindholm J, et al. Increasing incidence of paediatric inflammatory bowel disease in northern Stockholm County, 2002–2007. J Pediatr Gastroenterol Nutr 2013; 57:29–34.

2. Jakobsen C, Wewer V, Urne F, et al. Incidence of ulcerative colitis and Crohn's disease in Danish children: still rising or levelling out? J Crohns Colitis 2008; 2:152–157.

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 2009; 44:446–456.

4. Lehtinen P, Ashorn M, Iltanen S, et al. Incidence trends of pediatric inflammatory bowel disease in Finland, 1987–2003, a nationwide study. Inflamm Bowel Dis 2011; 17:1778–1783.

5. Hope B, Shahdadpuri R, Dunne C, et al. Rapid rise in incidence of Irish paediatric inflammatory bowel disease. Arch Dis Child 2012; 97:590–594.

6. Qin X. Etiology of inflammatory bowel disease: a unified hypothesis. World J Gastroenterol 2012; 18:1708–1722.

7. Pfeffer M, Ziesenitz SC, Siebert G. Acesulfame K, cyclamate and saccharin inhibit the anaerobic fermentation of glucose by intestinal bacteria. Z Ernahrungswiss 1985; 24:231–235.

8. Leth T, Fabricius N, Fagt S. Estimated intake of intense sweeteners from non-alcoholic beverages in Denmark. Food Addit Contam 2007; 24:227–235.

9. Leth T, Jensen U, Fagt S, et al. Estimated intake of intense sweeteners from non-alcoholic beverages in Denmark, 2005. Food Addit Contam Part A Chem Anal Control Expo Risk Assess 2008; 25:662–668.

10. Ilback NG, Alzin M, Jahrl S, et al. Estimated intake of the artificial sweeteners acesulfame-K, aspartame, cyclamate and saccharin in a group of Swedish diabetics. Food Addit Contam 2003; 20:99–114.

11. Husoy T, Mangschou B, Fotland TO, et al. Reducing added sugar intake in Norway by replacing sugar sweetened beverages with beverages containing intense sweeteners—a risk benefit assessment. Food Chem Toxicol 2008; 46:3099–3105.

12. Loos R, Gawlik BM, Boettcher K, et al. Sucralose screening in European surface waters using a solid-phase extraction-liquid chromatography-triple quadrupole mass spectrometry method. J Chromatogr A 2009; 1216:1126–1131.

© 2013 by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology,

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