IBS in twins: genes and environment

May-Bente Bengtson ^1*, Thorbjorn Ronning ², Morten Vatn ¹ and Jennifer Harris ²

¹ University of Oslo, Norway
² The Norwegian Institute of Public Health, Norway

^* To whom correspondence should be addressed. E-mail: trolabe{at}online.no.

Accepted 15 August 2006

Abstract

Background and aims: Both environmental and genetic factors may contribute to irritable bowel syndrome (IBS). Nutrition in fetal life, an early environmental factor, seems to influence the development of chronic diseases later in life, like coronary heart disease, hypertension and non-insulin diabetes. This population-based twin study evaluated the association between intrauterine growth, measured by weight and gestational age, and IBS. Structural equation analyses were conducted to analyse genetic and environmental sources of variation in liability to IBS.

Methods: A postal questionnaire was sent to 12700 Norwegian twins born between 1967 and 1979. The questionnaire included a checklist of 31 illnesses and symptoms, including IBS. The influence of birth weight on developing IBS was tested in four weight groups. Disease discordant monozygotic (MZ) pairs were analysed to test the association between intrauterine growth and IBS.

Results: Concordance for IBS was significantly greater (p=0,011) in monozygotic (22,4%) than in dizygotic (9,1%) twins. The heritability of IBS was estimated to be 48,4% among females. Birth weight below 1500g (adjusted OR=2.4, 95% CI:1.1, 5.3)contributed significantly to development of IBS, which appeared 7.7 years earlier than in higher weight groups. In the MZ group with birth weights lower than 2500g, twins with IBS were significantly lighter than the twins without disease (190,6g, p=0,02).

Conclusion: The present study demonstrates that restricted fetal growth, has a significant influence on the development of IBS later in life. Weight below 1500 g influences age at onset. Genetic contribution appears to be important for IBS among females.

Keywords: genetic factors, irritable bowel syndrome, population based, restricted birth weight, twins

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

Relevant Articles

Digest

Robin Spiller and Alastair Watson
Gut 2006 55: 1685. [Extract] [Full Text] [PDF]

This article has been cited by other articles:

• Saito, Y. A., Strege, P. R., Tester, D. J., Locke, G. R. III, Talley, N. J., Bernard, C. E., Rae, J. L., Makielski, J. C., Ackerman, M. J., Farrugia, G. (2009). Sodium channel mutation in irritable bowel syndrome: evidence for an ion channelopathy. Am. J. Physiol. Gastrointest. Liver Physiol. 296: G211-G218 [Abstract] [Full Text]  
• Zoetendal, E G, Rajilic-Stojanovic, M, de Vos, W M (2008). High-throughput diversity and functionality analysis of the gastrointestinal tract microbiota. Gut 57: 1605-1615 [Abstract] [Full Text]  
• Kapeller, J., Houghton, L. A., Monnikes, H., Walstab, J., Moller, D., Bonisch, H., Burwinkel, B., Autschbach, F., Funke, B., Lasitschka, F., Gassler, N., Fischer, C., Whorwell, P. J., Atkinson, W., Fell, C., Buchner, K. J., Schmidtmann, M., van der Voort, I., Wisser, A.-S., Berg, T., Rappold, G., Niesler, B. (2008). First evidence for an association of a functional variant in the microRNA-510 target site of the serotonin receptor-type 3E gene with diarrhea predominant irritable bowel syndrome. Hum Mol Genet 17: 2967-2977 [Abstract] [Full Text]  
• McOmber, M. A., Shulman, R. J. (2008). Pediatric Functional Gastrointestinal Disorders. Nutr Clin Pract 23: 268-274 [Abstract] [Full Text]