Psychosocial risk markers for new onset irritable bowel syndrome - results of a large prospective population-based study

Nicholl, B.I., Halder, S.L., Macfarlane, G.J., Thompson, D.G., O'Brien, S., Musleh, M. and McBeth, J. (2008) Psychosocial risk markers for new onset irritable bowel syndrome - results of a large prospective population-based study. Pain, 137 (1), 147-155. (doi:10.1016/j.pain.2007.08.029).

Abstract

Irritable bowel syndrome (IBS) affects up to 22% of the general population. Its aetiology remains unclear. Previously reported cross-sectional associations with psychological distress and depression are not fully understood. We hypothesised that psychosocial factors, particularly those associated with somatisation, would act as risk markers for the onset of IBS. We conducted a community-based prospective study of subjects, aged 25–65 years, randomly selected from the registers of three primary care practices. Responses to a detailed questionnaire allowed subjects’ IBS status to be classified using a modified version of the Rome II criteria. The questionnaire also included validated psychosocial instruments. Subjects free of IBS at baseline and eligible for follow-up 15 months later formed the cohort for this analysis (n = 3732). An adjusted participation rate of 71% (n = 2456) was achieved at follow-up. 3.5% (n = 86) of subjects developed IBS. After adjustment for age, gender and baseline abdominal pain status, high levels of illness behaviour (odds ratio (OR) = 5.2; 95% confidence interval (95% CI) 2.5–11.0), anxiety (OR = 2.0; 95% CI 0.98–4.1), sleep problems (OR = 1.6; 95% CI 0.8–3.2), and somatic symptoms (OR = 1.6; 95% CI 0.8–2.9) were found to be independent predictors of IBS onset. This study has demonstrated that psychosocial factors indicative of the process of somatisation are independent risk markers for the development of IBS in a group of subjects previously free of IBS. Similar relationships are observed in other “functional” disorders, further supporting the hypothesis that they have similar aetiologies.

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Contributors

Author: J. McBeth

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