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Bidirectional associations between depression/anxiety and bowel disease in a population based cohort
  1. Carsten Leue1,
  2. Jim van Os1,5,
  3. Jan Neeleman2,
  4. Ron de Graaf3,
  5. Wilma Vollebergh3,
  6. R W Stockbrügger4
  1. 1Department of Psychiatry and Neuropsychology, South Limburg Mental Health Research and Teaching Network, EURON, Maastricht University, Maastricht, Netherlands
  2. 2Julius Center for Health Sciences and Primary Care, University Medical Center, Utrecht, Netherlands
  3. 3The Netherlands Institute of Mental Health and Addiction, Trimbos Institute, Utrecht, Netherlands
  4. 4Department of Gastroenterology and Hepatology, University Hospital of Maastricht, Maastricht, Netherlands
  5. 5Division of Psychological Medicine, Institute of Psychiatry, London, UK
  1. Correspondence to:
 Professor J van Os
 Department of Psychiatry and Neuropsychology, Maastricht University, PO Box 616 (DRT 10), 6200 Maastricht, Netherlands;

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Kurina and colleagues1 reported that neurotic disorders preceded inflammatory bowel disease (IBD), adding credence to the suggestion that depression/anxiety may either play an aetiological part in the onset of IBD or that both conditions share a common abnormality.2 As their findings were based on record linkage of people with neurotic disorder who received treatment in mental health services, representing only a small minority of such cases, replication independent of mental health service treatment setting is necessary to exclude the well known bias attributable to selection of the most severely ill with the highest comorbidity rates.

This analysis is a part of the Netherlands mental health survey and incidence study (NEMESIS), a longitudinal study of the prevalence, incidence, course, consequences, and somatic comorbidities of psychiatric disorders in the Dutch general population, approved by a recognised ethics committee. The sample consists of 7076 people who were examined at three measurement points (baseline, T1, and T2) over a period of three years.3,4 Subjects were seen at home by trained interviewers using the composite international diagnostic interview (CIDI),5 yielding DSM-III-R diagnoses. At baseline and at T2, trained interviewers asked subjects about a range of somatic conditions in the past 12 months. The question on bowel disease was: “did you suffer, in the past 12 months, from severe bowel disease for a period of longer than 3 months?”

There were 3428 people with complete data on depression and somatic conditions, including cancer, at both baseline and T2. At baseline, 88 people (2.6%) reported “severe bowel disease” (SBD), for which 76% received medical treatment, and 525 (15.3%) reported a history of depression according to CIDI interview. There was significant comorbidity of SBD and depression at baseline (OR = 2.3, 95% CI: 1.4 to 3.6) (table 1).

Table 1

 Prospective associations between depression and severe bowel disease

After three years, when assessments were repeated, the incidences for SBD and depression were 1.5% (of which 85% in receipt of medical treatment) and 4.0% respectively. A baseline composite variable was made indicating presence of any of 29 somatic illnesses other than SBD. Cases with cancer were excluded from the SBD case definition.

People with depression who did not have a history of SBD at baseline had a greater risk than those without depression of reporting SBD at follow up, independent of other baseline somatic illnesses, medication use, age, class, sex, and depression at follow up (logistic regression adjusted OR = 2.0, 95% CI: 1.01 to 3.8). Similarly, people with SBD at baseline who were free of depression had a greater risk than those without SBD of having depression at follow up, independent of any other baseline somatic illness at baseline, age, class, and sex (adjusted OR: 2.5, 95% CI: 1.1 to 5.8).

The measures of SBD were not precise, and probably included not only people with IBD but also people with severe irritable bowel syndrome (IBS). However, IBD and IBS themselves are associated with each other over time6 and therefore the bidirectional gut-brain relations shown in this study are compatible with the hypothesis that severe non-cancerous bowel disease and depressive illness have reciprocal aetiological influences or, more parsimoniously, are varying expressions of a partly shared aetiological process. In support of the latter hypothesis is recent work showing that IBD is associated with familial transmission of an endophenotype characterised by subclinical inflammation7 that may predispose to no only IBD, but also to depression.8