Patients with depression are more likely to develop inflammatory bowel disease (IBD), but antidepressant treatment appears to reduce that association, a recent study found.
The retrospective study used data on more than 5 million patients from the Health Improvement Network to identify a cohort of 403,665 patients who developed new-onset depression in 1986 to 2012. The rate at which these patients developed Crohn's disease or ulcerative colitis was compared to that in a reference group of patients in the database without depression, after controlling for age, sex, socioeconomic status, comorbid conditions, smoking, anxiety, and antidepressant use. Median follow-up was 6.7 years. Results were published by Gut on Oct. 18.
Patients with depression had a significantly greater risk of developing Crohn's disease (adjusted hazard ratio [HR], 2.11; 95% CI, 1.65 to 2.70) or ulcerative colitis (adjusted HR, 2.23; 95% CI, 1.92 to 2.60) than those without depression. Taking selective serotonin reuptake inhibitors (SSRIs) or tricyclic antidepressants appeared to be protective against both Crohn's disease (HRs, 0.63 [95% CI, 0.50 to 0.78] and 0.77 [95% CI, 0.61 to 0.97], respectively) and ulcerative colitis (HRs, 0.48 [95% CI, 0.42 to 0.55] and 0.59 [95% CI, 0.51 to 0.68], respectively). Use of mirtazapine, serotonin norepinephrine reuptake inhibitors (SNRIs), or serotonin modulators appeared to be protective against ulcerative colitis (HRs, 0.34 [95% CI, 0.15 to 0.77], 0.46 [95% CI, 0.25 to 0.83], and 0.46 [95% CI, 0.23 to 0.92], respectively).
The authors believe this is the first study to explore the temporal relationship between depression and IBD, including the effect of antidepressants. They noted that the association between depression and inflammation is well established and that another recent study showed that the relationship between IBD and mood disorders is bidirectional.
The protective effect of SSRIs and SNRIs might be explained by the drugs increasing tissue levels of norepinephrine and serotonin, which are decreased in the inflamed mucosa of patients with IBD, the authors said. The differing effectiveness in the two conditions is unexplained but might result from different neurotransmitter-related immune modulatory responses. Strengths of the study include its large sample size, and limitations include the fact that the effects of other depression therapies, such as cognitive behavioral or electroconvulsive therapy, and prognostic factors, such as social support, were not explored.
The authors recommended that their findings be replicated using other datasets that specify the severity of depression. Based on the results, clinicians should increase their suspicion for IBD in patients with depression and gastrointestinal symptoms and consider treatment with antidepressants, they advised.