Taking antidepressants could help people who suffer from inflammatory bowel disease (IBD), a new Canadian study has found.
Researchers at McMaster University Medical Centre's Intestinal Disease Research Program induced depression in mice and then treated them with antidepressants.
They found that while the mice displayed depression-related symptoms, they had an increased likelihood of inflammation of the digestive system. In turn, the risk of inflammation decreased after the mice were given antidepressants.
The researchers found that the vagus nerve (which runs from the brain stem to the gastrointestinal tract) releases nicotine, which itself guards against inflammation. Without this action, the antidepressants did not improve stomach inflammation.
Jean-Eric Ghia, lead study author and a post-doctoral fellow in McMaster's program, said that the effect is cyclical.
"If patients are depressed, the vagus nerve is probably not working properly because it is not going to release nicotine, and probably that is why depressed patients have a greater sensitivity to inflammation," Ghia told CTV.ca.
So when patients are given antidepressants, Ghia speculated, the action in the brain re-stimulates the vagus nerve to produce nicotine, which in turn reduces the stomach inflammation.
The findings are published online in The Journal of Clinical Investigation.
"The results of this study have clinical relevance," the study's authors write.
"First, they prompt close consideration of the relationship between depression and disease activity in patients with IBD. Second, if there is indeed a correlation, then depressed patients with IBD might be selected for novel treatment strategies."
They noted that the treatment of IBD could now include antidepressants, vagus-nerve stimulation or nicotine therapy.
According to the Crohn's & Colitis Foundation of Canada, nearly 200,000 Canadians suffer from IBD, which doesn't have a cause or a cure. IBD encompasses two diseases: Crohn's disease and ulcerative colitis. They are characterized by inflammation of the intestines, which can lead to bleeding sores. Symptoms include abdominal pain, cramping, fatigue and diarrhea.
Scientists have long believed that depression can exacerbate IBD. Previous studies have linked the two, but it is not known if depression causes IBD, or the IBD leads to depression.
Abstract:
Impaired parasympathetic function increases susceptibility to inflammatory bowel disease in a mouse model of depression/>
Jean-Eric Ghia, Patricia Blennerhassett, and Stephen M. Collins/>
Clinical and experimental evidence indicates that intestinal inflammatory conditions can be exacerbated by behavioural conditions such as depression. The recent demonstration of a tonic counterinflammatory influence mediated by the vagus nerve in experimental colitis provides a potential link between behaviour and gut inflammation. Here we show that experimental conditions that induced depressive-like behaviours in mice increased susceptibility to intestinal inflammation by interfering with the tonic vagal inhibition of proinflammatory macrophages and that tricyclic antidepressants restored vagal function and reduced intestinal inflammation. These results show that reserpine-induced monoamine depletion and maternal separation, 2 models for depression, produced a vulnerability to colitis by a mechanism involving parasympathetic transmission and the presence of gut macrophages. The tricyclic antidepressant desmethylimipramine protected against this vulnerability by a vagal-dependent mechanism. Together these results illustrate the critical role of the vagus in both the vulnerability to inflammation induced by depressive-like conditions and the protection afforded by tricyclic antidepressants and rationalize a clinical evaluation of both parasympathomimetics and tricyclic antidepressants in treatment of inflammatory bowel disease.
