These findings (based on repeated measures of IL6 over a period of time ) support the hypothesis that persistently elevated levels of IL-6 contribute to the development of common mental disorder.The fact that previous studies relied on a single measurement of IL-6 may partially explain the mixed findings: a one-off measure does not reliably capture the chronicity of inflammation. The present study has limitations: common mental disorder measured by a questionnaire is not the same as clinical diagnosis of depression or anxiety. Our data are from an occupational cohort where participants are likely to be healthier than the general population. Loss to follow-up accumulated over the extended follow-up; however, there was no evidence of major differences between the analytic sample and the sample at study recruitment.
Our findings have important clinical implications. If the observed association is causal, then targeting chronic inflammation with anti-inflammatory drugs could be useful in prevention of common mental disorder. Further studies are needed to clarify the underlying mechanisms, such as activation of the tryptophan-degrading enzyme, changes in indoleamine 2,3-dioxygenase, and abnormalities of the hypothalamic–pituitary–adrenal axis. Future investigations should also test the side effects, since anti-inflammatory strategies might increase the risk of infection and malignancy
Our findings have important clinical implications. If the observed association is causal, then targeting chronic inflammation with anti-inflammatory drugs could be useful in prevention of common mental disorder. Further studies are needed to clarify the underlying mechanisms, such as activation of the tryptophan-degrading enzyme, changes in indoleamine 2,3-dioxygenase, and abnormalities of the hypothalamic–pituitary–adrenal axis. Future investigations should also test the side effects, since anti-inflammatory strategies might increase the risk of infection and malignancy
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