tweet). Of course depression is related to stress. But a recent meta-analysis of inflammatory markers in depression didn't make this point clear. Instead, it indicated (as I've said in a previous post) that the motivation for studying the role of inflammation in depression is to identify a novel therapeutic target. It concluded that depression is a pro-inflammatory state (without being very precise about what that means).
Actually, the meta-analysis is useful as it provides evidence that the inflammatory marker elevations are not due to an inflamed sub-group as such. Nonetheless, if we ever get as far as anti-inflammatory agents being marketed for depression (see previous post), I suspect this will, at least initially, be focused on those with raised markers or those with physical illness as well as depression (see another previous post).
Despite attempts to eliminate confounders, such as smoking and obesity, there are questions about how effective these strategies are. More importantly, any increases in inflammatory markers in depression are generally not of the same order as in autoimmune or inflammatory diseases (see another previous post). Psychosocial stress itself raises inflammatory markers. So, why don't we just stick with the obvious explanation that the increase in inflammatory markers in depression is due to psychosocial stress?