JESS Seminar: C-reactive protein, antidepressant use, and trajectories of psychological distress in UKHLS

Since its proposal a decade ago, the Inflammatory Theory of Depression has generated substantial interest and a multi-disciplinary research programme, based on the idea that low-grade or ‘systemic’ inflammation forms part of the aetiology of depression in otherwise healthy humans. However, at odds with laboratory-based studies in which manipulated inflammation is clearly shown to produce depression-like symptoms, epidemiological studies have been mixed in their support for an inflammation-depression link. In this analysis, I consider whether inconsistency of epidemiological studies results from failure to take into account recent findings from a third body of research: clinical studies of depressed patients. These increasingly suggest that inflammation may be aetiologically important only for a distinct atypical form of depression, one characterised by resistance to antidepressant treatment. Using UKHLS data, I examine relationships between the inflammatory marker C-reactive protein, antidepressant use, and GHQ score (a measure of psychological distress) cross-sectionally and at three repeated outcome points. Substantial modification of CRP-GHQ associations by antidepressant use, I argue, supports existence of an atypical, inflammatory-depressive subtype, and further suggests that relationships may differ by antidepressant type