Childhood and young adult-onset depression are associated with similar psychosocial risk factors.

ED FROM Shanahan L, Copeland WE, Costello EJ, et al. Child-, adolescentand young adult-onset depressions: differential risk factors in development? Psychol Med 2011;41:2265–74. Correspondence to: L Shanahan, University of North Carolina at Greensboro, Department of Psychology, PO Box 26170, Greensboro, NC 27402, USA; lilly_ [email protected] Sources of funding: National Institute of Mental Health, National Institute on Drug Abuse and the William T Grant Foundation. OM M EN TA RY Environmental adversity is a long-established risk factor for the onset of depressive disorder. Evidence to date has suggested that psychosocial risk factors for childhood-onset depression are not associated with adult-onset depression. Some have interpreted this to mean that there are different aetiological risk factors for childhoodand adult-onset depression, here termed the ‘risk differences’ hypothesis. Shanahan et al propose an alternative explanation, the ‘recency’ hypothesis: the depressogenic effects of environmental adversity are mostly time limited, and so childhood adversity has little effect on the risk of onset of adult depression due to the time interval. The authors used the Great Smoky Mountains Study to compare the two hypotheses: similar environmental adversities were measured at all age groups, as were depression onsets. This study demonstrated that all categories of concurrent adversity were associated with onset of depression at all ages, disproving the risk differences hypothesis. While there were some associations between childhood adversity and adult depression (even when controlling for early–late adversity correlations), these were weaker than for adult adversity-adult depression, supporting the recency hypothesis. The authors limited risk of information bias by only including adversities and symptoms within the last 3 months. This was appropriate and power was adequate for the main analysis. However, the resultant reduction in power meant that this paper was unable to answer some important questions. First, are the positive adolescent concurrent adversity-depression associations non-signifi cant due to different aetiological pathways in this age group, or type II errors? Second, is the association between childhood adversity and depression signifi cantly greater than that between childhood adversity and adult depression, thus adding further support to the recency hypothesis? Third, what are the comparative associations between childhood versus adult adversity and persistent/recurrent adult depression, a subtype found to be particularly associated with childhood adversity?1 Further, larger studies are needed to answer these questions. Overall, this well-conducted study demonstrates that similar aetiological risk factors operate for childhood and adult depression, with more recent risks having a stronger effect. Clinically, we still need to enquire about childhood adversity. From a public health perspective, reducing childhood adversity should reduce adult depression.