Is low cognitive functioning a predictor or consequence of major depressive disorder? A test in two longitudinal birth cohorts
Published online by Cambridge University Press: 16 November 2017
Cognitive impairment has been identified as an important aspect of major depressive disorder (MDD). We tested two theories regarding the association between MDD and cognitive functioning using data from longitudinal cohort studies. One theory, the cognitive reserve hypothesis, suggests that higher cognitive ability in childhood decreases risk of later MDD. The second, the scarring hypothesis, instead suggests that MDD leads to persistent cognitive deficits following disorder onset. We tested both theories in the Dunedin Study, a population-representative cohort followed from birth to midlife and assessed repeatedly for both cognitive functioning and psychopathology. We also used data from the Environmental Risk Longitudinal Twin Study to test whether childhood cognitive functioning predicts future MDD risk independent of family-wide and genetic risk using a discordant twin design. Contrary to both hypotheses, we found that childhood cognitive functioning did not predict future risk of MDD, nor did study members with a past history of MDD show evidence of greater cognitive decline unless MDD was accompanied by other comorbid psychiatric conditions. Our results thus suggest that low cognitive functioning is related to comorbidity, but is neither an antecedent nor an enduring consequence of MDD. Future research may benefit from considering cognitive deficits that occur during depressive episodes from a transdiagnostic perspective.
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The first two authors contributed equally to this article. The Dunedin Multidisciplinary Health and Development Research Unit is funded by the New Zealand Health Research Council and the New Zealand Ministry of Business, Innovation, and Employment. Additional support was provided by US National Institute on Aging (NIA) Grants R01AG032282, R01AG049789, and R01AG048895; UK Medical Research Council Grants MR/P005918/1 and MR/K00381X; Economic and Social Research Council Grant ES/M010309/1; and the Jacobs Foundation. The Environmental Risk (E-Risk) Longitudinal Twin Study is funded by UK Medical Research Council Grant G1002190. Additional support was provided by US National Institute of Child Health and Human Development (NICHD) Grant HD077482, the Jacobs Foundation, and the Duke Social Science Research Institute. We thank the Dunedin and E-Risk Study members, their peer informants, and Dunedin Study founder Phil Silva. Support was also provided by NIA Grant T32-AG000139 and NICHD Grant T32-HD007376 (to J.D.S.), by a National Science Foundation Graduate Research Fellowship (to M.A.S.), and by NIA Grant P30-AG028716 (to D.W.B.).