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Childhood IQ and Adult Mental Disorders: A Test of the Cognitive Reserve Hypothesis

机译:儿童智商和成人心理障碍:认知储备假说的检验

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Cognitive reserve has been proposed as important in the etiology of neuropsychiatric disorders. However, tests of the association between premorbid IQ and adult mental disorders other than schizophrenia have been limited and inconclusive. The authors tested the hypothesis that low childhood IQ is associated with increased risk and severity of adult mental disorders. Participants were members of a representative 1972-1973 birth cohort of 1,037 males and females in Dunedin, New Zealand, who were followed up to age 32 with 96% retention. WISC-R IQ was assessed at ages 7, 9, and 11. Research diagnoses of DSM mental disorders were made at ages 18, 21, 26, and 32. Lower childhood IQ was associated with increased risk of developing schizophrenia spectrum disorder, adult depression, and adult anxiety. Lower childhood IQ was also associated with greater comorbidity and with persistence of depression; the association with persistence of generalized anxiety disorder was nearly significant. Higher childhood IQ predicted increased risk of adult mania. Lower cognitive reserve, as reflected by childhood IQ, is an antecedent of several common psychiatric disorders and also predicts persistence and comorbidity. Thus, many patients who seek mental health treatment may have lower cognitive ability; this should be considered in prevention and treatment planning.
机译:已经提出认知储备在神经精神疾病的病因中很重要。但是,对病前智商与精神分裂症以外的成年精神障碍之间关联的测试仍然有限且尚无定论。作者检验了儿童智商低与成人精神障碍的风险和严重性增加相关的假设。参加者为新西兰但尼丁市1972-1973年代表性的1037名男性和女性出生队列的成员,对他们进行随访,直至32岁,保留率达96%。 WISC-R智商在7、9和11岁时进行评估。DSM精神障碍的研究诊断是在18、21、26和32岁时进行的。儿童智商低下与患精神分裂症谱系障碍,成人抑郁症的风险增加相关和成人焦虑症。儿童智商低下还与合并症和抑郁持续存在有关。与广泛性焦虑症持续存在的相关性几乎是显着的。儿童智商较高可预测成人躁狂症的风险增加。如儿童期智商所反映的那样,较低的认知储备是几种常见精神疾病的先决条件,并且还预测了持续性和合并症。因此,许多寻求心理健康治疗的患者可能具有较低的认知能力。在预防和治疗计划中应考虑到这一点。

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    《The American Journal of Psychiatry》 |2009年第1期|p.50-57|共8页
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    Karestan C. Koenen, Ph.D.Terrie E. Moffitt, Ph.D.Andrea L. Roberts, Ph.D.Laurie T. Martin, Sc. D., M. P.H.Laura Kubzansky, Ph.D., M. P.H.HonaLee Harrington, B.A.Richie Poulton, Ph.D.Avshalom Caspi, Ph.D.Received March 5, 2008, revisions received June 13 and July 24, 2008, accepted Aug. 21, 2008. From the Department of Society, Human Development, and Health and the Department of Epidemiology, Harvard School of Public Health, the Social, Genetic, and Developmental Psychiatry Research Centre, Institute of Psychiatry, King's College London, the Department of Psychology and Neuroscience, the Department of Psychiatry and Behavioral Sciences, and the Institute for Genome Sciences and Policy, Duke University, Durham. N.C., RAND Health, the RAND Corporation, Washington, D.C., and the Dunedin Multidisciplinary Health and Development Research Unit, University of Otago, Dunedin, New Zealand. Address correspondence and reprint requests to Dr. Koenen, Department of Society, Human Development, and Health, Harvard School of Public Health, Kresge 613, 677 Huntington Ave., Boston, MA 02115, kkoenen@hsph.harvard.edu (e-mail).The authors report no competing interests.Supported by NIMH grants MH-45070, MH-49414, and MH-077874, by U.K. Medical Research Council grants G0100527 and G0601483, by the Esther Katz Rosen Grant for Research and Programs on Giftedness in Children, by the William T. Grant Foundation, by funding for the Dunedin Multidisciplinary Health and Development Research Unit from the New Zealand Health Research Council, by partial support of Dr. Koenen by NIMH grants K08 MH-070627 and MH-078928, and by the Royal Society-Wolfson Merit Award to Dr. Caspi.The authors thank the Dunedin Study members and study founder Phil Silva.,;

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