Sullivan P F, Neale M C, Kendler K S
Department of Psychiatry, Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, 23298-0126, USA.
Am J Psychiatry. 2000 Oct;157(10):1552-62. doi: 10.1176/appi.ajp.157.10.1552.
The authors conducted a meta-analysis of relevant data from primary studies of the genetic epidemiology of major depression.
The authors searched MEDLINE and the reference lists of previous review articles to identify relevant primary studies. On the basis of a review of family, adoption, and twin studies that met specific inclusion criteria, the authors derived quantitative summary statistics.
Five family studies met the inclusion criteria. The odds ratios for proband (subjects with major depression or comparison subjects) versus first-degree relative status (affected or unaffected with major depression) were homogeneous across the five studies (Mantel-Haenszel odds ratio=2.84, 95% CI=2.31-3.49). No adoption study met the inclusion criteria, but the results of two of the three reports were consistent with genetic influences on liability to major depression. Five twin studies met the inclusion criteria, and their statistical summation suggested that familial aggregation was due to additive genetic effects (point estimate of heritability of liability=37%, 95% CI=31%-42%), with a minimal contribution of environmental effects common to siblings (point estimate=0%, 95% CI=0%-5%), and substantial individual-specific environmental effects/measurement error (point estimate=63%, 95% CI=58%-67%). The literature suggests that recurrence best predicts the familial aggregation of major depression.
Major depression is a familial disorder, and its familiality mostly or entirely results from genetic influences. Environmental influences specific to an individual are also etiologically significant. Major depression is a complex disorder that does not result from either genetic or environmental influences alone but rather from both. These findings are notably consistent across samples and methods and are likely to be generally applicable.
作者对重度抑郁症遗传流行病学的原始研究相关数据进行了荟萃分析。
作者检索了MEDLINE以及先前综述文章的参考文献列表，以确定相关的原始研究。在对符合特定纳入标准的家族、收养和双生子研究进行综述的基础上，作者得出了定量汇总统计数据。
五项家族研究符合纳入标准。在这五项研究中，先证者（患有重度抑郁症的受试者或对照受试者）与一级亲属状态（受重度抑郁症影响或未受影响）的比值比是同质的（Mantel-Haenszel比值比=2.84，95%置信区间=2.31-3.49）。没有收养研究符合纳入标准，但三份报告中的两份结果与遗传因素对重度抑郁症易感性的影响一致。五项双生子研究符合纳入标准，其统计汇总表明家族聚集是由于加性遗传效应（易感性遗传度的点估计值=37%，95%置信区间=31%-42%），同胞共有的环境效应贡献最小（点估计值=0%，95%置信区间=0%-5%），以及显著的个体特异性环境效应/测量误差（点估计值=63%，95%置信区间=58%-67%）。文献表明，复发最能预测重度抑郁症的家族聚集情况。
重度抑郁症是一种家族性疾病，其家族性主要或完全由遗传因素影响所致。个体特异性的环境影响在病因学上也具有重要意义。重度抑郁症是一种复杂的疾病，并非仅由遗传或环境因素单独导致，而是两者共同作用的结果。这些发现显著地在不同样本和方法中保持一致，并且可能具有普遍适用性。
