Do the genetic or environmental determinants of anxiety and depression change with age? A longitudinal study of Australian twins
Do the genetic or environmental determinants of anxiety and depression change with age? A longitudinal study of Australian twins
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DOI：
10.1375/13690520460741435
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发表时间：
2004-02-01
期刊：
影响因子：
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通讯作者：
Martin, NG
中科院分区：
文献类型：
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作者：
Gillespie, NA;Kirk, KM;Martin, NG
由于青春期晚期和成年早期焦虑和抑郁的决定因素可能与以后的生活不同，因此我们研究了整个生命周期中焦虑和抑郁症状的时间稳定性以及遗传和环境相关性的程度。数据收集自以澳大利亚人口为基础的样本，其中包括 4364 对完整双胞胎和 777 名年龄在 20 至 96 岁之间的单身人士，这些样本在 1980 年至 1996 年间通过三项研究进行了随访。每项研究都包含 14 项自我报告 DSSI/sAD 量表，用于测量最近经历的焦虑和抑郁症状。然后根据每个受试者参与时的年龄对症状评分进行划分并分配到年龄区间。我们拟合遗传单纯形模型以考虑数据的纵向性质。对于男性焦虑和抑郁，最合适的单纯形模型包含 20 岁时传播的单一遗传创新，并解释了 30、40、50 和 60 岁时焦虑和抑郁的遗传变异。女性焦虑和抑郁的大多数终生遗传变异也可以通过 20 岁时传播到所有其他年龄段的创新来解释；然而，30 岁时焦虑症、40 岁和 70 岁抑郁症也存在较小的年龄依赖性基因创新。尽管焦虑和抑郁的遗传决定因素在男性和女性的整个生命周期中似乎相对稳定，但有一些证据支持女性中年和晚年的抑郁基因有额外的作用。事实上，中年焦虑症的发病早于抑郁症十年，这一事实也与这些病症之间的因果关系（焦虑导致抑郁症）相一致。这些发现对于大规模抑郁症预防项目具有重要意义。
Because the determinants of anxiety and depression in late adolescence and early adulthood may differ from those in later life, we investigated the temporal stability and magnitude of genetic and environmental correlates of symptoms of anxiety and depression across the life span. Data were collected from a population-based Australian sample of 4364 complete twin pairs and 777 singletons aged 20 to 96 years who were followed-up over three studies between 1980 and 1996. Each study contained the 14-item self-report DSSI/sAD scale which was used to measure recently experienced symptoms of anxiety and depression. Symptom scores were then divided and assigned to age intervals according to each subject's age at time of participation. We fitted genetic simplex models to take into account the longitudinal nature of the data. For male anxiety and depression, the best fitting simplex models comprised a single genetic innovation at age 20 which was transmitted, and explained genetic variation in anxiety and depression at ages 30, 40, 50 and 60. Most of the lifetime genetic variation in female anxiety and depression could also be explained by innovations at age 20 which were transmitted to all other ages; however, there were also smaller age-dependent genetic innovations at 30 for anxiety and at 40 and 70 for depression. Although the genetic determinants of anxiety and depression appear relatively stable across the life-span for males and females, there is some evidence to support additional mid-life and late age gene action in females for depression. The fact that mid-life onset for anxiety occurs one decade before depression is also consistent with a causal relationship (anxiety leading to depression) between these conditions. These findings have significance for large scale depression prevention projects.