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Genetic and environmental contributions to stability and change in social inhibition across the adolescent and adult life span.
Developmental Psychology ( IF 3.1 ) Pub Date : 2022-05-05 , DOI: 10.1037/dev0001379
Ruifang Li-Gao 1 , Dorret I Boomsma 2 , Conor V Dolan 2 , Eco J C De Geus 2 , Johan Denollet 1 , Nina Kupper 1
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Feeling inhibited and socially not at ease is reflected in the trait social inhibition (SI). SI is associated with psychopathology that arises in young adulthood, such as anxiety. We aim for a better insight into the genetic and environmental contributions to SI across the life span, and as such examine their contributions to SI stability and change across adolescent and adult life span. We analyzed cohort-sequential longitudinal data from the Netherlands Twin Register (NTR), spanning a period of 25 years (Men (N, %): 17855, 37.4%; Age (Median, IQR): 19 years, 16-26 years; 7474 complete MZ twins and 8799 complete DZ twins). The data were organized into 7 age groups: < 14 (preadolescence), 15-16 (early adolescence), 17-18 (mid adolescence), 19-20 (late adolescence), 21-30 (young adulthood), 31-40 (adulthood), 41 + (middle-age-older adulthood). SI was assessed with the ASEBA-based proxy questionnaire. Phenotypic stability was established across the entire age range. Next, a longitudinal genetic simplex model was fitted to estimate the genetic and environmental contributions to the observed phenotypic stability. Results showed SI correlated well across follow-up of a single decade (.44 ≤ r ≤ .59) and moderately across the 25 years (.23 - .32) from adolescence to middle-age and older. Broad-sense heritability (h²) was between 40 and 48% across the 7 age groups. Additive and nonadditive genetic effects together explained most of the stability of SI across the life span (about 60-90% of the phenotypic correlation between ages), whereas environmental effects played a lesser role (about 10-40%). Concluding, SI, known to increase the risk of internalizing psychopathology, is phenotypically stable across the life span, which is largely attributable to genetic contributions to individual differences in SI. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

中文翻译:

遗传和环境对青春期和成年期社会抑制的稳定性和变化的贡献。

感觉压抑和社交不自在反映在特质社交抑制(SI)中。SI 与青年期出现的精神病理学有关,例如焦虑。我们的目标是更好地了解遗传和环境对 SI 在整个生命周期中的贡献,并因此检查它们对 SI 稳定性和青少年和成年生命周期变化的贡献。我们分析了来自荷兰 Twin Register (NTR) 的队列序列纵向数据,跨越 25 年(男性(N,%):17855,37.4%;年龄(中位数,IQR):19 岁,16-26 岁; 7474 个完整的 MZ 双胞胎和 8799 个完整的 DZ 双胞胎)。数据分为 7 个年龄组:< 14(青春期前)、15-16 岁(青春期早期)、17-18 岁(青春期中期)、19-20 岁(青春期后期)、21-30 岁(青年期)、31-40 岁(成年), 41 + (中老年)。SI 使用基于 ASEBA 的代理问卷进行评估。在整个年龄范围内建立了表型稳定性。接下来,拟合纵向遗传单纯形模型以估计遗传和环境对观察到的表型稳定性的贡献。结果显示,SI 在单个十年的随访中具有良好的相关性 (.44 ≤ r ≤ .59),并且在从青春期到中年及以上的 25 年 (.23 - .32) 中具有适度的相关性。7 个年龄组的广义遗传力 (h²) 介于 40% 和 48% 之间。加性和非加性遗传效应共同解释了 SI 在整个生命周期中的大部分稳定性(大约 60-90% 的年龄之间的表型相关性),而环境影响的作用较小(大约 10-40%)。结论是,已知 SI 会增加内化精神病理学的风险,在整个生命周期中表型稳定,这主要归因于遗传对 SI 个体差异的贡献。(PsycInfo 数据库记录 (c) 2022 APA,保留所有权利)。
更新日期:2022-05-05
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