Wichers M, Schrijvers D, Geschwind N, Jacobs N, Myin-Germeys I, Thiery E, Derom C, Sabbe B, Peeters F, Delespaul Ph, van Os J
Department of Psychiatry and Neuropsychology, South Limburg Mental Health Research and Teaching Network, EURON, Maastricht University, Maastricht, The Netherlands.
Psychol Med. 2009 Jul;39(7):1077-86. doi: 10.1017/S0033291708004388. Epub 2008 Oct 6.
Previous work suggests that daily life stress-sensitivity may be an intermediary phenotype associated with both genetic risk for depression and developmental stress exposures. In the current analysis we hypothesized that genetic risk for depression and three environmental exposures over the course of development [prenatal stress, childhood adversity and adult negative life events (NLEs)] combine synergistically to produce the phenotype of stress-sensitivity.
Twin pairs (n=279) participated in a momentary assessment study using the Experience Sampling Method (ESM), collecting appraisals of stress and negative affect (NA) in the flow of daily life. Prospective data on birthweight and gestational age, questionnaire data on childhood adversity and recent NLEs, and interview data on depression were used in the analyses. Daily life stress-sensitivity was modelled as the effect of ESM daily life stress appraisals on ESM NA.
All three developmental stress exposures were moderated by genetic vulnerability, modelled as dizygotic (DZ) or monozygotic (MZ) co-twin depression status, in their effect on daily life stress-sensitivity. Effects were much stronger in participants with MZ co-twin depression and a little stronger in participants with DZ co-twin depression status, compared to those without co-twin depression. NLE main effects and NLE genetic moderation were reducible to birthweight and childhood adversity.
The findings are consistent with the hypothesis that adult daily life stress-sensitivity is the result of sensitization processes initiated by developmental stress exposures. Genes associated with depression may act by accelerating the process of stress-induced sensitization.
先前的研究表明，日常生活应激敏感性可能是一种中间表型，与抑郁症的遗传风险和发育应激暴露均相关。在当前分析中，我们假设抑郁症的遗传风险与发育过程中的三种环境暴露因素[产前应激、童年逆境和成人负面生活事件（NLEs）]协同作用，产生应激敏感性表型。
双胞胎对（n = 279）参与了一项使用经验取样法（ESM）的即时评估研究，收集日常生活中应激和负性情绪（NA）的评估数据。分析中使用了出生体重和孕周的前瞻性数据、童年逆境和近期NLEs的问卷数据以及抑郁症的访谈数据。将日常生活应激敏感性建模为ESM日常生活应激评估对ESM NA的影响。
所有三种发育应激暴露在对日常生活应激敏感性的影响上，均受到遗传易感性的调节，遗传易感性以异卵（DZ）或同卵（MZ）双胞胎的抑郁状态来建模。与没有双胞胎抑郁的参与者相比，MZ双胞胎抑郁的参与者效应更强，DZ双胞胎抑郁状态的参与者效应稍强。NLE的主效应和NLE遗传调节可归结为出生体重和童年逆境。
这些发现与以下假设一致，即成人日常生活应激敏感性是由发育应激暴露引发的致敏过程的结果。与抑郁症相关的基因可能通过加速应激诱导的致敏过程起作用。
