Comasco Erika, Sylvén Sara M, Papadopoulos Fotios C, Sundström-Poromaa Inger, Oreland Lars, Skalkidou Alkistis
Department of Neuroscience, Uppsala University Hospital, Uppsala, Sweden.
Psychiatr Genet. 2011 Feb;21(1):19-28. doi: 10.1097/YPG.0b013e328341a3c1.
Postpartum depression (PPD) is an under diagnosed and under treated mood disorder, with negative impact on both the mother and the infant's health. The aim of this study is to examine whether genetic variations in the monoaminergic neurotransmitter system, together with environmental stressors, contribute to the development of PPD symptoms.
This nested case-control study included 275 women from a population-based cohort of delivering women in Sweden. A questionnaire containing the Edinburgh Postnatal Depression Scale was collected at 6 weeks and 6 months postpartum. Three functional polymorphisms were genotyped, catechol-O-methyltransferase (COMT)-Val158Met, monoamine oxidase A (MAOA)-upstream variable number tandem repeat (uVNTR) and serotonin transporter linked polymorphic region (5HTT-LPR). Stressful life events, maternity stressors and previous psychiatric contact were considered as potential risk factors.
COMT-Val158Met was significantly associated with PPD symptoms at 6 weeks, but not at 6 months postpartum. A significant gene-gene interaction effect was present between COMT-Val158Met and MAOA-uVNTR. In a gene-environment multivariate model, COMT-Val158Met, psychiatric contact and maternity stressors were significantly associated with PPD symptoms. Among those with history of psychiatric problems, the COMT-Val158Met and 5HTT-LPR risk variants were associated with PPD symptoms, whereas in the absence of previous psychiatric contact only maternity stressors were related to PPD symptoms.
The interaction effect between monoaminergic genes and environmental stressors is likely to contribute to vulnerability for PPD. The different patterns of association according to history of psychiatric problems, if replicated, might be helpful in screening strategies.
产后抑郁症（PPD）是一种诊断不足且治疗不足的情绪障碍，对母亲和婴儿的健康均有负面影响。本研究旨在探讨单胺能神经递质系统的基因变异与环境应激源是否共同导致PPD症状的发生。
这项巢式病例对照研究纳入了瑞典一个基于人群的分娩女性队列中的275名女性。在产后6周和6个月收集了一份包含爱丁堡产后抑郁量表的问卷。对三个功能多态性进行基因分型，即儿茶酚-O-甲基转移酶（COMT）-Val158Met、单胺氧化酶A（MAOA）-上游可变数目串联重复序列（uVNTR）和5-羟色胺转运体连锁多态性区域（5HTT-LPR）。生活应激事件、孕产应激源和既往精神科接触被视为潜在风险因素。
COMT-Val158Met在产后6周时与PPD症状显著相关，但在产后6个月时无此关联。COMT-Val158Met与MAOA-uVNTR之间存在显著的基因-基因交互作用。在一个基因-环境多变量模型中，COMT-Val158Met、精神科接触和孕产应激源与PPD症状显著相关。在有精神疾病史的人群中，COMT-Val158Met和5HTT-LPR风险变异与PPD症状相关，而在无既往精神科接触的人群中，只有孕产应激源与PPD症状相关。
单胺能基因与环境应激源之间的交互作用可能导致PPD易感性。根据精神疾病史的不同关联模式若能得到重复验证，可能有助于筛查策略。
