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.
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Departments of aNeuroscience, Pharmacology
bWomen's and Children's Health
cDepartment of Neurosciences, Psychiatry, Uppsala University Hospital, Uppsala
dCentre for Clinical Research Västera˚s, Uppsala University, Central Hospital, Västera˚s, Sweden
Correspondence to Erika Comasco, PhD, Department of Neuroscience, Unit of Pharmacology, Uppsala University, BMC, Box 593, Uppsala 751 24, Sweden Tel: +46 18 471 5020; fax: +46 18 51 1540; e-mail: email@example.com
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Received March 22, 2010
Accepted August 9, 2010