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Abstract

Objective:

The authors investigated the relative importance of genetic and environmental influences on perinatal depression, and the genetic overlap between perinatal depression and nonperinatal depression.

Method:

Analyses were conducted using structural equation modeling for 1) the lifetime version of the Edinburgh Postnatal Depression Scale in 3,427 Swedish female twins and 2) clinical diagnoses of depression separated into perinatal depression and nonperinatal depression in a Swedish population-based cohort of 580,006 sisters.

Results:

In the twin study, the heritability of perinatal depression was estimated at 54% (95% CI=35%−70%), with the remaining variance attributable to nonshared environment (46%; 95% CI=31%−65%). In the sibling design, the heritability of perinatal depression was estimated at 44% (95% CI=35%−52%) and the heritability of nonperinatal depression at 32% (95% CI=24%−41%). Bivariate analysis showed that 14% of the total variance (or 33% of the genetic variance) in perinatal depression was unique for perinatal depression.

Conclusions:

The heritability of perinatal depression was estimated at 54% and 44%, respectively, in separate samples, and the heritability of nonperinatal depression at 32%. One-third of the genetic contribution was unique to perinatal depression and not shared with nonperinatal depression, suggesting only partially overlapping genetic etiologies for perinatal depression and nonperinatal depression. The authors suggest that perinatal depression constitutes a subset of depression that could be prioritized for genomic discovery efforts. The study findings have direct translational impact that can assist clinicians in the counseling of their patients regarding risk and prognosis of perinatal depression.

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Supplementary Material

File (appi.ajp.2015.15010085.ds001.pdf)

Information & Authors

Information

Published In

Go to American Journal of Psychiatry
Go to American Journal of Psychiatry
American Journal of Psychiatry
Pages: 158 - 165
PubMed: 26337037

History

Received: 21 January 2015
Revision received: 1 June 2015
Accepted: 15 June 2015
Published online: 4 September 2015
Published in print: February 01, 2016

Authors

Affiliations

Alexander Viktorin, M.Sc.
From the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm; the Departments of Psychiatry and Genetics, University of North Carolina School of Medicine, Chapel Hill; and the Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden.
Samantha Meltzer-Brody, M.D., M.P.H.
From the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm; the Departments of Psychiatry and Genetics, University of North Carolina School of Medicine, Chapel Hill; and the Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden.
Ralf Kuja-Halkola, Ph.D.
From the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm; the Departments of Psychiatry and Genetics, University of North Carolina School of Medicine, Chapel Hill; and the Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden.
Patrick F. Sullivan, M.D., F.R.A.N.Z.C.P.
From the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm; the Departments of Psychiatry and Genetics, University of North Carolina School of Medicine, Chapel Hill; and the Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden.
Mikael Landén, M.D., Ph.D.
From the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm; the Departments of Psychiatry and Genetics, University of North Carolina School of Medicine, Chapel Hill; and the Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden.
Paul Lichtenstein, Ph.D.
From the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm; the Departments of Psychiatry and Genetics, University of North Carolina School of Medicine, Chapel Hill; and the Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden.
Patrik K.E. Magnusson, Ph.D.
From the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm; the Departments of Psychiatry and Genetics, University of North Carolina School of Medicine, Chapel Hill; and the Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden.

Notes

Address correspondence to Mr. Viktorin ([email protected]).
Presented as an abstract at the 44th annual meeting of the Behavior Genetics Association, Charlottesville, Va., June 18–21, 2014.

Competing Interests

Dr. Meltzer-Brody has received research support from Sage Therapeutics. Dr. Landén has received compensation for lectures from AstraZeneca, Bayer, Biophausia, Bristol Myers-Squibb, Lundbeck, Eli Lilly, Wyeth, and Servier and has served as an advisory board member for AstraZeneca and Lundbeck. The other authors report no financial relationships with commercial interests.

Funding Information

The Swedish Twin Registry is financially supported by Karolinska Institutet. The present study was supported by grants from the Swedish Medical Research Council (K2014-62X-14647-12-51 and K2010-61P-21568-01-4), the Swedish Foundation for Strategic Research, the Swedish Brain Foundation, and NIMH (K23 MH085165).

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