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Continuity of genetic and environmental influences on clinically assessed major depression from ages 18 to 45

Published online by Cambridge University Press:  28 November 2018

Fartein Ask Torvik*
Affiliation:
Department of Mental Disorders, Norwegian Institute of Public Health, Oslo, Norway Department of Psychology, University of Oslo, Oslo, Norway
Kristin Gustavson
Affiliation:
Department of Mental Disorders, Norwegian Institute of Public Health, Oslo, Norway Department of Psychology, University of Oslo, Oslo, Norway
Eivind Ystrom
Affiliation:
Department of Mental Disorders, Norwegian Institute of Public Health, Oslo, Norway Department of Psychology, University of Oslo, Oslo, Norway PharmacoEpidemiology and Drug Safety Research Group, School of Pharmacy, University of Oslo, Oslo, Norway
Tom H. Rosenström
Affiliation:
Department of Mental Disorders, Norwegian Institute of Public Health, Oslo, Norway
Nathan Gillespie
Affiliation:
Department of Psychiatry, Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA
Ted Reichborn-Kjennerud
Affiliation:
Department of Mental Disorders, Norwegian Institute of Public Health, Oslo, Norway Institute of Clinical Medicine, University of Oslo, Oslo, Norway
Kenneth S. Kendler
Affiliation:
Department of Psychiatry, Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA Department of Human and Molecular Genetics and Department of Psychiatry, Virginia Commonwealth University, Richmond, VA, USA
*
Author for correspondence: F. A. Torvik, E-mail: fato@fhi.no

Abstract

Background

Studies on the stability of genetic risk for depression have relied on self-reported symptoms rather than diagnoses and/or short follow-up time. Our aim is to determine to what degree genetic and environmental influences on clinically assessed major depressive disorder (MDD) are stable between age 18 and 45.

Methods

A population-based sample of 11 727 twins (6875 women) born between 1967 and 1991 was followed from 2006 to 2015 in health registry data from primary care that included diagnoses provided by treating physicians. Individuals with schizophrenia or bipolar disorder (n = 163) were excluded. We modelled genetic and environmental risk factors for MDD in an accelerated longitudinal design.

Results

The best-fitting model indicated that genetic influences on MDD were completely stable from ages 18 to 45 and explained 38% of the variance. At each age, the environmental risk of MDD was determined by the risk at the preceding observation, plus new environmental risk, with an environmental correlation of +0.60 over 2 years. The model indicated no effects of shared environment and no environmental effects stable throughout the observational period. All long-term stability was therefore explained by genetic factors.

Conclusions

Different processes unfolded in the genetic and environmental risk for MDD. The genetic component is stable from later adolescence to middle adulthood and accounted for nearly all long-term stability. Therefore, molecular genetic studies can use age-heterogenous samples when investigating genetic risk variants of MDD. Environmental risk factors were stable over a short span of years with associations rapidly decreasing and no evidence of permanent environmental scarring.

Type
Original Articles
Copyright
Copyright © Cambridge University Press 2018 

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Footnotes

*

These authors are joint senior authors.

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Continuity of genetic and environmental influences on clinically assessed major depression from ages 18 to 45
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