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A developmental twin study of symptoms of anxiety and depression: evidence for genetic innovation and attenuation

Published online by Cambridge University Press:  26 June 2008

K. S. Kendler ,
C. O. Gardner  and
P. Lichtenstein
K. S. Kendler*
Affiliation:
Virginia Institute of Psychiatric and Behavioral Genetics, Medical College of Virginia/Virginia Commonwealth University, Richmond, VA, USA Department of Psychiatry, Medical College of Virginia/Virginia Commonwealth University, Richmond, VA, USA Department of Human and Molecular Genetics, Medical College of Virginia/Virginia Commonwealth University, Richmond, VA, USA
C. O. Gardner
Affiliation:
Virginia Institute of Psychiatric and Behavioral Genetics, Medical College of Virginia/Virginia Commonwealth University, Richmond, VA, USA Department of Psychiatry, Medical College of Virginia/Virginia Commonwealth University, Richmond, VA, USA
P. Lichtenstein
Affiliation:
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
*
*Address for correspondence: K. S. Kendler, M.D., Department of Psychiatry, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA, USA. (Email: kendler@vcu.edu)
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Abstract

Background

Little is known about the pattern of genetic and environmental influences on symptoms of anxiety and depression (SxAnxDep) from childhood to early adulthood.

Method

Parental- and self-reported levels of SxAnxDep were assessed at ages 8–9, 13–14, 16–17 and 19–20 years in 2508 twins from the Swedish Twin Study of Child and Adolescent Development (TCHAD). Analysis conducted using the Mx program included SxAnxDep by parental and self-report.

Results

The best-fit model revealed one genetic risk factor for SxAnxDep acting at ages 8–9, 13–14, 16–17 and 19–20, and new sets of genetic risk factors ‘coming on line’ in early adolescence, late adolescence and early adulthood. Together, these genetic factors were very strong influences on the levels of SxAnxDep reported in common by parents and twins with heritability estimates, correcting for rater- and time-specific effects, ranging from 72% to 89%. The first genetic factor, which accounted for 72% of the variance in SxAnxDep at ages 8–9, attenuated sharply in influence, accounting for only 12% of the variance by ages 19–20. No evidence was found for shared environmental influences. Although not statistically significant, the correlation between genetic risk factors for SxAnxDep in males and females declined with advancing age.

Conclusions

Genetic effects on SxAnxDep are developmentally dynamic from middle childhood to young adulthood, demonstrating both genetic innovation and genetic attenuation. The attenuation might explain the low levels of continuity observed for anxiety and depressive disorders from childhood to adulthood. Differences in genetic risk factors for SxAnxDep in males and females may increase during development.

Keywords

Anxietydepressiondevelopmentgenetic effectstwins
Type
Original Articles
Information
Psychological Medicine , Volume 38 , Issue 11 , November 2008 , pp. 1567 - 1575
Copyright
Copyright © 2008 Cambridge University Press

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