K S Kendler1, C O Gardner, P Lichtenstein. 1. Virginia Institute of Psychiatric and Behavioral Genetics, Medical College of Virginia/Virginia Commonwealth University, Richmond, VA, USA. kendler@vcu.edu
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.MethodParental- 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.
BACKGROUND: Little is known about the pattern of genetic and environmental influences on symptoms of anxiety and depression (SxAnxDep) from childhood to early adulthood.MethodParental- 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.
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