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

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.

Fig. 1

The model used in these analyses presented for one source of liability such as additive genetic effects. The model contains four latent scores for symptoms of anxiety and depression (SxAnxDep) (T₁–T₄) reflecting the true level of SxAnxDep at time 1 (age 8–9), time 2 (age 13–14), time 3 (age 16–17) and time 4 (age 19–20). These latent variables are indexed by ratings of SxAnxDep by parental report (P) (available for times 1–3) and by self-report (S) (available for times 2–4). The degree to which the parent- and self-reported ratings of SxAnxDep index the true latent level of symptoms is reflected by the paths λ_P and λ_S. The genetic and environmental influences on the latent SxAnxDep scores are modeled as a Cholesky decomposition. See text article for further details.

Fig. 2

The proportion of total variance in symptoms of anxiety and depression (SxAnxDep) accounted for by genetic factors through development. The y axis represents the total phenotypic variance so the sum of all the factors equals the total heritability. The first genetic factor, which starts at ages 8–9, is represented in dark grey. An intermediate grey represents the second genetic factor starting at ages 13–14. Light grey represents the third genetic factor starting at ages 16–17 and white represents the fourth genetic factor acting only at ages 19–20.