Symptoms of Anxiety and Depression in Young Adults: Genetic and Environmental Influences on Stability and Change

AbstractEtiological factors for stability and change in symptoms of anxiety and depression, including sex differences, are largely unexplored in young adults. Using biometric modeling and two-wave longitudinal data from 4393 Norwegian twins aged 18 to 31 we explored (i) heritabilities of symptoms of anxiety and depression, (ii) effects of genetic and environmental factors on the stability and change of such symptoms, and (iii) sex-specific effects. The phenotypic cross-time correlations for symptoms of anxiety and depression were estimated to .54 and .49 for males and females, respectively. The best fitting longitudinal model specified additive genetic and individual environmental influences and emerging effects from the shared environment for females only. For both males and females, long-term stability was mainly attributable to stable additive genetic factors, whereas change was essentially related to environmental influences. Minor time-specific genetic effects were indicated, and some stable variance was due to the individual environment. Additive genetic risk factors explained 87% and 68% of the phenotypic cross-time correlation for males and females, with the unique environment accounting for the remaining covariance. The results provide strong evidence for the temporal stability of genetic risk factors for symptoms of anxiety and depression in young adults, and substantial sex-specific influences on heritability, stability and change.

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

Psychological Medicine ◽

10.1017/s003329170800384x ◽

2008 ◽

Vol 38 (11) ◽

pp. 1567-1575 ◽

Cited By ~ 130

Author(s):

K. S. Kendler ◽

C. O. Gardner ◽

P. Lichtenstein

Keyword(s):

Risk Factors ◽

Twin Study ◽

Genetic Risk ◽

Depressive Disorders ◽

Early Adulthood ◽

Environmental Influences ◽

Genetic Risk Factors ◽

Self Report ◽

Anxiety And Depression ◽

Males And Females

BackgroundLittle 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.ResultsThe 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.ConclusionsGenetic 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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Genetic risk factors in young adults with ‘cryptogenic’ ischemic cerebrovascular disease

Blood Coagulation & Fibrinolysis ◽

10.1097/00001721-200210000-00002 ◽

2002 ◽

Vol 13 (7) ◽

pp. 583-590 ◽

Cited By ~ 19

Author(s):

R. Grossmann ◽

U. Geisen ◽

G. Merati ◽

W. Müllges ◽

C. M. Schambeck ◽

...

Keyword(s):

Risk Factors ◽

Young Adults ◽

Cerebrovascular Disease ◽

Genetic Risk ◽

Genetic Risk Factors ◽

Ischemic Cerebrovascular Disease

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A longitudinal twin study of cluster A personality disorders

Psychological Medicine ◽

10.1017/s0033291714002669 ◽

2014 ◽

Vol 45 (7) ◽

pp. 1531-1538 ◽

Cited By ~ 8

Author(s):

K. S. Kendler ◽

S. H. Aggen ◽

M. C. Neale ◽

G. P. Knudsen ◽

R. F. Krueger ◽

...

Keyword(s):

Risk Factors ◽

Personality Disorders ◽

Genetic Risk ◽

Temporal Stability ◽

Genetic Risk Factors ◽

Structured Interview ◽

Parameter Estimates ◽

Environmental Correlations ◽

Cluster A ◽

The Cross

BackgroundWhile cluster A personality disorders (PDs) have been shown to be moderately heritable, we know little about the temporal stability of these genetic risk factors.MethodParanoid PD (PPD) and schizotypal PD (STPD) were assessed using the Structured Interview for DSM-IV Personality in 2793 young adult twins from the Norwegian Institute of Public Health Twin Panel at wave 1 and 2282 twins on average 10 years later at wave 2. Using the program Mx, we fitted a longitudinal latent factor model using the number of endorsed criteria for PPD and STPD.ResultsThe stability over time of the criteria counts for PPD and STPD, estimated as polychoric correlations, were +0.34 and +0.40, respectively. The best-fit longitudinal model included only additive genetic and individual-specific environmental factors with parameter estimates constrained to equality across the two waves. The cross-wave genetic and individual-specific environmental correlations for a latent cluster A factor were estimated to equal +1.00 and +0.13, respectively. The cross-time correlations for genetic and environmental effects specific to the individual PDs were estimated at +1.00 and +0.16–0.20, respectively. We found that 68% and 71% of the temporal stability of PPD and STPD derived, respectively, from the effect of genetic factors.ConclusionShared genetic risk factors for two of the cluster A PDs are highly stable in adults over a 10-year period while environmental risk factors are relatively transient. Over two-thirds of the long-term stability of the common cluster A PD liability can be attributed to genetic influences.

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

Psychological Medicine ◽

10.1017/s0033291718003550 ◽

2018 ◽

Vol 49 (15) ◽

pp. 2582-2590

Author(s):

Fartein Ask Torvik ◽

Kristin Gustavson ◽

Eivind Ystrom ◽

Tom H. Rosenström ◽

Nathan Gillespie ◽

...

Keyword(s):

Risk Factors ◽

Environmental Risk ◽

Genetic Risk ◽

Longitudinal Design ◽

Environmental Influences ◽

Environmental Risk Factors ◽

Shared Environment ◽

Term Stability ◽

Long Term Stability

AbstractBackgroundStudies 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.MethodsA 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.ResultsThe 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.ConclusionsDifferent 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.

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