Legrand, L. N., M. McGue, et al. (1999). "A twin study of state and trait anxiety in childhood and adolescence." J Child Psychol Psychiatry 40(6): 953-8.
- The amount of anxiety and worry that one typically feels seems to be largely a consequence of inherited predispositions. On the other hand, the amount of anxiety that one is feeling at a particular point in time appears to be determined only by the environment (i.e., situational stressors and prior unique experiences) rather than genes.
Legrand, L.N., McGue, M., & Iacono, W.G. (1999). A twin study of state and trait anxiety in childhood and adolescence. Journal of Child Psychology & Psychiatry, 40, 953-958.
- Little research has addressed the relative influence of genetic and environmental factors on subclinical levels of anxiety in children. Of the two twin studies to date, one concluded that measures of adolescents' self-reported trait anxiety were best explained by shared environmental factors (Thapar & McGuffin, 1995), while the second determined that approximately half the variance was attributable to genetic effects (Topolski et al., 1997). The present study, using a sample of 547 twin pairs, reached conclusions similar to those of Topolski et al. Heritability was estimated at 45%. Measures of state anxiety conformed more closely to Thapar and McGuffin's findings, with environmental factors accounting for the variance.
Keel, P. K., Klump, K. L., Miller, K. B., McGue, M., & Iacono, W. G. (2005). Shared transmission of eating disorders and anxiety disorders. International Journal of Eating Disorders, 38, 99-105.
- Objective Eating disorders have high comorbidity with mood, anxiety, and substance use disorders. Using twins from the population-based Minnesota Twin Family Study (MTFS), we examined comorbidity and shared transmission between eating pathology and these disorders. Method Female twins (N = 672), ages 16–18 years, completed structured clinical interviews assessing anorexia nervosa and bulimia nervosa (as described in the 4th ed. of the Diagnostic and Statistical Manual of Mental Disorders [DSM-IV; American Psychiatric Association, 1994]), as well as mood, anxiety, and substance use disorders (as described in the 3rd Rev. ed. of the Diagnostic and Statistical Manual of Mental Disorders [DSM-III-R]). Shared transmission was examined using a discordant monozygotic (MZ) twin design. Results Significant comorbidity was found between eating disorders and major depression, anxiety disorders, and nicotine dependence. Within MZ twin pairs discordant for eating disorders (n = 14), non–eating-disordered cotwins demonstrated increased risk for anxiety disorders compared with controls. Similarly, within MZ twin pairs discordant for anxiety disorders (n = 52), non–anxiety-disordered cotwins demonstrated increased risk for eating disorders compared with controls. Discussion Findings support shared transmission between eating disorders and anxiety disorders. However, the nature of this shared diathesis remains unknown.
Hicks, B.M., DiRago, A.C., Iacono, W.G., & McGue, M. (2009). Gene-environment interplay in internalizing disorders: Consistent findings across six environmental risk factors. Journal of Child Psychology and Psychiatry, 50(10), 1309-1317. PMCID: PMC2758614
- Background: Behavior genetic methods can help to elucidate gene-environment (G-E) interplay in the development of internalizing (INT) disorders (i.e., major depression and anxiety disorders). To date, however, no study has conducted a comprehensive analysis examining multiple environmental risk factors with the purpose of delineating general mechanisms of G-E influence in the development of INT disorders. Methods: The sample consisted of 1315 male and female twin pairs participating in the age 17 assessment of the Minnesota Twin Family Study. Quantitative G-E interplay models were used to examine how genetic and environmental risk for INT disorders changes as a function of environmental context. Multiple measures and informants were employed to construct composite measures of INT disorders and six environmental risk factors including: stressful life events, mother-child and father-child relationship problems, antisocial and prosocial peer affiliation, and academic achievement and engagement. Results: Significant moderation effects were detected between each environmental risk factor and INT such that in the context of greater environmental adversity, nonshared environmental factors became more important in the etiology of INT symptoms. Conclusion: Our results are consistent with the interpretation that environmental stressors have a causative effect on the emergence of INT disorders. The consistency of our results suggests a general mechanism of environmental influence on INT disorders regardless of the specific form of environmental risk.