To examine the genetic and/or environmental origin of variation and covariation of perceived stressful life events and two stress-related coping styles, anger expression and John Henryism.
Data were available from 306 European American (EA) and 213 African American (AA) twin pairs, including monozygotic and dizygotic of same as well as opposite sex (mean age, 14.8 ± 3.1 years; range, 10.0–25.9 years). Anger expression, John Henryism, and life events were measured with the Anger Expression Scale (subscales: Anger-in, Anger-out, and Anger-control), the John Henryism Active Coping Scale, and the Adolescent Resources Challenges Scale, respectively.
Model fitting showed no ethnic or sex differences for any of the scales. All traits showed at least some degree of familial resemblance, best explained by shared environment for Anger-in (18%), heritability for Anger-control (34%), John Henryism (34%), and life events (47%), and a combination of heritability (14% and 15%) and shared environment (10% and 20%) for Anger-out and overall anger expression, respectively. The remaining part of the variation for all traits was explained by environmental influences that are unique to the individual. Anger expression and life events were correlated (r = 0.28), and bivariate genetic modeling showed that 61% of this correlation was mediated by common genetic factors.
Individual differences in coping styles and life events in youth can be explained by moderate genetic and substantial environmental influences, of which most are idiosyncratic to the individual. The association between anger expression and life events is largely the result of common genes.
AA = African American; A = additive genetic component; AIC = Akaike’s information criterion; ARCS = Adolescent Resources Challenges Scale; C = common environmental component; CVD = cardiovascular disease; D = dominant genetic component; DZ = dizygotic; E = unique environmental component; EA = European American; MZ = monozygotic.
From the Georgia Prevention Institute, Department of Pediatrics, Medical College of Georgia, Augusta, Georgia (X.W., R.T., F.T., H.S.); the Department of Psychiatry, Duke University Medical Center, Durham, North Carolina (R.T.); and the Twin Research & Genetic Epidemiology Unit, St. Thomas’ Hospital, London, U.K. (H.S.).
Address correspondence and reprint requests to Harold Snieder, PhD, Georgia Prevention Institute, Medical College of Georgia, Building HS-1640, Augusta, GA 30912. E-mail: email@example.com
Received for publication October 31, 2003; revision received July 28, 2004.
This study was supported by grant HL56622 from the National Heart Lung and Blood Institute.