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Genetic and Environmental Influences on Anger Expression, John Henryism, and Stressful Life Events: The Georgia Cardiovascular Twin Study

Xiaoling Wang, PhD, Ranak Trivedi, MS, Frank Treiber, PhD and Harold Snieder, PhD

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.).



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  		Figure 1. Path diagram for a univariate scalar model. An opposite-sex twin pair is shown, twin 1 being male and twin 2 female. Observed phenotypes (P) for twin 1 and twin 2 are shown in squares; latent (ie, unmeasured) factors are shown in circles. Correlations between additive genetic factors are 1 in MZ twins and 0.5 in DZ twins. Path coefficients (or factor loadings) of observed variables on the different latent factors are shown in lower case: h = additive genetic effect; c = shared environmental effect; e = unique environmental effect;k = scalar factor. D, the dominance genetic influence, was also tested but is omitted to simplify the diagram.

 


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  		Figure 2. Genetic and environmental correlations and factor loadings of the best fitting bivariate model for Anger expression and life events. For clarity, only one twin is depicted. Factor loadings (or path coefficients) are expressed as square roots to make clear that squaring those factor loadings yields estimates of genetic and environmental variance components as shown in text. A = additive genetic factor; E = unique environmental factor.

 




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