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Depression and manifestations of cardiovascular disease (CVD), including coronary artery disease (CAD), myocardial infarction (MI), ischemic stroke, heart failure, and atrial fibrillation, are strongly comorbid.1 Given their high prevalence and the many years lost to disability caused, establishing the causality underlying their comorbidity is of huge public health value. This is not a simple mission. Apart from chance, which is nonnegligible with 2 highly prevalent conditions, several mechanisms could underlie the co-occurrence of depression and CVD, ranging from biological (inflammatory processes, dysfunction in the hypothalamic-pituitary-adrenal and autonomic nervous systems, and endothelial and platelet dysfunction) and behavioral mechanisms (physical inactivity, poor eating habits, smoking, and drinking) to a shared genetic vulnerability or chronic stress linked to socioeconomic status, both of which could independently affect the risk of developing depression and CVD. Of note, these mechanisms are not mutually exclusive, and the depression-CVD comorbidity is likely a composite of all of them. The exact mixture may differ across people and possibly be symptom specific.2.

OBJECTIVE: To quantify the influence of genes and environment on individual differences in type-D status, and the type-D subcomponents negative affectivity and social inhibition. Type-D personality independently predicts poor prognosis in patients with cardiovascular disease. However, no previous study has determined the heritability of type-D personality. METHODS: This study determined type-D personality by applying the "combination of scales" method to survey data collected by the Netherlands Twin Register in 3331 healthy, young adult twins. Using structural equation modeling (SEM), the relative contributions of additive genetic, nonadditive genetic, and nonshared environmental factors to the variance in type-D and its subcomponents were determined. RESULTS: SEM indicated that type-D personality was substantially heritable (52%). The subcomponents negative affectivity and social inhibition were equally heritable, with broad heritability estimates of 46% and 50%. Although negative affectivity was determined by additive genetic effects and nonshared environment, individual differences in social inhibition were predominantly determined by nonadditive genetic effects and nonshared environment. CONCLUSIONS: This study provides strong evidence that genes are important in determining individual differences in type-D personality and the type-D subcomponents negative affectivity and social inhibition. Copyright © 2007 by American Psychosomatic Society.