Genetic Analysis of Anger: Genetic Dominance or Competitive Sibling Interaction

Abstract

The knowledge of the causes and development of anger is still scarce. Previous studies on the sources of variance on Type A Behavior Pattern (TABP) related measures found variable heritability estimates ranging from 0.12 to 0.68, and large differences between MZ and DZ correlations. Some authors considered dominance genetic effects, competitive sibling interaction and sex differences as possible mechanisms to explain the results, but most studies lacked power. The present study uses a large sample of more than 2500 families, with longitudinal data from MZ and DZ pairs as well as their parents, to disentangle the sources of variance on anger. Model Fitting results showed that the sources of variance differ across sexes. For males 23% of the variance is due to additive genetic effects, and 26% to dominance genetic effects. For females 34% of the variance is due to additive genetic effects, and no dominance effects are found. There was no consistent evidence to confirm the presence of competitive sibling interaction as an alternative explanation for the low correlations in DZ males. The focus of research on the prediction of coronary heart disease (CHD) risk through psychological characteristics has recently changed from the multidimensional TABP to its emotional component: Anger. Understanding the sources of individual differences on anger can help to clarify the mechanisms that link it with CHD and its possible implications for treatment and prevention.

Nonadditive Genetic Effects on Hostility in South Korean Adolescent and Young Adult Twins

“…Sex differences in the magnitude of additive and nonadditive genetic influences found in the Dutch twin family study by Rebollo and Boomsma (2006) were not observed in the present sample, however. Several factors might contribute to the discrepancy between the results from the Dutch twin family study and the present findings.…”

“…In the present study, a lack of statistical power associated with small twin samples, especially the small DZ twin samples, may be responsible for a failure to detect sex differences in additive and nonadditive genetic factors. However, one should note that additive and nonadditive genetic estimates for the full scalar sex-limitation model (Model 1) differed in males and females, and the pattern of sex difference was consistent with that found in the study by Rebollo and Boomsma (2006). The SKTR is planning to collect data from siblings of twins to complement DZ twins.…”

“…Furthermore, the authors found sex differences in dominance genetic effects, favoring males (26% vs. 0%). In the Rebollo and Boomsma (2006) study, additive genetic effects were higher for females than for males (34% vs. 23%). The authors speculated that these sex differences in additive and nonadditive genetic effects might be related to sex differences in the risk for cardiovascular diseases.…”

“…Recently, Rebollo and Boomsma (2006) studied the genetic etiology of anger, an emotional component of hostility, in a large sample of adolescent and young adult twins (age range 12 to 25 years) and their parents. The authors administered the Spielberger's Trait Anger Scale (TAS) to 2664 twin families.…”

Biological Systems and the Development of Self-Regulation: Integrating Behavior, Genetics, and Psychophysiology

“…63,[73][74][75] This genetic influence is seen even for forms of fear that are highly conditioned and context or stimulus dependent, such as the strength of fear conditioning underlying the formation of some phobias. 76 As we have noted above, the regulatory aspects of attention and working memory have been implicated in modulation of negative affect, implying separate but interconnected biological systems for affect and cognitive control.…”