Genetic and Environmental Influences on Type A Behavior Pattern: Evidence From Twins and Their Parents in The Netherlands Twin Register

Abstract

Objective: There is a dose-response positive relationship between type A behavior (TABP) and cardiovascular disease-related symptoms. Estimates of heritability for TABP from previous studies vary; this might be explained by limitations in the sizes and compositions of the samples. Methods: This study combines a large sample size, twin and parental, data from males and females, two generations of young adults and older adults, and the use of structural equation modeling (SEM) and full information maximum likelihood (FIML) estimation. To assess TABP, the Jenkins Activity Survey (JAS) was collected from MZ and DZ twins and their parents (n ϭ 1670 twin families). Structural equation modeling is used to evaluate and estimate the effects of additive and nonadditive genetic effects, nonshared environmental effects, and competitive sibling interaction. Results: Forty-five percent of the variance in TABP was the result of genetic factors (28% were additive and 17% were nonadditive). The remaining 55% of the variance was explained by environmental factors not shared by the members of the same family. Competitive sibling interaction effects were not significant. There was no evidence of sex differences either in variances or means. Conclusion: Understanding the sources of variance on TABP is important for therapy and prevention. According to the present results, the relevant environmental factors for the development of TABP are not shared by the members of the same family. The genetic portion of the variance is also worth considering for therapeutic purposes. Although the genetic code cannot be altered, its effects on behavior may be modifiable through the treatment of the biological mediators. Key words: type A behavior pattern, risk of CHD, JAS, sibling interaction, twin studies, parents-offspring.TABP ϭ type A behavior pattern; JAS ϭ Jenkins Activity Survey; FIML ϭ full information maximum likelihood; CVD and CHD ϭ Cardiovascular and Coronary Heart Disease; MZM ϭ monozygotic males; MZF ϭ monozygotic females; DZM ϭ dizygotic males; DZF ϭ dizygotic females; OSMF ϭ opposite sex male first born and female second born; OSFM ϭ opposite sex female first born and male second born; DF ϭ degrees of freedom; SEM ϭ structural equation modeling; ADEi:A ϭ additive genetic effects; D ϭ dominance genetic effects; E ϭ nonshared environmental effects; i ϭ sibling interaction effects; CI ϭ confidence interval.

How fair treatment affects saliva cortisol release in stressed low and high type‐A behavior individuals

“…In particular, individuals who differ in proneness to heart failure (as measured by Jenkins Activity Scale; see Palmero, Diez & Breva, 2001) react differently to stress. High type-A individuals have a tendency to cardiovascular disease-related symptoms, that is a high proneness to heart failure (see e.g., Robello & Boomsma, 2006) and can be characterized as having an easily aroused hostility, a sense of time urgency and competitive achievement strivings. This hostility might make them more responsive to stress and less responsive to palliative treatment in response to stress (Taylor, 1995).…”

An Extended Twin-Pedigree Study of Neuroticism in the Netherlands Twin Register

“…This has led to a database with roughly equal proportions of participants who are and who are not twins. In genetic studies, the simultaneous analysis of all data from extended twin families can offer substantial gains in statistical power, when, for example, estimating non-additive genetic components of variance or when considering the effects of a shared family environment (Posthuma and Boomsma 2000 ; Rebollo and Boomsma 2006a , b ; Keller et al 2010 ). Here, we analyzed a large dataset on neuroticism from twins, their biological relatives and non-biological family members, including spouses (N > 30,000 subjects), after constructing the extended pedigrees (see “ Methods ”), that link all nuclear families from the Netherlands Twin Register to each other within larger pedigrees.…”

Genetic and environmental causes of variation in perceived loneliness in young people

“…The main part of the genetic variation in the latent perceived loneliness factor came from additive genetic sources, that is, contributions of genes that are independent of each other. Non‐additive effects have been reported in other personality traits in adolescents [Rebollo et al, 2006; Rettew et al, 2008; Waaktaar and Torgersen, 2011]. Although dominant genetic effects were not specifically tested in this study due to the confounding of the shared environment effects in the classic twin reared together design [Rijsdijk and Sham, 2002], the correlations matrix did not indicate any effect of different genes interacting with each other.…”