Hostname: page-component-7c8c6479df-ph5wq Total loading time: 0 Render date: 2024-03-28T12:37:34.347Z Has data issue: false hasContentIssue false

Genetics of testosterone and the aggression-hostility-anger (AHA) syndrome: a study of middle-aged male twins

Published online by Cambridge University Press:  21 February 2012

F Sluyter*
Affiliation:
Department of Psychoneuropharmacology, University of Nijmegen, Nijmegen, The Netherlands. F.Sluyter@psy.vu.nl
JN Keijser
Affiliation:
Department of Animal Physiology, University of Groningen, Haren, The Netherlands.
DI Boomsma
Affiliation:
Department of Biological Psychology, Vrije Universiteit, Amsterdam, The Netherlands.
LJP van Doornen
Affiliation:
Clinical and Health Psychology, Utrecht University, Utrecht, The Netherlands.
EJCG van den Oord
Affiliation:
Department of Child and Adolescent Psychology, Utrecht University, Utrecht, The Netherlands.
H Snieder
Affiliation:
Twin Research & Genetic Epidemiology Unit, St Thomas' Hospital, London, UK.
*
*Correspondence: Dr F Sluyter, Department of Biological Psychology, De Boelelaan 1111, 1081 HV Amsterdam, The Netherlands. Tel: + 31 20 4448817; Fax: + 31 20 4448832

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

The aim of this study was to determine the genetic contribution to the variation in testosterone and the aggression-hostility-anger (AHA) syndrome in middle-aged twins. Moreover, the relation between testosterone and this syndrome, and possible common genetic mechanisms were investigated. Towards this end, blood samples were collected at two time points; the AHA syndrome was measured using three questionnaires: the Buss-Durkee Hostility Inventory with seven subscales, the Jenkins Activity Survey and the Spielberger State-Trait Anger Scale. The results showed substantial heritabilities for testosterone (approximately 60%) and moderate to fair heritabilities for the nine measures of the AHA syndrome (23–53%). The best fitting model for testosterone at two time points included a small age component and additive genetic and unique environmental factors, while a multivariate analysis of the nine AHA subscales resulted in an independent pathway model with two common additive genetic and two common unique environmental factors. No correlation between the common genetic factor influencing testosterone and the AHA subscales was found. We did, however, detect a negative correlation between the common environmental factor underlying testosterone and both common environmental factors influencing the nine AHA subscales, which may reflect a tendency for testosterone levels to rise and hostility to drop (or vice versa) after repeatedly experiencing success (or failure). Twin Research (2000) 3, 266–276.

Type
Articles
Copyright
Copyright © Cambridge University Press 2000