Understanding and Preventing Violence, Volume 2: Biobehavioral Influences (1994)
Chapter: INTRODUCTION
polymorphisms influence individual differences in aggression and agonistic behavior in rodents. This genetic liability toward aggression, however, is to a certain degree situation specific (Jones and Brain, 1987). For example, in dyadic male encounters, mice of the BALB/cBy strain are more aggressive than those of the C57BL/6By strain when tested against members of their own strain, but C57BL/6By are more aggressive when tested against mice of other strains. As Maxson (1990) notes, the genetics of aggression in a dyadic encounter depend not only on the individual's own genes but also on the genes of the conspecific partner. Similarly, diurnal variation, season of the year, arena size, test duration, and the operational definition of aggression are but a few of the variables that may change the rank order of aggression in strains (Maxson, 1990).
Similar specificity may occur for sex-appropriate aggression. Early selection studies selected for aggression among males only and did not report differences in aggression among females of the selected lines (Ebert and Sawyer, 1980). However, later researchers argue that females from high aggressive lines demonstrate their aggression in sex-appropriate settings such as postpartum tests (Hood and Cairns, 1988). Similarly, there also appears to be genetic sensitivity to the effects of early neonatal androgens on aggression in mice (e.g., Michard-Vanhee, 1988; Vale et al., 1972).
The recent trend in behavioral genetic research is aimed less at demonstrating the fact of inheritance than at elucidating its genetic correlates and identifying genetic loci that underlie agonistic behavior. Here, polymorphic loci on the Y chromosome may contribute to individual differences in male aggression in the mouse, at least in some strains (Carlier et al., 1990; Maxson et al., 1989; Selmanoff et al., 1976). Given the homology of the mammalian genome, such work may offer insight into the genetics of human behavior.
HUMAN BEHAVIORAL GENETIC STUDIES
INTRODUCTION
Before embarking on a critical overview, the terms of human behavioral genetics require definition. With respect to sibships, phenotypic (i.e., observed) variability is often decomposed into three major components: genetic variance, common environmental variance, and unique environmental variance. The difference between common and unique environmental variance is purely statistical: Common environment includes all environmental factors
that contribute to sibling similarity, whereas unique environment subsumes all environmental mechanisms that promote sibling differences . To express similarity for vertical relationships such as parent and offspring, two major variance components are usually identified: genetic variance and vertical environmental transmission variance. Technically, vertical environmental transmission variance includes all environmental mechanisms, even those outside the home, that correlate with parental antisocial behavior and at the same time influence individual differences in offspring antisocial behavior.
Genetic influence is usually quantified by either of two estimates of heritability. Broad sense heritability is the total genetic variance divided by the phenotypic variance; usually, the only population to permit estimation of broad sense heritability is a large series of identical twins raised apart in random environments. Narrow sense heritability is the additive genetic variance divided by the phenotypic variance. The difference between additive genetic variance and total genetic variance is a complicated function of allele frequencies, allelic action, and interaction among difference genetic loci. Precise heritability estimates are seldom possible with human behavioral phenotypes. Narrow sense estimates are usually reported, with little or no empirical data to justify the validity of their assumptions.
One does not inherit behavior as one inherits eye color. Hence, when the behavioral phenotype is dichotomized (e.g., criminal offender versus nonoffender), behavioral genetic analysis is aimed at liability. Liability is a latent, unobserved variable that is at least ordinally related to risk—the higher an individual's score on the liability scale, the greater is the relative probability that the individual will be an offender. The latent variable of liability is analyzed, not the dichotomized phenotype. Hence, it is appropriate to speak of heritability of liability to criminal offending; it is not technically correct to refer to the heritability of criminal offending.
One important specific application of the concept of liability is the multifactorial model. The central assumption of this model is that a large number of factors (many genes, parenting, schooling, peers, etc.) contribute to liability in roughly equal amounts so that some mathematical transformation will be able to scale liability to resemble a multivariate normal distribution within families. In this case, the tetrachoric correlation is the appropriate statistical index used to quantify familial resemblance for liability.
