Genetics and Violence

Gregory Carey

ANIMAL STUDIES

There is no behavioral genetic literature on violence in infrahuman species. Rather, the phenotype (i.e., observable behavior) is termed aggression or agonistic behavior, often occurring as an appropriate, adaptive response to a particular set of environmental circumstances. The extrapolation of such evolutionarily preadapted responses to human homicide or robbery is, of course, tenuous. Nevertheless, the ability to control matings and the intrauterine and postnatal environment dictates that the study of behavioral biology in animals may yield clues to the conditions for onset and cessation of some violent encounters in humans.

The behavioral genetic literature on animal aggression focuses almost exclusively on rats and mice. It has been documented for more than half a century that there are strain differences in the agonistic behavior of male mice (Ginsburg and Allee, 1942; Scott, 1942). The extensive literature on these differences has been reviewed elsewhere (e.g., Brain et al., 1989; Maxson, 1981). Selection studies have also demonstrated significant heritability for murine aggression (e.g., Ebert and Sawyer, 1980; van Oortmerssen and Bakker, 1981). Hence, there is abundant evidence that genetic

Gregory Carey is at the Department of Psychology and the Institute for Behavioral Genetics, University of Colorado, Boulder.



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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences Genetics and Violence Gregory Carey ANIMAL STUDIES There is no behavioral genetic literature on violence in infrahuman species. Rather, the phenotype (i.e., observable behavior) is termed aggression or agonistic behavior, often occurring as an appropriate, adaptive response to a particular set of environmental circumstances. The extrapolation of such evolutionarily preadapted responses to human homicide or robbery is, of course, tenuous. Nevertheless, the ability to control matings and the intrauterine and postnatal environment dictates that the study of behavioral biology in animals may yield clues to the conditions for onset and cessation of some violent encounters in humans. The behavioral genetic literature on animal aggression focuses almost exclusively on rats and mice. It has been documented for more than half a century that there are strain differences in the agonistic behavior of male mice (Ginsburg and Allee, 1942; Scott, 1942). The extensive literature on these differences has been reviewed elsewhere (e.g., Brain et al., 1989; Maxson, 1981). Selection studies have also demonstrated significant heritability for murine aggression (e.g., Ebert and Sawyer, 1980; van Oortmerssen and Bakker, 1981). Hence, there is abundant evidence that genetic Gregory Carey is at the Department of Psychology and the Institute for Behavioral Genetics, University of Colorado, Boulder.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences 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

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences 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.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences MENDELIAN DISORDERS Molecular genetic studies of rare, well-defined disorders can elucidate basic physiologic mechanisms. Familial hypercholesterolemia, for example, unraveled aspects of lipoprotein receptor synthesis and transport. Are there any such exploitable models for human violence? A search through Mendelian Inheritance in Man (MIM), a computerized data base of known or suspected heritable disorders, revealed eight disorders of potential relevance in the sense that the words ''aggression," "rage," "violence," or "antisocial" were mentioned in the MIM description. Table 1 lists these disorders, their current MIM numbers, and comments. Except for alcoholism, the genetics of which are unclear, the disorders are only tangentially associated with violence. An appropriate model disorder (e.g., one with presenting symptoms such as inexplicable rage) has yet to be described, although this feature was present in one sibship from a consanguineous mating for Urbach and Wiethe's disease (Newton et al., 1971). Although seizure disorders did not appear in the search, emotional lability is a typical feature of Unverricht and Lundborg myoclonus epilepsy (MIM number 254800), a form of seizure disorder found largely in Finland. At the other extreme, the genetics of some rare phenotypes associated with violence (e.g., repetitive rapists, pedophiles) have never been studied. It is possible that heritable forms may be uncovered among these rare individuals and that molecular genetics may be used to elucidate basic mechanisms of violence. A potentially important finding that emerged after this review was completed deserves mention. Brunner et al. (1993a,b) reported on a single, large Dutch kindred in which an unusual number of males were affected with moderate intellectual deficiency and aggression. The pattern of transmission was consistent with X-linkage and perfectly correlated with a deficiency in the gene for the enzyme monoamine oxidase-A. Studies on the frequency of this gene and its association with aggression in the general population have yet to be conducted. CHROMOSOMAL ANOMALIES The report by Jacobs et al. (1965) of a high prevalence of men with an extra Y chromosome (karyotypes 47,XYY and 48,XXYY) among incarcerated males sparked research (and debate) into the issue of whether supernumerary Y individuals are at high risk for

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences TABLE 1 Known or Suspected Genetic Disorders Associated With Aggression Disorder MIM Numbera Comments Urocanase deficiency 276880 Vaguely defined disorder; aggression noted in one pedigree. Gilles de la Tourette symptom 137580 Neurologic disorder with involuntary motoric and vocal tics. Both aggression and self-mutilation have been reported, but neither is symptomatic of the disorder. Precocious puberty, male limited 176410 Gonadotropin-independent gonadal testosterone secretion; male-limited, autosomal dominant transmission with onset of sexual precocity as early as 1 year; blockage of both androgen and estrogen synthesis was associated with a reduction of aggression in a series of nine boys. a-Mannosidosis 248500 Aggressive tendency noted in cattle with a-mannosidase deficiency, but not known to be associated with the deficiency in humans. Alcoholism 103780 Not known to follow strict Mendelian transmission patterns; well-established phenotypic correlation with aggression. Lipoid proteinosis of Urbach and Wiethe 247100 One pedigree reported in which a sib suffered with attacks of rage. Deafness-hypogonadism syndrome 304350 Only a single pedigree reported, consistent with X linkage; antisocial and immature behavior noted in males of the pedigree. Fragile X syndrome 309550 Variable expression with frequent mental retardation; antisocial tendencies noted but not a central part of the syndrome. a Mendelian Inheritance in Man.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences violence, crime, and other psychopathology. Early research compared the prevalence of sex chromosome aneuploidy among selected samples (e.g., prisoners, psychiatric patients) with the prevalence among newborn screens or other controls. The initial reviews of 47,XYY and 48,XXYY syndromes by Owen (1972) and Hook (1973) stressed that prospective research on well-defined populations was necessary for accurate assessment of any relationship between XYY and violence. Several prospective studies have now followed aneuploid children into adolescence. Results on 47,XYY suggest behavioral development well within the normal range, but with minor deficits in intelligence, other cognitive skills, and perhaps, in emotional and social skills (Bender et al., 1987). Study of a Danish birth cohort (Witkin et al., 1976) found a high prevalence of criminal registration among XYY individuals (5 of 12) that is not statistically different from the prevalence among 47,XXY (3 of 16) but is greater than the base rate among normal XY males of the same height (9% of slightly more than 4,000 men). Criminal histories of the five XYY individuals were not characterized by violence and aggression. Convictions were for minor offenses adjudicated by mild penalties, prompting the investigators to suggest that the relationship was likely due to nonspecific factors such as lowered intelligence. Personal follow-up revealed that the 12 XYY individuals had statistically significant but clinically minor differences from controls in sexuality, aggression, and testosterone levels (Schiavi et al., 1984, 1988; Theilgaard, 1984). The prospective results dispel the myth of the XYY as a "hyperaggressive, supermasculine sociopath" and, in its place, portray a group of individuals within the normal range but with an array of relatively nonspecific behavioral differences in attention and cognition, motoric skills, and personality. For example, the sexuality of XYY individuals is characterized more by insecurity and difficulty in developing and maintaining satisfying relationships with women than by stereotyped hypermasculinity (Schiavi et al., 1988). It is possible that nonspecific behavioral problems may increase risk among these individuals for later criminal offenses. GENETICS AND PERSONALITY TRAITS Given that genes do not code directly for crime and violence, it might be reasonable to suspect that genetic diathesis is mediated through personality traits and cognitive styles. Kinship correlations for intelligence have been summarized by Bouchard and

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences McGue (1981), and the general pattern suggests important contributions from both genes and family environment. A survey of the genetic literature on personality traits is too vast to report here. Hence, this review is limited to two major domains of personality. First, scales purporting to measure aggression are reported, with the name of the scale dictating acceptance of a study for review. In some studies, the exact items bear strong content resemblance to the concept of violence used by the Panel on the Understanding and Control of Violent Behavior (e.g., Tellegen et al., 1988); in other cases, the content appears related more to a broader, almost psychoanalytic, notion of intrapunitiveness (e.g., Partanen et al., 1966); and in yet other studies, item content was not fully specified (e.g., Rushton et al., 1986). The second area for review is scales specifically constructed to predict juvenile delinquency. These scales include the Psychopathic-deviate (Pd) scale of the Minnesota Multiphasic Personality Inventory (MMPI; Hathaway and McKinley, 1940); the Socialization (So) scale of the California Psychological Inventory (CPI; Gough, 1969); and the aggression scale of the Missouri Children's Picture Series (MCPS). Table 2 summarizes the results of this review. The studies are broadly classified into twin and adoption strategies. The twin results are consistent with the overall twin literature on personality: on the average, identical twins correlate higher than fraternal twins. A notable exception is reported by Plomin et al. (1981), the only study using blind ratings of aggression in a test situation (ratings of child's aggression against a Bobo doll). All other studies used self-report inventories or parental ratings. Unfortunately, sample sizes in Plomin et al. (1981) are too small to detect whether this difference is attributable to method of assessment, to aggression in childhood versus adulthood, or to sampling error from a trait with modest heritability. In the Minnesota series of twins raised apart (Gottesman et al., 1984; Tellegen et al., 1988), the correlations are as great as those for adult twins raised in the same household. Although standard errors for these correlations are large, they suggest that the great similarity of twins raised together is not due exclusively to such processes as imitation or reciprocal interaction (Carey, 1986) that might invalidate the twin design. There is little relevant adoption data. Different scales were administered to the Texas Adoption Project sample (Loehlin et al., 1985, 1987) in adolescence (the CPI in Loehlin et al., 1985) and in early adulthood (the MMPI in Loehlin et al., 1987). The patterning here is very similar to that of other adoption studies

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences TABLE 2 Genetics Studies of Personality Measures Related to Delinquency or Aggression     Males Females Study Measure Group N R Group N R Genders Analyzed Separately Owen and Sines (1970) MCPS aggression MZ 10 .09 MZ 8 .58     DZ 11 -.24 DZ 13 .22 Gottesman (1966) CPI socialization MZ 34 .32 MZ 45 .52     DZ 32 .06 DZ 36 .26 Scarr (1966) ACL n aggression MZ 24 .35           DZ 28 -.08       Partanen et al. (1966) Aggression items MZ 157 .25           DZ 189 .16       Loehlin and Nichols (1976) CPI socialization MZ 202 .52 MZ 288 .55     DZ 124 .15 DZ 193 .48   ACL aggressive MZ 216 .20 MZ 293 .24     DZ 135 -.05 DZ 195 .06 Rowe (1983) Number of delinquent acts MZ 61 .62 MZ 107 .66 DZ 38 .52 DZ 59 .46 Rushton et al. (1986) 23 aggression items MZ 90 .33 MZ 106 .43     DZ 46 .16 DZ 133 .00     DZ-OS 98 .12           MZ DZ Study Measure N R N R Genders Pooled           Gottesman (1963, 1966); Reznikoff and Honeyman (1967) MMPI psychopathy 120 .48 132 .27 Plomin et al. (1981) Median (three objective aggression ratings) 53 .39 31 .42 Ghodsian-Carpey and Baker (1987) CBC aggression 21 .78 17 .31   MOCL aggression 21 .65 17 .35 Pogue-Geile and Rose (1985) MMPI psychopathy 71 .47 62 .15     71 .23 62 .20 Rose (1988) MMPI psychopathy 228 .47 182 .23 Tellegen et al. (1988) MPQ aggression 217 .43 114 .14     MZ DZ Study Measure N R N R Twins Raised Apart (Minnesota Sample)         Tellegen et al. (1988) MPQ aggression 44 .46 27 .06 Gottesman et al. (1984) MMPI psychopathy 51 .64 25 .34 Study Measure Relationship N R Adoption Studies         Loehlin et al. (1985) CPI socialization Adoptive father-child 241 -.03     Adoptive mother-child 253 -.02     Biological father-child 52 .16     Biological mother-child 53 .06     Adoptive-adoptive sibs 76 .03     Adoptive-biological sibs 47 .10     Biological-biological sibs 15 -.01 Loehlin et al. (1987) MMPI psychopathy Adoptive father-child 180 .07     Adoptive mother-child 177 .01     Biological father-child 81 .12     Biological mother-child 81 .07     Birth mother-adopted child 133 .27     Adoptive-adoptive sibs 44 .02     Adoptive-biological sibs 69 .06     Biological-biological sibs 20 -.06 Parker (1989) CBC aggression items Adoptive sibs (age 4) 45 .54     Natural sibs (age 4) 66 .42     Adoptive sibs (age 7) 17 .28     Natural sibs (age 7) 19 .55 NOTE: ACL = adjective checklist; CBC = child behavior checklist; CPI = California Psychological Inventory; MCPS = Missouri Children's Picture Series; MMPI = Minnesota Multiphasic Personality Inventory; MOCL = Mothers' Observational Checklist; MPQ = Multidimensional Personality Questionnaire.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences (e.g., Scarr et al., 1981)—zero-order correlations with adoptive parents and small positive correlations with biological parents. This is consistent with the twin data in suggesting heritability, although estimates of the genetic effect are lower in the adoption than in the twin studies. The fact that adoptive relatives bear little resemblance to one another suggests that processes such as imitation and common family environment have weak effects on these psychometric predictors of delinquency. Parker's (1989) recent analysis of data from the Colorado Adoption Project (Plomin et al., 1981) gives a very different picture. Based on maternal ratings of aggression, both adoptive and biological siblings show strong, roughly equal, resemblance. These data agree with the Plomin et al. (1981) results in suggesting important common environment effects for childhood aggression, but do not agree with the small twin studies of Owen and Sines (1970) and Ghodsian-Carpey and Baker (1987). Together, the personality data imply a genetic contribution to individual differences for important correlates of violence. This inference is stronger for older adolescents and adults than for children. A glaring lack in this literature (as well as in the genetic literature on criminal offenders) is the absence of data to permit multivariate genetic analysis of personality traits such as aggression and criminal offending. Since this review was completed, several important studies of parental ratings of childhood aggression and delinquency in child and adolescent twins have been completed and initial results suggest important heritability. Gottesman and Goldsmith (in press) should be consulted for a review. Juvenile Antisocial Behavior Here, research on actual crime or antisocial behavior during adolescence is reviewed. Early twin studies of juvenile delinquency, summarized in Table 3, gave strong evidence of important common environment effects and weak evidence for heritability. Many of these early studies did not select samples or define phenotypes with the rigor required by modern research standards (see Slater and Cowie, 1971; Christiansen, 1977, for reviews). More recently, Rowe (1983, 1985, 1986) analyzed the number of self-reported antisocial behaviors from junior and senior high school twins. The twin correlations (given previously in Table 2) demonstrate significant heritability and, agreeing with the concordances

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences TABLE 3 Pooled Twin Concordance Rates for Juvenile Delinquency in Identical and Same-Sex Fraternal Twinsa   Identical Fraternal Gender Number of Pairs Percent Concordant Number of Pairs Percent Concordant Female 12 92 9 100 Male 55 89 30 73 a Based on the review by Cloninger and Gottesman (1987), eliminating pairs studied by Kranz (1936) in which concordance was not reported separately by gender. in Table 3, implicate common environment, albeit without reaching statistical significance. Adoption studies support the importance of family environment in early antisocial behavior. Cadoret et al. (1983) reported a significant main effect for an adverse adoptive home and some form of gene-environment interaction in three different adoptee samples. Bohman (1971) and colleagues (Bohman and Sigvardsson, 1985; Bohman et al., 1982) prospectively studied Swedish children from unwanted pregnancies. At age 15, those who remained with their own biological parents or who were placed as foster, but unadopted, children had almost twice the rate of antisocial-like behavior problems (truancy, running away, misuse of alcohol and drugs, repeated thefts) as their classmate controls. Children who were formally adopted, however, showed slightly lower rates than their controls and much lower rates than both the foster children and those remaining with their parents, despite a high frequency of criminality and alcohol abuse among their birth parents. Bohman suggested that any adverse genetic liability was neutralized by the benefits provided by secure adoption. Together, the early twin studies, the nonsignificant trend in Rowe's study, the Cadoret analyses, and the Bohman results provide strong evidence for a family environment effect on juvenile antisocial behavior. Both the Rowe and the later Cadoret studies suggest that genetics cannot be ignored during this period. Perhaps the most important research question for the future is the investigation of genetic and family environmental contributions to adolescent antisocial behavior that persists into adulthood and the detection of reasons why this behavior ceases in many adolescents.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences differences. The r-strategy is associated with relative ecological instability and tends to promote such qualities as small body size, rapid sexual maturation, short life span, and profligate reproduction. The K-strategy is associated with environmental stability and gives advantage to large body size, delayed maturation with parental care, longevity, and economical reproduction. By extrapolating the r/K between-species distinction to a continuum of within-species variability, human aggression is viewed as part of the r end and law abidingness as part of the K end of the dimension. A second research thrust has been the study of familial homicide by Daly and Wilson (1988a,b). Based largely on the concept of inclusive fitness, they predict that homicide (and presumably other aggression) should vary inversely with the degree of genetic relatedness of assailant and victim and with the reproductive capacity of the victim. This present round of sociobiological/evolutionary research is more empirical than many previous attempts to extrapolate from other species to human behavior. The research is also relatively new, so a large body of well-controlled studies has yet to be developed to permit assessment of the predictions. For example, Daly and Wilson present Canadian homicide data suggesting that filicide victimization is considerably greater for infants who have yet to reach their first birthday than for older children. To what extent is this due to inhibition because of the reproductive and temporal investment already made in an older child, to what extent is it a consequence of maternal postpartum psychoses, and to what extent is it due to the physical vulnerability of the young infant to a punitive blow that might injure but not kill an older child? For theories about the r/K-strategies, the relevant multivariate data that would permit one to assess the proportion of variance in violent criminal participation attributable to the latent r/K-variable have not been reported. Presumably, individual differences in these strategies have some heritable component. The requisite twin or adoption data must be gathered and subjected to multivariate analysis. GENETICS, RACE, AND VIOLENCE Racial differences in arrests, homicides, etc., have sometimes been interpreted in terms of mean genetic differences among human groups (Rushton, 1988a,b). From a genetic perspective, race differences fall into the general category of group differences. There

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences are two distinct questions that may be asked about genetics and violence in different groups. First, is the heritability of violence large within each group? Within-group heritabilities may be derived through adoption or twin studies of each group. Second, to what extent are differences in violence between groups due to the genetic differences between them? This question addresses between-group heritability. Empirical data suggest the possibility of important within-group heritability in European populations and some American populations of European ancestry. There are no comparable twin or adoption data to document within-group heritability among American minorities. Even in the presence of such data, it would be incorrect to infer that genetic differences contribute to differences between groups. Within-group heritabilities are insufficient to predict the extent to which mean group differences are genetic (DeFries, 1972; Loehlin et al., 1975). For example, the demonstration of within-group heritability among Danes and among Iowa whites does not imply that differences in crime rates between Denmark and Iowa are due to gene pool variance. Differences in prevalence and incidence of violence between Northern and Southern Ireland might be explained more easily by social and political milieus than by DNA variation. Wilson and Herrnstein (1985) consider it inconceivable that the rapid historical changes in homicide could be accounted for by changes in allelic frequencies. The two- to threefold increase in homicide rates that occurred between the 1960s and 1970s (Zahn, 1989) is almost certainly due to environmental factors, not all of which have been identified. Hence, it is plausible that large mean group differences could be perpetuated by environmental factors. Despite the fact that there are analytical models in genetics that attempt to account for such types of environmental diffusion (e.g., Boyd and Richerson, 1984; Cavalli-Sforza and Feldman, 1981; Lumsdem and Wilson, 1981), little is known about their empirical validity, let alone their direct application to human violence. It is not clear that it would even be possible to research the genetics of group differences in violence without first identifying these mechanisms for environmental diffusion and their prevalence and impact in different groups. On the genetic side, it is also improbable that various human

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences populations, reproductively isolated for millennia, will evolve genetic liabilities equal to the last decimal place. What do we know about mean genetic differences? Studies of red cell polymorphisms, proteins, and isozymes have consistently shown considerably more variability within a race than between races (Hartl, 1980; Nei, 1985; Nei and Roychoudhury, 1974, 1982). To put this in different terms, the "average" U.S. Oriental, "average" U.S. black, and "average'' U.S. white are genetically more similar to one another than three randomly selected individuals within, say, the U.S. white population. Hence, if these results can be extrapolated to a polygenic system contributing to liability for violence, then the genetic effects on race differences in violence are probably small and secondary to the genetic differences within races. Faced with a literature equivocal on whether there is a significant genetic effect on violence in Scandinavian samples, the absence of data on within-group heritability for minorities, abrupt historical trends largely unexplainable by genetic drift or natural selection, and molecular genetic evidence suggesting a low between-to-within ratio of genetic group differences, one might conclude that models attributing racial differences mostly to environmental factors have more plausibility than those that explain them mostly in terms of genetics. At the very least, there is no positive evidence to suggest that heritability plays an important role in group differences in violence within the United States. REFERENCES Baker, L.A. 1986 Estimating genetic correlations among discontinuous phenotypes: An analysis of criminal convictions and psychiatric-hospital diagnoses in Danish adoptees. (Special Issue: Multivariate behavioral genetics and development.) Behavior Genetics 16:127–142. Baker, L.A., W. Mack, T.E. Moffitt, and S. Mednick 1989 Sex differences in property crime in a Danish adoption cohort. Behavior Genetics 19:355–370. Bender, B.G., M.G. Linden, and A. Robinson 1987 Environment and developmental risk in children with sex chromosome abnormalities. Journal of the American Academy of Child and Adolescent Psychiatry 26:499–503. Bohman, M. 1971 A comparative study of adopted children, foster children and children in their biological environment born after undesired pregnancies. Acta Paediatrica Scandinavica 60(Suppl 221):5–38.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences 1978 Some genetic aspects of alcoholism and criminality: A population of adoptees. Archives of General Psychiatry 35:269–276. Bohman, M., and S. Sigvardsson 1985 A prospective longitudinal study of adoption. Pp. 137–155 in A.R. Nicol, ed., Longitudinal Studies in Child Psychology and Psychiatry . Somerset, N.J.: John Wiley & Sons. Bohman, M., C.R. Cloninger, S. Sigvardsson, and A.-L. von Knorring 1982 Predisposition to petty criminality in Swedish adoptees: I. Genetic and environmental heterogeneity. Archives of General Psychiatry 39:1233–1241. Bouchard, T.J., and M. McGue 1981 Familial studies of intelligence: A review. Science 212:1055–1958. Boyd, R., and P.J. Richerson 1984 Culture and the Evolutionary Process. Chicago: University of Chicago Press. Brain, P.F., D. Mainardi, and S. Parmigiani 1989 House Mouse Aggression: A Model for Understanding the Evolution of Social Behavior. London: Harwood Academic Publishers. Brunner, H.G., M. Nelen, X.O. Breakfield, H.H. Ropers, and B.A. Van Oost 1993a Abnormal behavior associated with a point mutation in the structural gene for monoamine oxidase A. Science 262:578–580. Brunner, H.G., M.R. Nelen, P. van Zandvoort, N.G.G.M. Abeling, A.H. Van Gennip, E.C. Wolters, M.A. Kuiper, H.H. Ropers, and B.A. Van Oost 1993b X-linked borderline mental retardation with prominent behavioral disturbance: Phenotype, genetic localization, and evidence for disturbed monoamine metabolism. American Journal of Human Genetics 52:1032–1039. Cadoret, R.J. 1978 Psychopathology in adopted-away offspring of biologic parents with antisocial behavior. Archives of General Psychiatry 35:176–184. Cadoret, R.J., and C.A. Cain 1980 Sex differences in predictors of antisocial behavior in adoptees. Archives of General Psychiatry 37:1171–1175. Cadoret, R.J., L. Cunningham, R. Loftus, and J. Edwards 1975 Studies of adoptees from psychiatrically disturbed biologic parents: II. Temperament, hyperactive, antisocial, and developmental variables. Journal of Pediatrics 87:301–306. Cadoret, R.J., C. Cain, and R.R. Crowe 1983 Evidence for a gene-environment interaction in the development of adolescent antisocial behavior. Behavior Genetics 13:301–310. Cadoret, R.J., T. O'Gormon, E. Troughton, and E. Heywood 1985 Alcoholism and antisocial personality: Interrelationships, genetic

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences Crowe, R.R. 1972 The adopted offspring of women criminal offenders: A study of their arrest records. Archives of General Psychiatry 27:600–603. 1974 An adoption study of antisocial personality. Archives of General Psychiatry 31:785–791. Dalgard, O.S., and E. Kringlen 1976 A Norwegian twin study of criminality. British Journal of Criminology 16:213–232. Daly, M., and M. Wilson 1988a Homicide. Hawthorne, N.Y.: Aldine de Gruyer. 1988b Evolutionary social psychology and family homicide. Science 242:519–524. DeFries, J.C. 1972 Quantitative aspects of genetics and environment in the determination of behavior. Pp. 5–16 in L. Ehrman, G.S. Omenn, and E. Caspari, eds., Genetics, Environment, and Behavior: Implications for Educational Policy. New York: Academic Press. Eaves, L.J. 1976 A model for sibling effects in man. Heredity 36:205–214. Eaves, L.J., J.L. Silberg, J.K. Hewitt, M. Rutter, J.M. Meyer, M.C. Neale, and A. Pickles 1993 Analyzing twin resemblance in multisymptom data: Genetic applications of a latent class model for symptoms of conduct disorder in juvenile boys. Behavior Genetics 23:5–19. Ebert, P.D., and R.G. Sawyer 1980 Selection for agonistic behavior in wild female Mus musculus. Behavior Genetics 10:349–360. Ellis, L. 1982 Genetics and criminal behavior: Evidence through the end of the 1970s. Criminology 20:43–66. 1987 Criminal behavior and r/K selection: An extension of gene-based evolutionary theory. Deviant Behavior 8:149–176. Gabrielli, W.F., Jr., and S.A. Mednick 1984 Urban environment, genetics, and crime. Criminology 22:645–652. Ghodsian-Carpey, J., and L.A. Baker 1987 Genetic and environmental influences on aggression in 4- to 7-year-old twins. Aggressive Behavior 13:173–186. Ginsburg, B.E., and W.C. Allee 1942 Some effects of conditioning on social dominance and subordination in inbred strains of mice. Physiological Zoology 15:485–506. Gottesman, I.I. 1963 Heritability of personality: A demonstration. Psychological Monographs: General and Applied 77(9):1–21. 1966 Genetic variance in adaptive personality traits. Journal of Child Psychology and Psychiatry 7:199–208.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences Loehlin, J.C., and R.C. Nichols 1976 Heredity, Environment, and Personality: A Study of 850 Sets of Twins. Austin: University of Texas Press. Loehlin, J.C., G. Lindzey, and J.N. Spuhler 1975 Race Differences in Intelligence. San Francisco: W.H. Freeman. Loehlin, J.C., L. Willerman, and J.M. Horn 1985 Personality resemblances in adoptive families when the children are late-adolescent or adult. Journal of Personality and Social Psychology 48:376–392. 1987 Personality resemblance in adoptive families: A 10 year follow-up. Journal of Personality and Social Psychology 53:961–969. Lumsdem, C., and E.O. Wilson 1981 Genes, Mind, and Culture. Cambridge, Mass.: Harvard University Press. Lyons, M.J., L. Eaves, M.Y. Tsuang, S.E. Eisen, J. Goldberg, and W.T. True 1993 Differential heritability of adult and juvenile antisocial traits. Psychiatric Genetics 3:117. Maxson, S.C. 1981 The genetics of aggression in vertebrates. In P.F. Brain and D. Benton, eds., The Biology of Aggression. Amsterdam: Sijthoff & Noordhoff International Publishers 1990 Methodological issues in genetic analyses of an agonistic behavior (offense) in male mice. In D. Goldowitz, R.E. Wimer, and D. Wahlsten, eds., Techniques for the Genetic Analysis of Brain and Behavior. Amsterdam: Elsevier Science Publishers. Maxson, S.C., A. Didier-Erickson, and S. Ogawa 1989 The Y chromosome, social signals, and offense in mice. Behavioral and Neural Biology 52:251–259. Mednick, S.A. 1987 Introduction—Biological factors in crime causation: The reactions of social scientists. In S.A. Mednick, T.E. Moffitt, and S.A. Stack, eds., The Causes of Crime: New Biological Approaches. New York: Cambridge University Press. Mednick, S.A., W.F. Gabrielli, Jr., and B. Hutchings 1983 Genetic influences in criminal behavior: Evidence from an adoption cohort. Pp. 39–56 in K.T. Van Dusen and S.A. Mednick, eds., Prospective Studies of Crime and Delinquency. Boston: Kluwer-Nijhoff Publishing. 1984 Genetic influences in criminal convictions: Evidence from an adoption cohort. Science 224:891–894. 1987 Genetic factors in the etiology of criminal behavior. Pp. 74–91 in S.A. Mednick, T.E. Moffitt, and S.A. Stack, eds., The Causes of Crime: New Biological Approaches . New York: Cambridge University Press.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences Mednick, S.A., P. Brennan, and E. Kandel 1988 Predisposition to violence. (Special Issue: Current theoretical perspectives on aggressive and antisocial behavior.) Aggressive Behavior 14:25–33. Michard-Vanhee, C. 1988 Aggressive behavior induced in female mice by an early single dose of testosterone is genotype dependent. Behavior Genetics 18:1–12. Miles, D., and G. Carey 1993 The genetics of antisocial personality disorders: A psychiatric sample. Behavior Genetics 23:558–559. Moffitt, T.E. 1987 Parental mental disorder and offspring criminal behavior: An adoption study. Psychiatry 50:346–360. Nei, M. 1985 Human evolution at the molecular level. In T. Ohta and K. Aoki, eds., Population Genetics and Molecular Evolution. Tokyo: Japan Scientific Societies Press. Nei, M., and A.K. Roychoudhury 1974 Genetic variation within and between the three major human races of man, Caucasoids, Negroids, and Mongoloids. American Journal of Human Genetics 26:421–443. 1982 Genetic relationship and evolution of human races. Evolutionary Biology 14:1–59. Newton, F.H., R.N. Rosenberg, P.W. Lempert, and J.S. O'Brien 1971 Neurological involvement in Urbach-Wiethe's disease (lipoid proteinosis): A clinical, ultrastructural, and chemical study. Neurology 21:1205–1213. Owen, D.R. 1972 The 47,XYY male: A review. Psychological Bulletin 78:209–233. Owen, D.R., and J.O. Sines 1970 Heritability of personality in children. Behavior Genetics 1:235–247. Parker, T. 1989 Television Viewing and Aggression in Four and Seven Year Old Children. Paper presented at Summer Minority Access to Research Training meeting, University of Colorado, Boulder. Partanen, J., K. Bruun, and T. Markkanen 1966 Inheritance of Drinking Behavior: A Study on Intelligence, Personality, and Use of Alcohol of Adult Twins. Helsinki: Keskuskirjapaino. Plomin, R., T.T. Foch, and D.C. Rowe 1981 Bobo clown aggression in childhood: Environment, not genes. Journal of Research in Personality 15:331–342.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences Plomin, R., J.C. Loehlin, and J.C. DeFries 1985 Genetic and environmental components of "environmental" influences. Developmental Psychology 21:391–402. Pogue-Geile, M.F., and R.J. Rose 1985 Developmental genetic studies of adult personality. Developmental Psychology 21:547–557. Reznikoff, M., and M.S. Honeyman 1967 MMPI profiles of monozygotic and dizygotic twin pairs. Journal of Consulting Psychology 31:100. Rose, R.J. 1988 Genetic and environmental variance in content dimensions of the MMPI. Journal of Personality and Social Psychology 55:302–311. Rowe, D.C. 1983 Biometrical genetic models of self-reported delinquent behavior: A twin study. Behavior Genetics 13:473–489. 1985 Sibling interaction and self-reported delinquent behavior: A study of 265 twin pairs. Criminology 23:223–240. 1986 Genetic and environmental components of antisocial behavior: A study of 265 twin pairs. Criminology 24:513–532. Rowe, D.C., and D.W. Osgood 1984 Heredity and sociological theories of delinquency: A reconsideration. American Sociological Review 49:526–540. Rushton, J.P. 1988a Race differences in behavior: A review and evolutionary analysis. Personality and Individual Differences 9:1009–1024. 1988b The reality of race differences: A rejoinder. Personality and Individual Differences 9:1035–1040. Rushton, J.P., D.W. Fulker, M.C. Neale, D.K. Nias, and H.J. Eysenck 1986 Altruism and aggression: The heritability of individual differences. Journal of Personality and Social Psychology 50:1192–1198. Scarr, S. 1966 The origins of individual differences in adjective check list scores. Journal of Consulting Psychology 30:354–357. Scarr, S., P.L. Webber, R.A. Weinberg, and M.A. Wittig 1981 Personality resemblance among adolescents and their parents in biologically related and adoptive families. Journal of Personality and Social Psychology 40:885–898. Schiavi, R.C., A. Theilgaard, D.R. Owen, and D. White 1984 Sex chromosome anomalies, hormones, and aggressivity. Archives of General Psychiatry 41:93–99. 1988 Sex chromosome anomalies, hormones, and sexuality. Archives of General Psychiatry 45:19–24. Schulsinger, F. 1972 Psychopathy: Heredity and environment. International Journal of Mental Health 1:190–206.

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