c CHAPTER 4 Evidence from Behavioral Genetics for Environmental Contributions to Antisocial Conduct TERRIE E. MOFFITT and AVSHALOM CASPI DesPite assiduous efforts to eliminate it, antisocial behavior is still a problem. Approximately 20% of people in the developed world experience victimization by perpetrators of violent and nonviolent illegal behavior each year (U.S. Bureau of Justice Statistics, 2002; World Health Organization, 2002). Behavioral science needs to achieve a more complete understanding of the causes of antisocial behavior to provide an evidence base for effectively controlling and preventing antisocial behavior. A new wave of intervention research in the last decade has demonstrated clear success for a number of programs designed to prevent antisocial behavior (www.preventingcrime.org; Heinrich, Brown & Aber, 1999; Sherman et aI., 1999; Weissberg, Kumpfer, & Seligman, 2003). Nevertheless, the reduction in antisocial behavior brought about by even the best prevention programs is, on average, modest (Dodge, 2003; Wasserman & Miller, 1998; Olds et aI., 1998; Heinrich et aI., 1999; Wandersman & Florin, 2003; Wilson, Gottfredson, & Najaka, 2001). The best-designed intervention programs reduce serious juvenile offenders' recidivism only by about 12% (Lipsey & Wilson, 1998). This modest success ot interventions that were theory-driven, well designed, and amply funded sends a clear message that we do not yet understand the causes of antisocial behaVIOr well enough to prevent it. Simultaneous with the new wave of research evaluating interventions is a wave of research pointing to the concentration of antisocial behavior in families. In the 19705, the astounding discovery that fewer than 10%, of individuab perpetrate more than 50%, of crimes (Wolfgang, FigJio, & Sellin, 1972) prompted researchers to investigate individual 96 \ I ~ I \ f t 97Environmental Behavioral Genetics t:imnIIllal~ (Blumstein & Cohen, 1987) and examine the childhood origins of such reoffenders (Moffitt, 1993). This research constructed the evidence base supnew wave of preventive intervention trials (Yoshikawa, 1994). Recently jourdrawn public attention to certain families that across several generations . far more than their share of criminal family members (Butterfield, 1996,.LU'H~'··· familial concentration of crime has been confirmed as a characteristic of the population (Farrington, Barnes, & Lambert, 1996; Farrington, Jolliffe, Loeber, Loeber, & Kalb, 2001; Rowe, & Farrington, 1997). In general, fewer than families in any community account for more than 50(1~ of that community's In.'lJU'''U''~W' The family concentration of antisocial behavior could be explained by influence on antisocial behavior, but it could just as easily be explained by social transmission of antisocial behavior within families. Again, causation is nderstood. Studies that cannot disentangle genetic and environmental influ­ help. IAL BEHAVIOR RESEARCH IS STUCK IN THE RISK-FACTOR STAGE reviewers have concluded that the study of antisocial behavior has been stuck stage (Farrington, 1988, 2003; Hinshaw, 2002; Rutter, 2003a, ":01::<.«1,,,,,, so few studies have used designs that are able to document causality Murray, & Eaves, 2001). A variable is called a risk factor if it has a docu­ relation with antisocial outcomes, whether or not the association is causal status of most risk factors is unknown; we know what statistically pre­ .,..~"' ...'" ogy outcomes but not how or why (Kraemer, 2003; Kraemer et aI., are consequences to the field's failure to push beyond the risk factor stage to understanding of causal processes. Valuable resources have been wasted be­ programs have proceeded on the basis of risk factors, without suffito understand causal processes. barrier to interpreting an association between an alleged environmental and antisocial outcome as a cause-effect association is, of course, the old bugcorrelation is not causation. Some unknown third variable may account for the and that third variable may well be heritable. During the 1990s, the assumpnurture" influences behavior came under fire. Traditional socialization studies behavior, which could not separate environmental influences from their corwere challenged by four important empirical discoveries: (1) ostensible enmeasures are influenced by genetic factors (Plomin & Bergeman, 1991); (2) heritable traits influence the environments they provide for their children 1996; PIomin, 1994); (3) people's genes influence the environments they eni'-'-llU.IC1_ 1996; Plomin, DeFries, & Loehlin, 1977); and (4) environmental influnot seem to account for the similarity among persons growing up in the ~ame 1994). It was said that although non-behavioral-genetic studies might certain rearing experiences predict young people's antisocial outcomes, theo. based on findings from such designs were guilty of a fundamental logical -~~'"'u''' correlation for causation (Scarr, 1992). These challenges culminated in that so far the evidence for genetic influences outweighed the evidence ·nn,.,..~~._ influences within the family (Harris, 1998; Rowe, 1994). Many social 98 SOCIALIZATION WITHIN BIOLOGICAL FRAMEWORKS scientists responded to this claim, reasserting evidence for environmental influences (CoJlim, Maccoby, Steinberg, Hetherington, & Bornstein, 2000; Reid, Patterson, & Snyder, 2002; Yandell, 20(0). However, the reason there is all this controversy about the importance of the family environment in the first place is that the evidence base was not decisive enough to compel both camps. The best way forward to resolve the debate is to use research designs that can provide leverage to test environmental causation. Ordinary studies cannot test whether a risk factor is causal, and it would be unethical to assign children to experimental conditions expected to induce aggression. Fortunately, researchers can use three other methods for testing causation: natural-experiment studies of within-individual change (Cicchetti, 2003; Costello, Compton, Keeler, & Angold, 2003), treatment experiments (Howe, Reiss, & Yuh, 2002), and the focus of this review: behavioral-genetic designs (Moffitt, 2005). None of the three alone can provide deciSive proof of causation, but if all supply corroborative evidence by ruling out alternative noncausal explanations about a risk factor, then a strong case for causation can be made. TESTING HYPOTHESES ABOUT ENVIRONMENTAL CAUSATION Inference from Different Types of Behavioral-Genetic Designs Antisocial behavior has been studied in twins reared together, adoptees, and twins reared apart. Behavioral-genetics research is not limited to exotic samples; researchers also examine ordinary families whose members vary in genetic relatedness full siblings, half-siblings, step-siblings, cousins, and unrelated children reared in the same family) (Rowe, Almeida, & Jacobson, 1999). This variety of research designs offers a special advantage for inference, because comparing their estimates tells us that the environmental effect sizes for antisocial behavior are robust across different designs; they are not biased by the limitations and flaws peculiar to one design. A number of potential flaws are unique to adoption studies. First, adoption agencies could attempt to maximize similarity between the adoptee's biological and adoptive families to increase the child's chance of fitting in with the new family ("selective placement"). Relatedly, biological mothers who intend to give their baby away may neglect prenatal care and continue to abuse substances during pregnancy, and many unwanted babies experience institutionalization before they are adopted. If adoptive homes, prenatal care, and institutional care were selectively worse for the babies given up by antisocial biological mothers, this could bias estimates of heritability upward and estimates of environment effects downward, by misattributing the criminogenic influences of these three unmeasured nongenetic factors to a criminogenic influence of genes (Mednick, Moffitt, Gabrielli, & Hutchings, 1986). Second, both adoptees and twins reared apart are likely to be reared in home environments that are unusually good for children because adoptive parents are carefully screened. Adoption breaks up the association between genetic risk and environmental risk naturally occurring in ordinary families by removing genetically at-risk children from damaging homes and placing them in salutary homes. As a result, interactions between environmental adversity and genetic vulnerability that exacerbate behavioral problems in ordinary children (and twins) are uncommon among adoptees (Stoolmiller, 1999). The restricted range of rearing environments resulting from screening of adoptive parents could suppress estimates of environmental effects and thus bias heritability estimates upward (Fergusson, Lynskey, & Horwood, 1995; Stoolmiller, ----------------~ 99 (Coi­ Iyder, lpor­ deci) use ethi­ )rtu­ oent ,& this ride 'na- be ed x­ ~s, y) J­ 11 d s Environmental Behavioral Genetics 1999). However, this flaw of adoption studies is offset by studies of national twin registers (e.g., Cloninger & Gottesman, 1987) or stratified high-risk twin samples (e.g., Moffitt & E-risk Study Team, 2002), because such sampling frames represent the complete population range of environme~taJ and genetic ~ackgro~nds. Studies of tWillS aVOId the potential flaws of adoptIOn studies, but they suffer several potential flaws of their own. First, the logic of the twin desi~ assumes that all the greater similarity between monozygotiC (MZ) compared to dizygotIC (DZ) tWillS can safely be ascribed to MZ twins' greater genetic similarity. This "equal environments assumption" requires that MZ twins are not treated more alike than DZ twins on the causes of antisocial behavior (Kendler, Neale, Kessler, Heath, & Eaves, 1994). Because MZ twins look identical, they might be treated more similarly than DZ twins in some way that promotes antisocial behavior, and as a result, estimates of heritability from studies of twins reared together could be biased upward, and estimates of environmental effects could be biased downward, relative to the correct population value (DiLalla, 2002). However, studies of adoptees do not suffer this flaw, and neither do studies of twins reared apart, because MZ twins reared apart do not share environments (unless their genetically influenced behaviors evoke similar reactions from caregivers in their separate rearing environments, which is a genetic effect). Second, in studies of twins, MZ twins differ more than DZ twins in prenatal factors affecting intrauterine growth; for example, MZ twins sharing the same chorion appear to suffer more fetal competition for nutrients. These intrauterine factors also violate the assumption that environments are equal for MZ and DZ twins, but intrauterine differences tend to make MZ twins less alike than their genotypes and thus would bias heritability estimates downward and environmental effects upward (Rutter, 2002). Third, genomic factors that make some MZ twin pairs' genotypes less than perfectly identical (such as random inactivation of genes on one of each girl's two X chromosomes; Jorgensen et al., 1992) could in theory affect twin-study estimates, but so far no evidence shows that these processes influence behavior. Fourth, parental assortative mating can bias heritability estimates. Coupled partners are known to share similarly high or low levels of antisocial behaviors (Galbaud du Fort, Boothroyd, Bland, Newman, & Kakuma, 2002; Krueger, Moffitt, Caspi, Bleske, & Silva, 1998). When parents of twins mate for similarity, it should increase the genetic similarity of DZ twins, but MZ twins' genetic similarity cannot increase beyond its original 100%, and as a result heritability estimates will be biased downward and environmental estimates upward, relative to the correct population value. The implication of biological-parent assortative mating for adoption studies is the opposite; biological-parent similarity for antisocial behaviors would bias adoptees' heritability upward relative to the correct population value (because adoptee/biological-parent correlations would represent a double dose of parental genes). Fifth, twin studies using adult reports to measure behavior sometimes suffer from rater artifacts; for example, adults may mix up or conflate the behavior of MZ twins and they may exaggerate differences between DZ twins. Such a rater artifact does not afflict adoption studies (nor twin studies using the twins' self-reports, as twins do not confuse them­ selves). In any case, comparisons between designs have revealed that studies of twins reared together yield estimates that are more similar than different to the estimates from studies of twins reared apart or of adoptees (Rhee & Waldman, 2002). On the one hand, this is because any bias arising from factors such as selective adoptee placement, violations of the equal-environment assumption, intrauterine twin differences, or assortative mating, is only very small (Miles & Carey, 1997; Rutter, 2002). On the other hand, these factors 100 SOCIALIZATION WITHIN BIOLOGICAL FRAMEWORKS bias esnmare, u~,\\arll a, otten Lh thn bias them JOWl1\\ ard, lanlelmg ealh other Out. The bottom line i, that it is lmportanr tor tests of environmental nsk to exploit a \'al'lety of beho\'ioral-genetics de:-,igns, as well as experimental designs and studie, of Withinllldividu effects are environmentally mediated, it is useful to mention that some known risk factors do not appear to be causal. First, as noted previously, we found that children's genes accounted for virtually all the association between their corporal punishment (i.e., spanking) and their conduct problems. This indicated a "child effect," in which children's bad conduct provokes their parents to use more corporal punishment, rather than the reverse (Jaffee, Caspi, Moffit, Polo-Tomas, et al.,2004). Second, studies have reponed that mothers' smoking during pregnancy is correlated with children's conduct problems, but pregnancy smoking is known to be concentrated among mothers who are antisocial, have mental health problems, mate with antisocial men, and rear children in conditions of social deprivation. When the family liability for transmission of psychopMhology from parents to children was controlled through statistical controls for the parents' antisocial behavior, mental health, and social deprivation, the effect of even heavy smoking during pregnancy disappeared. This study suggests that although pregnancy smoking undoubtedly has undesirable effects on outcomes such as infant hirthweight, it is probably not a cause of conduct problems (Maughan, Taylor, Ca~pi, & Moffitt, 2004). A third finding of nil environmental influence concerned father absence. In families h;)\'ing ab~ellt fathers, the children are known to have more conduct problems. However, absent fathers are more antisocial on average than fathers who stay with their children, and antisocial beha\'ior can be genetically' transmitted, \Vhen we controlled for mother's and father's antisocial history, we found that the association between father absence and children's conduct prohlell1s disappeared. 1'his suggests that father ahsence is not a direct cause of conduct problem~ hut, rather, is a proxy indicator for famllialliahilitv to antisocial behavior !.Jaffee t't al._ 20()3). z 113 liabil_ )r. 'oking It any ding, :ative e to- be- OUt vior the reEnvironmental Behavioral Genetics What Research Is Needed? To date, question 5, "Does bad parenting have an environmentally mediated causal effect on children's aggression?," has been answered in the affirmative by behavioral-genetics reports from several twin samples, finding such effects for family adaptability: parentchild conflict, parental momtonng, bad fathermg, maternal depresslOn, phySiCal maltreatment, and mothers' negative expressed emotions. These studies share an Achilles' heel; because different forms of parenting risk are concentrated in the same families, the particular parenting measure targeted in a study may be a proxy for some other, correlated risk factor. Research is needed that isolates the effects of one risk factor from its correlates. Nevertheless, whatever the most influential parenting behaviors are, the studies attest that parents can have environmentally mediated effects. It may surprise some developmentalists to learn that when familial liability and child effects are controlled, parenting influences on children drop to small effect sizes. However, small effects ought to be expected, for three reasons. First, it must be remembered that these small effects reflect true environmental associations after they have been purged of the confounding influences that inflate effect sizes in nongenetic studies. Associations between risk factors and behavior outcomes tend to shrink by at least half when genetic confounds are controlled (Turkheimer & Waldron, 2000). This shrinkage suggests that the risk-outcome correlations that social scientists are accustomed to seeing are inflated to about double their true size. Second, small effects for any particular risk factor make sense, in view of evidence that clear risk for antisocial behavior accrues only when a person accumulates a large number of risks (Rutter, Giller, & Hagell, 1998), each of which may individually have only a small effect (Daniels & Plomin, 1985). A third reason why small effects should not be too surprising is that they represent the main effects of measured environments, apart from any environmental effects involved in gene-environment (G x E) interactions. Recall that adoption studies found no effects of bad adoptive parenting in the absence of genetic liability, but bad adoptive parenting was associated with elevated antisocial outcomes for adoptees at genetic risk (Cadoret, Yates, Troughton, Woodworth, & Stewart, 1995; Mednick, Gabrielli, & Hutchings, 1984). In twin designs, when testing whether the shared experience of bad parenting enhances twin similarity in aggression over and above genetic influences on similarity, G x E interactions are controlled along with other genetic influences. In twin designs testing whether differential experiences of bad parenting are associated with MZ twin differences in aggression, differential outcomes arising from G x E interactions are ruled out by the twins' identical genotypes. In contrast, genetic risk and bad parenting are not usually disentangled in real life as they are in behavioral-genetics studies. In ordinary lives, genetic and environmental risks often coincide. It is possible in theory that environmental effects conditional on genetic vulnerability could be quite large. We next turn to the question of G x E interactions influencing antisocial behavior. 6. Testing the Hypothesis of Interaction between Genes and Environments The study of G x E interaction entails substantial methodological challenges. It requires measured environments that are truly environmental, measured genetic influence, some means of separating them from each other, and enough statistical power for a sensitive test of interaction (Rutter & Silberg, 2002). Despite the challenges, theory-driven hypotheses of G x E interaction are well worth testing, because where measured G x E is found 114 SOCIALIZATION WITHIN BIOLOGICAL FRAMEWORKS to influence hehavior di~order." both '>peutic gene'> and specIfic ennronmenta] flsb can concei\'ably have moderate-co-large effect!>, as oppo,>ed to the very sI11311 expected from prior quantitative generic research. SpecifIc genes revealed to he stronger in the presence of enVironmental risk would guide strategic research into those gene,' expres_ sion, possibh' leading to genetic diagnostics and improved pharmacological inten'entions (Evans &.: Reliing, 1999), Specific enVIronmental effects revealed to be stronger in the presence of generic risk would prompt a new imperus for specific envmmmental preven_ tion efforts, and would help to identify who needs the prevention program!> most. The study of G F is especially exciting in antisocial behavior research, where investigations have pioneered the way for all behavioral di<,orders. Studies of antIsocial behavior were first to report evidence of interaction between latent genetic and latent environmental risks ascertained in adoption studies, and also first to report evidence of an interaction between a measured genetic polymorphism and a measured environmental riSK. Four research designs have been used. Adoption Studies of Latent Gx E The first evidence that genetic and environmental risks influence antisocial beha vior in a synergistic way came from adoption studie~. Among the 6,000 families of male adoptees in the Danish Adoption Study, 14% of adoptees were convicted of crime though neither their biological nor their adoptive parents had been convicted, whereas 15°/', were convicted if their adoptive parent alone was convicted, 20% were convicted if their bIOlogical parent alone was convicted, and 25% were convicted if both biological and adoptive parents \vere convicted, although there were only 143 such cases (Mednick &.: Christiansen, 1977). This pattern of percentages did not represent a statistically significant cross-over interaction term, but it did illustrate clearly that the effects of genetic and environmental risk acting together were greater thal1 the effects of either factor acting alone. The finding was buttressed by two studies from American and Swedish adoption registers completed about the same time (Cadoret et aI., 1983; Cloninger, Sigvardsson, Bohman, & von Knorring, 1982). Adoption Studies of Latent G x Measured E In a pool of 500 adoptees from the Iowa and Missouri adoption studies, adoptees had the most elevated antisocial behaviors when they experienced "adverse circumstances" in their adoptive homes as well as having birth mothers with antisocial personality problems or alcoholism (Cadoret et aI., ] 983). This landmark study documented that the interaction was statistically significant and replicated across two independent samples. This finding was replicated and extended in another Iowa adoption cohort of 200 families (Cadoret, et aI., 1995). Adoptive parents' adversity was defined according to the presence of marital problems, legal prohlems, substance ahuse, or mental disorder, and it imeracted significmtly with biological parents' antisocial personality disorder to predict elevated rates of childhood aggression, adolescent aggression, and diagnosed conduct disorder in the adoptees. This same Iowa adoption study was creatively analyzed to demonstrate that adversity in the adoptive home can moderate the genetic child effect in which children's aggression provokes bad parenting (Riggins-Caspers et aI., 20(3). Adoptees' genetic liability for antisocial behavior (defined as hiological parents' psycho­ 115Environmental Behavioral Genetics provoked more harsh discipline from the adoptive parents in homes in which doptive parents suffered adversity (marital, legal, substance, or psychopathology ). There is one prohlem with studying G x E in adoption designs, and it is that itself breaks up the naturally occurring processes of rGE that characterize the nn,rm",,"u majority population, thereby precluding the possibility of G x E. This sepaallows the empirical study of G x E, but paradoxically, it probably results in an un.re:;L11U""~ of the influence of G x E on antisocial outcomes in the general population. this reason, adoption G x E studies should be complemented with twin studies. ... Twin Study of Latent Gx Measured E E-risk twin study also yielded evidence that genetic and environmental risks interact '(Jaffee et a!., 2005). Because we already knew that conduct problems were highly heritaIble in the E-risk twin sample at age 5 years (Arseneault et a!., 2003), we were able to estimate each child's personal genetic risk for conduct problems by considering whether his or her co-twin had already been diagnosed with conduct disorder, and whether he or she shared 100% versus 50% of genes with that diagnosed co-twin. This method's usefulness bad been demonstrated previously in a landmark G x E study showing that the risk of depression following life-event stress depends on genetic vulnerability (Kendler et a!', 1995). For example, an individual's genetic risk is highest if his or her co-twin sibling already has a diagnosis of disorder and the pair is monozygotic. Likewise, an individual's gene~ic risk is lowest if his or her co-twin has been free from disorder and the pair is monozygotic. Individuals in DZ twin pairs fall between the high and low genetic risk .groups. In our study an interaction was obtained such that the effect of maltreatment on conduct problem symptoms was significantly stronger among children at high genetic risk than among children at low genetic risk. (Because there was no genetic child effect provoking maltreatment, the genetic risk groups did not differ on concordance for maltreatment or the severity of maltreatment.) In addition, the experience of maltreatment was associated with an increase of 24% in the probability of diagnosable conduct disorder among children at high genetic risk, but an increase of only 2% among children at low risk. Studies of Measured Gx Measured E: Testing a Measured Gene The aforementioned adoption and twin studies established that genotype does interact with bad parenting in the etiological processes leading to antisocial behavior. However, the studies did not implicate any particular genes. We conducted one study to test the hypothesis of G x E interaction using a measured environmental risk, child maltreatment, and an identified gene, the monoamine oxidase A(MAOA) polymorphism (Caspi et aI., 2002). We selected the MAOA gene as the candidate gene for our study for four reasons (supporting research is cited in Caspi et aI., 2002). First, the gene encodes the MAOA enzyme, which metabolizes the neurotransmitters linked to maltreatment victimization and aggressive behavior by previous research. Second, drugs inhibiting the action of the MAO enzyme have been shown to prevent animals from habituating to chronic stressors analogous to maltreatment and to dispose animals toward hyperreactivity to threat. Third, in studies of mice having the MAOA gene deleted, increased levels of neurotransmitters and aggressive behavior were observed, and aggression was normalized by restoring MAOA 116 SOCIALIZATION WITHIN BIOLOGICAL FRAMEWORKS gene expressIOn. Fourth, an extremeh- rare mutation causing a null allele at the MAOA locus was associated with aggressive psychopathology among some men in a Dutch farn_ ily pedigree, although no relation between MAOA genotvpe and aggression had been detected for people in the general population. We selected maltreatment for this study for four reasons (supporting research is cited in CaspI et aI., 2002). First, childhood maltreatment is a known predictor of antisocial outcomes. Second, not all maltreated children become antisocial, suggesting that vulnera_ bility to maltreatment is influenced by heretofore unstudied individual characteristics. Third, our abovementioned twin research had established that maltreatment's effect on children's aggression is environmentally mediated (i.e., the association is not an artifact of a genetic child provoking maltreatment or of transmission of aggression-prone genes from parents). As such, maltreatment can serve as the environmental variable in a test of G x E interaction. Fourth, animal and human studies suggest that maltreatment in early life alters neurotransmitter systems in ways that can persist into adulthood and can influence aggressive behavior. Based on this logic to support our hypothesis of G x E, we measured childhood maltreatment history (8'1., severe, 28% prohable, 64% not maltreated) and MAOA genotype (37% low-activity risk allele, 63'Yo high-activity allele) ll1 the 442 caucasian males of the longitudinal Dunedin Multidisciplinary Health and Development Study. We found that maltreatment history and genotype interacted to predict four different measures of antisocial outcome: an adolescent diagnosis of conduct disorder, an age-26 personality assessment of aggression, symptoms of adult antisocial personality disorder reported by informants who knew the study members well, and court conviction for violent crime up to age 26, the latest age of follow-up. Among boys having the combination of the lowMAOA-activity allele and severe maltreatment, 85% developed some form of antisocial outcome. Males having the combination of the low-activity allele and severe-to-probable maltreatment were only 12% of the male birth cohort, but they accounted for 44 % of the cohort's violent convictions, because they offended at a higher rate on average than other violent offenders in the cohort. Replication of this study was of utmost importance, because the study reported the first instance of interaction between a measured gene and a measured environment in the behavioral sciences, and because reports of connections between measured genes and disorders are notorious for their poor replication record (Hamer, 2002). One initial positive replication and extension has emerged from the Virginia Twin Study for Adolescent Behavioral Development (Foley et aI., 2004). This team studied 514 caucasian male twins and measured environmental risk using an adversity index comprised of parental neglect, interparental violence, and inconsistent discipline. MAOA genotype and adversity interacted significantly such that 15% of boys having adversity but the highMAOA-activity allele developed conduct disorder, in comparison to 35 'X, of boys having adversity plus the low-activity allele. This study went a step further, controlling for maternal antisocial personality disorder to rule out the possibility that passive rGE might have resulted in the co-occurrence of environmental and genetic risk. TI1is study thus replicated the original G x E between the MAOA polymorphism and maltreatmenr, extended it to other forms of parental treatment, and showed that it is not an artifact of passive rGE. Another study has tested the MAOA G x E effect, and although the pattern of findings was consistent with the interaction, it did not attain statistical significance (Haberstick et aI., 20(5). 117Environmental Behavioral Genetics Genes as Protective Factors Promoting Resilience An intriguing finding from the two MAOA G x E studies was that, in contrast to the G x E interaction's marked effects on antisocial outcomes, the unique effects of maltreatment apart from its role in the Gx E interaction were very m,odest. ~altreatment initially predicted antisocial outcomes III the full cohorts, but wIthlll the high-MAOA-actlvity genotype group its effects were reduced by more than half (Caspi ,et al., 2002; Foley et al., 2004). This pattern IS III keeplllg WIth the fllldlllgs ,from adopnon and tWill studles clted earlier in this section, all of which found that measured bad parenting had relatively little effect on children who were at low genetic risk (Cadoret et al., 1983; Cadoret et aI., 1995; Cloninger et al., 1982; Jaffee et aI., 2005; Mednick et ai., 1984). Taken together, these findings suggest the novel notion that genotype can be a protective factor against adversity. Some people respond poorly to adversity while others are resilient to it, and the reason for this variation has been a holy grail in developmental research. The search for sources of resilience has tended to focus on social experiences thought to protect children, overlooking a potential protective role of genes (but see Kim-Cohen, Moffitt, Caspi, & Taylor, 2004). The potential protective effect of genes deserves more attention (Insel & Collins, 2003). CONCLUSION In this chapter we reviewed the first studies in a new generation of research that exploits behavioral-genetics designs to address the interplay between measured environmental risks and genetic risks in the origins of antisocial behavior. This work has only recently accelerated, and more of it is needed before drawing conclusions (Dick & Rose, 2002; Kendler, 2001). However, even the few studies so far counteract prior claims that associations between family risk factors and child antisocial outcome might be nothing more than a spurious artifact of familial genetic transmission. This argument can be subjected to empirical test, and such tests need to address both child effects on environments (involving children's genes) and gene-environment correlations (involving parents' genes). Further, although the "residual main effects" of environmental risk factors may appear small after controlling for genetic transmission, that is not the whole story. Emerging evidence about G x E interactions suggests that environmental risks can affect people more strongly than previously appreciated, in genetically vulnerable segments of the population. Although this chapter has argued that twin and adoption studies together can provide a good evidence base, the most compelling information about gene-environment interplay will come from converging findings from behavioral-genetics designs, treatment experiments, and longitudinal natural experiments showing within-individual change. ACKNOWLEDGMENTS Work on this chapter was supported by grants from the U.S. National Institute of Mental Health (Nos. MH45070 and MH49414) and the U.K. Medical Research Council (Nos. G9806489 and G0100527), and by a Royal Society-Wolfson Research Merit Award. 118 SOCIALIZATION WITHIN BIOLOGICAL FRAMEWORKS REFERENCES Arseneault, L, l'v1offitt, T E.. (aspl, A., Ta\'lol, A., Ri)sdiik. F. V., Jaffee, S., et al. i 2003 J. '>tf(Jng genetic ef. fects on cross-sitllational antisocial behaviour among 5-year-old children accordrng to mothers. teach_ er,. examll1er-ohservers, :lI1d tWlIlS' self-repoft,·l(}umal ()f Child Pswhul, >,1{)' and Pswhhltrl', 44, 832_ 84li. Asbury, K., Dunn, j., Pike. A., & Piomin, R. (2003 J. ;-';onshared enYlronmel1tal lI1fluenccs on indlvldual dif. ferences in earlv behavioral develupment: A TllOllOZ\'gOt!c twin diffen:nces stud\'. Child /)el'eluj!lllent, 74, 933-943. Belsky, .I., & Barends, N. (2002). Personality and parenting. In M.H. Bornstein (Ed.). /-hmdhook of l!clrelliing: V()I. 3. Helll,!.: and hecoming a Illlrellt i2nd ed.• pp. 415-43X). Mahwah, N,I: Erlbaum. Blumstein, A., & Cohen, J i 1'-)X7). Char:lctenzlI1g criminal CHeers. Seiella', 237. 985-99 J. Bohman, M., Clolllnger, R.• Sigvardsson. S., & von Knorring, A.L (1902). Predlsposnion to pnn cnminalIty in Swetbh adpotces. I. Genetic and environmental heterogeneity. Archil/('s o( (;"l1er.11 Psychiatry, 3<),1233-]241. Braungart, J. M .• PJomin, R., & hilker, D, W. (J 992). Genetic medl~lti()n'()f the home environment dUring infancy: A sibling adoption study of the HOME. Deve/opme11t£1/ Psyc/w/ogl', 28, 104i\-\05S. Burt, A. S., Krueger, R. E, ,\-kGue, M., & Iacono, W. (2003). Parent-child conflict and the comorbidity among childhood exwrl1alizing disorders. Archiues of General Ps),chiatry, MI, 505-S J:l. Butterfield, F. (1996). All God's chi/drew Thl' Buskel t~lInil)' .md the Al1Il'n(.111 tr,ldltwl1 uf l'iolC1lCe. :-Jew York: Avon. Bmterfield, F. (2002, August 21). Father stea Is best: Crime in an American family. The Ncw York Tl1nes IOn· line]. Avaibble: www.nytimes.com/2002/08/21/nationalJ21FAMLhnnl. Cadoret, R. j., Cain, C. A., & Crowe, R. R. (1983). Evidence' for gene-environment interaction in tht development of adolescent antisocial behavior. Behauior Genetics, 13. 301-310. Cadoret, R. J" Yates, W. R., Troughton, E., Woodworth, G., & Stewart, M. A. S. (1995). Genetic-environmental interaction in the genesis of aggressivity and conduct disorders. Archir1es of General P"y'c/Jiatry, .12, 916-924. Caspi, A., McClay, j, Moffitt, T. E., Mill, J., Martin, J., Craig, I., et al. (2002). Role of genotype in the cycle of violence in maltreated children. Science, 297,851-854. Caspi, A., & Moffitt, T. E. (1995). The continuity of maladaptive behavior. In D. Cicchetti & D. Cohen (Eds.), Manual of developmental psychopathology (Vol. 2, pp. 472-511). New York: Wiley. Caspi, A., Moffitt, T., Morgan,.J., Rutter, M .. Taylor, A., Arseneault, L., et al. (2004). Maternal expressed emotion predicts children's antisocial behavior problems: Using MZ-twin differences to identifv environmental effects on hehavioral development. Deuelopmental Psychology, 40(2) 149-161. Caspi, A., Taylor, A., Moffitt, T. E., & Plomin, R. (2000). Neighborhood deprivation affects children's mental health: Environmental risks identified using a genetic design. Psychological Scwnce, 11,338-342. Caspi, A., Taylor, A., Smart, M. A.,Jackson,J., Tagami, S., & Moffitt, T. E. (2001). Can women provide reli:lble information about their children'$ fathers? Cross-informant agreement about men '5 antisocial behaviour. Journal Child Psychology and Ps),chiatry, 42, 915-920. Cichetti, D. (2003). Experiments of nature: Contributions to developmental theory. DC!Jel()pment and Psych()pathology, is, 833-835. Cloninger, C. R., & Gottesman I. L i 1n7). Genetic and environmental factors in antisocial behavior dIsorders. In 5. A. Mednick, T. E. Moffitt, & S. A. Stack (Eds.), The CJllses (ltcrime: Nell' Inolngical tll!pruac/ies (pp. 92-109). New York: Cambridge University Press. Cloninger. C. R., Sigv;Jrdssoll. S.. R"hnwn, M .. &: von Knorring, A. L (1 9 82). Pt'(·dispositlol1 to petty crill1inality in Swedish <1doptees. 11. Cross-fostering <1!1alysis ot gene-environll1ent interaction. Archil'''s (lj' C;CI1('T,r/ PsyciJitltr),,-I'J, 1242-1247. Collins, W. A.. Maceob)', E. E., Steinberg, L, Hcth~rington, E. M., & BornstclI1, M. H. (2000). C:ontcmpomry research on parenting. Allier/Call Psychol()gist. 55, 218-232. Conger, K. ,I., & Conger. R. D, ( [994). Differential parenting and change In ,ibling dJfh.-rence, In dclin'-jucncy. J()ltnhll Family l'sY('h%g)', 8, 2X7-302. Costello, E. ./., Compton, S. N., Keeler. G., & Angold, A. (200.';). R<:'lationships between poverty and psychopathology: A natural exp('rIment. ./oum.rl of I/J(' A1I11'l'ic2, 833-1:)42, KendleI', K. S., Ne3le, M. C. Kessler, R. C, Heath. A. C, & Eaves, L.J- (19Sl2). Childhood parental loss and adult psychopathology in women: A twill smdv perspective. ArciJiues 0/Gel1er.;z/ Psychiatry', 4'1.109­ 116. Kendler, K. S., Neale, Iv1. C, Kessler, R. C, Heath, A. c., & Eaves, L. J. (1994), Parental treatment and the equal environments assumption in twin studies of psychiatric illness. Psychological Medicine. 24. 579-590, Kendler, K, S., Prescott, C A" Myers,J" & Neale, M, C. (2003). The structure of genetic and environmental risk factors for common psychiatric and substance use disorders in men and women. Al'chiues orGen· eral Ps)'chiat7)~ 60, 929-937. Kim-Cohen.J.. Moffitt, 1'. E.. Caspi, A., & Taylor, A, (2004). Genetic and environmental processes in young children's resilience and vulnerability to socio-economic deprivation, Child Development, 7S(3), 651­ 668, Kim-Cohen, J., Moffitt, 1'. E., Taylor, A" Pawlby, S. .J., & Caspi, A. (2005). Maternal Depression and children's antisocial behavior: Nature and nurture effects, Archives o/General Psychiatry, 62, 173-] 81, Ktaemer, H. C (2003). Current concepts of risk in psychiatric disorders. Current Ophzi{)n in Ps)!chiatry', 16, 421-430. Kraemer, H. C, Kazdin, A. E., Offord, D. R., Kessler, R. C, Jensen, P. S., & Kupfer, D. J (1997). Coming to terms with the terms of risk. Archives 0/ General Psychiatry, 54. 337-343. Krueger R, E, Markon K, E., Bouchard T. J. (2003). The extended genotype: The heritability of personality accounts for the heritability of recalled family environments in twins reared apart. Joumal 0/Person· ality, 71, 809-833. Krueger, R, E, Moffitt, T, E., Caspi, A" Blesh, A., & Silva, P. A. (J 998). Assortative mating for antiSOCIal be· havior: Development:I1 and methodological implications. Behavior GenetiCS, 28, 173-186. Lahey, B, B., Moffitt, 1: E., & Caspi, A, (Eds.), (2003), Causes 0/conduct disurder and ;ul'cl1ile delinquellc)', New York: Guilford Press, Laub.]. H., & Sampson, R, J. (20U3). Sbared bl'gi1l11111gS, diverge11f liues: Delinquellt boys to age 70, Cambridge, MA: HarvJrd University Press. Lipsey. M. W,. & Wilson. D, B. (1998). Effective intervention for serious and violent juvenile offenders: Synthesis of research, In R. Locher IX D, P. hlrrington (Eds,), SCriOUS LInd lIiolCllt ;HuclIile nt!CI1ders (pp. 313-345), Thousand Oaks, CA: Sage, Losoya. S. H .. Callor. S.• Rowe. D, C, IX Goldsmith, H. H. (1997). Origins of familia! similarity in parenting: A study of twins and adoptive siblings. Dcvc/otJmental Psychology. .13. 1012-1023. Maughan, B" Taylor, A., Caspi, A.. & Moffitt, 1'. E, (2004). Prenawl smoking and child conduct problems: testing genetic and environmental explanation of the association. Archi!les (}(Gellcr,lI Psychiatl')" 61. 836-843. McGue, M .• Sharma, A., & Benson, P. (1996). The dfcct of common rearing on Jdolescent adjusrmeIH: Evi~ dence from a U.S. adoption cohort, DC1'elu/lmellhll Psychology. 32. 604-613. ----_11 121 hUd; '5. f liv­ 74, ~vi­ win )i£­ 8, III .1 d Environmental Behavioral Genetics S. (2003). The heritability of parenting. Parenting: Science and Practice, 3, 73-94. 'Mednick, S. A., & Christiansen, K. O. (1977). Biosocial bases of criminal behavi01: New York: Gardner Press. Mednick, S. A., Gabrielli, W. E, & Hutchings, B. (19,84). Genetic factors In criminal behavior: Evidence from an adoptlon cohort. SCIence, 224,891-89.>. . Mednick, S. A., Moffitt, T. E., Gabrielli, W. E, & Hutchings, B. (1986). Generic factors in criminal behavior: A review. In J. Block, D. Olweus, & M. R. Yarrow (Eds.), The development ofantiSOCIaland prosoclal behaVIOr (pp. 33-50). New York: Academic Press. Meyer,]. M., Rutter, M., Silberg,]. L., Maes, H., Simonoff, E., Shillady, L. L., er al. (2000). Familial aggregation for conduct disorder symptomatology; The role of genes, mantal discord, and family adaptability. psychological Medicme, 30, 7S9-774. Miles, D. R., & Carey, G. (1997). Genetic and environmental architecture of human aggression. Journal of Personality and Social Psychology, 72,207-217. Moffitt, T. E, (1993). "Life-course-persistent" and "adolescence-limited" antisocial behavior: A developmental taxonomy. Psychological Review, 100, 674-701. Moffitt, T. E. (200S). The new look of behavioral-genetics in developmental psychopathology. Psychological Bulletin, 131,533-554. Moffitt, T. E., Caspi, A., Rutter, M., & Silva, p, A. (2001). Sex differences in amisocial behm'lOur: Conduct disorder, delinquenc)', and violence in the Dunedin longitudinal study. Cambridge, UK: Cambridge University Press. Moffitt, T. E., & E-risk Study Team (2002). Teen-aged mothers in contemporary Britain. Journal of Child Psychology and Psychiatry, 43, 1-16. Neiderhiser, J. M., Reiss, D., Hetherington, E. M., & Plomin, R. (1999). Relationships between parenting and adolescent adjustment over time; Genetic and environmental contributions. Developmental Psychology, 35, 680-692. Neiderhiser,J. M., Reiss, D., Pederson, N., Lichtenstein, P., Spotts, E. L, Hansson, K., et al. (2004). Genetic and environmental influences on mothering of adolescents: A comparison of two samples. Developmental Psychology, 40, 335-351. O'Connor, T. G., Deater-Deckard, K., Fulker, D., Rutter, M., & Plomin, R. (1998). Genotype-environment correlations in late childhood and early adolescence: Antisocial behavioral problems in coercive parenting. Developmental Psychology, 34,970-981. O'Connor, T. G., Heatherington, E. M., Reiss, D., & Plomin, R. (1995). A twin-sibling study of observed parent-adolescent relations. Child Development, 66, 812-829. Olds, D., Henderson, C R. Jr., Cole, R., Eckenrode,J., Kitzman, H., Luckey, D., et al. (1998). Long-term effects of nurse home visitation on children's criminal and antisocial behavior: IS-year follow-up of a randomized trial. Journal of the American Medical Association, 280, 1238-1244. Perusse, D., Neale, M. C., Heath, A. C, & Eaves, L. J. (1994). Human parental behavior: Evidence for genetic influence and potential implications for gene-culture transmission. Behavior Genetics, 24, 327­ 336. Pike, A., McGuire, S., Hetherington, E. M., Reiss, D., & Plomin, R. (1996). Family environment and adolescent depressive symptoms and antisocial behavior: A multivariate genetic analysis. Developmental Psychology, 32, 590-603. Pike, A., Reiss, D., Hetherington, E. M., & Plomin, R. (1996). Using MZ differences in the search for nonshared environmental effects. Journal of Child Psychology and Psychiatry, 37, 695-704. Plomin, R. (1994). Genetics and experience: The interplay between nature and nurture. Thousand Oaks, CA: Sage. Plomin, R., & Bergeman, C S. (1991). The nature of nurture: Genetic influences on "environmental" measures. BehaVIOral and Brain Sciences, 14,373-427. Plomin, R., & Caspi, A. (1999). Behavior genetics and personality. In L. A. Pervin & O. P. John (Eds.), Handbook ofpersonality (2nd ed., pp. 251-276). New York: Guilford Press. Plomin, R., & Daniels, D. (1987). Why are children in the same family so differentfrom each other? Behavioral and Brain Sczences, 10, 1-16. Plomin, R., DeFries,]. C, & Loehlin, J. C (1977). Genotype-environment interaction and correlation In the analysis of human behavior. Psychological Bulletin. 84, 309-322. Plomin, R., DeFries, J. C, McClearn, G. E., & McGuffin, P. (2001). Behavioral genetics, (4th ed.). New York: Freeman. 122 SOCIALIZATION WITHIN BIOLOGICAL FRAMEWORKS Plomin, R., .\kClcarn, (1. E., I'edcr,on, 1':. L, ]'\;c"clroadc, J. R., /:( llergenun, C. ~. (I ':If)'! J. (.",l1cttc lIliiuCl1ce on adult,' ratings or their currenr lamilv ell\'ironmenL .Irlllrlidi of iV/dlTiclgc .1Ild the }ellwh" 11, -':11-803. Purcell, S, 120(2). Variance (Ol11pOllenrs model;. fur gelle-CIl\'lronmcnr Il1teractHlI1 in twin analysi;" Tluin ReSCdrcl). S, 554-S71, ReId, J., PaHerson CJ, R., /:( Snyder J. (2002', Am/suelell bciJclL'iul' III dJildl'l'lI .lIld dd()11!5C1!l1t s, \X'a shington, DC: Amencan Ps\chologicai i\s;.ociatiol1, Rei", D., 1':eiderhiser, J. JvL Hetherillgton, L ,\1., 0:. Plol11il1, R. 120(lO I. The reieuwllslJ/f! (ode: lJl:(i/l/Jcl'lJIg genetic c/lld soodimfJuellU:" UII dt/u/escellt del,e/o/llJ!t'IIt. Camhndgt" MA: H;:1f\'ard Uni\'tr'lty Pres" Rendt;', R, D" Slomkowski, C. L., Stocker, C., Fulker, D. \X'., &. I'lomlll, R, 11';)':12), C,cllctlC Jnd environmental influence, on maternal and sibling inrerJcrion in middle childhood: A sibling adoption stud\, Del'ciu/Jlnentd/ Psvcboil)g)" 28, 4a4-4';)O. Rh~e, ~, H .. &. WoldJ11;lll, L D, (2002), (,cnerie Jnd environmental II1fiucnccc, on anri:.ocial behaViOr: A meta-analysis of tWlI1 and adoption studie" I'syc/w/of:!,lcal Bu//etll1, 128, 4~()-Sl'!, Riggrn,,-Caspers, K. !vL Cadoret, R. J" Knurson, J. E, &: Langbehn, D. 120U3 j, lliolog\'-ClH'irolll11enr lI1t(;raction and evocative hlol()g)'-~nvironll1ent correlation: Contri hutiom of harsh dl:.ciplllll' ,llld p,w':lItul psychopathology to problem adolescent behaviors. Bchal'w)' Gellctlcs, ll, 205-22(), Rodger",!. L, Rowe, D, C, &: Li, CII ';1':14), Beyond nature ver"us nurture: DI' analv'I'> of nonshan:d influ, ences nil problem behaviors. iJCl'e/o/JlII<'lItail's:vc/w/ogY,iI), 374-384, Rowe, D, C, : I ':lIn), A biometric anal),sls of pcrceptJons of tamrlv CI1\'lronment. Child J)cl'c/()lmrellt, \4, 416-423, Rowe, D. C. (19';)4), The limit, mfiuence: Gelles, expcriellce, alld "ehdl/IO)'. New York: GLlilford Press. Rowe, D. C, Almeida, D. M., &. Jacobson, K, C. (199':1), School context and genetic mfiuences on aggression in adolescence. Psych()/oglc,d Snc/lce, 10,2:'7-280, Rowe, D, C, 0:. Farrington, D. P. (1997), The familial transmission of criminal cOllvictlOl1S, CrilllJl1()logy, 35,177-201. Rutter, M. (2002). Nature, nurture, and development: From evangelism through science tow,lfd policy and practice, Child Deue/upll1C'nt, 73, 1-21. ' Rutter, M, (2ll03a), Commentary: Causal processes leadmg to antisocial behavior. lJel'elopmental Psychedogy (Speeral issue], 39, 372-378, Rutter, M. (200.3b). Crucial parhs from risk mdicaror to c311salmechanism. In B. B. Lahey, T. E. Moffitt, & A, Caspi (Eds.), Causes (Onduct disorder and ju1'1'11iie delinque1lcy (PP. 3-241. New York: Guilford Press, Rutter, M., Giller, H., & Hagel!, A. IJ9(8), Al1tisocia//Jchdl'lOlir hy young /leutlle, Cambridge, UK: Camhridge University Press, Rutter, M" Pickles, A., Murrav, R., & Eaves, L (2001). Tesring hyporheses on specific environmental causal effects on behavior. Psychological Bulletin, 127, 2'!]-324. Rutter, M" &. Silberg, J, (20021, Gene-environment Interplav in relation to emotional and behavioral disturb'lllce. Amilia/ Rel'icu.' fit Psychulog)', 5'3, 463-490, Scarr, S, (]9'! 1 The constrllctlon of the family reality. Behdt'i(Jr<1i ,1I1d Bruill Sciences, /-4,403-404, Scarr, S, (1 ':192). Dev'elopmenral theories for the 1':190',: Deveiopmem and indlvidll~11 differences. Child Del'c/opmellf, 63, J-I 9. Scarr, S., &: McCartney, 1(, (1983 I, How people make rheir own enVironments, Child DCl'e/O/,IIlCII[, 54, 424-435. Sherman, L. W., (;otrlredsoll, D. C, MacKenzie, D. L, Eck, J" Rellter, p" &. BLlshwa\" S, D, i 1';)';)9), I'rel'el1til1g aillle: \Vbaf works, Idhlt doesN't, II'lhlt:' 1mJI1I1SlI1g, New York: RLlsseli :,age hJlllld:ltIon ialso ;1\';IILrblc from thl' U,S, Department of Justice, www,ojp.usdoj,gov/nip, Silberg, J. L. (2002J. l'drcllf,i/ eti,'cts OIl depressioll dl/d di,m/,tll'c /J"hal'w)' ill the dJlldrCII ot tll'ills: A t1l'"pos,!1 to the US N,lIiollallllstlfllte of Mel/hI/ Heedt/;, Rlchmond: Medical College 01 VirginIa, Silberg. l L" 0:. blves, L J {2004L An:.rlvsing the contrihutiolls of genes and parent-child interacrion [(l childhood hehavioural and emotional problems: A modd for the children of rwim" I'syc/ml()gi(etl AiedlCIIIL'. 34, ]-10. Spinarh, E M .. &. O'Connor, 1. G. (20()31, A behavioral generic stud\' of rht' overlap between pLTsonalrry and parenting, J()umal oi {'{,!'SOlie/lit)'. -:1, 785-1'01'. Srnolmillcr. M, 119(9). Il11plicariom of rhe restrictcU range of Llll1ih- t'mirol1ment, for estimates of ...~ 123Environmental Behavioral Genetics ....rl:£a.)U"'l and nonshared environment m behavior-genetic adoption studies. Psychological Bulletin, 392-409. T.P. (Ed.). (1996). Advances in aiminological them'),: Developmental theories ofcrime and de· 'lillIl1U,fm,-",,' London: Transactions. H E. L, & Neiderhiser, J. (200] ). Genetic and environmental influences on parenting and ., relationships: Current findings and future directions. Marriage and Famil)' Review, 33, 1]-29. E., & Waldron, M. (2000). Nonshared environment: A theoretical, methodological, and quanrltative review. psychologIcal Bulletin, 126, 78-108. Bureau of Justice Statistics. (2002). Criminal victimization 2001 (::-.JC] Repof[ ]94610). Washington, DC: U.S. Department of Justice (Available: www.oJP·usdof.gov/bjs). D. L (2000). Parents, peer groups, and other socializing influences. Developmental Psychology, 36,699-710. K., Mednick, S. A., Gabrielli, W. E, & Hutchings, B. (1983). Social class and crime in an adop· tion cohort. Journal of Criminal Law and Criminology, 74, 249-269. T. D., & Kendler, K. S. (2000). The genetic epidemiology of parental discipline, Psychological Medi­ 30, 1303-1313. LllaerSlnaJ:I,A., & Florin, P. (2003). Community interventions and effective prevention. American Psychologist, 58, 441-448. G. A., & Miller, L S. (1998). The prevention of serious and violent juvenile offending. In R. Loeber & D. P. Farrington (Eds.), Serious and violent juuenile offenders (pp. 197-247). Thousand Oaks, CA: Sage. R.l~, Kumpfer, K. L, & Seligman, M. E. P. (2003). Prevention that works for children and youth. American Psychologist, 58, 425-432. D. B., Gottfredson, D. c., & Najaka, S. S. (200]). School-based prevention of problem behaviors: A meta-analysis. Journal ofQuantitatilJe Criminology, 17, 247-272. .W()lfg~n!~, M. E., Figiio, R. M., & Sellin, T. (1972). Delinquency in a birth cohort. Chicago: University of Press. Health Organization. (2002). World report 011 l'iolence and health. Geneva: Author. ;