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Genetic risk factors correlate with county-level violent crime rates and collective disadvantage
... 36,37 Taken together, the current evidence underlines the importance of adequately addressing unmeasured confounding in studies of adverse outcomes in released prisoners and possibly other high-risk populations. Given the relative lack of such controls in the contemporary criminological literature examining the consequences of adverse neighborhood conditions, 38,39 it could be the case, as some critics have argued, 18,40,41 that such studies may have overemphasized the etiological role played by socioeconomic factors in explaining why violent criminality and other antisocial behaviors tend to aggregate within specific types of geographical areas. ...
Released prisoners diagnosed with psychotic disorders have elevated rates of violent reoffending risk and their exposure to adverse neighborhood environments may contribute to this risk. We identified all released sentenced prisoners in Sweden between 2003 and 2013 (n = 47 226) and followed them up for a median period of 4.4 years. We identified prisoners who had ever been diagnosed with a psychotic disorder (n = 3782) or prescribed antipsychotics (n = 7366). We examined 3 neighborhood characteristics: income, proportion of welfare recipients, and crime rate. By fitting generalized mixed-effects and negative bino-mial regression models and adopting within-individual designs that controlled for all time-invariant unmeasured confounders within each individual, we estimated neighborhood intraclass correlations (ICCs) and associations between specific neighborhood characteristics and violent reoffending. Neighborhood factors explained 13.5% (95% CI: 10.9%; 16.6%) of the violent reoffending risk among released prisoners diagnosed with psychotic disorders. This contrasted with 4.3% (95% CI: 3.7%; 4.9%) in all released prisoners. However, after controlling for unmeasured confounding, these estimates were not statistically significant (ICC psychotic disorders = 0.9%; 95% CI: −0.8%; 2.3%; ICC all prisoners = 0.3%; 95% CI: −0.02%; 0.6%). Similarly, none of the within-individual correlations between the specific neighborhood factors and violent reoffending were significantly different from zero. We found consistent results when we investigated prisoners with other psychiatric and substance use disorders. These findings suggest that placing released prisoners with psychotic disorders in less deprived neighborhoods might not reduce their violent reoffending risk, which may also apply to other psychiatric disorders. The assessment , treatment, and community linkage of high-risk prisoners as a strategy to reduce reoffending needs further research.
... Individual level resilience was not considered. This latter point is significant since recent research has shown the importance of individual level genetic risk factors in predicting neighborhood level collective disadvantage (Barnes, Boutwell, & Beaver, 2013). It could be that other individual level genetic factors increase resilience among those residing in disadvantaged neighborhoods. ...
Purpose: Drawing on theories from environmental criminology, this article identifies neighborhood-level characteristics that promote resiliency in neighborhoods in New Zealand with disadvantageous socioeconomic settings. Methods: We used neighborhood-level crime (2008-2010) and socio-economic data to develop a Crime Resilience Index for New Zealand (CRINZ) to quantify neighborhood level resilience to crime across the country. We then examined relationships between the index and a suite of built and social neighborhood-level characteristics. Results: Access to built environment factors generally decreased across neighborhoods stratified by resiliency. That is, resilient neighborhoods had decreased access to a range of healthcare, education, and living infrastructures. Very little difference was found in the social environment of high resilient and low resilient neighborhoods in New Zealand. Conclusions: Understanding why communities respond differently in similar environments can enable communities to respond better or more effectively to such stressful environments and consequently build resilience. Identifying 'place-specific' resilience factors can be effective in reducing crime in neighborhoods.
... Several polymorphisms that mediate the HPA axis, neurotransmission, immune response, brain development, serotonin synthesis, and other processes are also shown. Many of the polymorphisms, such as MAOA, SLC6A4, DRD4, OXTR, COMT, and others, are extensively studied in behavior genetics and in criminology and have been linked to an assortment of antisocial behavioral phenotypes (Barnes, Boutwell, & Beaver, 2013;Caspi et al., 2002Caspi et al., , 2008Reif et al., 2007;Wu & Barnes, 2013). In addition, the environmental pathogens that appear in Table 1 include a range of deprivations (e.g., sexual abuse, physical abuse, antenatal exposure to depression, antenatal toxicity exposure, and others) that are commonly included in cycle of violence studies showing the intergenerational transmission of parental environmental traumas to offspring behavior. ...
Research on epigenetic mechanisms is gaining traction, yet is poorly understood by criminologists and behavioral scientists. The current objective is to review relevant studies of interest to behavioral scientists who study crime, and to translate admittedly challenging scientific information into text that is digestible to the average criminologist. Using systematic search procedures the authors identified and reviewed 41 studies of epigenetic mechanisms in psychiatric and behavioral phenotypes among humans. Findings revealed significant epigenetic effects in an assortment of genes that are implicated in the etiology of depression, suicidality, callous-unemotional traits, and chronic and intergenerational aggressive behavior. Several polymorphisms that mediate the HPA axis, neurotransmission, immune response, brain development, serotonin synthesis, and other processes were found. Although prescriptive knowledge based on epigenetic findings to date is premature, epigenetics is a new and exciting scientific frontier not too different in spirit from Lamarck's observations centuries ago. Copyright © 2015 John Wiley & Sons, Ltd.
... The low-activity alleles of MAO-A interacts with maladaptive childhood environment and has been associated with aggression, violent delinquency, externalizing behavior, and lower inhibitory control (Brunner et al., 1993;Guo et al., 2008). Barnes et al. (2013) examined whether genetic risk factors (DAT1, DRD2, and DRD4) for antisocial behavior were predictive of exposure to disadvantage and violent crime measured at the county level. Data were drawn from the National Longitudinal Study of Adolescent Health; N = 2,212-2,268. ...
Multiple scientific disciplines have weighed in with different viewpoints regarding the origins of criminal behavior among human beings. What is lacking, however, is a framework capable of uniting the theoretical viewpoints into a single overarching perspective. The current article offers such a framework. Drawing on a variety of influences, we argue that many types of crime can be understood in the evolutionary context of human life history. Along these lines, we present a framework capable of explaining different patterns of criminal offending both at the individual level as well as the macro-level. Although the current article offers only a starting point, the way forward in the study of crime should involve a multi-disciplinary, multilevel explanatory framework. The evolutionary taxonomy we propose represents a step in that direction.
In the United States Black citizens are more residentially segregated from Whites than other racial and/or ethnic group. Prior studies have found that these patterns of segregation result in part from feelings of resentment and racial stereotypes that Whites hold toward Blacks. In this study, we further explore this idea by assessing the relevance of criminal and economic stereotypes, along with an extensive set of community and individual-level controls in understanding White citizens preferences for segregation. Utilizing a sample of 1,222 White citizens we explore factors that shape their residential preferences. Our results demonstrate that Whites who view Black citizens as criminal and economic liabilities are less willing to desire them as neighbors. The results also suggest that the growth of the Black population further erodes White’s willingness to reside in communities with Black residents.
This article critiques theChild Developmentspecial issue on poverty. First, we argue that the special issue has understated the variation observed within social class groups. Second, we believe that a confounding of genetic and environmental effects in biological families weakens the case for environmental effects as presented in the special issue. Our conclusion is that behavior genetic research designs are required for studies of poverty.
A thorough understanding of factors that influence aggression in children cannot be achieved without including behavior genetic studies that allow us to examine the effects of shared versus non-shared environment, as well as genes, on aggressive behaviors. This review details the growing body of evidence on the genetic effects on aggression. The majority of twin and adoption studies on antisocial behavior in children suggest that genetic effects are important influences, but most of these studies utilize parent reports rather than observational data. Some recent studies of non-parent raters are beginning to suggest that aggression in childhood may indeed be heritable and that this may not be a function simply of parent reporting bias. Future studies will need to focus on gene–environment correlations and interactions to begin to disentangle the myriad ways that children and the people in their environments inter-relate and mutually affect each other.
This study tests the specific hypothesis that the 9R/9R genotype in the VNTR of the dopamine transporter gene (DAT1) exerts a general protective effect against a spectrum of risky behaviors in comparison to the 10R/9R and 10R/10R genotypes, drawing on three-time repeated measures of risky behaviors in adolescence and young adulthood on about 822 non-Hispanic white males from the Add Health study. Our data have established two empirical findings. The first is a protective main effect in the DAT1 gene against risky behaviors. The second finding is that the protective effect varies over age, with the effect prominent at ages when a behavior is illegal and the effect largely vanished at ages when the behavior becomes legal or more socially tolerated. Both the protective main effect and the gene-lifecourse interaction effect are replicated across a spectrum of most common risky behaviors: delinquency, variety of sexual partners, binge drinking, drinking quantity, smoking quantity, smoking frequency, marijuana use, cocaine use, other illegal drug use, and seatbelt non-wearing. We also compared individuals with the protective genotype and individuals without it in terms of age, physical maturity, verbal IQ, GPA, received popularity, sent popularity, church attendance, two biological parents, and parental education. These comparisons indicate that the protective effect of DAT1*9R/9R cannot be explained away by these background characteristics. Our work demonstrates how legal/social contexts can enhance or reduce a genetic effect on risky behaviors.
Both genes and environment contribute to individual differences in aggression. Surveys of the pathways implicated in the physiological and neuronal processes involved highlight the potential role of genes regulating sexual differentiation, anxiety, stress response and neurotransmission. To date, however, association studies have provided little evidence of a substantially significant role for any single candidate gene in such pathways. This may be because genes function against a background in which other genetic and environmental factors are crucial. A series of recent studies, particularly concentrating on monoamine oxidase A , has emphasised the necessity of examining gene by environmental interactions if the contributions of individual loci are to be understood. These findings have major significance for the interpretation of data, both from individual gene and whole genome association studies. Functional imaging studies of genetic variants affecting serotonin pathways have also provided valuable insights into potential links between genes, brain and aggressive behaviour.
Key Concepts
Aggression is an evolutionarily advantageous trait with input from one of the most primitive brain regions, the amygdala.
There is significant disparity between aggressive behaviour in males and females.
Genes and environment both influence aggressive behaviour and there is evidence that stressful life events can interact with specific genetic variants.
DBH , COMT , adrenergic receptors, NET1 and SLC6A2 have been studied as possible candidate genes linking stress and aggression.
In the serotonin system, genetic polymorphisms in MAOA , SLC6A4 , TPH1/2 and the serotonin receptor genes have been linked with aggression.
Studies have shown a potential link between diet and its effects (e.g. on glucose levels) and aggression.
Brain imaging studies are beginning to assist an interpretation of the links between genetic variation and aggression.
Imagine that the neighborhood you are living in is covered with graffiti, litter, and unreturned shopping carts. Would this
reality cause you to litter more, trespass, or even steal? A thesis known as the broken windows theory suggests that signs
of disorderly and petty criminal behavior trigger more disorderly and petty criminal behavior, thus causing the behavior to
spread. This may cause neighborhoods to decay and the quality of life of its inhabitants to deteriorate. For a city government,
this may be a vital policy issue. But does disorder really spread in neighborhoods? So far there has not been strong empirical
support, and it is not clear what constitutes disorder and what may make it spread. We generated hypotheses about the spread
of disorder and tested them in six field experiments. We found that, when people observe that others violated a certain social
norm or legitimate rule, they are more likely to violate other norms or rules, which causes disorder to spread.
Emerging evidence suggests that variants of specific genes may influence some youths to seek out or associate with antisocial peers. Using genotypic data (N= 1,816) from the National Longitudinal Study of Adolescent Health (J. R. Udry, 1998, 2003), the authors tested this possibility. They found that the 10R allele of the dopamine transporter (DAT1) gene was associated with self-reported delinquent peer affiliation for male adolescents from high-risk environments (beta range = .13-.14) despite controlling for delinquent involvement, self-control, and drug and alcohol use. The authors discuss the importance of using a biosocial framework to examine issues related to adolescent development.
Since 1979, a continuing study of monozygotic and dizygotic twins, separated in infancy and reared apart, has subjected more
than 100 sets of reared-apart twins or triplets to a week of intensive psychological and physiological assessment. Like the
prior, smaller studies of monozygotic twins reared apart, about 70% of the variance in IQ was found to be associated with
genetic variation. On multiple measures of personality and temperament, occupational and leisure-time interests, and social
attitudes, monozygotic twins reared apart are about as similar as are monozygotic twins reared together. These findings extend
and support those from numerous other twin, family, and adoption studies. It is a plausible hypothesis that genetic differences
affect psychological differences largely indirectly, by influencing the effective environment of the developing child. This
evidence for the strong heritability of most psychological traits, sensibly construed, does not detract from the value or
importance of parenting, education, and other propaedeutic interventions.
The main threats to adolescents' health are the risk behaviors they choose. How their social context shapes their behaviors is poorly understood.
To identify risk and protective factors at the family, school, and individual levels as they relate to 4 domains of adolescent health and morbidity: emotional health, violence, substance use, and sexuality.
Cross-sectional analysis of interview data from the National Longitudinal Study of Adolescent Health.
A total of 12118 adolescents in grades 7 through 12 drawn from an initial national school survey of 90118 adolescents from 80 high schools plus their feeder middle schools.
The interview was completed in the subject's home.
Eight areas were assessed: emotional distress; suicidal thoughts and behaviors; violence; use of 3 substances (cigarettes, alcohol, marijuana); and 2 types of sexual behaviors (age of sexual debut and pregnancy history). Independent variables included measures of family context, school context, and individual characteristics.
Parent-family connectedness and perceived school connectedness were protective against every health risk behavior measure except history of pregnancy. Conversely, ease of access to guns at home was associated with suicidality (grades 9-12: P<.001) and violence (grades 7-8: P<.001; grades 9-12: P<.001). Access to substances in the home was associated with use of cigarettes (P<.001), alcohol (P<.001), and marijuana (P<.001) among all students. Working 20 or more hours a week was associated with emotional distress of high school students (P<.01), cigarette use (P<.001), alcohol use (P<.001), and marijuana use (P<.001). Appearing "older than most" in class was associated with emotional distress and suicidal thoughts and behaviors among high school students (P<.001); it was also associated with substance use and an earlier age of sexual debut among both junior and senior high students. Repeating a grade in school was associated with emotional distress among students in junior high (P<.001) and high school (P<.01) and with tobacco use among junior high students (P<.001). On the other hand, parental expectations regarding school achievement were associated with lower levels of health risk behaviors; parental disapproval of early sexual debut was associated with a later age of onset of intercourse (P<.001).
Family and school contexts as well as individual characteristics are associated with health and risky behaviors in adolescents. The results should assist health and social service providers, educators, and others in taking the first steps to diminish risk factors and enhance protective factors for our young people.
The 7-repeat allele of the dopamine receptor D4 gene (DRD4) and the 10 repeat allele of the dopamine transporter gene (DAT1) have shown association and linkage with symptoms of attention deficit hyperactivity disorder (ADHD) in childhood. The parents of ADHD children (clinic group, n = 80 fathers and 107 mothers) and control children (control group, n = 42 fathers and 51 mothers) were the focus of this study. These parents reported retrospectively on their level of ADHD Inattention and Conduct Disorder symptoms in adolescence. In analyses of the relation of symptom levels to the DRD4 and DAT1 genotypes, fathers possessing the 7 repeat DRD4 allele had greater levels of both inattention and conduct disorder symptoms. Mothers with the 10/10 genotype had higher levels of inattention symptoms. Thus, genetic associations found in children may be replicable in their parents.
As far as we know, this is the first national study that reports compelling evidence for the main effects of genetic variants on serious and violent delinquency among adolescents and young adults. This study investigated the association between the self-reported serious and violent delinquency and the TaqI polymorphism in the DRD2 gene and the 40-bp VNTR in the DAT1 gene. The study was based on a cohort of more than 2,500 adolescents and young adults in the National Longitudinal Study of Adolescent Health in the United States. The trajectories of serious delinquency for the DAT1*10R/10R and DAT1*10R/9R genotypes are about twice as high as that for the DAT1*9R/9R genotype (LR test, P = 0.018, 2 df). For DRD2, the trajectory of serious delinquency for the heterozygotes (A1/A2) is about 20% higher than the A2/A2 genotype and about twice as high as the A1/A1 genotype, a phenomenon sometimes described as heterosis (LR test, P = 0.005, 2 df). The findings on violent delinquency closely resemble those on serious delinquency. The trajectories of violent delinquency for the DAT1*10R/9R and DAT1*10R/10R genotype are again about twice as high as that for DAT1*9R/9R (LR test, P = 0.021, 2 df). The two homozygotes of DRD2*A1/A1 and DRD2*A2/A2 scored lower (LR test, P = 0.0016, 2 df) than the heterozygotes. The findings in the models that consider DAT1 and DRD2 jointly (serious delinquency P = 0.0016, 4 df; violent delinquency P = 0.0006, 4 df) are essentially the same as those in the single-gene models, suggesting the absence of a significant correlation between the two genetic variants. These results only apply to males. Neither variant is associated with delinquency among females.
This article describes the design and data availability for samples of genetic pairs in the National Longitudinal Study of Adolescent Health (Add Health). Add Health provides unique samples of genetic pairs that are nationally representative and followed longitudinally from early adolescence into young adulthood with 3 in-home interviews and a 4th interview planned for 2007 to 2008. The design of Add Health included an embedded genetic sample of more than 3000 pairs of individuals with varying genetic resemblance, including monozygotic twins, dizygotic twins, full siblings, half siblings, and unrelated siblings who were raised in the same household. Add Health has collected rich longitudinal social, behavioral, and environmental survey data, as well as buccal cell DNA from a subsample of the genetic sample (N = 2612). Add Health has an enlightened dissemination policy and to date has released phenotype and genotype data to more than 3000 researchers in the scientific community.
Antisocial behaviors are complex polygenic phenotypes that are due to a multifactorial arrangement of genetic polymorphisms. Little empirical research, however, has been undertaken that examines gene x gene interactions in the etiology of conduct disorder and antisocial behavior. This study examined whether adolescent conduct disorder and adult antisocial behavior were related to the dopamine D2 receptor polymorphism (DRD2) and the dopamine D4 receptor polymorphism (DRD4).
A sample of 872 male participants from the National Longitudinal Study of Adolescent Health (Add Health) completed self-report questionnaires that tapped adolescent conduct disorder and adult antisocial behavior. DNA was genotyped for DRD2 and DRD4.
Multivariate regression analysis revealed that neither DRD2 nor DRD4 had significant independent effects on conduct disorder or antisocial behavior. However, DRD2 interacted with DRD4 to predict variation in adolescent conduct disorder and in adult antisocial behavior.
The results suggest that a gene x gene interaction between DRD2 and DRD4 is associated with the development of conduct disorder and adult antisocial behavior in males.
This paper analyzes the method of social experiments. The assumptions that justify the experimental method are exposited. Parameters of interest in evaluating social programs are discussed. The authors show how experiments sometimes serve as instrumental variables to identify program impacts. The most favorable case for experiments ignores variability across persons in response to treatments received and assumes that mean impacts of a program are the main object of interest in conducting an evaluation. Experiments do not identify the distribution of program gains unless additional assumptions are maintained. Evidence on the validity of the assumptions used to justify social experiments is presented. Copyright 1995 by American Economic Association.
"The Truly Disadvantagedshould spur critical thinking in many quarters about the causes and possible remedies for inner city poverty. As policy makers grapple with the problems of an enlarged underclass they—as well as community leaders and all concerned Americans of all races—would be advised to examine Mr. Wilson's incisive analysis."—Robert Greenstein,New York Times Book Review "'Must reading' for civil-rights leaders, leaders of advocacy organizations for the poor, and for elected officials in our major urban centers."—Bernard C. Watson,Journal of Negro Education "Required reading for anyone, presidential candidate or private citizen, who really wants to address the growing plight of the black urban underclass."—David J. Garrow,Washington Post Book World Selected by the editors of theNew York Times Book Reviewas one of the sixteen best books of 1987. Winner of the 1988 C. Wright Mills Award of the Society for the Study of Social Problems.
Biological causes of human social behavior will be invisible to those who follow the Durkheimian injunction to seek the causes
of social facts in preceding social facts. Sociologists ignore or deny these biological causes at peril of grievous error.
Biological causes can be integrated with traditional sociological models, but this approach will require sociologists to incorporate
into their thinking the knowledge of disciplines whose paradigms offer biological explanations of the behaviors important
to sociologists. I take examples of such knowledge from evolutionary biology, behavior genetics, and behavioral endocrinology.
The Moving to Opportunity (MTO) housing experiment has proven to be an important intervention not just in the lives of the poor, but in social science theories of neighborhood effects. Competing causal claims have been the subject of considerable disagreement, culminating in the debate between Clampet-Lundquist and Massey (2008) and Ludwig et al. (2008). This paper assesses the debate by clarifying analytically distinct questions posed by neighborhood-level theories, reconceptualizing selection bias as a fundamental social process worthy of study in its own right rather than as a statistical nuisance, and reconsidering the scientific method of experimentation, and hence causality, in the social world of the city. I also analyze MTO and independent survey data from Chicago to examine trajectories of residential attainment. Although MTO provides crucial leverage for estimating neighborhood effects on individuals, as proponents rightly claim, I demonstrate the implications imposed by a stratified urban structure and how MTO simultaneously provides a new window on the social reproduction of concentrated inequality.
First published in 1895: Emile Durkheim's masterful work on the nature and scope of sociology--now with a new introduction and improved translation by leading scholar Steven Lukes.The Rules of the Sociological Method is among the most important contributions to the field of sociology, still debated among scholars today. Through letters, arguments, and commentaries on significant debates, Durkheim confronted critics, clarified his own position, and defended the objective scientific method he applied to his study of humans. This updated edition offers an introduction and extra notes as well as a new translation to improve the clarity and accessibility of this essential work. In the introduction, Steven Lukes, author of the definitive biography Emile Durkheim: His Life and Work, spells out Durkheim's intentions, shows the limits of Durkheim's view of sociology, and presents its political background and significance. Making use of the various texts in this volume and Durkheim's later work, Lukes discusses how Durkheim's methodology was modified or disregarded in practice--and how it is still relevant today. With substantial notes on context, this user-friendly edition will greatly ease the task of students and scholars working with Durkheim's method--a view that has been a focal point of sociology since its original publication. The Rules of the Sociological Method will engage a new generation of readers with Durkheim's rich contribution to the field."
The concentration of delinquency in certain areas in large cities has been established, but not yet completely explained. It may be the result of conditions found in such areas or of selective forces, or of both. The study of selection has been neglected. Mr. Clifford Shaw's tests of the selection of nationalities for residence in such areas seem inconclusive. A survey of crime in the city of Danville, Ilinois, offered oppportunity to test indirectly selective processes. It shows that over two-fifths of adult felons resident in Danville and committed during three years to prison or reformatory had a criminal record before coming to the city and that probably over half of them cannot be called "Danville products" or products of its delinquency areas. Racial and economic isolation in delinquency areas, the concentration of crime in rooming-house areas, the transient residence of delinquent as compared with non-delinquent families in delinquency areas, the existence of conflicting group patterns of behavior within the areas, and data from case histories seem partially to confirm this finding. The conclusion, though confined to this one study, is that areas of delinquency not only produce delinquency but act as selective forces attracting delinquents and predelinquents. Therefore criminological surveys should study this factor of selection and enlist the service of psychologists and psychiatrists as well as sociologists.
This book presents the results of 20 years of ecological research into the nature of the relationship between the distribution of delinquency and the pattern of physical structure and social organization of 21 American cities. Uniform findings in every city confirm the hypothesis that the physical deterioration of residential areas accompanied by social disorganization is greatest in a central zone in the business district, intermediate in a middle zone, and lowest in the other zones, and that there is a progressive decline in the incidence of delinquency from the innermost zone where it is most concentrated to the peripheral areas. Delinquency is found to be highly correlated with changes in population, inadequate housing, poverty, presence of Negroes and foreign-born, tuberculosis, mental disorders, and adult criminality. The common basic factor is social disorganization or the absence of community effort to cope with these conditions. Causation of juvenile delinquency is to be sought more in terms of the community than of the individual. 107 maps pertaining to the cities studied and 118 tables relating to population and delinquency rates are included as well as a chapter describing the Chicago Area Project as a demonstration of the effective mobilization of community forces to combat delinquency and crime. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
The author argues that it is what children experience outside the home, in the company of their peers, that matters most. Parents don't socialize children: children socialize children. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
The general failure of sociologists to understand, much less accept, an evolutionary perspective on human behavior transcends mere ignorance and ideological bias, although it incorporates a good deal of both. It also includes a general anthropocentric discomfort with evolutionary thinking, a self-interested resistance to self-understanding, and a trained sociological incapacity to accept the fundamental canons of scientific theory construction: reductionism, individualism, materialism, and parsimony.
"This is a book about Chicago. It is also, and for that very reason, a book about every other American city which has lived long enough and grown large enough to experience the transformation of neighborhoods and the contact of cultures and the tension between different types of individual and community behavior. . . . Here is a type of sociological investigation which is equally marked by human interest and scientific method."âChristian Century
Theoretical models concerning how neighborhood contexts adversely influence juvenile antisocial behavior frequently focus on urban neighborhoods; however, previous studies comparing urban and rural areas on the prevalence of youth antisocial behavior have yielded mixed results. The current study uses longitudinal data on the offspring of a nationally representative sample of mothers (N = 4,886) in the US. There was no relation between density and mother-reported child conduct problems across ages 4-13 years, but youth living in areas of greater population density exhibited more youth self-reported delinquency across 10-17 years. Families often moved to counties with greater or lesser population density, but longitudinal analyses treating population density as a time-varying covariate did not support the hypothesis that living in densely populated counties influenced youth delinquency. Rather, the association between population density and delinquency appears to be due to unmeasured selection variables that differ between families who live in more or less densely populated counties.
Two issues that complicate behavioral genetic analyses are the interaction and correlation between genetic and environmental influences. In the present report, the effects of genotype-environment interaction and correlation on behavioral genetic studies (twin and adoption studies) are examined. The analysis suggests that genotype-environment interaction may bias twin study estimates of genetic and environmental influence but need not affect adoption studies. On the other hand, genotype-environment correlation may affect both twin and adoption study estimates of genetic and environmental influence, the direction of the effect depending on the sign of the correlation. New tests of genotype-environment interaction and correlation, using adoption data, are proposed. (27 ref) (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Understanding both typical human development and indivdual differences within the same theoretical framework has been difficult because the 2 orientations arise from different philosophical traditions. It is argued that an evolutionary perspective can unite the study of both species-typical development and individual variation. Research on determininants of development from many perspectives can be understood within an evolutionary framework in which organism and environment combine to produce development. Species-normal genes and environments and indidividual variations in genes and environments both affect personality, social, and intellectual development. These domains are used as examples to integrate theories of normal development and individual differences. Within the usual samples of European, North American, and developed Asian countries, the results of family and twin studies show that environments within the normal species range are crucial to normal development. Given a wide range of environmental opportunities and emotional supports, however, most children in these societies grow up to be individually different based on their individual genotypes. Understanding the ways in which genes and environments work together helps developmentalists to identify children in need of intervention and to tailor interventions to their particular needs.
We propose a theory of development in which experience is directed by genotypes. Genotypic differences are proposed to affect phenotypic differences, both directly and through experience, via 3 kinds of genotype leads to environment effects: a passive kind, through environments provided by biologically related parents; an evocative kind, through responses elicited by individuals from others; and an active kind, through the selection of different environments by different people. The theory adapts the 3 kinds of genotype-environment correlations proposed by Plomin, DeFries, and Loehlin in a developmental model that is used to explain results from studies of deprivation, intervention, twins, and families.
It is hypothesized that collective efficacy, defined as social cohesion among neighbors combined with their willingness to
intervene on behalf of the common good, is linked to reduced violence. This hypothesis was tested on a 1995 survey of 8782
residents of 343 neighborhoods in Chicago, Illinois. Multilevel analyses showed that a measure of collective efficacy yields
a high between-neighborhood reliability and is negatively associated with variations in violence, when individual-level characteristics,
measurement error, and prior violence are controlled. Associations of concentrated disadvantage and residential instability
with violence are largely mediated by collective efficacy.
Family, twin, and adoption studies show attention deficit hyperactivity disorder (ADHD) to have a substantial genetic component. Although several studies have shown an association between ADHD and the 7-repeat allele of the dopamine D(4) receptor gene (DRD4), several studies have not. Thus, the status of the ADHD-DRD4 association is uncertain.
Meta-analysis was applied to case-control and family-based studies of the association between ADHD and DRD4 to assess the joint evidence for the association, the influence of individual studies, and evidence for publication bias.
For both the case-control and family-based studies, the authors found 1) support for the association between ADHD and DRD4, 2) no evidence that this association was accounted for by any one study, and 3) no evidence for publication bias.
Although the association between ADHD and DRD4 is small, these results suggest that it is real. Further studies are needed to clarify what variant of DRD4 (or some nearby gene) accounts for this association.
We have analyzed genetic data for 326 microsatellite markers that were typed uniformly in a large multiethnic population-based sample of individuals as part of a study of the genetics of hypertension (Family Blood Pressure Program). Subjects identified themselves as belonging to one of four major racial/ethnic groups (white, African American, East Asian, and Hispanic) and were recruited from 15 different geographic locales within the United States and Taiwan. Genetic cluster analysis of the microsatellite markers produced four major clusters, which showed near-perfect correspondence with the four self-reported race/ethnicity categories. Of 3,636 subjects of varying race/ethnicity, only 5 (0.14%) showed genetic cluster membership different from their self-identified race/ethnicity. On the other hand, we detected only modest genetic differentiation between different current geographic locales within each race/ethnicity group. Thus, ancient geographic ancestry, which is highly correlated with self-identified race/ethnicity--as opposed to current residence--is the major determinant of genetic structure in the U.S. population. Implications of this genetic structure for case-control association studies are discussed.
There is a robust relationship between the experience of maltreatment in childhood and later antisocial behaviors amongst adolescents and adults. Animal and human studies suggest that variation in monoamine oxidase A (MAOA) genotype may moderate the effects of maltreatment. Self-reported conduct problems and criminal convictions amongst sibling-pairs from the National Longitudinal Study of Adolescent Health were tested for association with reports of maltreatment before and after the age of 12. MAOA promoter polymorphisms were tested for possible moderation effects. Maltreatment predicted conduct problems and criminal convictions. MAOA genotype did not have a significant moderating effect in any of the six analyses that were conducted. We did not replicate a previous report that MAOA polymorphisms moderated the relationship between maltreatment and conduct problems. There was, however, a non-significant trend in the predicted direction. Additional studies will be needed before firm conclusions can be drawn about this hypothesized genotype-environment interaction.
To examine genetic and environmental influences on drinking in a nationally representative study of genetically informative adolescents followed into young adulthood.
The average quantity of alcohol used per drinking episode during the past year was analyzed in 4432 youth assessed during adolescence (mean age of 16) and then 1 and 6 years later. The variance of quantity of alcohol consumed was decomposed into three components: additive genetic (a2), shared environmental (c2), non-shared environmental (e2). Four candidate genes were tested for association.
Wave 1 a2-0.52e2-0.48, Wave 2 a2-0.28e2-0.72, Wave 3 a2-0.30e2-0.70. Genetic correlations between Waves 1 and 2 were 0.85, Waves 1 and 3 were 0.34. The DAT1 440 allele was associated at Wave 1 (p=0.007). DRD2 TaqI A1/A2 was associated at Wave 3 (p=0.007). DRD4 and 5HTT were not associated. The DAT1 and DRD2 polymorphisms accounted for 3.1% and 2.0% of the variation, respectively.
Genetic influence on drinking behavior was common in adolescents longitudinally assessed 1 year apart, but was less correlated between these adolescents and their assessment as young adults at a subsequent time point. Polymorphisms in genes of the dopaminergic system appear to influence variation in drinking behavior.
Traditional models of psychiatric epidemiology often assume that the relationship between individuals and their environment is unidirectional, from environment to person. Accumulating evidence from developmental and genetic studies has made this perspective increasingly untenable.
Literature search using Medline, PsycINFO, article references and contact with experts to identify all papers examining the heritability of measures of environments of relevance to psychiatry/psychology.
We identified 55 independent studies organized into seven categories: general and specific stressful life events (SLEs), parenting as reported by child, parenting reported by parent, family environment, social support, peer interactions, and marital quality. Thirty-five environmental measures in these categories were examined by at least two studies and produced weighted heritability estimates ranging from 7% to 39%, with most falling between 15% and 35%. The weighted heritability for all environmental measures in all studies was 27%. The weighted heritability for environmental measures by rating method was: self-report 29%, informant report 26%, and direct rater or videotape observation (typically examining 10 min of behavior) 14%.
Genetic influences on measures of the environment are pervasive in extent and modest to moderate in impact. These findings largely reflect 'actual behavior' rather than 'only perceptions'. Etiologic models for psychiatric illness need to account for the non-trivial influences of genetic factors on environmental experiences.
Families, primarily female-headed minority households with children, living in high-poverty public housing projects in five U.S. cities were offered housing vouchers by lottery in the Moving to Opportunity program. Four to seven years after random assignment, families offered vouchers lived in safer neighborhoods that had lower poverty rates than those of the control group not offered vouchers. We find no significant overall effects of this intervention on adult economic self-sufficiency or physical health. Mental health benefits of the voucher offers for adults and for female youth were substantial. Beneficial effects for female youth on education, risky behavior, and physical health were offset by adverse effects for male youth. For outcomes that exhibit significant treatment effects, we find, using variation in treatment intensity across voucher types and cities, that the relationship between neighborhood poverty rate and outcomes is approximately linear. Copyright The Econometric Society 2007.
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