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Perceptions of crime detection risk (e.g., risk of arrest) play an integral role in the criminal decision-making process. Yet, the sources of variation in those perceptions are not well understood. Do individuals respond to changes in legal policy or is perception of detection risk shaped like other perceptions—by experience, heuristics, and with biases? We applied a developmental perspective to study self-reported perception of detection risk. We test four hypotheses against data from the Dunedin Longitudinal Study (analytic sample of N = 985 New Zealanders), a study that spans 20 years of development (Ages 18–38, years 1990–2011). We reach four conclusions: (1) people form their perception of detection risk early in the life course; (2) perception of detection risk may be general rather than unique to each crime type; (3) population-level perceptions are stable between adolescence and adulthood; but (4) people update their perceptions when their life circumstances change. The importance of these findings for future theoretical and policy work is considered. [ABSTRACT FROM AUTHOR]

Background: Midlife adults are experiencing a crisis of deaths of despair (i.e. deaths from suicide, drug overdose, and alcohol-related liver disease). We tested the hypothesis that a syndrome of despair-related maladies at midlife is preceded by psychopathology during adolescence. Methods: Participants are members of a representative cohort of 1037 individuals born in Dunedin, New Zealand in 1972–73 and followed to age 45 years, with 94% retention. Adolescent mental disorders were assessed in three diagnostic assessments at ages 11, 13, and 15 years. Indicators of despair-related maladies across four domains – suicidality, substance misuse, sleep problems, and pain – were assessed at age 45 using multi-modal measures including self-report, informant-report, and national register data. Results: We identified and validated a syndrome of despair-related maladies at midlife involving suicidality, substance misuse, sleep problems, and pain. Adults who exhibited a more severe syndrome of despair-related maladies at midlife tended to have had early-onset emotional and behavioral disorders [ β = 0.23, 95% CI (0.16–0.30), p < 0.001], even after adjusting for sex, childhood SES, and childhood IQ. A more pronounced midlife despair syndrome was observed among adults who, as adolescents, were diagnosed with a greater number of mental disorders [ β = 0.26, 95% CI (0.19–0.33), p < 0.001]. Tests of diagnostic specificity revealed that associations generalized across different adolescent mental disorders. Conclusions: Midlife adults who exhibited a more severe syndrome of despair-related maladies tended to have had psychopathology as adolescents. Prevention and treatment of adolescent psychopathology may mitigate despair-related maladies at midlife and ultimately reduce deaths of despair. [ABSTRACT FROM AUTHOR]

What are the major sources of worldwide variability in subjective well-being (SWB)? Twin and family studies of SWB have found substantial heritability and strong effects from unique environments but virtually no effects from shared environments. However, extant findings are not necessarily valid at the global level. Prior studies have examined within-countries variability but did not take into account mean differences across nations. In this article, we aim to estimate the effects of genetic factors, individual environmental exposures, and shared environments for the global population. We combine a set of knowns from national well-being studies (means and standard deviations) and behavioral-genetic studies (heritability) to model a scenario of twin studies across 157 countries. For each country, we simulate data for a set of twin pairs and pool the data into a global sample. We find a worldwide heritability of 31% to 32% for SWB. Individual environmental factors explain 46% to 52% of the variance (including measurement error), and shared environments account for 16% to 23% of the global variance in SWB. Worldwide, well-being is somewhat less heritable than within nations. In contrast to previous within-countries studies, we find a notable effect of shared environments. This effect is not limited to within families but operates at a national level. [ABSTRACT FROM AUTHOR]

Objectives Individuals with more education are at lower risk of developing multiple, different age-related diseases than their less-educated peers. A reason for this might be that individuals with more education age slower. There are 2 complications in testing this hypothesis. First, there exists no definitive measure of biological aging. Second, shared genetic factors contribute toward both lower educational attainment and the development of age-related diseases. Here, we tested whether the protective effect of educational attainment was associated with the pace of aging after accounting for genetic factors. Methods We examined data from 5 studies together totaling almost 17,000 individuals with European ancestry born in different countries during different historical periods, ranging in age from 16 to 98 years old. To assess the pace of aging, we used DunedinPACE, a DNA methylation algorithm that reflects an individual's rate of aging and predicts age-related decline and Alzheimer's disease and related disorders. To assess genetic factors related to education, we created a polygenic score based on the results of a genome-wide association study of educational attainment. Results Across the 5 studies, and across the life span, higher educational attainment was associated with a slower pace of aging even after accounting for genetic factors (meta-analysis effect size = −0.20; 95% confidence interval [CI]: −0.30 to −0.10; p =.006). Further, this effect persisted after taking into account tobacco smoking (meta-analysis effect size = −0.13; 95% CI: −0.21 to −0.05; p =.01). Discussion These results indicate that higher levels of education have positive effects on the pace of aging, and that the benefits can be realized irrespective of individuals' genetics. [ABSTRACT FROM AUTHOR]

Adverse childhood experiences (ACEs) are associated with poorer health, which has spurred public health efforts to reduce the number of adverse events children experience. Unfortunately, it is unlikely that all ACEs can be prevented. For adults who already experienced ACEs in childhood, what psychological, social, and behavioral intervention targets might reduce risk for negative health outcomes? To provide insight into the "black box" of psychosocial mechanisms linking ACEs to poor health, our study used data from the Dunedin Study, a longitudinal cohort assessed from birth to age 45. Mediation models (N = 859) were used to examine whether candidate psychosocial variables in adulthood explained the association between childhood ACEs and health in midlife. Potential psychosocial mediators included stressful life events, perceived stress, negative emotionality, and health behaviors. Children who experienced more ACEs had poorer health in midlife. They also had significantly more stressful life events, more perceived stress, more negative emotionality, and unhealthier behaviors as adults. These mediators were each independently associated with poorer health in midlife and statistically mediated the association between ACEs and midlife health. Health behaviors evidenced the strongest indirect effect from ACEs to midlife health. Together, these psychosocial mediators accounted for the association between ACEs in childhood and health three decades later. Public health efforts to mitigate the health consequences of ACEs could aim to reduce the stressful life events people experience, reduce negative emotionality, reduce perceived stress, or improve health behaviors among adults who experienced childhood adversity. [ABSTRACT FROM AUTHOR]

Neuropsychological evidence supports the developmental taxonomy theory of antisocial behavior, suggesting that abnormal brain development distinguishes life-course-persistent from adolescence-limited antisocial behavior. Recent neuroimaging work confirmed that prospectively-measured life-course-persistent antisocial behavior is associated with differences in cortical brain structure. Whether this extends to subcortical brain structures remains uninvestigated. This study compared subcortical gray-matter volumes between 672 members of the Dunedin Study previously defined as exhibiting life-course-persistent, adolescence-limited or low-level antisocial behavior based on repeated assessments at ages 7–26 years. Gray-matter volumes of 10 subcortical structures were compared across groups. The life-course-persistent group had lower volumes of amygdala, brain stem, cerebellum, hippocampus, pallidum, thalamus, and ventral diencephalon compared to the low-antisocial group. Differences between life-course-persistent and adolescence-limited individuals were comparable in effect size to differences between life-course-persistent and low-antisocial individuals, but were not statistically significant due to less statistical power. Gray-matter volumes in adolescence-limited individuals were near the norm in this population-representative cohort and similar to volumes in low-antisocial individuals. Although this study could not establish causal links between brain volume and antisocial behavior, it constitutes new biological evidence that all people with antisocial behavior are not the same, supporting a need for greater developmental and diagnostic precision in clinical, forensic, and policy-based interventions. [ABSTRACT FROM AUTHOR]

Background: A recent genome‐wide association study identified molecular‐genetic associations with age‐at‐first‐birth. However, the meaning of these genetic discoveries is unclear. Drawing on evidence linking early pregnancy with disinhibitory behavior, we tested the hypothesis that genetic discoveries for age‐at‐first‐birth predict disinhibition. Methods: We included participants with genotype data from the two‐decade‐long Environmental Risk (E‐Risk) Study (N = 1,999) and the four‐decade‐long Dunedin Study (N = 918). We calculated a genome‐wide polygenic score for age‐at‐first‐birth and tested whether it was associated with a range of disinhibitory outcomes across the life course, including low childhood self‐control; risk for externalizing psychopathology; officially recorded criminal offending; substance dependence; informant reports of disinhibitory problems; and number of lifetime sexual partners. We further tested whether associations were attributable to accelerated pubertal maturation. Results: In both cohorts, the age‐at‐first‐birth polygenic score predicted low childhood self‐control, externalizing psychopathology, officially recorded criminal offending, substance dependence, and number of sexual partners. Associations were modest, but robust across replication. Childhood disinhibition partly mediated associations between the polygenic score and reproductive behaviors. In contrast, associations were not attributable to accelerated pubertal timing. Conclusions: Genomic discoveries for age‐at‐first‐birth are about more than reproductive biology: They provide insight into the disinhibitory traits and behaviors that accompany early parenthood. Age‐at‐first‐birth is a useful proxy phenotype for researchers interested in disinhibition. Further, interventions that improve self‐regulation abilities may benefit young parents and their children. [ABSTRACT FROM AUTHOR]

This study tested implications of new genetic discoveries for understanding the association between parental investment and children's educational attainment. A novel design matched genetic data from 860 British mothers and their children with home-visit measures of parenting: the E-Risk Study. Three findings emerged. First, both mothers' and children's education-associated genetics, summarized in a genome-wide polygenic score, were associated with parenting-a gene-environment correlation. Second, accounting for genetic influences slightly reduced associations between parenting and children's attainment-indicating some genetic confounding. Third, mothers' genetics were associated with children's attainment over and above children's own genetics, via cognitively stimulating parenting-an environmentally mediated effect. Findings imply that, when interpreting parents' effects on children, environmentalists must consider genetic transmission, but geneticists must also consider environmental transmission. [ABSTRACT FROM AUTHOR]

Twin studies have documented that parenting behavior is partly heritable, but it is unclear how parents' genetics shape their caregiving. Using tools of molecular genetics, the present study investigated this process by testing hypotheses about associations between a genome-wide polygenic score for educational attainment and parental caregiving in 702 members of the Dunedin Study, a population-representative birth cohort. Data have been prospectively collected from when Study members were born through to midlife, and include assessments of the caregiving they provided once they became parents. Results showed that parents' polygenic scores predicted warm, sensitive, and stimulating caregiving, both in personal interactions with their young children (as captured on video) and through the home environ- ments they created for their families (as observed by home visitors). The magnitude of this effect was small. Polygenic-score associations were independent of well-established predictors of parenting, such as parents' own childhood experiences of parenting and the age at which they became parents. Polygenic-score associations were mediated by parents' early-emerging cognitive abilities and self-control skills. Findings have implications for theory and research about genetic influences on caregiving and child development. [ABSTRACT FROM AUTHOR]

Background: Childhood risk factors are associated with elevated inflammatory biomarkers in adulthood, but it is unknown whether these risk factors are associated with increased adult levels of the chronic inflammation marker soluble urokinase plasminogen activator receptor (suPAR). We aimed to test the hypothesis that childhood exposure to risk factors for adult disease is associated with elevated suPAR in adulthood and to compare suPAR with the oft‐reported inflammatory biomarker C‐reactive protein (CRP). Methods: Prospective study of a population‐representative 1972–1973 birth cohort; the Dunedin Multidisciplinary Health and Development Study observed participants to age 38 years. Main childhood predictors were poor health, socioeconomic disadvantage, adverse childhood experiences (ACEs), low IQ, and poor self‐control. Main adult outcomes were adulthood inflammation measured as suPAR and high‐sensitivity CRP (hsCRP). Results: Participants with available plasma samples at age 38 were included (N = 837, 50.5% male). suPAR (mean 2.40 ng/ml; SD 0.91) was positively correlated with hsCRP (r 0.15, p < .001). After controlling for sex, body mass index (BMI), and smoking, children who experienced more ACEs, lower IQ, or had poorer self‐control showed elevated adult suPAR. When the five childhood risks were aggregated into a Cumulative Childhood Risk index, and controlling for sex, BMI, and smoking, Cumulative Childhood Risk was associated with higher suPAR (b 0.10; SE 0.03; p = .002). Cumulative Childhood Risk predicted elevated suPAR, after controlling for hsCRP (b 0.18; SE 0.03; p < .001). Conclusions: Exposure to more childhood risk factors was associated with higher suPAR levels, independent of CRP. suPAR is a useful addition to studies connecting childhood risk to adult inflammatory burden. [ABSTRACT FROM AUTHOR]

In both child and adult psychiatry, empirical evidence has now accrued to suggest that a single dimension is able to measure a person's liability to mental disorder, comorbidity among disorders, persistence of disorders over time, and severity of symptoms. This single dimension of general psychopathology has been termed "p," because it conceptually parallels a dimension already familiar to behavioral scientists and clinicians: the "g" factor of general intelligence. As the g dimension reflects low to high mental ability, the p dimension represents low to high psychopathology severity, with thought disorder at the extreme. The dimension of p unites all disorders. It influences present/absent status on hundreds of psychiatric symptoms, which modern nosological systems typically aggregate into dozens of distinct diagnoses, which in turn aggregate into three overarching domains, namely, the externalizing, internalizing, and psychotic experience domains, which finally aggregate into one dimension of psychopathology from low to high: p. Studies show that the higher a person scores on p, the worse that person fares on measures of family history of psychiatric illness, brain function, childhood developmental history, and adult life impairment. A dimension of p may help account for ubiquitous nonspecificity in psychiatry: multiple disorders share the same risk factors and biomarkers and often respond to the same therapies. Here, the authors summarize the history of the unidimensional idea, review modern research into p, demystify statistical models, articulate some implications of p for prevention and clinical practice, and outline a transdiagnostic research agenda. [AJP AT 175: Remembering Our Past As We Envision Our Future October 1910: A Study of Association in Insanity Grace Helen Kent and A.J. Rosanoff: "No sharp distinction can be drawn between mental health and mental disease; a large collection of material shows a gradual and not an abrupt transition from the normal state to pathological states."(Am J Psychiatry 1910; 67(2):317-390 )]. [ABSTRACT FROM AUTHOR]

The geroscience hypothesis posits that therapies to slow biological processes of aging can prevent disease and extend healthy years of life. To test such "geroprotective" therapies in humans, outcome measures are needed that can assess extension of disease-free life span. This need has spurred development of different methods to quantify biological aging. But different methods have not been systematically compared in the same humans. We implemented 7 methods to quantify biological aging using repeated-measures physiological and genomic data in 964 middle-aged humans in the Dunedin Study (New Zealand; persons born 1972-1973). We studied 11 measures in total: telomere-length and erosion, 3 epigenetic-clocks and their ticking rates, and 3 biomarker-composites. Contrary to expectation, we found low agreement between different measures of biological aging. We next compared associations between biological aging measures and outcomes that geroprotective therapies seek to modify: physical functioning, cognitive decline, and subjective signs of aging, including aged facial appearance. The 71-cytosine-phosphateguanine epigenetic clock and biomarker composites were consistently related to these aging-related outcomes. However, effect sizes were modest. Results suggested that various proposed approaches to quantifying biological aging may not measure the same aspects of the aging process. Further systematic evaluation and refinement of measures of biological aging is needed to furnish outcomes for geroprotector trials. [ABSTRACT FROM AUTHOR]

Objective: Individuals reporting a history of childhood violence victimization have impaired brain function. However, the clinical significance, reproducibility, and causality of these findings are disputed. The authors used data from two large cohort studies to address these research questions directly.Method: The authors tested the association between prospectively collected measures of childhood violence victimization and cognitive functions in childhood, adolescence, and adulthood among 2,232 members of the U.K. E-Risk Study and 1,037 members of the New Zealand Dunedin Study who were followed up from birth until ages 18 and 38 years, respectively. Multiple measures of victimization and cognition were used, and comparisons were made of cognitive scores for twins discordant for victimization.Results: Individuals exposed to childhood victimization had pervasive impairments in clinically relevant cognitive functions, including general intelligence, executive function, processing speed, memory, perceptual reasoning, and verbal comprehension in adolescence and adulthood. However, the observed cognitive deficits in victimized individuals were largely explained by cognitive deficits that predated childhood victimization and by confounding genetic and environmental risks.Conclusions: Findings from two population-representative birth cohorts totaling more than 3,000 individuals and born 20 years and 20,000 km apart suggest that the association between childhood violence victimization and later cognition is largely noncausal, in contrast to conventional interpretations. These findings support the adoption of a more circumspect approach to causal inference in the neuroscience of stress. Clinically, cognitive deficits should be conceptualized as individual risk factors for victimization as well as potential complicating features during treatment. [ABSTRACT FROM AUTHOR]

Background: To prevent onset of age-related diseases and physical and cognitive decline, interventions to slow human aging and extend health span must eventually be applied to people while they are still young and healthy. Yet most human aging research examines older adults, many with chronic disease, and little is known about aging in healthy young humans.Method: This article explains how this knowledge gap is a barrier to extending health span and puts forward the case that geroscience should invest in researching the pace of aging in young adults. As one illustrative example, we describe an initial effort to study the pace of aging in a young-adult birth cohort by using repeated waves of biomarkers collected across the third and fourth decades to quantify the pace of coordinated physiological deterioration across multiple organ systems (eg, pulmonary, periodontal, cardiovascular, renal, hepatic, metabolic, and immune function).Results: Findings provided proof of principle that it is possible to quantify individual variation in the pace of aging in young adults still free of age-related diseases.Conclusions: This article articulates research needs to improve longitudinal measurement of the pace of aging in young people, to pinpoint factors that slow or speed the pace of aging, to compare pace of aging against genomic clocks, to explain slow-aging young adults, and to apply pace of aging in preventive clinical trials of antiaging therapies. This article puts forward a research agenda to fill the knowledge gap concerning lifelong causes of aging. [ABSTRACT FROM AUTHOR]

Background: Adverse childhood experiences (ACEs; e.g. abuse, neglect, and parental loss) have been associated with increased risk for later-life disease and dysfunction using adults’ retrospective self-reports of ACEs. Research should test whether associations between ACEs and health outcomes are the same for prospective and retrospective ACE measures. Methods: We estimated agreement between ACEs prospectively recorded throughout childhood (by Study staff at Study member ages 3, 5, 7, 9, 11, 13, and 15) and retrospectively recalled in adulthood (by Study members when they reached age 38), in the population-representative Dunedin cohort (N = 1,037). We related both retrospective and prospective ACE measures to physical, mental, cognitive, and social health at midlife measured through both objective (e.g. biomarkers and neuropsychological tests) and subjective (e.g. self-reported) means. Results: Dunedin and U.S. Centers for Disease Control ACE distributions were similar. Retrospective and prospective measures of adversity showed moderate agreement (r = .47, p < .001; weighted Kappa = .31, 95% CI: .27–.35). Both associated with all midlife outcomes. As compared to prospective ACEs, retrospective ACEs showed stronger associations with life outcomes that were subjectively assessed, and weaker associations with life outcomes that were objectively assessed. Recalled ACEs and poor subjective outcomes were correlated regardless of whether prospectively recorded ACEs were evident. Individuals who recalled more ACEs than had been prospectively recorded were more neurotic than average, and individuals who recalled fewer ACEs than recorded were more agreeable. Conclusions: Prospective ACE records confirm associations between childhood adversity and negative life outcomes found previously using retrospective ACE reports. However, more agreeable and neurotic dispositions may, respectively, bias retrospective ACE measures toward underestimating the impact of adversity on objectively measured life outcomes and overestimating the impact of adversity on self-reported outcomes. Associations between personality factors and the propensity to recall adversity were extremely modest and warrant further investigation. Risk predictions based on retrospective ACE reports should utilize objective outcome measures. Where objective outcome measurements are difficult to obtain, correction factors may be warranted. [ABSTRACT FROM AUTHOR]

A previous genome-wide association study (GWAS) of more than 100,000 individuals identified molecular-genetic predictors of educational attainment. We undertook in-depth life-course investigation of the polygenic score derived from this GWAS using the four-decade Dunedin Study (N = 918). There were five main findings. First, polygenic scores predicted adult economic outcomes even after accounting for educational attainments. Second, genes and environments were correlated: Children with higher polygenic scores were born into better-off homes. Third, children's polygenic scores predicted their adult outcomes even when analyses accounted for their social-class origins; social-mobility analysis showed that children with higher polygenic scores were more upwardly mobile than children with lower scores. Fourth, polygenic scores predicted behavior across the life course, from early acquisition of speech and reading skills through geographic mobility and mate choice and on to financial planning for retirement. Fifth, polygenic-score associations were mediated by psychological characteristics, including intelligence, self-control, and interpersonal skill. Effect sizes were small. Factors connecting DNA sequence with life outcomes may provide targets for interventions to promote population-wide positive development. [ABSTRACT FROM AUTHOR]

Background: Toxoplasma gondii (T. gondii) is a protozoan parasite present in around a third of the human population. Infected individuals are commonly asymptomatic, though recent reports have suggested that infection might influence aspects of the host’s behavior. In particular, Toxoplasma infection has been linked to schizophrenia, suicide attempt, differences in aspects of personality and poorer neurocognitive performance. However, these studies are often conducted in clinical samples or convenience samples. Methods/Results: In a population-representative birth-cohort of individuals tested for presence of antibodies to T. gondii (N = 837) we investigated the association between infection and four facets of human behavior: neuropsychiatric disorder (schizophrenia and major depression), poor impulse control (suicidal behavior and criminality), personality, and neurocognitive performance. Suicide attempt was marginally more frequent among individuals with T. gondii seropositivity (p = .06). Seropositive individuals also performed worse on one out of 14 measures of neuropsychological function. Conclusion: On the whole, there was little evidence that T. gondii was related to increased risk of psychiatric disorder, poor impulse control, personality aberrations or neurocognitive impairment. [ABSTRACT FROM AUTHOR]

Objective: Despite a prevailing assumption that adult ADHD is a childhood-onset neurodevelopmental disorder, no prospective longitudinal study has described the childhoods of the adult ADHD population. The authors report follow-back analyses of ADHD cases diagnosed in adulthood, alongside follow-forward analyses of ADHD cases diagnosed in childhood, in one cohort.Method: Participants belonged to a representative birth cohort of 1,037 individuals born in Dunedin, New Zealand, in 1972 and 1973 and followed to age 38, with 95% retention. Symptoms of ADHD, associated clinical features, comorbid disorders, neuropsychological deficits, genome-wide association study-derived polygenic risk, and life impairment indicators were assessed. Data sources were participants, parents, teachers, informants, neuropsychological test results, and administrative records. Adult ADHD diagnoses used DSM-5 criteria, apart from onset age and cross-setting corroboration, which were study outcome measures.Results: As expected, childhood ADHD had a prevalence of 6% (predominantly male) and was associated with childhood comorbid disorders, neurocognitive deficits, polygenic risk, and residual adult life impairment. Also as expected, adult ADHD had a prevalence of 3% (gender balanced) and was associated with adult substance dependence, adult life impairment, and treatment contact. Unexpectedly, the childhood ADHD and adult ADHD groups comprised virtually nonoverlapping sets; 90% of adult ADHD cases lacked a history of childhood ADHD. Also unexpectedly, the adult ADHD group did not show tested neuropsychological deficits in childhood or adulthood, nor did they show polygenic risk for childhood ADHD.Conclusions: The findings raise the possibility that adults presenting with the ADHD symptom picture may not have a childhood-onset neurodevelopmental disorder. If this finding is replicated, then the disorder's place in the classification system must be reconsidered, and research must investigate the etiology of adult ADHD. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article "Pulling back the curtain on heritability studies: Biosocial criminology in the postgenomic era" by Callie H. Burt and Ronald L. Simons in the volume 52, 2014 issue.

Background: We investigated the importance of indicators of parental socio-economic status (SES) for getting an official drug charge, while we controlled for self-reported drug law infractions (use of illegal drugs and/or drug trafficking) and potential variables confounding the association.Methods: We used data from the long-term, population based longitudinal Young in Norway Study (N = 2,549). Participants were followed up over four survey-based data collections with linkages to crime registers from adolescence to adulthood. Data on drug charges were assessed based on official registers. The use of illegal substances, involvement with drug trafficking and potential covariates such as involvement with other types of crime, academic resources, and risk factors in the family, were assessed by means of self-reports.Results: Two per cent had been charged for drug-related offences, and 37% reported drug offending. Use of cannabis was the primary infraction statistically related to a criminal charge. Having parents with 4+ years university education (14% of the sample) was associated with lower risk for being charged than having parents with no higher education (OR 4.87; 95% CI: 1.16-20.52) or with a short university education (OR 4.76; 1.05-21.48). The association between parental education and drug charges remained stable when controlling for self-reported drug law infractions and other potential covariates.Conclusion: In Norway, adolescents who have parents with higher university education, may be protected from getting a drug charge, even though they report similar levels of drug law infractions as other adolescents. [ABSTRACT FROM AUTHOR]

Childhood cruelty to animals is thought to indicate that a child may have been maltreated. This study examined: (a) prevalence of cruelty to animals among 5- to 12-year-old children; (b) the association between cruelty to animals, child physical maltreatment, and adult domestic violence; and (c) whether cruelty to animals is a marker of maltreatment taking into account age, persistence of cruelty, and socioeconomic disadvantage. Data were from the Environmental Risk (E-Risk) Longitudinal Twin Study, an epidemiological representative cohort of 2,232 children living in the United Kingdom. Mothers reported on cruelty to animals when children were 5, 7, 10, and 12 years, on child maltreatment up to age 12, and adult domestic violence. Nine percent of children were cruel to animals during the study and 2.6% persistently (≥2 time-points). Children cruel to animals were more likely to have been maltreated than other children (OR =3.32) although the majority (56.4%) had not been maltreated. Animal cruelty was not associated with domestic violence when maltreatment was controlled for. In disadvantaged families, 6 in 10 children cruel to animals had been maltreated. In other families, the likelihood of maltreatment increased with age (from 3 in 10 5-year-olds to 4.5 in 10 12-year-olds) and persistence (4.5 in 10 of those persistently cruel). Although childhood cruelty to animals is associated with maltreatment, not every child showing cruelty had been maltreated. The usefulness of cruelty to animals as a marker for maltreatment increases with the child's age, persistence of behavior, and poorer social background. [Copyright &y& Elsevier]

The rising number of newly insured young adults brought on by health care reform will soon increase demands on primary care physicians. Physicians will face more young adult patients, which presents an opportunity for more prevention-oriented care. In the present study, we evaluated whether brief observer reports of young adults' personality traits could predict which individuals would be at greater risk for poor health as they entered midlife. Following the cohort of 1,000 individuals from the Dunedin Multidisciplinary Health and Development Study (Moffitt, Caspi, Rutter, & Silva, 2001), we show that very brief measures of young adults' personalities predicted their midlife physical health across multiple domains (metabolic abnormalities, cardiorespiratory fitness, pulmonary function, periodontal disease, and systemic inflammation). Individuals scoring low on the traits of Conscientiousness and Openness to Experience went on to develop poorer health even after accounting for preexisting differences in education, socioeconomic status, smoking, obesity, self-reported health, medical conditions, and family medical history. Moreover, personality ratings from peer informants who knew participants well, and from a nurse and receptionist who had just met participants for the first time, predicted health decline from young adulthood to midlife despite striking differences in level of acquaintance. Personality effect sizes were on par with other well-established health risk factors such as socioeconomic status, smoking, and self-reported health. We discuss the potential utility of personality measurement to function as an inexpensive and accessible tool for health care professionals to personalize preventive medicine. Adding personality information to existing health care electronic infrastructures could also advance personality theory by generating opportunities to examine how personality processes influence doctor-patient communication, health service use, and patient outcomes. [ABSTRACT FROM AUTHOR]

Many young people who are mistreated by an adult, victimized by bullies, criminally assaulted, or who witness domestic violence react to this violence exposure by developing behavioral, emotional, or learning problems. What is less well known is that adverse experiences like violence exposure can lead to hidden physical alterations inside a child's body, alterations that may have adverse effects on life-long health. We discuss why this is important for the field of developmental psychopathology and for society, and we recommend that stress-biology research and intervention science join forces to tackle the problem. We examine the evidence base in relation to stress-sensitive measures for the body (inflammatory reactions, telomere erosion, epigenetic methylation, and gene expression) and brain (mental disorders, neuroimaging, and neuropsychological testing). We also review promising interventions for families, couples, and children that have been designed to reduce the effects of childhood violence exposure. We invite intervention scientists and stress-biology researchers to collaborate in adding stress-biology measures to randomized clinical trials of interventions intended to reduce effects of violence exposure and other traumas on young people. [ABSTRACT FROM PUBLISHER]

Translational research is needed to leverage discoveries from the frontiers of genome science to improve public health. So far, public health researchers have largely ignored genetic discoveries, and geneticists have ignored important aspects of population health science. This mutual neglect should end. In this article, we discuss 3 areas where public health researchers can help to advance translation: (1) risk assessment: investigate genetic profiles as components in composite risk assessments; (2) targeted intervention: conduct life-course longitudinal studies to understand when genetic risks manifest in development and whether intervention during sensitive periods can have lasting effects; and (3) improved understanding of environmental causation: collaborate with geneticists on gene-environment interaction research. We illustrate with examples from our own research on obesity and smoking. INSET: Genetic Risk Scores and Family History Scores for Obesity.... [ABSTRACT FROM AUTHOR]

Why do more intelligent people live healthier and longer lives? One possibility is that intelligence tests assess health of the brain, but psychological science has lacked technology to evaluate this hypothesis. Digital retinal imaging, a new, noninvasive method to visualize microcirculation in the eye, may reflect vascular conditions in the brain. We studied the association between retinal vessel caliber and neuropsychological functioning in the representative Dunedin birth cohort. Wider venular caliber was associated with poorer neuropsychological functioning at midlife, independently of potentially confounding factors. This association was not limited to any specific test domain and extended to informants’ reports of cohort members’ cognitive difficulties in everyday life. Moreover, wider venular caliber was associated with lower childhood IQ tested 25 years earlier. The findings indicate that retinal venular caliber may be an indicator of neuropsychological health years before the onset of dementing diseases and suggest that digital retinal imaging may be a useful investigative tool for psychological science. [ABSTRACT FROM PUBLISHER]

Using data from the large, 30-year prospective Dunedin cohort study, we examined whether preexisting individual differences in childhood temperament predicted adulthood disordered gambling (a diagnosis covering the full continuum of gambling-related problems). A 90-min observational assessment at age 3 was used to categorize children into five temperament groups, including one primarily characterized by behavioral and emotional undercontrol. The children with undercontrolled temperament at 3 years of age were more than twice as likely to evidence disordered gambling at ages 21 and 32 than were children who were well-adjusted at age 3. These associations could not be explained by differences in childhood IQ or family socioeconomic status. Cleanly demonstrating the temporal relation between behavioral undercontrol and adult disordered gambling is an important step toward building more developmentally sensitive theories of disordered gambling and may put researchers in a better position to begin considering potential routes to disordered-gambling prevention through enhancing self-control and emotional regulation. [ABSTRACT FROM PUBLISHER]

Policy-makers are considering large-scale programs aimed at self-control to improve citizens' health and wealth and reduce crime. Experimental and economic studies suggest such programs could reap benefits. Yet, is self-control important for the health, wealth, and public safety of the population? Following a cohort of 1,000 children from birth to the age of 32 y, we show that childhood self-control predicts physical health, substance dependence, personal finances, and criminal offending outcomes, following a gradient of self-control. Effects of children's self-control could be disentangled from their intelligence and social class as well as from mistakes they made as adolescents. In another cohort of 500 sibling-pairs, the sibling with lower self-control had poorer outcomes, despite shared family background. Interventions addressing self-control might reduce a panoply of societal costs, save taxpayers money, and promote prosperity. [ABSTRACT FROM AUTHOR]

The authors examined the role of food insecurity in the etiology of children's cognitive and mental health problems. Data from a prospective longitudinal study of 1,116 United Kingdom families with twins (sample constructed in 1999–2000) were used to test associations among household food insecurity; income; maternal personality; household sensitivity to children's needs; and children's cognitive, behavioral, and emotional development. Food-insecure children had lower IQs and higher levels of behavioral and emotional problems relative to their peers. After differences in household income, the personalities of children's mothers, and the sensitivity of household organization to children's needs were accounted for, food-insecure children had moderately higher levels of emotional problems relative to food-secure children (β = 0.22, P = 0.02). Differences in children's cognitive development were accounted for by household income, and differences in their behavioral development were accounted for by their mothers’ personalities and their households’ sensitivity to children's needs. Results suggest that food insecurity was associated with school-aged children's emotional problems but not with their cognitive or behavioral problems after accounting for differences in the home environments in which children were reared. Mothers’ personality and household sensitivity to children's needs may present challenges to improving outcomes of children with food insecurity. [ABSTRACT FROM PUBLISHER]

This article reports on the influence of neighborhood-level deprivation and collective efficacy on children's antisocial behavior between the ages of 5 and 10 years. Latent growth curve modeling was applied to characterize the developmental course of antisocial behavior among children in the E-Risk Longitudinal Twin Study, an epidemiological cohort of 2,232 children. Children in deprived versus affluent neighborhoods had higher levels of antisocial behavior at school entry (24.1 vs. 20.5, p < .001) and a slower rate of decline from involvement in antisocial behavior between the ages of 5 and 10 (-0.54 vs. -0.78, p < .01). Neighborhood collective efficacy was negatively associated with levels of antisocial behavior at school entry (r = -.10, p < .01) but only in deprived neighborhoods; this relationship held after controlling for neighborhood problems and family-level factors. Collective efficacy did not predict the rate of change in antisocial behavior between the ages of 5 and 10. Findings suggest that neighborhood collective efficacy may have a protective effect on children living in deprived contexts. [ABSTRACT FROM AUTHOR]

Objective: Cognitive reserve has been proposed as important in the etiology of neuropsychiatric disorders. However, tests of the association between premorbid IQ and adult mental disorders other than schizophrenia have been limited and inconclusive. The authors tested the hypothesis that low childhood IQ is associated with increased risk and severity of adult mental disorders. Method: Participants were members of a representative 1972-1 973 birth cohort of 1,037 males and females in Dunedin, New Zealand,.who were followed up to age 32 with 96% retention. WISC-R 10 was assessed at ages 7, 9, and 11. Research diagnoses of DSM mental disorders were made at ages 18, 21, 26, and 32. Results: Lower childhood 10 was associated with increased risk of developing schizophrenia spectrum disorder, adult depression, and adult anxiety. Lower childhood IQ was also associated with greater comorbidity and with persistence of depression; the association with persistence of generalized anxiety disorder was nearly significant. Higher childhood 10 predicted increased risk of adult mania. Conclusions: Lower cognitive reserve, as reflected by childhood 10, is an antecedent of several common psychiatric disorders and also predicts persistence and comorbidity. Thus, many patients who seek mental health treatment may have lower cognitive ability; this should be considered in prevention and treatment planning. [ABSTRACT FROM AUTHOR]

This article reports on the childhood origins and adult outcomes of female versus male antisocial behavior trajectories in the Dunedin longitudinal study. Four antisocial behavior trajectory groups were identified among females and males using general growth mixture modeling and included life-course persistent (LCP), adolescent-onset, childhood-limited, and low trajectory groups. During childhood, both LCP females and males were characterized by social, familial and neurodevelopmental risk factors, whereas those on the adolescent-onset pathway were not. At age 32, women and men on the LCP pathway were engaging in serious violence and experiencing significant mental health, physical health, and economic problems. Females and males on the adolescent-onset pathway were also experiencing difficulties at age 32, although to a lesser extent. Although more males than females followed the LCP trajectory, findings support similarities across gender with respect to developmental trajectories of antisocial behavior and their associated childhood origins and adult consequences. Implications for theory, research, and practice are discussed. [ABSTRACT FROM PUBLISHER]

This article charts a strategic research course toward an empirical foundation for the diagnosis of conduct disorder in the forthcoming DSM-V. Since the DSM-IV appeared in 1994, an impressive amount of new information about conduct disorder has emerged. As a result of this new knowledge, reasonable rationales have been put forward for adding to the conduct disorder diagnostic protocol: a childhood-limited subtype, family psychiatric history, callous-unemotional traits, female-specific criteria, preschool-specific criteria, early substance use, and biomarkers from genetics, neuroimaging, and physiology research. This article reviews the evidence for these and other potential changes to the conduct disorder diagnosis. We report that although there is a great deal of exciting research into each of the topics, very little of it provides the precise sort of evidence base required to justify any alteration to the DSM-V. We outline specific research questions and study designs needed to build the lacking evidence base for or against proposed changes to DSM-V conduct disorder. [ABSTRACT FROM AUTHOR]

The article presents a study of the relationship between low self-control and the four dimensions of criminal careers which include participation, frequency, persistence and desistance from crime. It investigates whether self-control differentiates between persistence and desistance. Based on data from 985 participants, the authors found that low self-control equally predicts all dimensions of criminal behavior and that its effects hold study across all types of individual.

Gene–environment interaction research in psychiatry is new, and is a natural ally of neuroscience. Mental disorders have known environmental causes, but there is heterogeneity in the response to each causal factor, which gene–environment findings attribute to genetic differences at the DNA sequence level. Such findings come from epidemiology, an ideal branch of science for showing that a gene–environment interactions exist in nature and affect a significant fraction of disease cases. The complementary discipline of epidemiology, experimental neuroscience, fuels gene–environment hypotheses and investigates underlying neural mechanisms. This article discusses opportunities and challenges in the collaboration between psychiatry, epidemiology and neuroscience in studying gene–environment interactions. [ABSTRACT FROM AUTHOR]

Objective: The association between violence between intimate partners and psychiatric disorders is assumed to reflect a causal link. This assumption is now questioned because several longitudinal studies have documented that adolescents with psychiatric disorders grow up to be overrepresented among adults involved in partner violence. Method: The study followed a representative birth cohort prospectively. Adolescent mental disorders were diagnosed at age 18 years. Between ages 24 and 26 years, the authors identified individuals involved in nonabusive relationships versus those involved in clinically abusive relationships (i.e., resulting in injury and/or official intervention). At age 26 years, mental disorders were again diagnosed. Results: Male and female adolescents with psychiatric disorders were at greatest risk of becoming involved in abusive adult relationships. After the authors controlled for earlier psychiatric history, women who were involved in abusive relationships, but not men, had an increased risk of adult psychiatric morbidity. Conclusions: 1) Psychiatric disorders pose risk for involvement in abusive relationships for both sexes; 2) partner abuse is a contributing source of psychiatric disorders among women but not among men. [ABSTRACT FROM AUTHOR]

There is much curiosity about interactions between genes and environmental risk factors for psychopathology, but this interest is accompanied by uncertainty. This article aims to address this uncertainty. First, we explain what is and is not meant by gene-environment interaction. Second, we discuss reasons why such interactions were thought to be rare in psychopathology, and argue instead that they ought to be common. Third, we summarize emerging evidence about gene-environment interactions in mental disorders. Fourth, we argue that research on gene-environment interactions should be hypothesis driven, and we put forward strategies to guide future studies. Fifth, we describe potential benefits of studying measured gene-environment interactions for basic neuroscience, gene hunting, intervention, and public understanding of genetics. We suggest that information about nurture might be harnessed to make new discoveries about the nature of psychopathology. [ABSTRACT FROM AUTHOR]

Gene–environment interplay is a general term that covers several divergent concepts with different meanings and different implications. In this review, we evaluate research evidence on four varieties of gene–environment interplay. First, we consider epigenetic mechanisms by which environmental influences alter the effects of genes. Second, we focus on variations in heritability according to environmental circumstances. Third, we discuss what is known about gene–environment correlations. Finally, we assess concepts and findings on the interaction between specific identified genes and specific measured environmental risks. In order to provide an understanding of what may be involved in gene–environment interplay, we begin our presentation with a brief historical review of prevailing views about the role of genetic and environmental factors in the causation of mental disorders, and we provide a simplified account of some of the key features of how genes ‘work’. [ABSTRACT FROM AUTHOR]

Previous studies have reported, but not explained, the reason for a robust association between reading achievement and antisocial behavior. This association was investigated using the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally representative 1994-1995 birth cohort of 5- and 7-year-olds. Results showed that the association resulted primarily from environmental factors common to both reading and antisocial behavior and was stronger in boys. Environmental factors also explained the relation between reading disability and conduct disorder. Leading candidate environmental risk factors weakly mediated the association. For boys the best explanation was a reciprocal causation model: poor reading led to antisocial behavior, and vice versa. In contrast, the relation between reading achievement and attention deficit hyperactivity disorder was best explained by common genetic influences. [ABSTRACT FROM AUTHOR]

This article reviews behavioral-genetic research to show how it can help address questions of causation in developmental psychopathology. The article focuses on studies of antisocial behavior, because these have been leading the way in investigating environmental as well as genetic influences on psychopathology. First, the article illustrates how behavioral-genetic methods are being newly applied to detect the best candidates for genuine environmental causes among the many risk factors for antisocial behavior. Second, the article examines findings of interaction between genes and environments (G × E) associated with antisocial behavior, outlining steps for testing hypotheses of measured G × E. Third, the article envisages future work on gene-environment interplay, arguing that it is an interesting and profitable way forward for psychopathology research. [ABSTRACT FROM AUTHOR]

Background: Recent evidence documents that cannabis use by young people is a modest statistical risk factor for psychotic symptoms in adulthood, such as hallucinations and delusions, as well as clinically significant schizophrenia. The vast majority of cannabis users do not develop psychosis, however, prompting us to hypothesize that some people are genetically vulnerable to the deleterious effects of cannabis. Methods: In a longitudinal study of a representative birth cohort followed to adulthood, we tested why cannabis use is associated with the emergence of psychosis in a minority of users, but not in others. Results: A functional polymorphism in the catechol-O-methyltransferase (COMT) gene moderated the influence of adolescent cannabis use on developing adult psychosis. Carriers of the COMT valine158 allele were most likely to exhibit psychotic symptoms and to develop schizophreniform disorder if they used cannabis. Cannabis use had no such adverse influence on individuals with two copies of the methionine allele. Conclusions: These findings provide evidence of a gene × environment interaction and suggest that a role of some susceptibility genes is to influence vulnerability to environmental pathogens. [Copyright &y& Elsevier]

Some children exposed to socioeconomic (SES) deprivation are resilient and function better than expected, given the level of deprivation they have experienced. The present study tested genetic and environmental contributions to young children's resilience and vulnerability to SES deprivation. Children's resilience was assessed by the difference between their actual score and the score predicted by their level of SES deprivation in the E-Risk Study, an epidemiological cohort of 1,116 five-year-old twin pairs. Consistent with previous research, results showed that maternal warmth, stimulating activities, and children's outgoing temperament appeared to promote positive adjustment in children exposed to SES deprivation. Findings add new information by demonstrating that resilience is partly heritable and that protective processes operate through both genetic and environmental effects. [ABSTRACT FROM AUTHOR]

In an unselected birth cohort (N = 980, age 24-26 years), individuals in abusive relationships causing injury and/or official intervention (9% prevalence) were compared with participants reporting physical abuse without clinical consequences and with control participants who reported no abuse, on current characteristics and prospective developmental risks. In nonclinically abusive relationships, perpetrators were primarily women. In clinically abusive relationships, men and women used physical abuse, although more women needed medical treatment for injury. Women in clinically abusive relationships had childhood family adversity, adolescent conduct problems, and aggressive personality; men had disinhibitory psychopathology since childhood and extensive personality deviance. These findings counter the assumption that if clinical abuse was ascertained in epidemiological samples, it would be primarily man-to-woman, explained by patriarchy rather than psychopathology. [ABSTRACT FROM AUTHOR]

If maternal expressed emotion is an environmental risk factor for children's antisocial behavior problems, it should account for behavioral differences between siblings growing up in the same family even after genetic influences on children's behavior problems are taken into account. This hypothesis was tested in the Environmental Risk Longitudinal Twin Study with a nationally representative 1994-1995 birth cohort of twins. The authors interviewed the mothers of 565 five-year-old monozygotic (MZ) twin pairs and established which twin in each family received more negative emotional expression and which twin received more warmth. Within MZ pairs, the twin receiving more maternal negativity and less warmth had more antisocial behavior problems. Qualitative interviews were used to generate hypotheses about why mothers treat their children differently. The results suggest that maternal emotional attitudes toward children may play a causal role in the development of antisocial behavior and illustrate how genetically informative research can inform tests of socialization hypotheses. [ABSTRACT FROM AUTHOR]

Background: Early childhood antisocial behaviour is a strong prognostic indicator for poor adult mental health. Thus, information about its etiology is needed. Genetic etiology is unknown because most research with young children focuses on environmental risk factors, and the few existing studies of young twins used only mothers' reports of behaviour, which may be biased. Method: We investigated genetic influences on antisocial behaviour in a representative-plus-high-risk sample of 1116 pairs of 5-year-old twins using data from four independent sources: mothers, teachers, examiner-observers previously unacquainted with the children, and the children themselves. Results: Children's antisocial behaviour was reliably measured by all four informants; no bias was detected in mothers', teachers', examiners', or children's reports. Variation in antisocial behaviour that was agreed upon by all informants, and thus was pervasive across settings, was influenced by genetic factors (82%) and experiences specific to each child (18%). Variation in antisocial behaviour that was specific to each informant was meaningful variation, as it was also influenced by genetic factors (from 33% for the children's report to 71% for the teachers' report). Conclusions: This study and four others of very young twins show that genetic risks contribute strongly to population variation in antisocial behaviour that emerges in early childhood. In contrast, genetic risk is known to be relatively modest for adolescent antisocial behaviour, suggesting that the early-childhood form has a distinct etiology, particularly if it is pervasive across situations. [ABSTRACT FROM AUTHOR]

Background: Previous studies that have examined the long-term effects of infertility and assisted reproductive technology on parenting and child behaviour in families with twins have suffered from methodological problems. This study compared measures of parental adjustment, parenting and child behaviour in families with 5-year-old twins who were conceived after in vitro fertilisation (IVF) or ovulation induction (OI) with families whose twins were naturally conceived (NC). Methods: The families who conceived via IVF/OI ( N=121) were identified from an epidemiological study of twins and matched to families who were conceived naturally ( N=121) on the basis of eleven child and family variables. Mothers were interviewed in their homes for the study. Results: No significant differences were observed between the IVF/OI families and the NC families on measures of parental adjustment or parent and teacher ratings of the twins' behaviour. IVF/OI mothers and their partners agreed with each other about discipline more than NC couples, but otherwise no other differences in parenting were found. Conclusions: Overall, this study provides evidence that families who conceive twins following IVF/OI are functioning well and that the experience of fertility treatment does not lead to long-term difficulties for parents or children. [ABSTRACT FROM AUTHOR]

Objective: Externalizing and internalizing problems may aggregate in families because (1) siblings share genetic risks for problem behaviors or (2) siblings are exposed to similar environmental risks. A genetically sensitive design was used to determine whether domestic violence accounted significantly for the variation and covariation of externalizing and internalizing problems, independent of additive genetic effects on these behavior problems. Method: Using the Achenbach family of instruments, mothers and teachers reported internalizing and externalizing problems for 1,116 monozygotic and dizygotic 5-year-old twin pairs in the United Kingdom (93% response rate). Mothers reported their experiences of domestic violence in the previous 5 years. Structural equation models were tested to determine the effect of mothers' experiences of domestic violence on children's emotional and conduct problems, controlling for latent genetic and environmental effects on these behaviors. Results: A multivariate model showed that adult domestic violence accounted for 2% and 5% of the variation in children's internalizing and externalizing problems, respectively, independent of genetic effects. The co-occurrence of externalizing and internalizing scores was accounted for by genetic (62.6%) and shared environmental (29.2%) factors and by domestic violence (8%). Conclusions: Because domestic violence affects children's behavior problems beyond genetic influences, programs that successfully reduce domestic violence should also prevent children's psychopathology. [ABSTRACT FROM AUTHOR]

Background: This paper describes the circumstances of contemporary young mothers and their children from a nationally representative sample, and compares them to the circumstances of mothers who delayed childbearing beyond age 20. Methods: The participants are members of the Environmental Risk (E-risk) Longitudinal Twin Study, which follows an epidemiological sample of 1,116 women who became mothers in England and Wales in 1994-95, and their children, and contains an over-sample of young mothers. Home visits were conducted when the children were aged 5 years. Data were collected from mothers via interviews, from children via experimental tasks and observations, and from teachers via postal questionnaires. Results: Young mothers encountered more socio-economic deprivation, had significantly less human and social capital, and experienced more mental health difficulties. Their partners were less reliable and supportive, both economically and emotionally, and were more antisocial and abusive. The children of young mothers showed reduced educational attainment, were rated by multiple informants as having more emotional and behavioural problems, were at increased risk of maltreatment or harm, and showed higher rates of illnesses, accidents, and injuries. Conclusions: Young mothers today face difficulties known to have long-lasting effects for women and their children. Preventions that target young mothers may reduce harm to the physical health, mental health, and social status of future generations. [ABSTRACT FROM AUTHOR]

Background: Estimates of who is most at risk from violence by people with mental illness rest mainly on identified patient samples. This study, without such selection bias, examined the targets of violence committed by young adults with as-yet untreated alcohol dependence, marijuana dependence, or schizophrenia-spectrum disorders, to determine the extent to which their victims were co-residents or non-household members.Methods: In a total birth cohort of 21-year-olds (n=956), past-year prevalence of alcohol dependence, marijuana dependence and schizophrenia-spectrum disorders were diagnosed using standardized DSM-III-R interviews. None of the people with schizophrenia-spectrum disorder has been hospitalized in the past year. Past-year violence and victim targets were measured using self-reports.Results: Compared with controls, cohort members with substance dependence or schizophrenia-spectrum disorders had higher prevalence and frequency rates of assault against co-residents, against non-household members, and also robbery and gang fights. Out of 39, five individuals with schizophrenia-spectrum disorder committed violent street crimes. Persons with substance dependence had similar proportions of violence against co-resident and non-household members, but persons with schizophrenia-spectrum disorders tended to victimize co-residents more than others.Conclusions: At the age when they are most likely to contribute to the community's violence burden, young untreated offenders with alcohol or marijuana dependence or with schizophrenia-spectrum disorders assault not only co-residents, but others as well, and commit violent street crimes. Families, schoolteachers and primary care physicians have an important potentially preventive role in early identification and treatment of the disorders. [ABSTRACT FROM AUTHOR]

Both partner abuse and general crime violate the rights and safety of victims. But are these phenomena the same or are they distinct, demanding their own research and intervention specialties? Are persons who abuse their partners the same people who commit other criminal behavior? Do partner abuse and general crime share the same correlates? We investigated these questions in a birth cohort of over 800 young adults, by testing whether a personality model known to predict general crime would also predict partner abuse. Personality data were gathered at age 18, and self-reported partner abuse and general criminal offending were measured at age 21. Results from modeling latent constructs showed that partner abuse and general crime represent different constructs that are moderately related; they are not merely two expressions of the same underlying antisocial propensity. Group comparisons showed many, but not all, partner abusers also engaged in violence against nonintimates. Personality analyses showed that partner abuse and general crime shared a strong propensity from a trait called Negative Emotionality. However, crime was related to weak Constraint (low self-control), but partner abuse was not. All findings applied to women as well as to men, suggesting that women's partner abuse may motivated by the same intra-personal features that motivate men's abuse. The results are consistent with theoretical and applied arguments about the "uniqueness" of partner violence relative to other crime and violence. [ABSTRACT FROM AUTHOR]