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Objective: Cannabis use is increasing among midlife and older adults. This study tested the hypotheses that long-term cannabis use is associated with cognitive deficits and smaller hippocampal volume in midlife, which is important because midlife cognitive deficits and smaller hippocampal volume are risk factors for dementia.Methods: Participants are members of a representative cohort of 1,037 individuals born in Dunedin, New Zealand, in 1972-1973 and followed to age 45, with 94% retention. Cannabis use and dependence were assessed at ages 18, 21, 26, 32, 38, and 45. IQ was assessed at ages 7, 9, 11, and 45. Specific neuropsychological functions and hippocampal volume were assessed at age 45.Results: Long-term cannabis users showed IQ decline from childhood to midlife (mean=-5.5 IQ points), poorer learning and processing speed relative to their childhood IQ, and informant-reported memory and attention problems. These deficits were specific to long-term cannabis users because they were either not present or were smaller among long-term tobacco users, long-term alcohol users, midlife recreational cannabis users, and cannabis quitters. Cognitive deficits among long-term cannabis users could not be explained by persistent tobacco, alcohol, or other illicit drug use, childhood socioeconomic status, low childhood self-control, or family history of substance dependence. Long-term cannabis users showed smaller hippocampal volume, but smaller hippocampal volume did not statistically mediate cannabis-related cognitive deficits.Conclusions: Long-term cannabis users showed cognitive deficits and smaller hippocampal volume in midlife. Research is needed to ascertain whether long-term cannabis users show elevated rates of dementia in later life. [ABSTRACT FROM AUTHOR]

Objective: Neuroimaging research has revealed that structural brain alterations are common across broad diagnostic families of disorders rather than specific to a single psychiatric disorder. Such overlap in the structural brain correlates of mental disorders mirrors already well-documented phenotypic comorbidity of psychiatric symptoms and diagnoses, which can be indexed by a general psychopathology or p factor. The authors hypothesized that if general psychopathology drives the convergence of structural alterations common across disorders, then 1) there should be few associations unique to any one diagnostic family of disorders, and 2) associations with the p factor should overlap with those for the broader diagnostic families.Methods: Analyses were conducted on structural MRI and psychopathology data collected from 861 members of the population-representative Dunedin Multidisciplinary Health and Development Study at age 45.Results: Study members with high scores across three broad diagnostic families of disorders (externalizing, internalizing, thought disorder) exhibited highly overlapping patterns of reduced global and widely distributed parcel-wise neocortical thickness. Study members with high p factor scores exhibited patterns of reduced global and parcel-wise neocortical thickness nearly identical to those associated with the three broad diagnostic families.Conclusions: A pattern of pervasively reduced neocortical thickness appears to be common across all forms of mental disorders and may represent a transdiagnostic feature of general psychopathology. As has been documented with regard to symptoms and diagnoses, the underlying brain structural correlates of mental disorders may not exhibit specificity, and the continued pursuit of such specific correlates may limit progress toward more effective strategies for etiological understanding, prevention, and intervention. [ABSTRACT FROM AUTHOR]

Objective: Self-harm is associated with violent offending. However, little is known about young people who engage in "dual-harm" behavior. The authors investigated antecedents, clinical features, and life characteristics distinguishing dual-harming adolescents from those who self-harm only.Methods: Participants were from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally representative U.K. cohort of 2,232 twins born in 1994 and 1995. Self-harm in adolescence was assessed through interviews at age 18. Violent offending was assessed using a computer questionnaire at age 18 and police records through age 22. Risk factors were assessed between ages 5 and 12. Adolescent mental health, victimization, personality functioning, and use of support services were measured at age 18.Results: Self-harm was associated with violent crime (odds ratio=3.50, 95% CI=2.61-4.70), even after accounting for familial risk factors. Dual harmers had been victims of violence from childhood and exhibited lower childhood self-control and lower childhood IQ than self-only harmers. Dual harmers experienced higher rates of concurrent psychotic symptoms and substance dependence. They also exhibited distinct personality styles characterized by resistance to change and by emotional and interpersonal lability. However, dual harmers were not more likely than self-only harmers to have contact with mental health services.Conclusions: Dual harmers have self-control difficulties and are immersed in violence from a young age. A treatment- rather than punishment-oriented approach is indicated to meet these individuals' needs. Connecting self-harming adolescents with delinquency-reduction programs and transdiagnostic approaches that target self-regulation may reduce harmful behaviors. Preventing childhood maltreatment and implementing strategies to reduce victimization exposure could mitigate risk for both internalized and externalized violence. [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]

Objective: DNA methylation has been proposed as an epigenetic mechanism by which early-life experiences become "embedded" in the genome and alter transcriptional processes to compromise health. The authors sought to investigate whether early-life victimization stress is associated with genome-wide DNA methylation.Method: The authors tested the hypothesis that victimization is associated with DNA methylation in the Environmental Risk (E-Risk) Longitudinal Study, a nationally representative 1994-1995 birth cohort of 2,232 twins born in England and Wales and assessed at ages 5, 7, 10, 12, and 18 years. Multiple forms of victimization were ascertained in childhood and adolescence (including physical, sexual, and emotional abuse; neglect; exposure to intimate-partner violence; bullying; cyber-victimization; and crime).Results: Epigenome-wide analyses of polyvictimization across childhood and adolescence revealed few significant associations with DNA methylation in peripheral blood at age 18, but these analyses were confounded by tobacco smoking and/or did not survive co-twin control tests. Secondary analyses of specific forms of victimization revealed sparse associations with DNA methylation that did not replicate across different operationalizations of the same putative victimization experience. Hypothesis-driven analyses of six candidate genes in the stress response (NR3C1, FKBP5, BDNF, AVP, CRHR1, SLC6A4) did not reveal predicted associations with DNA methylation in probes annotated to these genes.Conclusions: Findings from this epidemiological analysis of the epigenetic effects of early-life stress do not support the hypothesis of robust changes in DNA methylation in victimized young people. We need to come to terms with the possibility that epigenetic epidemiology is not yet well matched to experimental, nonhuman models in uncovering the biological embedding of stress. [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]

The article presents a research study on clinical use of intranasal ketamine for treatment-resistant or acutely suicidal patients with depression. Topics discussed include the therapeutic effect of overusing ketamines for mood elevation; the guidelines made for marketing and distribution of ketamine by the Food & Drug Administration (FDA) in U.S.; and education of the public and physicians about the risk of drug abuse.

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]

Objective: Despite the widespread belief that neuropsychological decline is a cardinal feature of the progression from the premorbid stage to the chronic form of schizophrenia, few longitudinal studies have examined change in neuropsychological functioning from before to after illness onset. The authors examined whether neuropsychological decline is unique to schizophrenia, whether it is generalized or confined to particular mental functions, and whether individuals with schizophrenia also have cognitive problems in everyday life. Method: Participants were members of a representative cohort of 1,037 individuals born in Dunedin, New Zealand, in 1972 and 1973 and followed prospectively to age 38, with 95% retention. Assessment of IQ and specific neuropsychological functions was conducted at ages 7, 9, 11, and 13, and again at age 38. Informants also reported on any cognitive problems at age 38. Results: Individuals with schizophrenia exhibited declines in IQ and in a range of mental functions, particularly those tapping processing speed, learning, executive function, and motor function. There was little evidence of decline in verbal abilities or delayed memory, however, and the developmental progression of deficits in schizophrenia differed across mental functions. Processing speed deficits increased gradually from childhood to beyond the early teen years, whereas verbal deficits emerged early but remained static thereafter. Neuropsychological decline was specific to schizophrenia, as no evidence of decline was apparent among individuals with persistent depression, children with mild cognitive impairment, individuals matched on childhood risk factors for schizophrenia, and psychiatrically healthy individuals. Informants also noticed more cognitive problems in individuals with schizophrenia. Conclusions: There is substantial neuro-psychological decline in schizophrenia from the premorbid to the postonset period, but the extent and developmental progression of decline varies across mental functions. Findings suggest that different pathophysiological mechanisms may underlie deficits in different mental functions. [ABSTRACT FROM AUTHOR]

Objective: Retinal and cerebral micro-vessels are structurally and functionally homologous, but unlike cerebral micro-vessels, retinal micro-vessels can be non-invasively measured in vivo by retinal imaging. The authors tested the hypothesis that individuals with schizophrenia exhibit microvascular abnormality and evaluated the utility of retinal imaging as a tool for schizophrenia research. Method: Participants were members of the Dunedin Study, a population-representative cohort followed from birth with 95% retention. Study members underwent retinal imaging at age 38. The authors assessed retinal arteriolar and venular caliber for all members of the cohort, including individuals who developed schizophrenia. Results: Study members who developed schizophrenia were distinguished by wider retinal venules, suggesting microvascular abnormality reflective of insufficient brain oxygen supply. Analyses that controlled for confounding health conditions suggested that wider retinal venules are not simply an artifact of co-occurring health problems in schizophrenia patients. Wider venules were also associated with a dimensional measure of adult psychosis symptoms and with psychosis symptoms reported in childhood. Conclusions: The findings provide initial support for the hypothesis that individuals with schizophrenia show microvascular abnormality. Moreover, the results suggest that the same vascular mechanisms underlie subthreshold symptoms and clinical disorder and that these associations may begin early in life. These findings highlight the promise of retinal imaging as a tool for understanding the pathogenesis of schizophrenia. [ABSTRACT FROM AUTHOR]

Objective: The binding protein FKBP5 is an important modulator of the function of the glucocorticoid receptor, the main receptor of the stress hormone system. This turns the FKBP5 gene into a key candidate for gene-environment interactions, which are considered critical for pathogenesis of stress-related disorders. The authors explored gene-environment interactions between FKBP5 gene variants and adverse life events in predicting the first occurrence of a major depressive episode. Method: The analyses were based on 884 Caucasians in a 10-year prospective community study. At baseline, they were 14-24 years old and did not fulfill criteria for a major depressive episode. The DSM-IV-based Munich Composite International Diagnostic Interview was used to assess adverse life events preceding baseline and major depressive episodes during follow-up. On the basis of previous findings, five single-nucleotide polymorphisms (SNPs) within the FKBP5 gene were selected for genotyping. Results: While the authors did not observe genetic main effects, they found interactions between the five SNPs and traumatic (but not separation) events, with the strongest effect for severe trauma. The effect of trauma on incident major depressive episodes was evident among subjects homozygous for the minor alleles but not subjects with other genotypes. The findings were replicated in the U.K. Environmental Risk Longitudinal Twin Study. Conclusions: These hypothesis-driven results suggest that an interaction between FKBP5 genotype and trauma is involved in the onset of depression. Subjects homozygous for the minor alleles of the investigated FKBP5 SNPs seem to be particularly sensitive to effects of trauma exposure in terms of triggering depression onset. [ABSTRACT FROM AUTHOR]

Objective: Using longitudinal and prospective measures of trauma during childhood, the authors assessed the risk of developing psychotic symptoms associated with maltreatment, bullying, and accidents in a nationally representative U.K. cohort of young twins. Method: Data were from the Environmental Risk Longitudinal Twin Study, which follows 2,232 twin children and their families. Mothers were interviewed during home visits when children were ages 5, 7, 10, and 12 on whether the children had experienced maltreatment by an adult, bullying by peers, or involvement in an accident. At age 12, children were asked about bullying experiences and psychotic symptoms. Children's reports of psychotic symptoms were verified by clinicians. Results: Children who experienced mal-treatment by an adult (relative risk=3.16, 95% Cl=1.92-5.19) or bullying by peers (relative risk=2.47, 95% Cl=1.74-3.52) were more likely to report psychotic symptoms at age 12 than were children who did not experience such traumatic events. The higher risk for psychotic symptoms was observed whether these events occurred early in life or later in childhood. The risk associated with childhood trauma remained significant in analyses controlling for children's gender, socioeconomic deprivation, and 10; for children's early symptoms of internalizing or externalizing problems; and for children's genetic liability to developing psychosis. In contrast, the risk associated with accidents was small (relative risk=1.47, 95% Cl=1.02-2.13) and inconsistent across ages. Conclusions: Trauma characterized by intention to harm is associated with children's reports of psychotic symptoms. Clinicians working with children who report early symptoms of psychosis should inquire about traumatic events such as maltreatment and bullying. [ABSTRACT FROM AUTHOR]

Objective: Premorbid cognitive deficits in schizophrenia are well documented and have been interpreted as supporting a neurodevelopmental etiological model. The authors investigated the following three unresolved questions about premorbid cognitive deficits: What is their developmental course? Do all premorbid cognitive deficits follow the same course? Are premorbid cognitive deficits specific to schizophrenia or shared by other psychiatric disorders? Methods: Participants were members of a representative cohort of 1,037 males and females born between 1972 and 1973 in Dunedin, New Zealand. Cohort members underwent follow-up evaluations at specific intervals from age 3 to 32 years, with a 96% retention rate. Cognitive development was analyzed and compared in children who later developed schizophrenia or recurrent depression as well as in healthy comparison subjects. Results: Children who developed adult schizophrenia exhibited developmental deficits (i.e., static cognitive impairments that emerge early and remain stable) on tests indexing verbal and visual knowledge acquisition, reasoning, and conceptualization. In addition, these children exhibited developmental lags (i.e., growth that is slower relative to healthy comparison subjects) on tests indexing processing speed, attention, visual-spatial problem solving ability, and working memory. These two premorbid cognitive patterns were not observed in children who later developed recurrent depression. Conclusions: These findings suggest that the origins of schizophrenia include two interrelated developmental processes evident from childhood to early adolescence (ages 7-13 years). Children who will grow up to develop adult schizophrenia enter primary school struggling with verbal reasoning and lag further behind their peers in working memory, attention, and processing speed as they get older. [ABSTRACT FROM AUTHOR]

Objective: It is unclear how many people in the community have obsessions and compulsions and associated levels of interference. It is also unknown what variables predict help-seeking for these syrup toms, whether they are developmentally stable, and whether they increase the risk of mental disorders, Method: The authors analyzed data from the prospective longitudinal Dune din study of an unselected birth cohort, The presence of obsessions and compulsions and mental disorders was assessed using the Diagnostic Interview Schedule (DIS) at ages 11, 26 and 32. Data on interference and help-seeking were obtained at ages 26 and 32. Results: Obsessions and compulsions were frequent in individuals with mental disorders other than obsessive-compulsive disorder (OCD) and among people without mental disorders, Even in the latter group. these symptoms caused significant interference. The presence of anxiety/depression and of obsessions (particularly aggressive and shameful thoughts), but not compulsions, was associated with help seeking. Harm/checking was the most prevalent symptom dimension. Symptom dimensions were temporally stable and associated with increased comorbidity. Obsessive-compulsive symptoms at age 11 predicted a high risk of an adult OCD diagnosis as well as elevated adult symptom dimensions. Conclusions: Obsessions and compulsions are common in the adult population. have their roots in childhood, and are associated with interference, risk for disorders, and help-seeking, Subclinical obsessions and compulsions should be taken into account in research, intervention. and DSM-V. [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]

Objective: Information about the psychiatric histories of adults with anxiety disorders was examined to further inform nosology and etiological/ preventive efforts. Method: The authors used data from a prospective longitudinal study of a representative birth cohort (N=1,037) from ages 11 to 32 years, making psychiatric diagnoses according to DSM criteria. For adults with anxiety disorders at 32 years, follow-back analyses ascertained first diagnosis of anxiety and other juvenile disorders. Results: Of adults with each type of anxiety disorder, approximately half had been diagnosed with a psychiatric disorder (one-third with an anxiety disorder) by age 15. The juvenile histories of psychiatric problems for adults with different types of anxiety disorders were largely nonspecific, partially reflecting comorbidity at 32 years. Histories of anxiety and depression were most common. There was also specificity. For example, adults with panic disorder did not have histories of juvenile disorders, whereas those with other anxiety disorders did. Adults with posttraumatic stress disorder had histories of conduct disorder, whereas those with other anxiety disorders did not. Adults with specific phobia had histories of juvenile phobias but not other anxiety disorders. Conclusions: Strong comorbidity between different anxiety disorders and lack of specificity in developmental histories of adults with anxiety disorders supports a hierarchical approach to classification, with a broad class of anxiety disorders having individual disorders within it. The early first diagnosis of psychiatric difficulties in individuals with anxiety disorders suggests the need to target research examining the etiology of anxiety disorders and preventions early in life. [ABSTRACT FROM AUTHOR]

Objective: Many depressed women have a history of antisocial behavior, but research into maternal depression has not ascertained if this has implications for children of depressed mothers. This study compared the developmental outcomes in and caregiving environments provided to children by depressed mothers with or without an antisocial history.Method: In the Environmental Risk Longitudinal Twin Study, a nationally representative study of 1,106 families, mothers were administered the Diagnostic Interview Schedule for Major Depressive Disorder and interviewed about their lifetime history of antisocial personality disorder symptoms. Mothers and teachers provided information regarding the children's behavior problems at 5 and 7 years of age. The authors assessed the quality of the caregiving environment through maternal reports and interviewer observations.Results: Compared with children of mothers with depression only, the children of depressed and antisocial mothers had significantly higher levels of antisocial behavior and rates of DSM-IV conduct disorder, even after the authors controlled for numbers of symptoms and chronicity of maternal major depressive disorder. The children of depressed and antisocial mothers were at an elevated risk of experiencing multiple caregiving abuses, including physical maltreatment, high levels of maternal hostility, and exposure to domestic violence.Conclusions: If one ignores the common co-occurrence of an antisocial history in depressed mothers, it may obscure the significantly elevated risks in children's development. Clinicians treating women's depression should be aware that children of depressed and antisocial mothers constitute a group at extremely high risk for early-onset psychopathology. [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]

Objective: This longitudinal study of a nonreferred, population-based sample tested the concurrent, convergent, and predictive validity of DSM-IV conduct disorder in children 4(1/2)-5 years of age.Method: In the Environmental Risk Longitudinal Twin Study, a representative birth cohort of 2,232 children, the children's mothers were interviewed and the teachers completed mailed questionnaires to assess the children's past 6-month conduct disorder symptoms. Children with three or more symptoms were diagnosed with conduct disorder, and a subset with five or more symptoms was diagnosed with "moderate-to-severe" conduct disorder.Results: The prevalence of conduct disorder and moderate-to-severe conduct disorder were 6.6% and 2.5%, respectively. Children diagnosed with conduct disorder were significantly more likely than comparison subjects to self-report antisocial behaviors, to behave disruptively during observational assessment, and to have risk factors known to be associated with conduct disorder in older children (effect sizes ranging from 0.26 to 1.24). Five-year-olds diagnosed with conduct disorder were significantly more likely than comparison subjects to have behavioral and educational difficulties at age 7. Increased risk for educational difficulties at age 7 persisted after control for IQ and attention deficit hyperactivity disorder diagnosis at age 5.Conclusions: Behavioral problems of preschool-age children meeting diagnostic criteria for conduct disorder should not be ignored. Appropriate intervention should be provided to prevent ongoing behavioral and academic problems. [ABSTRACT FROM AUTHOR]

The article contemplates on the worldwide prevalence of childhood attention deficit hyperactivity disorder (ADHD). The author stresses that a uniform prevalence rate worldwide shows that ADHD is not caused by the avarice of American psychiatric profession or by permissive Western culture. It has been noted that geographical variation will not offer fresh clues to the causation of ADHD.

Objective: The purpose of this study was to report the prevalence, risk, and implications of comorbidity between partner violence and psychiatric disorders.Method: Data were obtained from a representative birth cohort of 941 young adults through use of the Conflict Tactics Scales and Diagnostic Interview Schedule.Results: Half of those involved in partner violence had a psychiatric disorder; one-third of those with a psychiatric disorder were involved in partner violence. Individuals involved in severe partner violence had elevated rates of a wide spectrum of disorders.Conclusions: The findings support the importance of mental health clinicians screening for partner violence and treating victims and perpetrators before injury occurs. [ABSTRACT FROM AUTHOR]