Different Characteristics and Heritabilities of Alcohol Use Disorder Classes: A Population-Based Swedish Study.

AIMS: The aims of the present study are to identify alcohol use disorder (AUD) classes among a population-based Swedish sample, determine if these classes differ by variables known to be associated with AUD and determine whether some AUD classes have stronger genetic influences than others. METHODS: A latent class analysis (LCA), based on types of registrations, was conducted on Swedish individuals with an AUD registration born between 1960 and 1990 (N = 184,770). These classes were then validated using demographics; patterns of comorbidity with drug abuse, psychiatric disorders and criminal behavior; and neighborhood-level factors, i.e. peer AUD and neighborhood deprivation. The degree of genetic and environmental influence was also investigated. RESULTS: The best-fit LCA had four classes: (a) outpatient/prescription, characterized by a mix of outpatient medical and prescription registrations, (b) low-frequency inpatient, characterized entirely by inpatient medical registrations, with the majority of individuals having one AUD registration, (c) high-frequency mixed, characterized by a mix of all four registration types, with the majority having four or more registrations and (d) crime, characterized almost entirely by criminal registrations. The highest heritability for both males and females was found for Class 3 (61% and 65%, respectively) and the lowest for Class 1 (20% for both), with shared environmental influences accounting for 10% or less of the variance in all Classes. CONCLUSIONS: Using comprehensive, nationwide registry data, we showed evidence for four distinct, meaningful classes of AUD with varying degrees of heritability.

Geographic proximity is associated with transmission of suicidal behaviour among siblings.

OBJECTIVE: The aim of this study was to clarify the role of 'contagion', or social transmission, in risk of suicidal behaviour (SB) among siblings. METHODS: We followed Swedish sibling pairs until one of them (S1; N = 111,848) was registered for a suicide attempt or completion. We tested the effect of geographic proximity between siblings on risk of a first SB registration of S1's sibling (S2). To control for familial confounding, we conducted complementary analyses of sibling trios (N = 701), comparing risk in different siblings as a function of their respective proximity to S1. RESULTS: The best-fitting model across sibling pairs included an effect of distance between siblings (HR = 0.96, 95% CI = 0.93-0.99). Hazard ratios declined quickly up to 25 km and largely stabilized beyond 150 km. Across all pairs, a larger age difference between siblings was associated with reduced SB risk (HR = 0.96 95% CI = 0.93-0.98). Findings were consistent within the sibling trios. CONCLUSIONS: Consistent with the concept of suicide contagion, risk of suicidal behaviour subsequent to a sibling's suicide completion or attempt is higher as a function of sibling closeness. These findings are robust to potentially confounding familial factors.

The role of parent and offspring sex on risk for externalizing psychopathology in offspring with parental alcohol use disorder: a national Swedish study.

PURPOSE: The substantial literature showing that offspring of parents with alcohol use disorder (AUD) is at increased risk for externalizing psychopathology rarely examines the differential effects of parental and offspring sex. This literature also has other important limitations, such as modest sample sizes and use of unrepresentative samples. Using a large, nationwide Swedish sample, we aim to investigate the roles of parental and offspring sex in externalizing psychopathology among offspring with parental AUD. METHODS: AUD diagnosis and externalizing measures were obtained from national registries. Associations between outcomes and parental AUD were examined using logistic regressions. Parental and offspring sex effects were examined with interaction terms. RESULTS: Risks for externalizing disorders were increased in sons and daughters with parental AUD, with significant differences between sons and daughters for criminal behavior; maternal AUD had a greater impact than paternal AUD (regardless of offspring sex), but having two parents with AUD increased risk for all outcomes substantially more than having one parent; and maternal AUD increased risk of drug abuse for daughters more than sons, while paternal AUD increased risk of AUD and criminal behavior for sons more than daughters. CONCLUSIONS: Offspring of parents with AUD are at increased risk for externalizing psychopathology. Maternal and paternal AUD differentially affected sons' vs. daughters' risks for AUD, drug abuse, and criminal behavior. The transmission of psychopathology within the externalizing spectrum appears to have sex-specific elements.

The joint impact of cognitive performance in adolescence and familial cognitive aptitude on risk for major psychiatric disorders: a delineation of four potential pathways to illness.

How do joint measures of premorbid cognitive ability and familial cognitive aptitude (FCA) reflect risk for a diversity of psychiatric and substance use disorders? To address this question, we examined, using Cox models, the predictive effects of school achievement (SA) measured at age 16 and FCA-assessed from SA in siblings and cousins, and educational attainment in parents-on risk for 12 major psychiatric syndromes in 1 140 608 Swedes born 1972-1990. Four developmental patterns emerged. In the first, risk was predicted jointly by low levels of SA and high levels of FCA-that is a level of SA lower than would be predicted from the FCA. This pattern was strongest in autism spectrum disorders and schizophrenia, and weakest in bipolar illness. In these disorders, a pathologic process seems to have caused cognitive functioning to fall substantially short of familial potential. In the second pattern, seen in the internalizing conditions of major depression and anxiety disorders, risk was associated with low SA but was unrelated to FCA. Externalizing disorders-drug abuse and alcohol use disorders-demonstrated the third pattern, in which risk was predicted jointly by low SA and low FCA. The fourth pattern, seen in eating disorders, was directly opposite of that observed in externalizing disorders with risk associated with high SA and high FCA. When measured together, adolescent cognitive ability and FCA identified four developmental patterns leading to diverse psychiatric disorders. The value of cognitive assessments in psychiatric research can be substantially increased by also evaluating familial cognitive potential.

Polygenic risk for severe psychopathology among Europeans is associated with major depressive disorder in Han Chinese women.

BACKGROUND: Previous studies have demonstrated that several major psychiatric disorders are influenced by shared genetic factors. This shared liability may influence clinical features of a given disorder (e.g. severity, age at onset). However, findings have largely been limited to European samples; little is known about the consistency of shared genetic liability across ethnicities. METHOD: The relationship between polygenic risk for several major psychiatric diagnoses and major depressive disorder (MDD) was examined in a sample of unrelated Han Chinese women. Polygenic risk scores (PRSs) were generated using European discovery samples and tested in the China, Oxford, and VCU Experimental Research on Genetic Epidemiology [CONVERGE (maximum N = 10 502)], a sample ascertained for recurrent MDD. Genetic correlations between discovery phenotypes and MDD were also assessed. In addition, within-case characteristics were examined. RESULTS: European-based polygenic risk for several major psychiatric disorder phenotypes was significantly associated with the MDD case status in CONVERGE. Risk for clinically significant indicators (neuroticism and subjective well-being) was also associated with case-control status. The variance accounted for by PRS for both psychopathology and for well-being was similar to estimates reported for within-ethnicity comparisons in European samples. However, European-based PRS were largely unassociated with CONVERGE family history, clinical characteristics, or comorbidity. CONCLUSIONS: The shared genetic liability across severe forms of psychopathology is largely consistent across European and Han Chinese ethnicities, with little attenuation of genetic signal relative to within-ethnicity analyses. The overall absence of associations between PRS for other disorders and within-MDD variation suggests that clinical characteristics of MDD may arise due to contributions from ethnicity-specific factors and/or pathoplasticity.

Transmission of alcohol use disorder across three generations: a Swedish National Study.

BACKGROUND: While risk for alcohol use disorder (AUD) is correlated in twins, siblings and parent-offspring pairs, we know little of how this syndrome is transmitted across three generations. METHOD: We examined 685 172 individuals born in Sweden from 1980 to 1990 with four grandparents, and both parents alive in 1980. AUD was assessed in all these individuals from nationwide medical, criminal and pharmacy registries. RESULTS: AUD was stably transmitted across three generations. Parent-child and grandparent-grandchild tetrachoric correlations equaled +0.25 and +0.12, respectively. Grandchild AUD risk did not vary as a function of the sex of the parent or grandparent. However, from grandparents and parents, transmission to grandchildren was stronger in same-sex than opposite-sex pairs. Compared with a grandchild with unaffected parents and grandparents, risk for AUD with a grandparent but no parent affected, a parent but no grandparent affected or both affected increased approximately 70% and 3 and 4-fold, respectively. Grandchildren with ⩾2 grandparents affected had a 40% greater AUD risk than those with only one affected. Tetrachoric correlations for AUD between offspring and great-aunts/uncles, and aunts/uncles equaled +0.06 and +0.13, respectively. CONCLUSIONS: The transmission of AUD in Sweden across three generations is relatively stable. An orderly pattern of resemblance is seen with correlations declining by approximately 50% between first and second, and second and third-degree relatives. While the transmission of risk from affected male and female relatives does not differ, we find consistent evidence for greater resemblance in same-sex v. opposite-sex across generational pairs of relatives.

Prediction of drug abuse recurrence: a Swedish National Study.

BACKGROUND: Relapse from drug abuse (DA) is common, but has rarely been studied in general population samples using a wide range of objective predictors. METHOD: Using nationwide registries, we ascertained 44 523 subjects first registered for DA between the ages of 15 and 40 in 1998 to 2004 and followed for 8 years. We predicted relapse in subjects defined as a second DA registration. We also predicted DA relapse in relative pairs concordant for DA but discordant for relapse. RESULTS: In multivariate regression analyses, the strongest predictors for relapse were prior criminal behavior, male sex, being on social welfare, low school achievement, prior alcoholism, and a high-risk father. A risk index trained from these analyses on random split-halves demonstrated a risk ratio of 1.11 [95% confidence intervals (CIs) 1.10-1.11] per decile and an ROC value of 0.70 (0.69-0.71). Co-relative analyses indicated that a modest proportion of this association was causal, with the remainder arising from familial confounders. A developmental structural equation model revealed a complex interviewing of risk pathways to DA with three key mediational hubs: low educational attainment, early age at first registration, and being on social welfare. CONCLUSIONS: In a general population sample, using objective registry information, DA relapse is substantially predictable. However, the identified risk factors may not be valid targets for interventions because many index familial risk and may not impact causally on probability of relapse. Risk for DA relapse may reflect an inter-weaving, over developmental time, of genetic-temperamental vulnerability, indices of externalizing behaviors and social factors reflecting deprivation.

The genealogy of the clinical syndrome of mania: signs and symptoms described in psychiatric texts from 1880 to 1900.

In 1800, mania was conceptualized as an agitated psychotic state. By 1900, it closely resembled its modern form. This paper reviews the descriptions of mania in Western psychiatry from 1880 to 1900, when Kraepelin was training and developing his concept of manic-depressive illness. Psychiatric textbooks published 1900-1960 described 22 characteristic manic symptoms/signs the presence of which were recorded in 25 psychiatric textbooks and three other key documents published 1880-1900. Descriptions of mania in these nineteenth century textbooks closely resembled those in the twentieth century, recording a mean (s.d.) of 15.9 (2.3) and 17.0 (2.3) of the characteristic symptoms, respectively (p = 0.12). The frequency with which individual symptoms were reported was substantially correlated in these two periods (r = +0.64). Mendel's 1881 monograph, Kraepelin's first description of mania in 1883 and the entry for mania in Tuke's Dictionary of Psychological Medicine (1892) described a mean (s.d.) of 19 (1.7) of these characteristic symptoms. These descriptions of mania often contained phenomenologically rich descriptions of euphoria, hyperactivity, grandiosity, flight of ideas, and poor judgment. They also emphasized several features not in DSM criteria including changes in character, moral standards and physical appearance, and increased sense of humor and sexual drive. Fifteen authors described key symptoms/signs of mania most reporting elevated mood, motoric hyperactivity and accelerated mental processes. By 1880, the syndrome of mania had been largely stabilized in its modern form. In the formation of his concept of manic-depressive illness, Kraepelin utilized the syndrome of mania as described in the psychiatric community in which he was trained.

Diagnostic and genetic overlap of three common mental disorders in structured interviews and health registries.

OBJECTIVE: To investigate whether diagnostic data from structured interviews, primary care and specialist care registries on major depressive disorder (MDD), anxiety disorders (AD) and alcohol use disorder (AUD) identify the same individuals, yield comparable comorbidity estimates and reflect the same genetic influences. METHODS: Registry data from primary and specialist care were available for 11 727 twins and diagnostic interview data for 2271 of these. We used logistic regression analyses and biometric modelling to investigate the overlap between the data sources. RESULTS: Most individuals meeting diagnostic criteria at interview were not registered with a corresponding diagnosis. The rates of registration were higher for MDD (36% in primary care and 15% in specialist care) and AD (21% and 18%) than for AUD (3% and 7%). Comorbidity estimated as odds ratios, but not as polychoric correlations, was higher in the registries than in the interviews. Genetic influences on the disorders were highly correlated across data sources (median r = 0.81), bordering unity for MDD and AD. CONCLUSION: Prevalence and comorbidity estimates differ between registries and population-based assessment. Nevertheless, diagnoses from health registries reflect the same genetic influences as common mental disorders assessed in the general population, indicating generalizability of aetiological factors across data sources.

Robust symptom networks in recurrent major depression across different levels of genetic and environmental risk.

BACKGROUND: Genetic risk and environmental adversity-both important risk factors for major depression (MD)-are thought to differentially impact on depressive symptom types and associations. Does heterogeneity in these risk factors result in different depressive symptom networks in patients with MD? METHODS: A clinical sample of 5784 Han Chinese women with recurrent MD were interviewed about their depressive symptoms during their lifetime worst episode of MD. The cases were classified into subgroups based on their genetic risk for MD (family history, polygenic risk score, early age at onset) and severe adversity (childhood sexual abuse, stressful life events). Differences in MD symptom network structure were statistically examined for these subgroups using permutation-based network comparison tests. RESULTS: Although significant differences in symptom endorsement rates were seen in 18.8% of group comparisons, associations between depressive symptoms were similar across the different subgroups of genetic and environmental risk. Network comparison tests showed no significant differences in network strength, structure, or specific edges (P-value > 0.05) and correlations between edges were strong (0.60-0.71). LIMITATIONS: This study analyzed depressive symptoms retrospectively reported by severely depressed women using novel statistical methods. Future studies are warranted to investigate whether similar findings hold in prospective longitudinal data, less severely depressed patients, and men. CONCLUSIONS: Similar depressive symptom networks for MD patients with a higher or lower genetic or environmental risk suggest that differences in these etiological influences may produce similar symptom networks downstream for severely depressed women.

The genealogy of major depression: symptoms and signs of melancholia from 1880 to 1900.

How deep are the historical roots of our concept of major depression (MD)? I showed previously that psychiatric textbooks published in 1900-1960 commonly described 18 characteristic depressive symptoms/signs that substantially but incompletely overlapped with the current DSM (Diagnostic and Statistical Manual of Mental Disorders) MD criteria. I here expand that inquiry to the key years of 1880-1900 during which our major diagnostic categories of manic-depressive illness (MDI) and dementia praecox were developed. I review the symptoms of depression/melancholia in 28 psychiatric textbooks and 8 other relevant documents from this period including monographs, reviews and the first portrayal of melancholia Kraepelin in 1883. Descriptions of melancholia in the late nineteenth and twentieth century textbooks closely resembled each other, both reporting a mean of 12.4 characteristic symptoms, and emphasizing core features of mood change and alterations in cognitive content and psychomotor behavior. The detailed monographs, reviews and the early description of Kraepelin were more thorough, reporting a mean of 16.6 of these characteristic symptoms. These nineteenth century texts often contained phenomenologically rich descriptions of changes in mood and cognition, loss of interest and anhedonia and emphasized several features not in DSM including changes in volition/motivation, posture/facial expression and derealization/depersonalization. In the early nineteenth century, melancholia was often defined primarily by delusions or as the initial phase of a unitary psychosis transitioning to mania and then dementia. By 1880, the concept of depression as an independent mood disorder with characteristic symptoms/signs and a good prognosis had stabilized. Kraepelin incorporated this syndrome into his diagnostic concept of MDI, changing its name to 'Depressive States', but did not alter its underlying nature or clinical description.

Contributions of Genes and Environment to Developmental Change in Alcohol Use.

The precise nature of how genetic and environmental risk factors influence changes in alcohol use (AU) over time has not yet been investigated. Therefore, the aim of the present study is to examine the nature of longitudinal changes in these risk factors to AU from mid-adolescence through young adulthood. Using a large sample of male twins, we compared five developmental models that each makes different predictions regarding the longitudinal changes in genetic and environmental risks for AU. The best-fitting model indicated that genetic influences were consistent with a gradual growth in the liability to AU, whereas unique environmental risk factors were consistent with an accumulation of risks across time. These results imply that two distinct processes influence adolescent AU between the ages of 15-25. Genetic effects influence baseline levels of AU and rates of change across time, while unique environmental effects are more cumulative.

The association between psychotic experiences and disability: results from the WHO World Mental Health Surveys.

OBJECTIVE: While psychotic experiences (PEs) are known to be associated with a range of mental and general medical disorders, little is known about the association between PEs and measures of disability. We aimed to investigate this question using the World Mental Health surveys. METHOD: Lifetime occurrences of six types of PEs were assessed along with 21 mental disorders and 14 general medical conditions. Disability was assessed with a modified version of the WHO Disability Assessment Schedule. Descriptive statistics and logistic regression models were used to investigate the association between PEs and high disability scores (top quartile) with various adjustments. RESULTS: Respondents with PEs were more likely to have top quartile scores on global disability than respondents without PEs (19.1% vs. 7.5%; χ2  = 190.1, P < 0.001) as well as greater likelihood of cognitive, social, and role impairment. Relationships persisted in each adjusted model. A significant dose-response relationship was also found for the PE type measures with most of these outcomes. CONCLUSIONS: Psychotic experiences are associated with disability measures with a dose-response relationship. These results are consistent with the view that PEs are associated with disability regardless of the presence of comorbid mental or general medical disorders.

Do DSM-5 Section II personality disorders and Section III personality trait domains reflect the same genetic and environmental risk factors?

BACKGROUND: DSM-5 includes two conceptualizations of personality disorders (PDs). The classification in Section II is identical to the one found in DSM-IV, and includes 10 categorical PDs. The Alternative Model (Section III) includes criteria for dimensional measures of maladaptive personality traits organized into five domains. The degree to which the two conceptualizations reflect the same etiological factors is not known. METHODS: We use data from a large population-based sample of adult twins from the Norwegian Institute of Public Health Twin Panel on interview-based DSM-IV PDs and a short self-report inventory that indexes the five domains of the DSM-5 Alternative Model plus a domain explicitly targeting compulsivity. Schizotypal, Paranoid, Antisocial, Borderline, Avoidant, and Obsessive-compulsive PDs were assessed at the same time as the maladaptive personality traits and 10 years previously. Schizoid, Histrionic, Narcissistic, and Dependent PDs were only assessed at the first interview. Biometric models were used to estimate overlap in genetic and environmental risk factors. RESULTS: When measured concurrently, there was 100% genetic overlap between the maladaptive trait domains and Paranoid, Schizotypal, Antisocial, Borderline, and Avoidant PDs. For OCPD, 43% of the genetic variance was shared with the domains. Genetic correlations between the individual domains and PDs ranged from +0.21 to +0.91. CONCLUSION: The pathological personality trait domains, which are part of the Alternative Model for classification of PDs in DSM-5 Section III, appears to tap, at an aggregate level, the same genetic risk factors as the DSM-5 Section II classification for most of the PDs.

DSM disorders and their criteria: how should they inter-relate?

While the changes in psychiatric diagnosis introduced by Diagnostic and Statistical Manual third edition (DSM-III) have had major benefits to the field of psychiatry, the reification of its diagnostic criteria and the widespread adoption of diagnostic literalism have been problematic. I argue that, at root, these developments can be best understood by contrasting two approaches to the relationship between DSM disorders and their criteria. In a constitutive relationship, criteria definitively define the disorder. Having a disorder is nothing more than meeting the criteria. In an indexical relationship, the criteria are fallible indices of a disorder understood as a hypothetical, tentative diagnostic construct. I trace the origins of the constitutive model to the philosophical theory of operationalism. I then examine a range of historical and empirical results that favor the indexical over the constitutive position including (i) evidence that individual criteria for DSM-III were selected from a broader pool of possible symptoms/signs, (ii) revisions of DSM have implicitly assumed an indexical criteria-disorder relationship, (iii) the indexical position allows DSM criteria to be wrong and misdiagnose patients while such a result is incoherent for a constitutive model, an implausible position, (iv) we assume an indexical criteria-scale relationships for many personality and symptom measures commonly used in psychiatric practice and research, and (v) empirical studies suggesting similar performance for DSM and non-DSM symptoms for major depression. I then review four reasons for the rise of the constitutive position: (i) the 'official' nature of the DSM criteria, (ii) the strong investment psychiatry has had in the DSM manual and its widespread use and success, iii) lack of a clear pathophysiology for our disorders, and (iv) the absence of informative diagnostic signs of minimal clinical importance. I conclude that the constitutive position is premature and reflects a conceptual error. It assumes a definitiveness and a literalism about the nature of our criteria that is far beyond our current knowledge. The indexical position with its tentativeness and modesty accurately reflects the current state of our field.

Clarifying the role of neuroticism in suicidal ideation and suicide attempt among women with major depressive disorder.

BACKGROUND: Prior research consistently demonstrates that neuroticism increases risk for suicidal ideation, but the association between neuroticism and suicidal behavior has been inconsistent. Whereas neuroticism is recommended as an endophenotype for suicidality, the association of neuroticism with attempted suicide warrants clarification. In particular, prior research has not distinguished between correlates of attempted suicide, correlates of suicidal ideation, and correlates of comorbid psychopathology. METHODS: The present study used the CONVERGE study, a sample of 5864 women with major depressive disorder (MD) and 5783 women without MD throughout China. Diagnoses, suicidal ideation, and attempted suicide were assessed with the Composite International Diagnostic Interview (CIDI). Neuroticism was assessed with the neuroticism portion of the Eysenck Personality Questionnaire. RESULTS: Results replicate prior findings on the correlates of suicidal ideation, particularly elevated neuroticism among individuals who report prior suicidal ideation. Moreover, as compared with individuals who reported having experienced only suicidal ideation, neuroticism was associated with decreased likelihood of having attempted suicide. CONCLUSIONS: The association of neuroticism with suicidality is more complicated than has been previously described. Whereas neuroticism increases risk for suicidal ideation, neuroticism may decrease risk for a suicide attempt among individuals with suicidal ideation. These results have implications for the assessment of risk for a suicide attempt among individuals who report suicidal ideation and addresses prior discordant findings by clarifying the association between neuroticism and attempted suicide.

David Skae and his nineteenth century etiologic psychiatric diagnostic system: looking forward by looking back.

The Kraepelinian syndromal approach to diagnosis taken by DSM-III and its successors, which defines disorders by their clinical phenomenon, has come under rising criticism with increasing calls for an etiologically based nosology. The relative virtues of a syndromal versus etiologic psychiatric nosology have actually been debated within our field for a long time. To deepen and historically contextualize our current discussion, I review in detail the proposal for etiologic diagnostic systems for insanity by David Skae (1814-1873). While his proposal was intuitive and appealing to some, others questioned its viability and utility pointing out a number of potential problems in its implementation that remain relevant today. Something critical might be lost for psychiatric disorders, they argued, if mental symptoms were removed from diagnostic criteria. Etiologically based diagnoses work best for mono-causal disorders and those where the causes all operate on the same scientific level. However, psychiatric disorders are highly multifactorial with a wide diversity of risk factors spread across biological, psychological and social-environmental domains so identification of a particular cause on which to base diagnoses would be difficult. Not only do individual risk factors contribute to many different disorders but most disorders are influenced by many etiologic factors. With respect to causes and disorders, psychiatry is characterized by a 'many to many' relationship which would make an etiologic nosologic system inherently problematic. Finally, causes and effects can be devilishly difficult to distinguish for psychiatric illness and, while clinically based nosologies aid in differential diagnosis, etiologically based system might not operate similarly.

The association between personality disorders with alcohol use and misuse: A population-based twin study.

BACKGROUND: A clearer understanding of the etiological overlap between DSM-IV personality disorders (PDs) and alcohol use (AU) and alcohol use disorder (AUD) is needed. To our knowledge, no study has modeled the association between all 10 DSM-IV PDs and lifetime AU and AUD. The aim of the present study is to identify which PDs are most strongly associated with the phenotypic, genetic, and environmental risks of lifetime AU and AUD, and to determine if these associations are stable across time. METHODS: Participants were Norwegian twins assessed at two waves. At Wave 1, 2801 twins were assessed for all 10 DSM-IV PD criteria, lifetime AU, and DSM-IV AUD criteria. At Wave 2, six of the 10 PDs were again assessed along with AU and AUD among 2393 twins. Univariate and multiple logistic regressions were run. Significant predictors were further analyzed using bivariate twin Cholesky decompositions. RESULTS: Borderline and antisocial PD criteria were the strongest predictors of AU and AUD across the two waves. Despite moderate phenotypic and genetic correlations, genetic variation in these PD criteria explained only 4% and 3% of the risks in AU, and 5% to 10% of the risks in AUD criteria, respectively. At Wave 2, these estimates increased to 8% and 23% for AU, and 17% and 33% for AUD. CONCLUSIONS: Among a large Norwegian twin sample, borderline and antisocial PD criteria were the strongest predictors of the phenotypic and genotypic liability to AU and AUD. This effect remained consistent across time.

Genetic and environmental influences on last-year major depression in adulthood: a highly heritable stable liability but strong environmental effects on 1-year prevalence.

BACKGROUND: This study seeks to clarify the contribution of temporally stable and occasion-specific genetic and environmental influences on risk for major depression (MD). METHOD: Our sample was 2153 members of female-female twin pairs from the Virginia Twin Registry. We examined four personal interview waves conducted over an 8-year period with MD in the last year defined by DSM-IV criteria. We fitted a structural equation model to the data using classic Mx. The model included genetic and environmental risk factors for a latent, stable vulnerability to MD and for episodes in each of the four waves. RESULTS: The best-fit model was simple and included genetic and unique environmental influences on the latent liability to MD and unique wave-specific environmental effects. The path from latent liability to MD in the last year was constant over time, moderate in magnitude (+0.65) and weaker than the impact of occasion-specific environmental effects (+0.76). Heritability of the latent stable liability to MD was much higher (78%) than that estimated for last-year MD (32%). Of the total unique environmental influences on MD, 13% reflected enduring consequences of earlier environmental insults, 17% diagnostic error and 70% wave-specific short-lived environmental stressors. CONCLUSIONS: Both genetic influences on MD and MD heritability are stable over middle adulthood. However, the largest influence on last-year MD is short-lived environmental effects. As predicted by genetic theory, the heritability of MD is increased substantially by measurement at multiple time points largely through the reduction of the effects of measurement error and short-term environmental risk factors.

The role of marriage in criminal recidivism: a longitudinal and co-relative analysis.

AIMS: Marriage is associated with a reduced rate of criminal recidivism, but the underlying mechanisms have only partly been elucidated. We seek to clarify the nature of the association between marriage and recidivism and how that relationship may be moderated as a function of gender, deviance of spouse, a history of violence and familial risk. METHOD: We utilise a longitudinal cohort design consisting of Swedish men (n = 239 328) and women (n = 72 280), born between 1958 and 1986, who were convicted of at least one crime before age 20 and were not married prior to age 20. The analyses used Cox regression with marriage as a time-dependent covariate. We also perform co-relative analyses in sibling and first cousin pairs. RESULTS: Marriage after a first crime substantially reduces risk of recidivism in both males (hazard ratio (HR) with key covariates and 95% confidence intervals 0.55, 0.53-0.57) and females (HR = 0.38, 0.34-0.42), although the effect is stronger in females. Marriage to a deviant spouse increases recidivism rates in males. In males, a history of violent criminality and high familial risk, respectively, decrease and increase sensitivity to the protective effect of marriage on recidivism. Consistent with a causal effect of marriage on recidivism, marriage was associated with a decline in risk for criminal relapse comparable with that in the population in both male-male sibling pairs (raw HR = 0.53, 0.45-0.62) and cousin pairs (HR = 0.55, 0.47, 0.65) concordant for prior convictions. CONCLUSIONS: The protective effect of marriage on risk for criminal recidivism is likely largely causal and is of importance in both males and females. Those at high familial risk for criminal behaviour are more sensitive to the protective effects of marriage.