A Danish Twin Study of Schizophrenia Liability: Investigation from Interviewed Twins for Genetic Links to Affective Psychoses and for Cross-Cohort Comparisons.

We studied schizophrenia liability in a Danish population-based sample of 44 twin pairs (13 MZ, 31 DZ, SS plus OS) in order to replicate previous twin study findings using contemporary diagnostic criteria, to examine genetic liability shared between schizophrenia and other disorders, and to explore whether variance in schizophrenia liability attributable to environmental factors may have decreased with successive cohorts exposed to improvements in public health. ICD-10 diagnoses were determined by clinical interview. Although the best-fitting, most parsimonious biometric model of schizophrenia liability specified variance attributable to additive genetic and non-shared environmental factors, this model did not differ significantly from a model that also included non-additive genetic factors, consistent with recent interview-based twin studies. Schizophrenia showed strong genetic links to other psychotic disorders but much less so for the broader category of psychiatric disorders in general. We also observed a marginally significant decline in schizophrenia variance attributable to environmental factors over successive Western European cohorts, consistent perhaps with improvements in diagnosis and in prenatal and perinatal care and with a secular decline in the prevalence of schizophrenia in that region.

Mortality predictors in a 60-year follow-up of adolescent males: exploring delinquency, socioeconomic status, IQ, high-school drop-out status, and personality.

OBJECTIVE: To examine whether socioeconomic status (SES), high school (HS) completion, IQ, and personality traits that predict delinquency in adolescence also could explain men's delinquency-related (Dq-r) mortality risk across the life span. METHODS: Through a 60-year Social Security Death Index (SSDI) follow-up of 1812 men from Hathaway's adolescent normative Minnesota Multiphasic Personality Inventory (MMPI) sample, we examined mortality risk at various ages and at various levels of prior delinquency severity. We examined SES (using family rent level), HS completion, IQ, and MMPI indicators simultaneously as mortality predictors and tested for SES (rent level) interactions with IQ and personality. RESULTS: We ascertained 418 decedents. Dq-r mortality peaked between ages 45 years to 64 years and continued through age 75 years, with high delinquency severity showing earlier and higher mortality risk. IQ and rent level failed to explain Dq-r mortality. HS completion robustly conferred mortality protection through ages 55 years and 75 years, explained IQ and rent level-related risk, but did not fully explain Dq-r risk. Dq-r MMPI scales, Psychopathic Deviate, and Social Introversion, respectively, predicted risk for and protection from mortality by age 75 years, explaining mortality risk otherwise attributable to delinquency. Wiggins' scales also explained Dq-r mortality risk, as Authority Conflict conferred risk for and Social Maladjustment and Hypomania conferred protection from mortality by age 75 years. CONCLUSIONS: HS completion robustly predicts mortality by ages 55 years and 75 years. Dq-r personality traits predict mortality by age 75 years, accounting, in part, for Dq-r mortality.

The etiology of mathematical and reading (dis)ability covariation in a sample of Dutch twins.

The genetic etiology of mathematical and reading (dis)ability has been studied in a number of distinct samples, but the true nature of the relationship between the two remains unclear. Data from the Netherlands Twin Register was used to determine the etiology of the relationship between mathematical and reading (dis)ability in adolescent twins. Ratings of mathematical and reading problems were obtained from parents of over 1500 twin pairs. Results of bivariate structural equation modeling showed a genetic correlation around .60, which explained over 90% of the phenotypic correlation between mathematical and reading ability. The genetic model was the same for males and females.

Trauma, PTSD, and the course of severe mental illness: an interactive model.

Traumatic life events, as defined by DSM-IV, are common among persons with severe mental illnesses (SMI) such as schizophrenia. Limited evidence suggests concomitantly high rates of posttraumatic stress disorder (PTSD) in this population. However, conceptual models do not exist for understanding the interactions between trauma, PTSD, and SMI. We propose a model, which is an extension of the stress-vulnerability model, in which PTSD is hypothesized to mediate the negative effects of trauma on the course of SMI. Our model posits that PTSD influences psychiatric disorders both directly, through the effects of specific PTSD symptoms including avoidance, overarousal, and re-experiencing the trauma, and indirectly, through the effects of common correlates of PTSD such as retraumatization, substance abuse, and difficulties with interpersonal relationships. We discuss the evidence supporting this model, and consider several intervening variables that are hypothesized to moderate the proposed relationships between PTSD and SMI, including social support, coping and competence, and antisocial personality disorder. Theoretical and clinical implications of the model are considered, as well as several methodological and nosological issues. We conclude with a brief discussion of directions for future research aimed at evaluating components of the model.

Marriage and genetic variation across the lifespan: not a steady relationship?

The prevalence of marriage varies across the lifespan, as does its importance to reproduction and the nurturance of children. We examined genetic and environmental influences on self-reported marriage at each decade from 20 through 70 years of age, using data collected for the Duke Dementia Study, a followed-up subset of the World War II Veteran Twin Registry. Genetic influences best fit a common factor model, supplemented by another, age-specific, genetic factor at age 30. Broad heritability increased from age 20 through 40, and then decreased to zero by ages 60 and 70. A longitudinal Cholesky model best described environmental influences on marriage across the lifespan. Shared environmental factors showed their greatest influence at age 20, no influence at 30 or 40 years, and then, reappeared with influence at 60 and 70. Variance due to error and unique environmental influences increased steadily to age 50 years and then declined slightly.

The Washington University Twin Study of alcoholism.

Genetic contributions to the liability to develop alcoholism in males of Northern and Western European ancestry are well-established. However, questions remain concerning the role of genetic variation in the etiology of alcoholism among non-white populations, among women, and the possibility of etiological heterogeneity in subtypes of alcoholism. The answers to these questions are needed to help define phenotypes for molecular genetic studies searching for QTLs for alcoholism. Twins from 295 pairs were consecutively ascertained at inpatient and outpatient psychiatric and alcohol treatment facilities in St. Louis, MO in 1981-1986. Probands and willing cotwins were evaluated by structured psychiatric interviews, psychometric assessment, and lifetime treatment records. One hundred fifty-four probands met criteria for alcohol abuse/dependence (AAD), including twins from 45 MZ, 50 same-sex DZ, and 59 opposite-sex pairs. Twin-pair resemblance was evaluated for AAD and alcohol dependence (AD), as well as for subsets defined by gender, patterns of comorbidity, ethnic background, and clinical features. Among males, heritability of AAD and AD was substantial, with little evidence for common environmental contributions to family resemblance. Pair resemblance among females was also substantial, but similar for MZ and DZ pairs, yielding near-zero heritability estimates. However, based on these sample sizes, the sex differences were not statistically significant. The results confirm prior studies of strong genetic influences on alcoholism in males, but suggest lower genetic influence in females. Power to test other sources of heterogeneity was limited, but the results suggest no evidence for higher heritability for male early onset alcoholism or for alcoholism with comorbid antisocial personality.