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This study investigated the stability of genetic and environmental effects on the common liability to alcohol, tobacco, and cannabis dependence across adolescence and young adulthood. DSM-IV symptom counts from 2,361 adolescents were obtained using a structured diagnostic interview. Several sex-limited longitudinal common pathway models were used to examine gender differences in the magnitude of additive genetic (A), shared environment, and non-shared environmental effects over time. Model fitting indicated limited gender differences. Among older adolescents (i.e., age > 14), the heritability of the latent trait was estimated at 0.43 (0.05, 0.94) during the first wave and 0.63 (0.21, 0.83) during the second wave of assessment. A common genetic factor could account for genetic influences at both assessments, as well as the majority of the stability of SAV over time [rA = 1.00 (0.55, 1.00)]. These results suggest that early genetic factors continue to play a key role at later developmental stages.

Background: There is extensive evidence of statistical associations between family discord/ maladaptation and antisocial behaviour in the children, but questions remain on the extent to which the psychopathological risks are genetically or environmentally mediated., Methods: Twin pairs (N = 1,350), aged 8 to 16 years, in the general population-based Virginia Twin Study of Adolescent Behavioral Development were assessed using the Child and Adolescent Psychiatric Assessment interview administered separately to both twins and both parents. Structured interviews for parental lifetime psychiatric disorders were also administered to the mothers and fathers. Maternal reports on Olsson's Family Adaptability and Cohesiveness questionnaire and the Dyadic Adjustment Scale were used as indices of the family environment. A path analytical model based on an extended twin-family design was used to test hypotheses about parent offspring similarity for conduct disorder symptomatology., Results: Family discord and maladaptation, which intercorrelated at 0.63, were associated with a roughly two-fold increase in risk for conduct disorder symptomatology. When parental conduct disorder was included in the model the environmental mediation effect for family maladaptation remained, but that for family discord was lost., Conclusion: It is concluded that there is true environmental mediation from family maladaptation, operating as a shared effect, which accounts for 3.5 % of the phenotypic variance. The assumptions underlying this genetic research strategy are made explicit, together with its strengths and limitations.

Genetic studies have shown that both childhood and adult body mass index are substantially heritable. The evidence for shared family environmental influences is largely absent, even though there are clear indications that secular changes in energy expenditure have brought about a significant increase in the prevalence of obesity. This apparent inconsistency may be explained by the dual phenomena of the near-universality of access to environments that facilitate reductions in energy expenditure (e.g., TV as a recreational pastime), together with heritable individual differences in the response to or utilization of these environments. The impact of changes in nonshared environments on body weight can be estimated from biometrical genetical studies and is found to be both small and relatively short-lived. Genetic and environmental results from longitudinal studies are consistent with what is known about the changing distribution of adiposity during adulthood and clinical experience of the difficulty of maintaining behavioral-induced weight loss.

The genetic and environmental etiology of low general cognitive ability (g) during infancy and early childhood has not previously been investigated. The current study examined the genetic etiology of low cognitive ability at 14, 20, 24, and 36 months with twins from the MacArthur Longitudinal Twin Study. Low g groups were formed from the lowest 10th percentile at each age. Univariate probandwise concordance rates and DeFries-Fulker (J. C. DeFries & D. W. Fulker, 1985, 1988) multiple regression techniques suggest genetic etiology in low general cognitive ability groups. The stability of low general cognitive ability over time also appears to be primarily due to genetic factors. Although replication is necessary, these results suggest that the genetic etiology of low g during infancy and early childhood is at least as great as the heritability of g in the unselected population.

Genetic and environmental influences in the determination of individual differences in self-reported symptoms of separation anxiety (SAD), overanxious disorder (OAD), and manifest anxiety (MANX) were evaluated in children and adolescents for three age groups (8-10, 11-13, and 14-16). Symptom counts for SAD and OAD were assessed for 1,412 twin pairs using the children's version of the Child and Adolescent Psychiatric Assessment, and MANX scores were based on child report from the Revised Children's Manifest Anxiety Scales. Despite significant age and gender differences in thresholds of liability for child reports of symptoms of SAD and OAD, additive genetic and environmental effects could be set equal across age and gender for these variables. For MANX, however, the best-fitting model was a common effects sex-limitation model with estimates of heritability varying dependent upon age and gender. Parameter estimates from the ACE models of OAD and SAD showed that additive genetic variation was a necessary component in the explanation of individual differences in child-reported symptoms of OAD (h2 = .37) across gender, but does not appear to be a major contributor to the explanation of individual differences in symptoms of SAD reported by children. Shared environmental effects (c2 = .40) were found to play a moderate role for SAD but could be dropped from the model for OAD and from all of the age groups for MANX, although the parameter approached significance among 11 yr to 13-year-old males.

Few studies have employed genetically informative designs to study the causes of alcohol-related problems in nonclinical populations. We report patterns of alcohol abuse in a community-based U.S. volunteer sample of 3,049 female and 1,070 male twins aged 50 to 96. Significant gender and age effects were found for self-report measures of current and lifetime alcohol-related problems, with higher prevalence among males and lower frequency among older birth cohorts. Significant associations were found between severity of alcohol abuse (adapted from Feighner criteria) and age of drinking onset, parental history of alcohol problems and, among males, lower educational attainment. Model-fitting analyses based on data from 650 identical and 479 fraternal twin pairs indicate substantial family resemblance for a variety of definitions of lifetime alcohol abuse and alcohol problems. The median estimate of genetic variance across several definitions of alcohol problems was 38.5%, while that for shared environmental influence was 15.5%. Gender heterogeneity was not found for magnitude of genetic and environmental influences, but these comparisons were limited by low statistical power. Findings are discussed with reference to the literature on alcohol abuse among older adults and the genetic epidemiology of alcoholism.

A growing literature supports genetic contributions to familial resemblance for alcohol use characteristics, but few studies have focused on the mechanisms underlying alcohol use among older persons. We report patterns of alcohol use in a U.S. volunteer sample of 3,049 female and 1,070 male twins aged 50 to 96. Significant gender and age effects were found for self-report measures of current and lifetime alcohol use, with greater intake among males and current and lifetime abstinence more common among older participants. Comparisons with data obtained 4 years previously revealed high stability for quantity and frequency of alcohol consumption. Twin pairs with more frequent social contact tended to be more similar for lifetime and current alcohol use. Biometrical genetic modeling results indicate that use of alcohol is highly familial, with both genetic and shared environmental factors contributing to initiation of alcohol use among men and women. Among drinkers, however, the degree of twin resemblance for consumption behaviors is low to moderate and appears to be regulated by shared genes rather than shared environments. These data are consistent with a multidimensional process, suggesting that the determinants of whether one drinks in older age differ from those underlying how much or how often alcohol is consumed.

We review the conditions under which cross-sectional family data (e.g., data on twin pairs or adoptees and their adoptive and biological relatives) are informative about direction of causation. When two correlated traits have rather different modes of inheritance (e.g., family resemblance is determined largely by family background for one trait and by genetic factors for the other trait), cross-sectional family data will allow tests of strong unidirectional causal hypotheses (A and B are correlated "because of the causal influence of A on B" versus "because of the causal influence of B on A") and, under some conditions, also of the hypothesis of reciprocal causation. Possible sources of errors of inference are considered. Power analyses are reported which suggest that multiple indicator variables will be needed to ensure adequate power of rejecting false models in the presence of realistic levels of measurement error. These methods may prove useful in cases where conventional methods to establish causality, by intervention, by prospective study, or by measurement of instrumental variables, are unfeasible economically, ethically or practically.

Young male twins in The Netherlands and England completed the Jenkins Activity Survey (Dutch and English versions, respectively), a measure of Type A behavior. Separate model fitting analysis revealed a similar pattern of variance estimates and associated goodness of fit across the two countries. The data were then analyzed concurrently, with a scalar parameter included to account for differences in variance due to the disparity of the measurement scales. A model including additive genetic and individual environmental effects gave a good explanation to the data. The heritability estimate was 0.28. Models of social interaction and dominance explained the data even better, the former being preferred. The twins' parents were included in the analysis to examine population variation for Type A behavior intergenerationally. There was evidence for individual environmental experiences having a greater influence on Type A behavior in the older generation.

Four inbred strains of mice, DBA/2J, C57BL/10J, BALB/cJ, and SJL/J, were mated in a diallel cross. The cerebella of the F1 generation were examined for the presence (Type I) or absence (Type II) of an intraculminate fissure between vermian lobule IV and vermian lobule V (the ventral and dorsal lobules of the culmen). One strain (DBA/2J) consistently expressed the Type I pattern. Another strain (SJL/J) expressed predominantly the Type II pattern. The other two strains (C57BL/10J and BALB/cJ) and many of the hybrids exhibited variability in their expression of the foliation patterns. The results were analyzed using biometrical genetic procedures and showed significant additive and dominance genetic effects and a maternal effect. Correlations of these cerebellar anatomical variants with the development of behavior are discussed.

This report of a pilot study examines 29 pairs of twins from a population-based registry on whom four domains of schizotypy have been measured: personal interview using the Structured Interview for Schizotypy, self-report questionnaire formed from eight published self-report scales, attentional battery of eight individual tests, and root mean square error on smooth pursuit eye tracking. Analyzing the twins as individuals revealed two independent dimensions of clinically rated schizotypy (positive symptom schizotypy and negative symptom schizotypy) and two independent dimensions of self-rated schizotypy (positive trait schizotypy and trait anhedonia). Positive symptom schizotypy was highly correlated with positive trait schizotypy, but not with attentional dysfunction or eye-tracking error. By contrast, negative symptom schizotypy was significantly related to trait anhedonia, attentional dysfunction, and eye-tracking error. Correlations in monozygotic and dizygotic twins suggested that genetic factors were important in all four domains of schizotypy. Except for eye-tracking error, the results are more consistent with a dimensional than a "disease" model of schizotypy. Replication of these results with a larger group of subjects is needed.

Grayson (see the preceding paper) discusses some circumstances in which estimates of genetic and environmental parameters derived from the study of twins reared together may be biased and documents in those circumstances what the magnitude of the biases may be. As Grayson suggests, the points he makes have been made previously by various authors and issues such as the power to detect dominance have been analyzed at some length. This paper draws attention to some other sources of variation which Grayson does not consider but which have been considered by other writers and which might have somewhat different consequences for the estimation of shared environmental effects. The classical twin study has never been an end in itself, but it is the nucleus of a systematic genetic approach to the study of human behavior.