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Studies have suggested both adverse and protective associations of obesity with depressive symptoms. We examined the contribution of environmental and heritable factors in this association. Participants were same-sex twin pairs from two population-based twin cohort studies, the Older Finnish Twin Cohort (n = 8,215; mean age = 44.1) and the US Midlife Development in the United States (MIDUS; n = 1,105; mean age = 45.1). Body mass index (BMI) was calculated from self-reported height and weight. Depressive symptoms were assessed using Beck's Depression Inventory (BDI; Finnish Twin Cohort), and by negative and positive affect scales (MIDUS). In the Finnish Twin Cohort, higher BMI was associated with higher depressive symptoms in monozygotic (MZ) twins (B = 2.01, 95% CI = 1.0, 3.0) and dizygotic (DZ) twins (B = 1.17, 0.5, 1.9) with BMI >22. This association was observed in within-pair analysis in DZ twins (B = 1.47, CI = 0.4, 2.6) but not in within-pair analysis of MZ twins (B = 0.03, CI = -1.9, 2.0). Consistent with the latter result, a bivariate genetic model indicated that the association between higher BMI and higher depressive symptoms was largely mediated by genetic factors. The results of twin-pair analysis and bivariate genetic model were replicated in the MIDUS sample. These findings suggest an association between obesity and higher depressive symptoms, which is largely explained by shared heritable biological mechanisms. [ABSTRACT FROM AUTHOR]

BackgroundClinically ascertained reports suggest that boys and girls with attention deficit hyperactivity disorder (ADHD) may differ from each other in their vulnerability to substance use problems.MethodA total of 1545 Finnish adolescents were assessed for DSM-IV-based ADHD symptoms by their parents and classroom teachers using standardized rating scales at age 11–12 years. At age 14, substance use disorders and psychiatric co-morbidity were assessed with the Semi-Structured Assessment for the Genetics of Alcoholism, providing DSM-III-R/DSM-IV diagnoses for Axis I disorders. At age 17.5, substance use was assessed by multi-item questionnaire.ResultsAlthough baseline ADHD symptoms were less common among females, they were more predictive of adverse substance use outcomes once conduct disorder and previous substance use were controlled for. Only in females were baseline ADHD symptoms significant predictors of alcohol abuse and dependence and illicit drug use at age 14. At the age of 17.5, parents' reports of inattentiveness and hyperactivity were significant predictors for frequent alcohol use in both sexes, but they were more predictive of frequent alcohol and illicit drug use in girls. Impulsivity in teachers' ratings predicted frequent alcohol use and illicit drug use in boys. Parental reports of inattentiveness in their 11-/12-year-old daughters were a consistent predictor for illicit drug use across adolescence.ConclusionsInattentiveness and hyperactivity may be more predictive of alcohol use disorders and maladaptive patterns of alcohol and illicit drug use among girls than boys. The importance of these behavioural symptoms should be assessed further in the community, as they could jeopardize adolescents' successful transitioning into adult roles. [ABSTRACT FROM PUBLISHER]

We analyzed the association between mean height and old age cognition in two Nordic twin cohorts with different childhood living conditions. The cognitive performance of 4720 twin individuals from Denmark (mean age 81.6 years, SD = 4.59) and Finland (mean age 74.4 years, SD = 5.26) was measured using validated cognitive screens. Taller height was associated with better cognitive performance in Finland (β-estimates 0.18 SD/10cm, p value < .001, for men and 0.13 SD, p = .008, for women), but this association was not significant in Denmark (β-estimates 0.0093 SD, p value = .16, for men and 0.0075 SD, p value = .016, for women) when adjusted for age and education/social class. Among Finnish participants higher variability of cognitive performance within shorter height quintiles was observed. Analysis using gene-environment interaction models showed that environmental factors exerted a greater impact on cognitive performance in shorter participants, whereas in taller participants' it was explained mainly by genetic factors. Our results suggest that shorter participants with childhood adversity are more vulnerable to environmental risk factors for cognitive impairment. [ABSTRACT FROM PUBLISHER]

We enrolled more than 3500 same-sex twinsfrom 5 consecutive Finnish birth cohorts into a longitudinal study as each cohort reached age 16. Twins completed the Psychopathic Deviate (Pd) Scale of the Minnesota Multiphasic Personality Inventory at baseline, Sensation Seeking Scale items as each cohort reached age 17, and later, at average ages 18.5 and 25, the Rutgers Alcohol Problem Index (RAPI). Using raw maximum likelihood estimation, we fit a Cholesky model to the 4 variables assessed at 4 ages across the 4 twin types; we estimated genetic and environmental influences on the stability of alcohol problems across development and the genetic and environmental contributions to predictive correlations between adolescent personality and later alcohol-related behavior problems. With one exception, the phenotypic, genetic, and environmental correlations were very similar for males and females. The exception was that the lagged associations of Pd and RAPI reflect a higher genetic correlation among males than females and a higher environmental correlation among females than males. Our analyses suggest that developmental changes underlying variation in alcohol problems from late adolescence to early adulthood differ for males and females. In males, the main change is decreased variation due to shared environmental effects; the magnitude of genetic effects is stable over time, and the high genetic correlation, .95, suggests that the same genetic influences are important at both ages. Among females, in contrast, genetic influences decline in magnitude from age 18 to 25, and at least part of the genetic effect evident at age 25 differs from the genetic effect evident at age 18. [ABSTRACT FROM AUTHOR]