Suchergebnisse

This study examined whether promotive factors (future expectations, family warmth, school attachment, and neighborhood cohesion) moderated relationships between community violence exposure and youth delinquency. Analyses were conducted using N = 2,980 sixth to eighth graders ( Mage = 12.48; 41.1% males) from a racially, ethnically, and socioeconomically diverse sample. After controlling for demographic factors, delinquency was positively associated with community violence exposure and inversely associated with each of the promotive factors. When interaction effects between all promotive factors and community violence exposure were examined simultaneously, only future expectations moderated the relationship between community violence exposure and delinquency. Specifically, community violence exposure had a weaker association with delinquency for youth reporting high versus low levels of future expectations. Results indicate that while promotive factors from family, school, and neighborhood domains are related to lower rates of delinquency, only future expectations served as a protective factor that specifically buffered youth from the risk effects of community violence exposure.

Molecular genetic research has provided some evidence for the association between depression and metabolic disorders. We sought to determine if molecular findings are reflected in twin analyses testing if common genetic and environmental risk factors contribute to the co-occurrence of diabetes and depression. Data to derive depression and diabetes were collected from 1,237 male-male twins who participated in the 2005 Vietnam Era Twin Study of Aging (VETSA). The 1,237 twins were comprised of 347 MZ pairs, 3 MZ singletons, 267 DZ pairs and 6 unpaired twins. Depression was defined as a score below 46 on the Short Form-36 mental component summary score. Diabetes was defined by self report, use of anti-diabetic medications and insulin. Twin models were fit to estimate the correlation of genetic and environmental contributions to depression and diabetes. Consistent with other studies these data support the association between depression and diabetes (OR = 1.7; 95%CI: 1.1–2.7). Genetic vulnerability accounted for 50% (95%CI: 32%–65%) of the variance in risk for depression and 69% (95%CI: 52%–81%) of the variance in risk for diabetes. The genetic correlation between depression and diabetes was r = 0.19 (95%CI: 0–0.46) and the non-shared environmental correlation was r = 0.09 (95% CI: 0–0.45). Overall there is little evidence that common genetic and environmental factors account for the co-occurrence of depression and diabetes in middle aged men. Further research in female twins and larger cohorts is warranted.

AbstractWe examined the contributions of genetic and environmental factors to body mass index (BMI) over approximately 28 years. Participants were 693 male, predominantly middle-class, twins (355 monozygotic, 338 dizygotic) from the Vietnam Era Twin Registry. The phenotypic correlation between age 20 and age 48 BMI was 0.52; the genetic correlation was 0.60. Most of the remaining variance at both times was accounted for by nonshared environmental factors. Since genetic factors are not perfectly correlated, this indicates that other genes affect BMI at one or both time points, leaving room for further exploration of the genetics of body mass stability. Mean BMI increased significantly from 22.7 (normal) to 27.8 (overweight). Overweight BMI at age 20 predicted midlife adult onset diabetes (adjusted odds ratio = 4.62, 95% CI 1.91 to 11.18), but not hypertension. Depending on one's vantage point, the results indicate elements of both stability and change in BMI. Very similar phenotypic and genetic correlations were observed over a similar time period in a WW II twin sample, but without the substantial mean increase in BMI. It seems unlikely that different genes influence BMI in the two cohorts. Therefore, we argue that nonshared environmental factors are probably primarily responsible for the secular increase in midlife BMI. Our results also provide prospective evidence that early excess BMI may have serious long-term health consequences, and that this risk is not limited to minorities or adults of lower socioeconomic status.

In this longitudinal study we examined the stability of general cognitive ability (GCA), as well as heterogeneity and genetic and environmental influences underlying individual differences in change. We investigated GCA from young adulthood through late midlife in 1,288 Vietnam Era Twin Study of Aging participants at ages ~20, ~56, and ~62 years. The correlations among the three occasions ranged from .73 to .85, reflecting substantial stability. The heritability was significant on each of the three occasions and ranged from .59 to .66. The influence of the shared environment was not significant at any of the ages. The genetic correlations across the three occasions ranged from .95 to .99 and did not differ significantly from 1.0. The nonshared environmental correlations ranged from .21 to .47. Latent growth curve analysis was applied to characterize trajectories over the 42 year period. Slope was significantly different from 0 and indicated that there was modest change over time. There was a significant genetic influence on initial level of GCA (h2 = .67), but not change (h2 = .23). Genetic factors primarily contribute to stability, while change reflects the influence of nonshared environmental influences. There was a significant negative correlation between initial level of GCA and change (r = −.31). Latent class growth analysis identified four trajectories. In general, the four groups followed parallel trajectories and were differentiated mainly by differences in AFQT performance level at the time of military induction.