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Previous research links risky sexual behavior (RSB) to externalizing problems and to substance use, but little research has been conducted on relationships between internalizing problems (INT) and RSB. The current study addresses that literature gap, using both a twin sample from Colorado (N = 2567) and a second twin sample from Minnesota (N = 1131) in attempt to replicate initial results. We explored the hypothesis that the latent variable INT would be more strongly associated with the latent variable RSB for females than for males, examining relationships between INT and RSB via phenotypic confirmatory factor analysis and multivariate twin analyses. We found a small but significant phenotypic association between the latent variables. However, despite using two large twin samples, limited power restricted our ability to identify the genetic and environmental mechanisms underlying this association. Our sex differences hypothesis was not fully supported in either sample and requires further investigation. Our findings illustrate the complexity of the relationship between internalizing problems and risky sexual behavior. [ABSTRACT FROM AUTHOR]

Aims: To estimate the effect of recreational legalization on cannabis use frequency and sources of variance across legal environments. Design: Longitudinal discordant twin and gene–environment interaction models in twins recruited from birth records and assessed prospectively. Setting: The United States, including states with different recreational cannabis policies before and after 2014, when recreational cannabis was first legalized. Participants: Two longitudinal, prospectively assessed samples of American twins aged 24–47 (n = 1425 in legal states, n = 1996 in illegal states), including 111 monozygotic pairs discordant for residence. Measurements Current cannabis use frequency (measured continuously and ordinally) was the primary outcome, and the predictor was recreational status of cannabis (legal/illegal) in the participant's state of residence at the time of assessment. Covariates include age, sex and cannabis use frequency prior to 2014. Findings Accounting for pre‐2014 use, residents of legal states used cannabis more frequently than residents of illegal states (b = 0.21, P = 8.08 × 10−5). Comparing 111 pairs of monozygotic twins discordant for residence confirmed the effect (b = 0.18, P = 0.014). There was inconclusive evidence for genetic influences on cannabis use frequency that were specific to the legal environment [χ2 = 2.9 × 10−9, degrees of freedom (d.f.) = 1, P > 0.999]. Existing genetic influences were moderated by the legal environment, as the genetic correlation between marijuana use before and after legalization was lower in states that legalized (rgenetic = 0.24) compared with states that did not (rgenetic = 0.78, Pdifference = 0.016). Conclusions: In the United States, there appears to be a ~ 20% average increase in cannabis use frequency attributable to recreational legalization, consistent across increasingly rigorous designs. In addition, the heritability of cannabis use frequency appears to be moderated by legalization. [ABSTRACT FROM AUTHOR]

Externalizing psychopathology in early adolescence is a highly heritable risk factor for drug use, yet how it relates to marijuana use development is not well-characterized. We evaluate this issue in independent twin samples from Colorado (N = 2608) and Minnesota (N = 3630), assessed from adolescence to early adulthood. We used a biometric latent growth model of marijuana use frequency with data from up to five waves of assessment from ages 14 to 30, to examine change in marijuana use and its relationship with a factor model of adolescent externalizing psychopathology. The factor structure of adolescent externalizing psychopathology was similar across samples, as was the association between that common factor and early marijuana use (Minnesota r = 0.67 [0.60, 0.75]; Colorado r = 0.69 [0.59, 0.78]), and increase in use (Minnesota r = 0.18 [0.10, 0.26]; Colorado r = 0.20 [0.07, 0.34]). Early use was moderately heritable in both samples (Minnesota h2 = 0.57 [0.37, 0.79]; Colorado h2 = 0.42 [0.14, 0.73]). Increase in use was highly heritable in Minnesota (h2 = 0.82 [0.72, 0.88]), less so in Colorado (h2 = 0.22 [0.01, 0.66]), and shared environmental effects were larger in Colorado (c2 = 0.55 [0.14, 0.83]) than Minnesota (c2 = 0 [0, 0.06]). We found moderate genetic correlations between externalizing psychopathology and early use in both samples. Finally, additional analyses in the Minnesota sample indicated that marijuana use decreased during the late 20s. This decline is strongly heritable (h2 = 0.73 [0.49, 0.91]) and moderately negatively correlated with adolescent externalizing psychopathology (r = − 0.41 [− 0.54, − 0.28]). Adolescent externalizing psychopathology is genetically correlated with change in late adolescent marijuana use (late teens, early 20s), as well as maintenance of use in early adulthood (late 20 s) even after controlling for the effects of early use. [ABSTRACT FROM AUTHOR]

Background: Research indicates that early tobacco initiation increases risk for dependence, but despite this, early initiation is associated with slower transitions to escalated tobacco use. In contrast to these findings, other studies suggest that rapid escalated tobacco use is associated with increased dependence outcomes.Methods: Our sample was comprised of 5668 twins (2834 twin-pairs, mean age: 26.89, s.d = 4.42, 53.67% female, 57.69% monozygotic) from Colorado and Minnesota twin cohorts. We assessed the associations between 1) age of tobacco initiation and the speed of transitions (latency) to tobacco problem use and dependence and the associations between 2) age of initiation and latencies to tobacco problem use and dependence with tobacco dependence symptom severity. To further understand the etiological unfolding of these processes, we conducted univariate twin models and causally informative co-twin control models.Results: After adjustment for covariates, we found that early tobacco initiation was associated with a slower transition from initiation to problem use but a faster transition from problem use to dependence. Additionally, we found that earlier initiation and faster transitions to tobacco problem use and dependence predicted greater tobacco dependence severity within twin pairs (consistent with causal influences). The contribution of shared genetic and environmental factors was also evident for these relationships.Conclusions: Our study further disentangles the role of early initiation with transition times to tobacco problem use and dependence. In addition to common risk factors, we found potential causal roles for early tobacco initiation and rapid escalated tobacco use with increased risk for tobacco dependence severity. [ABSTRACT FROM AUTHOR]