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Background: Effective policies that can reduce alcohol use behaviors and impaired driving among young people at a population level are needed. Graduated driver licensing (GDL) laws increase the driving privileges of young novice drivers as they age and gain more driving experience. In this study, we seek to determine the effects of GDLs on risky driving behaviors of youth and to assess if GDLs have an unintended effect on underage drinking behaviors., Methods: We utilized 2000 to 2013 data on 12th grade students from the Monitoring the Future (MTF) study, an ongoing, annual national survey (since 1975) that studies the substance use behaviors of adolescents, as well as data on GDL laws obtained via the Insurance Institute for Highway Safety (IIHS). We conducted a series of regular logistic regression models that included fixed effects for year and state, and adjusted for demographic characteristics, school characteristics, and other state alcohol policies., Results: Total weighted sample size was 129,289 12th graders. Past month alcohol use and binge drinking (i.e., ≥5 drinks on one occasion) in the past 2 weeks were 45 and 26%, respectively. Seventeen percent of respondents reported riding with a driver who drank alcohol. Nearly 12% reported driving in the past 2 weeks after drinking alcohol, and 7% reported driving after binge drinking. Over half of the students lived in a state with a "good" GDL law. The logistic regression models suggest a link between restrictive GDL policies and a reduction of alcohol use behaviors and risky driving behaviors among youth., Conclusions: Our findings indicate that the effects of GDLs extend beyond driving-related risks and into other drinking-related behaviors that pose immediate or delayed health risks for young people. We speculate that GDLs may dictate social norms and expectations for youth risk behaviors, and should be maximized throughout the United States., (Copyright © 2016 by the Research Society on Alcoholism.)

A coding variant in alcohol dehydrogenase 1B (ADH1B) (rs1229984) that leads to the replacement of Arg48 with His48 is common in Asian populations and reduces their risk for alcoholism, but because of very low allele frequencies the effects in European or African populations have been difficult to detect. We genotyped and analyzed this variant in three large European and African-American case-control studies in which alcohol dependence was defined by the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria, and demonstrated a strong protective effect of the His48 variant (odds ratio (OR) 0.34, 95% confidence interval (CI) 0.24, 0.48) on alcohol dependence, with genome-wide significance (6.6 × 10(-10)). The hypothesized mechanism of action involves an increased aversive reaction to alcohol; in keeping with this hypothesis, the same allele is strongly associated with a lower maximum number of drinks in a 24-hour period (lifetime), with P=3 × 10(-13). We also tested the effects of this allele on the development of alcoholism in adolescents and young adults, and demonstrated a significantly protective effect. This variant has the strongest effect on risk for alcohol dependence compared with any other tested variant in European populations.

Background: Research suggests that individuals who start drinking at an early age are more likely to subsequently develop alcohol dependence. Twin studies have demonstrated that the liability to age at first drink and to alcohol dependence are influenced by common genetic and environmental factors, however, age at first drink may also environmentally mediate increased risk for alcohol dependence. In this study, we examine whether age at first drink moderates genetic and environmental influences, via gene x environment interactions, on DSM-IV alcohol dependence symptoms., Methods: Using data on 6,257 adult monozygotic and dizygotic male and female twins from Australia, we examined the extent to which age at first drink (i) increased mean alcohol dependence symptoms and (ii) whether the magnitude of additive genetic, shared, and nonshared environmental influences on alcohol dependence symptoms varied as a function of decreasing age. Twin models were fitted in Mx., Results: Risk for alcohol dependence symptoms increased with decreasing age at first drink. Heritable influences on alcohol dependence symptoms were considerably larger in those who reported an age at first drink prior to 13 years of age. In those with later onset of alcohol use, variance in alcohol dependence was largely attributable to nonshared environmental variance (and measurement error). This evidence for unmeasured gene x measured environment interaction persisted even when controlling for the genetic influences that overlapped between age at first drink and alcohol dependence symptoms., Conclusions: Early age at first drink may facilitate the expression of genes associated with vulnerability to alcohol dependence symptoms. This is important to consider, not only from a public health standpoint, but also in future genomic studies of alcohol dependence.