Adolescence is a time that can set the course of alcohol abuse later in life. Sensitivity to reward on multiple levels is a major factor in this development. We examined 736 adolescents from the IMAGEN longitudinal study for alcohol drinking during early (mean age=14.37) and again later (mean age=16.45) adolescence. Conducting structural equation modeling we evaluated the contribution of reward-related personality traits, behavior, brain responses and candidate genes. Personality seems to be most important in explaining alcohol drinking in early adolescence. However, genetic variations in ANKK1 (rs1800497) and HOMER1 (rs7713917) play an equal role in predicting alcohol drinking two years later and are most important in predicting the increase in alcohol consumption. We hypothesize that the initiation of alcohol use may be driven more strongly by personality while the transition to increased alcohol use is more genetically influenced.
BACKGROUND AND OBJECTIVE: Internet alcohol marketing is not well studied despite its prevalence and potential accessibility and attractiveness to youth. The objective was to examine longitudinal associations between self-reported engagement with Internet alcohol marketing and alcohol use transitions in youth.
METHODS: A US sample of 2012 youths aged 15 to 20 was surveyed in 2011. An Internet alcohol marketing receptivity score was developed, based on number of positive responses to seeing alcohol advertising on the Internet, visiting alcohol brand Web sites, being an online alcohol brand fan, and cued recall of alcohol brand home page images. We assessed the association between baseline marketing receptivity and both ever drinking and binge drinking (>/=6 drinks per occasion) at 1-year follow-up with multiple logistic regression, controlling for baseline drinking status, Internet use, sociodemographics, personality characteristics, and peer or parent drinking.
RESULTS: At baseline, ever-drinking and binge-drinking prevalence was 55% and 27%, respectively. Many (59%) reported seeing Internet alcohol advertising, but few reported going to an alcohol Web site (6%) or being an online fan (3%). Higher Internet use, sensation seeking, having family or peers who drank, and past alcohol use were associated with Internet alcohol marketing receptivity, and a score of 1 or 2 was independently associated with greater adjusted odds of initiating binge drinking (odds ratio 1.77; 95% confidence interval, 1.13-2.78 and odds ratio 2.15; 95% confidence interval, 1.06-4.37 respectively) but not with initiation of ever drinking.
CONCLUSIONS: Although high levels of engagement with Internet alcohol marketing were uncommon, most underage youths reported seeing it, and we found a prospective association between receptivity to this type of alcohol marketing and future problem drinking, making additional research and ongoing surveillance important.
BACKGROUND: The association between Parkinson's disease and lifestyle exposures such as smoking, coffee and alcohol consumption have been the focus of research for several decades, with varying and often conflicting results.
OBJECTIVE: This paper reviews the key features of observational studies investigating the relationship between alcohol drinking and PD risk, to determine potential sources of variability between the results.
METHODS: Relevant literature from 2000-2014 was systematically retrieved using three databases. Primary research articles were included if they reported a measure of association between quantity and frequency of alcohol intake and PD risk, and adjusted at least for the potential confounding factors of smoking and age.
RESULTS: Sixteen articles were identified. The seven case-control studies were more likely to report a weak protective association by level of alcohol consumption compared to the studies with prospective designs. Two studies reported the relationship between heavy (harmful to health) drinking and PD. There was weak evidence that associations varied by type of alcoholic beverage. Smoking may modify the association between alcohol intake and PD risk, however, the evidence does not support the theory that a confounder (such as an addiction-avoiding personality trait) produced the inverse associations between smoking, coffee and alcohol intake and PD risk. Methodological weaknesses of the studies, including selection and recall bias, residual confounding and lack of statistical power may in part account for their differences.
CONCLUSION: The weak association between alcohol drinking and PD risk was found in studies at greater risk of selection and recall bias.