Introduction: Adolescence and young adulthood are periods of continued biological and psychosocial maturation. Thus, there may be deleterious effects of consuming large quantities of alcohol on neural development and associated cognition during this time. The purpose of this mini review is to highlight neuroimaging research that has specifically examined the effects of binge and heavy drinking on adolescent and young adult brain structure and function.

Methods: We review cross-sectional and longitudinal studies of young binge and heavy drinkers that have examined brain structure (e.g., gray and white matter volume, cortical thickness, white matter microstructure) and investigated brain response using functional magnetic resonance imaging (fMRI).

Results: Binge and heavy-drinking adolescents and young adults have systematically thinner and lower volume in prefrontal cortex and cerebellar regions, and attenuated white matter development. They also show elevated brain activity in fronto-parietal regions during working memory, verbal learning, and inhibitory control tasks. In response to alcohol cues, relative to controls or light-drinking individuals, binge and heavy drinkers show increased neural response mainly in mesocorticolimbic regions, including the striatum, anterior cingulate cortex (ACC), hippocampus, and amygdala. Mixed findings are present in risky decision-making tasks, which could be due to large variation in task design and analysis.

Conclusions: These findings suggest altered neural structure and activity in binge and heavy-drinking youth may be related to the neurotoxic effects of consuming alcohol in large quantities during a highly plastic neurodevelopmental period, which could result in neural reorganization, and increased risk for developing an alcohol use disorder (AUD).

Published in Drinking Patterns

OBJECTIVE: A recent study suggested that college students who combined alcohol and energy drinks were more likely than students who consumed only alcohol to drive when their blood alcohol concentration (BAC) was higher than the .08% limit and to choose to drive despite knowing they had too much alcohol to drive safely. This study sought to replicate those findings with a larger sample while also exploring additional variables related to impaired driving.

METHOD: College students (N = 549) completed an anonymous online survey to assess differences in drinking and driving-related behaviors between alcohol-only users (n = 281) and combined alcohol-energy drink users (n = 268).

RESULTS: Combined users were more likely than alcohol-only users to choose to (a) drive when they perceived they were over the .08% BAC limit (35.0% vs. 18.1%, p < .001), (b) drive despite knowing they had too much alcohol to drive safely (36.3% vs. 17.0%, p < .001), and (c) be a passenger when they knew the driver had too much alcohol to drive safely (44.1% vs. 23.6%, p < .001). Combined users were significantly more likely (p < .001) to report indicators of high-risk alcohol use, such as larger number of drinks consumed, number of days drinking, number of days drunk, number of heavy episodic drinking episodes, greatest number of drinks on one occasion, and average hours of consumption.

CONCLUSIONS: Combined use of alcohol and energy drinks may place drinkers at greater risk when compared with those who consume only alcohol. College students in this sample who combined alcohol and energy drinks were more likely to participate in high-risk driving behaviors than those who consumed only alcohol.

Published in Drinking Patterns

BACKGROUND: Adolescent selective intervention programs for alcohol have focused on the identification of youth at risk as a function of personality and associated alcohol-related cognitions. Research into the role of personality, drinking motivations, and alcohol-related outcomes has generally focused exclusively on motives to drink. We expand on this literature by focusing on both motives to drink and motives not to drink across time from adolescence to early adulthood in a community sample.

METHODS: Using 3 waves of data from 3 cohorts from the Rutgers Health and Human Development Project (n = 1,380; 49.4% women), we modeled the influence of baseline alcohol consumption, disinhibition (DIS), and harm avoidance (ages 15, 18, and 21 years) on drinking motives and motives not to drink 3 years later (ages 18, 21, and 24 years) and alcohol use and drinking-related problems 7 years subsequently (ages 25, 28, and 31 years).

RESULTS: Path analytic models were relatively invariant across cohort. Across cohorts, DIS and baseline alcohol consumption related to later positive reinforcement drinking motives, but less consistency was found for the prediction of negative reinforcement motives to drink. While positive reinforcement motives were associated with greater alcohol consumption and problems 7 years later, negative reinforcement motives were generally associated with problems alone. Positive reinforcement motives for drinking mediated relations between baseline consumption and later consumption. However, results were mixed when considering DIS as a predictor and drinking problems as an outcome. Similarly, personality and baseline consumption related to later motives not to drink and such motives predicted subsequent alcohol-related problems. However, mediation was not generally supported for pathways through motives to abstain.

CONCLUSIONS: The results of this study replicate and extend previous longitudinal findings with youth and add to the growing literature on motivations not to engage in alcohol use.

OBJECTIVE: Epidemiological studies indicate that higher bone mass is associated with moderate alcohol consumption in postmenopausal women. However, the underlying cellular mechanisms responsible for the putative beneficial effects of alcohol on bone are unknown. Excessive bone turnover, combined with an imbalance whereby bone resorption exceeds bone formation, is the principal cause of postmenopausal bone loss. This study investigated the hypothesis that moderate alcohol intake attenuates bone turnover after menopause.

METHODS: Bone mineral density was determined by dual-energy x-ray absorptiometry in 40 healthy postmenopausal women (mean +/- SE age, 56.3 +/- 0.5 y) who consumed alcohol at 19 +/- 1 g/day. Serum levels of the bone formation marker osteocalcin and the resorption marker C-terminal telopeptide (CTx) were measured by immunoassay at baseline (day 0) and after alcohol withdrawal for 14 days. Participants then consumed alcohol and were assayed on the following morning.

RESULTS: Bone mineral density at the trochanter and total hip were positively correlated to the level of alcohol consumption. Serum osteocalcin and CTx increased after abstinence (4.1 +/- 1.6%, P = 0.01 and 5.8 +/- 2.6%, P = 0.02 compared with baseline, respectively). Osteocalcin and CTx decreased after alcohol readministration, compared with the previous day (-3.4 +/- 1.4%, P = 0.01 and -3.5 +/- 2.1%, P = 0.05, respectively), to values that did not differ from baseline (P > 0.05).

CONCLUSIONS: Abstinence from alcohol results in increased markers of bone turnover, whereas resumption of alcohol reduces bone turnover markers. These results suggest a cellular mechanism for the increased bone density observed in postmenopausal moderate alcohol consumers. Specifically, the inhibitory effect of alcohol on bone turnover attenuates the detrimental skeletal consequences of excessive bone turnover associated with menopause.

Published in Osteoporosis
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