INTRODUCTION: Age of first drink is a key risk factor for adolescent high-risk alcohol use. The current study examined whether speed of escalation from first drink to first intoxication is an additional risk factor, and whether these two factors are associated with binge and high-intensity drinking among adolescents.
METHODS: Data collected in 2005-2017 from a nationally-representative sample of 11,100 U.S. 12th grade students participating in the Monitoring the Future study were coded to indicate grade of first drink, grade of first intoxication, and speed of escalation from first drink to first intoxication. Logistic regression models estimated bivariate and multivariable odds of past 2-week binge (5+ drinks in a row) and high-intensity (10+ drinks in a row) drinking in 12th grade.
RESULTS: Of those who reported intoxication by 12th grade, almost 60% reported first drunkenness in the same grade in which they first drank. The likelihoods of 12th grade binge and high-intensity drinking were significantly associated with both grade of first drink and speed of escalation to intoxication. Past two-week high-intensity drinking prevalence was 17.4% among those with immediate (same-grade) escalation from first drink to first intoxication; 15.8% among those with a 1-grade delay, and 12.6% among those with a 2+ grade delay to intoxication.
CONCLUSIONS: The majority of students escalate quickly from having their first drink to being intoxicated for the first time. Both earlier age of first drink and a faster escalation from first drink to first intoxication are important indicators of binge and high-intensity drinking risk among adolescents.
AIM: This paper systematically reviews the literature on the effects of prenatal alcohol exposure on early child development from birth to 5 years with the aim to synthesize the developmental outcomes associated with prenatal alcohol exposure, and inform further research to improve our knowledge of the manifestations of prenatal alcohol exposure.
METHODS: Electronic databases (MEDLINE, Psych INFO, and Psych ARTICLES) were searched to find papers on the developmental outcomes of prenatal alcohol exposure in neonates, infants and toddlers and pre-school aged children. Studies were selected based on participants self-reporting alcohol consumption during pregnancy (either prospectively or retrospectively) and/or children being diagnosed with FASD based on a standardized assessment that includes a dysmorphology examination. The search was limited to peer-reviewed, English language studies involving human subjects, up to 5.5 years old.
RESULTS: Out of the 1,684 titles screened, a total of 71 papers were identified as relevant and included in this review. The majority of studies were prospective longitudinal studies. A range of assessment modalities (or tools) was used to determine neurodevelopmental outcomes of prenatal exposure to alcohol in the age group under review, the most frequently described being the Bayley Scales of Infant and Toddler Development (BSID) (n = 19). Studies varied in terms of the dose, frequency, and timing of alcohol consumption during pregnancy and methodology used to assess alcohol consumption. Findings demonstrate extensive evidence for poor global developmental outcomes in children prenatally exposed to alcohol, particularly with moderate to severe levels of prenatal alcohol exposure.
CONCLUSION: The outcomes related to lower levels of prenatal alcohol exposure as well as outcomes in specific developmental domains, are poorly understood. Further research should aim to clarify the more subtle or less easily measurable manifestations of prenatal alcohol exposure on early development when the potential for greatest impact of interventions is highest.
BACKGROUND: Some of the previously reported health benefits of low-to-moderate alcohol consumption may derive from health status influencing alcohol consumption rather than the opposite. We examined whether health status changes influence changes in alcohol consumption, cessation included.
METHODS: Data came from 571 current drinkers aged >/=60 years participating in the Seniors-ENRICA cohort in Spain. Participants were recruited in 2008-2010 and followed-up for 8.2 years, with four waves of data collection. We assessed health status using a 52-item deficit accumulation (DA) index with four domains: functional, self-rated health and vitality, mental health, and morbidity and health services use. To minimise reverse causation, we examined how changes in health status over a 3-year period (wave 0-wave 1) influenced changes in alcohol consumption over the subsequent 5 years (waves 1-3) using linear/logistic regression, as appropriate.
RESULTS: Compared with participants in the lowest tertile of DA change (mean absolute 4.3% health improvement), those in the highest tertile (7.8% worsening) showed a reduction in alcohol intake (beta: -4.32 g/day; 95% CI -7.00 to -1.62; p trend=0.002) and were more likely to quit alcohol (OR: 2.80; 95% CI 1.54 to 5.08; p trend=0.001). The main contributors to decreasing drinking were increased functional impairment and poorer self-rated health, whereas worsening self-rated health, onset of diabetes or stroke and increased prevalence of hospitalisation influenced cessation.
CONCLUSIONS: Health deterioration is related to a subsequent reduction and cessation of alcohol consumption contributing to the growing evidence challenging the protective health effect previously attributed to low-to-moderate alcohol consumption.
PURPOSE: To study the association between coffee and alcoholic beverage consumption and alcoholic liver disease mortality.
METHODS: In total, 219,279 men and women aged 30-67 years attended cardiovascular screening in Norway from 1994 to 2003. Linkage to the Cause of Death Registry identified 93 deaths from alcoholic liver disease. Coffee consumption was categorized into four levels: 0, 1-4, 5-8, and greater than or equal to 9 cups/d and alcohol consumption as 0, greater than 0 to less than 1.0, 1.0 to less than 2.0, and greater than or equal to 2.0 units/d, for beer, wine, liquor, and total alcohol consumption.
RESULTS: The hazard ratios per one category of consumption were 2.06 (95% confidence interval 1.62-2.61), 0.68 (0.46-1.00), and 2.54 (1.92-3.36) for beer, wine, and liquor, respectively. Stratification at 5 cups/d (the mean) revealed a stronger association between alcohol consumption and alcoholic liver disease at less than 5 versus 5 or more cups/d. With less than 5 cups/d, 0 alcohol units/d as reference, the hazard ratio reached to 25.5 (9.2-70.5) for greater than or equal to 2 units/d, whereas with greater than or equal to 5 cups/d, it reached 5.8 (1.9-17.9) for greater than or equal to 2 units/d. A test for interaction was significant (P = .01).
CONCLUSIONS: Coffee and wine consumption were inversely associated with alcoholic liver disease death. Total alcohol consumption was adversely associated with alcoholic liver disease mortality and the strength of the association varied with the level of coffee consumption.