Hazardous drinking is prevalent among college students, yet few seek treatment. Anxiety sensitivity AS is one factor with relevance to drinking. Yet, there are no known estimates of the prevalence of elevated AS among hazardous drinkers. The current study sought to estimate the prevalence of elevated AS among hazardous drinking college students and to examine relations between AS and hazardous drinking. Data from 1257 students Mage = 22.08; 80.4 % female; 76.8 % racial/ethnic minorities was employed. Approximately one third (30.7 %) of the sample met criteria for hazardous drinking. Among hazardous drinkers, 77.5 % had clinically elevated AS; similar rates were evidenced across sex and race/ethnicity. Hazardous drinkers reported significantly greater AS scores than moderate drinkers and non-drinkers (p < 0.001; η2 = 0.09). Those with elevated AS were more than three times more likely to be hazardous drinkers (p < 0.001). Among hazardous drinkers, those with elevated AS had more severe drinking levels (p < 0.001; Cohen's d=0.07) as well as greater likelihood, number, and disturbance related to use of other substances (p's from <0.001-0.005; Cohen's d's from 0.01 to 0.02). Findings from this study suggest that most hazardous drinkers have elevated AS, and that elevated AS is associated with a substantially higher likelihood of being a hazardous drinker. Hazardous drinkers with elevated AS report more severe drinking and other substance use than those with normative AS. There may be practical clinical benefit of implementing focus on AS to reduce hazardous drinking in college settings.

Ethanol (EtOH) consumption is a primary health risk worldwide, which generally starts during adolescence in a binge pattern (i.e., the episodic consumption of high amounts). Binge EtOH consumption can lead to modifications of the innate and adaptive immune responses, including fever. The present study evaluated the febrile response that was induced by lipopolysaccharide (LPS) and prostaglandins E2 (PGE2) and the mechanisms of thermoregulation in adolescent rats that were exposed to EtOH in a binge-like pattern. Male Wistar rats were treated with an intraperitoneal (i.p.) injection of EtOH or saline on postnatal days (PND) 25, 26, 29, 30, 33, 34, 37, and 38. On PND 51, they received a pyrogenic challenge with LPS (i.p.) or PGE2 (intracerebroventricular) to induce a febrile response. Interscapular brown adipose tissue (BAT) mass and uncoupling protein (UCP) activity in isolated mitochondria were evaluated on PND 51. The rats were then subjected to cold challenges to analyze adaptive thermogenesis. Intermittent EtOH exposure during adolescence impaired the LPS- and PGE2-induced febrile response 12 days after the end of EtOH exposure. Ethanol exposure decreased interscapular BAT mass, oxygen consumption, and UCP activity in isolated mitochondria, resulting in an impairment in thermogenesis at 5 °C. No morphological changes in BAT were observed. These findings indicate that binge-like EtOH exposure during adolescence impairs thermoregulation by reducing BAT mass and function. This reduction may last for a prolonged period of time after the cessation of EtOH exposure and may affect both cold defenses and the febrile response during the development of infectious diseases.