Research participants who conceal or fabricate information to gain admission to and participate in clinical research can undermine the reliability and reproducibility of study findings, and may contribute to false conclusions. This review identifies strategies for improving recruitment, assessment, and study implementation, and advances specific approaches that may be helpful to alcohol and drug researchers for reducing the impact of deceptive participants. It is time for each of us to assume greater responsibility for mitigating this source of research contamination.

Proposed hypothetical model of enhanced PEth formation in advanced liver disease. As liver disease progresses, the enzymatic activity of alcohol dehydrogenase and aldehyde dehydrogenase is decreased [1]. As a consequence oxidative metabolism of ethanol may be impaired yielding higher blood ethanol levels being shunted towards non-oxidative PEth pathway via phospholipase D (PLD) [2]. PLD has a greater affinity for ethanol than its usual substrate phosphatidylcholine [3], suggesting the possibility of intrinsic PEth formation in erythrocytes [4].

The induction of Cytochrome P4502E1 (CYP2E1) by chronic ethanol consumption results in the production of reactive oxygen species (ROS) which leads to lipidperoxidation and finally to the generation of carcinogenic etheno DNA-adducts. Since the intensity of CYP2E1 induction due to alcohol correlates with hepatic fibrosis and etheno DNA-adduct formation, CYP2E1 may be a driving force in alcohol mediated fibrogenesis and carcinogenesis. Thus, inhibition of hepatic CYP2E1 may be protective for alcoholic liver disease.

When alcohol is consumed with other fluids, as occurs in many drinking situations, blood alcohol content (BAC) early in the drinking interval is more closely related to alcohol concentration in the stomach (ratio of alcohol to total fluid) than it is to the amount of alcohol consumed. This nonlinear relationship between alcohol intake and BAC may have important implications for predicting the degree of alcohol-induced impairment since brain alcohol content mirrors BAC.

The potential therapeutic benefit of a ketogenic diet in managing alcohol withdrawal symptoms during detoxification was investigated. Rats fed either ketogenic or regular diets were administered ethanol or water orally, and abstinence symptoms were rated after the last alcohol administration. Maintenance on a ketogenic diet caused a significant decrease in the alcohol withdrawal symptoms ‘rigidity’ and ‘irritability’, suggesting that a ketogenic diet may be a novel approach for treating alcohol withdrawal symptoms in humans.

Excessive binge drinking is associated with increased risk for cardiovascular (CV) disease risk. Endogenous microRNA-21 is increased in the microcirculation of young adult binge drinkers and leads to reduced flow and acetylcholine-induced vasodilation. Local inhibition of miRNA-21 restores microvascular function in binge drinkers.

The incidence of binge drinking by women has recently increased, but the biological factors that promote binge drinking are not well understood. In this study, we compared female and male mice in a binge-drinking test (drinking in the dark). Female mice consumed more alcohol than males, an effect that was abolished by ovary removal (OVX). This study demonstrates that ovarian hormones, in particular estradiol, promote binge drinking, and provides a framework for understanding sex-specific mechanisms that contribute to binge drinking.

Moderate prenatal alcohol exposure (PAE) elevates histamine H₃ receptor-effector coupling in the dentate gyrus of adult rat offspring (Panel A) and increases H₃ receptor-mediated inhibition of excitatory neurotransmission in dentate gyrus slices from PAE rats compared to controls (Panel B). We speculate that this increased H₃ receptor-mediated inhibition contributes to the synaptic plasticity and behavioral deficits observed in our PAE rats, and provides a mechanistic basis for the efficacy of H₃ receptor inverse agonists in ameliorating these deficits.

Understanding the synaptic signaling mechanisms that change in response to sustained ethanol consumption and ethanol withdrawal can identify targets for improved treatments to prevent alcohol abuse and/or relapse drinking. Here we clarify the time courses of ethanol consumption and withdrawal that induce changes in ethanol and glutamate sensitivity in the mammalian circadian clock, and demonstrate that changes in NMDA receptor subunit expression/phosphorylation, TrkB receptor phosphorylation, and mBDNF expression accompany some but not all the changes in ethanol and glutamate sensitivity.

In vivo PET study confirmed the modulatory role of ethanol, administered acutely or chronically, in [1-¹¹C]-acetate kinetics and metabolism in the rat brain. Acute ethanol intoxication may inhibit the transport and metabolism of acetate in the brain, whereas chronic ethanol exposure may lead to the adaptation of the rat brain to ethanol in acetate utilisation. [1-¹¹C]-Acetate PET imaging is a feasible approach to study the effect of ethanol on acetate metabolism in rat brain.

Rats were drinking alcohol (two-bottle choice intermittent-access to 20% ethanol) or water (two-bottle choice) for 3 months. The densities of dopamine D2 receptor (D2R) complexes in the NAc shell were measured using in situ proximity ligation assay (PLA). Alcohol-drinking reduced the density of D2R-D2R and increased the density of adenosine A2AR-D2R complexes. This shift from D2R-D2R to A2AR-D2R complexes could result in decreased D2R transmission, based on the previously found antagonism between the A2AR and D2R within the receptor complex.

Between 2006 to 2014, the number of acute alcohol-related emergency department visits in the United States increased 51.5% from 1,801,006 to 2,728,313 and the rate increased 40% from 720.9 to 1009.6 per 100,000 population. The number of chronic alcohol-related visits increased 75.6% from 1,279,208 to 2,247,823 and the rate increased 57.9% from 502.2 to 792.9 per 100,000. Per capita consumption remained stable during this time. The overall increases in rates were larger for females than males.

Risk of injury was found to increase with both hours of exposure to a BAC ≥ 0.05 and average monthly volume of consumption among males, but not among females. Males aged 18 to 29 showed the largest increase in risk associated with an elevated BAC, with risk doubling at one hour of exposure. Data suggest the importance of preventive efforts aimed at moderate drinkers who may only rarely achieve elevated BAC levels, but who may be especially at risk on those occasions.

We examined the effect of hazardous alcohol use among pregnant South African women on infant growth outcomes. Thirteen percent of mothers reported hazardous alcohol use. Recent exposure to intimate partner violence and hazardous tobacco use were associated with hazardous alcohol use during pregnancy. Hazardous alcohol use predicted lower infant weight, height, and head circumference for age z-scores. Findings demonstrate that interventions to reduce hazardous alcohol use among pregnant women in South Africa are needed to prevent alcohol-related infant growth restrictions.

Amount of alcohol intake with regard to ALDH2 genotype (A) and the alcohol flushing response (B): All subjects with ALDH2*2/*2 were light drinkers with an average alcohol intake <4 units per week, but heterozygotes (ALDH2*1/*2) had a wider range of alcohol intake from 0 to 64 units per week (A). In addition, alcohol flushing evaluated by flushing questionnaire negatively correlated with alcohol intake (B). Data were presented as mean and standard deviation. One unit equals 14 g of ethanol.

We determined the best cutoff of the MoCA screening tool of cognition defects in alcoholics. It can be used with or without correction for education level. However, as using the correction increases the cutoff score by one point, it is suggested that the uncorrected score be used with the usual cutoff, i.e. 26. [ROC analysis for the corrected (empirical and smoothed = black and gray dotted lines) (AUC = 0.84; p < 0.001) and the uncorrected MoCA scores (black and gray full lines) (AUC = 0.87; p < 0.001)].

Cisternal CSF concentrations of the serotonin metabolite 5-HIAA were obtained from adolescent alcohol-naïve rhesus monkeys. Shortly after, they were infused with an intravenous dose of ethanol (EtOH) and rated for intoxication. Subjects rated as low in intoxication exhibited low CSF 5-HIAA concentrations. This finding suggests an association between impaired central serotonin functioning and relative insensitivity to EtOH, and that impaired central serotonin functioning may lead to a low level of response to alcohol, both of which are characteristics of Type 2 alcoholism.

Alcohol and tobacco are often co-abused in humans. We investigated the effects of repeated nicotine-alcohol co-exposure on binge-like alcohol drinking in mice. High (HAP2) and low alcohol-preferring (LAP2) mice were used to test potential interactions between nicotine treatment and genetic predisposition for alcohol preference. We found that repeated nicotine increased binge-like alcohol drinking in HAP2 mice only. This finding suggests that repeated co-abuse of alcohol and tobacco/nicotine may increase binge-like drinking in humans with a genetic predisposition for alcoholism.

High alcohol intoxication levels among spectators at sporting events are of great concern. Professional actors portraying a scene of obvious alcohol intoxication were used to assess rates of denied alcohol service at licensed premises (LPs) outside and inside football arenas, and denied entry to arenas. The rates of denied service at LPs inside arenas and denied entry to arenas were lower than denial rates at LPs outside arenas. These results underscore the need for training among staff at the arenas.

Varenicline is FDA approved for smoking cessation treatment and reduces alcohol craving. This experiment utilized a paradigm that procedurally separates appetitive from consummatory responding. Varenicline attenuated ethanol self-administration, but experience with ethanol consumption while varenicline was “on board” was not sufficient to alter subsequent ethanol-seeking. Overall, varenicline blocked the rewarding properties of ethanol while not substituting for ethanol, non-specific effects on an alternate reinforcer were negligible, and blood levels of varenicline needed to be maintained for treatment to remain effective.