Low Drinkers Research Articles

Coping responses and alcohol outcome expectancies in alcohol abusing and nonabusing social phobics

This study examined coping responses and alcohol outcome expectancies in alcohol abusing and nonabusing social phobics. The sample consisted of social phobics with current alcohol abuse or dependence (SPAs, n = 19), social phobics without lifetime alcohol use disorders (SPs, n = 19), and normal controls (NCs, n = 21). As predicted, SPs reported less problem-focused coping than did NCs in nonalcohol social situations and rated themselves as less skillful in interpersonal role-plays. However, observers did not rate SPs as less skillful than NCs in these role-plays. Consistent with the predicted situation-specific effects, SPAs reported less problem-focused coping than did SPs during alcohol-accessible social situations, but not during alcohol-inaccessible social situations. However, observer-rated and self-report results from role-plays of high-risk alcohol situations did not show the predicted lower drink refusal skills among SPAs compared to SPs. SPAs reported higher positive alcohol expectancies of tension reduction than did SPs but did not differ in negative alcohol expectancies of cognitive and behavioral impairment. These results are in several ways consistent with cognitive and social-learning theories of social phobia and alcohol abuse.

Neurophysiological Findings and Drinking Levels in High‐Alcohol‐Drinking (HAD) and Low‐Alcohol‐Drinking (LAD) Rats

Specific neurophysiological profiles, such as reduced P300 amplitude or altered spectral power in the EEG, have been associated with a risk for alcoholism in several clinical populations. In certain rodent models, high versus low alcohol consumption is associated with similar neurophysiological differences. For example, alcohol-preferring (P) rats have increased spectral power and decreased P300 amplitudes compared with alcohol-nonpreferring (NP) rats. In the present study, the neurophysiological profiles of high-alcohol-drinking (HAD) and low-alcohol-drinking (LAD) rats were assessed (1) to determine if their electrophysiological profiles are similar to P and NP rats and (2) to examine the relationship of these neurophysiological indices to ethanol drinking. Ethanol-naive HAD and LAD rats were implanted with cortical and amygdalar recording electrodes. Baseline EEG and event-related potentials (ERPs) then were assessed. Subsequently, all rats were trained to self-administer ethanol by using a sucrose-substitution procedure. Baseline EEG and ERP (i.e., pre-ethanol exposure) were assessed based on line (HAD versus LAD) and actual ethanol consumption (high drinkers versus low drinkers). At baseline, ethanol-naive HAD rats displayed significantly greater power in the cortical EEG and decreased amygdala N1 ERP amplitude compared with ethanol-naive LAD rats. Similar EEG and ERP profiles have been observed when P and NP rats are compared. No differences in P300 between lines were observed, but high-drinking rats, independent of line, had significantly decreased P300 amplitude in the amygdala compared with low-drinking rats. These data suggest there are some similarities in EEG and ERP profiles of P and HAD rats compared with NP and LAD rats. Furthermore, the data suggest that decreased P300 amplitude in the amygdala is associated with increased limited access ethanol drinking.

An individual in context: predictors of alcohol use and drinking problems among Greek and residence hall students.

Fraternity, sorority, and residence hall residents were compared on drinking rates and patterns, drinking-related problems, family history of alcohol problems, alcohol outcome expectancies, and high school drinking patterns. Results indicated residence in a fraternity was related to more frequent alcohol consumption and greater negative consequences even after accounting for family history, expectancies, and high school drinking rates. Family history of alcohol problems was only related to negative consequences for men. Only high school drinking rates were related to amount of alcohol consumed per occasion, for both men and women. Fraternity residence was found to be related to more negative consequences even after accounting for current drinking habits. However, sorority residence was found to moderate the relationship between current drinking and negative consequences. Both high and low drinkers in sororities indicated similar rates of alcohol-related negative consequences, whereas high frequency female drinkers in the residence hall sample reported significantly more problems.

Problem drinking from young adulthood to adulthood: patterns, predictors and outcomes.

Many young adults engage in heavy or problem drinking, but it is unclear who will continue problem drinking into adulthood. This study followed a general population sample in order to study patterns of problem drinking over time, to identify differences among drinking groups, to test a model differentiating youth-limited from developmentally-persistent problem drinkers, and to examine adult outcomes. Data were from the Health and Human Development Project; subjects (N = 1,073) were in three age cohorts (age 18-25; age 21-28; age 24-31). Based on use and consequences data from two assessment intervals, cluster analyses were performed. Cluster analyses yielded four drinking groups: youth-limited problem drinkers, stable moderate drinkers, stable low drinkers and developmentally-persistent problem drinkers. Rates of youth-limited problem drinking peaked in the middle cohort and rates of developmentally-persistent problem drinking decreased in the oldest cohort. Discriminant analysis revealed that developmentally-persistent problem drinkers in each age cohort are more likely to be male, to show high disinhibition, and to experience a high level of problem behaviors. Youth-limited problem drinkers were similar to developmentally-persistent problem drinkers on many young adult characteristics and adult outcomes. Developmentally-persistent problem drinkers in each age cohort continued to show higher levels of problem behaviors in adulthood than youth-limited problem drinkers. Most young adults show continuity of drinking patterns. Although developmentally-persistent problem drinkers did not differ from youth-limited problem drinkers in adopting adult roles, their continued experience of many problem behaviors suggests that they fail to adopt the role of greater conventionality in adulthood.

Changes in serum apolipoprotein and lipoprotein profile induced by chronic alcohol consumption and withdrawal: determinant effect on heart disease?

The effects of alcohol consumption on serum concentrations of apolipoproteins (apo) A-I, C-III, B, and E and of lipoproteins (Lp) A-I, A-I:A-II, C-III, C-III:B, and (a) were studied in 132 healthy subjects, including 55 low drinkers of alcohol (<20 g/day), 36 moderate drinkers (20-50 g/day), and 41 heavy drinkers (>50 g/day), and in 97 hospitalized alcoholic patients (> 100 g/day) without severe liver disease (especially functional insufficiency), before and after 21 days of withdrawal treatment. Serum concentrations of apo A-I, LpA-I, LpA-I:A-II, apo C-III, and LpC-III significantly (P </= 0.01) increased with alcohol intake (mean +/- SE in low drinkers vs in alcoholics)--1.45 +/- 0.03 vs 1.78 +/- 0.05 g/L; 0.45 +/- 0.02 vs 0.56 +/- 0.02 g/L; 0.99 +/- 0.02 vs 1.22 +/- 0.04 g/L; 27.6 +/- 1.5 vs 39.7 +/- 1.7 mg/L; and 8.4 +/- 0.9 vs 24.7 +/- 1.7 mg/L, respectively-whereas apo B and LpC-III:B concentrations tended to decrease--1.20 +/- 0.04 vs 1.06 +/- 0.04 g/L and 19.3 +/- 1.2 vs 14.9 +/- 1.0 mg/L, respectively. No significant difference between these four types of alcohol consumption was noticed for cholesterol, triglycerides, apo E, and Lp(a). After withdrawal, the concentrations of serum apo A-I, apo C-III, LpA-I, LpA-I:A-II, and LpC-III decreased significantly (P </= 0.01), reaching values comparable with those in low drinkers; concentrations of triglycerides, apo B, apo E, and Lp(a) rose; and cholesterol concentration was unaffected. In multiple regression analysis, after adjustment for serum concentrations of albumin, aspartate aminotransferase, and gamma-glutamyltransferase and for the Quetelet index, alcohol consumption remained positively correlated to apo A-I, LpA-I:A-II, apo C-III, and LpC-III concentrations. Study of other determinants of serum apo and lipoprotein concentrations suggests that alcohol-related variations in some of them, especially apo A-I, might depend on the metabolic ability of the liver to synthesize proteins and on induction phenomena. Finally, although the increase of antiatherogenic apo- and lipoproteins and the decrease of those known to be atherogenic were generally marked in alcoholics, alcohol-related modifications of these markers were very limited in our sample of French healthy men. We conclude, therefore, that moderate alcohol consumption (20-50 g/day) is unlikely to protect against ischemic heart disease through an effect on the proteins measured in this study.

Lack of effect of dopamine d 2 blockade on ethanol intake in selected and unselected strains of rats

Previous research has suggested that brain catecholamines may be involved in regulating ethanol intake. This study was designed to look more specifically at dopamine (DA) and whether DA D 2 receptor blockade with the antagonist pimozide would alter ethanol consumption in rats. Subjects were male Maudsley Reactive and Wistar rats, the former previously shown to consume larger amounts of ethanol than the latter. Both strains were screened for ethanol intake by presentation of ethanol solutions (free choice with water) in increasing steps from 2% to 10% (v/v) on an alternate-day schedule. Following the screening period, animals were switched to a schedule of everyday presentation of the 10% (v/v) ethanol solution (free choice with water) for 10 baseline days. Animals were then divided into high and low drinking levels according to whether their mean baseline ethanol intake (g/kg) fell within ±0.5 SD of the mean intake of their group (Maudsley Reactives: mean = 2.55 g/kg, low drinkers < 1.63, high drinkers > 3.47; Wistars: mean = 2.17 g/kg, low drinkers < 1.53, high drinkers > 2.82). The animals were assigned to one of five treatment groups for 5 subsequent days where they received IP injections of pimozide (0.08, 0.24, or 0.48 mg/kg), tartaric acid, or saline. Following the treatment period, ethanol consumption was recorded for 5 posttreatment days. No significant differences due to treatment were observed for either intake or preference of ethanol across treatments, drinking groups, or strains. The results obtained in the present study suggested that interference in DA neurotransmission through administration of the D 2 antagonist pimozide does not significantly alter ethanol consumption in either MR or Wistar animals.

Interference effects on verbal memory function, following oral lorazepam

Previous studies have consistently reported deficits in verbal memory following oral lorazepam administration. The possible role of susceptibility to interference effects as a contributory mechanism in benzodiazepine amnesia has not been examined as an independent variable. In addition, most studies of benzodiazepine amnesia have not controlled for the possible confounding effects of alcohol consumption, recently reported to affect the degree of amnesia produced by lorazepam. The present study assessed the verbal memory capabilities of 24 low social drinkers (MAST score < 3) receiving either oral lorazepam (2 mg) or placebo. Interference effects on verbal memory were assessed using the Auditory herbal Learning Test, with either the interference word list (trial B) or a counting backwards task. Lorazepam significantly reduced the recall scores for list B, compared to the first presentation of list A, suggesting lorazepam may increase susceptibility to proactive interference. There was no drug effect on retroactive interference. With regard to recall per se, lorazepam impaired verbal learning for initial acquisition trials (trials 2 and 3) but not subsequent trials, where learning was comparable to the placebo. Lorazepam did not produce significant impairment in immediate and delayed recall trials. This pattern of recall does not conform to the classic profile of benzodiazepine-induced amnesia; potential explanations for this are discussed.

Ethanol-Related Cues and Behavioral Tolerance to Ethanol in Humans

The present study examined the effect of ethanol-related cues in the natural environment of the social drinker (e.g., a bar setting) upon performance on a behavioral task. Fourteen male social drinkers participated in the study. Half were designated low drinkers (3 or fewer drinks per week and little or no experience in bars) and half of the subjects comprised a moderate drinking group (8 to 15 drinks per week and drinking in bars at least 4 times per month). Subjects played a computer-controlled video game prior to and following consumption of a drink containing ethanol and orange juice. Each subject participated for one session in two different environmental settings, a standard experimental room and a room decorated to resemble a bar situation. The results showed significantly more detrimental effect of the ethanol upon performance in the standard experimental room than in the bar setting, that is, more tolerance was exhibited in the bar setting. However, no difference was observed between groups, that is, no effect of drinking experience and bar experience upon the relative amount of tolerance exhibited.

Schedule-induced drinking is not ubiquitous: Effect of water-bottle location

After adaptation and shaping, barpresses of two groups of 4 food-deprived rats were reinforced at fixed intervals of 30 sec (FI-30) for 27 sessions, each one 25 min long. Water bottles were available, 16 cm from the food source for one group and 29 cm from it for the other group. Three animals in the first group but only 1 in the second developed polydipsia. When the bottle positions were reversed for the groups for a further 10 sessions, high drinkers remained high drinkers but the low drinkers did not become polydipsic. These data show that schedule-induced drinking is not ubiquitous, and they also suggest that once an alternative adjunctive behavior is acquired, drinking does not easily displace it.

EEG fast frequency activity in the sons of alcoholics

The EEGs of young (21–25-year-old) sons of alcoholics and their matched controls ( n = 24 pairs) were computer evaluated to assess activity in the 12–20 Hz (beta) range. Subjects were blindly exposed to ethanol and placebo drinks while EEG was gathered at baseline and 90 min postconsumption. Men with alcoholic fathers [family history positive (FHP)] displayed significantly more beta activity at 90 min postethanol consumption than the men who had no alcoholic relatives [family history negative (FHN)]. In addition, when subjects were sorted into “low” and “moderate” drinkers depending on their drinking practices, additional differences were found between groups. Within the FHN subjects, moderate drinkers were found to have significantly more energy in the beta frequencies at both baseline and at 90 postdrug than low drinkers. However, though family history positive subjects had overall increases in 12–20 Hz activity compared with the FHN subjects, no significant differences were found between moderate and low drinkers within the FHP population. Taken together, these studies suggest that drinking practices and a familial history for alcoholism can modify the beta content of the EEG in the 12–20 Hz range in young men.

Naloxone alters alcohol drinking induced in the rat by tetrahydropapaveroline (THP) infused ICV

In male rats of the Sprague-Dawley or Long-Evans strain, intracerebroventricular (ICV) cannulae were implanted permanently using stereotaxic techniques. Tetrahydropapaveroline (THP) was infused ICV for up to 14 days either chronically around the clock or acutely once per day in doses previously found to induce an abnormally high intake of alcohol. During these periods, alcohol preference for individual rats was determined by a self-selection procedure in which the concentration of alcohol was increased from 3 to 30% on each day of a 12-day interval. Those rats which displayed a substantial increase in their intake of alcohol were selected for naloxone treatment and subsequently assigned a fixed concentration of alcohol at which maximum consumption occurred. Naloxone was administered subcutaneously two to six times per day for three consecutive days in total daily doses ranging from 1.5 to 3.0 mg/kg. Each rat served as its own control and was given 0.9% saline isovolumetrically according to the same temporal schedule. Naloxone generally suppressed alcohol intake in animals by 20% to 45%, but the reduction in drinking depended upon the injection regimen as well as the prior level of alcohol consumption. In “high drinking” rats, the mean alcohol intake of 6.2 g/kg/day was reduced to 3.7 g/kg/day by naloxone whereas in “low drinkers” the mean intake of 3.5 g/kg/day was suppressed to 2.8 g/kg/day by the opiate antagonist. These results further support the suggestion of a possible opiate receptor link in the pathogenesis and maintenance of aberrant drinking of alcohol, the mechanism of which may involve the endogenous action of an amine-aldehyde condensation product in the brain.

Relationship between alcohol preference and biogenic aldehyde metabolizing enzymes in rats

Rats were presented water and alcohol solutions [up to 30 per cent (v/v)] in a free choice screening test. High drinkers ingested the equivalent of ca. 6 g/kg day of pure ethanol, at any concentration offered. Low drinkers consumed only ca. 2/kg. day, but stopped drinking alcohol solutions at concentrations higher than 7.5%. Males and females exhibited similar drinking habits. As measured by incubations of tissue slices and analysis of the components formed, high as well as low drinkers metabolize serotonin and dopamine at the same rate and produce identical metabolites. However, some small differences in the metabolism of these biogenic amines exist between males and females. The isozyme patterns of both aldehyde reductase (ALRed) and aldehyde dehydrogenase (ALDH) from the brain of high and low drinkers are identical. The levels of activity and isozymes of liver ALRed are the same, as are those of liver ALDH from the matrix of mitochondria which is responsible for the oxidation of acetaldehyde. Though the level of liver ALDH from the cytosol fraction is unaltered, the isozyme pattern is very different. Low drinkers always have three isozymes at pi 5.9, 6.0 and 6.2, while high drinkers have only one isozyme in this range, either at pi 5.9 or 6.2. Both animals have many more isozymes of the enzyme.

Physiological correlates of ethanol self-selection by rats

High-drinker and low-drinker rats were given 1.2g/kg of ethanol intraperitoneally. Subsequent blood-alcohol measurement showed that low-drinker rats had a significantly higher level than high-drinker rats at 15 min postinjection. Previous studies measured ethanol levels starting at 60 min postinjection and reported no differences for high drinkers and low drinkers. The present results are interpreted to account for the observed behavioral differences between high-drinker and low-drinker rats.