Zelig S. Dolinsky

Elevated endogenous breath acetaldehyde levels among abusers of alcohol and cigarettes

Endogenous (fasting) breath acetaldehyde levels were assessed as a discriminator between alcoholic and non-alcoholic subjects. The influence of smoking as a potential confounding variable on breath acetaldehyde was determined. Individuals with a history of smoking and/or drinking had higher endogenous breath acetaldehyde levels as compared to controls. Mean acetaldehyde levels revealed an additive (noninteractive) pattern associated with combined abuse of these substances. The similarity in acetaldehyde levels between alcoholic non-smokers and non-alcoholic smokers limits the usefulness of endogenous breath acetaldehyde for the purpose of early diagnosis of alcoholism. Results support hypotheses that elevations in acetaldehyde could be a common factor in disease associated with alcohol and cigarette abuse.

Alcohol Reinforcement: Biobehavioral and Clinical Considerations

When compared with stimulants, opioids, and barbiturates (Schuster and Thompson, 1969; Schuster and Villareal, 1968; Winger et al., 1983; Yanagita et al., 1969) in intravenous self-administration paradigms in monkeys and rats, ethanol is a relatively weak reinforcer. The delay in reinforcement associated with oral self-administration of ethanol further inhibits its reinforcing efficacy. A relatively prolonged period of exposure to frequent high doses of ethanol is necessary for the development of alcohol dependence in humans. In contrast, in vulnerable individuals, intravenous opiate self-administration, and intravenously self-administered or smoked cocaine are associated with the rapid development of dependence. The risk of developing alcohol dependence is strongly influenced by factors in the individual (e.g., genetics, temperament, psychopathology) and the environment (e.g., culture).

Dietary ascorbic acid deficiency in guinea pigs: No effect on ethanol preference, spiroperidol binding, or monoamine oxidase activity

Ascorbic acid levels are commonly reported to be decreased in alcoholics. Although this deficiency could be due to dietary factors, there is evidence that ascorbic acid may be involved in the metabolism and acute effects of ethanol, possibly related to the pathogenesis of alcoholism. Therefore, we examined ethanol preference in guinea pigs receiving an ascorbate deficient vs a normal diet. Brain and spleen ascorbic acid levels were dramatically decreased, but ethanol preference was not altered by the acute dietary deficiency of this vitamin. In addition, an acute stressor (cold water swim), alone or in combination with ascorbate deficiency, had no effect on ethanol preference. At termination of the experiment, two measures of brain aminergic function (MAO activity and 3H-spiroperidol binding), purportedly altered by ethanol or ascorbic acid or both, were not associated with tissue ascorbate levels.

Discriminant Function Analysis of Clinical Laboratory Data Use in Alcohol Research

There has been a growing interest in the use of discriminant function analysis of routinely collected laboratory data to differentiate between alcoholic and nonalcoholic individuals. However, no consensus has been reached concerning the validity and reliability of this form of analysis regarding the diagnosis of, or screening for, alcoholism. In addition, this technique may provide important information concerning the multivariate nature of the pathophysiological effects of alcohol. However, this issue is seldom discussed. Because of differences in methodology across studies and the growing confusion regarding conceptual issues associated with this statistical technique, there have been few critical reviews. This chapter is directed at critically evaluating the current literature, particularly with respect to the methodological and conceptual issues associated with the use of discriminant function analysis in alcohol research. As part of this approach we suggest guidelines for future research in this area.