Sex differences in spatial visualization and episodic memory as a function of alcohol consumption.

AIMS: Sex differences in visuospatial ability as well as episodic memory have been reliably demonstrated, irrespective of alcoholism. Studies in alcoholics have consistently documented cognitive deficits in visuospatial ability, problem solving and memory function. This cross-sectional, population-based study examined if sex differences in cognitive performance could be impacted by alcohol consumption. METHODS: Drinking data were collected from 2224 randomly sampled adults, aged between 35 and 85 years, who participated in the Betula study on memory, health and aging. Participants were classified into non-, light, moderate and heavy drinking subgroups based on sex-adjusted normative values. Cognitive tasks demonstrating clear sex differences, such as episodic memory tasks (favouring women) and spatial visualization tasks (favouring men), were conducted and performance was assessed by sex and the drinking group. RESULTS: After controlling for age and education, overall analyses found expected sex differences in episodic memory and spatial visualization that were apparent across the entire population. When these sex differences were examined by drinking group, visuospatial performance favouring men disappeared for the moderate to heavy drinking groups, but higher performance by women on episodic memory tasks was consistent across all levels of alcohol consumption. Traditional biomarkers of increased alcohol consumption (GGT and MCV) correlated with the reported drinks/day. CONCLUSIONS: These results lend support to the theory that moderate alcohol intake may be beneficial to cognitive function in women, but not necessarily in men.

Intra- and inter-individual relationships between central and peripheral serotonergic activity in humans: a serial cerebrospinal fluid sampling study.

Data are lacking concerning the longitudinal covariability and cross-sectional balance between central and peripheral 5-HIAA concentrations in humans and on the possible associations between tobacco smoking or post-traumatic stress disorder (PTSD) and CSF and plasma 5-HIAA concentrations. Using serial cerebrospinal fluid (CSF) and blood sampling, we determined the concentrations of 5-HIAA in CSF and plasma over 6 h, and examined their relationships in healthy volunteers and patients with PTSD-both smokers and nonsmokers. Patients with PTSD and healthy volunteers had very similar CSF 5-HIAA concentrations. Significant and positive correlations between CSF and plasma 5-HIAA levels were observed within individuals, but this CNS-peripheral 5-HIAA relationship was significantly reduced in smokers (nonsmokers: mean r = 0.559 +/- 0.072; smokers: mean r = 0.329 +/- 0.064 p < 0.038). No significant cross-sectional, interindividual correlation of mean CSF and mean plasma 5-HIAA was seen (r = 0.094). These data show that changes in CSF 5-HIAA levels within an individual over time are largely reflected in plasma 5-HIAA, albeit significantly less so in smokers. The present results therefore suggest that clinically, longitudinal determination of plasma 5-HIAA concentrations within an individual patient can be used to make inferences about relative changes in integrated CSF 5-HIAA concentrations. However, plasma 5-HIAA concentrations provide no significant information about absolute levels of the serotonin metabolite in the CSF.

Stress hormone dysregulation at rest and after serotonergic stimulation among alcohol-dependent men with extended abstinence and controls.

BACKGROUND: Alcohol dependence has been associated with long-lasting alterations in limbic-hypothalamic-pituitary-adrenal (LHPA) axis and serotonin (5-hydroxytryptamine [5-HT]) function. Other conditions that are associated with alcoholism (cigarette smoking and antisocial personality disorder [ASPD]) have been linked with disturbances in these interrelated systems. We evaluated the stress hormone response to 5-HTergic stimulation in alcohol-dependent men with extended abstinence (average abstinence duration, 4.3 months) and controls to determine the relative contributions of alcoholism, cigarette smoking, and ASPD on baseline and provoked plasma cortisol and adrenocorticotropin hormone (ACTH) concentrations. METHODS: One hundred nine alcohol-abstinent men with alcohol dependence (62%), habitual smoking (70%), and ASPD (43%) received D,L-fenfluramine (100 mg po) in a randomized, double-blind, placebo-controlled, crossover trial. The group of recovering alcohol-dependent individuals included abstinent primary alcohol-dependent men and alcohol-dependent men with ASPD, whereas the group of non-alcohol-dependent men comprised healthy controls and non-alcohol-dependent men with ASPD. Plasma cortisol and ACTH levels were obtained at AM baseline and at half-hour intervals after drug administration. Subjective ratings of drug response and physiological measures were also obtained at baseline and every 30 min. RESULTS: Abstinent alcohol-dependent men had significantly lower (approximately 20%) AM baseline plasma cortisol concentrations than non-alcohol-dependent men on both challenge days; however, no differences between the groups were observed with regard to resting AM plasma ACTH levels. After adjusting for these baseline differences, recovering alcohol-dependent men (area under curve = 35.6 +/- 37.4 [microg/dl] x min) had a twofold greater cortisol response to fenfluramine than non-alcohol-dependent men (area under curve = 17.5 +/- 32.5 [microg/dl] x min) (F = 5.1; df = 1,105; p < 0.03). The elevated cortisol response, which occurred primarily along the descending limb of the response curve, was paralleled by a nonsignificant statistical trend for alcohol-dependent men to also exhibit a greater ACTH response to fenfluramine at the 210-min (p < 0.07) and 240-min (P < 0.09) time points as compared with non-alcohol-dependent men. Cigarette smoking and ASPD did not affect hormonal responses, nor could the groups' subjective ratings and physiological measures be distinguished. CONCLUSIONS: Alcohol-dependent men with extended abstinence differed from age- and race-matched non-alcohol-dependent men in resting AM and fenfluramine-induced plasma cortisol levels. This dysfunction in glucocorticoid homeostatic mechanisms was associated with alcoholism and not with smoking or ASPD. We also observed a nonsignificant statistical trend for plasma ACTH levels to be elevated among alcohol-dependent men along the descending limb of the response curve. Alcohol-dependent men seemed to have inherited or acquired damage to 5-HT-regulated LHPA axis function, the precise mechanisms and sites of which remain to be determined.

Monoamine oxidases and tobacco smoking.

Although nicotine has been identified as the main ingredient in tobacco responsible for aspects of the tobacco dependence syndrome, not all of the psychopharmacological effects of smoking can be explained by nicotine alone. Accumulating preclinical and clinical evidence has demonstrated that smoking also leads to potent inhibition of both types (A and B) of monoamine oxidase (MAO). Smokers have 30-40 % lower MAOB and 20-30 % lower MAOA activity than non-smokers. Reduced MAO activity in smokers has been shown by direct measures (platelets, positron emission tomographic studies) or by indirect measures (concentration of monoamine catabolites in plasma or CSF). We examine the hypothesis that chronic habitual smoking can be better understood in the context of two pharmacological factors: nicotine and reduced MAO activity. We speculate that MAO inhibition by compounds found in either tobacco or tobacco smoke can potentiate nicotine's effects. Based on this concept, more effective anti-smoking drug strategies may be developed. As a practical consequence of tobacco smoke's MAO-inhibitory properties, comparative psychiatric research studies need to screen and control for tobacco use.

A bootstrapped commingling analysis of platelet monoamine oxidase activity levels corrected for cigarette smoking.

Monoamine oxidase (MAO) activity levels have been suggested as a possible biological marker for alcohol dependence and abuse, as well as for schizophrenia and other psychiatric conditions. Using platelet MAO activities in the Collaborative Study on the Genetics of Alcoholism data set, we applied bootstrapping methods as a novel way to test for admixture in families. This bootstrapping involved resampling in family units and hypothesis testing of the resampled datasets for commingling in the distribution of MAO activity levels. Prior to commingling analysis, we used linear models to find covariates of greatest effect on MAO activity levels. While an alcoholism diagnosis was significant in men (n = 1151, P < 0.0001) and women (n = 1254, P = 0.0003), the effect lost significance after controlling for cigarette smoking, indicating alcoholism and smoking behavior to be highly confounded. When smoking histories were compared, former smokers had levels (mean = 7.1) closer to those who never smoked (mean = 7.0) than to current smokers (mean = 5.4). Furthermore, current daily smoking and time since smoking cessation were significantly related to MAO levels, indicating smoking probably has a direct effect on MAO levels, rather than the reverse. These results suggest that studies using MAO levels as a biological marker should consider smoking as an important covariate. Finally, admixture was found in MAO levels controlled for smoking and sex, possibly indicating a major genetic locus; this confirms previous evidence for admixture.

Cigarette smoking decreases the prolactin response to serotonergic stimulation in subgroups of alcoholics and controls.

BACKGROUND: The prolactin response to serotonergic stimulation has been used as an index of central nervous system serotonin function. We evaluated the prolactin response to d,l-fenfluramine to determine whether subtypes of alcoholics differed in prolactin responsivity compared with nonalcoholics and whether cigarette smoking affected prolactin response. METHODS: One hundred ten healthy, abstinent men across four groups (controls [23% smokers]; alcoholics [72% smokers]; alcoholics with antisocial personality disorder [94% smokers]; nonalcoholic antisocials [88% smokers]) received d,l-fenfluramine (100 mg orally) in a randomized, double-blind, placebo-controlled study. Plasma prolactin levels were obtained at baseline and at half-hour intervals for 5 hr after fenfluramine/placebo administration. Plasma fenfluramine and norfenfluramine levels were obtained hourly. RESULTS: Smokers had a blunted prolactin response to fenfluramine compared with nonsmokers without any alcoholism or antisocial personality effects. Using a cutoff point of delta peak prolactin < 10 ng/ml, more smokers (41/76, 54%) had a dampened response to fenfluramine than did nonsmokers (7/34, 21%) [chi2(1) = 10.6, p < 0.003]. The percentage of low responders was greatest among smokers regardless of whether they were healthy controls, alcoholics, or antisocial. Multiple regression revealed that three variables--(1) number of pack-years of smoking, (2) actual dosage of fenfluramine received, and (3) plasma norfenfluramine level obtained--explained 43% of the variance (R2 = 0.43) in delta prolactin area under the curve. Variables that included alcoholism diagnostic status, antisocial personality diagnostic status, and impulsive aggressive personality, depressive, and suicidal traits failed to explain any additional unique variance. CONCLUSIONS: Cigarette smoking blunted the prolactin response to a pharmacological challenge with d,l-fenfluramine. Pharmacodynamic and pharmacokinetic factors related to smoking both appear to influence fenfluramine-induced prolactin secretion. Phenotypes of alcoholics did not differ in their prolactin response to this serotonergic probe.

Use of health services by men with and without antisocial personality disorder who are alcohol dependent.

In a sample of 104 medically stable male veterans with alcohol dependence, rates of health service utilization were compared for 48 patients with a primary diagnosis of antisocial personality disorder and 56 patients without this diagnosis. Patients were diagnosed using DSM-IV lifetime criteria; previous utilization of health services was based on self-reports. Although a similar proportion of both groups reported previous service use, patients with antisocial personality disorder reported using more substance abuse treatment services than those with a primary diagnosis of alcohol dependence. Between-group multiple regression analysis showed that an earlier age at onset of alcoholism and a history of a comorbid substance-induced mental disorder best predicted higher rates of use of substance abuse treatment.

Platelet monoamine oxidase activity in subgroups of alcoholics and controls: results from the Collaborative Study on the Genetics of Alcoholism.

OBJECTIVE: Platelet monoamine oxidase (MAO) B activity levels were evaluated to determine whether low platelet MAO activity is a marker for alcoholism, correlates of alcoholism (e.g., cigarette smoking), or a subtype of alcoholism. METHODS: Adult women (n = 788) and men (n = 685) participating in the Collaborative Study on the Genetics of Alcoholism study were evaluated with a semistructured interview, and blood samples were obtained for determination of platelet MAO activity using tryptamine (0.1 mM) as substrate. DSM-III-R alcohol-dependent individuals were subgrouped using four currently available methods (e.g., two variations of the type 1/type 2 scheme, primary versus secondary typology, type A/type B dichotomy). RESULTS: In the overall sample, subjects' gender, cigarette smoking status, and the Collaborative Study on the Genetics of Alcoholism site at which their platelets were prepared explained 22% of the variance in platelet MAO activity levels, and multivariate analysis showed that carrying a broad diagnosis of alcohol dependence did not uniquely explain any additional variance in platelet MAO activity levels. Furthermore, within each of the alcoholic subgrouping methods tested, there were no significant differences in platelet MAO activity for type 1 versus type 2, type A versus type B, or primary versus secondary alcoholics. CONCLUSIONS: Cigarette smoking and male gender are associated with decreased platelet MAO activity levels. After considering these factors, a diagnosis of alcohol dependence does not predict any additional variance in MAO-B activity. Phenotypes of alcoholics (e.g., type 1 versus type 2, type A versus type B, primary versus secondary) do not differ in platelet MAO activity. The results suggest that decreased platelet MAO activity is not a trait marker of alcoholism or one of its subtypes; but, rather, is a state marker of cigarette smoking.

Cerebrospinal fluid neuroendocrinology of alcohol misusers.

Cerebrospinal fluid (CSF) neurohumors reflect central nervous system physiology in a way that peripheral indices can not. We reviewed clinical studies of CSF biogenic amines and neurohormones in alcohol misusers during various stages of withdrawal or abstinence and found them difficult to compare because of highly variable experimental methods, reliance on single time collections (lumbar punctures) that fail to control for potential stress-induced effects of the procedure, lack of control for tobacco use, and a paucity of non-alcoholmisusing controls. However, taken together, the data thus far show that a variety of neuroactive substances are reduced in concentration in the CSF of some alcohol misusers. Low CSF levels of corticotropinreleasing hormone, beta-endorphin, norepinephrine, diazepam-binding inhibitor, 5-hydroxyindoleacetic acid and somatostatin have all been reported. Whether the decreased CSF levels of these neurohormones and neurotransmitters are a cause or consequence of alcoholism has not been determined. In fact, further studies using serial or continuous CSF sampling techniques with homogeneous, better-characterized patients and normal volunteers are still needed to establish the precise CSF neurochemical abnormalities in alcohol misusers.

Alcohol challenges in young men from alcoholic pedigrees and control families: a report from the COGA project.

OBJECTIVE: Alcoholism is a complex disorder that demonstrates genetic heterogeneity. Genetic linkage studies of alcohol dependence also suffer from the probability that many individuals who inherit an enhanced risk never develop the clinical syndrome. Thus, studies of genetic influences in alcohol abuse or dependence would benefit from the identification of characteristics of an individual that are associated with the probability of developing the disorder. A reduced responsivity to alcohol has been reported to characterize almost 40% of sons of alcoholics and to predict future alcohol abuse or dependence a decade later. This study explores the existence of this characteristic in a more heterogeneous sample that is part of a genetic pedigree study of families of alcoholics. METHOD: Eighteen to 30 year old subjects who were sons of alcohol dependent fathers and who were drinkers but not alcohol dependent were selected from pedigrees of alcoholics at all six sites of the Collaborative Study on the Genetics of Alcoholism (COGA) study. Family history negative controls matched on demography and substance use histories were selected for each subject. Data were obtained on 20 pairs of high-risk and low-risk men (40 subjects) following a challenge with 0.72 g/kg (0.9 ml/kg) of ethanol. Evaluations included measures of subjective feelings of intoxication and body sway, and changes in cortisol, ACTH and prolactin. RESULTS: The data corroborate a lower level of intensity of response to alcohol in the sons of alcoholics especially as measured by changes in cortisol, with similar but less robust changes in subjective feelings and other measures. CONCLUSIONS: The results expand upon earlier studies by using a more heterogeneous population of men at high alcoholism risk. The data highlight the possible usefulness of the reduced response to alcohol as an adjunct to future linkage analyses.

Anorexia nervosa and bulimia nervosa in alcohol-dependent men and women and their relatives.

OBJECTIVE: Many of the studies linking anorexia nervosa and bulimia nervosa to substance use disorders suffer from problems with small samples; some lack rigorous definitions of the syndromes, and it is difficult to determine whether eating problems were primarily temporary consequences of heavy substance use or drugs were temporarily used in an effort to control appetite. The goal of this study was to evaluate the relationship between alcohol dependence and eating disorders. METHOD: Structured interviews were carried out with 2,283 women and 1,982 men as part of the Collaborative Study on the Genetics of Alcoholism. Data on drug abuse and dependence, psychiatric disorders, and symptoms of anorexia and bulimia were evaluated among alcohol-dependent probands, their relatives, comparison probands, and their relatives. RESULTS: Lifetime rates for anorexia and bulimia were 1.41% and 6.17%, respectively, for the alcohol-dependent women, and bulimia was observed in 1.35% of the alcoholic men. However, once the impact of additional primary diagnoses was controlled for, anorexia was seen in only 1.26% of the women with primary alcohol dependence and none of the alcohol-dependent men; the rates for bulimia were 3.46% and 0.72%, respectively. There was no evidence of a strong familial crossover between alcohol dependence and anorexia or bulimia. CONCLUSIONS: While the rate of anorexia was not elevated in alcoholics after controlling for other disorders, bulimia did occur at a greater than expected rate. However, both eating disorders were relatively rare, and much of the association with alcoholism occurred in the context of additional preexisting or secondary psychiatric disorders.

Platelet monoamine oxidase activity levels in subgroups of alcoholics: diagnostic, temporal, and clinical correlates.

Platelet monoamine oxidase (MAO) activity levels were measured in 47 male inpatient alcoholics to determine whether this biological marker might be useful in differentiating subtypes of alcoholics. Of the subgrouping methods tested, only type 2 alcoholics defined by the criteria of Gilligan et al had significantly lower platelet MAO activity than type 1 alcoholics at intake, but this finding was not stable over time in a subset of subjects. Neither separating male veteran alcoholics into either of two other variations of the type 1/type 2 subtypes, nor classifying the sample into primary alcoholics versus primary ASPD with secondary alcoholism categories, yielded significant differences between subgroups. Generally, enzyme activity levels (Vmax) were higher about 10 days after stopping drinking compared to platelet MAO values determined in thrombocytes obtained after approximately 4 weeks abstinence; these levels remained relatively stable 3 months later in a cohort of subjects. Tobacco smoking was significantly negatively correlated to platelet MAO activity levels.

The prevalence of major anxiety disorders in relatives of alcohol dependent men and women.

OBJECTIVE: The relationship between alcohol dependence and lifelong major anxiety disorders is complex. The literature indicates a close association between anxiety symptoms and drinking behavior. However, it is difficult to determine whether the anxiety conditions are lifelong disorders or if they represent temporary organic conditions related to alcohol intoxication and withdrawal. One approach to understanding more about the relationships between alcohol dependence and major anxiety disorders is to observe the rate of anxiety-related diagnoses in close relatives of alcoholics. This approach evaluates whether alcoholism and major anxiety disorders might share a common genetic basis. METHOD: The data presented here describe the rates of four major anxiety disorders in 591 interviewed first-degree relatives of alcohol dependent men and women. The data were gathered through face-to-face structured standardized interviews. RESULTS: The analyses reveal that after focusing on DSM-III-R anxiety disorders, controlling for the potential presence of temporary organic conditions in the subject and considering the impact of assortative mating in their parents, the life-time risk for panic disorder in close biological family members of alcoholics is 3.4%; for agoraphobia, 1.4%; for social phobia, 2.3%; and for obsessive-compulsive disease, 1.4%. CONCLUSIONS: These data do not indicate an exceptionally high rate of anxiety disorders among close relatives of alcoholics. While other mechanisms might contribute to relationship between alcoholism and major anxiety disorders, the results do not support evidence of a common genotype for the two disorders.

The time course of development of alcohol-related problems in men and women.

OBJECTIVE: A predictable sequence of alcohol-related problems has been hypothesized to be applicable to the clinical course of alcoholism. However, few recent data are available on this question. METHOD: The age of first occurrence of 44 alcohol-related life experiences was determined for 478 DSM-III-R defined alcohol-dependent (alcoholic) individuals (317 men and 161 women), and for 444 drinking but not alcohol-dependent subjects (183 men and 261 women). Data were gathered through personal interviews with alcohol-dependent subjects and their relatives using a structured psychiatric interview (SSAGA). RESULTS: A high level of similarity (Spearman's rho = .81, p = .0004) was found for the retrospective reports of the order of appearance of alcohol-related problems between the present sample and an analysis of 636 alcoholic male inpatients who participated in a prior study. Within the present group of 478 alcoholics, the order of appearance of alcohol-related problems was similar for men and women (rho = .84, p < .0001), and the time course of development of problems was similar for treated and untreated alcoholic subgroups (rho = .86, p < .001). Analyses of 19 alcohol-related life experiences in 444 drinking but not alcohol-dependent individuals indicated an overall rank order for occurrence of problems similar to those observed for alcohol-dependent individuals (rho = .76, p < .001). CONCLUSIONS: These data corroborate the high level of predictability regarding the order of occurrence of major alcohol-related life problems among alcohol-dependent men and women, extending the previous findings to women with alcohol dependence and to alcoholics who have never received inpatient treatment.

A comparative study of criteria for subgrouping alcoholics: the primary/secondary diagnostic scheme versus variations of the type 1/type 2 criteria.

OBJECTIVE: This study compared three methods for identifying type 1 and type 2 alcoholism to determine how well the methods agree. It also evaluated the comparability of each of these schemes to the primary/secondary approach to subgrouping alcoholics. METHOD: Fifty male alcoholic inpatients were given diagnoses of primary alcoholism without antisocial personality disorder or primary antisocial personality disorder with secondary alcoholism on the basis of data from structured interviews. Operationalized criteria for type 1 and type 2 alcoholism from three groups of researchers (Gilligan et al., von Knorring et al., and Sullivan et al.) were also used to designate subgroups of the same subjects. RESULTS: Subgroups of subjects classified as having type 1 or type 2 alcoholism according to the criteria of von Knorring et al. and of Sullivan et al. showed good levels of agreement, but the criteria of Gilligan et al. yielded poor agreement with those of the other two schemes. Subgroups with type 1 or type 2 alcoholism according to the criteria of Sullivan et al. showed significant overlap with subgroups diagnosed according to the primary/secondary alcoholism scheme: there was 73% concordance between the type 1 subgroup and the subgroup with primary alcoholism and 73% concordance between the type 2 subgroup and the subgroup with primary antisocial personality disorder and secondary alcoholism. CONCLUSIONS: There is variability in assigning diagnoses of type 1 and type 2 alcoholism with the use of current methods. Also, type 1/type 2 classifications based primarily on age-at-onset factors significantly overlap with the primary/secondary classifications of alcoholics.

The prognostic importance of blackouts in young men.

In order to test the commonly held perception that blackouts are an early diagnostic sign of alcoholism, we evaluated a sample of 230 nonalcoholic young men longitudinally over an 8-12 year follow-up period. Consistent with the literature, blackouts were a common occurrence in this cohort, with 26% of the men reporting blackouts by their early twenties, and 30% of the subjects experiencing blackouts over the approximately 10-year follow-up. Alcohol-related amnestic episodes were associated with the quantity and frequency of drinking, and men with blackouts (especially four or more) were more likely to have other problems related to their heavy drinking. Although few alcoholics will report not having had such amnestic spells, blackouts are not sensitive indicators of the risk for developing alcoholism. The data suggest that blackouts should be viewed as an important warning sign of problem drinking, but not as the "hallmark" of alcoholism.

Predictors of drinking and driving in healthy young men: a prospective study.

This paper explores the ability of information about alcohol use and problem patterns in men's early 20s to predict drinking and driving by their early 30s. The sample consisted of 231 healthy young men who were students or nonacademic staff at a university. Subjects were evaluated initially with questionnaires and interviews, and subsequently followed-up using interviews with themselves and with a resource person. The reported rate of drinking and driving at follow-up was nearly 38%. Using logistic regression, the combination of variables that best predicted drinking and driving included prior alcohol-related auto accidents, a measure of typical drinking, and a measure of drinking-related problems. The overall prediction employing this combination was 72%, the specificity was 86%, and the sensitivity was 48%.

Affective and anxiety disorders and alcohol and drug dependence: diagnosis and treatment.

Depression and anxiety frequently coexist in patients with substance use disorders. This clinically-oriented article examines the relationship between these conditions and emphasizes data showing that substances of abuse can cause signs and symptoms of both depression and anxiety. These substance-related syndromes appear to have a different course and prognosis than uncomplicated, independent anxiety and major depressive disorders, and clinicians should consider the role of alcohol and other drugs in all patients presenting with these complaints. The authors also outline an approach for diagnosing and managing patients with the combination of a substance use and depressive or anxiety disorder.

Amnestic effects of intravenous diazepam in healthy young men.

Changes in a test of memory performance were evaluated in 103 healthy young men after challenges with placebo and two different doses of intravenous diazepam (0.12 and 0.20 mg/kg). Both diazepam doses significantly impaired free recall in a dose-dependent manner. Within each dose challenge there was no significant correlation between the average serum diazepam or desmethyldiazepam levels and the average number of words recalled across the time points. The data expand our current understanding of the amnestic effects of benzodiazepines and suggest that patients abusing these drugs in large doses may develop profound degrees of memory impairment.

Genetic studies of alcoholism.

This paper reviews recent developments in the evaluation of genetic factors in alcoholism. After presenting the results of family, twin, and adoption studies, the authors turn to investigations focusing on children of alcoholics. An emphasis is placed on the finding of a decreased intensity of reaction to alcohol in sons and daughters of alcoholics. The potential implications of these findings are discussed.