Alcoholism and Occupation: A Review

The post-war literature associating alcoholism with specific occupations is reviewed. It is concluded that some occupations do have particularly high alcoholism rates, though whether these are due to selection factors, or job pressure, remains unclear.     

A Medical Audit of Acute Alcoholism and Chronic Alcoholism

A medical audit for acute alcoholism was done in a large private general hospital where the cases are admitted to and treated on the general medical service. Another medical audit was done for chronic alcoholism for patients admitted to an alcoholism rehabilitation unit in a large general hospital in a teaching center.     

Alcoholism: A systemic proinflammatory condition

Excessive ethanol consumption affects virtually any organ, both by indirect and direct mechanisms. Considerable research in the last two decades has widened the knowledge about the paramount importance of proinflammatory cytokines and oxidative damage in the pathogenesis of many of the systemic manifestations of alcoholism. These cytokines derive primarily from activated Kupffer cells exposed to Gram-negative intestinal bacteria, which reach the liver in supra-physiological amounts due to ethanol-mediated increased gut permeability. Reactive oxygen species (ROS) that enhance the inflammatory response are generated both by activation of Kupffer cells and by the direct metabolic effects of ethanol. The effects of this increased cytokine secretion and ROS generation lie far beyond liver damage. In addition to the classic consequences of endotoxemia associated with liver cirrhosis that were described several decades ago, important research in the last ten years has shown that cytokines may also induce damage in remote organs such as brain, bone, muscle, heart, lung, gonads, peripheral nerve, and pancreas. These effects are even seen in alcoholics without significant liver disease. Therefore, alcoholism can be viewed as an inflammatory condition, a concept which opens the possibility of using new therapeutic weapons to treat some of the complications of this devastating and frequent disease. In this review we examine some of the most outstanding consequences of the altered cytokine regulation that occurs in alcoholics in organs other than the liver.     

Alcoholism Treatment: A Ten-Year Follow-Up Study

Two hundred male and female patients, selected at random from all patients admitted to an inpatient alcoholism treatment facility in 1973-1974, were surveyed 10 years following treatment. Response rate was 80%, and a validity check was done. Of the 158 unstable responses, 61% reported complete or stable remission of their alcoholism for at least 3 years prior to the survey and 84% reported stable psychosocial status. Successful outcome was possible regardless of severity of drinking history or psychosocial status. Seventy-six percent (76%) of those still alive at follow-up reported remission; at most, 23% of the deceased were reported in remission prior to death. Involvement in Alcoholics Anonymous (AA) predicted abstinence, suggesting successful outcome for patients who undergo a treatment regimen, which bridges patients into AA involvement. Of those respondents who continued to sponsor other AA members throughout the follow-up period, 91% were in remission at the time of survey.     

Impact of Chronic Alcoholism on the Aging Rat: Changes in Nutrition, Liver Composition, and Mortality

The adverse effects of chronic alcohol consumption (mean 6.68 g/kg/d) were assessed in 150 male Sprague-Dawley rats over their life span (25 months). Evaluations were performed at 2, 3, 8, 13, 19, and 25 months of age for changes in nutrition status, biochemical tests for liver injury, compositional changes in liver, and hepatic regenerative capacity. In spite of nearly identical caloric intake, alcohol treatment was associated with nutritional levels 10-30% lower than controls.
Maximal changes were observed at the two extremes of ages (2-3 months and 19-25 months). Hence, a nutritional contribution to other adverse changes could not be excluded. Fatty compositional increases (triglycerides) occurred early (5-fold increases after 1 month of treatment) then declined to levels only slightly above controls. Biochemical tests on sera for liver injury (AST and total bilirubin) were consistently higher with alcohol treatment. Regenerative capacity measured by [³H]thymidine uptake after partial hepatectomy was initially elevated in the alcoholic then rapidly declined beyond 7 months of age. In control animals, an age-related decline was also observed but occurred later beyond 12 months of age. Consistent with these adverse effects, ethanol diet survival was poorer than the pair-fed control groups by 15% (median survival for alcoholics, 17 months vs. 20 months in controls).     

Alcoholism: allostasis and beyond

Alcoholism is a chronic relapsing disorder characterized by compulsive drinking, loss of control over intake, and impaired social and occupational function. Animal models have been developed for various stages of the alcohol addiction cycle with a focus on the motivational effects of withdrawal, craving, and protracted abstinence. A conceptual framework focused on allostatic changes in reward function that lead to excessive drinking provides a heuristic framework with which to identify the neurobiologic mechanisms involved in the development of alcoholism. Neuropharmacologic studies in animal models have provided evidence for specific neurochemical mechanisms in specific brain reward and stress circuits that become dysregulated during the development of alcohol dependence. The brain reward system implicated in the development of alcoholism comprises key elements of a basal forebrain macrostructure termed the extended amygdala that includes the central nucleus of the amygdala, the bed nucleus of the stria terminalis, and a transition zone in the medial (shell) part of the nucleus accumbens. There are multiple neurotransmitter systems that converge on the extended amygdala that become dysregulated during the development of alcohol dependence, including gamma-aminobutyric acid, opioid peptides, glutamate, serotonin, and dopamine. In addition, the brain stress systems may contribute significantly to the allostatic state. During the development of alcohol dependence, corticotropin-releasing factor may be recruited, and the neuropeptide Y brain antistress system may be compromised. These changes in the reward and stress systems are hypothesized to maintain hedonic stability in an allostatic state, as opposed to a homeostatic state, and as such convey the vulnerability for relapse in recovering alcoholics. The allostatic model not only integrates molecular, cellular, and circuitry neuroadaptations in brain motivational systems produced by chronic alcohol ingestion with genetic vulnerability but also provides a key to translate advances in animal studies to the human condition.     

Alcoholism and Cocaine Addiction:

No abstract available for this article.     

Physicians Treated for Alcoholism: A Follow-Up Study

Studying alcoholism and chemical dependency among members of the medical profession, the authors discovered that, despite the special problems associated with alcoholic physicians, the number responding to treatment and showing improvement is high, and the overall results are encouraging.     

Static Ataxia: A Predictor of Alcoholism?*

Non-alcoholic college-aged males with and without a family history of alcoholism were compared on a measure of static ataxia (body sway). In two separate studies, subjects with alcoholic biological relatives showed significantly greater body sway than those without such relatives. This effect was independent of alcohol influence and subjects' typical drinking pattern. To the extent that subjects with a family history of alcoholism are at risk to become alcoholic, these results suggest that the previously reported motor impairment of alcoholics may exist prior to chronic alcohol intake. This possibility should be considered cautiously, due to two methodological issues: (a) differences between the two studies in measurement procedures and (b) the use of subjects' self reports for family history classifications. Methodological improvements and future research directions were discussed.     

Immune Function in Alcoholism: A Controlled Study

Several studies have shown an increased risk for infection and cancer in alcoholic patients. The mechanisms for such observations remain largely unknown. In an effort to investigate the possibility of immunological dysfunction in alcoholism, we studied three immune parameters in 47 hospitalized chronic alcoholic patients and 47 age-and sex-matched normal controls. The immune measures were: (1) lymphocyte phenotyping, with estimates of percentages of T cells, B cells, T helpers, T suppressors, natural killer (NK) cells, and cells carrying the activation markers IL₂R₁ and l₂; (2) NK cell activity; and (3) lymphokine-activated killer cell activity. Results indicate a significant increase in the IL₂R and l₂ lymphocyte markers in alcoholic patients compared with matched controls. We also found a nonsignificant trend for a decrease in the percentage of suppressor T cells in the alcoholic group, as well as a trend for a negative correlation between the percentage of T suppressor cells and age. There were no significant differences in either NK or lymphokine-activated killer cell activities between the two groups. Furthermore, there were no significant associations between duration and intensity of alcohol consumption and any of the immune measures. These results suggest subtle alterations in immune regulation in alcoholic patients that cannot be explained solely on the basis of duration and/or amount of alcohol consumed.     

Lithium and the Treatment of Alcoholism: A Critical Review

Lithium has been tried in many psychiatric conditions but its efficacy has been firmly established only in the case of certain affective disorders. Many alcoholics are also clinically depressed and it therefore seems possible that lithium could be of benefit in treating alcoholics who have concurrent affective disturbances; this suggestion is supported by the results of studies so far reported. For the moment however, evidence from long-term investigations on alcoholics indicate that therapeutic effects of lithium are not simply caused by an alleviation of associated affective disorders, and the role of the mood disturbance in treatment response is not clear. Observations in acute studies suggest a possible mechanism of action, as lithium can attenuate the mood-elevating effects of alcohol in subjects who abuse drugs or are depressed. Unfortunately many of these clinical reports are uncontrolled and can be criticized on other methodological grounds, and further double-blind studies which include comparisons with other drug treatments are required. Studies on rodents show that alcohol drinking is often reduced by lithium, but these results must be interpreted cautiously because lithium may produce conditioned aversion to alcohol and such a mechanism of action is unlikely in long-term studies on man.     

Genetic and Experiential Antecedents of Alcoholism: A Prospective Study

The present work builds on an extensively studied obstetrical cohort that includes a group of individuals, now in their midteens, who had a parent treated for alcoholism. To generate a comparable sample today would not only require a very large effort (many years and considerable expense), but might not be possible in most countries because of lack of records or restricted access to them, as well as difficulty in, locating people after long periods. Such a study is still possible in Denmark, which has a long tradition of cooperation between public officials and scientific investigators and invaluable centralized population and psychiatric registers. Since such an opportunity may not present itself again, and since it is difficult to anticipate which avenues of investigation will be more profitable, the study is designed as a collaborative effort by investigators from a number of disciplines: psychiatric, psychological, neurologic, sociologic, biochemical, and electrophysiologic. From the enormous amount of data collected, genetic and experiential antecedents of alcoholism and associated psychopathology can be identified.