An Enquiry into the Role of Cobalt in the Heart Disease of Chronic Beer Drinkers

Abstract

The natural history of a new disease entity in chronic beer drinkers consisting of pericardial effusion, a low cardiac output, and in about half of the cases of polycythemia is presented. Normalization of the heart volume, the hemoglobin value, and the hemodynamic state was obtained in patients who stopped drinking. Further evidence of the importance of cobalt in the development of the disease is presented. All patients drank beer to which cobalt was added and the disease was not seen in chronic alcoholics drinking wine or other alcoholic beverages. In view of the rather small quantity of cobalt consumed, an hypothesis is formulated which attributes the cobalt toxicity in chronic alcoholics, to a dietary deficiency of sulfhydryl-groups containing amino acids and a dietary deficiency of protein.

Cardiovascular diseases and the work environment. A critical review of the epidemiologic literature on chemical factors.

“…The cause of the epidemic was relatively quickly established. Several beer manufacturers had begun to add cobalt sulfate to the beer in order to stabilize the foam (156)(157)(158)(159)(160)(161). Nearly half the patients examined in the various studies died from their cardiomyopathy.…”

Chronic alcohol consumption disrupts myocardial protein balance and function in aged, but not adult, female F344 rats

“…When the excessive alcohol consumption is longstanding, a nonischemic cardiomyopathy develops, which is referred to as alcoholic cardiomyopathy (59). Whereas the etiology of this distinct disease entity is poorly understood, it is most certainly influenced by both genetic and environmental components (13,33) and is more symptomatic in individuals where alcohol consumption is increased with regard to amount and duration (71). Gender may also be a factor as women develop an asymptomatic form of alcoholic cardiomyopathy with a lower total lifetime consumption of alcohol (12,70).…”

Alcoholic Cardiomyopathy: A Review

“…Environmental factors (cobalt, arsenic) and genetic predisposition (HLA-B8, alcohol dehydrogenase alleles) have been proposed as triggers or abettors in the etio-pathogenesis of alcoholic heart disease. For example, 'Quebec beer-drinkers' cardiomyopathy appeared as an epidemic among heavy beer drinkers in Canada in mid-1960s 28 . It resembled typical a dilated cardiomyopathy except for purplish skin coloration and high early mortality rate (42%).…”