Abstract

There has been increasing attention recently to the possible role of alcohol consumption in the development of cardiovascular disease.’ A considerable body of evidence now indicates that the consumption of alcoholic beverages is associated with two factors known to be related to cardiovascular risk. On the one hand, alcohol consumption is associated with elevations of blood pressure2m5; that is, presumably, with an increased risk of cardiovascular disease. On the other, alcohol consumption tends to increase the concentration of high density lipoprotein (HDL) and perhaps decrease that of low density lipoprotein,6 which implies a decreased risk of coronary heart disease (CHD). Moreover, there is also evidence that alcohol when consumed in large quantities may induce heart arrhythmias, and that chronic alcohol abuse may lead to myocardial damage.7 Thus it would not be surprising if alcohol consumption increased the risk of certain cardiovascular events and decreased the risk of others. The literature is ambivalent. Some studies report a negative association of alcohol consumption with CHD*-12; others report no association’3-15 or a positive association.“v’6-‘8 One study reported a positive association of drinking with strokeIs; another study did not.20 Since the cardiovascular diseases are multifactorial in origin and are interrelated, and since alcoholic beverages have a variety of physiologic effects and these effects vary with the amount of alcohol consumed, it is not surprising to find apparently paradoxical relationships between drinking and the cardiovascular diseases. A careful exploration of the available data seems to be in order. This report explores relevant data derived from 24 years of follow-up of the Framingham Study

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