The major established risk for stroke is high blood pressure (BP) which in the human male is more closely correlated with alcohol consumption than with salt intake or stress (2). Ethanol contributes to hypertension both directly and via obesity (3). Adiposity in the human male (except genetic adiposity) is not always simply due to overeating or sedentary existence. Up to the age of 50 years it in-creases in parallel with alcohol consumption (3). A pathological mechanism linking alcohol to obesity is hyperinsulinaemia, promoting the lipogenetic effects of insulin (I). Hyperinsulinaemia may also contribute to high BP via increased renal sodium retention. However, hepatic steatosis is associated with hyperinsulinaemia, even in slender men. The importance of this process is, however, difficult to estimate because alcohol consumption is usually concealed, and reliable laboratory tests for hepatic steatosis are not currently available. Even the gamma glutamate transferase (gamma-GT) level is normal in most patients with fatty livers.