The dangers of alcohol have been exaggerated by mainstream medicine and this fear has been fanned by the mainstream media. Many populations around the world drink large amounts of alcohol and have few social problems and do not suffer from Western diseases. However, the difference between these populations and the West is that alcohol is generally consumed over time with a high quality diet. That being said alcohol is a metabolic poison, and in this respect does cause physiological changes to some important metabolic pathways. In particular, alcohol consumption appears to alter the absorption, metabolism and excretion rates of certain micronutrients. It is well known that alcoholics frequently have vitamin B deficiencies, and this can cause secondary hypovitaminosis if supplements are not taken or dietary improvements not implemented. Less well known is the ability of alcohol to increase the excretion of zinc, with hyperzincuria being associated with the consumption of alcohol.
The mean serum zinc concentrations of alcoholics has been reported to be lower than those of non-alcoholic controls (10.7 μmol/L versus 10.7 μmol/L, respectively). While zinc excretion rates are undoubtedly increased with frequent alcohol consumption, and may explain some of this discrepancy, there is also evidence that chronic alcohol can decrease zinc absorption. Following a meal postprandial zinc levels fall in both alcoholic (19%) and in non-alcoholic controls (23 %). However, when 25 mg of zinc are supplemented with an identical meal, a rise in plasma zinc concentrations is seen in both alcoholic and non-alcoholic subjects1. When the same meal is given but with 50 mg of zinc, the non-alcoholic control subjects experience a larger postprandial rise in serum zinc concentrations compared to the alcoholic subjects. These results therefore suggests that there might be some inhibitory effects of regular alcohol on the absorption of zinc in alcoholics, or that zinc concentrations have reached a saturation point in the alcoholic subjects.
It could be that chronic alcohol consumption might therefore contribute toward the lower serum zinc concentrations reported in alcoholic subjects. It should be noted however, that 50 mg of zinc is larger than might be found in food and at lower more physiologically relevant intakes of zinc the response of the alcoholic subjects was normal. The fall in postprandial zinc concentrations in both healthy and alcoholic subjects is also interesting, and other studies have reported similar findings. The reason for this fall is not fully understood, however a number of explanations are possible. The fall could relate to the release of pancreatic secretions during digestion, which are known to be rich in zinc containing enzymes. This zinc may bind to metallothionein in the small intestine, which may act as a temporary store of zinc. As digestion proceeds this zinc is then released and absorbed, allowing serum zinc levels to return to normal following the postprandial period. The rise in postabsorptive serum zinc concentrations support this hypothesis.
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