Alcohol abuse pathophysiology

The relationship between alcohol abuse and suicide has been recognized for many years, with at least one in five suicide victims being intoxicated at the time of their death. Alcohol may lower inhibitions, serving as a precipitant to the act, or the disease of alcoholism itself could be a risk factor. Alcohol also induces biochemical changes (e.g., lowers CSF 5-HIAA and decreases 5-HT2 receptors in the neocortex), similar to changes observed in at least a subset of depressive disorders. Thus, alcohol may aggravate or contribute to the pathophysiology that mediates the depressive syndrome and leads to suicide completions. 

A rise in the NADH/NAD ratio and the associated increase in the redox potential as well as the formation of acetaldehyde result in a variety of metabolic disturbances in the hepatocellular oxidation processes, so that pathophysiological consequences can be observed. This large variety of alcohol-induced metabolic disturbances is responsible for many situations of clinical importance, and thus acute and chronic alcohol abuse will eventually result in additional metabolic complications, (s. tab. 28.2)... 

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