There is growing evidence that chronic
alcoholism is associated with a derangement in the
sulfur amino acid metabolism. Excitatory aminoacids such as
glutamate,
aspartate, and
homocysteine have been shown to be increased in patients with chronic
alcoholism who underwent alcohol withdrawal. Furthermore, sustained
hyperhomocysteinemia occurred in chronic alcoholics with active drinking pattern. Excitotoxicity can be induced by increased hormocysteine levels via rebound activation of
NMDA receptor-mediated glutamatergic neurotransmission upon the removal of
ethanol-evoked inhibition. Therefore,
hyperhomocysteinemia may be responsible for the higher incidence of complications during alcohol withdrawal (e.g.
stroke,convulsions). In addition, an association between brain
atrophy and increased levels of
homocysteine in chronic
alcoholism was shown. This may have important implications for the pathogenesis of brain
atrophy in alcoholics. Taking into account that high plasma
homocysteine levels are helpful in the prediction of
alcohol withdrawal seizures, early anti-convulsive therapy could prevent this severe complication. Supplementation of
folate, a cofactor of the
homocysteine metabolism, lowers raised
homocysteine levels and therefore could be established as a new therapeutic strategy in alcohol withdrawal treatment. The results of various studies highlight the need for further research to prove whether alcoholics benefit from a reduced
homocysteine level with respect to both,
alcohol-related disorders and alcohol
withdrawal symptoms.