This study was supported in part by the Medical Research Council of Canada and the Alcoholic Beverage Medical Research Foundation.
Zinc Deficiency and Corticosteroids in the Pathogenesis of Alcoholic Brain Dysfunction—A Review
Article first published online: 11 APR 2006
Alcoholism: Clinical and Experimental Research
Volume 18, Issue 4, pages 895–901, August 1994
How to Cite
Menzano, E. and Carlen, P. L. (1994), Zinc Deficiency and Corticosteroids in the Pathogenesis of Alcoholic Brain Dysfunction—A Review. Alcoholism: Clinical and Experimental Research, 18: 895–901. doi: 10.1111/j.1530-0277.1994.tb00057.x
- Issue published online: 11 APR 2006
- Article first published online: 11 APR 2006
- Received for publication March 10, 1993; accepted March 7, 1994
- Brain Dysfunction;
- Zn Deficiency;
- Free Radicals
Chronic alcoholism is associated with hypercortisolemia and low serum zinc (Zn). Hypercortisolernia could be responsible for alcoholic cerebral atrophy and is also associated with enhanced NMDA neurotoxicity. It is hypothesized that low brain Zn, noted in chronic alcoholics, enhances NMDA excitotoxicity and ethanol withdrawal seizure susceptibility. Also, Zn deficiency can produce neuronal damage through increased free radical formation. Clinically, Zn replacement therapy may be a rational approach to the treatment of alcohol withdrawal seizures and alcohol-related brain dysfunction.