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Chronic Consumption of Ethanol Alcohol and Neurological Dysfunction

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Chronic Consumption of Ethanol Alcohol and Neurological Dysfunction
Chronic Consumption of Ethanol Alcohol and Neurological Dysfunction

Ethanol Alcohol, commonly known as Alcohol is the primary mood altering drug used in the United States of America. When alcohol is consumed it is absorbed unaltered by the stomach and the small intestines. Then the ethanol molecules are distributed evenly to all of the tissues and fluids of the body. The alcohol present in the bloodstream is metabolized by the liver through three pathways. The major pathway involves an enzyme of the cytosol, hepatic alcohol dehydrogenase (ADH). This enzyme assists in converting ethanol alcohol into acetaldehyde and free radicals. The two accessory pathways use to catalyze ethanol into acetaldehyde are the microsomal P-450 pathway and the catalase. The microsomal P-450 pathway is dependent on a super family of enzymes, cytochrome P-450. This pathway is only “turned on” when ethanol levels are high in the bloodstream. All three of these pathways convert alcohol into acetaldehyde which puts a lot of stress on the liver causing liver cirrhosis. (McCance & Huether, 2006)
Advanced alcoholic liver disease is called portal-systemic encepthalophy (PES). Patients who suffer from this disease have livers so damaged by cirrhosis that the venous blood flow is obstructed. This allows toxic substances to build up in the bloodstream which transports these toxins all over the body. Toxic substances in the brain interfere with the actions of many neurological transmitters and do neurological damage . (Oscar-Berman, Shagrin, Evert, & Epstein, 1997)
Alcohol also has other indirect effects on certain neurological transmitters. Excessive alcohol use has major consequences on the nutritional health of people causing major nutritional deficiencies. Alcoholics experience nutritional deficiencies in thymine, Vitamin B, magnesium, and phosphorus. Some neurological dysfunction present in alcoholics is due to poor nutrition. Poor nutrition is a major factor in the dysfunction



Cited: Danbolt, N. (2001). Glutamate as a Neuro Transmitter. The Neurotrasporter Group, 100-105. Gorelick, P. (1986). Alcohol and Stroke. current Conceptes of Cardiovascular Disease, 268-271. McCance, K., & Huether, S. (2006). Pathophysiology: The Biological Basis for Disease in Adults and Children. Moseby Inc. Osacar-Berman, M., & Bowirrat, A. (2005). Genetic influnces in emotional dysfunction and alcoholism-related brain damage. Nuropsychiatric Disease and Treatmant, Dove Press. Oscar-Berman, M., Shagrin, B., Evert, D., & Epstein, C. (1997). Imparments if the Brain and Behavior: The Neurological Effects of Alcohol. Alcohol Health and Research World, 65-75. Sullivan, E., & Pfefferbaum, A. (2009). Pontocerebellar Volume Deficits and Ataxia in Alcoholis Man and Women: No Evidence of Telescoping. psychopharmacology, 279-290. .

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