Chronic Consumption of Ethanol Alcohol and Neurological Dysfunction

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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 of certain neurotransmitters. (Oscar-Berman, Shagrin, Evert, & Epstein, 1997) Alcohol can alter the action of neurotransmitters both directly and indirectly. Alcohol affects neurotransmitters directly by interfering with receptor proteins. Receptor proteins on the surface of neurons normally recognize neurotransmitters and initiate a cell response. With extended exposure to drugs such as alcohol the levels of these receptor proteins change. Genes in the DNA of the neuron are affected causing both increases and decreases to the synthesis of these receptor proteins. The extensive regulation required by the body to obtain equilibrium can lead to many negative neurological side effects. This negative neurological side effect can present as seizers, imbalance, sedation, and behavioral disorders (Oscar-Berman, Shagrin, Evert, & Epstein, 1997) Alcohol can also alter the action of neurotransmitters in the brain by inhibiting the brain from processing glutamate. (Oscar-Berman, Shagrin, Evert, & Epstein, 1997) Glutamate is major facilitator of expiatory signals in the human brain. Glutamate functions as a neurotransmitter because of glutamate receptor protein on the surfaces of neurons. Glutamate binds to this protein receptor which initiates a response in the neuron. These receptors are found in both nerve and glial cells. (Danbolt, 2001) Even small amounts of alcohol consumption can affect the glutamate action as a neurotransmitter. This interference affects memory, cognition and learning. (Oscar-Berman, Shagrin, Evert, & Epstein, 1997) A symptom of theses neurological deficits appear in other chronic and acute alcoholics as “alcoholic blackouts”.

Alcohol effects many neurotransmitters because of its effects on several ligand-gated ionophores; such as, an isotropic glutamate receptor NMDA (N-methyl-D-aspartate, 5-HT3 receptors, and an acetylcholine receptor cholinergic. the neurotransmitter serotonin 5-HT3, also known a, hydroxytrptamine is a manoamine...
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