ALCOHOL

R.A.S HEMAT, MB;BCh, FRCSI, DUL.

The excessive consumption of alcoholic beverages is associated with numerous serious medical, social, and legal problems. Alcohol is a drug that produces a dual effect on the body. Withdrawal symptoms of alcohol are usually far more dangerous than those after withdrawal from the opiates or other drugs to which physical dependence may be developed. Withdrawal symptoms begin within the first 24 hours after the last drink, reach their peak intensity within 2-3 days, and disappear within one or two weeks. Aside from withdrawal itself, alcohol has a pervasive effect on the body's gastrointestinal tract, liver, bloodstream, brain and nervous system, heart, muscles, and endocrine system.

Alcoholism, one of the most common chronic disorders in the western world, causes or promotes a plethora of diseases and injuries. Ethanol is a hydrophilic and lipophilic substance, it may harm nearly every organ. Stress influences ethanol consumption and relapse in abstinent alcoholics.

Heavy alcohol consumption is associated with abnormalities of the menstrual cycle, sterility, miscarriages, and loss of female sexual characteristics, all of which are affected by the hormonal balance in women. Acute alcohol intake leads to decreased levels of testosterone in normal healthy men.

A genetic contribution to alcoholism has been firmly established. It has been evaluating that a roughly 40% rate of lifetime alcohol dependence among individuals who started drinking at age 14 or younger. The early exposure to alcohol causes an increase in alcohol use and misuse in subsequent years. Alcohol abuser have threefold increased risk of postoperative morbidity.

Gangliosides present a massive target for attracting both water and alcohol. Gangliosides may interact with each other, especially if ethanol influences dispersion. The displacement of hydrogen-bonded water is part of the mechanism of alcohol-induced intoxication. Acute ethanol can decrease the level of brain sialic acid, the acidic sugar that is a key component of gangliosides and many glycoproteins. The sugar of complex lipids and alcohol may share some similar properties. Alcohol displaces hydrogen-bonded water from membrane surfaces.

Ethanol consumption induces an oxidative stress in the liver and in extrahepatic tissues. CYP2E1, which is induced by administration of a large ethanol dose or after chronic ethanol ingestion, has a high oxidase activity and plays a crucial role in the microsomal generation of reactive oxygen species which have the capability of initiating membranous lipid peroxidation. Ethanol administration has been shown to induce an oxidative stress either by enhancing the production of oxygen reactive species and/or by decreasing the level of endogenous antioxidants. Tobacco smoking, which is very often associated with alcohol consumption, also produces free radicals and thus participates in the generation of oxidative stress. Ceramide may interact with mitochondria leading to generation of ROS. TNF activation of NF-kB requires mitochondrial ROS participation. Circulating levels of TNF and other cytokines are increased in patients with acute alcoholic hepatitis and chronic alcohol liver disease.

Ethanol excreted from the kidney may influence the detrusor function. In human, the ratio of urine alcohol to blood alcohol is 1.35. Acute ethanol intoxication can cause urinary retention in patients with BPE.

Chronic alcoholics are more prone to infections with a variety of pathogens. Altered inflammatory neutrophil, leukocyte, and macrophage functions after acute or chronic alcohol use contribute to impaired host defence against microbial infections. Acute alcohol inhibits monocyte phagocytic functions, antimicrobial activity, and expression of FcR-type II, which is involved in phagocytosis of antibody-coated particles. Ethanol may inhibit induction of ROS and NO in alveolar macrophages where these mediators play a crucial role in microbial killing. Alcohol use (potentially both acute and chronic) is likely to increase host susceptibility to HIV-1 infection and to contribute to an accelerated progression of HIV disease. Ethanol may accelerate the development of AIDS by disrupting cytokine production. Acute alcohol consumption may significantly modulate responses to subsequent challenges to the immune system, whether it is a bacterial, viral pathogen or trauma injury. The BCG infection in both alcoholics and non-alcoholic is associated with a significant increase in both CD4 and CD8 splenic T lymphocytes. BCG infection increases TNF, IFN, & IL-10 and decreases IL-4.

Alcoholic beverages are made from many plants and plant by-products that contain phytoestrogens. Alcoholism is associated with cardiomyopathy, arrhythmias, hypertension, and strokes. Alcohol may disrupt the NFkB function. The quantity of antioxidants consumed in wine may not reach sufficiently high plasma levels to prevent the oxidation of LDL. When alcohol consumption is chronic, platelet function is significantly reduced, and clotting time increases. Even after alcohol intake ceases, these effects persists for several weeks.

April, 2002

Note: The information in this article has been excerpted from the following books: urotext-ebook simplifying urology, Principles of modern urology, Principles of Orthomolecularism, Andrology, by Dr. R.A.S HEMAT. Permission is granted to copy and redistribute this document electronically as long as it is unmodified. This article may not be sold in any medium, including electronic, CD-ROM, or database, or published in print, without the explicit, written permission of Dr. R. A. S. Hemat.

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Dr. R.A.S HEMAT declares no conflicts of interest or financial interests in any product or service mentioned in this article, including grants, employment, stock holdings, gifts, or honoraria.