Alcohol vitamin interactions

Leo MA, Lieber CS. Alcohol, vitamin A, and beta-carotene adverse interactions, including hepatotoxicity and carcinogenicity. Am J Clin Nutr 1999 69(6) 1071-85. 

Beta-adrenoceptor antagonists arthralgia, 11.164 sexual function, 15.188 Beta-carotene, see also Vitamin A alcohol, vitamin A, interaction, 24.442 tumorigenicity, 25.454 Beta-lactam antibiotics effects on eukaryotic cells, 13.212 immediate hypersensitivity reactions, 14.211 pregnancy, 25.280 Blood, see Transfusions Botulinum toxin A, use in primary axillary hyperhidrosis, 27.161... 

At first glance it may seem that like dissolves like does not apply here. Certainly, none of these complex molecules looks like water, and the resemblance to simple hydrocarbons such as cyclohexane also is remote. Keep in mind, however, that the basis for the principle is that similar compounds dissolve in each other because they have common patterns of intermolecular interactions. Example indicates that alcohols containing large nonpolar segments do not dissolve well in water. We can categorize vitamins similarly by the amounts of their stmctures that can be stabilized by hydrogen bonding to water molecules. 

Cholestyramine use is not without limitations. It does not bind chlordecone alcohol, a metabolite of chlordecone that is also excreted in the bile (Guzelian 1981). It has a gritty texture in the mouth, and it causes several gastrointestinal disturbances, which may limit the willingness of patients to take it. It may also interfere with the absorption of fat-soluble vitamins and interact with other medications (Goldfrank 1990). 

Thiamine (vitamin B1 ) Essential vitamin required for synthesis of the coenzyme thiamine pyrophosphate Administered to patients suspected of having alcoholism (those exhibiting acute alcohol intoxication or alcohol withdrawal syndrome) to prevent Wernicke-Korsakoff syndrome Administered parenterally Toxicity None Interactions None... 

Lipid peroxidation of biological membranes is a destructive process, proceeding via an autocatalytic chain reaction mechanism [73]. Membrane phospholipids contain hydrogen atoms adjacent to unconjugated olefinic bonds, which make them highly susceptible to free radical oxidation. This is characterised by an initiation step, one or more propagation steps and a termination step [1], which may involve the combination of two radical species or interaction with an antioxidant molecule such as vitamin E. The products formed from such reactions include lipid peroxides, lipid alcohols and aldehydic by-products such as malondialdehyde and 4 hydroxynonenal [73]. 

As the reader is no doubt aware, we could fill up volumes on medical data surrounding alcohol use, abuse and interactions with other chemicals in the body. (In fact. Do It Now, publishes other works relating to alcohol in greater depth besides this one.) So what we will touch on are some basics involving vitamins, some basics regarding nutrition, and alcohol-related illnesses and physiological problems. 

Although workers are often exposed to a variety of solvents with Stoddard solvent, there are no available studies specifically characterizing the interactions of Stoddard solvent with other chemicals. Since Stoddard solvent may have adverse effects on the nervous system, it may compound the effects of other chemicals that cause central nervous system depression, such as alcohol, barbiturates, benzodiazepines, or medical anesthetics. Guinea pigs with a diet high in vitamin C survived a high exposure to Stoddard solvent vapors better than those with a diet low in vitamin C (Jenkins et al. 1971) however, it is not known how vitamin C levels might affect humans exposed to Stoddard solvent. 

The interaction between alcohol and vitamin A is complex. They have overlapping metabolic pathways a similar 2-step process is involved in the metabolism of both alcohol and vitamin A, with alcohol dehydrogenases and acetaldehyde dehydrogenases being implicated in the conversion of vitamin A to retinoic acid. Alcohol appears to act as a competitive inhibitor of vitamin A oxidation. In addition, chronic alcohol intake can induce cytochrome P450 isoenzymes that appear to increase the breakdown of vitamin A (retinol and retinoic acid) into more polar metabolites in the liver, which can cause hepatocyte death. So chronic alcohol consumption may enhance the intrinsic hepatotoxicity of high-dose vitamin A. Alcohol has also been shown to alter retinoid homoeostasis by increasing vitamin A mobilisation from the liver to extrahepatic tissues, which could result in depletion of hepatic stores of vitamin A. ... 

Among humans, abnormal dark adaptation is reported in both vitamin A deficiency and zinc deficiency and is especially prevalent in alcoholic cirrhotics (Patek and Haig, 1939 Russell et aL, 1973 Morrison et aL, 1978 McClain et aL, 1979). In the former but not in the latter deficiency, treatment with vitamin A reverses the abnormality (Russell et aL, 1978) only after correcting the zinc deficiency does dark adaptation become normal in the latter case (Morrison et aL, 1978 McClain et aL, 1979). The molecular basis for these observations may be associated, at least in part, with the activity of retinaldehyde reductase in the retina which, as already mentioned, Huber and Gershoff (1975) showed to be especially sensitive to the level of zinc nutriture and Mezey and Holt (1971) showed was competitively inhibited by the presence of ethanol. In the alcoholic cirrhotic, however, the zinc-vitamin A interaction may be further complicated by a defective hepatic synthesis of transport proteins (Mobarhan et aL, 1981) or failure to sequester or retain zinc Nutrition Reviews, 1982) and/or vitamin A (Sato and Lieber, 1981 Leo and Lieber, 1982) in the appropriate tissues. The implications for human nutrition of the interaction of vitamin A and zinc were reviewed by Solomons and Russell (1980). 

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