Alcohol vitamin deficiencies

Alcohol dextrose solutions are used cautiously in patients with hepatic and renal impairment, vitamin deficiency (may cause or potentate vitamin deficiency),... 

Delirium tremens (the D.T.s ) resulting from alcohol withdrawal is slightly different in that it is usually preceded by the shakes, convulsions and occasionally by alcoholic hallucinosis - characterized by accusatory auditory hallucinations. As observed 60 years ago by Maurice Victor, an expert on alcohol problems, delirium tremens usually does not appear until day 3 or 4 following abrupt withdrawal from alcohol. The patient is generally malnourished and grossly deficient in vitamin Bj (thiamine) as the result of a diet consisting of little but alcohol. This deficiency ftirther compromises mental function. 

Nutritional Deficiency-Related Dementias. We have already mentioned that chronic alcoholics are subject to thiamine deficiency that can cause dementia. It usually occurs only after heavy, prolonged abuse of alcohol. In developed countries, the other key nutritional concern is vitamin deficiency. Vitamin deficiency can surprisingly strike even those with a healthy diet. Such people are missing a vital protein, intrinsic factor, which would enable them to absorb it from their digestive tract. 

A healthy diet usually covers average daily vitamin requirements. By contrast, malnutrition, malnourishment (e.g., an unbalanced diet in older people, malnourishment in alcoholics, ready meals), or resorption disturbances lead to an inadequate supply of vitamins from which hypovitaminosis, or in extreme cases avitaminosis, can result. Medical treatments that kill the intestinal flora—e. g., antibiotics—can also lead to vitamin deficiencies (K, Bi2, H) due to the absence of bacterial vitamin synthesis. 

Chronic excessive consumption of alcohol can result in physical dependence or alcoholism. There is often a steady progress in the need to drink, so that the person starts drinking early in the day to maintain blood alcohol levels and avoid withdrawal effects. Alcoholism often results in a variety of organ system effects, some of which are related to accompanying malnutrition. Treatment for alcoholism must address the withdrawal effects as well as associated vitamin deficiencies associated with malnutrition. 

Vitamin deficiency of Bj leads to the disease known as Beriberi. However, nowadays in the Western hemisphere, vitamin Bj deficiency is mainly found as a consequence of extreme alcoholism. In fact, the vitamin absorption by the gut is decreased and its excretion is increased by alcohol. Alcohol also inhibits the activation of vitamin Bj to its coenzyme form, thiamine pyrophosphate ester (TPP). There is no evidence of adverse effects of oral intake of thiamine [417]. The main food sources of vitamin Bj are lean pork, legumes, and cereal grains (germ fraction). It is soluble in water and stable at higher temperature and at pH lower than 5.0, but it is destroyed rapidly by boiling at pH 7.0 or above. 

Recommended dietary allowances for vitamins have proved to be useful guidelines however it has to be appreciated that these guidelines are not more than estimates made from experiments on only a limited number of subjects. These recommended dietary allowances also need periodic reevaluation. While vitamin deficiencies due to inadequate intakes are encountered in developing countries, few cases are seen in the Western world apart from patients with an increased risk for deficiencies such as diabetics or alcoholics. On the contrary, the widely held belief that vitamins promote better health is deceptive and may lead to overdose disorders. 

Individuals with chronic alcoholism are prone to gastritis and have increased susceptibility to blood and plasma protein loss during drinking, which may contribute to anemia and protein malnutrition. Alcohol also reversibly injures the small intestine, leading to diarrhea, weight loss, and multiple vitamin deficiencies. 

Malnutrition from dietary deficiency and vitamin deficiencies due to malabsorption are common in alcoholism. 

Folic acid (or folate), which plays a key role in one-carbon metabolism, is essential for the biosynthesis of several compounds. Folic acid deficiency is probably the most common vitamin deficiency in the United States, particularly among pregnant women and alcoholics. 

Vitamin B Three substances are classed under the term pyridoxine or adermine pyridoxol, pyridoxal and pyridoxamine. Pyridoxine was isolated by various study groups in 1938. Its structure was described by Folkers and Kuhn in 1939. Pyridoxal and pyridoxamine were discovered by Snell in 1942. Pyridoxal phosphate and pyridoxamine phosphate are biologically active substances. Intestinal absorption of Bg is dose-dependent and not limited. In alcoholism, a deficiency of vitamin Bg is encountered in 20—30% of cases, whereas the respective percentage is 50—70% in alcoholic cirrhosis. Vitamin Bg is an important coenzyme for transaminases, which transfer amino groups from amino adds to keto acids. In this way, biochemical pathways between the dtiic acid cycle and carbohydrate and amino acid metabolisms are created. (104)... 

The manifold relationships between the metabolic functions of the liver and the vitamins fulfil vital tasks in helping the organism to stay healthy. Nutrition low in vitamins or age-related reduction in intestinal vitamin resorption as well as chronic alcoholism may be responsible for the development of hypovitaminosis. Standard values of vitamins (including fat-soluble vitamins) in the serum do not exclude a deficit. Deficiency is often recognized for the first time owing to the manifestation of clinical symptoms, and now requires substitution. Substitution therapy may be recommended, even if no vitamin deficiencies have become manifest at this stage, (s. p. 47) (s. tab. 28.2 )... 

The population thought to be nxost at risk for Bf, deficiency comprises chronic alcoholics. The deficiency arises fixim a low intakt of the vitamin as well as from alcoho[-induced impairments in the metabolism of the vitamin. An alcoholic deriving of his or her energy requirement from whiskey might be expected to be consuming only 20% of the KDA for vitamin 8, as well as for other nutrients such as protein, folate, and thiamin. 1 he symptoms of deficiency are not specific for this nutrient- They include depression, confusion, and sometimes convulsions. 

Thus, high-dose intravenous therapy should be given with caution to patients with prior vitamin deficiency or a history of alcohol abuse (103). 

Severe riboflavin deficiency is known as ariboflavinosis. Its major symptoms include cheilosis,. seborrheic dermatitis, and vascularization of the cornea. Ariboflavinosis occurs in chronic alcoholism in combination with other vitamin deficiencies. It has also resulted from phenothiazine, tricyclic antidepressant, and probenecid therapy. Riboflavin has no pharmacological action and is relatively nontoxic. The only approved indication is in the treatment and prevention of ariboflavinosis. 

Riboflavin is a nutritional supplement used during periods of deficiency known as ariboflavinosis. Riboflavin deficiency usually occurs in association with malabsorption, alcoholism, or protein-calorie deficiency, and is rarely the sole vitamin deficiency. Riboflavin needs are increased during chronic debilitative stress to the body such as malabsorption diseases of the small intestine, liver disease, hyperthyroidism, alcoholism, and during pregnancy and lactation. Neonates undergoing phototherapy for hyperbiliru-binema also have increased nutritional needs. 

Rodriguez-Martin JL, Qizilbash N, and Lopez-Arrieta JM (2001) Thiamine for Alzheimer s disease. Cochrane Database of Systematic Reviews 2 CD001498. Thomson AD (2000) Mechanisms of vitamin deficiency in chronic alcohol misusers and the development of the Wernicke-Korsakoff syndrome. Alcohol Alcoholism 35(Suppl 1) 2-7. 

A vitamin deficiency occurs when there is an insufficient quantity of vitamins for metabolism, such as when the patient s intake of vitamins is less than that required for his or her metabolism. Patients such as alcoholics and elderly people may not have a well-balanced diet or have difficulty absorbing food. Patients who have conditions that increase metabolism may use up their vitamin supply quicker than they can absorb food. 

Thompson AD. Mechanisms of vitamin deficiency in chronic alcohol misuse and the development of the Wernicke-Korsakoff syndrome. Alcohol Alcohol 2000 35 Suppl 1 2-7. 

Chronic overdrinking or binge-drinking alcoholism causes deficiencies of folate, thiamine, pyridoxine, vitamin A, and zinc, the combination of which causes multiple risks for disease, but mostly for cancer. 

The two most common vitamin deficiencies seen in patients chronically consuming alcohol are folic acid and thiamine. 

Folic acid deficiency is one of the most common vitamin deficiencies in the United States, largely due to its association with excessive alcohol intake and pregnancy. Requirements for folate in pregnancy are about five times higher than normal daily requirements. 

As a matter of fact, ethanol serves to deplete the body of what nutrition it had to begin with. Many of the complications arising from alcoholism can be associated more or less directly to a vitamin deficiency. For example, B Complex vitamins, which ethanol all but depletes completely, act as co-factors or as parts of a whole coehzyme molecule in specific enzymatic systems. This means that enzymatic and metabolic defects can exist as a result of chronic alcoholism. 

Cirrhosis, alcoholic hepatitis, pancreatitis, gastric or duodenal ulcer, esophageal varices, middle-age onset of diabetes, gastrointestinal cancer, hypertension, peripheral neuropathies, myopathies, cardiomyopathy, cerebral vascular accidents, erectile dysfunction, vitamin deficiencies, pernicious anemia, and brain disorders including Wemicke-Korsakoff syndrome (mortality rate of untreated Wernicke is 50% treatment is with thiamine)... 

Precipitate Factor Elvehjem90 and coworkers found a dietary factor in liver, yeast, and milk, which they called the alcohol-ether precipitate factor. This factor can be adsorbed by activated carbon, but difficulty has been experienced in eluting the active substance. However, when carbon that contained the adsorbed factor was fed to vitamin-deficient animals, good growth was obtained. This suggests that elution In vitro could be accomplished under appropriate conditions. 

In Western societies, gross thiamine deficiency is most often associated with alcoholism. The mechanism for active absorption of thiamine is strongly and directly inhibited by alcohol. Subclinical deficiency of thiamine from malnutrition or anorexia may be common in the general population and is usually associated with multiple vitamin deficiencies. 

AST were significantly below those seen in acute viral hepatitis. In addition, the ratio of the absolute values for serum ALT and AST often differ in the two diseases, tending to be greater than 1 in acute viral hepatitis and less than 1 in chronic alcohol-induced cirrhosis. The reason for the difference in ratio of enzyme activities released is not understood, but a lower level of ALT in the serum may be attributable to an alcohol-induced deficiency of pyridoxal phosphate. In addition, serologic tests for viral hepatitis were nonreactive. Her serum folate, vitamin B12, and iron levels were also slightly suppressed, indicating impaired nutritional status. 

Likewise, patients who do not have a well-balanced diet (such as the elderly, alcoholics, children, and those who go on fad diets) might also develop a vitamin deficiency. That would require the patient to take vitamin supplements to assure there are sufficient vitamins to support his or her metabolism. 

Wernicke Korsakoff syndrome (WKS) is the neurological disorder most clearly linked to thiamine deficiency in humans. WK develops in a subset of chronic alcoholics, who are vitamin deficient because so many calories are consumed as alcohol instead of normal diet, and a diet rich in carbohydrates increases the metabolic demand for thiamine. Thiamine dependent enzymes were diminished in the brains of patients who died with WKS, but not in alcoholic controls (Butterworth et al., 1993). Transketolase in fibroblasts from those patients who develop WKS syndrome binds TPP more avidly than the control lines. The Km was nearly ten times higher in patients with WKS. Thus, these patients have an abnormahty of transketolase that would be clinically unimportant if the diet was adequate (Blass and Gibson, 1977, 1979). The latter demonstrate a predisposing biochemical mutation to a neurological diseases that is only revealed by inadequate diet. 

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