To document the profile and role of malnutrition in alcoholic hepatitis, compared with chronic alcoholics and nonalcoholic chronic liver disease.
Alcoholic and nonalcoholic calories were calculated and percentage dietary and nutritional deficiencies computed. Anthropometric indices, nitrogen balance, and immune status of the patients were assessed.
Alcohol constituted about 48% of daily caloric intake in patients with ALD. The percentage mean intake of carbohydrate, protein, and energy was decreased in all three study groups compared with controls. The deficiencies were more pronounced in patients with severe than with moderate ALD.
1) protein energy malnutrition is common in both alcoholic and nonalcoholic cirrhotics, but is more pronounced in the latter;
2) the degree and profile of malnutrition in chronic alcoholics and in alcoholic cirrhotics are comparable;
3) based on our results, we hypothesize that malnutrition may not play a primary role in the pathogenesis of ALD.
Sarin SK et al., Dietary and nutritional abnormalities in alcoholic liver disease: a comparison with chronic alcoholics without liver disease [see comments]. Am J Gastroenterol, 1997 May, 92:5, 777-83.
In one of the first controlled trials using acupuncture in the treatment of alcoholism there was success in achieving sobriety. Forty alcoholics were treated with appropriate acupuncture points while 40 alcoholic controls who were treated at nonacupuncture points. A current of at least 50 uA could be detected at specific acupuncture points while there was no current detectable at the nonacupuncture points. Twice as many patients receiving authentic acupuncture treatment reported their need for alcohol was virtually gone at 1, 3 and 6 month follow-ups. They reported fewer drinking episodes and half the number of admissions to detoxification centers. It is noted acupuncture treatment is significantly less costly than traditional alcohol treatments.
"Acupuncture For Alcoholism?", Bullock, M.L, et al, Lancet, 1989; 1:1435-1438.
Nineteen percent of patients with liver disease were below the 5th percentile for arm fat area and 35% were below the 5th percentile for arm muscle area. Malnutrition was seen equally among patients with alcoholic and nonalcoholic liver disease. Nutritional status of patients with liver disease was similar to that of patients with carcinoma.
Anthropometric measurements correlated significantly with measurements of albumin concentration but not with other liver-function tests or with the severity of liver disease as assessed by Child-Pugh score. Data suggest that malnutrition is common in patients with both alcoholic and nonalcoholic liver disease.
Evaluation of nutritional status by using anthropometry in adults with alcoholic and nonalcoholic liver disease.
Thuluvath-PJ; Triger-DR. Am-J-Clin-Nutr. 1994 Aug; 60(2): 269-73.
Folate and Thiamin
Fifty-two patients, who were not taking folic acid supplements for 4 months, were evaluated for folate status in relationship to alcohol-related illness or injury and were seen in the emergency department. Out of 52 patients, 3 were found to be folate deficient. Out of 48 controls, 2 were found to be folate deficient. There was no statistical significance. The authors conclude folate deficiency in patients seen in this emergency department with alcohol-related illness or injury is low, and does not differ from the general emergency department population. Empiric folate therapy is not warranted in these patients. It was noted in the previous year, routine empiric administration of thiamine (vitamin B1), magnesium, and folate to patients presenting with alcohol-related illness or injury was discontinued in this hospital study emergency room department. Now these treatments are done on a selective basis, depending on the patient's living situation, diet, and recent medical history.
"Prevalence of Folate Deficiency in Emergency Room Department Patients With Alcohol-Related Illness or Injury", Schwab, Robert A., M.D. and Powers, Robert D., M.D., American Journal of Emergency Medicine, 1992;10:203-207.
Alcoholics are at risk for malnutrition since 50% of their calories may come from ethanol at the expense of other nutrient dense foods. Malabsorption can many times be traced to chronic pancreatic insufficiency and deficiency of folic acid is frequent. This is due to lower intakes of folic acid rich foods. Folic acid can affect the structure and function of the cells lining the intestines and even shorten the intestinal villi. This can impair absorption of glucose, sodium, water and other nutrients. Thiamine (Vitamin B1) deficiency is also associated with excess ethanol consumption. The author recommends dietary supplements of folic acid and thiamine for all heavy drinkers.
"Dietary Supplements Recommended in Alcohol Drinkers", Osteopathic Medical News, June 1990;8/Alcohol Health and Research World, 1989;13:207-210.
Epidemiological studies reveal that chronic alcoholics exhibiting liver disease are generally malnourished.
The mechanism by which malnutrition manifests in chronic alcoholism is, however, not clear. Recent studies have demonstrated, a) an inverse relationship between alcohol and non-alcohol energy intake and its impact on alcohol-induced effects in chronically alcoholic rats, b) a synergism between malnutrition and high doses of alcohol intake in the induction of alcoholemia, and c) that chronic alcoholemia significantly prolongs the delay in gastric emptying.
Abnormal prolongation of gastric emptying in alcoholics with chronic alcoholemia may initiate macronutrient deficiencies leading eventually to malnutrition.
Sankaran-H; Larkin-EC; Rao-GA: Induction of malnutrition in chronic alcoholism: role of gastric emptying. Med-Hypotheses. 1994 Feb; 42(2): 124-8.
The biological significance of Mallory bodies is still a mystery: whether Mallory bodies represent an epiphenomenon or play a role themselves in the initiation and continuation of liver damage.
The Mallory body: theories on development and pathological significance (Part 2 of a literature survey). Jensen-K; Gluud-C. Hepatology. 1994 Nov; 20(5): 1330-42.
Advances in genetics and molecular biology indicate that susceptibility to chronic diseases such as coronary artery disease (CAD), hypertension, diabetes, obesity, osteoporosis, alcoholism, cancer, etc., to a great extent is genetically determined.
Studies have shown that 50% of the variance in plasma cholesterol concentration is genetically determined, whereas 30%-60% of the variance in blood pressure is genetically determined.
Genetic variation influences the response to diet. For example, individuals with ApoE4 have higher cholesterol levels and a higher risk of CAD than those with ApoE3. Additional studies show that women of the ApoE 3/2 phenotype stand to benefit the least from a high polyunsaturate: saturate (P:S) diet because of reduction in the more 'protective' high density lipoprotein cholesterol (HDL-C), whereas men of the ApoE 4/3 phenotype showed the greatest improvement in the LDL/HDL ratio. Therefore a general recommendation to increase the polyunsaturated content of the diet in order to decrease the risk for CAD is not appropriate for women with ApoE 3/2 phenotype.
Thus, specific information is needed to define the optimal diet for an individual.
Simopoulos AP: Genetic variation and nutrition. Biomed Environ Sci, 1996 Sep, 9:2-3, 124-9.
Reviews the toxicologic manifestations of ethanol abuse. Hepatotoxicity of ethanol results from alcohol dehydrogenase-mediated excessive hepatic generation of nicotinamide adenine dinucleotide and acetaldehyde.
Alcohol also alters the degradation of key nutrients, thereby promoting deficiencies as well as toxic interactions with vitamin A and beta-carotene. Conversely, nutritional deficits may affect the toxicity of ethanol and acetaldehyde, as illustrated by the depletion in glutathione, ameliorated by S-adenosyl-L-methionine.
Lieber-CS: Mechanisms of ethanol-drug-nutrition interactions. J..Tox. Clin. Toxicol. 1994; 32(6): 631-81.
Thirteen healthy male subjects were evaluated for the ability of ascorbic acid to clear plasma alcohol levels. .5 and .8 g/kg body weight of alcohol were utilized and blood samples were taken at 0, .5 and then every 6 hours after alcohol consumption to assess plasma alcohol, ascorbic acid levels, RBC glutathione levels and plasma alanine aminotransferase activity.
Pretreatment with ascorbic acid short and long term resulted in a significantly enhanced clearance of alcohol. There was no significant effect on red cell reduced glutathione concentrations or plasma alanine aminotransferase activity. Subjects were used as their own controls and were studied three times. The first was with no ascorbic acid supplementation. The second was with two grams of ascorbic acid given orally 1 hour before alcohol consumption and the third was two grams (500 mg 4 times daily) of ascorbic acid for two weeks with the last dose of the vitamin taken the night before the test.
Long term vitamin C supplementation resulted in better alcohol clearance. Ascorbic acid may work by functioning as an electron donor sparing the NAD/NADH system and accelerating the conversion of alcohol to its metabolites.
"Effect of Ascorbic Acid on Plasma Alcohol Clearance", Chen, Marianne F., ScD, et al, Journal of The American College of Nutrition, 1990;9(3):185-189.
The objective of the present study was to assess zinc nutritional status in alcoholic patients with pellagra using plasma, hair, urine and nail zinc levels, as well as the zinc tolerance test.
The study was conducted on 81 patients, 73 males and eight females. Zinc parameters were compared with those of 84 individuals with no apparent disease aged 23-45 years. Plasma zinc levels were lower in patients with pellagra than in the controls.
The results of the zinc tolerance test showed that:
1. basal zinc levels were 69.7 +/- 16.8 micrograms/100 ml in pellagrins and 82.3 +/- 34.0 micrograms/100 ml in the controls;
2. after 1 h the increase in plasma levels was similar in the pellagrin and control groups;
3. during the second hour the increase was more marked in the controls, and the same was observed during the third and fourth hours.
Urinary zinc excretion (mg/24 h) was higher in pellagrins. Zinc concentration in hair and toenails did not differ between pellagrins and controls. We conclude that pellagrins present zinc deficiency as demonstrated by plasma and urine zinc levels and by their abnormal response to the zinc tolerance test.
Hair and nail zinc levels should not be used to assess zinc nutritional status in patients with pellagra.
Vannucchi H et al., Assessment of zinc nutritional status of pellagra patients. Alcohol Alcohol, 1995 May, 30:3, 297-302.
Relationships of nutritional status with ethanol consumption and diet were studied in 33 chronic alcoholics with no clinical or laboratory evidence of liver disease.
Nutritional assessment included subjective global assessment, weight-height index, body mass index, and serum albumin measurements. Dietary intake included estimates of daily intake of substrates, folic acid, vitamins B1, B5, B6, and B12. Circulating concentrations of folate, pyridoxal-phosphate and vitamin B12 were evaluated as well.
Only 18% of patients were considered malnourished, with body mass indices lower than those with an average or good nutritional status. Body weight was under 90% of the ideal in 8/33 (24%) patients. Serum albumin values were within normal range in all patients.
Low circulating concentrations of pyridoxal-phosphate and red blood cell folate were found in 51.5% and 60.6% of alcoholics, respectively. These were not correlated with vitamin dietary intake or ethanol consumption, but there was a trend toward malnourished patients to present lower concentrations of red blood cell folate.
Although over malnutrition is infrequent in this group of chronic alcoholics, specific vitamin deficiencies are present in a substantial proportion of patients and are more likely related to alcohol consumption.
Gloria L et al., Nutritional deficiencies in chronic alcoholics: relation to dietary intake and alcohol consumption. Am J Gastroenterol, 1997 Mar, 92:3, 485-9.
To determine the influence of chronic ethanol intake on the central nervous system, we studied 40 asymptomatic, well-nourished, chronic alcoholics (mean age, 42.6 +/- 9.1 years) and 20 age-, sex-, and education-matched control subjects.
Studies included neuropsychological testing, visual and short-latency auditory evoked potentials, and morphometric analysis of computed tomography scans. The mean daily ethanol consumption of the alcoholics was 204 gm over an average of 26.4 years.
Compared to control subjects, chronic alcoholics exhibited a significant prolongation of the P100 latency of visual evoked potentials, and a prolongation and reduction in the amplitude of the latency of the V wave of short-latency auditory evoked potentials. These abnormalities were related to the lifetime dose of ethanol consumed.
Brain morphometric analysis showed that alcoholics had a significantly greater degree of brain shrinkage with age, compared to control subjects. The cortical atrophy index correlated significantly with the lifetime ethanol consumption.
In conclusion, well-nourished chronic alcoholics exhibited significant brain impairment, as demonstrated by neuropsychological testing, evoked potentials, and brain morphometric analysis, which was correlated with the lifetime dose of ethanol consumed.
Nicolas JM et al., Brain impairment in well-nourished chronic alcoholics is related to ethanol intake. Ann Neurol, 1997 May, 41:5, 590-8.
Magnesium & Vascular Damage
Magnesium & Alcohol-Induced Vascular Damage
According to this study, magnesium may possess unique cerebral vascular protective properties against the vasculotoxic effects of alcohol. In a rat model, it was shown that magnesium acts as a local vasodilator on brain microvessels and has antispasmodic properties on brain arterioles and venules. In addition, this study showed that ethanol-induced cerebrovasospasm and vascular damage appear to be associated with a rapid loss of magnesium ion from cerebral vascular muscle cells.
Ema, Makoto, et al: Alcohol-Induced Vascular Damage of Brain Is Ameliorated by Administration of Magnesium, Alcohol, 1998;15(2):95-103.
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