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Available from: William E M Lands, Aug 23, 2015
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    • "Body mass index (BMI) is related to mortality, a relation that fits into a J-shaped curve; a relation also exists between lean mass and mortality, and between fat amount and mortality. Alcoholics usually showed altered nutritional status, partly because of the calorie-wasting effect of ethanol itself (Lands and Zakhari, 1991), partly because of the irregular style of life of alcoholics, partly because of the nutritional impairment produced by the accompanying disease, such as cirrhosis, cancer, pancreatitis or infection (Morgan, 1982; Simko et al. 1982; Romero et al., 1994; Seitz et al., 2005). Several studies have pointed out the clinical significance of deranged nutritional status in alcoholics, especially in those affected by chronic liver disease (Merli et al., 1996; Addolorato et al., 1998; Stickel et al., 2003; Halsted, 2004; Leevy and Moroianu, 2005). "
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    ABSTRACT: This study was performed in order to assess nutritional status of 77 alcoholic patients. Patients underwent a total body double-energy X-ray absorptiometry (DEXA) analysis, with estimation of lean and fat mass at different parts of the body. Lean mass, but not fat mass, was significantly reduced among alcoholics, compared to 31 age-matched controls, especially at right arm, legs, and total body. Lean mass at both arms was significantly related to liver function parameters (albumin, prothrombin activity, bilirubin) and, inversely, with ethanol consumption. The 24 patients who died during a follow-up period of 88 months showed less lean mass at both arms, trunk, and left leg, and also less fat at the left arm, than survivors. When right and left arm lean mass were classified in quartiles, Kaplan-Meier curves showed significant differences between dead and survivors. Left arm lean mass was the parameter which was independently related to mortality when encephalopathy was not included in a stepwise Cox regression analysis, but was displaced by this last parameter when it was also introduced in the analysis. Lean mass is reduced in alcoholics, is related to liver function derangement and ethanol consumption, and is related to mortality.
    Alcohol and Alcoholism 03/2008; 43(3):314-9. DOI:10.1093/alcalc/agn011 · 2.09 Impact Factor
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    • "Both ethanol and carbohydrate are metabolized by a common pathway to fatty acids from acetyl-coenzyme A by lipogenic enzymes (Guthrie et al., 1990). Humans are stated to have no regulatory or satiation point either for ethanol (Lands and Zakhari, 1991) or lipids and neither substrate can be metabolized to produce glucose. The large primate brain, and, in particular the unusually large human brain, utilizes considerable glucose each day. "
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    ABSTRACT: Humans and apes are placed together in the superfamily Hominoidea. The evolutionary trajectory of hominoids is intimately bound up with the exploitation of ripe, fleshy fruits. Fermentation of fruit sugars by yeasts produces a number of alcohols, particularly ethanol. Because of their pre-human frugivorous dietary heritage, it has been hypothesized that humans may show pre-existing sensory biases associating ethanol with nutritional rewards. This factor, in turn, could influence contemporary patterns of human ethanol use. At present, there seems little evidence to support a view of selection specifically for ethanol detection or its utilization over the course of hominoid evolution. Ethanol concentration in wild fruits consumed by monkeys and apes is predicted to be low. Wild monkeys and apes avoid consumption of over-ripe fruits, the class showing notable ethanol concentrations, and for this reason, ethanol plumes may act as deterrents rather than attractants. Any energetic benefits to wild primates from ingested ethanol appear negligible, at best. Mice and rats show patterns of ethanol self-administration similar to humans, indicating that a frugivorous dietary heritage is not necessary for such behaviors. In the natural environment, ethanol is predicted to be just one of many alcohols, esters and related compounds routinely encountered by frugivorous primates and of no particular significance. The strong attraction ethanol holds for some individuals could be due to a broad range of genetic and environmental factors. In some humans, the appetite for ethanol appears related to the appetite for sugar. The predisposition some individuals display toward excessive ethanol consumption could involve features of their genetics and biochemical similarities of ethanol and carbohydrate. Regular low ethanol intake is hypothesized to lower the incidence of cardiovascular disease in humans, perhaps through its effects on body fat distribution. Such a benefit, if confirmed, would appear to relate to features of the contemporary human rather than pre-human diet.
    Integrative and Comparative Biology 08/2004; 44(4):304-14. DOI:10.1093/icb/44.4.304 · 2.97 Impact Factor
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    ABSTRACT: To evaluate the effects of social subordination stress and chronic moderate alcohol consumption on indices of breast and endometrial cancer risk. Forty-six adult, ovariectomized, cynomolgus monkeys (Macaca fascicularis) were trained to voluntarily drink a placebo or a two-drink/day equivalent of ethanol (0.5 g/kg), 5 days a week for 26 months, the latter resulting in average blood alcohol levels of 42 mg/100 mL. Indices of cell proliferation and sex steroid receptor abundance were measured. Compared with dominants, socially subordinate females had increased cell proliferation and proportions of glandular (P < 0.02) and epithelial tissue (P = 0.009) and less stroma (P < 0.02) in endometrium, and increased tissue thickness in breast (P < 0.05). There was no evidence of increased risk of breast or endometrial cancer with chronic moderate alcohol consumption, as indicated by markers of cell proliferation and sex steroid receptor abundance. Chronic moderate alcohol consumption did not effect circulating sex steroid concentrations (all P > 0.10). The adipocyte hormones leptin and adiponectin were correlated with indices of cell proliferation and sex steroid receptor abundance. These observations suggest that social status was more important than chronic moderate alcohol consumption in endometrial and breast biology of surgically postmenopausal females. Endogenous sex steroid metabolism was not significantly affected by chronic moderate alcohol exposure consistent with the lack of estrogen-like effects on breast and endometrium. Social subordination stress was associated with initial cellular changes that may increase endometrial cancer risk. Ovariectomized cynomolgus monkeys may be a useful model for the study of effects of social factors and obesity on breast and endometrial cancer risk.
    Menopause 01/2004; 11(4):389-99. DOI:10.1097/01.GME.0000109312.11228.62 · 2.81 Impact Factor
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