The case of the missing calories

Division of Basic Research, NIAAA, Rockville, MD 20857.
American Journal of Clinical Nutrition (Impact Factor: 6.77). 08/1991; 54(1):47-8.
Source: PubMed
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Available from: William E M Lands
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    • "This is in contrast to epidemiological studies that report a negative association between alcohol consumption and adiposity [137]. This may be explained by the induction of unregulated futile metabolic cycles that appear to significantly aid in the disposal of excess calories [138]. In general, it appears that the effects of alcohol on body weight are controversial and it is likely that moderate consumption of alcohol that replaces calories from carbohydrates and fat is unlikely to result in weight gain [139]. "
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    ABSTRACT: Caffeine, nicotine, ethanol and tetrahydrocannabinol (THC) are among the most prevalent and culturally accepted drugs in western society. For example, in Europe and North America up to 90% of the adult population drinks coffee daily and, although less prevalent, the other drugs are also used extensively by the population. Smoked tobacco, excessive alcohol consumption and marijuana (cannabis) smoking are addictive and exhibit adverse health effects. These drugs are not only common in the general population, but have also made their way into elite sports because of their purported performance-altering potential. Only one of the drugs (i.e., caffeine) has enough scientific evidence indicating an ergogenic effect. There is some preliminary evidence for nicotine as an ergogenic aid, but further study is required; cannabis and alcohol can exhibit ergogenic potential under specific circumstances but are in general believed to be ergolytic for sports performance. These drugs are currently (THC, ethanol) or have been (caffeine) on the prohibited list of the World Anti-Doping Agency or are being monitored (nicotine) due to their potential ergogenic or ergolytic effects. The aim of this brief review is to evaluate the effects of caffeine, nicotine, ethanol and THC by: 1) examining evidence supporting the ergogenic or ergolytic effects; 2) providing an overview of the mechanism(s) of action and physiological effects; and 3) where appropriate, reviewing their impact as performance-altering aids used in recreational and elite sports.
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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.
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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.
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