Wine versus ethanol in human nutrition. I. Nitrogen and calorie balance

McDonald, Janet; Margen, Sheldon

doi:10.1093/ajcn/29.10.1093

Cited by 68 publications

(7 citation statements)

References 43 publications

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“…The majority of observational studies show that alcohol usually provides additional energy to the diet, but that its use is not associated with higher levels of adiposity (Bebb et al 1971 ; Jones et al 1982;Fisher & Gordon, 1985;HiIIers & Massey, 1985;Camargo et al 1987). In concordance with these findings are the results of various experimental studies (Pirola & Lieber, 1972;McDonald & Margen, 1976;Crouse & Grundy, 1984). In these studies it was found that isoenergetic substitution of non-alcoholic energy by alcohol resulted in weight loss in volunteers and that alcohol added to the diet did not result in weight gain.…”

mentioning

confidence: 83%

Alcohol and its acute effects on resting metabolic rate and diet-induced thermogenesis

1990

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The impact of alcohol (ethanol) on resting energy expenditure of male non-obese volunteers was determined in two studies. In the first study the thermic effect of alcohol on resting metabolic rate (RMR) was assessed in ten male non-obese volunteers. In the second study the impact of alcohol on diet-induced thermogenesis (DTT) was determined in twelve male non-obese volunteers. Energy expenditure was measured with a ventilated-hood system. RMR was measured for 60 min with the subjects in a fasting state. In the first study subjects received in random order 20 g alcohol in concentrations of 75, 180 and 300 ml/l water respectively. After measurement of the RMR the thermic effect of alcohol was measured for 90 min. In the second study volunteers received in random order and in duplicate either a meal of food (2 M J ) plus an alcoholic aperitif (20 g alcohol in a 180 ml/l solution) or an isoenergetic meal of food alone (2.55 M J ) plus a placebo aperitif containing no alcohol. DIT was measured for 240 min. Alcohol induced a significant thermic effect, which varied between 0.22 and 0.30 kJ/min. No systematic difference in DIT was observed among the different concentrations. DIT was not significantly affected by the ingestion of alcohol. Total DIT was 219 (SE 14) kJ for the alcohol treatment and 185 (SE 20) k J for the control treatment. The results do not support the suggestion that alcohol is less efficiently used as an energy source in comparison with, for example, fats and carbohydrates. Alcohol: Resting metabolic rate: Diet-induced thermogenesisIn most Western countries total per capita alcohol consumption has increased dramatically over the last few decades (Sulkunen, 1976; World Health Organization, 1980). A recent nationwide food consumption study in The Netherlands showed that alcohol contributes on average 3 % to total daily energy intake in women and 5.4 YO in men aged 2 2 4 9 years (Ministerie van Welzijn, Volksgezondheid en Cultuur & Ministerie van Landbouw en Visserij, 1988). Similar values have been reported for men and women in other Western countries (Spring & Buss, 1977;Gruchow et al. 1985). The health effects of excessive alcohol intake are well documented (Klatsky, 1979;Mercy, 1980;Lieber, 1982), but the metabolic consequences and relation to the incidence of disease of moderate alcohol use remain to be definitely assessed. In this respect there is a general interest in the utilization of alcohol as an energy source. The issues that receive most attention are whether alcohol energy is added to or substituted for non-alcoholic energy in the diet, and whether energy intake from alcohol is related to increased levels of adiposity in the same way as energy intake from non-alcoholic sources.The majority of observational studies show that alcohol usually provides additional energy to the diet, but that its use is not associated with higher levels of adiposity (Bebb

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confidence: 83%

Alcohol and its acute effects on resting metabolic rate and diet-induced thermogenesis

1990

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“…The effect of EtOH on protein metabolism has, up to the present time, received little attention and has not been thoroughly investigated in human subjects. In a classic well-controlled study performed more than two decades ago in a metabolic ward, isoenergetic replacement of food energy by EtOH, given in the form of wine or pure EtOH, resulted in a persistent negative N balance, suggesting an effect of EtOH on fatfree-mass losses (MacDonald & Margen, 1976). More recently, it was demonstrated that elevation of blood EtOH following social drinking increased leucine turnover (Berneis et al 1997) and influenced hepatic protein metabolism (De Feo et al 1995;Volpi et al 1998).…”

Section: Other Metabolic Effects Of Alcoholmentioning

confidence: 99%

Role of substrate utilization and thermogenesis on body-weight control with particular reference to alcohol

Schütz

2000

Proc. Nutr. Soc.

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Alcohol (ethanol; EtOH) provides fuel energy to the body (29·7 kJ (7·1 kcal)/g, 23·4 kJ (5·6 kcal)/ml), as do other macronutrients, but no associated essential nutrients. The thermogenic effect of EtOH (on average 15 % of its metabolizable value) is much greater than that of the main substrates utilized by the body, i.e. fat and carbohydrates (CHO), suggesting a lower net efficiency of energy utilization for EtOH than for fat and CHO. EtOH cannot be stored in the body and is toxic, so that there is an obligatory continuous oxidation of EtOH and it becomes the priority fuel to be metabolized. In contrast to CHO, its rate of oxidation does not depend on the dose ingested. As with CHO intake, it engenders a shift in postprandial substrate utilization (decrease in fat oxidation), but by a non-insulin-mediated mechanism. A limited amount of EtOH can be converted to fatty acids by hepatic de novo lipogenesis (as occurs with high levels of CHO feeding) from acetate production, which inhibits lipolysis in peripheral tissues. There is no evidence that EtOH consumed under normoenergetic conditions (i.e. isoenergetically replacing CHO or fat) leads to greater body fat storage than fat or CHO. However, there is still a lack of experimental studies on the influence of EtOH on the level of spontaneous physical activity in man. This effect may well depend on the dose of EtOH consumed as well as other intrinsic factors.

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“…Chronic ethanol feeding results in increased urinary excretion of nitrogen in rats (140) and in man (90). The increased excretion of nitrogen in man was associated with a negative nitrogen balance and weight loss.…”

Section: Nitrogen Balancementioning

confidence: 99%

Liver Disease and Protein Needs

Mezey

1982

Annu. Rev. Nutr.

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Protein deficiency is often associated with liver disease. The principal cause of protein deficiency is decreased dietary intake. Deficiencies in digestion and absorption that are common in alcoholics contribute to protein deficiency in alcoholic liver disease. The protein requirements in most patients with compensated chronic liver disease are not different from normal, but increase during episodes of hepatocellular deterioration. An increased demand for protein after liver injury drains nitrogen from other organs such as muscle. Aromatic amino acids released from muscle in increased amounts accumulate in the circulation of patients with chronic liver disease because of their decreased hepatic metabolism. By contrast branched chain amino acids decrease in the circulation because of their preferential uptake by extrahepatic tissues. Decreases in urea synthesis in liver disease result in the accumulation of ammonia. The causes of the decrease in urea synthesis include decreases in the enzymes and substrates of the urea cycle, alterations in portal blood flow, and a decrease in total hepatic mass. The resulting increase in ammonia in association with an increased accumulation and entry of aromatic amino acids into the brain are important factors in the pathogenesis of hepatic encephalopathy. Circulating proteins synthetized by the liver, such as albumin and clotting factors, are frequently decreased in chronic liver disease. Vitamin deficiencies that are common in liver disease contribute to abnormalities of protein metabolism. Hepatic regeneration following hepatic resection or injury is adversely affected by protein and vitamin deficiencies and by alcohol ingestion.

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Wine versus ethanol in human nutrition. I. Nitrogen and calorie balance

Cited by 68 publications

References 43 publications

Alcohol and its acute effects on resting metabolic rate and diet-induced thermogenesis

Alcohol and its acute effects on resting metabolic rate and diet-induced thermogenesis

Role of substrate utilization and thermogenesis on body-weight control with particular reference to alcohol

Liver Disease and Protein Needs

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