The case of the missing calories.

Division of Basic Research, NIAAA, Rockville, MD 20857.
American Journal of Clinical Nutrition (Impact Factor: 6.92). 08/1991; 54(1):47-8.
Source: PubMed
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    ABSTRACT: The number of days of food intake data needed to estimate the intake of 29 male (n = 13) and female (n = 16) adult subjects, individually and as a group, was determined for food energy and 18 nutrients. The food intake records were collected in a year-long study conducted by the U.S. Department of Agriculture's Beltsville Human Nutrition Research Center. Each individual's average intake of nutrients and standard deviation over the year were assumed to reflect his or her "usual" intake and day-to-day variability. Confidence intervals (P less than 0.05) for each individual's usual intake were constructed, and from these the number of days of dietary records needed for estimated individual and group intake to be within 10% of usual intake was calculated. The results indicated that the number of days of food intake records needed to predict the usual nutrient intake of an individual varied substantially among individuals for the same nutrient and within individuals for different nutrients; e.g., food energy required the fewest days (averaging 31) and vitamin A the most (averaging 433). This was considerably higher than the number of days needed to estimate mean nutrient intake for this group, which ranged from 3 for food energy to 41 for vitamin A. Fewer days would be needed for larger groups.
    Journal of Nutrition 10/1987; 117(9):1638-41. · 4.23 Impact Factor
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    ABSTRACT: To define the effects of moderate alcohol intake on cholesterol and triglyceride metabolism in man, twelve patients were hospitalized on a metabolic ward and were fed defined diets for 10 weeks. Each patient underwent testing of plasma lipid and lipoprotein levels, of cholesterol metabolism (absorption, fecal excretion, bile saturation), and of triglyceride metabolism [turnover of triglycerides in chylomicrons and very low density lipoproteins (VLDL)]. This testing was done twice, first during a 4-week control period and then during a 4-week period in which 630 calories of alcohol were either added to or substituted for baseline calories. This increased the average baseline caloric intake by only 24% (range 20% to 30% depending on the initial caloric intake). Addition of alcohol to the baseline diet did not cause weight gain in lean individuals. Obese individuals' responses were more variable, and 3/6 definitely gained weight when the diet was supplemented with alcohol. In addition, obese subjects appeared to be more susceptible to the hyperlipidemic effects of alcohol; whereas 4/6 obese patients developed increased total triglyceride and VLDL-triglyceride concentrations when alcohol was administered, concentrations increased with alcohol administration in only 1/6 lean individuals. High density lipoprotein (HDL) cholesterol increased in all volunteers. Low density lipoprotein (LDL) levels did not change. Metabolic studies showed increased transport of VLDL-triglycerides in overweight patients but not in normal weight individuals; increased transport of VLDL-triglycerides in the former was associated with delayed clearance of chylomicron triglycerides. Alcohol consumption did not affect lipoprotein lipase or hepatic triglyceride lipase in six patients in whom these enzyme activities were measured. In the amounts of alcohol taken in this study, no changes were observed in absorption, synthesis, or excretion of bile acids, or percent saturation of gallbladder bile with cholesterol.
    The Journal of Lipid Research 06/1984; 25(5):486-96. · 4.73 Impact Factor
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    ABSTRACT: Rates of exchange catalysed by alcohol dehydrogenase were determined in vivo in order to find rate-limiting steps in ethanol metabolism. Mixtures of [1,1-2H2]- and [2,2,2-2H3]ethanol were injected in rats with bile fistulas. The concentrations in bile of ethanols having different numbers of 2H atoms were determined by g.l.c.-m.s. after the addition of [2H6]ethanol as internal standard and formation of the 3,5-dinitrobenzoates. Extensive formation of [2H4]ethanol indicated that acetaldehyde formed from [2,2,2-2H3]ethanol was reduced to ethanol and that NADH used in this reduction was partly derived from oxidation of [1,1-2H2]ethanol. The rate of acetaldehyde reduction, the degree of labelling of bound NADH and the isotope effect on ethanol oxidation were calculated by fitting models to the found concentrations of ethanols labelled with 1-42H atoms. Control experiments with only [2,2,2-2H3]ethanol showed that there was no loss of the C-2 hydrogens by exchange. The isotope effect on ethanol oxidation appeared to be about 3. Experiments with (1S)-[1-2H]- and [2,2,2-2H3]ethanol indicated that the isotope effect on acetaldehyde oxidation was much smaller. The results indicated that both the rate of reduction of acetaldehyde and the rate of association of NADH with alcohol dehydrogenase were nearly as high as or higher than the net ethanol oxidation. Thus, the rate of ethanol oxidation in vivo is determined by the rates of acetaldehyde oxidation, the rate of dissociation of NADH from alcohol dehydrogenase, and by the rate of reoxidation of cytosolic NADH. In cyanamide-treated rats, the elimination of ethanol was slow but the rates in the oxidoreduction were high, indicating more complete rate-limitation by the oxidation of acetaldehyde.
    Biochemical Journal 08/1985; 229(2):315-22. · 4.78 Impact Factor

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