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Biomedical subjects

M Hegsted

Publications and source records attributed to M Hegsted.

27 records · Page 2Linked to original sources
PubMed1986

Factors related to blood pressure in a biracial adolescent female population.

Blood pressure levels, anthropometric parameters, and dietary intakes were assessed in 1981 and 1983 in a population of black (n = 236) and white (n = 296) adolescent girls, aged 14 and 16 years in 1983. The 14-year-old black girls exhibited significantly higher mean systolic and diastolic blood pressures than whites in both years. Body weight and Quetelet index were more strongly associated with blood pressure than were height and triceps skinfold thickness. Correcting blood pressures for weight, Quetelet index, 2-year changes in height, and age at menarche decreased in each case (but did not negate) the observed race differences in blood pressure. Dietary calcium and potassium intakes were inversely related to blood pressure, and a race difference in the intake of these nutrients (whites greater than blacks) was observed. Covariate adjustment for calcium, but not for potassium, decreased the magnitude of race differences in blood pressure. Family type (single-parent vs nuclear) and place of residence (urban vs nonurban) appeared to be the most important confounding variables for race differences in blood pressure, since differences largely were eliminated by controlling for these factors. Conflicting reports in the literature regarding the age range during which race differences in blood pressure become apparent may be partially attributed to the complex interrelationships among these factors and the potential influence of other genetic-environmental interactions that may also play a role in blood pressure regulation.

Adolescent↗
PubMed1985

Evaluation of zinc and copper nutritional status and effects upon growth of southern adolescent females.

A biracial sample of twenty-nine 14-yr old and thirty 16-yr old females was evaluated for zinc and copper nutritional status. Socioeconomic, demographic, anthropometric and 24-h dietary recall data were collected and plasma zinc and copper and erythrocyte zinc levels determined. Mean plasma zinc was 83 +/- 15 micrograms/dl; racial differences were significant (p less than 0.05) with plasma zinc levels at 87 +/- 3 micrograms/dl for whites and 79 +/- 3 micrograms/dl for blacks. Mean plasma copper was 119 +/- 24 micrograms/dl and was slightly higher for blacks than for whites. Mean erythrocyte zinc was 8.3 +/- 2.7 micrograms/g and represented 10 times the level of zinc in plasma. Plasma copper levels were positively (p less than 0.05) related to body size. Plasma copper was negatively (p less than 0.05) related to dietary fiber. Other dietary and economic factors did not affect mineral status.

Adolescent↗
PubMed1981

Renal acid, urinary cyclic AMP, and hydroxyproline excretion as affected by level of protein, sulfur amino acid, and phosphorus intake.

Two 51-day human studies were conducted to investigate the effects of level of protein and phosphorus intake on the various components of renal acid excretion and on urinary sulfate, cyclic AMP and hydroxyproline; the role of the sulfur amino acids (Saa) of the protein was also evaluated. Dietary treatments included: 1) a 50 g protein diet; 2) a 150 g protein diet; and 3) a 50 g protein diet plus Saa to equal that of the 150 g protein diet, each given at 2 levels of phosphorus (1010 and 2525 mg). Calcium intake was 500 mg. Subjects were 16 young adult males. The results are discussed in relationship to calcium data previously reported (1, 2). Changes in renal acid and calcium excretion are not directly related for these reasons: a) the Saa accounted for all of the protein-induced increase in urinary sulfate and acid but for only 43% of the increase in urinary calcium and b) the acid phosphate supplement decreased urinary calcium but increased total acid excretion. The phosphorus supplement increased cyclic AMP but not hydroxyproline excretion. In fact, protein and Saa caused increases in hydroxyproline that were greatly reduced by the phosphorus supplement. Increases in urinary hydroxyproline and calcium were well correlated indicating that, at low calcium intakes, protein or Saa-induced increases in urinary calcium result in increased bone resorption which is reduced by the administration of phosphorus.

Acids↗
PubMed1981

Long-term effects of level of protein intake on calcium metabolism in young adult women.

The long-term effect of level of protein intake on calcium metabolism, renal function and renal acid excretion was determined during a 75-day metabolic study. Six women consumed a diet containing either 46 or 123 g protein for 60 days; they then consumed the alternate diet for 15 days. Calcium, phosphorus and magnesium intakes were maintained constant at 500, 900 and 350 mg, respectively, throughout the 75-day study. Urinary calcium was remarkably constant with time at both levels of protein intake but was approximately twice as high when the 123 g protein diet was consumed. Level of protein intake had no effect on calcium absorption; the increase in urinary calcium found when the high protein diet was given, therefore, caused a markedly negative calcium balance. Glomerular filtration rate (GFR) and renal acid excretion were higher and fractional renal tubular reabsorption of calcium was lower when the high protein diet was given. The hypercalciuria caused by the high protein intake was due primarily to the decrease in fractional tubular reabsorption of calcium and, to a lesser extent, to the increase in GFR. Neither GFR, fractional renal tubular reabsorption of calcium nor any of the components of renal acid excretion exhibited any tendency to change with time over the 60-day experimental period.

Absorption↗
PubMed1981

Role of the sulfur-containing amino acids in protein-induced hypercalciuria in men.

A human metabolic study was conducted to determine what part sulfur-containing amino acids play in protein-induced hypercalciuria. The effects on the renal handling of calcium of increasing dietary protein from 50 to 150 g protein were compared with those of increasing the sulfur amino acids to simulate the amounts present in the 150 g protein diet; we also evaluated the effects of adding a 1.5 g supplement of phosphorus to the 50 g protein diet containing the sulfur amino acids. An increase in protein intake caused urinary calcium to double, increased glomerular filtration rate and decreased fractional renal tubular reabsorption of calcium and urinary sodium. Sulfur amino acids added to the low protein diet also caused urinary calcium to increase and fractional tubular reabsorption of calcium and urinary sodium to decrease, but the changes were only 43, 44 and 66%, respectively, those caused by the increase in protein. The phosphorus supplement effectively prevented the hypercalciuria caused by adding the sulfur amino acids to the low protein diet.

Absorption↗
PubMed1981

Urinary calcium and calcium balance in young men as affected by level of protein and phosphorus intake.

Eight young adult males were subjects in a 51-day metabolic study conducted to examine the effects of level of protein and of phosphorus intake on urinary calcium and calcium balance. Two levels of protein (50-150 g) were given at each of two levels of phosphorus intake (1,010 and 2,525 mg). Dietary calcium and magnesium were maintained at 500 and 350 mg, respectively. Raising the protein intake from 50 to 150 g caused a calciuresis at both phosphorus intakes, but the actual increase in urinary calcium was 71 mg/day greater at the low than at the high phosphorus intake and calcium balance was changed from 24 to -116 mg/day at the low phosphorus intake and from 8 to -25 mg/day at the high. When the phosphorus intake was raised, urinary calcium decreased from 156 to 93 mg/day at the low protein intake and from 334 to 200 mg/day at the high protein intake and the markedly negative calcium balance found at the high protein intake was greatly improved. Simultaneous increases in protein and phosphorus intakes caused a 28% increase in urinary calcium whereas the increase in protein intake alone caused a 115% increase.

Absorption↗
PubMed1981

Protein-induced hypercalciuria.

Under controlled dietary conditions the level of dietary protein has a profound and sustained effect on urinary calcium and calcium retention of man. Young adults achieve calcium balance at low intakes of 500 mg calcium and 700 to 1,000 mg phosphorus when protein intake is 50 g. Large calcium losses occur at the same calcium and phosphorus intakes when the protein intake is increased approximately threefold. The protein-induced hypercalciuria is due mainly to a decrease in fractional renal tubular reabsorption of calcium, although an increase in glomerular filtration rate is also involved. The changes in kidney function appear to result from the catabolism of excess dietary sulfur amino acids to sulfate and the subsequent excretion of sulfate in the urine. An increase in both protein and phosphorus intakes has a much less dramatic effect on urinary calcium and calcium retention than an increase in protein intake alone. An increase in dietary phosphorus greatly reduces urinary calcium by increasing the fractional renal tubular reabsorption of calcium. It appears therefore that high protein intakes may increase the requirements for both calcium and phosphorus.

Calcium↗