scholarly journals Lowering Dietary Protein to U.S. Recommended Dietary Allowance Levels Reduces Urinary Calcium Excretion and Bone Resorption in Young Women

2004 ◽  
Vol 89 (8) ◽  
pp. 3801-3807 ◽  
Author(s):  
B. Avery Ince ◽  
Ellen J. Anderson ◽  
Robert M. Neer
1999 ◽  
Vol 84 (3) ◽  
pp. 1052-1055 ◽  
Author(s):  
Jane E. Kerstetter ◽  
MaryAnn E. Mitnick ◽  
Caren M. Gundberg ◽  
Donna M. Caseria ◽  
Alice F. Ellison ◽  
...  

Although high protein diets are known to increase urinary calcium excretion and induce negative calcium balance, the impact of dietary protein on bone turnover and fractures is controversial. We therefore evaluated the effect of dietary protein on markers of bone turnover in 16 healthy young women. The experiment consisted of 2 weeks of a well balanced diet containing moderate amounts of calcium, sodium, and protein followed by 4 days of an experimental diet containing one of three levels of protein (low, medium, or high). On day 4, serum and urinary calcium, serum PTH, 1,25-dihydroxyvitamin D, serum osteocalcin, bone-specific alkaline phosphatase, and urinary N-telopeptide excretion were measured. Urinary calcium excretion was significantly higher on the high than on the low protein diet. Secondary hyperparathyroidism occurred on the low protein diet. Urinary N-telopeptide excretion was significantly greater during the high protein than during the low protein intake (48.2 ± 7.2 vs. 32.7 ± 5.3 nM bone collagen equivalents/mM creatinine; P < 0.05). There was no increase in osteocalcin or bone-specific alkaline phosphatase when comparing the low to the high diet, suggesting that bone resorption was increased without a compensatory increase in bone formation. Our data suggest that at high levels of dietary protein, at least a portion of the increase in urinary calcium reflects increased bone resorption.


1998 ◽  
Vol 18 (3) ◽  
pp. 475-487 ◽  
Author(s):  
Susan J Whiting ◽  
Timothy J Green ◽  
Evelyn P MacKenzie ◽  
Shawna J Weeks

1997 ◽  
Vol 83 (4) ◽  
pp. 1159-1163 ◽  
Author(s):  
Noriko Ashizawa ◽  
Rei Fujimura ◽  
Kumpei Tokuyama ◽  
Masashige Suzuki

Ashizawa, Noriko, Rei Fujimura, Kumpei Tokuyama, and Masashige Suzuki. A bout of resistance exercise increases urinary calcium independently of osteoclastic activation in men. J. Appl. Physiol. 83(4): 1159–1163, 1997.—Metabolic acidosis increases urinary calcium excretion in humans as a result of administration of ammonium chloride, an increase in dietary protein intake, and fasting-induced ketoacidosis. An intense bout of exercise, exceeding aerobic capacity, also causes significant decrease in blood pH as a result of increase in blood lactate concentration. In this study we investigated changes in renal calcium handling, plasma parathyroid hormone concentration, and osteoclastic bone resorption after a single bout of resistance exercise. Ten male subjects completed a bout of resistance exercise with an intensity of 60% of one repetition maximum for the first set and 80% of one repetition maximum for the second and third sets. After exercise, blood and urine pH shifted toward acidity and urinary calcium excretion increased. Hypercalciuria was observed in the presence of an increased fractional calcium excretion and an unchanged filtered load of calcium. Therefore, the observed increase in urinary calcium excretion was due primarily to decrease in renal tubular reabsorption of calcium. Likely causes of the increase in renal excretion of calcium are metabolic acidosis itself and decreased parathyroid hormone. When urinary calcium excretion increased, urinary deoxypyridinoline, a marker of osteoclastic bone resorption, decreased. These results suggest that 1) strenuous resistance exercise increased urinary calcium excretion by decreasing renal tubular calcium reabsorption, 2) urinary calcium excretion increased independently of osteoclast activation, and 3) the mechanism resulting in postexercise hypercalciuria might involve non-cell-mediated physicochemical bone dissolution.


1972 ◽  
Vol 71 (2) ◽  
pp. 313-320 ◽  
Author(s):  
O. Helmer Sørensen ◽  
Inge Hindberg ◽  
S. Nistrup Madsen

ABSTRACT Bone resorption, intestinal absorption of calcium, and urinary calcium excretion were studied in young rats given prolonged calcitonin treatment. The animals soon developed a resistance to the hypocalcaemic effect of calcitonin, probably due to a secondary hyperparathyroidism. In one of the experiments the rats were given 45Ca 2 weeks before the start of the calcitonin treatment in order to label the deep parts of bone. The release of isotope from bone was inhibited after the first injections of the hormone, but even after a few days of calcitonin treatment no differences could be detected between the treated animals and their corresponding controls. An increased release of isotope from bone was registered as soon as the treatment was interrupted, indicating the presence of a secondary hyperparathyroidism. No conclusive changes could be detected in the intestinal absorption of calcium. A transitory reduction in the excretion of calcium in the urine was followed by a considerable loss of calcium.


2014 ◽  
Vol 144 (3) ◽  
pp. 282-288 ◽  
Author(s):  
Jessica D. Bihuniak ◽  
Rebecca R. Sullivan ◽  
Christine A. Simpson ◽  
Donna M. Caseria ◽  
Tania B. Huedo-Medina ◽  
...  

1992 ◽  
Vol 12 (1) ◽  
pp. 17-26 ◽  
Author(s):  
Roma R Bell ◽  
Michelle M Eldrid ◽  
P Grad Dip Hlth Sc ◽  
Felicity R Watson ◽  
Grad Dip Diet

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