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Objectives: Sarcopenia, the involuntary loss of skeletal muscle with age, affects up to one-quarter of older adults. Evidence indicates a positive association between dietary protein intake and lean muscle mass and strength among older persons, but information on dietary protein's effect on physical performance in older adults has received less attention., Design: Cross-sectional observational analysis of the relationship of dietary protein on body composition and physical performance., Setting: Clinical research center., Participants: 387 healthy women aged 60 - 90 years (mean 72.7 ± 7.0 y)., Measurements: Measures included body composition (fat-free mass, appendicular skeletal mass and fat mass) via dual x-ray absorptiometry (DXA), physical performance (Physical Performance Test [PPT] and Short Physical Performance Battery [SPPB]), handgrip strength, Physical Activity Scale in the Elderly (PASE), quality of life measure (SF-8), falls, fractures, nutrient and macromolecule intake (four-day food record). Independent samples t-tests determined mean differences between the above or below RDA protein groups., Statistical Analysis: Analysis of covariance was used to control for body mass index (BMI) between groups when assessing physical performance, physical activity and health-related quality of life., Results: The subjects consumed an average of 72.2 g protein/day representing 1.1 g protein/kg body weight/day. Subjects were categorized as below the recommended daily allowance (RDA) for protein (defined as less than 0.8 g protein/kg) or at or above the RDA (equal to or higher than 0.8 g protein/kg). Ninety-seven subjects (25%) were in the low protein group, and 290 (75%) were in the higher protein group. Women in the higher protein group had lower body mass, including fat and lean mass, and fat-to-lean ratio than those in the lower-protein group (p <0.001). Composite scores of upper and lower extremity strength were impaired in the group with low protein intake; SPPB score was 9.9±1.9 compared to 10.6±1.6 in those with higher protein intake and PPT was 19.8± 2.9 compared to 20.9± 2.1 in the low and higher protein groups, respectively. The results were attenuated by correction for BMI, but remained significant. The physical component of the SF-8 was also lower in the low protein group but did not remain significant when controlling for BMI. No significant differences were found in hand grip strength or reported physical activity., Conclusion: Healthy, older postmenopausal women consumed, on average, 1.1 g/kg/d protein, although 25% consumed less than the RDA. Those in the low protein group had higher body fat and fat-to-lean ratio than those who consumed the higher protein diet. Upper and lower extremity function was impaired in those who consumed a low protein diet compared to those with a higher protein intake. Protein intake should be considered when evaluating the multi-factorial loss of physical function in older women.

Background: We reported previously that lowering dietary protein intake in young healthy women to 0.7 g/kg depressed intestinal calcium absorption and was accompanied by elevations in parathyroid hormone (PTH). Moderate amounts of dietary protein (1.0 g/kg) did not appear to perturb calcium homeostasis., Objective: The purpose of this study was to evaluate the effect of graded intakes of dietary protein (0.7, 0.8, 0.9, and 1.0 g/kg) on calcium homeostasis., Design: The experiment consisted of 2 wk of a well-balanced diet containing moderate amounts of calcium, sodium, and protein followed by 4 d of an experimental diet containing 1 of 4 amounts of protein. Eight young healthy women received the 4 amounts of protein in random order. The average age of the subjects was 23.1 +/- 2.3 y, their weight was 64 +/- 3 kg, and their body mass index (in kg/m(2)) was 24.3 +/- 0.9., Results: Elevations in PTH developed by day 4 of the diets containing 0.7 and 0.8 g protein/kg but not during the diets containing 0.9 or 1.0 g protein/kg. By day 4 of the 0.7- and 0. 8-g/kg diets, midmolecule PTH, calcitriol, and nephrogenous cyclic adenosine monophosphate were 1.5-3.5-fold higher than on day 0. Calcitropic hormones on day 4 of the diets containing 0.8 and 0.9 g protein/kg were within the normal range and 23-57% lower than values observed with the 0.7- and 0.8-g/kg diets (P < 0.005). Mean 24-h urinary calcium was 3.29 +/- 0.35 mmol with the diet containing 0.7 g protein/kg and 3.54 +/- 0.46 mmol with the diet containing 1.0 g protein/kg., Conclusions: Our data suggest that in young healthy women consuming a well-balanced diet, the current recommended dietary allowance for protein (0.8 g/kg) results in short-term perturbations in calcium homeostasis.

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.

Background: Changes in dietary protein in adults are associated with changes in urinary calcium excretion. The mechanisms underlying this effect are not completely understood, but alterations in intestinal absorption of calcium are not thought to be involved., Objective: We reexamined this mechanism by evaluating the effect of 2 amounts of dietary protein (low: 0.7 g/kg; and high: 2.1 g/kg) on fractional calcium absorption in 7 healthy, young women., Design: The experiment consisted of 2 wk of a well-balanced diet containing moderate amounts of calcium, sodium, and protein followed by 5 d of an experimental diet that contained 1 of 2 amounts of protein and constant amounts of other nutrients known to influence calcium metabolism. Seven subjects received both amounts of dietary protein in random order. Blood and urine were sampled at baseline and on day 4. Fractional calcium absorption was measured by dual-stable calcium isotopes on day 5. In a second study of 5 additional women, we evaluated the effects of dietary fiber on calcitropic hormones., Results: Subjects developed hypocalciuria and secondary hyperparathyroidism on day 4 of the low-protein diet. Urinary calcium excretion and the glomerular filtration rate were elevated significantly by day 4 of the high-protein compared with the low-protein diet. Fractional calcium absorption after the low-protein diet was 0.19+/-0.03, which was significantly lower than that after the high-protein diet (0.26+/-0.03, P=0.05)., Conclusion: These data provide evidence that depressed intestinal calcium absorption explains, in part, low-protein-induced secondary hyperparathyroidism.

Increasing dietary protein induces hypercalciuria and a negative calcium balance. Despite this, the influence of dietary protein on the parathyroid hormone (PTH) I-a-hydroxylase axis is not well understood. We therefore examined the effect of three amounts of dietary protein: low (0.7 g/kg), medium (1.0 g/kg), and high (2.1 g/kg) on mineral metabolism and the PTH-1-alpha-hydroxylase axis in 16 healthy women aged 26.7 +/- 1.3 y. By day 4, urinary calcium decreased significantly with the low-protein diet and increased significantly with the high-protein diet compared with the medium-protein diet (control). Also by day 4, there were striking elevations in serum PTH and calcitriol [1,25-dihydroxyvitamin D] in subjects consuming the low-protein diet. Serum PTH, by two different assays, was 1.5-2.4 times higher and by day 14 1.6-2.7 times higher during the low-protein diet compared with the medium-protein diet. This was accompanied by a significant increase in both nephrogenous cyclic adenosine monophosphate (cAMP), a sensitive and specific indicator of PTH bioactivity, and serum calcitriol by day 14. In comparison, there were relatively minor changes in the calcitropic hormones with the medium- and high-protein diets. The stimulus for the elevation in PTH induced by protein restriction is unclear, but probably does not involve a simple renal mechanism and could reflect either a decline in intestinal calcium absorption, a reduction of bone turn-over, or both. Our data indicate that dietary protein is a powerful regulator of calcium metabolism. Further study is needed to both clarify the mechanisms by which these changes are induced and to better define the amount of dietary protein that will optimize skeletal health in young women.