By Zamzam K. (Fariba) Roughead, Ph.D., R.D.
It has been hypothesized that a high protein diet is a risk for osteoporosis through an increased endogenous acid production from catabolism of sulfur amino acids and subsequent increase in urinary calcium excretion (hypercalciuria). 1 Hypercalciuria has been observed with both purified2 and common food sources of protein when phosphorus intakes were held constant.3 However, with an increased intake of common protein foods, without manipulation of the phosphorus content, hypercalciuria is not observed.4-6 This suggests that phosphorus inhibits thehypercalciuric effect of protein. However, it has been suggested that the favorable effects of phosphorus on urinary calcium may be offset by increased fecal calcium losses.7 In a recent controlled feeding study, using sensitive radiotracer methodology, increasing protein intake (as meat) from 12-20 percent of energy for eight weeks, in a randomized crossover design, did not affect calcium retention measured during weeks 4-8 of the study (retention at week 8: 15.6 vs. 17.1 percent, ± 0.6 percent/dose, respectively), indicating that near doubling of protein intake for several weeks did not increase calcium loss through any of the excretory routes.8 Although renal acid excretion was about 45 percent higher during week 3 of the high protein period, this difference abated to 18 percent by week 8, indicating adaptation in renal acid excretion over time.8
All Proteins Not Created Equal
The effect of animal vs. plant proteins on bone health has been the subject of much scientific debate.9-12 Observational studies have indicated both negative13 and positive effects on bone status from animal protein12 and positive association with plant protein consumption. 9,14 However, with respect to calcium homeostasis, this distinction based on origin may not be appropriate as the sulfur amino acid and phosphorus content of proteins, and any counteracting alkali, vary greatly among commonly consumed proteins (Table 1). Therefore, the net effect of any protein source on calcium balance is determined by co-existing factors in the protein and the total diet, and cannot be predicted merely based on protein origin. This concept was demonstrated in a recent controlled feeding study of 13 healthy postmenopausal women (age 52-69) in which calcium retention was similar after 8 weeks from diets that were the same except that 25 g of soy protein was substituted for an equivalent amount of meat protein.15 Urinary calcium was also similar despite a consistently lower renal acid excretion (by about 15-20 percent) with soy consumption indicating that changes in urinary acidity, within the range that results from common dietary practices, do not reach a “threshold” which triggers use of calcium as a buffering agent.
Synergists
Several supplementation studies have suggested a bone sparing effect for high-isoflavone soy protein compared to milk proteins. 16-18 Although these studies were of limited duration and sample size, the favorable effect of soy protein on bone implies improved calcium retention as compared to milk proteins. This difference may be related to the higher calciuric effect of milkbased proteins vs. soy protein.18 Again, because of the use of isolated proteins instead of milk as a whole food, these results must be interpreted with caution. Furthermore, encouraging (although still preliminary) results16-20 suggest that the isoflavone component of soy may exert a favorable effect on bone health. In regard to calcium and protein, recent findings suggest that the two dietary components may synergistically interact to favorably affect bone mass.21, 22 The mechanism for this interaction may be related to an increase in the serum IGF-1, an osteotrophic growth factor. A recent study18 indicated that supplemental soy protein may be more potent in increasing serum IGF-1 than milkbased proteins in postmenopausal women, suggesting that the source of protein may modify the protein effect on serum IGF-1.
Conclusion
Recent evidence has demonstrated that increased intake of common proteins does not necessarily affect bone health adversely. The composition of the protein source as well as co-existing factors in the total diet determines the renal acid load. In healthy individuals consuming high protein foods, in the context of typical mixed diets, the renal acid load does not seem to reach a “threshold” that affects calcium homeostasis.
ABOUT THE AUTHOR
Z. K. (Fariba) Roughead, Ph.D., R.D. directs research in the Mineral Nutrition and Bone Health Laboratory at the USDA-ARS, Grand Forks Human Nutrition Research Center in North Dakota, where she is currently investigating the role of dietary protein and trace minerals in calcium homeostasis and bone health. She received her doctorate in nutrition at Clemson University in South Carolina.
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