Abstract
We disagree with Hunt's statement that the “scientific evidence does not support” an effect of dietary protein on the calcium requirement. Much of what Hunt says is quite correct, but she is wrong on one aspect of a key point, namely the effect of the phosphorus in food protein sources. Phosphorus does lower urine calcium. It has been used therapeutically for that purpose in patients with kidney stone disease for many years. We have shown this effect in controlled trials ((1)Heaney R.P. Recker R.R. Calcium supplements anion effects.Bone Miner. 1987; 2: 433-439Google Scholar), as well as in our cross-sectional study of healthy, perimenopausal women ((2)Heaney R.P. Recker R.R. Effects of nitrogen, phosphorus, and caffeine on calcium balance in women.J Lab Clin Med. 1978; 92: 953-963Google Scholar). So have many other investigators. Why is it, then, that the phosphorus content of protein sources does not neutralize the negative effect of protein on the calcium economy? Very simply: Phosphorus increases the secretion of calcium into the digestive tract ((3)Heaney R.P. Recker R.R. Determinants of endogenous fecal calcium in healthy women.J Bone Miner Res. 1994; 9: 1621-1627Google Scholar). The effect is just about numerically equal to the hypocalciuric effect. Thus, when you ingest a purified protein source, your urine calcium goes up; but when you ingest a food protein source, your fecal calcium goes up and the urine calcium stays about the same. Note that there is no hypocalciuric effect, as you would find with a pure phosphorus source. This was pointed out in the Journal several years ago ((4)Heaney R.P. Protein intake and the calcium economy.J Am Diet Assoc. 1993; 93: 1261-1262Google Scholar). It is true that Spencer ((5)Spencer H, Kramer L, Osis D. Do protein and phosphorus cause calcium loss? J Nutr. 1988; 118:657-660.Google Scholar) looked for the effect of phosphorus on endogenous fecal calcium loss and was unable to find it. However, she did not use calcium tracer methods, the only tools sensitive enough to detect the effect against the background variability inherent in measurement of total fecal calcium. Lest that be considered special pleading, recall that phosphorus does not improve calcium balance. (In fact, there has been concern that phosphorus might cause deterioration in calcium balance.) Obviously if balance is unchanged, but urine calcium is reduced, fecal calcium must increase. We disagree that “more controlled experimental designs” support the conclusion that protein has no effect on calcium economy. Rather, we conclude that the evidence supports the conclusion that increased protein intake increases the calcium requirement. PATRICIA PACKARD, MS, RD ROBERT P. HEANEY, MD Creighton University, Omaha, Neb
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