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Letter to the Editor |
Centre for Nutrition and Food Safety, School of Biomedical and Life Sciences, University of Surrey, Guildford, Surrey GU2 7XH, United Kingdom, E-mail: s.new{at}surrey.ac.uk
Dear Sir:
The recent paper by Dawson-Hughes and Harris (1) suggests that an increase in dietary protein is beneficial to the skeleton, provided that dietary intakes of calcium and vitamin D meet recommended amounts (2). Because the calcium supplement used provided an alkali source (citrate and malate), a point noted by the authors, it might be prudent to examine further the relation between total potassium and alkali intakes and rates of bone loss in this data set. Frassetto et al (3) showed that the ratio of protein to potassium predicts net acid excretion and, in turn, net renal acid excretion predicts calcium excretion. They propose a simple algorithm for determining the net rate of endogenous noncarbonic acid production by calculating both the acidifying effect of protein (mainly through sulfate excretion) and the alkalizing effect of potassium (resulting from the dietary intake of potassium as salts of weak organic acids). The baseline results of the Aberdeen Prospective Osteoporosis Screening Study were reanalyzed (4, 5); those women with a high intake of endogenous noncarbonic acid (ie, a higher protein intake but a lower potassium intake) had a lower peripheral and axial bone mineral density and a higher level of bone resorption than did women who had a low intake of endogenous noncarbonic acid (ie, a lower protein intake but a higher potassium intake) (6). These findings have also been confirmed in the longitudinal Aberdeen Prospective Osteoporosis Screening Study (7).
Furthermore, the article by Hannan et al (8) is cited by Dawson-Hughes and Harris as providing evidence that dietary protein is beneficial to bone mass; subjects with higher total and animal protein intakes had lower rates of bone loss than did subjects consuming less protein. However, in previous analyses of this cohort, high intakes of potassium (and fruit and vegetables) were associated with lower rates of bone loss in men and of greater bone mass in women (9). This suggests, therefore, that in the Framingham cohort, dietary protein intake was beneficial to bone, at least in part because its potential acidifying influence was balanced by the alkalizing effect of the dietary potassium intake.
As argued by Heaney (10) in the editorial accompanying the article by Dawson-Hughes and Harris, the magnitude and importance of the bone protein pool is such that, considered in isolation, a positive effect of protein on bone is not surprising. Indeed there is considerable evidence for a limitation on the synthesis of glycine (11), which accounts for 25% of collagen, so that competition for glycine between collagen and its other important metabolic demands might prevent its reutilization during bone collagen turnover. However, it is now becoming clear that in maintaining the bone matrix, the amino acid supply is as important as is the sufficient stimulation of appropriate concentrations of insulin-like growth factor I and other important growth factors through the regulatory influence or anabolic drive of dietary protein (12). In the past, this was mainly discussed in the context of bone length growth stimulation (13). What is not yet clear is the relation between these insulin-like growth factor I–mediated anabolic influences acting on the matrix and the parathyroid hormone–mediated responses to any protein-derived, acid-stimulated increased urinary calcium loss. We suggest that, in the absence of sufficient dietary alkali to neutralize the protein-derived acid, net calcium loss ensues and the anabolic drive of dietary protein on the bone matrix is ineffective in maintaining bone mineral density. However, provision of dietary alkali (either in the type of calcium supplement used in the current study by Dawson-Hughes and Harris or as fruit and vegetables) prevents urinary calcium loss and enables the full expression of the dietary protein–mediated anabolic drive on bone. This is supported by previous work by this group, which showed that calcium supplementation in the form of calcium citrate malate was more effective in reducing bone loss than was supplementation in the form of calcium carbonate (14).
Thus, the exciting findings of Dawson-Hughes and Harris (1) further support the arguments that maintenance of acid-base homeostasis is crucial to preserving skeletal health (15). Hence, calcium supplements may be favorable to bone health, not just through the additional mineral that they supply but also (and possibly more so) through their provision of additional alkali salts. Indeed, the challenge remains to establish the extent of any need for additional calcium in the presence of adequate dietary protein and fruit and vegetable intakes.
REFERENCES
This article has been cited by other articles:
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  S. A. Bowman and B. T. Vinyard Fast Food Consumption of U.S. Adults: Impact on Energy and Nutrient Intakes and Overweight Status J. Am. Coll. Nutr., April 1, 2004; 23(2): 163 - 168. [Abstract] [Full Text] [PDF]
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 S. A New, H. M MacDonald, M. K Campbell, J. C Martin, M. J Garton, S. P Robins, and D. M Reid Lower estimates of net endogenous noncarbonic acid production are positively associated with indexes of bone health in premenopausal and perimenopausal women Am. J. Clinical Nutrition, January 1, 2004; 79(1): 131 - 138. [Abstract] [Full Text] [PDF]
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