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Letters to the Editor

High Meat Diet, Acid-Base Status and Calcium Retention

Forschungsinstitut für Kinderernährung, 44225 Dortmund, Germany

Dear Editor,

In a recent paper in the April 2003 issue of The Journal of Nutrition, Roughead et al. (1) examined the effects of a high meat compared with a low meat diet on calcium retention and calciuria in healthy postmenopausal women. No differences in calcium status were observed after 3–8 diet wk. These findings concur with earlier studies showing that high meat or high protein intake does not necessarily result in elevated urinary calcium losses. Furthermore, the study of Roughead et al. suggests that an increase in dietary potential renal acid load (PRAL) and net endogenous acid production does not seem to have relevant effects on calcium homeostasis as long as the acid load increase is moderate and the respective net endogenous acid production varies in the average range of common Western diets. Average net endogenous acid production of common mixed diets, measured as urinary net acid excretion (NAE), varies from 40 to 80 mEq/d (2,3). Roughead et al. observed NAE values [sum of titratable acidity and ammonium minus bicarbonate (at urine pH levels < 6.2, bicarbonate can be neglected)] of 57 and 82 mEq/d in their subjects after 3 wk on the low meat and 3 wk on the high meat diet, respectively. This NAE difference of 25 mEq/d between low and high meat diet corresponds closely to the change in PRAL of 24 mEq/d that can be estimated from the mere difference in protein intake (49 g/d) (3,4). Elimination of protein-induced surplus acid loads of that magnitude are managed by the kidney at least partly through an (protein-dependent) improvement of NAE capacity (5). Consequently, there is no clear additional renal acid stimulation with the high meat diet that could have affected calcium balance. That renal acid stimulation is actually similar with both diets can be directly read from the comparable urine pH values measured by Roughead et al.

In a previous controlled short-term study in which the NAE produced by adults was analyzed and estimated for several isoenergetic diets (each provided for 5 d), we also examined the effect of daily addition of 3.0 g (20 mmol) of L-methionine to one of the diets (6). After the 5-d period with methionine, NAE was 113 mEq/d compared with 70 mEq/d without the methionine supplement. Re-evaluation of the data showed that methionine addition had increased urinary calcium excretion significantly (P < 0.05) by nearly 1 mmol/d (40 mg/d) (7). This increase occurred despite constant calcium intake and despite a relatively high phosphorus intake of 1730 mg/d. A high phosphorus intake has been repeatedly shown to exert hypocalciuretic effects (8–9).

Based on the above observations it appears possible that increases in daily acid load which exceed 25 mEq (measurable as -NAE and calculable as -PRAL) may affect calcium homeostasis, particularly if the final NAE is higher than 100 mEq/d. This additional condition seems to be important because especially NAE values > 100 mEq/d can result in so-called maximum renal acid stimulation, a physiological border zone in which further increases in renal free H⁺ excretion will no longer involve appropriate increases in acid load elimination (7,10). Probably, in such situations the plasma bicarbonate level falls and the largest alkali pool of the body, the skeleton, releases increasing amounts of calcium to buffer excessive endogenous acid production. Correspondingly, negative calcium balances have been observed at high renal NAE levels in young healthy adult males, even after hypercalciuria had been largely prevented by an excessive phosphorus intake (8–9).

High meat or high protein diets can easily result in clearly higher NAE values than those observed for the controlled high meat diet of Roughead et al. This is the case if the acidifying potential of elevated protein is not counterbalanced by an adequate intake of base-forming minerals like potassium or magnesium. Although NAE reduction by an increased intake of alkalizing nutrients is certainly a desirable dietary practice, it does not seem to be the optimal way to specifically study potential adverse effects of high meat or high protein diets on calcium balance. For this, NAE values > 100–120 mEq/d (PRAL > 70–80 mEq/d) appear to be an adequate target area (3,7).

Another aspect of the paper of Roughead et al. should also be mentioned. The authors argued that the increase in renal acid load that occurred with the high meat diet adapted over time. Indeed, NAE fell from 82.3 mEq/d at wk 3 to 77.9 mEq/d at wk 8. However, the parallel increase in urinary potassium excretion from 42.2 to 45.6 mmol/d can almost completely explain this fall in NAE. Thus, the NAE decrease does not seem to be an adaptation in renal acid excretion, but rather indicates that food composition or dietary compliance may have slightly varied.

Manuscript received 10 June 2003.

LITERATURE CITED

1. Roughead, Z. K., Johnson, L. K., Lykken, G. I. & Hunt, J. R. (2003) Controlled high meat diets do not affect calcium retention or indices of bone status in healthy postmenopausal women. J. Nutr. 133:1020-1026.[Abstract/Free Full Text]

2. Manz, F., Kalhoff, H. & Remer, T. (1997) Renal acid excretion in early infancy. Pediatr. Nephrol. 11:231-243 Review.[Medline]

3. Remer, T., Dimitriou, T. & Manz, F. (2003) Dietary potential renal acid load and renal net acid excretion in healthy, free-living children and adolescents. Am. J. Clin. Nutr. 77:1255-1260.[Abstract/Free Full Text]

4. Remer, T. & Manz, F. (1995) Potential renal acid load of foods and its influence on urine pH. J. Am. Diet. Assoc. 95:791-797.[Medline]

5. Remer, T. & Manz, F. (1995) Dietary protein as a modulator of the renal net acid excretion capacity: Evidence that an increased protein intake improves the capability of the kidney to excrete ammonium. J. Nutr. Biochem. 6:431-437.

6. Remer, T. & Manz, F. (1994) Estimation of the renal net acid excretion by adults consuming diets containing variable amounts of protein. Am. J. Clin. Nutr. 59:1356-1361.[Abstract/Free Full Text]

7. Remer, T. (2000) Influence of diet on acid-base balance. Semin. Dial. 13:221-226.[Medline]

8. Hegsted, M., Schuette, S. A., Zemel, M. B. & Linkswiler, H. M. (1981) Urinary calcium and calcium balance in young men as affected by level of protein and phosphorus intake. J. Nutr. 111:553-562.

9. Schuette, S. A., Hegsted, M., Zemel, M. B. & Linkswiler, H. M. (1981) Renal acid, urinary cyclic AMP, and hydroxyproline excretion as affected by level of protein, sulfur amino acid, and phosphorus intake. J. Nutr. 111:2106-2116.

10. Kalhoff, H., Manz, F., Diekmann, L., Kunz, C., Stock, G. J. & Weisser, F. (1993) Decreased growth rate of low-birth-weight infants with prolonged maximum renal acid stimulation. Acta Paediatr. 82:522-527.[Medline]

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