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Clinique Bois-Cerf, Lausanne, Switzerland
* To whom correspondence should be addressed. E-mail: p_burckhardt{at}bluewin.ch.
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ABSTRACT |
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 TOP ABSTRACT Introduction and DiscussionLITERATURE CITED |
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Introduction and Discussion |
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TOPABSTRACTIntroduction and DiscussionLITERATURE CITED |
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Therefore, it seemed interesting to us to examine the question of whether an alkali load by natural nutritional means can influence bone metabolism. For this a series of interventional trials have been performed in human volunteers under variable dietary conditions. They are summarized in Table 1. After the demonstration by a short-term study that diets that are different in their alkali load but not in their calcium content have different effects on bone resorption markers (3), it became evident that mineral waters represent a practical vector of nutritional alkali. Indeed, in that short-term study in normal volunteers on a very strict diet, mineral water contributed essentially to the nutritional alkali load.
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For quantifying the alkali load of a mineral water, the content of bicarbonate was used as an indirect parameter. As a biologically weak anion, bicarbonate decreases the acid load. Calcium in mineral waters is most frequently associated with sulfates. There is a significant correlation between calcium and sulfate in mineral waters, as discussed below, and only a few waters, especially those rich in bicarbonate, deviate from this rule. These considerations led to further analysis of the results of these trials and to the use of potential renal acid load (PRAL) instead of bicarbonate. PRAL assesses directly the content of the acidifying or alkalizing components of food. The more negative the PRAL, the more alkaline the food. PRAL values were calculated with the formula of Remer and Manz (6), adapted to mineral waters. The original PRAL formula could not be applied to mineral waters because of the sulfates. In food, sulfates stem from cysteine and methionine, which are consumed with dietary proteins. In mineral waters, where sulfates are in solution, the molecular weight and the resorption rate of sulfate alone have to be taken into account and not those of the amino acids stemming from dietary proteins (T. Remer, personal communication, 2007).
In the above-mentioned controlled study (3), significant inhibition of bone resorption was obtained with a special diet and 2 L of a mineral water providing 4868 mg bicarbonate and a PRAL of –124 mEq/d, whereas the control diet containing the same amount of calcium, protein, salt, and energy and a less alkaline mineral water had no such effect. Whether this inhibition of bone resorption was caused by the increased bicarbonate or potassium intake could not be determined. Both are reported to have a positive effect (7), but the effect of potassium on calcium excretion is linked to potassium in the urine (8), and this was not elevated in this study. In any case, this short-term study showed that it was possible to decrease bone resorption by a nutritional alkali load.
However, in this particular study the diet was strictly controlled and could not be applied to a longer trial. For a long-term trial and for the prevention of osteoporosis, it would be easier to propose a given mineral water. Mineral waters have a prolonged metabolic effect. When 1 L is consumed during the day, pH and calcium content of the fasting urine of the next morning are still increased, depending on the bicarbonate and calcium content of the consumed water (M. Jeanneret-Ramos and P. Burckhardt, unpublished data). This explains why the consumption of a bicarbonate-rich mineral water in a study over 4 wk decreased the bone resorption markers in the 24-h urine by 25%. Calciuria did not rise despite the increased calcium intake, another sign of probably improved calcium balance. Interestingly, a calcium-rich water used as control, which increased urinary calcium excretion by 31%, had no effect on bone resorption (9). In other words, the bicarbonate-rich water lowered the markers of bone resorption despite the fact that it contained less calcium than the control water. The high sulfate content of the latter might have contributed to the extent that it eventually enhanced renal calcium losses. The observed effect of the bicarbonate-rich water on bone resorption could also be caused at least partially by the higher potassium content in the mineral water. The potassium concentration was 50 mEq/L, but the urinary potassium excretion did not increase above that on the control water.
This advantage of an alkaline, bicarbonate-rich water could further be demonstrated when such a water was compared with a water that contained the same high amount of calcium but was acid, even in a situation of calcium and estrogen sufficiency (10). Although the latter had no effect on bone resorption over 4 wk, the bicarbonate- and calcium-rich water significantly decreased the bone resorption markers C-telopeptides (CTX) by 16% and PTH by 17%. This could be explained by the high intake of bicarbonate (3.258 g/d) and the important difference in PRAL. In addition, the concentration of sulfates was high in the acid water, which reportedly has a calciuric effect. This may have prevented a beneficial effect of the calcium on bone resorption, but urinary calcium excretion did not increase more in this group. Therefore, it could not be confirmed that sulfates enhance calcium excretion.
These studies have shown that alkali, bicarbonate-rich mineral waters, especially waters with a strongly negative PRAL value, decrease bone resorption, even when compared with mineral waters with a higher calcium content, and even in the situation of a sufficient calcium intake. This could lead to the recommendation that certain mineral waters that contain calcium and bicarbonate, i.e., calcium-rich waters with a strongly negative PRAL, can contribute to the prevention of bone loss.
A partial demonstration of that was made by a study (11) in which a bicarbonate- and calcium rich water decreased bone resorption markers and PTH, whereas the control water, rich in calcium, had no such effect. But this study was performed in calcium-deficient postmenopausal women on a calcium intake of only 400 mg/d. In such a situation, the mineral water rich in calcium only should have a beneficial effect. This was not the case because it was extremely rich in sulfates and had an exceptionally high PRAL value.
The results obtained with mineral waters must be sufficiently analyzed with respect to the other components and not only to calcium and bicarbonate. Potassium plays a role because it decreases calciuria (8), but its concentration is usually low in mineral waters. Sulfates should also be considered as acid components in addition to the acid or alkali load expressed by PRAL.
It has to be kept in mind that the PRAL values do not include bicarbonate because of its quick metabolization. When the PRAL values of mineral waters are calculated, it first appears that they are positive in waters with a high concentration of sulfates. The effect of sulfates may counterbalance the effect of calcium because sulfates are reported to increase calcium excretion in animals. In humans, the reports are conflicting (12,13), but even if such a calciuric effect exists, it was not seen in the studies presented here. It must at least be assumed that high concentrations of sulfates may counterbalance the beneficial effect of calcium, but not totally, otherwise a calcium- and sulfate-rich water would not have shown beneficial effects in calcium deficiency (5). In addition, there is a significant positive correlation between the calcium and the sulfate concentration in mineral waters (P < 0.001 in 21 randomly chosen European mineral waters), which contributes to confounding results. A few exceptional waters have a high calcium and a relatively low sulfate concentration but are rich in bicarbonate, such as the French Quezac and the Polish Kryniczanka waters. These waters may be of particular interest.
Considering all that, it appears that alkali mineral waters with a low PRAL value and a high content of bicarbonate exert an inhibitory effect on bone resorption that exceeds the effect of mineral waters that are only rich in calcium.
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FOOTNOTES |
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2 Author disclosure: P. Burckhardt, no conflicts of interest.
3 Abbreviations used: BMD, bone mineral density; CTX, C-telopeptides; PRAL, potential renal acid load, a value for acid/alkaline balance in foods, calculated as PRAL = [0.00049 SO4 (mg)] + [0.027 Cl (mg)] + [0.037 P (mg)] – [0.021 K (mg)] – [0.026 Mg (mg)] – [0.0413 Na (mg)] – [0.013 Ca (mg)]; PTH, parathyroid hormone.
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LITERATURE CITED |
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TOPABSTRACTIntroduction and DiscussionLITERATURE CITED |
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1. Sebastian A, Harris S, Ottaway J, Todd K, Morris C. Improved mineral balance and skeletal metabolism in postmenopausal women treated with potassium bicarbonate. N Engl J Med. 1994;330:1776–81.
2. Jehle S, Zanetti A, Muser J, Hulter H, Krapf R. Partial neutralization of the acidogenic Western diet with potassium citrate increases bone mass in postmenopausal women with osteopenia. J Am Soc Nephrol. 2006;17:3213–22.
3. Buclin T, Cosma M, Appenzeller M, Jacquet AF, Décosterd L, Biollaz J, Burckhardt P. Diet acids and alkalis influence calcium retention in bone. Osteoporos Int. 2001;12:493–9.[Medline]
4. Guillemant J, Le HT, Accarie C, Tézenas du Montcel S, Delabroise A-M, Arnaud M, Guillemant S. Mineral water as a source of dietary calcium: acute effects on parathyroid function and bone resorption in young men. Am J Clin Nutr. 2000;71:999–1002.
5. Meunier P, Jenvrin C, Munoz F, De la Gueronnière V, Garnero P, Menz M. Consumption of a high calcium mineral water lowers biochemical indices of bone remodelling in postmenopausal women with low calcium intake. Osteoporos Int. 2005;16:1203–9.[Medline]
6. Remer T, Manz F. Potential renal acid load of foods and its influence on urine pH. J Am Diet Assoc. 1995;95:791–7.[Medline]
7. Lemann J Jr, Pleuss JA, Gray RW. Potassium causes calcium retention in healthy adults. J Nutr. 1993;123:1623–6.
8. Lemann J Jr. Relationship between urinary calcium and net acid excretion as determined by dietary protein and potassium: a review. Nephron. 1999;81: Suppl 1:18–25.[Medline]
9. Burckhardt P, Waldvogel Abramowski S, Aeschlimann JM, Arnaud MJ. Bicarbonate in mineral water inhibits bone resorption. J Bone Mineral Res. 2002;17:(S1):S107–M360.
10. Wynn Dumartheray E, Krieg MA, Burckhardt P. Bicarbonate from mineral water lowers bone resorption even in calcium sufficiency. In Burckhardt P, Heaney RP, Dawson-Hughes B, editors. Nutritional aspects of osteoporosis Amsterdam: Elsevier; 2006. p. 303–9.
11. Roux S, Baudoin C, Boute D, Brazier M, De la Gueronnière V, De Vernejoul M. Biological effects of drinking-water mineral composition on calcium balance and bone remodeling markers. J Nutr Health Aging. 2004;8:380–4.[Medline]
12. Walser M, Browder A. The effect of sulfate infusion on calcium excretion. J Clin Invest. 1959;38:1404–11.[Medline]
13. Guéguen L, Besançon P. Effect of sulfates on phosphorus and calcium metabolism. Utilization of calcium sulfate by sheep. Ann Biol Anim Biochim Biophys. 1972;12:589–98.[Medline]
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