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Letter to the Editor |
Department of Medicine (L.F., R.C.M., A.S.) and General Clinical Research Center (L.F., A.S.), University of California, San Francisco, San Francisco, California 94143
Address correspondence to: Lynda Frassetto, University of California, San Francisco, Box 0126, San Francisco, California 94143. E-mail: frassett{at}gcrc.ucsf.edu.
To the editor:
Heaney et al. (1) doubt that long-term reduction of urine calcium excretion induced by chronic dietary potassium bicarbonate supplementation, which we showed (2), will translate to prevention/reversal of bone mass reduction in postmenopausal women. In support, they cite their own study in postmenopausal women, in which they found that a lower rate of intestinal calcium absorption offsets the lower rate of urine calcium excretion associated with higher potassium intakes. They conclude that higher potassium intakes do not lead to greater net calcium balance (3).
Heaney et al. (1), however, failed to provide evidence that, in the subjects they studied, the intakes of bicarbonate or bicarbonate-generating anions amounted to a large fraction of the subjects’ higher potassium intakes. Indeed, in the conclusion to their paper, they assert the following caveat about the interpretation of their findings: "We note, however, that since the high K intakes in our studies come more from milk and meat than from fruits and vegetables, we cannot exclude a possible balance effect for different food sources of K [potassium]". In fact, such "different food sources of K" as fruits and vegetables, which supply potassium with approximately commensurate amounts of bicarbonate-generating anions, might induce a different calcium balance effect. Indeed, epidemiological studies demonstrate a positive association of lifelong fruit and vegetable intake (hence, high K+ and alkali intake) with bone mineral density in women (4, 5, 6).
In view of the caveat of Heaney et al. (1) and in view of their targeting their skepticism to our paper, we find surprising the concluding remark in their letter to the editor: "A high potassium intake remains important for its cardiovascular benefits. Unfortunately, our data suggest that there is little or no corresponding skeletal benefit."
But the issue of skeletal benefit from high potassium intakes turns critically on whether or not bicarbonate-generating anions accompany potassium to a large extent. Two independent investigative groups demonstrated significant improvements in net calcium balance during potassium bicarbonate administration, as studied with the classic metabolic balance technique in a metabolic ward setting (7, 8). Heaney et al. (1) dismiss the results of metabolic balance studies because of potential errors in the methodology, but the large magnitude of the induced improvement in net calcium balance in the studies cited tend to remove doubt about such potential errors. Moreover, both cited studies provided evidence of concomitant reductions in bone resorption rate accompanying administration of potassium bicarbonate, suggesting a positive bone effect.
Another group has shown that months of treatment of postmenopausal women with supplemental potassium citrate, which metabolizes to potassium bicarbonate, significantly decreased urine levels of two biochemical markers of bone resorption (9). Our group found that potassium citrate prevented the otherwise predictable increase in calcium excretion and in bone resorption rate that accompanies sodium chloride loading (10). In kidney stone formers treated long term with potassium citrate for their stone-forming tendency, Pak et al. (11) observed a significant increase in mineral density of the spine occurring over an extended period of time when spine density ordinarily would have, if anything, decreased.
It seems to us that the weight of evidence from interventional studies indicates that potassium alkali supplementation can improve calcium balance by lowering urine calcium excretion and can reduce bone resorption rates and increase bone mineral density—and that the epidemiological data suggest positive bone effects with high potassium intakes supplied by foods rich in bicarbonate-generating anions. We suggest that, in the subjects of Heaney et al. (1), the lower urine calcium excretion rates associated with higher potassium intakes failed to improve calcium balance because relatively few bicarbonate-generating anions accompanied the higher potassium intakes provided mainly by milk and meat (3). We hesitate, therefore, to credit their skepticism that urine calcium lowering with potassium alkali can lead to "skeletal benefit."
Received April 11, 2005.
References
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  A. Sebastian, L. Frassetto, and R. C. Morris Jr. Authors' Response: Long-Term Persistence of the Urine Calcium-Lowering Effect of Potassium Bicarbonate in Postmenopausal Women J. Clin. Endocrinol. Metab., July 1, 2005; 90(7): 4417 - 4418. [Full Text] [PDF]
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