Extract

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 (4–6).

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