Potassium Citrate, but not Chloride, Increases Bone Density in Postmenopausal Women


Partial neutralization of the acidogenic Western diet with potassium citrate increases bone mass in postmenopausal women with osteopenia.

Chronic acid loads are an obligate consequence of the high animal/grain protein content of the Western diet. The effect of this diet-induced metabolic acidosis on bone mass is controversial. In a randomized, prospective, controlled, double-blind trial, 161 postmenopausal women (age 58.6 +/- 4.8 yr) with low bone mass (T score -1 to -4) were randomly assigned to 30 mEq of oral potassium (K) citrate (Kcitrate) or 30 mEq of K chloride (KCl) daily. The primary end point was the intergroup difference in mean percentage change in bone mineral density (BMD) at lumbar spine (L2 through L4) after 12 mo. Compared with the women who received KCl, women who received Kcitrate exhibited an intergroup increase in BMD (+/-SE) of 1.87 +/- 0.50% at L2 through L4 (P < 0.001), of 1.39 +/- 0.48% (P < 0.001) at femoral neck, and of 1.98 +/- 0.51% (P < 0.001) at total hip. Significant secondary end point intragroup changes also were found: Kcitrate increased L2 through L4 BMD significantly from baseline at months 3, 9, and 12 and reached a month 12 increase of 0.89 +/- 0.30% (P < 0.05), whereas the KCl arm showed a decreased L2 through L4 BMD by -0.98 +/- 0.38% (P < 0.05), significant only at month 12. Intergroup differences for distal radius and total body were NS. The Kcitrate-treated group demonstrated a sustained and significant reduction in urinary calcium excretion and a significant increase in urinary citrate excretion, with increased citrate excretion indicative of sustained systemic alkalization. Urinary bone resorption marker excretion rates were significantly reduced by Kcitrate, and for deoxypyridinoline, the intergroup difference was significant. Urinary net acid excretion correlated inversely and significantly with the change in BMD in a subset of patients. Large and significant reductions in BP were observed for both K supplements during the entire 12 mo. Bone mass can be increased significantly in postmenopausal women with osteopenia by increasing their daily alkali intake as citrate, and the effect is independent of reported skeletal effects of K.

Jehle S, Zanetti A, Muser J, Hulter HN…
J. Am. Soc. Nephrol. Nov 2006
PMID: 17035614 | Free Full Text

Despite more than 70 yr of sustained interest in the possibility that chronic metabolic acidosis might decrease bone mass, central questions regarding the effect of acid-base alterations on human bone physiology and pathophysiology remain unanswered (4,27,28). First, does chronic metabolic acidosis of any magnitude decrease bone mass? Second, does the low-grade chronic metabolic acidosis that is induced by the acidogenic Western diet result in osteoporosis? Third, can neutralization of dietary acid result in increased bone mass in normal humans or those with osteopenia?

Indirect support for a possible role of chronic metabolic acidosis to reduce bone mass comes from small, uncontrolled studies in humans with nonazotemic renal disease (distal renal tubular acidosis [29,30]). Chronic dietary acid loads were shown to result in significant and reversible negative calcium balance (6), and experimental increases in animal protein intake or its chief acidogenic constituent, methionine, within the range that is characteristic of the Western diet were shown to cause both negative calcium balance and increased systemic acid load (31,32). Compatible with and strongly supportive of these observations, short-term neutralization of endogenous acid production by oral ingestion of bicarbonate for 7 to 18 d in both postmenopausal women and young healthy adults resulted in calcium retention and—on the basis of analysis of bone markers—in inhibition of bone resorption (13,14).


This study establishes that bone mass can be increased significantly in postmenopausal women with osteopenia by increasing their daily alkali intake as Kcitrate and that this effect is independent of reported in vitro skeletal effects of co-administered K. The magnitude of the effect is large, and the safety profile was found to be excellent, albeit based on a limited sample size. The results strongly support the thesis that neutralization of the modern Western diet will promote skeletal health. The associated BP effects of the K supplement provide additional incentive to move forward with controlled outcome trials using long-term Kcitrate treatment.

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