Background In normal subjects, a low level of metabolic acidosisand positive acid balance (the production of more acid thanis excreted) are typically present and correlate in degree withthe amount of endogenous acid produced by the metabolism offoods in ordinary diets abundant in protein. Over a lifetime,the counteraction of retained endogenous acid by base mobilizedfrom the skeleton may contribute to the decrease in bone massthat occurs normally with aging.
Methods To test that possibility, we administered potassiumbicarbonate to 18 postmenopausal women who were given a constantdiet (652 mg [16 mmol] of calcium and 96 g of protein per 60kg of body weight). The potassium bicarbonate was given orallyfor 18 days in doses (60 to 120 mmol per day) that nearly completelyneutralized the endogenous acid.
Results During the administration of potassium bicarbonate,the calcium and phosphorus balance became less negative or morepositive -- that is, less was excreted in comparision with theamount ingested (mean [±SD] change in calcium balance,+56 ±76 mg [1.4 ±1.9 mmol] per day per 60 kg;P = 0.009; change in phosphorus balance, +47 ±64 mg [1.5±2.1 mmol] per day per 60 kg; P = 0.007) because of reductionsin urinary calcium and phosphorus excretion. The changes incalcium and phosphorus balance were positively correlated (P<0.001).Serum osteocalcin concentrations increased from 5.5 ±2.8to 6.1 ±2.8 ng per milliliter (P<0.001), and urinaryhydroxyproline excretion decreased from 28.9 ±12.3 to26.7 ±10.8 mg per day (220 ±94 to 204 ±82µmol per day; P = 0.05). Net renal acid excretion decreasedfrom 70.9 ±10.1 to 12.8 ±21.8 mmol per day, indicatingnearly complete neutralization of endogenous acid.
Conclusions In postmenopausal women, the oral administrationof potassium bicarbonate at a dose sufficient to neutralizeendogenous acid improves calcium and phosphorus balance, reducesbone resorption, and increases the rate of bone formation.
Source Information
From the Department of Medicine and the General Clinical Research Center, Moffitt-Long Hospitals, University of California, San Francisco.
Address reprint requests to Dr. Sebastian at Box 0126, University of California, San Francisco, CA 94143.
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