This study compared magnesium oxide and magnesium citrate with respect to in vitro solubility and in vivo gastrointestinal absorbability. The solubility of 25 mmol magnesium citrate and magnesium oxide was examined in vitro in solutions containing varying amounts of hydrochloric acid (0-24.2 mEq) in 300 ml distilled water intended to mimic achlorhydric to peak acid secretory states. Magnesium oxide was virtually insoluble in water and only 43% soluble in simulated peak acid secretion (24.2 mEq hydrochloric acid/300 ml). Magnesium citrate had high solubility even in water (55%) and was substantially more soluble than magnesium oxide in all states of acid secretion. Reprecipitation of magnesium citrate and magnesium oxide did not occur when the filtrates from the solubility studies were titrated to pH 6 and 7 to stimulate pancreatic bicarbonate secretion. Approximately 65% of magnesium citrate was complexed as soluble magnesium citrate, whereas magnesium complexation was not present in the magnesium oxide system. Magnesium absorption from the two magnesium salts was measured in vivo in normal volunteers by assessing the rise in urinary magnesium following oral magnesium load. The increment in urinary magnesium following magnesium citrate load (25 mmol) was significantly higher than that obtained from magnesium oxide load (during 4 hours post-load, 0.22 vs 0.006 mg/mg creatinine, p less than 0.05; during second 2 hours post-load, 0.035 vs 0.008 mg/mg creatinine, p less than 0.05). Thus, magnesium citrate was more soluble and bioavailable than magnesium oxide.

Calcium supplementation is recommended as a prophylaxis against bone loss. This study was performed to determine the dose dependency of calcium absorption in an attempt to derive an optimum dose schedule. Using the well-described oral calcium load technique, we measured the calcium absorption from three different calcium doses (0.5, 1.0, and 2.0 g) of both calcium carbonate and calcium citrate administered to 21 normal subjects (4 men and 17 women, 22-60 years). Nine subjects underwent two additional loads with 0.2 g of elemental calcium as calcium carbonate and as calcium citrate. The intestinal calcium absorption from calcium carbonate and calcium citrate was estimated from the rise in urinary calcium following oral ingestion of the respective calcium salt. The increment in urinary calcium post-load, reflective of intestinal calcium absorption, rose rapidly from 0 to 0.5 g calcium loads with only slight subsequent increases from the 0.5 g to 2.0 g calcium doses. Thus, results indicate that 0.5 g of calcium is the optimum dose of either calcium salt. Moreover, the increment in urinary calcium post-load was higher from calcium citrate than from calcium carbonate at all four dosage levels. The increment in urinary calcium (during the second 2 hr) following calcium citrate load (0.5 g calcium) was 0.104 +/- 0.096 mg/dl glomerular filtrate (GF), which was higher than that of 0.091 +/- 0.068 mg/dl GF obtained from 2.0 g calcium as calcium carbonate. These results confirm the superior calcium bioavailability from calcium citrate as compared with calcium carbonate.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of calcium citrate (800 mg calcium/day in 4 divided doses) on urinary biochemistry and crystallization of calcium salts was examined in 18 normal subjects. During treatment, urinary calcium increased significantly (from 150 +/- 65 (SD) to 248 +/- 77 mg/day). Urinary citrate rose from 611 +/- 208 to 730 +/- 225 mg/day, owing largely to the alkali load. The urinary saturation of calcium oxalate rose by only 41% during calcium citrate treatment, due mainly to citrate complexation of calcium (rather than by 62% without such complexation). Moreover, the formation product of calcium oxalate rose during treatment, indicating that the enhanced citrate excretion augmented the inhibitor activity against calcium oxalate crystallization. Thus, calcium citrate may not be attendant with the risk for stone formation usually associated with calcium supplementation.

The bioavailability of citrate from two different preparations of potassium citrate was examined in eighteen normal volunteers during three phases of study. After stabilization on a constant metabolic diet, subjects took a single dose of placebo, “slow‐release” potassium citrate tablets (60 meq) or rapid‐release liquid potassium citrate preparation (60 meq). Timed urine specimens were collected for 24 hours and analyzed for citrate, potassium, and pH. Similar biochemical findings were observed following administration of the two different preparations with the onset and decline of changes being slightly more rapid for the liquid potassium citrate than the tablet preparation. These equivalent bioavailability data indicate that the liquid preparation is a comparable therapeutic alternative to the tablet form.