Calcium has a tightly regulated homeostasis rendering it unsuitable for comparing fasting calcium concentrations for the purpose of determining the effect of supplementation on calcium status. Although, there are some studies in the literature in which the calcium concentration was determined following a short time interval after calcium intake [12–16]. For instance, Heaney et al. compared the bioavailability of calcium from two fortification systems. A combination of tricalcium phosphate and calcium lactate (500 mg calcium, orange juice) led to an increase in serum calcium of almost 0.35 mg/dl (0.09 mmol/l) after two hours . In the study of Green et al., the change in the calcium concentration after tricalcium phosphate (1200 mg calcium, powder mixed in water) was 0.1 mmol/l . In present study, plasma calcium concentration rose by approximately 0.06 mmol/l in four hours after single administration and by about 0.1 mmol/l after repeated administration. The significantly higher calcium concentration at 240 min after single and repeated CaP administration and the significantly higher AUC for the increment in calcium concentration after repeated CaP administration compared to placebo suggest that part of the calcium from the CaP supplement was absorbed. Supplementation with CaP led to an increase in blood calcium concentration, which is comparable to other studies.
Because hyperphosphatemia is linked with vascular calcification, cardiovascular mortality, and progression of chronic kidney disease, phosphate intake is an aspect that is controversially discussed [17–19]. In the present study, there was no difference in the plasma phosphate concentration between CaP and placebo after 240 min. In another study by Reginster et al. comprising 10 male subjects, the serum phosphorus concentration did not change after supplementation with tricalcium phosphate (1000 mg Ca) within a time frame of 360 min . In contrast, both Yang et al. and Shires et al. showed an increase in phosphorus concentration after an intake of 1200 mg calcium [21, 22].
Interestingly, after all administrations (single CaP and placebo administration, repeated CaP and placebo administrations), phosphate concentration significantly decreased at first, followed by a rise to basal concentration (Figure 2). Karp et al. showed similar results for plasma phosphate concentration after supplementation with different calcium supplements and potassium citrate . Because of a decrease in bone resorption, the authors assumed a decrease in the release of phosphate from bone for potassium citrate only . Moreover, hypophosphatemia can be a result of phosphate shifts from the blood into the cells, such as after ingestion of glucose, fructose, and feeding following starvation (phosphorylation processes) . A glucose load can induce a transient reduction in serum phosphate levels , probably due to secretion of gastrointestinal hormones and subsequent stimulation of calcitonin . Calcitonin induces an inhibition of osteoclasts and a reduction in the release of phosphorus from bone into blood. However, the association between gastrointestinal hormones and calcitonin has only been shown in rodents and not in humans .
Alternatively, the decreasing concentration of phosphate in the present study can also be explained by a dilution effect as participants were allowed to drink water ad libitum after the test meal. Between time points 60–120 min, the phosphate concentration increased again to baseline levels indicating that intestinal phosphate absorption took place within this time frame. Indeed, in the study by Karp et al., the participants were also allowed to drink water ad libitum. In contrast, studies in which liquid intake were restricted showed either an immediate increase or a constant phosphate concentration [20–22].
Hence, the present results indicate that the increased phosphate intake due to the CaP supplementation, did probably not lead to an increased phosphate absorption in the gut. This conclusion is supported by comparably postprandial phosphate concentrations and the similar AUC for the increment in phosphate concentration after CaP and placebo administrations. In order to confirm these results, isotopic tracer studies are indicated. However, the results show that phosphate from this CaP supplement did not lead to an increase in plasma phosphate concentration.