A high dietary P intake is suggested to have negative effects on bone through increased parathyroid hormone secretion, as high serum parathyroid hormone (S-PTH) concentration increases bone resorption. In many countries the P intake is 2- to 3-fold above dietary guidelines, whereas Ca intake is too low. This combination may not be optimal for bone health. In a previous controlled study, we found that dietary P dose-dependently increased S-PTH and bone resorption and decreased bone formation. The aim of the present study was to investigate the dose–response effects of Ca intake on Ca and bone metabolism with a dietary P intake higher than recommended. Each of the twelve healthy female subjects aged 21–40 years attended three 24-h study sessions, which were randomized with regard to a Ca dose of 0 (control day), 600 or 1200 mg, and each subject served as her own control. The meals on each study day provided 1850 mg P and 480 mg Ca. S-PTH concentration decreased (P < 0·001) and serum ionized Ca concentration increased (P < 0·001) with increasing Ca doses. The bone formation marker, serum bone-specific alkaline phosphatase, did not differ significantly (P = 0·4). By contrast, the bone resorption marker, urinary N-terminal telopeptide of collagen type I, decreased significantly with both Ca doses (P = 0·008). When P intake was above current recommendations, increased Ca intake was beneficial for bone, as indicated by decreased S-PTH concentration and bone resorption. However, not even a high Ca intake could affect bone formation when P intake was excessive.

Ca and P are both essential nutrients for bone and are known to affect one of the most important regulators of bone metabolism, parathyroid hormone (PTH). Too ample a P intake, typical of Western diets, could be deleterious to bone through the increased PTH secretion. Few controlled dose–response studies are available on the effects of high P intake in man. We studied the short-term effects of four P doses on Ca and bone metabolism in fourteen healthy women, 20–28 years of age, who were randomized to four controlled study days; thus each study subject served as her own control. P supplement doses of 0 (placebo), 250, 750 or 1500mg were taken, divided into three doses during the study day. The meals served were exactly the same during each study day and provided 495mg P and 250mg Ca. The P doses affected the serum PTH (S-PTH) in a dose-dependent manner (P=0·0005). There was a decrease in serum ionized Ca concentration only in the highest P dose (P=0·004). The marker of bone formation, bone-specific alkaline phosphatase, decreased (P=0·05) and the bone resorption marker, N-terminal telopeptide of collagen type I, increased in response to the P doses (P=0·05). This controlled dose–response study showed that P has a dose-dependent effect on S-PTH and increases PTH secretion significantly when Ca intake is low. Acutely high P intake adversely affects bone metabolism by decreasing bone formation and increasing bone resorption, as indicated by the bone metabolism markers.

Brown trout and rainbow trout (average weight 100 g) were reared in fresh water at 12 °C under the same conditions before transferring brown trout to sea water, in order to compare phosphorus utilisation in both species. Apparent phosphorus availability, orthophosphate excretion and phosphorus accretion in the fish were directly determined. Thus, actual phosphorus mass balance was built. Rainbow trout raised in fresh water had a higher phosphorus retention coefficient (maximum 50 %) than brown trout reared in fresh water (maximum 45 %). Transferring brown trout to sea water induced a reduction in phosphorus retention (maximum 39 %). Orthophosphate excretion, ranging 7-20 mg phosphorus per kg wet weight per day, represented 10-20 % of ingested phosphorus. Phosphorus availability was lower in brown trout raised in sea water (65 %) than brown trout raised in fresh water (76 %). Phosphorus balance measurements showed that 90 to 98 % of phosphorus flow could be accounted for.