Impact of Phosphorus-Based Food Additives on Bone and Mineral Metabolism

Abstract

Context: Phosphorus-based food additives can substantially increase total phosphorus intake per day, but the effect of these additives on endocrine factors regulating bone and mineral metabolism is unclear.

Objective: This study aimed to examine the effect of phosphorus additives on markers of bone and mineral metabolism. Design and Setting, and Participants: This was a feeding study of 10 healthy individuals fed a diet providing ∼1000 mg of phosphorus/d using foods known to be free of phosphorus additives for 1 week (low-additive diet), immediately followed by a diet containing identical food items; however, the foods contained phosphorus additives (additive-enhanced diet). Parallel studies were conducted in animals fed low- (0.2%) and high- (1.8%) phosphorus diets for 5 or 15 weeks.

Main outcome measures: The changes in markers of mineral metabolism after each diet period were measured.

Results: Participants were 32 ± 8 years old, 30% male, and 70% black. The measured phosphorus content of the additive-enhanced diet was 606 ± 125 mg higher than the low-additive diet (P < .001). After 1 week of the low-additive diet, consuming the additive-enhanced diet for 1 week significantly increased circulating fibroblast growth factor 23 (FGF23), osteopontin, and osteocalcin concentrations by 23, 10, and 11%, respectively, and decreased mean sclerostin concentrations (P < .05 for all). Similarly, high-phosphorus diets in mice significantly increased blood FGF23, osteopontin and osteocalcin, lowered sclerostin, and decreased bone mineral density (P < .05 for all).

Conclusions: The enhanced phosphorus content of processed foods can disturb bone and mineral metabolism in humans. The results of the animal studies suggest that this may compromise bone health.

Trial registration: ClinicalTrials.gov NCT01394146.

Figures

Figure 1.

Percent change in circulating FGF23, osteopontin, sclerostin and osteocalcin relative to the immediate preceding dietary period. Results are depicted as means ± SDs.

Figure 2.

A, Femurs and vertebrae from the C57BL/6 mice fed HPD (1.8%) and LPD (0.2%) diets for 5 weeks were analyzed by DXA (n = 10). B, Percent change in femur BMD relative to LPD was calculated for the 5-week (n = 10) and 15-week (n = 7) mice fed HPD. Vertebrae from the C57BL/6 mice fed HPD and LPD for 5 weeks were analyzed by μCT. C, Images of representative vertebrae. D, Quantitative indices generated by μCT analysis; BV/TV (%);Tb.N, trabecular number (1/mm); Tb.Th, trabecular thickness (1/mm3); Tb.SP, trabecular spacing (mm) (N = 5). E, Images of representative femurs from the same mice as in panel C at the mid-diaphysis. F, Femurs were analyzed for cortical quantitative indices; cortical thickness (Ct.Th), total cross-sectional area (Tt.Ar), cortical area (Ct.Ar), and percent porosity (Ct.Po) (N = 9). Results are average ± SEM. *, P < .05 relative to LPD; #, P < .05 relative to 5-week HPD; Student t test.