Adult Americans typically consume on average 1400 mg, or more, of phosphorus (P) daily in meals, which almost doubles the recommended dietary allowance. After a meal phosphorus is rapidly absorbed at a high efficiency and hormonal mechanisms act swiftly to maintain the serum inorganic phosphate (Pi) concentration within fairly narrow limits. Both parathyroid hormone (PTH) and fibroblast growth factor-23 (FGF-23) reduce serum phosphate during postprandial periods through homeostatic actions on the kidney. However, it is speculated that exposure of cells to a brief high-serum Pi concentration may signal alterations in cell functions that lead to deleterious effects. Elevation of serum FGF-23 or PTH may also be harmful to specific cell types. Examples of possible adverse health effects include cancer, obesity, and hypertension. Here I review potential mechanisms through which high-P intake may contribute to cell metabolic abnormalities and the development of chronic disease; high-dietary phosphorus, especially from foods processed with phosphate salts, may be associated with these chronic diseases. Further investigation is needed to establish the significance of high-phosphate diets within a large segment of the U.S. population with normal renal function.
Keywords: chronic diseases; high-P diets; hormones; metabolic abnormalities.
© 2013 New York Academy of Sciences.