title: Increasing dietary phosphorus intake from food additives: potential for negative impact on bone health.
abstract: It is important to consider whether habitual high phosphorus intake adversely affects bone health, because phosphorus intake has been increasing, whereas calcium intake has been decreasing in dietary patterns. A higher total habitual dietary phosphorus intake has been associated with higher serum parathyroid hormone (PTH) and lower serum calcium concentrations in healthy individuals. Higher serum PTH concentrations have been shown in those who consume foods with phosphorus additives. These findings suggest that long-term dietary phosphorus loads and long-term hyperphosphatemia may have important negative effects on bone health. In contrast, PTH concentrations did not increase as a result of high dietary phosphorus intake when phosphorus was provided with adequate amounts of calcium. Intake of foods with a ratio of calcium to phosphorus close to that found in dairy products led to positive effects on bone health. Several randomized controlled trials have shown positive relations between dairy intake and bone mineral density. In our loading test with a low-calcium, high-phosphorus lunch provided to healthy young men, serum PTH concentrations showed peaks at 1 and 6 h, and serum fibroblast growth factor 23 (FGF23) concentrations increased significantly at 8 h after the meal. In contrast, the high-calcium, high-phosphorus meal suppressed the second PTH and FGF23 elevations until 8 h after the meal. This implies that adequate dietary calcium intake is needed to overcome the interfering effects of high phosphorus intake on PTH and FGF23 secretion. FGF23 acts on the parathyroid gland to decrease PTH mRNA and PTH secretion in rats with normal kidney function. However, increased serum FGF23 is an early alteration of mineral metabolism in chronic kidney disease, causing secondary hyperthyroidism, and implying resistance of the parathyroid gland to the action of FGF23 in chronic kidney disease. These findings suggest that long-term high-phosphorus diets may impair bone health mediated by FGF23 resistance both in chronic kidney disease patients and in the healthy population.
authors.affiliation: Department of Clinical Nutrition, Institute of Health Biosciences, University of Tokushima Graduate School, Tokushima City, Tokushima, Japan.
authors.forename: Eiji
authors.initials: E
authors.lastname: Takeda
authors.forename: Hironori
authors.initials: H
authors.lastname: Yamamoto
authors.forename: Hisami
authors.initials: H
authors.lastname: Yamanaka-Okumura
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Taketani
mesh_terms: D000818:Animals; D001862:Bone Resorption / Q000209:etiology* / Q000378:metabolism; D001842:Bone and Bones / Q000378:metabolism*; D003226:Congresses as Topic; D057140:Fast Foods / Q000009:adverse effects; D005247:Feeding Behavior; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors / Q000378:metabolism; D005503:Food Additives / Q000008:administration & dosage / Q000009:adverse effects*; D006801:Humans; D010280:Parathyroid Glands / Q000378:metabolism; D010281:Parathyroid Hormone / Q000378:metabolism; D016226:Phosphorus, Dietary / Q000008:administration & dosage / Q000009:adverse effects*
chemical_list: C000717427:FGF23 protein, human; D005503:Food Additives; C470125:PTH protein, human; D010281:Parathyroid Hormone; D016226:Phosphorus, Dietary; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23