Takeda Eiji, Yamamoto Hironori, Yamanaka-Okumura Hisami, Taketani Yutaka
Department of Clinical Nutrition, Institute of Health Biosciences, University of Tokushima Graduate School, Tokushima City, Tokushima, Japan.
Adv Nutr. 2014 Jan 1;5(1):92-7. doi: 10.3945/an.113.004002.
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.
考虑习惯性高磷摄入是否会对骨骼健康产生不利影响很重要,因为在饮食习惯中,磷的摄入量一直在增加,而钙的摄入量却在减少。在健康个体中,较高的习惯性膳食总磷摄入量与较高的血清甲状旁腺激素(PTH)和较低的血清钙浓度有关。食用含磷添加剂食品的人血清PTH浓度较高。这些发现表明,长期的膳食磷负荷和长期的高磷血症可能对骨骼健康产生重要的负面影响。相比之下,当磷与足够量的钙一起提供时,高磷饮食并不会导致PTH浓度升高。摄入钙磷比接近乳制品的食物对骨骼健康有积极影响。几项随机对照试验表明,摄入乳制品与骨矿物质密度之间存在正相关关系。在我们为健康年轻男性提供的低钙、高磷午餐的负荷试验中,血清PTH浓度在1小时和6小时出现峰值,餐后8小时血清成纤维细胞生长因子23(FGF23)浓度显著升高。相比之下,高钙、高磷餐抑制了餐后8小时内PTH和FGF23的第二次升高。这意味着需要足够的膳食钙摄入量来克服高磷摄入对PTH和FGF23分泌的干扰作用。在肾功能正常的大鼠中,FGF23作用于甲状旁腺,降低PTH mRNA和PTH分泌。然而,血清FGF23升高是慢性肾脏病矿物质代谢的早期改变,导致继发性甲状旁腺功能亢进,这意味着慢性肾脏病患者甲状旁腺对FGF23的作用产生抵抗。这些发现表明,长期高磷饮食可能会损害慢性肾脏病患者和健康人群中由FGF23抵抗介导的骨骼健康。