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再探酸灰假说:重新评估饮食酸度对骨骼的影响

The acid-ash hypothesis revisited: a reassessment of the impact of dietary acidity on bone.

作者信息

Nicoll Rachel, McLaren Howard John

机构信息

Department of Public Health and Clinical Medicine and Heart Centre, Umea University, Umeå, Sweden,

出版信息

J Bone Miner Metab. 2014 Sep;32(5):469-75. doi: 10.1007/s00774-014-0571-0. Epub 2014 Feb 21.

DOI:10.1007/s00774-014-0571-0
PMID:24557632
Abstract

The acid-ash hypothesis states that when there are excess blood protons, bone is eroded to provide alkali to buffer the net acidity and maintain physiologic pH. There is concern that with the typical Western diet, we are permanently in a state of net endogenous acid production, which is gradually reducing bone. While it is clear that a high acid-producing diet generates increased urinary acid and calcium excretion, the effect of diet does not always have the expected results on BMD, fracture risk and markers of bone formation and resorption, suggesting that other factors are influencing the effect of acid/alkali loading on bone. High dietary protein, sodium and phosphorus intake, all of which are necessary for bone formation, were thought to be net acid forming and contribute to low BMD and fracture risk, but appear under certain conditions to be beneficial, with the effect of protein being driven by calcium repletion. Dietary salt can increase short-term markers of bone resorption but may also trigger 1,25(OH)2D synthesis to increase calcium absorption; with low calcium intake, salt intake may be inversely correlated with BMD but with high calcium intake, salt intake was positively correlated with BMD. With respect to the effect of phosphorus, the data are conflicting. Inclusion of an analysis of calcium intake may help to reconcile the contradictory results seen in many of the studies of bone. The acid-ash hypothesis could, therefore, be amended to state that with an acid-producing diet and low calcium intake, bone is eroded to provide alkali to buffer excess protons but where calcium intake is high the acid-producing diet may be protective.

摘要

酸灰假说认为,当血液中质子过量时,骨骼会被侵蚀以提供碱来缓冲净酸度并维持生理pH值。有人担心,按照典型的西方饮食,我们会一直处于内源性净产酸状态,这会逐渐削弱骨骼。虽然高产酸饮食确实会增加尿酸和钙的排泄,但饮食对骨密度、骨折风险以及骨形成和骨吸收标志物的影响并不总是如预期那样,这表明还有其他因素在影响酸碱负荷对骨骼的作用。高膳食蛋白质、钠和磷的摄入,虽然这些都是骨骼形成所必需的,但曾被认为是净产酸的,会导致骨密度降低和骨折风险增加,但在某些情况下似乎是有益的,蛋白质的影响受钙补充情况的驱动。膳食盐会增加骨吸收的短期标志物,但也可能会触发1,25(OH)2D的合成以增加钙的吸收;钙摄入量低时,盐摄入量可能与骨密度呈负相关,但钙摄入量高时,盐摄入量与骨密度呈正相关。关于磷的影响,数据存在矛盾。纳入钙摄入量分析可能有助于调和许多骨骼研究中出现的相互矛盾的结果。因此,酸灰假说可以修正为:在产酸饮食且钙摄入量低的情况下,骨骼会被侵蚀以提供碱来缓冲过量的质子,但在钙摄入量高的情况下,产酸饮食可能具有保护作用。

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损伤后肌肉骨骼组织中的早期 pH 值变化——有氧分解代谢途径活性与局部 pH 值的个体间差异有关。
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