This article [Whybro et al., 1998: (http://www.ncbi.nlm.nih.gov/pubmed/9481529)] is great, and the authors found that 1000 mg of extra phosphorus, provided by a sodium phosphate supplement that was administered for a week, didn't significantly decrease serum calcium or increase serum phosphate (there were nonsignificant decreases and increases, respectively) and didn't produce very large increases in serum parathyroid hormone (PTH) concentrations. There are other articles showing similarly-marginal effects of not-excessively-high phosphate supplements, and one interesting thing that Whybro et al. (1998) noted is that an increase in PTH in the presence of an increase in phosphate availability to osteoblasts and to the extracellular fluid in the bone tissue, for example, has been shown to suppress the bone resorption induced by PTH. Phosphate supplementation could conceivably cause electrolyte abnormalities in the long term and could deplete magnesium or prevent its absorption or cause other problems, but the problems I see with phosphate supplementation don't really have to do with the supposed effects on the bones but with the fact that all of these awful effects can emerge, in the long term, as a result of phosphate depletion. And phosphate supplementation, as I've discussed in previous postings, could, in the short term, exacerbate some of those problems.
The arguments that many authors make about phosphate homeostasis are not compelling, in part because such large percentages of people are overtly or almost-overtly deficient in vitamin D or have low dietary intakes of utilizable phosphate (phytates do not provide much usable phosphate, as discussed in past postings). Vitamin D depletion tends to reduce phosphate absorption and retention by multiple mechanisms, many of which do not have to do with the regulation of serum hormonal vitamin D, as discussed below, but have to do with the actions of hormonal vitamin D that is produced and that acts locally, in many (or most) different tissues, in an autocrine and paracrine manner. And, as Whybro et al. (1998) noted, one can't simply look at an increase in serum PTH and say that bone resorption is occurring, in part because phosphate can suppress the "undesirable" effects of PTH. Very high PTH levels are undesirable, but Whybro et al. (1998) discussed research showing that an adequate concentration of extracellular phosphate can inhibit osteoclast differentiation from osteoclast progenitor cells. The authors also note that PTH levels tend to increase after meals and to fluctuate significantly throughout the day, and some of the markers that have been used as indicators of bone resorption have not been especially reliable or "bone-specific" (Whybro et al., 1998).
Another important thing is that the decreases in serum calcium that may occur in response to phosphate supplementation are thought to result from the phosphate-induced decreases in renal 1alpha-hydroxylase activity, thereby lowering the levels of serum 1alpha,25-dihydroxyvitamin D (serum hormonal vitamin D), and the phosphate-induced inhibition of calcium absorption. I've seen articles in which the authors simply state that phosphate, given in small dosages, decreases serum calcium by causing ectopic calcification, immediately. That's not true, in my opinion, and the [Ca] x [Pi] product has to be something like 58, usually, localized in the extracellular fluid of a given tissue, before that effect occurs. That's not to say that phosphate supplementation couldn't conceivably contribute to calcification, because I think it could, particularly in the kidneys, at higher dosages, especially. But, for example, Kemi et al. (2006) [Kemi et al., 2006: (http://www.mm.helsinki.fi/mmkem/RAV/tutkimus/calcium/dokumentit/2006/06_high_phosphorus_intakesf.pdf)(http://www.ncbi.nlm.nih.gov/pubmed/16925861)] used large, single dosages of phosphate in people on diets very low in calcium and noted, in table 2, that the Ca:P ratio decreased drastically as the doses of phosphate and total daily phosphorus intakes increased. One has to actually do the calculations, based on the ratios and not on the wording in the methods section, to see that the total, daily calcium intake, for all of the dosages of phosphate, was roughly 250 mg per day. That's very low, and it's almost a given that most of the people in the study were probably vitamin D deficient. In view of the extreme and potentially devastating aspects of phosphate depletion, I think that there is a real danger in pronouncing judgment on phosphate and drawing hasty conclusions. There's a considerable amount of research showing that low phosphate intakes or vitamin D deficiency can actually contribute to osteomalacia and osteoporosis. The effects of calcium supplementation don't impress me at all, and I don't supplement with calcium anymore, personally. There's also the potential for thrombogenic effects from elevations in serum calcium, even within the reference range. Researchers should be focusing on ways of safely supplementing with magnesium and phosphate and vitamin D and focus less on the overrated effects of calcium supplementation. I do think sodium phosphate supplementation is potentially problematic, and a person would obviously not want to supplement with phosphate or vitamin D or magnesium or anything else before discussing that with his or her doctor.
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