Phosphate as a "Magnesium-Binder"

I was looking at the amounts of calcium that can bind to a given amount of dietary phosphate and form an insoluble precipitate [Heaney, 2004: (http://www.mayoclinicproceedings.com/content/79/1/91.full.pdf)(http://www.ncbi.nlm.nih.gov/pubmed/14708952)]. That quantitative relationship is likely to be important in determining the amounts of supplemental magnesium that would, in theory, in my opinion, be required to compensate for the formation of insoluble complexes of magnesium and phosphate (Pi) in the GI tract. Magnesium is probably just as effective as calcium (a recent article shows it to be more "effective" than calcium) as a "phosphate binder" [here are some of the older articles: (http://scholar.google.com/scholar?q=%22Long-term+use+of+magnesium+hydroxide+as+a+phosphate+binder+in+patients+on+hemodialysis%22&hl=en)], but, assuming magnesium and calcium are equipotent as phosphate binders, the quantitative relationship that Heaney (2004) mentioned would mean that 1,000 mg of supplemental phosphate (I'm assuming phosphorus means phosphate, given the convention) could theoretically bind up to 1,827 mg of magnesium (or 3012 mg calcium). In reality, it wouldn't be that high, and the articles on phosphate binding (it's used to treat hyperphosphatemia in people who have renal failure) discuss those discrepancies between in vitro data and in vivo data, etc. And the effect could be minimized through the use of chelated magnesium asparate, assuming one can tolerate it, or by separating the phosphate intake from the magnesium intake or by using organic phosphate compounds, such as ATP or fructose-1,6-diphosphate (if those phosphorylated sugar compounds were actually available). The organic phosphate compounds can be absorbed intact, to some extent, and any complexes formed with magnesium would still be soluble (in all likelihood, in my opinion), meaning that the complex could also be absorbed intact by solvent-drag-facilitated passive diffusion, etc.

But the point is that, in the case of magnesium oxide, there could conceivably be a really significant reduction in the absorption of magnesium. I think it would probably be more pronounced with something like disodium phosphate than with ATP or dietary phosphate. There's a lot of research in this area, and it's really interesting. In any case, it's almost impossible for a person who does not have kidney failure to become hypermagnesemic, and a couple of those articles discussed the use of dosages of up to 3000 mg of magnesium hydroxide, which is about 42 percent elemental magnesium (966-1260 mg elemental Mg), as a phosphate binder in people with renal failure. Those dosages didn't cause hypermagnesemia, even in people with renal failure. But the main concern is not necessarily the potential for hypermagnesemia, in my opinion, but the disturbances in electrolytes or in nerve fiber conduction or in the short-term regulation of blood pressure, etc., in susceptible individuals, and so one would want to discuss these things with one's doctor. The main thing is to be aware of the potentially large magnitude of the "interaction" with magnesium oxide or other magnesium salts. A lot of the magnesium might not be absorbed. That's what I mean when I refer to an "interaction." Chelated magnesium aspartate (this is a chelated form that has been researched a lot and that doesn't provide massive amounts of glycine) is thought to be largely absorbed intact, through dipeptide transporters or passive diffusion, and its solubility in chelated form would probably prevent it from precipitating with phosphate. It's conceivable that there could still be some binding to phosphate or pyrophosphate, but, anyway, "it's a wrap" for tonight: quantitative estimate of the maximal magnesium-binding capacity of phosphate in the intestinal luminal fluid.