The authors of these articles [Thumfart et al., 2008: (http://www.ncbi.nlm.nih.gov/pubmed/18701629); Wei et al., 2006: (http://www.pdiconnect.com/cgi/reprint/26/3/366.pdf)(http://www.ncbi.nlm.nih.gov/pubmed/16722031)] have discussed the evidence that serum magnesium (Mg) levels tend to be inversely correlated with serum parathyroid hormone (PTH) levels, and Wei et al. (2006) discussed all of the evidence that magnesium repletion can be protective against calcification and thrombosis and markers of cardiovascular disease. The inverse relationship between the serum Mg and PTH levels is not widely known in the literature, and I've only recently even seen research on it. It's really important, and Mg is just really important, in general, in my opinion. Most of the research and articles on Mg and PTH have focused on the hypocalcemic hypoparathyroidism that can occur in severe Mg deficiency, but repletion of Mg in severely-deficient animals or humans only increases serum calcium (Ca) back to normal levels, by increasing (restoring) the normal capacity of the parathyroid glands to release PTH in response to decreases in serum Ca. At serum Mg levels or dietary Mg supplies that are higher than those that are required for those most basic functions, Mg is thought to suppress PTH levels by acting as a "weak" activator, like a partial agonist, almost, of the calcium-sensing receptor(s) that mediate the suppression of PTH release in response to increases in serum Ca (Thumfart et al., 2008). Paradoxically, Mg can also increase urinary calcium excretion by reducing the reabsorption of calcium in the renal tubules (Thumfart et al., 2008). It's important to note that that increase in urinary Ca excretion would be likely to occur in conjunction with the decreases in the risk of nephrocalcinosis that researchers have generally found in response to increases in Mg intake. In the case of phosphate (Pi) repletion, the decreases in urinary Ca excretion are thought to result from the suppression of PTH-mediated bone resorption. Thus, Pi is thought to actually reduce the amount of Ca that is filtered in the glomeruli, and Mg may partially act by inhibiting Ca reabsorption in the renal tubules (proximal tubules and distal tubules). But the research I cited above suggests that Mg can increase the rate of urinary Ca excretion and even decrease the serum Ca levels and exert a concomitant, suppressive effect on PTH release. That's a really unusual set of effects. Pi can decrease serum Ca (an effect that is probably undesirable) and decrease urinary calcium excretion but can also elevate PTH levels, and that's an effect that could be attenuated, for better or worse, by an increase in Mg availability to the parathyroid glands or the Ca sensing proteins in the renal tubules, etc. Additionally, many of the bizarre derangements in the homeostatic regulation of Ca and Pi that have been found in response to long-term, excessive Pi supplementation could result, in some cases, from Mg depletion. I also get the general sense that a "high" Pi intake will tend to produce plasma volume expansion and lead to a reduction in urinary sodium excretion, and that could tend to oppose the natriuretic effect that high doses of Mg can sometimes produce. Another way of looking at it would be to say that a high or excessive Pi intake may produce plasma volume expansion by reducing Mg absorption or by increasing Mg turnover by other mechanisms, and Mg has sometimes produced low-level diuretic effects [Walker et al., 1998: (http://www.ncbi.nlm.nih.gov/pubmed/9861593?dopt=Abstract)], by mechanisms that aren't clear.
Incidentally, this is another article that includes a discussion of the antithrombotic effects that increases in Mg availability can produce [Maier et al., 2004: (http://www.ncbi.nlm.nih.gov/pubmed/15158909)], and I've been meaning to collect some of the articles that show the antithrombotic effects of Mg repletion or of elevations in the extracellular Mg levels (the steady-state, extracellular Mg levels are not necessarily or even usually going to be elevated much or at all, even in response to Mg supplementation that increases intracellular Mg levels).
What's really interesting is that low serum Mg and low serum Pi tend to go hand in hand and produce many of the same manifestations, including rhabdomyolysis and decreases in red blood cell (RBC) deformability and hemolytic anemia and decreases in RBC 2,3-DPG and ATP, etc. Oken et al. (1971) [Oken et al., 1971: (http://www.bloodjournal.org/cgi/reprint/38/4/468.pdf)(http://www.ncbi.nlm.nih.gov/pubmed/5571433)] found that Mg deficiency caused hemolytic anemia, reticulocytosis in combination with erythroid hyperplasia in the bone marrow (basically meaning that some erythroid colony-forming units in the bone marrow may be enlarged and hyperresponsive to erythropoietin and that the immature RBC's are more numerous and are also undergoing apoptosis at a high rate, because of Mg depletion), decreases in serum phosphorus (and, hence, serum Pi, also), and decreases in the RBC 2,3-DPG and ATP concentrations and in the overall glycolytic activity in RBC's. Piomelli et al. (1973) [Piomelli et al., 1973: (http://www.bloodjournal.org/cgi/reprint/41/3/451.pdf)(http://www.ncbi.nlm.nih.gov/pubmed/4690142)] also found hemolytic anemia in Mg depleted rats and cited research that had shown hypophosphatemia and hypomagnesemia to occur concomitantly in animals and humans.
It's also really important to note that a lot of articles have shown that Mg supplementation at dosages that would produce "desirable" effects, in my opinion, can decrease serum Pi or produce outright hypophosphatemia. And Pi supplementation can produce hypomagnesemia and intracellular Mg depletion. I think that the amounts of supplemental Mg that might be required to compensate for those effects of Pi repletion could be large and could be too high for many people to easily "accept." But, if the Mg is binding to Pi in the GI tract and precipitating, it's not going to be absorbed (there could be some solubilization in response to pH changes along the GI tract, but, for the most part, the precipitation is going to be permanent and is going to mean that the Mg and Pi are "lost"). One way of considering this would be to say that some percentage of a dose of Pi, from the diet or low-dose supplement, under a doctor's supervision, is going to be absorbed and some percentage is going to not be absorbed and probably bind some amounts of Mg and Ca. The intestinal absorption of Ca and the maintenance of serum Ca and renal Ca reabsorption are much more effectively maintained and regulated, in my opinion. Researchers have noted that the serum Ca is relatively stable, even in terms of circadian changes, than the serum Pi. The serum Pi fluctuates wildly throughout the day and in response to exercise, etc. I think the serum Mg levels are not as unstable as the serum Pi levels are, but the intracellular Mg concentrations are very easily depleted, such as in response to catecholaminergic stimulation, etc. Assuming one is using any supplemental Mg and Pi under a doctor's supervision, there's really a need to not be afraid to increase the supplemental intake of Mg, from Mg salts (such as magnesium hydroxide or magnesium oxide) slowly but relatively freely, to compensate for the reductions in absorption that are likely to result from the extra Pi. It wouldn't be a good idea to increase the Pi as freely as one might increase one's Mg intake, but part of the point of this is that an adequate degree of Mg availability is really obligatory for many of the effects of Pi repletion to be sustained in the longer term. One way to approach this type of problem would be to decide on some dosage of supplemental Mg that is tolerable and safe, under a doctor's supervision, and then to increase the ratio of Pi to Ca, assuming one would want to do this, in the first place. That would allow one to evaluate the effect of the Pi increase, from food or low-dose supplements, with the "knowledge" of the baseline effects that the initial Mg dosage produced. There's still a tendency for a lot of the research to focus on the most severe manifestations of the depletion of Mg or Pi or both (hypophosphatemia or hypomagnesemia), but intracellular Pi and Mg depletion tend to occur long before overt hypomagnesemia and hypophosphatemia occur. In any case, those articles I cited are just the tip of the iceberg. Resistance exercise that is done correctly, for example, can drastically deplete intracellular Mg and Pi concentrations, but the tendency has been to focus, in the case of Pi and RBC 2,3-DPG, on the short-term, post-exercise increases in RBC 2,3-DPG or serum Pi. But the more important issues have to do with the changes that occur in the days after the workout. It doesn't make sense to say that resistance exercise that correctly emphasizes the eccentric movement is going to increase RBC 2,3-DPG in the hours after exercise and then cause those levels and the intracellular Pi levels in skeletal or cardiac myocytes to also remain persistently elevated. Where would the Pi come from. It's likely that intense exercise can produce drastic depletions in intracellular Pi levels, but I haven't seen a lot of data on that. The increases in catecholaminergic transmission during resistance exercise would be expected to produce a significant depletion of intracellular Mg, and this has been shown to occur. And beta-adrenoreceptor agonists can produce hypophosphatemia and hypomagnesemia in the long term, etc. Even lowly L-methylfolate could reasonably be expected to increase Pi and Mg turnover, in my opinion, as a result of its apparent catecholaminergic effects.
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