These articles [Ruttmann et al., 2007:(http://www.anesthesiaanalgesia.org/cgi/content/full/104/6/1475) (http://www.ncbi.nlm.nih.gov/pubmed/17513645); Seelig, 1990: (http://www.ncbi.nlm.nih.gov/pubmed/2132751)] discuss the potential for high dietary calcium intakes, particularly in the absence of abundant magnesium intake, to produce hypercoagulability. Finding articles on hypercoagulability produced by something like calcium is difficult, but there's a great deal of research on the antithrombotic and mild antiplatelet actions of magnesium. A lot of articles mention that calcium is required for "normal blood coagulation" or something like that, but the pathological side of this tends to be glossed over by all of the osteoporosis-related discussion, etc. This is the type of thing that is worth considering in the context of something like vitamin D supplementation. There's a great deal of research on the association of low plasma 25-hydroxyvitamin D [25(OH)D] with increases in the risk of breast cancer and other epithelial cell cancers, and vitamin D3 has been shown to be safe up to about 2,000-4,000 IU/d (providing the source is a reputable manufacturer). But both vitamin D and calcium can increase serum calcium slightly, and the issue is not even if this causes hypercalcemia. Calcium is normally at a very high concentration in the blood, and those articles suggest that small changes in the serum calcium may be able to affect processes such as the coagulation cascade (and calcium is fairly directly involved in that). This is not usually the way the modulation of serum calcium is even researched, and it's sort of an obscure concept. But it clearly can occur. It's almost surprising, given the way the regulation of serum calcium is discussed, that dietary calcium supplements can increase serum calcium levels. But they can. I can put up articles showing that, but many articles have shown that to be the case.
In the case of vitamin D and calcium supplementation in the context of the prevention of osteoporosis or osteomalacia, the usual mechanistic explanation has been that both calcium and vitamin D reduce the risk of osteoporosis by reducing the serum parathyroid hormone (PTH) concentration. The serum PTH levels vary inversely with plasma 25(OH)D up to 200 nM, in a roughly linear manner, and it seems like using vitamin D supplementation without a great deal of extra calcium supplementation would be reasonable. Obviously, this would be a decision that would be different for everyone. But the supplemental intakes of calcium are getting enormous. I don't think the business of ratios of calcium to magnesium is useful, and it's really necessary to think of each thing like that individually. The zinc-to-copper ratio concept is very problematic and is not valid at all, in my opinion. The range of dosages for magnesium is very large, and some research has shown that 1,000 mg/d of Mg2+ is necessary to even maintain positive "magnesium balance" in someone who is exercising. The effects of magnesium can be complex, and its effects on PTH are difficult to understand.
It also makes sense to use the serum albumin correction equations for serum calcium. Their use is controversial and tends to be most necessary in people with renal failure or renal disease, given that renal disease impairs calcium homeostasis. I'll collect them, but the general idea, as far as I understand it, is that a low serum albumin will increase the proportion of serum calcium that is ionized (free) and not bound to albumin. That's the fraction that would be likely to increase the coagulation cascade, in theory, and perhaps produce excessive calcium influx into cells, thereby deranging insulin metabolism, etc.
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