In past postings, I've discussed this article about the potentially-nonexistent utilizability of dietary phytates (such as myo-inositol hexakisphosphate, or IP6) [Letcher et al., 2008: (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2605958)(http://www.ncbi.nlm.nih.gov/pubmed/18684107)], and I've since looked at this [Wise et al., 1982: (http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=241913&blobtype=pdf)(http://www.ncbi.nlm.nih.gov/pubmed/7081983)] and other articles about supposed phytate absorption. Wise et al. (1982) found that the percent of phytate that was hydrolyzed (it actually looks like the numbers could indicate percent absorption, but the implications are similar, in that case, to the implications of a very low percent hydrolysis), to yield inorganic phosphate, was at most between 4 and 9 percent in germ-free rats and was 22-56 percent in rats maintained under normal conditions. Germ-free rats are kept in plastic isolation cages and fed irradiated food [it sounds like the controls' food was also irradiated in the article by Wise et al. (1982), but it's not possible to tell, based on the description of the methods] and sterilized water, to prevent much or most of the ingestion of bacteria and other microbes that are capable of hydrolyzing phytates (organisms that can supply "microbial phytase" activity) [Djouzi et al., 1997: (http://jn.nutrition.org/cgi/content/full/127/11/2260)(http://www.ncbi.nlm.nih.gov/pubmed/9349856?dopt=Abstract)]. So, assuming a mammal isn't ingesting bacteria-laden food and water, the microbial phytase activity in the small intestine may be almost nonexistent. The key point, really, that Letcher et al. (2008) made is that the assays that researchers had previously used to measure serum and urinary IP6 levels, in humans and animals, and to show variations in those values, in response to changes in dietary IP6 intakes, may have been inappropriately measuring phosphate-containing organic compounds, etc. The assays may have been "spiked" with other compounds, and those organic phosphate compounds may have been released during the processing of the blood, etc. Letcher et al. (2008) found basically zero urinary IP6 and found that the serum IP6 levels of humans eating foods, such as cereals, containing abundant IP6 were 200-500 times lower than the levels that had previously been found in humans who had been consuming no IP6 at all. That led the authors (Letcher et al., 2008) to suggest that some of the past assays had been flawed. Letcher et al. (2008) go through the complex process they used to assay the plasma IP6 levels, and I tend to think they're right that very little or no IP6 is likely to be absorbed or to be retained, following any absorption, and metabolized so as to yield utilizable inorganic phosphate to humans. The whole idea that microbial phytase would be a reliable source of phytase activity has always sounded really far-fetched to me, but that's just my opinion. The idea that IP6 would be transported into cells sounds far-fetched to me, too. After small-molecule compounds are phosphorylated, upon entry into cells, the phosphorylated compounds don't tend to be transported out of cells as easily. I think that phosphorylated, small molecule compounds also may not be transported into cells as easily as non-phosphorylated/dephosphorylated compounds are, but I don't know how generalizable or valid that concept may be. Also, I saw one article referring to the possibility that mixtures of D-myo-inositol phosphates and L-myo-inositol phosphates could be formed by the activities of microbial phytase enzymes [Brearly and Hanke, 1996: (http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1217619&blobtype=pdf)]. But I don't see any of the nutritional articles addressing the significance of that, given that some human enzymes that display inositol phosphate kinase activity exhibit stereoselectivity and can only phosphorylate some inositol phosphates [Riley et al., 2006: (http://www.ncbi.nlm.nih.gov/pubmed/16376887)]. Supposing that some IP6 is actually absorbed and transported into human cells, it's not clear to me that human enzymes could necessarily hydrolyze many of those inositol phosphates. Moreover, the fact that no one seems to address that type of detail is another reason I'm seriously questioning the commonly-accepted notion that 50 percent of the phosphate contained in phytates (inositol phosphates, including IP6) is utilizable. Just because phytates are absorbed and transported into cells [and Letcher et al. (2008) argue that they may not be, to any meaningful extent] doesn't mean they won't just be exported and excreted an hour or a day later. I doubt phytates provide much utilizable phosphate at all. For the sake of estimating my dietary phosphate intake, I'd go with some kind of low estimate, such as 5-10 percent, but that's just me. I mean that if a food is grain-based, for example, and supposedly provides 100 mg of phosphate (this would be the phosphate that could potentially be derived from the hydrolysis of IP6 and other phytates, in the grain-based food), I'd assume it actually provides 10 mg of phosphate. Assuming I wanted to make a "conservative" estimate and avoid underestimating my "phosphate intake," I might estimate that 25 percent of the phosphate is utilizable. I wouldn't be surprised if it's 5 percent a lot of the time, when I look at those problems with assays for serum IP6. I can't give anyone else advice about the types of assumptions that he or she should make, however.
But that's a really important point that Letcher et al. (2008) make, and it means that a person on a vegetarian diet who doesn't eat dairy products and takes a calcium supplement could have something like one 20th or one 30th or less of the "true" phosphate intake (of available phosphate) that a person eating a lot of meat and/or milk would. Meat contains phosphate additives and provides about 800 mg phosphate per 50 grams of meat protein (I linked to an article, in a past posting, that showed that). The authors of other articles have reported similarly-large amounts of phosphate in meats. As I've discussed in past postings, Heaney (2004) [Heaney, 2004: (http://www.mayoclinicproceedings.com/content/79/1/91.full.pdf)(http://www.ncbi.nlm.nih.gov/pubmed/14708952)] used some calculations to make the argument that a person who takes 1200 mg of calcium, from calcium carbonate or citrate, may cause all of the potentially-utilizable phosphate in the GI tract to precipitate as calcium phosphates (CaHPO4 or other crystalline or amorphous calcium phosphates or mixed Ca/Mg phosphate crystals) and cease to be potentially-absorbable. When one adds in the fact that phytates may provide no meaningful amounts of utilizable, inorganic phosphate (Letcher et al., 2008), the issues surrounding phosphate nutrition and metabolism have the potential to become even more serious, in my opinion, than the article by Heaney (2004) implies that the "issues" may be.
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