These articles [Fang et al., 2007: (http://www.ncbi.nlm.nih.gov/pubmed/17910512); Debon and Tester, 2001: (http://cat.inist.fr/?aModele=afficheN&cpsidt=987245); Leroux et al., 2003: (http://cat.inist.fr/?aModele=afficheN&cpsidt=14819835); Nasir et al., 2008: (http://www.ncbi.nlm.nih.gov/pubmed/18267216)] show that gum arabic and other gums (comprising high-molecular-weight polysaccharides and glycoproteins, etc.) contain significant amounts of "occult" calcium (Ca2+) and magnesium, primarily, and also small amounts of copper and zinc. The amounts of zinc and copper listed in the table on page 4 of Debon and Tester (2001) are actually (ug zinc or iron)/(g of "gum") (micrograms Zn or Cu/g gum), not mg/g. The authors mention that in the text on that page, and those values are consistent with the values reported in other articles. Debon and Tester (2001) found that the gum arabic (also known as gum acacia or acacia fiber, etc.) samples contained a mean of 7.82 mg Ca2+/g gum, and the values for pectin, guar gum, and carrageenan are, respectively, 1.53 mg Ca2+/g, 0.79 mg Ca2+/g gum, and 30.3 mg Ca2+/g gum. Fang et al. (2007) found that a 20 % (w/w) aqueous solution (20 g gum arabic/100 g solution) of gum arabic contained 1417 ppm Ca2+. One ppm = 1 ug/g. So that works out to about 7.1 mg Ca2+/g gum arabic. Leroux et al. (2003) found that sugar beet pectin contained 5700 ppm Ca2+, and that's 5.7 mg Ca2+/g sugar beet pectin. That gives one an idea of the amounts of unlabeled calcium that some of these things might contain. If one applies the 7.82 mg/g number, for example, one sees that 30 g of gum arabic might contain up to about 235 mg Ca2+. There's also magnesium, but there's research that implies that some of these gums may sequester magnesium and increase the gums' intestinal (and urinary) excretion [Eby and Eby, 2009: (http://www.ncbi.nlm.nih.gov/pubmed/19944540); Nasir et al., 2008]. Acacia gums of the family Gummiferae (similar to gum acacia, which is from the family Leguminosae) contained mean copper contents of 4.36 and 13.0 ug copper/g of Acacia gum (4.36 and 13.0 ppm) and 6 and 9.5 mg calcium/g gum [Mhinzi, Mghweno, and Buchweishaija, 2008: (http://linkinghub.elsevier.com/retrieve/pii/S0308814607009983)] . That works out to about 131-390 ug copper per 30 g of gum acacia or gum arabic, assuming that the "inter-family" similarities in calcium contents imply that the two families contain similar copper concentrations. Harmuth-Hoene and Schelenz (1980) [Harmuth-Hoene and Schelenz, 1980: (http://www.ncbi.nlm.nih.gov/pubmed/6251185)] found that the endogenous copper concentration in guar gum was 0.40 ppm (0.40 ug/g), and it looks like guar gum might contain less copper than some of these other fibers. In general, however, it looks like some of these soluble fibers might contain smaller amounts of copper (and, perhaps, also calcium) per gram of fiber (insoluble or soluble) than even some of the "best" commercial "whole-grain" "goodness-filled" cereals contain. There's nothing terrible about cereal, but some of these cereals that are "healthy" in relation to their glycemic indices have unsettlingly-large amounts of copper in them, in my opinion. The USDA nutrient tables are useful for estimating one's copper intake (http://www.nal.usda.gov/fnic/foodcomp/Data/SR17/wtrank/sr17a312.pdf), but there's a typo in that document on the copper contents of foods. The numbers given are in milligrams, not micrograms. For example, a number like 0.345 means 345 micrograms (mcg) of copper per mass given, and that's equivalent to 0.345 milligrams copper. (To find the USDA documents for other nutrients/minerals, search on google with the terms USDA copper content" or whatever other nutrient, and the title will be something God-awful, along the lines of "release 18 December 23rd 1993" or the like.) It's appalling that one has to keep trying to check to see what the RDA is now, and I don't even know if they mean for males or females. I personally make every attempt to avoid dealing with numbers that are based on the RDAs, given that, for example, the RDA for copper for adult males is different from the RDA for adult females. The way to use a USDA table is to convert all of the numbers into ug nutrient/g food (mcg/g) or mg nutrient/g food. Take a copper content of 345 mcg or whatever, and divide by the mass of the serving of food in question. When one does that, the numbers are relatively consistent across similar foods. If I'm looking at a nutrition label on a food and can't tell what RDA "thing" the label is referring to, I'll just type the name of the food into google scholar and add the words "copper content" or whatever. The articles usually provide the concentrations in ppm (ug/g) or mg/g or % (w/w) (which is g nutrient/g food, or g/g, unless otherwise specified).
These types of issues could be relevant to the treatment of depression or other psychiatric disorders, given the potential that exists, in my opinion, for small changes in dietary calcium and copper to produce low-level hemostatic effects and, by that and other mechanisms, in my view, to exacerbate depression or brain functioning in a more general sense, at least in some people. It's worthwhile to note that the soluble fibers can sequester small amounts of metals, and that effect could, in theory, offset the supposed increases in copper or calcium absorption that one might expect to see in response to the ingestion of one or more of the fibers. I was going to discuss some of the research on depression and psychiatric symptoms in relation to copper and calcium metabolism, but this posting is getting too long. One of the points I was going to make is that one could replace a healthy cereal with some source of soluble fiber and conceivably get less copper, less calcium, and substantially more soluble fiber than one would get from the cereal itself, with milk. Another downside of milk is that manufacturers are still adding preformed vitamin A to it, and preformed vitamin A can produce toxic effects on the liver and parts of the brain, among other tissues, in relatively small amounts. Another approach would be to dilute the milk with water. I'm not suggesting that these are likely to be practical approaches for most people, but I just throw the ideas out. As discussed in past postings, there's research that suggests that excesses of dietary calcium can produce increases in platelet activation, either by increasing the rates of calcium influx into platelets or simply serving its functions in the coagulation cascade. In my opinion, excesses of dietary copper have the potential to exacerbate depression, in part by producing hemostatic effects. Copper is incorporated into coagulation factor V and factor VIII during the post-translational processing of those proteins (http://scholar.google.com/scholar?hl=en&q=copper+%22factor+VIII%22+OR+%22factor+V%22&btnG=Search&as_sdt=2000&as_ylo=&as_vis=0), and there's abundant evidence that excesses of intracellular copper have been associated with exacerbaions of symptoms of depresssion and other psychiatric conditions, etc. Essentially, it's well-known, and I'm not going to collect a lot of references at this point. But it's interesting that there's all this research focusing on the increases in platelet activation that can occur in association with depression (http://scholar.google.com/scholar?hl=en&q=depression+platelet&btnG=Search&as_sdt=2000&as_ylo=&as_vis=0), and the assumption seems to generally be that this platelet activation is going to mainly have relevance as an explanation for the association of heart disease with depression [for example, see Nemeroff and Musselman, 2000: (http://www.ncbi.nlm.nih.gov/pubmed/11011349)]. But there's a lot of research showing, for example, that elevations in serum antiphospholipid autoantibody titers can occur in people who have been diagnosed with depression or some other disorder (http://scholar.google.com/scholar?hl=en&q=depression+antiphospholipid&btnG=Search&as_sdt=2000&as_ylo=&as_vis=0); (http://scholar.google.com/scholar?hl=en&q=antiphospholipid+psychiatry&btnG=Search&as_sdt=2000&as_ylo=&as_vis=0)]. Elevations in serum antiphospholipid autoantibody titers are very well known to produce hemostasis and increases in platelet activation or platelet-dependent thrombosis (http://scholar.google.com/scholar?hl=en&q=antiphospholipid+hemostatic+OR+hemostasis+OR+platelet+OR+thrombogenic+OR+thrombosis&btnG=Search&as_sdt=2000&as_ylo=&as_vis=0). Thus, the increases in platelet activation could be a cause of the depression. I want to emphasize, however, that using any old platelet-anti-aggregatory approach is likely to be problematic, at best, and could be disastrous, given the association of a lot of these plant (herb)-derived or other antiplatelet compounds with hemorrhages and whatnot. There's a lot of other indirect evidence that I'm not going to get into now.
These types of issues could be relevant to the treatment of depression or other psychiatric disorders, given the potential that exists, in my opinion, for small changes in dietary calcium and copper to produce low-level hemostatic effects and, by that and other mechanisms, in my view, to exacerbate depression or brain functioning in a more general sense, at least in some people. It's worthwhile to note that the soluble fibers can sequester small amounts of metals, and that effect could, in theory, offset the supposed increases in copper or calcium absorption that one might expect to see in response to the ingestion of one or more of the fibers. I was going to discuss some of the research on depression and psychiatric symptoms in relation to copper and calcium metabolism, but this posting is getting too long. One of the points I was going to make is that one could replace a healthy cereal with some source of soluble fiber and conceivably get less copper, less calcium, and substantially more soluble fiber than one would get from the cereal itself, with milk. Another downside of milk is that manufacturers are still adding preformed vitamin A to it, and preformed vitamin A can produce toxic effects on the liver and parts of the brain, among other tissues, in relatively small amounts. Another approach would be to dilute the milk with water. I'm not suggesting that these are likely to be practical approaches for most people, but I just throw the ideas out. As discussed in past postings, there's research that suggests that excesses of dietary calcium can produce increases in platelet activation, either by increasing the rates of calcium influx into platelets or simply serving its functions in the coagulation cascade. In my opinion, excesses of dietary copper have the potential to exacerbate depression, in part by producing hemostatic effects. Copper is incorporated into coagulation factor V and factor VIII during the post-translational processing of those proteins (http://scholar.google.com/scholar?hl=en&q=copper+%22factor+VIII%22+OR+%22factor+V%22&btnG=Search&as_sdt=2000&as_ylo=&as_vis=0), and there's abundant evidence that excesses of intracellular copper have been associated with exacerbaions of symptoms of depresssion and other psychiatric conditions, etc. Essentially, it's well-known, and I'm not going to collect a lot of references at this point. But it's interesting that there's all this research focusing on the increases in platelet activation that can occur in association with depression (http://scholar.google.com/scholar?hl=en&q=depression+platelet&btnG=Search&as_sdt=2000&as_ylo=&as_vis=0), and the assumption seems to generally be that this platelet activation is going to mainly have relevance as an explanation for the association of heart disease with depression [for example, see Nemeroff and Musselman, 2000: (http://www.ncbi.nlm.nih.gov/pubmed/11011349)]. But there's a lot of research showing, for example, that elevations in serum antiphospholipid autoantibody titers can occur in people who have been diagnosed with depression or some other disorder (http://scholar.google.com/scholar?hl=en&q=depression+antiphospholipid&btnG=Search&as_sdt=2000&as_ylo=&as_vis=0); (http://scholar.google.com/scholar?hl=en&q=antiphospholipid+psychiatry&btnG=Search&as_sdt=2000&as_ylo=&as_vis=0)]. Elevations in serum antiphospholipid autoantibody titers are very well known to produce hemostasis and increases in platelet activation or platelet-dependent thrombosis (http://scholar.google.com/scholar?hl=en&q=antiphospholipid+hemostatic+OR+hemostasis+OR+platelet+OR+thrombogenic+OR+thrombosis&btnG=Search&as_sdt=2000&as_ylo=&as_vis=0). Thus, the increases in platelet activation could be a cause of the depression. I want to emphasize, however, that using any old platelet-anti-aggregatory approach is likely to be problematic, at best, and could be disastrous, given the association of a lot of these plant (herb)-derived or other antiplatelet compounds with hemorrhages and whatnot. There's a lot of other indirect evidence that I'm not going to get into now.
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