In this article [Ko, 2008: (http://www.ncbi.nlm.nih.gov/pubmed/18289201)], Ko (2008) discussed this article (the article the editorial accompanies) [Tsai et al., 2008: (http://socgastro.com/biblioteca/rev-articulos/pdf/magnesio200802.pdf)(http://www.ncbi.nlm.nih.gov/pubmed/18076730)]. Tsai et al. (2008) found that higher intakes of dietary magnesium (Mg2+) intakes were associated with a decrease in the risk of developing symptomatic gallstones. I guess they looked at men only (?). It's not just relevant to men, of course. But Ko et al. (2008) cited some of that old research showing that intraduodenal Mg2+, in the form of Mg2+ salts and not chelates, induces gallbladder contractions by inducing cholecystokinin CCK release (http://scholar.google.com/scholar?hl=en&q=cholecystokinin+magnesium+gallbladder) from, I guess, enterocytes. I haven't read enough of all that research to get a sense of the mechanism, but the site of action is apparently localized. They've used large doses of Mg2+ in some of those articles, but I did some quick searching and reading and found a dose-response study in dogs that would tend to argue against the need for massive dosages. Ko (2008) was basically saying that normal amounts of Mg2+ could exert the same effect on a smaller scale.
On the surface, that research doesn't look like much, and the same effect can supposedly be shown for other electrolytes. I don't know, though. This article [Colombato et al., 1977: (http://www.ncbi.nlm.nih.gov/pubmed/835560)] shows a 17-fold increase in the rate of bilirubin output from the gallbladder/common bile duct in normal people, in response to Mg2+. That's significant, but the main thing I was thinking, in view of that editorial by Ko (2008), is that changes in the relative abundances of bile acids or increases in the biliary and intestinal-luminal-fluid concentrations of unconjugated bilirubin occur in people with liver disease and can bind massive amounts of magnesium [see here for some articles: (http://hardcorephysiologyfun.blogspot.com/2009/09/heterogeneous-precipitationnucleation.html)]. In one of those articles in the past posting [Heubi et al., 1997: (http://www.ncbi.nlm.nih.gov/pubmed/9285381)], the authors found that the equivalent of an adult's intake of 1100-2300 mg of Mg2+ per day was necessary to just prevent overt Mg2+ deficiency in children with liver disease, and that was attributed mainly to the sequestration of Mg2+ in the GI tract. In any case, in theory, that Mg2+ would exist mainly as mixed precipitates, bound to free fatty acids or bile salts or bilirubin, etc., and wouldn't be capable of participating in osmoregulatory disturbances. So the people might be able to tolerate much higher dosages of Mg2+ than people who do not have liver disease would. Some authors have remarked on the drastic differences in the amounts of Mg2+ that people can tolerate. That type of precipitation could be one reason for the large amount of variation. I think Ko (2008) also mentioned the anti-nucleating effect that Mg2+ could have. Magnesium binds to bilirubin or otherwise interacts with it in complex ways, also (http://scholar.google.com/scholar?hl=en&q=magnesium+bilirubin+binding), and can apparently prevent bilirubin from binding to precipitated calcium phosphate [Van der Veere et al., 1995: (http://www.jlr.org/cgi/reprint/36/8/1697.pdf)(http://www.ncbi.nlm.nih.gov/pubmed/7595091)]. In general, Mg2+ has an "anti-nucleating" effect, in different contexts, even though I've seen articles discussing the capacity of Mg2+ to promote amorphous calcium phosphate formation but to also help to prevent, to a significant degree, soft-tissue hydroxyapatite/apatite crystallization. Amorphous calcium phosphate is basically innocuous, as far as I know, particularly in comparison to hydroxyapatite (in soft tissues). Anyway, the point is that people who have liver disease could require large amounts of Mg2+ to just to prevent deficiency (there's a lot of research showing that Mg2+ depletion contributes to exercise intolerance in liver disease, etc.), and even larger dosages could be required to produce the CCK-releasing effects that would occur in normal people at lower dosages. They used to say that CCK suppresses the appetite and used to suggest that people use L-phenylalanine to release CCK, etc. I don't think that's a good idea, but, in view of the problematic quality of much of the research on Mg2+ (research that is plagued by the use of miniscule and arbitrary dosages of oral Mg2+ and massive dosages of intravenous Mg2+ for everything under the sun), I wouldn't be surprised if the regulation of gallbladder contraction by Mg2+ is another thing that people stopped paying attention to in the 1980's, after the Bayh-Dole Act was passed or something. Bayh and Dole told them to buy influence in Universities via special interest groups and dole out advertising money for endless tv ads, and they "Bayh-ed it." No, that's nonsense.
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