So the "bottom-line," "take-home" message of that last posting is that, in susceptible individuals or individuals in whom the coagulation cascade has been transiently or mildly activated by infectious mono or influenza, an increase in serum calcium within the normal range could produce depression or psychiatric symptoms by producing low-level thrombogenic effects (effects that essentially disturb mitochondrial functioning, as the feed-forward activation of the coagulation cascade essentially always does), and reducing serum calcium by reducing the dietary calcium or vitamin D intake could ameliorate those effects. Increasing the ratio of the phosphate to calcium intake could be a superior way of addressing those potentially-thrombogenic effects (and calcium influx promoting effects, in neurons) of increases in serum calcium. And idiosyncratic effects of glutamine supplementation might be addressed by decreasing the vitamin D or calcium intake or increasing the relative intake of phosphate, to some small extent, given the potential for slight "calcemic" and hypophosphatemic effects of glutamine. It's possible that an increase in serum phosphate would reduce calcium influx into platelets, given that increases in phosphate availability have reduced stimulus-induced intracellular calcium influx in beta-cells, for example, if memory serves (see past postings), and in other cell types. That's thought to be one mechanism underlying magnesium's antithrombotic effects (and relative absence of hemorrhagic effects).
I don't have time to go into the research, but, in my opinion, some of the research that would seem to rule out a role for the activation of the coagulation cascade in depression (http://scholar.google.com/scholar?q=coagulation+psychiatry&hl=en) does not rule it out, given that research in people with lupus and research on the coagulation cascade in general have shown that localized endothelial cell activation, such as in cerebral blood vessels, can occur and can cause localized microthrombi or low-level thromboses without producing measurable changes in the systemic coagulation parameters. Blood tests of coagulation parameters are notoriously insensitive and problematic, in my opinion. This is not a scientific statement, but, if it were possible to easily evaluate coagulation function, then monitoring people on warfarin wouldn't be so difficult and complex for both doctors and patients (the people taking warfarin, etc.), in my opinion. The coagulation cascade is extremely complex, and quantitative data on coagulation parameters are not going to tell one all that much about the individual and tissue-restricted effects of that state in any one person. The INR, for example, is very insensitive and displays a semi-logarithmic relationship with changes in the serum prothrombin levels, etc. I tend to think the ex vivo tests on platelet function are also not always going to have relevance to tissue-restricted (or endothelial-site-restricted) thrombogenic effects in the brain, for example. Benign intracranial hypertension/idiopathic intracranial hypertension commonly produces psychiatric symptoms, but that type of disease state may just be a slightly more extreme state along a spectrum of low-level thrombogenic changes that could potentially contribute to some forms of severe depression or chronic fatigue syndrome, etc. Those articles about visual dimming in depression could also indicate that low-level activation of the coagulation cascade is occurring, given the common occurrence of visual dimming in idiopathic intracranial hypertension (and the fact that idiopathic intracranial hypertension is thought to be not-infrequently caused, in part, by venous sinus thrombosis). Magnesium can also produce antithrombotic effects and may, in my opinion, be a lot less likely to cause bleeding, upon adjustment to a dose increase in 1-2 days, than many or most of the many other compounds that influence platelet activation and the coagulation cascade. In any case, it's worthwhile to remember that the use of Ginkgo biloba extracts has been associated with intracranial hemorrhages in many case reports (http://hardcorephysiologyfun.blogspot.com/2008/12/ginkgo-biloba-extracts-and-intracranial.html), and many compounds can reduce coagulation by mechanisms that could be very dangerous and unpredictable. So one would want to talk to one's doctor about this type of thing. Purines have produced antithrombotic effects in a lot of animal studies and appear to be a lot less likely to cause bleeding than most of these other physiological approaches, but that's just my opinion, based on my experiences during infectious mono, several years ago. These are all, obviously, just my opinions.
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