Professor & patients' paper on the solvable biological challenge of ME/CFS: reader-friendly version
Simon McGrath provides a patient-friendly version of a peer-reviewed paper which highlights some of the most promising biomedical research on ME/CFS ...
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Hypoxic ishemic encephalopathy

Discussion in 'General ME/CFS Discussion' started by wastwater, Apr 8, 2015.

  1. wastwater

    wastwater Senior Member

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  2. Eeyore

    Eeyore Senior Member

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    Calcium levels in the body are tightly regulated. They shouldn't move up or down much over a wide variety of vitamin D. The vitamin D3 you buy in the drugstore (or make in response to sunlight) is not active at the VDR (vitamin D receptor). Levels of the active form (calcitriol, available for supplementation only by prescription, as too much is very dangerous, aka 1,25 dihydroxy vitamin D) are often a thousand fold lower than the inactive form.

    Activation of Vitamin D is accomplished in a stepwise fashion in the liver and kidneys, and the rate of this conversion is controlled so as to prevent hypocalcemia or hypercalcemia.

    How much D you take isn't really going to significantly affect calcium influx through glutamate channels (NMDA and AMPA are different types of glutamate channels - NMDA has a much greater permeability to Ca++ than AMPA, which is more selective for monovalent cations such as Na+ and K+).

    I don't think this has anything to do with the role of Vitamin D, and whether or not higher or lower levels may or may not be protective in ME.

    I do think there is a good body of evidence suggesting a role for overactivation of glutamate channels. A number of mechanisms may be involved in this.
     
    wastwater likes this.

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