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

  2. Eeyore

    Eeyore Senior Member

    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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