Lipkin's Monster ME/CFS Study: Microbes, Immunity & Big Data
The Microbe Discovery Project outlines an ambitious new study by top researchers that has collected patient samples, but needs desperately funds to complete the work.
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Medcation & Supplement Regime for those in acute Suffering or Crisis

Discussion in 'General Treatment' started by energyoverload, Apr 3, 2012.

  1. energyoverload

    energyoverload Senior Member

    I have just completed a blog post about what has helped me when I have been most disabled by this illness and in such poor a state that I felt I could not go on any longer. I have tried what must be over a hundred different interventions for this illness. So few have been of any use. In this blog I outline the ones that have not changed my life but have at least maintained my head above the water life. I focus principally on the Glutamate, NMDA and GABA systems and the severe impact these can have on symptoms.

    I hope this may help some people. For the many of whom are drug sensitive always start with half or quarter tablets, or by breaking a capsule open and taking roughly half of the contents. I take LIV 52 tablets and SAM-e to help the liver metabolize these compounds without any undue hepatic effects.
  2. Jenny

    Jenny Senior Member

    Your blog is very interesting energyoverload. Presumably you've found a doctor in the UK who will prescribe these meds?

    Would you be able to pm me with details?

    Many thanks.

  3. ramakentesh

    ramakentesh Senior Member

    I enjoyed the blog and found it refreshingly well informed, however I take one section out of your etiological mechanism - I believe there is evidence that rather than there being a chronic infection as a trigger for inflammatory cytokine activation, the problem might actually just be the cytokine activation as occurs in rheumatic diseases like Ankylosing Spondylitis (many CFS and POTS patients actually test positive to HLA-B27).

    that is innate immune system activation results in perhaps CNS alterations, perhaps upregulation of certain sodium channels that increase innervation from the sympathetic system - either as increased substance P mediated pain reception as in Fibro, or perhaps as sympathoexcitation as in CFS.

    There is some subjective evidence that the blood brain barrier is comprimsed in CFS and there is certainly evidence that cerebral blood flow autoregulation is very wacky.

    Otherwise what im reading and what research seems to be point to supports an etiological mechanism perhaps along those lines.

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