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New video: Is acetylcholine toxicity the cause of CFS?

Discussion in 'Autonomic, Cardiovascular, and Respiratory' started by Emootje, Apr 18, 2011.

  1. Lotus97

    Lotus97 Senior Member

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    That might be acetylcholine overload since huperzine acts sort of like an SSRI, but for ACh. Especially if you're also getting a lot of choline from your diet. Unless you really want the algal based DHA, Swanson has the same thing for half the price. (If you're a first time customer PM me for a discount. Otherwise use SAVETODAY for 10% off $75 or more. Ends midnight 3/26) http://www.swansonvitamins.com/swanson-ultra-herbal-extract-memory-complex-60-caps
  2. Sushi

    Sushi Moderator and Senior Member Albuquerque

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    Thanks for the link to the Swanson product. The dosing is slightly different--who knows what is best. As far as acetylcholine, I seem to be the opposite from most patients. I have already ordered the ProHealth product so I'll give it a try.

    Sushi
  3. Lotus97

    Lotus97 Senior Member

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    I'm not sure what you mean by opposite, but wasn't Rich saying that a deficiency in ACh is what causes the sensitivity? (assuming he's right of course). I haven't read through the entire thread, but here's what he said about it at the beginning.
    For what it's worth, if my hypothesis about ME/CFS is valid, it is more likely that there will be a deficiency of acetylcholine, rather than too much, producing toxicity. The reason is that the production of phosphatidylcholine in the body, from which choline can be derived to make acetylcholine, is one of the two main users of methylation, and there appears to be a methylation deficit in most cases of ME/CFS, due to a partial block of methionine synthase in the methylation cycle.

    I think that a deficiency of acetylcholine is consistent with the high sensitivity to acetylcholine that was observed by Vance Spence's group in Scotland a few years ago. I also think that the MRS experiments that were interpreted as showing elevation of choline in ME/CFS were misinterpreted by assuming that creatine is at normal levels. The problem is that creatine synthesis is the main user of methylation in the body, and creatine is also likely to be low.

    Best regards,

    Rich
  4. sregan

    sregan Senior Member

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    This fits my experience. After my last 2 Amalgams were removed last June I have been experiencing a significant increase in symptoms including brain fog. Acetylcholine boosters have helped. I try to take as little as possible. DMAE is my first line of defense, then Pregnenolone if DMAE doesn't work. Pregnenolone is supposed to boost NMDA and helps if I believe I have too much GABA (after theanine).

    I also want to add that since I've started on the SMP the brain Fog has significantly lessened.[/quote]
  5. Lotus97

    Lotus97 Senior Member

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    Too much GABA? What's that like?:lol:
  6. Azrael

    Azrael

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    This is surely a heavy thread, having difficulties getting the big picture. I guess im extra tired today. But im wondering. If someone have problems with those symptoms, would it be beneficial with a supplement of citicholine ?

    I know methionine is not working correctly, and the same goes for creatine as I dont feel strong in my muscles any longer.

    I know many years ago when I was young I took creatine on a regular basis which I felt great from but with my history I believe that the creatine fueled the methylation in a way that would not last, consuming other pathways.

    I have seen some positive effects of taking regular choline, but for some reasons it has not been helful the whole way, and I guess thats the way with a sluggish methylation.

    So seeing some if only some positive effects I might see better ones with a stronger choline like citicholine.

    Any suggestions or comments to my message?

    Thanks
  7. Theresa S

    Theresa S

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    I have a pseudocholinesterase deficiency, homozygous.
    I came upon this site because of your discussion thread. I believe my pervasive fatigue and diminished cognitive function (I taught grades7&8, all subjects for 25 years) is due to acetylcholine toxicity.

    There is no family history of Alzheimer's or dementia in my family. I do not have depression.

    Any thoughts?
  8. Valentijn

    Valentijn Activity Level: 3

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    Which SNP?
  9. lansbergen

    lansbergen Senior Member

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  10. xks201

    xks201 Senior Member

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    What SNP?
  11. xks201

    xks201 Senior Member

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    DMAE is a false choline uptake substrate. It does not increase choline levels. It is used in experiments to block choline uptake.

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