New Atmosphere, New Vision: Gibson and Whittemore Kick Off Invest in ME Conference 2016
Mark Berry reports on Dr. Gibson's introduction and Dr. Whittemore's keynote speech, at the 11th Invest in ME International ME Conference in London.
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From brain fog to clarity in 30 minutes

Discussion in 'General Treatment' started by nanonug, Mar 8, 2018.

  1. nanonug

    nanonug Senior Member

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    First of all, let me clarify that I take much more stuff than the things I am about enumerate. They are important in their own right and include support for methylation and glutathione production, for example. Also, the disclaimer applies that these things work for me and there is absolutely no guarantee that they will work for anyone else. That being said, there are good reasons why they might work for others as well.

    There is nothing revolutionary here, and there is most likely room for improvement, but the following are the things that appear to have a quick effect on my brain fog:
    • Ubiquinol
    • Nicotinamide Riboside
    • Fursultiamine
    • Dichloroacetate
    Ubiquinol, nicotinamide riboside and fursultiamine are all involved in mitochondrial oxidative phosphorylation. Nicotinamide riboside is a precursor to NAD+ and fursultiamine is a thiamine analog and precursor to thiamine pyrophosphate (aka, cocarboxylase.) Dichloroacetate inhibits pyruvate dehydrogenase kinase, therefore "forcing" pyruvate (via acetyl-CoA) through the Krebs cycle. Dichloroacetate is potentially toxic so care with dosage of this substance is of utmost importance.

    I also find it important to supplement with pyrroloquinoline quinone (PQQ) in a long term basis as this promotes mitochondrial biogenesis. Without a sufficient number of mitochondria, the above four substances wouldn't be able to do much.
     
  2. Runner5

    Runner5 Senior Member

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    PNW
    Are those supplements or prescription? I've never heard of them.
     
  3. nanonug

    nanonug Senior Member

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    None of them is prescription, at least not in the US. Dichloroacetate is really not a supplement but to my knowledge doesn't require a prescription anywhere.
     
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  4. rodgergrummidge

    rodgergrummidge Senior Member

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    Hi @nanonug, very interesting. Be careful with the DCA. Clinical trials have basically stopped for DCA because of the toxicities, but it is still used in cases of congenital PDH deficiencies where kids can die if left untreated. Probably a good idea to monitor toxicities. For example, clinicians treating with DCA will sometimes measure the accumulation of maleylacetone and delta-aminolevulinate (heme precursor) which are potentially are toxic to the liver and peripheral nerves.

    What dosing regimens do you use? And where do you buy Nicotinamide Riboside, Fursultiamine and PQQ?

    Do you have mitochondrial defect? PDH? lactic acidosis? If so, how did you diagnose it?

    Rodger
     
  5. nanonug

    nanonug Senior Member

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    Yes, I'm aware of the dangers, something I mentioned in my original post. Based on my research, there has been no issues with toxicity when dosages are kept under 5mg/kg BID. I currently take 333mg BID which is below that threshold.

    Nicotiname riboside (250mg BID): https://www.amazon.com/gp/product/B072R2LVLV/
    Fursurtiamine (150mg morning / 50mg night): https://www.amazon.com/gp/product/B0058AB268
    PQQ (10mg BID): https://www.amazon.com/gp/product/B00GXC9OHE

    Don't know. Don't know. Don't know. I didn't diagnose it, I'm using the research by Naviau et al and Fluge et al (hypometabolic state/PDH dysfunction) as guide and assuming that it applies in my case as well.
     
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  6. rodgergrummidge

    rodgergrummidge Senior Member

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    Very interesting @nanonug, the Fursurtiamine (aka TTFD) is a modified version of Thiamine or Vit B1 (Med Sci Monit, 2004; 10(9): RA199-203). It has a disulfile 'linker' that helps with the uptake of the drug into cells. When TTFD comes into contact with cell membranes, the disulfide is fractured and it remains outside the cell. The remainder of the molecule passes through the cell membrane, the thiazolium ring closes and the cell now has an intact molecule of free thiamine in the cytosol.

    The disulfide makes TTFD more powerful in its actions compared with the readily available water-soluble thiamine salts, since it does not require the rate limiting transport system required for thiamine (Med Sci Monit, 2004; 10(9): RA199-203). Essentially, there is a rapid buildup of intracellular thiamine and so the effective concentration of B1 is much higher than achieved by conventional B1 supplements.

    The pharmacologic activity of the disulfide link in TTFD or its toxicities are not known. After oral administration of TTFD to human subjects, urinary recovery of the labelled disulfide was 90% and so it might be prudent to monitor kidney toxicity.

    Rodger
     
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  7. sb4

    sb4 Senior Member

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    I'm pretty interested in dichloroacetate. I have looked at the side effects and it seems that neurophathy is one, presumably from the increased PDH using up B1. So taking B1 should be a remedy, and gastrointestinal. Are there more extreme side effects I'm missing?

    How do you think it will interact with those on ketogenic diets? Might it push too of already low levels of sugar, down into Acetyl CoA instead of into oxaloacetate causing blood sugar issues?
     
  8. nanonug

    nanonug Senior Member

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    To my knowledge, neuropathy is the only one, at least within the dosages normally used in humans. Also, to my knowledge, all cases of neuropathy have been reversible.

    That's a good question. I don't know!
     
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  9. CFS_for_19_years

    CFS_for_19_years Hoarder of biscuits

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    I agree that PQQ helps a lot with energy and being more alert. It should be taken no later than noon since it is energizing. Several people here on PR said that it was like speed to them, so I recommend starting at 5mg per day, then if no improvement in 3 days, increase to 10mg per day, etc.

    This is the brand I use because it is a 20mg TABLET that can be broken into quarters (a 5mg dose) with a pill-splitter:
    https://www.amazon.com/SOURCE-NATURALS-Mind-Tablet-Count/dp/B00BQS87D2
     
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  10. dreamydays

    dreamydays

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    http://www.medical-hypotheses.com/article/S0306-9877(18)30105-1/fulltext#s0040
     
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  11. nanonug

    nanonug Senior Member

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  12. RustyJ

    RustyJ Contaminated Cell Line 'RustyJ'

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    Hi nanonug, could you also provide brand and dosage for your Ubiquinol, and brand for the Dicholoacetate.
     
  13. rodgergrummidge

    rodgergrummidge Senior Member

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    some information on DCA can be found here

    some information on DCA toxicity and the risks of self-medication can be found here

    In terms of combinnig DCA with a ketogenic diet, it wouldnt really make much biochemical sense unless there was a really serious PDH defect such as sometimes occurs in congenital disorders. The reasoning would be that:

    On a carbohydrate diet, the glycolytic pathway converts carbohydrates and sugars into pyruvate which is then converted by PDH into acetyl CoA to fuel the TCA cycle. Thus, on a carbohydrate diet, PDH provides a vital link that funnels the product of glycolysis (pyruvate) into the mitochondrial where the TCA and oxidative phosphorylation (OXPHOS) convert it into energy (ATP). If PDH is only weakly active in an individual (as can occur in congenitial diseases), then there will be insufficient Acetyl CoA to fuel the TCA and OXPHOS and so not enough ATP to fuel tissue functions. In such a situation, DCA might be used therapeutically to activate PDH activity and increase Acetyl CoA production in order to increase aerobic energy production from carbohydrates.

    A ketogenic diet provides a 'short-cut' that skirts around PDH to allow the generation of energy from fatty acids and amino acids rather than pyruvate. On a ketogenic diet lacking significant amounts of carbohydrates and sugars, glycolysis is largely inactive and so there is little pyruvate produced. Under these conditions, fatty acids and amino acids enter the TCA cycle at steps 'after' PDH. Thus, activating PDH activity using DCA under conditions where there is little glycolysis and pyruvate production wouldnt make biochemical sense (one exception might be really serious congenital defects in PDH where the patient has gone into lactic acidosis). Thats because the whole purpose of the ketogenic diet is to 'skirt around PDH' and provide alternative fuels (fatty acids and amino acids) to the TCA.

    Rodger
     
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  14. researcher

    researcher

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    So you guys think that brainfog is a consequence of a dysfunctional mitochondria?
     
  15. nanonug

    nanonug Senior Member

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  16. nanonug

    nanonug Senior Member

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    Not necessarily. Most likely cause is inhibition of pyruvate dehydrogenase complex in the mitochondria due to physiological stresses, such as excessive reactive oxygen/nitrogen species (ex: superoxide, peroxynitrite.)
     
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  17. Frenchguy

    Frenchguy Senior Member

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    @nanonug

    Thanks for sharing,
    What's your function level ?
     
  18. nanonug

    nanonug Senior Member

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    With the amount of stuff that I take, close to normal. But I still need to be careful not to overexert myself. So I guess I'd put myself in the mild SEID category.
     
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  19. redrachel76

    redrachel76 Senior Member

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    @nanonug Did you ever try DCA alone or only part of the whole protocol you listed in the opening post?

    Can you remember how long it took before this whole protocol or DCA alone started helping?

    I assume you need to be on these supplements permanently to stay functioning near normal?
     
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  20. nanonug

    nanonug Senior Member

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    Never alone, only part of the complete protocol.

    It took me a few days to start feeling a difference. I no longer recall exactly how many but I'd say after 7 days I was "feeling it."

    At this point, that's my understanding. It's not a permanent fix, it's a band-aid.
     
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