The 12th Invest in ME Research Conference June, 2017, Part 2
MEMum presents the second article in a series of three about the recent 12th Invest In ME International Conference (IIMEC12) in London.
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Metabolic defect in pentose metabolism

Discussion in 'Genetic Testing and SNPs' started by out2lunch, Jun 20, 2015.

  1. out2lunch

    out2lunch Senior Member

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    My apologies if this has been discussed at length in other threads. But my PR site search proved fruitless for the specific questions I'm about to ask our resident experts. :cool:

    Can anyone explain what Dr Weyrich is referring to in these two paragraphs about elevated arabinose in the OAT:

    http://drweyrich.weyrich.com/disorders/autism.html

    "It is not clear whether elevated urinary levels of arabinose detected in by the Organic Acid Test" are simply a marker for yeast dysbiosis, or are pathogenic in their own right.

    In some cases, it appears that a metabolic defect in the processing of pentose sugars such as arabinose may be the cause, since it is reported that in some children, eating fruits rich in arabinose (apples and pears) rapidly induces an exacerbation of autistic symptoms [Shaw2008].
    "

    I'm asking about this "metabolic defect" because my latest OAT results show elevated arabinose like I had two years ago, but without elevation in the other yeast markers, tartaric and carboxcitric. Those were hugely elevated two years ago, but are now in the normal range. In fact, carboxcitric barely registers; it's near zero.

    Quick background:

    OAT test from 2013 showed high elevation for tartaric (14; s/b < 4.5), arabinose (70; s/b < 29), and carboxycitric (113; s/b < 29). Genova fecal testing showed high levels of fungus in gut at the time.

    Fast forward to 2015 after many months of Nystatin therapy. Fungus now gone per Genova repeat testing. Latest OAT test shows normal tartaric (3.6) and carboxycitric (0.41). But arabinose is actually higher (77).

    I should also note that I went on off high arabinose foods before testing (apples, pears, grapes). Actually, I don't eat these anymore, nor their juice products, so it wasn't a problem.

    I've also returned to NADH and D-Ribose supplements for the past three months, which I stopped taking five years ago. D-Ribose helps to lower my blood sugar, but I don't really notice much energy improvement (which is why I originally stopped taking them).


    If someone has a pentose metabolism defect… will D-Ribose not be assimilated properly and potentially drive arabinose higher? Is that possible?

    And how, exactly, does the pentose metabolic defect affect someone?

    The fungus in my gut is gone yet the arabinose continues merrily on. It doesn't add up, at least to me.
     
    helen1 likes this.
  2. out2lunch

    out2lunch Senior Member

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    Did some more detective work…

    The most common defect in the pentose phosphate pathway (PPP) involves our good buddy glucose-6-phopsphate dehydrogenase, resulting in G6PDH deficiency.

    Thanks to 23andMe raw data hosed through MTHFR Support, I now know I don't have this inherited condition.

    However… I still believe something is dragging down my G6PDH which is leading to elevated arabinose.

    I'm still investigating this, but reading sites like Heartfixer are less like :bulb: for my head and more like :fire: .


    Any and all info about G6PDH and metabolizing pentose sugars is much appreciated! :)
     
    JaimeS likes this.
  3. JaimeS

    JaimeS Senior Member

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    @out2lunch ,

    The quotation is from Shaw, who works for Greater Plains Laboratories.

    I ended up reading this article, which was interesting because it discussed arabinose as a measure of infectious autism, but also because it noted low IgA (which I have - or do not have, depending on your POV) in conjunction with high arabinose and high creatinine (which has been observed to be high in the urine of ME patients). [Edit: arabinose helps regulate blood sugar, but at this point I'm biased enough that I'm seeing it everywhere... too much attention to one article. ;) ]

    How is your dairy/gluten intake? These seem to be associated, according to the article.

    [Edit: Vitamin K is necessary to break this down, and so are certain bacteria in the appendix. A deficiency in the former or a lack of the latter?]

    -J
     
    Last edited: Jun 20, 2015
  4. dannybex

    dannybex Senior Member

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    @out2lunch -- I don't have an answer for you but just a suggestion from personal experience to not rely on the Heartfixer site for reliable information. Most of it is ancient Yasko-related info, some of which has turned out to be incorrect. Others here on PR know more about it than myself however.

    And @JaimeS, Shaw OWNS Great Plains Labs, and there are others who disagree w/him (Susan Owens for one) when it comes to his interpretations. That doesn't mean she's right or he's wrong, but he at least has a vested interest, which ties in with your comment about too much attention to one article. :)

    Very interesting about Vitamin K and arrabinose -- do you have a study or other reference for that?
     
    Valentijn likes this.
  5. out2lunch

    out2lunch Senior Member

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    Thanks for the response, JaimeS. I'll address these one by one.

    I've got one of the three. My IgA isn't low, but my urine creatinine is. I've only got high arabinose.

    I know that D-Ribose, another pentose sugar, helps to lower blood glucose. In fact, it works so well in me, that I can see my glucose drop as much as 20 points from just 5 grams. Which is a good thing in the morning when
    my fasting glucose is 110. But very much a bad thing when it's 90 and I get hypoglycemic shakes.

    I've been 99% gluten free for five years. I'm not celiac but gluten sensitive; gliadin antibodies showed up in fecal testing. Getting off gluten has helped the IBS significantly. And I've been mildly allergic to whey my whole life, so dairy is reduced to small amounts of cheddar cheese. I use coconut milk and occasionally almond instead of moo juice.

    Vitamin K is something I supplement because of osteoporosis. Genova testing last year showed good levels, so no deficiency. As for bacteria in the appendix, I have no idea. Maybe I am lacking.
     
    Gondwanaland likes this.
  6. Critterina

    Critterina Senior Member

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    Does this article help? http://www.researchgate.net/publica...cts_of_the_pentose_phosphate_pathway_a_review
    You asked
    and I think it answers it.
    It's funny because you ask what symptoms a PPP defect would have. I was wondering the converse: what symptoms do you have that you think might be associated with the high arabinose in your urine?
     
  7. JaimeS

    JaimeS Senior Member

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    Thanks for this! I can't take therapeutic sugars like inositol or ribose at all, I feel awful when I do, and this might be why. :)
     
    out2lunch likes this.
  8. out2lunch

    out2lunch Senior Member

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    I don't know if I have any symptoms. I'm wondering if I have a PPP defect because my latest OAT test shows elevated arabinose while the other yeast markers are low normal. Those other markers were elevated on my last OAT before I did several months of anti fungal treatment. They came down but the arabinose did not. That makes me think the PPP might not be functioning normally.
     
  9. Critterina

    Critterina Senior Member

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    What I understood from the article was that there are symptoms for the identified PPP dysfunction. If you don't have those, then you might be right, but science hasn't caught up with you. The arabinose is elevated, but not the tartaric acid, you said. So, I don't know who might know what that means. Sorry not to be more helpful.
     
  10. JaimeS

    JaimeS Senior Member

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    Yes! That's why I mentioned from whence the info came...

    Yesss, what I have is someone mentioning a section in the textbook Advanced Nutrition and Human Metabolism, but I can't get my hands on the original...

    The '1' leads to the textbook that I can't find.


    Hmm, Vitamin K induces arabinose resistance in gut flora... also there are a lot of articles about arabinose and bacteria, as it makes up their cell walls...

    ....hmm. Not sure if any of that was helpful, but I hope so...

    -J
     
  11. South

    South Senior Member

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    Good lord, my brain can't understand this stuff.

    • I have a longstanding candida problem.
    • I also have a longstanding tendency to low blood sugar.
    • Somewhere I read that arabinose binds to lysine, and that the liver needs lysine to prevent low blood sugar.
    That's as far as I got with understanding my situation.
    Then I read little bits about vitamin K having something to do with arabinose, but I don't understand what.

    Maybe I'll just try taking vitamin K and see if my low blood sugar problems fades away.
     
  12. JaimeS

    JaimeS Senior Member

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    Not a terrible idea. Give it a go, and report back!

    (I love how we're all our own guinea pigs...)

    -J

    [Edit: however, be aware that what the quoted text was saying is:

    1) We can't metabolize L-arabinose.

    2) Our gut flora can.

    3) These gut flora that can, also produce Vitamin K.

    ...the implication being:

    4) If you pee out a lot of L-arabinose, you may be lacking the gut bacteria that help you break it down.

    5) This would also possibly imply low Vitamin K...

    6) And poor sugar metabolism, since L-arabinose absorption slows glucose metabolism.

    ...I think. <3

    -J
     
    South likes this.
  13. JaimeS

    JaimeS Senior Member

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    Hmm, I wonder if candida 'produces' arabinose or competitively inhibits those other bacteria that can break it down?

    Both? Both is also an option.

    -J
     
  14. out2lunch

    out2lunch Senior Member

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    Actually, I might have a problem, thanks to this thread:

    http://forums.phoenixrising.me/inde...se-6-phosphate-dehydrogenase-deficiency.13173

    I'm homozygous for two SNPs, one that's been linked to risk for hemolytic anemia.

    If I have a deficiency, even mild, that could explain the arabinose elevations in my OAT results. It could also explain my difficulties overcoming iron deficiency because G6PD deficiency elevates hepcidin, which inhibits iron absorption in the gut.

    Now I wonder if the iron deficiency problems so many of us have are actually deficiencies in G6PD which lead to elevations in hepcidin and poor iron absorption.

    Smells like an interesting research project to me! :cool:
     
    JaimeS likes this.

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