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Aspirin Inhibits Tryptophan Absorption From The Intestine

Discussion in 'Scientific Studies' started by haidut, Jun 19, 2015.

  1. haidut

    haidut Member

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    Peat has written about the benefits of tryptophan restriction for overall health and metabolism. Unfortunately, there are few reliable methods of reducing tryptophan absorption and most people have to resort to simply limiting consumption of foods high in tryptophan. It would be nice if there was a way to inhibit the absorption of the amino acid even in cases when one eats a high tryptophan food like muscle meats or fish. While BCAA delays tryptophan absorption from the intestine and reduces its contents in brain, BCAA does not actually inhibit tryptophan absorption.
    Well, it looks like aspirin and especially its metabolite salicylic acid can do that trick. The first study states that this inhibition of tryptophan absorption may be behind the ability of drugs like aspirin to uncouple oxidative metabolism.

    http://onlinelibrary.wiley.com/doi/10.1 ... 3/abstract
    "...Indomethacin (5 mM), phenylbutazone (5 mM), and salicylate (15 mM) prevent the active transport of the amino acid, L-tryptophan, across the small intestine of the rat. Aspirin (15 mM) appears to inhibit somewhat, but does not prevent, this process. Salicylate (15 mM) significantly inhibits the active transport of L-tryptophan across the hamster small intestine; aspirin (15 mM) has no inhibitory effect. These results are consistent with the relative effectiveness of these drugs as uncouplers of oxidative phosphorylation."

    http://onlinelibrary.wiley.com/doi/10.1 ... x/abstract

    "...In normal persons, ingestion of aspirin causes a release of tryptophan from its binding site on serum albumin. There is a fall in bound and total serum tryptophan concentrations and a rise in free tryptophan concentrations. The urinary excretion of 3-hydroxyanthranilic acid is decreased, that of xanthurenic acid is increased and that of 3-hydroxykynurenine was increased in 4 out of 6 subjects, indicating an effect on the enzyme systems involved in the metabolism of tryptophan. Conjugates of these metabolites were shown to interfere with the method of assay of the unconjugated hydroxy acids by column chromatography. To overcome this difficulty all urine samples were first boiled in molar hydrochloric acid to hydrolyse any conjugates present. Any results obtained using non-hydrolysed urines would be misleading. This work shows that it is important to take account of the drugs used in treatment before ascribing changes in tryptophan metabolism to pathological states."
     
  2. artemis

    artemis Member

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    Great to know, thanks!
    I'm going to start taking aspirin with my meat/fish meals.
     
  3. narouz

    narouz Member

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    Cool, haidut.
    Thanks!

    How much, roughly, would you do for this effect?
     
  4. OP
    haidut

    haidut Member

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    The concentration used in the first study (15mM) is a LOT! Ingesting 6g-9g aspirin daily would achieve about 3mM concentration in humans. But the second study is a human one and the doses used were quite small (<1g a day) and that also lowered total tryptophan and changed levels of biomarkers suggesting tryptophan depletion.
     
  5. miles

    miles Member

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    Would salicylates in foods have the same effect?
     
  6. sugar daddy

    sugar daddy Member

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    I wish I could take aspirin but it really sets off gout in my foot!! :oops:

    What about drinking a lot of juice would that have enough Salicylic acid?
     
  7. lexis

    lexis Member

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    The benefits are due to reduced iron levels. Cupping therapy helps too.
     
  8. OP
    haidut

    haidut Member

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    To the people asking about salicylic acid from food - yes, it should work. The first study even says that aspirin itself was not very effective (in vitro) but it does get metabolized into acetic acid and salicylic acid and the study found salicylic acid to be very effective. The second study, which I would put even more weight on, found that aspirin was effective in vivo, and it was a human study so you can't get much better than that. Yet another reason to load up on ripe fruit.
     
  9. tara

    tara Member

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    Salicylic acid from fruit may reduce tryptophan absorption, but vit-C from fruit increases iron absorption, right? So a bit of a trade off with meat.
     
  10. milk_lover

    milk_lover Member

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    So would you recommend taking Aspirin after eating muscle meat to reduce tryptophan? So Aspirin+gelatin+coffee+simple sugars combo with muscle meat will reduce any stressful reaction from muscle meat? Like Aspirin for tryptophan reduction and possibly iron reduction, gelatin for amino acid balance, coffee for iron reduction, and simple sugars for low blood sugar avoidance. Thanks haidut.
     
  11. tara

    tara Member

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    True.
     
  12. Peata

    Peata Member

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    I thought the aspirin would help the amino acid balance too?
     
  13. FiveAsh

    FiveAsh Member

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    Sorry @haidut, im sure im being stupid but the 2nd study seems to be indicating that aspirin is displacing Tryptophan from albumin, causing a rise in free Tryptophan???

    -doesnt this intrinsically mean more Serotonin would be synthesised in the brain?

    Or does the decreased excretion of 3-hydroxyanthranilic acid indicitate upregulation of this enzyme showing that the T is being diverted away from metabolism into Serotonin?

    I cant work it out...
     
  14. OP
    haidut

    haidut Member

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    I supposed you are right, the second study concerns already absorbed tryptophan. So, it has no bearing to the absorption of trypophan for which only the first study is relevant. But the first study does show inhibition of tryptophan absorption from intestine, which is what we want.
     
  15. FiveAsh

    FiveAsh Member

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    Ok, i see, thanks. Are you not concernedabout its displacement of T from albumin? Similar to that of PUFA...
     
  16. FiveAsh

    FiveAsh Member

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    Can anyone clarify this?? Does anyone have access to this study??

    Pubmed 4396888
     
  17. conhnore

    conhnore Member

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    PM me, I've got a .pdf
     
  18. Terma

    Terma Member

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    Landed on this by accident, but maybe this suggests aspirin actually lowers B6, as has been "commonly" thought? NSAIDs Deplete Body's Vitamin B-6 Levels - Heal Naturally Aspirin stops B vitamins' benefit | Patrick Holford's Blog

    Don't worry those aren't serious quotes, but this old research suggests that high Xanthurenic acid, low 3-HA and high Hydroxykynurenine reflects a B6 depletion pattern (low Kynureninase activity), which you can also achieve with high-dose Leucine or acetoacetate:
    https://www.researchgate.net/public...acid_and_other_tryptophan_metabolites_in_rats
    Now Xanthurenic acid (XA) in the CNS has become sought-after, since:
    Xanthurenic acid - Wikipedia
    and it's responsible for some therapeutic effects of ketosis. But all this is curious, because it essentially suggests part of the benefit of ketosis is actually B6 depletion, at least locally.

    I don't personally seek this metabolite, being Trp-derived and all, although some of them like Anthranilic acid are close cousins of Salicylic acid and Benzoic acid, which raises a few questions and makes it hard to damn the whole pathway; but regardless, I can probably do without.... However, since mGlu2R antagonizes 5-HT2A (5HT2A-mGlu2R heterocomplex), everyone else is interested in it (XA is also in red wine, though no idea if it gets anywhere near the brain from oral ingestion), though I'm pretty sure that combo or simply high XA would utterly destroy my cognition.

    It's striking how closely all this ties together... although I didn't pay close attention to dosages in all of these, which is why I'm not raising any alarms, messing around with these probably calls for some B6 (+B2 also needed for KP) and even B3 just to be safe.

    Going on a tangent, if you follow the dots, it's clear T4 (not sure about T3) increases Quinolinic Acid, toward niacin, which isn't a surprise. But this innocent old research might actually explains several of the problems with thyroid supplementation: Quinolinic Acid -> Niacin by QPRT enzyme requires PRPP from the pentose phosphate pathway (PPP) (NADPH), which becomes compromised in many serious disease, except cancer. Interestingly numerous articles clearly show hyperthyroidism increasing the PPP, but now I wonder if this isn't so much a consequence of increased ROS but could even be part of the programmed response (but this is a wild guess), because otherwise thyroid would risk leading to QUIN buildup every single time if PRPP can't keep up with QPRT/niacin. In turn perhaps anything that spares PRPP would alleviate the problem (there's even Ribose supplements and people use them with success, but it's highly reactive; I'm not sure to what extent purines like inosine can work due to the degradation to uric acid and gut). Finally, sick people give up on thyroid because there's no way it can succeed on its own and just pushes up QUIN levels. So they turn to ketosis to increase Xanthurenic acid which is the most potent glutamate-inhibiting Trp metabolite (stronger than KYNA) and then we're back to the top. In fact, I traditionally I did badly taking B6 or P5P, giving a sort of depression, which I suspect could be QUIN, so we end up in this strange situation where B6 deficiency is desirable in the scope of modulating the Trp pathway (of course it's not a great idea - unless it's purely local, which is doubtful - but you'd make up with ingested B3).
     
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