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CFS/ME as a Liver issue

Discussion in 'Alternative Therapies' started by undcvr, Aug 5, 2012.

  1. undcvr

    undcvr Senior Member

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    No I didn't. I can't find it. Did he remove it ?
  2. undcvr

    undcvr Senior Member

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    One of the recommendations for pyroluria is arachidonic acid, a pro inflammatory omega 6 oil that the body produces from linoleic acid and gamma linoleNic acid. They say that people with pyroluria need more of this. I realise that this is true in general and may extend to pple with CFS/ME.
    Sometime ago I had ESR (erythrocyte sedimentation rate) tests done. It is supposed to test the body's inflammation responses. My values were always in the single digits 2 or 5 with the normal value starting at 10 or 25. My doctor could not explain this. Back then, I thought that this was a good thing but a healthy inflammation response in also important for the immune system to work well.

    Nowadays I take about 200mg of arachidonic acid a day along with gla and aa high foods. It may also be a reason why I am doing better in general. It is worth knowing that in the brain, the ratio of aa to dha is almost one to one.
  3. roxie60

    roxie60 Senior Member

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    but out of range AST and ALT must mean something????
  4. Little Bluestem

    Little Bluestem Senescent on the Illinois prairie, USA

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    Sorry, I just saw this. I have been spending a lot of time on the Burnout Bench.

    Dog Person is no longer a member, so her posts are difficult to find. They are also long and contentious, so you may not want to read them now. She said if you were low in a mineral, including zinc, that you were supplementing, it could mean that you are deficient in something needed to metabolize that mineral. She thought that Riboflavin (B2) was often the culprit. You might want to look into what is needed to utilize zinc.
    xks201 likes this.
  5. xks201

    xks201 Senior Member

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    If you are undermethylating then the liver can't detox things as fast. Combine that with potential hypovolemia and there is less fluid to circulate toxins out of the liver. That is my opinion on the matter. Combine that with nervous system dysfunction and bile flow gets jammed and stones form and then the liver becomes even worse.
  6. undcvr

    undcvr Senior Member

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    Methylation has nvr really quite helped me the way I hoped it would.
    xks201 likes this.
  7. xks201

    xks201 Senior Member

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    Not saying it helps everyone. It didn't do anything for me.
  8. merylg

    merylg Senior Member

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    I have been thinking about common substances which damage the liver:

    http://en.wikipedia.org/wiki/Hepatotoxins

    These Blue-Green algae are common in my local environment:

    http://en.wikipedia.org/wiki/Cyanobacteria
    "Health risks

    See also: Cyanotoxin
    Some cyanobacteria produce toxins, called cyanotoxins. These include anatoxin-a, anatoxin-as, aplysiatoxin,cylindrospermopsin, domoic acid, microcystin LR, nodularin R (from Nodularia), or saxitoxin. Cyanobacteria reproduce explosively under certain conditions. This results in algal blooms, which can become harmful to other species if the cyanobacteria involved produce toxins.
    These toxins can be neurotoxins, hepatotoxins, cytotoxins, and endotoxins, and can be toxic and dangerous to humans as well as other animals and marine life in general. Several cases of human poisoning have been documented but a lack of knowledge prevents an accurate assessment of the risks.[28][29][30] Recent studies suggest that significant exposure to high levels of some species of cyanobacteria producing toxins such as BMAA can cause amyotrophic lateral sclerosis(ALS, also known as Lou Gehrig's Disease). The Lake Mascoma ALS cluster [31] and Gulf War veteran's cluster are two notable examples.[29][30][32]"
    MishMash likes this.
  9. alex3619

    alex3619 Senior Member

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    Excess arachidonic acid can be a huge problem for people with ME. It depends on the activity state of the enzyme cyclooxygenase, how much inflammation they have, what other disease states they have, and probably even what type of ME they have. I have commented elsewhere that we both don't make enough arachidonic acid and use too much. This puts us in a deficiency state (all other things being equal), but if we take more the body might just do the wrong thing with it. I have benefited from evening primrose oil ... for a while. At some point it starts driving inflammation and pain. We are deficient in arachidonic acid, and we use too much arachidonic acid. Directly supplementing with it can be a huge problem.

    One of the things that arachidonic acid can trigger in me is massive pain levels, everywhere. I collapse to the floor, very quickly. Arachidonic acid is an essential fat, without it you die, but its also one of the most toxic. Inject a little into a rabbit and some minutes later after the rabbit is done convulsing its dead. This is not a nice acid in excess, it needs to be tightly regulated. All NSAIDs do this, so does cortisol. Indirect inhibition also occurs via omega-3 fish oil (EPA) and to a limited extent I think (I have not proven this) by monounsaturated fats. We make more arachidonic acid if we correct oxidative stress, particularly when we raise glutathione levels. Lately I am experimenting with resveratrol to control arachidonic utilization, though its not without its problems as the arachidonic acid derivative PGD2 is essential to sleep.

    If someone is wanting to take evening primrose oil or increase arachidonic acid intake, it should be done very very carefully. If anything goes wrong, particularly inflammation or pain, then stopping extra arachidonic acid or evening primrose oil intake is the first step to try.

    There is one time that extra arachidonic acid is useful though. If you contract a new infection and are in the early stages then increased arachidonic acid might help you fight it off.

    Bye, Alex
    Little Bluestem and merylg like this.
  10. Michael

    Michael

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    This is a VERY helpful site.. thanks!
    merylg likes this.
  11. Little Bluestem

    Little Bluestem Senescent on the Illinois prairie, USA

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    Yes, very helpful. I haven't read it all yet, but I have already learned one new, interesting thing.
    merylg likes this.
  12. Old Salt

    Old Salt Rowing the boat

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    So, Alex, are you saying too much Omega 3 is hard on the liver? What's too much? Thanks
  13. merylg

    merylg Senior Member

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    Yes interesting Little Bluestem...so any impairment of the liver including parenchyma, ducts, circulation & supporting structure would impair that function of removing microorganisms.

    Michael you're welcome!
    Little Bluestem likes this.
  14. Little Bluestem

    Little Bluestem Senescent on the Illinois prairie, USA

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    I am also wondering, merylg, if long-term microorganism removal could tax the liver and lead to liver impairment.
    merylg likes this.
  15. alex3619

    alex3619 Senior Member

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    I do not think omega-3 is likely to be hard on the liver. It can cause excessive blood thinning, and there is some vague and so far as I know unproven potential to reduce gut healing. Eicosanoids come in three flavours. Series 1, 2, and 3 - they didn't have much imagination. So if you see something like PGE2, thats prostaglandin, E (the type), series 2. The 2 tells you its made from arachidonic acid. Series 1 is made from DGLA which is a precursor to arachidonic acid. Series 3 is from omega-3s. That one is easier to remember obviously.

    Now these eicosanids have many functions, from regulating blood vessels to the immune system. Some are pro-inflammatory, some are anti-inflammatory. The balance of pro- and anti-inflammatory factors, including impact from factors that are not eicosanoids, is what determines the level of inflammation. I have not investigated the science behind that recently - and I am sure its very complicated.

    Now its a common misconception that omega-3s are anti-inflammatory. They are not particulary anti-inflammatory. They are also pro-inflammatory. The issue though is, I think (doh, its been too long now since I researched this), that an enzyme called cyclooxygenase prefers (preferentially processes) omega-3 fats to omega-6 fats. Omega-3 derived eicosanoids are less inflammatory on the whole than arachidonic acid derived eicosanoids. So when you take omega-3s you still make repair, anti-inflammatory and pro-inflammatory eicosanoids, but the impact of the pro-inflammatory eicosanoids is much less. That decline is a relative decline, rather than an increase in anti-inflammatory action, I think. This science changes so rapidly though, and I am now very out of date, so my explanation should be regarded as tentative.

    The take home message though is that arachidonic acid tends to be inflammatory but isn't always. One useful impact of inflammation is to assist fighting off pathogens. So its good stuff in the early stages of infection, and its good stuff in us due to our tendency to be deficient (though this varies patient by patient) but its bad stuff in that it can make us feel more ill and drive inflammation. Its the balance that counts.

    Bye, Alex

    PS On the liver, one of the main functions of it is to purify the blood coming from the gut, including removing bacterial toxins such as LPS. The fact that LPS is found in our blood tells you the liver is not working properly or is overwhelmed.
    merylg likes this.
  16. Old Salt

    Old Salt Rowing the boat

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  17. Old Salt

    Old Salt Rowing the boat

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    I was diagnosed CFS in the early eighties, a heart attack in 1998. Not a candidate for coumadin. Was on aspirin for a few years to thin the blood but gut dysbiosis caused Afib, got off the aspirin, on to fish oil to prevent platelet aggregation and with minerals, controlled the Afib very well. For me, the CFS is all due to dysbiosis in the gut, the propensity of which, is inherited. Now, my liver is in rough shape from so many years of toxins from the gut.
    I attribute fish oil for still being alive but I don't think it helped the dysbiosis.
    merylg likes this.
  18. Old Salt

    Old Salt Rowing the boat

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  19. Old Salt

    Old Salt Rowing the boat

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    I used to believe gut permeability (leaky gut) was the major issue but know I think it's more a liver detox issue, or rather the liver not detoxing, due to damage in the same way the gut is damaged, including the immune system that resides there-in. A genetic propensity is most likely a requirement, as well as a triggering event. Alex?
    merylg likes this.
  20. alex3619

    alex3619 Senior Member

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    Hi Old Salt, I think there might be genetic risk factors, but I am unsure of this. Its probable, from my current perspective, that some of us might have genetic issues, while others have aquired issues. My best guess is that its a combination of factors that are responsible, and that combination might vary person to person.

    I view blood bacterial toxins like LPS the same way I view excess salicylates getting into the blood. Salicylates should be neutralized by gut bacteria somewhat, and in the case of LPS its either shedding or death of bacteria that releases it.

    Then it has to go through the gut wall. The gut wall is semipermiable naturally to allow absorption of nutrients. Note we are talking molecules not whole bacteria here. The gut has a sizeable immune capacity. It should neutralize both toxins and salicylates. If that fails it makes it to the blood. The blood then takes it via the portal vein to the liver. The liver is a massive immunological filter. Layer after layer of immune cells that are supposed to detox the blood so that toxic substances do not make it into the general circulation. For it to get into the blood then both the gut immune system and the liver have to be functioning sub par, but that is more likely if there is too much LPS being released into the blood stream.

    I hope to post a blog on this three or four blogs from now. The next three are political, then I am planning to return to biochemistry, looking at bacterial toxins and the gut immune system.

    To function correctly the immune cells have to be healthy. They need various substrates including glutathione. They require that they not be receiving immune signals which tell them to stop working, and require normal mitochondrial function. Furthermore for any individual toxin it requires the right form of the detox and associated enzymes to be there for optimal effect. That is where the genetics comes in. If your enzyme forms (called isoforms) are not optimal for a given toxin, then more will get through. Generally though there is a trade-off in that they are better adapted to other toxins.

    We know we have immune issues. We know that NK cells have substandard function. I wonder what the result would be if we started investigating liver biopsies? Not a pleasant non-invasive procedure, but we might learn something.

    The final stage of defence is in the tissues. For salicylates that defence is often glutathione. For LPS I am still unsure. I do know that selenium is associated with improved tolerance, but I do not know that we really understand the mechanism (presuming this association is causally linked, which it might not be). I can speculate, link it back to glutathione, but I want to do more investigation of this first and I am busy writing up political stuff.

    So I don't think genetics is an absolute requirement, but I am fairly sure it can increase risk, and in some cases may severely increase risk. I also think it takes multiple failures in the immune system to see a problem. So, are there multiple events causing it, and it only occurs when these are combined? Or is there a single underlying cause somewhere that starts all these processes off? That cause could of course be genetic.

    Bye, Alex
    merylg likes this.

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