Acetaldehyde As A Cause For Chronic Migraines In Candida Patients

Discussion in 'Testimonials' started by burtlancast, Sep 6, 2017.

  1. burtlancast

    burtlancast Member

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  2. Makrosky

    Makrosky Member

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    She doesn't provide a protocol?
     
  3. Amazoniac

    Amazoniac Member

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    Non-alcoholic fatty liver disease?
     
  4. haidut

    haidut Member

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    Vitamin B6 and glycine are the most effective acetaldehyde scavengers, and I know B6 has been used for migraines clinically but why it helped was not known.
     
  5. gbolduev

    gbolduev Member

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    There are 2 enzymes in the body that break down acetaldehyde. Acetaldehyde scavengers? What is it?

    AO and ALDH are the 2 enzymes.. B6 is not a part of any of those. What B6 does is it lowers zinc, when zinc goes down ethanol cant be turned into acetaldehyde.(Alcohol dehydrogenase ) This is not scavenging anything. This makes you toxic in alcohols. Candida ferments sugar into ethanol.

    B2 and molybdenum = AO

    NAD= ALDH

    end result is acetic acid for both enzymes, and if you are in acidosis both will be inhibited.

    Georgi, this is another example of how reading studies does not give the proper picture.

    This is exactly why b2 and magnesium are used for migraines. Since magnesium lowers zinc, so your production of acetyldehyde goes down, and b2 breaks down acetaldehyde into acetic acid. This is a wrong regimen though. You dont want to be left toxic in alcohols.
     
  6. ecstatichamster

    ecstatichamster Member

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    Do you have any cites?
     
  7. gbolduev

    gbolduev Member

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    Cites for what? for enzymes?. Just go look them up. I dont read any studies. this is biochemstry 101.
     
  8. opiath

    opiath Member

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    If both enzymes are inhibited in acidosis how do you clear the Acetaldehyde to clear candida?
    I am stuck in anaerobic metabolism and I have huge candida load.

    You recommended I use bifidus bacteria to reduce my lactic acid load.
    I understand your reasoning but I can't get them to settle.
    Felt some transient improvements but it doesn't last.
    I don't think I can repopulate my colon without fixing digestion and candida first.

    What is the way out of this?
    I think my metabolism improves as I burn out the PUFA but I have a long way to go still.
    Currently I'm high adrenaline, high lactic acid, high acetaldehyde.
    Cholesterol is low. Bile is not flowing.
    Liver and pancreas are slow. They can't work in this acidosis.
    I know it because if I take biotin and thiamine high doses PH goes up but it is not sustainable (burn and crash).
    I can digest max 30grams protein or fat on my own.
    Rest I have to fill out with amino acids and sugar. I have no other choice.

    Egg yolks for cholesterol, taurine for glycogen repletion and red light for aerobic metabolism work but I can't eat enough to support it.

    I have read all of your posts and I am trying to see things from your perspective but I can't figure out what is applicable in my case.
     
  9. Amazoniac

    Amazoniac Member

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    LIsten , buds. You take tons of vitamin A only to kill your remaning potential. And you start writing about endotoxin poisoning LMAO
    You take loads of it and you put pressure on NAD, while eating all this sugar non stop and sitting on your asses all day long.This must be a joke.

    For the first time , you DONT test, you guess. There are at least 12 body chemistries, Peat is ONE. I know my stuff so dont come tell me what he thinks,Im simply NOT interested)) Im no t fooled by studies anymore

    People are not just deficient in vitamin A.LOL Now tell me how is it going to be active if peoples pancreas are shot for running low on SODs and their digestion is ZERO? Cortisol goes UP so you dont die .Its there to save you)) This is when people take hormones to shut down stress. Guys ,FOOD needs to be balanced.

    BOdy is regulatory, you give retinol and you lower all the cofactors BIG TIME.its not even funny
     
  10. allblues

    allblues Member

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    @Amazoniac :D:D or should i say ))

    I will study your post thoroughly and report back with results
     
  11. Amazoniac

    Amazoniac Member

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    gbolduev's writing style is so striking that it's contagious..
     
  12. Amazoniac

    Amazoniac Member

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    Zeus mentioned some time ago that the ratio of NAD+ to NADH is a good indicator of health. But the ratio can vary simply by alterting what's happening to NADH. If you're congested, NADH will accumulate and the ratio will decrease, contrary to what would happen if there was a proper flow. And it's about the proportion but amounts as well. If the problem isn't a deficiency of NAD, but something clogging up the subsequent reactions, increasing NAD can make the congestion worse in the long run: reducing the overall state even more.

    Some time ago I had the brilliant idea of trying Energin (could've been any other B-complex supplement for that matter) with gelatin, which I don't react well. It potentiated the reaction beyond my expectations. After experimenting with each vitamin isolated to find out, it turned out to be indeed niacin. Organisms depend on it to generate energy. But it doesn't do anything by itself, it just increases the potential/ability to burn fuel. As soon as fuel is supplied, the reactions can occur.

    It shouldn't be a good idea to ingest plenty of it or precursors when someone has bacterial overgrowth: it would probably make it worse.
    It's also risky to give it to someone that is struggling to get enough calories and nutrients, it can drain the person even more. It's likely to have a "wasting" effect. It reminds me of Max Gerson's book and how he recommended only vit C and niacin, but feedings had to be frequent with plenty of nutrients.

    That's why I mentioned that it's the NAD that organisms are after, and it can be obtained through tryptophan, which some of it happens to always be escaping protein digestion anyway.

    I created a thread about the low niacin content of milk, and I guess there's more than the fact that it's low to not suppress fatty acid oxidation. If there wasn't an advantage in keeping it so low, it would have some more niacin (after all some is needed) and less of everything involved in the conversion.

    Can someone mutilate my ignorance on this, supply me some Diokinone, and buy me a ticket to knowledgeland instead?
     
  13. Amazoniac

    Amazoniac Member

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    by Lawrence Wilson, MD:

    http://orthomolecular.org/library/jom/1984/pdf/1984-v13n02-p066.pdf

    "It is possible that most strains of Candida albicans produce ethanol in the human intestine, but in an amount too small to be detectable in the peripheral blood. That the intestinal environment is sufficiently anaerobic for this to occur is indicated by the fact that, if adequate sugar is available, certain strains of Candida albicans can produce ethanol in quantities sufficient to induce a rising blood-alcohol level, and clinical drunkenness (Iwata, 1972). Thus such strains can efficiently accomplish the final step in ethanol production, i.e., the conversion of acetaldehyde to ethyl alcohol."

    "The major mechanism for the disposition of aldehydes in the body is oxidation by means of aldehyde dehydrogenase. This takes place primarily in the liver, although other tissues to some extent aid in this process. When the aldehyde is acetaldehyde, the oxidation product is acetate, which binds to Co-enzyme A (CoA). The acetyl CoA so formed may undergo any of the normal fates of acetyl CoA."

    "the presence of acetaldehyde in the intestine, the intestinal wall, and in the portal blood would afford many opportunities for its binding to such substances as nutrients, enzymes, vitamins, and polypeptides. If formed high in the intestinal tract, acetaldehyde could react with digestive enzymes in the small intestine. The possiblities are many."

    "Many of the metabolic disturbances caused by acetaldehyde have been attributed to its strong affinity for sulfhydryl (-SH) and amine groups, and to the increase in the ratio of NADH to NAD that results from the oxidation of acetaldehyde by aldehyde dehydrogenase."

    "PLP [Zeus' pyridoxal phosphate] is normally protected from degradation by its binding to the amine group of lysine residues of proteins, including serum proteins and hemoglobin. Acetaldehyde may, by binding preferentially to these residues, displace PLP and result in its increased destruction, and in abnormally low blood levels of this co-enzyme (Lumeng and Ting-Kai Li, 1974; Veitch et al., 1975)."

    "When the ratio of NADH/NAD increases, many secondary abnormalities occur. An uninterrupted supply of NAD is necessary in many areas of metabolism. NAD is converted to NADH when this nucleotide serves as hydrogen receptor in glycolysis, in the citric acid cycle, and elsewhere in metabolic reactions.
    The amount of NAD in the body is quite limited. It is therefore imperative that it be regenerated continually for these processes to continue. Normally, by means of oxidative phosphorylation and the electron-transport chain, molecular oxygen eventually accepts the hydrogen from NADH, yielding ATP and NAD. The latter thus is again available for pathways that utilize it, such as glycolysis and the citric acid cycle. When either ethanol or acetaldehyde is oxidized by its respective dehydrogenase, NAD is converted to NADH. When the necessity exists for the removal of these toxins in large amount over an extended period of time, the resulting shift to NADH decreases the amount of available NAD.
    The many metabolic transformations that utilize NAD as hydrogen receptor cannot proceed normally under these conditions. An increased NADH/NAD ratio leads to many metabolic abnormalities. Some of the more important are listed. Lieber has recently reviewed the biochemical abnormalities that may occur in this situation (Lieber, 1980).
    1. Increase in the ratio of lactate to pyruvate.
    2. Increase in the ratio of plasma hydroxy-steroids to ketosteroids.
    3. Decreased galactose tolerance. The conversion of galactose to glucose is inhibited by NADH.
    4. Alterations in amine metabolism. Where alternate pathways exist, reduced metabolites may be excreted at the expense of oxidized metabolites.
    5. The citric acid cycle is inhibited by NADH.
    6. Inhibition of glycolysis by NADH at the first oxidative step (conversion of glyceraldehyde 3-P04 to 1,3 diphosphoglycerate). This inhibits energy release (ATP formation) as well as pyruvate formation.
    7. Elevation of blood uric acid secondary to the elevated lactate levels caused by NADH excess. Lactate and uric acid compete for excretion in the kidney tubule.
    8. Abnormalities in porphyrin metabolism.
    9. Oxidative phosphorylation is inhibited by acetaldehyde. This is reversed by NAD.
    10. Decreased protein synthesis and increased proteolysis."

    "In addition to the effects of the high NADH/NAD ratio, Lieber lists the following toxic effects of acetaldehyde:
    1. Reduction in the number of microtubules in the liver.
    2. Decreased protein secretion, with protein retention in the liver.
    3. Engorgement of the Golgi apparatus with VLDL particles.
    4. Accumulation of lipid and protein, causing increased size of hepatocytes.
    5. Depression of glutathione in the liver, possibly as a result of the binding of acetaldehyde to its cysteine component. Glutathione is important in the removal of toxic free-radicals; a reduction in glutathione may damage membranes. Lipid peroxidation and decreased GSH (reduced glutathione) occurred in animals following chronic ethanol intake.
    6. Stimulation of hepatic smooth endoplasmic reticulum, leading to an increase in the rate of metabolism of alcohol and of drugs and, less desirably, to an increased rate of conversion of various substances to more toxic compounds.
    7. The mitochondrial ethanol oxidizing system (MEOS) produces acetaldehyde in the endoplasmic reticulum, in contrast to that produced by alcohol dehydrogenase in the cytosol. This leads to greater acetaldehyde concentration at this site (i.e., endoplasmic reticulum), possibly with induction of enzymes that are important in carcinogenesis and in lipid peroxidation.
    8. Increased collagen deposition in the liver (detectable only chemically in its early stages, but later by light microscopy). This is thought to be due in part to the increased lactate associated with the high NADH/NAD ratio. This leads to an increase in peptidyl proline hydroxylase activity, favoring collagen deposition in other tissues as well as in the liver."

    --
    Protective action of ascorbic acid and sulfur compounds against acetaldehyde toxicity: Implications in alcoholism and smoking

    @Zeus
     
  14. Amazoniac

    Amazoniac Member

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    Guys, regarding this type of intestinal fermentation, and as mentioned on the other thread: it's mostly a problem with fructose that escapes digestion, all depending on digestive capability, microbial composition and especially transit time. Many indigestible carbs have plenty of fructose in their fiber (even if not stated on nutritional labels) and are more troubling in general for obvious reasons. But the amount of sugars that someone can tolerate varies, so even from balanced sources such as fruits they can become a problem if you exceed your ability or ignore bad reactions; since fruits have an abundance of fructose, they can be particularly troubling when exceeded. Starches such as rice and white potatoes, which lack fructose in their composition, won't provide substrate for alcoholic fermentation because to reach that point, they require a much stabler environment, such as extreme constipation. It's all about intuition and tolerance.

    Fructose And Endotoxin [edwardjedmonds]
    Sorbitol, Xylitol, Mannitol
     
  15. gbolduev

    gbolduev Member

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    You got it.
     
  16. Amazoniac

    Amazoniac Member

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    Check out the Gershom post on the second link..
     
  17. Amazoniac

    Amazoniac Member

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    I forgot to comment that ripe apples seem unique, even for those that can't handle much sugar, and despite its relatively high fructose content, they should help to restore a healthy intestinal balance. The whole fruit provides a type of fiber than when fermented, will release acids with antimicrobial properties (on top of the already present compounds) throughout the entire tract. The juice is pretty useless for this purpose. It goes way beyond any malic acid discussion.

    That doesn't mean that eating more will be better, because they are still fermentable and excess fermentation is always a problem. But in small amounts it's a safer fermentation with possibly some benefits.
    I suggested a few times the addition of diced apples to the carrot salad, it's quite refreshing and goes well with its cider vinegar. The combination also gets rid of any concern with fermentation.
    Another suggestion is a potato puree with cooked apples. This combination is great, here's a shameless plug:

    People with slow metabolisms can't handle sugars very well, digestion is impaired and a lot of these sugars starts to escape it: the environment becomes favorable for the development of fungal overgrowths (fructose is feast). Apple cider vinegar is one of the first things that comes to mind when you talk about foods with antifungal properties.
    If you let the fruit rot, it doesn't smell as nasty as the majority. The antimicrobial compounds are just powerful.

    Perhaps the "one apple a day keeps the doctor away" isn't unjustified.
     
  18. tara

    tara Member

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    Very interesting thread!

    I've tried supplementing B2. Could it be that adding molybdenum could be the missing link that could make it effective?

    Thanks. If that is all or mostly accurate, it seems like lots of reasons for me to take this seriously.

    Hmm. So I get little obvious gut distress/discomfort these days, but I could potentially be getting enough sugar fermentation to be producing more than enough ethanol and acetaldehyde that gets through the blood brain barrier easily, and messes with me in various ways.
    So that could be at least part of an explanation for me feeling sick/foggy/poisoned if I overeat sugar - acetaldehyde.
    It could have been causing damage to the liver, so making it harder to clear these and other toxins.
    And it messes with cellular energy production.

    Grated carrot with grated apple is a delicious salad. Grated beetroot with it can be good too, if you like that.

    It's not making me any keener to follow the advice on other threads to eliminate starch. Potatoes and rice seem to digest well for me, and and I can eat more of them at a sitting and last longer before the next meal. Following cravings, I'm still wanting some fruit or juice etc at this time. But as I've increased the starchy foods, I've gradually lost interest in most of the refined sugar foods - only a little from time to time now, and it feels increasingly wrong when I do. It's nice to be doing it by taste rather than by theory, restrictive mindset and control.
     
  19. Amazoniac

    Amazoniac Member

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    Not only the fruit exerts antimicrobial activity but it has little vitamins. Even if they're fermented, they're not supplying the growth-factors, unlike most other fruits. And supplying something fermentable without those growth-factors along with carrots, which by themselves would be mostly antibiotic and unnatractive, can help to eradicate that sort of problem.
     
  20. haidut

    haidut Member

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    Actually, better acetaldehyde scavengers are NAC and alpha lipoic acid. They are direct scavengers as they can bind acetaldehyde and prevent its effects.
    N-acetyl cysteine attenuates ethanol induced hypertension in rats. - PubMed - NCBI
    "...All known pathways of ethanol metabolism result in the production of acetaldehyde, a highly reactive compound. N-acetyl cysteine, an analogue of the dietary amino acid cysteine, binds acetaldehyde, thus preventing its damaging effect on physiological proteins."

    Glycine and B6 are more of protectors against acetaldehyde, but glycine is also a direct scavenger.
    Metadoxine - Wikipedia
    "...Metadoxine is an ion pair salt of pyridoxine and pyrrolidon carboxilate (PCA).[1] Pyridoxine (vitamin B6) is a precursor of coenzymes including pyridoxal 5’-phosphate (PLP), which accelerates the metabolic degradation of ethanol and prevents adenosine triphosphate (ATP) inactivation by acetaldehyde."

    Effects of Glycine on the Catecholamine Levels and Activities of Alcohol-Metabolizing Enzymes in Rats with Alcohol Intoxication and Addiction
    "...We studied in rats the effects of peroral glycine introduction on the contents of catecholamines (CA) – noradrenaline (NA) and dopamine (DA) – in different brain structures (hypothalamus, midbrain, and neocortex), as well as the levels of adrenaline (A), NA, and DA in the blood and the activity of alcohol-metabolizing (AlM) enzymes – alcohol dehydrogenase (AlDH) and aldehyde dehydrogenase (AdhDH) – in the blood serum. The experimental group included animals with a disposition to alcohol consumption under conditions of free choice for drinking between an alcohol solution and water. The measurements were performed in animals in the state of acute alcohol intoxication (i.p. injection of 4 g/kg ethanol) or chronic alcohol addiction (formed due to a 3-month-long free access to ethanol solution). Introduction of 150 mg/kg glycine increased the NA and DA contents (the latter, to a lesser extent) in all examined brain structures; the NA level in the blood increased, while that of DA decreased. Under conditions of acute alcohol intoxication and chronic alcohol addiction, the ratio of the activities of AlM enzymes, AdhDH/AlDH, was significantly shifted toward values indicative of accumulation of acetaldehyde (AcAdh) in the tissues. This was accompanied by noticeable modifications of the CA contents in the brain structures and blood of the rats; in particular, the [DA]/[NA] ratio in the brain significantly increased. Introduction of glycine under conditions of acute alcohol intoxication provided normalization of the AdhDH/AlDH activity ratio. Obvious trends toward normalization of the CA levels in the brain structures were also observed in both acute and chronic experiments. In the latter case, the glycine treatment course resulted in a drop in the daily alcohol consumption by the animals. We conclude that glycine, which binds AcAdh and modifies the metabolism of CA transmitters, exerts a significant corrective influence on the pathogenetic mechanisms of alcohol addiction. Our experimental findings demonstrate that there are contact points between the “acetaldehyde” and “catecholamine” hypotheses of pathogenesis of alcoholism."

    [The new anti-alcohol preparation medikhronal: changes in the level of ethanol, acetaldehyde and monoamines during the treatment of alcoholism pati... - PubMed - NCBI
    The last study above talks about medikhronal (MEDICHRONAL®-DARNITSA), which is basically glycine and glucose.

    And yes, I am quite aware that just reading studies does not give the complete picture. That's why I work with people and have access to hospital data, to confirm or refute those studies. NAD is just a cofactor for ALDH but does not affect levels of the enzyme. That's why raising NAD levels does very little to improve alcohol intoxication in older people with low ALDH levels or in some people of Asian descent with genetically low levels of this enzyme. However, giving thyroid to older people does improve/accelerate alcohol metabolism. So, I do not agree with "NAD = ALDH".
    Finally, B2 is a cofactor for MAO and accelerates degradation of serotonin. Serotonin is the primary cause of migraines and that is why anti-serotonin drugs are used as well. The case of migraines in Candida patients is very specific and cannot be used to generalize to all migraine patients.
     
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