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Acetaldehyde As A Cause For Chronic Migraines In Candida Patients

  1. She doesn't provide a protocol?
     
  2. Non-alcoholic fatty liver disease?
     
  3. 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.
     
  4. 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.
     
  5. Do you have any cites?
     
  6. Cites for what? for enzymes?. Just go look them up. I dont read any studies. this is biochemstry 101.
     
  7. 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.
     
  8. 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
     
  9. @Amazoniac :D:D or should i say ))

    I will study your post thoroughly and report back with results
     
  10. gbolduev's writing style is so striking that it's contagious..
     
  11. 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?
     
  12. 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
     
  13. 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
     

  14. You got it.
     
  15. Check out the Gershom post on the second link..
     
  16. 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.
     
  17. 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.
     
  18. 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.
     
  19. 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.
     
  20. Not as effective as Molybdenum
     
  21. Man oh man. this is not true what you posted. I have done extensive testing. and I know enzymatic interactions. What I posted is correct. NAC is not acetaldehyde scavenger, Acetaldehyde scaverngers dont exist. These studies are bogus.

    All the results of your studies can be explained by enzymatic interactions. It seems the conclusions of these studies are a bro science which you then take and extrapolate. I posted to you how it is , why your claim this or not that.
    If you want to use the word scavenger, I have no idea what that means. Scavengers dont exist. IT is used when people cant't explain the interaction.

    Georgi, I like you and we are on good terms, I ' m not trying to argue with you and make you feel bad. But this is just bogus stuff. Study enzymatic interactions, then you will not need to read these bogus studies. About their imaginary scavengers and other bs.
    Stick with the biochemistry

    Study acetaldehyde pathway and ethanol pathway then you will understand where NAC plays part of it. and why NAD does not help people in acidosis to get rid of acetaldehyde. and how b6 works at " scavenging " acetaldehyde which it does not.

    You answering me these questions telling me that you dont know this. And this is the base of medical information, without this you should not even start reading studies or even analyze anything. You simply can't

    You make conclusions which are already known and researched and taught in medical schools.
    Only you make them yourself from some bogus studies that use word scavenger.

    I can write out the acetaldehyde pathway for you and you will see that every thing you say is wrong. And that all these substances that you mentioned are not scavengers . They are just a part of this pathway and do certain things -- they either stop acetaldehyde from forming or allow it to to be converted further down the line faster. This is PH dependant
    I think you did not see what I wrote to you , that ALDH will be inhibited by acidic PH and no matter how much NAD you will feed it won't work. NAD is pH dependant.

    giving thyroid increase CO2 and causes venous blood to get more alklaline. thus it allows acetaldehyde metabolism to go further

    ALDH is PH dependant. and ALDH= nad . NAD is PH dependant.

    I have most enzymes in my system all tied together in one huge algo. I know the overall interactions. The sooner you start going this route, the sooner you will understand that reading studies or even looking at some hospital results dont give you anything#

    At first I tried to do the same with hospital data and studies database from pubmed and 3 hospitals. EPIC FAIL. Since most of the data contradicted itself and even the computer could not find a proper model using latest state of the art AI algos that kill for me in the market.

    When I started to do the same with enzymes, everything got together. That was 4 years ago.
    Now I dont read one study because of this. Since I not only read them all, I understood , that they are wrong, and most of these are done not even by real scientists.

    You are still going at Peats conclusions. Just snap out of it. Look at Peat. He is aging man, and aging rapidly , nowhere near the top of this age group. If you contact me on Skype I can show you my grandparents, you will see what 87 should look like. And Peat is nowhere near that age.

    So anti aging did not work for him. since anti aging is only possible when you have ideal PH, and your not using any buffer systems. This will be never achieved by going after certain hormones . Lets say you go after serotonin, you will create an imbalance and this imbalance will start using buffering. And you age. You go after cortisol, you also create an imbalance, this imbalance will also use the buffer system and will age you

    By going after certain hormones you get rid of certain things or symptoms , but then you create other imbalances that you dont even know about, And then you just patch patch patch and patch . It won't work, brother.

    You will need to be so good at it like GOD to patch your self up.

    I really like that you research and look at things and try to systemize it. but I am telling you as a super systemic guy , that approach with the studies will fail. Do your own studies otherwise you will never create a matrix that you want. It is impossible.

    to study something you dont even need many people. You need to study and test something all at once all interactions at once. This is why you can never use hospital data or studies, Since hospital data has patients tested separately and studies do the same, it is like a test out of the matrix. You cant use results for progesterone from this patient, estrogen from this and serotonin from another study.

    As an example Eck's computer probably has 20 enzymes for each mineral and cofactor. This has many many complex interactions like millions. With all different outcomes. like ALDH will work like this in this case, like that in that case. Progesterone will work like this in this case, like that in that case.

    I now have probably 100 times more interactions. Eck was a pioneer of this approach and I think his approach is correct. PH controls everything first, then and only then you go further





    Good luck , man. Why don't we talk some on skype. Haven't heard from you for a while there.
     
  22. because scavengers don't exist. LOL Cysteine( NAC) simply converts acetic acid down the line into coenzym A pathway LOL, so more acetaldehyde is allowed to be converted into acetic acid. This is biochemistry 101

    Scavengers LOL
     
  23. This is probably a fungal infection problem, which can generate CO2 in the intestines, bacterias don't posses mitochondria to do so, what they do is generate other nasty gases and acids, and affect CO2 levels in the body, but not as a direct contribution. And I believe that they can rob people of many nutrients before they're even absorbed. Magnesium is possibly an example, and when supplements are given in excess, they can worsen these problems.
     
  24. Agree
     
  25. I have been studying Candida for years. I have it since I was born and let me tell you: caffeine pills and tobacco have been the best tools to have it under control. B1, B2, niacin and biotin are great for Candida sufferers. Just my 2 c.

    Edit: b6 feeds it like gasoline to a fire. I don't know why but I'm really suspicious about that vitamin. Some people claims that it's not a true vitamin, just a surrogate for niacin. It's one of the few vitamins that can create irreversible damage in high doses and everything is fortified with it from government orders...
     
  26. Candida Article #3: Conquering Candida

    "Candida toxins interfere with acetyl coenzyme A activity,(3) which could inhibit the synthesis of adrenal steroids, and further, it is believed that Candida possesses receptor sites that can bind adrenal steroids thus competing with host cells, producing apparent adrenal insufficiency.(3)"

    "The functioning of the thyroid gland is one of the first activities interfered with by Candida,(9) and it has been observed that 90% of Candida victims have low thyroid function.(8) As with adrenal hormones, it appears that Candida receptor sites can bind thyroxine and render it physiologically unavailable.(8) This may help explain the common finding of a normal blood level of thyroxine in a person who is clinically very obviously hypothyroid. Moreover, candidiasis is commonly associated with zinc deficiency, and since zinc is necessary for the conversion of thyroxine to its active form, tri-iodothyronine, such a deficiency could produce symptoms of hypothyroidism (which also could occur in the presence of normal blood levels of thyroxine).(10)"
    Increased transit time is classic. I know it's possible to keep kefir cultures with low numbers of yeasts just by not letting it ferment for too long and by renewing the milk more often. It won't become alcoholic: it's a yogurt. And you can even prevent grain colony growth if you change it too often, they start to rarefy to eventually disappear. Carless analogy.

    "The relationship between food allergies and candidiasis is well-known. Candida damages the gastrointestinal mucosa with its invading hyphae and secretory products such as phospholipase and acetaldehyde, which leads to an increase in the permeability of the mucosa ("leaky gut" syndrome). This allows large molecules of incompletely digested food protein to enter the bloodstream, thus provoking an immune response.(6) Additionally, irritation and inflammation of the intestine caused by Candida may impair local immunological defence mechanisms, which could result in food allergies, as could the more general immune dysfunctioning that is normally associated with candidiasis.

    The liver takes the full brunt of Candida toxins emanating from the bowel (at least one of which - acetaldehyde - is a known hepatotoxin) and also, Candida itself is likely to disseminate to the liver readily. Liver function might therefore be expected to be disturbed in candidiasis, and this could encourage the development of food allergies since the liver is responsible for removing foreign proteins from the circulation. Candida-induced hypoadrenia might also be part of the picture. (Adrenal hormones modulate allergic responses.)

    The other side of the coin is that food allergies distract the immune system,(6,7) and further, produce immunosuppressive chemicals such as histamine and prostaglandin E2,(4) and therefore could predispose to candidiasis."

    "The relationship between Candida and hypoglycaemia is complex. Both conditions can independently give rise to similar symptoms (fatigue, headaches, anxiety/depression, forgetfulness, poor concentration, carbohydrate craving);(11) hypoglycaemia, by impairing immunity (particularly neutrophil activity) can contribute to the development of candidiasis;(12) and candidiasis is implicated as a cause of hypoglycaemia.(2)

    In candidiasis, Magnesium, vitamin B6 (pyridoxal phosphate), zinc, and fatty acid deficiencies are all likely to occur and could predispose to the development of hypoglycaemia. Hypothyroidism, hypoadrenia, and liver dysfunction induced by Candida could also give rise to hypoglycaemia. Further, there is no doubt that hypoglycaemia can result from food allergies, which, as noted above, are common in candidiasis. Additionally, sugar metabolism at the cellular level may be impaired by Candida (Candida toxins interfere with acetyl coenzyme A activity,(3) thus reducing citric acid production), and this could give rise to hypoglycaemic-like symptoms."

    "Candida infection disrupts the metabolism of vitamin B6 and essential fatty acids, and is associated with low levels of Magnesium, all of which could be relevant to premenstrual tension. Further, Candida can apparently secrete oestrogens,(5) which could contribute to the oestrogen overload that characterizes most women with premenstrual tension.(14) It is also possible that Candida-induced liver dysfunction impairs the liver's ability to degrade oestrogen."
    Rayzord suggests to be careful with nutritional yeast as frequent supplement, one of the reasons being its estrogen. Talk about an internal factory..

    "We commonly note the existence of candidiasis in children with learning disability and hyperactivity. Mothers of hyperactive children often give a history of candidal vaginitis, particularly during pregnancy, and the children have often been exposed to antibiotics early in life. A low income is frequently part of the picture and leads to poor nutrition and a high-sugar diet. It can therefore be postulated that the hyperactivity results from the effect of Candida toxins on brain function, the ingress of food allergens and exorphins through a gut rendered leaky by Candida, Candida-induced chemical sensitivities, and Candida-induced nutritional deficiencies (Magnesium, zinc, pyridoxal phosphate, and gamma-linolenic acid). Magnesium and zinc deficiencies could predispose to the heavy metal toxicity (lead,(15) copper,(15) and aluminium(16)) implicated by some authors. Dyslectic tendencies appear to be related to Candida-derived acetaldehyde interfering with corpus callosum function.(5)"

    "The ileocaecal valve (ICV) comprises a sphincter-like thickening of the circular muscle at the distal end of the ileum and a pair of transverse folds or lips that project into the lumen of the caecum. The purpose of the valve is to prevent the contents of the ileum (chyme) from passing into the caecum before nutrient and water absorption is complete, and to prevent the reflux of colonic contents into the ileum.(17,18)

    In kinesiology, the ICV is commonly found to be malfunctioning: often it is inappropriately open and occasionally it is inappropriately closed. The causes of such dysfunction are considered to be food sensitivities, intestinal acid/alkaline imbalance, psychological stress, and adrenal gland dysfunction.(18)

    When the ICV is inappropriately open, toxic colonic waste can regurgitate into the ileum from where it can readily be absorbed. Thus an open ICV leads to symptoms of autointoxication, which include headache, dizziness, faintness, nausea, and general achiness. It has been pointed out in these columns (1985, March issue, p. 21) that such symptoms bear a close resemblance to those attributed to Candida, and the relationship between these two conditions therefore needs clarifying.

    Stimulated by this observation we attempted to analyse the situation kinesiologically, and concluded that the two conditions almost always co-exist, and that candidiasis is a major cause of ICV dysfunction."

    "Candida toxins are undoubtedly the cause of much of the symptomatology associated with candidiasis. Pre-eminent among these is acetaldehyde, which poisons by irreversibly binding to tissues and destroying them by free-radical activity.(3,19)"

    "depending on the level of Candida toxins (we have developed a test vial for use with Vega testing or kinesiology that measures the level), we might also give zinc in ultra-pure form (NS 1) and molybdenum since the enzymes that degrade acetaldehyde (aldehyde dehydrogenase and aldehyde oxidase) are dependent on these two minerals. In theory, taking a fibre supplement should help lower the level of Candida toxins in the intestine by binding them and by encouraging frequent bowel movements. In practice, however, fibre supplements may not be well tolerated in those suffering from established candidiasis and/or a toxic bowel, perhaps because they stir up toxins by stimulating bowel motility, leading to their increased absorption. Fibre supplements should therefore be introduced with some care, and taken along with plenty of water to assist in the detoxification and excretion of any mobilized toxins.

    In the brain, acetaldehyde interferes with cholinergic mechanisms, inducing a relative shortage of acetylcholine (which produces problems with thinking, reading, concentration, memory, and behaviour), (5) and this can sometimes be helped by giving dimethylaminoethanol (DMAE), a choline precursor that readily penetrates the blood-brain barrier, and vitamin B5, which is necessary for the acetylation of choline. Additionally, cross-crawl techniques are useful to re-establish left-right brain coordination impaired through acetaldehyde-induced corpus callosum dysfunction."

    "Inadequate production of digestants (gastric acid, pancreatic enzymes, and bile) is common and predisposes to intestinal candidiasis. Our initial approach here is to give betaine hydrochloride and digestive enzymes."

    "Dysbiosis and digestive insufficiency encourage intestinal parasites other than Candida. These include enteroviruses, protozoa, and nematodes. Enteroviruses, if allowed to establish themselves in the colon can spread systemically to cause a myalgic encephalomyelitis (M.E.) situation. Protozoa and nematodes can cause a whole array of intestinal and systemic symptoms, and all three types of infection activate and burden the immune system."

    "For reasons that are not entirely clear, candidiasis is associated with a number of nutrient deficiencies. These include vitamin A, pyridoxal phosphate (Vitamin B6), Magnesium , zinc, and Omega-6 and Omega-3 fatty acids.(3,4)

    One unifying hypothesis is that acetaldehyde displaces pyridoxal phosphate from its binding sites on albumin, resulting in its rapid metabolism.(19) Since magnesium and zinc appear to be dependent on pyridoxal phosphate for their assimilation, this could lead to a deficiency of these minerals. In turn, this would further deplete pyridoxal phosphate, and also deplete the phosphate coenzyme forms of vitamins B1, B2, and B5, since phosphate transfer is a magnesium-dependent process."

    "Alternatively, it could be argued that the Magnesium deficiency is "primary" (itself resulting from impaired renal reabsorption of magnesium consequent upon chloride retention due to the binding of chloride by leukotrienes produced as part of the inflammatory response to Candida).(4) The magnesium deficiency could then cause a depletion of the phosphate coenzyme forms of vitamins B1, B2, B5, and B6, with vitamin B6 being the most affected because pyridoxal phosphate formation is dependent on riboflavin (vitamin B2) phosphate and zinc (depleted as described above), in addition to magnesium.

    With regard to vitamin A deficiency, it is theorized that the conversion of carotene to vitamin A is inhibited by Candida-induced hypothyroidism or by Candida-induced impairment of carotene dioxygenase in the intestine or liver.(4) It may be relevant that Candida binds iron, and that carotene dioxygenase is an iron-dependent enzyme.

    Whatever the mechanisms of these deficiencies, they should all be investigated and corrected where appropriate, particularly since they undoubtedly contribute to the symptomatology of candidiasis. In view of the preceding considerations, vitamin A deficiency should be corrected with retinol rather than with carotene, and the pre-formed coenzyme forms of the B-vitamins should be preferred to the usual precursor forms."
     
  27. @haidut , have you changed your mind on NAC? I remember you advised against it a few times.
     
  28. Hey bud, as an expert I wonder if you can help me. I have a little athletes foot and have recently stared to get nail fungus on both hands and feet. I ate raw garlic thinking this may a) kill some stomach candida on the assumption I may well have some and b) help to fight the nail fungus. I had some tiredness and then a day or so later the most horrific smelling wind. I put this down to a small die off perhaps? I really dont know if i have stomach candida. Thoughts?thanks in advance
     
  29. Raw garlic does nothing. I have tried every other antifungal/vitamin/supplement out there. The only thing that has kept me sane in all this years is tobacco, but it seems that caffeine (pills) is even better (for me at least). The B vitamins would.be up there at the top and after them the fat-solubles.

    I used to have athletes foot and it dissapeared when I was using Estroban. It's the easiest fungus to cure. The rest of the skin fungus are getting better with the B's and caffeine pills. Good luck.
     
  30. Thanks, appreciate it.
     
  31. Lol, yes we are on good terms. I am just responding to your post about B6 and glycine not being acetaldehyde scavengers. I do not dispute the role of PH in alcohol metabolism and toxicity. When you say something I don't agree with I respond to it, but you take it as arguing :): As far as NAC and lipoic acid, they are indeed scavengers and I have seen it both in a lab and in people injected with NAC to prevent liver damage from alcohol intoxication. Why do you think they inject them NAC and this is a standard practice in emergency rooms?
    All chemicals that have sulfhydryl groups can bind to and inactivate acetaldehyde. This is basic biochemistry too. NAC has one such group and alpha lipoic acid two, so it is even better than NAC for scavenging acetaldehyde.
    Alpha-lipoic acid ameliorates oxidative stress by increasing aldehyde dehydrogenase-2 activity in patients with acute coronary syndrome. - PubMed - NCBI
    Molecular Mechanisms of Aldehyde Toxicity: A Chemical Perspective
    The reaction of sulfhydryl groups with carbonyl compounds. - PubMed - NCBI
    "...The sulfhydryl groups of L-cysteine and reduced glutathione (GSH) react nonenzymatically with formaldehyde (F), acrolein (Al), acetaldehyde (AA), malondialdehyde (DAM), pyruvate (P), oxoglutarate (oxo-G) and glucose (G) to form thiazolidine derivatives. These reactions show different velocities and the adducts formed show different stabilities. The equilibrium constants K, as well as the rate constants kr for the reverse reaction, show considerable variation. The carbonyls reveal higher reactivity with sulfhydryl group of L-Cys than with those of GSH, and the stability of the adducts is higher than that of GSH. Al, F and AA react more rapidly with both thiol compounds than the other carbonyls, but the adducts are less stable. The sulfhydryl groups level of bovine serum albumin as well as those of high- and low-molecular thiols of human plasma is reduced in the presence of Al, F or DAM."

    Cysteine - Wikipedia
    "...Cysteine has been proposed as a preventative or antidote for some of the negative effects of alcohol, including liver damage and hangover. It counteracts the poisonous effects of acetaldehyde."

    I actually don't agree with Peat 100%, maybe closer to 70%. Some of his dietary recommendations on calcium and dairy have to be applied very carefully as they can be dangerous for some people. There are a few people here who got true iron deficiency from eating too much dairy and a lot of copper from seafood or taking supplements.
    ...but the overall approach of Peat about metabolism and disease being always related to excess of free electrons is pretty solid in my personal experience. His metabolic approach (and a LOT of personal experimentation) helped me recover from pretty serious health issues. I have the data to prove it, and can send over to you.

    But, let's forget about diet for a minute. The main approach of Peat is keeping stress under control because it leads to inefficient metabolism and build up of NADH, which ultimately leads to disease. That excessive buildup of electrons leads to disease is very hard to argue with, as the evidence for it is extraordinary. The faster the metabolism, the less NADH (and more NAD) you have and the less you are in reductive state (the more oxidized you are), and as a consequence the more CO2 you produce, which results in better oxygenation of tissue. ALL degenerative diseases have an excessive reductive component, especially cancer. As an extension to that there are things in our diet that either promote or inhibit metabolism, and thus redox balance. All of Peat's dietary recommendations stem from that basic principle. Does not mean that every single recommendation, like eat more dairy/calcium, will work for everybody.
    In my experience, the metabolic types Eck and you talk about are simply maladapted states that will be different for different people. But it does not mean we should aim to keep people in those states. That being said, it may be very difficult to get some people out of that maladapted state and into "fast oxidizer" state. I have some examples in mind and I will mentioned over Skype.
    I volunteer in a hospital now and contract a lab to run some experiments. People send me their blood work and scan results every day. Seventeen doctors (MD) communicate with me on a daily basis and share (anonymous) patient data. So, it is not all studies and I see results from Peat's approach every day.
    Anyway, I will reach out on Skype so we can talk more.
     
  32. Zeus, if you ever need a third opinion, invite Travisord to a group conversation as well. It will get interesting)))
    Hope that you're doing great.
     
  33. Woa didn't know that you only agree 70% of what Peat said, I thought you've always been 100% in through and through. Can you elaborate more on the 30% beside the ones above?
     
  34. I already hinted to the gap - some dietary recommendations related to dairy, and also things like niacinamide doses (in my experience 100mg dose will do nothing to stop excessive lipolysis, 500mg+ may be needed), avoidance of drugs which for some severely compromised people may be the only recourse to break out of the vicious cycle, pregnenolone effects in high doses (he claims no antiandrogenic effects in ANY dose, and used to recommend 150mg+ which I think may be excessive for most people), etc. But the theory that people here ascribe to him (which is simply his take on metabolic primacy over genetics) is about as close to the truth as we currently have, so I am 100% behind it. I think it is unfair to criticize Peat for "his" metabolic vs. genetics theory, as that battle has in fact been an extension of the Cold War for more than 7 decades. The book "Cold War in Biology" sums up that ideological battle pretty well. He just did a great job of collecting most/all known work on metabolism and environmental influence, the relation of the organism to its environment, etc and synthesized it pretty well in English. His unique work I think is mostly related to progesterone and vitamin E, which he fused excellently into the metabolic theory of disease.
    So... considering all of this I think the people criticizing Peat are probably doing so out of personal reasons. "His" theory was the dominant field in the Eastern Block, and is well-backed up by evidence but mostly unknown in the West due to ideological reasons. I suppose it is easy to attack one person than to refute 7 decades of research...
     
  35. The idea that someone's metabolic type is set in stone seemed like an epitome of rationalism.

    At some point, it would be great if you would share more about calcium metabolism. One of the random quotes from a yummy Amazoniac citing was, "Mg depletion exacerbates intracellular K loss and increases intracellular Na. [..]the increase in intracellular Na is followed by a Na-Ca exchange and results in increased intracellular Ca." I would love to understand this later stage of Na-Ca exchange. I've shared how successful kuinone was at, seemingly, giving me all new joints. Now, I would like to peer wider to these interactions of Mg, Na, K and Ca. Thank you!
     
  36. I can't help noticing while your first quote (1) suggests magnesium supplementation being potentially harmful for candida patients, no such suggestion is made at any point in your second one (2), which actually strongly advises magnesium supplementation for candida patients.

    Could it be because (1) is made by a supplements merchant defrauding the scientific publishing system while himself without scientific training, and (2) is made by a career pharmacologist?
     
  37. I stand by it because excess nutrients is a problem, regardless of how safe they are, but especially if dealing with chronic infections such as this case. All I'm questioning the idea that magnesium can only do good. If you spread this notion, people are not careful with supplementation and start chugging it down. And if it fails, people turn the blame to themselves.

    As you note from the last post, it's a systemic depletion. Once problems start to appear, one part tries to compensate for the other until a point where the person is trapped for the lack of various nutrients that are interdependent. It's not a fixed state, it's just depletion on various levels.
    The person then becomes deenergized and you can't just force more and more magnesium in because it's not that simple. Sometimes the body rejects it because even a small amount can be excessive for its state and it wouldn't be able to handle, it's the same process when digestion becomes impaired: the excess in turn can feed these type of infections, but people persist and keep ignoring the reactions trying to overcome the problem.
     
  38. Except there has been millions of people supplementing with magnesium for the past 60 years, and neither scientific nor epidemiological or clinical evidence ever surfaced in that whole period of excess magnesium supplementation triggering candida overgrowth.

    There's simply nothing there.

    Absolutely nothing.

    Notwithstanding a shrewd businessman and his deep pockets able to corrupt the scientific journals.
     
  39. The idea of supplementing magnesium for yeast infections is to replenish a common deficiency in this situation, it can be a sign of nutrients being robbed or a depleted and inviting susceptible environment; either way, I'm not aware of people eradicating them with plain oral magnesium. In other words, it isn't a yeast antibiotic. But even if there are successful reports, you can't disconsider that it can go bad as well. There are reports on forums such as Curezone from people noticing the same symptoms they get from yeasts, flaring up after supplementation, the reaction made them search for a connection, not the opposite.
     
  40. We already got over that; the only post on curezone stating magnesium triggered candida symptoms was the one research article published by Eby and cited (with cautions!) by Narouz.
    Further down that curezone discussion, there's even a post responding to the Eby article and stating the exact opposite.

    "I haven't found any evidence magnesium feed candida. Instead, people with CRC are very low in magnesium and need this supplement.
    Jorge."
    Magnesium Feeds candida. at Candida & Dysbiosis Forum, topic 1884809
     
  41. As I mentioned, what prompted their search was the negative effects from supplementation, they searched for a connection later.

    Why do you think that there can't be adverse effects from something that is part of their metabolism? They can withstand very harsh insults from something that's completely toxic to them. Especially because the state of the person is probably already weakened to allow their overgrowth.
    If it was indeed a cure, this should be the simple and successful route since it's used for a long time as you stated. When you search for "magnesium yeast" what actually appears right away are the possible negative interactions and the fact that it's a common deficiency, but read the previous post again.

    And read this as well, disconsider the experiment part and focus instead on how general yeast metabolism works:
    http://www.aulibrary.au.edu/multim1/ABAC_Pub/Au-Journal-of-Technology/v3-n3-3.pdf
     
  42. We're running in cercles here.

    Test tubes aren't living conditions; petri dishes only contain microrganisms; there's no immune cells in petri dishes.

    Magnesium enhances the replication of polio virus in petri dishes; in a human being infected by polio, magnesium supplementation cures the infection in 100% of the cases.

    No scientific article stating magnesium feeds candida or yeasts IN VITRO makes the inference to living conditions.

    No magnesium supplementation ever triggered clinical candida overgrowth. In 60 years of supplementation with millions of people.

    And it's not the trolls on curezone or the deep pockets of Mr Eby who will change any of that.
     
  43. Each one of those points were already addressed on the other thread, not sure why you're bringing them up again))

    Since you need formal proof that magnesium supplementation is not a cure and considering that no one here will be injecting themselves with it, here it is:
    The treatment of chronic fatigue syndrome by complementary medicine - ScienceDirect
    "one exception is magnesium, which has been demonstrated to be the single most effective treatment for CFS. It was demonstrated that CFS sufferers are significantly deficient in magnesium (shown by red cell magnesium levels) compared to healthy controls, and that parenteral administration of magnesium was significantly helpful in 80% of patients.15 At present it is unclear whether magnesium deficiency is part of the cause of the condition or a result. However, as oral magnesium is relatively ineffective, it would appear that reduced absorption and/or increased excretion is probably the cause. Patients with yeast overgrowth appear to be particularly susceptible to magnesium deficiency, possibly because the yeasts themselves extract magnesium from the diet or interfere more directly with absorption."

    If the body is being unable to control the infection as is, and a lot of people just can't handle supplemental magnesium well judging by reactions, and as stated on the passage being ineffective for repletion purposes, why can't there be a negative outcome from supplementation in this case? Unabsorbed nutrients are food for microbes.
     
  44. Magnesium is needed to detox the products of yeast metabolism, acetaldehyde essentially; that's why its deficient.

    Candida also prevents you from absorbing nutrients, magnesium being one of them.

    But there's no evidence of magnesium supplementation worsening an already existing candida overgrowth or triggering it.

    You keep coming out empty handed even though you don't realize it.
     
  45. Explain to me then why parenteral is effective and oral is not.
     
  46. Also explain me what's the meaning of something that isn't nourishing you well while feeding your germs.
     
  47. I believe oral magnesium chloride is effective in an overwhelming number of cases.
     
  48. And I believe that you will reply one day to one of my PMs.
    I think that there's truth to it but we can't generalize, that's my point. If you ever find such cases, please share. It's good to know that it's an effective tool indeed for some, no sarcasm, burtlan!
     
  49. Hey guys, let me give you my take on this.
    I've been dealing with candida overgrowth for 2 years.
    Coated white tongue and digestion ****88 up beyond what you can imagine.
    Antifungals like Nystatin make my liver literally stop (jaundice, gallbladder attacks and intestinal inflammation).

    I think you can both agree Candida is an energy deficiency problem.
    Antibiotics may very well start it but insufficient energy for the repair of the digestive system sustains the overgrowth.

    While magnesium doesn't directly feed it, I can attest it can make the condition much much worse.
    You see, one of the things magnesium does when it goes inside the body is that it decreases adrenaline sensitivity.
    This may sound like a good thing but unless you have a severe Mg deficiency I can assure you, it is not.
    Adrenaline is usually always there for a reason.
    If you have a disrupted aerobic metabolism like I do, adrenaline is very much needed to maintain energy production.
    So when you put magnesium inside, you downregulate adrenaline sensitivity and then you actually need MORE adrenaline to do the same job.
    This is why you see everywhere that stress depletes magnesium. Body is getting rid of it fast in order to increase sensitivity.
    It wants to have the minimum amount of adrenaline and MAX sensitivity.
    Why? Because adrenaline upkeep is expensive and destructive.
    High adrenaline floods your blood with free fatty acids which you very well know.
    Also more MAO and COMT are going to be needed to break down that adrenaline.
    MAO and COMT break it to aldehyde which is thing you are trying to get rid of.
    Salt works because it increases adrenaline sensitivity and helps you retain magnesium without this negative effect.

    I've supplemented tons of magnesium over the past 2 years and I now think it was a big mistake.
    I know healthy people don't believe sick people but this is my personal observation and conclusion.
     
  50. Did you ever test magnesium levels?
    Do you have happen to have any studies on this?
     
  51. "auto-brewery syndrome"
     
  52. Opposing actions of calcium and magnesium ions on the metabolic effects of epinephrine in rat heart - ScienceDirect
    Magnesium inhibits the hypertensive but not the cardiotonic actions of low-dose epinephrine — Experts@Minnesota
    Effect of intravenous epinephrine on serum magnesium and free intracellular red blood cell magnesium concentrations measured by nuclear magnetic re... - PubMed - NCBI
    Effects of magnesium on contractile responses induced by electrical transmural stimulation and noradrenaline in rabbit thoracic aorta
    Beta-adrenergic desensitization reduces the sensitivity of adenylate cyclase for magnesium in permeabilized lymphocytes. - PubMed - NCBI

    Make of those what you will.
    I'm not trying to convince anyone here.
    I'm just sharing my n=1.
    I know @gbolduev mentioned this also.
    Soaking in epsom salts or taking magnesium makes me feel really good and sedated for 1-2 hours and then my heart starts beating
    harder and my feet get colder.
    I know this because I'm really sensitive to those two symptoms.

    Also Ray Peat himself says that good thyroid function is needed to retain magnesium.
    And when does thyroid go up? When the need for adrenaline goes down.
     
  53. None of the papers you cited discuss an increased adrenaline secretion following magnesium supplementation.

    They merely analyze the antagonistic effects of adrenaline and other various cations to magnesium.

    Magnesium and adrenaline have antagonistic effects of the neuro-muscular junction, and other energy processes. That's been known for 80 years.

    You must have mistaken the articles.


    just sharing my n=1. :wink
     
  54. That's simply not true.
    It's the other way around.
     
  55. You are correct. I cannot bring up a study that shows increased adrenaline levels.

    But I do wonder what a study would show that measures the adrenaline after Mg heavy dose in a person that is reliant on that adrenaline.
    I agree it is very hypothetical but I'm going by my bro science and my instincts on this one.
     
  56. Good you mention is bro science and your intuition. Helps put things in perspective. Thanks @burtlancast
     
  57. I have no doubt that serotonin is a significant player in migraine.
    If serotonin is elevated there will be reasons for that. Understanding more about the presumably multifactorial causes and seeing if any of them are practically avoidable would be nice. I'm not completely opposed to using drugs - I've used quite a lot over the years, including some anti-serotonin ones. There seem to always be downsides to long term or frequent drug use.

    Peat has also mentioned that typically migraines occur on a background of high estrogen, histamine and serotonin.
    They are all hormones that rise to deal with stresses of various kinds.
    Struggling liver and high stress levels also seem to be common factors.

    Candida may be a special case, but acetaldehyde is not just an issue with candida, right? Acetaldehyde can arise from fermentation of sugars by other microbes too, right? And acetaldehyde, and difficulties with eliminating it, is a stressful burden on the the system, right?

    Do you have reason to think that serotonin, for instance, is completely independent of acetaldehyde?

    Resolving those would be nice.
     
  58. Pretty dense thread here. This is interesting: #13
    And the most essential for microtubule formation is probably guanidine triphosphate (GTP). This interacts with tubulin directly and is essential to the polymerization process.
    Almost certainly. Methylglyoxal is another aldehyde which binds to gluathione forming S-linked adduct. It then goes on to enzyme glyoxylase I, where it is dehydrogenated and hydroxylated to S-lactoyl glutathione. This is now lactic acid S-linked to glutathione and a second enzyme glyoxylase II then splits this apart regenerating glutathione.

    Analogues of the intermediate, S-lactoyl glutathione, can be designed to be powerful inhibitors of the enzyme glyoxylase I – effectively inhibiting methylglyoxal degradation and increasing intracellular levels. This inhibits cancer. Small natural glyoxylase-inhibitorslike lapachol, lapachone, and some flavanoidsstrongly inhibit cancer. This is often explained by either free radical mechanisms or DNA/topisomerase interactions, which I doubt. I think it's cancerostatic effect is achieved by raising methylglyoxal.
    inhibitor.png
    I pretty sure that the glyoxylase system turns all S-linked aldehydes into their corresponding carboxylic acids.
    Ray Peat has written an article on collagen formation and cancer, which is often associated with high lactate concentrations but I don't remember him mentioning this mechanism.


    *Douglas, Kenneth T., et al. "Partial transition-state inhibitors of glyoxalase I from human erythrocytes, yeast and rat liver." Biochimica et Biophysica Acta (BBA)-Protein Structure and Molecular Enzymology (1985)
    The Cancer Matrix ―Ray Peat
    ‡If anyone looks into lapachol, you will be confronted with scaremongering. Look at the real toxicological data, realize that it has a lower LD₅₀ than aspirin, and then disregard this pathetic NCI scaremongering and ponder why they habitually create unscientific fear over safe, cheap, natural, and effective drugs such as lapachol and laetrile.
     
  59. Acetaldehyde is a liver burden and anythign that burdens the liver will reduce its ability to excrete serotonin and estrogen. I was just saying that for migraine sufferers acetaldehyde is probably not the main cause. I know quite a few people with migraines who never drink and have tested negatively for Candida, so it has to be something else.
     
  60. I think many people in the field consider migraines to be typically multifactorial and diverse. Just because it's clearly not the cause for some people doesn't demonstrate that it isn't causal for others. It could be acetaldehyde for some people, and/or other liver burdens for others, couldn't it?

    I thought part of the point above was that you can get acetaldehyde without drinking alcohol if the microbes get a chance to work on sugars. Surely candida are not the only gut microbes that can do that?
     
  61. It is possible, but aside from Candida most other fungi that can infect humans are quite lethal so I doubt somebody lives with chronic infection like that and worries about migraines. I am not downplaying the link, I am saying that for an anti-serotonin to help there must be more than acetaldehyde even if it one of the factors.
     
  62. Aren't there other common yeasts that can produce acetaldehyde too - only seriously dangerous fungi?

    I agree that there are likely other factors too.
     
  63. Well, the ones that can colonize the gut are usually pretty serious. Mouth and other mucous membrane openings can probably harbor less harmful ones. I maybe wrong, so if you know of other chronic yeast infections in the gut that can linger for years and overload with acetaldehyde please share.
     
  64. Are you talking about systemic (and therefore dangerous) candida or other fungal infections?

    From the posts on the first page of this thread, I wasn't thinking just of those serious infections, but of the variety of normal yeasts and bacteria that commonly hang out in most people's guts, in larger or smaller numbers. I thought the point of @Amazoniac 's posts was that if they get fed lots of sugar (because in some circumstances it doesn't all get digested further up-tube), they'll be fermenting it, and possibly producing a little alcohol and/or acetaldehyde in the gut, and that could be contributing to trouble?
     
  65. It is possible there is always some acetaldehyde floating around from smaller fungal colonies. As I posted in another thread, chronic alcohol consumption increases Candida overgrowth and thus acetaldehyde on top of what alcohol will already do by itself. So, maybe this is a good test - if even a little alcohol gives you bad headaches maybe there is a fungal issue that needs addressing.
     
  66. I don't like destructive testing. :)
     
  67. :cool:
     
  68. Well, one of your older posts stated the following:
    On another note, does anybody know of an english translation of Warburg's works? It seems nobody has taken the time to translate his books from german.
     
  69. I haave read that pantothene, not pantothenic acid, is good for lowering acetaldahyde levels in people with candida. Don't have anymore info off the top of my head, but you can find it on a search.
     
  70. I've come across a few references to molybdenum over the last while - wondering if it could be a relevant one for me. I wonder if anyone here has noticed benefit from supplementing it?

    I think I could enjoy a serving of cauliflower every week or so - looks like a rich source, and occasional buckwheat.
     
  71. Somebody had translated a few of his articles. This looks like a good one:
     
  72. @haidut Bringing back on old thread here, but this comment peaked my interest due to personal experience... I was curious if you could expand on your recommendations on calcium intake and how they differ from Peat's. Either through too heavy of an effort at blocking iron absorption, low thyroid/PFS leading to nutrient absorption issues, and/or leaky gut symtoms I've developed extremely low ferritin (my level is 10) and bottom of the range serum iron, and %saturation. As I try to bring my iron back up and hopefully stop my excessive hair shedding and fatigue, I'm trying to figure out what to do with calcium. I don't tolerate dairy well and have tested positive on food allergy to egg yolk and whites so egg shell calcium probably isn't the best idea. In fact, when I did try it I reacted poorly to it (as well as other forms of supplemental calcium) such as nausea/anxiety, general feeling of unwellness for 3-4 hours after supplementing.

    As of now, I've been doing fine with small doses of Calcium Orotate from Bulk Supplements and Brer Rabbit Blackstrap molasses (20% calcium, 25% magnesium, 4% iron RDA per serving). To make a long question short, I'm curious to your recommendations and sources for calcium intake in general and any thoughts/concerns given my situation/sources of calcium intake?

    I'm also now taking OptiFerin-C (iron bis-glycinate) from Pure Encapsulations with food away from high calcium intake.

    Thanks in advance.
     
  73. I was speaking just based on what people on the forum reported. Maybe those who got iron deficiency were already hypo and avoiding iron tanked it even more. Not sure, but it certainly happened to maybe 7-8 people posting here. Also, quite a few people here report issues with milk/calcium when intake reaches say half a gallon of milk daily. Could be from magnesium deficiency or something else, but again, I was just mentioning what others reported.
     
  74. I’d want to know something, Haidut. As you know chemical fonctionnement and industrial business in chemical purview, do you know if this is reliable and clean of all industrial stains? It’s about crystalline glycine, a French society. Thanks in advance.