Acetaldehyde As A Cause For Chronic Migraines In Candida Patients

Madato

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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.

Not as effective as Molybdenum
 

gbolduev

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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.

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.
 
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gbolduev

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Not as effective as Molybdenum

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
 

Amazoniac

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SIBO is making tons of CO2
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.
 
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gbolduev

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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.

Agree
 

Lucenzo01

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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...
 
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Amazoniac

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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."
 
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dibble

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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...

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
 

Lucenzo01

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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

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.
 

dibble

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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.
Thanks, appreciate it.
 

haidut

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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.

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.
 
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Jarman

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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.

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?
 

haidut

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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?

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...
 

Regina

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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.
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!
 
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burtlancast

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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.

Candida Article #3: Conquering Candida:
"Magnesium is a vitally important mineral, a deficiency of which can lead to multiple biochemical and physiological perturbations, including immune impairment. It is, at the best of times, a difficult mineral to replete. As well as eliminating Candida overgrowth it is essential to give Magnesium in a form that is well absorbed. Over the years we have found that Magnesium Citrate citrate is one of the most bioavailable forms of magnesium but noted that citrus-derived magnesium citrate is not always acceptable to those intolerant of citrus fruit."

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?
 
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Amazoniac

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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?
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.
 
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burtlancast

burtlancast

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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.

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.
 
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Amazoniac

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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 establishment.
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.
 
EMF Mitigation - Flush Niacin - Big 5 Minerals

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