Panquinone - Liquid Triquinoyl/Quinone Mix For Lab/R&D

[Ell]

Possibly too much meabolism boost. The Koch recommendation was to use the quinones at most 2-3 times weekly, and taking every day with caffeine and other stimulants may be too much.

Hi, my understanding is that "the Koch recommendation" was to only administer a single injection, and that repetition of the dose would only be undertaken under certain particular circumstances. If the patient is properly prepared and has the diet down, the first febrile reaction should occur within three days, or on the 14th day. My view is that 2x, 3x weekly goes against Koch's teaching. However, I've seen quite a few folk repeating on a frequent basis, with more or less success also. Go figure....

 

[haidut]

Hi, my understanding is that "the Koch recommendation" was to only administer a single injection, and that repetition of the dose would only be undertaken under certain particular circumstances. If the patient is properly prepared and has the diet down, the first febrile reaction should occur within three days, or on the 14th day. My view is that 2x, 3x weekly goes against Koch's teaching. However, I've seen quite a few folk repeating on a frequent basis, with more or less success also. Go figure....

The reference I posted in the original thread, which claims to be Koch's own words, states that taking once every few days was also a protocol Koch used. It a long read but if you do Ctrl+F for "weekly" or "twice" or "days" you should be able to find it.
Dr. William Frederich Koch USA/Brazil, Drs. Erich & Dieter Reinstorff, Germany - Continued Research

 

[Ell]

Thanks. Apparently there is confusion on this. Keep in mind that all six late-stage patients done before the Detroit Medical Association were all cured with a single injection. Moreover, Dr. Koch repeatedly mentioned that the dose is only repeated in certain particular circumstances. The text below is all taken from "The Survival Factor in Neoplastic and Viral Diseases" published by Dr. Koch in 1961, after his having learned 40 years experience of his own technology. It may be true that for most people in the modern world, repetition will be necessary owing to myriad of factors most folk do routinely, that would tend to disrupt the free radical chain depolymerization reactions once started. Moreover, absolute purity of the water used is essential, and few appreciate how absolutely difficult it can be to produce such water, it is not simply to triple distill it, we have a lot more organic volatiles in our water these days than back then. The following are Dr. Koch's words from 1961, not mine. If you'd like a page number for any of the text, just ask :)

REPEATING THE TREATMENT

If the curative chemistry is started it must be allowed to go as far as it can before the dose is repeated.

Good medical judgment will tend rather to delay, than to repeat Treatment; for, if the Treatment is effective, like a key in a lock, one does not repeat the dose any more than one would stick another key in the hole while turning the key already there. Recovery may take months or years, and one dose has demonstrated its ability to act equally long. The dose is practically never repeated before the twenty-fourth week. Yet patients that have been heavily radiated may require a second dose on the fifteenth day, but only if they have given no response by way of reaction or improvement after the first dose.

Recovery is generally secured on one or two doses, but if the dose is to be repeated this is done during a negative phase only and at one of the divisional periods, such as the third, sixth, ninth, twelfth, twenty-fourth, thirty-sixth, sixtieth, and seventy-second week periods.

Lytic changes manifested by failure to crenate and their counterpart, the failure to build up the correct cell structure, point to a lack of energy production of the high efficiency type by the FCG. These changes mean that the FCG is blocked, and hence the Super FCG (the SSR) is needed to release it. This is a straight indication that either the Survival Super FCG (the SSR) administered has not finished its work to a safe point or that there is none working. One must decide between the two.

If there is reason to believe the SSR was blocked right at the start, the Treatment can be repeated right away three days to two weeks after the first dose. It may even be good policy to give a second dose at the end of the second week as a routine if no heavy febrile reaction was had 24 hours, 36, 72, or 84 hours after the Treatment. Repeating on the 14th or 15th day is good policy even if the crenation test shows only slight change.

Also, after the third week reaction is passed, failure of an improvement in the crenation test and in other changes in the patient indicate the need to repeat the dose. In that length of time it will not be much and there is much room for more. This is a different matter from repeating the dose at the sixth week or later since the improvement in the crenation test may be definite, but not 100%. But it may be the maximum for the patient at the time. So repeating the dose would then overload him. Therefore, never repeat if the patient is improving.

Repeating the dose in the first few days or at the end of the second week is more like giving a double dose at the start. It is better than that, as in these two weeks interferences may have neutralized or destroyed a big part of the Remedy, and repeating at the end of the second week would restore the lost part so the second dose would have cleaner ground to work on.

Nevertheless, one must balance up all the factors, the crenation test, the reduction in the size of the growth, the color change in the patient, that is, the loss of the hemolytic color, the gain in red cells and hemoglobin, improvement in the sedimentation test, etc. The appetite and gain in strength may be the best indicators as they speak for many specific changes such as those just mentioned. The quality of the pulse and respirations are also most valuable as is the ability to have a refreshing sleep. The improvements in taste, smell, and even in hearing, have the greatest significance. The old-fashioned doctor who knew how to observe his patient as a physiological complex knows what to look for. When such data is balanced with the crenation of the red cells, a correct decision on the need for dose-repetition can be reached. It is better to take one’s time and think.

 

[Obi-wan]

The first impression that one will probably have when looking at enzalutamide is that it could also be a PPAR agonist.

View attachment 7306

The ring in the middle is both similar to the prostaglandin J₂ ring (the endogenous high‐affinity ligand), and a thiazolidinedione—the classic PPAR agonist drugs.

View attachment 7308 click to embiggen

Its ability to bind the androgen receptor with high‐affinity is undeniable (Figure 2a), but it could also have undefined effects on the PPAR receptors. After all, there has to be way to explain why different antiandrogens have slightly different effects.

The activation of the PPAR receptors can be considered a good thing, and their first described function was to upregulate peroxisomes—small subcellular organelles which metabolize excessive prostaglandins and fats. I get the impression that the activation of these could represent the 'resolution stage' of inflammation—an idea which may depend on exactly which subtype of PPAR is activated. I am aware of four types: PPARα, PPARβ, PPARγ, and PPARδ. Of these four, PPARγ get the most attention . . . by far.


As a strong androgen receptor agonist, I would expect the dose to be rather small. The website indicates that 40 milligrams is commonly used, probably not enough for any pro-metabolic electron transfer to be perceptible. And if fact, the image above shows the thee known metabolites—metabolites that show no change in electron count or redox activity.

I think it would be safe to assume that the vast majority of changes noticed after taking it come from it's binding to the androgen receptor, but perhaps also a PPAR receptor—a suspicion supported by the close similarity of its inner thioxo-imidazolinone ring both to the thiazolidinedione drugs and the cyclopentanone prostaglandins.

Thanks @Travis.

So PPARs play essential roles in the regulation of cellular differentiation, development, and metabolism (carbohydrate, lipid, protein),[2] and tumorigenesis[3] of higher organisms and Cyclopentenone prostaglandins are a subset of prostaglandins (PGs) or prostenoids (see eicosanoid#classic eicosanoids and eicosanoid#nonclassic eicosanoids) that has 15-deoxy-Δ12,14-prostaglandin J2 (15-d-Δ12,14-PGJ2), Δ12-PGJ2, and PGJ2 as its most prominent members but also including PGA2, PGA1, and, while not classified as such, other PGs. 15-d-Δ12,14-PGJ2, Δ12-PGJ2, and PGJ2 share a common mono-unsaturated cyclopentenone structure as well as a set of similar biological activities including the ability to suppress inflammation responses and the growth as well as survival of cells, particularly those of cancerous or neurological origin. Consequently, these three cyclopentenone-PGs and the two epoxyisoprostanes are suggested to be models for the development of novel anti-inflammatory and anti-cancer drugs. The cyclopenentone prostaglandins are structurally and functionally related to a subset of isoprostanes viz., two cyclopentenone isoprostanes, 5,6-epoxyisoprostane E2 and 5,6-epoxisoprostane A2.

In laymen terms enzalutamide can metabolize PUFA and prostaglandins and cause cancer cell apoptosis with the only concern of a mutated AR while blocking androgens from attaching to the receptor. I am assuming it is the aromatizable androgens like testosterone and DHEA that need to be blocked even though all androgens would be blocked. This is being done at the same time Firmagon blocks LH (testosterone production) and FSH (aromatase production). My interpretations of LH and FSH.

A past Pub Med study indicated that Prostate cancer represents a mixture of androgen-dependent and androgen independent cells. Regarding androgen-independent tumor cells, beta-lapachone demonstrated very promising apoptosis-inducing affects. Would this apply to other Quinone's as well? Trying to cover my bases.

 

[Travis]

Thanks @Travis.

So PPARs play essential roles in the regulation of cellular differentiation, development, and metabolism (carbohydrate, lipid, protein),[2] and tumorigenesis[3] of higher organisms and Cyclopentenone prostaglandins are a subset of prostaglandins (PGs) or prostenoids (see eicosanoid#classic eicosanoids and eicosanoid#nonclassic eicosanoids) that has 15-deoxy-Δ12,14-prostaglandin J2 (15-d-Δ12,14-PGJ2), Δ12-PGJ2, and PGJ2 as its most prominent members but also including PGA2, PGA1, and, while not classified as such, other PGs. 15-d-Δ12,14-PGJ2, Δ12-PGJ2, and PGJ2 share a common mono-unsaturated cyclopentenone structure as well as a set of similar biological activities including the ability to suppress inflammation responses and the growth as well as survival of cells, particularly those of cancerous or neurological origin. Consequently, these three cyclopentenone-PGs and the two epoxyisoprostanes are suggested to be models for the development of novel anti-inflammatory and anti-cancer drugs. The cyclopenentone prostaglandins are structurally and functionally related to a subset of isoprostanes viz., two cyclopentenone isoprostanes, 5,6-epoxyisoprostane E2 and 5,6-epoxisoprostane A2.

In laymen terms enzalutamide can metabolize PUFA and prostaglandins and cause cancer cell apoptosis with the only concern of a mutated AR while blocking androgens from attaching to the receptor. I am assuming it is the aromatizable androgens like testosterone and DHEA that need to be blocked even though all androgens would be blocked. This is being done at the same time Firmagon blocks LH (testosterone production) and FSH (aromatase production). My interpretations of LH and FSH.

A past Pub Med study indicated that Prostate cancer represents a mixture of androgen-dependent and androgen independent cells. Regarding androgen-independent tumor cells, beta-lapachone demonstrated very promising apoptosis-inducing affects. Would this apply to other Quinone's as well? Trying to cover my bases.

I know that β-lapachone is cyclooxygenase inhibitor, but also the most powerful glyoxylase I inhibitor ever tested. Perhaps this means that some of this cellular transcription partially under the control of methylglyoxal? Thornally proved that methylglyoxal could modify an arginyl residue in a transcription factor leading to decreased VEGF, so I suppose it's possible.

Research in methylglyoxal is taboo, since it holds the key for cancer. Letting this cat out of the bag would collapse billion-dollar industries and dry-up research funds for thousands.

By your paragraph I'm almost left with the impression that the androgen receptor is under transcriptional control of one of the PPAR receptors? This could make more sense, since enzalutamide does not look like it would bind to the androgen receptor. But on reflection, I'm fairly certain that I saw a direct binding assay indicating that it does.

These nuclear receptors aren't as straightforward as we'd like to believe. They dimerize with other receptors, an can even chaperone heat shock proteins and immunophilins into the nucleus. These are also transcription factors, despite the fact they're not commonly referred to as such.

Perhaps the most logical idea is that the androgen receptor can be blocked by prostaglandin-like molecules in a separate, yet overlapping, binding domain. Assuming this to be true, this would make the androgen receptor itself under control of both steroid hormones and cyclopentenone prostaglandins. Even if false, this is an interesting thought.. . .

 

[Ell]

That's a great reply, and its great how much the understandings have been progressing. I admit I don't quite understand all the enzymes and language, but on the brighter side, I don't have to. :) Our good genius Dr. Koch laid it plain and simple about the FCG, its function, and how to prep and admin the remedy, and how the patients respond stastically re the febrile reaction, the periodicity of the positive and negative phases, the timelines, and even how photochromic effects from reflected circularly polarized light from the heavens may play a role. I truly appreciate postings like the one above, on the other hand, I don't need to know all those details, the answer is pretty simple :) The toughest part is preparing ultra pure water, wow, what a lesson that provides. What amazes me is that few who write on many forums ever expound on the real deal of what Dr. Koch did, I mean, its not that complicated. D6 with the benzoquinone, D9 or 12 or even D30 with glyoxal / methylglyoxal, and do it in pure water, 2cc's. Why is that so hard to comprehend for the masses, I'll never understand. The recipient is "prepared" a week in advance of the treatment by cecal cleansing and then the diet restriction, no big deal. The ampuoles from commercial sources are isotonic, which won't work. I won't name company names who peddle carbonylgruppen and other like substances having NaCl in the formula, but that is totally wrong obvioiusly to anyone with a brain cell. Here is wisdom for you - what happens when pure water hits a cell, it bursts, spewing its contents, reverse crenation, the cell wall explodes and all the protoplasm and other unknowns become to be in contact with the D6, D12 material, etc. THAT is where the remedy begins - the nascently-released protoplasms react with the glyoxylide, and that is whenceforth you get the actives that do the work. The isotonic remedies peddled by various companies containing NaCl, are NOT Koch remedies. Like... duh. :) The hypotonic nature of the triply-distilled water combined with the infinitesimal amounts of reagent is what gets the goat. See Wagner, Kreher, Jurcic in Arzneimittel-Forschung 38(1): 273-275 (1988). No big deal there, we saw a lot of Dr. Koch's genius later proven, most of the "cancer" diets are based on his writings. :))))) Its only the isotonic solutions peddled by the companies that need repeat doses mostly, except for the cases Dr Kock wrote about which I put up in my message above. This totally works on 85+% of what most people encounter, be it "cancer", MS, diabetes, or whatever, which is exactly why "they" hounded him so long, losing three (3) times in a "federal" court. "They" don't hound true "quacks", that's how you know, - "by their actions, ye shall know them" - someone once wrote.

 

[Travis]

That's a great reply, and its great how much the understandings have been progressing. I admit I don't quite understand all the enzymes and language, but on the brighter side, I don't have to. :) Our good genius Dr. Koch laid it plain and simple about the FCG, its function, and how to prep and admin the remedy, and how the patients respond stastically re the febrile reaction, the periodicity of the positive and negative phases, the timelines, and even how photochromic effects from reflected circularly polarized light from the heavens may play a role. I truly appreciate postings like the one above, on the other hand, I don't need to know all those details, the answer is pretty simple :) The toughest part is preparing ultra pure water, wow, what a lesson that provides. What amazes me is that few who write on many forums ever expound on the real deal of what Dr. Koch did, I mean, its not that complicated. D6 with the benzoquinone, D9 or 12 or even D30 with glyoxal / methylglyoxal, and do it in pure water, 2cc's. Why is that so hard to comprehend for the masses, I'll never understand. The recipient is "prepared" a week in advance of the treatment by cecal cleansing and then the diet restriction, no big deal. The ampuoles from commercial sources are isotonic, which won't work. I won't name company names who peddle carbonylgruppen and other like substances having NaCl in the formula, but that is totally wrong obvioiusly to anyone with a brain cell. Here is wisdom for you - what happens when pure water hits a cell, it bursts, spewing its contents, reverse crenation, the cell wall explodes and all the protoplasm and other unknowns become to be in contact with the D6, D12 material, etc. THAT is where the remedy begins - the nascently-released protoplasms react with the glyoxylide, and that is whenceforth you get the actives that do the work. The isotonic remedies peddled by various companies containing NaCl, are NOT Koch remedies. Like... duh. :) The hypotonic nature of the triply-distilled water combined with the infinitesimal amounts of reagent is what gets the goat. See Wagner, Kreher, Jurcic in Arzneimittel-Forschung 38(1): 273-275 (1988). No big deal there, we saw a lot of Dr. Koch's genius later proven, most of the "cancer" diets are based on his writings. :)))))

Yeah. Koch and Szent-Györgyi were right; Warburg was right; Thronally and Ray were right. I have read dozens of cancer studies and methylglyoxal is the best. Also very effective is inhibiting the enzyme which normally destroys it. I think most people are trained by public school to be subservient, and fall into the archetypes that mass media promotes. Most probably can't wrap their head around the idea that modern medicine is actually profit driven and archaic—not archaic in terms of technology, a the technology is highly advanced, but archaic in terms of biological paradigms and understanding. People in the '60s knew more useful things about cancer than most anyone today; ideas that were simply not included in textbooks. Like Linus Pauling, they couldn't argue against Szent-Györgyi—he was right, and he had a Nobel Prize. All they could do is get people to look the other way.

They've been doing it ever since. You just have to have enough faith in yourself to trust your instincts, the obvious science, the undeniable data, and realize that many oncologists are capable of lying to people's face—with no remorse.. . . ..Or at least be extremely misleading.

So how does methylglyoxal work? It's up to us to decide. Nobody is working on this, and nobody is creating mechanisms. Thornally will explain all that is known, but there's much left to explain. Methylglyoxal will add to arginine forming an imidazolone ring; pretty amazing. This means that any enzyme or transcription factor with an arginine in its active site could be under the control of methylglyoxal. The cell has a steady-state concentration of methylglyoxal, and nothing correlates with cell growth and cancer better. What is amazing about it is that high levels do not effect normal cells, but simply transform cancerous cells to normal. There is really nothing quite like it.

All enzymes that bind NADH have an argine residue which interacts with the cofactor's diphosphate. High levels of methylglyoxal could prevent this binding, releasing the cofactor, and slowing down the entire citric acid cycle. This could be a simple way in which methylglyoxal throttles metabolism—by disabling glycolytic enzymes when the glycolytic products (methylglyoxal) become too high.

Koch started it all, and Szent-Györgyi was well-aware of him. Thornally followed after Szent-Györgyi and still publishes articles. The one published just a few years ago was the most amazing methylglyoxal study yet.

I realize that the quinones are important—and you'd need the B vitamins of course—but I find methylglyoxal the most interesting. I see it as a cellular control mechanism that nobody sees as such—a way for the cell to sense its glycolytic rate through key arginine residues on proteins.

 

[Ell]

Lets get straight on this. Szent-Georgyi only went the free-radical mechanism way, after Koch , but S-G and everybody else in the gang saw what Fishbeind did to Koch. After Hoxsey had Fisbein step down, a short window of "free speech" opened, but S-G stepped cautiously. That's all I need to know. I don't need historical political details, only thing I needed was to know the political dweebs wouldn't have gone after Koch for 40 friggin years, had Koch had nothing. And I've seen proven over and over, Koch realy does cure cancer and all those other conditions that lack oxidative vigor. There is NO mystery about this, it works 80+ % and you can kick it up to 99% if you've been reading. Simple. Prepare the patient. Then D6 BZQ. Or D9 with glyoxal / me-glyoxal. Many other reagents work but Koch used the gly/me-gly at D9 over 40 years with the same curative resluts. No need to talk about enzymes, blah blah. For $35 worth of reagent, I could treat the entire population of the USA. Duh. Now you understand why they cut him, because its a $1 trillion a year cockammammie industry that is based on fraud and falsehood. Those people who pulled this sht off should be HUNG FOR TREASON, against the People of the United States of America , and the whole world, they need to be brought to Justice. that's why they're so gung ho to go after people's .22 rifles, et cet. Its as if they expect to be brought down, which they should and will be for covering up Dr. Koch's great works, by our Lord, I do ask


Edit, please forgive me for not having mentioned, that Dr. Koch proved Warburg wrong, on his thesis of the irreversibility of cancer.
The good German Koch presented it philosophically at first by noting that some cases went into "remission" by themselves. That in itself proves that Our Lord had shown us that it is definitely reverisble, and those who can't conceive that cognitively, don't belong in this Field. All that remained was the "why" about it. For that, all that needs be looked at are the early studies on the parathyroidectomies of the dogs. Those not up on this, I'd implore for them to look further, there is a gold mine there with the guanadines, that even a simple BS such as myself can see :)

 

[Travis]

Lets get straight on this. Szent-Georgyi only went the free-radical mechanism way, after Koch , but S-G and everybody else in the gang saw what Fishbeind did to Koch. After Hoxsey had Fisbein step down, a short window of "free speech" opened, but S-G stepped cautiously. That's all I need to know. I don't need historical political details, only thing I needed was to know the political dweebs wouldn't have gone after Koch for 40 friggin years, had Koch had nothing. And I've seen proven over and over, Koch realy does cure cancer and all those other conditions that lack oxidative vigor. There is NO mystery about this, it works 80+ % and you can kick it up to 99% if you've been reading. Simple. Prepare the patient. Then D6 BZQ. Or D9 with glyoxal / me-glyoxal. Many other reagents work but Koch used the gly/me-gly at D9 over 40 years with the same curative resluts. No need to talk about enzymes, blah blah. For $35 worth of reagent, I could treat the entire population of the USA. Duh. Now you understand why they cut him, because its a $1 trillion a year cockammammie industry that is based on fraud and falsehood. Those people who pulled this sht off should be HUNG FOR TREASON, against the People of the United States of America , and the whole world, they need to be brought to Justice. that's why they're so gung ho to go after people's .22 rifles, et cet. Its as if they expect to be brought down, which they should and will be for covering up Dr. Koch's great works, by our Lord, I do ask


Edit, please forgive me for not having mentioned, that Dr. Koch proved Warburg wrong, on his thesis of the irreversibility of cancer.
The good German Koch presented it philosophically at first by noting that some cases went into "remission" by themselves. That in itself proves that Our Lord had shown us that it is definitely reverisble, and those who can't conceive that cognitively, don't belong in this Field. All that remained was the "why" about it. For that, all that needs be looked at are the early studies on the parathyroidectomies of the dogs. Those not up on this, I'd implore for them to look further, there is a gold mine there with the guanadines, that even a simple BS such as myself can see :)

Yeah. They ran Koch out of the country because he was actually curing cancer. He would have put them all out of a job, so they attacked him with slander and back-handed tactics—the same way the always do.

Koch was a medical doctor, and also had a PhD in chemistry. Albert Szent-Györgyi only had a PhD in (bio)chemistry, so he couldn't have legally treated people if he had tried.* He certainly got the word-out more than anyone had, and had published over ten articles on methylglyoxal alone. This is more than anyone besides Thornally.

Adding the Koch approach to the Gerson diet would be the best, I would think. You could do something similar with all-natural glyoxylase I inhibitors and L-threonine, which can raise natural methylglyoxal levels without having to source it externally. Our bodies make our own methylglyoxal from either glucose, glycerol, or L-threonine.

What happened to the dogs given parathyroidectomies? and why do you mention guanidines?

(Methylglyoxal selectively reacts with guinidine to form an imidazolone. You might expect higher levels of guinidines in the urine of cancer patients due to low methylglyoxal.)


*Although he did cure rats with methylgloxal (after giving them cancer first).

 

[Koveras]

@Obi-wan @Travis

2pence here

I posted this study on oxandrolone below previously -

It seems that an "empty/unbound androgen receptor" is the worst thing as far as glucocorticoid signalling - and that even androgen antagonists interacting with the androgen receptor can reduce that glucocorticoid signalling.

Tempting to speculate that part of the benefit seen with both androgens and androgen antagonists in prostate cancer is through that mechanism.

Oxandrolone blocks glucocorticoid signaling in an androgen receptor-dependent manner. - PubMed - NCBI

The anabolic steroid oxandrolone is increasingly used to preserve or restore muscle mass in those with HIV infection or serious burns. These effects are mediated, in part, by the androgen receptor (AR). Anti-glucocorticoid effects have also been reported for some anabolic steroids, and the goal of our studies was to determine whether oxandrolone had a similar mechanism of action. Studies with in vitro translated glucocorticoid receptor (GR), however, showed no inhibition of cortisol binding by oxandrolone. Conversely, experiments in cell culture systems demonstrated significant antagonism of cortisol-induced transcriptional activation by oxandrolone in cells expressing both the AR and GR. Inhibition was not overcome by increased cortisol concentration, and no inhibition by oxandrolone was observed in cells expressing GR alone, confirming that non-competitive mechanisms were involved. AR-dependent repression of transcriptional activation by oxandrolone was also observed with the synthetic glucocorticoids dexamethasone and methylprednisolone. Furthermore, the AR antagonists 2-hydroxyflutamide and DDE also repressed GR transactivation in an AR-dependent manner. A mutant AR lacking a functional nuclear localization signal (AR(4RKM)) was active in oxandrolone-mediated repression of GR even though oxandrolone-bound AR(4RKM) failed to enter the nucleus and did not affect nuclear import of GR. These data indicate a novel action of oxandrolone to suppress glucocorticoid action via crosstalk between AR and GR.

Very interesting, thanks. So, based on the study both AR agonists and antagonists may be able to suppress glucocorticoid effects and without directly displacing cortisol from the receptor. Btw, pregnenolone does something similar in a receptor independent way - i.e. it does not block cortisol from binding to the receptor but blocks translocation of the bound steroid/receptor complex to the cell nucleus, which in effects prevents cortisol's genomic effects. Progesterone does both - displaces cortisol from the receptor and blocks translocation to the nucleus. DHEA is 11b-HSD1 inhibitor and 11b-HSD2 activator. I guess the androgen receptor crosstalk is yet another mechanism for opposing cortisol, which means that a progesterone + DHEA + strong androgen combo would be really good as it address all of these pathways.

 

[Ell]

Adding the Koch approach to the Gerson diet would be the best, I would think. You could do something similar with all-natural glyoxylase I inhibitors and L-threonine, which can raise natural methylglyoxal levels without having to source it externally. Our bodies make our own methylglyoxal from either glucose, glycerol, or L-threonine.

I think to look at the timing of publication of the diet of Dr. Koch, and Gerson's work, it might be found that Gerson derived his diets from Dr. Koch. On the methylglyoxal, keep in mind that Koch employed it hypotonically in the range of between at one part per billion and one part per 10(^ -14). In view of the Wagner et al. article I cited above, more me-glyoxal is not better, if it is too much it will not function the same as if in those ranges and employed hypotonically. There are many works concerning me-glyoxal but they do not operate in the way Koch's reagents function.
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What happened to the dogs given parathyroidectomies? and why do you mention guanidines?

In general they all convulsed and died, the urine contained elevated levels of Ca, Phos. and guanadine and me-guanadine, which Dr. Koch identified as toxins able to react with the functional carbonyl groups of the natural immunity of the reticulo-endothelial system by imine condensation to form azomethine bonds. When molecular oxygen is absent locally, this leads to the toxins also binding to the unsaturated bond adjacent to the functional carbonyls. This results in loss of charge transfer to the blood colloid, and the destruction of the blood zeta potential, which was the cause of the coagulation found in the dogs post mortem. This was all verified by another group in Edinburg, who were awarded some academic prize or other. These articles are published on the williamfkoch(dot)com website.
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(Methylglyoxal selectively reacts with guinidine to form an imidazolone. You might expect higher levels of guinidines in the urine of cancer patients due to low methylglyoxal.)

I don't personally believe that is the mechanism responsible for the recoveries, although those reactions can occur. It is the tiny amounts of the reagents in the presence of nascently-released protoplasm and other material from the ruptured cells in the presence of the reagents. "More" is not always "better", especially in this case. Again, seek the Wagner et al. article that verified Koch's work 70 years after Koch discovered it.
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*Although he did cure rats with methylgloxal (after giving them cancer first).
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That might be, but he didn't need to use rats, the six stage IV patients before the Detroit Medical Board were cured in 1920, and he had plenty of human subjects to work on both then and thereafter.. Given the reagents being 99.999999999% water, harm could not have been done. Those interested will find the same reagents worked on a myriad of other conditions, and the common denominator was established between ailments such as cancer, diabetes, ms, bubonic plague, syphillis, gonnorhea, sarcomae, hoof and mouth, cholera, etc. Its all in his case histories, some in the Congressional Record, and the Canadian cattleman's association.
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The modus operandi of the forces against Koch was the same as used against Roy Rife and Harry Hoxsey. Typically, those naughty people will not go after modalities which are ineffective, so the mere fact they went after these people is strong suggestion itself that there was efficacy present in each instance.

 

[Wagner83]

, except for the cases Dr Kock wrote about which I put up in my message above.

???

 

[Ell]

In the link below, provided by T. Hesselink, MD , one can click on #8 at the left, and then scroll down to see a graphic from the Wagner et al. article referenced above, which illustrates that more is not always better. What we find for example is that benzoquinone is cytotoxic at higher concentrations, whereas when employed at the concentrations used by W.F. Koch MD, the effect was immunostimulating. So, for example, throwing a bunch of me-glyoxal at something, is not the same as a nanogram dilution of the same substance in water of extreme purity administered i.m. or subcutaneously. Oxidative Catalytic Therapy

 

[Travis]

In the link below, provided by T. Hesselink, MD , one can click on #8 at the left, and then scroll down to see a graphic from the Wagner et al. article referenced above, which illustrates that more is not always better. What we find for example is that benzoquinone is cytotoxic at higher concentrations, whereas when employed at the concentrations used by W.F. Koch MD, the effect was immunostimulating. So, for example, throwing a bunch of me-glyoxal at something, is not the same as a nanogram dilution of the same substance in water of extreme purity administered i.m. or subcutaneously. Oxidative Catalytic Therapy

Methylglyoxal is different, since it's made all the time in the body. We have two enzymes which get rid of it called glyoxylase I & II. These enzymes are expressed everywhere and exists in such high amounts that methylglyoxal barely works when taken internally, because it's detoxified so fast. This is why injections are much more effective, and also why using a glyoxylase I inhibitor (lapachol) could be a better approach; raising natural concentrations within the cell. There's little to be afraid of when it comes to methylglyoxal, we all probably made kilograms of it ourselves from glucose over the last year.

But I can see how quinones can be abused. We need electron transfer, but I'd think that to much could cause noise. A low methionine and linoleic acid diet coupled with B vitamins, quinones, and methylglyoxal seems to be a winning combination. Koch was the first to realize this, so everyone who came later—Albert Szent-Györgyi an Paul Thornally—owes him a debt of gratitude.

Cancer has been understood for decades, and not nearly as terrifying as they try to make you believe (to scare you out of thousands of dollars before you can even begin to think rationally about your circumstance.)

 

[Travis]

@Obi-wan @Travis

2pence here

I posted this study on oxandrolone below previously -

It seems that an "empty/unbound androgen receptor" is the worst thing as far as glucocorticoid signalling - and that even androgen antagonists interacting with the androgen receptor can reduce that glucocorticoid signalling.

Tempting to speculate that part of the benefit seen with both androgens and androgen antagonists in prostate cancer is through that mechanism.

That's bizarre: the way that androgens inhibit the glucocorticoid receptor. I was thinking at first that they are inhibiting it in the nucleus by completing for DNA or transcription factors, but it works even when the androgen receptor doesn't even enter the cell. The effects of androgens seem totally confusing.. . .

Perhaps it's binding to one of the PPAR receptors; scientists unaware, as the PPARs are not being measured. I there any other way to explain that paragraph above? I have the suspicion that testosterone binds to PPARδ.

Perhaps examining the effects of this drug could give insights into this.

Ye, Ji‐Ming. "PPARδ agonists have opposing effects on insulin resistance in high fat‐fed rats and mice due to different metabolic responses in muscle." British journal of pharmacology (2011)
​

Vitamin D appears to be a ligand for PPARδ. This could help explain some of its anabolic effects.

Dunlop, Thomas W. "The human peroxisome proliferator-activated receptor δ gene is a primary target of 1α, 25-dihydroxyvitamin D₃ and its nuclear receptor." Journal of molecular biology (2005)​

 

[Obi-wan]

Hi @Travis,

Since we are on the Panquinone thread, what are your thoughts on
Triquinoyl hydrate: 3 mcg
Naphthoquinones: 1 mg

which are the ingredients.

And while we are the subject how about Methylene Blue?

Lapodin also has emodin as well as Lapachol.

Since you stated that Lapachol "is the most powerful glyoxylase I inhibitor ever tested" is their synergy with the others I mentioned or will it just create "noise"?

By the way, the price tag on Xtandi is $9700/month. Luckily my co-pay is $20/month. I like that it is a PPAR agonist. I don't understand how androgen receptor blocking works other than blocking aromatase. PSA did come down quickly

Interesting what @Koveras said "It seems that an "empty/unbound androgen receptor" is the worst thing as far as glucocorticoid signalling - and that even androgen antagonists interacting with the androgen receptor can reduce that glucocorticoid signaling. When would the androgen receptor ever be unbound?

Further discussions could involve modulation of signal transduction pathways such as intracellular Ca2+ levels and PKC. Also Bcl-2 and p53.

Looking for discussions on all of the ways that induce or enhance the apoptotic response of prostate cancer cells.

Sorry for all the questions but I feel that this thread has attracted some superstars! Sometimes It s hard to decipher what you guys say but I do my best as a laymen to keep up.

 

[Travis]

Hi @Travis,

Since we are on the Panquinone thread, what are your thoughts on
Triquinoyl hydrate: 3 mcg
Naphthoquinones: 1 mg

which are the ingredients.

And while we are the subject how about Methylene Blue?

Lapodin also has emodin as well as Lapachol.

Since you stated that Lapachol "is the most powerful glyoxylase I inhibitor ever tested" is their synergy with the others I mentioned or will it just create "noise"?

By the way, the price tag on Xtandi is $9700/month. Luckily my co-pay is $20/month. I like that it is a PPAR agonist. I don't understand how androgen receptor blocking works other than blocking aromatase. PSA did come down quickly

Interesting what @Koveras said "It seems that an "empty/unbound androgen receptor" is the worst thing as far as glucocorticoid signalling - and that even androgen antagonists interacting with the androgen receptor can reduce that glucocorticoid signaling. When would the androgen receptor ever be unbound?

Further discussions could involve modulation of signal transduction pathways such as intracellular Ca2+ levels and PKC. Also Bcl-2 and p53.

Looking for discussions on all of the ways that induce or enhance the apoptotic response of prostate cancer cells.

Sorry for all the questions but I feel that this thread has attracted some superstars! Sometimes It s hard to decipher what you guys say but I do my best as a laymen to keep up.

Methylene blue can act as a methyl donor. Under my theory of neutrotransmitter action, this could potentially give it slight stabilizing and anesthetic effects.

I don't think that methylene blue can transfer two electrons like the quinones, but I think it can transfer one. Albert Szent-Györgyi's book called "Bioenergetics" has much information on 'charge transfers.' All this simply means is two molecules interacting and transferring one electron only. Their electronic orbitals must overlap for this to occur, and is more selective that the redox two-electron transfers. I would guess that it interacts with flavin, or some other molecule capable of one-electron charge transfer. I think I remember Szent-Györgyi having written something similar himself. The ability of methylene blue to rescue respiration in the presence of inhibitors proves that it can transfer electrons, to something, somehow—probably one-at-a-time.

I think it's neat that you have triquinoyl. That molecule looks like one hell of an electron acceptor. It makes you wonder how it's metabolized?

But I think that methylglyoxal is unique because it's a dicarbonyl, giving it the ability to add to arginyl and guinidine residues. I think this is it's main function, and I think so does Thornally. This is a bit different idea than how Koch and Szent-Györgyi had imagined it worked. I think it inhibits cancer by interacting directly with the glycolytic enzymes. All glycoltic enzymes have an arginyl group which attracts the phosphodiester bridge of their cofactor NADH. This is a simple interaction: the positive charges of arginine attracting the negative charges of the phosphodiester. I have looked, and all of the NADH enzymes appear to have the arginyl residue in this location. Methylglyoxal covalently binds to arginyl residues forming a fluorescent imidazolone. You would expect this, if it would occur, to disable an NADH-containing enzymes ability to bind its cofactor. These methylglyoxal—argine covalent adducts (imidazolone) have been well characterized and certainly exist. This is, after all, why blood proteins of diabetics are fluorescent. There has even been talk of using L-arginine to mop-up excessive methylglyoxal in the blood of diabetics.

Diabetics don't have less cancer rates because the extra methylgloxal isn't within the cell, of course, but without.

Lapachol binds glyoxylase I very strongly, but β-lapachone does even slightly more. These both come from the same tree, and there is much more elaborate data on β-lapachone (if you would like to search for one of them.) You can find scientific studies on β-lapachone by straight-laced, hard-headed East Coast academics showing it's superiority over anything else.

I know that emodin is a descent 11β-HSD₁ inhibitor, but it looks like it's redox active as well. The more I read about drugs the more I get the impression that they often interact in multiple ways. Keep in mind that the 11β-HSD₁ enzyme is bidirectional, and can work in either direction depending on what body site it's found.

I've been noticing a few relationships between PPARδ receptors and androgens, and nonpolar steroids. The PPARδ receptor has a relatively large binding domain and appears far less selective than the steroid receptors. I am getting the impression that some PPARs can bind steroids, and I just came across a study showing that PPARδ can bind vitamin D. The nuclear receptor PPARδ is not very well studied, so I'm kind of alone with this idea—but I plan on keeping it in the back of my head, keeping an eye out for other connections (should I see any).

 

[Koveras]

Interesting what @Koveras said "It seems that an "empty/unbound androgen receptor" is the worst thing as far as glucocorticoid signalling - and that even androgen antagonists interacting with the androgen receptor can reduce that glucocorticoid signaling. When would the androgen receptor ever be unbound?

When androgen levels are low

 

[Travis]

When androgen levels are low

Like in finasteride-induced chemical castration?

 

[Koveras]

That's bizarre: the way that androgens inhibit the glucocorticoid receptor. I was thinking at first that they are inhibiting it in the nucleus by completing for DNA or transcription factors, but it works even when the androgen receptor doesn't even enter the cell. The effects of androgens seem totally confusing.. . .

Perhaps it's binding to one of the PPAR receptors; scientists unaware, as the PPARs are not being measured. I there any other way to explain that paragraph above? I have the suspicion that testosterone binds to PPARδ.

Perhaps examining the effects of this drug could give insights into this.

Ye, Ji‐Ming. "PPARδ agonists have opposing effects on insulin resistance in high fat‐fed rats and mice due to different metabolic responses in muscle." British journal of pharmacology (2011)
​

Vitamin D appears to be a ligand for PPARδ. This could help explain some of its anabolic effects.

Dunlop, Thomas W. "The human peroxisome proliferator-activated receptor δ gene is a primary target of 1α, 25-dihydroxyvitamin D₃ and its nuclear receptor." Journal of molecular biology (2005)​

"Recently, Schug et al. showed that when the cellular retinoic acid binding protein-II (CRABP-II) expression levels were higher than FABP5 in the cells, retinoic acid (RA) bound to CRABP- II. Subsequently, CRABP-II relocated to the nucleus and delivered RA to RAR, resulting in inhibition of cell proliferation and induction of apoptosis. On the contrary, when the FABP5 to CRABP-II ratio is high, RA serves as a physiological ligand for PPARδ, which induces cell survival and proliferation. Therefore, it is important to identify the cytosolic ligand binding proteins and the expression levels of the proteins for defining the physiological effects of ligands.

The Role of PPARs in Cancer