Travis

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I had a typo in the above comment.

It should have read : OPT (ortho-phospho-tyrosine as a metastatic cancer marker.

Eggs are no longer a concern for polyunsaturates. Separate out the yolks and blend the raw egg whites with orange juice, delicious.

The best way to separate out the yolks is using the egg shells, altering between cracked halves until the egg white is fully gone. Then place the shell and yolk back into the carton.
Someone needs to get a tallow‐fed chicken. (Their eggs are only ~8% linoleic acid!)
 

Amazoniac

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Ahh! So the right intestinal bacteria could form polyamines and then donate them to the human intestine in a relay fashion!

Interesting, but I think extracellular polyamines are less dangerous than intracellular methionine because they are destroyed by monoamine oxidase and polyamine oxidase. I am pretty sure that there are studies showing selenomethione inhibiting polyamine synthesis in the human cell:


Ah, here we go. Any doubts instilled by your comment will evaporate after viewing this table:

View attachment 8197

We have massive—massive!—reductions in the concentrations of polyamines spermidine and spermine (putrescine is just a diamine), two molecule types shown to increase dNA synthesis through inducing a left‐handed helix; these molecules take it halfway towards complete unfurlment.* The housekeeping genes cannot replicate quickly without spermine and proliferation is always inhibited by their absence (I have seen no exception to this). Spermidine is less effective at catalyzing dNA replication than spermine, and putrescine is ineffective—a paper tiger, dangerous only to the degree that it can later be polymerized to spermidine/spermine.

* Is that really a word?
de Fabolous,

The experiment shows you the endogenous effect, but there can be impairment of oxidation without action of the biogenic amines, the noxious smell tells you how toxic those compounds can be. Now perhaps 200mcg is too little to make a difference over time if you're addressing it the savage way, but the toxins can still react with the oxidative substances and render them useless, from nutrients to the bark quinones.

It makes no sense to push the ingestion that high if the person keeps ingesting plenty of methionine, I still think up to 100mcg is safer. But with methionine restriction, it can be another interesting experiment. Perhaps a period of restriction of methionine and selenomethionine is worth before starting the supplementation.
 

Travis

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de Fabolous,

The experiment shows you the endogenous effect, but there can be impairment of oxidation without action of the biogenic amines, the noxious smell tells you how toxic those compounds can be. Now perhaps 200mcg is too little to make a difference over time if you're addressing it the savage way, but the toxins can still react with the oxidative substances and render them useless, from nutrients to the bark quinones.

It makes no sense to push the ingestion that high if the person keeps ingesting plenty of methionine, I still think up to 100mcg is safer. But with methionine restriction, it can be another interesting experiment. Perhaps a period of restriction of methionine and selenomethionine is worth before starting the supplementation.
I think you found the answer to why selenomethionine is less toxic than selenide—per gram Se²⁻ atom. Since there appears to be no limit to how much methionine can be safely substituted by selenomethionine in the body (the Japanese have ~7× tissue levels), the toxicity appears to be dependent on Se²⁻ itself upon cleavage. I think its easy to get this this feeling from the the material we'd read in the past on selenium toxicity, where selenomethionine is about half as toxic and only when used in large amounts. If you keep the dose small, much more will be incorporated into the tissues and there will be less Se²⁻ release—perhaps the frantic effort by the body to metabolize the amino acid for energy; eliminating excess.

But the 200‧μg dose can probably be safely exceeded, what is essentially the upper limit for inorganic selenium. Selenomethionine seems to be about half as toxic as Se²⁻ in extreme doses, yet only about ¹⁄₅ as toxic in more reasonable doses. So perhaps 800‧μg would represent a fair upper limit?
 
OP
haidut

haidut

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Ahh! So the right intestinal bacteria could form polyamines and then donate them to the human intestine in a relay fashion!

Interesting, but I think extracellular polyamines are less dangerous than intracellular methionine because they are destroyed by monoamine oxidase and polyamine oxidase. I am pretty sure that there are studies showing selenomethione inhibiting polyamine synthesis in the human cell:


Ah, here we go. Any doubts instilled by your comment will evaporate after viewing this table:

View attachment 8197

We have massive—massive!—reductions in the concentrations of polyamines spermidine and spermine (putrescine is just a diamine), two molecule types shown to increase dNA synthesis through inducing a left‐handed helix; these molecules take it halfway towards complete unfurlment.* The housekeeping genes cannot replicate quickly without spermine and proliferation is always inhibited by their absence (I have seen no exception to this). Spermidine is less effective at catalyzing dNA replication than spermine, and putrescine is ineffective—a paper tiger, dangerous only to the degree that it can later be polymerized to spermidine/spermine.

* Is that really a word?

What is the active moiety in selenomethionine - is it selenium? If it is, that would explain the rapid regressions of cancer with high doses sodium selenide. There are several spectacular case reports on PubMed with 5mg selenium from soidum selenite.
 

Travis

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What is the active moiety in selenomethionine - is it selenium? If it is, that would explain the rapid regressions of cancer with high doses sodium selenide. There are several spectacular case reports on PubMed with 5mg selenium from soidum selenite.
For cancer, I think the active moiety is the entire amino acid. This is similar to methionine, can take its place in proteins, yet it cannot form polyamines. When added to cells directly, it will actually lower polyamine levels by about 50% simply due to competition.

But the Se⁻ is cleaved off and can effect redox status, so this limits the amount you can consume. This is a really good cancer drug regardless, and greatly lowers prostate cancer in studies. The fact that inorganic selenium also inhibits cancer but to lesser extent makes a strong case for the involvement of polyamines.
 

Obi-wan

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Selenomethionine induces apoptosis in cancer cells independent of polyamine restriction which it does as well!
 

Amazoniac

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Supporting Kochzord's observations. The guy is a beast.

http://www.tandfonline.com/doi/full/10.1080/03079450600711045

"Fermentative bacteria produce organic acids when oxygen is not available as a terminal electron acceptor, but they differ greatly in the types of acids that they produce. Because the oxidation of one molecule must be coupled to the reduction of another, anaerobic bacteria often produce several acids. The simplest fermentation is conversion of sugar to lactate, and many lactobacilli, streptococci, lactococci and enterococci have a scheme that is virtually homolactic when sugar is plentiful. However, when sugars are scarce, all of these bacteria are capable of switching to a fermentation that produces acetate, formate and ethanol, so ATP production can be enhanced. Butyric acid-producing bacteria typically utilize the hydrogenases of butyrate (or other even longer chain fatty acid) production as a mechanism of reducing equivalent disposal. If the bacterium has a hydrogenase, the interspecies hydrogen transfer to a methanogen decreases the need for dehydrogenase activity and acetate production typically is enhanced. Bacteria capable of utilizing fatty acids are found in stagnant anaerobic environments, but these bacteria grow very slowly, and fermentative environments are typically acidic. Fermentation acids are inhibitory when the pH is low but some bacteria are much more resistant than others."

"For many years it was assumed that bacteria maintained a slightly alkaline intracellular pH, but this assumption was largely based on work with laboratory cultures of E. coli (Padan et al., 1981). It is now clear that many fermentative bacteria have the ability to let their intracellular pH decline when the extracellular pH becomes highly acidic."

"The antimicrobial activity of organic acids on other bacterial species has not been correlated with intracellular pH regulation, but bacteria that could be classified as neutrophils seem to be more sensitive than those that are acid tolerant. For example, the minimal inhibitory concentration (MIC) of acetic acid is 250 times lower for Bacillus subtilis than for lactobacilli (Hsiao & Siebert, 1999).

The anion model of organic acid toxicity explains why bacteria differ in their sensitivity to organic acids, but it does not provide information on the antibacterial effect of one acid versus another. The MIC values for acetic, butyric, lactic and caprylic acid in E. coli are less than 4 g/l, but this same bacterium is approximately 10 times more resistant to malic acid, tartaric acid and citric acid (Hsiao & Siebert, 1999). This observation indicates that factors such as chain length, side chain composition, pKa values and hydrophobicity could affect the antimicrobial activity."

"It appears that supplemental acids are most apt to affect in the crop and gizzard rather than in the intestine. This point is illustrated in a study of Thompson & Hinton (1997), who fed laying hens a feed supplemented with a commercial mixture of formic and propionic acids. In these animals, pH values of the crop, gizzard, jejunum, caecum and colon were not altered relative to control animals, but formic acid and propionic acid concentrations in the crop and gizzard were significantly increased. At the same time, the lactic acid concentration in the crop decreased significantly, suggesting that lactobacilli were either inhibited or killed (Thompson & Hinton, 1997)."

"Recently, researchers have attempted to transport the organic acids further down in the gastrointestinal tract by micro-encapsulation, which should prevent absorption of the acids in the upper tract and ensure release further down in the gastrointestinal tract. Van Immerseel et al. (2004c) examined the effect of microbeads containing formic acid, acetic acid, propionic acid and butyric acid on colonization of S. Enteritidis in the caeca, liver and spleen. Animals were infected (day 5 post-hatch) with 5×103 cfu S. Enteritidis and samples were taken 3 days post-infection. Caecal colonization was significantly increased when acetic acid was added to the feed, but decreased when butyric acid was added. Internal organ colonization was increased if either formic acid or acetic acid were added to the feed, and this result is consistent with the idea that acids can enhance the virulence of Salmonella (see earlier)."

"Feed and drinking water sanitation, and the addition of acid to the crop, appears to prevent pathogen colonization in the live animals, but the type of acid and its concentration can be very important. Salmonella colonization of the caeca and internal organs is not always affected by these treatments, especially if the infection pressure is high. Acids from feed or drinking water are not effective further down in the intestinal tract because Salmonella colonization is mainly in the caeca (Desmidt et al., 1997). Because the caecum is the main fermentation site, the concentrations of SCFA are already higher there than in other intestinal segments (Engberg et al., 2002)." "If SCFA production in the caeca could be altered by changes in feed composition, producers would have a very cost-effective and efficient way of controlling Salmonella."

__
Gut Bacteria and Hydrogen Sulfide: The New Old Players in Circulatory System Homeostasis

"The proportion of H2S synthesis derived from bacteria and colonic tissue was examined by Flannigan et al. [84]. They have found that fecal samples of germ-free mice contained half of H2S in comparison to feces of controls. Furthermore, it was shown that the absence of vitamin B6, a CSE and CBS cofactor, in the diet resulted in a 50% reduction of fecal H2S. The deficiency of vitamin B6 in the diet significantly reduced fecal H2S levels, likely due to the inhibition of enzymatic H2S synthesis in colonic tissues. Interestingly, after six weeks of a vitamin B6-deficient diet, the fecal H2S levels returned to the same levels as in controls. This suggests that the H2S generation in the gut of germ-free mice was shifted towards nonenzymatic pathways by increasing the SRB activity [84]."

"In our studies, rats treated with neomycin (an antibiotic that does not cross the GBB and is used for intestinal decontamination in liver failure patients to reduce microbiota-produced NH3) exhibited significantly decreased levels of thiosulfate and sulfane sulfur, products of H2S oxidation, in portal vein blood plasma but not in peripheral blood plasma [11]. Furthermore, we found that intracolonic administration of Na2S (a H2S donor) increases portal blood levels of thiosulfate and sulfane sulfur, while no such significant effect was observed in peripheral blood. These findings imply that the liver may buffer the thiosulfate and sulfane sulfur pools in the organism, and suggest that systemic effects of colon-derived H2S and/or its derivatives may be in part due to some liver-dependent mechanisms [11]."

"it has been suggested that high colonic H2S levels may be responsible for colonic inflammation and cancer [73,85]."

"gut dysbiosis induced by chronic administration of nonsteroidal anti‑inflammatory drugs was reversed by exogenous H2S [88]."

"Interestingly, sulfate reduction and methanogenesis compete for the mutual substrate, which is H2. The methanogenesis/sulfate reduction ratio is dependent on substrate availability, thermodynamics and pH. In human colon, the ratio is in the favor of methanogenesis, due to neutral pH of stool and low sulfate levels in diet. However, in certain conditions, such as high availability of sulfate substrates in a diet (bread, beer, wine) and hypochlorhydria, sulfate reduction may become the major process [131,132]."

"Various bacteria, more than 85 species, can metabolize trypthophane and form indole. For example, the conversion of tryptophan into indole, pyruvate and ammonia is catalyzed by tryptophanase in E. coli [149]. Indole was detected in mammalian feces [150,151,152], and gut bacteria produce indole presumably by enzymes homologous to tryptophanases [33]. In the gut, indole is either oxidized by bacterial oxygenases or by cytochrome P450 to form indoxyl, which is further sulfonated in the liver to indoxyl sulfate (IS) and excreted with urine [149]."

__
Contribution of dietary protein to sulfide production in the large intestine: an in vitro and a controlled feeding study in humans 1 – 3 | The American Journal of Clinical Nutrition | Oxford Academic

"Although a variety of sulfur compounds are metabolized by gut bacteria, sulfide is generated in the human large intestine by 2 principal routes: first, by the action of sulfate-reducing bacteria on inorganic sulfur (sulfate and sulfite) (7) and second, through the fermentation of sulfur-containing amino acids (SAAs). The chief sources of sulfur in the diet are inorganic sulfate and the SAAs methionine, cysteine, cystine, and taurine. Sulfur also occurs naturally in the form of sulfur-containing glucosinolates in Brassica vegetables. Daily intake of inorganic sulfate is estimated to range from 1.5 to 16.0 mmol (8). Inorganic sulfur in the form of sulfite, sulfur dioxide, bisulfate, or metabisulfite is used routinely in the preservation of processed foods and beverages (9). SAA intake may vary with protein consumption. In addition to dietary sources, sulfated polysaccharides, such as mucin and chondroitin sulfate, are produced endogenously by the gastrointestinal tract."

"The biology of sulfur in the human gut has escaped serious attention until recently. Thus, little is known about the amounts and sources of sulfur in the diet and about the subsequent digestion and absorption of sulfur from the intestine. However, the microbial metabolism of sulfur is well understood and in anaerobic ecosystems, such as the large intestine, reduced sulfur compounds such as hydrogen sulfide, which are highly toxic, can be formed. Sulfide has been implicated in the pathogenesis of ulcerative colitis (23, 24) and may damage the colonic epithelium in several ways. The purpose of this study was to begin to ascertain which dietary components contribute to sulfide generation in the large bowel. Because SAAs are probably the major source of sulfur in the diet, we examined their effect."

"The main finding of this study was the significant, dose-related increase in fecal sulfide concentrations with meat intake, confirmed by in vitro modeling of protein fermentation. The main dietary contributor to protein intake in the present study was meat, but this relation between sulfide concentrations and meat may hold true for any protein source. Meat provides a ready source of protein for use in experimental studies. Silvester and Cummings (25) showed that it is the amount of protein in the diet rather than its source that determines the amount of protein reaching the colon."

"sulfide concentrations can increase dramatically with dietary change"

"The mean fecal sulfide concentration of the present group of volunteers with the 600-g[212g of proteid]/d diet was 3.38 mmol/kg. Deleterious effects of sulfide within the human colon, such as mucosal ulceration, goblet cell loss, apoptosis, and distortion of the crypt architecture, have been observed with concentrations of 0.5–1 mmol/L (3). Although the amount of meat consumed with the 600-g/d diet was much higher than the average UK intake of 150 g/d (EAM Magee, V Blokdijk, CJ Richardson, JH Cummings, unpublished observations, 1999), it is possible that a combination of dietary protein and sulfur oxoanion [S(IV)] additives in food may lead to fecal sulfide concentrations of this order."

"As early as 1905, Wendt (31) emphasized the importance of measuring urinary sulfur in studies of protein metabolism. Several studies showed that most of the sulfur excreted as urinary sulfate in humans results from the oxidation of the SAAs methionine and cysteine absorbed in the intestine and generated from tissue breakdown (32). Animal proteins are rich in both methionine and cysteine. When methionine and cysteine are metabolized, sulfate is released and excreted in urine."
 

Sheila

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Dear Amazoniac,

Some extraordinary finds here, thank you. Much to think upon.

Dr Koch suggested onions daily I believe and also small amounts of sodium sulphate to relieve constipation if necessary (whilst making sure that the real cause was being addressed). He was also not adverse to small amounts of vinegar, presumably to assist likely hypochlorhydria (?) in his patients.

I have taken sodium sulphate to see what it was like (at 195mg mane or BD) as it had an old, but competent, reputation for oedema, jaundice and biliary conditions. (Initially, it was used back then as the homeopathic: Nat. sulph)

It seems that sulphates can bat for either team depending on the context? Whodathoughtit? The dose response curve once again. Not too much, not too little, just right: like porridge.

Thank you dear one, your finds are a great help to me.
Sincerely,
Goldilocks.
 
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Amazoniac

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Dear Amazoniac,

Some extraordinary finds here, thank you. Much to think upon.

Dr Koch suggested onions daily I believe and also small amounts of sodium sulphate to relieve constipation if necessary (whilst making sure that the real cause was being addressed). He was also not adverse to small amounts of vinegar, presumably to assist likely hypochlorhydria (?) in his patients.

I have taken sodium sulphate to see what it was like (at 195mg mane or BD) as it had an old, but competent, reputation for oedema, jaundice and biliary conditions. (Initially, it was used back then as the homeopathic: Nat. sulph)

It seems that sulphates can bat for either team depending on the context? Whodathoughtit? The dose response curve once again. Not too much, not too little, just right: like porridge.

Thank you dear one, your finds are a great help to me.
Sincerely,
Goldilocks.
One of the challenges when the body has been congested for too long is that it harbors infections. The longer you stay congested, the more likely it's to get secondary ones, sometimes one cooperating with the other. This establishes a pattern that holds angelords back and prevents recovery. I've been thinking for quite some time on how to reverse this pattern in the intestines with direct intervention, and there's one possibility: through guavas.

Like it was mentioned maaany times, when carbs are exhausted from constipation, there are fatty and amino acids left to decay. When this occurs there's an adaptation to different fuels and microbes become very efficient in thriving on whatever happens to be around. Whenever a scarce carb comes in, the effect is a sharp consumption because it's rapid and available energy and there's a growth spur likely resulting in the generation of lactic acid as a consequence. Extreme food restriction will only serve to specialize any infection, I have already suggested that it's best to provide diverse tolerable fibers than single ones repetitively. At that point where carbs were constantly absent, they tend to specialize on the sulfur compounds. At the same time the intestines are being poisoned, and devitalized tissue should fuel the issue. These bacteria aren't as dependent on iron as others, so prolonged iron restriction won't work at all. A diet with milk as staple is not good for this pattern, it doesn't work. I've never read such thing being recommended by cancer shakals. As you read above, restoring balance through organic acid manipulation is difficult because they don't reach the infected areas, they're absorbed much earlier. In healthy gurus these acids are usually derived from leafy greens, but in unhealthy people the same fibers serve to feed the infections; especially if cooked since the plant defenses are destroyed.

I won't bother posting the miraculous properties of guavas because when we read these, the text sounds standardized for all fruits. However they're excellent: plenty of potassium and even an unusual amount of niacin. Some dates contain even more of both, the only problem is that they can feed present infections, it's no wonder they're classified as fermentable ("dates fodmap"). The vit C in guavas is the limiting factor though, it contains so much that it's possible to exceed, but thankfully not much is needed. They contain a lot of fiber, a safe type of fiber. When dehydrated it constitutes about 40-45% of its composition if I'm not wrong.

Warning, anthroquinorphism ahead:
Mild antimicrobials work best when combined with food because on the fasted state there's nothing interesting out there, so there's no point in lowering the guard. But when fuel is available, it's a choice: keep protected and starve or to drop the guard and feed (the gap in which antimicrobials work best). I think the leg gap from the other thread infected my thoughts.

In brief: whenever intestinal problems with sulfur are present, guavas are definitely worth considering. The detail is that they can't be cooked, and mature ones (instead of overripe) tend to be the best ones, they must be firm. If they're not available, it's possible to find them powdered, which I suspect it can work as well; must be good when combined with citrus juice.

Herb Doctors - Breast Cancer
Blesser said:
The foods that naturally contain anti-aromatases I think are very important. I always mention orange juice and guavas but there are lots of fruits and vegetables that contain similar chemicals.

Another big one, lisa!
 
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Sheila

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Messages
374
Dear Amazoniac,

Thank you for taking the time to write one of the best and most succinct expositions I have read on this subject, a matter that affects a great many people today and one which I have observed repeatedly.

When I first read this:-
Mild antimicrobials work best when combined with food because on the fasted state there's nothing interesting out there, so there's no point in lowering the guard. But when fuel is available, it's a choice: keep protected and starve or to drop the guard and feed (the gap in which antimicrobials work best).

I thought you meant initially the half-starved young women I have encountered who keep slim and SIBO at bay - seemingly - by very low calorie intake until they start eating properly once more and then their whole world changes and often, not for the better. Then I realised you meant the microbes. But, either way!

There does seem to me to be a difference in using potassium, calcium and sodium sulphates as opposed to multi-thiol natural products/supplements (as Andrew Cutler points out), as these were used for the deep seated infections of crevices; blind eruptions of skin and burdened liver conditions respectively. Thus we have potentially the remedy and the toxin. That Koch suggested onions - if tolerated - hints, perhaps, of the goldilocks nature of sulphur compounds here as well. Though I appreciate onions are poor wrt FODMAP considerations and many people are sensitive to this family. My mind then turns back to Mo. And disappointingly, I don't mean these FIVE.

I had never thought of guavas, but we do grow feijoas, a close relative and they are rather nice. Not sure if we'll get any this year given the dry conditions.
Thank you again for shining another light in dark crevices, most illuminating. My experiments will continue.
Sincerely
Sheila
 
L

lollipop

Guest
One of the challenges when the body has been congested for too long is that it harbors infections. The longer you stay congested, the more likely it's to get secondary ones, sometimes one cooperating with the other. This establishes a pattern that holds angelords back and prevents recovery. I've been thinking for quite some time on how to reverse this pattern in the intestines with direct intervention, and there's one possibility: through guavas.

Like it was mentioned maaany times, when carbs are exhausted from constipation, there are fatty and amino acids left to decay. When this occurs there's an adaptation to different fuels and microbes become very efficient in thriving on whatever happens to be around. Whenever a scarce carb comes in, the effect is a sharp consumption because it's rapid and available energy and there's a growth spur likely resulting in the generation of lactic acid as a consequence. Extreme food restriction will only serve to specialize any infection, I have already suggested that it's best to provide diverse tolerable fibers than single ones repetitively. At that point where carbs were constantly absent, they tend to specialize on the sulfur compounds. At the same time the intestines are being poisoned, and devitalized tissue should fuel the issue. These bacteria aren't as dependent on iron as others, so prolonged iron restriction won't work at all. A diet with milk as staple is not good for this pattern, it doesn't work. I've never read such thing being recommended by cancer shakals. As you read above, restoring balance through organic acid manipulation is difficult because they don't reach the infected areas, they're absorbed much earlier. In healthy gurus these acids are usually derived from leafy greens, but in unhealthy people the same fibers serve to feed the infections; especially if cooked since the plant defenses are destroyed.

I won't bother posting the miraculous properties of guavas because when we read these, the text sounds standardized for all fruits. However they're excellent: plenty of potassium and even an unusual amount of niacin. Some dates contain even more of both, the only problem is that they can feed present infections, it's no wonder they're classified as fermentable ("dates fodmap"). The vit C in guavas is the limiting factor though, it contains so much that it's possible to exceed, but thankfully not much is needed. They contain a lot of fiber, a safe type of fiber. When dehydrated it constitutes about 40-45% of its composition if I'm not wrong.

Warning, anthroquinorphism ahead:
Mild antimicrobials work best when combined with food because on the fasted state there's nothing interesting out there, so there's no point in lowering the guard. But when fuel is available, it's a choice: keep protected and starve or to drop the guard and feed (the gap in which antimicrobials work best). I think the leg gap from the other thread infected my thoughts.

In brief: whenever intestinal problems with sulfur are present, guavas are definitely worth considering. The detail is that they can't be cooked, and mature ones (instead of overripe) tend to be the best ones, they must be firm. If they're not available, it's possible to find them powdered, which I suspect it can work as well; must be good when combined with citrus juice.

Herb Doctors - Breast Cancer


Another big one, lisa!
LoL @Amazoniac. I soooooo was thinking that a few paragraphs up and how excellent the explanation. A few sentences later, I was sooo determined that I needed to comment and thank you :):
 
L

lollipop

Guest
thought you meant initially the half-starved young women I have encountered who keep slim and SIBO at bay - seemingly - by very low calorie intake until they start eating properly once more and then their whole world changes and often, not for the better. Then I realised you meant the microbes. But, either way!
I have seen this repeatedly @Sheila! Even at times on this forum. People come, early we’ll and suddenly all “problems” occur and they blame Ray’s diet...
 

Amazoniac

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LoL @Amazoniac. I soooooo was thinking that a few paragraphs up and how excellent the explanation. A few sentences later, I was sooo determined that I needed to comment and thank you :):
Both of you have clients, right?

I know it sounds too simple, but in theory it has many aspects in favor of being effective. I'm curious now to know if it works in practice indeed. For instance, the fruit can be consumed along with milk (or the powder added to it) to help overcome problems related to lactic acid bacteria. It even prevents the adhesion of problematic bacteria to the intestines.

One hint is that Danny Roddy posted on his Instagram a pic of guava jam. It can cause such a drastic change that it might explain why he can only tolerate them cooked.

I'm posting these because they discuss its composition in more details (it changes depending on the variety though and I suspect that white guavas are almost as good as red ones in terms of effectiveness):
- Chemical Components and Bioactivities of Psidium guajava
- Nutritional Composition and Volatile Compounds in Guava
- Psidium guajava: A review of its traditional uses, phytochemistry and pharmacology
- Flavonoid (Myricetin, Quercetin, Kaempferol, Luteolin, and Apigenin) Content of Edible Tropical Plants
- Thermal and structural study of guava (Psidium Guajava L) powders obtained by two dehydration methods
 
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L

lollipop

Guest
Both of you have clients, right?

I know it sounds too simple, but in theory it has many aspects in favor of being effective. I'm curious now to know if it works in practice indeed. For instance, the fruit can be consumed along with milk (or the powder added to it) to help overcome problems related to lactic acid bacteria. It even prevents the adhesion of problematic bacteria to the intestines.

One hint is that Danny Roddy posted on his Instagram a pic of guava jam. It can cause such a drastic change that it might explain why he can only tolerate them cooked.

I'm posting these because they discuss its composition in more details (it changes depending on the variety though and I suspect that white guavas are almost as good as red ones in terms of effectiveness):
- Chemical Components and Bioactivities of Psidium guajava
- Nutritional Composition and Volatile Compounds in Guava
- Psidium guajava: A review of its traditional uses, phytochemistry and pharmacology
- Flavonoid (Myricetin, Quercetin, Kaempferol, Luteolin, and Apigenin) Content of Edible Tropical Plants
- Thermal and structural study of guava (Psidium Guajava L) powders obtained by two dehydration methods
Definitely interesting and worth experimenting with...
 

Sheila

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Joined
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Messages
374
My dear Amazoniac,
Simple works for me and so I will experiment before tending to my remaining flock.
I appreciate you sharing your find and will report back in due course.
Sincerely,
Sheila
 

Amazoniac

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Joined
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Messages
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Location
Not Uganda
My dear Amazoniac,
Simple works for me and so I will experiment before tending to my remaining flock.
I appreciate you sharing your find and will report back in due course.
Sincerely,
Sheila
Quinones should help:
- A Quinone Formulation which Inhibits Evolution of Hydrogen Sulfide Because of Sulfate Reducing Bacteria

Salicylic acid derivatives:
- The Effect of 5-Aminosalicylic Acid–Containing Drugs on Sulfide Production by Sulfate-Reducing and Amino Acid–Fermenting Bacteria
- Antimicrobial effect of salicylamide derivatives against intestinal sulfate-reducing bacteria - ScienceDirect
- Activity of selected salicylamides against intestinal sulfate-reducing bacteria

- Salicylates in foods
apricots
berries (strawberries, etc)
cantaloupe
dates
grapes
guava
orange
pineapple
prunes

celery
cinnamon
dill
ginger
oregano
paprika
rosemary
turmeric
thyme

And finally, Lifepbuoy:
"nothing less than 99.9% germ protection"
 

Amazoniac

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Messages
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Not Uganda
Meat physiology, stress, and degenerative physiology.

"Muscle physiologists and endocrine physiologists know that fatigue, stress and excess estrogen can cause the tissues to swell hugely, increasing their weight and water content without increasing their protein content."

"There are many ways to increase the water content of meat, besides feeding estrogen to the animal and soaking the meat after slaughter. Everything that causes water retention and tissue swelling in the living animal, that is, every kind of stress, fatigue, poisoning, malnutrition and injury, will make the animal gain weight, without consuming expensive nutritious food. Crowding, fright, and other suffering increase water retention and accelerate the breakdown of fats and proteins."

"When grains and soybeans are used for fattening animals, their characteristic fatty acids are present in the meat, and are harmful to the consumer, but their complex degradation products, such as isoprene, acrolein, and isoprostanes, remain, along with the complex changes they induce in every aspect of the tissue. The reactive products of oxidative fat degradation stimulate, among other things, the adaptive/defensive production of polyamines, small molecules derived from amino acids. The polyamines, in turn, can be oxidized, producing highly toxic aldehydes, including acrolein (Sakata, et al., 2003). These molecules stimulate cell multiplication, and alter, at least temporarily, the way the cell's genes function.
An excess of water stimulates cell division, and an important mechanism in producing that effect is the increased production of polyamines by the enzyme ornithine decarboxylase. This enzyme is activated by an excess of water (hypotonicity), by estrogen, and by stress."

"Besides stimulating cell division and modifying the cell's state of differentiation (including developmental imprinting), the polyamines also contribute to nerve cell excitation and excitotoxicity."

"The polyamines are increased in cancers, and therapies to block their formation are able to stop the growth of various cancers, including prostate, bowel, and breast cancer. Metabolites of the polyamines in the urine appear to be useful as indicators of cancer and other diseases. (In pancreatic cancer, Yamaguchi, et al., 2004; in cervical cancer, Lee, et al., 2003; in adult respiratory stress syndrome, Heffner, et al., 1995.) The quantity of polyamines in the urine of cancer patients has been reported to be 20 times higher than normal (Jiang, 1990). Polyamines in the red blood cells appear to indicate prognosis in prostate cancer (Cipolla, et al., 1990)."

"In protein catabolism, one fate of the protein's nitrogen is to be converted to the polyamines, rather than to urea. In plants, at least, these small molecules help cells to balance osmotic stresses."

Commercial meat:
"Both the liver and the muscles contain a significant amount of glycogen when they are fresh, if the animal was healthy. At first, the lack of oxygen causes the glycogen to be metabolized into lactic acid, and some fatty acids are liberated from their bound form, producing slight changes in the taste of the meat. But when the glycogen has been depleted, the anaerobic metabolism accelerates the breakdown of proteins and amino acids."

"In the absence of oxygen, no carbon dioxide is produced, and the result is that the normal disposition of ammonia from amino acids as urea is blocked, and the polyamines are formed instead. The chemical names of two of the main poly-amines are suggestive of the flavors that they impart to the aging meat: Cadaverine and putrescine. After two or three weeks of aging, there has been extensive breakdown of proteins and fats, with the production of very complex new mixtures of chemicals."

"There is a lot of theorizing about the role of meat in causing cancer, for example comparing Japan's low mortality from prostate cancer, and their low meat consumption, with the high prostate cancer mortality in the US, which has a higher meat consumption. But Argentina and Mexico's prostate cancer mortality ranks very favorably with Japan's.

If meat consumption in the US contributes to the very high cancer rate, it clearly isn't the quantity of meat consumed, but rather the quality of the meat."

"Polyamines are increased in stressed and stored vegetables, as in aged meats. This defensive reaction retards tissue aging, and researchers are testing the application of polyamines to fruits to anyonebutdiokine their ripening."

"Although the diffusion of these stimulating factors from stressed tissues normally functions to accelerate healing and tissue regeneration, under less optimal conditions they are undoubtedly important factors in tissue degeneration and tumor formation. For example, the bystander effect (contributing to delayed radiation damage, and producing a field of precancerous changes around a cancer), in which substances diffusing from injured tissues damage surrounding cells, involves disturbances in polyamine metabolism.

The direct, optimal effects of the polyamines are protective, but when excessive, prolonged, or without maintained cellular energy, they become harmful."

"The brain is extremely different from a malignant tumor, and the derangements produced by stress, by high cortisol and estrogen and an excess of water, are different in the two types of organ (considering the tumor as an ad hoc organ), but the polyamines have central roles in the degenerating brain and in the divergent disorganization of tumors."

"Because of the great generality of genetic processes, it wouldn't be surprising if cold storage of vegetables turned out to produce polyamine patterns similar to those of cold storage meats. Air pollution and other stressful growing conditions cause vegetables to have very high levels of polyamines."

"Increasing carbon dioxide will tend to direct ammonia into urea synthesis, and away from the formation of polyamines. Bicarbonate protects against many of the toxic effects of ammonia, and since carbon dioxide spontaneously reacts with amino groups, it probably helps to inactivate exogenous polyamines. This could account for some of the protective effects of carbon dioxide (or high altitude), for example its anti-seizure, anticancer, and antistress effects.

Other things that protect against excessive polyamines are procaine and other local anesthetics (Yuspa, et al., 1980), magnesium, niacin, vitamin A, aspirin, and, in some circumstances, caffeine. Since endotoxin stimulates the formation of polyamines, a diet that doesn't irritate the intestine is important. Tryptophan and methionine contribute to the formation of polyamines, so gelatin, which lacks those amino acids and is soothing to the intestine, should be a regular part of the diet."
 
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