Problems With Sulphur

[LUH 3417]

I seem to have problems with sulphur--both in terms of food and supplements.

I am continual problems with low copper and low selenium, to the point that my thyroid swells if I do not consume enough and I get very strong low copper symptoms. If I eat high sulphur foods, it is a constant struggle to get enough selenium and copper. My experiments with whey protein have had me feeling like my memory is completely going. I am only 28.

I am a rock climber and train 4-5 times a week. Whenever I have consumed taurine I end up with quire severe finger tendon injuries. I react poorly to garlic, b1, cruciferous veg, egg (very bad). I often can have gas that is very smells strongly of sulphur.

Any ideas, solutions, recommendations? I am vaguely familiar with concepts such as CBS mutation, methylation but there are many schools of thought that dismiss CBS mutations as false.

I really need to keep my selenium and copper high. My thyroid really suffers otherwise.

Have you made any progress or discovered anything regarding your problems with sulfur?

 

[chrismturner89]

Nope. Other than selenium brings my thyroid swelling down.

Im sure its related to some kind of cbs gene mutation or bacterial composition in my gut but it is really hard to tell.

 

[LUH 3417]

Nope. Other than selenium brings my thyroid swelling down.

Im sure its related to some kind of cbs gene mutation or bacterial composition in my gut but it is really hard to tell.

I suspect I may have something similar. Did you ever experiment with the flower of sulfur remedy?

 

[Dave Clark]

Does anyone know if using MSM will antagonize copper, and possibly reduce ceruloplasmin? When you look at what minerals oppose each other I notice it is stated that sulfur and copper are supposed to, according to what I read. So, if one is trying to increase their bio-available copper, should they not use MSM or eat high sulfur foods? I haven't been able to get a good answer to this question. I am wondering if all the people using high dosses of MSM are unwittingly lowering their copper/ceruloplasmin? Most report good effects in the near term for joints, pain, energy, detoxing, etc., but are they eventually going to pay the price, similarly to what high zinc would do.

 

[LUH 3417]

Last year I did the flower of sulfur remedy and came down with a flu like fever and body ache syndrome soon after. The fatigue seemed to last for months, I went for a labs and had elevated viral titers. It took me a long time to get out of that fatigue, was feeling significantly more energetic after taking sublingual b12, a b complex and getting lots of sun and walking.
I had a bag of MSM at home and decided to try it. I know MSM is not the same as flowers of sulfur but it did not make me feel very good, wired feeling and night sweats plus I woke up smelling like cat pee from I guess ammonia.
To further my experiment and test my sulfur capacity, a few days later I took flowers of sulfur 1/2 tspn similar to what I did last year. I felt horrible, had hydrogen sulfide smelling gas and BM, the worst headache, and terrible thoughts. I think it is clear I have a bacterial overgrowth, but like @Amazoniac posted regarded restricting foods, I do not want to make the bacteria more resilient. I also don’t want to induce a copper deficiency which I may have done last year when I took the flowers of sulfur and had extensive bruising all over my legs.

 

[Amazoniac]

Last year I did the flower of sulfur remedy and came down with a flu like fever and body ache syndrome soon after. The fatigue seemed to last for months, I went for a labs and had elevated viral titers. It took me a long time to get out of that fatigue, was feeling significantly more energetic after taking sublingual b12, a b complex and getting lots of sun and walking.
I had a bag of MSM at home and decided to try it. I know MSM is not the same as flowers of sulfur but it did not make me feel very good, wired feeling and night sweats plus I woke up smelling like cat pee from I guess ammonia.
To further my experiment and test my sulfur capacity, a few days later I took flowers of sulfur 1/2 tspn similar to what I did last year. I felt horrible, had hydrogen sulfide smelling gas and BM, the worst headache, and terrible thoughts. I think it is clear I have a bacterial overgrowth, but like @Amazoniac posted regarded restricting foods, I do not want to make the bacteria more resilient. I also don’t want to induce a copper deficiency which I may have done last year when I took the flowers of sulfur and had extensive bruising all over my legs.

- The inhibition of mitochondrial cytochrome oxidase by the gases carbon monoxide, nitric oxide, hydrogen cyanide and hydrogen sulfide: chemical mechanism and physiological significance

 

[Amazoniac]

- Philippe Haouzi | ResearchGate
↳ Hydrogen Sulfide Toxicity: Mechanism of Action, Clinical Presentation, and Countermeasure Development

@haidut - This guy is working on an article that might interest you, entitled 'Methylene blue as an antidote against hydrogen sulfide intoxication'.

 

[Amazoniac]

- Dietary Factors in Sulfur Metabolism and Pathogenesis of Ulcerative Colitis

"In IL-10 knockout mice, a common murine model of IBD, a diet high in saturated fat increases the presence of taurine-conjugated bile acids, leading to an expansion of the sulphite-reducing pathobiont Bilophila wadsworthia and a greater severity of inflammation [20]. High fat diets also promote intestinal inflammation in rats as well as adenoma formation in the presence of a mutagen [44]. A high protein diet in a similar model increases SRB abundance and sulfide production and decreases the abundance of bacterial taxa associated with SCFA production and the amount of butyrate in stool [45]. Similarly, a high protein diet has been associated with post-weaning diarrhea in piglets [46]. Taken together, a high protein and saturated fat diet (characteristic of a western, animal-based diet) seems to result in an increased capacity for H2S production, decreased capacity for butyrate production, and a potential to cause intestinal inflammation."

"[..]low dietary sulfur interventions generally emphasize transitions to a plant-based, semi-vegetarian diet. While all these experiences describe positive outcomes, conclusions are limited given the small patient numbers."

"Dietary input and small intestinal absorption are considered the main determinants of sulfur delivery to the colon [19]. The small intestine has an efficient but saturable dietary sulfate absorptive capacity of ~5–7 mmol/day [62]. Once dietary sulfate intake exceeds ~5–7 mmol/day the amount reaching the colon increases linearly with intake. Therefore, the amount of dietary sulfur that reaches the colon, particularly with increasing levels, can be generally assumed to parallel dietary intake. A number of additional factors, however, such as food preparation (e.g., cooked versus uncooked, cooking temperature and method, ground versus whole), meal consumption habits (e.g., chewing), and transit time have been shown to influence small intestinal absorption of sulfur-containing molecules and the total amount of sulfur reaching the colon [63–67]."

"Intestinal mucins are glycoproteins that form a mucus barrier along the epithelial surface of the gastrointestinal tract. The primary intestinal mucin MUC2 contains cysteine amino acids as core components of its structure [39,70]. Glycosylation of mucin proteins makes up a substantial portion of their size and provides protection of the peptide backbone and the gel-forming capacity [70]. The glycosylation pattern of mucin varies along the intestinal tract with increasing sulfation moving distally through the small intestine and into the colon [71,72]. The colonic mucus barrier is predominately composed of sulfomucins with a trend toward slightly diminished sulfation moving distally (100% sulfation in the right colon and 86% in the rectum) [73]. The normal sulfation pattern is altered in UC and is associated with the concentration of SRB [73]."

"The genus Desulfovibrio is regarded as the most abundant SRB in humans [83]. Despite the focus on Desulfovibrio spp. as the primary producer of H2S in the human gut, the number of microbial groups known to be capable of dissimilatory sulfate reduction continues to expand [82,84]. Many of these microbes can also reduce sulfite, dithionite, thiosulfate, elemental sulfur, and several thionates."

"Although sulfate intake and quantity of SRB has been the primary focus of the H2S toxin hypothesis, there is a growing appreciation for the contribution of protein intake to H2S production. The efficiency of protein degradation is greatest in the distal colon and at neutral to alkaline pH, which suggests a possible relationship with the pathogenesis of UC [90]. A cross-over diet study conducted by Magee and colleagues demonstrated that dietary protein intake positively correlates with fecal sulfide concentrations in healthy individuals [78]."

"A recent in vitro study that profiled gas production from incubated fecal samples implicated cysteine specifically as a primary driver of H2S production—conversely, the effect of sulfate was small [81]."

"Fermentation of digestible carbohydrate results in the production of SCFA and a drop in luminal pH in the colon relative to the small intestine [102–104]. Increased dietary fiber also results in faster intestinal transit [105]. Indeed, the colon pH is lowest proximally and increases distally, which is likely driven by the decreasing availability of digestible carbohydrate [102]. Mildly acidic pH, characteristic of the proximal colon, is inhibitory to the growth of SRB, but favors the growth of methanogens and some butyrate producers [30,106,107]. In contrast, sulfate reduction and H2S production are optimal at an alkaline pH [108]."

"Although a small amount of H2S present in the lumen of the colon is able to be cleared through flatus [110], the primary pathway for H2S clearance is via intracellular sulfide oxidation. Interestingly, this pathway may be facilitated by cyanide, which has been proposed by Levitt and colleagues to explain the well-documented beneficial role of smoking in UC [111]."

"The addition of fermentable fiber to healthy human feces in an in vitro setting drastically reduces H2S production from any source (e.g., cysteine, sulfate) [81]. Lower pH associated with microbial carbohydrate fermentation also leads to inhibition of dissimilatory aromatic amino acid metabolism [125]. Interestingly, stool pH is lower in vegan and vegetarian individuals relative to omnivores, consistent with greater abundance of carbohydrates in the proximal colon, faster colon transit, and higher delivery of SCFA to the distal colon [126]. This finding underscores the importance of overall diet composition when considering the relative proportions of dierent end-products of microbial metabolism."

"Although there is little data supporting a direct role of dietary fat in the H2S toxin hypothesis, animal fat was shown in a murine model to result in increased production of taurine-conjugated bile acids and a bloom of the sulfite-reducer Bilophila wadsworthia in the colonic microenvironment [127]. A high fat diet in mice is associated with lesser production of SCFA and greater production of H2S, even when the protein content of high fat chow is lower relative to regular chow [128]."

"The most significant source of endogenous sulfur (both as sulfate and cysteine) is intestinal mucin. The mucous layer of the colon is composed of two layers [40], the microbiota is abundant in the outer loose mucous layer, while the inner dense mucous layer—largely devoid of bacteria—maintains a barrier between the colonic microbiota and colonocytes [39,40]."

"The role of carbohydrate, and more specifically fermentable carbohydrate, intake within the H2S toxin hypothesis may be its overall impact on protein degradation by colonic bacteria. These findings are supported by a diet study in healthy volunteers [148], where administration of metronidazole effectively reduced SRB counts, but fecal concentration of H2S remained unchanged. In contrast, consumption of fermentable fiber (oligofructose) resulted in a decrease in fecal H2S, concomitant increase in SCFA concentrations, but failure to influence SRB counts. The impact of fiber on microbial H2S production is further supported by recent data demonstrating a decrease in SRB with a high brassica diet (sulfur-containing vegetables) [149]. Although brassica vegetables are technically considered to be high sulfate foods, they also have a high fiber content."​

They also discussed means of detoxification, which involve coenzyme Q and glutathione.

But starving this kind of infection is a lost battle, these microbes will turn to bile/mucus without difficulty. What needs to be done instead is restoration of bowel movements and reacidification. I suspect that temporary use of anything that works as laxative is helpful but the diet must provide safe fermentable carbs along.

Magnesium hydroxide is an example of common laxative but it can backfire. There are alternatives that are preferable such as orange juice with sodium bicarbonate or renew'd antidote C doses until bowling intolerance.

These options can be useful (and you'll know when they're not):

• Pineapple
• Celery root/stalk
• Beetroots
  
• Apple (or its juiceless fiber added to other recipes)
• Berries
• Custard apple family fruits (even soursop)
• Bell pepper (the deeper the color, the stronger it tends to be)
• Cocoa (you can experiment with low-fat options if normal is punishing, goes well with milch)
• Incidental resistant starch
  
• Supplemental lactose with edible fruit skins

It's worth considering legumes as well, some people do fine with them and the ones with less demanding preparation are usually milder.
Vinegar is great, and will make up for a possible deficiency of acetate, but won't reach the affected regions.

 

[Amazoniac]

- Carrageenan - Wikipedia

"Carrageenans or carrageenins [] are a family of linear sulfated polysaccharides that are extracted from red edible seaweeds. They are widely used in the food industry, for their gelling, thickening, and stabilizing properties. Their main application is in dairy and meat products, due to their strong binding to food proteins. There are three main varieties of carrageenan, which differ in their degree of sulfation. Kappa-carrageenan has one sulfate group per disaccharide, iota-carrageenan has two, and lambda-carrageenan has three."​

 

[Amazoniac]

Regarding the previous post, given that most of iodine is adsorbed from the stomach or upper small intestine, if the indigestible parts of seaweed happen to contain some iodine, it's a good way to deliver it farther down the intestines to function as antimicrobial. This could also minimize the problems that occurs when it's used isolated as gum.

 

[Amazoniac]

@Kartoffel, remember this post?

I was thoughting the other day that perhaps it's a viable approach to try to identify our most problematic fermentable foods and what's the common element in them. Later, try to find out if raw plants containing them improve the situation. If they don't, search if there's anything available on the market that sort of extracts the fermentable component while leaving the antimicrobials, because it's precisely these that will be the most beneficial for targeting the infection, those that protect what yerms are using to thrive.

Maybe the antimicrobials could've contributed to the shaping noted here:

- Consumption of a diet rich in Brassica vegetables is associated with a reduced abundance of sulphate-reducing bacteria: A randomised crossover study

"Brassica vegetables are a rich source of fibres and vitamins, and contain relatively high amounts of sulphur-containing compounds[,]" "are a significant source of inorganic sulphate in the diet [17], and it is conceivable that diets rich in these vegetables may encourage the growth of SRB, with potentially negative health consequences due to the proinflammatory activity of H2S."

"Florin et al. reported that ~0.22 g of dietary sulphate per day can be absorbed in the small intestine, with any additional dietary sulphate reaching the colon where it would be available for utilisation by SRB [25]."

"This study found that the Brassica-rich diet was not associated with an increase in lactobacilli, but was associated with a decrease in the relative proportions of SRB, compared to the low-Brassica diet (Fig. 1)."

"A high-protein diet has been reported to lead to proportional increases in SRB and faecal sulphide [30], which have been linked with an increased likelihood of relapse in ulcerative colitis patients [31, 32]. Conversely, a study investigating the effects of inorganic sulphate-supplemented drinking water in mice did not find significant increases in intestinal sulphate or H2S concentration, suggesting no significant increase in SRB activity [33]. The authors postulated that inorganic sulphate (as is found in Brassica vegetables) was not a determining factor in H2S production associated with SRB, and that H2S generated from sulphur-containing amino acid dissimilation may be primarily responsible for the majority of intestinal H2S [33]. It was also reported that increased supplementation of drinking water with inorganic sulphate correlated with an increased density of sulphomucin-containing goblet cells in mice, linking dietary inorganic sulphate with an increase in the sulphation of mucins within the large intestine. The results of this study suggest that the high consumption of Brassica vegetables reduced the abundance of SRB. Further studies could examine whether a high-Brassica diet may also be associated with a regeneration of the human intestinal mucosa."​

Unexpect'd, isn't it?

 

[Kartoffel]

@Kartoffel, remember this post?


Maybe the antimicrobials could've contributed to the shaping noted here:

- Consumption of a diet rich in Brassica vegetables is associated with a reduced abundance of sulphate-reducing bacteria: A randomised crossover study

"Brassica vegetables are a rich source of fibres and vitamins, and contain relatively high amounts of sulphur-containing compounds[,]" "are a significant source of inorganic sulphate in the diet [17], and it is conceivable that diets rich in these vegetables may encourage the growth of SRB, with potentially negative health consequences due to the proinflammatory activity of H2S."

"Florin et al. reported that ~0.22 g of dietary sulphate per day can be absorbed in the small intestine, with any additional dietary sulphate reaching the colon where it would be available for utilisation by SRB [25]."

"This study found that the Brassica-rich diet was not associated with an increase in lactobacilli, but was associated with a decrease in the relative proportions of SRB, compared to the low-Brassica diet (Fig. 1)."

"A high-protein diet has been reported to lead to proportional increases in SRB and faecal sulphide [30], which have been linked with an increased likelihood of relapse in ulcerative colitis patients [31, 32]. Conversely, a study investigating the effects of inorganic sulphate-supplemented drinking water in mice did not find significant increases in intestinal sulphate or H2S concentration, suggesting no significant increase in SRB activity [33]. The authors postulated that inorganic sulphate (as is found in Brassica vegetables) was not a determining factor in H2S production associated with SRB, and that H2S generated from sulphur-containing amino acid dissimilation may be primarily responsible for the majority of intestinal H2S [33]. It was also reported that increased supplementation of drinking water with inorganic sulphate correlated with an increased density of sulphomucin-containing goblet cells in mice, linking dietary inorganic sulphate with an increase in the sulphation of mucins within the large intestine. The results of this study suggest that the high consumption of Brassica vegetables reduced the abundance of SRB. Further studies could examine whether a high-Brassica diet may also be associated with a regeneration of the human intestinal mucosa."​

Unexpect'd, isn't it?

I think the bacteria specialize in using the organic compounds from amino acids to reduce the sulphur. However, in this study with pigs they found that adding inorganic calcium-sulfate to their diet increased the amount of SBR in the colon, but curiously not in the small intestine. The high-sulphur diet also increased inflammation quite a bit. Unfortunately, they didn't measure H2S but it seems reasonable to assume that it was increased, at least in the colon. The difference to the study that is mentioned in your paper (reference 33) might be that they fed the pigs a lot of CaSO4 (5%).
The production of H2S from protein is why changed my mind on protein quite a bit. Eating less protein energizes me and eating to much at a time (>20g) gives me tremendous brain fog.

Sci-Hub | | 10.2527/jas.2010-3228

Sci-Hub | | 10.2527/jas.2010-3228

 

[Amazoniac]

I think the bacteria specialize in using the organic compounds from amino acids to reduce the sulphur. However, in this study with pigs they found that adding inorganic calcium-sulfate to their diet increased the amount of SBR in the colon, but curiously not in the small intestine. The high-sulphur diet also increased inflammation quite a bit. Unfortunately, they didn't measure H2S but it seems reasonable to assume that it was increased, at least in the colon. The difference to the study that is mentioned in your paper (reference 33) might be that they fed the pigs a lot of CaSO4 (5%).
The production of H2S from protein is why changed my mind on protein quite a bit. Eating less protein energizes me and eating to much at a time (>20g) gives me tremendous brain fog.

Sci-Hub | | 10.2527/jas.2010-3228

Sci-Hub | | 10.2527/jas.2010-3228

Guru, left and right where I live there's a case of carbon monoxide poisoning; people are not used to heaters, so when they travel to cold places, they don't know the precautionary measures. A family just recently deaded themselves due to this.

From the link posted here, only hydrogen sulfide is malodorous, the rest can be irritating but they don't give an off odor (including methane, which is odorless), making it unreliable to use as guide to unsafe levels of exposure (hence the unsuspect'd carbon monoxide poisonings).

- Methane production in anaerobic digestion of organic waste from Recife (Brazil) landfill: evaluation in refuse of diferent ages

"Although the landfill odor is the result of a complex mixture of several compounds (Stretch et al., 2001), the most representative among them in terms of odor is hydrogen sulfide (H2S) (Kim et al., 2005; Kim, 2006), together with other organosulphur compounds, aldehydes and carboxylic acids. The combination of the individual odors of these compounds (all with different limits of detection) gives the characteristic odor of the landfill gas (Karnik et al., 2003; Odorizzi et al., 2003). USEPA (1991) observed that the landfill odor originates both from the refuse degradation process (decomposition anaerobic phases) and from the previously disposed refuse in the landfill (painting products, solvents, pesticides, adhesives, etc.). This odor results mainly from chemical groups such as organosulphur compounds, esters, alkylbenzenes, limonene (Inaut, 2019), among other hydrocarbons responsible for the characteristic landfill odor. For Senante et al. (2003), the odor of landfills has as main sources the leachate, fresh refuse and biogas. In this case, the odorant compounds can belong to the following chemical groups: sulphur compounds, nitrogen compounds, aldehydes, acids, ketones, alcohols, aromatic compounds, esters, and chlorinated compounds. Still, although hydrogen sulfide is the main odorant present in landfill gas, due to its very low limit of odorant perception, other compounds are also responsible for the characteristic landfill odor (Haarstad et al., 2003)."

"Sulfate, for example, during the methanogenic phase (in anaerobic conditions), is reduced to sulfide (Reinhart and Townsend, 1998), which subsequently combines with hydrogen in the environment to form hydrogen sulfide (H2S) (Tchobanoglous et al., 1993). In the acid phase, a phase prior to the methanogenic, the microbiological activity accelerates the produc-tion of organic acids, generating hydrogen gas in low concentrations. When the methanogenesis takes place in the biodigestion process, these acids, as well as the H2 (H2S precursor), are gradually converted into CH4 and CO2. This reduction in acids and hydrogen concentrations raises the pH in the environ-ment, leading it to neutrality (range of 6.8 to 8.0) (Tchobanoglous et al., 1993)."

"It is relevant to highlight that the H2S is an odorant in its molecular form, while under basic con-ditions H2S formation is inhibited (the ionized forms of sulfide are prevalent), controlling the formation of odor due to sulphur compounds (Gostelow and Parsons, 2001)."

"Because the process in the biodigesters was anaerobic since the beginning of the experiment, high concentrations of H2S (a reduced compound) were simultaneously verified; this fact was confirmed by the strong rotten egg smell, characteristic of this gas (Gostelow et al., 2003; Mbuligwe, 2005), observed in all samplings. Even with the reduction in H2S gas concentrations along the biodigestion, the values observed remained far above the olfaction perception limit (0.0011 ppm, according to Summer, 1971) and toxicity for this compound (10 ppm – time weighted average, according to OSHA, 2012). As the human olfaction system is able to detect extremely low concentrations of odorant gases, many times below the detection limits of analytical instruments (Senante et al., 2003), considering the H2S concentration values observed here, one can see that the olfactometric analysis in this study (if this option was made as a complement to the analytical instrumental determination) would be unnecessary, given that the concentration values are hundreds of times superior to the threshold odor. The permanent strong intensity odor could even be dangerous to the health of the olfactometric jury because the concentration values were tens of times above the toxicity limit in all phases of the biodigestion evaluated.

"Besides the odor issue, it is important to emphasize that elements such as sulfide act as inhibitory agents in the anaerobic digestion process (Chen et al., 2008). Under anaerobic conditions, sulfate is reduced to sulfide through the action of sulfate-reducing bacteria (SRB), which will compete for the substrate with the methane-producing bacteria (MPB), resulting in lower methane production during the methanogenic phase (Harada et al., 1994; Isa and Anderson, 2005; Karhadkar et al., 1987)."​

Why has we evolved such a low threshold for detection of hydrogen sulfide? To shy us away from stuff that's under significant decomposition by microbes that thrive on flesh?

If you search for those phases of decomposition, there's first the acetogenic phase where vinegary bacteria thrive on acidic conditions, later developing to the methanogenic and sulfidogenic phase when there's more extensive organic matter decay. It's as if beings are being (?) degraded and returned to their environment to restart the pboyologic cycle. Whatever is going on in the source of smell, it can't be good, so let's avoid it.

I think it was CLASH that was doing flavored enemas, and acetic/butyric acid are worth considering (very low doses initially).

 

[Amazoniac]

People that use massive doses of antidote C will have a great portion escaping digestion serving to acidify the intestines.
- What Would You Do To Heal Your Microbiome?

 

[Amazoniac]

From Koch's 'Neoplastic And Viral Parasitism -- Their Basic Chemistry And Its Clinical Reversal':

"The initiating toxin could be one of the sulfydryl products of certain bacteria, trapped within occluded tonsilar crypts, the apical infection of teeth, or some occluded scarred sinus of long standing. Sulfydryl readily forms free radicals upon dehydrogenation by the FCG; and it also has the ability to add to the double bonds of ethylenic linkages conjugated with Carbonyl groups. It can therefore interfere with oxidations in several ways, for it can inactivate the quinone type co-enzymes as Co-enzyme Q-10, which is an electron carrier or transfer agent. As when one closes a culture of such bacteria taken from a focus of infection, just mentioned, it soon shows the development of malodorous mercaptans. In like manner, it may also add to the FCG’s activating system to initiate pathogenesis."

"The practical meaning of the vegetarian diet is seen in the cases of the leukemia blood depletion, where 50 transfusions could not keep the blood up to a normal or even half of a normal level, but without even one transfusion, each of these cases gained to a normal blood count only on vegetables, fruits, and cereals, without any medications whatever. Their gain took a few months, but it was observable within one month after the Treatment was given and the diet put into action. Mr. J. K. gained two pounds a day for a month. Mrs. Mac A. did as well and so have countless others.

On this same diet patients have reduced to a healthier weight after the Treatment gave the oxidation they needed. So diet and oxidation capacity determine tissue efficiency and health. Nature is always beautiful when unimpeded. It is joyous and rewards one for dietary care.

Early in our experience, we noted that patients whose homes were in Mt. Clemens, just 20 miles from Detroit, did not do well under Treatment for cancer after they returned to their homes. The recovery process was reversed. This we found was due to the sulfides in the water, and we noted that asparagus that contains methyl mercaptan was as obstructive to recovery, too. The sulfydryl group adds readily to the double bond that activates the FCG of energy production and of energy acceptance, and not only is its function thus blocked, but the addition serves, as we believe, the synthetic carcinogens act to initiate carcinogenesis, as is explained earlier. Very small amounts of mercaptans are physiologically active. Methyl mercaptan is active in one part per 50 billion, and in more concentrated doses, causes blistering and paralytic effects. It blocks the production of rhodopsin in the retina from vitamin A. Like other sulfydryls, it can inactivate such essential electron carriers as the quinones now known to be oxidation co-enzymes. And they readily reduce Oxidizing Agents to become disulfides. They easily inactivate iodine and thus, cripple the oxidation mechanism and serve as do its sister compounds containing selenium, to block oxidations of surviving tissue slices in the Warburg Chamber. Needless to say, the diet and bowel hygiene must be guarded against the sulfydryl group, and groups that inactivate sulfydryl, will prove helpful in combating cancer. Potassium iodide, and such plants as the dandelion, and the chamomile flowers are thus good intestinal aids."

"One great function of bacteria is to convert dead animal tissues into food for plants, whether the dead animal product is in the ground or in the colon. And it is certain that a large part of the ingested meat is not digested and absorbed completely before it reaches the colon. The toxins evolved paralyze the bowel wall and cause diverticulae. These hold putrid material for varying periods among which the toxic amines are transition bodies. Diamine oxidase present in the intestinal wall and liver combats them, more or less successfully. But in the presence of excessive sulfydryl groups also formed during the putrefaction, the diamine oxidase may also be inactivated."​

 

[Kartoffel]

From Koch's 'Neoplastic And Viral Parasitism -- Their Basic Chemistry And Its Clinical Reversal':

"The initiating toxin could be one of the sulfydryl products of certain bacteria, trapped within occluded tonsilar crypts, the apical infection of teeth, or some occluded scarred sinus of long standing. Sulfydryl readily forms free radicals upon dehydrogenation by the FCG; and it also has the ability to add to the double bonds of ethylenic linkages conjugated with Carbonyl groups. It can therefore interfere with oxidations in several ways, for it can inactivate the quinone type co-enzymes as Co-enzyme Q-10, which is an electron carrier or transfer agent. As when one closes a culture of such bacteria taken from a focus of infection, just mentioned, it soon shows the development of malodorous mercaptans. In like manner, it may also add to the FCG’s activating system to initiate pathogenesis."

"The practical meaning of the vegetarian diet is seen in the cases of the leukemia blood depletion, where 50 transfusions could not keep the blood up to a normal or even half of a normal level, but without even one transfusion, each of these cases gained to a normal blood count only on vegetables, fruits, and cereals, without any medications whatever. Their gain took a few months, but it was observable within one month after the Treatment was given and the diet put into action. Mr. J. K. gained two pounds a day for a month. Mrs. Mac A. did as well and so have countless others.

On this same diet patients have reduced to a healthier weight after the Treatment gave the oxidation they needed. So diet and oxidation capacity determine tissue efficiency and health. Nature is always beautiful when unimpeded. It is joyous and rewards one for dietary care.

Early in our experience, we noted that patients whose homes were in Mt. Clemens, just 20 miles from Detroit, did not do well under Treatment for cancer after they returned to their homes. The recovery process was reversed. This we found was due to the sulfides in the water, and we noted that asparagus that contains methyl mercaptan was as obstructive to recovery, too. The sulfydryl group adds readily to the double bond that activates the FCG of energy production and of energy acceptance, and not only is its function thus blocked, but the addition serves, as we believe, the synthetic carcinogens act to initiate carcinogenesis, as is explained earlier. Very small amounts of mercaptans are physiologically active. Methyl mercaptan is active in one part per 50 billion, and in more concentrated doses, causes blistering and paralytic effects. It blocks the production of rhodopsin in the retina from vitamin A. Like other sulfydryls, it can inactivate such essential electron carriers as the quinones now known to be oxidation co-enzymes. And they readily reduce Oxidizing Agents to become disulfides. They easily inactivate iodine and thus, cripple the oxidation mechanism and serve as do its sister compounds containing selenium, to block oxidations of surviving tissue slices in the Warburg Chamber. Needless to say, the diet and bowel hygiene must be guarded against the sulfydryl group, and groups that inactivate sulfydryl, will prove helpful in combating cancer. Potassium iodide, and such plants as the dandelion, and the chamomile flowers are thus good intestinal aids."

"One great function of bacteria is to convert dead animal tissues into food for plants, whether the dead animal product is in the ground or in the colon. And it is certain that a large part of the ingested meat is not digested and absorbed completely before it reaches the colon. The toxins evolved paralyze the bowel wall and cause diverticulae. These hold putrid material for varying periods among which the toxic amines are transition bodies. Diamine oxidase present in the intestinal wall and liver combats them, more or less successfully. But in the presence of excessive sulfydryl groups also formed during the putrefaction, the diamine oxidase may also be inactivated."​

Guru, are you secretly phantasizing about becoming a vegan?

 

[Amazoniac]

- Novel enzyme discovered in intestinal bacteria

Guru, are you secretly phantasizing about becoming a vegan?

 

[Kartoffel]

- Novel enzyme discovered in intestinal bacteria

Have you seen this one? I bet Travis would love it. I instincitvely threw away the cup of milk I was drinking while reading this.


Nature. 2012 Jul 5;487(7405):104-8. doi: 10.1038/nature11225.
Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10-/- mice.
Devkota S1, Wang Y, Musch MW, Leone V, Fehlner-Peach H, Nadimpalli A, Antonopoulos DA, Jabri B, Chang EB.

Abstract
The composite human microbiome of Western populations has probably changed over the past century, brought on by new environmental triggers that often have a negative impact on human health. Here we show that consumption of a diet high in saturated (milk-derived) fat, but not polyunsaturated (safflower oil) fat, changes the conditions for microbial assemblage and promotes the expansion of a low-abundance, sulphite-reducing pathobiont, Bilophila wadsworthia. This was associated with a pro-inflammatory T helper type 1 (T(H)1) immune response and increased incidence of colitis in genetically susceptible Il10(−/−), but not wild-type mice. These effects are mediated by milk-derived-fat-promoted taurine conjugation of hepatic bile acids, which increases the availability of organic sulphur used by sulphite-reducing microorganisms like B. wadsworthia. When mice were fed a low-fat diet supplemented with taurocholic acid, but not with glycocholic acid, for example, a bloom of B. wadsworthia and development of colitis were observed in Il10(−/−) mice. Together these data show that dietary fats, by promoting changes in host bile acid composition, can markedly alter conditions for gut microbial assemblage, resulting in dysbiosis that can perturb immune homeostasis. The data provide a plausible mechanistic basis by which Western-type diets high in certain saturated fats might increase the prevalence of complex immune-mediated diseases like inflammatory bowel disease in genetically susceptible hosts.

"While milk fat (MF) and PUFA had similar effects on Bacteroidetes and Firmicutes, a significant bloom of a member of the Deltaproteobacteria, Bilophila wadsworthia, was consistently observed only with MF

MF did not affect wild-type mice, but increased the onset and incidence of colitis in IL-10 −/− mice, driving it from a spontaneous rate of 25–30% (on LF) to over 60% in a 6-month period (Fig. 1b). In contrast, the incidence of colitis in IL-10−/− mice fed PUFA was no different than those fed LF. The colitis seen in mice fed MF was also more severe and extensive

To explore whether MF was necessary for B.wadsworthia’s survival and proliferation, we
monoassociated germ-free (GF) IL-10−/− mice with B. wadsworthia (ATCC 49260) tha twere consuming either LF, PUFA, or MF. Five-weeks post-gavage, colonization of the
colon could only be established in mice fed MF.

These changes were not observed in mice consuming MF in the absence of B. wadsworthia, indicating that the diet itself is not immunogenic. Moreover, when Lactobacillus murinus, which is also promoted by MF, was monoassociated in GF IL-10
−/−mice, no evidence of colitis or immune activation was seen (data not shown).

B. wadsworthia flourishes in the presence of taurine-conjugated (TC) bile acid (a propertyfrom which it got its name), a rich source of organic sulfur, which is used as the terminal electron acceptor of the electron transport chain resulting in the formation of H2S as a byproduct 17. Because of their hydrophobicity, milk fats will promote increased hepatic taurine conjugation of bile acids which are more efficient for micelle formation and fat emulsification 18–20.

When 10^7 CFU B. wadsworthia in taurine-free liquid growth media supplemented with 20ul of gall bladder aspirates obtained from SPF C57BL/6 mice fed the three test diets (n=5 pooled). B. wadsworthia growth was selectively and robustly stimulated only by bile from MF-fed mice (Fig. 3b). To determine whether the dietary effect was in fact mediated by TC, SPF IL-10 −/− mice were fed LF and gavaged with either TC or GC daily for two weeks. This resulted in a bloom of B. wadsworthia with TC.

We find the dependence of B. wadsworthia on diet-induced taurocholic acid intriguing and possibly representative of how certain gut microbes utilize bile to their advantage. Bile formation is unique to vertebrates, providing the host with the ability to digest and utilize a far greater variety of dietary substrates. Bile also has potent anti-microbial properties thatcan contribute to the selection or exclusion of many potential gut microbiota. However, several intestinal pathogens, including protozoa such as Giardia, Microsporidia and Cryptosporidia, and bacteria such as B. wadsworthia, H. hepaticus, and L. monocytogenes,are not only bile-resistant, but highly favored in the presence of bile [...]
Once established, the byproducts of these bacteria, whether H2S or secondary bile acids, can serve as gut mucosal “barrier-breakers” allowing for increased immune cell infiltration and thus acts synergistically with the bacterial antigen specific immune response to induce tissue damage.​

 

[Amazoniac]

Have you seen this one? I bet Travis would love it. I instincitvely threw away the cup of milk I was drinking while reading this.


Nature. 2012 Jul 5;487(7405):104-8. doi: 10.1038/nature11225.
Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10-/- mice.
Devkota S1, Wang Y, Musch MW, Leone V, Fehlner-Peach H, Nadimpalli A, Antonopoulos DA, Jabri B, Chang EB.

Abstract
The composite human microbiome of Western populations has probably changed over the past century, brought on by new environmental triggers that often have a negative impact on human health. Here we show that consumption of a diet high in saturated (milk-derived) fat, but not polyunsaturated (safflower oil) fat, changes the conditions for microbial assemblage and promotes the expansion of a low-abundance, sulphite-reducing pathobiont, Bilophila wadsworthia. This was associated with a pro-inflammatory T helper type 1 (T(H)1) immune response and increased incidence of colitis in genetically susceptible Il10(−/−), but not wild-type mice. These effects are mediated by milk-derived-fat-promoted taurine conjugation of hepatic bile acids, which increases the availability of organic sulphur used by sulphite-reducing microorganisms like B. wadsworthia. When mice were fed a low-fat diet supplemented with taurocholic acid, but not with glycocholic acid, for example, a bloom of B. wadsworthia and development of colitis were observed in Il10(−/−) mice. Together these data show that dietary fats, by promoting changes in host bile acid composition, can markedly alter conditions for gut microbial assemblage, resulting in dysbiosis that can perturb immune homeostasis. The data provide a plausible mechanistic basis by which Western-type diets high in certain saturated fats might increase the prevalence of complex immune-mediated diseases like inflammatory bowel disease in genetically susceptible hosts.

"While milk fat (MF) and PUFA had similar effects on Bacteroidetes and Firmicutes, a significant bloom of a member of the Deltaproteobacteria, Bilophila wadsworthia, was consistently observed only with MF

MF did not affect wild-type mice, but increased the onset and incidence of colitis in IL-10 −/− mice, driving it from a spontaneous rate of 25–30% (on LF) to over 60% in a 6-month period (Fig. 1b). In contrast, the incidence of colitis in IL-10−/− mice fed PUFA was no different than those fed LF. The colitis seen in mice fed MF was also more severe and extensive

To explore whether MF was necessary for B.wadsworthia’s survival and proliferation, we
monoassociated germ-free (GF) IL-10−/− mice with B. wadsworthia (ATCC 49260) tha twere consuming either LF, PUFA, or MF. Five-weeks post-gavage, colonization of the
colon could only be established in mice fed MF.

These changes were not observed in mice consuming MF in the absence of B. wadsworthia, indicating that the diet itself is not immunogenic. Moreover, when Lactobacillus murinus, which is also promoted by MF, was monoassociated in GF IL-10
−/−mice, no evidence of colitis or immune activation was seen (data not shown).

B. wadsworthia flourishes in the presence of taurine-conjugated (TC) bile acid (a propertyfrom which it got its name), a rich source of organic sulfur, which is used as the terminal electron acceptor of the electron transport chain resulting in the formation of H2S as a byproduct 17. Because of their hydrophobicity, milk fats will promote increased hepatic taurine conjugation of bile acids which are more efficient for micelle formation and fat emulsification 18–20.

When 10^7 CFU B. wadsworthia in taurine-free liquid growth media supplemented with 20ul of gall bladder aspirates obtained from SPF C57BL/6 mice fed the three test diets (n=5 pooled). B. wadsworthia growth was selectively and robustly stimulated only by bile from MF-fed mice (Fig. 3b). To determine whether the dietary effect was in fact mediated by TC, SPF IL-10 −/− mice were fed LF and gavaged with either TC or GC daily for two weeks. This resulted in a bloom of B. wadsworthia with TC.

We find the dependence of B. wadsworthia on diet-induced taurocholic acid intriguing and possibly representative of how certain gut microbes utilize bile to their advantage. Bile formation is unique to vertebrates, providing the host with the ability to digest and utilize a far greater variety of dietary substrates. Bile also has potent anti-microbial properties thatcan contribute to the selection or exclusion of many potential gut microbiota. However, several intestinal pathogens, including protozoa such as Giardia, Microsporidia and Cryptosporidia, and bacteria such as B. wadsworthia, H. hepaticus, and L. monocytogenes,are not only bile-resistant, but highly favored in the presence of bile [...]
Once established, the byproducts of these bacteria, whether H2S or secondary bile acids, can serve as gut mucosal “barrier-breakers” allowing for increased immune cell infiltration and thus acts synergistically with the bacterial antigen specific immune response to induce tissue damage.​

View attachment 13645

Thank you. For some reason I skimmed through it one day but forgot about it..

I just did a search and found a few links that were still 'purple,' indicating that I've clicked on them before and haven't cleared my history.

The adsorption of fat-soluble vitamins from leaves is poor (especially if raw, uncrushed and without fat), but this has a positive side in terms of protection throughout the intestines. It's common here for people to load up on foods rich in antioxidant carotenoids that provide little of the oxidizing quinones. To be fair they do get both, but purified quinones won't be present along with dietary carotenoids throughout the intestines.

I believe this was already post'd somewhere:
- Sweet discovery in leafy greens holds key to gut health

Therefore dark leafy greens should be helpful if tolerated, and it's worth trying cooked or raw.


- A Multihit Model: Colitis Lessons from the Interleukin-10–deficient Mouse

I guess that small amounts of dairy fat in meals are protective and shouldn't trigger these issues in susceptible people, yet if they is going to consume substantial quantities, it's preferable to favor cheese or milch over ice cream. Cheese, because of the discussion about soap formation on the calcium thread; same for milk, but in this case although its carbs won't help in eradication and might even contribute to a mild degree, they will at least acidify the intestines and minimize the protein feast, contrary to strained yogurt that provides an insignificant amount of carbs and is concentrated in proteid high in cysteine (they're after sulfur after all).


I think that now you're getting why @Captain_Coconut has a point. By the way, selenium is one of the responsibles for the characteristic coconut flavor, it's easy to perceive this when you happen to pick a spoiled one; it develops into a foul smell similar to white potatoes when they expire (but in this case more due to the sulfur-containing amino acids).

The advantage of eating whole foods is the protective array of substances that should minimize to a great extent, avoid and sometimes even correct the problem. This crappy poem is legit: coconut meat instead of just the oil, chocolate instead of cocoa butter, milk instead of butter sprinkled with a meal, olives instead of the oil, avocados, corn, nuts, and so on.

Koch (above and in his writings in general) was always cautious about selenium compounds. At first I thought it was due to some environmental excess at his time or where he lived, but later I realized that it's because intestinal bactaeria can act on them as replacement for sulfur. Hence why even within this thread you can find problematic experiences in spite of clearly needing and benefiting from it.
If supplementation is required, it's safer at first to concentrate the dose and decrease the frequency because the body should be able to retain the excess for a few days and you can avoid this issue for the most part.

 

[Kartoffel]

Therefore dark leafy greens should be helpful if tolerated, and it's worth trying cooked or raw.

I still doubt that. Basically none of the traditional living cultures and tribes ever ate significant amounts of leafy greens, especially not raw. I think there is a reason for that. I know lots of people that get horrible gas and bloating from any greens, even cooked. I tolerate them better now, but anything more than a little bit for extra flavor in my meal gives me discomfort and bad digestion. I still like you argument on insoluble fibers best: Everything that keeps stuff moving is good. I write this while cooking some bamboo shoots on my stove.

I think that now you're getting why @Captain_Coconut has a point.

No, not really. Why? Coconut oil has been shown in many experiments to restore eubiosis and to reduce the amount of harmful proteobacteria, and they even noted in their study that other "saturated" fats such as lard didn't produce the same result as milk fat. Also, I should mention that I am not really convinced of the study I posted because some things don't make much sense. Saturated fats don't increase the bile acid pool more than PUFA, as far as I can see. In fact, the ω-6 seem to increase total bile pool the most, and they used safflower oil in that paper. Also, their explanation for the effect of MF on bilophila is unconvincing to say the least. As I quoted above, they say the greater hydrophobicity of long chain saturated fatty acids increases taurine conjugation. In another paper, they specifiy that a little further and say this:

"The primary impact of the saturated milk fat lies in the unique fatty acid composition consisting of high levels of hydrophobic stearate that places demand on the host for efficient emulsification by bile salts. The body adapts and shifts the composition of bile toward a greater taurocholate:glycocholate ratio— taurocholate being the much more efficient emulsifier for hydrophobic fats."

Sci-Hub | Diet-induced expansion of pathobionts in experimental colitis. Gut Microbes, 4(2), 172–174 | 10.4161/gmic.23589
​

So, according to this argument, stearic acid would be the worst for your gut microbiome. Thus, cocoa butter and beef fat should be the worst. I simply don't buy this when I see all the studies showing these fats can successfully treat colits and cirrhosis. Their only useful reference for the claim on saturated fatty acids and taurochlorate is this paper.(1) They fed people either coconut oil or corn oil and saw that the ratio of glycine:taurine conjugates was greater in the corn oil group. But coconut oil contains very little stearic acid, and not even that much palmitic acid. (Btw, did you know that nutmeg, allthough not really beeing a nut, is the second most saturated nut on the planet after coconuts? It's allmost pure myristic acid.) Lard, for example contains much more of the suspected causative fatty acids, and they already mentioned that it did not promote bilophila. What am I to make of this? Maybe @haidut @CLASH have something useful to add with all their vast knowledge.

In the their reference paper the authors also state that a higher glycine:taurine conjugate ratio is not always neccessarily better:

"In hypothyroid patients ,a relative increase in the glycine conjugates hasbeen found."​

You are a very bad poet. Continue focusing on witty word plays instead.


1)
J Clin Invest. 1965 Nov;44(11):1754-65.
The effect of dietary fat on the turnover of cholic acid and on the composition of the biliary bile acids in man.
Lindstedt S, Avigan J, Goodman DS, Sjövall J, Steinberg D.