Problems With Sulphur

[Amazoniac]

There was a recent video from a local Youtube channel describing this compound:
- Thioacetone - Wikipedia

- Chemists and bad smells (and sulfur): A productive pairing | Scientific American

"[..]if you think that thiols are the worst of all [odors], think again. I will leave you with a conversation between two great twentieth-century scientists that illustrates just how bad compounds purportedly similar to thiols can be. Sulfur is followed in the periodic table by selenium and tellurium. Hydrogen sulfide smells awful and we know that elements in the same column in the table behave similarly. How might hydrogen selenium and hydrogen telluride smell? Linus Pauling (LP), widely acknowledged as the greatest chemist of the century, offered some helpful perspective to Matt Meselson (MP), inventor of the most beautiful experiment in biology.

LP: Well, Matt, you know about tellurium, the group VI element below selenium in the periodic chart of the elements?
MM: Uh, yes. Sulfur, selenium, tellurium ...
LP: I know that you know how bad hydrogen sulfide smells. Have you ever smelled hydrogen selenide?
MM: No, I never have.
LP: Well, it smells much worse than hydrogen sulfide.
MM: I see.
LP: Now, Matt, Hydrogen telluride smells as much worse than hydrogen selenide as hydrogen selenide does compared to hydrogen sulfide.
MM: Ahh ...
LP: In fact, Matt, some chemists were not careful when working with tellurium compounds, and they acquired a condition known as "tellurium breath." As a result, they have become isolated from society. Some have even committed suicide.
MM: Oh.
LM: But Matt, I'm sure that you would be careful. Why don't you think it over and let me know if you would like to work on the structure of some tellurium compounds?​

I suspect that most graduate students would not embark on this project, even if it meant they got to work for Linus Pauling."​

Spoiler: How To Make An Easy And Effective Stink Bomb | Klye

View: https://www.youtube.com/watch?v=daxjMLCOVTM

 

[gaze]

You mean problems with sulfur once it's absorbed?
- Molybdenum, Hard To Pronounce, Harder Still To Obtain


If it involves gut imbalances and it's the constipation type, vigorous intestinal activity is the priority; if you correct it, the rest might follow, and if there hasn't been much time since initiation, it shouldn't be rooted and harmful microbes should be outcompeted. The diarrheal types tend to be more complicated to solve because microbes aren't merely overgrowing due to a favorable conditions, you would have to attempt to modulate it somehow, larger doses of killcium should help to control it.


The things that have been suggested:

- Acidification with safe fermentable carbs.
- Sun exposure.
- Ubiquinone. Should we call mk-4, MeQ4; or CoQ10, uq-10? Confusing and dangerous. Again, IUPAC/FAO/WWF/FDA (Lemonoil, 2020) to it.
- Methylene blue. [C16H18ClN3S]
- Extra ascourgic acid (if I'm not wrong, Raj suspected industrial sulfur residues in some supplements).
- Creatine/choline/cobalamins (preferably together with protein, collagen and adequate magnesium). They can worsen the state in case of existing nutrient deficiencies.
- Hydrolyzed collagen instead of gelatin.
- Troubling supplements can be consumed at a higher dose less often, or topically.
- Topical B-vitamins, magnesium, and vitamin E with K2.
- Anthocyanin-rich foods.
- Sodium 'hydrogen carbonate' before meals (waiting until appetite returns).
- Vinegar (neutralized or not).
- Trace minerals: copper, molybdenum, manganese, zinc, selenium (inorganic forms may be alternatives, probably unnecessary and fatal), boron, silicon.
- Problematic foods at the end of the day with a hefty killcium dose. Roughage with meals depends on the type of condition, but more at evening if you want to encourage fermentation and acidification.
- Trying problematic foods on their own (for the sake of experiment) and avoid starting your day with them.
- Combining troubling ones with nitrate-rich foods (celery root/stalk, beetroots, and so on; depends on what you're dealing with, check out text below).
- Dark leafy greens mixed.
- Venom D with meals (prevents microbial action).
- Green apple (or its juiceless fiber added to other recipes).
- Custard apple family fruits (even soursop).
- Berries.
- Edible fruit skins (may try supplemental lactose with them).
- Incidental resistant starch.
- Bell pepper.
- Ginger, cinnamon, hibiscus, pepper, (dried) herbs (some are sources, such as oregano, cooking helps, but the only spice that's really concerning in terms of fueling the problem is turmeric).
- Beneficial fats such as butter and coconut can be inducers: better consumed with complex meals that make their impact in this regard negligible.
- Walking (moderate activity) sipping magnesium water (improves its utilization).
- Counteracting the stress response to troubling foods with as much clothing as it's necessary to keep you comfortable (putting on or taking out).
- Cascara sagrada for relief.


Limiting the intake of the most troubling foods is advisable, but excluding all potential sources not only is impractical, but won't work. This toxin is everywhere:
- Organosulfur compounds - Wikipedia
- Volatile sulfur compounds in tropical fruits

Foods are complex enough to not justify restriction of any without being sure that the one in question is doing more harm than good. It may contain enough reasons to be contraindicated, yet it ends up not being detrimental in practice because there's something else in it that's protective. Dairy, pineapple, cocoa/chocolate and cruciferous vegetables are examples that may have more valuable compounds in them than the potential troubling ones. Their quality also varies a lot, it's a the worth exploring your available options. For example, cheeses might behave differently, there are ones whose proteins are easy to digest, provide a lot of salts that will be protective; white and opaque pineapples are harsh, the others are not; some dark chocolate bars have a fart.. taste, others are naturally sweet; a mild fermentation of cruciferous vegetables can be advantageous; and so on.

In general, it's the indigestible sulfur-containing compounds in high concentrations that are fueling.

Some traditional condiment recipes call for complementary ingredients with balancing fibers, it's rarely just one class.

The major source of sulfur in the diet are the amino acids containing them (not a reason to restrict them, it's not necessarily proportional to content). If I remember it right, about 25% of their weight is sulfur. Requirements vary, but you can use the RDA as guide to be sure that the intake of sulfur is decent.

@Amazoniac would these still be your up-to-date life hacks ?

basically, dont be constipated ?

Nietzsche right again:

“The abdomen is the reason why man does not easily take himself for a god.”​

 

[Dr. B]

@Amazoniac would these still be your up-to-date life hacks ?

basically, dont be constipated ?

Nietzsche right again:

“The abdomen is the reason why man does not easily take himself for a god.”​

whats that mean mate

 

[Amazoniac]

whats that mean mate

Reminder of invincibility. It's known that pretty women don't defecate.

 

[Amazoniac]

- Presentation #13064805 | slideplayer.com

Spoiler

Same principle with chlorine:

Has to be considered the distribution of molecular iodine and the concentration that it can reach in relation to hydrogen sulfide. If you want to increase the chances of them interacting, use molecular iodine during a crisis, not beforehand.

With Lugol's solution, there's the issue of having to deal with iodide:

- Mega Dosing Iodine = Bad, Destroys Thyroid Tissue Permanently
- Mega Dosing Iodine = Bad, Destroys Thyroid Tissue Permanently (last quote)

 

[Dr. B]

- Presentation #13064805 | slideplayer.com

Spoiler

View attachment 25958

Spoiler

​

Same principle with chlorine:​

​

View attachment 25959​

​

​

Has to be considered the distribution of molecular iodine and the concentration that it can reach in relation to hydrogen sulfide. If you want to increase the chances of them interacting, use molecular iodine during a crisis, not beforehand.

With Lugol's solution, there's the issue of having to deal with iodide:

- Mega Dosing Iodine = Bad, Destroys Thyroid Tissue Permanently
- Mega Dosing Iodine = Bad, Destroys Thyroid Tissue Permanently (last quote)

mate can you please mention what the last quote says there.

 

[Amazoniac]

It would be interesting to compare the tissue expression and activity of enzymes involved in metabolizing pyridoxine because, depending on differences between pyridoxol and pyridoxal, if pyridoxine happens to fuel infections, it may be advantageous to take transdermally the form that's preferentially processed by the liver for regulation purposes.

---

- A Comprehensive Review of Infectious Granulomatous Diseases of the Gastrointestinal Tract

"ITB usually affects one single location, and the most commonly affected area is the ileocecal region. One possible explanation is due to the slow transit and relatively static physiological environment that occurs in the ileum, which allows for prolonged contact between the bacillus and mucosa [5, 12, 14, 15]."​

---

mate can you please mention what the last quote says there.

?

Iodide wouldn't be part of Lugol's solution if molecular iodine had good solubility on its own, there's this hassle to consider when using it. It's a matter of deciding to obtain the desired dose of molecular iodine and ignoring the presence of iodide or factor iodide in and let it limit.

 

[Dr. B]

It would be interesting to compare the tissue expression and activity of enzymes involved in metabolizing pyridoxine because, depending on differences between pyridoxol and pyridoxal, if pyridoxine happens to fuel infections, it may be advantageous to take transdermally the form that's preferentially processed by the liver for regulation purposes.

---

"ITB usually affects one single location, and the most commonly affected area is the ileocecal region. One possible explanation is due to the slow transit and relatively static physiological environment that occurs in the ileum, which allows for prolonged contact between the bacillus and mucosa [5, 12, 14, 15]."​

---

?

Iodide wouldn't be part of Lugol's solution if molecular iodine had good solubility on its own, there's this hassle to consider when using it. It's a matter of deciding to obtain the desired dose of molecular iodine and ignoring the presence of iodide or factor iodide in and let it limit.

you said this " Mega Dosing Iodine = Bad, Destroys Thyroid Tissue Permanently (last quote)"

which quote in that thread?

 

[Amazoniac]

The ratio of glycine to taurine is all over the place:
- Bile Acids Conjugation in Human Bile Is Not Random: New Insights from 1H-NMR Spectroscopy at 800 MHz (Fig. 4a; absolute values are shown in Fig. 3)

The absorption of taurine is good, the concern is the aftermath if it enriches bile, which can serve to deliver it to distal parts of the abdominal brain. Two options that have been discussed as potential measures to migitate harm that this may cause are: extra killcium (in particular with meals that stimulate bile output) or consuming a minimal amount of fat. These would have to be employed for as long as it takes for bile composition to normalize. A taurochocalate bar would require this warning on the label.

you said this " Mega Dosing Iodine = Bad, Destroys Thyroid Tissue Permanently (last quote)"

which quote in that thread?

The titles was automatic, each link directs you to a specific post (not random).

 

[Amazoniac]

- Why Nature Chose Selenium

The authors were asked by the Editors of ACS Chemical Biology to write an article titled “Why Nature Chose Selenium” for the occasion of the upcoming bicentennial of the discovery of selenium by the Swedish chemist Jöns Jacob Berzelius in 1817 and styled after the famous work of Frank Westheimer on the biological chemistry of phosphate [Westheimer, F. H. (1987) Why Nature Chose Phosphates, Science 235, 1173−1178]. This work gives a history of the important discoveries of the biological processes that selenium participates in, and a point-by-point comparison of the chemistry of selenium with the atom it replaces in biology, sulfur. This analysis shows that redox chemistry is the largest chemical difference between the two chalcogens. This difference is very large for both one-electron and two electron redox reactions. Much of this difference is due to the inability of selenium to form π bonds of all types. The outer valence electrons of selenium are also more loosely held than those of sulfur. As a result, selenium is a better nucleophile and will react with reactive oxygen species faster than sulfur, but the resulting lack of π-bond character in the Se−O bond means that the Se oxide can be much more readily reduced in comparison to S-oxides. The combination of these properties means that replacement of sulfur with selenium in nature results in a selenium-containing biomolecule that resists permanent oxidation. Multiple examples of this gain of function behavior from the literature are discussed.

 

[Amazoniac]

After Juan y Miguel's class, I was reading again some of these publications.

- Dietary fat-induced taurocholic acid production promotes pathobiont and colitis in IL-10−/− mice

Spoiler

"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]."

"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)."

"Altogether these observations suggest that the bloom of sulfite-reducing Deltaproteobacteria, particularly B. wadsworthia, is associated with colitis in hosts that are genetically susceptible or have compromised mucosal barrier function."

↳ [18] The effect of dietary fat on the turnover of cholic acid and on the composition of the biliary bile acids in man

Spoiler

"Our studies show that the ratio of glycine- to taurine-conjugated bile acids in duodenal bile is influenced both by the form of the diet (solid or liquid) and by the nature of the dietary fat (coconut oil versus corn oil)."

Spoiler

"The values obtained in the subjects studied on a solid diet were close to those found previously in healthy young subjects on regular diets (31) (corn oil, 2.6 and coconut oil, 2.3 in the present study, compared to 3.2 in the previous study). The ratio was consistently lower in the present series of subjects studied on liquid formula diets (corn oil, 2.2; coconut oil, 1.1). There was in four cases a marked increase in the ratio on changing from coconut oil to corn oil; in the other three the increase was smaller but probably significant. The mechanism underlying these changes is not clear. Several factors are known to influence the relative abundance of glycine and taurine conjugates. For example, feeding large amounts of taurine can lead to a twofold increase in taurine conjugates; on the other hand, large increases in glycine intake do not change the proportion of two types of conjugates (32). In hypothyroid patients, a relative increase in the glycine conjugates has been found (33). Impairment of liver function leads to a diminished capacity of the liver to conjugate bile acids with glycine in vitro (34). Thus, changes in the glycine:taurine ratio can be effected either by changes in the available amounts of taurine or its precursors, or by changes in the activity of the conjugating systems in the liver. Of course, it is also possible that alterations in bacterial flora could lead to differences. For example, changes in the rates of hydrolysis of the different conjugates or in the rates of their reabsorption would result in changes in the ratios observed in bile."

In some subjects the bile acid pool was also increased, so there's more glycine relative to taurine, but the total amount of taurine was elevated.

↳ [19] Conjugated bile acids and intestinal flora during the preruminant stage in goat: Influence of a lamb milk replacer
- Bile salt evolution

Spoiler

"There is an obvious association between mammalian bile salt type and diet. Carnivores have taurine conjugates of cholic or other trihydroxycholanoic acids, herbivores generally have dihydroxy or ketohydroxy acids with, frequently, a high proportion of glycine conjugates, and omnivores have a good proportion of these various types. Bovids are an exception to this generalization, for these herbivores seem to have bile salts of the “omnivorous” type, rich in cholic acid and taurine conjugates as well as in chenodeoxycholic and deoxycholic acids and conjugates of glycine. The omnivorous laboratory rats and mice (Murinae) have taurocholate as the chief bile salt and possess liver enzymes that rehydroxylate deoxycholic acid at C-7Diokine to re-form cholic acid (60), which suggests that these rodents, like carnivores, “prefer” trihydroxy bile acids."

For the classification:
- Manipulating the Microbiome: An Alternative Treatment for Bile Acid Diarrhoea

↳ [16] Bilophila wadsworthia Isolates from Clinical Specimens

Spoiler

"The preferred ecological niche of Bilophila sp. is unknown but is presumably the lower gastrointestinal tract. However, the organism is occasionally found in the oral and vaginal floras. It is felt to be virulent, since it is the third most common anaerobic isolate in studies of gangrenous and perforated appendicitis, although it is present in the feces of about 50% of humans in mean counts of only 10^5 to 10^6/g (with total flora counts of 10^11/g). Studies are in progress in the Wadsworth Anaerobe Laboratory to characterize its virulence mechanisms. The genus was originally thought to be resistant to antimicrobial agents used to treat anaerobic infections because of difficult-to-interpret growth patterns on agar dilution susceptibility plates. Bilophila species are now felt to be susceptible to imipenem, cefoxitin, and ticarcillin on the basis of tests performed with the spiral gradient method with endpoint determination enhanced by a triphenyltetrazolium chloride overlay (9). Contrary to earlier reports, most Bilophila strains produce 13-lactamase and are resistant to penicillins and other P-lactam antibiotics that are not resistant to this enzyme (10)."

- Bilophila wadsworthia aggravates high fat diet induced metabolic dysfunctions in mice

Spoiler

"HFD had been consistently associated with increased abundance of B. wadsworthia, a bacterium implicated in increased colitis severity of Il-10-/- mice [5⇈]. However, the impact of B. wadsworthia on non-genetically susceptible host, and whether and how its expansion could promote an impaired metabolic function remains poorly understood. Here, we utilized a hypothesis-driven approach, using a combination of host trancriptomics, metatrancriptomics and gnotobiotic techniques, to dissect how B. wadsworthia is able to modulate host metabolic response to HFD. We then tested our hypotheses in conventional HFD murine model. Our results showed that, beside intestinal pro-inflammatory effects, B. wadsworthia promotes intestinal barrier defect, systemic inflammation, bile acid dysmetabolism and changes in microbiome functional profile, leading to the worsening of HFD-induced metabolic effects. Moreover, we showed that L. rhamnosus CNCM I-3960 was able to inhibit most of the B. wadsworthia-driven host metabolic and inflammatory impairments."

"We showed that B. wadsworthia increased HFD-induced metabolic syndrome, which is a condition often associated with low degree of systemic inflammation [26]. At the same time, B. wadsworthia had been demonstrated to exacerbate intestinal inflammation in genetically susceptible mice [5] and also to induce systemic inflammation in wild type animals [27]. Higher state of inflammation is characterized by wasting and weight loss while metabolic syndrome is characterized by low grade inflammation and higher body mass index. Thus, a key question is how can B. wadworthia affect both opposing pathologies. Moreover, the contribution and relative importance of B. wadworthia’s pro-inflammatory properties in disturbing host metabolic status in HFD setting is unknown. By pharmacologically suppressing the inflammation, we unmasked the capacity of B. wadsworthia to directly induce a negative impact on host metabolic function. Specifically, we were able to discriminate distinct metabolic impairments, namely reduced glucose clearance and fatty liver phenotype, influenced by B. wadworthia that do not completely rely on its pro-inflammatory properties. Nonetheless, B. wadworthia-driven inflammation remains an important factor that further tip the balance to stronger metabolic dysfunctions. Accordingly, this may explain why B. wadworthia is able to play a pathological role on two contrasting settings. It is also important to note that although we showed in this study that B. wadsworthia promoted heightened immune response, this did not translate to patent colitis development compared to previous reports [5]. This might be due to the fact that our murine model is not a genetically susceptible host, and therefore have intact compensatory mechanism that prevents the development of overt intestinal inflammation. Hence, B. wadsworthia’s effect on metabolic function in our system outweighs its effect on development of overt inflammation due to lack of additional stimuli. As a result, the phenotype we achieved is a model by which B. wadsworthia potentiates the deleterious effect of HFD on host metabolic homeostasis. Taken all together, the effect of B. wadsworthia to the host can be pleiotropic, but the combination of genetics, host and environmental factors ultimately dictate the degree of inflammation and type of pathologies B. wadworthia will exacerbate or influence."

"Overall, we demonstrated that B. wadworthia augments some of the deleterious host metabolic effects of HFD by modifying multiple targets: altering the functional potential of intestinal microbes, promoting higher intestinal permeability, development of heightened immune response both at mucosal and systemic level, and disproportionate bile acid concentrations. All these pathways ultimately converge to further disturb the host metabolic function in HFD setting (Supplementary Figure 8). Importantly, we also unraveled that B. wadsworthia, independent of its pro-inflammatory properties, has the capacity to negatively affect glucose and hepatic homeostasis. These results suggest that the carriage of high levels of Bilophila species or strains might modulate the susceptibility to not only inflammatory but also metabolic diseases. Collectively, our study provides a conceptual framework to further test this hypothesis in human and warrants the evaluation of preventative strategies, such as probiotics use, to suppress the expansion of Bilophila."

- Diet rapidly and reproducibly alters the human gut microbiome

Spoiler

"Our study provides several lines of evidence confirming that B. wadsworthia growth in humans can also be promoted by a high-fat diet. First, we observed B. wadsworthia to be a major component of the bacterial cluster that increased most strongly while on the animal-based diet [Supplementary Table 1 for this hardcore royal diet] (C28; Fig. 2 and Supplementary Table 8). This Bilophila-containing cluster also showed significant positive correlations with both long-term dairy (p<0.05; Spearman correlation) and baseline saturated fat intake (Supplementary Table 20), supporting the proposed link to milk-associated saturated fats [6]. Second, the animal-based diet led to significantly increased fecal bile acid concentrations (Fig. 5c and Extended Data Fig. 9). Third, we observed significant increases in the abundance of microbial DNA and RNA encoding sulfite reductases on the animal-based diet (Fig. 5d,e). Together, these findings are consistent with the hypothesis that diet-induced changes to the gut microbiota may contribute to the development of inflammatory bowel disease. More broadly, our results emphasize that a more comprehensive understanding of diet-related diseases will benefit from elucidating links between nutritional, biliary, and microbial dynamics."

Beyond the fatty acids profile:

- Virgin coconut oil improves hepatic lipid metabolism in rats–compared with copra oil, olive oil and sunflower oil

Spoiler

"Coconut palm (Cocos nucifera L.) grown at the Kerala University campus were used for the extraction of VCO and CO. Extraction of oils as follows: For extracting VCO, solid endosperm of mature coconut (West coast tall variety) was crushed, made in to viscous slurry and squeezed through cheese cloth to obtain coconut milk which was refrigerated for 48 h, then subjected to mild heating (50°C) in a thermostat oven. The obtained VCO filtered through cheesecloth was used for the present study [14]. CO was extracted from coconut meat, which was dried in sunlight continuously for 4 days to remove moisture and the resulting copra was pressed in a mill to obtain CO [14]."

"For estimating the degradation of cholesterol, we analyzed the concentration of total hepatic bile acids, which was found to be significantly increased in rats fed with VCO (47.18 mg /100 g liver) compared to CO (36.74 mg /100 g liver), OO (30.31 mg /100 g liver) and SFO (40.65 mg /100 g liver) (Fig. 3). In addition, there was a significant increase in the concentration of fecal bile acids (27.38 mg /100 g feces) and neutral sterols (6.75 mg /100 g feces) were observed in VCO fed rats, which indicating higher rate of its excretion in VCO fed rats compared to other oil fed groups (Table 5)."

 

[Amazoniac]

- Dietary Glycine and Taurine on Bile Acid Conjugation in Man

Spoiler

"Because of the striking effect of taurine on conjugation of bile acids in the patient described [..], the effect of giving glycine and taurine to healthy persons was investigated. Various amounts of the amino acids were given for 5 days and bile acids in duodenal contents were determined before and after administration. The results are shown in Fig. 2."

"Even when given in large amounts, glycine did not affect the ratio between glycine and taurine conjugated bile acids."

"In contrast to results obtained with glycine, 0.5 g of taurine 3 times a day gave a pronounced increase in the proportion of taurine conjugated bile acids. This proportion tended to increase further when larger amounts of taurine were given. Five to 7 days after last administration of taurine, the proportion between glycine and taurine conjugates had usually returned to starting value."

"To test the effect of prolonged taurine administration, 3 patients were given 3 g of taurine daily for 3 weeks. All patients had stones in the gallbladder. The proportion of taurine conjugates was increased at end of experimental period (Fig. 3)."

 

[Sani]

"To test the effect of prolonged taurine administration, 3 patients were given 3 g of taurine daily for 3 weeks. All patients had stones in the gallbladder. The proportion of taurine conjugates was increased at end of experimental period (Fig. 3)."

Hello Amazoniac, interesting stuff you have found again. I can't access that study and that quotation seems a little odd. Does it mean that taurine caused gallbladder stones? That would be very odd because taurine is a major component of the bile acids and helps to keep bile salts dissolved.

What's your take on supplementing taurine?

 

[Dr. B]

Hello Amazoniac, interesting stuff you have found again. I can't access that study and that quotation seems a little odd. Does it mean that taurine caused gallbladder stones? That would be very odd because taurine is a major component of the bile acids and helps to keep bile salts dissolved.

What's your take on supplementing taurine?

is taurine a sulfur based amino acid since cysteine is? or does the sulfur get removed in the process of turning cysteine to taurine.
taurine has an anti anxiety, constipating, sedative effect, and is completely opposite to beta alanine which has a pro anxiety, laxative, and energizing or wiring effect. it seemed like it could be making me colder, but it caused some constipation or at least difficulty with stools so i stopped using it. some sites/sources say it helps digestion or fixes constipation, im not sure, in my case it turns normal bowel movements difficult

 

[Sani]

is taurine a sulfur based amino acid since cysteine is? or does the sulfur get removed in the process of turning cysteine to taurine.
taurine has an anti anxiety, constipating, sedative effect, and is completely opposite to beta alanine which has a pro anxiety, laxative, and energizing or wiring effect. it seemed like it could be making me colder, but it caused some constipation or at least difficulty with stools so i stopped using it. some sites/sources say it helps digestion or fixes constipation, im not sure, in my case it turns normal bowel movements difficult

Taurine is a sulfur compound. Your constipation could be just temporary effect because taurine affects so many things like your microbiome. Probiotics sometimes cause constipation too at start but after couple of weeks it improves, I would think taurine can have the same effect.

 

[Dr. B]

Taurine is a sulfur compound. Your constipation could be just temporary effect because taurine affects so many things like your microbiome. Probiotics sometimes cause constipation too at start but after couple of weeks it improves, I would think taurine can have the same effect.

im confused its made from cysteine, but Ray advises avoiding cysteine, and not using supplements,
Peaty foods contain taurine but youd get a few hundred milligrams.
the constipation like effect lasted months. im not sure, and i did get the effect from probiotics
probiotics also cause acne.
i assumed probiotic supplements have some issues with them or maybe shouldnt be supplemented at all?

 

[Amazoniac]

- Impaired Butyrate Oxidation in Ulcerative Colitis Is Due to Decreased Butyrate Uptake and a Defect in the Oxidation Pathway

"Inhibition of butyrate oxidation induces an energy-deficient state ultimately resulting in reduced absorption of sodium, reduced secretion of mucin, and a shorter life of the colonocytes."

"Putative mechanisms for the impaired butyrate oxidation in those patients may include a decreased availability of butyrate in the colonic lumen, decreased uptake of butyrate in the colonocytes, and/or abnormalities in the b-oxidation pathway.[11]"

"[..]we provide evidence that the butyrate metabolism is not only a consequence of a reduced butyrate transport, but also of a reduced butyrate oxidation. In addition, the reduction of uptake and oxidation is situated at the level of gene expression and not at the functional level. This also implies that local application of higher concentrations of butyrate does not overcome the mucosal energy deficiency in UC and that stimulation of butyrate production through indigestible carbohydrates or butyrate enemas may not be effective in the treatment of this disease. Inflammation is clearly associated with the observed butyrate oxidation deficiency in UC. An upregulation of the expression levels after antiinflammatory therapy was observed. However, for most genes involved in the butyrate metabolism, the expression levels in UC remained significantly lower as compared with the expression level of healthy controls, suggesting that there might be a genetic deficit."​

Hello Amazoniac, interesting stuff you have found again. I can't access that study and that quotation seems a little odd. Does it mean that taurine caused gallbladder stones? That would be very odd because taurine is a major component of the bile acids and helps to keep bile salts dissolved.

What's your take on supplementing taurine?

You can tell from the first quote that there was healthy and unhealthy subjects involved and from the last that the stones was there before treatment, they haded them.

The concern with taurine in cases of intestinal sulfur issues must not be its absorption since it's good, but when it enriches bile, for working as a taurine carrier to distal sites. Given that hydrogen sulfide can be synthesized endogenously, the advantages of a compensatory adaption to let sulfidogenic microbes grow would be to maximize the extraction of sulfur from protein that's not digested, getting the person close to 100% of utilization, and recovering what would otherwise be lost from sloughed cells. They can feast on this extra sulfur, adding up to the irritation caused by modified bile.

 

[Amazoniac]

- Coconut milk gavage enhanced fecal bile excretion by modulating hepatic Fxr expression but failed to improve fasting serum cholesterol profile in C57BL/6 mice

Spoiler

"In recent years, studies have shown that mice supplemented with virgin coconut oil registered the highest hepatic and fecal bile acid content as compared to other oil, i.e. copra oil, sunflower oil, or olive oil (Arunima and Rajamohan, 2012 [last]). Nonetheless, the molecular link leading to such observation has not been investigated. The main molecular modulator of bile metabolism is a nuclear receptor known as the farnesoid X receptor (Fxr). This receptor is bile sensitive and is triggered by bile acids (e.g. chenodeoxycolate and deoxycholate) to regulate its own synthesis. Fxr controls the biosynthesis of bile salt by regulating the expression of Cyp7a1 – the rate-limiting enzyme in bile acid synthesis (Chiang, 2009). Activation of FXR will negatively affect the expression of CYP7A1, which consequently represses the formation of bile salt (Chiang, 2009). The shutdown of this process is usually accompanied by the buildup of cholesterol in hepatocytes, and this will impact the plasma cholesterol level."

"This study was aimed to investigate the molecular relationship between coconut milk, bile excretion, and serum cholesterol using an in vivo model system, C57BL/6 mice. Coconut milk was chosen as the source of coconut fat since it is used extensively in the South East Asia but it has received lesser attention than coconut oil." "[..]the coconut oil used in [some] studies was hydrogenated – a modification that would strip coconut oil off its original properties (Enig, 1996; Foale, 2003; Amarasiri and Dissanayake, 2006)."

"The nutritional composition of the commercial light whipped cream used is presented in Table 1A. Light cream was included as a control since this food product shares comparable nutrition profile and calorie contents as coconut milk (Tab. 1C). Saturated fat in dairy products is generally rich in long-chain fatty acid (LCFA), consisting mostly of palmitic acid (C16:0), followed by stearic acid (C18:0) and myristic acid (C14:0) (Jost, 2007), which ideally contrasted the high MCFA content found in coconut milk."

"As expected, the fecal bile concentration of the coconut milk group had increased significantly by 1.68-fold, from the basal level of 33.5 uM/g to 56.4 uM/g during the 8th week as compared to water control (Fig. 1b). Intriguingly, though the coconut milk and light cream groups shared similar serum cholesterol progression throughout the study, the fecal bile acid content of the latter group did not change significantly after the gavage (Fig. 1b). This suggests that the light cream group had adopted an entirely different homeostatic strategy to stabilize the increase in serum cholesterol levels."

"To investigate whether bile metabolism is truly involved in the response to coconut milk intervention, the hepatic expression of four bile acid metabolism genes in the mice subject were analyzed. Consistently, the bile acid synthetic genes – Cyp7a1, Cyp7b1, and Akr1d1 – were elevated in the liver of coconut-milk-fed mice, in conjunction with a significant down-regulation of the Fxr mRNA (Fig. 1c). Likewise, the Fxr protein level of the coconut milk group was also downregulated significantly (Fig. 1d). This shows that the increased bile acid excretion in the coconut milk group is modulated through the suppression of Fxr. Such changes were not observed in the light cream group, which further validated our earlier hypothesis."

 

[Amazoniac]

- Desulfovibrio Isolate from the Microbiote of Children with Autistic Spectrum Disorders Immobilizes Iron in Poorly Soluble Crystalline Sulfides

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- Sulfur-Containing Compounds in Butter and their Influence on Butter Aroma

Spoiler

 

[Amazoniac]

- Nutritional essentiality of sulfur in health and disease (!)