Problems With Sulphur

[Amazoniac]

Very interesting. Didn't know about the inhibitory effect of flavonoids on SULT. Is orange juice and cheese the perfect way to sulphite your gut to hell?

Good to know that you're around.

It would be interesting to compare fresh and matured cheese. I suspect that there isn't going to be much difference between them in terms of taxing sulfate, although it doesn't help that the vitamin losses when milk is processed might eventually impair sulfur metabolism. Perhaps the carbs that are also lost could promote the growth of bacteria that contribute to a steady supply of those vitamins, would be another hit.

How people's craving for the Brassica foods would be affected if it was possible to decontaminate them of sulfate?

Ingesting preformed sulfate might be worth a shot for attempting to skip impairments in conversion and because a greater share of the dose will target the liver compared to transdermal use, that bypasses the first regulatory steps of normal digestion and requires the person to exceed. Despite limitations, microbes that thrive on sulfur tend to be flexible, if it's not sulfate, they're going to attack something else. When people start viewing sulfate salts as sulfate supplements rather relegating it, dosing is more likely to be appropriate and according to sulfate needs. They repeated above that absorption is easily saturated (making it a great as laxative), smaller doses at a time must prevent adversities, this includes feeding bacteria.

In case the sulfate ingestion gets overwhelming, there are the copper complexes:

- Simple Copper Complexes Are A Powerful Alternative To Antibiotics​

It's possible for the person to consume meals from copperware (bowls, mugs, etc) and it should be protective; it's difficult to obtain a reasonable dose when dissolving in advance. This has been suggested before, what wasn't commented is that people with sulfur issues might benefit from the opposition of copper on the dietary sulfur that's being reduced (in state), the reactive sulfur groups in molecules might interact with copper and either carry it further down the intestines where it may be antimicrobial, facilitate its uptake (sulfur compounds are important copper ligands) or aid in cycling.
- NAC (cysteine) Increases Melanoma Spread

I don't remember the region where the bulk of sulfate is adsorbed, how fast symptoms appear may help in diagnose. For example, if it's very fast, it can be at the stomach, that could in turn be stemming from a hidden infection in mouth. However, it might affect distal parts indirectly, so it can be confusing. By the way, search for 'sulfide pylori/halitosis'.

After heat lamp sessions I notice an increased need for acetate and sulfate to the point where I have to make up for it or else deficiencies are induced; might be related to a boost in liver acetylation and sulfation, perhaps involving hormones. With sun exposure it happens to a lesser degree, Steph believes that there's something in sunlight that can oxidize sulfur to sulfate, this may occur ('sulfide photooxidation'). If others have a similar experience, heat lamps can be useful in rescuing from too much copper, more so than sun exposure.

Regarding the 'composition of intestinal gases', based on an exhaustive search of a couple of minutes, only oxygen and waste productide appear to be denser than hydrogen sulfide. Nevertheless, physical activity may help to distribute sulfide and prevent its buildup on a spot, exercises that involve bouncing might be necessary.
- Intestinal gases: influence on gut disorders and the role of dietary manipulations

I know that activated charcoal is used to remove hydrogen sulfide from the environment, but I haven't looked at it in detail. Sometimes they refer to it as activated carbon, so it's rich in carbon, followed by oxygen and sulfur (need to confirm this and I guess it depends on the source). If there is sulfur and it's not removed, a typical dose can yield a fair amount while being constipating: fatal. On the bright side, the oxygen in it is claimed to oxidize sulfur, perhaps it can react with sulfide that happens to be absorbed on the surface too.

 

[Memento]

Sunlight and Vitamin D: They're Not the Same Thing! - Seneff

Have you been told by your dermatologist to "stay out of the sun and take vitamin D." Sunlight and vitamin D are not the same.

stephanieseneff.net

The book mentioned above can be found at z lib, someone with more chemistry knowledge should give us plebs a tldr from Stephanies theory.

 

[Amazoniac]

- Intestinal metabolism of sulfur amino acids
- Emerging aspects of gut sulfur amino acid metabolism (also by Doug and Barbie)
- Nutritional and Functional Importance of Intestinal Sulfur Amino Acid Metabolism
- Nutrition and health relevant regulation of intestinal sulfur amino acid metabolism

- Why You Should Eat Raw Meat ('lentils' are one of the best sources of morbydenum)

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- The role of hydrogen sulfide in gastrointestinal tract functioning (review)

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- Recent Advances in Metabolic Pathways of Sulfate Reduction in Intestinal Bacteria
- Rapid hydrogen sulfide consumption by Tetrahymena pyriformis and its implications for the origin of mitochondria

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They've mentioned in a publication from another post that upping 'NDF' is useful for ruminants dealing with sulfidogenic microbes. It's worse for them because issues at the initial steps of digestion might compromise everything that follows.

- Back to Basics: Ruminant Digestive System | Amy Radunz - University of Wisconsin–Madison
- Rumen - Wikipedia

"Microbes in the reticulorumen eventually flow out into the omasum and the remainder of the alimentary canal. Under normal fermentation conditions the environment in the reticulorumen is weakly acidic and is populated by microbes that are adapted to a pH between roughly 5.5 and 6.5; since the abomasum is strongly acidic (pH 2 to 4), it acts as a barrier that largely kills reticulorumen flora and fauna as they flow into it. Subsequently, microbial biomass is digested in the small intestine and smaller molecules (mainly amino acids) are absorbed and transported in the portal vein to the liver. The digestion of these microbes in the small intestine is a major source of nutrition, as microbes usually supply some 60 to 90% of the total amount of amino acids absorbed."​

- plant carbohydrates classification ndf - Google Search

 

[Amazoniac]

- Metabolism of dietary sulphate: absorption and excretion in humans

Spoiler

The diagonal line below is for 1:1, where absorption would be complete since nothing could be recovered. However, there are the internal losses to account for (total sulfate = free + bound). Once we add the difference (total − free = bound) to that line (dotted line on top), it's easier to realize that it varies little depending on sulfate intake, it's the free that reflects the intake.

Both curves start paralleling the diagonal line, indicating that absorption is approaching saturation. The vertical distance between total ileal sulfate and the equivalence line eventually levels at 500 mg (not the intake), which is the claimed adsorptive capacity, the rest escapes digestion. Therefore, the efficient range is brief.

A teaspoon of magnesium sulfate (heptahydrate) is claimed to contain 5 grams.

Spoiler

Source: World-Wide Web, the online.

The ratio of magnesium to sulfate in magnesium sulfate salts is about 1:4. Sulfate ocurring as 4x the magnesium content won't vary depending on the degree of hydration. The usual salt is the heptahydrate, where magnesium is responsible for ~10% of the weight, therefore sulfate should be around 40%. A teaspoon provides something close to 2 grams of sulfate.

The experiment above graphed according to the total amount ingested in a day. Although the changes in sulfate intake were mostly based on dietary manipulation (rather than supplementation), there were specific foods in each diet making the greatest contribution. This means that a single meal could be responsible for the majority of the intake, which could be surpassing the range where capability to absorb is maximized in spite of not involving supplements. Spacing it out might allow the person to consume a greater amount at the end of the day without increasing wastefulness (and potentially feeding microbes). Over time, it may also be possible to adapt and improve tolerance.

If the presence of these microbes is compensatory, the person can expect a period of discomfort when correction starts until the body senses that they is no longer useful. The strategy of adding copper might be protective, but if consumption of sulfate in low doses continues being overwhelming, transdermal supplementation is preferable. Regardless of the route, it's possible that sulfate will make mucus richer in it and microbes keep attacking it, making extra copper still valuable when sulfate is not ingested. Upping selenium may be needed since there's risk of oxidative stress from plenty of copper.

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- Copper Touch, LLC (copper surfaces probably deodorize sulfurous compounds)

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- Enzymatic sulfation of mucin in gastric mucosa: effect of sofalcone, sucralfate and aspirin
- Inhibition of phenolsulphotransferase by salicylic acid: a possible mechanism by which aspirin may reduce carcinogenesis
⬑ [16] Sulphation catalysed by the human cytosolic sulphotransferases - chemical defence or molecular terrorism?

- Emerging Sulfated Flavonoids and other Polyphenols as Drugs: Nature as an Inspiration

Removed notes from figures, they were distracting.​

 

[Amazoniac]

Below, subjects supplemented 2x ~950 mg of sulfate as sodium sulfate. They rarely use killcium or magnesium in these experiments, and considering the daily needs of each, sodium is the least interferring. If it was killcium, it would provide about 400 mg at a time, which is an amount that people could be taking and the sulfate content being overlooked, yet that's what they refer to as 'high sulfate'. For example, if you check out the graphs from the previous post, where the area below total sulfate in ileum represents what wasn't absorbed, you'll notice that even if only a single 950 mg dose was ingested, it would yield a fair amount of unabsorbed sulfate.

- Alteration of Sulfate and Hydrogen Metabolism in the Human Colon by Changing Intestinal Transit Rate

"Normal volunteers underwent four interventions while taking a low-sulfate diet: placebo, sulfate supplements, or sulfate supplements with either senna [] or loperamide [?]."

"Decreased intestinal transit time or increased dietary intake of sulfate or protein may overwhelm ileal absorption (20, 42) and results in increased colonic concentrations of fecal sulfate (43) and thus exposure to H2S."

"The addition of sulfate alone increased fecal and urinary excretion of sulfate, fecal sulfide, sulfate reduction rates, and acetic acid production rates; it reduced fecal methanogenic bacterial concentrations. Faster intestinal transit increased fecal sulfate, sulfide, bile acids, the reduction rates of sulfate, and methionine and the production rates of acetic acid. Reduction in fecal methanogens and methane production was seen. The reverse effects were seen with loperamide."

"In this study sulfate reduction rates were higher in those harboring sulfate-reducing bacteria, but fecal H2S concentrations did not depend on their presence or absence. It is possible that other bacteria such as E. coli (45) produce produce significant amounts of H2S. Another possibility is that the efficacy of H2S absorption and metabolism has a greater influence on fecal concentrations than production rates."

"[..]in humans, despite the sensitivity of sulfate-reducing bacteria to ciprofloxacin and metronidazole (55), evidence for benefit is lacking (56–58). Metronidazole does not reduce fecal H2S concentrations in normal volunteers (55) suggesting that the raised concentrations seen in active disease reflect disordered removal rather than increased bacterial production."

"Sulfate-reducing bacteria have a greater affinity for H2 than methanogenic bacteria; thus, given an adequate supply of sulfate, sulfate-reducing bacteria should predominate (64). Unlike some previous studies (47, 62) we and others (48, 65) have shown that both sulfate-reducing bacteria and methanogens can be metabolically active at the same time. It is possible that with changing availability of substrate (e.g., mucin, cystine, taurocholate) and local conditions (the optimum pH for sulfate-reducing bacteria is 7.5, for methanogenesis is 7.0, and for acetogenesis is 6.5 (66)) along the colon, the relative efficacy of each of the hydrogen consuming processes may vary. Methanogenic bacteria outcompete acetic acid-producing bacteria for CO2 (67). While acetic acid production rates changed inversely with the concentration of methanogenic bacteria, molar ratios of acetic, butyric, and propionic acidwere similar suggesting that reductive acetogenesis contributes minimally to total acetate formation (12, 46)."​

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- The Nutritional Relationship Linking Sulfur to Nitrogen in Living Organisms

 

[Amazoniac]

- Decreased phenol sulfotransferase activities associated with hyperserotonemia in autism spectrum disorders

Hyperserotonemia is the most replicated biochemical abnormality associated with autism spectrum disorders (ASD). However, previous studies of serotonin synthesis, catabolism, and transport have not elucidated the mechanisms underlying this hyperserotonemia. Here we investigated serotonin sulfation by phenol sulfotransferases (PST) in blood samples from 97 individuals with ASD and their first-degree relatives (138 parents and 56 siblings), compared with 106 controls. We report a deficient activity of both PST isoforms (M and P) in platelets from individuals with ASD (35% and 78% of patients, respectively), confirmed in autoptic tissues (9 pineal gland samples from individuals with ASD—an important source of serotonin). Platelet PST-M deficiency was strongly associated with hyperserotonemia in individuals with ASD. We then explore genetic or pharmacologic modulation of PST activities in mice: variations of PST activities were associated with marked variations of blood serotonin, demonstrating the influence of the sulfation pathway on serotonemia. We also conducted in 1645 individuals an extensive study of SULT1A genes, encoding PST and mapping at highly polymorphic 16p11.2 locus, which did not reveal an association between copy number or single nucleotide variations and PST activity, blood serotonin or the risk of ASD. In contrast, our broader assessment of sulfation metabolism in ASD showed impairments of other sulfation-related markers, including inorganic sulfate, heparan-sulfate, and heparin sulfate-sulfotransferase. Our study proposes for the first time a compelling mechanism for hyperserotonemia, in a context of global impairment of sulfation metabolism in ASD.

 

[GelatinGoblin]

Very informative thread. Thanks you, @Amazoniac

 

[Amazoniac]

- Modulation of colonic hydrogen sulfide production by diet and mesalazine utilizing a novel gas-profiling technology

Spoiler

"[..]one of the possible mechanisms of 5-aminosalicylic acid (5-ASA), a first-line drug therapy, in inducing remission in UC, is the inhibition of H2S production.[3]"

"Limited data suggest that readily fermentable fibers, such as resistant starch and fructo-oligosaccharides (FOS), may influence H2S production by shifting fermentation away from sulfur-amino acids.[6,7]"

"The two major pathways of H2S production by the colonic microbiota comprise fermentation of amino acid or dissimilatory sulfate reduction utilizing hydrogen as an electron donor.[18] The current [artificial] study found that the sulfur-amino acid, cysteine, was a more powerful and reliable stimulator of H2S production than inorganic sulfur. This information could be used to speculate that, quantitatively, sulfate reduction in the large bowel by sulfate-reducing bacteria may not be the major pathway of generating free luminal H2S, although further experiments may be needed to examine factors that increase its activity. It is possible that a larger quantity of sulfate is needed to stimulate a larger response of H2S in our study. Lewis et al.[19] observed an almost 2-fold increase in faecal sulfide concentrations following a 14-day dietary supplementation with 20 mmol/day of sodium sulfate in a small cohort of healthy volunteers,[20] but their findings likely reflected an increase in both free and bound H2S levels. In contrast, our findings are in agreement with those of two other studies. Levine et al.[16] observed a 300-fold stimulation of free faecal H2S production by cysteine relative to that of an unspiked faecal slurry and this was much greater than the two fold stimulation with sodium sulfate at the end of the 24-h experiment.[16] Similarly, Florin et al.[21] found sulfate to be a poor stimulant of H2S production in vitro compared to cysteine, or another sulfur-containing substrate, mucin. One of the reasons for the ineffective production of H2S by sulfate could be related to the greater presence of protein-fermenting bacterial species within the colonic microbiota, whereas the process of sulfate-reduction is highly specialized and limited to the less abundant sulfate-reducing bacteria. Hence, it may be prudent for dietary strategies to reduce excessive H2S production in the large bowel to target a reduction in the fermentation of sulfur-amino acids rather than sulfate-reduction."

- Amino Acid Content And Profile Of Some Proteinaceous Foods (pot cheese appears to contain 2/3 of what poor sources have)​

"The administration of 5-ASA has previously been postulated to inhibit the genesis of luminal H2S. Initial observations were based on the lower content of total faecal sulfide (both bound and unbound) in patients with active UC and who were taking 5-ASA than those not on 5-ASA therapy. The inhibitory effects of 5-ASA appear to be mediated by interfering with both the rate of dissimilatory sulfate reduction and, to a lesser extent, the fermentation of sulfur-amino acids. This has been demonstrated in two studies in vitro with a reduction of 30–60% in H2S production being observed after 18-h incubation periods with 20 mmol/ L 5-ASA.[3,22] one with faecal cultures of amino-acid fermenting bacteria.[22] and the other measuring dissimilatory sulfate-reduction rates. Somewhat in contrast, we did not see such potent inhibitory effects at the end of our 4-h experiments whether with the incubations of faecal slurries was with 5-ASA alone or in combination with cysteine. Reasons for this discrepancy could potentially lie in the differences in experimental time courses or the methodology employed for H2S measurement." "[The] fermentation period was limited to 4 h, as pH dropped below 5 following this timeframe. As most metabolic activities of the colonic bacteria change (mostly inhibited) when the pH is 5 or lower.35 the drop in pH below 5 would have significantly affected the metabolic ability of the faecal bacteria in our study." "A longer incubation period could have provided more time for adsorption of H2S by 5-ASA compared to our experiments. Alternatively, 5-ASA may exert its effects mostly on bound H2S as seen in the earlier studies,[3,22] which may be less relevant to its pathogenicity. This suggests that, in patients with UC, the efficacy of 5-ASA therapy is less likely to be via reduction in metabolically active H2S in the large bowel."

"Of great interest, and potential therapeutic importance, are the findings that resistant starch and, to a lesser extent, FOS, modulate H2S production in vitro. Only a few studies have observed such effects of these fermentable fibers on reducing bacterial H2S production. In in vitro fermentation experiments using colonic content of pigs as the inoculum,[23] both inulin and FOS added to cecal content (as the ‘control’ substrate) reduced H2S levels by 15% and 5% respectively at the end of 24 h. Lewis and co-workers.[19] also observed a reduction in faecal sulfide concentrations following a 12-day supplementation with oligofructose, a type of FOS, in healthy controls. No changes in concentrations of faecal sulfate, populations of sulfate-reducing bacteria or sulfate-reducing rates were observed in their study. It is possible that the mechanism of action for oligofructose was via reducing fermentation of sulfur-amino acids. This was demonstrated in a study in ruminants where increasing overall carbohydrate fermentation via a decrease in colonic pH effectively decreased ruminant production of H2S.[24] This is highly likely as resistant starch and FOS have previously been shown to reduce biomarkers of colonic protein fermentation, including faecal ammonia, phenols and branched-chain fatty acids in animal studies,[25,26] and several human interventional studies.[27-29] An increase in nitrogen disposal[26] or utilization of nitrogen to support increased bacteria mass following increased carbohydrate fermentation shifts the colonic microbiota away from utilizing protein as substrates for fermentation.[27,29] The reduction in protein fermentation by supplying readily fermentable carbohydrate to increase carbohydrate fermentation and thus, divert ‘attention’ of bacteria to protein as a fermentative substrate most likely explains the current findings that, following the addition of FOS to cysteine, the production of H2S is actively and markedly reduced (by 90%) in comparison to cysteine alone. The shift to carbohydrate fermentation was confirmed by a concurrent 12- to 16-fold increase in both CO2 and H2 production during the experiment following the addition of FOS to cysteine compared to cysteine alone. The corollary of this finding is that effective suppression of H2S production by faecal microbiota requires active carbohydrate fermentation with concurrent reduction in protein fermentative activity."

"A small effect on H2S suppression was also seen with slowly or poorly fermentable fibers despite minimal participation in bacterial fermentation. As poorly fermentable but highly soluble and viscous carbohydrates, both sterculia and psyllium can exert other gel-forming effects.[30] It is quite possible that these carbohydrates ‘mop up’ H2S produced spontaneously by faecal microbiota as they attract water to form a viscous gel within the faecal slurries. This would explain the passive H2S suppression by these fibers. No other data are available to corroborate these observations."

 

[Amazoniac]

I think this one was referenced in a previous publication:
- Increasing dietary neutral detergent fiber concentration decreases ruminal hydrogen sulfide concentrations in steers fed high-sulfur diets based on ethanol co-products

 

[Kvothe]

"The sulphotransferase enzymes are potentially modulated by dietary components. Flavonoids, polyphenolic compounds found in fruits and vegetables, inhibit the SULT 1A1 isoform competitively and partially inhibit SULT 1A3, although other compounds may also be involved. Studies with fruit and vegetable cytosols showed that radishes, spinach, broccoli, bananas, elderberries, red cabbage, grapes, and red wine inhibit SULT 1A1 and also SULT 1A3

I was referring to this part. If flavonoids and polyphenos inhibit SULT, drinking lots of OJ or eating vegetables might not be so good for people with established dysbiosis favoring the production of H2S and an increased ratio of H2S to sulphate. Ray used to tell people with dysbiosis to take a good pinch of pure sulphure (flowers of sulphur). I haven't heard from anybody trying it, but it might be that some people just need a few good doses to activate detoxification processes.

 

[Amazoniac]

I was referring to this part. If flavonoids and polyphenos inhibit SULT, drinking lots of OJ or eating vegetables might not be so good for people with established dysbiosis favoring the production of H2S and an increased ratio of H2S to sulphate. Ray used to tell people with dysbiosis to take a good pinch of pure sulphure (flowers of sulphur). I haven't heard from anybody trying it, but it might be that some people just need a few good doses to activate detoxification processes.

I think that if sulfate is being produced normally and there's enzyme inhibition (from those foods), it should be excreted without trouble, unless this somehow signals shortage, extra production, toasts cofactors and eventually forces the body to resort to sulfide gas that may lead to buildup of environmental toxins such as sulfite. Some people will experience issues from small amounts of sulfide and its production isn't necessarily at the expense of sulfate. What do you have in mind?

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Have you listened to this interview? It's a matter of sulfide intoxicating some microbes earlier than ourselves (yet can select organisms than thrive on it).

- Ray Peat - Menopause & Estrogen; Thyroid; Coronavirus; Glaucoma; Food Combining and More (55:45) | Patrick Timpone

- Sulphur metabolism. I. The absorption and excretion of flowers of sulphur

For people that can oxidize it fine, it may indeed help in detoxification.

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Dissimilatory/assimilatory sulfate reduction..

- Molecular Pharmacology: The Mode of Action of Biology Active Compounds (978-0-12-395640-8)

"Metabolism is usually divided into catabolism and anabolism. Catabolic processes lead to dissimilation, the degradation or breakdown of the metabolites, which in this way are eliminated. Anabolic processes lead to assimilation, the incorporation of the metabolites in the body consitutients. For drug metabolism a similar differentiation is useful: (a) Dissimilation leads to biochemical changes in the drug molecule with, as a final result, the elimination of the drug; (b) Assimilation leads to an incorporation of the drug in the body constituents and, therefore, a fixation of the drug."​

Some organisms will disappear with it after embodying it.

Apparently sulfide farts aren't a cool thing, here they point out that the reaction is exothermic:
- 3'-Phosphoadenosine-5'-phosphosulfate - Wikipedia

I forgot to mention that casein digesting slowly might be another advantage that combined with its poor cysteine content must prevent problems. Egg whites are rich in cysteine and are known for fouling even healthy intestines when in excess; selenium may play a role too, the content per egg white is relatively low (7 mcg/egg), but some bodybuilders consume them in large quantities. It's worth experimenting cheese with varying amounts of fat because I presume that some people here will fare better when it's low, in particular if killcium is wasted in processing.

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- Biotransformation Reactions and their Enzymes

Spoiler

"Sulfonation reactions (also less correctly known as sulfation reactions) consist in a sulfate being transferred from the cofactor 3'-phosphoadenosine 5'-phosphosulfate (PAPS) to the substrate under catalysis by a sulfotransferase. Sulfotransferases, which catalyze a variety of physiological reactions, are soluble enzymes [24,5862]. The most significant for drug metabolism are listed in Table 24.5. The sulfate moiety in PAPS is linked to a phosphate group by an anhydride bridge whose cleavage is exothermic and supplies enthalpy to the reaction. The nucleophilic -OH or -NH- site in the substrate will react with the leaving SO3− moiety, forming an ester sulfate or a sulfamate. Some of these conjugates are unstable under biological conditions and will form electrophilic intermediates of considerable toxicological significance [2].

The sulfoconjugation of alcohols leads to metabolites of different stabilities. Endogenous hydroxysteroids (i.e., cyclic secondary alcohols) form relatively stable sulfates, while some secondary alcohol metabolites of allylbenzenes (e.g., safrole and estragole) form highly genotoxic carbenium ions. In contrast to alcohols, phenols form stable sulfate esters. The reaction is usually of high affinity (i.e., rapid), but the limited availability of PAPS restricts the amounts of conjugate being produced. Typical drugs undergoing limited sulfonation (Box C in Figure 24.8) include paracetamol and diflunisal (6). Aromatic hydroxylamines and hydroxylamides are good substrates for some sulfotransferases and yield reactive sulfate esters [48]. In contrast, significantly more stable products are obtained upon N-sulfoconjugation of amines. An intriguing and rare reaction of conjugation (Box D in Figure 24.8) occurs for minoxidil (7). This drug is an N-oxide, and the actual active form responsible for the different therapeutic effects is the N,O-sulfate ester."

- Sulphate in Pregnancy

 

[Amazoniac]

- Understanding the role of sulfur–thiamine interaction in the pathogenesis of sulfur-induced polioencephalomalacia in beef cattle

Spoiler

"Brain thiamine may increase in cattle with excessive dietary exposure to S in order to protect the brain tissue from increased S toxicity by scavenging sulfide or sulfite ions (Olkowski, 1997). The increased thiamine in HS brains in the present study fits this hypothesis. Another possible factor for the increased thiamine and TPP in the HS brains might be that sulfide or sulfite toxicity may result in pathologically increased energy consumption. The increased energy consumption may lead brain tissue to requiremore TPP to meet its increased energy demand. The results of brain thiamine variables in heifers fed high dietary S indicate that excess dietary S may increase the metabolic demand for thiamine, possibly to offset toxic effects of S on brain tissue."

"The causes of insufficiency of TPP in the brain tissue of PEM affected cattle in the present study could be due to the inhibition of TPP synthesis and/or enhanced TPP degradation. Thiamine pyrophosphate is synthesized from free thiamine by pyrophosphokinase (TPK) (Liu and Hurley, 2011). This phosphorylation process is only accomplished under the conditions where there is enough free thiamine, ATP, Mg2+, and normal function of TPK (Ramanaet al., 2012). Hence the inhibition of TPP synthesis can occur when any one of the required conditions is altered. Free thiamine was abundant in the PEM brains and thus it can be ruled out as a factor inhibiting TPP synthesis. However, it is possible that alteration of ATP (Raghavendra Rao et al., 1993; Mastrogiacomo et al., 1996), Mg2+ (Johnson, 2001), or TPK activity (Raghavendra Rao et al.,1993; Mastrogiacomo et al., 1996) inhibited TPP synthesis from free thiamine. Adverse effects of sulfite on mitochondrial ATP production (Zhang et al., 2004) and Mg2+ absorption from the rumen (Ferreira et al., 1966a,b; Martens and Blume, 1986) have been reported. Thus, the adverse effects of S on these substances required for TPP synthesis may result in inhibition of TPP synthesis."

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- Hydrogen sulfide: An endogenous regulator of the immune system
- H2S promotes a glycometabolism disorder by disturbing the Th1/Th2 balance during LPS-induced inflammation in the skeletal muscles of chickens

 

[Amazoniac]

- Sulfide as a Mucus Barrier-Breaker in Inflammatory Bowel Disease?

Spoiler

Spoiler: Box 1. Mucins as the First Line of Defense Against Pathogens and Bacteria

"The gut microbiota is [] involved in the progression and, possibly, the initiation of IBD [28]. The gut microbiome is diverse and consists of 500-1000 species, with Bacteroidetes and Firmicutes being the dominant phyla [29]. The role of the gut microbiota in IBD is further supported by the fact that gnotobiotic animals (germ-free or colonized only with selected bacteria) do not develop intestinal inflammation in genetic animal models of colitis, in contrast to animals recolonized with normal commensal intestinal microbiota [30-32]."

"[..]the percentage of the epithelium covered by mucus is significantly decreased in IBD patients [21], presenting a discontinuous and thinner mucus layer [24,25]."

"[..]increased levels of fecal sulfatase and mucinase activity have been found in the intestine of IBD patients relative to healthy individuals [50,51], suggesting that bacteria with a capacity to degrade mucus are more elevated and/or more active."

This may not be a reason to avoid dietary sulfate, mucus has to be repaired as fast as it's degraded, but the compromised region must be after the absorption sites.​

"The enzymatic detoxification of sulfide was shown to be normal in the intestine of IBD patients, indicating that elevated sulfide levels are not a consequence of defective detoxification [52]."

"5-aminosalicylic acid, an anti-inflammatory drug commonly prescribed for the treatment of IBD, inhibits the growth of SRB and suppresses sulfide production in IBD patients [48,53]. IBD patients who do no use 5-aminosalicylic acid have higher fecal sulfide levels [48]."

"Previously, potential mechanisms linking hydrogen sulfide to IBD focused mainly on the possibility that sulfide damages the epithelium by its genotoxic properties [38,39] and/or by its inhibitory effect on intestinal short-chain fatty acid metabolism [58-60]. This could lead to the initiation of chronic inflammation and/or colon cancer. We propose here a novel, not mutually exclusive mechanism by which sulfide may contribute to the etiology and severity of IBD based on our previous work [16]."

"Sulfide is produced by particular gut bacteria [..] and potently reduces disulfide bonds in the mucus, thereby lysing the polymeric MUC2 network [16] (Figure 1, Key Figure). Consequently, the mucus layer becomes less viscous and more permeable, allowing toxic compounds and bacteria present in the gut lumen to contact the surface of epithelial cells, inducing damage and/or an immune response."

Spoiler

"Reduction of disulfide bonds in the mucus leads to the formation of trisulfides [16]."

"The mechanism of disulfide bond splitting by sulfide is supported by Devkota et al. [56]. In this study, mono-association of germ-free mice with the sulfide-producing proteobacterium Bilophila wadsworthia in the presence of taurocholate, but not glycocholate, resulted in a bloom of the bacterium, causing mucus barrier breakage, inflammation, and increased colitis scores. Both taurocholate and glycocholate are metabolized to deoxycholate; however, only catabolism of taurocholate by Bilophila wadsworthia can lead to sulfide production [55]. We believe that sulfide is responsible for the mucus barrier breakage and increased colitis scores observed in their study."

"To increase the mucus barrier as a therapeutic option for IBD is not new, but the mechanism(s) by which sulfide breaks down the mucus layer opens up exciting new possibilities that could facilitate the inhibition of mucus degradation, and this warrants further attention."

- Association Between Sulfur-Metabolizing Bacterial Communities in Stool and Risk of Distal Colorectal Cancer in Men

Spoiler

"Processed meats, a key component of the sulfur microbial diet, are viewed as particularly problematic due to their high sulfur content from both sulfur-containing amino acids and the inorganic sulfurs found in preservatives.[9] In contrast, plant-based sulfur sources, such as those found in legumes and vegetables, two food groups associated with the relative depletion of sulfur-metabolizing bacteria, are distinct from animal-based sources, and may include compounds called glucosinolates. Non-sulfur metabolizing bacteria may produce myrosinases that hydrolyze glucosinolates to isothiocyanates, which have been extensively studied for their cancer preventative properties.[59-61] Thus, the source of sulfur, rather than quantifiable sulfur content of foods, may be more strongly predictive for sulfur-metabolizing bacterial abundance, a plausible explanation for prior inconsistent findings relating overall sulfur content with CRC risk."

- Adaptation of Candida albicans to Reactive Sulfur Species

Spoiler

"In humans, sulfite is generated during oxidative catabolism of the sulfur-containing amino acid cysteine and is also released by neutrophils (Mitsuhashi et al. 2002; Stipanuk et al. 2006). The release of sulfite by neutrophils occurs in response to activation by bacterial lipopolysaccharides, suggesting that sulfite acts as an antimicrobial agent (Mitsuhashi et al. 1998)."

 

[Amazoniac]

"Low blood sulfate coupled with high levels in urine is likely due to poor reabsorption in the kidney. Waring notes that the proximal tubule of the kidney contains transporter proteins necessary for sulfate reabsorption. Loss of these transporters leads to renal sulfate wasting and reduced blood sulfate level. In particular, two proteins deserve mention, NaS1 (sodium-sulfate co-transporter SLC13A1) and SAT1 (anion exchanger SLC26A1). Located in the kidney, they move sulfate from urine at the apical membrane, then back into the bloodstream at the basolateral membrane. It is interesting to note that NaS1 expression is regulated by vitamin D. In a study of VDR knockout mice with diminished vitamin D levels, urinary sulfate excretion increased by 42% and blood serum sulfate decreased by 50% (Bolt et al. 2004). Since vitamin D deficiency is quite common, affecting 41.6% of the US population as shown in the National Health and Nutrition Examination Survey of 2005/2006, it may be an environmental factor for dysfunctional sulfate levels (Forrest and Stuhldreher 2011)."​

 

[Amazoniac]

- Problems With Sulphur

Apparently, sulfite oxidase doesn't require riboflavin. It was while reading something related to poison/"vitamin" A that I came across the following:

- Advanced Nutrition and Human Metabolism (978-1-337-11555-1)

Spoiler

"Cytochrome c is the physiological electron acceptor for the reaction."

I asked Brenda what she thinks, as usual, she didn't reply, but her tattoos reinforced:
- BRENDA - Information on EC 1.8.3.1 - sulfite oxidase

 

[Mrscorpion360]

- Decreased phenol sulfotransferase activities associated with hyperserotonemia in autism spectrum disorders

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I know this is a month old post, but damn I was about to post it and you beat me to it. Lol

 

[Amazoniac]

- Kenneth R. Olson | Google Scholar (!)

Spoiler: A red-purple–blue therapeutic diet?

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- Disruption of sulphated glycosaminoglycans in intestinal inflammation ?? (sulphate)
- Nitric Oxide Products Degrade Chondroitin Sulfates ?? (sulfate)

 

[Amazoniac]

- The Nutritional Relationship Linking Sulfur to Nitrogen in Living Organisms

- Subclinical protein malnutrition is a determinant of hyperhomocysteinemia
- The essentiality of sulfur is closely related to nitrogen metabolism: a clue to hyperhomocysteinaemia

Sulfur in molecules has to be derived from somewhere and we know that extreme losses can occur. Having it conserved for methionine synthesis in cases of shortage is one more reason to experiment with sulfate ingestion (in conservative doses) to verify if sulfate isn't missing.

 

[Amazoniac]

- GutSelf: Interindividual Variability in the Processing of Dietary Compounds by the Human Gastrointestinal Tract

Spoiler

⬑ [19] Digestibility of Cooked and Raw Egg Protein in Humans as Assessed by Stable Isotope Techniques
- Amount and fate of egg protein escaping assimilation in the small intestine of humans

 

[Amazoniac]

- Endogenous Hydrogen Sulfide Production Is Essential for Dietary Restriction Benefits
- Calorie restriction and methionine restriction in control of endogenous hydrogen sulfide production by the transsulfuration pathway