Problems With Sulphur

[Amazoniac]

- Role of hydrogen sulfide in duodenal HCO3(-) secretion

"Mucosal application of H2S donor, NaHS, increases gastric and duodenal alkaline secretion in a concentration-dependent manner (Fig. 1). Interestingly, these reactions were markedly suppressed by the previous administration of the cyclooxygenase (COX) inhibitor indomethacin, suggesting that endogenous PGs may be involved in the increase in alkaline secretion by H2S. Endogenous PG is important for local regulation of alkaline secretion, and E-type PG (PGE2) has a strong alkaline secretagogue action. PGE2 has been shown to promote gastric and duodenal alkaline secretion via EP1 and EP3/EP4 receptors, respectively (5). In fact, the effects of NaHS are suppressed by selective EP3 and EP4 receptor antagonists, indicating that this response is mediated by endogenous PG. H2S has been reported to increase PGE2 production through induction of COX-2 in cardiomyocytes (9), and inhibition of H2S production in large intestine mucosa leads to decreased COX-2 expression and PGE2 synthesis (10). The authors have also confirmed that mucosal application of NaHS increases the PGE2 content of the duodenal mucosa. These findings suggest that H2S promotes duodenal alkaline secretion through increased mucosal PGE2 production."

"The promotion of duodenal alkaline secretion by topical application of NaHS is also significantly suppressed by the NO synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME). This suggests that NO is involved in H2S-induced increase in alkaline secretion in addition to endogenous PG. H2S has been shown to promote NO production in the vascular endothelium (11), but similarly mucosal application of NaHS increases NO release into the duodenal lumen. The authors have previously reported that the NO donor, NOR3, promotes duodenal alkaline secretion via an increase in mucosal PGE2 (12). Since this reaction was suppressed by pretreatment with indomethacin, it is speculated that the promotion of alkaline secretion by NO is mediated by endogenous PG. Since the increase of alkaline secretion by NaHS is suppressed by indomethacin and L-NAME, it is considered that H2S increases NO release and PGE2 production, and as a result, promotes duodenal alkaline secretion."​

- Diet and relapsing ulcerative colitis: take off the meat?

"It has been proposed that sulphide toxicity may be important in the pathogenesis of UC.[9,10] The initial evidence in this regard was demonstration that experimental exposure of colonic tissue to sulphide causes inhibition of butyrate use (see below), a defect similar to that observed in mucosal biopsies obtained from UC patients.[11] UC patients have significantly higher luminal concentrations of hydrogen sulphide than controls, and disease activity correlates with sulphide production rates.[12] Hydrogen sulphide induces hyperproliferation of colonic mucosa and this effect is antagonised by butyrate.[13] Treatment with 5-aminosalicylates and bismuth subsalicylates has been shown to reduce hydrogen sulphide production in the colonic lumen.[12,14] Apart from the direct toxicity of hydrogen sulphide, it has been speculated that thiols may react with sulfhydryl containing compounds to form persulfides, which may alter protein function as well as antigenicity, which could theoretical lead to a chronic immune mediated process, as known in UC.6"

"Patients with active extensive UC have decreased colonic butyrate oxidation. As remission of disease is associated with normalisation of butyrate oxidation, UC mucosa is not intrinsically altered in butyrate oxidation.[19]"

"So, how to increase faecal butyrate levels? In animal and human studies, ingestion of resistant fibre has resulted in an increase in the population of Bifidobacillus and Lactobacillus in the colon and an increase in faecal butyrate concentrations. Administration of oat bran over three months to UC patients in remission (corresponding to 20 g dietary fibre) has recently been shown to result in increased faecal butyrate levels and in this pilot study no relapses were observed.[22] Alternative strategies of delivering short chain fatty acids to the inflamed colon are by providing a substrate, a “prebiotic”, for short chain fatty acid production by colonic bacteria, or directly delivering probiotics to the intestinal lumen." "Butyrate enemas have been shown to be of benefit in the management of distal UC.[20,21]"​

- https://www.google.com/search?q=butyrogenic+fiber

 

[Amazoniac]

- Adverse reactions to the sulphite additives (intermediate product when sulfide is oxidized to sulfate)
- Sulfites inhibit the growth of four species of beneficial gut bacteria at concentrations regarded as safe for food


- Sulfate Deficiency as a Risk Factor for Autism

- Chondroitin, Dermatan, Heparan, and Keratan Sulfate: Structure and Functions
- Proteoglycans and Glycosaminoglycan Modification in Immune Regulation and Inflammation

- Heparan Sulfate Modulates Neutrophil and Endothelial Function in Antibacterial Innate Immunity

- Emerging Roles of Heparanase in Viral Pathogenesis
- Sulfotransferase and Heparanase: Remodeling Engines in Promoting Virus Infection and Disease Development

 

[Amazoniac]

Hydrogen selenide is actually closer to incorporation into selenoproteins than dietary selenocysteine:

- Postgraduate symposium: Epigenetic and antioxidant effects of dietary isothiocyanates and selenium: Potential implications for cancer chemoprevention

Spoiler

Sometimes you'll find it represented as HSe(−) or Se(2−). You can broaden your search by using only 'selenide' or 'sulfide' because it will include the other forms.

- Biogenesis of reactive sulfur species for signaling by hydrogen sulfide oxidation pathways

"H2S is used in this article to refer collectively to all three species that exist in solution: the diprotonated (H2S), monoanion (HS−) and dianion (S2−) forms."​

- Sulfate Deficiency as a Risk Factor for Autism

Spoiler

"One characteristic of autism is dysfunctional sulfur metabolism." "An English study reports the urine of those with autism contains 50 times the sulfite and double the sulfate of neurotypicals (Waring and Klovrza 2000). In an Arizona study that investigated blood sulfate levels in a cohort with autism, free sulfate was 35% and total sulfate was 72% of non-autistic individuals (Adams et al. 2011). In addition, a French study of nasal stem cells found decreased expression of either the molybdenum cofactor sulfurase or aldehyde oxidase genes (MOCOS or AOX) in 91% of a small group (n = 11/12) of autistic participants (Feron et al. 2016). Both of these genes are part of the molybdenum cofactor pathway, responsible for sulfite oxidase enzyme, among several others. Impaired sulfite oxidase production results in an increase of sulfite []."

"Sulfate is a common nutrient and functions in a variety of chemical processes including the development of tissue structure for important organs. During human pregnancy, maternal circulating sulfate levels double during the final trimester. This highlights the importance of sulfate in fetal development (Dawson et al. 2015). In particular, heparan sulfate is essential for neuron regulation. In studies of mice with compromised heparan sulfate synthesis, symptoms similar to those found in autism resulted, including impairments in social interaction, expression of repetitive behavior and difficulties with vocalization (Irie et al. 2012). In humans, the examination of postmortem brain tissue in young individuals showed reduced levels of heparan sulfate for those with autism vs neurotypicals (Pearson et al. 2013). Finally, sulfate supports sulfonation and sulfotransferase enzymes which help to remove xenobiotics and certain pharmacological drugs. Through a sulfonate intermediary, 3′-phosphoadenosine 5′-phosphosulfate (PAPS), sulfate is attached to unwanted chemicals increasing water solubility to facilitate removal (Gamage et al. 2005). Without sufficient sulfate, developing children may be at heightened risk from xenobiotics and environmental factors that require metabolism via sulfonation."

"How could a deficit of a few hundred milligrams of sulfate make any difference in the diet of a pregnant woman? There are some clues in the medical literature. In Waring’s English study 19 years ago, urine was analyzed for those with autism and compared against neurotypicals. The results showed autistic urine to contain 6800 uM sulfate compared to a normal reading of 3000. Assuming daily urine discharge at 1.4 L, the extra sulfate in urine for those with autism was 510 mg per day. This suggests that tissue in those with autism may be starved for sulfate. And this assumption is confirmed by Adam et al.’s (2011) Arizona study showing blood levels are below normal, only 35% in the case of free sulfate. Note that sulfate in drinking water is typically in the form of a free ion, exactly what seems to be missing in those with autism."

"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)."

"Bottled water is an interesting modern phenomenon, rare 70 years ago when autism was virtually unknown but very common in today’s world. If participants in the Southwest region had rejected bottled water and had drunk 2 L of local tap water instead, 222 mg of sulfate would have been added to their diet. Bottled water is not the only factor that has reduced sulfate in the modern world. Since the enactment of the Clean Water Act of 1972, the EPA has been tasked with cleaning up public water in the United States. Clearly, this is good for the country as it minimizes the microbes and toxins that pose health hazards. Of course, water that has been cleaned to contain fewer contaminates will naturally contain less sulfate. The reduced sulfate content of some tap water and most purified bottled water may be relevant when considering the potential role of a low sulfate supply in autism."

"Many simple steps may be taken to reverse this trend and increase sulfate in the diet of pregnant women. As discussed above, if local tap water is mineral rich, it could be used instead of purified, bottled water. If taste is an issue, the use of simple carbon filters like Brita effectively improves the flavor while leaving sulfate largely intact."

"Sulfate supplements are inexpensively available. Most common are the heptahydrate versions of ferrous and zinc sulfate. Ferrous sulfate is often sold at a strength of 65 mg iron, providing 112 mg of sulfate. Zinc sulfate is usually sold at a strength of 50 mg zinc, resulting in 74 mg sulfate. However, they provide about three times the daily value of iron or zinc which may limit their usefulness. Another option is Epsom salts (magnesium sulfate) used for both drinking and bathing. One quarter level teaspoon (1.33 g) of the common heptahydrate version yields 518 mg sulfate and 131 mg magnesium. When dissolved in 2 L of purified water, a mineralized water is created with a sulfate concentration similar to that of the Colorado River. To circumvent digestive issues, Epsom salts may be added to bath water. Transdermal absorption has been anecdotally reported to increase body sulfate levels (Adams et al. 2018)."

"Some food contains significant amounts of sulfate and may offer a natural choice for increasing sulfate in the diet. Table 5 lists the foods and beverages with the highest levels of dietary sulfate upon digestion. The data are from Florin’s study which preps samples using acid hydrolysis to simulate gastric acid. The table entry “Reference at 24 mg/L” refers to the EPA published median for sulfate in public water. Using a combination of tap water, bottled mineral water and select foods or beverages, it’s not difficult or inconvenient to make up for the additional 510 mg of sulfate measured in the urine of individuals with autism."

 

[Amazoniac]

- Hydrogen sulfide intoxication induced brain injury and methylene blue

"[..]one of the first measurable symptoms of toxicity to an exposure to H2S is a stimulation of breathing, long identified as a result of a stimulation of the arterial chemoreceptors by H2S (Haouzi, 2012; Heymans et al., 1931). As the intoxication progresses this stimulation of breathing is replaced by a depression of breathing always associated with a coma (Beauchamp Jr, et al., 1984; Guidotti, 2010). This coma may be associated with seizures, although generalized seizures appears, at least in un-sedated rats, much less frequent than during cyanide intoxication (Haouzi et al., 2017)."

Other antidotes are based on empirical observations, such as sodium bicarbonate (Almeida and Guidotti, 1999; Guidotti, 2010) and hyperoxia (Bitterman et al., 1986; Haouzi et al., 2011; Smilkstein et al., 1985; Smith et al., 1976).

⬑ [Guidotti] Hydrogen Sulfide: Advances in Understanding Human Toxicity

"In healthy, fit human volunteers, hydrogen sulfide exposure as low as 5 ppm during exercise (30 minutes) is associated with an early shift from aerobic to anaerobic metabolism, as indicated by increasing blood lactate levels, but without symptoms.[69]"

"There is a potentially promising lead involving 2 readily available agents, bicarbonate and glucose.[113] Almeida investigated the toxicity of dimethyl sulfide (Me2S), a less potent and more easily handled analogue of hydrosulfide, in Sprague Dawley rats. The incidence and duration of coma (the rat equivalent of knockdown) induced by this agent over a range of dose was determined and with this model the efficacy of purported antidotes for H2S was determined. Using a standard dose of dimethyl sulfide that reliably induced the coma effect, 3 agents proposed to protect against lethality from hydrogen sulfide, nitrite, pyruvate, and dithiothreitol, were found to have no significant effect in shortening duration of coma and preventing lethality, whether given at onset of coma or as pretreatment. Bicarbonate, however, reduced duration of coma by about 28% but did not affect lethality. Bicarbonate and glucose administered together, however, reduced coma duration 37% and mortality 50% if given at onset and the effect was even greater when given as a pretreatment, reducing coma duration by 80% and preventing mortality altogether. Sulfide toxicity in the central nervous system may therefore be associated in some way with the metabolism of glucose. Perhaps cellular hypoglycemia and carbonic anhydrase activity play a role in the pathophysiology of sulfide toxicity, although earlier studies have suggested a hyperglycemic response,[116] perhaps due to stress and catecholamine release."

"Sulfide disappears quickly from the circulation under conditions of good oxygenation anyway."​

 

[Amazoniac]

Foulium cycle (simplified):

Spoiler

Source: couldn't track.

- Metabolism of Natural Polymeric Sulfur Compounds

Spoiler

- Hydrogen Sulfide (H2S) - The Relationship of Bacteria to its Formation, Prevention, and Elimination

Spoiler

- The Microbial World - Winogradsky column: perpetual life in a tube
- The Colorless Sulfur Bacteria

 

[Amazoniac]

- Estimation of bacterial hydrogen sulfide production in vitro

"Periodontal disease is believed to be associated with an anaerobic and proteolytic bacterial metabolism but the pathogenesis is still largely unknown. Hydrogen sulfide (H2S) is a toxic, bacterial waste product in the subgingival pocket and up to 1.9 mM H2S has been detected in gingival crevicular fluid (1, 2). Due to its proinflammatory properties, it has been suggested that H2S may participate in the bacteria-induced inflammatory response in the periodontal diseases (36)."

"The H2S-producing capacity is commonly tested by blackening of lead acetate paper (10) or with gas chromatography (1, 11) and sensors (1214). These methods are either rough or require complex equipment and are therefore expensive. Simple chair-side methods for semiquantification of bacterial H2S, which could further facilitate the investigation of H2S production and presence, are lacking."

"The aim of the present study is to examine oral bacterial H2S production in vitro comparing two colorimetric methods in microtiter plate format."

"Bacterial hydrogen sulfide (H2S) production from cysteine measured with two colorimetric methods in microtiter plate format, recorded as black bismuth sulfide (BS) precipitation and methylene blue (MB) formation":

Spoiler

"The bacterial species tested for H2S-producing capacity are given in Table 1. The species were grown on appropriate agar plates under optimal conditions."

"Both methods, based on BS precipitation and MB formation, respectively, had a high reproducibility, reliability, and simplicity. The highest rate to maximal detectable production of H2S was found for Fusobacterium spp. Different findings from the two methods for some bacteria may reflect different pathways used for H2S production and, therefore, the BS and MB methods may complement one another. The BS method was more sensitive than the MB method and may be suitable for in vivo estimation of H2S production, using, for example, plaque samples from bacterial infections, such as in the periodontal pockets and other anaerobic infection sites. The production of H2S is complex and needs more attention in future studies to enhance the knowledge of the mechanisms involved in H2S production and its impact in vivo."​

 

[Amazoniac]

The quality of the article below isn't the best, but it has interesting bits. Some parts are repeated, it's for the sake of clarity.

- Sulphurous Mineral Waters: New Applications for Health

Spoiler

"Being a gas, H2S can be absorbed by numerous routes. It is able to penetrate the skin and mucosae and can therefore act at the cell level both in the skin and in internal organs of our organism. This means that the topical application of sulphurous mineral waters rich in hydrogen sulphite has the potential to treat disorders of the internal organs such as high blood pressure, ischemia, and conditions affecting the kidneys or nervous system. Further, if sulphurous mineral water is applied to the skin in the form of a matured mud, or peloid, its effects may be potentiated. Many authors have examined the mechanisms of action of medicinal waters and their therapeutic effects, and certain inorganic components have been linked to the effects of curing baths [3–7] and muds [8–11]."

"Its stability depends on the pH, temperature, and the oxygen concentration of the environment.

Sulphur forms change at two critical pHs, pKa = 7.04 and pKa = 11.96. At physiological pH, the ratio of hydrogen sulphide to bisulphide (HS−) is 1:3. Thus, two identical solutions of H2S show different concentrations at different ambient temperature and the presence of oxygen will promote the reduction of hydrogen sulphide to hydrogen sulphate.

At acidic pH, H2S is the only form of sulphur. At a pH of 7.04, sulphur salts occur at a 50% concentration and when the pH is around 9.5 only bisulphide will exist (HS−). Beyond pH 9.5, sulphides (S2−) start to form and as pH increases, this anion is the only viable form of sulphur (Figure 1)."

Spoiler

"The composition of sulphurous mineral water has been well-established. However, regardless of accompanying salts, for this mineral water to exert its beneficial effects, it must contain a reasonable amount of H2S or HS− and thus have a relatively acidic pH. In contrast, S2− usually found in alkaline waters are inert or do not exert the same activity [14]."

"Another factor to consider is that although H2S is a gas, HS− and S2− are salts. This means that H2S will be more easily absorbed through the skin and mucosa than its soluble salts. Further, given that the reactivity of dissociated HS− is greater than that of H2S, it may be assumed that [15] (1) both the gas and anions coexist in vivo; (2) dissociated bisulphide is more reactive than H2S and peaks at pH 11 [16]; and (3) the presence of oxygen could diminish the reduction force. This means that H2S molecules will more actively penetrate the skin rather than remaining on the surface."

"In nature, H2S is generated by the decomposition of organic matter, whereby it is aerobically oxidized to elemental sulphur and then transformed to sulphates through the activity of bacteria and other microorganisms. Likewise, sulphates can be anaerobically reduced to H2S through their assimilation by living organisms or their decomposition by microorganisms, thus closing the sulphur cycle [18]. Thus, in simple terms, anaerobically reduced sulphates give rise to H2S, which is aerobically oxidized to sulphate."

"In balneology, medicinal muds (peloids) can be generated through these reactions [9]. This mud has similar properties to water [19] and matures over time improving their properties of granulometry, specific heat, caloric retentivity, inertia time, relaxation time, hardness, adhesiveness, cohesion, and springiness [20, 21]. Mud treatments have been used for wounds produced by trauma. In this application, water remains in contact with the skin surface for a long time and absorption of the active principle is enhanced due to occlusion and ion exchange at temperatures slightly above physiological [22]. For this purpose, the use of peloids produced from sulphurous mineral waters is common. These peloids have their own peculiar characteristics [11]."

"According to the data available so far, balneotherapy using thermal-mineral waters and peloids has proved to be an effective remedy for lower back pain and knee and hand osteoarthritis [23–26]."

"There are [] three nonenzymatic ways to produce H2S: through sulphurous proteins, sulphite, or thiosulphate. Conversely, there are five ways of removing H2S in the organism: by its conversion into thiocyanate via rhodanese; by its transformation into sulphurous proteins; through thiol molecules; by converting haemoglobin into sulfhaemoglobin; and by its transformation into methanethiol."

"Sulphurous mineral water may be absorbed through the skin causing vasodilation, analgesia, immune response inhibition, and keratolytic effects that reduce skin desquamation [47]. It is also known that the topical application of H2S will also have an effect on the internal organs [48]."

"The therapeutic action of sulphurous mineral waters is related mainly to sulphur’s keratolytic, or peeling, effect. Sulphurous mineral water exerts beneficial anti-inflammatory, keratoplastic, and antipruritic effects [49]. Its bactericidal and antifungal properties have determined its use for the treatment of infected leg ulcers, tinea versicolor, tinea corporis, and tinea capitis [50]. Further, within the epidermis, H2S is transformed into sulphur, which may also interact with oxygen radicals in the deeper layers of the epidermis. Here, sulphur may be converted into pentathionic acid (H2S5O6), which could explain the antibacterial and antifungal properties of sulphurous mineral waters [51]."

"Skin treatments based on mineral water or muds derived from mineral waters have been traditionally used in Europe [52]. Some of the cutaneous activity of sulphurous mineral waters is based on the formation of colloidal sulphur inside the skin via chemical reactions or microbial metabolism, where it then acts as a keratolytic agent. Accordingly, sulphur eliminates disulphide cystine bonds between corneocytes. This gives rise to two cysteine molecules, promoting desquamation of the stratum corneum (Figure 3)."

"Sulphurous spa baths have been used successfully for immunomediated conditions such as contact dermatitis, psoriasis, and atopic dermatitis, and it has been recently suggested that the active principles of sulphurous mineral waters could play a role in immune regulation in the skin [59]."

"Sulphurous mineral water inhalations and irrigations have been traditionally used to treat airway diseases [60–63]. According to Keller et al. [64], compared to isotonic saline solution, sulphurous mineral water shows benefits and should be investigated further."

"The inhalation of sulphurous mineral waters has been shown to improve the health state of patients with chronic obstructive pulmonary disease (COPD) [67]."

"The topical use of H2S is not free of complications. The use of concentrated sulphurous mineral water and especially bathing in hot springs can produce skin conditions ranging from irritative dermatitis to chemical burns."

"Long-term exposure to even low levels of H2S at the workplace has been reported to raise mean methaemoglobin and sulfhaemoglobin levels [72]."

"In mammalian cells, H2S passes through the cell membrane and its salts pass through bisulphide channels, where they are exchanged for Cl− (by anion exchange protein AE1). In the extracellular matrix, under physiological conditions of pH 7.4 and 37°C, only approximately 20% H2S exists as a gas. H2S dissociates to HS− with a trace amount of S2−. This means it is mostly absorbed as bisulphide (Figure 4)."

"[..]within the epidermis, the extracellular environmental pH is much lower than inside the cell (4.5–6.5) and the temperature is also slightly lower (35°C)." "[..]virtually all sulphur occurs as H2S."

"Yang et al. [78] reported that the newly synthesized H2S donor is capable of protecting human skin keratinocytes from methylglyoxal-induced injury and dysfunction. Thus, it could be that H2S-releasing molecules will improve wound healing in patients with diabetes mellitus. Suzuki et al. [79] have found differences in plasma levels of hydrogen sulphide in diabetic patients."

"Pharmacological molecules that release H2S too quickly do not adequately mimic the physiological effects of the gas. Hence, slow-releasing H2S donors are a more appropriate source of hydrogen sulphide than even a sulphur salt solution. In addition, the beneficial effects of H2S on inflammation are concentration and time-dependent and may involve bell-shaped dose-response curves."

"In conclusion, several new lines of evidence indicating a role of hydrogen sulphide as a cell messenger with cytoprotective effects anticipate promising perspectives for treatments with sulphurous mineral waters [104]."

 

[Amazoniac]

For cases that are overwhelming, I think that reserving a couple of times a week to obtain most of the share of your dietary taurine and selenium may be a positive measure. If the overgrowth is not merely infectious, but compensatory, it's important to prevent their deficiency and arrest it.

Sulfate isn't included because it's easily supplemented transdermally. Even though it might affect bile composition (that in turn can be acted upon in the intestine), the excess should leave through urine.

It might be possible to supplement taurine or selenium topically, but I'm not confident in how well it works. Taurine has to affect bile nevertheless, it's something that you'll to deal with one way or another. Selenium occurs in small amounts and the body is capable of retaining for longer than taurine/sulfate, justifying the attempt to sneak in and get both together.

Since it's usual for magnesium to promote and calcium suppress bacterial activity, a hefty calcium dose along should be protective. As far as I know, it doesn't compromise the absorption of taurine or selenomethionine (prioritized over inorganic forms, but these can be inferior alternatives that end up being less problematic).

By consuming them as the last meal of the day (provided that it doesn't disturb sleep), it avoids anything that could sustain a negative reaction while leaving a long window for the immune system to act.

White chocalate would be it. The typical ingredients are cocoa butter, powdered milk and fine sugar. Eggshells (watchout for adverse effects from the proteins that hold them together or membrane residues) or calcium carbonate could replace milk to miminize issues, sieving would be needed to avoid large pieces just like it's done with sugar. Taurine is tasteless and dispersed selenium is mild. I haven't tried, but it should work. Excluding the fat, substituting sugar for honey and consuming them as a tea would be something to try if there's still trouble from this.

Spoiler

What's important is to not run low on those nutrients because they're critical.

It would be ideal to have a steady availability of taurine with bacteria cooperating for its production, but we can't count on this to be functioning. Decreasing the requirements of cysteine can be advantageous in these cases.
- Gut Microbiota And B-vitamins: An Estimation Of Its Contribution To Daily Intakes

 

[ecstatichamster]

For cases that are overwhelming, I think that reserving a couple of times a week to obtain most of the share of your dietary taurine and selenium may be a positive measure. If the overgrowth is not merely infectious, but compensatory, it's important to prevent their deficiency and arrest it.

Sulfate isn't included because it's easily supplemented transdermally. Even though it might affect bile composition (that in turn can be acted upon in the intestine), the excess should leave through urine.

It might be possible to supplement taurine or selenium topically, but I'm not confident in how well it works. Taurine has to affect bile nevertheless, it's something that you'll to deal with one way or another. Selenium occurs in small amounts and the body is capable of retaining for longer than taurine/sulfate, justifying the attempt to sneak in and get both together.

Since it's usual for magnesium to promote and calcium suppress bacterial activity, a hefty calcium dose along should be protective. As far as I know, it doesn't compromise the absorption of taurine or selenomethionine (prioritized over inorganic forms, but these can be inferior alternatives that end up being less problematic).

By consuming them as the last meal of the day (provided that it doesn't disturb sleep), it avoids anything that could sustain a negative reaction while leaves a long window for the immune system to act.

White chocalate would be it. The typical ingredients are cocoa butter, powdered milk and fine sugar. Eggshells (watchout for adverse effects from the proteins that hold them together or membrane residues) or calcium carbonate could replace milk to miminize issues, sieving would be needed to avoid large pieces just like it's done with sugar. Taurine is tasteless and dispersed selenium is mild. I haven't tried this, but it should work. Excluding the fat, substituting sugar for honey and consume it as a tea would be something to try if there's still trouble from this.

Spoiler

What's important is to not run low on those nutrients because they're critical.

It would be ideal to have a steady availability of taurine with bacteria cooperating for its production, but we can't count on this to be functioning. Decreasing the requirements of cysteine can be advantageous in these cases.
- Gut Microbiota And B-vitamins: An Estimation Of Its Contribution To Daily Intakes

your posts are amazing. Thank you so much.

 

[LLight]

Maybe you have already posted this one, but just in case:

Sulfate’s Critical Role for Maintaining Exclusion Zone Water: Dietary Factors Leading to Deficiencies

"In this paper we equate interfacial water with Exclusion Zone (EZ) water described by Pollack and propose that it is the sulfate molecule that plays a fundamental role in providing the interfacial negative charge that builds and maintains the EZ in biological systems."​

 

[Amazoniac]

- Fructose: A Dietary Sugar in Crosstalk with Microbiota Contributing to the Development and Progression of Non-Alcoholic Liver Disease

"Short-chain fatty acids are able to reduce the pH of the gut, altering the composition of microbiota. Changing the pH from 5.5 to 6.7 favors the population of gut microbiota that produces propionate, while reducing the pH to 5.5 favored bacteria producing butyrate (35). This process maintains the gut homeostasis and economy. As outlined [], butyrate is already more effective at lower concentrations than propionate and acetate, and it need to be considered that butyrate at higher concentrations may provide too much energy which can promote obesity."

"An increased production of intestinal bile acid occurs in a high fat diet." "As a consequence, bile-sensitive bacteria [..] will be less prevalent, and more bile-tolerant bacteria will be predominant."​

--
- Sulfide:quinone reductase - Wikipedia

"Sulfide:quinone reductase contains FAD. Ubiquinone, plastoquinone or menaquinone can act as acceptor in different species."​

 

[Amazoniac]

- Growth and activities of sulphate-reducing bacteria in gut contents of healthy subjects and patients with ulcerative colitis

"Almost all persons with ulcerative colitis (96%) seem to harbour significant populations of SRB compared to healthy individuals, where the carriage is only 50% [7]. Sulphate reducer counts and activities were markedly different in healthy and colitic faeces (Table 1)."

Spoiler

"Although overall transit rates through the colon of ulcerative colitis patients differ little from healthy individuals [26], these persons often have proximal colonic stasis [27]." "The distal part of the gut is always affected, although the inflammation often spreads backwards to the ileo-caecal junction [6]." "Their disorder is probably due to colonic irritation in the left colon which would tend to disperse populations of slow growing organisms. As MB [methylene blue] generally have slower growth rates compared to SRB, this may partly explain the high prevalence of sulphate reducers found in colitic patients. The continuous culture experiments made in this study showed that desulfovibrios growing in the colitic bowel were best able to grow at high dilution rates. In contrast, Desulfovibrio desulfuricans isolated from healthy colon contents could not be maintained at these growth rates in continuous culture. This indicates that fast growing strains had been selected for in the guts of the patients with ulcerative colitis."

"Although activities of SRB, as shown by H2S production and sulphate reduction rates in faecal slurries were relatively high in the colitic group, viable counts were low (Table 1). These data indicate that bacteria growing in the colitic colon do so at a higher rate with a more rapid turnover of substrate. Their numbers remain low however, due to the high volume of material passing through the left colon."

"A number of sulphated polysaccharides such as mucins or chondroitin sulphate are endogenously produced in the human large intestive. Mucin is a highly sulphated glycoprotein that is secreted by goblet cells lining the gut epithelium [28]. Table 3 shows how SRB activity may be influenced by the degree of substrate sulphation. SRB do not contain enzymes that enable them to directly metabolize sulphated carbohydrates. However, some fermentative bacteria in the colonic ecosystem are able to produce sulphatases that can release free sulphate from such substrates and include Bacteroides fragilis group bacteria and clostridia [29-31]. In this case, SRB activities in the gut would not only be related to the sulphate content of diet, but also to the retative amount of sulphated polysaccharides secreted in vivo, the degree of sulphation of these polymers and the activities of sulphatase containing bacteria that are able to utilize the substrates."

Spoiler

"In the healthy group of volunteers, none of the subjects had taken antibiotics for at least eight weeks prior to the study. In contrast, the drug sulfasalazine is widely used in the management of ulcerative colitis [32]. The compound consists of the antibiotic sulphapyridine linked by a diazo bond to the anti-inflammatory agent 5-aminosalicylic acid. The diazo bond is broken by bacteria in the colon releasing the two agents, either of which may become pharmacologically active [33,34]. It was considered that this could have consequences for the growth and activities of SRB in the colitic individual. However, experiments to test this showed that the drug had no effect on sulphate reduction in faecal slurries (Table 5)."

"In the event of high mucus production, as may occur in colitis, SRB activity would be stimulated, leading to an over-production of H2S. This could then impair mucus structure, either by direct action or the formation of mercaptans [9], Thus, SRB may perpetuate epithelial damage in ulcerative colitis, without necessarily being involved in initiation of the disease."​

One thing that I forgot to mention regarding chocalate is to be wary that taurine supplementation will enrichen bile in it, so for a few days anything that triggers a significant bile release can be in effect similar to taking taurine with the meal. Lowering temporarily the factors that increase secretion, supporting internal synthesis to decrease the dose or increasing glycine intake to change bile composition (I don't remember if it's going to be displacing or both will end up high) can be tried.

 

[Amazoniac]

Whenever eggshells are boiled for sterilization, there's the characteristic odor of sulfur compounds. The presence of organic residues becomes noticeable again after storing the powder for days, they start decomposing and giving off a pungent smell that intensifies with time.

About 4% of the eggshell are maked of proteins, but not all are potentially problematic. If we assume that 0.5% can be so (it's possible for the troubling compounds to belong to bigger structures and the whole component ends up being an issue if it's not broken down) and that killcium is responsible for about 35% of its weight, someone supplementing 350 mg could be consuming along 5 mg of fermentable proteins.

It sounds negligible, but I wouldn't dismiss it:
- We is capable of detecting odors for these compounds that occur in tiny amounts, which hints at potency and biological effect that they can have.
- There are persons who react poorly to 0.1-0.2 mg of selenomethionine (and only 40% being selenium), Travisord's signature amino acid.
- People tend to supplement more killcium than that.

The outer part of the eggshell may be acted upon by stomach acid, yet the inner part might escape intact attached and protected by membrane residues (concentrates a great deal of protein, it's easy to remove but takes patience, the task often ends up incomplete).

Dissolving cracked eggshells in acids (Jennifer, 2018) without pulverizing makes it possible to avoid the larger undesireable stuff, it's worth a try in case of doubt. However, some people are allergic to egg proteins and they might be found within the eggshells as well, traces must remain after processing. It's then valuable to compare with purified killcium craponate.

This is speculation, I don't know how concerning it is in practice and you'd have to be susceptible because there are persons who (for example) supplement the membranes and are not bothered by them. Sometimes it's good to have a mild trigger to keep signaling what has to be corrected without being overwhelming, but if there's no improvement, it can add to the chronic low-grade inflammation burden and complicate things unnecessarily.

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- Toxicology of Sulfur in Ruminants: Review
- High-sulfur in beef cattle diets: a review

 

[Amazoniac]

- Polioencephalomalacia in ruminants caused by excessive amount of sulphur - A review

 

[Amazoniac]

- A review of polioencephalomalacia in ruminants: is the development of malacic lesions associated with excess sulfur intake independent of thiamine deficiency?

Spoiler

- Biobehavioral variation in human water needs: How adaptations, early life environments, and the life course affect body water homeostasis (@Collden)

"[..]the external nose was an important adaptation for Homo to dry environments by providing the ability to retrieve moisture from exhaled air and then using this moisture to humidify the next breath to help conserve and reduce body water loss (Franciscus & Trinkaus, 1988; Lieberman, 2015)."​

--
- Metabolic acidosis after sodium thiosulfate infusion and the role of hydrogen sulfide
- Broad-Range Antiviral Activity of Hydrogen Sulfide Against Highly Pathogenic RNA Viruses

 

[Amazoniac]

- Polioencephalomalacia in ruminants caused by excessive amount of sulphur - A review

Spoiler

"The cause of the disease can be a single component diet fed over a sustained period and containing ingredients with high sulphur content, especially by-products from the mining and food industries. Mining and industrial water, cruciferous plants, some concentrates and milk substitutes, and also molasses and spent grain have high sulphur content (5, 13, 17, 20, 21, 24, 29). The ingestion of sulphur with water can be exceptionally high in situations of drought and high temperature when animals drink heavily (14, 23, 34)."

"Water with a high concentration of sulphates easily induces PEMES symptoms both in natural and experimental conditions (2, 12, 14). Similarly, an acute course of the disease leading to deaths was observed in single-component feeding with cruciferous plants (24), in which sulphur content is 3-5 times higher than in other plants commonly used in cattle feeding. In cruciferous plants it is about 1.5 % of dry matter, but only slightly lower concentrations can be found in fodder plants from industrial areas. PEMES was observed also in cattle kept in barns with a high H2S concentration in the air (9). High content of this gas is found in barns with residual slurry, which are inadequately ventilated. A concentration of H2S in the air higher than 150 ppm causes mucosal layer irritation, respiratory disturbances, and can induce PEMES (5). As H2S is heavier than air, it has a tendency to stay in barns, especially those with windows and ventilators placed high (5)."

"The speed of reduction of sulphur largely depends on the activity of different anaerobic bacteria which exist in the rumen. Various factors probably influence the reductive activity of the bacteria; among them the amount and kind of sulphur compound in the diet, diet composition, and the pH of rumen contents (4, 28)."

"Initially the reduction process of sulphur to H2S predominates. H2S in large concentrations causes dysfunction of the nervous and respiratory systems with the possibility of death. But quite fast acidosis of rumen develops, which inhibits proliferation and activity of microorganisms including reduction by bacteria. The concentration of H2S decreases and thus symptoms are limited or inexistent. With time there occurs a relative adaptation of the organism and reduction of bacteria to the excessive sulphur, followed by a moderate re-increase of H2S concentration with the possibility of PEMES development."

"Normally H2S is quickly utilised for synthesis of amino acids and sulphides. Absorbed sulphides are also quickly oxygenated to sulphates in the liver and they are in turn passed to extracellular fluids and eliminated with urine or return to the intestines or the rumen with saliva."

"Beside H2S, a large concentration of soluble sulphides in the rumen is also pathogenic. Sulphides given to lambs in large amounts via the oesophagus cause clinical signs of nervous system dysfunction in the form of lethargy, spasms, and poor vision after a short period of time as 20 h (22). Some role can be played by deficiency in Cu, Mo, Zn, and Ca, which bind sulphur producing poorly soluble sulphides (5)."

"The necropsy of the animal died of PEMES has no defining peculiarity with the exception of the characteristic smell of hydrogen sulphide from rumen contents (if the necropsy is performed shortly after death) and the presence of degenerative necrotic foci in the brain. Quite often hyperaemia and inflammation of mucosal membranes, a light yellow liver, and dark coloured kidneys are observed (5). Morphological and histological changes in the brain are relatively distinctive. They occur very early, before clinical symptoms appear. They are noted in animals seemingly healthy and without specific subclinical symptoms in herds with a few clinical cases of the disease (8) and in experimental animals before symptoms appear (29). Typical changes are as follows: diffused degenerative necrotic foci undergoing malacia or liquefaction, and changes with spongious structure in the cerebral cortex, but also in the interbrain and brain stem (14). Degeneration and necrosis of neuron cells, leucocyte infiltrations around small blood vessels, and hypertrophy of gliomatous tissue dominate in the foci with spongious structure. Excavasations, capillary vessels hypertrophy, and fibrous degeneration of arterioles are also observed. (19)."

"It is recommended to administer vitamin B1, which improves metabolism in the brain and therefore protects animals from the development of degenerative necrotic lesions and facilitates their healing (24). In acute cases, it is recommended to administer orally alkalising preparations, such as sodium bicarbonate, calcium carbonate, or magnesium oxide, to increase pH and remove acidosis (5). Neutralisation of acid components of the diet with a 2% solution of sodium hydroxide is advised."

- Toxicology of Sulfur in Ruminants: Review

Spoiler

"Hydrogen sulfide poisoning in ruminants can be treated successfully either with glucose saline, followed with glycerine by mouth and bismuth carbonate, or with bismuth carbonate mixed into the feed in the form of cubes for those animals willing to eat (53). This treatment limits absorption of sulfide from the rumen by reducing the absorption rate constant by increasing rumen pH. In White's report (53) all ailing ewes were drenched daily with saline and .140 liters of glycerine. In addition, hydrogen sulfide poisoning in cattle has been treated with intramuscular injection of camphor in oil or calcium gluconate solution intravenously (18). Coghlin (18) recommended as a chemical antidote for sulfuretted hydrogen the following mixture: 31.1 g of iron sulfate [justification below] and 15.6 g of liquor ammonia fortis, dissolved in 1.135 liters of warm water. The mixture was prepared extemporaneously and given as one dose."

- High-sulfur in beef cattle diets: a review

Spoiler

"Bacterial sulfate reduction may be classified as either dissimilatory, also known as sulfate respiration, or assimilatory. In assimilatory reduction, bacteria reduce sulfate to hydrogen sulfide (H2S) which is then utilized to produce S containing amino acids or co-factors such as biotin and pantothenic acid; while in dissimilatory reduction the bacteria reduce sulfate and produce H2S as an end product of their metabolism (Bradley et al., 2011). These dissimilatory sulfate reducing bacteria (SRB) utilize anaerobic respiration pathways for their bioenergetic processes, and depend on the dissimilatory sulfite reductase enzyme activity to do so (Bradley et al., 2011). Many SRB can also reduce other oxidized inorganic S compounds (sulfite, thiosulfate, or elemental S) as well as S-containing amino acids (Coleman, 1960; Barton and Fauque, 2009)."


"The etiology of S-PEM has not yet been fully elucidated, but it is speculated that eructated H2S gas is inhaled by the animal ultimately allowing H2S to enter the brain, which may then cause necrosis of the grey matter (Figure 1). Dougherty and Cook (1962) observed that 70 to 80% of gas eructated from the rumen is subsequently inhaled by the ruminant, which would allow the eructated gases to enter circulation without being detoxified by the liver. Further, when Dougherty et al. (1965) infused H2S into the rumen of sheep, they observed that sheep with an open trachea collapsed after several eructations, whereas those with a blocked trachea produced no clinical signs. These data suggest that the mechanism of toxicity is not through ruminal absorption of sulfide or H2S, but through the inhalation of eructated H2S."

- The effect of dietary sulfur on performance, mineral status, rumen hydrogen sulfide, and rumen microbial populations in yearling beef steers (!)

"At lower concentrations, ruminants may experience toxicity as a result of eructation. But if H2S concentrations become high enough, the amount absorbed through the rumen epithelia may result in toxicity. This toxicity by the epithelial route may be because the amount of H2S crossing the rumen epithelia exceeds the ability of the liver to detoxify H2S prior to entering the blood supply to the rest of the body."​

"In the ruminant, S is a major trace mineral antagonist. In the rumen, S can interact with molybdate to form complexes called thiomolybdates, which have very high affinity for Cu. Copper bound to thiomolybdates is unavailable for absorption and use by the animal, thus feeding high S diets causes a decrease in Cu status of the ruminant, potentially resulting in severe deficiency if not properly addressed (Suttle et al., 1991). In addition, S as sulfide, can bind to Cu and prevent absorption in the intestine (Suttle et al., 1991). Spears et al. (2011) reported that not only was liver Cu decreased in steers fed 0.31 or 0.46% S compared with 0.13% S, but also that activity of whole blood glutathione peroxidase, a Se-dependent enzyme, was lesser in 0.31% and 0.46% S-fed steers compared with 0.13% S-fed steers. In dairy cattle, Ivancic and Weiss (2001) reported that true Se digestibility was decreased as dietary S increased from 0.21% to 0.4% and 0.7%, regardless of Se concentration of the diet (0.13 or 0.27 mg Se/kg DM). Sulfur and Se share some similar chemical properties and there is evidence that the two elements compete for a common intestinal transporter (Ardüser et al., 1985). Additionally, S may compete for incorporation into selenoenzymes, thus decreasing enzyme activity (Lee et al., 2000)."

"Pogge et al. (2014a) found that steers receiving 0.68% S diets retained less Cu and Mn when compared with steers fed 0.20% S diets during a 5-d collection period. The maximum tolerable limit for S in cattle diets is not reflective of the concentrations of S which would negatively impact trace mineral status. Trace minerals such as Cu, Se, Mn, and Zn likely need to be included in the diet at greater than NRC recommendations when diet S concentration exceeds 0.30%. Decreased trace mineral status may contribute to decreased performance of cattle fed high S diets; however, the effects of S on trace mineral status will take some time and thus may have greater implication for ruminants fed high-S diets for long periods."

"Preliminary data by D. J. Pogge, J. Roth, and S. L. Hansen (unpublished) found that blood neutrophils isolated from non-stressed steers consuming a 0.55% S diet for 143 d had greater myeloperoxidase degranulation, indicating greater neutrophil fragility and oxidative stress, compared to neutrophils isolated from steers consuming a diet containing 0.22% S. Interestingly, the addition of vitamin C to the 0.55% S diet returned myeloperoxidase degranulation to values that were less than the control steers, indicating an increase in neutrophil membrane strength. These data support the idea that the capacity of cattle to cope with high S diets may potentially be improved by antioxidant supplementation to the diet. Particularly in light of new receiving cattle protocols where high dietary concentrations of wet DGS are utilized as cattle transition to high grain diets, further research on the impact of increased S diets on cattle immune function is warranted."

"[..]inorganic S such as calcium sulfate or ammonium sulfate would also be expected to be 100% available [in the rumen] for reduction by SRB."

"At one time it was thought that S-PEM was due to thiamine deficiency caused by ruminal destruction of thiamine (Goetsch and Owens, 1987; Gooneratne et al., 1989). However, when a semi-synthetic thiamine-free diet was fed to weaned lambs to test the effect of high S on the microbial production of thiamine, neither rumen thiamine concentration or thiaminase activity were modified by the dietary S content (0.2 vs. 0.6% S; Alves de Oliveira et al., 1996). Although Alves de Oliveira et al. (1997) reported that high S slightly decreased microbial thiamin production (326 vs. 266 nmol/d) in vitro, they concluded that it was unlikely to result in a substantial effect on thiamine status of the animal. In his review on S-PEM, Gould (1998) summarized data that suggests experimentally induced S-PEM (Sager et al., 1990; Gould et al., 1991) as well as some field cases of S-PEM (Mella et al., 1976) were not caused by thiamine deficiency. This is not the only evidence that high dietary S can induce PEM independent of a systemic or local thiamine deficiency. Olkowski et al. (1992) found that sheep fed a 0.63% S diet had slightly increased liver and blood thiamine concentrations compared to sheep fed a 0.19% S diet and that brain thiamine concentrations were unaffected by S concentration. Furthermore, baseline activity of the thiamine-dependent enzyme erythrocyte transketolase, and erythrocyte transketolase activity measured after addition of thiamine pyrophosphate (often used as a diagnostic marker of thiamine deficiency), were not affected by dietary S concentration in this study (Olkowski et al., 1992). In addition, feedlot cattle consuming high sulfate water (2,200 and 2,800 mg sulfate/L) exhibiting acute signs of PEM were found to have blood thiamine concentrations within normal reference ranges (McAllister et al., 1997). Likewise, Loneragan et al. (2005) reported that blood thiamine concentration was not affected by consumption of water with increased concentrations of sulfate (136, 583, or 2,360 mg sulfate/L water)."

"So why do many nutritionists feed supplemental thiamine in situations of high dietary S consumption? This may be because thiamine has nonspecific therapeutic benefits in cerebral diseases (Gould, 1998). Thiamine injections are the primary method of treatment for animals afflicted with PEM, regardless of cause (Ensley, 2011). Indeed PEM induced by acute Pb poisoning has been shown to be thiamine responsive (Gould, 1998). Thiamine plays a key role in the tri-carboxcylic acid cycle and pentose shunt and thus may increase energy availability to the diseased brain. Additionally, thiamine may reduce edema in the brain through thiamine-dependent enzymes (Olkowski et al., 1992)."

"[..]the depletion of GSH by S suggests the importance of GSH in detoxification of excess S. Depleting GSH may increase strain on other body antioxidants such as vitamin C, vitamin E, and trace mineral-dependent enzymes such as superoxide dismutase, catalase, and glutathione peroxidase; which, under normal conditions are able to neutralize radical species through the donation of electrons. As noted earlier, the absorption of some trace minerals necessary for the catalytic activity of many antioxidants is lessened when cattle consume high S diets, potentially increasing the likelihood of oxidative stress in these animals. While it is well established that S negatively affects trace mineral status (Suttle, 1991), no research addresses the repercussions of high S diets on the integrity of the trace mineral-dependent antioxidant enzymes."


"Research regarding mitigation of the toxic effects of high S in ruminant diets has centered around three basic strategies: inhibiting the metabolism of SRB, binding sulfide in the rumen fluid, or increasing ruminal pH in order to decrease the amount of sulfide that remains as H2S."

"With a pKa of 7.04, H2S can be converted to the HS- ion in the rumen (Schoonmaker and Beitz, 2012). As pH decreases, the amount of sulfide remaining in its gaseous form will increase."

"Decreased ruminal pH of cattle that consume high concentrate diets may partially contribute to increased S toxicity by increasing the amount of sulfide that remains as H2S. There is also evidence that the uptake of sulfate by SRB may be in symport with H+ (Cypionka, 1989), indicating that sulfate uptake and subsequent production of H2S would likely increase at the lower pH associated with concentrate diet-feeding of ruminants."

"Rumen pH taken immediately after H2S measures was found to be strongly negatively correlated with rumen H2S concentrations, until rumen pH exceeded 5.8, above which rumen pH was a poor predictor of H2S concentrations."

- The role of pH on the survival of rumen protozoa in steers

"Rumen pH can vary from 5.5 to 7.5 and this variation is influenced by the type of diet and the feeding frequency according to different ruminant species (Franzolin et al., 2010)."​

- Advances in Oral Drug Delivery for Regional Targeting in the Gastrointestinal Tract - Influence of Physiological, Pathophysiological and Pharmaceutical Factors

Spoiler

"Recently, Nichols et al. (2013) conducted a meta-analysis of finishing studies conducted at the University of Nebraska feedlots over a 7 yr period and suggested that there is a strong effect of the concentration of roughage NDF within a concentration of dietary RAS [Ruminally-available Sulfur] on the incidence of S-PEM. Risk of S-PEM decreased approximately 19% for each 1% increase in roughage NDF in the diet, within a given concentration of RAS."

"Decreased ruminal pH of cattle that consume high concentrate diets may partially contribute to increased S toxicity by increasing the amount of sulfide that remains as H2S. There is also evidence that the uptake of sulfate by SRB may be in symport with H+ (Cypionka, 1989), indicating that sulfate uptake and subsequent production of H2S would likely increase at the lower pH associated with concentrate diet-feeding of ruminants."

"Morine et al. (2014) tested two different roughage sources, chopped corn stalks and chopped bromegrass hay, at three concentrations of roughage NDF (4, 7, or 10% added NDF from roughage) using a Latin square design with cannulated steers fed DDGS-based diets (0.45% S). The authors observed that ruminal H2S was lesser in steers fed 7 or 10% roughage NDF, compared with those consuming 4% roughage NDF, regardless of roughage source. Rumen pH taken immediately after H2S measures was found to be strongly negatively correlated with rumen H2S concentrations, until rumen pH exceeded 5.8, above which rumen pH was a poor predictor of H2S concentrations."

"While in many studies ruminal pH is well correlated with H2S concentrations of ruminants fed high S diets, pH does not explain all of the variation in H2S measures."

"It is unclear if the decrease in ruminal H2S due to increasing effective NDF is strictly due to increased ruminal pH or whether shifts in microbial ecology of the rumen or changes in eating behavior may also be contributing factors. Increasing effective NDF in a high concentrate, high S diet, may have decreased H2S and increased pH in part due to increasing chewing and saliva production."

"More work is necessary to clarify this complex relationship between ruminal pH and H2S as not all authors have noted a significant correlation between ruminal pH and ruminal H2S concentrations (Sarturi et al., 2013b), which may be due to differences in H2S measurement methodology and sensitivity."


"Kung et al. (1998*) found that adding 10 mg/L of 9, 10 anthraquinone to in vitro culture fluid decreased sulfide production by 71%. Regrettably, the use of this compound is likely limited by its availability and cost."

- Inhibition of Sulfate Reduction to Sulfide by 9,10-Anthraquinone in In Vitro Ruminal Fermentations*

- Effects of various compounds on in vitro ruminal fermentation and production of sulfide

Spoiler

"[..]sulfide is readily absorbed through the rumen wall into the blood stream (Bray, 1969). Once absorbed, sulfide inhibits the functions of carbonic anhydrase, dopa-oxidase, catalases, peroxidases, dehydrogenases, and dipeptidases, adversely affecting oxidative metabolism and the production of ATP (Short and Edwards, 1989). Specifically, sulfide is also thought to block the enzyme cytochrome c-oxidase. Sulfide also binds to hemoglobin creating sulfhemoglobin, reducing the ability of the blood to carry oxygen to tissues. In addition, sulfide also has a paralyzing effect on the carotid body and, therefore, may also inhibit normal respiration (Bulgin et al., 1996). In the environment, iron and steel structures are prone to corrosion in the presence of sulfides (Odom and Singleton, 1993). In the work place, the presence of hydrogen sulfide gas at low concentrations (50±200 ppm) is an irritant to the human respiratory tract, and at higher concentrations (200±500 ppm) it can cause hemorrhagic pulmonary edema that is often fatal (Green et al., 1991). Broad-spectrum biocides, such as hypochlorite (Odom and Singleton, 1993), methylenebis thiocyanate (Zhou and King, 1995) and gentamicin (Tanimoto et al., 1989) have been used to control sulfide production. Most, if not all, of these biocides would be impractical to use in ruminant diets because their broad antimicrobial spectrums would negatively impact ruminal fermentation."

- Hydrogen sulfide as a novel biomarker of asthma and chronic obstructive pulmonary disease

"Others have evaluated the use of clay minerals such as zeolite (Knight et al., 2008) or clinoptilolite (Cammack et al., 2010) as hydrogen sinks to lessen H2S production in cattle fed high S diets, but in both cases, the clay mineral had no effects on cattle performance."

"Molybdate has been shown to inhibit SRB in many environments, including rumen fluid (Gawthorne and Nader, 1976; Kung et al., 2000). Kung et al. (2000 [⇈]) showed that the addition of 10 mg/L of Mo to in vitro culture fluid decreased H2S by 11% and 25 mg Mo/L decreased H2S by 77%. Unfortunately, Mo can bind to Cu in the rumen causing the formation of an insoluble complex, thereby decreasing the availability of Cu to the animal, and causing potential for Cu deficiency. To achieve concentrations of 10 mg Mo/L of rumen fluid the Mo concentration in the diet would need to be at least four times the maximum tolerable level of 10 mg of Mo/kg of diet DM, which was determined based on the deleterious effects of Mo on Cu metabolism in the ruminant (NRC, 2005). Kessler et al. (2012) reported that supplementing Mo at a rate of 187.5 mg/kg DM to steers consuming high sulfate water (2,218 mg sulfate/L; ~0.073% S) substantially decreased liver Cu concentrations, and unfortunately, resulted in greater ruminal H2S concentrations than steers receiving the high sulfate water alone."

"Copper has the potential to bind with sulfide in the rumen."

"Some researchers have tested manganese oxide (Mn(II)O) as a potential mitigator of ruminal H2S production (Kelzer et al., 2010). When the effects of adding various concentrations of Mn(II)O to in vitro fluid was tested, the results were inconclusive as H2S production responses were inconsistent (Kelzer et al., 2010)."

"Sulfate reducing bacteria, most prominently Desulfovibrio, are also referred to as dissimilatory metal reducing bacteria because of their capability to reduce heavy metals (at certain states) such as Au, Cr, Fe, Mn, Mo, and Se, to name a few (Barton and Fauque, 2009). Recently, inclusion of ferric Fe was evaluated as a method of decreasing H2S concentration (Drewnoski et al., 2013; Drewnoski and Hansen, 2013b; Drewnoski et al., 2014). It was theorized that dissimilatory ferric Fe reduction could inhibit sulfate reduction and that the resulting ferrous Fe could also bind with some of the sulfide in the rumen fluid. Since ferric Fe has a greater redox potential than sulfate, adding a soluble form of ferric Fe could decrease ruminal sulfate reduction by competing for the same electron donors. Furthermore, some species of Desulfovibrio can carry out ferric Fe reduction, thus these SRB could potentially transfer their activity from sulfate reduction to Fe reduction. When the effect of ferric citrate and ferric ammonium citrate on in vitro production of H2S was tested, it was found that inclusion of either source of ferric Fe at 71 mg/L resulted in a 51% reduction of H2S."


"Currently, no magic bullet exists in the battle against S toxicity. However, sound cattle management and an understanding of ruminal S metabolism and how dietary factors affect H2S are the best weapons against S toxicity. To date, the most valuable tools for a nutritionist or cattle feeder in the prevention of S-induced toxicity appear to be a strong understanding of the ruminal availability of the S in the diet and inclusion of sufficient dietary roughage. A minimum of 7 to 8% NDF from a roughage source should be included in diets containing 0.4% or more S, to minimize risk of S-PEM. Alternative means to cope with the negative effects of S on cattle health and performance need to be identified. Future research in this area should focus on identifying additional factors which affect H2S production by SRB in the rumen of cattle fed high S diets as targets for mitigation strategies. Since H2S cytotoxicity may be because of oxidative damage, and the trace mineral status of cattle fed high S diets may be compromised due to ruminal antagonisms, future research should focus on antioxidants as potential ameliorators of S-toxicity."

 

[Amazoniac]

Contribution of dietary protein to sulfide production in the large intestine: an in vitro and a controlled feeding study in humans

Spoiler

"Five healthy men were housed in a metabolic suite and fed a sequence of 5 diets for 10 d each." "All subjects had [..] no history of gastrointestinal disease."

"Meat intake ranged from 0 g/d with a vegetarian diet to 600 g/d with a high-meat diet, with intermediate amounts of 60 g/d, 240 g/d, and 420 g/d."

"Fecal sulfide and urinary sulfate were measured in samples collected on days 9 and 10 of each diet period."

"Individual mean transit time ranged from 25 to 172 h across the diets with a group mean (±SEM) of 75.8 ± 18.6 h; there was no significant variance between dietary treatments."

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

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

 

[Amazoniac]

- Amino acid - Wikipedia

- Physiological actions of taurine

Spoiler

"Taurine is an amino acid that differs from the more familiar substances of that class in being a sulfonic rather than a carboxylic amino acid and in being a b-amino acid rather than an a-amino acid. Compared with carboxylate groups, the sulfonate group is a strong acid, having an acidic dissociation constant (pKa) equivalent to that of a mineral acid, such as hydrochloric acid (Table 2). The high acidity makes taurine almost completely zwitterionic over the physiological pH range. In contrast, a significant fraction of carboxylic amino acids exist unionized over this range (Fig. 1). At pH 7.4, the fractions of b-alanine and GABA having unionized acid functions are 125 and 340 times greater than the fraction of taurine."

"The zwitterionic nature of taurine gives it high water solubility and low lipophilicity. Consequently, compared with carboxylic amino acids, diffusion through lipophilic membranes is slow for taurine."

"The sulfur in taurine is in the form of a sulfonate and may be further oxidized to sulfate. The lowest oxidation state for sulfur is -2, and the highest is +6. The sulfur in taurine, at +4, has a free energy content of ~260 kJ/mol relative to sulfate (Fig. 4)."

 

[Amazoniac]

'Buffoon'

- The Plasma Cysteine/Sulphate Ratio: A Possible Clinical Biomarker

Spoiler

"Sulphation is a major detoxification pathway for a wide range of endogenous compounds, including phenols, bile acids, catecholamines, serotonin and steroids. Exogenous substrates such as ascorbic acid, paracetamol and various other drugs are also conjugated with sulphate [1, 2] and the process requires the involvement of the sulphotransferase enzymes (SULT isoforms) together with PAPS (3’-phosphoadenosine-5’-phosphosulphate) as the activated sulphate donor [3]. Neurotransmitters such as dopamine are inactivated by this pathway; sulphation accounts for approximately 80% of dopamine metabolism in man, and also removes dietary neurotransmitters such as tyramine from cheese, serotonin from bananas, and p-phenylethylamine from chocolate. Failure to carry out this reaction leads to neurotransmitter imbalances which may have clinical consequences; patients with migraine usually have reduced activity of SULT 1A1 (PST) and sometimes also SULT 1A3 (MST) [4]. Generally, sulphation is a high-affinity but low-capacity process [5] limited by the supply of PAPS. This is in turn controlled by the levels of free organic sulphate. Absorption of this anion across the gut occurs via a 2Na(+)/SO4(2−) sodium/sulphate transporter, which is easily saturated."

"The amino acid cysteine is obtained from the breakdown of dietary protein, and from transulphuration of another dietary amino acid, methionine. Most of the sulphate in vivo (approximately 80–90%) is formed via oxidation of cysteine. This reaction sequence involves an initial (and rate-determining) step using the enzyme cysteine dioxygenase to convert the cysteine to cysteine sulphinic acid. This is degraded by transamination and subsequent fission to form sulphite, which is oxidized to sulphate by the enzyme sulphite oxidase, which has a molybdopterin complex as cofactor (Fig. 1)."

"Reduced supplies of sulphate not only affect the removal of drugs and neurotransmitters, they also alter the synthesis of biocomponents such as the mucin proteins which line the gastrointestinal tract. These have a protein core with peptide branches, which have many sialic acid and sulphate residues. The sulphation has been shown to be essential for the initial stages in mucin formation, and also for the twin functions of lubrication and protection of tissues from the gut contents. Sulphation here is controlled by another member of the sulphotransferase family, tyrosyl protein sulphotransferase and it has been shown [6] that reduced sulphation of gut mucin is linked with increased permeability and irritable bowel disease. Other proteins and peptides require sulphation for optimal function."

"Both gastrin and the peptide cholecystokinin (CCK) need to be sulphated before being activated. Gastrin is involved in the release of stomach acid and pepsin. CCK is involved in the release of digestive enzymes. CCK and gastrin potentiate the action of secretin, which is also involved in the release of digestive enzymes. If protein digestion is inefficient, peptides can enter the bloodstream before being broken down into amino acids [7]. This process is exacerbated if the gut wall is leaky, as increased numbers of large peptides will reach the blood, causing allergic reactions."

"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 [9, 10]. Other substances, like chlorophenols and chloro-nitrophenols, also inhibit sulphotransferases, and other chemicals may inhibit PAPS formation."

"The ability to conjugate with sulphate is variable, and requires both active sulphotransferase enzymes and adequate supplies of sulphate [11, 12]. Poor ability to conjugate amines and phenols with sulphate appears to be implicated in a variety of conditions, like food sensitivity, chemical susceptibility, Parkinson’s disease, motor neurone disease, Alzheimer’s disease, chronic fatigue syndrome, migraine, rheumatoid arthritis, lupus erythematosus, inflammatory bowel disease, asthma, depression, hyperactivity, systemic primary biliary cirrhosis, adverse drug reactions, and autism [1, 7, 13–21]."

"The oxidation of cysteine, eventually forming sulphate, appears to be a critical process which is tightly controlled. Cysteine levels are rate determining in glutathione synthesis, so that their concentration effectively determines the major part of the thiol redux system. If cysteine levels are too low, the organism will be more subject to damage from reactive oxygen species, which are generally removed either by thiols or by glutathione-linked enzymes."

"Viruses can react with thiol-containing compounds, and this may explain why low plasma cysteine levels have been found in patients who are HIV positive [22]. N-acetyl cysteine alone, or combined with vitamin C, was found to be effective in HIV patients [23–26], as was a cysteine-rich whey protein formula [27, 28]. Possible mechanisms for the action of cysteine in HIV patients are the release of anti-HIV cytokines [29], the disruption of membranes by anti-microbial cysteine-rich protegrins [30] and the inactivation of HIV protease [31]."

"However, other problems may arise if cysteine levels are high, as cysteine is an excitotoxin acting at the N-methyl-D-aspartic acid (NMDA) subtype of the glutamate receptor, and hence alters neuronal transmission [19, 32]. Cysteine levels are raised in Alzheimer’s and Parkinson’s diseases [14, 33] and have been implicated in memory loss consequent on hippocampal damage. Increased concentrations of plasma cysteine also drive the synthesis of the pro-inflammatory leukotriene–cysteine adducts [34–36] which form complexes with complement C4 and inhibit its action; they are found in rheumatoid arthritis and other autoimmune conditions [37]."


"Checking plasma levels of sulphate and cysteine and the ratio between them can, therefore, be helpful when assessing how to treat a variety of people with chronic problems, as these parameters may give information on the underlying biochemical disease processes. A group of patients with chronic illness, often affecting multiple body systems, was therefore studied to determine how many were affected by abnormal cysteine and sulphate levels and how many had abnormal cysteine/sulphate ratios."

"The patients were divided into categories, according to whether their cysteine and sulphate levels and (cysteine × 1000)/sulphate ratio were above, below or within the reference range."

Grouped:

- Group A: patients with high cysteine, low sulphate and high ratio
- Group B: patients with low cysteine, low sulphate and high ratio
- Group C: normal cysteine, low sulphate and high ratio
- Group D: high cysteine, normal sulphate and high ratio
- Group E: normal cysteine, normal sulphate and high ratio
- Group F: low cysteine, normal sulphate and high ratio
- Group G: low cysteine, normal sulphate and low ratio
- Group H: low cysteine, normal sulphate and normal ratio

Groups A-H:

"The combination of high cysteine and low sulphate levels, as seen in group A, the most numerous subset, may reflect the presence of inflammatory cytokines, as tumour necrosis factor-a (TNF-a) and transforming growth factor-b have been shown to inhibit the expression of cysteine dioxygenase, the enzyme catalysing the initial step in cysteine conversion [39, 40]. Another possibility is that there are mutations in the DNA coding for the enzyme, or in the flanking regions, which lead to a less efficient isozyme of cysteine dioxygenase. Patients in group A often had a family history of chronic illness, suggesting that this could be a susceptibility factor. Research to determine to what extent abnormalities of sulphur metabolism are inherited would be useful. Patients in group B (low cysteine, low sulphate) might have some fault in cysteine synthesis or some viral infection, while group C patients (normal cysteine, low sulphate) could be linked with poor conversion from cysteine to sulphate. Group D, with high cysteine and normal sulphate levels, could reflect increased tissue breakdown or protein consumption; other problems in sulphur metabolism may also be involved here. Groups E, F, G and H had too few individuals to draw any tentative conclusions."

"The measles vaccination has been found to increase the levels of the Th1 cytokines, interferon-c, soluble interleukin-2 receptor (sIL-2R) and TNF-a [41]."

"Corticosteroids upregulate cysteine dioxygenase. As pantothenate is required to produce cortisol, an inadequate level of pantothenate may cause poor conversion of cysteine to sulphate."

"If conversion from cysteine to sulphate is poor, molybdenum and vitamin B2 can be supplied, to improve the conversion from sulphite to sulphate by the enzyme sulphite oxidase [49]. Epsom salt baths can also be used to provide sulphate, as it passes through the skin. Vitamin B6 can be supplemented, in order to reduce a high level of cysteine by converting it to taurine. Magnesium, zinc and vitamin B2 are required with vitamin B6."

"Foods high in the toxic mineral boron, like tomatoes and apricots, cause excretion of vitamin B2 [50, 51] and may therefore inhibit the enzyme sulphite oxidase that converts sulphite to sulphate. Diets high in purines, caffeine or alcohol may reduce the quantity of sulphite oxidase, by competing for molybdenum and vitamin B2 [49]."

"In depression there may be high levels of histamine in the brain, and reducing this by inactivation with sulphate may improve mood [52]."

"Testing cysteine and sulphate levels may become a useful technique for investigating chronic health problems including multiple sclerosis, myalgic encephalomyelitis, irritable bowel syndrome, autism, depression, motor neurone disease, Parkinson’s, Alzheimer’s, haemolytic anaemia, and also other conditions that are difficult to define. Double-blind clinical trials would be valuable to determine how effective it is to treat patients with molybdenum, vitamins B2, B6 and C, pantothenate, fish or flax oil, Epsom salt baths, N-acetyl cysteine, zinc and/or magnesium. Testing sulphate levels could be used to determine who is likely to be particularly susceptible to environmental chemicals, so as to advise them against employment in particularly polluted environments, against using unnecessary drugs and against using pesticides. Inoculations may contain phenol [53–55] and might need to be avoided where possible."

"The results of the 81 patients tested [were] summarized in Table 10, together with suggestions for possible treatment. Those with inefficient sulphate production could be advised to use diets with lower quantities of amines and bioflavonoids than the rest of the population. Advice to drink red wine may protect against coronary heart disease, but at the expense of other symptoms in susceptible people. High amine and bioflavonoid foods are listed in Tables 11 and 12. The nutritional and dietary suggestions are based on the biochemistry discussed above."

"It is important for patients who do not have a clear diagnosis to have tests that show that their problems are real. The cysteine/sulphate test can contribute to this. Then their families, friends, doctors, employers, or benefit agencies can take them seriously."

"Those already on supplements and a diet were less likely to have a very high ratio, suggesting that supplements and a special diet might be helping them. It would therefore be useful to test a series of patients before starting nutritional supplements and a diet, and then to repeat the test a few months later, to determine how successful the programme has been in improving the ratio, and thus the conversion of cysteine to sulphate."

 

[Kvothe]

'Buffoon'

- The Plasma Cysteine/Sulphate Ratio: A Possible Clinical Biomarker

Spoiler

"Sulphation is a major detoxification pathway for a wide range of endogenous compounds, including phenols, bile acids, catecholamines, serotonin and steroids. Exogenous substrates such as ascorbic acid, paracetamol and various other drugs are also conjugated with sulphate [1, 2] and the process requires the involvement of the sulphotransferase enzymes (SULT isoforms) together with PAPS (3’-phosphoadenosine-5’-phosphosulphate) as the activated sulphate donor [3]. Neurotransmitters such as dopamine are inactivated by this pathway; sulphation accounts for approximately 80% of dopamine metabolism in man, and also removes dietary neurotransmitters such as tyramine from cheese, serotonin from bananas, and p-phenylethylamine from chocolate. Failure to carry out this reaction leads to neurotransmitter imbalances which may have clinical consequences; patients with migraine usually have reduced activity of SULT 1A1 (PST) and sometimes also SULT 1A3 (MST) [4]. Generally, sulphation is a high-affinity but low-capacity process [5] limited by the supply of PAPS. This is in turn controlled by the levels of free organic sulphate. Absorption of this anion across the gut occurs via a 2Na(+)/SO4(2−) sodium/sulphate transporter, which is easily saturated."

Spoiler

​

"The amino acid cysteine is obtained from the breakdown of dietary protein, and from transulphuration of another dietary amino acid, methionine. Most of the sulphate in vivo (approximately 80–90%) is formed via oxidation of cysteine. This reaction sequence involves an initial (and rate-determining) step using the enzyme cysteine dioxygenase to convert the cysteine to cysteine sulphinic acid. This is degraded by transamination and subsequent fission to form sulphite, which is oxidized to sulphate by the enzyme sulphite oxidase, which has a molybdopterin complex as cofactor (Fig. 1)."​

​

View attachment 20809​

​

"Reduced supplies of sulphate not only affect the removal of drugs and neurotransmitters, they also alter the synthesis of biocomponents such as the mucin proteins which line the gastrointestinal tract. These have a protein core with peptide branches, which have many sialic acid and sulphate residues. The sulphation has been shown to be essential for the initial stages in mucin formation, and also for the twin functions of lubrication and protection of tissues from the gut contents. Sulphation here is controlled by another member of the sulphotransferase family, tyrosyl protein sulphotransferase and it has been shown [6] that reduced sulphation of gut mucin is linked with increased permeability and irritable bowel disease. Other proteins and peptides require sulphation for optimal function."​

​

"Both gastrin and the peptide cholecystokinin (CCK) need to be sulphated before being activated. Gastrin is involved in the release of stomach acid and pepsin. CCK is involved in the release of digestive enzymes. CCK and gastrin potentiate the action of secretin, which is also involved in the release of digestive enzymes. If protein digestion is inefficient, peptides can enter the bloodstream before being broken down into amino acids [7]. This process is exacerbated if the gut wall is leaky, as increased numbers of large peptides will reach the blood, causing allergic reactions."​

​

"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 [9, 10]. Other substances, like chlorophenols and chloro-nitrophenols, also inhibit sulphotransferases, and other chemicals may inhibit PAPS formation."​

​

"The ability to conjugate with sulphate is variable, and requires both active sulphotransferase enzymes and adequate supplies of sulphate [11, 12]. Poor ability to conjugate amines and phenols with sulphate appears to be implicated in a variety of conditions, like food sensitivity, chemical susceptibility, Parkinson’s disease, motor neurone disease, Alzheimer’s disease, chronic fatigue syndrome, migraine, rheumatoid arthritis, lupus erythematosus, inflammatory bowel disease, asthma, depression, hyperactivity, systemic primary biliary cirrhosis, adverse drug reactions, and autism [1, 7, 13–21]."​

​

"The oxidation of cysteine, eventually forming sulphate, appears to be a critical process which is tightly controlled. Cysteine levels are rate determining in glutathione synthesis, so that their concentration effectively determines the major part of the thiol redux system. If cysteine levels are too low, the organism will be more subject to damage from reactive oxygen species, which are generally removed either by thiols or by glutathione-linked enzymes."​

​

"Viruses can react with thiol-containing compounds, and this may explain why low plasma cysteine levels have been found in patients who are HIV positive [22]. N-acetyl cysteine alone, or combined with vitamin C, was found to be effective in HIV patients [23–26], as was a cysteine-rich whey protein formula [27, 28]. Possible mechanisms for the action of cysteine in HIV patients are the release of anti-HIV cytokines [29], the disruption of membranes by anti-microbial cysteine-rich protegrins [30] and the inactivation of HIV protease [31]."​

​

"However, other problems may arise if cysteine levels are high, as cysteine is an excitotoxin acting at the N-methyl-D-aspartic acid (NMDA) subtype of the glutamate receptor, and hence alters neuronal transmission [19, 32]. Cysteine levels are raised in Alzheimer’s and Parkinson’s diseases [14, 33] and have been implicated in memory loss consequent on hippocampal damage. Increased concentrations of plasma cysteine also drive the synthesis of the pro-inflammatory leukotriene–cysteine adducts [34–36] which form complexes with complement C4 and inhibit its action; they are found in rheumatoid arthritis and other autoimmune conditions [37]."​

​

​

"Checking plasma levels of sulphate and cysteine and the ratio between them can, therefore, be helpful when assessing how to treat a variety of people with chronic problems, as these parameters may give information on the underlying biochemical disease processes. A group of patients with chronic illness, often affecting multiple body systems, was therefore studied to determine how many were affected by abnormal cysteine and sulphate levels and how many had abnormal cysteine/sulphate ratios."​

​

"The patients were divided into categories, according to whether their cysteine and sulphate levels and (cysteine × 1000)/sulphate ratio were above, below or within the reference range."​

​

View attachment 20810​

​

Grouped:​

​

- Group A: patients with high cysteine, low sulphate and high ratio​

- Group B: patients with low cysteine, low sulphate and high ratio​

- Group C: normal cysteine, low sulphate and high ratio​

- Group D: high cysteine, normal sulphate and high ratio​

- Group E: normal cysteine, normal sulphate and high ratio​

- Group F: low cysteine, normal sulphate and high ratio​

- Group G: low cysteine, normal sulphate and low ratio​

- Group H: low cysteine, normal sulphate and normal ratio​

​

Groups A-H:​

​

View attachment 20811​

​

"The combination of high cysteine and low sulphate levels, as seen in group A, the most numerous subset, may reflect the presence of inflammatory cytokines, as tumour necrosis factor-a (TNF-a) and transforming growth factor-b have been shown to inhibit the expression of cysteine dioxygenase, the enzyme catalysing the initial step in cysteine conversion [39, 40]. Another possibility is that there are mutations in the DNA coding for the enzyme, or in the flanking regions, which lead to a less efficient isozyme of cysteine dioxygenase. Patients in group A often had a family history of chronic illness, suggesting that this could be a susceptibility factor. Research to determine to what extent abnormalities of sulphur metabolism are inherited would be useful. Patients in group B (low cysteine, low sulphate) might have some fault in cysteine synthesis or some viral infection, while group C patients (normal cysteine, low sulphate) could be linked with poor conversion from cysteine to sulphate. Group D, with high cysteine and normal sulphate levels, could reflect increased tissue breakdown or protein consumption; other problems in sulphur metabolism may also be involved here. Groups E, F, G and H had too few individuals to draw any tentative conclusions."​

​

"The measles vaccination has been found to increase the levels of the Th1 cytokines, interferon-c, soluble interleukin-2 receptor (sIL-2R) and TNF-a [41]."​

​

"Corticosteroids upregulate cysteine dioxygenase. As pantothenate is required to produce cortisol, an inadequate level of pantothenate may cause poor conversion of cysteine to sulphate."​

​

"If conversion from cysteine to sulphate is poor, molybdenum and vitamin B2 can be supplied, to improve the conversion from sulphite to sulphate by the enzyme sulphite oxidase [49]. Epsom salt baths can also be used to provide sulphate, as it passes through the skin. Vitamin B6 can be supplemented, in order to reduce a high level of cysteine by converting it to taurine. Magnesium, zinc and vitamin B2 are required with vitamin B6."​

​

"Foods high in the toxic mineral boron, like tomatoes and apricots, cause excretion of vitamin B2 [50, 51] and may therefore inhibit the enzyme sulphite oxidase that converts sulphite to sulphate. Diets high in purines, caffeine or alcohol may reduce the quantity of sulphite oxidase, by competing for molybdenum and vitamin B2 [49]."​

​

"In depression there may be high levels of histamine in the brain, and reducing this by inactivation with sulphate may improve mood [52]."​

​

"Testing cysteine and sulphate levels may become a useful technique for investigating chronic health problems including multiple sclerosis, myalgic encephalomyelitis, irritable bowel syndrome, autism, depression, motor neurone disease, Parkinson’s, Alzheimer’s, haemolytic anaemia, and also other conditions that are difficult to define. Double-blind clinical trials would be valuable to determine how effective it is to treat patients with molybdenum, vitamins B2, B6 and C, pantothenate, fish or flax oil, Epsom salt baths, N-acetyl cysteine, zinc and/or magnesium. Testing sulphate levels could be used to determine who is likely to be particularly susceptible to environmental chemicals, so as to advise them against employment in particularly polluted environments, against using unnecessary drugs and against using pesticides. Inoculations may contain phenol [53–55] and might need to be avoided where possible."​

​

"The results of the 81 patients tested [were] summarized in Table 10, together with suggestions for possible treatment. Those with inefficient sulphate production could be advised to use diets with lower quantities of amines and bioflavonoids than the rest of the population. Advice to drink red wine may protect against coronary heart disease, but at the expense of other symptoms in susceptible people. High amine and bioflavonoid foods are listed in Tables 11 and 12. The nutritional and dietary suggestions are based on the biochemistry discussed above."​

​

"It is important for patients who do not have a clear diagnosis to have tests that show that their problems are real. The cysteine/sulphate test can contribute to this. Then their families, friends, doctors, employers, or benefit agencies can take them seriously."​

​

"Those already on supplements and a diet were less likely to have a very high ratio, suggesting that supplements and a special diet might be helping them. It would therefore be useful to test a series of patients before starting nutritional supplements and a diet, and then to repeat the test a few months later, to determine how successful the programme has been in improving the ratio, and thus the conversion of cysteine to sulphate."​

​

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?