In mei 2009 kwam de Belgische professor Kenny de Meirleir (zeer bekende ME expert) met het nieuws naar buiten dat bij de meerderheid van zijn ME patiënten hoge waterstofsulfide waarden in de darmen een cruciale rol bij de chronische klachten konden spelen.
Deze zwavelvorm is normaal een afweerreaktie op schimmels zoals Candida, verkeerde bacteriën (darmflora verstoring), virussen en toxines zoals zware metalen. Wordt deze belasting chronisch en vele malen hoger dan bij een normaal gezonde persoon dan gaat deze neurotoxische stof van alles slopen en uitputten.
Het kan je darmwand aantasten (lekkende darm), poliepvorming bevorderen (darmkanker), je zenuwgestel en hersenen belasten maar ook voor allerlei vage klachten zorgen zoals spierpijnen, chronische vermoeidheid, geheugenverlies, problemen met ontstekingen door uitputting van het immuunsysteem en voedselintoleranties. Kortom een scala aan ellende.
Na wat googlen ben ik erachter dat deze stof ook een belangrijke rol kan spelen bij ziekten als colitis ulcerosa (chronische ontsteking dikke darm), darmkanker en celdood in de hartspier (!)
Professor Meirlier kondigde ook aan met een goedkope urinetest te komen waarmee je dit in je urine kan testen. Voor 18 euro heb je het setje in huis. Omdat ik zelf na blootstelling aan lijmdampen ook allerlei vage klachten heb overgehouden wilde ik deze test wel eens doen.
Tot mijn stomme verbazing sloeg de urine paars/zwart uit dus behoorlijk wat van deze sloper in mijn urine. Aangezien urine gefilterde rommel uit je bloed (via de nieren) is zit deze ziekmaker dus door je hele lichaam. Ik was al via Novelcure erachter gekomen dat ik een lekkende darm zou hebben dus dit gaf mij weer een stukje vd puzzel.
Ik heb al zo vaak tegen mensen gezegd dat ik iets in mijn bloed had dat pijnen gaf in goed doorbloede plaatsen zoals geslachtsdeel, darmen, armen, romp, nek, schouders en hoofd maar niemand die me de oorzaak kon vertellen. Deze neurotoxische stof (giftig voor de hersenen en zenuwen dus) schijnt te worden gestimuleerd door toxines in de darmen. Zaak dus om de darm weer gezond te maken, ik neem nu zelf Gastrint (Novelcure), dit is een middel wat zowel probiotica als prebiotica bevat en nog een aantal stoffen die gunstig zijn voor de darmwand en maag.
Mijn vermoeden is dat gluten de darmwand kunnen beschadigen. Daarnaast heeft het eiwit in zuivel (caseïne) een negatief effect op de afweer van de darm (IGA) en vermijd ik dus beide en leef op rijst(wafels), aardappels, kip, kalkoen, vis, groente, fruit, olijfolie, kokosolie, noten, koudgeslingerde honing, jam, appelstroop etc.
Ik vermijd rood vlees omdat het ijzer (haem) in vleed ook de darmwand kan beschadigen, verder knoflook en ei omdat deze laatste twee ook waterstofsulfide (eierstank) bevatten. Via Pubmed (database klinische studies) heb ik ontdekt dat de Yucca plant, houtskool en Zink de waterstofsulfide kunnen verlagen. Dit werd namelijk onderzocht bij honden die last van stinkwinden hebben. Ook is er in Amerika een diaree remmer op recept verkrijgbaar die het gas met 96% kan reduceren.
Ik vermoed dat dit probleem wel eens bij heel veel mensen kan spelen, zeker als het om vermoeidheid zonder echte oorzaak gaat, om chronische spierpijnen, slaapproblemen etc etc. Ik heb nu wat testen besteld voor familieleden omdat darmproblemen bij de familie een bekend euvel zijn. Zou wel heel veel zaken/chronische klachten kunnen verklaren.
Naast toxines zal antibiotica gebruik ook een rol spelen, deze sloopt namelijke je goede darmflora en kan voor een schimmelprobleem zorgen (candida groei) die op haar beurt weer voor extra waterstofsulfide vorming (dus meer klachten) zorgt.
De aanpak van professor Meirlier is die van het het herstellen van de darmen door een voedingsintolerantie test te doen en de darmen te helpen met goede pre- en probiotica. Daarnaast wordt er voor mensen met schade aan de hersenen en problemen met de hartspier zuurstoftherapie toegepast.
Frappante is nu dat je in de VS steeds meer hoort over zuurstoftherapie bij kids met autisme. En laat nu juist die kinderen vaak ook schimmel/darmproblemen hebben dus is het cirkeltje weer rond.
Naast waterstofsulfide is er nog een gas dat een rol speelt bij veel chronische aandoeningen. Dit is NO (nitric oxide) dat ook weer in hogere hoeveelheden giftig voor het lichaam wordt. Ik heb daar op deze pagina (link) uitgebreid over geïnformeerd
Is dit alles nieuw? Nee, maar wel de eerste keer dat de relatie met ME wordt gelegd. Ga je nl spitten dan is al langer bekend dat waterstofsulfide oa een rol speelt bij darmontstekingen, darmpoliepen, problemen met de hartspier en meer. Net zoals NO heeft deze stof voordelen maar in hogere hoeveelheden wordt het een toxine die zelf DNA kan slopen.
Ken je mensen met chronische vermoeidheid, spierpijnen, hartspierproblem of darmproblemen geef dan deze link eens door. Doel van de site is elkaar helpen en zo onze gezondheid weer op order te krijgen.
Ik zal hieronder de resultaten van mijn zoektocht samenvatten, aanvullende informatie kan naar mij gemailed worden.
Sterkte met jouw zoektocht
ME zit niet tussen de oren !
Uitgebreid artikel van de Belgische krant de Morgen over de ziekte ME/CVS. Ik heb toestemming gekregen om dit artikel over te nemen en wil de hoofdredactie van de krant hierbij bedanken voor hun medewerking.
(C) De Morgen
en wederom geen woord hierover in de media in Nederland. Hier blijven we volgzaam achter de aanpak van het Radboud Ziekenhuis protocol aanlopen. Want het wondermiddel hier tegen deze ziekte is jawel, cognitieve gedragstherapie…….wat kan het leven toch simpel zijn….
The Neurotoxic metabolite test
R.E.D. Laboratories focuses on clinical laboratory activities, commercializing specific diagnostics assays for chronic immune dysfunctions, including the proprietary tests developed by PROTEA biopharma.
ME: End of an Era of Medical Negation
In conclusion, ME is a disorder which is caused by increased endogenous H2S production. For the latter many factors can be present. Because of the effects of H2S in the body a chain of events will develop which have more and more negative effects on the aerobic metabolism and depression of the immune system leading to more and more infections and reactivation of endogenous viruses. In its final stage aberrant transmissible prions develop which put the patients in a total energy depleted state.
Function of H2S in the body
Hydrogen sulfide is produced in small amounts by some cells of the mammalian body and has a number of biological functions. It is produced from cysteine by various enzymes. It acts as a vasodilator and is also active in the brain, where it increases the response of the NMDA receptor and facilitates long term potentiation which is involved in the formation of memory. Eventually the gas is converted to sulfites and further oxidized to thiosulfate and sulfate. Due to its effects similar to NO (without its potential to form peroxides by interacting with superoxide), hydrogen sulfide is now recognized as a potential cardioprotective agent. Vasoactivity of garlic is caused by catabolism of the polysulfide group in allicin to H2S, a reaction which could depend on reduction mediated by glutathione. In trisomy 21 (the most common form of Down syndrome) the body produces an excess of hydrogen sulfide.
H2S verlagende kruiden
Als ik het goed heb zou uit onderstaande studie blijken dat in varkens voortsgenoemde kruiden een verlagend effect hebben op de H2S-productie: Perilla frutescens (Soyou), Mentha piperita (Peppermint), Ajuga decumbens (Kiransou).
Influence of dietary supplementation of herb extracts on volatile sulfur production in pig large intestine.
Volatile sulfur compounds (VS) are generated in the large intestine by the bacterial metabolism of sulfate and sulfur amino acids. VS are potentially harmful to the host. The effect of dietary supplementation of herb extracts on volatile sulfur production in the large intestine of pig was evaluated in this study. The extracts Perilla frutescens (Soyou), Mentha piperita (Peppermint), and Ajuga decumbens (Kiransou) were fed to pigs equipped with a permanent cannula at the cecum. Cecal digesta were sampled and analyzed for ammonia and short-chain fatty acids (SCFA). Sampled digesta were incubated anaerobically either
with or without L-methionine for 24 h to estimate volatile sulfur production in vivo. L-Methionine was supplemented to enhance methanethiol (MeSH) production. At the end of the incubation, head space concentrations of volatile sulfur compounds such as hydrogen sulfide (H2S), MeSH, and dimethyl sulfide (DMS) were determined by flame-photometric gaschromatography after the addition of 6 N HCl. Sampled digesta were also subjected to the most probable number estimations for sulfate-reducing bacteria (SRB), sulfide producer from L-methionine, and MeSH producers from L-methionine. All three herb extracts significantly decreased H2S (p<0.05), MeSH (p<0.05), and ammonia (p<0.05) production, but SCFA production was not affected (p>0.05). The number of volatile sulfur-producing bacteria did not vary among groups by the dietary supplementation of these herb extracts. Serial solvent extraction was done on these herb extracts to specify the active fractions that reduce volatile sulfur production. n-Butanol fraction of all three extracts significantly reduced volatile sulfur production in vitro.
Tip: Frank Op de Beeck
Actions and interactions of nitric oxide, carbon monoxide and hydrogen sulphide in the cardiovascular system and in inflammation – a tale of three gases!
Nitric oxide (NO), carbon monoxide (CO) and hydrogen sulphide (H(2)S) together make up a family of biologically active gases (the so-called ‘gaseous triumvirate’) with an increasingly well defined range of physiological effects plus roles to play in a number of disease states. Over the years, most researchers have concentrated their attention on understanding the part played by a single gas in one or more body systems. It is becoming more clear that all three gases are synthesised naturally in the body, often by the same cells within the same organs, and that all three gases exert essentially similar biological effects albeit via different mechanisms. Within the cardiovascular system, for example, all are vasodilators, promote angiogenesis and vascular remodelling and are protective towards tissue damage in for example, ischaemia-reperfusion injury in the heart. Similarly, all exhibit complex effects in inflammation with both pro- and anti-inflammatory effects recognised. It seems likely that cell function is controlled not by the activity of single gases working in isolation but by the concerted activity of all three of these gases working together.
Endogenous and Exogenous Hydrogen Sulfide Promotes Resolution of Colitis in Rats
Hydrogen sulfide (H(2)S) is an endogenous gaseous mediator of mucosal defense with antiinflammatory effects that promote ulcer healing. The effects of H(2)S during the pathogenesis of colitis have not been established. We analyzed the contribution of H(2)S to inflammation and ulceration of the colon in a rat model of colitis. In rats, H(2)S modulates physiological inflammation and contributes to the resolution of colitis.
Fecal hydrogen sulfide production in ulcerative colitis.
Sulfide, a product of sulfate-reducing bacteria, has been proposed to play an etiologic role in ulcerative colitis. Ulcerative colitis feces have increased numbers and activity of sulfate-reducing bacteria, but only modestly increased sulfide. However, fecal sulfide exists largely in the volatile, highly toxic H2S form that moves rapidly from feces to surrounding gas. Our aim was to quantify the fecal release of H2S and other volatiles (CO2, H2, CH4, methanethiol, and dimethylsulfide). METHODS: Fecal samples from 25 subjects with ulcerative colitis and 17 controls were incubated in 4-L containers, and gas release was assessed at intervals over 24 h. RESULTS: H2S release by ulcerative colitis feces was elevated 3-4-fold at every measurement point compared with normal feces (p < 0.003 at 24 h). The only other significant difference was increased CO2 release by ulcerative colitis feces at 1 h. Supplementation of fecal homogenates with sulfur-containing substrates showed that organic compounds (mucin, cysteine, taurocholate) provided more readily utilizable substrate for H2S production than did sulfate. CONCLUSIONS: Increased H2S release is a relatively localized metabolic aberration of ulcerative colitis feces. This increased H2S may reflect abnormalities of the fecal bacteria and/or substrate availability.
Hydrogen sulfide induces direct radical-associated DNA damage
Hydrogen sulfide (H(2)S) is produced by indigenous sulfate-reducing bacteria in the large intestine and represents an environmental insult to the colonic epithelium. Clinical studies have linked the presence of either sulfate-reducing bacteria or H(2)S in the colon with chronic disorders such as ulcerative colitis and colorectal cancer, although at this point, the evidence is circumstantial and underlying mechanisms remain undefined. We showed previously that sulfide at concentrations similar to those found in the human colon induced genomic DNA damage in mammalian cells. The present study addressed the nature of the DNA damage by determining if sulfide is directly genotoxic or if genotoxicity requires cellular metabolism. We also questioned if sulfide genotoxicity is mediated by free radicals and if DNA base oxidation is involved. Naked nuclei from untreated Chinese hamster ovary cells were treated with sulfide; DNA damage was induced by concentrations as low as 1 micromol/L. This damage was effectively quenched by cotreatment with butylhydroxyanisole. Furthermore, sulfide treatment increased the number of oxidized bases recognized by formamidopyrimidine [fapy]-DNA glycosylase. These results confirm the genotoxicity of sulfide and strongly implicate that this genotoxicity is mediated by free radicals. These observations highlight the possible role of sulfide as an environmental insult that, given a predisposing genetic background, may lead to genomic instability or the cumulative mutations characteristic of colorectal cancer.
Evidence that hydrogen sulfide is a genotoxic agent
Hydrogen sulfide (H2S) produced by commensal sulfate-reducing bacteria, which are often members of normal colonic microbiota, represents an environmental insult to the intestinal epithelium potentially contributing to chronic intestinal disorders that are dependent on gene-environment interactions. For example, epidemiologic studies reveal either persistent sulfate-reducing bacteria colonization or H2S in the gut or feces of patients suffering from ulcerative colitis and colorectal cancer. However, a mechanistic model that explains the connection between H2S and ulcerative colitis or colorectal cancer development has not been completely formulated. In this study, we examined the chronic cytotoxicity of sulfide using a microplate assay and genotoxicity using the single-cell gel electrophoresis (SCGE; comet assay) in Chinese hamster ovary (CHO) and HT29-Cl.16E cells. Sulfide showed chronic cytotoxicity in CHO cells with a %C1/2 of 368.57 micromol/L. Sulfide was not genotoxic in the standard SCGE assay. However, in a modified SCGE assay in which DNA repair was inhibited, a marked genotoxic effect was observed. A sulfide concentration as low as 250 micromol/L (similar to that found in human colon) caused significant genomic DNA damage. The HT29-Cl.16E colonocyte cell line also exhibited increased genomic DNA damage as a function of Na2S concentration when DNA repair was inhibited, although these cells were less sensitive to sulfide than CHO cells. These data indicate that given a predisposing genetic background that compromises DNA repair, H2S may lead to genomic instability or the cumulative mutations found in adenomatous polyps leading to colorectal cancer.
Sudden infant death syndrome: the colon connection
The etiology of sudden infant death syndrome (SIDS) is not known. Various maternal and infant risk factors have been identified. Adoption of the non-prone position has reduced the incidence of SIDS but has not eliminated the problem. Some sulfate reducing bacteria in the colon produce hydrogen sulfide (H2S) which is as toxic as hydrogen cyanide. Normally, the colonic mechanism for metabolizing and detoxifying H2S is very effective and no H2S appears in the exhaled breath although small amounts are present in the flatus. We are putting forth the hypothesis that in some cases of SIDS colonocytic mechanism for detoxifying H2S may not have matured by the age of 3 months and H2S may be absorbed resulting in SIDS. The hypothesis can be tested by in vitro evaluation of colonic tissue from SIDS cases for its ability to detoxify H2S.
Hydrogen sulfide protects colon cancer cells from chemopreventative agent beta-phenylethyl isothiocyanate induced apoptosis.
Hydrogen sulfide (H(2)S) is a prominent gaseous constituent of the gastrointestinal (GI) tract with known cytotoxic properties. Endogenous concentrations of H(2)S are reported to range between 0.2-3.4 mmol/L in the GI tract of mice and humans. Considering such high levels we speculate that, at non-toxic concentrations, H(2)S may interact with chemical agents and alter the response of colonic epithelium cells to such compounds. The GI tract is a major site for the absorption of phytochemical constituents such as isothiocyanates, flavonoids, and carotenoids, with each group having a role in the prevention of human diseases such as colon cancer. The chemopreventative properties of the phytochemical agent beta-phenyethyl isothiocyanate (PEITC) are well recognized. However, little is currently known about the physiological or biochemical factors present in the GI tract that may influence the biological properties of ITCs. The current study was undertaken to determine the effects of H(2)S on PEITC mediated apoptosis in colon cancer cells. METHODS: Induction of apoptosis by PEITC in human colon cancer HCT116 cells was assessed using classic apoptotic markers namely SubG1 population analysis, caspase-3 like activity and nuclear fragmentation and condensation coupled with the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrasodium bromide) viability assay and LDH leakage. RESULTS: PEITC significantly induced apoptosis in HCT116 cells as assessed by SubG1 population formation, nuclear condensation, LDH leakage and caspase-3 activity after 24 h, these data being significant from control groups (P<0.01). In contrast, co-treatment of cells with physiological concentrations of H2S (0.1-1 mmol/L) prevented PEITC mediated apoptosis as assessed using the parameters described. CONCLUSION: PEITC effectively induced cell death in the human adenocarcinoma cell line HCT116 in vitro through classic apoptotic mechanisms. However, in the presence of H(2)S, apoptosis was abolished. These data suggest that H(2)S may play a significant role in the response of colonic epithelial cells to beneficial as well as toxic agents present within the GI tract.
Production and elimination of sulfur-containing gases in the rat colon
Highly toxic sulfur-containing gases have been pathogenetically implicated in ulcerative colitis. Utilizing a rat model, we studied the production and elimination of sulfur-containing gases within the unperturbed colon. The major sulfur-containing gases were hydrogen sulfide (H2S), methanethiol, and dimethyl sulfide with cecal accumulation rates of 2.6, 0.096, and 0.046 microliter/min, respectively. The dependence of H2S production on dietary components was demonstrated via a sixfold reduction with fasting and a fivefold increase with carrageenan (a nonabsorbable, sulfur compound) feeding. Zinc acetate reduced cecal H2S by fivefold, indicating the importance of H2S binding by divalent cations. During passage from the cecum to the rectum, > 90% of the sulfur gases were absorbed or metabolized. An H2 35S turnover of 97%/min was observed in the isolated cecum. Thus mucosal exposure is > 10 times the measured accumulation rate. Cecal mucosal tissue very rapidly metabolized H2S and methanethiol via a nonmethylating reaction.
The emerging roles of hydrogen sulfide in the gastrointestinal tract and liver
Hydrogen sulfide, like nitric oxide, was best known as a toxic pollutant before becoming recognized as a key regulator of several physiologic processes. In recent years, evidence has accumulated to suggest important roles for hydrogen sulfide as a mediator of several aspects of gastrointestinal and liver function. Moreover, alterations in hydrogen sulfide production could contribute to disorders of the gastrointestinal tract and liver. For example, nonsteroidal anti-inflammatory drugs can reduce production of hydrogen sulfide in the stomach, and this has been shown to contribute to the generation of mucosal injury. Hydrogen sulfide has also been shown to play a key role in modulation of visceral hyperalgesia. Inhibitors of hydrogen sulfide synthesis and drugs that can generate safe levels of hydrogen sulfide in vivo have been developed and are permitting interventional studies in experimental models and, in the near future, humans.
Gastrointestinal safety and anti-inflammatory effects of a hydrogen sulfide-releasing diclofenac derivative in the rat
Gastrointestinal damage caused by nonsteroidal anti-inflammatory drugs (NSAIDs) remains a significant clinical problem. Hydrogen makes an important contribution to mucosal defense, and NSAIDs can suppress its synthesis. In this study, we evaluated the gastrointestinal safety and anti-inflammatory effects of a novel “HS-NSAID” (ATB-337) that consists of diclofenac linked to a hydrogen sulfide-releasing moiety. RESULTS: Diclofenac (10-50 micromol/kg) dose-dependently damaged the stomach, while ATB-337 did not. Repeated administration of diclofenac caused extensive small intestinal damage and reduced hematocrit by 50%. ATB-337 induced >90% less intestinal damage and had no effect on hematocrit. Diclofenac, but not ATB-337, elevated gastric granulocyte infiltration and expression of tumor necrosis factor alpha, lymphocyte function-associated antigen 1, and intercellular adhesion molecule 1. ATB-337 inhibited cycloxygenase-1 and cyclooxygenase-2 activity as effectively as diclofenac. ATB-337 did not induce leukocyte adherence, whereas diclofenac did, and was more potent at reducing paw edema. CONCLUSIONS: An HS-NSAID spares the gastric mucosa of injury despite markedly suppressing prostaglandin synthesis. This effect may be related to hydrogen sulfide-mediated inhibition of tumor necrosis factor-alpha expression and of the leukocyte adherence to vascular endothelium normally induced by cyclooxygenase inhibitors.
Hydrogen sulfide-releasing anti-inflammatory drugs.
Non-steroidal anti-inflammatory drugs are among the most commonly used drugs. Despite efforts to produce non-steroidal anti-inflammatory drugs that do not cause gastrointestinal ulceration and bleeding, these adverse effects remain major limitations to their use. In recent years, physiological roles of hydrogen sulfide (H2S) have been recognized, and there is emerging evidence that this endogenous gaseous substance can modulate inflammatory processes. Indeed, H2S donors have been shown to reduce edema formation and leukocyte adherence to the vascular endothelium, and to inhibit pro-inflammatory cytokine synthesis. Moreover, H2S donors can increase the resistance of the gastric mucosa to injury and accelerate repair. Taken together, these observations and others suggest that anti-inflammatory drugs that are modified to release H2S will exhibit improved efficacy and reduced toxicity. Such compounds have now been synthesized and shown to be markedly improved in many respects over the parent anti-inflammatory drugs.
Hyperbaric oxygen therapy in the management of two cases of hydrogen sulfide toxicity from liquid manure
These cases suggest that hyperbaric oxygen therapy is safe when applied early in patients with severe hydrogen sulfide exposure. It is impossible to know whether our patients’ favourable outcomes were the result of HBO treatment; however, based on these cases and previous data, we believe that, in addition to supportive care and nitrite administration, hyperbaric oxygen therapy, if available, may be considered as early as possible in cases of moderate to severe hydrogen sulfide poisoning.
ToxFAQs™ for Hydrogen Sulfide
Hydrogen sulfide (H2S) occurs naturally in crude petroleum, natural gas, volcanic gases, and hot springs. It can also result from bacterial breakdown of organic matter. It is also produced by human and animal wastes. Bacteria found in your mouth and gastrointestinal tract produce hydrogen sulfide from bacteria decomposing materials that contain vegetable or animal proteins. Hydrogen sulfide can also result from industrial activities, such as food processing, coke ovens, kraft paper mills, tanneries, and petroleum refineries.
Brain hydrogen sulfide is severely decreased in Alzheimer’s disease
Although hydrogen sulfide (H2S) is generally thought of in terms of a poisonous gas, it is endogenously produced in the brain from cysteine by cystathioninebeta-synthase (CBS). H2S functions as a neuromodulator as well as a smooth muscle relaxant. Here we show that the levels of H2S are severely decreased in the brains of Alzheimer’s disease (AD) patients compared with the brains of the age matched normal individuals. In addition to H2S production CBS also catalyzes another metabolic pathway in which cystathionine is produced from the substrate homocysteine. Previous findings, which showed thatS-adenosyl-l-methionine (SAM), a CBS activator, is much reduced in AD brain and that homocysteine accumulates in the serum of AD patients, were confirmed. These observations suggest that CBS activity is reduced in AD brains and the decrease in H2S may be involved in some aspects of the cognitive decline in AD.
Hypothesis ME CFS hydrogen sulfide metabolism
Recent research has demonstrated that at low, non-toxic doses, exogenous H2S produces a reversible state of hibernation-like deanimation in mice, causing a decrease in core body temperature, an apnea-like sleep state, reduced heart and respiration rates, and a severe metabolic drop . These characteristics are not unlike the symptoms and extreme “de-animation” experienced by CFS/ME patients. Moreover, H2S affects biological networks that are disrupted by CFS including neurologic, endocrine and immunologic systems. Therefore, a plausible etiology of CFS is an increase in the activity of endogenous H2S, thereby inhibiting mitochondrial oxygen utilization.
The most common form of food intolerance, lactose intolerance is the manifestation of the inability to digest dairy products. Lactose, the main sugar in diary products, is broken down in the small intestine by the enzyme lactase. Many older children and adults lack adequate lactase, resulting in incomplete digestion of ingested milk sugar. Colonic bacteria then ferment the sugar into carbon dioxide (CO2), methane (CH4), hydrogen (H2) and hydrogen sulfide (H2S), resulting in the unpleasant gastrointestinal effects associated with food intolerance.
Comments on hydrogen sulfide and the methylation cycle in CFS
It is quite common in CFS that there is dysfunction in the digestive system. This can include low stomach acid, slow gastric motility, insufficient secretion of pancreatic enzymes, insufficient secretion of bile, gluten or casein sensitivity, fructose or lactose intolerance, candidiasis, dysbiotic bacteria, intestinal permeability (leaky gut), a variety of other food sensitivities, secretory IgA deficiency, protozoal or helminthic parasites, and others.
Hydrogen sulfide-induced apoptosis of human aorta smooth muscle cells via the activation of mitogen-activated protein kinases and caspase-3
The endogenous production of hydrogen sulfide (H2S) and its physiological functions, including membrane hyperpolarization and smooth muscle cell relaxation, position this gas well in the family of gasotransmitters together with nitric oxide (NO) and carbon monoxide (CO). In this study, we demonstrate that H2S at physiologically relevant concentrations induced apoptosis of human aorta smooth muscle cells (HASMCs). Exposure of HASMCs to H2S did not induce necrosis as verified with Trypan blue exclusion and LDH release analysis. After inhibiting endogenous H2S production, exogenous H2S induced much more significant apoptosis, which was not altered by the presence of albumin or glutathione. H2S treatment increased the activities of ERK and p38 mitogen-activated protein kinase (MAPK), but not c-Jun N-terminal kinase activity. Suppression of extracellular signal-regulated kinase (ERK) activity, but not of p38 activity, inhibited the H2S-induced apoptosis of HASMCs. The activation of ERK by H2S in HASMCs was accompanied by increased caspase-3 activity. Inhibition of caspase-3 by AC-DEVD-CHO attenuated the H2S-induced cell apoptosis. Inhibition of ERK by U0126 decreased caspase-3 activity, whereas AC-DEVD-CHO did not alter ERK activity. In conclusion, exogenous H2S induces apoptosis of HASMCs, which is significantly affected by the endogenous H2S level. Of the three investigated MAPKs, only ERK played an active role in mediating H2S-induced apoptosis of HASMCs by activating caspase-3. These findings may help reveal novel mechanisms for many diseases linked to H2S-related abnormal cellular proliferation and apoptosis.
Mercury and Hydrogen Sulfide (H2S)
“When gut bacteria or fungi are attacked by something like a heavy metal molecule (e.g. mercury), they have a special defense mechanism (called a “resistance gene”) that produces Hydrogen Sulfide (H2S) gas, which binds to the attacker and neutralizes it. Subsequently this highly toxic and poisonous H2S gas is created in the gut. H2S can impair the immunity system, especially in the area of neutrophil function, which is used to fight the original yeast in the gut, and hence one can hit a vicious cycle. H2S is very similar to mercury, in that it can bind to many of the things that mercury binds to and inactivate them. In other words, all the bad things that mercury can do, as described here, H2S can do. H2S can also convert the safer Inorganic mercury to the more dangerous Organic mercury, as described here.
TOXICOLOGICAL REVIEW OF HYDROGEN SULFIDE
Inflammatory Bowel Disease, Colititis, and IBS
Kenny De Meirleir : ME/CFS, hydrogen sulfide and aberrant prion disease
Bismuth subsalicylate markedly decreases hydrogen sulfide release in the human colon
The ability of bismuth subsalicylate to dramatically reduce H2S could provide a clinically useful means of controlling fecal and/or flatus odor and of decreasing the putative injurious effects of H2S on the colonic mucosa.
Hydrogen sulfide induces apoptosis in epithelial cells derived from human gingiva
Hydrogen sulfide (H2S) is not only one of the main causes of halitosis but is also an agent of toxicity against periodontal cells and tissues in biofilm-related periodontal diseases. Also, apoptosis of gingival epithelial cells may play an important role in the onset and progress of periodontitis. We examined the effect of H2S on the induction of apoptosis, using human gingival fibroblasts (HGF) and keratinocyte-like Ca9-22 cells derived from human gingiva. The cells were incubated with H2S (100 ng ml-1) for 24, 48 or 72 h by adding H2S to air containing 5% CO2, supplied constantly to the culture environment during incubation. The incidence of apoptosis caused by H2S was determined with Annexin V staining by flow cytometry. The proportion of apoptotic cells was significantly increased by exposure to H2S for 48 h in comparison with the control in both Ca9-22 cells and HGF. A concentration of 100 ng ml-1 H2S in air is possible in the gingival sulcus. This study indicates that apoptosis in gingival epithelial cells and HGF by H2S may occur in the oral cavity, which may cause a periodontal condition.
Is ME/CFS caused by dysregulation of hydrogen sulfide metabolism
H2S plays a pivotal role in both aerobic and non-anaerobic organisms as a signaling molecule. Bacteria in the gut both produce H2S and utilize it as a substrate alternative to oxygen. This is of particular relevance in the gastrointestinal tract, where unusually high levels of gram-negative bacteria, which increase intestinal permeability, have been found in patients with CFS/ME . In addition to bacteria, yeast, mold and other fungi also emit H2S. CFS/ME is a model disease for multisystem disturbance. It is my hypothesis that mitochondria, organelles required by every cell to sustain life, are unable to adequately utilize oxygen. This mitochondrial disturbance could be due to the combined effects of anaerobic conditions known to occur in CFS and associated low-level H2S toxicity. This increase in H2S alters fine signaling necessary for body homeostasis, and causes CFS. Understanding the role of H2S in the body, and, in particular, in mitochondrial function, may provide a unifying lens through which to view the diverse manifestations of this complex disease.
Bismuth subsalicylate reduces H2S
According to Dr. de Meirleir, a major cause of ME/CFS is a high level of the chemical hydrogen sulfide (H2S). H2S can build up after antibiotic use, salmonella infection, or too much mercury exposure. Treatment of subjects with bismuth subsalicylate produced a >95% reduction in fecal H2S release. Conclusions: The ability of bismuth subsalicylate to dramatically reduce H2S could provide a clinically useful means of controlling fecal and/or flatus odor and of decreasing the putative injurious effects of H2S on the colonic mucosa.
Manganese and H2S
I am also going to keep juicing my beets, because not only do beets have small amounts of B12 in them, but they are also high in manganese, which is another antidote to H2S.
Administration of charcoal, Yucca schidigera, and zinc acetate to reduce malodorous flatulence in dogs
Total gas production and number and frequency of flatulence episodes were unaffected by any of the agents. Production of hydrogen sulfide in vitro was significantly reduced by charcoal, Yucca schidigera, and zinc acetate by 71, 38, and 58%, respectively, and was reduced by 86% by the combination of the 3 agents. Consumption of the 3 agents was associated with a significant decrease (86%) in the percentage of flatulence episodes with bad or unbearable odor and a proportional increase in the percentage of episodes of no or only slightly noticeable odor. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that activated charcoal, Yucca schidigera, and zinc acetate reduce malodor of flatus in dogs by altering the production or availability of hydrogen sulfide in the large intestine.