Hoge waterstofsulfide (H2S) in de
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 patiŽnten 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 bacteriŽn (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 (caseÔne) 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 geÔnformeerd
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
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
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
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
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
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
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.
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
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
Hypothesis ME CFS hydrogen sulfide
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
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
TOXICOLOGICAL REVIEW OF HYDROGEN
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
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
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.