Serum H2S is increased in Coxsackie B3 virus-induced myocarditis in mice and a

[Emootje]

Serum H2S is increased in Coxsackie B3 virus-induced myocarditis in mice

"The present study found that serum H2S level, H2S production rate, CSE mRNA and CSE protein levels were increased in CVB3-induced myocarditis."
http://www.beyotime.com/reference/a...fp30-1-p0013g-7-p0018-26-st505-st506-ref1.pdf

"Hydrogen sulfide (H2S), better known as a poisonous gas, has emerged as the third gaseous transmitter in mammals, next to nitric oxide (NO) and carbon monoxide (CO). Increased production and higher serum concentrations were shown in inflammatory diseases, septic shock and stroke"
http://clinicaltrialsfeeds.org/clinical-trials/show/NCT01088490

Could DML be wrong? H2S not from the gut but from inflammation?

 

[Athene]

Emootje,
This is really interesting - thank you so much for posting it!

Do you mean K De Meirler? (by DML)? Having had a year of antibiotic treatment from him for gut bacteria, I still have H2S at level 3 (max level is 4) and my son has level 4. His treatment reduced my H2S level from 4, but didn't reduce my son's level at all.
SO
I definitely think that this explanation of H2S production could be the reason. I think that probably his theory of H2S being produced by gut bacteria is correct, but only part of the story. His treatment improved gut symptoms in myself (very slightly) and my son (a lot), but there is still this H2S problem.

My CFS began with very severe myocarditis. I have been able to feel that whatever infection caused that has remained permanently in my body, and is eating away at my heart, slowy damaging it over the years. I also find that in periods where the rate of damage accelerates, this corresponds with periods of raised H2S symptoms - by which I mean, very badly aching muscles and extreme/constant sleepiness.
(CFS in general causes tiredness, but high H2S causes sleepiness, which is different).

Anyway I am going to read these articles very carefully and, again, thank you for posting. If you find anything else on this topic, please post it also!

 

[Athene]

Interestinger and interestinger!

The first article talks about cystathionine being a major factor in H2S production.

It is derived from methionine, which is a fundamental part of the methylation cycle. Many people with methylation breakdowns have severely worsened symptoms when they take supplements that form part of that chain.

It also says that H2S reacts with zinc citrate to form a new compound. Nearly all people with CFS are zinc deficient but they often remain zinc deficient even if they take massive doses.

H2S also works by stimulating ATP sensitive potassium channels. ATP plays a key role in energy production in cell mitochondria, so I am wondering if excess H2S could be what causes mitochondrial dysfuction in CFS?

Could these nutrients be getting siphoned off for other purposes, in the presence of a pathogen that causes excessive production of H2S?

This certainly makes me understand why KDM was so certain that his H2S discovery was THE explanation of CFs - it ties in with absolutely all the abnormalities:
vasorelaxation, (i.e. dysautonomia)
inflammation,
apoptosis,
ischemia/reperfusion
and oxidative stress.
(listed in article)

 

[Emootje]

Farts

Thank you Anthene!
Indeed DML=KDM
My H2S level is 6 but my farts never smell like H2S (rotten eggs). My healthy girlfriend H2S level is 1 and she is the queen of H2S farts. This difference in H2S level does not make any sense unless mine H2S is endogenously produced by CSE or CBS. Another explanation could be that my gut is more permeable for H2S But I think it more likely that a chronic inflammation is the reason of my increased H2S.
Interesting about the methylation cycle. Thank you for mention that.
More on H2S:
http://www3.interscience.wiley.com/cgi-bin/fulltext/121662221/PDFSTART
http://journals.lww.com/shockjourna...lfide_and_Sulfite__Novel_Mediators_in.17.aspx

Emootje

 

[Athene]

My healthy husband does those deadly farts too, and I never do!

KDM says this is because we absorb the H2S into our body tissues rather than eliminating it as gas. Healthy people produce it in the last part of the colon, where the relevant bacteria are "allowed" to live, whereas we make it in the small intestine, which should not really contain many bacteria at all, so maybe it gets absorbed simply because it is not produced anywhere near the "exit." I think it also makes great sense that we produce it in internal organs and thus it is diffused in the body tissues as well as comiong from the gut.

I am surprised about the H2S level being 6, because the nurse who did out H2S test said the maximum is 4. Does this mean they have changed the measurement? When he did the test on my son he said he had never seen such an extreme and immediate reaction, and that the real level was completely off the scale.

Also, I forgot to mention that KDM did an H2S test for me from a vaginal swab and that also went black immediately, so that proves that either we are also making H2S in other parts of the body than the gut, or else that it is totally diffused through our bodies and not concentrated in the gut.

 

[Emootje]

Shame on your H2S husband!

After 3 minutes my tube looks like this:



I assumed it was level 6 but it is possible KDM uses another gradation.

I updated my CFS theory and added the inflammation/CSE/CBS/H2S pathway.
It now looks like this:



I'm very curious about the publication of KDM's H2S theory. I'm waiting almost a year now. Maybe the paper can take away the doubt of the origin of H2S.
In my case I think cosackie B viruses and maybe XMRV are the cause of the disease but I have not been tested for these viruses.
By the way, did you ever tested for CO, ZPP or COP? And do you know what virus caused the myocarditis? And did you developed any valve disease afterwards?

Greetings

 

[Emootje]

Best H2S paper:
http://www.if-pan.krakow.pl/pjp/pdf/2007/1_4.pdf

Some highlights:

H2S is synthesized from L-cysteine by either cystathionine beta-synthase (CBS) or cystathionine gamma-lyase (CSE), both using pyridoxal 5- phosphate (vitamin B6) as a cofactor.

CBS is a predominant source of H2S in the central nervous system whereas CSE is a major H2S-producing enzyme in the cardiovascular system.

S-adenosyl-methionine (SAM), an intermediate product of methionine metabolism and a major donor of methyl groups, is an allosteric activator of CBS.

The physiological significance of NO in the regulation of H2S production is also supported by the observation that circulating H2S level as well as CSE gene expression and enzymatic activity in the cardiovascular systemare reduced in rats chronically treated with NOS inhibitor. Thus, NO is probably a physiological regulator of H2S production in the cardiovascular system.

Moreover, H2S has been demonstrated to stimulate heme oxygenase expression and CO production, and to have bidirectional effects on the extracellular signal-regulated kinases (ERK) and inducible NO synthase.

H2S may also have some effects in the peripheral nervous system. In particular, accumulating body of evidence suggests that H2S stimulates the capsaicinsensitive sensory nerves and evokes the release of tachykinins such as substance P (SP) and neurokinin-A.

Dello Russo et al. [21] have demonstrated that H2S donor, NaHS, as well as H2S precursor and CBS activator, S-adenosylmethionine, decreased potassium stimulated release of corticotropin releasing hormone (CRH) by the rat hypothalamic slices. In addition, SAM attenuated stress-induced increase in plasma glucocorticoids suggesting that H2S may be a negative regulator of hypothalamo-pituitary-adrenal axis.

H2S should be expected to be overproduced in the brain of patients with Down syndrome.

H2S exerts a toxic effect on neurons through the inhibition of cytochrome c oxidase and/or overstimulation of NMDA receptors.

NaHS decreases myocardial contractility.

The currently available data indicate that H2S relaxes blood vessels mostly, if not exclusively, by opening ATP-regulated potassium channels in the vascular smooth muscle cells. First, glibenclamide, a KATP channel antagonist, attenuated the hypotensive effect of H2S in vivo and vasodilatory effect in vitro.

H2S is also overproduced in vascular tissue of rats with experimental septic shock induced by coecal ligation and puncture, as well as in endotoxemic shock induced by lipopolysaccharide (LPS) administration In addition, H2S level negatively correlates with blood pressure and myocardial contractility, suggesting its pathogenic role in the hemodynamic collapse. Notably, at least one study has demonstrated that LPS-induced hypotension is attenuated by glibenclamide suggesting the involvement of abnormal activation of KATP channels.

 

[Joopiter76]

I wonder why pyridoxal-5-phosphate improves my symtoms especially muscle shrugging (I hope you understand my english..) if p5p activates CBS and CSE. Otherwise it lowers NMDA acivity. And Pall describes p5p as effective. Any idea??

 

[alex_nk]

Is beta actin expressed in cardiac myocytes?

"The present study found that serum H2S level, H2S production rate, CSE mRNA and CSE protein levels were increased in CVB3-induced myocarditis."
http://www.beyotime.com/reference/a...fp30-1-p0013g-7-p0018-26-st505-st506-ref1.pdf

"Hydrogen sulfide (H2S), better known as a poisonous gas, has emerged as the third gaseous transmitter in mammals, next to nitric oxide (NO) and carbon monoxide (CO). Increased production and higher serum concentrations were shown in inflammatory diseases, septic shock and stroke"
http://clinicaltrialsfeeds.org/clinical-trials/show/NCT01088490

Could DML be wrong? H2S not from the gut but from inflammation?

 

[aquariusgirl]

Yes,that last study is comprehensive. Raises more questions than it answers...
I have massively elevated cystathionine...so now I'm a bit alarmed.

And did anyone notice the linke between H2S & NK cell death?

From this study, bottom of page 597/top of page 598

http://www.beyotime.com/reference/a...fp30-1-p0013g-7-p0018-26-st505-st506-ref1.pdf

"H2S facilitates NK cell death which may also be related to its early pro-viral effects"

 

[Athene]

Long delay...

Hi Emootje,

I just realised I never answered your questions, please forgive me, I went into a very bad decline before leaving for Lyme disease treatment in Germany.

By the way, did you ever tested for CO, ZPP or COP? And do you know what virus caused the myocarditis? And did you developed any valve disease afterwards?

I've never been tested for CO, ZPP or COP.

As for the myocarditis, they never found out what caused it, but it was most likely to have been either Borrelia, or chlamydia pneumonia, or mycoplasma pneumonia. I definitely had these illnesses at the time and I definitely didn't have either herpes virus or EBV, which I do have now. I still haven't been tested for XMRV, so I don't know about that one.

I didn't develop valve disease at the time, but I did during my pregnancy years later, when the original heart problem worsened. Basically the acute infection I got never went away, I could feel it damaging my heart slowly over the years. When my CFS was bad the damage would be faster, when I was better it would calm down. My valves are leaky but still working reasonably well. Since I have started a massive antibiotic therapy for borrelia and co-infections (listed above) I am not feeling any bad things in my heart at all, which makes me feel all the more convinced that the infection causing the problem is one of the above.

If H2S is predominantly produced by inflammation in the body, then theoretically it should be reduced by reducing inflammation. At the moment I am taking green tea extract to reduce inflammation and following the anti-inflammation diet (trying to, my allergies greatly limit what I can do) in "The Lyme Solution" so it would be interesting to find out if this is having any effect on my H2S level. Maybe some stronger pharmaceutical grade anti-inflamamtory would be necessary??

 

[Emootje]

Hi Athene,

Of course I forgive you. I'm glad your heart is doing better.
I was wondering if there is a connection between heart valve disease and coxsackie B viruses.
http://eurheartj.oxfordjournals.org/content/23/7/567.full.pdf
But in your case a Lyme carditis is more likely.

Last Monday I spoke with KDM. He thinks endogenous H2S is not an important factor. He also mentioned that acids (vitamin C, short-chain fatty acids from soluble fiber) in the gut could increase H2S production. NaHCO3 or KHCO3 could decrease H2S production. The next day I tested negative for H2S (after a diet of 3 days with low fiber and no vitamin C) Maybe it is only in the gut.....

Emootje

 

[Athene]

Hi Emootje,
That is really interesting that you tested negative for H2S when you stopped fibre and vitamin C. It is worrying to think that these bacteria could parasitise even our prebiotics and the most essential nutrient for the immune system!
I think I really need to repeat the test to find out what level I have now...
Also, I am convinced this H2S level varies a lot from one day to the next, even from one hour to the next.

I am also beginning to think that a lot of our problems are caused by acidity in general, and which specific acid is less important than the aggregate level. I am trying to follow the alkaline diet and I also take bicarbonate of soda to alkalise my body, and I think this helps.

 

[Hip]

Very interesting speculation of yours, Emootje, that in chronic fatigue syndrome, hydrogen sulfide (H2S) may not come from the gut, but rather come from inflammation, and/or from coxsackievirus B infection in the body.

Also very interesting is your observation that, in spite of high H2S readings on the De Meirleir Neurotoxic Metabolite Test, often people with CFS produce no H2S smell in their farts; and moreover, that other healthy people without CFS can have very odorous H2S farts.

I had a very high reading for H2S on the Neurotoxic Metabolite Test, but my farts are almost always odorless (this usually means they are mainly methane, which is a gas that has no smell).

Not only that, but also I notice on the rare occasions when, due to the food I have eaten, I do produce some H2S farts, during these times I generally feel better, not worse, as a result of the H2S being produced in my guts. My whole digestion seems better when I produce H2S flatus, in fact.

In my case, it seems like H2S in my flatus improves my CFS symptoms.

So what is going on here?

One possible answer is the following.

It is known that increased levels of H2S in the colon causes the colon mucosa to secrete more H2S detoxification enzymes, which neutralize H2S by converting it to thiosulfate. Colonic mucosa tissues possess a specialized detoxification system for this H2S detoxification (references here and here). Other non-colonic tissues are much less efficient at neutralizing H2S.

So, could it be that, when H2S is produced at high levels in the gut (by bacteria digesting food), the detoxification enzymes then produced by the colon mucosa serve not only to neutralize H2S in the gut, but these enzymes may go on working to generally lower H2S in the body as a whole?

This may be why I often feel better, not worse, when I have H2S in my flatus.

Assuming that H2S is a cause of CFS, then it follows from this that perhaps people with CFS should be eating the right foods to increase H2S production in the guts, in order to increase the production of the H2S detoxification enzymes generated in the colonic mucosa. At least this would be an interesting experiment.

Another possibly might be to take these H2S detoxification enzymes as a supplement (if they were available in future, and safe); or try take herbs or supplements that might increase the natural production of these H2S detoxification enzymes in the body.

From what I have discovered, one major H2S detoxification enzyme is thiosulfate sulfurtransferase (TST), which is a component part of the enzyme rhodanese (reference here). I am not sure if this is the only H2S detoxification enzyme generated in the colonic mucosa, or whether there are other H2S detoxification enzymes also generated.

Incidentally, hydrogen sulfide in the gut seems to be involved in ulcerative colitis too.

 

[richvank]

Hi, Hip.

There is also a sulfide oxidase in the wall of the gut (Not the same as the sulfite oxidase that converts sulfite to sulfate). I think it handles most of the H2S. When it gets overwhelmed, H2S is able to enter the blood.

Rich

 

[Hip]

Thanks Rich.

I think possibly one way to increase H2S production in the gut (as an experiment) would be to include some sulfur in the diet. I know that dogs do well on rock sulfur supplements (which is pure elemental sulfur)....

"Elemental sulfur is considered to be of low toxicity. Compounds such as carbon disulfide, hydrogen sulfide, and sulfur dioxide are toxic."