Boosting Mitochondria Increases Energy, Leads To Viral Clearance

globalpilot

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Excellent research and explanations Hip. Have you tested positive for enterovirus ? So I guess if the daughters can carry the infection non-cytolytic cells can essentially infect new cells then.

I went to my doctor Thursday and showed him Dr Chias findings. He is not on board and does not think this is a causal factor. He pointed to Lyme and mycoplasma as possibilities. And the enterovirus as an outcome of having Lyme (suppressed immune system I guess). How does one respond to this ?

Chia's research focused on enteroviruses in the gut (both the cytolytic and non-cytolytic subsets) because the gut is a main reservoir of enteroviruses in the body, and because it is relatively easy to take tissue sample from the gut. However, the mental symptoms of CFS are probably underpinned by these same cytolytic and non-cytolytic infection in the brain (but of course nobody living with CFS is going to donate a part of their brain in order to test this...).

It is known that enteroviruses can ascend the vagus nerve that runs from the gut to brain in three days. So this is one route of entry that enteroviruses have into the brain.

Coxsackievirus B seems able to infect the astrocyte cells in the brain (an astrocyte is a type of glial cell), according to this recent paper from China. And a postmortem examination of the brain, performed on a deceased CFS patient of the late Dr John Richardson (who had studied enteroviruses in CFS for 50 years), found lots of enterovirus infection in the outer (exterior) lining of the blood vessels in the brain, and some enterovirus infection in the glial cells.

The difference between a cytolytic and a non-cytolytic enterovirus is simply that the non-cytolytic version has had a tiny part of its genome deleted and removed the part that encodes for the shell of the virus (capsid). Thus the non-cytolytic version is identical, except that it has no shell. The analogy think of for this is that a non-cytolytic enterovirus is like a snail without its shell.

In essence, the non-cytolytic enterovirus is just a naked RNA genome.

I am not sure whether this shell-less non-cytolytic enterovirus can jump into new cells or not (I have not seen any research that confirms or refutes this possibility). However, since there are likely thousands of copies of this naked RNA an infected cell, presumably if that cell divides to create daughter cells (mitosis), the daughters will also carry the infection.

Refs:

Coxsackievirus Infection Induced Cytopathy and Cytokine Secretion in Astrocyte.
J. Richardson. (2001). Viral Isolation from Brain in Myalgic Encephalomyelitis (A Case Report).
 

Lou

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While I do think that Mitochondria have their role in this disease, I don't think that the treatment recommendations here will help us. PWME and people on this board tried these supplements over and over again and none got cured. Posts about mitochondria appear on a regular basis, they all blame the mitochondria as cause of ME and they all recommend some supplements and all the treatment recommendations don't work for most people.

Couldn't agree with this more. My reaction to supplements like glutamine, d-ribose, reversatrol, and some others mentioned is toxic. Glutamine, think I'd rather be beat with a major league bat than try that again.
 

heapsreal

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I have not seen this, but if you have a link, I'd like to read it.

At the moment I have just started a new antiviral strategy that involves boosting the killer T-cell (CD8 T cell) response. I managed to find several supplements that boost killer T-cells, namely:

CD8 Boosting:
Siberian ginseng
Echinacea
Licorice
B12 methylcobalamin
Ecklonia Cava
Astragalus
Proboost (thymic protein A)

So I thought, why not take them all simultaneously, and see what happens?

This should increase killer T-cell surveillance, which may make up for the down-reulation of the number of MHC infection markers.

The only problem is that killer T-cell are involved in autoimmunity, so these CD8 boosting supplements are probably not be a good strategy for people with autoimmune tendencies; and these supplements might even precipitate autoimmunity in some people.

See here: Activation of Autoimmunity Following Use of Immunostimulatory Herbal Supplements.

I have also experimented in boosting natural killer cell function, using a different set supplements, and this does seem to give me more energy.
Astragalus and echinacea i have found helpful for cold/flu stuff. Thymic protein intrigues me but seems expensive, also AHCC looks good on paper but again price is high for long term use. Maybe we need to put our heads together to get the cheapest sources.

This link info on cd8 and nk cell activity starts on page 4 http://www.translational-medicine.com/content/pdf/1479-5876-9-81.pdf

Lymphocyte Cytotoxic Activity
NK and CD8+T (n = 71) cytotoxic activity measured as
the ability of NK and CD8+T cells to effectively lyse
K562 and P815 cells respectively was significantly
decreased (p < 0.05) among the CFS/ME patients compared
to the control subjects (Figure 2). Similarly granzyme
A expression was significantly decreased in both
the NK and CD8+T cells in the CFS/ME population.
However, IFN-g and granzyme K were decreased only in
the NK cells of the CFS/ME group compared to the
healthy controls as shown in Figure 3A and 3B.

cheers!!!
 

Hip

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Thanks heapsreal. I did not know that CD8 T cell activity is also low in CFS, in addition to NK cell activity.


Boosting CD8 T cell activity might conceivably help target the cells infected with normal cytolytic enteroviruses, but whether it targets the more surreptitious side of this infection the cells infected with non-cytolytic enteroviruses well that's another question. In fact, Dr Chia suggests that you don't want to target and kill off these cells infected with non-cytolytic enteroviruses, because there are too many of these cells, and there would be too much co-lateral damage.

Though help may be at hand, as Chia thinks that a new hepatitis C drug in clinical trials may be able to clear out non-cytolytic enteroviruses from cells, presumably without killing the cell (reference: see about halfway down this page)
 

Hip

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Excellent research and explanations Hip. Have you tested positive for enterovirus ? So I guess if the daughters can carry the infection non-cytolytic cells can essentially infect new cells then.

I went to my doctor Thursday and showed him Dr Chias findings. He is not on board and does not think this is a causal factor. He pointed to Lyme and mycoplasma as possibilities. And the enterovirus as an outcome of having Lyme (suppressed immune system I guess). How does one respond to this ?
Unfortunately on the only lab capable of detecting the very low levels of enterovirus antibodies present in the chronic infections of CFS patients is ARUP Lab, Salt Lake City, but they do no accept blood samples sent internationally, so I have not been able to test. But by the specific symptoms produced by the virus I caught (in me and in the others around me who also caught the same virus), I looks like it is an enterovirus, such as coxsackievirus B.

I always get the feeling that ME/CFS is not caused by just one pathogen, but by the combined action of several. I think it is no co-incidence that many people that developed CFS from a respiratory virus also had pre-existing conditions like irritable bowel syndrome, recurrent kidney or bladder infections, overactive-bladder, interstitial cystitis, most of which are caused or at least suspected to be caused by infections of some sort.

So CFS may work on the "straw that broke the camel's back" principle: you just get one infection too many, and that it, you get CFS.

So if your doctor does not consider enterovirus to be a causal factor, that's fine, just go with the infection he is testing your for, as these may play some small role in your CFS.

In any case, enteroviruses are probably not be the only "major hitter" infection that precipitate CFS ; the herpesviruses are also major hitters, it would appear.




ARUP Lab Enterovirus Antibody Tests:
http://www.aruplab.com/guides/ug/tests/0060055.jsp
http://www.aruplab.com/guides/ug/tests/0060053.jsp
 

globalpilot

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I agree but I don't know what those other infections would be in me - I tested -ve for HHV6, CMV, EBV, mycoplasma.

You can send your biopsy sample to Dr Chia. That is the definitive test. The antibodies may or may not pick up the strain one has. I live in Canada and both my fiance and i have talked at length to the people at ARUP regarding their policy of not accepting samples from Canada. It turns out their concern is that the sample gets held up in customs and doesn't arrive in time for it to still be viable. We have explained to them that we send samples to US from Canada regularly and have never had a problem....never. And doctors we have been to have also said they do this regularly and have not had a problem. Perhaps they will change their minds if they can come to the terms iwth the fact that the samples will (generally) arrive on time. In the meantime they have agreed to make a one time exception for me. But at this point I don't think they'd do this routinely. But I do plan to tell them that a lot of people outside the US could benefit from their testing.


Unfortunately on the only lab capable of detecting the very low levels of enterovirus antibodies present in the chronic infections of CFS patients is ARUP Lab, Salt Lake City, but they do no accept blood samples sent internationally, so I have not been able to test. But by the specific symptoms produced by the virus I caught (in me and in the others around me who also caught the same virus), I looks like it is an enterovirus, such as coxsackievirus B.

I always get the feeling that ME/CFS is not caused by just one pathogen, but by the combined action of several. I think it is no co-incidence that many people that developed CFS from a respiratory virus also had pre-existing conditions like irritable bowel syndrome, recurrent kidney or bladder infections, overactive-bladder, interstitial cystitis, most of which are caused or at least suspected to be caused by infections of some sort.

So CFS may work on the "straw that broke the camel's back" principle: you just get one infection too many, and that it, you get CFS.

So if your doctor does not consider enterovirus to be a causal factor, that's fine, just go with the infection he is testing your for, as these may play some small role in your CFS.

In any case, enteroviruses are probably not be the only "major hitter" infection that precipitate CFS ; the herpesviruses are also major hitters, it would appear.




ARUP Lab Enterovirus Antibody Tests:
http://www.aruplab.com/guides/ug/tests/0060055.jsp
http://www.aruplab.com/guides/ug/tests/0060053.jsp
 

Hip

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I agree but I don't know what those other infections would be in me - I tested -ve for HHV6, CMV, EBV, mycoplasma.

You can send your biopsy sample to Dr Chia. That is the definitive test. The antibodies may or may not pick up the strain one has. I live in Canada and both my fiance and i have talked at length to the people at ARUP regarding their policy of not accepting samples from Canada. It turns out their concern is that the sample gets held up in customs and doesn't arrive in time for it to still be viable. We have explained to them that we send samples to US from Canada regularly and have never had a problem....never. And doctors we have been to have also said they do this regularly and have not had a problem. Perhaps they will change their minds if they can come to the terms iwth the fact that the samples will (generally) arrive on time. In the meantime they have agreed to make a one time exception for me. But at this point I don't think they'd do this routinely. But I do plan to tell them that a lot of people outside the US could benefit from their testing.
Yes, Chia's stomach biopsy is more definitive (though it won't tell you which enterovirus you have).

And you can send a sample to him from any country I believe. At the moment, though, I generally too tired to try to find and organize a local gastroenterologist to snip off a bit of my stomach wall and send it to Chia's lab. But I will do this at some point.

I also have emailed ARUP (twice now), and explained to them that they have pretty much the only commercially available antibody test suitable for ME/CFS patients, but they just gave me some spiel about regulations not permitting sending blood samples to them internationally. Though with the UK being about 4 times the distance from Salt Lake City than Canada, I guess the longer flight time adds extra risk to the sample arriving unviable. Though I am sure there must be ways of sending samples on ice, in some thermally insulated package.

I also explained to ARUP the political circumstances of ME/CFS that the disease is often not believed, in part because there is often no evidence for viral infection (mainly in the enterovirus subset of CFS). So, since ARUP is the only lab that can offer a straightforward convenient antibody test for enteroviruses in CFS patients (thus indicating an infection is present), it would be nice and politically expedient if this test were more widely available.

I also wrote to the Health Protection Agency (HPA), the UK's equivalent of the CDC, again explaining to them the need to have a test for enterovirus available for CFS patients in the UK, if just for scientific validation purposes of this illness, but got a less than enthusiastic response, saying to me "that enterovirus is not a definitive marker for CFS, it is a common virus that can appear in healthy people too".
 

snowathlete

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All very interesting posts. Thanks everyone.

I guess we need a treatment that can either clear out the infected cells without killing them, or a treatment that kills them but that you have to take small doses of over a period of time, so that your body can deal with the damage as it happens, rather than having to generate new cells throughout your body all at once.

I am currently focusing on herpes viruses, but other infections, including enteroviruses are next on my life if i dont get lucky with my current plans.
 

globalpilot

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Don't you love vague responses like that ? Without any science.

When I was calling ARUP the people answering the phone kept repeating they don't accept samples from outside canada. After awhile of this we got in touch with someone higher up in teh organization and that is when we were able to get somewhere. I can give you her name once I get my blood drawn ... I don't want to do anything to mess this up as she did say this is a ONE TIME only. But I think if a few of us can convince them that testing samples outside US isn't the concern they think it is, we can all benefit.

Regarding the collateral damage Chia mentioned, I was looking for information on enterovirus and the Th1/Th2 response. I was wondering if the infection influenced that. Well I didn't find that specific information but did find information that the perforin secreted by cytolytic T cells during coxsackie caused fibrosis. This is disturbing since a goal of treatments like the methylation protocal and possibly others is to increase the Th1 response of which cytotoxic response is part of.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1852975/

So perhaps in light of that, the best approach would be to stop replication instead of measures to increase killing activity.

Yes, Chia's stomach biopsy is more definitive (though it won't tell you which enterovirus you have).

And you can send a sample to him from any country I believe. At the moment, though, I generally too tired to try to find and organize a local gastroenterologist to snip off a bit of my stomach wall and send it to Chia's lab. But I will do this at some point.

I also have emailed ARUP (twice now), and explained to them that they have pretty much the only commercially available antibody test suitable for ME/CFS patients, but they just gave me some spiel about regulations not permitting sending blood samples to them internationally. Though with the UK being about 4 times the distance from Salt Lake City than Canada, I guess the longer flight time adds extra risk to the sample arriving unviable. Though I am sure there must be ways of sending samples on ice, in some thermally insulated package.

I also explained to ARUP the political circumstances of ME/CFS that the disease is often not believed, in part because there is often no evidence for viral infection (mainly in the enterovirus subset of CFS). So, since ARUP is the only lab that can offer a straightforward convenient antibody test for enteroviruses in CFS patients (thus indicating an infection is present), it would be nice and politically expedient if this test were more widely available.

I also wrote to the Health Protection Agency (HPA), the UK's equivalent of the CDC, again explaining to them the need to have a test for enterovirus available for CFS patients in the UK, if just for scientific validation purposes of this illness, but got a less than enthusiastic response, saying to me "that enterovirus is not a definitive marker for CFS, it is a common virus that can appear in healthy people too".
 

Hip

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All very interesting posts. Thanks everyone.

I guess we need a treatment that can either clear out the infected cells without killing them, or a treatment that kills them but that you have to take small doses of over a period of time, so that your body can deal with the damage as it happens, rather than having to generate new cells throughout your body all at once.
As treatment for chronic enterovirus CFS, my guess is that antivirals may be helpful for targeting full viral particles (cytolytic enteroviruses) floating in the blood, etc; but at the same time, you may need a drug that specifically targets the non-cytolytic viral infection within cells. I would not be surprised if these two co-existing types of enterovirus infection the cytolytic and the non-cytolytic mutually support each other.

In fact, we know that cytolytic viruses underpin non-cytolytic viruses, as cytolytic viruses infect cells, and then in some situations, turn into these non-cytolytic virus that live inside the cell.

But I often wonder if the non-cytolytic viruses, in turn, also support the cytolytic viruses, in some way?


The genes of this non-cytolytic virus RNA remain functional, and so able to express viral proteins (including no-doubt immunomodulating proteins) so the presence of non-cytolytic virus RNA in a cell may radically alter cellular functioning, even if it does not kill the cell.


Don't you love vague responses like that ? Without any science.

When I was calling ARUP the people answering the phone kept repeating they don't accept samples from outside canada. After awhile of this we got in touch with someone higher up in teh organization and that is when we were able to get somewhere. I can give you her name once I get my blood drawn ... I don't want to do anything to mess this up as she did say this is a ONE TIME only. But I think if a few of us can convince them that testing samples outside US isn't the concern they think it is, we can all benefit.

Regarding the collateral damage Chia mentioned, I was looking for information on enterovirus and the Th1/Th2 response. I was wondering if the infection influenced that. Well I didn't find that specific information but did find information that the perforin secreted by cytolytic T cells during coxsackie caused fibrosis. This is disturbing since a goal of treatments like the methylation protocal and possibly others is to increase the Th1 response of which cytotoxic response is part of.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1852975/

So perhaps in light of that, the best approach would be to stop replication instead of measures to increase killing activity.
Thanks globalpilot. It might be a good idea to write sort of join letter, from several of us on PR, to this chap you mention (once you have test results back), and see if he can do something for us CFS patients.

If you look at the ARUP's coxsackievirus B test, you see that it says: "Stability (collection to initiation of testing): Ambient: 2 days; Refrigerated: 2 weeks; Frozen: 1 year".

So there should be no problems sending frozen samples from abroad.


I have also looked for research on whether enteroviruses like coxsackievirus B can alter the Th1/Th2 balance, but have not seen anything. It may be that other co-infections in the body are responsible for a shift to Th2 (LPS toxin from bacteria shifts Th2, for example), and so if you have these co-infections as prior conditions, once you catch Coxsackie B, the body is less able to fight it off. These prior infection might help explain why only certain people develop CFS from a Coxsackie B infection.


Regarding perforin, I think there is one theory that CFS may result from perforin deficiency.
 
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Hip

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Tentacles Sprout from Virally Infected Cells

I also discovered recently that coxsackievirus B infected cells can grow tentacle-like protrusions that connect to adjacent cells.

See this video of tentacle-like protrusions sprouting out of Coxsackie B virus infected cells.

More videos here.

Quite amazing, really. I wonder how coxsackievirus is able to change the shape of the cellular membrane like that.

One might guess that these cellular protrusions are mechanisms to infect adjacent cells with the virus.

The study abstract is here: Coxsackievirus B3-Induced Cellular Protrusions: Structural Characteristics and Functional Competence
 

globalpilot

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I just read this paper in its entirety. They measured 3 cytokines : TNFalpha, TGFbeta and IL1beta. They found they increased in both cases above controls but in the coxsackie permissive case, they didn't rise enough to eliminate the infection. They said the cytokines correlate with the increase in the C1 and C3 activity. It would be interesting to know why the cytokines are not increasing enough - a genetic polymorphism perhaps.

Also, what I'm curious about is ... why aren't the other forms of apoptosis , namely NK cell activity and cytotoxic T cell activity not able to eliminate the infection when the mitochondira pathway fails.

I think you have found something significant here. I didn't realize this pathway of apoptosis even existed. I have a few papers here to read now regarding apoptosis. Maybe something useful will fall out of the learning process. Some of us may have polymorphisms in this area although I'm not aware of any studies done in this area yet.

Boosting Mitochondria May Not Only Increase Energy, But Also Lead To Complete Viral Clearance

New study: The mitochondrial respiratory chain has a critical role in the antiviral process in Coxsackievirus B3-induced myocarditis.

This new study (Oct 2011) compared mice strains that were able to completely clear the CVB infection, against mice strains that could not, and so had lingering infection/immune activation.

The study context was coxsackievirus B3-induced myocarditis, but I think CVB myocarditis may be an excellent model for studying chronic fatigue syndrome; the symptoms are very different, but chronic, lingering CVB infection often seems to be a common denominator in both diseases.

After 90 days, the study authors found that the non-clearing mice showed permanently restricted mitochondrial complex I activity, whereas the mice that cleared the virus normalized all four mitochondrial complexes.

Note that these authors say that replicating viruses were no longer detectable after 90 days in both mice strains, but in fact, it is known form the work of Dr Nora Chapman et al, and Dr Chia, that non-cytolytic Coxsackie B viruses can remain indefinitely in cells, even when replicating virus particles are no longer detectable. This likely explaining the lingering immune activation observed in chronic myocarditis, as well as in chronic fatigue syndrome, even when replicating viruses cannot been seen anymore.

In general, the authors found that reduced CVB3 titers correlated with increased complex I and III activity.

So mitochondrial complexes I and III are possibly the ones you want to boost the most, to try to get viral clearance, if you have enterovirus / coxsackievirus B related chronic fatigue syndrome.

Supplements that boost or protect mitochondrial complexes I and III include: pyrroloquinoline quinone, gingko biloba, and melatonin (at night).

The paper concluded: "the regulation of energy metabolism appears crucial for an effective virus elimination and may be of prognostic and therapeutic significance"

So intriguingly, it seems that low energy output from mitochondria not only likely cause fatigue, but worse still, it seems to prevent the clearance of enterovirus from the tissues.

So boosting mitochondria, particularly complexes I and III, may not only provide a welcome increase in energy, but may also help clear viral infections.


Supplements That Boost Various Mitochondrial Complexes (unverified):

Pyrroloquinoline quinone stimulates complex I. http://www.ncbi.nlm.nih.gov/pubmed/16424117
Gingko biloba stimulates complexes I and III. http://www.annclinlabsci.org/cgi/reprint/31/1/25.pdf
Melatonin stimulates complexes I and IV.
Methylene blue stimulates complex IV.
Deprenyl stimulates complex IV

MDMA ("ecstasy") inhibits complex I activity in mice.
Pyrethroid pesticides like permethrin, often used as pet flea killer, is a potent inhibitor of complex I. How many people with CFS have a dog or cat that they use permethrin on, I wonder?
The organophosphate pesticide malathion inhibits complex IV.


Supplements That Boost Mitochondrial Function (I think):

Creatine.
Glutamine protects mitochondrial structure and function in oxygen toxicity.
High doses of nicotinamide prevent oxidative mitochondrial dysfunction in a cellular model and improve motor deficit in a Drosophila model of Parkinson's.
Piracetam improves mitochondrial dysfunction following oxidative stress.
Q10 Take co-enzyme Q10 with food! Q10 facilitates the conversion of nutrients into energy in the mitochondria. So take with meals.
Alpha lipoic acid + acetyl-L-carnitine.
Magnesium.
Malic acid.
Coconut oil / MCT oil.
Taurine.
D-ribose.


Supplements That Boost Mitochondrial Biogenesis:

Mitochondrial biogenesis = birth of new mitochondria. There are around a few hundred to a few thousand mitochondria in each cell. Some people think that CFS may not just be linked to reduced mitochondrial function, but also to reduce mitochondrial numbers. So generating new mitochondria may be a good idea.

Quercetin promotes mitochondrial biogenesis.
Resveratrol.
Leucine (and Branched Chain Amino Acids).
R-alpha-lipoic acid and acetyl-L-carnitine.
Isoflavones (daidzein, genistein, biochanin A).
Caffeine.
Hydroxytyrosol (from olive oil, and olive leaf extract). Commercial name: Hidrox.
Pioglitazone (Actos), an antihyperglycemic, antidiabetic drug.
Estradiol (hormone).
Pyrroloquinoline quinone (possibly a new vitamin).
Caloric Restriction (fasting) promotes mitochondrial biogenesis.
Erythropoietin.
Cold exposure.
Hypoxia.
SRT1720 (new drug from Sirtris Pharmaceuticals).
Telmisartan enhances mitochondrial biogenesis in human endothelial cell.
Triiodothyronine (T3).
DHEA.
Pyruvate.
Lactate.
Lithium.



Also of interest: Wikipedia's article on complex III says: "mutations in complex III cause exercise intolerance".

Given this, I wonder if virally induced restrictions in complex III might explain the post exertional malaise (PEM) in CFS, which is an exercise intolerance?

It possibly adds weight to the idea of boosting complex I and III as a CFS treatment.
 

Hip

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I just read this paper in its entirety. They measured 3 cytokines : TNFalpha, TGFbeta and IL1beta. They found they increased in both cases above controls but in the coxsackie permissive case, they didn't rise enough to eliminate the infection. They said the cytokines correlate with the increase in the C1 and C3 activity. It would be interesting to know why the cytokines are not increasing enough - a genetic polymorphism perhaps.

Also, what I'm curious about is ... why aren't the other forms of apoptosis , namely NK cell activity and cytotoxic T cell activity not able to eliminate the infection when the mitochondira pathway fails.

I think you have found something significant here. I didn't realize this pathway of apoptosis even existed. I have a few papers here to read now regarding apoptosis. Maybe something useful will fall out of the learning process. Some of us may have polymorphisms in this area although I'm not aware of any studies done in this area yet.
Well spotted. I did not realize that there was this intrinsic pathway for apoptosis either, and had not noticed that it's the intrinsic pathway that this paper refers to.

Though I think this intrinsic pathway of apoptosis is what that new DRACO antiviral treatment devised at MIT works on.
 

globalpilot

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That could be a very promising treatment. I don't have any information on when it will be available or the cost, do you ?
I also wonder too if you can get reinfected again if the root problem isn't fixed.


Well spotted. I did not realize that there was this intrinsic pathway for apoptosis either, and had not noticed that it's the intrinsic pathway that this paper refers to.

Though I think this intrinsic pathway of apoptosis is what that new DRACO antiviral treatment devised at MIT works on.
 

Hip

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That could be a very promising treatment. I don't have any information on when it will be available or the cost, do you ?
I also wonder too if you can get reinfected again if the root problem isn't fixed.
DRACO is only in the very early stages of research, so if it ever does see the light of day, it won't be for 15 years or so.
 

alex3619

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On DRACO, I think it might be good for healthy people with new onset infection. For a long term ME sufferer I think it will most probably be lethal. They might be able to get around this, but I very much doubt it. One of the big reasons for this is that many of the cells likely to be infected either cannot be replaced, or are replaced very slowly. So expect the best outcome from DRACO to be permanent paralysis and brain damage, though death is more probable. Bye, Alex
 

globalpilot

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This is a new report on a drug called DCA that shrunk tumors in mice w/o side effects.
They mention it works by increasing energy - I just wonder if this might be applicable to enterovirus and the study reported in this thread.
I have to go reread the study now and think about this drug in the context of the study. Might be some promise here.
 

Radio

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Hi Marian

Thanks very much for those links.

I find your H2S theory very thought provoking, especially since the H2S neurotoxic metabolite test I took a couple of years ago came out a strong positive. I did some experiments at that time with taking orally some H2S absorbers such as zinc acetate, hydroxocobalamin, zeolite, and even small amounts of sodium nitrite (which you have to be very careful with, as a fatal dose of sodium nitrite can be as a little as 1 gram).

However, even after a few weeks on this anti-H2S regimen, I did not get much in the way of results, in terms of improved CFS symptoms. Since in experiments, mice emerged very quickly from their H2S-induced low energy "suspended animation" state, I assume the same thing would happen to CFS patients once the H2S has been removed: ie, you'd return to normal health within hours or days, rather than weeks or months.

It's also interesting that some perfectly healthy people can have digestions that regularly produce odorous flatulence (which generally means they are producing H2S in their gut), but experience no ill effects. I myself occasionally have this odorous H2S flatus (usually, like many people, when I have a meal with lots of beans); however I don't feel any worse on those days; in fact, I usually feel noticeably better when my digestion is more odorous, for some reason.

This could of course be a paradoxical result, and this is something I did think about: ie, it may be that increased H2S in the gut spurs some H2S detoxification system into action in the body, thus actually lowering overall bodily H2S (in which case, an experimental treatment for CFS might be a very low level exposure to H2S - though that's not easy to do, given that breathing H2S can be fatal).



It may be that the source of the H2S is as intracellular one, in which case, perhaps a different strategy may be needed to absorb or to block its production. It says in the above link you gave on CVB viral myocarditis that cystathionine gamma-lyase is the enzyme involved in manufacturing H2S in coxsackievirus B infection. I am not sure if this is an intracellular enzyme, but if so, then perhaps the impact of H2S in CFS patients is indeed confined to within the cells.

I am not sure how easily H2S can diffuse in and out of cells across the plasma membrane. If it can diffuse very easily, then perhaps this distinction made here between intracellular and extracellular H2S is not really correct.


Do you know if there are intracellular enzymes that break down H2S? If so, could the it be that CFS patients have a lack of these enzymes, thus leading to H2S toxicity?
The Vicious Cycle To Recovery (Synopsis)

Chronic Fatigue Syndrome is a complex condition involving multiple processes and pathways in the body. There are many theories involving a single cause. However, we propose that there are multiple root causes which compound and reinforce each other, leading to the viscous cycle of CFS.

Inflammatory conditions can affect many functions in the body such as the liver's detoxification process. Chronic fatigue, and many other chronic illnesses can be aggravated by a buildup of toxins. The Sulfotransferase metabolism is a key factor in Phase II detoxification which is responsible for the detoxification of many compounds. Some of these compounds are phenols, amines, sulfide, and many other toxic molecules and nutritious food considered very healthy. These enzyme's are also responsible for the oxidization of sulfur to sulfate. Malfunction of the Phenol-Sulfotransferase (PST) enzyme, as well as other contributing factors can cause an overload of phase 2 toxins in the liver. These toxins can damage mitochondria, as well as lead to a functional sulphur transferase and sulphite oxidase deficiency. These insufficiency can have a impact on intercellular sulfate needed for proper cell function, without it a myriad of health problems occur. We believe inherited metabolic liver genetic factors can be a contributing causes of this viscous cycle.

Hydrochloric acid and bile acid production are needed to maintain a proper balance of gut flora, as well as liberate key nutrients such as B-12. We have identified that these imbalances can lead to developing dysbiosis in the small intestine, leading to malabsorption and leaky gut. Intestinal permeability opens the door to autoimmune conditions, silent viral infections, bacterial infections, and immune system dysfunction. Once chronic viral infections have been established they can cause chronic inflammation of the liver and kidneys, further inhibiting PST enzyme as well as sulfate recycling. Mercury toxicity is also a possible issue in this metabolic pathway. Sulfate is also required for mucus production need for many protective functions in human organism. Bacteria and yeast overgrowth can also produce hydrogen sulfide (H2S) that can bind to the mitochondrial enzyme cytochrome c oxidase, part of the electron transport chain in the krebs cycle. This can also impair oxidative phosphorylation and ATP production. When mitochondria become damaged due to a buildup of toxins, energy production is greatly impaired. The mitochondria pays the ultimate price for our weak detoxification ability.

There are many contributing factors that can overwhelm the body's metabolism such ; lyme disease, viruses and non-cytolytic viruses, mold, toxic exposure as well as dysbiosis, endotoxins and even physical exertion can dramatically affect the liver's detoxification process. We are work on a synopsis that will be identifying critical research needed to help us understand this viscous cycle. See more here: http://www.newtreatments.org/fromweb/sulfur.html





Sulphationhttp://www.allnaturaladvantage.com.au/Sulphation_diagram.htm
 
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godlovesatrier

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Old thread this but really interesting. My dizziness has definitely got better the more and more I've been able to address the fatigue. Ubiquinol currently has had the largest and most protracted effect of anything I've ever taken. I wonder if vitamin c has any effect on mitchondrial function. I've recently discovered magnesium ascorbate so finally able to get about 1600mg of vit c per day. I wonder if this combined with a few other supplement changes over the last 2 months has caused the body to get more control over viral load and therefore reduce the dizziness, which feels like possible viral attack in the brain.