All plausible causes of ME

[redo]

Waverunner. When it comes to the enterovirus hypothesis, is there a specific virus in the group that's a suspect, or is it the group as a whole. Do you or alex3619 know of a study that highly indicates that such mechanisms may be involved?

I totally agree with your last paragraph. IMO, research such as the horrible Tuskegee syphilis experiment have contributed strongly to shifting the ethics guidelines from "everything is OK" to "almost nothing is OK". When the pros clearly outweigh the cons, then permission should naturally be granted - but I know many valid research projects which have been killed in the cradle by an ethics committee - even totally harmless research regarding analysis of blood samples.

 

[Waverunner]

I totally agree with your last paragraph. IMO, research such as the horrible Tuskegee syphilis experiment have contributed strongly to shifting the ethics guidelines from "everything is OK" to "almost nothing is OK". When the pros clearly outweigh the cons, then permission should naturally be granted - but I know many valid research projects which have been killed in the cradle by an ethics committee - even totally harmless research regarding analysis of blood samples.

Some of the people in these ethic committee just massage their ego's. They are much too stupid in order to understand the science behind most of the compounds but in their eyes, they need to save the patient from greedy companies and a new Dr. Mengele who only wants to abuse his patients and doesn't care about their lives. It's the same with politicians, most things work a lot better without them.

Bastiat said, that it not only counts what you see but especially what you don't see. In the medical approval field this means, that you can see, that less patients die of toxic drug side effects. What you don't see, is the number of patients who suffer and die, because new compounds never reached the market, because companies cannot afford the approval process.

Regarding the virus test, I would go for Enterovirus (species A-D) and Adenovirus (Species A-F) and maybe even Rhinovirus if you have access to a Nanosphere test. The problem is, that lots of PCR tests have been done but yielded no useful results. Dr. Chia for example uses PCR but only tests stomach/gut biopsies.

 

[redo]

Excluding the misdiagnosed patients, I think it's safe to assume that most of the CCC diagnosed ME patients have at least one common denominator.

In my opinion, the way to get the best clues as to what can lie behind this disease is to try to answer the following question. Pieces which must fit the puzzle:
1) Mononucleosis, giardisis and the flu are among triggers for the disease. What can be triggered by so wildly different things such as the aforementioned infections?
2) If the Mella/Fluge results hold true, that what, has to be able to cause symptoms mediated via autoimmunity/autoinflammation – further narrowing the list of possible suspects.
3) The cause(s) leading to ME has to be more prevalent in women than men.
4) What's causing the disease must be able to produce a wide array of symptoms (brainfog, joint paint, visual problems, fatigue etc).

If you have any other things you'd like to add to the list, then please do weigh in.

One more thing I'd like to add to the list of pieces which must fit the puzzle:
*) The mechanisms behind the rather characteristic PEM must be explained in some way.

This is just as important to rule out some theories as it is to confirm others. For example; people whom are depressed and the likes often get better from exercise, not worse...

 

[Allyson]

Excluding the misdiagnosed patients, I think it's safe to assume that most of the CCC diagnosed ME patients have at least one common denominator.
.....
4) What's causing the disease must be able to produce a wide array of symptoms (brainfog, joint paint, visual problems, fatigue etc).

If you have any other things you'd like to add to the list, then please do weigh in.


. Does anyone else know of other viable candidates?


I am hoping we can get a debate going about this in the weeks to come. I'm working on getting a list ready for early March, which will be discussed with a person who's got several hundred thousands of dollars disposable, which can be used for ME research.

My health is really frail, so I wont pop by daily to the forums, but please do drop some lines if you've got some thoughts on the matter. Both on what pieces must fit the puzzle, and also on possible candidates matching that list.

Hi Redo,
so sorry to hear aboutyour poor health, and thanks for the thread.

I will weigh in with this to match your point 4, namely:
What's causing the disease must be able to produce a wide array of symptoms (brainfog, joint paint, visual problems, fatigue etc).

connective tissue disease such as Ehlers- Danlos Syndrome would do this as CT is all throughout the body and EDS explains almost ALL my symtoms to my satisfaction ... which nothing esle does in oer 5 years of researching it.
I have started a liin in it here .. note that on the EDS pages they are all complaining aout ALL the same symtoms as we do.
The CTD also affects blood and blood vessels ( both CTs) leading to POT OI and gut issues. Brain fog is due to resulting lack of blood to the brain and the effect of excess adrenaline secretion in an attempt to constrict the blood vessels to get blood up to the brain. ( brain fog is like a hangover - research shows hangovers to be due to dehydration of the brain due to the effects of alcohol)

http://forums.phoenixrising.me/index.php?threads%2Fis-me-due-to-ehlers-danlos-syndrome-stretchy-veins.20351%2F

 

[kurt]

If I had a friend with money to test a group of CFS patients, the test I would run would be something that has not been done yet. And that seems obvious to me, based on many discussions here over multiple years. What is missing? Full genomic sequencing of a group of ME/CFS patients. That's it, nothing else in my opinion is likely to yield as much rapid evidence at this point in time. I realize that full genomic sequence costs several thousand dollars, if a lab has access to efficient tools anyway, it can cost a lot more. But still, even a group of 20 patients, with full sequencing, something would be discovered.

 

[kurt]

A plausible cause of ME/CFS?

Based on the 4 points made in the OP:

1. all the mentioned infections and many others create high chronic reactive oxygen species (ROS) load. This oxidative stress puts pathological detoxifiers at risk of poisoning their own mitochondria.

2. autoimmunity that leads to poor immune function may perpetuate the chronic infections, increasing oxidative load. autoimmunity also can be destructive and inflammatory, both increasing oxidative load.

3. women have higher natural oxidative load due to hormonal differences, thus any condition involving pathological detoxification will put them at greater risk, if they have the underlying bad immune and/or detox genes.

4. oxidative stress can occur in any system in the body, and any area of the brain, any tissue anywhere. Thus there is probably no symptom that can not be activated with pathological detoxification, particularly if there are problems in the brain regions that regulate neurological function.

So I think chronic oxidative stress, combined with bad genes for detox and immune function is the likely common element to explain everything. Pretty much every CFS trigger involves high oxidative stress load, including the psychogenic (adrenal looping or PTSD), infectious, toxin exposure, immune over-stimulation, etc.

More evidence of the combination of oxidative stress and a detox problem is the fact that many people have pathologies associated with CFS but they do not all get CFS. Only a few percentage of people who have mono develop CFS, for example. Most people with leaky gut, candidiasis, metals problems, enteroviruses, etc., do not appear to have CFS. Clearly these triggers are not the sole cause of CFS.

And even more interesting evidence is the diseases that create temporary CFS generally are known to produce high oxidative load. I have seen this personally as my mother and one sister have battled cancer. Before treatment both had a type of CFS, my mother had many the classic CFS symptoms, including PEM, low energy levels, intolerance of noise, people, etc. After treatment started working, both have seen remission of the CFS type symptoms.

I suspect most CFS patients fit this model, poor detoxifiers under an oxidative stress load. But we have different causes of our oxidative stress, I believe that is why the research has been so disappointing, we are just too diverse in the causes of our personal oxidative stress.

So in my view, a great area for research right now is identify deoxification and immune factors that are common to CFS patients. Those types of studies, including looking at genetics, might reveal why we have such a hard time with ROS.

And great areas for treatment exploration would be to find your personal source of oxidative stress and treat that, while at the same time identifying detoxification problems and treat them (methylation support, etc).

 

[Helen]

If I had a friend with money to test a group of CFS patients, the test I would run would be something that has not been done yet. And that seems obvious to me, based on many discussions here over multiple years. What is missing? Full genomic sequencing of a group of ME/CFS patients. That's it, nothing else in my opinion is likely to yield as much rapid evidence at this point in time. I realize that full genomic sequence costs several thousand dollars, if a lab has access to efficient tools anyway, it can cost a lot more. But still, even a group of 20 patients, with full sequencing, something would be discovered.

I agree, this is the study I am waiting for too. And good news from Nielk and others that Dr. Derek Enlander at Mt Sinai Hospital is conducting a study on ME/CFS people including full genomic sequencing of 300 people , half of them healthy controls. The study is planned to be completed in autumn (grammar?) this year. Analysed by Dr. Eric Schadt that is said to be an outstanding researcher.

If I , or a friend, had the money I would let everyone with ME/CFS also be tested for an eventual blockage of the methylation; the test that Rich suggested as the first to take. He found only a few normal panels among more than 200 people that had been tested.

I would also investigate how many that had been exposed to mercury from vaccines and/or amalgam fillings as mercury might affect every cell and process in the body.

 

[Young&sick]

Excluding the misdiagnosed patients, I think it's safe to assume that most of the CCC diagnosed ME patients have at least one common denominator.

In my opinion, the way to get the best clues as to what can lie behind this disease is to try to answer the following question. Pieces which must fit the puzzle:
1) Mononucleosis, giardisis and the flu are among triggers for the disease. What can be triggered by so wildly different things such as the aforementioned infections?
2) If the Mella/Fluge results hold true, that what, has to be able to cause symptoms mediated via autoimmunity/autoinflammation – further narrowing the list of possible suspects.
3) The cause(s) leading to ME has to be more prevalent in women than men.
4) What's causing the disease must be able to produce a wide array of symptoms (brainfog, joint paint, visual problems, fatigue etc).

If you have any other things you'd like to add to the list, then please do weigh in.

The only candidate I know of, which fulfills the four criteria, are ERVs. Does anyone else know of other viable candidates?

I recently stumbled across these graphics from the company of which Perron works for. It pretty much falls in line with everything I've thought about how ME erupts: I find it really hard to believe that a exogenous retrovirus can be the culprit of the disease, when we know all too well how mononucleosis, giardisis or a flu (and more things which are pretty unrelated) can trigger the disease.

(see an article about Perron's work here)

I am hoping we can get a debate going about this in the weeks to come. I'm working on getting a list ready for early March, which will be discussed with a person who's got several hundred thousands of dollars disposable, which can be used for ME research.

My health is really frail, so I wont pop by daily to the forums, but please do drop some lines if you've got some thoughts on the matter. Both on what pieces must fit the puzzle, and also on possible candidates matching that list.

I feel like point 3 is only applicable for ME/CFS in adults. Teens who get it seem to be most mono generated inceptions and is equally prevalent in both genders as far as i can tell.

 

[golden]

I think Dr Ray Perrins theory is relevant. The lymphatic system is not working correctly.

I wonder if this maybe because of a virus or mercury caused glutathione depletion.

The lymphatic system is all encompassing. Perrins theory was something about a reverse lymph theory. The lymph gets blocked and backs up , gets clogged in the brain. Posture worsens this.

Toxins in the brain are responsible for symptoms. It affects the hypothalamus and gas a knock on effect through the pituitary gland, then the thyroid which governs all functions.

It includes the parasympathetic nervous system too and is more complex than I can remember.

It does make me wonder about the guaresferin treatment protocol too which may link in with getting the lymph working properly again.

The idea is to manually drain the lymph in the proper direction thus enabling the correct functioning of the body to begin again.

 

[Seven7]

Full genomic sequencing of a group of ME/CFS patients.

If is a couple thousand I would pay for it myself (my own sequencing) if we can get a few more people maybe we can start a self funded study. If anybody is interested I am in.

 

[Navid]

If is a couple thousand I would pay for it myself (my own sequencing) if we can get a few more people maybe we can start a self funded study. If anybody is interested I am in.

i think kurts theory is 100% right on...but the mystery remains what is causing the oxidation issues, the detox issues and how do we treat them? i know what caused mine...anecdotally; not scientifically but have no idea how to fix. i am too ill right now to even tolerate methlyation...but i do know where my defects lie.

inester
i would be interested in this.

thanks

 

[Navid]

i think kurts theory is 100% right on...but the mystery remains what is causing the oxidation issues, the detox issues and how do we treat them? i know what caused mine...anecdotally; not scientifically but have no idea how to fix. i am too ill right now to even tolerate methlyation...but i do know where my defects lie.

inester
i would be interested in this.

thanks

A plausible cause of ME/CFS?

Based on the 4 points made in the OP:

1. all the mentioned infections and many others create high chronic reactive oxygen species (ROS) load. This oxidative stress puts pathological detoxifiers at risk of poisoning their own mitochondria.

2. autoimmunity that leads to poor immune function may perpetuate the chronic infections, increasing oxidative load. autoimmunity also can be destructive and inflammatory, both increasing oxidative load.

3. women have higher natural oxidative load due to hormonal differences, thus any condition involving pathological detoxification will put them at greater risk, if they have the underlying bad immune and/or detox genes.

4. oxidative stress can occur in any system in the body, and any area of the brain, any tissue anywhere. Thus there is probably no symptom that can not be activated with pathological detoxification, particularly if there are problems in the brain regions that regulate neurological function.

So I think chronic oxidative stress, combined with bad genes for detox and immune function is the likely common element to explain everything. Pretty much every CFS trigger involves high oxidative stress load, including the psychogenic (adrenal looping or PTSD), infectious, toxin exposure, immune over-stimulation, etc.

More evidence of the combination of oxidative stress and a detox problem is the fact that many people have pathologies associated with CFS but they do not all get CFS. Only a few percentage of people who have mono develop CFS, for example. Most people with leaky gut, candidiasis, metals problems, enteroviruses, etc., do not appear to have CFS. Clearly these triggers are not the sole cause of CFS.

And even more interesting evidence is the diseases that create temporary CFS generally are known to produce high oxidative load. I have seen this personally as my mother and one sister have battled cancer. Before treatment both had a type of CFS, my mother had many the classic CFS symptoms, including PEM, low energy levels, intolerance of noise, people, etc. After treatment started working, both have seen remission of the CFS type symptoms.

I suspect most CFS patients fit this model, poor detoxifiers under an oxidative stress load. But we have different causes of our oxidative stress, I believe that is why the research has been so disappointing, we are just too diverse in the causes of our personal oxidative stress.

So in my view, a great area for research right now is identify deoxification and immune factors that are common to CFS patients. Those types of studies, including looking at genetics, might reveal why we have such a hard time with ROS.

And great areas for treatment exploration would be to find your personal source of oxidative stress and treat that, while at the same time identifying detoxification problems and treat them (methylation support, etc).

kurt: wht kind of cancer treatment did our mom and sister have. i think your theory is right on. i have had my methylation checked thru yasko's testing and i have tons of defects in detoxing. i know causes in my life that would have lead to oxidation problems also....an their are others in my famiy with similar issues...so the perfect storm....ihave a case of textbook me/cfs: PEM, Fractured, Unrefreshing sleep. POTS/OI/NMH/Viruses/Bacterial Infections, body pain...etc.

i would be very interested in being part of a group to have genomic testing done. If we can get the right number of ppl to make the cost reasonable pls count me in.

thanks,

 

[kurt]

kurt: wht kind of cancer treatment did our mom and sister have.

Navid: my mom and sister are both on chemotherapy. My mom is elderly and was stage IV to begin with and had about 2 months expected to live if she had no treatments. At that point she had classic CFS type symptoms. Fortunately she has responded well to chemo and also an adjunctive therapy, so it looks like she will live, and her CFS is decreased now, but she will be on regular or intermittent chemo for life.

My sister is middle-age and has also responded well to the chemo fortunately, she is also using the adjunctive therapy (chlorine dioxide, ClO2). My mom has proven that chlorine dioxide works against cancer. When she neglects to take regular doses her tumor markers increase. But when she takes the adjunctive chlorine dioxide the tumor markers plummet quickly. My sister has a different cancer without those types of markers, so the effect of the ClO2 on her is harder to measure. And yes, I have also tried the chlorine dioxide and it does help, gives me a bit more energy in a day, but nothing dramatic like what happens with my mom and sister.

i think your theory is right on. i have had my methylation checked thru yasko's testing and i have tons of defects in detoxing. i know causes in my life that would have lead to oxidation problems also....an their are others in my famiy with similar issues...so the perfect storm....ihave a case of textbook me/cfs: PEM, Fractured, Unrefreshing sleep. POTS/OI/NMH/Viruses/Bacterial Infections, body pain...etc.

i would be very interested in being part of a group to have genomic testing done. If we can get the right number of ppl to make the cost reasonable pls count me in.

That's good you know some of the defects. Do you have MTHFR? I only have functional lab results showing the detox problems (full liver detox profile). But should probably take the Yasko profile.
Yes, I've been thinking along those lines for awhile now, of helping put together a group of CFS/ME patients who share that type of testing data. Basically, self-funded research into topics that are being neglected but are showing promise.

 

[Stretched]

Having had this DD since 1986, I have of course followed the science and various theories, but
as we all know none of the protocols have 'cured' or turned around ME/CFS, sic as far as we know.

I was young then now I'm older, and the illness has progressed. I'm a pragmatist - if eating pine
cones will make me feel better I don't care how it came to be. Maybe later... .

So, and I hope I'm not unintentionally restating anything from someone else's thoughts but I turned
the science debates around and started to question a macro perspective. To date I have backed in
to needing an answer to essentially one question: how can 4-10+ million disparate people suddenly become plagued with essentially the same illness (in a short historical span)?

We can't all have communicably 'picked up' a bug, i.e there are more than 6 degrees of separation. There are those of us who know we have 'it'. and those who don't... .

Is it then that all humans have the same anatomical seed and the growth to ME is precipitated by something to which we all have in common? I come up with massive answers such environmental conditions, exposure to emotional and/or physical changes around the globe (or at least in those areas report the malaise), or physiologically, as in perception of reality, sic leading to stress. Everyone fits the 'n' of this statistical consideration.

Maybe ME is precipitated by global warming, tears in the ozone layer...leading to build up of
carbon dioxide or other biology and changes from earlier historical eras. This plague is certainly not from flea born rats at the water source; and it's more than condensation around an air conditioner on
a ship. Or maybe it is the water source - we all get rain?

Perhaps by examining the bigger questions we can get today's science (or tommorrow's)
refocused...to the point we see at least one cure. Anyone care to expand?

 

[Young&sick]

Having had this DD since 1986, I have of course followed the science and various theories, but
as we all know none of the protocols have 'cured' or turned around ME/CFS, sic as far as we know.

I was young then now I'm older, and the illness has progressed. I'm a pragmatist - if eating pine
cones will make me feel better I don't care how it came to be. Maybe later... .

So, and I hope I'm not unintentionally restating anything from someone else's thoughts but I turned
the science debates around and started to question a macro perspective. To date I have backed in
to needing an answer to essentially one question: how can 4-10+ million disparate people suddenly become plagued with essentially the same illness (in a short historical span)?

We can't all have communicably 'picked up' a bug, i.e there are more than 6 degrees of separation. There are those of us who know we have 'it'. and those who don't... .

Is it then that all humans have the same anatomical seed and the growth to ME is precipitated by something to which we all have in common? I come up with massive answers such environmental conditions, exposure to emotional and/or physical changes around the globe (or at least in those areas report the malaise), or physiologically, as in perception of reality, sic leading to stress. Everyone fits the 'n' of this statistical consideration.

Maybe ME is precipitated by global warming, tears in the ozone layer...leading to build up of
carbon dioxide or other biology and changes from earlier historical eras. This plague is certainly not from flea born rats at the water source; and it's more than condensation around an air conditioner on
a ship. Or maybe it is the water source - we all get rain?

Perhaps by examining the bigger questions we can get today's science (or tommorrow's)
refocused...to the point we see at least one cure. Anyone care to expand?

I think you are looking too big here, no offense. We could all very well have 'picked up' a bug, look at how ubiquitous certain viruses are. I dont know that this illness is any more prevalent today than it was at other times in history, we just have the technology to record its presence and connect the community today, remember the internet as we know it has only been around for a decade and change. This means that millions of what seemed like isolated cases now have a forum and it seems like its suddenly an illness that has picked up steam.

The most likely theory to me is that we have a genetic or acquired predisposition to immune related issues that would go unnoticed were our immune systems not put under extreme duress by something (it can be different for different people, mono, the flu, etc). This would explain how so many different paths lead to this illness.

For example there is a history of b-cell related immune issues in my family (RA mostly). I am going to have my 5th infusion of rituximab in a few weeks here and after my last one while i had no b-cells, i felt the best ive felt since falling ill three years ago. I felt almost normal, and i feel as though the remaining illness i felt was due to having spent three years sitting around being ill, not the illness itself. I became ill after having mono and then returning to training for my sport much too soon which between mono, training, and living a college lifestyle put a ton of stress on my immune system (which it seems may have a systemic issue due to genetics, remember my family history).

Just my 2 cents.

 

[cigana]

Excluding the misdiagnosed patients, I think it's safe to assume that most of the CCC diagnosed ME patients have at least one common denominator.

In my opinion, the way to get the best clues as to what can lie behind this disease is to try to answer the following question. Pieces which must fit the puzzle:
1) Mononucleosis, giardisis and the flu are among triggers for the disease. What can be triggered by so wildly different things such as the aforementioned infections?
2) If the Mella/Fluge results hold true, that what, has to be able to cause symptoms mediated via autoimmunity/autoinflammation – further narrowing the list of possible suspects.
3) The cause(s) leading to ME has to be more prevalent in women than men.
4) What's causing the disease must be able to produce a wide array of symptoms (brainfog, joint paint, visual problems, fatigue etc).

If you have any other things you'd like to add to the list, then please do weigh in.

I like this thread
I would say (4) needs to be in there but is less important than the others, because it seems to me that you can always find ways of explaining the myriad symptoms from any hypothesis, eg. heavy-metal poisoning, thyroid resistance, Lyme, mast cell disorders, methylation disorder etc etc....none of these have a hard time explaining a route to symptoms.

I would probably add in a (6) that the model has to explain why successful treatments are successful, eg. ampligen, rituximab, gc-maf, antibiotics etc. Obviously these don't lead to complete cures, so maybe they are just removing the "perpetuators" (as Alex puts it) that are listed in piece (1).

Maybe we should not be shy of including more and more pieces, and just rank them in order of importance.

Personally I think immune dysfunction is the most important element. All of the big gun treatments seem to treat this.

Let's assume it is one thing, or that there are at least some necessary preconditions. We all must have been exposed to these preconditions. Some of us have tick-borne infections, some enteroviruses, etc., (arguably all of us if testing improves), but the only thing that really has changed in the past 50 years that we can say for sure is all of us have definitely been exposed to is the modern diet. I don't think it's as simple as leaky gut or dysbiosis, but I can't help thinking it has a key role. Perhaps the western diet is a necesary precondition that sets the scene for immune dysfunction and then the triggers and perpetuators come along.

So currently I go for:

necessary precondition(s) + immune dysfunction + trigger(s) + perpetuator(s)

 

[alex3619]

thanks, Alex

now I'm confused whether this explains sudden onset of OI?

Darn, the date of the last post I made was when I broke my leg and spent nearly two months in hospital, so I never got to reply.

I think viral infection of the blood vessels can explain sudden onset OI. The concept here is that of what in chaos theory is called a catastrophe. The system is under stress, but copes. Then more stress, and it tries harder to cope. Suddenly something happens to the balance, and the entire system changes. The coping mechanisms fail. The body then achieves a new stable state, but you now have a new symptom: OI.

All of this is of course speculation. As I said much earlier, donor blood vessel tissue could be tested for enteroviral or other viral infection in the muscle bands. I would not suggest taking such biopsies from a live patient due to the potential damage.

On another topic, leaky gut testing is not required to prove it. The presence of LPS proves it, unless you consider that patients have occult bacterial infections producing LPS. That is the only other explanation. What is needed though is a better understanding of what is meant by leaky gut in the case of ME patients. We just don't know enough. That might mean, again, using deceased donors to supply tissue for study. While superficial gut biopsies are simple and usually not very dangerous, the kind we really need are probably deep cross-sections. That is not something a live patient should be even asked to volunteer for.

 

[heapsreal]

Darn, the date of the last post I made was when I broke my leg and spent nearly two months in hospital, so I never got to reply.

I think viral infection of the blood vessels can explain sudden onset OI. The concept here is that of what in chaos theory is called a catastrophe. The system is under stress, but copes. Then more stress, and it tries harder to cope. Suddenly something happens to the balance, and the entire system changes. The coping mechanisms fail. The body then achieves a new stable state, but you now have a new symptom: OI.

All of this is of course speculation. As I said much earlier, donor blood vessel tissue could be tested for enteroviral or other viral infection in the muscle bands. I would not suggest taking such biopsies from a live patient due to the potential damage.

On another topic, leaky gut testing is not required to prove it. The presence of LPS proves it, unless you consider that patients have occult bacterial infections producing LPS. That is the only other explanation. What is needed though is a better understanding of what is meant by leaky gut in the case of ME patients. We just don't know enough. That might mean, again, using deceased donors to supply tissue for study. While superficial gut biopsies are simple and usually not very dangerous, the kind we really need are probably deep cross-sections. That is not something a live patient should be even asked to volunteer for.

Infections affecting the ticker could also explain pots/oi, as in dr lerners theory??

 

[alex3619]

Infections affecting the ticker could also explain pots/oi, as in dr lerners theory??

These viruses affect heart as well as other muscle, so yes. However what I am saying is its probably the heart and blood vessels, the entire vascular system, not just the heart.

 

[Guido den Broeder]

It can't be both? Viruses can trigger autoimmune disease.

They can, but I don't think that's happening in ME. Our immune system is fighting a real intruder, only it does so ineffectively because our B-cells have been repogrammed, as it were.