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Why does Kenny De Meirleir diagnose almost every patient with bacterial infections?

pattismith

Senior Member
Messages
3,941
Rituximab.
Rituximab works for autoimmune-induced CFS/ME, but CFS/ME is only a syndrome with mitochondrial involvment,and not all the patients respond to immunomodulators.

It may be that mitochondrial deficiency (either primary or secondary) can alter immunity and favors intolerance to infectious agents that are usually under control like Chlamydia or Mycoplasma species.

This is my understanding of the disease, and this is the way I understand the improvment I felt with some of my painful symptoms under azithromycin/doxycycline, although the treatment made my mitochondria worse.

In France very few doctors believe these chronic infections does exist, but one published online his results
(he treats CFS/ME, Lyme, co-infections, FM, Autism, (all with minimal testing) based on symptoms , and recorded improvments rates:

http://www.psychostrategy.net/artic...omatis-et-mycoplasma-pneumoniae-67077855.html

http://www.psychostrategy.net/artic...omatis-et-mycoplasma-pneumoniae-67078656.html

It's in french but I could translate it if you wish.
 
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snowathlete

Senior Member
Messages
5,374
Location
UK
No, I am not, but ME is not the only field where politics has an impact on ´scientific´ approval, hence my mention of the IDSA and ILADS. I think you are right about some of the treatments though, but that´s what happens when you try to help patients despite the fact that many of the issues that affect them have been underfunded in terms of research.

I agree, and I am in support of adult patients being able to access unproven treatments. I do think that some patients are unaware how unproven some of the treatments are though, which I don't think is good, and that brings us back to what I think is the primary issue, that patients aren't properly informed of the risks.
 

ivorin

Senior Member
Messages
152
I agree, and I am in support of adult patients being able to access unproven treatments. I do think that some patients are unaware how unproven some of the treatments are though, which I don't think is good, and that brings us back to what I think is the primary issue, that patients aren't properly informed of the risks.
This!
 

Cheshire

Senior Member
Messages
1,129
In France very few doctors believe these chronic infections does exist, but one published online his results
(he treats CFS/ME, Lyme, co-infections, Autism, (all with minimal testing) based on symptoms , and recorded improvments rates:

http://www.psychostrategy.net/artic...omatis-et-mycoplasma-pneumoniae-67077855.html

http://www.psychostrategy.net/artic...omatis-et-mycoplasma-pneumoniae-67078656.html

It's in french but I could translate it if you wish.

This website, chronimed, is linked with discredited Nobel price Jean-Luc Montagnier.
 

pattismith

Senior Member
Messages
3,941
This website, chronimed, is linked with discredited Nobel price Jean-Luc Montagnier.

Yes, Luc Montagnier had some very strange theory lately as getting old, and I'm not sure that his support to Chronimed GPs really help them :confused:
 

pattismith

Senior Member
Messages
3,941
We have no convincing evidence for immunosuppression in ME, as you know.

maybe no evidence yet Jonathan, but it would make sense that mitochondria issues create immune deficit.

Mitochondria are the powerhouses of immunity.
https://www.ncbi.nlm.nih.gov/pubmed/28418387

Powering the Immune System: Mitochondria in Immune Function and Deficiency
https://www.hindawi.com/journals/jir/2014/164309/

"Concurrently, immunodeficiencies arising from perturbation of mitochondrial elements are increasingly recognized. Recent observations of immune dysfunction and increased incidence of infection in patients with primary mitochondrial disorders further support an important role for mitochondria in the proper function of the immune system. Here we review current findings."

So if CFS/ME has a link with a mito dysfunction, immune deficit may be involved on the long run.

The immune system of the Hibernating animals is at rest, and doesn't fight pathogens...

Periodic arousal from hibernation is necessary for initiation of immune responses in ground squirrels.

https://www.ncbi.nlm.nih.gov/pubmed/11893609

and other study on that subject:

"Hibernation may therefore increase infection risk, as illustrated by the currently emerging WNS in hibernating bats."
https://www.ncbi.nlm.nih.gov/pubmed/20519639

https://www.ncbi.nlm.nih.gov/pubmed/23527062

Also in primary mitochondrial diseases:

"What is the impact of illness or infection on a patient with mitochondrial disease?
Patients, parents, and healthcare providers with firsthand experience of mitochondrial disease have probably experienced the consequences of an illness or infection. Illnesses and infections have a more dramatic and prolonged impact on children and adults who suffer from mitochondrial disorders, often causing long periods of fatigue, regression in developmental milestones, skills or baseline function, and exacerbation or complaints of additional (unrelated) symptoms during and after the period of illness. In addition, some physicians and families notice an increased susceptibility to illness for patients with mitochondrial disease"
http://www.mitoaction.org/blog/immune-function-and-mitochondrial-disease

 
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Jonathan Edwards

"Gibberish"
Messages
5,256
maybe no evidence yet Jonathan, but it would make sense that mitochondria issues create immune deficit.

Mitochondria are the powerhouses of immunity.
https://www.ncbi.nlm.nih.gov/pubmed/28418387

That is bit like saying that the mains supply causes your computer to crash. Mitochondria are the powerhouses of everything - the mains supply. So if they are not working you get something called death.

And we do not yet have any real evidence there is anything wrong with the mitochondria in ME.
 

Learner1

Senior Member
Messages
6,305
Location
Pacific Northwest

JES

Senior Member
Messages
1,322
I think most of us would agree that mitochondria are involved, but labeling CFS/ME as a mitochondrial disease is another matter. With CFS/ME there are several things that do not fit well with classic mitochondrial diseases, such as possible sudden onset (rarely in childhood) and the spontaneous recovery that is sometimes witnessed, check for example Ken Lassesen's blog, he is a patient who recovered three times. To give another example, myself and some others on this forum notice big improvements after getting a cold/flu. If the mitochondria are fundamentally not working, I have a hard time understanding the mechanism behind such rapid improvements that many of us have experienced.
 
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Alvin2

The good news is patients don't die the bad news..
Messages
3,024
I think most of us would agree that mitochondria are involved, but labeling CFS/ME as a mitochondrial disease is another matter. With CFS/ME there are several things that do not fit well with classic mitochondrial diseases, such as possible sudden onset (rarely in childhood) and the spontaneous recovery that is sometimes witnessed, check for example Ken Lassesen's blog, he is a patient who recovered three times. To give another example, myself and some others on this forum notice big improvements after getting a cold/flu. If the mitochondria are fundamentally not working, I have a hard time understanding the mechanism behind such rapid improvements that many of us have experienced.
Indeed, and the biggest thing to me is the cell serum experiments from Dr Davis, he was able to reverse the "block" by filtering the serum, suggesting something signals cells to reduce energy output. I would really like to know what the identity of that molecule is, it could be a huge piece of this condition.
 

Learner1

Senior Member
Messages
6,305
Location
Pacific Northwest
If the mitochondria are fundamentally not working, I have a hard time understanding the mechanism behind such rapid improvements that many of us have experienced.
Mitochondria have to be working, or we'd be dead. That's not to say that they aren't in top working condition, having complexes that aren't performing optimally, missing key inputs, filled with toxins, or damaged.

Here are a couple of examples. We are all unique individuals with unique environmental factors, and we have billions of mitochondria, so its likely they are in a variety of states. They do have repair mechanisms and they can be recycled, generally every couple of months, so their status can vary with time and external influences.


https://goo.gl/images/x2vWKk
 

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Valentijn

Senior Member
Messages
15,786
That is bit like saying that the mains supply causes your computer to crash. Mitochondria are the powerhouses of everything - the mains supply. So if they are not working you get something called death.
Not really. There are a lot of ways that mitochondria can dysfunction, resulting in different severity.

Even if we just look at genetic causes, mitochondrial mutations can result in death shortly after birth, or good health well into adulthood. And in later-onset cases, death is less likely and takes a lot longer. There are different mitochondrial genes which affect different stages of the electron-transport chain, with some problems at some stages being more severe than mutations at other stages. And within each stage, there are different genes where mutations will have a different impact. And within those genes, different mutations will be more or less severe than others.

Mitochondrial mutations can also be heteroplasmic, meaning only certain tissues will be affected, and those tissues vary from case to case. Obviously some of those will be more deadly than others. Eg, MELAS is bad news because malfunctioning mitochondria in the muscles result in elevated lactate in the CNS which can trigger strokes and seizures. Whereas MIDD results in diabetes and deafness, and while that obviously sucks, it isn't deadly.

Then there are nuclear DNA mutations which are also involved in mitochondrial function. While some mutations would be deadly before or soon after birth, other mutations are known to only start causing problems when under physiological stress, such as hypoxia or infection.

And then there can be non-genetic factors. I'm not particularly clear on what these might be, but mitochondrial specialists seem to be quite sure that they exist.

And we do not yet have any real evidence there is anything wrong with the mitochondria in ME.
I'm less confident of that. There are a lot of patients on the forum with a maternal history of similar symptoms, and many are mothers with similarly sick children. And there are more than I'd expect with a history of extra non-ME symptoms suggestive of mitochondrial disease, such as hemiplegia, seizures, progressive eye problems, progressive hearing problems, trouble swallowing, diabetes, thyroid dysfunction, etc.

I certainly don't think mitochondrial disease is the same thing as ME. But I suspect that many classic mitochondrial disease patients are misdiagnosed with ME. And I'd be quite surprised if there wasn't mitochondrial dysfunction involved in most other patients with PEM.

Also, SNPs known or suspected of causing mitochondrial disease were about 10x more common in ME patients than the general public in a recent study from South Africa and England. And that was with using a testing method which made it extremely unlikely that any heteroplasmic mutations would be detected. Unfortunately the researchers were either very incompetent or determined to get a negative result, so didn't mention the evidence regarding most of those mutations, and retested positive patients with the undeniably pathogenic mutations to make sure they disappeared the 2nd time around.
 
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heapsreal

iherb 10% discount code OPA989,
Messages
10,099
Location
australia (brisbane)
I am not quite following the logic. Could you give me an example of how a doctor would directly treat CFS?

No. Because i dont think anyone can treat cfs directly. One may get lucky and an active infection is treated thats the cause of everything but generally infections are like comorbities or abnormal hormones or anything else found abnormal is secondary to the unknown cause of ones cfs.

So most treatments for cfs are really secondary or downstream issues. Ampligen is one exception as its indicated directly for cfs in Argentina and probably a small number of other countries.
 

pattismith

Senior Member
Messages
3,941
@Learner1 , I would add to your mito-cocktail : Thiamine, CoQ10 and Riboflavine :)
I think most of us would agree that mitochondria are involved, but labeling CFS/ME as a mitochondrial disease is another matter. With CFS/ME there are several things that do not fit well with classic mitochondrial diseases, such as possible sudden onset (rarely in childhood) and the spontaneous recovery that is sometimes witnessed, check for example Ken Lassesen's blog, he is a patient who recovered three times. To give another example, myself and some others on this forum notice big improvements after getting a cold/flu. If the mitochondria are fundamentally not working, I have a hard time understanding the mechanism behind such rapid improvements that many of us have experienced.

You have to make the distinction between primary mitochondrial diseases (genetic mitoD, with either childhood or adult onset) and secondary mitoD (in that case, auto-immunity can be involved, or toxicity, or maybe some other factors I don't think about).

Ken Lassesen's recovery were not spontaneous. The first one was from a long ATBX treatment:

"Onset #1 1972-73
My first bout with chronic fatigue syndrome occurred over 40 years ago. Two more followed several decades later. I have fully recovered from all my bouts with ME/CFS.

Doing triple honors at University, working full time and family stress resulted in a sudden collapse of cognitive ability, tiredness and a persistent cough after a mild flu. This was before CFS or Lyme existed as a condition. The family MD (in his 60′s then) happened to have also treated my parents and grandparents and recognized some characteristics of my grandfather “stress cough”. The official diagnosis was “Antibiotic resistant walking pneumonia” which resulted in different antibiotics in high dosages for several months.

I also changed diet to lose weight, a high protein – no carbohydrates diet (which was effectively a gluten free diet before it was invented!). He advised me that stress is a real contributor and to minimize it. It took almost 4-5 years before cognitive ability returned fully. IMHO (in hindsight), I was lucky — the treatment was likely ideal although the reasons(model) may have been wrong."
 
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pattismith

Senior Member
Messages
3,941
I'm less confident of that. There are a lot of patients on the forum with a maternal history of similar symptoms, and many are mothers with similarly sick children. And there are more than I'd expect with a history of extra non-ME symptoms suggestive of mitochondrial disease, such as hemiplegia, seizures, progressive eye problems, progressive hearing problems, trouble swallowing, diabetes, thyroid dysfunction, etc.

I certainly don't think mitochondrial disease is the same thing as ME. But I suspect that many classic mitochondrial disease patients are misdiagnosed with ME. And I'd be quite surprised if there wasn't mitochondrial dysfunction involved in most other patients with PEM.

Also, SNPs known or suspected of causing mitochondrial disease were about 10x more common in ME patients than the general public in a recent study from South Africa and England. And that was with using a testing method which made it extremely unlikely that any heteroplasmic mutations would be detected. Unfortunately the researchers were either very incompetent or determined to get a negative result, so didn't mention the evidence regarding most of those mutations, and retested positive patients with the undeniably pathogenic mutations to make sure they disappeared the 2nd time around.

I agree with all you wrote Valentijn.

I would add that for Fibro and Autism, about 5% of them are missdiagnosed primary MitoD, so I suspect we are in the same range of missdiagnosed primary MitoD for ME/CFS, maybe more.:)
 

Jonathan Edwards

"Gibberish"
Messages
5,256
Er, not so fast...

https://www.healthrising.org/forums...-work-in-chronic-fatigue-syndrome-me-cfs.390/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4566449/

Many of us benefit from supplements that support mitochondria - carnitine, ALA, d-ribose, magnesium, manganese, copper, methylating nutrients, and NT Factor.

We don't know everything there is to know about mitochondria and CFS, but its pretty clear they're impacted somehow...

These citations are not serious science. We have no reliable evidence for anything wrong with mitochondria in ME. I think we can say that quite clearly. There might turn out to be but my point about being dead was a direct quote from Mike Murphy who is a mitochondrial expert at Cambridge who was invited to talk at an IiME conference a year or two ago. The symptoms of ME do not sound remotely like under performing mitochondria. Murphy was quite clear about that. It is possible that mitochondria harbour signalling molecules involved in generating symptoms but that would be quite separate from an 'energy deficit' which I think is a misconception.

I have looked after many people with failing energy supplies due to a range of illnesses and their condition does not remotely resemble ME.
 
Messages
21
That is bit like saying that the mains supply causes your computer to crash. Mitochondria are the powerhouses of everything - the mains supply. So if they are not working you get something called death.

And we do not yet have any real evidence there is anything wrong with the mitochondria in ME.

I do not believe the mitochondria are the cause of the illness either however it seems to be pretty clear that their functioning is affected by the illness. In mine and many others' experience taking supplements (in particular magnesium) to correct mineral imbalances can result in a significant increase in functioning. Magnesium of course is critical in the production of atp in the mitochondria. I also get a significant boost from taking coq10, b12 etc all which exert effects on the mitochondria.

Sarah Myhill through her mitochondrial function profiling has shown the very low levels of key mitochondrial nutrients in her patients. It has also been shown that there is a methylation block in ME patients, methylation of course being responsible for prodcuing many of those compounds that the mitochondria need to function.

There are countless indviduals and a lot of practioners who have documented their positive experiences in taking/prescribing these supplements in improving functioning. I'm sure many on this thread could attest to this. These are clearly symptomatic improvements, although I would bet that if we are to have a chance at actually healing the root cause of the illness then we will increase our chances of doing so from having our mitochondria functioning as optimally as possible.
 
Messages
21
This is not directed at anyone in particular but is more of a general point and is related to some of the themes spoken about in the thread. I think that merely using the term 'no evidence' to dismiss ideas is a lazy way of arguing against a proposed theory without an explanation as to why logically that idea would not be feasible.

A lot of GPs would go as far as saying that there is no evidence for the existence of ME itself, that doesn't mean it's not happening.

If we were to dismiss any treatment, particularly those that seem to be helping people, on the basis that there hasn't been numerous scientfic studies to confirm exactly what is helping them then we will be waiting around forever. I would be in a much worse position than I am now had I not taken nutraceuticals to help correct my mitochondrial imbalances. Logically it makes sense as to why they would help and the positive experience of others was enough for me to give them a try.

Of course we should aim to be as scientific as possible however I think we need to be aware of the limitations of our understanding of science/medicine. Human beings have probably accumulated less than 1% of the total knowledge about how the human body actually works - so whether there are multiple large/credible scientific studies to prove something or not we are all guessing somewhat and should be not so quick to dismiss patient experience.
 
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A.B.

Senior Member
Messages
3,780
This is not directed at anyone in particular but is more of a general point and is related to some of the themes spoken about in the thread. I think that merely using the term 'no evidence' to dismiss ideas is a lazy way of arguing against a proposed theory without an explanation as to why logically that idea would not be feasible.

As we have learned with the PACE/CBT/GET story, a lot of unreliable evidence doesn't add up to reliable evidence. I don't think anyone is arguing that chronic infection cannot exist but rather that the evidence for it playing a major role in ME/CFS just isn't there.