Interview with Dr. De Meirleir about ME/CFS/SEID and Lyme Oct, 2014

[duncan]

Edwards: "What do polemics and disputes have to do with measuring something in two groups of people under carefully unbiased conditions?"

and

"Polemics and disputes cannot play any part in tests that are validated by labs exchanging blinded samples and showing replicability."

I suspect your question would not have been be asked if you appreciated the contested nature of most TBD diagnostics.

Your declaration I quoted only demonstrates you are unfamiliar with the problems presented by validated Lyme labs.

I am sorry, I am not trying to insult you. I am simply observing that your statements show a complete lack of knowledge of the many challenges presented by Lyme and other TBD diagnostics.

I appreciate you may have a problem with Dr. DeMeirleir's claims. I would kindly suggest reading up on Lyme diagnostics before trying to characterize studies related to them.

 

[Jonathan Edwards]

We might reflect on the fact that a lot of KDMs patients are from Norway and Sweden, which might result in him having more Lyme patients than a ME researcher working in somewhere were there aren't any forests (not sure where that would be, but geography will have an influence on this).

But I thought somebody said there weren't many tics in Norway. It seems fair to assume that Dr De Meirleir is implying that his claim applies to ME in general - otherwise wouldn't he say 'I do not know much about the cause of ME because it seems that I get referred a rather unusual population who actually have Lyme (instead).'

 

[msf]

So lupus begins with an infectious episode? Or is it just it looks like an infectious episode?

 

[Jonathan Edwards]

Edwards: "What do polemics and disputes have to do with measuring something in two groups of people under carefully unbiased conditions?"

and

"Polemics and disputes cannot play any part in tests that are validated by labs exchanging blinded samples and showing replicability."

I suspect your question would not have been be asked if you appreciated the contested nature of most TBD diagnostics.

Your declaration I quoted only demonstrates you are unfamiliar with the problems presented by validated Lyme labs.

I am sorry, I am not trying to insult you. I am simply observing that your statements show a complete lack of knowledge of the many challenges presented by Lyme and other TBD diagnostics.

I appreciate you may have a problem with Dr. DeMeirleir's claims. I would kindly suggest reading up on Lyme diagnostics before trying to characterize studies related to them.

No, Duncan, I am very aware that there are terrible problems about validating Lyme tests but this is non sequitur to the proposal I am making. It cancels out. And so the details are of no interest to me - or to anybody here as far as I can see. Whether or not a test has high or low specificity or sensitivity for some other indicator of Lyme persistence or post Lyme symptoms does not matter. If there is no difference between positivity rates in PWME and controls then we have no reason to think Lyme is relevant to ME. If there is a difference then it might not in fact turn out to be due to Lyme but at least there would be an indication that it was worth further investigation. As long as the tests are replicable we do not need to know what they actually mean. As an example, we used a rheumatoid factor test in RA for years without having any idea what its significance was but because it was different in RA and controls it led us to understand what was going on.

All the politics can be factored out of the experiment. What I find telling is that nobody has taken this simple route to provide new evidence that the tests really do indicate Lyme. If they correlate with ME they are not just random fluctuations in a laboratory. When people do not do the basic control experiments it is usually a sign that there is no solid base.

 

[duncan]

You are wrong. The best you can hope for is to demonstrate exposure between the two groups. That is it.

 

[Jonathan Edwards]

So lupus begins with an infectious episode? Or is it just it looks like an infectious episode?

The clinical history may start with what looks like an infectious episode. (It may not.) When it looks like an infectious episode sometimes there is evidence of infection and sometimes not. Sometimes there are features over and above what you expect from that sort of infection or it is much more severe than in a normal person. Almost any combination of options can occur. Nothing is simple in lupus. My way of looking at it is that most autoimmune diseases involve a cyclical loop. Lupus is more like a Swiss watch with lots of loops, and each patient has a different make of watch with different numbers of hands and features.

 

[Jonathan Edwards]

You are wrong. The best you can hope for is to demonstrate exposure between the two groups. That is it.

But how could one demonstrate exposure if we are not sure if the test reflects exposure or chronic persistence or whatever. I am not even suggesting that we need to claim exposure - we just need some different results on some tests that seem likely to have something to do with Lyme.

 

[msf]

http://www.gmv.gu.se/digitalAssets/...s---concept-note-dec-2011---daniel-slunge.pdf

This study mentions the increase in tick-borne diseases in Scandinavia in the last few decades, as KDM mentioned in the interview. There might still be fewer ticks there than elsewhere (though I doubt it) but other factors will affect this, such as how close people live to nature, etc.

I was referring to the 95% quote, not the quote about Lyme and ME being the same - perhaps he sees ME as being poorly defined, and he feels that as someone who has treated 'ME' patients for over 20 years, he able to say that the 'ME' he is seeing in his patients is mostly actually Lyme.

 

[msf]

Thanks for the explanation. I still find it easier to understand a infection unveiling an existing auto-immune problem than the symptoms of an existing auto-immune problem suddenly manifesting themselves, but I guess that's why we have experts in auto-immunity, if it was simple there would be no need for them!

 

[Undisclosed]

Sorry, Jonathan Edwards, but I need to disagree with you. You are oversimplifying. It is just not that easy. To suggest otherwise seems to me to be ignoring (or unaware) of the profound polemics and disputes at play in diagnostics.

Could you explain why you think J. Edwards is oversimplifying @duncan

 

[duncan]

The reason that you must only speak to exposure is PRECISELY because you cannot distinguish between chronic and acute and late and active etc. You must reduce to the lowest assumption, and that is exposure. Also, you must exclude from your healthy controls any individuals who were ever diagnosed with or treated for Lyme.

 

[duncan]

Kina, he is oversimplifying because he is not factoring in everything. He understands that specificity and sensitivity play a role, but I don't get the sense that Edwards appreciates the rules that are overlayed on top of those two issues further complicate the situation.

Also, there is the enormous gulf in diagnostics that fail to pick up different strains and species.

When you incorporate all these and other considerations, you realize that people like De Meirleir are coming at this from, in part, clinical diagnoses, and also, only in part, labs support - because the labs suck in so many ways.

So crafting a study to verify what is in great measure reduced to clinical dynamics is a dicey proposition.

ETA: Oh, and I doubt very much that politics can be sifted from this process; that holds particularly true in the US and UK. If it were possible to conduct such a study, I suspect it would not get published in a regarded peer-review journal - again, because politics do assume such a large role. The best of intentions are frequent casualties in the Lyme Wars.

 

[duncan]

I don't mean to be vague, and I apologize if I appear too general. There are landmines with just about every recognized Bb metric. When Jonathan Edwards suggests controlled tests that isolate (my wording) or highlight certain markers, the problem is there just aren't any I can think of that are universal, across species, across strains, or across stages.

On top of that, you have forced onto these limitations "rules" that may or may not apply to late stage Bb or chronic Lyme or PTLDS. I believe Professor Edward has his background in immunology, so he can appreciate when mainstream Lyme people say that an IgM positive after say, three months, must be a false positive because the body should have converted to IgG's by then, roughly speaking. I'm not sure how relevant that rule is in a compromised immune sytem - one that is challenged by a varying surface antigen that is constantly reshaping itself to fool the immune system. For some, that arguably is being interpreted, perpetually, as a new infection, therefore only IgM's are being mustered.

There are lots of issues that are presented by the peculiar nature of the spirochete that confound diagnostics.

I will use the C6 Peptide test as an example of how immunological rules are either undefined or hazy, or even virtually undone by Bb. Personally, I like the C6. It is Bb-specific. It has a good record of identifying acute infections. Better still, it purportedly can track the efficacy of treatments: You get sick, they test you with the C6; if it comes up above a 1.09 value, you have a positive Lyme hit. Your clinician treats you with two weeks doxy. As you improve, as the doxy knocks back the infection, your C6 value should actually decline. The doctor can run periodic labs until he sees the C6 level is back below that 1.09 threshold.

Sounds good. But the problem is, once the bacteria disseminates and progresses to late stage, the values for C6 are not going where some experts believe they should, ie, those values frequently tell a story that demonstrates treatment is NOT successful, as they do not decline, and may in fact rise even after treatment.

So what happens? Well, mainstream Lyme promotes the test for acute cases, but often discounts it for late stage.cases.

Doesn't sound quite fair to me.

This is just a single test. There are many.

So, a big problem that emerges is, what markers and associated tests does one embrace that covers all the different obstacles? What marker that holds true for the different stages, for the different species etc? The different co-infections that mimic Lyme?

That's why I suggest the prudent thing that might be done is look for a correlation between Bb exposure and ME/CFS- cuz you may mitigate the active vs post-treatment vs acute vs late stage hurdles.

I know I am leaving out important stuff. But as much as I hate to make excuses, my brain is baked. I just didn't want to leave anyone with the idea I had given a short crappy answer in a dissmissive fit. It really is a complicated multi-level issue.

 

[Jonathan Edwards]

ETA: Oh, and I doubt very much that politics can be sifted from this process; that holds particularly true in the US and UK. If it were possible to conduct such a study, I suspect it would not get published in a regarded peer-review journal - again, because politics do assume such a large role. The best of intentions are frequent casualties in the Lyme Wars.

Just on this point for the moment I do not think we have a problem here. Somebody has already published a negative study of borrelia testing in ME and normals and negative studies are always harder to publish than positive. The journal does not need to be 'regarded' and there are now journals that will publish more or less anything. I never take any interest in the name of the journal, even if the trendsetters like to.

 

[Jonathan Edwards]

That's why I suggest the prudent thing that might be done is look for a correlation between Bb exposure and ME/CFS- cuz you may mitigate the active vs post-treatment vs acute vs late stage hurdles.

In a sense I think I agree with you even more than you do, Duncan, but I think you are raising a hare because you are confusing interpretation of a test in an individual and in a population.

If we do a test in an individual all we can hope to do is interpret it in terms of some specific relation to borrelia (exposure, persistent carriage, persistent damage or whatever) for that individual. To do that the test has to be vlidated against a gold standard such as proof of exposure, or proof of persistent live organism by culture, or inoculation into guinea pigs or histopathology or whatever, none of which seem to be straightforward. So I agree that the best one can hope for in an individual is get some evidence for at least exposure. But there may still be false positives and we cannot bring to bear statistics on probabilities because you cannot do that on one case.

For a population the question is quite different so the evidence needed is quite different. The question is 'is the population we call ME consistent with being just a sample of normal people, on standard statistical analysis of probability, in terms of any biological relation to borrelia you like, as evidenced by as many tests as one thinks is replicable. To deal with Bonferoni it might be good to do an initial screen and then do a confirmation cohort if p values come up <0.05. For this question there is no need to be specific about what each test might mean - all that is being tested is whether or not PWME, as a population appear to be 'just normal people in terms of borrelia tests'.

And as I indicated before we might not even need to require that the tests indicated a relation to borrelia. Just showing that PWME are not just normal in terms of any test would be a major breakthrough if it proved replicable. Lupus patients were found to have positive tests for syphilis and nobody knew what it meant but it proved a useful tool for delineating lupus, especially when it was shown that it was due to anti-phospholipid antibodies.

So I really do not think we should mind what tests people like De Meirleir compare in PWME and controls. It would just be nice to have one test reported as different in an ME population. A positive test in an individual cannot be used to argue causal role without all the back up we do not have. A different rate of positivity in a population can be used to indicate a causal relation because we can bring in probabilities. What we could not do at first is indicate whether the causal relation was direct, indirect or 'bystander' as in linkage disequilibrium for genes but it would still indicate that there was a causal story for ME that we had a foothold on.

The fact that Dr De Meirleir is using clinical aspects for individual cases is probably a relection of the problems of using the tests for individuals, as you say, but it does not impact on the population question. So there is no reason not to report the positivity rate for his tests in an ME population with matched controls.

 

[duncan]

Maybe. I am trying to understand what you have written. This reflects on me, and only me.

Relative to that negative ME/Borrelia study - I'll wager it didn't have a cohort drawn from any Lyme endemic area, unless it was an exceptionally small sample. Regardless, I'd want to know who the authors were, who they were affiliated with, and who they were looking at relative to how they defined positive/negative signs of Borrelia in PWME. By the sheer virtue they found no Bb in ME patients, I am inclined to be highly skeptical.

By the way, I agree it should not matter what test De Meirleir uses, although I would tend to think it should be some Lyme test. The problem isn't necessarily with the accuracy either. It's he will likely get sliced and diced by the individuals who think of themselves as Stewards of Lyme .

 

[MeSci]

Certainly, I have explained this a number of times on PR and for those who know that please ignore this repeat, but not everyone reads every thread and people come and go.

Here is a detailed post in which Jonathan explains a possible link between infection and autoimmunity/ME.

My ME brain has trouble grasping it, but I think it goes:

• Infection raises gamma-interferon levels (and higher levels are indeed seen in the first 3 years according to the Hornig/Lipin cytokine study)
• This gamma-interferon primes something - I didn't quite get that - but in some way it increases the binding of (non-specific?) antibodies to CD64 on microglial cells in the brain.
• Then I can't remember how this could lead to the production of autoantibodies...

I wish I could get this straight in my head, as it interests me a lot.

 

[abporter]

Anyway Yolanda is doing Ozone Therapy now... Wonder how that will turn out, that's one of the few alternative therapies I actually think it's legit.

@Folk, I've been reading some positive things about ozone. Could you tell the source where you heard Yolanda is doing it now? Curious, thanks.

 

[Folk]

@Folk, I've been reading some positive things about ozone. Could you tell the source where you heard Yolanda is doing it now? Curious, thanks.

I don't really remember where I saw it but if you google it you find i bet. Also check her instagram, she keeps updating daily every step she takes heheh if you can't fins it Isearch for you when I get home cause now I'm on the cel and traveling

 

[frederic83]

Does anyone know how Dr Kenny De Meirleir treats his patient with Epstein-Barr (EBV)?

Thanks...