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

[duncan]

Gary Wormser and Suzanne Vernon are among the authors noted.

Interesting collaboration. Wormser is one of the go-to peeps for hardcore IDSA dogma.

 

[paolo]

Sorry but the silence, in terms of lack of evidence for any association between borrelia and ME, seems to be particularly deafening!

According to Sam Donta, the chronic form of Lyme disease shares many symptoms with Chronic Fatigue Syndrome, and in many cases the two conditions may be clinically indistinguishable. With his own words:

"As there is overlap in symptomatology between patients who are diagnosed as having chronic fatigue syndrome, fibromyalgia, and those who have persisting symptoms with Lyme disease, there is great difficulty clinically in knowing who amongst those with chronic fatigue and fibromyalgia might have persisting Lyme disease." (Donta, S.; Open J Neurology, 2012)

On the other hand we have that some patients with persisten Lyme disese are seronegative:

"We conclude that antibodies to B. burgdorferi often are present in only low levels or are even absent in culture or PCR positive patients who have been suffering for years from symptoms compatible with LB." (Oski, Uksila, Marjamaki et al; J Clinical Microbiology, 1995)

So we have

• a group of patients with persistent Lyme disease (which is called Chronic Lyme Disease by some Authors, as Montoya or Sam Donta and Post Lyme Disease by others as Brian Fallon) that fills in the Criteria for ME/SEID from a clinical point of view, let's call them Group A;
• a sub group of Group A which is seronegative, let's call it Group B.

We can conclude then that people in Group B (seronegative Chronic Lyme Disease) are diagnosed with ME. How many? I don't know. What I know is that I am among them.

The fact that in ME population the incidence of Lyme disease serology is the same than in general population leads me to speculate that those with Lyme who develop the ME clinical picture are mainly seronegative, as I am.

This is the same idea -I guess- that Kenny De Meirleir presented in the following slides, from the debate in Dutch Parliament:

http://nelelijnen.be/images/nele_afbeeldingen/laatste_nieuws/2014/Presentatie_De_Meirleir.ppt

 

[Jonathan Edwards]

Sorry, Dr. Edwards, but when discussing any possible link between Lyme and ME and all the noise associated with both, you opined "...I think we have to assume that some other researchers have looked in to this..."

I cannot say what has been published. But it's common practice in the US at least to take someone who had been diagnosed and treated for Lyme, and who remained symptomatic, but eventually turned sero-negative (or not), and re-brand that individual with ME/CFS.

The thing is, perhaps that old case of Lyme HAS morphed into ME/CFS. Right? Like EBV or an enterovirus, Bb triggered ME/CFS. There is no reason to believe this would be any less a valid occurrence.

Perhaps Lyme lingers but diagnostics fail. The patient tests negative via the CDC's 2T system. It happens. So, Borrelia, in stealth mode, sickens the patient, while clinicians diagnose that individual with ME/CFS, because until SEID has been accepted, it is still primarily a diagnosis of exclusion. Or, maybe, in an ultimate twist, an individual meets the requirements for BOTH diseases - I know at least a few of the members of this forum are a part of that fraternity.

However you approach these possibilities, Borrelia assumes more than just a tad of a correlation, and coincidence does not factor in at all.

Sorry, Duncan, but none of that changes my point. If there was a biological relation between borrelia and ME then at least something ought to turn up on tests. OK the tests may be poor or unreliable but a test that shows absolutely no correlation (across a population I am talking about) does not support any relation. The fact that nobody has published a study showing a correlation, despite having treated patients as if there were some correlation either means that nothing could be found even with twisting the statistics as much as possible and so nothing was published because it would be rather embarrassing, or the people involved were too lazy to even gather the data. If we are to take this forward seriously in scientific terms we need published data. And asking for scientific publication is not asking for anything that an ordinary physician cannot perfectly well do - it just requires careful recording of results that must be there because the patients are having the tests - a decent secretary could do it.

 

[duncan]

Sorry the medical research community has let you down, but that does not change anything I have written. You speak to the lack of publications, while I am telling you this is the real world, and this is what happens between ME/CFS and Lyme communities.

This is the bible written in gutter Greek, and no less authentic. I am puzzled how you cannot know that this is happening every hour of every day.

Very simply: This is the way it is done, and it is done in many, many cases throughout every state in the US, and I suspect throughout much of Europe. You can cite lack of journal ink till you are blue in the face, but I fear your protestations will have little effect on the realities of Lyme and ME/CFS diagnoses, and the dragooned relationship those two diseases share.

 

[voner]

I have access to "Anti-neural antibody response in patients with post-treatment Lyme disease symptoms versus those with myalgic encephalomyelitis/chronic fatigue syndrome". The ME/CFS patients were provided by the Solve ME/CFS Initiative.

here you go: (PTLDS is the acronym for: Post treatment Lyme disease symptoms, or it is commonly known, chronic Lyme disease)

We found a significantly increased level and frequency of IgG anti-neural antibody reactivity in the PTLDS patients (41 of 83; 49.4%) both in comparison to patients who had been treated for Lyme disease previously but did not have residual symptoms (5 of 27; 18.5%) and to healthy controls who never had Lyme disease (3 of 20; 15.0%) (p < 0.01 for both compar- isons). The anti-neural antibody response in the patients with PTLDS was independent of serologic positivity for antibodies to Borrelia burgdorferi (the etiologic agent of Lyme disease).

.......

In contrast to the findings of our prior study on PTLDS patients (Chandra et al., 2010), we found no significant difference in the prevalence of anti-neural antibody reactivity between ME/CFS patients (4 of 51; 7.8%) and healthy controls (7 of 53; 13.2%) (p = 0.5).

.

then at the end of the letter (@Jonathan Edwards), this statement:

Further inquiry into B cell activation mechanisms and autoantibody response may be useful to gaining a better understanding of differences between PTLDS and ME/CFS, and might provide potential markers for the identification of disease subsets.

 

[NK17]

@voner Can you tell us how big was the study? And did they test blood and/or spinal fluid? Which kind of labs/tests did they use?

 

[PDXhausted]

@voner thank you so much for satisfying my curiosity.

Any of the Lyme experts out there know much about anti-neural antibodies? Is this something researchers are trying to use to show like some kind of post-Lyme autoimmune response?

 

[duncan]

Yeah, Wormser and Klempner tried this back about five years ago, i.e. explain PTLDS via a corrupted immune response, i.e. anti-neural antibodies. I'm not quite sure what they were referencing when they discussed neural proteins back then. It's a body's antibody response to these proteins they are trying to suggest may be significant. I think. They seemed to believe the antibody result had nothing to do with Bb, because it was observed it both sero-positive and sero-negative patients. But if you speculate that their sero-negative cases were actually NOT negative....I'd want to see the WB results of those they characterized as sero-negative. If any of them have bands Bb specific, I wouldn't bother any further.

Now this collaboration with Vernon?

I'd approach this very carefully, very guardedly.

 

[PDXhausted]

@duncan hope I didn't step on any toes bringing this up. If anti-neural antibodies is junk science, I only brought it up on sheer ignorance I just happened across the article and hadn't heard of them.

 

[duncan]

Naw! There may be merit to this. I just would want to examine some of the methodology in detail, and have a look at those labs of individuals that were qualified as sero-negative.

God knows I can be too skeptical of some of the things that emerge....No, I cannot say that with a straight face. I cannot be too skeptical of some of these studies.

 

[PDXhausted]

If I'm reading the snippet of results correctly, then it sounds like if you have ME/CFS, they aren't something to be concerned with anyway. Which is really what I was curious about.

 

[duncan]

If you assume the sample provided by Vernon was representative.

 

[voner]

@voner Can you tell us how big was the study? And did they test blood and/or spinal fluid? Which kind of labs/tests did they use?

NK17,

you can PM me and I can supply you with more information or someone can request the paper in the members only " request a paper" thread and I can supply it. The Study patient numbers are in the quotes I supplied. The results for the chronic Lyme patients or from a previous study. here's what they say:

In a previous study published in BBI, we developed a semi- quantitative immunoblot assay to compare antibody reactivity to neural antigens in a group of PTLDS patients and controls (Chandra et al., 2010)

 

[voner]

here's the 2011 paper published on differences in spinal fluid from chronic Lyme patients and ME/CFS.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0017287

 

[SOC]

It appears that some people here need reminding that absence of evidence is not evidence of absence.

The fact that we don't have published evidence of something doesn't mean it doesn't exist. It simply means that one of the following is true: 1) we haven't looked yet, 2) we haven't found it yet, 3) someone has evidence but hasn't published it yet, or 4) it doesn't exist. Lack of published documentation is not a reason to dismiss something out of hand. The best we can say based on a lack of published documentation is that we don't know yet -- the jury is still out. If we don't have published research on a subject we have to, by necessity, fall back on the next level of evidence -- the clinical experience of those working extensively in the field.

 

[NK17]

@SOC couldn't agree more with you!

 

[Valentijn]

The fact that nobody has published a study showing a correlation, despite having treated patients as if there were some correlation either means that nothing could be found even with twisting the statistics as much as possible and so nothing was published because it would be rather embarrassing, or the people involved were too lazy to even gather the data.

A third possibility is that this correlation was clinically observed recently (it was), and that publication is underway. Dr de Meirleir seems to be pretty good about publishing whatever he finds, and very recently gave a presentation which was not put online due to containing material due to be published soon. I wouldn't be surprised if his upcoming publication is exactly about the correlation between ME diagnosis and the presence of Lyme.

It might be worthwhile for someone to go look over the relevant threads to see if there was a bit more detail about what he's working on. But I'm off for a nap now, so it isn't going to be me

 

[msf]

Prof. Edwards, given that even the NHS cite Lyme as one of the illnesses that have to be excluded before a diagnosis of ME can be made, and given that a number of ME physicians (KDM, Lerner, etc) have found significant numbers of Lyme cases in their patients, and that Lyme tests are notoriously insensitive, how confident can you be that the Lyme and the ME populations have been completely seperated out?

The study cited above will have the same drawbacks that I pointed out the Lyme vs ME spinal fluid study must have. This was in the thread about the Lipkin spinal fluid study. Basically, if the authors did a good job of seperating out the two populations, then what their hypothesis is a tautology. If they haven´t, then the significance of their findings can be called into question.

 

[msf]

Damn, separate is one of those ones that always gets me.

 

[msf]

To clarify, I meant if they did a good job of seperating out the two populations before the study. As I pointed out in the other thread, the ME definition that they were using will also have had an effect on the results. That is, if they have found a test that distinguishes between most patients with the Fukuda criteria and some PTLDS patients, then I wouldn´t be that surprised. It would be even less surprising if they first excluded those with any sign of Lyme infection from the Fukuda group, using the most sensitive tests available (Western Blot or LTT).