Lipkin and Hornig ME/CFS Monster Study: Microbes, Immunity & Complex Data

[Sasha]

P.S. I'm pretty sure that <3 is the international symbol for "Hercule Poirot is taking a nap."

 

[barbc56]

Just my opinion folks, so don't get mad...

At this point in time, if I had to choose the research team I thought was most likely to actually crack ME/CFS, it would be Lipkin, Hornig and the CII.

Yes! As far as I'm concerned, KDM, Mikovitz, et. al. don't even come close to Lipkin, Hornage, Davis, etc. as far as credibility as researchers.

I'm not trivializing Lyme and it's impact but it is NOT me/cfs unless a co morbid condition and I think that's pretty rare. The conflating of the two is a step backwards and there's no credible evidence they are the same.

I guess if others want to study lyme, thats fine. But take off the blinders that every symptom means lyme. THATS, trivializing to the patients who truely do have it and only distracts from research that gets closer to understanding me/cfs.

The same symptoms do not necessarily mean the same disease.

I think this sounds like very exciting research and have also just donated!

 

[duncan]

I'm not trivializing Lyme and it's impact but it is NOT me/cfs unless a co morbid condition and I think that's pretty rare. The conflating of the two is a step backwards and there's no credible evidence they are the same.

Apparently there will be no new research one way or the other emerging from this research crop come harvesting time.

Regardless, I think most here agree that Lipkin is putting together good research. That is not the issue.

The issue is, for some, the glaring omissions. They are hard to explain away, except for $'s, and cost is a very real consideration. Still, NO targeted evaluations at the role of prominent TBD's when you have prominent ME/CFS clinicians like Bell and KDM asserting their role? Aren't they worth at least, say, a token Western Blot to check for prior exposure? It doesn't even have to be 2T compliant - just a specific band or two...?

I feel like that little Dicken's waif asking for a bit more porridge, "Please, Sir..."

@barbc56 , you are right, of course, that not everything boils down to Lyme. You know I differentiate between ME/CFS and Lyme. We agree here. I just cannot get my brain around why he would decide not to take a look at TBD's given A) the similariities in presentations, B) the leading clinicians who think there is a tie, C) the extensive media coverage being generated about Lyme & Company recently, and D) the almost daily recalibrating of tick topography.

It seems to me this would have had to have been deliberate. It would be great if I could ask him. I suppose I can dredge up his email address somewhere; maybe I will.

 

[Cheesus]

I had to google "<3" and find it's supposed to be a heart. I always thought it was a bare bottom wearing a dunce's hat, and wondered why you were applying it to this study, so that's a relief!

Or perhaps a pair of testicles pitching a tent.

 

[JES]

The Dr Ian Lipkin group found in their study, inflammation in CFS halts after 3 years, a bizarre finding when other ME researchers generally find the opposite finding, to the extent patients themselves can now order Cytokine panels and look aghast that they are living on a day to day basis in a 'Cytokine Storm'' worsened by stress (such as exercise) - as Dr Nancy Klimas demonstrated years ago. Initially when I read that Dr Lipkin/Dr Horning paper I thought was a hatchet job, until I realized it was the isolated truth.

How? Because their CFS patients didn't have high cytokines after 3 years. How is this possible? Study design.
The rules were that ME sufferers (called CFS in America) who displayed signs of ANY existing organic disease are excluded from the study (a common phenomena of all Fukuda CFS criteria studies). So if you have Fatigue? You're in, if you display signs of chronic ME (such as developing POTS, Autoimmune Thyroid disease, Cancer, Infections that cause Fatigue ontop of your ME? - You're out of the study, and that is how no inflammation is found after 3 years.

It's very plausible to me why patients don't have high cytokine levels after three years, and it's explained by the authors:

Lead author Dr Mady Hornig said this was down to the way viral infections could disrupt the immune system.

"It appears that ME/CFS patients are flush with cytokines until around the three-year mark, at which point the immune system shows evidence of exhaustion and cytokine levels drop."

If anything, this finding proves that ME is a physical disorder and that there are distinct stages in ME. It also tells us that after the three year mark, any kind of recovery might be much harder, as your immune system has partly shut itself down by then.

Apparently there will be no new research one way or the other emerging from this research crop come harvesting time.

Regardless, I think most here agree that Lipkin is putting together good research. That is not the issue.

The issue is, for some, the glaring omissions. They are hard to explain away, except for $'s, and cost is a very real consideration. Still, NO targeted evaluations at the role of prominent TBD's when you have prominent ME/CFS clinicians like Bell and KDM asserting their role? Aren't they worth at least, say, a token Western Blot to check for prior exposure? It doesn't even have to be 2T compliant - just a specific band or two...?

Some definitions of ME and some ME researchers apparently consider ME to be specifically a disease onset by a viral trigger. For example, there are mycoplasma outbreaks in my country, which can cause chronic fatigue and long-term illness in some people, but these would not be classified as ME here. So it could be a matter of how they define the illness.

 

[Cheesus]

Apparently there will be no new research one way or the other emerging from this research crop come harvesting time.

Regardless, I think most here agree that Lipkin is putting together good research. That is not the issue.

The issue is, for some, the glaring omissions. They are hard to explain away, except for $'s, and cost is a very real consideration. Still, NO targeted evaluations at the role of prominent TBD's when you have prominent ME/CFS clinicians like Bell and KDM asserting their role? Aren't they worth at least, say, a token Western Blot to check for prior exposure? It doesn't even have to be 2T compliant - just a specific band or two...?

I feel like that little Dicken's waif asking for a bit more porridge, "Please, Sir..."

@barbc56 , you are right, of course, that not everything boils down to Lyme. You know I differentiate between ME/CFS and Lyme. We agree here. I just cannot get my brain around why he would decide not to take a look at TBD's given A) the similariities in presentations, B) the leading clinicians who think there is a tie, C) the extensive media coverage being generated about Lyme & Company recently, and D) the almost daily recalibrating of tick topography.

It seems to me this would have had to have been deliberate. It would be great if I could ask him. I suppose I can dredge up his email address somewhere; maybe I will.

We have no reason to believe it is a tick borne disease, particularly as many patients have a definitive viral onset. If patients routinely reported being bitten prior to falling ill I would sing a different tune, but as it stands we should search in the area that the etiological clues suggest will likely produce answers.

Having an overlap in non-specific, multi-system and highly heterogenous symptoms does not appear to me to be particularly good evidence that Lyme disease and CFS/ME share an aetiology, and is certainly insufficient to warrant investigation given how much it costs.

 

[msf]

Yes! As far as I'm concerned, KDM, Mikovitz, et. al. don't even come close to Lipkin, Hornage, Davis, etc. as far as credibility as researchers.

I'm not trivializing Lyme and it's impact but it is NOT me/cfs unless a co morbid condition and I think that's pretty rare. The conflating of the two is a step backwards and there's no credible evidence they are the same.

I guess if others want to study lyme, thats fine. But take off the blinders that every symptom means lyme. THATS, trivializing to the patients who truely do have it and only distracts from research that gets closer to understanding me/cfs.

The same symptoms do not necessarily mean the same disease.

I think this sounds like very exciting research and have also just donated!

Heehee, Hornage lost a lot of credibility when she changed her name.

So you know that ME is not Lyme. Does that mean you know for certain what ME is, or do you just know what it isn´t? And how do you know that? Perhaps you could pass your insights along to Dr. Knox, who is part of the Stanford research group and is investigating TBIs in ME.

 

[duncan]

Got a good handle on ME/CFS aetiology, @Cheesus? As for "definitive", the word has little credibility when it comes to both Lyme and ME/CFS.

So, yeah, the issue as to why Lyme and other TBD's were not included remains, well, an issue, at least for me.

@JES, yes, how one defines ME/CFS would matter. But as the definition has yet to be nailed down, not to mention the etiology, doesn't it strike you as a little presumptive or premature to exclude an entire category of pathogens?

 

[msf]

We have no reason to believe it is a tick borne disease, particularly as many patients have a definitive viral onset. If patients routinely reported being bitten prior to falling ill I would sing a different tune, but as it stands we should search in the area that the etiological clues suggest will likely produce answers.
Having an overlap in non-specific, multi-system and highly heterogenous symptoms does not appear to me to be particularly good evidence that Lyme disease and CFS/ME share an aetiology, and is certainly insufficient to warrant investigation given how much it costs.

Definitive viral onset...hmm, how is that proven exactly?

Your second point is a tautology. If people know they have been bitte by a tick, they will suspect Lyme Disease, and have this investigated. If they fail to get better with antibiotics they will be diagnosed with PLDS by IDSA doctors, and with Chronic Lyme by ILADS doctors, rather than with ME.

Re: your third point, see my post above - Stanford don´t seem to agree with you!
I do not want to make this debate just about Lyme though. I am disappointed that they do not seem to be testing for things like Yersinia, which triggered my illness, and for which a small proportion of people on this forum are IgA positive. I am not sure this and other enteric pathogens will be detected by the Microbiome study, and things like Chlamydia definitely won´t be.

 

[Cheesus]

Got a good handle on ME/CFS aetiology, @Cheesus?

To the extent that I know a large bulk of people develop ME/CFS following a viral illness.

 

[msf]

You don´t know that. You know a lot of people believe that, or have been told that by doctors. A small proportion will have some proof of an active virus at the time they fell ill, but then a small proportion have proof of an active bacteria when they fell ill, so why not study both?

 

[Cheesus]

You don´t know that. You know a lot of people say that, or have been told that by doctors. A small proportion will have some proof of an active virus at the time they fell ill, but then a small proportion have proof of a active bacteria when they fell ill, so why not study both?

Because no one reports being bitten at the point of becoming ill with ME/CFS. If they reported both, I would suggest both. As they report only one, I suggest only one (given the expense and limited resources).

 

[duncan]

Can anyone imagine the shitstorm if Lipkin or Davis demonstrate that a quarter or a third or half or more of their respective cohorts have evidence of at least prior exposure to a Borrelia? Who would want to deal with the potential implications? It would be a political nightmare dealing with the Lyme establishment.

Needless to say, that isn't likely to happen with the study at hand.

 

[A.B.]

Stop before this degenerates into another Lyme discussion.

 

[msf]

Because no one reports being bitten at the point of becoming ill with ME/CFS. If they reported both, I would suggest both. As they report only one, I suggest only one (given the expense and limited resources).

See my post above and the definition of tautology.

 

[msf]

I won´t mention Lyme again (apart from then), but I am still disappointed by the Hornig´s constant use of ´viruses´ instead of ´pathogens´ and I feel that the design of this study is a result of that perhaps unconscious bias.

I guess ´the virus hunter´ has more of a ring to it than ´the pathogen hunter.´

 

[Forbin]

Are we certain that tick borne bacteria in the blood will not be included in the study?

The study intends to test the hypothesis that ME/CFS cases and controls have different bacterial, fungal or viral microflora in the oropharynx (mouth and throat regions), lower gastrointestinal tract (gut) and blood in a massive, well-powered study. http://microbediscovery.org/2016/08/05/ciis-mecfs-monster-study-microbes-immunity-complex-data/

 

[msf]

Well, shut my face. I guess I shouldn´t read summaries of something and then reply to them. I really hope the above quote is accurate.

 

[duncan]

Stop before this degenerates into another Lyme discussion.

Or ascends, depending on one's perspective...

 

[msf]

Immunology
To identify biomarkers for diagnosis, prognosis, as well as potential therapeutic targets, and to determine the history of exposure to infectious agents that may trigger onset or exacerbation of ME/CFS.

I guess this might include antibody testing for different bacteria.

So, Cheesus and Barb56, what will you say if they are testing for bacteria, including the one from Connecticut?