NIH post-infectious CFS study

[Comet]

Because they're asymptomatic but may have similar/identical history of an immune onslaught as ME patients.

This makes a lot of sense to me. Any thoughts on the FMD control group?

 

[Scarecrow]

Actually, I'm pretty sure that it was clear that the controls did have to have an earlier active Lyme infection that had resolved.

Active infection, yes. Active disease, not necessarily (according to the now removed inclusion criteria).

Antibiotics are the standard treatment for Lyme. I don't know the stats relating to how many patients recover from Lyme naturally vs with treatment, but I had assumed that anyone presenting to their doctor with Lyme would automatically be treated? So I assume it's just a case of it being the standard treatment for anyone presenting with Lyme.

So you get a course of antibiotics because you were either sero positive or because you had an EM rash. The antibiotics eradicate the infection without ever developing a fever or any other symptom. How do you tell the difference between someone who would have ultimately been symptomatic and those who were never destined to develop the disease?

 

[Bob]

Active infection, yes. Active disease, not necessarily (according to the now removed inclusion criteria).

The patients have to have previously tested positive for infection. You might be right about them not having to have had any symptoms, but then it's unlikely they would have sought treatment.

So you get a course of antibiotics because you were either sero positive or because you had an EM rash. The antibiotics eradicate the infection without ever developing a fever or any other symptom. How do you tell the difference between someone who would have ultimately been symptomatic and those who were never destined to develop the disease?

I don't think it's important. The point is that the patients were subjected to a similar immune onslaught as ME patients but no longer have symptoms. We want to know why ME patients have symptoms i.e. we're looking at the immunological differences between ME patients and ex-Lyme patients. Why do ME patients have symptoms but ex-Lyme patients don't have symptoms?

 

[Cheshire]

The patients have to have previously tested positive for infection. You might be right about them not having to have had any symptoms, but then it's unlikely they would have sought treatment.


I don't think it's important. The point is that the patients were subjected to a similar immune onslaught as ME patients but no longer have symptoms. We want to know why ME patients have symptoms i.e. we're looking at the immunological differences between ME patients and ex-Lyme patients. Why do ME patients have symptoms but ex-Lyme patients don't have symptoms.

Why don't they take people with a documented glandular fever who recovered? GF is known for being a trigger for MECFS, whereas I don't know of any link made in the scientific literature between ME and Lyme (which doesn't mean there is none).

 

[viggster]

But when the psychobabbler is a lead investigator (Dr. Brian Walitt), the damage done can be tremendous. I've seen it in his prior studies in Fibromyalgia, post-chemo fatigue, etc, as discussed in the Details on NIH Study thread.

Wallitt is not the lead investigator. Nath is in charge, and his hypothesis is that ME is a post-infectious neuroimmune illness. The study design is as far as you can get from trying to show ME is psychosomatic. It's the anti-Pace trial.

Patients will be referred to NIH by the expert clinicians. Unger and Lipkin will have a role in patient selection as well.

I'm guessing that anybody at NIH who had previously worked in "CFS" was invited to participate. That does not mean the study is useless or that the hidden agenda is to show it is psychosomatic. Patients are getting a million dollars worth of deep biological testing - that would not be happening if this was a "CFS is psychosomatic and we're trying to fool everyone" study.

 

[Bob]

Why don't they take people with a documented glandular fever who recovered? GF is known for being a trigger for MECFS, whereas I don't know of any link made in the scientific literature between ME and Lyme (which doesn't mean there is none).

Good idea, Cheshire! I'd go along with that. What do other folk think? Perhaps that's a suggestion we could make in any letters we send them?

 

[Denise]

I'm guessing that anybody at NIH who had previously worked in "CFS" was invited to participate.

I am not sure what you mean by this.
Occupy CFS has this to say about
Leorey Saligan who presented at the P2P meeting last year
"Dr. Leorey Saligan received $117,707 for his NIH intramural project on cytokines and physical or emotional correlates of fatigue in ME/CFS and other diseases."

 

[Valentijn]

Wallitt is not the lead investigator.

I said he's "a" lead investigator, not "the" lead investigator. The slide from the NIH presentation has him labeled as "Lead Clinical Investigator".

 

[searcher]

Leorey Saligan is one of the investigators on the study.

 

[Scarecrow]

I don't think it's important. The point is that the patients were subjected to a similar immune onslaught as ME patients but no longer have symptoms. We want to know why ME patients have symptoms i.e. we're looking at the immunological differences between ME patients and ex-Lyme patients. Why do ME patients have symptoms but ex-Lyme patients don't have symptoms?

Because the ex-Lyme patients were treated with antibiotics and if they still have symptoms after that, they are excluded from this study.

 

[Scarecrow]

Good idea, Cheshire! I'd go along with that. What do other folk think? Perhaps that's a suggestion we could make in any letters we send them?

I think that's why we are so perplexed about the Lyme group. Glandular fever is the obvious choice, so what are the NIH thinking of?

I don't think we need to make the suggestion. The NIH have surely considered it and ditched it in favour of Lyme. Why?

 

[ukxmrv]

I think that's why we are so perplexed about the Lyme group. Glandular fever is the obvious choice, so what are the NIH thinking of?

I don't think we need to make the suggestion. The NIH have surely considered it and ditched it in favour of Lyme. Why?

Not necessarily. If one of the lead investigators has as one his area of study Lyme disease and has a free rein (he thinks) to design a study why not throw in the areas he actually wants to study.

 

[Bob]

Because the ex-Lyme patients were treated with antibiotics and if they still have symptoms after that, they are excluded from this study.

But as far as we know, some of the ex-Lyme patients had potential to develop an ME-like illness if they were left untreated for a period of time. Its impossible to find a cohort who had 100% potential to develop an ME-like illness, but didn't. I can't think of one anyway. So this seems like the next best thing. And, of course, mononucleosis (glandular fever) patients.

 

[Bob]

BTW, glandular fever is what we call mono (infectious mononucleosis) in the UK.

 

[Valentijn]

But as far as we know, some of the ex-Lyme patients had potential to develop an ME-like illness if they were left untreated for a period of time.

Sure, it's in the realm of possibility. But there has never been a study showing that Lyme infection ever results in ME. It seems like an inappropriate time for investigators to be jumping to conclusions in that regard.

EBV has been shown to trigger ME in some, but people who recover from that are basically a "healthy controls" group anyhow, since pretty much everyone has had it. People completely recovered from Q-fever and ross-river virus might be sensible controls if the purpose truly was to compare those who go chronic and those who don't.

 

[Sasha]

Wallitt is not the lead investigator. Nath is in charge, and his hypothesis is that ME is a post-infectious neuroimmune illness. The study design is as far as you can get from trying to show ME is psychosomatic. It's the anti-Pace trial.

Patients will be referred to NIH by the expert clinicians. Unger and Lipkin will have a role in patient selection as well.

I'm guessing that anybody at NIH who had previously worked in "CFS" was invited to participate. That does not mean the study is useless or that the hidden agenda is to show it is psychosomatic. Patients are getting a million dollars worth of deep biological testing - that would not be happening if this was a "CFS is psychosomatic and we're trying to fool everyone" study.

I don't see the study as designed, in some "evil plot" way to show that ME is psychosomatic but my concern is that it's going to do that by accident.

The investigators appear convinced that FMD is a psychosomatic disorder, and my/our worry is that this is according to the same logic that psychiatrists have used to put all sorts of diseases in that category, including ours - namely, that they couldn't find objective findings. That doesn't mean that there aren't any to find.

So, suppose FMD is in fact an organic neurological disorder and that when it gets the same tests that the ME group get, similar things show up? Do we risk being classed as a psychosomatic disorder because we have similarities to the FMD group? That's the big worry.

I simply cannot understand why there's a "psychosomatic" control condition. Even if one could be definitive that FMD is psychosomatic (and in principle, I don't see how that's possible), what's the logic? What exactly is being controlled for? The belief that one is ill? If so, why doesn't every disease have such a control condition?

We need an explanation of this from Dr Nath.

Brian, I understand your frustration at people thinking that this is a study designed with ill intent but I think we need to be vigilant that it doesn't do bad things as a result of conceptual screw-ups.

 

[Sasha]

I think that's why we are so perplexed about the Lyme group. Glandular fever is the obvious choice, so what are the NIH thinking of?

I don't think we need to make the suggestion. The NIH have surely considered it and ditched it in favour of Lyme. Why?

I think it's a reasonable question to put to Dr Nath. We shouldn't be left guessing. We need to open up a line of communication.

 

[ukxmrv]

Was is the difference between comparing the FMD group to CFS and the research already done comparing depression and CFS?

 

[Scarecrow]

I think it's a reasonable question to put to Dr Nath. We shouldn't be left guessing. We need to open up a line of communication.

Question, yes, absolutely. What I meant was that we didn't need to suggest it because the NIH must have considered it.

 

[viggster]

There's no way this study will "accidentally" show that ME is psychosomatic. In regards to comparing ME with FMD: FMD patients do not have POTS, PEM, cognitive problems, or severe immune dysfunction. Also, FMD responds dramatically to placebo - ME does not. So I'm not buying into the worries being expressed here. Further clarification on why both control groups were chosen would be good...we're still working out channels of communication and the best way to move info back and forth.