CDC Patient Outreach Call starts in 30 min

[Ember]

I was kind of asking a question above. This is a bit of an assumption on my part, which could be unwarranted. Came from a small comment that lumping as well as splitting was valuable, (lumping to find commonalities which might exist across the "broad group" of this disease, splitting to find the differences)

Your assumption makes sense though. The terms “lumpers” and “splitters” have been used for a long time in connection with our illness. “Splitters” refers to the likes of the ICC and CCC authors, who claim that there is a separate neurological disease embedded within the CFS cohorts. “Lumpers” includes the Reeves definition and NICE Guidelines authors, who claim that it's all one illness entity with differences mainly in severity.

Dr. Unger has been loathe to acknowledge the position of the splitters, a position that might be bolstered by the test-retest protocol. She's been keen on using instruments that differentiate only in terms of severity.

If we jump to the wrong conclusions here, Dr. Unger has only herself to blame. It's hard to imagine that nobody taped the call. What would be the reason for such an oversight?

 

[Dolphin]

For those on Facebook, Kati did a short report: https://www.facebook.com/permalink.php?story_fbid=10150985829403251&id=216740433250

 

[peggy-sue]

sorry, I posted in the wrong thread!

 

[Dolphin]

For those on Facebook, Kati did a short report: [URL='https://www.facebook.com/permalink.php?story_fbid=10150985829403251&id=216740433250[/quote]It's']https://www.facebook.com/permalink.php?story_fbid=10150985829403251&id=216740433250[/URL]

It's also available now away from Facebook: https://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind1208b&L=co-cure&F=&S=&P=7588

 

[Ember]

From Patient transcript of CDC CFS Patient-centered outreach and communication activity conference call:

Today on August 9th 2012 the CDC chief of the CFS program, Dr Unger made history by reaching out to patients and organizing the first conference call aimed at informing patients about their research program.

How differently we frame things! I think of Dr. Unger's recent conference call as an exercise in public relations. Dr. Unger believes that Dr. Reeves expressed his opinions with too little tact, and she doesn't want to make the same mistake.

If anyone should be in a position to know the challenges faced by this patient population though, you'd think that person would be Dr. Unger. She must have been aware of the patient response to the lack of live video feed at the November CFSAC meeting. Yet her omissions were far more egregious.

The CFSAC organizers wouldn't risk photocopying the ME/CFS Primer twice so that committee members could be prepared for their June meeting. Dr. Unger has surely outdone them. Sometimes, as Marshall McLuhan said, “The medium is the message.”

 

[richvank]

Hi, all.

With regard to lumping and splitting, I would like to express the view that there is a place for both in research on ME/CFS.

The reason, in my opinion, is that there are differing etiologies in the ME/CFS population, but they have the same core pathophysiology. This feature is what has made it so difficult to understand ME/CFS, in my opinion.

In other words, there are several types of stressors that can bring the onset of ME/CFS, especially in those who are genetically predisposed. These include physical, chemical. biological and emotional/psychological stressors. In many cases, it is a combination of more than one stressor that leads to the onset. This is an area where "splitting" is relevant, especially where it can identify infections or toxins that may need to be specifically treated, and that differ from one case to another.

All of these stressors place a demand on glutathione. If it goes low enough, this leads to a functional B12 deficiency, a partial block in the methylation cycle, and folate loss from the cells, forming a vicious circle mechanism that makes this disorder chronic. I suggest that everyone with ME/CFS has this core vicious circle mechanism going on. This is where "lumping" is relevant. All PWCs/PWMEs can benefit from methylation treatment to break this vicious circle.

So I believe that a combination of approaches makes sense for ME/CFS,and that continuing to argue for one or the other is counterproductive.

Best regards,

Rich

 

[WillowJ]

hi, Rich,

I agree with you in general terms.

But I don't believe that the Georgia cohort (or a typical Oxford group, either) has much to tell us about any condition, because the grouping is illogical. People with CF/ICF/NSF/Reeves Disease should be re-diagnosed with (and treated for!) the various other conditions that they would have. I believe they probably are mostly diagnosable. The only way I could see that approach useful is if someone could come up with enough money to do vast enough studies to be studying illness in general and still pick out various different diseases (including relatively less prevalent ones within the set) with sophisticated analyses.

best,
Willow

 

[Ember]

This is an area where "splitting" is relevant, especially where it can identify infections or toxins that may need to be specifically treated, and that differ from one case to another....
I suggest that everyone with ME/CFS has this core vicious circle mechanism going on. This is where "lumping" is relevant..

I wonder too what definition you're using when you describe “everyone with ME/CFS,” Rich. In their case definitions, the authors of the ICC and CCC, those who would be identified as “splitters,” focus on symptom clusters, along with their presumed underlying pathophysiology. Does that then make them “lumpers” to you?

 

[richvank]

Hi, Ember.

I would suggest that everyone who has post-exertional malaise/fatigue and who shows a partial methylation cycle block on the methylation pathways panel has ME/CFS or whatever the actual physiological disorder is going to be called, as distinguished from clinical depression or other psychiatric conditions. Might have to throw in some other common symptoms as well, but that's how I would define it.

I don't think it's possible to come up with meaningful subsets by looking only at symptom clusters, without a hypothesis covering the etiologies, pathogenesis, and pathophysiology. People have been trying to do that for a long time, going back at least to the 2004 conference in Madison, where I argued against it. I believe that to make progress, you have to do hypothesis-driven research. Just looking at symptoms without having a working hypothesis has not led to much progress in understanding subsets, in my opinion, because there's no real basis for defining the subsets.

Many of the people who have been doing ME/CFS research are M.D.'s M.D. training does not really equip people to do hypothesis-driven research, although a few have been able to do it without formal training. Mostly they have collected some clinical data and have reported it, without attempting to say how it fits into the bigger picture. Also, they mostly stay within their particular specialty box and cannot be coaxed out of it. I know, because I have tried! In the physical sciences, a trained researcher is expected to try to make the connection between his or her work and the bigger scientific picture, regardless of boundaries between disciplines.

I'm not going to label people as lumpers or splitters. They will have to decide that for themselves.

Best regards,

Rich

 

[Ember]

I would suggest that everyone who has post-exertional malaise/fatigue and who shows a partial methylation cycle block on the methylation pathways panel has ME/CFS or whatever the actual physiological disorder is going to be called, as distinguished from clinical depression or other psychiatric conditions. Might have to throw in some other common symptoms as well, but that's how I would define it.

Thanks, Rich. PENE (or PEM), along with its complex manifestation of symptom clusters, does seem to be at the heart of an ME definition. It distinguishes ME from other forms of CFS, as well as from depression. Both the ICC and the CCC represent hypothesis-driven ways of defining a subset:

Why was this maneuver of the Canadian criteria so effective in separating out this subgroup? By recognizing that fatigue showing the specific dynamical patterns of ME characterized a large subset of fatigued patients, and thus was different in kind from the patterns underlying the majority of severe, chronic and unexplained fatigues (CFS). It thus pointed to a different underlying causality- a natural kind or real pattern...(http://investinme.org/Documents/Journals/Journal of IiME Vol 6 Issue 1 Screen.pdf)

The rationale of the ICC document advances the successful strategy of the Canadian Consensus Criteria of not viewing symptoms isolated in a nominal list, but rather as coordinated patterns of symptoms that directly reflect the regulatory interactions of the underlying systems involved. If the same symptoms consistently flare in response to exertion, they are more likely to share a common cause (http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.2011.02499.x/full).

The ICC also suggests further subgroups within the diagnosis of ME:

Classifying patients by subgroups to enable the comparison of patients within the diagnosis of ME may be helpful in some studies.

1 Onset: acute infectious or gradual.
2 Onset severity may be a good predictor of severity in the chronic phase.
3 Symptom severity: mild, moderate, severe, very severe.
4 Criterial subgroups: neurological, immune, energy metabolism/transport or eclectic.

Wouldn't you consider the international panels of experts involved in these definitions to include medical doctors working in the name of hypothesis-driven research?

 

[justinreilly]

Hi, Ember.

I would suggest that everyone who has post-exertional malaise/fatigue and who shows a partial methylation cycle block on the methylation pathways panel has ME/CFS or whatever the actual physiological disorder is going to be called, as distinguished from clinical depression or other psychiatric conditions. Might have to throw in some other common symptoms as well, but that's how I would define it.

I don't think it's possible to come up with meaningful subsets by looking only at symptom clusters, without a hypothesis covering the etiologies, pathogenesis, and pathophysiology. People have been trying to do that for a long time, going back at least to the 2004 conference in Madison, where I argued against it. I believe that to make progress, you have to do hypothesis-driven research. Just looking at symptoms without having a working hypothesis has not led to much progress in understanding subsets, in my opinion, because there's no real basis for defining the subsets.

Many of the people who have been doing ME/CFS research are M.D.'s M.D. training does not really equip people to do hypothesis-driven research, although a few have been able to do it without formal training. Mostly they have collected some clinical data and have reported it, without attempting to say how it fits into the bigger picture. Also, they mostly stay within their particular specialty box and cannot be coaxed out of it. I know, because I have tried! In the physical sciences, a trained researcher is expected to try to make the connection between his or her work and the bigger scientific picture, regardless of boundaries between disciplines.

I'm not going to label people as lumpers or splitters. They will have to decide that for themselves.

Best regards,

Rich

I really like this post. It seems like a great insight to me. This sort of thing helps me contextualize all the mess of info that we are exposed to when we try to learn about the disease and all the messy sausage-making of the science and politics. Do you have a blog? If not, pls start one! : )

 

[richvank]

Thanks, Rich. PENE (or PEM), along with its complex manifestation of symptom clusters, does seem to be at the heart of an ME definition. It distinguishes ME from other forms of CFS, as well as from depression. Both the ICC and the CCC represent hypothesis-driven ways of defining a subset:

The ICC also suggests further subgroups within the diagnosis of ME:

Wouldn't you consider the international panels of experts involved in these definitions to include medical doctors working in the name of hypothesis-driven research?

Hi, Ember.

I would say that they are trying. My criteria for hypotheses may be different from that of most biomedical researchers. Their hypotheses tend to be one-liners, and granted, that is better than no hypothesis at all, but progress is very slow if that is all one does in terms of hypothesis development. I'm talking about a comprehensive hypothesis that is consistent with everything known about this disorder in one self-consistent, concatenated, logical, cause and effect sequence, covering etiology, pathogenesis, and pathophysiology, and that explains the various symptoms and abnormal test results, regardless of which specialty they appear to fit into. That's what I'm attempting to develop.

Best regards,

Rich

 

[Ember]

Their hypotheses tend to be one-liners, and granted, that is better than no hypothesis at all, but progress is very slow if that is all one does in terms of hypothesis development.

Are we talking about the same hypotheses, Rich? I was referring to the ICC and CCC case definitions.

I'm not going to label people as lumpers or splitters. They will have to decide that for themselves.

To my mind, this quotation helps to explain the distinction that Dr. Unger and Dr. Jason made between “lumpers” and “splitters:”

The more general and stereotypic the criteria, the less useful they become because lumping together patients whose chronic fatigue is an integral part of many other diseases skews both clinical and research findings.