Which disease is HHS studying? - Mary Dimmock

[Nielk]

From OccupyCFS - http://www.occupycfs.com/2013/11/27/which-disease-is-hhs-studying/

 

[Nielk]

HHS recently issued an FAQ about the IOM contract. As Jennie Spotila, Erica Verillo, Lois Ventura and Jeannette Burmeister pointed out, the FAQ falls far short of providing useful answers, is misleading and leaves critical questions unanswered.

Like the fundamental question: “What disease is HHS developing definitions for – ME or the diverse conditions that meet the overly broad “CFS” criteria?

I recently asked that question of both IOM’s Kate Meck and HHS’ Dr. Nancy Lee. From their answers, which I summarized below, the only possible conclusion is that the IOM study is intended to establish diagnostic criteria for the diverse conditions that meet the overly broad “CFS” criteria and that ME will be treated as a subgroup.

All of us, patients, advocates and experts alike, must reject this as completely unacceptable. We must call on HHS to acknowledge that ME is not part of the overly broad CFS. We must continue to call on HHS to adopt the Canadian Consensus Criteria.

We all know the problem. ME, the neurological disease characterized by post-exertional malaise, cognitive issues and immunological dysfunction has been buried inside of “CFS”, a diverse collection of medically unexplained fatiguing conditions. Numerous authors, especially Dr. Jason of DePaul, have reported extensively on the serious research and clinical problems caused by these overly broad CFS definitions, definitions that lump biologically unrelated conditions together. Dr. Bruce Carruthers summed it up simply, “There is a poignant need to untangle the web of confusion caused by mixing diverse and often overly inclusive patient populations in one heterogeneous, multi-rubric pot called ‘chronic fatigue syndrome.”

Having rejected the Canadian Consensus Criteria as unacceptable, HHS is conducting three separate initiatives to develop its own criteria. But what does HHS intend to do about the “web of confusion” that ha been created by “CFS”? What disease will these new criteria describe?

The ME/CFS IOM Statement of Work is ambiguous on this point as it uses the same jumbled, non-specific disease labels that have gotten us into this mess to begin with. The SOW states:

the Committee will consider the various existing definitions and recommend consensus clinical diagnostic criteria for this disorder [ME/CFS]. . .
The Committee will also distinguish between disease subgroups . . .
For the purposes of this document, ME/CFS shall be used to refer to Myalgic Encephalomyelitis (ME), Chronic Fatigue Syndrome (CFS), Chronic Fatigue and Immune Dysfunction Syndrome (CFIDS), Neuroendocrine Immune Disorder, and other terminologies in use for this illness.

I asked both Kate Meck at the IOM and Dr. Lee, the designated federal official for the CFS Advisory Committee (CFSAC) to clarify what “scope of disease” had been specified in the IOM contract. Has the IOM been contracted to develop clinical criteria specifically for ME? Or has IOM been contracted to develop clinical criteria for the range of unrelated fatiguing conditions that meet the “CFS” criteria? I asked Dr. Maier of NIH and Dr. Beth Collins-Sharp of AHRQ a similar question on the NIH Evidence Based Methodology Workshop process and am waiting on a promised response.

Here’s a summary of the responses I received from Dr. Lee of HHS and Kate Meck of the IOM:

Both Dr. Lee and Ms. Meck said that the scope of disease to be covered by the new clinical criteria has not been specifically defined at this point and that this will need to be defined as the process goes forward.

Dr. Lee indicated that the panel itself would need to resolve this issue and that possible outcomes could be ME as a subgroup of the broader CFS, ME as part of a spectrum that includes these other conditions, or ME as a separately defined disease. Ms. Meck indicated that HHS would be asked to clarify what scope of disease was intended at the first meeting. I raised the concern with Ms. Meck that the scope of disease directly affects panel selection and evidence base selection but she felt that the panel and process would be able to adjust as needed.

In a follow-up email, Dr. Lee confirmed the above statements but also reiterated an earlier point she had made that the IOM task list specifies that the “committee will also distinguish between disease subgroups”. She also said that in order for the target audience – defined as the primary care physicians – to effectively use the resultant guidance, “it is important to start a bit broad and then have criteria which distinguishes between subgroups.”

These answers are profoundly disturbing.

First, the statement that the scope of disease has not yet been defined is frankly hard to believe. This is a million dollar contract and panel selection is due to be announced soon. How can such a critical issue as the scope of disease to be covered by the new criteria be undecided at this point? If it really is undecided, who will decide and how? What criteria have been used to select the panel? And will that panel still be the appropriate one once a decision is reached on what disease or diseases the new criteria will cover?

But the statements about subgroups and spectrum of illnesses are much more disturbing.

Yes, ME is a complex disease that needs to be broken down into legitimate subgroups in order to better understand the disease and the treatment options. Perhaps those subgroups are based on whether onset is sudden or not, the level of severity of the disease or the nature of the immune profile and viral load. But let’s be realistic. What is the likelihood that the panel selected for the IOM study is going to be able to identify proper subgroups of ME itself when our experts are still working through that? Or when the evidence base lacks the ME specific studies – studies done with proper ME definitions – that would be needed to substantiate ME subgroups?

At the same time, we have an agency with a long-term commitment to studying medically unexplained chronic fatigue as the single clinical entity, “CFS”. We have an agency that has taken the position that Oxford, Fukuda and the Canadian criteria all describe the same set of patients for whom one set of clinical guidance is appropriate. We have an agency that questions the scientific evidence surrounding even post-exertional malaise and its measurement while simultaneously rejecting the Canadian Consensus Criteria because it does “not account for scientific evidence developed since 2003.” We have the CDC’s Dr. Unger, rhetorically asking at the May 2013 CFSAC “If a patient doesn’t have [PEM], wouldn’t you still manage them as a “CFS” patient?” And we have the IOM adopting the same overly broad view of CFS as HHS in recent IOM publications on Gulf War Illness.

Now we have Dr. Lee stating that the target audience of the new criteria is the primary care physicians and that they need criteria that start broader and then distinguish between subgroups. What about the patients who desperately need criteria that accurately reflect their disease?

What are we to conclude from all this? HHS has not committed to criteria specific to ME. HHS is not talking about the proper subgroups of ME that we all envision. HHS intends the IOM study to define criteria for the broader set of CFS conditions, with ME characterized as a subgroup. Or worse, ME becomes a subgroup of the even broader chronic multisymptom illness (CMI).

Either way, this will be a disaster that will degrade ME research and worsen the abysmal clinical care and stigma that ME patients receive today. This is the nightmare scenario that we all fear.

If HHS truly wants to reverse the chaos and the grievous harm to patients caused by years of sloppy definitions, it will first and foremost declare that ME, the disease described by the Canadian Consensus Criteria, is not the same disease as the overly broad “CFS” and should not be considered as either a subgroup of CFS or part of a spectrum of CFS diseases.

And if HHS cares not only about primary care physicians but also about the ME patients that they treat, it will acknowledge the harm done to patients by its clinical guidelines as reported at a recent Mount Sinai conference. CDC will immediately highlight PEM as a hallmark symptom of ME, will provide “black box warnings” about the adverse effects of exercise on ME patients and will point clinicians to the Canadian Consensus Criteria and the IACFS/ME primer.

Beyond that, HHS needs to immediately require that the Canadian Consensus Criteria be used in every study funded by NIH, even if it is used in parallel with Fukuda as an interim step.

Patients, advocates and experts alike must demand and accept no less, especially in the context of the IOM study and the NIH Evidence Based Methodology process.
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[Nielk]

Actually, this is the real reason why HHS refuses to adopt the CCC. It does not describe the broad fatiguing illnesses which they want the IOM to define for them.

 

[Ember]

I wish that Mary would use language consistent with that of the experts when she addresses which disease HHS is studying. She writes:

If HHS truly wants to reverse the chaos and the grievous harm to patients caused by years of sloppy definitions, it will first and foremost declare that ME, the disease described by the Canadian Consensus Criteria, is not the same disease as the overly broad “CFS” and should not be considered as either a subgroup of CFS or part of a spectrum of CFS diseases.

But the Canadian Consensus Criteria define ME/CFS; the ICC define ME. Mary quotes and purports to agree with Dr. Carruthers. She writes that ME should not be considered a subgroup of CFS. Dr. Carruthers also writes about untangling "the web of confusion" by segregating ME, but he nevertheless describes ME as a subset of CFS:

While it has always been essential, it has now also become urgent to segregate the subset that we are calling ME more clearly, using the ME International Consensus Criteria, so that researchers can confirm/disconfirm their results using patients who have chronic fatigue of this clearly bio-pathological origin. Otherwise the all-inclusive umbrella of “CFS”, in ambiguating natural and psychosocial kinds of fatigue, will continue to dilute the results of any investigations and maintain the pervasive confusion resulting when biopathological kinds are mixed indiscriminately (emphasis added).

Let's not add to "the chaos and the grievous harm to patients caused by years of sloppy definitions."

 

[medfeb]

Hi Ember

I'd take Dr. Carruthers' comments to mean that patients that meet ME-ICC are today lumped in with the diverse types of patients who meet CFS criteria. But he states that ME patients need to be segregated out. From my reading, he wouldn't agree with ME-ICC patients becoming a permanent and formally recognized subgroup of CFS patients.

Mary

 

[Ember]

Your words, @medfeb, seem to demonstrate the kind of either/or thinking that Dr. Carruthers cautions against, the kind of thinking that only adds to our tangled “web of confusion.” When it was first published, the ICC was used by the Coalition for ME/CFS in its NCHS reclassification request to argue that “when properly defined, CFS is the same as ME.” You've flipped that position now to argue instead that “ME...is not the same disease as the overly broad 'CFS' and should not be considered as either a subgroup of CFS or part of a spectrum of CFS diseases.”

In your current characterization, you seem to be regarding CFS and ME “as mutually exclusive dualistic entities and not complementary parts of a single disease concept.” Discussing the van der Meer and Lloyd critique, “A controversial consensus,” Dr. Carruthers writes:

All three of these contributions agree on one point - that whatever it is we are talking about, it is a complex disease/illness - but on little if nothing else. There was special confusion on whether we were talking about CFS or ME, regarding them as mutually exclusive dualistic entities and not complementary parts of a single disease concept.

Dr. Carruthers holds that CFS and ME are complementary parts of a single disease concept, just as mycoplasma pneumonia, in an analogous way, is part of the pneumonia disease concept and migraine is part of the headache disease concept. But for clinical and research purposes, ME patients need to be segregated and treated separately.

 

[Chris]

Ember, I agree with you on this; I think it is a mistake to strive for too much clarity and definition in a situation that is not yet clear or even very well described. Even the border between ME/CFS and FM in less than clear--some studies, like fairly recent proteomics one, showed a large area of overlaop, despite considerable difference.

I think that is behind some of the justified resistance to the IOM contract--we need more good research before sharp definitions become effective. Chris

 

[Ember]

Ember, I agree with you on this; I think it is a mistake to strive for too much clarity and definition in a situation that is not yet clear or even very well described.

Yet I do favour striving for clarity, Chris, even in the midst of complexity. Definitions drive the research, so without clear definitions we won't get good research.

In a situation that is not yet clear or even very well described, a definition needs to be part intelligent hypothesis. The CCC and (especially) the ICC both consider the presumed pathogenesis underlying our symptom clusters. But the IOM committee may instead focus on symptom lists alone, throwing up their collective hands at the state of the research. The implicit SOW directive that they consider ME/CFS to be another multi-symptom, complex disorder certainly does bode ill for us.

 

[Chris]

Ember, I take your point that "a definition needs to be part intelligent hypothesis." But what hypothesis do you hold to as to the "presumed pathogenesis underlying our symptom clusters"? Some bug? A stress sufficient to disrupt the HPA complex? Autoimmunity? (triggered by what?) The ANS (Julia Newton is focusing largely on this)--but what has disrupted its functioning? An environmental disrupter--vaccine, RF (my favourite guess at the moment)--or other? I think it is great that Lipkin suspects a bug, and would love to investigate a couple further if he had the money; that Newton pursues the ANS and sees links to metabolic (mito) dysfunction; but I don't yet see a clear winner, though I know where I would put my money right now. Which "intelligent hypothesis" do you want to underly the definition?
Chris

 

[Ember]

Ember, I take your point that "a definition needs to be part intelligent hypothesis." But what hypothesis do you hold to as to the "presumed pathogenesis underlying our symptom clusters"?

The ICC identify not triggers, but rather “patients who have neuroimmune exhaustion with a pathological low threshold of fatigability and symptom flare in response to exertion.” Abnormalities underlying the criteria (PENE, neurological impairments, immune impairments and energy production/transport impairments) are presented in the ME definition and ME Primer: “There is simply too much evidence of pathophysiologic neurological and immune dysregulation, immune activation and an imbalance between inflammatory and anti-inflammatory mediators to be ignored [32–56].”

According to its authors, the ICC “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.” They explain that “symptoms by definition are subjective; however, the clinician can observe visible signs that accompany symptoms...thus confirming symptoms.” The ICC identify patients who have “measurable and reproducible pathophysiological abnormalities in response to exertion,” and its authors call on researchers to confirm the specific biopathological mechanisms and biomarkers:

When advances in scientific technology are applied to patients who meet the more specific case definition of the ICC for ME, the current urgent need for identifying and confirming specific biopathological mechanisms and biomarkers will be facilitated, and our improved understanding of the pathophysiology can then be directed towards enhancing treatment efficacy.

Dr. Peterson urges clinicians to read the ICC because it emphasizes the presumed pathogenesis underlying the symptoms.

 

[Wally]

I may just be too exhausted right now to comprehend what is being discussed here, but I am really having a hard time understanding what people are talking about. So to see if I can simplify this for my very foggy brain - Is Mary, Ember, Chris are anyone else who is commenting on this thread in favor of the HHS adopting the CCC as an current research and/or clinical definition? If yes, clinical, research or both? If yes, do you advocate that this is just a starting point and would you want the HHS to work with ME/CFS experts (researchers, clinicians and patients) to refine the definition to accurately reflect the evolving areas of science/medicine that have developed in the last 10 years since the CCC definition was first introduced?

Thanks for any clarification you can provide me on this discussion.

 

[Ember]

I may just be too exhausted right now to comprehend what is being discussed here, but I am really having a hard time understanding what people are talking about.

I suggest relying on the open letter to Secretary Sebelius:

The expert biomedical community will continue to refine and update the case definition as scientific knowledge advances; for example, this may include consideration of the 2011 ME International Consensus Criteria (Carruthers et al, Journal of Internal Medicine, 2011). As leading researchers and clinicians in the field, however, we are in agreement that there is sufficient evidence and experience to adopt the CCC now for research and clinical purposes, and that failure to do so will significantly impede research and harm patient care. This step will facilitate our efforts to define the biomarkers, which will be used to further refine the case definition in the future.

All 50 experts and 171 advocates have supported that statement.

 

[Wally]

I suggest relying on the open letter to Secretary Sebelius:

All 50 experts and 171 advocates have supported that statement.

Yes, what you have quoted is what I agreed to support when I signed the advocates letter. So I think I was just confused if a new argument was being made that the CCC wasn't a sufficient starting point to get the federal government "off the pot" and move this definition out of the dark ages.

 

[Chris]

Ember, I don’t think we differ that much. I signed the advocate letter, and wrote twice to Sebelius in defence of the experts’ decision to use the CCC for the future. I think the ICC is probably the best document we could have at the moment, and am supported in that view by the fact that I fit into it, even though I regard myself as somewhat of an outlier in the ME world–very late onset, very aged, heavy concentration of symptoms on the cardio/ANS side, with only light representation from the immune and neurological sides. As VP of the local support group, I am frequently surprised by how differently the symptoms of many around me appear from my own. Julia Newton’s group has produced a little essay showing that ME is a somewhat different disease when it strikes the elderly, one focused on fatigue and OI. I think they may have a point. But are we a separate sub-group simply by virtue of age?
I am strongly in favour of trying to persuade HHS to spend the money on real research, rather than wasting it on the very dubiously connected IOM. But on this question of definitions... I do think many fundamental things are still unclear, and so deciding about subgroups etc. needs to be put on hold for the time being. We need more research to bring them into real visibility; we need more longitudinal research, since it is becoming clear that symptoms shift and change with time. Paul Cheney somewhere says that after about 3 years things usually quiet down somewhat, and he gives a characteristic quote: "I feel OK, but can’t do anything." I seem to be slowly moving towards that stage, and even PENE is changing; a few years ago, if I transgressed that invisible boundary, an hour or two later my BP would begin an inexorable climb towards the heights, accompanied by chest and/or mid pain, and so on. This would last a day or two, and then begin to quiet down. Now the same transgression brings a very mild rise in BP, no or very little pain, and in a day or so is over. I had some fairly heavy night sweats back then (only a few years ago)–now very seldom and very light. Am I slowly recovering? I sometimes think so, but maybe just changing. Many people claim both FM and ME. Do they really have two separable diseases, or one shaped a little differently from those who claim only one of the two? It seems from Julia Newton’s work that our form of fatigue has much in common with the fatigue found in Primary Biliary Cirrhosis, and from other work that our symptoms have a good deal in common with those of GWI–in fact, some work on us is being done under the cover of large grants for those two states.
What is driving those similarities? Is there one central driver producing different diseases in different folks? Or are there several and distinct drivers producing overlapping symptoms in different folks? What about the extraordinary parallels between us and kids in the Autistic Spectrum? Some of this has been known for years–the late and lamented Rich van Konynenberg’s methylation stuff derived from Amy Yasko’s work on autism, and the parallels were recently brought to my mind again by Martha Herbert’s 60pp. essay (plus 550 refs) in her Section 20 of the "BioInitiative 2012" document–available on the net, and her section is available separately there. I read it, and was constantly surprised by seeing our symptoms, and documented dysfunctions, appear again and again.
So I see the possibility that a lot of things will finally be seen in rather different groupings than the current one, and that is one large reason why I resist both the HHS attempt at a premature diagnostic definition, but also any overly rigid holding to the CCC or ICC. The experts make it clear that these definitions may well need to be further revised as research continues, and I say "Amen" to that. So I go with their brave and clear statement, but resist attempts to be overly tough in separating ME from CFS.

 

[Chris]

Perhaps this is a good moment to step back a bit and think about this business of "definitions" and what drives it. Way back there was Koch’s postulate stuff–one pathogen, one disease. Then genetics entered the scene–various genetic dysfunctions and/or variant forms might control specific symptoms. Then enter insurance companies, and medical textbooks and manuals–closely connected to available / authorized treatments.

Now look at cancer. A few years ago Siddhartha Mukherjee wrote "The Emperor of all Maladies: A Biography of Cancer." It is an excellent book, and provides a good overview of how the defining of multiple cancers–now into the hundreds, I think–is connected with the absolute domination of viral and genetic definitions of the main drivers of the disease.

The name "Warburg" does not appear at all in the Index, but right at the end of the p/b edition is an "Interview with the author," who responds to the question "What are some particularly promising areas of cancer biology where laboratory advances are becoming clinical realities?" with a short paragraph about Otto Warburg, who won a Nobel prize for his work in the 1920s on cancer metabolism, but who got swiftly buried by the prevailing definitions and the research they gave rise to.
Now we have Thomas Seyfried’s "Cancer as a Metabolic Disease," which threatens–the right word–to fundamentally shift basic paradigms. He returns to the Warburg hypothesis, removes some of the objections that were made earlier, and shows with–to me–devastating clarity that the genetic damage and variation in cancer cells is not the driver but a product of the disease–for one thing, one cancer can contain many different genetic variants. His focus is on the mitochondria, and a basic failure in energy production–basic metabolic function–sounds familiar?

He is too big and well-established a name to be brushed off–he has over 150 papers to his name–but don’t look to be offered his theories and solutions by the oncologist you meet with next week. His work is making some waves, but the whole cancer establishment will doubtless put up a long and stiff resistance. And doubtless there will be revisions and modifications to his views over the next years.

But one irritating feature of his book–some of which I frankly found to be too technical for my proper comprehension–is his repeated complaint that he has been publishing towards this overview for years, and the cancer establishment just keeps grinding on, despite having made only very modest gains over the many years since Nixon’s declaration of war, and despite the spending of many billions of dollars. I think his irritation is justified by the facts, but is itself an irritant to this reader. His basic views are also laid out in an earlier and much easier to read paper with the same title, freely available on the net, if you are interested.

One moral I draw from this is that an overly rigorous and focused diagnostic and research definition can hold back and repress really new ideas big time, and this lies behind my resistance to being too clear-cut about dividing ME from CFS at this moment in time.

I am not sure that there is a realistic chance of stopping the contract–the HHS has the power and it seems the will to just forge ahead anyway. But we can hope that the quality of the research now being done outside this monolithic organization, that has so flagrantly failed and foiled us, will eventually win out and make this whole thing irrelevant. Generous donors are keeping several US research groups alive and active, and the MRC has given Julia Newton’s group a substantial grant. There is still hope.

Or is there? I will share one dark thought. In my previous post I mentioned Martha Herbert’s paper in the "BioInitiative 2012" document. It carefully parallels the manifold forms of damage to cells and metabolism that can be caused by RF with the documented dysfunctions found among ASD bodies; the parallels are very disquieting, though Herbert carefully avoids making any claims to causality: as she comments, "the research has not been done." It should be done, but probably will not be done–the consequences would be too large for any government to contemplate. As you know, the latest CDC figure is that ADS now affects ca. 1 out of every 50 boys–that is, or should be, a terrifying figure. It is still rising rapidly, it seems–it was 1/88 only a few years ago. Genetics–the usual scapegoat for these conditions–cannot drive such a rate of increase. As I mentioned, the dysfunctions she describes very closely mirror the dysfunctions found among us.

When I search my personal history, the likeliest trigger for my capture by ME is my moving into an apartment building in Victoria that, since it is the highest point in the town, has a roof crowned by a forest of cell and other antennae. ME hit about 4 months after my move. When I became aware of the discussion about possible effects from RF, I rented a Stetzer meter, which recorded extremely high levels of high frequency pollution of my electrical power lines–around 400–they recommend trying for below 20. I bought some Stetzer filters, that brought the levels down to around 80. Three years ago I moved to a building in another part of town with a lower level of RF, and my levels here are considerably lower, and I seem to be slowly improving. Is there a connection?

I have a friend in town who sold her house when a large cell phone tower was built close by, and residents of the street began reporting cancers and other ill health–she came down with CFS. She moved to the same general area that I now inhabit, and is now pretty much well. Is there a connection?
The possibility has been strengthened recently by another Section in the "BioInitiative 2012" report, Section 16, Paul Héroux and Ying Li, "Plausible Genetic and Metabolic Mechanisms for the Bioeffects of Very Weak ELF Magnetic Fields on Living Tissues." This has since been supported by the same authors in a paper, "Extra-low-frequency magnetic fields alter cancer cells through metabolic restriction," PMID 23915261. It is behind a paywall, but I wrote to ask about the weight of "ELF" in relation to RF, and got in reply both a PFD of the full text and an assurance that the mechanism described would be effective up to around 10Gherz, which would encompass the full range of current cell and other uses.

The mechanism described, arrived at by very sophisticated lab work, is fascinating–it involves the observation that magnetic fields can act on the structure of water in the tubes passing through mitochondrial membranes in which are implanted those amazing proton pumps that are central to the generation of ATP. I shall not attempt an explanation–I am no scientist–but the paper is the work of serious McGill scientists, not amateurs.

If Seyfried’s hypotheses win the day, will the next step be to do serious research into the possible emvironmental and other drivers of the metabolic dysfunctions that drive cancer? and maybe ME and other conditions too? Could Health Canada and the HHS and other bureaucracies begin to demand serious control and even rollbacks in the level of RF emissions, or would industry simply steamroller any such attempt, probably before it became in any way public? There is a small group planning to record a documentary about us, "Canary in a Coal Mine." Maybe that is us–and maybe a lot of others too. And of course there are those vaccines....

This is purely a speculative hypothesis, thoughts of a dry brain in a dry season, but do I think current North American governments, in collusion with multinationals and controlled by "free" trade restrictions, capable of knowingly suppressing such information? Absolutely, and the IOM might be an agent.

In the meantime, I suspect that if by miracle we get a good and functional committee, it may not matter too much whether they look at ME or CFS–if they try to be serious about subgroups and issues like that, they will be able to make some sense of what is known, while waiting for better information. If we get the kind of committee we fear may be imposed, I suspect that it will not make too much difference.

 

[Ember]

Thanks for your insights, @Chris. A significant distinction seems to be that the CCC and ICC are driven by pathophysiology rather than by etiology. If ME were to remain lumped in with CFS for clinical and research purposes, wouldn't patients continue to receive harmful treatments (or no treatment at all) and research continue to serve up diluted and inconsistent findings? Unfortunately, an IOM committee, even if trying to be serious about subgroups, won't likely do for us what the ICC has done. Not given recent GWI history.

I'm nibbling away at your sources, but catching up will take me more time!