Jeffrez, thank you for making that last point, though I would still like to read that paper. I have many of the central, "classic" ME symptoms--PENE, fatigue, OI, sleep problems, fog, autonomic dysfunction ( blood pressure disregulation,etc)--but there is another group I have not had--swollen lymph nodes, fevers, sore throat, joint or muscle pain, and a few others. I too vote for keeping definitions purposely a bit loose until things are cleared up.
Chris
Very good points on the subgrouping. Based on the talk at June CFSAC the CDC is, for the first time, going outside of the CDC to define what is CFS. It was reported that the CDC was working with all 5 major ME/CFS groups to see if each doctor maybe working with a different subgroups and if CFS needs to be split up. For example; most of us have run into doctors that think Fibromyalgia and CFS are the same illness. However, per the Bateman/Light group Fibromyalgia, CFS and CFS with pain that does not have Fibro tender points, show 3 very distinct cytokine and chemokine signatures and are most likely different illness.
The five groups as I understand it are
Bateman/light - who seem to work with a lot of pain groups and per Dr. Bateman around 30% of her CFS patients are incorrectly diagnosed but are actually patients with Thyroid, Kidney, Diabetes, and Cancer rather than true CFS patients that have come to her after getting a CFS label elsewhere. The other 70% meet the CCC definition.
Dr. Kogolnik at Open Medicine is working with patients who have viral onset, PENE, and high IgG titers. (that may change based on what happens with the pilot study) He is looking for the group that respond to this treatment and how to define them from those who do not respond.
Dr. Montoya is looking a patients with high viral titers across the board and why some of the patients that he treats with antivirals get much much better while many see only mild improvements that plateau. What is the element that separates those groups?
Dr. Klimas is dividing out the fourth group and she is looking at high IL readings and TNF-a. She has a variety of protocols that she works with based on the individual patient but her baby or bias is immune dysfunction. Like Dr. Montoya she has about a 30% success rate (based on her talks only, not published) While other patients may respond mildly.Again the frustrating question these researchers are hitting is why only a small group are responding?
Dr. Karmoff is the fifth grouping. and you can take a look at the excellent link provided by Sing above for more information on his group and treatments. Dr. Karmoff was/is a huge backer of the EBV theory and recent work in Herpes virus mechanisms may vindicate him.HHV-1 and 2 cause mitochondrial damage reducing the energy that is available. ( I have the paper reference around here somewhere, I'll add the link when I find it, sorry big grins)
I have no clue how this will end up breaking down or how it will help with patient treatment. And it could as easily turn out that it's not subgroups at all but a lack of "complete" treatment for patients.
A Hypothetical for instance might be sleep, which is mostly ignored by many of the above doctors, except to admonish the patient to practice sleep hygiene. (big grins) And really there isn't a lot that can be done pharmacological to help produce quality sleep at least currently.So good advice is all these docs have in their tool kit to work with. But that may change.
There are dozens of papers that define the poor quality of sleep in ME/CFS patients. My favorite is one that Van Hoof et al which states:
(CFS) present a disordered sleep pattern and
frequently undergo polysomnography to exclude a primary
sleep disorder. Such studies have shown reduced
sleep efficiency, a reduction of deep sleep, prolonged
sleep initiation, and alpha-wave intrusion during deep
sleep. Deregulation of the 2-5A synthetase/RNase L antiviral
pathway and a potential acquired channelopathy
are also found in a subset of CFS patients
Bold is mine. Twitter version; we don't get to that deep sleep place where the body does it's healing and growing.
If patients are not reaching Delta sleep where all healing and growing takes place, then there is a chance that no matter how many vitamins, antivirals or antibiotics we take, the body will not be able to complete the healing process. So we get incomplete results instead of a cure.
Now there is recent evidence that
TNF-a antibodies can disturb the sleep system (rather than the cycle) causing the patient to not reach the much needed Delta sleep state. Drugs like Ebrel, which is the drug that Mella and Fluge are trying on the non responders to Rituxian, work to calm the TNG-a antibodies in effect resetting the system and allowing the brain to reach Delta sleep. The hope is that it will allow the healing cycle to be complete and the non responders will then respond.
I find their line of reasoning sound. I really look forward to the results. For the last century medicine has been about one problem, one drug and then move on to the next but it's changing. There is a better understanding that came about with AIDS that the systems are complex and interdependent and may need a more holistic approach.
In regards to the Morris/Maes paper I can't really say if their attempt to bring everything under one umbrella is correct or not since any hypothesis needs time to be proven or dis-proven or adjusted. There is a swing among Research/Clinicians right now to go back to looking at subgrouping and that is the way the CDC is moving right now. We haven't had much success with subgrouping in the past but we have a lot more information to work with now. We also haven't had much luck with one size fit's all. (big grins)
I'm leaning toward the Mella and Fluge approach of a tight definition, and a one two punch as a good hypothesis to try out!