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Is CDC Out to Bury PEM?

Discussion in 'Action Alerts and Advocacy' started by Mindy Kitei, Jul 8, 2014.

  1. shahida

    shahida

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    Totally agree with that. Surely asking the patient if they experience this counts for a great deal- im sure this is the case
    with other diseases where the aetiology may not be defined and so asking the patient, however 'subjective' this may seem, counts for something. Funny how it all gets so 'complicated' when it comes to ME. Although I don't think PEM is unique to ME- I think there are a few other diseases out there which have this, maybe MS, but not very many. Which makes it all the more important as a defining characteristic.
     
    WillowJ likes this.
  2. Scarecrow

    Scarecrow Senior Member

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    @Valentijn, how do you know this and is it any way linked to the IOM contract?
     
  3. Valentijn

    Valentijn Activity Level: 3

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    It's what they keep focusing on any time they talk about it publicly.
     
  4. Scarecrow

    Scarecrow Senior Member

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    How I wish for a name change. It might defocus their attention away from the F word.
     
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  5. NK17

    NK17 Senior Member

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    Totally, completely, utterly agree with you @Scarecrow: the F word has to go.

    I suggest we all do a virtual burying ceremony for the F word and make an oath to never use it ever again.

    Ban it from your personal vocabulary, I did.

    I've ME (by CCC and ICC), I've had it since I had a bad case of IM (mono) in my early teens, thirty years ago. Then came toxoplasmosis, then chickenpox and many other infections. Looking back I always had PEM and PENE and my current ME doctor (Dr. Kogelnik) is working hard to bring tests on biomarkers that, to my understanding, will make the 2 CPTE look inappropriate and barbaric for very ill PWME.

    A year ago I was going to do it, I was better, now I'm worse so I regret not doing it, but also wonder what would have the CPET done to me, health wise.

    I might still need to do it for disability. I might have to pay the price, both financially and physically speaking.

    It's a classic catch 22 situation.
     
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  6. Gingergrrl

    Gingergrrl Community Support Volunteer

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    @anciendaze I couldn't agree with you more re: HR being an appropriate measurement tool for ME/CFS patients and my situation sounds very similar to yours. When I went to the ER a few weeks ago for tachycardia and extreme shortness of breath, they totally dismissed me and only took measurements supine which were useless.

    I also wanted to ask you what you meant re: "Clumsy use of beta blockers to lower HR can lead to patients becoming essentially bedbound if cardiac output is low." In my case, I was put on beta blocker, Atenolol, at a very low dose (literally either a quarter or a half of the lowest pill) and it is one of the only things that has truly helped me. Without it, when I stand up from bed in the morning, my HR is in the 150's and with it, my HR is anywhere from the 70's to the 90's. Without it, it takes me several hours to recover and with it, I can go about my morning and semi-function.

    I do think however, that I have low cardiac output based on my symptoms but have not found an effective way to measure or prove this. My EKG's are normal and when I do the Zio Patch test (an extended holter monitor type test) and it captures the tachy, I was diagnosed with "Inappropriate Sinus tachycardia" and also "POTS" type reactions (that are not consistent.) I had none of this before mono and it is not life-long.

    I had an echocardiogram last Tues and am still waiting for the results. I keep reading that "Impedance Cardiography" is the true measure of cardiac output but cannot find any local MD who runs this test! Are you familiar with it?
     
  7. anciendaze

    anciendaze Senior Member

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    The dose of Atenolol you are taking seems to be appropriate for you. Had a doctor simply given you the same dose as a patient with an entirely different heart problem you would have trouble standing up at all. It does happen, and I've seen it.

    Unfortunately, cardiologists tend to see their job as keeping your heart beating as long as possible, regardless of what is taking place in other organ systems, or what restrictions they place on your activity. There's a reason your heart began behaving weirdly in common situations, and we don't have an answer for why.

    This brings us to a second blind spot in cardiology: recognition of degenerative processes prior to explicit heart damage. Part of this has to do with the drastic nature of the surgical interventions which are a major (and lucrative) part of the profession. About all they can do otherwise is to keep blood pressure or heart rate from going too high, or prescribe statins for evidence we are forming atherosclerotic plaques. Many of us have trouble tolerating statins and/or medication for bp.

    Despite many advances in the field, the ability to predict trouble prior to a heart attack or catheterization is still poor, in the absence of an annual echocardiogram and stress test. (These are required if your business has a multi-million dollar insurance policy on you as CEO. None of us here are likely in that situation. You can be sure the CDC will oppose such diagnostic tests because of cost.)

    Since we are likely to have low bp, we are not considered at risk. Diffuse problems with endothelial function are likely to be dismissed as trivial right up to the point where a blockage is detected and bypass is needed. (To the man who has only a hammer everything is either a nail or nothing.) Endothelial problems also affect the parts of the circulatory system inside the heart. While the muscle is fine on the systole it may be slow to relax during diastole. This results in reduced filling and reduced stroke volume. Measuring stroke volume accurately is tricky. This is where we run into the medical tendency to cast things in dichotomies based on thresholds: either you have a problem I need to do something about, or you don't have a problem at all.

    At one time diastolic dysfunction was considered a minor problem, and you can probably find cardiologists who have not changed their opinions. Research now shows that serious left-ventricular diastolic dysfunction is just as lethal as systolic dysfunction. Either one strongly predicts death within 3 years without intervention. Most of us fall in the category of mild diastolic dysfunction, which is not associated with increased mortality on that time scale. This is the point where cardiologists generally tune out. Whatever is wrong with us is somebody else's problem.

    You can probably see the catch here. We aren't going to die as long as we don't push ourselves far beyond our limits, but our limits are unusually narrow. If the condition is progressive there is a real danger to life, but we have apparently fought the pathological process to some kind of impasse. Many of us performed much, much better prior to onset, but we were not studied at that time. If a doctor had followed those changes the condition might have been considered progressive, until it leveled off after six months or more. With current definitions it is effectively impossible to study ME/CFS patients in that significant interval.

    All I've said here is the opinion of an educated layman. I've concentrated on heart function because that is where the discussion was going at the time. I want to emphasize that none of us, doctors or patients, know what causes the dramatic change in function so many of us have experienced. These changes affect the heart, but are certainly not limited to it. You can find weird stuff going on in a variety of organ systems.

    From my own perspective this illness resembles sudden aging. People in their teens, twenties or 30s, suddenly behave like they are 40 years older. It is likely the relevance to the rest of the population will be that it illuminates the processes which make aging degenerative. I strongly suspect this will shed light on the causes of "serious diseases" like heart problems which are now poorly predicted in the general population.
     
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  8. Gingergrrl

    Gingergrrl Community Support Volunteer

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    @anciendaze You are very wise re: the cardiac issues and I wish some doctors would take note.

    What did you mean re: "Endothelial function and problems?"
     
  9. taniaaust1

    taniaaust1

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    Good point and maybe I shouldnt assume but I very much doubt that is the reason why she doesnt support a 2 day CPET but Ive got the impression in the past that this wasnt the reason she didnt back 2 day tests (I got the impression she thought that was unneccessary, I cant remember now thou why I thought that).

    One has to weigh up a risk of a once of CPET test for an actual diagnoses, with the risk of no tests being done and people getting wrongly diagnosed with ME/CFS when they actually have other kinds of "fatiguing" illnesses some possibly serious. There is large harm done to those people wrongly diagnosed (as they then dont get the treatment they need and they could have something deadly or easily treatable) and the harm also done to our patient group when all kinds of illnesses start being put under the one name which messes up our studies etc etc.

    So yes harm may be done by a once of test for a diagnoses but maybe the alternative of wrong diagnoses is worst.
     
  10. taniaaust1

    taniaaust1

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    I liked this post above. It could be a simple check list with questions like.. Do you feel sick after exercise? and ask questions related to other malaise things after exercise too. If check lists of questions are good enough to diagnose all kinds of mental health issues, why arent they good enough to diagnose our illness too? (I guess the only issue with checklists is that it may make it easy for anyone who wants to fraud the system.. but then they could throw in some fake ridiculous questions to catch those out those who dont really fit).

    There's quite a few ways to find out if someone has PEM.
     
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  11. Valentijn

    Valentijn Activity Level: 3

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    Yup, but that's exactly the same issue which already exists with ME/CFS diagnosis, and it is just as vulnerable to abuse when using "fatigue" instead of PEM as the self-reported symptom. If we're stuck with self-reported symptoms for diagnosis, we might as well at least use the meaningful symptoms!
     
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  12. MeSci

    MeSci ME/CFS since 1995; activity level 6

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    Good post, @Scarecrow and I think I agree with all of it. My PEM has become so mild as to be (almost?) undetectable during mild phases, which have come between moderate phases. I didn't stop having ME then.

    I agree that CPET isn't actually a measure of PEM and that it should not be used clinically except in conditions of complete, unpressured and informed consent - i.e. the patient must be aware of the potential hazards and must not have to do it in order to access welfare support, etc. Even 2-day CPET doesn't strictly measure PEM - it measures the ability to perform an activity 2 days in a row and notes some biological correlates. Many of us don't get the actual PEM until at least 48 hours after activity, so maybe 2-day CPET could produce measurable biomarkers of precursors to PEM, thus it could to some extent predict PEM.
     
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  13. Nielk

    Nielk

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    I think there is a major difference here between the ability to test for a symptom and the inclusion of this symptom for a diagnostic criteria.

    Just because it is not easy to objectively test for a specific symptom doesn't mean itt should not be required for a diagnosis of the disease.

    Fatigue
    Pain
    Weakness
    Muscle soreness
    Headaches

    Are all symptoms of ME that cannot be objectively tested yet they are included as symptoms of the disease. They are based on patients' reportin them. Somehow the CDC and Unger have no problems with these.

    The reason for this is because these are vague symptoms that can mean any of many symptoms of multiple syndromes, including psychosomatic ones. The CDC's agenda is to keep this disease as a vague syndrome with psych overtone.

    The symptom of PEM is a distinguishing symptom. It would mean that it is not a psych syndrome. It would mean there are biological abnormalities going on. This is the reason why Beth Unger and the CDC are so reluctant to admit that it exists in this disease.
     
    Last edited: Jul 10, 2014
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  14. anciendaze

    anciendaze Senior Member

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    Here's a paper on the subject of endothelial dysfunction and cardiovascular disease. See also this paper. The simple explanation is that there are changes in the inside walls of blood vessels which precede the formation of atherosclerotic plaques. These are like relatively mild inflammation. They also result in decreased flexibility of arteries, which forces the heart to work harder. There is other research showing that cells of the immune system invade this tissue, as would be expected if there were some pathogen responsible. (This also happens with nerve tissue in our disease. The question then becomes "do these cells know what they are doing?" We could have an undetected pathogen, a pathogen which was detected but discounted because it is considered harmless, or an autoimmune disease.) Immune cells which may be at reduced concentrations in peripheral blood might be the ones invading endothelial tissues. When we test immune function via blood we are only measuring numbers in one physiological compartment.

    There are well-known correlations between either long-term inflammation due to infection or autoimmune disease and endothelial dysfunction leading to cardiovascular problems.
     
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  15. Ren

    Ren .

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    Re Unger and PEM:

    From Phoenix Rising, April 2011; "Who is CDC Research Chief Dr. Elizabeth Unger?" by Cort Johnson

    "Dr. Unger at the CFSAC Meeting... She [Unger] agreed that the disorder is heterogeneous... When Dr. Klimas asserted that a subset of exercise-induced relapse’ would produce a ‘clean group’ Dr. Unger ‘seemed’ to agree but the idea that postexertional malaise is a key determining factor does not seem to hold true for her and at one point during the presentation she [Unger] said that no symptoms are unique to the disorder."

    http://phoenixrising.me/archives/5434


    The above notes seem to correspond to the October 2010 CFSAC meeting*. See pages 35-6, using "Unger" as search term.

    "Dr. Arthur J. Hartz asked Dr. Unger if she could speak to her philosophy, in regards to having a more politically‐vulnerable broad definition, for research. Dr. Unger believes every study should make sure they characterize the dimensions of the illness in patients, not just a yes or no (for meeting criteria). The findings in CFS are not unique to the disease, but it’s the constellation of those varying parts which makes the disease." (p.36)

    *https://wayback.archive-it.org/3919...advcomcfs/meetings/minutes/viewattachment.pdf
     
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  16. caledonia

    caledonia

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    I think this might have possibilities. Patients are already using this for pacing purposes.
     
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  17. Nielk

    Nielk

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    Yes. It works for pacing but, how does it prove PEM?
     
  18. Keela Too

    Keela Too Senior Member

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    I have been using a Fitbit since Nov 2013.. I have data for every day. Not only does it measure steps but also gives me data for "active" time at 3 levels - Very / Fairly / Lightly.

    It is very obvious from this data when I have low periods (crashes) and the long term results of a crash afterwards on my abilities.

    So lets say a person undergoes some GET and the therapist thinks their activity levels are increasing... the fitbit might well show that other activities are reducing to compensate.

    I'm now trying to combine Fitbit data with info from using a HR monitor and Endomondo....

    I over did it slightly on Tuesday (gah I wanted to go and do something & did - felt good at the time doing it too), and the effects are noticeable in the Fitbit data of yesterday and today. Also in my elevated resting HRs. Clearly some PEM going on.

    I so want to do more. I so hate these days when activity is restricted. However past experience has taught me that if I push on now, during this PEM then I will be doubly worse down the line.

    The Fitbit is amazingly useful at giving real quantifiable data... not vague qualitative stuff where my opinion could be influenced by some CBT therapist who wants me to talk myself better by always being positive!!
     
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  19. Ren

    Ren .

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    Now that I've read a bit more about it, I understand that a device like Fitbit measures/documents an individual's activity levels, and so in this sense, it measures how PEM affects someone.

    Others are saying as well though that it doesn't prove that PEM is the mechanism that creates the pattern of activity levels. I don't know enough about it to say.

    On my part at least though, there was some confusion regarding what Unger meant by measuring PEM.
     
  20. Keela Too

    Keela Too Senior Member

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    My norms:
    HR monitor:

    Resting HR 75 or below.
    Fitbit:
    620 steps/day.
    Less 3 hrs lightly active.
    Less 0.2 hrs fairly active.
    zero very active.

    Yesterday & Today:
    HR monitor:

    Resting HR 90 yesterday 85 today
    Fitbit:
    550 steps yesterday, will be around 300 today
    0.85 hrs lightly active
    0.08 hrs fairly active
    0 very active
    (Edited as formatting was wonky)

    So yesterday and today shows PEM clearly to me.... Higher heart rate without higher exertion to justify it. No other stressful stimulations either.

    So the means to measure PEM is in our hands I think.
     

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