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Mary Schweitzer's Essays on CFIDS/M.E.
Mary Schweitzer's Testimony to CFSAC and CFSCC

Presentation to the CFSAC
(Chronic Fatigue Syndrome Advisory Committee)
U.S. Department of Health and Human Services
Mary M. Schweitzer, Ph.D.
Washington, DC - May 17, 2007

No matter how pretty the glossy handouts, no matter how lengthy the website, in the end we keep coming back to this single short statement. Everything that CDC sends out about CFS includes this sentence: "There are no tests and there are no treatments.”

That single, bleak sentence is very costly - in terms of disability denied, healthcare reimbursement refused, and the sheer difficulty getting pharmaceuticals interested in finding drugs that will treat our disease.

As I understand it, CDC does not consider anything useful as a test or treatment unless it works for every single person they have classified as having “chronic fatigue syndrome.” That has been difficult enough with the CFS (Fukuda, 1994) definition. As CDC shifts to a definition based primary on the single symptom “chronic fatigue,” it will be impossible.

  • Consequences of CDC’s decision to insist “there are no tests and there are no treatments”:

    There are perhaps unintended but nevertheless very real consequences to the CDC’s longstanding position that “there are no tests or treatments” for “CFS”.

  • It makes it harder to get disability, and it makes it harder to get medical coverage from your insurance company.
  • The default option in a “medically unexplained disease” is psychiatry. All somatic syndromes require that there be no evidence of physical causation of the symptoms experienced by the patient. Somehow that has been turned into the stronger transitive: If it cannot be proven that a symptom is caused by physical abnormalities, then it is open season for diagnosis by psychiatry. In England, the preferred psychiatric diagnosis is “neurasthenia” – in the United States, CDC tends to use the language of “handling stress” instead. Either way, the disease becomes reduced to a neurosis, a character flaw.
  • Pharmaceuticals are reluctant to spend the large amounts of money necessary to pass the FDA’s rigorous approval process when there is no objective measure of the positive impact of the drug on the patient. FDA judges far more harshly the possibility of placebo effect and/or mild adverse reactions when it is not clear that the benefits of the drug clearly outweigh the potential costs in terms of the health of the patient. If there “are no tests,” it makes it much more difficult to come up with treatments.
  • Ultimately, researchers are denied information that would help push knowledge about this secretive disease further; physicians are frustrated with high-maintenance patients whom they cannot seem to help; and patients are left bereft of medical care.
  • Let’s look at a case where both CDC and NIH agreed there was a test that, in general, was abnormal in patients with CFS (Fukuda, 1994). Stephen Straus and Mark Demitrack found that, when compared to controls, CFS patients had lower-than-average levels of the hormone cortisol. This was considered an important finding at the time because patients with major melancholic depression have higher-than-average levels of cortisol. After a cursory study concluding that hormone replacement therapy was too risky for the level of benefit (and not controlling for the patients’ continuing problems with sleep), the cortisol thread was dropped.

    Normally, when a patient presents to a doctor with abnormally low levels of cortisol, there will be a discussion of the condition called Addison’s Disease. According to Medline Plus, Addison’s Disease is a hormone deficiency caused by damage to the outer layer of the adrenal gland (the part known as the adrenal cortex). In one form, Addison’s Disease may be an autoimmune condition. That’s interesting, because usually patients with CFS (Fukuda, 1994) have an unusual number of comorbid autoimmune conditions.

    The discussion might not center on Addison’s Disease per se, but perhaps a version of it unique to patients with CFS (Fukuda, 1994). A disinterested observer might think that would be the most obvious place to start.

    When I tested positive for hypothyroidism and Hashimoto’s thyroiditis, we discussed the known treatments for the disorders. As it turned out, I have an unusual form of hypothyroidism in which my body fails to convert T4 (the hormone made by the thyroid and stored in the thyroid gland) to T3 (the hormone that is actually used by the body, most of the time). So I have to take Cytomel, which is T3 – the usual remedies for hypothyroidism, levithroid and synthroid, do not work. Thyroid replacement did not cure M.E./CFS – but it significantly helped my symptoms. Furthermore, there is always a danger that Hashimoto’s thyroiditis can lead to cancer. Appropriate treatment (focusing on TSH levels and T3) not only improved my quality of life, but also perhaps prevented a dangerous complication of the disease.

    However, in the world of CFS at CDC, NIH, and the Royal Colleges in London, the discovery of abnormal levels of cortisol did not lead to discussions of existing information about Addison’s Disease – or even use of the terminology.

    At first, the information was anathema because it had disproved a previous hypothesis that many patients with “CFS” were actually suffering from a mental illness. Then it became incorporated into an advanced model involving the entire HPA axis (hypothyroid, pituitary, and adrenal) axis. According to this theory, an abnormal HPA response is critical to understanding CFS. Some authors suggested that the disease itself caused the abnormal response – others that earlier events in a patient’s life (such as parental abuse) had stretched the HPA axis response beyond repair, and the result was CFS.

    Either way, the HPA axis theories quickly developed a large superstructure built upon a very slim foundation. When pressed, it appeared that the main source of evidence for these theories was the single observation that one of the glands – the adrenal gland – failed to produce sufficient output of a single hormone – cortisol.

    The U.S. CDC was so convinced of the power of this theory that when human genome studies sponsored in large part by CDC were conducted in 2005, using a sample of 43 patients gathered in a still-unclear manner [the reader is referred to the December 2005 description of the two-day Wichita hospital stay in Reeves et al, “Chronic fatigue syndrome - a clinically empirical approach to its definition and study,” BMC Medicine 3:19, 2005, available in full text at http://www.biomedcentral.com/1741-7015/3/19], researchers were asked to use only genomes already known to be connected to the HPA axis. No alternate possibilities were allowed.

    Physicians were never asked to check their CFS patients for hypocortisolism; never alerted to the possibility that some CFS patients might develop a form of Addison’s Disease; and never given the opportunity to decide for themselves whether the patient’s personal level of hypocortisolism was sufficiently severe to warrant treatment.

    The evidence of hyportisolism was torn from the realm of normal medicine, and a disease (Addison’s) accessible to most physicians. Ironically, given that the early research on hypocortisolism had failed to prove a relationship between a known major mental illness (major depression) and CFS, when subsumed into the large HPA theory, it enabled those government officials so disposed to position CFS as a type of neurosis: the inability to handle modern-day stress.

    The point is not that Addison's Disease is or is not a major component of ME/CFS - I truly have no idea. The point is that the language within which this medical discovery was framed led only to a psychiatric interpretation, completely obliterating the possibility that this could be a relatively simple endocrine abnormality within the access zone of most physicians.

    Focusing on an abnormal HPA response, instead of the stronger evidence of a form of Addison’s Disease, enabled a transition to the fuzzy world of neo-psychiatry. A physical disorder was thereby transformed into a character flaw with a behavioral solution. Once again it could be claimed that there was simply something wrong within the patients themselves – in this case, that they were suffering from a type of post-traumatic stress disorder. The evidence for PTSD in CFS-Fukuda patients is slim. Dr. Reeves has spoken internationally on his own conclusion that many patients are sick because they were abused as children - but that conclusion is based upon a single sample of 43 "CFS" patients (only 6 of whom had actually been diagnosed with CFS-Fukuda during the 3-year Wichita surveillance study).

    In 1999, I asked a representative from CDC why no one ever spoke to the media about the severity of the disease. I was told at the time that to do so would be irresponsible. Until the behaviors associated with developing chronic fatigue syndrome could be identified, there was no reason to tell the public about it. CDC could only inform the public when they could also tell the public how to avoid coming down with CFS. Apparently it occurred to no one that “CFS” might be a disease that did not have a behavioral component. If you could not tell patients not to smoke, not to have unsafe sex, and to put your seatbelt on when driving, what was the point? I thought that a most peculiar (if revealing) response.

    Now, eight years later, CDC has its behaviorist slant: CFS is either caused by, or creates, an inability on the patient’s part to “handle stress.” Of course, this has been Dr. William Reeves’ theory about the disease for some time. The addition of the “childhood trauma” and “post-traumatic stress” theories remain simply that – theories.

    So now we had the prize: evidence that CFS was a character flaw (physical in nature) that could be corrected by behavior modification (don’t get so stressed).

    I consider that to be a most bizarre approach to the scientific study of a disease about which little is known, except that it impacts roughly one million Americans and the majority of them are undiagnosed; of those who are diagnosed, a majority cannot work full time. This is not a minor illness. Yet we could not discuss it in public without being able to offer some type of personal behavior modification.


    Known treatments for CFS (Fukuda, 1994) and M.E.:

    How can CDC remain so convinced there exist “no tests and no treatments” for CFS? I have been given tests and receiving treatments for some time. Most of you may not remember when I would come here in a wheelchair – sometimes pushed by my aging mother – barely able to do anything except present my short little paper that had taken weeks to write.

    Here are tests which my own doctors used that were positive in my case:

  • Simple office tests: Romberg test, subtracting from 100 by 7's, remembering 3 items with a distractor;
  • NMH/POTS
  • Hashimito's thyroiditis/hypothyroidism
  • Oxygen reuptake during a treadmill test
  • Intestinal permeability
  • Low natural killer cell function
  • 37kDa Rnase-L; abnormally high levels of Rnase-L
  • Chronically reactivated Epstein-Barr Virus
  • Active HHV-6A
  • Cheney uses a different test for exercise tolerance – bicycle ergometry with gas analysis – but the purpose is the same as the one Peterson uses (oxygen reuptake during a treadmill test). Cheney found that most of his patients shifted to anaerobic metabolism within minutes of beginning the test. When I did the test for Peterson, my oxygen reuptake was 19, below the legal disability limit of 20 (that is, on the basis of that test alone I was disabled). Thankfully it is better than that now, because I have had treatment. However, any exercise program had to be tailored to my obvious disability – and my prior improvement with pharmaceutical treatment.

    If we are telling physicians to start exercise therapy for their CFS patients (as CDC does in the toolkit and on the website), should we not also tell them how to measure the impact of exercise on the patient? As a bare minimum, shouldn’t the physician have some idea about the ability of the patient to conduct normal aerobic exercise?

    Other patients have suggested tests that led to successful treatment (that alleviated symptoms and/or suggested a direction to head). Many tests that have helped others did not have positive results in my case. This is a disease that must be approached on an individual basis. But is that not true of most severe illnesses? Does every cancer patient receive the same treatment?

    For example, recently specialists have added more cardiological testing as evidence has appeared supporting a higher incidence in cardiological abnormalities in ME/CFS.

    I'm certain Dr Nancy Klimas (on the current CFSAC) can provide a list of other immunological tests and how physicians can use that information – cell aptosis, natural killer cell counts and measures of killer cell function, T-cell ratios, alpha and beta cell meausures, for example. Here is Dr. Klimas, sitting at the table, a longstanding researcher on the immunology of CFS and AIDS, yet there is no reference to her work at the CDC website or the content of her work in the CDC’s suggestions for physicians and patients. Over the years I have watched as numerous physician/researchers either participated in or presented evidence to the CFSAC (formally the CFSCC and the CFS-ICC) – Dr. Robert Suhadolnik on the Rnase-L Factor, Dr. David Bell on childhood CFS, Harvard researcher Anthony Komaroff on neurological testing. Komaroff has been a frequent member of this committee, yet his pathbreaking Journal of American Medicine article (2000) giving a brief survey of the biological testing available for CFS, has never been referenced in a CDC publication.

    Returning to my own case, should not physicians be told about treatments that physicians who are part of the CFSAC use in their own practice? If controversial, that can be acknowledged. In the case of a finding such as a low natural killer cell function, is there actually disagreement on the implications of those results?

    Why are we withholding this information, simply on the basis that it cannot be proven (and never will be) that every patient who has one or another of these abnormalities fits the ever-broadening description of CFS by Dr. Reeves at CDC?

    Finally, although I tested negative for these conditions, it was important to be tested for them anyway: tests for HHV-7 and 8, mycoplasma, Chlamydia pneumonae, cytomegalovirus, coxsackie viruses, adenoviruses. The toolkit does suggest that some diseases be ruled out: mononucleosis (glandular fever), Lyme disease, lupus, multiple sclerosis, primary sleep disorders, hypothyroidism, severe obesity, and major depressive disorders. My own physicians also ruled out leukemia, untreated anemia and diabetes, and heart disorders. I was given PET, SPECT, and MRI scans to rule out brain tumors and to detect the impact of the disease on my brain – because of the expensive of those tests, CDC does not recommend them, but I would think physicians should at least make certain that patients are not suffering from a containable brain tumor.

    Because I have private insurance and because my extended family was willing to chip in and help pay for whatever testing was available, I was able to find out that I had some things and not others, and I have received treatment for what I have. If I need more treatment, my physician looks for what is available and we do the best we can getting it and paying for it. We are still finding abnormalities and trying to treat them.

    Should patients be denied testing and treatment because insurance companies and Medicare don't want to have to pay for the testing?

    Should CDC be in the business of assisting insurance companies and Medicare in denying tests and treatments to patients?


    Questionnaires as “tests”

    CDC might respond that their questionnaires are a kind of "test". Keep in mind that although questionnaires can provide a comparatively quick way of beginning the diagnostic process, they are and will always be subjective. They may provide a numerical result that can be poured into a computer to crank out statistical results, but the information remains subjective. As for the CDC's own packet of questionnaires, I’ve had to answer most of them every other month since 1999 (as part of the Ampligen study I am on), and I do not believe they can pick up the severity of the symptoms that many of us experience. If it were up to me, I would add the following questions:

  • Do you have trouble with balance?
  • Can you cross the street unassisted?
  • Can you cross the room unassisted?
  • Do you use a wheelchair and/or a cane?
  • Can you stand up from a chair unassisted?
  • How many steps can you take up a stepladder without something to hold on to?
  • Can you read the newspaper or understand the evening news? Can you follow a simple sitcom plot?
  • How often have you mixed up where to put items away (e.g., milk in the cabinet, sugar bowl in the refrigerator)?
  • Can you drive a car?
  • Do you experience blackouts?
  • Do you pause in the middle of a sentence, unable to remember how to complete it?
  • Do you use the wrong word for things, or have so much trouble with word retrieval that you are blocked from being able to finish the sentence?
  • Do you speak in a halting, slow manner?
  • Do you walk in a halting, slow manner?
  • Was this questionnaire difficult for you to fill out? Did you require assistance in filling it out?
  • Of course, these questionnaires are designed to be filled out in person, with a nurse or other medical practitioner directly asking the questions to the patient – but in practice, the patient is generally handed questionnaires and told to fill them out himself/herself. In that case, it might be helpful to ask a family member, when possible, to help fill out the questionnaire.

    Those are questions I would ask, if I were writing the questionnaire.


    A questionnaire for M.E.

    Previously I have given testimony about Myalgic Encephalomyelitis (M.E.), the disease that was also called atypical polio and, in the United States, Epidemic Neuromyesthenia. When the Holmes committee came together in 1987, they rejected the notion that there was any relationship between M.E. and any of the cluster outbreaks that had occurred in the U.S. in the mid-1980s. However, by 1991 NIH had published a booklet stating that M.E. was an outdated term for CFS.

    More recently, CDC has added a sentence to the website that states M.E., like fibromyalgia, overlaps somewhat with CFS, but is not the same disease.

    Perhaps what we need is not yet another series of tests on “fatiguing diseases that are medically unexplainable,” but a questionnaire for M.E. The Canadian consensus criteria for ME/CFS, adopted in 2003, offer an excellent set of criteria for clinicians – and researchers – to diagnose this illness in all its complexity. They should be at least mentioned in the information handed out to physicians and patients. I guess not – they include tests and treatments.


    Conclusion

    “There are no tests and there are no treatments.”

    Twenty years after the Holmes meeting in 1987 chose the name CFS and the Holmes definition to go with it, that's all CDC and NIH have been able to come up with?

    Roughly one million people in the United States have “CFS”. The vast majority have no idea what is wrong with them, and few of those who do have the diagnosis have access to a physician with the slightest idea of how to treat them.

    After twenty years, that’s a pretty sad state of affairs.

    Mary M. Schweitzer, Ph.D.
    Presentation to the Chronic Fatigue Syndrome Advisory Committee (CFSAC)
    U.S. Department of Health and Human Services
    May 17, 2007


    Go to the CFIDS/M.E. Information Page
    Mary Schweitzer's Essays on CFIDS/M.E.
    Mary Schweitzer's Testimony to CFSAC and CFSCC