In the Princess Bride, Miracle Max says, "Your friend here is mostly dead....Mostly dead is slightly alive." And so we are. I have diagnoses of Myalgic Encephalomyelitis (M.E.) and CFS. I have immune dysfunctions and persistent viruses: HHV-6A, EBV, CMV, and Coxsackie. HHV-6 and CMV are in my spinal fluid. I've had abnormal SPECT scans and VO2 MAX scores. I am an Ampligen responder. One million Americans suffer in silence from my disease, undiagnosed, untreated, alone. Slightly Alive.
An Open Letter to Dr. Collins and Dr. Nath on the NIH internal ME/CFS study
Note: As of Sunday, March 6, NIH has dropped the somatoform comparison group. Thank heavens! But they are still looking for "the underlying physiology of fatigue." So I still wish they would spend as much time learning about M.E. as they have spent deciding on the [admittedly admirable] lineup of tests.
Dear Dr. Collins and Dr. Nath:
I echo the sentiments of many ME/CFS patients in expressing concerns about the way the in-house NIH study on ME/CFS is proceeding.
The stated hypothesis of this new study is that: “post-infectious ME/CFS is triggered by a viral illness that results in immune-mediated brain dysfunction." Is that really all there is to the hypothesis? Dr. Wallit's participation raises troubling questions as to whether that is so. The comparison groups chosen for this study also suggest there is more to the hypothesis than we have been told.
I beg you, Drs. Collins and Nath, please rethink the hypothesis - and Dr. Walitt's role in this study. I also ask you to rethink the comparison groups. This disease has been a serious problem in the US for 30 years, and for 30 years both NIH and CDC have obstructed the creation of a strong biomedical research community – nevertheless, it has existed.
What has happened here? A hypothesis created by people who know next to nothing about this disease is being plonked on top of us. If I may say so, yet again. Why?
Make no mistake about it, fellow patients: Dr. Walitt is playing with somatoform diseases here – he just thinks there’s a biological cause for them.
He seems insulted that we might be unhappy about his inclusion. All I can say is that anybody who uses the words "chronic fatigue syndrome," "fibromyalgia," and "somatoform illnesses" in the same sentence is unacceptable in a preliminary study of my disease sponsored by NIH.
Last March Dr. Walitt published an article containing the following sentence: "The discordance between the severity of subjective experience and that of objective impairment is the hallmark of somatoform illnesses, such as fibromyalgia and chronic fatigue syndrome." (Chemobrain: a critical review and causal hypothesis )
I really do not care if Dr. Wallit is looking for a physiological cause for what are called "somatoform" illnesses. The problem is that he thinks ME/CFS is a somatoform illness.
Then there are the comparison groups. Where did these come from? Two comparison groups: post-symptomatic Lyme Disease patients, and patients with physical somatic disorders. The choices of comparison groups themselves suggest that the research hypothesis for this project has not been fully revealed to patients.
With only enough money to put 40 ME/CFS patients in the study, may I ask why we are bothering with comparison groups at all? Does it not make more sense to do this first study with ME/CFS patients v. controls - and then use more ME/CFS patients?
Since 1998 I have known that i had the defective 37kDa Rnase-L and a severe case of HHV-6A. Later testing showed natural killer cell dysfunction (in my case, a natural killer cell function of 2-3%) and abnormal cytokine patterns. In 2009, Dr. Dan Peterson found active HHV-6A and CMV in my spinal fluid. Do you think that my serious encephalitic and neurological symptoms could have had something to do with that evidence? The immune defects and viruses go away on Ampligen and come back 7-12 months off it. I am a sample of 1, but there are more like me. Many more. We have patients improving on the antiviral Vistide at Dr. Peterson's (I cannot take Vistide; my liver markers shoot up). The late Martin Lerner had patients on both Vistide and another antiviral, Valcyte; Dr. Jose Montoya at Stanford has had success with Valcyte as well.
Please pay attention to this evidence. Talk to clinician/researchers.
If not – then please run that hypothesis past some non-psychiatric specialists in our field before running with it in the first NIH internal study on our disease since Straus discovered (to his dismay) that we have abnormally LOW levels of adrenaline (patients with major mood disorders tend to have abnormally HIGH levels of adrenaline) 20 years ago. Dr. Straus had planned to be able to say we really had depression; hence his disappointment. (Psychiatists in the UK - and CDC's CFS group - finally found a use for Straus's adrenaline study in the unsupported hypothesis that patients had too many stressors earlier in life and had, in effect, run out of mechanisms to cope with them. If that were true, wouldn't one expect to find this disease much more common in Kosovo, parts of Africa, and in the embattled mid-east? Why hasn't it popped up in refugee communities internationally?)
Perhaps you could put this off until you can hold a workshop with recognized ME/CFS experts. I am confident we could pull one together quickly.
The well-respected British organization, Invest in ME , is holding a research conference May 3 in London. I am certain they would include you if asked. Another international research organization for this disease, IACFS/ME (International Association for CFS/ME) is meeting in Miami in October. Put this on a workshop there, or let them help you set up an earlier one. Or ask the public members of CFSAC to help you create a workshop. Ask any of us to help you create a workshop. You need to discuss the hypothesis and comparison groups with the longstanding biomedical ME/CFS community before committing to them.
In the beginning of 2000, ignoring the existence of CFSCC, the late Stephen Straus of NIAID and CAM at NIH ran a "state of the science" meeting about "CFS" with the usual suspects (if you forgive my saying so) – the psychiatrists from the UK who have had an inordinate amount of influence on perceptions of this disease both abroad and within HHS. After pressure from Congress he relented to having ONE public member from CFSCC attend (Nancy Klimas). But Congress continued to ask for a more objective conference. Donna Dean had just been placed as head of CFSCC, and she ran a conference the next fall that was fantastic – full of science and discussions with researchers who had previously known nothing about the disease. Unfortunately, there was a presidential shift in 2001 and CFSCC was shut down (to emerge, weakened, as CFSAC almost three years later). Dr. Dean left, and nothing happened again until 2011, when Dennis Mangan ran another excellent State of the Knowledge conference at NIH, which then came to naught.
When researchers do not know the very long history of this disease (technically going back to atypical polio in 1934, but practically speaking, back 60 years to the Royal College outbreak and creation of the terms myalgic encephalomyelitis in the UK and epidemic neuromyesthenia in the US), they make blunders. They can be perfectly well-meaning, but this topic is a mine field and requires someone who knows the history to navigate it. I am discouraged that once again NIH is going off on its own, as if we were never here at all.
One last way to salvage this study. Simply ditch the hypothesis and comparison groups and run it as a study of potential biomarkers in ME/CFS, without prejudging their meaning.
This is a very raw hypothesis. I love the scientific evidence you want to bring to bear, but I wish you were working on biomarkers for ME/CFS – not the physiological basis for "somatoform" illnesses.