Sunday, December 29, 2013
NIH's P2P program's MECFS-Draft Report
Apparently NIH no longer believes in the scientific process, preferring, as one representative chirped happily, the "jury system! - it's the American way!"
Katharine Voss has two daughters with the disease. She presented testimony to the P2P because US government actions have international repercussions. I thought her testimony deserved a wider readership, so with her permission I have posted it here. I also wish to thank Jan Van Roijen for first widely posting Katharine's testimony on his private information list.
December 27, 2014
Public comment on the P2P Draft Statement by Katharina Voss, Dec 2014:
(Corresponding line numbers of the report are shown here in parentheses, reference numbers are shown here in brackets)
What does the NIH leadership really think about our disease?
"They hate you!"
This was the answer of a retired NIH scientist to a patient at a medical conference in New York City, Dec 2013.  And his answer was the first and only honest answer patients with ME ever got from NIH. This NIH scientist frankly expressed what patients with ME undergo every single day: they face a wall of hatred and scorn.
The NIH P2P Draft Statement clearly shows that he was right.
As many of ME activists predicted we got just the same bad recommendations given to Gulf war veterans (whose disease was “redefined” into the belittling “CMI”) and fibromyalgia patients.  NIH wants to put us off with ineffective harmful treatments like GET, CBT, antidepressants, and self-management. (Lines 113-116, 135-138, 344-350, 370-371).
Self-management – have we read correctly? What else are we doing now for decades in the absence of proper medical care? Self-management! And the NIH spends millions of taxpayers` dollars to recommend self-management? Are you kidding us?
These treatments like GET, CBT, antidepressants, and self-management ("multimodal therapy“) couldn't possibly be effective for some psychological disorders, but they do harm to patients with organic diseases like ME, a fact that is proven by true science but which is rejected by the P2P "experts“! 
Why does NIH neglect patients with ME?
Although men are also affected, the majority of ME patients are women. Hence this neglect is clearly a case of misogyny! I want to compare the situation with the early AIDS epidemic when mainly gay men fell ill and were discriminated against as homosexuals and AIDS was called "gay plague", "Gay Related Immune Deficiency“ (GRID), "Gay People’s Immuno Deficiency Syndrome“ (GIDS), the CDC`s creation “the 4H disease” (Haitians, homosexuals, hemophiliacs, heroin users)].  Racism, homophobia and misogyny impeded research much too long.
Today there is a big problem with the so-called "medically unexplained syndromes“, a term created by psychiatrists in order to cover and falsely include a lot of physical diseases. These psychiatrists - mostly the same psychiatrists who recommend CBT, GET and antidepressants for patients with "ME/CFS" - try to “prove” that exposure to childhood trauma is associated with significantly increased risk of “ME/CFS”. They try to “prove” that sexual abuse, emotional abuse and emotional neglect cause “ME/CFS”, and that these factors were most effective in distinguishing “ME/CFS” cases from healthy controls.  They try to “prove” this unscientific nonsense in spite of the very well-known results of biomedical research.
Their unscientific work results in falsely accusing mothers of children with ME of having a Munchausen by proxy syndrome. Parents, falsely accused of sexual abuse, emotional abuse and emotional neglect or of Munchausen by proxy syndrome lose custody and many children with ME have been separated from their families. They were mistreated with GET in psychiatric wards and their parents were wrongly criminalized. This is an ongoing praxis and this happens all due to the disregard of an organic disease. 
All these so-called "medically unexplained syndromes“ which are in reality physical diseases affect more women than men. Women are probably genetically more susceptible for these diseases. Actually these diseases are not psychological disorders and many biomedical abnormalities can be measured for diseases like ME, fibromyalgia and so on, falsely labeled as "medically unexplained syndromes."
We must not assume that these psychiatrists who assert that all these diseases are medically unexplained and caused by sexual abuse, emotional abuse and emotional neglect are stupid. We have to assume that they are well familiar with the results of biomedical research. Therefore, it is a deliberate misrepresentation by these psychiatrists, driven by misogyny.
This intentional misrepresentation is a violation of the AMERICAN DECLARATION OF THE RIGHTS AND DUTIES OF MAN, a violation of article I (Right to life, liberty and personal security), article VII (Right to protection for mothers and children), article XI (Right to the preservation of health and to well-being).
NIH consistently denies the fact that ME is an infectious disease. The report encourages more "biopsychosocial" studies. (Lines 275-276) Is that really what we need? More of these "biopsychosocial" studies from Wessely School and their worldwide followers which will "prove" that ME is a mental illness perpetuated by our "false illness beliefs"? No, we don`t need any single further study of this kind!
Why is NIH consistently denying the fact that ME is an infectious disease? There are so many clusters in families and among fellow workers and pupils proving that ME is indeed infectious.  Why is NIH hiding this very well-known fact? No actions have been taken to stop this epidemic. Why? A disease which was ""[not] numerically important on a national scale““ in the fifties has now evolved into the "most common chronic disease of young and middle-aged adults“ because NIH failed to recognize its epidemic character. 
Everyone who is able to read can read that Mikovits and Ruscetti found uncontaminated retroviral variants other than XMRV. Those variants were not XMRV. 
Only figure 1 of the Science paper was wrong. Figure 1 was the XMRV PCR sequencing/naming done by Silverman. Silverman was the one who sequenced XMRV in his lab, and these are the PCR data shown in figure 1 in the Science paper. 
GAll the other data on the Science paper still stand.  The serology information is well documented. The research also showed the dysfunctional immune profile, the cytokine signature, and microarray co-pathogens associated with those who were antibody positive in several studies. This data is all published. 
The prostate cancer paper by Silverman falsely claimed XMRV to be a human infection and was later retracted. However, no research came to a halt for prostate cancer because of Silverman`s error. Contrary to Dr. Judy Mikovits Silverman still has his career and the prostate cancer patients are still provided with research and treatment.
However, because of the original mistake made in XMRV prostate cancer research the ME patient population has been denied further research on Mikovits/Ruscettis original results and effective treatment. Silverman was wrong yet ME patients and Dr. Judy Mikovits are paying the price for his mistake.
And by the way, what about Maureen Hansons findings, her detection of MLV-like gag sequences in blood samples from a patient cohort? 
What about Sidney Grossberg`s isolation of the JHK retrovirus in ME patients? 
And what about Elaine De Freitas` HTLV II-like retroviral sequences found in ME patients? . Why had the CDC never tried to follow her protocol? 
Why did the NIH continue refusing unbiased and true science? Why did the NIH destroy future research for our disease because of the XMRV mistake made in prostate cancer? Why is NIH not pursuing the research for the variants and serology found in Ruscetti's lab? Why did the NIH destroy the hope of millions ME sufferers for effective antiretroviral, antiviral and anti-inflammatory treatments?
Shall my beloved daughters never have a life? Both developed mild ME, at least at the age of three. The elder one lost 2 years of education due to her disease before she got completely bedbound, the younger one lost nearly a whole year of education before she got bedbound. In 2009 my elder daughter received a Boostrix shot (polio, tetanus, dyphtheria) followed by a very severe relapse which continues to date. (100% bedbound, spoonfed, unable to wash, to brush her teeth without help, touch-sensitive, sensitive to the slightest noise and often unable to bear the presence of their beloved family members even for only a few minutes) In January 2011 my younger daughter relapsed after a series of viral infections. Being 90% bedbound, suffering from severe neurological and neurocognitive problems she is too severely affected to participate in any form of education, even at home. (My daughters are just the most severely affected members of our family! Many have/had other neuroimmunological diseases or/and cancer.)
My daughters clearly don`t suffer from a syndrome "characterized by extreme fatigue“ as "ME/CFS“ is described in the P2P draft. (Lines 2-4) My daughters suffer from a disease characterized by postexertional neuroimmune exhaustion (PENE). And PENE "is part of the body’s global protection response“ in a disease named Myalgic Encephalomyelitis in the fifties, recognized as a neurological disease from WHO in 1969. 
PENE, the cardinal symptom of ME, is an objectively measurable (i.e. Two-day Cardiopulmonal Exercise Test) abnormal biological response to exertion.  ME is not characterized by a subjective feeling of fatigue. Fatigue can be an accompanying symptom but many ME sufferers never experience fatigue. But every real ME sufferer experiences PENE. Without PENE – no ME!
My elder daughter is now 21 years old and spent 5 ½ years in a darkened room with no hope to ever get out of there. When will NIH research release her from prison? The younger one is now 14 years old, being severely ill nearly one third of her young life!
Both girls lost half of their childhood due to mild ME and her whole youth due to very severe ME. But all the NIH has to offer is self-management? Will NIH not allow them to have a future?
Oh yes, all the tests, medications and medical care we really need (and some of us probably lifelong) would be costly if the NIH would actually recognize ME as an infectious and transmissible disease.
But what is the alternative? The alternative is that we will further spread this disease. And many of our beloved ones will contract this disease, our friends and carers and physicians. And this disease will not stop in front of the doors of NIH.
Wake up, NIH! Break down the wall of hatred and scorn!
Wake up, America!
Thank you for your attention.
 Heckenlively, Kent, Mikovits, Judy. Plague: One Scientist's Intrepid Search for the Truth about Human Retroviruses and Chronic Fatigue Syndrome, Autism, and Other Diseases”. Foreword by Hillary Johnson, p. xxi, Skyhorse Publishing 2014.
 Gulf War and Health Volume 9: "Treatment for Chronic Multisymptom Illness”, Institute of Medicine.
 Snell, Christopher R., Stevens, Staci R., Davenport, Todd E., and Van Ness, J. Mark “Discriminative Validity of Metabolic and Workload Measurements to Identify Individuals With Chronic Fatigue Syndrome”, published online before print 27 June 2013 doi: 10.2522/ptj.20110368;
Monday, September 16, 2013
So Dr. Elizabeth Unger and the CDC have decided against a two-day exercise test in their supposedly all-encompassing, supposedly cooperative, upcoming CFS study.
Why am I not surprised?
When normal people go walking or bicycling or jogging, it is called "aerobic exercise" because while their body is exercising, it's using normal amounts of oxygen from air with carbon dioxide being expelled through their lungs. If you do aerobic exercise regularly, it is good for you. You get stronger and can go longer times or distances. For a normal person, aerobic metabolism can be measured with heart rate: (220 - your age) times 60% for the lower bound, (220 - your age) times 80% for the upper bound.
If your heart rate exceeds the upper bound, you're no longer operating in aerobic metabolism - your body will shift into what is called anaerobic exercise.
Weightlifting is an example of anaerobic exercise - you go past the point where the muscles can get enough oxygen from the lungs, and they start breaking down muscle to get it. That's okay - the muscle rebuilds stronger. But if you have to give the muscles a two-day rest, so in training, you either alternate working on upper body one day and lower body the next, or do weightlifting every other day.
If you push harder than that - even as an athlete - if you go too far with the supposedly aerobic exercise that your body switches into anaerobic, or do anaerobic exercises (like weightlifting) too frequently, the body starts living in anaerobic metabolism, and that is bad, because breaking down too many proteins this way poisons the body. If you don't have the good sense to stop, your body does - eventually it will MAKE you rest.
A gung-ho young athlete who is improperly trained can screw himself up with too much anaerobic exercise, and then his/her body will just refuse to keep going - for up to 3 weeks. That is called "over-training syndrome."
Professional and collegiate trainers keep close tabs on their athletes because of this.
For some reason our bodies shift into anaerobic metabolism (generally anything that sends our heart rates over 100) too soon. In my case, just walking does it when I'm sick. So you could say that our bodies are responding to "normal" activities as if we were athletes pushing too hard, that is, to a certain degree we are perpetually in the midst of "overtraining syndrome."
They use the VO2 MAX test (or CPET - Cardio-Pulmonary Exercise Testing) to measure this.
People with a bad heart have the same problem, and again they turn to the VO2 MAX stress test to measure it.
A recent set of studies* have found that those of us who are REALLY sick score badly on just one day of exercise - which then makes you wonder about the over-prevalence of heart attacks among us. So a score in the danger range (that would be me off Ampligen) should be taken seriously.
Most patients in this study are not going to score THAT low - they will score low-normal. The problem is, so do couch potatoes.
The amazing thing Staci Stevens and Chris Snell found was that high-functioning patients may score the same as deconditioned controls (the afore-mentioned couch potatoes) in one day of exercise - but on the SECOND day, the controls' scores don't change, whereas the patients' scores plummet IN HALF.
Which makes sense if you have a good understanding of this disease. But is really quite an astonishing finding for outsiders.
AND it is the best argument we have with which to make the case that graded exercise programs can hurt patients. Can make them worse. In some cases, can leave them paralyzed (something no one in government wants to talk about).
So if you want to measure that cardinal symptom of our disease that is often called post-exertional malaise (PEM), or post-exertional worsening of symptoms, you need a TWO-DAY test. Otherwise, we don't come off any different than someone who is not in shape.
Which means that by refusing to do the two-day test, CDC's results will make it look as if graded exercise was a good idea.
And that is bad. Bad enough that I think we are being set up. You can't say CDC doesn't KNOW that the two-day test has a different meaning - Chris Snell used to be president of CFSAC. And I've attended FDA meetings where Dr. Unger and Dr. Snell sat on the same dais. She knows. She is CHOOSING not to do the two-day test, knowing full well that it is the TWO-day test that demonstrates PEM.
Now, you're CDC. Supposedly the best in the world. You'd want to use the best methods, wouldn't you?
CDC's explanation for not dong the two-day test is that it would be an imposition for patients. But both Staci and Chris found that while the deconditioned controls could get whiney about having to do the test, patients with ME/CFS (Canadian) would walk on hot coals if it would move the science of this disease further along. So the supposition that the patients wouldn't want to have to come two days in a row does not fit what we already know.
The only time I ever saw Dr. Unger get angry in a CFSAC meeting was when we were all calling for a change in the CDC's recommendation of graded exercise. We asked not only that they quit recommending it, but also that they openly WARN physicians about the dangers. She was furious. She said that the emphasis on graded exercise was supported by scientists and was not negotiable. Those very words. Not negotiable.
Thus, by constructing this new study in such a way that patients will look like couch potatoes, Dr. Unger and CDC preserve their nonnegotiable stance of promoting graded exercise.
Why do I feel like I am being set up?
I think I'll ask Dr. Unger about that at the next CFSAC meeting. Oops! No can do - I'm not invited. The public is being excluded from the next CFSAC meeting, except for our pathetic little five-minute phone-in testimony.
I also noticed in the latest CFSAC announcement that CDC has returned to the IOM, where nobody knows anything about this disease except what CDC tells them, for the "new definition." The community of ME/CFIDS patients and clinicians had strenuously protested this through appropriate channels; CDC responded that they they heard us and were backing off - but not two weeks later, they have already gone back on their word.
Our position remains that it is currently active ME and CFIDS specialists and clinicians who should be drawing up that new definition. Like the ones on CFSAC. Not, well, strangers. They should put together a committee with John Chia (USC), Jose Montoya (Stanford), Dan Peterson (Simarron Institute), Lucinda Bateman (U of Utah), Alan and Kathleen Light (U of Utah), Nancy Klimas (Nova University), Mary Ann Fletcher (Miami), Martin Lerner, Paul Cheney, Maureen Hanson (Cornell), Gordon Broderick (U of Alberta), Charles Lapp (Duke), Anthony Komaroff (Harvard), Ben Natelson (NJ College of Medicine), Susan Levine, Ian Lipkin (Columbia), Derek Enlander (Mt. Sinai NYC) - and Chris Snell or Stavi Stevens. As a start. Not hired strangers.
These are VERY VERY BAD developments that roll things backwards to the early 1990s.
At least the insurance companies will be happy.
*For the most recent, see Christopher R. Snell, Staci R. Stevens, Todd E. Davenport, and J. Mark Van Ness. "Discriminative Validity of Metabolic and Workload Measurements to Identify Individuals With Chronic Fatigue Syndrome." Physical Therapy (2013). Click here for the abstract:
My apologies to those I missed, and those whose affiliations I missed. The larger point is that these are clinician-scholars working at top-level institutions. They should not be ignored.
Friday, May 24, 2013
Department of Health and Human Services
United States Federal Government
Washington, DC - 22 May 2013
Today I want to talk about two facts and one symptom. The facts are these:
1. Of the more than one million Americans who have CFS, up to 850,000 remain undiagnosed. Where are they? What happens to those people? Why is this not an urgent concern of CDC?
2. Of the more than one million Americans who have CFS, at least one-fourth are homebound, and one-tenth bedridden. One half cannot work at all. WHERE ARE THEY? Who takes care of them? What happens to them if there is no one to take care of them? What happens when there is no money because they cannot work and few make it through the social welfare maze? I can tell you. They end up on the street. You think that's an exaggeration? I personally know people who have ended up on the street because of this disease. I know others who ended up living in cars. What happens to a single mother when she is too sick to work and no one can care for her? She loses her children, and then she ends up on the street. Why is this not an urgent concern of CDC? City of Hope in Los Angeles was founded to get patients with tuberculosis off the streets. Where is the City of Hope for patients with ME or CFS?
Now I want to talk about one symptom: the symptom referred to on CDC's CFS website as "Post-exertional malaise lasting more than 24 hours." In the Fukuda (1994) definition, currently the official definition used by the federal government, PEM is one of eight symptoms, four of which have to be present for a diagnosis of CFS. Obviously it's not considered important.
But if you ask patients, and you ask their doctors, they will tell you it is important. Post-exertional malaise (PEM) is a defining symptom of this disease. Maes and Twisk have even suggested it be used to differentiate CFS from M.E.
In three minutes I do not have enough time to explain to you what this is. The word “malaise” is just as unrepresentative of the symptom as “fatigue” is unrepresentative of the disease. "Malaise" sounds vaguely ... unwell. My daughter, who had to take care of me from the age of 13, suggested Post-exertional dysfunction, because I would suddenly become completely dysfunctional. I could not talk intelligibly, could not understand much of what was said to me, had t o be helped to bed. I had a sudden increase in symptoms: light hurt; my head hurt. The pain behind my eyes and in the back of my neck, which never left me for a moment, got much worse. My glands ached. Most important, though, she said, “Mom, you just could not function.”
It does not take much to bring about what we patients all call a crash, depending on the condition of the patient. Just the activities of daily living - getting up, taking a shower, getting dressed - can do it. Mental exertion like reading or a long phone call can do it. But it is sudden, and it is unmerciful, and you are never quite sure how long it will last.
I want to differentiate PEM from post-exertional relapse. In post-exertional relapse, exercise makes you ratchet down to a worse level of the disease than before, and you stay there. In roughly 24 hours I had over 50 patients respond to a query about this symptom. One wrote that she was asked by her doctor to take a half-hour swim several times a week. She ended up bedridden for two years. Others told of being asked to take walks, or in one case, to run for 9 minutes a day. They all ended up bedridden.
Surely we already know this. Christopher Snell made an excellent presentation to the NIH State of the Knowledge Conference on CFS in 2011, describing the drop in performance by ME/CFS patients on the second day of CPET testing, in contrast to deconditioned controls and patients with other debilitating conditions. Alan and Kathleen Light et al at the University of Utah recently published research showing significant and unusual physiological abnormalities brought about by exercise in ME/CFS. As my own physician, Dr. Derek Enlander, recently wrote, “The notion that ME/CFS is caused by poor conditioning is no longer widely accepted.”
Most doctors believe that a patient who is “fatigued” is going to be made better by exercising. Make it an overweight female and they are even more convinced that exercise is just what is needed. But that is not true for this disease.
CDC's website on CFS gives the following advice for offering graded exercise to a bedridden patient:
A subset of patients with CFS are so severely ill that they're
largely housebound or bedridden. They require special
attention, including a modified approach to exercise. Hand
stretches and picking up and grasping objects may be all
that can be managed at first. Gradually increasing activity
to the point patients can handle activities of daily living –
getting up, personal hygiene, and dressing – is the next step.
[From the CDC's CFS Toolkit for Professionals ]
Listen to yourselves!! You see a bedridden teenager with a feeding tube, and all you can think of is how to get her to exercise? Shouldn't you try to find out why she is bedridden in the first place?
Until you have found the 85% of patients you have lost, until you find the patients who are lost because they cannot care for themselves and there is no one to care for them, you have no business talking about telling patients to practice grasping objects. As long as there are doctors casually telling patients to “just get some exercise and you'll be fine,” you have no business telling bedridden patients what exercise they should do.
If doctors need to know anything about our disease, it is this: exercise can make us very sick. It can make us bedridden. A bedridden patient is a very, very sick patient. Simple exercise that you think is easy can in fact be dangerous for us. It could very well be that what is happening with bedridden patients is that every activity sends them into over-exertion, into crash mode. They are that sick. Quit trying to figure out what exercise to give them and find out what's wrong with them.
As Irish patient and advocate Tom Kindlon puts it, “If graded exercise therapy were a drug instead of a treatment protocol, it would have long ago been banned by FDA.” There are too many adverse responses, and (frankly) not much evidence of success.
Post-exertional collapse, post-exertional dysfunction, post-exertional crash, post-exertional relapse – whatever you call it, is there really any debate any more over whether it exists?
Shouldn't that be the first thing you tell doctors?
I can tell you that it's the first thing we wish they knew.
And then, let's figure out why you can't find 850,000 missing patients.
Saturday, April 27, 2013
As often happens when I attend a government meeting on our disease, I am left with more questions than answers.
The purpose was to facilitate drug development for our disease, and I don't think we made very much progress there. There's always someone to say "no," to put down an idea. It gets frustrating.
So here are some random impressions that could be productive:
1. We were informed there is money at NIH to develop and validate tests, questionnaires, and endpoints for drug testing. If you could get something verified, the drug company can just go ahead and use it. Otherwise, they don't have much to go on. Perhaps patient groups should think about tests that should be verified and getting this accomplished.
2. In the absence of validated tests, particularly biomarkers, we're left with questionnaires. Questionnaires pose a LOT of problems, but more so with our disease because cognitive dysfunction is a primary symptom. I think FDA was beginning to "get" this. We should use that to emphasize the need for objective testing.
3. Sometimes we can be our own worst enemies. We need whatever biomarkers we can get. There were patients complaining that VO2 MAX testing is unethical. Well, just how are you going to show the significance of our disability without walking on the edge? Off Ampligen, my VO2 MAX score is 14-15 - which is in the seriously disabled, dangerous range. (More on that later.). But I'd do it tomorrow if it meant someone would take our symptoms seriously, or I could get a drug passed.
4. I don't know how to get around this one, but those of us who have been really sick for a very long time may require a long period of treatment before we show much improvement. That's expensive. But it needs to be taken into account nevertheless.
Now, those were thoughts on testing for drug approval. Here are a few things that occurred to me just listening to what was said.
1. IT'S ALL ABOUT THE DEFINITION. I think that's self-evident to anyone reading this, but it about drove me crazy on the second day. I do not want to be in a "cooperative" data sharing effort with someone (e.g., the CDC) who uses the Reeves or "empiric Fukuda (2003)" definition. I want to be in studies that use the M.E. (2011) international research definition or the M.E./CFS (2003) Canadian consensus definition. For those of you in the UK, that means beware of a research program being set up that cooperates with those who use the Oxford definition. It will really skew the results because the ill-defined Oxford cohort will outnumber and swallow up any group defined by a more biomedical definition. When it comes to drug approval, we need to convince drug companies to go for a definition that gives you the most homogeneity.
2. What is the REAL meaning of those VO2 MAX (CPET) scores? Everyone talks about using the VO2 MAX stress test to prove disability, or using the 2-day version to demonstrate the biological nature of post-exertional collapse. But I want to take this a step further. I knew I was really sick, but I was honestly shocked at how low I scored on that test. WHAT DOES IT MEAN TO SCORE 15 OR BELOW ON A VO2 MAX STRESS TEST? It means THERE IS SOMETHING SERIOUSLY WRONG WITH YOUR CARDIOPULMONARY FUNCTION.
To push this further, when I scored so badly I had a mess of active viruses in my blood serum (EBV, HHV-6A, CMV, HHV-7, and Coxsackie B). I had active CMV and HHV-6A in my spinal fluid and classic symptoms of encephalitis, so I think it's a good bet that I had viral encephalitis.
But did I also have viral myocarditis? Lenny Jason has suggested we are more likely to die of a heart attack prematurely than die of suicide. IS THERE MORE CARDIAC DAMAGE IN THS DISEASE THAN RESEARCHERS HAVE REALIZED? How do we get someone to pay attention to this information?
[For the record, most of the encephalitic symptoms clear up for me within six months on Ampligen. But my CPET scores don't budge for at least a year. Then they do start getting better, and after 4 years on Ampligen my CPET score was actually normal. Perhaps that helps explain why it seems to take much longer to get my stamina back.]
3. Where is the rest of the iceberg? How many years have we been told that only 15-20% of patients with this disorder have a diagnosis? Where is the 80-85%?
Someone asked a panel about the distribution of this disease by ethnicity. Beth Unger of CDC responded (and I agree with her response) that evidence shows this disease is at the equal opportunity - and that African-Americans and Latin Americans may actually have a slightly higher prevalence rate.
THERE WERE NO PEOPLE OF COLOR AT THIS CONFERENCE (AFAIK) except for one person who was not a patient. People of color are grossly under-represented in the diagnosed population; I don't want to think how badly they are represented in the practices of the handful of specialists who actually know what they are doing.
Could we find out? Could we get an accounting from the clinician experts as to what percent of their patient population with this disease are white? How about income? I think we already know the answer to this.
WHO WOULD BE INTERESTED IN THIS PROBLEM? Are there political groups who might be interested in the neglect of patients of color?
And WHERE ARE THE 80-85%? I was an invalid. Someone would have had to take care of me, and someone did. What happens to a single mother of two when she gets a serous case of this disease and remains untreated?
What has happened to patients I knew well online in the 1990s who have just disappeared?
The larger question, of course - the elephant in the room - has yet to be addressed by anyone in the government:
WHERE IS THE SENSE OF URGENCY? What is it going to take to hear that word spoken by someone in a position to actually change things?
Saturday, March 23, 2013
FDA, Washington, DC
From: Mary M. Schweitzer, Ph.D.
Date: December 5, 2012
Subject: My experiences with ME/CFS and 14 years on Ampligen
My name is Mary M. Schweitzer. I was a 44-year-old tenured professor of history at Villanova University when I suffered a blackout in my office on October 24, 1994. When I came to, at first I could not move at all. Once I could move, I was unable to understand a word in the papers on my lap that I had been grading. From that point on I was very sick, and my condition would continue to worsen for the next four years. I had no difficulty getting approved for private long-term disability and Social Security Disability Insurance because no one doubted how sick I was. I suffered from blackouts, ataxia, absence seizures, expressive dysphasia, disorientation, short-term memory loss, dyslexia, tinnitus, sensitivity to light and sound, and massive confusion to the extent that once I poured an entire pot of coffee into a silverware drawer, convinced it was a cup. I could not even pass a simple Romberg Test (I fell over as soon as I closed my eyes). I had intense pain behind my eyes and in the back of my neck 24/7, suffered intense headaches, and had constant muscle pain. Some times the pain was so bad all I could do was lie in a darkened room listening to a favorite movie.
My world grew smaller and smaller. I could not drive a car, but I could go places. In the summer of 1996 I started falling when we tried to walk to Camden Yards in Baltimore from the parking lot, and we had to start using a wheelchair whenever I left the house. I had a perfect score on my grad records in 1975, but now I could not understand a comic strip if I tried to read it in print. I found I could write on internet, although I had trouble reading much. In 1997 we added a riser to the toilet and a shower chair. I wrote several short essays and posted them; they all have a copyright date of 1997 because by 1998 even that was too difficult. Finally, in the fall of 1998 I was completely confined to bed, able only to make it on my own to the bathroom and back by holding on to furniture and walls and my golden retriever. By the end of 1998, I could not even brush my own teeth.
I had a good physician in Washington, DC (Marsha Wallace, who has since retired). I was diagnosed with NMH/POTS in 1995 and began taking florinef, and I developed Hashimoto’s thyroiditis in 1996 and began thyroid supplements. She introduced me to Dr. Dharam Ablashi, the co-discoverer of HHV-6 and its two variants. He found me positive for HHV-6, Variant A, in the fall of 1998; he told us that my lymphocytes were riddled with the virus. [Variant A was the strain of HHV-6 he had found in AIDS patients.] He also sent a PBMC pellet from my blood to Redlabs in Belgium, where they found me positive for the 37kDA Rnase-L defect. We now had two serious biomarkers.
I knew that Dr. Dan Peterson of Incline Village, NV, had found that patients with the 37kDa Rnase-L defect were more likely to respond to the experimental drug Ampligen, and I also knew that Drs. Ablashi and Paul Levine had run experiments with Ampligen and HHV-6A in vitro and found that Ampligen kept the virus from replicating. With those two biomarkers, I thought I stood a good chance of benefitting from the drug, so my family agreed to try it for one year. It would be a great strain to our finances but it would be worth it if it could stop the downward spiral I was in.
I began Ampligen with the late Dr. Joseph Bellesorte in Chadds Ford, PA, on February 4, 1999. In two months I could walk without a cane. In five months I could drive again. But I think the most remarkable moment was when I realized that for the first time in four and a half years, I didn’t FEEL SICK. We retested me for HHV-6A and the 37kDa Rnase-L defect at six months, and both biomarkers were gone. Six months into treatment I read an entire book. In September I was able to dance with my son at his wedding, and I walked barefoot on a beach for the first time in five years. I continued to improve on Ampligen.
After 20 months on Ampligen, we thought I had been cured and we ended treatment while I began negotiations to start teaching again. That was not to be, however. One year after I stopped taking Ampligen, on October 6, 2001, I had a blackout at Cal Ripken’s last baseball game and had to be taken out in a wheelchair. Dr. Ablashi tested me and HHV-6A was back.
It took seven months to get back on Ampligen, but since I had experienced no adverse side effects, my family and I agreed that I should stay on it indefinitely. Now I received it at the I. Brodsky hematology-oncology practice at Hahnemann Hospital in Philadelphia. The cost had come down in half because the drug no longer needed to be prepared by a pharmacist before each use, and with co-pays, the entire cost (roughly $22,000/year) was covered by my after-tax disability pay. We lived on my husband’s salary as a chaired professor of finance at the University of Delaware.
I remained on Ampligen this time for over five years. My health improved more slowly, but eventually substantially. I was able to publish 2 history essays and I wrote a 650-page draft for a book manuscript on this disease; my husband and I crossed the country five times by car because our daughter was now at USC; in the summer of 2007 I could even take short hikes with my brother in California.
However, in January 2008, Dr. Brodsky died, and although he was not my doctor at the practice, permission to continue receiving Ampligen there was denied. They reapplied twice and were denied twice. Now there was no place on the East Coast where I could get Ampligen. You have to have it twice a week by IV – you cannot travel far to get it. We guessed that a two-hour radius from our home in Delaware was reasonable – and covered most of the mid-Atlantic, one of the most populous areas in the nation. There was no Ampligen available.
I thought I would have a year or longer, but I only had seven months before the crash came in September, 2008. Thanks to Southwest Airlines, I was already seeing Dr. Peterson in Nevada once a year for my specialist, and I was scheduled to see him September 23. By the time I got there, I was running a fever and had active cases of Epstein-Barr (EBV) and cytomegalovirus (CMV). My natural killer cell function was 3%. I had an abnormal SPECT scan, Halter Monitor Test, and cytokine pattern, and my VO2 MAX score was so low that it fit social security’s definition for permanent disability.
We tried Vistide, which Dr. Peterson had experienced success with in patients who had both HHV-6 and CMV, but after three doses my liver rejected it. He halved the dose, then halved it again, and both times my liver markers immediately spiked. I could not take Vistide. [During the period I was on Vistide, we asked a local (Delaware) infectious disease practice to give me the infusions every other week. They agreed, but when I came for my infusion, stopped me. “You have CFS, dear,” the doctor said. Uh, yes, but I have a recognized disease, CMV, and Vistide is an approved treatment for CMV (Cytomegalovirus, or HHV-5). “Vistide is too strong a drug for you because all you have is CFS. If you had AIDS or cancer, we could see giving it to you. But you aren’t sick enough to warrant taking such a strong drug.” I had to fly overnight to Reno to get that dose!]
My condition continued to deteriorate. In July 2009 Dr. Peterson had me get a spinal tap in Reno; my daughter came up from L.A. to take care of me, because by this point I was no longer capable of taking care of myself. The spinal tap showed that in my spinal fluid, I had active HHV-6 and CMV as well as the 37kDa Rnase-L defect. After consulting with my husband, Dr. Peterson concluded that I had to get back on Ampligen, which would mean moving to Nevada. However, my ataxia was so great that I fell in a motel room and suffered a slipped disk; we had to have that fixed before he would start the Ampligen, so there were more delays and I got still worse.
I moved out to Incline Village in March, 2010, and began Ampligen treatment again. My daughter and her boyfriend stayed with me the first two months to help take care of me. After they left, I leaned on the kind services of other clinic patients and their families, two generous taxi drivers who would get me fresh groceries, and my brother, who would drive from Santa Rosa once a month and make sure I had enough paper products, water, detergent, etc., for the next month. It helped that the apartment was only one floor.
Once again I no longer needed my cane after two months. I began to recover, but it was slower than before. However, by the summer I was walking along the lake (starting at 6 minutes a day, then adding 2 minutes a day each week), and in August my husband shipped my car out to me because I was well enough to drive again. I began working on the book manuscript again. I was doing well, but
I missed my husband of 35 years – 3,000 miles east. I wanted to go home, but I knew I could not go off Ampligen. Then, in the spring of 2011, I learned that Dr. Derek Enlander would be starting Ampligen treatment in New York City. I drove home from Nevada at the end of April, 2011.
It took longer to get back on Ampligen than we had thought, but I restarted it October 3, 2011, in New York City and have remained on it since. I have to commute the 100 miles north to New York twice a week, but I use local Philadelphia area and Amtrak trains, and there is a NY Metro bus that goes from Penn Station in Manhattan right to Dr. Enlander’s office, so although it is a long commute (3 hours one way), it’s not uncomfortable. And it has given me back a life.
As long as I can remain on Ampligen, I can take care of myself (although I have very little stamina). Our daughter has moved back in with us, because my husband has an aggressive form of bladder cancer and now he needs to be cared for. Without Ampligen, my family would have to take care of me as well – instead, I can be of help.
I have a great fear of losing Ampligen. It is difficult for a person who had been so successful in her life to be so dependent on a single drug, a single company, and a single decision by a government agency, but there I am.
Please do not take the drug away from me again.
Mary M. Schweitzer, Ph.D.
Coda: My husband died of bladder cancer at the age of 63 in July 2013. In December, 2014, I moved back to Lake Tahoe at Incline Village, where I now live and continue to get Ampligen at Dr. Peterson's. It is a good place to heal both body and soul.
Saturday, February 2, 2013
CFSCC, or the Chronic Fatigue Syndrome Coordinating Committee, existed through from 1996-2001; CFSAC, the Chronic Fatigue Syndrome Advisory Committee, replaced CFSCC in 2003. The purpose of each was slightly different - one was supposed to coordinate activities; the other only to advise the Secretary of the Department of Health and Human Services, or HHS, on how to approach the disease. Since all CFSAC can do is advise, the committee sends recommendations to the Secretary of HHS. There has been little response. Consequently, and without involvement from the public, the committee has issued a new list of the recommendations they want to receive the highest priority. Jennifer's blog essay, "Highest Priority," discusses both the new list and the process by which it came about.
The committee is the only interaction Washington has with patients with Myalgic Encephalomyelitis (M.E.), or those diagnosed with the insipidly named Chronic Fatigue Syndrome (CFS). Because I live 90 minutes north of Washington by Amtrak, I have attended all but a couple of meetings of both CFSCC and CFSAC. It can be an exercise in frustration.
The biggest difference between the two isn't really that one coordinated and the other advises - the first never did much anyway. Rather, I find it very problematic that when it was CFSCC, back in the 1990s, there was a microphone at the head of the aisle and we were permitted to line up and ask questions – we, the public, the patients, parents, doctors. We could point out an obvious contradiction in a report by one of the ex officio members (representatives from the health agencies – CDC, NIH, FDA, HRSA …) and ask about information that was missing from their report, or simply wrong. Without that privilege – which is a standard right in all other public meetings, just not for us – the reports from the agencies since 2003 have been sawdust, bland comments with little meaning and sometimes blushingly misleading.
For example, the essential problem with NIH is that they allocate less than $6 per year per patient to this disease (compared to $500 per patient per year for MS). So a meeting never passes without NIH blaming the absence of funding for our disease on the researchers – saying they don’t fill out funding requests effectively, but assuring us that they’ll hold seminars to fix that. The statement is not only insulting, it’s not really true, because most “CFS” researchers have had no trouble getting funding for something other than CFS. They suddenly become all thumbs when it comes to our disease? Sounds like the fault lies within NIH, not the researchers.
But there's no one to say that.
Without the ability to ask questions, we can’t verbalized a misstatement when we catch one, or ask a meaningful question and get it answered. I would really like to know why it is okay for CDC’s website to omit information about the large body of research into CFS regarding biomarkers (such as cytokine patterns); immune defects (particularly natural killer cell abnormalities and the 37kDa Rnase-L); viruses (particularly EBV, CMV, HHV-6A, and Coxsackie); cardiac abnormalities; hypothyroidism and hypocortisolism; the VO2 MAX stress test. The list goes on, but the bottom line is this: the first statement on CDC's website, that little is known about this disease, is simply not true. After 25 years of research NOT involving CBT or GET, you’d think some of it should find its way unto that website.
Or the website should not exist.
They tell us our moment for commenting is during the five minutes they give us to testify – which may occur before the ex officio testimony, in which case you cannot comment at all. But commenting is not the same as being able to communicate publicly with the ex officio members. I have testified innumerable times about CDC, and once we shifted to the CFSAC format, my comments were simply ignored by Dr. Reeves and Dr. Unger. Pat Fero has gone to a great deal of trouble to research the paltry funds given out by NIH and testifies to that – then the NIH representative will stand up and say the same thing as always, with no reference to Pat’s findings.
It has become a comedy of the absurd – we exist in parallel universes, with a glass wall between the committee and the public. I used to pass notes to friendly members of the committee who would then ask my question for me, but now they are actually FORBIDDEN to do that!
Saddest of all would be the seriously ill patient, earnestly testifying to the ravages of the disease, speaking slowly and haltingly because of neurological dysfunction, being cut off at precisely 5 minutes - so the committee can spend 25 minutes chatting about whether to go to lunch yet.
And yet, CFSAC did pretty well, because public members of the committee such as Lenny Jason and David Bell worked hard to get serious recommendations up to the Secretary of HHS. It was frustrating that the only response we ever got from the Secretary, back in the last administration, was to have each ex officio member recite uncritically how their agency was responding to the public’s wishes – the same silly parade as before.
Attending these meetings is not unlike the scene in “Animal House” where the undesirable at an open fraternity rush party keeps getting sent back to the same spot with the rest of the “undesirables”.
Now we’ve lost the one thing we had in our favor at CFSAC – committee membership who actually wanted to change things. For that reason, it is disconcerting that they have gone back to re-prioritize the previous recommendations. The first recommendations in 2004 were just fine. Start there and demand answers, then move on to the next ones.
My mother – then in her mid-70s and in much better health than I have been – took me in my wheelchair to the first CFSCC meeting. I remember my mother listening for a few minutes to Bill Reeves say that the one thing we DID know about CFS was that it was not caused by a viral infection. Mom looked down at the Table of Contents for the meeting. “Who is this guy?” she asked. “It says here someone is supposed to speak from the CDC’s department of viruses and exanthums [diseases with pussy sores].” That’s right, I answered. That’s who’s talking. “But he is saying that this disease is basically psychological.” Yep. “Then why is he still in charge of it?”
Mom had not listened to an ex officio report for five minutes before immediately gerting to the crux of the matter, the problem that haunts us everywhere in the US federal government. Here are a bunch of guys taking about psychiatric causation and feel-good solutions – and every one of them is an expert in something OTHER THAN PSYCHIATRY. (At NIH we were housed for years within NIAID, the National Institute for Allergies and Infectious Diseases, where virologist Steve Straus prided himself on being able to prove CFS was not related to viruses.) What passes for “science” at HHS with regard to our disease is what I can only call psychobabble. It’s not even serious psychiatry. [I don't think a good psychiatrist would entertain the faux psychiatric theories put forward about our disease for an instant.] And when it comes to psychiatry, these heads of agencies are as unqualified as I would be – it is not and has never been their specialty. They are rank amateurs.
We are hidden in plain sight. At least for a while, we had a committee willing to fight that injustice. But the best way would be to once again allow the public REAL access to the agencies.
We need the right to ask questions ourselves of the agency representatives in public. We need the right to be able to point out discrepancies. We need the right to get ANSWERS.
And the questioning can start with why the government ignores all the existing evidence into pathogens, biomarkers, and objectively defined abnormalities, substituting instead popular psychiatry.