Comments for NIH Research Program on ME/CFS

1.  It is critical that we find a way to diagnose the 850,000 Americans with ME/CFS who have no diagnosis today.

In 1988, after a series of cluster outbreaks across the nation, US experts attended a meeting put together by NIH and CDC to give a name to the disease that had been called CEBV.  They chose “chronic fatigue syndrome,” or CFS.  

That was nearly 30 years ago.  In the intervening time, CDC has so misjudged the prevelence, severity, and urgency of the need to get a handle on this disease, that today, with a national prevalence of at least 1 million adult Americans, CDC admits that only 15% of patients even have a diagnosis.  

That tells me that the decision to focus on “fatigue” was a disaster.  And I wonder where the other 850,000 Americans are.  Since this is an equal opportunity disease - but that’s not true of those who are diagnosed - the population of undiagnosed patients with this disease is going to be skewed towards people of color, and I also suspect people of lower income.  They are suffering alone.  

2.  We need to go back and investigate the phenomenon of cluster outbreaks.

Once EBV was dismissed as a possible cause of this disease (prematurely, as it turns out), all interest in the possibility of cluster outbreaks disappeared.  Yet many patients experienced this disease in what appears to have been a cluster outbreak.  CDC and NIH responded to the experience of patients by saying (to me, personally), these were not outbreaks of disease - they were outbreaks of diagnosis.  It was the belief of Drs. Straus and Reeves that since this was obviously not a disease that was in any way contageous (decided in Washington, not after looking at statistics), then the evidence of outbreaks must be cases where patients found a friendly doctor willing to confirm their belief they had a “real" illness.  

That goes against the evidence.

More important, where we are today, I believe there has been a new set of cluster outbreaks.  Why?  Because I have been contacted by patients for twenty years, and starting around 2010 I began to be contacted by young people in their 20s and 30s and the parents of teenagers.  They had become sick SINCE 2010.  If there is indeed a new set of cluster outbreaks, let me suggest that we start to get a handle on it by looking at cases of EBV and asking for evidence of the long-run health of patients.  

3.  We need biomarkers now.

Both Items 1 and 2 are direct consequences of the absence of biomarkers.  It is hard to find out how many people have this disease when you are reduced to questionnaires.  It is hard to find out whether there are cluster outbreaks (or outbreaks of diagnosis) without biomarkers.  

I have had specialists who have been using biomarkers for two decades.  I see no reason to have to start from scratch.  We will at least catch a significant subset of patients.  NIH needs to look at natural killer cell function as both a marker showing THAT you have The Disease, and also a marker of the SEVERITY of The Disease.  

The 37kDA Rnase-L was a useful biomarker for some specialists until we lost the ability to send blood to Belgium.  A new lab was started in the US, but the group it was connected to had problems and it closed.  The patent was owned by Temple University, but they have said they do not care if they are reimbursed - anyone may use it.  

Dr. Robert Suhadolnik, now deceased, did a study in the 1990s of 100 patients from the Incline Village cluster outbreak, 100 patients with fibromyalgia but no symptoms of CFS (Fukuda 1994), 100 patients with major melancholic depression (at the urging of Dr. Straus), and 100 controls.  98 of the 100 patients from Incline Village had the defective protein.  Only 2-3% in each of the other three groups did.  That is profound, but it was ignored.  

In the meantime, Drs. Catherine Bisbal and Luc Montaigner tested patients with PVFS in France and Belgium, and had similar results.  This is even more fascinating given that Dr. Suhadolnik was using an electron microscope, but Drs. Bisbal and Montaigner weighed the protein (hence the name 37kDA Rnase-L).  

So two different sets of researchers, on two different continents, using two different methods, found the same thing.  The researchers switched blinded samples and got them all right.  So I think the 37kDa RNase-l biomarker is also another important characteristic of at least a subset of patients.

So many different specialists have worked with cytokine profiles that I can’t even list them all here.  But that is also an area for biomarkers.

As I write, biomarkers are being proposed by researchers from Griffith University in Australia to Stanford and Columbia universities, to the Simmaron Foundation, the NOVA clinic in David, FL - we need a systematic way to look at the existing evidence and start using biomarkers to find at least a subset of patients.

4.  We need treatments now,

Ampligen is already available and it has been shown to lead to dramatic improvements in 30-40% of patients.  I am one of them.  We ask that NIH help us get this drug provisionally approved.  The company does not have the money to do another large double-blind study.  I would contribute my own money towards such an effort.  In the meantime, the drug needs to be made more available because of the severe geographic restrictions it puts on those patients (such as myself) who would be vegetables without it.  

Rituxmab needs to be researched.  It has shown promise in Norway.

Patients have improved on gamma globulin and on antivirals, specifically Valcyte and Vistide.

We need to find other drugs to repurpose.  I believe there also needs to be a push to develop more antivirals, period, and more pharmaceuticals targeted to the immune system.

5.  We need to pay more attention to viruses.

From the first diagnosis of atypical polio (which became Myalgic Encephalomyelitis in the British commonwealth nations and Epidemic Neuromyesthenia in the US in the 1950s, CEBV in the 1980s, and then CFS in 1988), the evidence has strongly suggested that the disease is connected to a virus.  Which virus?  If you don’t test people, how do you know?  Now that there are better methods for finding viruses, we need an all-out push to find the viruses behind cases of ME/CFS in the United States.  [In my own case, both HHV-6A and CMV were in my spinal fluid in 2009, during a 2-year period when I could not get Ampligen.]

The earliest viruses suggested were those in the polio family, now called enteroviruses.  Coxsackie B was considered a prime candidate for the culprit in the UK (before the psychiatrists got involved), and it has also been found in patients in the US.  I also know patients whose illness began with an episode of adenovirus infection.

However, in the US, the viruses most commonly found are EBV (particularly at the start) [HHV-4], CMV [HHV-5}, HHV-6A, HHV-6B, and HHV-7.  

6.  Pay attention to 12 years of CFSAC recommendations.

Every year, CFSAC creates a list of recommendations for the Secretary of HHS.  I know that they go to a lot of trouble to do this.  Most of these are very good recommendations.  Please go back and compile them and take them into consideration. 

7.  Don’t start from scratch.  Use existing research.

Let me suggest the numerous websites that i referenced in my May 12 blog, “ME is not a mysterious disease.”  It would take too much space to write it all down here now!

http://slightlyalive.blogspot.com/2016/05/for-may-12-2016-me-is-not-mysterious.html

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This spring I lost 3 good friends whom I had known for 20 years as fellow patients with this disease.  One had been sick for 32 years; another died at 40 from breast cancer because her ME-battered body could not take the necessary chemotherapy regimen; one died in the hospital of pneumonia, again because his body was so weakened.  I look at a new generation of patients who got this disease as teenagers and wonder - will they still have it in their 40s, as is true for many patients I know?  Are they doomed?  Please stop this rolling epidemic now, because more and more people have it every time there are a series of outbreaks.  

I thank you for the opportunity to comment, and I am hopeful that with the will to do so, NIH can stop this unending tragedy.  

Mary M. Schweitzer, Ph.D.