Editor’s Note: On October 23-24, 2000, the Chronic Fatigue Syndrome State of the Science Conference (CFS-SOS) was held in Rosslyn, Virginia. Donna Dean of the National Institutes of Health, organized the conference. What follows is a personal account of the second day of the conference by Mary Schweitzer, Ph.D, CFS sufferer and author of several essays on living with Chronic Fatigue.
The professionalism was a welcome relief from what we have experienced in the past. There was a healthy respect for research done outside the government agencies, that was the most noticeable change, and also a willingness to allow a broad spectrum of topics to be covered without having them compete on “which is right.”
The two sessions I attended on medical issues – one on immunology and one on NMH/POTS (Neurally Mediated Hypotension/Postural Orthostatic Tachycardia Syndrome)- were both quite good. Dr. Nancy Klimas covered a lot of ground on immunological defects in U.S.-defined CFS and seemed to convince several of the non-CFS researchers there that the immune system clearly played an important role in the “condition.”
De Meirleir responded to a question I submitted about a report in the February 2000 issue of Journal of American Medicine. De Meirleir stated that it did seem that the 37kDa RnaseL factor (which I personally have) was implicated in a subset of CFS patients, and that it was time we tried to identify who those patients were, and what that meant. Others on the panel echoed a need to better identify the subsets of the condition.
Dr. Jerry Wolinsky
Dr. Jerry Wolinsky of the University of Texas at Houston, a specialist in MS, suggested that CFS shared much with what he called “organ-specific autoimmune diseases” There is a geographic variation if the person lived in the area before the age of 15, for example. He also noted that MS relapses are common two weeks after a viral onset.
Wolinsky said that it was hard to catch the MS patients with the relapse and remission variety at the point in time when whatever was causing their relapse had happened. Most interestingly, he said they found these patients worst symptoms did not occur at the same time that the de-myelization activity peaked. The situation was even more complex with patients with progressive type MS.
Where that would help us, he said, was to realize that we are probably catching patients too late to get the type of information we want if we are searching for causes. By the time we realize how sick the patient is, and get a diagnosis, it’s too late to find the cause.
Dr. Wolinsky went on to suggest that the CFS research community include markers that were statistically abnormal for CFS patients, (for example, the evidence on alpha and delta waves in sleep that had been presented the day before). Wolinsky suggested this should be without regard to whether it fit 100 percent or even 50 percent of the community, but also be willing to discard markers if they later proved unhelpful in sorting out patients who had the disease from those who didn’t, and also in finding subgroups.
Focus on earlier diagnosis
Wolinsky said they should focus more on early diagnosis. Long-established patients may give false leads, and treatment failures in long-established patients might discourage the use of treatments that would have helped had they caught the patient earlier. He had many other good suggestions and I managed to write down the phrase “metabolic storm,” which he thought also described what we were going through. An absolutely fascinating talk.
Dr. Wolinsky provides a good example of why “outsiders” were called in – precisely to offer suggestions for new research directions and to provide useful information that a CFS researcher may not have thought of, that could help lead to the breakthrough we all know this field needs. The “outsiders” never questioned that something was very wrong with patients diagnosed with CFS – which was a wonderful relief from some of the other “scientific” experts I have had to listen to.
Benefits of opinions from non-CFS researchers
I believe this was due in large part to the readings they were given ahead of time, which were generally peer-reviewed published studies solidly grounded in good research methodology. They accepted the evidence from the research they were given to read ahead of time, and then moved on to try to help us find answers as to why.
Similarity of CFS symptoms and chronic active hepatitis
In the same session, Dr. Bruce Rabin of the University of Pittsburgh noted there seemed to be many similarities between CFIDS symptoms and symptoms of patients with chronic active hepatitis. He said the immune system seemed to be trying to eliminate a virus; he also noted that there are some types of insulin-dependent diabetes that are the result of a viral assault on the pancreas. “Sickness behavior,” he argued, is cytokine-driven, and something had happened to extend the behavior of cytokines beyond normal responses. He was curious as to whether anyone knew what happened when patients with CFIDS had to have organ transplants. I believe he said that cytokine-reactive proteins can lead to heart problems, and he wanted to know about that in CFIDS too.
I found the NMH/POTS (Neurally Mediated Hypotension/Postural Orthostatic Tachycardia Syndrome)session very interesting and informative as well — and not just because I have particular problems with NMH/POTS! Dr. Roy Freeman, of the Beth Israel-Deaconess Medical Center, stood in for the late Dr. Streeten, who was to have keynoted this session. He provided a very useful presentation of the different terminologies – what I found most interesting was the number of ways in which the vasodilator reflex system could go wrong that could lead to the same results. This introduced me to a whole set of new terms from “alpha adrenoreceptor denervation” to “baroreceptors” and “baroreflex” — no, don’t ask me to explain it! It just suggests how immensely complex the topic is.
Dr. David Averill
In the NMH/POTS seminar, there was another interesting presentation by a total outsider, Dr. David Averill of Wake Forest. He knew even less about CFS than Dr. Wolinsky — he had ignored it altogether whenever it was brought up in the popular media, which was the only time he ever encountered it! Dr. Averill became very excited at the list of symptoms we were exhibiting, because he said that he can duplicate many of them by giving too much medication to hypertensive patients. For example, hypertensive patients on calcium channel blockers can have problems with tachycardia and a greater than average nocturnal drop in blood pressure. Dr. Averill also advised that we collect more information on diurnal fluctuations in blood pressure, heart rate, and cardiac output, in CFS patients. We were assuming too much from a single point in time, he suggested.
I was disappointed (I think a lot of us were) that the panelists all seemed to agree that low blood volume was not the answer. There was some niggling over the differences between POTS and NMH and other “ANS pathologies” in CFS – and the “proper” way to test for them – someone suggested just saying pan-dysautonomia — but that died down.
Not always a rosy picture
There were some unpleasant moments. One person asked whether there was evidence that CFS patients had higher-than-normal levels of child abuse in their history, and to my disappointment, a researcher stated that there was some evidence this was true. I thought this was a rather cruel and clueless thing to suggest in front of a number of parents of
However, Dr. David Bell quickly found a microphone and stated that the studies claiming to find such a link have only found a very weak correlation, and that he thinks that is due to the way the questions are asked rather than anything of use to researchers. He then stated very strongly that he has seen numerous adolescents and young people over a period of many years and has found no connection whatsoever between child abuse and the disease. It was a real change from the way things used to be that he was there to rebut that comment so quickly. No one else brought it up after that.
Again, when someone asked the usual question about whether the NMH/POTS
problems weren’t just due to “deconditioning,” Dr. Julian Stewart responded that he sees a lot of athletes with the disorder, and that clearly they weren’t deconditioned. Although orthostatic intolerance is associated with patients who are bedridden, it was also noted, the vast majority of CFS patients are able to be vertical at least 20 percent of their waking hours, which is enough to prevent that response. There were comments about different organs that could contribute to blood pooling as a problem — and then yet another call to recognize the ultimate heterogeneity of the category “CFS” itself.
The ‘Fatigue’ Question
I was personally unhappy with the Fatigue session — I did not want to see it on the docket at all, so I can’t say I was disappointed; it went rather as I expected. Once you start going into “fatigue” studies to deal with something that was named “Chronic Fatigue Syndrome,” then researchers begin looking at it as if CFS were just “chronic fatigue”
writ large, as if there was a linear model of fatigue-ness and we’re on the upper end of the scale. They are clueless as to the true aspects of the disease itself, frankly, and I found myself walking out of the session repeatedly, unable to sit and listen.
I believe that session lowered the quality of the whole conference — and it was a shame it was the last session, because it pretty much ended things on a sourer note than should have been necessary.
Later, I heard the hypertension specialist in an excited discussion with David Bell about what he thought might be causing “our problem”. He said that there are abnormalities of neurotransmitters that go on in the spine that cause symptoms like ours — I could not really follow it because in his excitement he got very technical, but this was a good sign, I thought – he had been engaged by the problem. Something that before was a nonexistent, or even silly, popular diagnosis (CFS) was now to him a very serious condition, and an area for new and exciting research, which is what we want outside scientists to find out.
Patient questions and answers
There was supposed to have been a session devoted to patient questions and responses, but because questions were submitted anonymously and edited in advance, and thus many were never asked at all, I was disappointed in the process. I would have rather seen people line up at the microphones (sitting down if necessary) in the usual fashion, each getting to ask their question in turn, than the method chosen, instead of being a patient-directed question-answer session, most of the time was wasted rehashing things already said.
At least one woman with diagnosed mycoplasma was able to say what she wanted -that she had improved significantly on medication (in contrast to the way her question was edited and asked to the panel) and thought that was important. The panelists agreed those sorts of things were important to keep track of. There should have – could have – been more of those moments.
Overall success promises future hope
Yes, there were problems, but it bears repeating: as a whole, the conference was definitely a success. I hope that the information and ideas presented will translate into action on the part of the NIH, CDC, and other agencies.
Even if there is no publicity, even if there is no direct action by the government – what happened was significant. There are now scientists with good reputations, in important specialties, who know that CFS (M.E.) is a serious condition meriting much more serious research. They didn’t know it before. From this meeting may come the spark that leads to that ‘Big Breakthrough’ – somewhere none of us could have expected. And that’s why the meeting was a success.
This account appears with the permission of Mary Schweitzer, Ph.D. She may be contacted at email@example.com