In an extraordinary turn of events, a noted Centers for Disease Control (CDC) scientist has publicly charged his own government agency with improperly diverting funds away from authorized CFIDS research. Dr. William Reeves, the CDC's pointman on CFIDS research, has filed a complaint with the U.S. Health and Human Services Inspector-General to demand an investigation. CDC administrators then canceled a scheduled study of CFIDS in youths. The CFIDS Association of America, a patient advocacy organization, has called for an additional investigation by the General Accounting Office (GAO), an agency of the U.S. Congress.
Dr. Reeves claims in a written statement that he was told by another CDC official when there were fiscal shortfalls in other programs, CDC administrator Dr. Brian Mahy "always made up such deficits with CFS and other similar monies." In his detailed account submitted to the Inspector-General's office, Reeves stated that in recent years as many as half or more of the millions of dollars specifically earmarked for CFIDS research has been secretly diverted to other programs. Reeves claims that the CDC's reports to Congress about these expenditures were in fact false statements and that his superiors have "intentionally misrepresented" CFIDS expenditures to Congress and to the patients. He further alleges that more than $5 million has been diverted from CFIDS research into other programs since 1995.
The Inspector-General of the U.S. Department of Health and Human Services has initiated an audit to look into these matters. Dr. Reeves has furthermore filed for protection under the "Whistleblower's Act," a law that protects the jobs of government employees while they report government waste, fraud or abuse.
In a newswlre story about these events, patient leader John Friedlich was quoted as saying that the predominant attitude among CDC scientists for years has been that CFIDS "is not important, is not a real illness, and they're not going to commit to try to learn more about it." These events were also reported on the front page of the Congressional Quarterly Daily Monitor (9 September 1998), an influential publication read by lawmakers in Washington, D.C.
The CFIDS Association of America has called on patients to write Congress to demand an investigation by the General Accounting Office, an investigative agency that is independent of the CDC and answers directly to the U.S. Congress.
Report of Erroneous Information from CDC on CFS Research Allocations 1996-98
I am Dr. William C. Reeves. I am Chief of the Viral Exanthems and Herpesvirs Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention. 1 am directly responsible for CDC's chronic fatigue syndrome (CFS) research program.
I believe CDC has provided erroneous information to Congress, DHHS and patient groups concerning support of CFS research. I have attempted to rectify this within CDC. I am noting for the record that my providing this testimony is covered by the Whistle Blower's Act, and I request protection under that Act.
In 1997, The CFIDS Association of America and Dr. Arthur Lawrence (Office of the Assistant Secretary for Health, DHHS) requested details concerning CDC's 1996-98 allocations for CFS. An appropriate response was not received until February 1998, and serious questions were immediately raised concerning the veracity of the figures. 1 believe CDC's replies to these questions contain intentional misrepresentations.
CFS Research Support Fiscal Year 1986
CDC's reports to DHHS, Congress, and the CFIDS Association of America state that $1.2 million was used to support CFS laboratory studies in 1996. Indeed, on the last day of FY '96, $1.2 million of laboratory equipment and supply costs incurred by the Measles and Polio Eradication Programs were charged to CFS. When Ms. Kenney asked Dr.. Brian Mahy (Division Director and my immediate supervisor) to justify this at the April 1998 DHHS CFS Coordinating Committee meeting, he told her the money was used to support CFS laboratory research. He asked me to verify this, and I stated that the 1996 CFS Research Program did not include a laboratory effort. When Congressman Porter asked CDC to explain this discrepancy, he was told that the 1996 CFS Research Program included studies of enteroviruses, Borna disease virus and herpesviruses. When Dr. [Claire] Broome (Acting Director of CDC) testified to Congress, she was queried as to CFS expenses for supplies and equipment and stated that 1996 costs were significantly higher because CDC was investigating the potential role of infectious agents in the etiology of CFS. She further stated that a portion of the costs were used to establish a new laboratory in my Branch.
This information is not true. CDC's most recent publication concerning laboratory studies of CFS was published in 1995. Actual laboratory work was accomplished between 1993-94. This work involved testing performed in 12 different CDC laboratories and was done at no cost to the CFS program. Analysis showed that there was no need to conduct similar laboratory studies. Dr. Mahy, my Division Director, was well aware of this because he conducts a detailed annual review of all programs. In addition, Dr. Mahy held a peer review of the CFS program in August 1996, during which we discussed laboratory studies and plans in detail. Finally, I informed Dr. Mahy on at least two occasions during preparation of the requested budget reports that no CFS laboratory work was conducted in 1996.
The $1.2 million that CDC falsely indicated was used to support CFS laboratory research in 1996 only represents part of the misrepresentation that fiscal year. Dr. Mahy's Division appears to have used an additional $1.4 million of monies they reported as supporting CFS research in my Branch for unrelated activities. These monies encompassed [approximately] $600,000-to support staff elsewhere in the Division (this was in addition to overhead staff shown in the materials given to Congress) and [approximately] $900,000 for various contracts ($200 000 measles program agreements with other agencies, $200,000 to the respiratory and Enterovirus Branch for management and professional services, $228,000 epidemiology and laboratory fellowships, $315,000 printing services contracts).
Unrelated projects have been charged as CFS in previous years. In 1995, CDC reported [approximately] $6 million was used to report CFS research. After overhead, about $4 million should have been available for program. Again on the last day of the fiscal year, Dr. Mahy's Division charged $2 6 million used in unrelated studies against CFS.
CFS Research Support Fiscal Year 1997
CDC's reports to DHHS, Congress, and the CFIDS Association of America state that my Branch used $3.4 million for CFS research during 1997. However, I can only account for $2.8 million. At the end of FY '97, Dr. Mahy's Division Administrator withdrew or withheld $340,000 to cover other programs ($150,000 in orders for equipment, $20,000 in supplies for the laboratory and $167,000 for personnel contracts). However, the withheld monies were shown as CFS research costs in the reports. The withheld monies represented about half of what was needed to fully establish a CFS Molecular Epidemiology Laboratory (recommended during 1996 peer review and suggested in FY '97 Congressional language). The withheld funds ($340,000) had to be covered by the CFS Research Program for the FY '98 allocation.
As with 1996 expenses, this was not. a simple accounting artifact or an oversight due to lack of information. My branch had worked throughout the year to provide Dr. Mahy with accurate 1997 budget estimates. This culminated on October 17, 1997, when Dr. Mahy asked me for a detailed breakdown of CFS research expenditures. I noted that what we had actually spent on CFS was significantly less than what the CDC was planning to put forward. He stated that "we were at cross purposes" and that the only figures that would be given out were $3.4 million in direct research costs.
Indeed, my Branch's entire FY '97 research allocation was $1.7 million, inclusive of CFS. On August 4, 1997,1 met with Dr. Mahy's Administrative Officer to clarify this. He told me, although they had received an allocation of $4.2 million for CFS, that he could not pass the entire allocation to the CFS program because some branches had insufficient budgets and Dr. Mahy had always made up such deficits with CFS and other similar monies. I can provide the names of the five individuals who attended this meeting.
CFS Research Support Fiscal Year 1998
An identical pattern is occurring in 1998. Dr. Broome reported to Congress that CDC had allocated $5.8 million for CFS and that $3.4 million would directly support research in my Branch. My entire Branch FY '98 allocation from Dr. Mahy is $2.5 million and this must support research involving 32 FTEs [full time equivalent staff members] in Papillomaviruses, Herpesviruses and Poxviruses, in addition to CFS. I sent. five memos to Dr. Mahy's Administrative Officer over the last week to obtain clarification and was finally told that he would drop by some time and discuss it with me.
In addition to these apparently intentional misrepresentations of CDC's allocations for CFS research., I believe CDC has grossly misrepresented overhead costs for Dr. Mahy's Division. During her testimony to Congress, Dr. Broome stated that a Committee Management Specialist was required full-time to support Dr. Mahy's duties as co-chair of the CFS Coordinating Committee. In my opinion, this reply is insulting. The Committee has met three times with Dr. Mahy as co-chair (May 1997, October 1997, April 1998). The Committee Management Specialist in question (Renee Ross) was not certified until July 1997 and left for another position at CDC before the April 1998 Committee meeting. Her principal daily duties during 1997 and 1998 were to serve as Dr. Mahy's secretary. In addition, a separate Committee Executive Secretary was responsible for many of the duties Dr. Broome indicated for the Committee Management Specialist. Finally, as a benchmark, CDC's CFS Research Program (for which I am responsible) charges 75% of a secretary and 10% of a Program Analyst FTEs to CFS. In addition to daily administration they cover responses to approximately 450 direct contacts monthly.
Summary and Conclusions
In summary, I believe that CDC has intentionally misrepresented monies allocated to CFS research and I cannot ethically support this. The misrepresentations "involve systematically charging between $400,000 and $2 million incurred by unrelated activities to CFS between 1995-97 and reporting to DHHS, Congress, and patients that the monies were used for CFS research. Previous administrators under Dr. Mahy could be interviewed to explore this in more detail for years in which Congress specified a CFS appropriation. The misrepresentations also involve charging inappropriate Division overheads to CFS. The misrepresentations have been compounded by intentionally ignoring technical information from Program concerning expenses and knowingly transmitting inaccurate figures and information. I am responsible for the CFS Research Program and cannot manage this responsibility in an acceptable fashion unless CDC provides Program the same support it tells the public is available,
The AACFS Conference coupled with the CFSCC meeting in Boston, city of our first "Freedom Fighters," should have produced results we have ALL been fighting for, but it didn't. More evidence was presented in the Research and Clinical Sessions to fuel the HOT, continuing fire of the many advocates and researchers who want the name changed - including myself!! Founders, Co-Founders. Presidents, Board Members, Officers of MANY PATIENT groups were THERE, FIGHTING FOR YOU ... NOT for their BANK accounts. They came in from all over the world, rode long hours in cars, planes and even trains. FOR YOU!!! They wheel-chaired or hobbled in with canes, and some even brought care-givers for paralyzing, painful "CFIDS crashes" after long, exhausting days of putting the well-known "psychobabblers" off guard with damaging questions and statements about their biased and discriminatory "research" papers, ... FOR YOU!!! They ate lunch and dinner with fellow advocates and doctors WHO FIGHT AND CARE FOR YOU!!! They passed out their hundreds of piles of newspapers, cards, articles, blue ribbons, mugs & badges with CHANGE THE NAME on them - FOR YOU!!! They escorted learning physicians and nurses by hand to introduce them to doctors who take CARE OF US and KNOW about this "DOOMSDAY" disease. They sat in hard, uncomfortable chairs listening for hours, taking notes with arms and fingers feeling like lead ... FOR YOU! They took naps at dinner-time, MAKING themselves get up to go to late night sessions - yes, for YOU. Many at home, lying on the couch, think "they must be less sick than me ..." They're not! Many at home, lying in their beds, think "they must have a lot of money, especially from their groups ..." They don't. We all are just as sick and poor as you. There's one big thing that makes us different ... we don't lie down and "take it" anymore! We can't UNDERSTAND all the losses we've been through AND have to put up with a totally DISCRIMINATORY NAME, all the while watching them hover around those who cause YOU and ME harm! There's a BIG difference in helping someone represent YOU vs. letting someone pretend to. There's also secondary gains in going, even though you KNOW you will pay dearly for it when you get home. You become friends with so many wonderful "Freedom Fighter" CFS advocates - patients and researchers alike. You get to really see and hear who cares, and who doesn't. Who fights for your rights as a human being, a patient, a dis-abled person, and who likes to drag your misery and money to their nearest savings account. You get to get your heads together and plan "hope" and strategy .. just like Paul Revere did in that same town. Our great government health institutions are failing the American People, and even more, us. Just like the "Freedom Fighters" we see those "Redcoats" all lining up to fight us. We may lose a battle here and there, but we have that "fighting spirit" in us, and in the long run, we will win. Our numbers are ever increasing and we may go home sicker than we came, our "pay," but we can smile and say "I did the right thing and went and fought for US, for YOU! WE need YOU, too!! We ask you to be a part of US ... to help US, too, ... to help YOURSELF ... to help the next little child who is going to get this and have their entire social foundation and formative years completely wiped out, and as Dr. Alan Gurwitt's story told, have these children "wish for purple spots," so their friends could see they "had" an illness and were sick. The next event is the April CFSCC meeting in Washington, DC, April 21-22; the Washington Rally for Awareness Day, May 9th at the Capitol Building; and May 12th Lobby Days, May 11-12 in Washington. The next AACFS meeting is October, 2000. (I heard that Denver may be the next place.) IF EVERYONE tried to make at least ONE of those, think of what we could GET DONE!!! Think of the CFS history YOU could help make! An AIDS ACT-UP activist was there and may show us how to get more attention for the disease. Dr. Lee even said to do it now - the NAME, workable DEFINITION, and new ICD-9/10 codes!! "AIDS now gets $1.7 Billion per year!" Dr. Lee reported to the audience. MOVE an agreement forward to the CFSCC!! WHAT ARE YOU WAITING FOR?
I attended an evening session with Dr. Lapp, Dr. Jason and Albert Donnay on these last two issues. Dr. James Jones was sitting right immediately behind us. Almost EVERY single time a PWC or anyone stated a good idea or made a or-CFIDS statement, he would immediately begin to moan loudly, and say, "no ... noooo .. no ... no ...... ". He told physicians (learning about CFIDS) in that room that "kids will get well and over CFS." That their "problem was basically hormones and peers!" He asked us Should we REALLY concentrate on an illness with no etiology, no treatment?" That we should ask, "What illness IS present?" ... "There is - NO - CFS!!!"
Dr. Jason, et al, has prepared a paper, "U.S. Case Definition of Chronic Fatigue Syndrome: Diagnostic and Theoretical Issues," a 55-page manuscript highlighting conceptual and operational difficulties inherent in the current definition of CFS, with suggestions to alternate approaches.
After the name panel and all the discussion was finished at another late night session for YOU, Kim Snyder showed us a portion of her work-in-progress documentary film, "I Remember Me." This is the kind of film you would want everyone you know to see.... For those of us barely hanging on from the day-long sessions. the banquet and the name panel, this was a sobering account of the reality of this illness and the horror stories that go with it. I met Kim in San Francisco at the 1996 AACFS Conference. Her film has come a long way since then, and she needs a connection for someone or company to help her finish producing it...and like most of us doing something FOR YOU. financial help. This is a great documentary and she deserves help in getting it finished and out so the public can understand this disease!! You can call Kim, if you can help, at 212/627-5277. Please.
Beth Honeycutt, Support Network Services Director, will be leaving the CFIDS Association of America on December 17, 1998. I will miss her compassionate help she has always given to me, and so many others. Thank you, Beth and I wish you much luck in your future pursuits.
I wish to thank Bonnie Gorman, Sara Bass, Jill McLaughlin and Tom Hennessy for their help and kindness at the Boston Conference. I also wish to thank Anita, Meghan and Lori for their support. And last, but not least, I wish to thank my Mother, Betty Spencer, for having to travel with me so I can try to help others with this disease, and for "watching over" all my friends there as well.
I urge you to read my speech I gave at the The Name Panel Session, as it is in serious conflict with my belief for a name change now, with a recent article in a well-known national CFIDS group's journal, especially since I have been at the last 4 CFSCC and AACFS meetings and have never seen this individual there - at all. My speech was taken out of context and used in bad faith. Also read my "Name Game" speech I gave at the
CFSCC last April before Surgeon General Dr. David Satcher. It's important for the CFIDS Community to know that the public testimonies were re-written, and shortened, while others were lengthened, and other public comments were not written in the minutes at all. This is NOT how public, government documents should be disseminated.
The following is a summary of a few of the over 90 presentations given at the biannual American Association for CFS scientific conference held during October, 1998, in Cambridge, Massachusetts. IA more in-depth and comprehensive report on this conference will appear in the Winter 1999 issue of UPWO News. -- Ed. note.]
Dr. Roben Suhadolnik presented much more extensive work on his possible biological marker for CEIDS.
The damaged protein is showing up significantly more often within a subset of CFIDS patients than in healthy controls.
\rery similar findings have bow been shown by two other studies. Professor Anthony Komaroff, a noted crms researcher and clinician from Brigham and Women's Hospital in Boston, commented that this is not yet proven as a diagnostic marker for CYIDS, and there needs to be more studies, in particular, studies that make comparisons to patients who have other illnesses.
New epidemiologic studies seem to show similar prevalence figures as did recent studies: between 1 and 4 per one thousand adults in the USA have a CEIDS-like illness. [See report on CDC prevalence study in this newsletter.]
A study by Dr. Nancy KImas shows low level immune activation in CFIDS, and in particular, that the level of activation of cytotoxic T-cells seems to correlate well with the patients' reports of how seven their illness feels.
Dr. Wilhelmina Behan presented a study showing that potassium may be leaking from cells in CFIDS patients. This may be related to noted energy loss.
Dr. Dharam Ablashi's paper showed that the HHV-6 virus seems to be re-awakened in CFIDS, hut also in multiple sclerosis. Dr. Konstance Knox also presented her work on BHV-6 in CFIDS, stating that her studies "demonstrate that a sizable proportion (30% to 70%) of patients with CFIDS suffer from an active persistent infection with HHv-6, which may account for all, or many, of the clinical manifestations of their disease. " She concludes that active HHV-6 infections "may be especially prevalent in patients with CNS [central nervous system] involvement, consistent with the highly neuroinvasive nature of HHV-6."
Dr. Bellanti conducted a randomized placebo-controlled study of NADH treatment in CEIDS. His results seemed to show a correlation with some improved health.
Dr. Greta Moorkens studied the use of growth hormone as a treatment which had previously been studied by other researchers In fibromyalgia. The CEIDS study seemed inconclusive, with standard measures showing no significant improvement, yet some patients were able to return to work and one reported a recovery. Prof Komaroff commented that these studies need further research.
Ampligen trials were reported on by Dr. David Strayer, Medical Director of Hemisplierx Blopharma, Inc. Improvements were indicated for a large number of patients, especially those that tested positive for the ItNase L marker being developed by Robert Suhadolnik.
A presentation by Ampligen trial patients in a separate session was enlivened by the presence of Manuel Asensio, the Wall Street investment advisor who is in a pitched financial and legal battle with the drug's manufacturer, and who is seeking to downplay the medical value of the drug. In contrast, Dr. Daniel Peterson of Incline Village, NV, stated at the session that his 12 years of experience with 70 patients in Ampligen trials shows the drug to be safe and effective, but good responses are seen only in selected patients and it is very important to select the right patients.
The "Name Change" session had about 50 attendees. Most people who testified urged that the name be changed as soon as possible, but a few stated that efforts would be better spent in promoting education campaigns using the current name. Several attendees commented in favor of Dr. Charles Shepherd's recommendation to use either "myalgic encephalopathy" or "chronic myalgic encephalopathy.'t Kim Kenney of the CrifiS Association of America gave results of a survey of doctors and scientists that was circulated at the conference. The results seemed to show an awareness of stigma issues but no strong interest in changing the name in the near future. The survey asked whether adding an eponym would be an effective step. Fewer than 10 percent of the respondents thought that would lead to positive changes. However, the survey did not ask about backing an eponym with a high-profile educational campaign to change the image of the illness as has been widely discussed. [Medical Professionals with CFIDS President and Co-Founder Gail Dahlen, R.N., presented testimony at the "Name Change" session.-- Ed. note.]
This is only a portion of the over 90 research topics and conclusions presented at the 4th AACFS Conference, October 1998. I have included only the proceedings which I found to be relevant, with only a few comments. Those papers which I felt deserved special attention have been marked with [***]. Many thanks to Mary Schweitzer, Ph.D. (and MPWC webmaster) for putting these proceedings on her website for ALL PWC's and other interested patients, physicians, and parties who were unable to attend the conference. The complete conference proceedings can be found at http://www.cfids-me.org/aacfs/. Links in the summaries below refer to the particular website with the complete session or paper abstracts from which the summaries were drawn.
-- Gail Dahlen, RN.
Authors: Leonard A. Jason, Karen M. Jordan, Judith A. Richman, Alfred Rakemaker, Cheng-Fang Huang, William McCready, Jennifer Shlaes, Caroline P. King, Dana Landis, Susan Torres, Trina Haney-Davis, Erin L. Frankenberry
Conclusion: Findings indicated that fatigue is common in urban populations, but that prolonged fatigue and chronic fatigue occurs in only about 5.0% to 7.7% and 2.6% to 4.1%, respectively, of the sample of the population.
Authors: Karen Jordan, Ph.D., Penny Ayers, Kari Taylor, and Leonard Jason, Ph.D.
Conclusion: Fatigue and symptoms of CFS do indeed strike children and adolescents. This preliminary research demonstrates that even younger children do display CFS symptoms and definable fatigue and that they are very similar to adolescents in number and frequency. Similarly, both boys and girls appear to be stricken by fatigue and CFS symptoms, although there are differences in the types of symptoms most commonly striking each gender. Further work is in progress to evaluate these children medically and psychiatrically in order to allow firm diagnoses to be made and for further description of this group.
Authors: Han K. Kan, Ph.D., Clare M. Mahan, Ph.D., Kyung Y. Lee, Ph.D., Carol A. Magee, Ph.D., Benjamin H. Natelson, M.D.
This survey is one of a few population-based studies of Gulf veterans and suggests that CFS may account for a significant portion of Gulf veterans who complained of medically unexplained constellation of symptoms.
Authors:KG Manu, Colby College, Waterville, Maine; S Pollack, St. John's University, Queens, New York; and P Manu, Albert Einstein College of Medicine, Bronx, New York
OUR NOTE: Dr. Peter Manu has disclosed that he is a paid consulant for Metlife Insurance Company (see the official Disclosure Statements listed above in the MPWC Conference Report). During the formal question and answer period after Dr. Manu's presentation, Judy Morris, M.D., asked Dr. Manu if Metlife had given him the cases he used in his study, and he answered yes. She then asked how Metlife selected the 112 cases that they sent him, and he said he had no idea. There is thus no way to judge whether or not the sample used for this study was collected in a statistically unbiased fashion, an omission which casts serious doubt on the validity of the conclusions of the study.]
Authors: M. Reyes Ph.D., R. Nisenbaum, Ph.D., G. Stewart, M.A., W.C. Reeves, M.D. [all of the U.S. Centers for Disease Control]
OUR NOTE: The abstract for this paper was printed in the proceedings booklet before the study was finalized. The research findings that were actually presented was released to the press, and picked up by both Reuters News Service and the Boston Globe. Both the study conclusions and the Globe article can be found at the CFIDS Association of America's website, at New CFS Prevalence Figures.
Conclusion: Analyses of these data will provide the first population-based estimate of the prevalence of fatiguing illness. We are longitudinally monitoring these respondents to study the clinical course of fatiguing illness and to identify incident cases of CFS. [At the actual session, principal investigator William Reeves, MD, chief of the CDC branch responsible for studying CFS, reported that earlier estimates published by the CDC of 6.4 to 10.8 cases per 100,000 adults must now be revised upward six-fold. The most recent evidence now indicates a CFS prevalence rate of 183 per 100,000 persons aged 18-69, which would indicate that at least 370,000 U.S. adults have the disease. This brings the CDC estimates more in line with other studies such as the one conducted by Lenny Jason et al (see above) and the study published in 1995 by Dr. Dedra Buchwald of the University of Washington and Dr. Anthony Komaroff of Harvard University. According to the CDC report as presented at the conference, CFS must be considered a significant health risk, particularly to women, among whom the prevalence rate was 303 per 100,000. "To put this into perspective, CFS is three times more common than HIV infection in women (125/100,000),
25 times the rate of AIDS among women (12/100,000), and is considerably higher than a
woman's lifetime risk of getting lung cancer (63/100,000)," Reeves stated at the Conference.]
Authors: Nancy F. Hill, Lana A. Tierskv, Vanessa R. Scavalla, Benjamin H. Natelson
Conclusion:This study shows that for the severely ill subset of CFS patients studied here, the majority show no symptom improvement and only 4% of the patients recovered. However, in the remaining 39%, improvement in CFS symptoms did occur. Further studies investigating the illness at closer and more numerous time periods is recommended.
Authors: L.M. Forsyth, M.D.; A.L. MacDowell-Carneiro, M.D.; G.D. Birkmayer, M.D., Ph.D.; H.O. Preuss, M.D. and J.A. Bellanti M.D. Departments of Pediatrics and Microbiology-Immunology and the Immunology Center, Qeorgetown University Medical Center, Washington, D.C.
The results of the present study not only suggest that NADH is a safe, naturally-occurring biologic substance which may be a useful therapeutic adjunct in the management of chronic fatigue syndrome, but also that the measurement of urinary 5-HIAA may serve as an important predictive marker of neurocognitive dysfunction, as well as an objective measure of improvement following therapy.
Authors: Nancy Klimas, Mary Ann Fletcher, Kevin Maher, Roberto Patarca, Jean Walling, Mack Smith, Lauren Vitek*, and Herb Bresler**, *Neoprobe Corp, Dublin Ohio; **Ohio State University, Columbus, Ohio; and University of Miami School of Medicine and the Miami Veterans Affairs Medical Center, Miami, Florida.
Conclusion: There have been no adverse events related to the lymph node resection itself. The final product in the pre-clinical and clinical subjects consists of highly activated polyclonal populations of memory CD4 and CD8 cells, expanded 10 to 100 fold from the initial sample. The initial 3 clinical subjects have had minimal-to-no adverse reactions in the initial weeks of therapy. Subjects' health status, phenotyping and cytokine expression of peripheral blood cells will be followed for 6 months.
[OUR NOTE: Dr. Klimas reported there have been no adverse side effects or health events related to the the biopsy or cell re-infusion seen in the patients tested at this time. This therapy has been successful in studies done with cancer and other chronic viral illness patients.]
Authors: G. Moorkens*, H. Wijnants*, R. Abs**
*Department of Internal Medicine0 and Endocrinology
**University Hospital Antwerp, Belgium
Conclusion: To our knowledge , this study is the first to use GH therapy in patients with CFS. The administration of GH induced important changes in body composition. Although all 17 patients reported feeling better no significant improvements were recorded in the NHP and QoL-AGHDA questionnaires. Further studies are necessary to confirm these findings and to investigate the changes in body composition and metabolism of amino acids.
Authors: David R. Strayer, William A. Carter, Thomas J. McCarron. Hahnemann/Allegheny University and Hemispher, Biopharma Inc.; Philadelphia, PA
Conclusions: In summary, a review of long-term results using Ampligen ® in CFS demonstrates the therapeutic advantages of the treatment as revealed in the magnitude of KPS improvement. The 22 patients in the extension phase had an average KPS change of 29.9 and a baseline standard deviation of 11.6. This KPS change represents a large physical improvement, which is highly significant (one-sided paired t-test, p < 0.0001). In conclusion, physical performance improved dramatically with the supplemental Ampligen ® treatment provided in the extension phase and the Ampligen ® treatment was generally well-tolerated.
Authors: H. Moldofskv, F.A. Lue, J. Dickstein, L. Poplonski, C.G. Jiang, R. Gorczynski;
University of Toronto Centre for Sleep and Chronobiology, Toronto, Ontario, Canada
Conclusions: In comparison to normal symptomatic and asymptomatic subjects, CFS patients show altered diurnal patterns in cortisol, prolactin, and NK cells that accompany the alpha EEG sleep disorder, and daytime fatigue, sleepiness and pain. These findings are consistent with the theory of chronobiological disturbances in CFS. [See Moldofsky H. Adv. in Neuroimmunology, 5:39-56, 1995.]
Authors: Konstantin Konstantinov, Mark Daniels, Li Yang, Larry Gerace and Eng M. Tan. Autoimmune Disease Center and Department of Cell Biology, The Scripps Research Institute, La Jolla, California.
Conclusion: CFS patients have autoantibody responses which target epitope or epitopes in the N-terminal region of lamin B1. An immuno-slot blot assay comparing reactivities between the N-terminal fragment and full-length lamin B1 appears to be the best discriminant to identify this auto antibody.
Authors: Aristo Vojdani, Paul Choppa, Cathy Tagle, Lilia Magtoto, and Charles Lapp; Immunosciences Lab., Inc. and the Hunter-Hopkins Center, Beverly Hills, CA and Charlotte, NC.
Conclusions: Enhancement of the interferon-induced enzyme PKR at the mRNA and protein level, along with elevated apoptotic cell population in CFS patients, may contribute to the pathogenesis and the fatigue symptomatology associated with CFS. [See Vojdani, A; Ghoneum, M; Choppa, PC; Magtoto, L; Lapp, CW; Elevated Apoptotic Cell Population in Patients with Chronic Fatigue Syndrome: The Pivotal Role of Protein Kinase RNA. J. Internal Medicine 242:465-478, 1997.]
Authors: S. Wagner, M.S.; L. Helder, Ph.D.; N. Klimas, M.D.; M. Antoni, Ph.D.; R. Keller, M.D.
Conclusion: These findings suggest that the degree of cellular immune activation is associated with the severity of CFS-related physical symptoms, cognitive complaints, and perceived impairment secondary to CFS. Specifically, elevations in T-helper/inducer cells, activated T-cells, activated cytotoxic/suppressor T-cells, and CD4/CD8 ratio are associated with greater disease severity. Furthermore, reductions in T-suppressor/cytotoxic cells also appear related to greater severity of CFS-related physical symptoms and illness burden, suggesting greater symptoms are associated with lower availability of regulatory T-cells.
[OUR NOTE: Dr. Klimas reported that lymph node morphology and cell activation status in CFS showed a predominance of activated T-cells which were higher in the lymph node samples than in the peripheral blood samples taken at the same time.]
Authors: O. Zhang, B.H. Natelson, X.D. Zhou, T. Denny, J.E. Ottenweller, W.C. Gause
Conclusions: The data provided support for the immune dysfunction hypothesis in the CFS veteran group, but not in the CFS civilians. However, instead of having Type II responses, the CFS veterans showed a general upregulation of cytokines and T cells and a decreased percentage of NK-cells. One interpretation of the immunological differences exhibited by CFS Gulf vets is that immune dysregulation plays a role in the genesis of this epidemic presentation of CFS. However, differences between the veteran groups in terms of sleep, chronic stress, and level of activity also could contribute to produce the differences.
Authors: D. Fairhurst*, M. Waterman*, S. Lynch**
*Cognitive Group, School of Psychology, University of Leeds, Leeds LS2 93T
**Dept. of Psychiatry, School of Medicine, University of Leeds, Leeds.
Conclusions: Perception of fatigue does vary with objective measures of performance speed. This appears to be independent of comorbid anxiety and depression. The CFS group appears to perform more slowly than controls in tests with a higher conceptual-processing load. These results are discussed within the framework of a more specific profile of cognitive slowing in CFS.
Authors: D.V. Ablashi*+, S. Marsh*, M. Handy*, J. Whitman*, D. Viza**, O. Krueger***, and P.H. Levine****
*Advanced Biotechnologies Inc, Columbia, MD
+Georgetown University School of Medicine, Washington, DC
**Laboratoire d'Immunobiologie, Faculte' de Medecine, Paris, France
***Laboratory of Immunopathology, Pathology Institute, University of Köln, Köln Germany
****George Washington University School of Medicine, Washington, DC
Conclusion: The above data support the concept that HHV-6 reactivation or persistent-latent infection is significantly higher in CFS patients compared to healthy donors, suggesting its role in the pathogenesis of CFS. Since IgG antibody prevalence and titers to HHV-7 and HHV-8 were similar to that of the controls, these two herpesviruses did not appear to be associated with CFS. Additional longitudinal studies are necessary to correlate HHV-6 infection and disease manifestation to assess the role HHV-6 plays as a co-factor in CFS.
Authors: Konstance K Knox Ph.D.*; Joseph H. Brewer, M.D.**, and Donald R. Carrigan, Ph.D*.
*Herpesvirus Diagnostics, Inc. and Institute for Viral Pathogenesis; 12346 W. Layton Ave.; Greenfield, Wisconsin 532281 and
**Infectious Diseases; St. Luke's Hospital; Kansas City, Missouri
Conclusion: These studies demonstrate that a sizable proportion (30% to 70%) of patients with CFS suffer from an active persistent infection with HHV-6, which may account for all, or many, of the clinical manifestations of their disease. Active HHV-6 infections may be especially prevalent in CFS patients with CNS involvement, consistent with the highly neuroinvasive nature of HHV-6.
Authors: Robert J. Suhadolnik*, Daniel L Peterson**, Paul R Cheney+, Susan E. Horvath*, Nancy L Reichenbach*, Karen O'Brien**, Vincent Lombardi**, Suzanne WeIsch++, Elizaoeth G. Furr+, Ramamurthy Charubala***, and Wolfgang Pfleiderer***
*Temple University School of Medicine, Philadelphia, PA
**Sierra Internal Medicine Associates, Incline Village, NV
+The Cheney Clinic, Charlotte, NC
++Sierra Nevada College, Incline Village, NV;
***Universität Konstanz, Konstanz, Germany.
Objective: We have previously demonstrated a statistically significant dysregulation in key components of the 2',5'-oligoadenylate [2-5A] synthetase / RNase L pathway in individuals with chronic fatigue syndrome (CFS) [1,2]. In CFS, 2-5A synthetase is present predominantly in its activated form, bioactive 2-5A levels are elevated, and RNase L activity is upregulated compared with healthy controls. A novel low molecular weight (LMW) RNase L (37 kDa) has been discovered in CFS . These studies were designed to determine the extent of these phenomena in less severely disabled individuals with CFS and to identify clinical correlates to these biochemical findings.
Summary: Our working hypothesis has been that the characteristic clinical signs and symptoms of CFS are associated with the dysregulation of the 2-5A synthetase / RNase L pathway. The results presented here confirm and extend our published reports on the biochemical dysregulation of the 2-5A synthetase / RNase L pathway in individuals who are severely disabled with CFS. Evidence is provided indicating that the RNase L enzyme dysfunction in CFS is more profound and complex than previously reported. [See R.J. Suhadolnik et al., Clinical Infectious Diseases 18: S96-S 104 (1994); R.J. Suhadolnik et al., In Vivo 8: 599-604 (1994); R.J. Suhadolnik et al., Journal of lnterfrron & Cytokine Research 17: 377-385 (1997).
Authors:Peter O. Behan*, Abhijit Chaudhuri*, Walter S. Watson**, John Pearn***
*University Department of Neurology, Institute of Neurological Sciences and
**Department of Nuclear Medicine, Southern General Hospital, Glasgow (UK),
***Department of Child Health, University of Queensland, Brisbane (Australia).
Conclusion: Abnormal thallium201-cardiac SPECT scans in CFS similar to those described in syndrome X suggest a common mechanism for both these conditions. An abnormality of membrane ion channel function is considered the underlying mechanism in syndrome X. Increased REETBK; in a subgroup of CFS patients suggests that some CFS patients spend more energy in maintaining essential body function at the expense of the energy available for other physical activities. Since 30% of REE is expended to maintain physiological ion gradients in normal health, cell membranes that leak ions increase REETBK Elevated REE and abnormal cardiac perfusion scans in CFS provide the first objective and indirect support to our hypothesis that symptoms in CFS could be the result of an acquired abnormality of
the voltage or ligand-gated ion channels. It is possible that such alteration of transmembrane ion traffic
could affect normal receptor sensitivity to neurochemicals and neurohormones such as acetylcholine, serotonin or other monoamines, accounting for the neuroendocrine abnormalities previously documented in CFS.
AuthorsK. De Meirleir*, LCLI, I. Campine+*, P. De Becker, B. Van Steenberge*, C. Bisbal**, T. Salehzada**, B. Lebleu**, C.V. Herst*
*Department of Human Physiology, Free University of Brussels, Brussels, Belgium
**Institute of Molecular Genetics, Montpellier University, Montpellier, France
+ I.Campine is supported by funds from the Foundation for Scientific Research, Belgium (F.W.O.).
Conclusion:The presence of a 37 kDa 2'.-5'A binding polypeptide in the PBMC pellets of CFS patients may objectively contribute to distinguish CFS patients from healthy individuals. These observations could provide the basis for the development of a biochemical assay for the differential
diagnosis of CFS and for follow up of its clinical evolution.
Authors: Susan B. Horvath*, Daniel L. Peterson**, and Robert J. Suhadolnik*
*Temple University School of Medicine, Philadelphia, PA;
**Sierra Internal Medicine Associates, Incline Village, NV.
Methods:CFS subjects who met the 1994 CDC criteria for CFS and age and sex-matched control subjects were selected from Incline Village, NV.
Summary: Competition experiments with [32P]pApAp(8-azidoA) and pApAp(8-azidoA) or p3A3 demonstrated that the 2-5A photoprobe is specific for the 2-5A binding site. The 6-fold difference in Kd between the 80 kDa and the LMW RNase L suggests that the LMW RNase L is responsible for the elevated RNase L activity observed in CFS PBMC.
Authors: L. Paul and L. Wood, Division of Physiotherapy and Department of Biological Science, Glasgow Caledonian University, Glasgow, Scotland.
Conclusions: CFS subjects have a 'normal' heart rate response during exercise although they perceive the workload to be significantly greater. A number of gait parameters were altered in the CFS group compared to the controls (step distance, step time, velocity and cadence). Gait analysis, therefore, may prove to be a valid outcome measure in the evaluation of treatment intervention in this group of patients. Gait was not adversely affected by exercise thus the results of this study do not support anecdotal evidence, from CSF sufferers, that activity can adversely affect functional abilities, as assessed by changes in gait pattern. Further studies in progress, using three dimensional motion analysis of gait, may provide more specific information on the kinetics of the gait pattern in CFS subjects.
Authors:Arnold Peckerman, John J. LaManca, Sharon L. Smith, and Benjamin H. Natelson;
NJ CFS Research Center, University of Medicine and Dentistry of New Jersey
Conclusion: These findings suggest the possibility of a low flow circulatory state in the most severe cases of CFS. In patients with a less severe form of CFS, a diminished blood pressure response to a
cognitive-behavioral (speech presentation), but not to an aversive-sensory (the cold pressor test) stressor may indicate a defect in the higher cortical modulation of cardiovascular autonomic control. In this latter group, situations may arise where a demand for blood flow to the brain may exceed the supply with a possibility of ischemia and a decrement of function.
Authors: S.A. Sisto, J.J. LaManca, A. Peckerman, B. Natelson
Conclusions: Patients with CFS demonstrate a hyporesponsiveness to a cognitive stressor
before exercise. Exercise produces the expected attenuation of the cardiovascular responses in the healthy group, but not for the CFS patients. Since CFS patients have lower systolic blood pressure and heart-rate responses compared to their healthy counterparts, they may not be able to exhibit the expected range of response to either cognitive or exercise stressor. This hyporesponsiveness may, in part, be responsible for CFS patients reporting detrimental effects of periods of psychological stressors or excess physical exertion.
Authors:Julian M. Stewart, Amy Weldon, Karl Li, Nina Arlievsky, Jose Munoz
Conclusion: We conclude that chronic fatigue syndrome in adolescents is highly related to orthostatic intolerance in adolescents. The orthostatic intolerance of CFS has heart-rate and blood pressure suggesting the orthostatic tachycardia syndrome and HRV abnormalities consistent with a partial autonomic defect. Such a defect may contribute to symptomatology in these patients.
Chronic Fatigue Syndrome. Like most of you, I cringe every time I have to tell someone what kind of disease I have...as I know I will have to go into explaining that this devastating disease involves a huge list of more serious symptoms than fatigue, as the name implies.
If you think the name of this disease is ok, then you haven't experienced the shocking and vast discrimination that the majority of us have had to endure because of the name. If you think we need to wait for a very specific cause to properly name this disease, at the rate our health institutions are studying the physical abnormalities of CFS, all of us here will probably be pushing up daisies before our federal scientists find an absolute, specific, physical cause. Today there are many abnormal, multiple organ and system research data available to suggest possible testing for CFS patients. Even with numerous tests that, now, can show physical abnormalities in patients, the name CFS continues to hamper a lot of money going into research studies for this terrible disease, thus delaying it's cause, markers, treatments and it's cure.
There is one internet site today that has over 1,200 studies listed in a bibliographic database. The AACFS site has " over 2,100 recent as well as historic references." It suggests to me that our federal scientists "studying" this disease has a case of "Chronic Lethargic Syndrome" with all the psychological implications they have branded patients with. Many of their "abnormal psychological studies" do not follow rigid, scientific methods, nor their very own diagnostic criteria. Our real CFS researchers many times not only use the CFS case definitions of this country, the United States, but of other countries as well. Yet, their studies continue to be "mysteriously" banned from "highly respected" medical journals.
Case in point, Dr. Thomas Glass' studies on our pets. This was a transmission study. He had to abandon these very important studies because he had no research monies. Our federal health officials would not grant him any money. This is what scientists DO in labs to research diseases like ours. They STUDY animals. How many of you have seen studies like this with our disease? How many of you have seen federal grants for such important and routine studies? Dr. Glass, also, was "mysteriously" banned from "respected" research journals, even though, these journals praised him for the high quality of scientific methods he had used. He went to a prominent, inter/national support group and waited three years to get his important findings published in their journal, and they turned him away, too. I had to track Dr. Glass down, and our small newsletter finally published his important research. Patients who had donated the bodies of their beloved pets, with all the other things they had lost, had been waiting for years to see his research.
We may be sick......but, we're not stupid. The word is out. If you see the name of a research study on Chronic Fatigue Syndrome wanting to be published, unless they are on "the list", forget it. The name has even affected our innocent, beloved pets.
Our disease has had numerous outbreaks in schools, hospitals, work places, communities with pain-staking documentation, including, careful, in-depth laboratory testing with abnormal results. DeFreitas, Bell, Cheney, Nicolson, Jason, Hyde, Martin, Goldstein, Glass, Klimas ...these are just a few dedicated, REAL CFS researchers who know how the name effects us, that this is a horrible physical disease, and with little or no help from our federal health institutions, continue their quest to help us. They STUDY our disease, some with the most advanced techniques and technology, sometimes under very difficult situations.
The name affects monies to special CFS Clinics. A San Francisco clinic recently, had to close down, because of lack of funds. Those patients are out on their own, now, sick, looking for help. This is abominable.
Re-naming this disease is a number one priority in my book. It always has been. I believe the most appropriate thing to do is to supply, add on, if you will, an appropriate, non-discriminatory eponym to our disease, until we can properly name it with a physiologic cause or marker. Such as with "Lou Gehrig's Disease." A name we can all live with in the CF(ID)S communities. The official name, CFS, has gone on for 10 years. It hasn't done us any good. It has influenced researchers from not researching, community charities from not helping us, delayed disability benefits (many times for years) to the point of PWC's losing everything they had worked for for decades, and insurance companies are cancelling and/or re-writing their policies to terminate CFS patients after a few years. So much for the "great" benefits we were promised. This is not the American way! The name has caused all of this! I know it! You know it! They know it!
Stephen Straus, M.D. and Janet Dale, R.N. wrote a 20 page article for the NIH in 1992, The Chronic Fatigue Syndrome: Considerations Relevant to Children and Adolescents. In their first sentence, they say "Increasing lay and professional attention has been placed over the past decade [my emphasis] upon an illness that is now commonly referred to as ...CFS. The salient feature...is...debilitating or easy fatigueability."
First of all, this paper suggests that children have this disease. We know they do! Yet I did not see their research, survellience studies or statistics. Did you? How do they come to the conclusion it is "a predominantly ...adult disorder," when in 1992, there were no published survellience studies done on kids with CFIDS.
Secondly, what is this statement saying "that it is commonly referred to as...CFS"? Commonly referred to, to me, would be something like ME (Myalgic Encephalomyelitis) or even CFIDS. The official name IS CFS, isn't it?
On pages 72-73 of this public document, there is "A Partial List of Differential Diagnoses for Protracted Fatigue." In this document, the NIH has actually included a list of disorders that include "protracted fatigue," such as: *Allergy, *Autoimmune-related rheumatologic disorders, *Cardiovascular, *Gastointestinal disorders, *Hematologic, *Infectious diseases, *Metabolic and endocrine, *Acute intermittent porphyria, *Neurologic, *Pharmacologic agents and other drugs, *Toxin exposure, *Psychiatric and behavioral, and *Lifestyle choices. Under these heading are some 73 diseases!!!.
Now, tell me, could any CFS symptoms and/or abnormal tests come under these headings? Of course they can! Because of the name, our physicians have to rule out seventy-three diseases which also happen to have "protracted fatigue" as a symptom among many, just to get to CFS! This is still going on today! Remember, this is only a partial list!!! None of these 73 diseases have the word "FATIGUE" in their official name, even though they do have "protracted fatigue" in their symptomatology, as do tens of hundreds of other diseases. And, many, many of these listed diseases do not have a cause, marker or cure.
Remember, Sir William Osler taught his students of medicine to listen most of all to their patients. I have heard it said that a fifth-grader can pick out CFS patients just by listening to them for about 15 minutes.
CFIDS replaced the name of CFS. Others will, too. It will only require our repeated use and education to the public and medical community. This, we have experience in. It will take persistence. This, we have experience in, too.
Let's put an end to the misconception and misunderstanding of this terrible disease. M/PWC's have been advocating for a name change for years now.
To those physicians on this CFSCC Committee, remember the Hippocratic Oath and the words "First, do no harm." Give this disease the respect it deserves. Give this disease a respectful name that will not harm patients any longer. Remember your oath!
Dr. Lee Accepts Rudy Perpich Award
Dr. Lee's Acceptance Speech
I am honored to receive the Rudy Perpich Award Particularly because Governor Perpich was a great public servant and CFS advocate and because the first recipient was my Stanford Medical school class mate, Dr. Alexis Shelokov. Sorry I can't be here Sunday with family.
In accepting this award, I want to acknowledge particularly the contributions of five individuals to my education: Dr. Shekolov, whose contributions to our understanding of chronic fatigue syndrome extend over more than 40 years; to Dr. Jay Levy of UCSF who has been an innovative and courageous investigator, not only of chronic fatigue but of HIV/AIDS; Elizabeth Roberts, a dear friend and one who has educated me about Chronic Fatigue Syndrome from a patient's perspective of the past 20 years; and Jan Montgomery and Marya Grambs for engaging me in CFS policy 10 years ago when I was president of the San Francisco Health Commission.
I also want to take this opportunity to express myself on an issue that you will be considering at a forum on Monday evening - the change of the name of chronic fatigue syndrome. It is time for a change.
Chronic Fatigue Syndrome, Wedner tells us, is neither a disease nor a syndrome. It is a committee definition. My own experience with CFS probably began in the 1950's. I was a fellow at the Mayo Clinic in 1953-1955. One of my most common diagnoses was clinical nervous exhaustion - was some of it CFS? The 1988 working case definition of Chronic Fatigue Syndrome was an important step in facilitating prevalence surveys but it did not differentiate CFS from other types of chronic fatigue.
In 1993, CDC convened the International Chronic Fatigue Syndrome Study Group, which developed a revised definition of Chronic Fatigue Syndrome. Chronic Fatigue Syndrome was defined as self-reported persistent or relapsing fatigue lasting six or more consecutive months. In addition, four or more of the following symptoms must be currently present:
impaired memory or concentration;
tender cervical or axillary lymph nodes;
multiple joint pains;
unrefreshing sleep; and
During the past decade there have been important developments related to CFS. Most important has been the knowledge gained from research, some funded by NIH and CDC, including prevalence surveys as well as a number of other surveys by CDC. Conferences on CFS in 1989 (San Francisco), 1990, 1992, 1994, and 1996 helped summarize research advances and disseminate information to researchers and practitioners. But there remained a great deal of uncertainty about CFS among clinicians, including academic clinicians specializing in infectious disease. In 1995, CDC published The Facts About Chronic Fatigue Syndrome, an excellent summary for clinicians. Also in 1995 an excellent paper by Sekuda and Gantz on management strategies for chronic fatigue was published. The publication in 1997 by the American Journal of Medicine of the proceedings of the 1996 research conference was another step forward. This week's meeting is further evidence of progress.
If there has been so much progress in the past ten years why is it time to change the name of CFS?
First and foremost, most physicians have no respect for the name and it sends the wrong message.
Second, the approach to CFS is now dominated by the biopsychosocial approach that gives excessive emphasis to the social, behavioral, and emotional factors in the presentation and perpetuation of symptoms. The "bio" seems to be missing. While I believe in the psychosocial determinants of health paradigm, this approach to CFS has gone too far.
The problem is evidence in the proposed ICD-9 codes for CFS, and the 1996 report of the Joint Working Group of the Royal Colleges of Physicians, Psychiatrists and General Practitioners on Chronic Fatigue Syndrome in the United Kingdom. The Royal Colleges convened a working group after a request from the UK's Chief Medical Officer. The group recommended that the term encephalomyelitis be dropped in the UK and that it be replaced by CFS.
In its editorial comment on the report of the working group, Lancet noted, "Psychiatry has won the day for now. A decade hence, when an organic cause for at least some cases of CFS have emerged, it would be tempting to ask the committee to reconvene. We believe that the report was haphazardly set up, biased, and inconclusive, and is of little help to patients or their physicians.
Dr. Stephen Straus of the NIH had a very different view and one that I strongly disagree with. He wrote in the British Medical Journal: "The report constitutes, arguably, the finest contemporary position statement in the field, and physicians and patients are well advised to read it, but it is sure to engender disagreement on both sides of the Atlantic." Indeed, it has engendered disagreement.
Third, the current approaches to CFS, except in a few hands, do not take sufficient cognizance of the research on brain positron emission tomography, cognitive function, possible biomarkers, electron microscopy, the evidence from past outbreaks, or a number of the studies presented here.
Finally, the overlap of symptoms with Gulf War Syndrome, fibromyalgia, and multiple chemical sensitivities merit a thorough re-examination and the development of a comprehensive strategic plan for research. We owe it to the thousands of individuals who suffer from these chronic debilitating diseases to place these issues squarely on the national research agenda.
As a first step, I hope the Association will debate the name issues actively on Monday, reach a conclusion, and strongly advocate a change before the Department of Healh and Human Services Chronic Fatigue Syndrome Coordinating Committee on Tuesday.
Let me close with [a story told by Lyndon Baines Johnson about Winston Churchill, concluding] "so little done, so much to do."
Dr. Philip Lee
Assistant Secretary of Health, US DHHS 1993-1997
Institute for Health Policy Studies
1388 Sutter Street, 11th Floor
San Francisco, CA 94109
MPWC'S WOULD LIKE TO CONGRATULATE DR. LEE FOR RECEIVING THIS AWARD AND THANK HIM FOR HIS DEDICATION AND COURAGE.
News from NIAID
Some CFIDS Patients Benefit from Low Dose Steroids,
Side Effects Risky
SOURCE: PRESS RELEASE, 22 SEPTEMBER 1998
Low doses of the steroid hydrocortisone can cause slight improvement in some CFS symptoms but at the risk of inducing adrenal suppression. This finding, say NIAID researchers, precludes the use of hydrocortisone in people with the illness. Their report appears in the September 23/30 issue of JAMA.
"The data show that about half the people on placebo and 2/3 of those taking hydrocortisone reported some improvement in well-being," comments Stephen Straus, MD, senior author of the study. "The greater benefit seen in the hydrocortisone group, however, was modest and there was clear evidence of adrenal suppression by the drug. It was manageable and completely reversible, but it's the kind of suppression that in the context of the minimal improvement afforded by the drug cannot in our minds, justify using this treatment for CFS."
A JAMA editorial accompanying the hydrocortisone report notes that some people with CFS manifest neurally mediated hypotension, an abnormality of blood pressure control. Preliminary published data suggest that treatment with fludrocortisone, a steroid drug that helps the body retain salt and water, may be beneficial.
Although the new JAMA report does not support the use of hydrocortisone, a second trial led by Dr. Straus at NIAID with scientists at Johns Hopkins is attempting to supplement a different class of steroid hormones produced by the adrenal gland.
"The fact that the treatment worked to some degree," says Straus, "was encouraging, but we would expect to see a greater benefit if low cortisol levels were directly responsible for symptoms of CFS. The amount of CRH [cortisol releasing hormone - Ed. note] may be more important than the amount of circulating cortisol because CRH receptors are located in the brain, and it is an important substance for stimulating mood, attention, and activity. Unfortunately, we don't have convenient ways of supplementing CRH."
However, supplementing other adrenal steroids, as is being done in the currently open trial of fludrocortisone may yield a more beneficial treatment effect, adds Straus, because the regulation of the hypothalamic-pituitary-adrenal axis is not as sensitive to changes in the circulating levels of these steroids.
For more information about participating in the NIH/Johns Hopkins study, call
NIAID at 1-800-772.5464 (extension 659) or
Johns Hopkins at 1-410-821-7253.
By Roger Burns, CFS-News, and Lori Clovis, MPWC News
In recent months the number of reports in the media and online of children diagnosed with CFIDS being forcibly removed from their families by local authorities has shockingly increased. According to noted author and CFIDS child advocate Jane Colby, there have been at least five cases in Great Britain alone in which children were removed from their parents' custody and placed in psychiatric institutions. Dozens more children live with the constant threat of removal and the uncertainty and terror associated with it.
Colby, in her efforts to fight this trend, is requesting that persons with CFIDS who have had any experience with Cognitive Behavioral Therapy, reportedly the treatment of choice at these institutions, send her a brief written account of their experiences so that they may be admitted as evidence in a pending court case.
Colby stated that there are certainly many more than five cases of children incarcerated against the will of their families. One case, about "Child X," was broadcast on Channel 4 News (Britain) on August 26, 1998. A court injunction has for now blocked any public discussion that would reveal the identities of the family or the psychiatric hospital involved in the case. The Channel 4 News report said in part:
The court has ordered that he be treated in a locked hospital ward. His parents had wanted to care for him at home. The police raided their house. Child X's [parent] was jailed until the boy was handed over for compulsory psychiatric treatment.
Channel 4 asked British psychiatrist Simon Wessely to comment on these kinds of cases. Wessely responded that they were so rare that discussing them distracts from the real business of how to manage and treat CFIDS.
Child expert Jane Colby stated that many parents whose children have, or are threatened to be, removed are afraid of speaking up about their cases in public or to advocacy organizations for fear that the authorities will deal more harshly with them.
If you have any information which could help Dr. Colby in her efforts to help these children, please contact her at the following address:
Ted Shaw reports that the situation is much the same in Australia. Shaw described a very ill 15-year-old young lady who is presently institutionalized in the psychiatric unit of a hospital in that country who was forcibly removed from her mother's care. He also stated that at the recent international CFIDS medical conference in Sydney, noted pediatrician and pediatric CFIDS expert David Bell, reported that he personally knew of over 20 cases in the United States where the parents of children with CFIDS had been threatened with the removal of their children from their care.
An article by Max Daly in the August 17- 23, 1998 issue of The Big Issue, a British weekly magazine, entitled "Inhuman Scheme Forces Children Into Psychiatric Units" describes several such cases in Britain. In one of these cases, a young girl's parental visits were dependent upon how often she was ill, and in another, a young boy told his parents that the treatment he was receiving was making him more ill. The article goes on to describe how children with CFIDS are removed from their families by local police and social workers despite the intervention of their doctors who have diagnosed them with the illness and prescribed treatments other than CBT. exercise, and psychotherapy, calling the practice "inhuman."
Another article which appeared in The Scotsman on 28 August 1998 reported that a twelve-year-old girl from East Lothian, Scotland, who had been diagnosed with CFIDS/ME had been forcibly removed from her mother's care because the mother insisted that her daughter's illness was physical rather than psychiatric and should be treated as such. The girl had been diagnosed by two physicians including noted CFIDS specialist Dr. Nigel Speight, but because the doctors were located a considerable distance from the girl's home and her local physician had refused to also make the diagnosis of CFIDS, she was sent. to the pediatric psychiatric unit at Newcastle General Hospital for three weeks. During that time her condition deteriorated so severely that she left the institution in a wheel chair.
There have been similar instances in the United States. One such case involved a 12-year-old boy from western New York. The child was diagnosed by at least two physicians as having CFIDS, including pediatric CFIDS specialist David Bell of Lyndonville, New York. Despite receiving the diagnosis and supporting documentation from the doctors prescribing the limitation of school attendance, the boy was forcibly removed from his mother by police on a street near the boy's home. The boy was placed in foster care, and his mother, who has also been diagnosed with CFIDS, spent several days in jail. Fortunately, this case has a happier ending: during a legal proceeding, a judge agreed with the family's physicians and returned the boy to his parents.
Such cases seem all too shocking when we read about them in the newspapers and hear about them on television news programs. Unfortunately, the recent ascendency of CBT and exercise therapy as the treatments of choice for the illness ensure that these will not be the last such cases we are likely to hear about.
[Thanks to Jane Colby Carole Lewis, Ted Shaw, Linda Clement, Steve Obispo, and Deborah Shearer for their assistance with this report.]
by Dr. Elizabeth Dowsett, Blue Ribbons for the Awareness of M.E.
The earliest definitions of Myalgic Encephalomyelitis (M.E.) were concise and descriptive and were based on a good history of the illness from patient observation accompanied by a check list. Wallis (1955)  provided a concise list of symptoms (with appropriate variations in children and adolescents) while Ramsay (1956)  introduced the descriptive name "Myalgic Encephalomyelitis" which has stood the test of time over 40 years in the U.K, Australia, Canada, and elsewhere.
The "fatigue" definitions, which first arose in the USA following the Lake Tahoe, NV, epidemic in 1984, have by contrast, caused universal confusion. The earliest of these (Holmes, et al., 1988) was based upon incorrect attribution of the epidemic to Epstein Barr Mononucleosis. Fatigue, sore throat, and lymphadenopathy were elevated to an unreal importance while the cardinal encephalic features of the illness were ignored. This definition was so exclusive of organic features that evidence for a psychiatric cause of the illness was grossly infatuated.
The 1988 definition was soon found unreliable for epidemiological studies, as it produces a gross underestimation of the true incidence.  Moreover, the use of different definitions by research groups in the same or different countries made any comparison between research findings and evaluation of treatment impossible.
A revised edition in 1994 [Fukuda, et al.] moved in the opposite direction and was so inclusive as to incorporate a heterogeneous population of psychiatric and non-psychiatric conditions without making any clear distinctions. Currently there is a significant demand coming mainly from the USA, but popular on both sides of the Atlantic, for dumping the "fatigue" definitions in favour of a scientifically based desert pure and distinctive name.
We now have a plethora of epidemiological, neuroanatomical, neuroendocrinological, and neuropsychological data either to support a change or to make a new definition of "Myalgic Encephalomyelitis" unnecessary. For example, it is acknowledged that M.E. has a unique neuroendocrinological profile, that molecular biology provides documentation of associated viral infections, and radiobiology points to specific anatomical areas of brain damage. Yet, the disease is now involved in fierce clan war between the biochemical, subcellular, brain imaging, and virological scientists who are challenging the centuries old imaginative world of psychiatrists. 
For the sake of our patients, no less, we need to gather doctors and scientists of all grades together now so that information and opinion, however divergent, can be brought to bear upon the urgent task of finding a suitable name and definition. A recent straw poll amongst the members of the USA's "Chronic Fatigue Syndrome" charities put "Myalgic Encephalomyelitis" in the lead with a slightly smaller proportion voting for "Myalgic Encephalopathy" on the grounds that inflammation is not usually associated with the chronic condition though it is undoubtedly a feature of the acute stage. Whether "itis" or "opathy" eventually wins the day, everybody hates "fatigue." A summit meeting incorporating all shades of opinion is urgently needed if we are to break the stalemate of entrenched opinion and do something practical to solve the dilemma of diagnosis, prevention, and evaluation of treatment before this century is over.
 Wallis, A.L. "An investigation into an unusual disease in epidemic and sporadic form in general practice In Cumberland in 1955 and subsequent years." University of Edinburgh. Doctoral Thesis, 1957.
 Ramsay, A.M., O'Sullivan, E. "Encephalomyelitis simulating poliomyelitis. Lancet 1 (1956):761-766.
 Jason, L.A., Richman, J.A., Friedberg, F., et al. "Politics, science and the emergence of a new disease: the case of chronic fatigue syndrome." American Psychologist 52 (9):973-983.
 Hyde, B.M, "The definitions of ME/CFS. A review." In Hyde, B.M., Goldstein, S., Levine, P., eds. The Clinical and Scientific Basis of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. Ottawa: The Nightingale Research Foundation (1992):5-7.
Medical Professionals/Persons with CFIDS represents the Blue Ribbon for the Awareness of M.E. (BRAME) campaign in the United States. Each future issue of MPWC News will contain an article or an update from BRAME to keep you informed on BRAME's progress in educating people in the United Kingdom about CFIDS/ME.
Servatius, R.J., et al. Impaired associative learning in chronic fatigue syndrome. Neuroreport, 20 April 1998.
Researchers studied CFIDS patients and sedentary controls with tests designed to measure instinctive and learned reaction to sensory stimulations using sound associated with a puff of air directed toward the eyeball in order to cause the subject to blink. They found that the persons with CFIDS (PWC's) reacted normally to the puff of air -- that is, they instinctively blinked -- but they were slow to make the association between the puff of air and the sound. The patients should have "learned" to blink at the sound alone after it was presented repeatedly at the same time as the puff of air. In other words, the PWC's reacted normally to the stimuli but were abnormally slow to learn new reactions to stimuli. The researchers say this indicates an "associative deficit" and that PWC's are probably suffering from "organic brain dysfunction within a defined neural substrate."
SOURCE: CFIDS Chronicle, July/August 1998
Saggini, R., et al. Alteration in spatial-temporal parameters of gait in chronic fatigue syndrome patients. Journal of Neurological Science, 21 January 1998.
Researchers studied the spatial (movement) and temporal (speed) parameters of gait of 12 PWC's. They found significant abnormalities in symmetry, which has to do with the movement of one side of the body as compared to the other, as well as other abnormalities. They also found that these abnormalities did not change from the beginning to the end of the exercise period and so could not have been produced by fatigue. The authors say that this study strengthens the hypothesis that a dysfunction of the central nervous system plays a part in the onset of CFIDS.
SOURCE: CFIDS Chronicle, July/August 1998.
Cannon, J.G., et al. Hormonal influences on stress-induced neutrophil mobilization in health and chronic fatigue syndrome. Journal of Clinical Immunology 18 (4):291-298.
A study of hormonal response to exercise in female CFIDS patients found abnormal responses by some measures and normal responses by other measures. Researchers studied eight CFIDS patients in each phase of the menstrual cycle who were matched against eight lutial-phase controls and seven follicular-phase controls. The study found no differences between patients and controls when measuring changes in post-exercise counts of circulating neutrophil, lactoferrin, plasma C3a des arg and creatine kinase. However, differences were seen in relationships between basal neutrophil counts and plasma progesterone concentrations and between exercise-induced neutrophilia correlated and both urinary cortisol and plasma creatine linase. The researchers conclude: " ... Contrary to the original hypothesis of this investigation, CFS patients did not exhibit greater systemic manifestations of an inflammatory response than healthy women as defined by the parameters evaluated in this study, i.e., neutrophil mobilization and activation, complement activation, and plasma creatine kinase activity. However, previously described endocrine relationships with the circulating neutrophil pool were observed in the control group but were absent in the patients." They further concluded that the study provided "additional evidence that CFS patients can be differentiated from healthy individuals by objective physiological and immunological measurements."
SOURCE: CFS-NEWS, 14 September 1998.
Krilov, L.R., et al. Course and outcome of chronic fatigue in children and adolescents. Pediatrics 102 (2):360-366.
This new study disputes the controversial perspective it presented last year in an article by Dr. Plioplys (August 1997) entitied "Chronic Fatigue Syndrome Should Not Be Diagnosed in Children." Dr. Plioplys argued that since there was no treatment, diagnosing CFIDS in children might cause a child to exhibit "illness behavior" that would artificially prolong the illness." The new report found that the medical care and social support children received as a result of their diagnosis was, in fact, helpful. Four years after they were first treated, 43% of the patients' parents said the children were "cured" and 52% said they had "improved" while only 5% considered their children to be "the same." The researchers attributed these recovery rates to the fact that half of the children were referred to them within six months of becoming ill. Because medical intervention started sooner, the children might have had a better chance at recovery, although this study could not prove that theory.
SOURCE: CFIDS Chronicle, September/October 1998
Demitrack, M.A. and Crofford, L.J. Evidence for and pathophysiologic implications of
hypothalamic-pituitary-adrenal axis dysregulation in fibromyalgia and chronic fatigue syndrome. Annals of the New York Academy of Science. 1 May 1998:684-697.
This research shows that the hypothalamic-pituitary-adrenal (HPA) axis function in CFIDS patients shows an abnormally low level of activity. The HPA axis plays a significant role in the neuroendocrine process through which the body responds to and recovers from stress -- including physical stress, emotional stress, and the stress from fighting off an infection. In this study. Demitrack and Crofford suggest that CFIDS is NOT caused by depression because patients who have depression but not CFIDS do not have this HPA axis abnormality. However, fibromyalgia patients DO have the same abnormality as the CFIDS patients which could indicate that CFIDS and FMS are related disorders. The researchers say that it isn't clear yet how the dysregulated HPA axis function develops, but his research shows that it seems to be due in part to an impaired central nervous system drive.
SOURCE: CFIDS Chronicle, September/October 1998
Natelson, B.H., et al. Single-blind, placebo phase-in trial of two escalating doses of selegiline in the chronic fatigue syndrome. Neuropsychobiology 37(3): 150-154.
The authors assessed the effect of selegiline, a specific monoamine oxidase (MAO) B receptor inhibitor in treating CFIDS. They concluded that this drug has "a small but significant therapeutic effect in CFS which appears independent of an antidepressant effect."
Lane, N.J., et al. Muscle fiber characteristics and lactate responses to exercise in chronic fatigue syndrome. Journal of Neurology, Neurosurgery, and Psychiatry 64(3):362-367.
Researchers used quadriceps needle biopsies to examine the muscles of 105 CFIDS patients to find out if abnormalities could be due to lack of activity. Muscle atrophy from inactivity would have resulted in an increased number of a particular type of muscle fiber, called muscle fiber type 2, as well as fiber atrophy. The researchers found that muscle fiber type 1, not type 2, was predominant and that fiber atrophy was only present in 10% of the patients. This means that there was no sign of abnormality which could have been due to inactivity. However, they did find that some CFIDS patients had an abnormal lactate response to exercise and that these patients had a lower proportion of mitochondria-rich type 1 muscle fibers.
SOURCE: CFS MAIL, 1 June 1998.
Lane, R.J., et al. Heterogeneity in chronic fatigue syndrome: evidence from magnetic resonance spectroscopy of muscle. Neuromuscular Disorders 83 (4):204-209.
Researchers wanted to study previously reported abnormally elevated plasma lactate levels in CFIDS patients after exercise and abnormally low numbers of Type 1 muscle fibers. The authors used the sub-anaerobic threshold exercise test (SATET) and then performed phosphorus magnetic resonance spectroscopy on the subjects' forearm muscles to look for other chemical abnormalities. The patients were divided into three groups: 10 patients with increased lactate responses to the SATET, 9 with no increased lactate response, and 13 sedentary healthy controls. The sedentary health controls were included to be sure that any abnormal exercise response was not due to normal muscle deconditioning from inactivity. Prior to exercise, spectroscopy on all three groups was about the same. However, after exercise, the CFIDS patients who had shown increased lactate response also exhibited lower intracellular pH and lower ATP synthesis rate during recovery from exercise. The researchers state that this indicates "impaired mitochondrial oxidative phosphorylation" and that this study provides further evidence that the disability of some CFIDS patients is related to abnormalities in their peripheral muscles.
SOURCE: CFS MAIL, 29 June 1998
Morehouse R.L., et al. Depression and short REM latency in subjects with chronic fatigue syndrome. Psychosomatic Medicine 60 (3):347-351.
Researchers at Dalhousie University, Nova Scotia, questioned why some CFIDS patients were depressed and others weren't. They gave a group of CF!DS patients the Diagnostic Interview Schedule to determine which ones had depression and which did not, then they tested the entire group in a sleep laboratory. REM, or Rapid Eye Movement Latency, is one possible indicator of depression because depressed persons tend to have shorter periods of REM sleep (dream sleep) than normal controls. The investigators found that the CFIDS patients who were depressed also exhibited short REM while the CFIDS patients who were not depressed did not.
SOURCE: CFS MAlL, 16 June1998
Streeten, D.H. and Anderson, G.H. The role of delayed orthostatic hypotension in the pathogenesis of chronic fatigue. Clinical Autonomic Research 8 (2)119-124.
David Streeten, who co-authored the recently published study of low blood volume in CFIDS with Dr. David Bell, co-authored this study which looked at various neurological and endocnne disorders to see if they can cause fatigue similar to that found in CFIDS. 431 CFIDS patients who had been diagnosed with various neurological or endocrine disorders were given a fatigue questionnaire. They found that delayed orthostatic hypotension (a blood pressure disorder involving delayed response to postural changes) and all forms of hypocorticolism (low levels of cortisol) always occurred in patients who said they had symptoms of chronic fatigue. On the other hand, patients with acute orthostatic hypotension (immediate and severe response to posture changes) only had fatigue some of the time and were more likely to feel light-headed or to faint. Patients with multiple system atrophy, pituitary disorders without hypocorticolism, and ideopathic hirsutism did not exhibit chronic fatigue. The researchers concluded that delayed orthostatic hypotension and all forms of hypocorticolism produce chronic fatigue.
SOURCE: CFS MAlL, 16 June 1998
Nisenbaum, R, et al. Factor analysis of unexplained severe fatigue and interrelated symptoms: overlap with criteria for chronic fatigue syndrome. American Journal of Epidemiology 148 (1):72-77.
Researchers at the Klemm Analysis Group in Atlanta surveyed people at random by telephone in San Francisco. They wanted to find out if there was a difference between the symptoms of simple chronic fatigue (defined as lasting less than 6 months) and chronic fatigue syndome (defined as lasting more than 6 months). They eliminated all the respondents who had other medical or psychiatric conditions, such as depression, which could cause fatigue. This left 1,510 people with chronic fatigue which could not be accounted for by depression or other medical or psychiatric conditions. The researchers found that the CFIDS patients had three symptoms which the chronic fatigue sufferers did not have: (1) "fatigue-mood-cognitions" symptoms, (2) "flu-type" symptoms, and (3) "visual impairment." These correlations were not found in the simple chronic fatigue subjects. The authors say that this provides empirical support for the CDC's CFS case definition which defines CFS as a disease which is distinct from simple chronic fatigue or depression. [Interestingly. one of the authors of this study is William C. Reeves of the CDC, who recently made news by alleging misappropriation of funds at the CDC, and also recently issued a press release stating that CFS should be considered a significant health risk to women in the U.S. --Ed. Note.]
SOURCE: CFS MAlL, 29 July1998
Scott, L.V., et al. Blunted adrenocorticotropin and cortisol responses to corticotropin-releasing hormone stimulation in chronic fatigue syndrome. Acta Psychiatr Scand 97 (6):450-457.
Previous research has suggested that a lowered functioning of the HPA axis may be a physical basis for CEIDS. Previous studies have also found blunted adrenocorticotropin (ACTH) responses but normal cortisol responses to exogenous corticotropin-releasing hormone (CRH) tn CFIDS. The researchers compared 14 CFIDS patients who did not have any psychiatric illness to 14 healthy controls, They administered 100 mcg of ovine CRH and measured the subjects' ACTH and cortisol responses. The authors say that "the blunted response of ACTH to exogenous stimulation may be due to an abnormality in CRH levels with a resultant alteration in pituitary CRH receptor sensitivity, or it may reflect a dysregulation of vasopressin or other factors involved in HPA regulation. A diminished output or neurotrophic ACTH, causing a reduced adrenocortical secretory reserve, inadequately compensated for by adrenoreceptor upregulation, may explain the reduced cortisol production demonstrated in this study."
SOURCE: CFS MAlL, 29 July 1998
Heller, U., et al. [Original Title in German; Paper about interrelationship between hearing loss and a cluster of antibodies that could be diagnostic for CFIDS or FMS]. HNO 46 (6):583-586.
Previous research found that some CFIDS and FMS patients have phospholipid, scratonin, and ganglioside antibodies which can cause fatigue, myalgia, arthralgia, depression, sicca symptoms, and diarrhea. The researchers in this study tested patients with hearing loss for these antibodies and found them in about half of their subjects. They noted that some of the patients also had the symptoms of CFIDS and FMS listed above and recommended that patients with inner ear disorders should be checked for CFIDS~FMS symptoms. They argue that these antibodies, when accompanied by the symptoms of CFIDS and/or FMS, are diagnostic for CFTDS or FMS and that the same antibodies may be a cause of hearing loss.
SOURCE: CFS MAlL, 29 July1998
Vollmer-Conna, U., Lloyd, A., Hickie, I., Wakeield, D. Chronic fatigue syndrome: an immunological perspective.
Australian-New Zealand Journal of Psychiatry 32 (4):523-527.
The authors reviewed the research examining an immunological basis for chronic fatigue syndrome and concluded that neuropsychiatric symptoms in patients with CFIDS may be more closely related to disordered cytokine production by glial cells within the central nervous system than to circulating cytokines.
SOURCE: CO-CURE, 29 August 1998
Kathy Houghton, LVN, from Anchorage, Alaska, and a long-time member of Medical Professionals with CFIDS, has agreed to act as the chair for the newly established MPWC Public Relations Network (PRN) and as a public speaker for MPWC's at conferences and in the media. The PRN was established to promote public education about CFIDS and to respond to both positive and negative portrayals of the illness in the public media. Kathy has always been very active in CFIDS advocacy and education issues. She has been a participant in a number of CFIDS conferences and activities in her area and has tenaciously pursued advocacy and educational activities in her state. Kathy has been instrumental in the creation and continued success of the Alaska CFIDS Association. She is currently working on a book which will contain "stories" of PWC's in an effort to educate the public about the illness. You can send your story to Kathy at
The Alaska CFIDS Association
6941 Caravelle Drive
Anchorage, Alaska 99502
or by email to GandK@Alaska.net.
We would like to welcome Kathy whole-heartedly as an active MPWC!!
Study of ill adolescents shelved by CDC: sick kids become casualty of internal CDC politics that drive federal research spending on CFIDS
Charlotte, N.C., 13 August 1998 -- Progress in a fundamental study of chronic fatigue syndrome in children and adolescents was halted when budget bureaucrats at the U.S. Centers for Disease Control and Prevention (CDC) refused to release $400,000 needed to start the study. The CDC's Procurement and Grants Office ordered all work stopped on a multi-site study to better understand CFIDS in youth because agency officials did not approve funding. Study scientists were told that overspending in other programs contributed to the decision to block this study which was to be the first of its kind. The youth study is just the latest casualty of fiscal misconduct at CDC involving CFIDS spending. In a compelling three-page statement, Dr. William C. Reeves, a veteran scientist who filed for protection under the Whistleblowers' Protection Act, reported that end-of-fiscal-year juggling often switched CFIDS research funds to other programs.
SOURCE: CFIDS Association of America, Press Release, 13 August 1998.
[See articles above: "CDC Scientist Charges Agency With Misappropriation of CFIDS Funds", and "Testimony of Dr. William Reeves of CDC".
Israeli Gulf War Illness study may have implications for CFIDS and FMS
The scientific journal Nature reported that Hermona Soreq and colleagues at the Hebrew University of Jerusalem have found that stress and inhibiting the brain enzyme acetylcholinesterase (AChE) in mice triggers complex changes in the brain that decrease mental ability and cause depression and irritability. AChE inhibitors have been used to treat Altzheimer's Disease, a degenerative brain disorder in which the cholinergic fibers in the brain are damaged, and were part of a cocktail of drugs given to Gulf War soldiers to protect them against Iraqi chemicals and nerve gas during the 1991 war. The researchers say that their discovery of anticholinesterase-promoted feedback mechanisms may help to explain " ... the delayed neurocognitive disturbances reported by soldiers exposed to [the drug] pyridostigmine or other cholinesterases dunng the Gulf War," Soreq said. The findings also explain how stress acts on gene regulation to disrupt learning and cognitive ability. The study concentrated on acetylcholine, a neurotransmitter which carries messages in the brain; when it is depleted, learning and memory are disrupted. In studies on mice, the researchers discovered that both AChE inhibitors and stress lead to a long-lasting decrease in acetylcholine. Robert Sapolsky, a biologist at Stanford University, said the Israeli research offers a " ... possible biological underpinning of some of the neuropsychological features of Gulf War Syndrome'" and provides support for both arguments. "First, Gulf War Syndrome cannot be discounted simply because of its heterogeneous symptoms, given the many and varied risk factors to which troops were exposed," he said in a commentary in Mature. "Second, sixty years of stress physiology undermines the view that a stress-related disease is "merely" psychological and thus grounds for discounting, stigmatizing, or denying medical benefits or treatment."
SOURCE: CO-CURE, 29 May 1998
Canadian teen finds potential enzyme deficiency in Chronic Fatigue Syndrome
Toronto teen Dilnaz Punjwani, 16, has won a national science award for research into Chronic Fatigue [Immune Dysfunction] Syndrome. The Branksome Hall student was awarded a top prize at the Canada-wide Science Fair in Timmins for her work identifying a possible enzyme deficiency in this illness. In simple terms, what the Toronto teen has done, according to the selection committee for the Manning Young Canadian Innovator Award, is discover a possible physiological basis for the illness. She has identified a "statistically highly significant" relationship between low levels of a blood enzyme called 2,3-diphosphoglycerate (2,3-DRG) and patients with CFIDS. That particular enzyme is believed to have a strong effect on the oxygen-carrying ability of the blood. If her results are supported by further research, her discovery could lead to a blood test for the disease. In an interview with the Toronto Star Panjwani recalled the growing excitement she felt late one night as she began to compute the results of the blood test. "I just kind of looked at [the statistical printout] and I looked more carefully at it, showed my father and my sister, and I got more excited when I realized what had happened," Panjwani said. "Being an athlete, I have friends who suffer from chronic fatigue syndrome, and everything they've worked toward goes to waste with it," Panjwani said, explaining why she chose to focus on the study which took more than 100 hours to complete. Panjwani said her inspiration came from a 1971 report by researcher William Oski, who speculated that low levels of the 2,3-DPG enzyme in one of his patients might be linked to chronic fatigue [syndrome]. Panjwani used Oski's passing thought as a hypothesis, and with the help of her psychiatrist father Dr. Dilkush Panjwani, she assembled a group of patients to test the theory. When her first group of 13 patients correlated her hypothesis, she got another set of is patients to replicate the results. The study parameters were guided by physicians from the Homewood Health Centre in Guelph. She now dreams of getting a pharmaceutical company to back her finding the cause of the low levels of the enzyme.
SOURCE: CFIDS Chronicle, July/August 1998
Workers Against Senseless Toxic Exposure (WASTE) group created to promote the safe use of chemicals such as glutaraldehyde.
Sharon Sowers and Janet Kenepp, two nurses who have been injured by a high level disinfectant containing glutaraldehyde, have created a group called Workers Against Senseless Toxic Exposure, or WASTE, to support and educate persons who have also been injured by such chemicals. They have found 100+ other medical personnel had been poisoned by glutaraldehyde across the country. The group's goals are to offer support and information on chemical poisoning to medical personnel who have been exposed to toxic chemicals and work toward the regulation of these substances in the workplace. They also hope to put mechanisms in place to help those who have also been injured. For more information on WASTE, contact either Sharon Sowers at
SSowersl@aol.com or Janet Kenepp at
Australian research could lead to diagnostic test for CFIDS
Research being conducted by Professor Gary Scroop at the Department of Physiology, University of Adelaide, Australia, may lead to the development of the world's first diagnostic test for CFIDS. Prof. Scroop and his team have spent the last two years studying 20 CFIDS patients matched with normal controls. They have found that persons with CEIDS release twice as much lactic acid into their bloodstream during exercise as healthy people so that they fatigue much earlier and have a significantly lower endurance level. Prof. Scroop noted that the Royal Australian College of Physicians' draft CFIDS Guidelines recommend exercise programs for patients and said he didn't know why because
" ... exercise training could not help them in any way" and in fact are "potentially damaging." He said that the lactic acid test will provide CFIDS patients with a sound scientific laboratory test to show that the illness is not "all in their heads." The abstracts of the two papers presented by Prof. Scroop at the International CFIDS Conference in Sydney in February 1998 can be viewed at the conference website at the
1998 Sydney CFS Conference Home Page
SOURCE: CO-CURB, 17 June 1998
CFIDS is highlighted in the national media
Over the past few months, CFIDS has been highlighted in the national media. On 29 July 1998, CFIDS patient advocate Wilhelmina Jenkins and her daughter Kamilah appeared on the nationally syndicated Oprah Winfrey Show. Jenkins described her 15 year battle with CFIDS and her efforts to obtain adequate medical treatment for her illness. Despite the fact that the show wasn't a comprehensive overview of CFIDS, it will help to educate the public about the illness and increase its legitimacy. Transcripts of the episode [titled "Illnesses That May Go Undetected For Years"] are available for $5 from Burell's Transcripts, P.O. Box 7, Livingston, NJ 07039. For credit card orders call
Microbe linked to CFIDS-like syndrome in Lancet medical journal
In a recent issue of the major medical journal Lancet, 17 August 1998, researchers in Maryland describe a disorder discovered among fishermen on Chesapeake Bay which involves cognitive dysfunction similar to that experienced by CFIDS patients. The disorder, which has not been named, is transmitted by exposure to a single-cell micro-organism called Pfiesteria piscicida which is responsible for killing millions of fish along the East Coast. The symptoms are caused by potent toxic chemicals which Pfiesteria secretes. "What this does," said lead researcher Dr. Glenn Morris of the University of Maryland, "is to open up a completely new field of research. We don't know what the toxins are or how they act. And we don't know how they are transmitted to the brain." Symptoms of the disorder include fatigue, headaches, diarrhea, impaired memory, disorientation, and learning difficulties. The researchers reported that their tests showed "deficits in learning and selective and divided attention in 19 people who were exposed to Pfiesteria on the Potomac River. The most severe cognitive deficits occurred in the people who were exposed for the longest time. The subjects also reported such difficulties as setting out on an errand by car and forgetting where they were going or what they planned to do when they got there and setting out in their fishing boats without their fishing equipment. The researchers say that their subjects' health problems began to fade after three months and were completely gone after 6 months. However, Jo Ann Burkholder, a lab technician at North Carolina State University who has been involved in studying Pfiesteria, says that she has suffered 11 bouts of pneumonia in the last 3 years and believes that her respiratory problems are due to the microbe. The authors of the study say that there is no evidence of any danger from eating fish.
SOURCE: Associated Press, Reuters
Persistent Viral Disease Research Foundation responds to Simon Wessely Article
Professor John Hughes, Chairman of the Research Committee of the Persistent Viral Disease Research Foundation, recently wrote a letter responding to Simon Wessely's article "I Run An M.E. Clinic" in a letter dated 14 May 1998. The text of the letter reads:
An article "I Run an M.E. Clinic" by Professor Simon Wessely has been drawn to my attention. I do not wish to enter into a debate about the causes or treatment of the illness, but I must correct a factual error. Prof. Wessely states that "we know now that it is not due to a virus that doesn't go away." He does not say who "we" are, but this implies that the scientific community holds this belief. The PVDRF is funding several studies exploring the behavior of the viruses implicated in this illness. They are all being carried out in universities and medical schools by scientists of proven calibre. Only research projects which reach the highest standards of ethical, clinical, and scientific research are accepted for funding. We have a research committee of scientists who are pre-eminent in the field. Their opinions must be taken seriously and. as evidence mounts for the existence of persistent viruses or parts of these viruses, we can now look to a time when we shall have the prospect of a cure in sight."
The Persistent Viral Disease Research Foundation can be reached by writing to:
4 One Tree Lane
Beaconsfield, Bucks HP9 2BU
or phoning 01494 674769.
SOURCE: CFS MAIL, 26 May 1998
Hemispherx Biopharma sponsors CFIDS Symposium in November, 1998
Hemispherx Biopliarma, Inc., announced that its European subsidiary, Hemispherx Biopharma Europe, with offices in Belgium and France, will sponsor an international meeting on new developments in chronic fatigue immune dysfunction syndrome (CFIDS) in Rome, Italy, November 6-7, 1998. Prominent physicians and researchers from more than fifteen countries are expected to attend to discuss the rapidly moving discoveries in diagnosis and medical management of the disorder. A spokesman for the company stated that the forum sponsorship was in response to the intense number of inquiries from medical researchers, doctors, and worldwide regulatory agencies seeking a comprehensive update of recent rapid advancements in diagnosis and therapeutics. The Symposium is expected to introduce new conclusions and expand on clinical data available at the October 1998 International AACFS Conference on CFIDS in Boston. The company's product, Ampligen ®, is in advanced (Phase III) clinical tests and treatments are being made available under certain accelerated access provisions for severely ill patients in the U.S., Canada, Belgium. and Austria.
SOURCE: PRNewswire, 19 September 1998
Factsheet on CFIDS for medical practitioners now available on-line
A new Chronic Fatigue Immune Dysfunction Syndrome factsheet for medical practitioners is available on-line at David Axford's website, "Axford's Abode," an excellent source of information on CFIDS for both medical professionals and patients. The factsheet is an update on the diagnosis and treatment which can be printed out by patients to take to their physician or other health care provider. The factsheet can be accessed at
Axford's Abode: Information on M.E. for Medical Professionals and Patients
SOURCE: CFS MAIL, 19 September 1998.
CFIDS Testing Available in Australia
Associate Professor Tim Roberts of the University of Newcastle, Australia, has been researching possible diagnostic tests for CFIDS for some years. His team recently found that there are different types of CFIDS and that the illness is definitely of a physical, organic nature. The team is also currently working on designing treatment protocols and making treatment recommendations to treating doctors. Dr. Roberts recently announced that his team would "be delighted to get samples from overseas" to test for both urinary metabolites and markers and blood plasma lipids (to determine essential and non-essential fatty acid levels.) Interested persons should contact him through the secretary of the Collaborative Pain Research Unit:
Collaborative Pain Research Unit
University of Newcastle
Department of Biological Sciences
Medical Sciences Building
Callaghan, New South Wales 2308
Fax: 0011 61 2024921 7282
Jason publishes on CFIDS in nurses
Leonard Jason, Ph.D., and Lynne I. Wagner, Ph.D., of DePaul University, have published the results of their research which indicates that there is a higher prevalence of CFIDS among nurses than in the general population. Jason has been conducting research on the incidence of CFIDS in medical professionals for a number of years, and his recent data confirms his previous findings. The researchers' data shows the prevalence rate of CFIDS among nurses to be 1,088 per 100,000, a number considerable higher than the currently accepted prevalence of about 200 cases per 100,000 among the general population. Jason's study appears in the American Journal of Nursing, May 1998. If you would like a copy of this study, send a self-addressed stamped envelope to:
P.O. Box 144
Hinsdale. NY 14743.
CDC Announces prevalence study results
On 10 October 1998, the CDC announced the results of their prevalence studies which suggest that CFIDS is a far greater public health problem than previously known. The study, the most extensive of its kind, estimated the overall prevalence in CFIDS in the US at 183 cases per 100,000 persons aged 18-69. As in other studies, there seems to be a higher prevalence in women. Data from this study was presented at the October 10 AACFS conference in Boston, MA.
SOURCE: CFIDS Association of America Press Release
AACFS Conference and CDC Study Reported on in the Boston Globe, 19 October 1998
Several articles on CFIDS appeared in the 19 October edition of the Boston Globe. The articles reported on the AACFS research conference in Boston as well as on the newly released CDC prevalence studies and the "change the name" efforts.
General Accounting Office asked to investigate CDC spending on CFIDS
Senator Harry Reid of Nevada recently sent a letter to the General Accounting Office (GAO) requesting that they conduct a comprehensive investigation into the CDC CFIDS research program. Reid is a member of the Senate's Labor, Health, and Human Services, Education, and Related Agencies Appropriations Subcommittee which provides funding for the CDC programs.
Surgeon General David Satcher shows interest in CFIDS, renews CFSCC charter
Dr. David Satcher, US Surgeon General, has asked representatives from the Department of Health and Human Services agencies and the Social Security Administration to participate in a private "state of the science" briefing about CFIDS. Although a date for the briefing has not yet been set, Satcher wrote in a September 9 letter to CAA's Kim Kenney, "I am very concerned about CF[ID]S issues." He also indicated that be has requested that the CFS Coordinating Committee charter, which he chairs in his position as Assistant Secretary for Health, be re-chartered.
SOURCE: CFIDS Association of America "Advocacy News"
"The more I do, the more I can do." - Christopher Reeve
DOROTHY KAYNER, MT(ASCP), B.S.
Dorothy Kayner, MT(ASCP), B.S., and MPWC, died of cancer on 8 August 1998. After becoming disabled by CFIDS in 1991 she was diagnosed with cancer 10 weeks before she died. Her commitment to helping other PWC's was profound. She started and was coordinator for Chicago's N/NW Suburban CFIDS support groups. She published an article about CFIDS in a major nursing journal and gave educational presentations to medical professionals and the general public. Much of her precious time and energy was spent on supporting and informing other PWC's. Dorothy strongly opposed the politics which has predominated in the CFIDS movement in recent years. She commented that "The only loss is to the patient, us, and none of us have the time and energy for this." Dorothy Kayner will be sadly missed by MPWC's and we extend our sympathy, condolences, and prayers to her family and friends.
JONNA LANNERT, M.Ed., Ph.D.
Jonna Lannert, M.Ed., Ph.D., and MPWC, a writer and counselor to many who shared her struggle with chronic migraines and CFIDS, died on 6 July 1998 at her daughter's home in Michigan. Her doctors were attempting to control her pain when she died. Dr. Lannert earned her Ph.D. in psychology after becoming ill with CFIDS more than 15 years ago. She was an accomplished artist and poet who campaigned on behalf of the CFIDS community and was active in a support group near her home in Culver City, CA. "Jonna was a courageous and determined woman," said her sister Jeri Rumsey. "Whenever she had a little strength, she had to be active. She just wouldn't stay in bed." Jonna's children have asked that memorial donations be made to the
CFIDS Association of America. Jonna Lannert will be greatly missed. MPWC's would like to extend our heartfelt condolences and prayers to Jonna's family and friends.
CFIDS ANNIVERSARY - ONSET: 10/88
By John Herd, formerly known as John Friedlich
October, for me, marks the passing of years
That I've had CFIDS, ground the advocacy gears
Seen so much suffering, so many tears
From those struggling so desperately, in the face of sneers
The ambiguity of the illness, and future, causing such fears
A legion of walking wounded, calling to seemingly deaf ears
While those who function in the government spheres
Drag their feet and debate amongst their peers
A puzzle of questions, answered with speculative veers
When will there he science instead of conjectural and obstructionist spears
Oh how wonderful it will be, when more effective treatment nears
When from the millions who have CFIDS, come resounding cheers.
MPWC's needs your information sheets
Any MPWC who has not yet filled out and returned their blue information sheet to Gail Dahlen is asked to please do so as soon as possible. The information you provide on these sheets is kept completely confidential and is used only for statistical analysis by MPWC's. Please send your completed information sheet to Gail at
50 North Cecil Avenue
Indianapolis, IN 46219
or fax it to her at (317)899-6033.
IFNa Study needs subjects for Phase II trials
Amarillo Biosciences will begin a Phase II clinical trial of low-dose oral interferon alpha (IFNa) in the treatment of Fibromyalgia. The company said that previous studies indicated that lFNa reduces pain and stiffness in some FMS patients. Treatment with amitriptyline [Elavil -- Ed. note] and either IFNa or placebo will last four months. Researchers are seeking 120 patients for the study, which will take place at the University of Texas Health Science Center in San Antonio under the direction of Dr. I. Jon Russell. Patient enrollment will be open until July 1999. Final results could be available in the first quarter of the year 2000. For information, write to
Dr. I. Jon Russell
University of Texas Health Science Center
7703 Floyd Curl Drive
San Antonio, Texas 782S4.
SOURCE: CFIDS Chronicle, September/October 1998
Johns Hopkins and NIH seek subjects for trial of fludrocortisone (Florinef)
Investigators at Johns Hopkins and the National Institutes of Health continue to recruit CFIDS patients for a trial of fludrocortisone (Florinef) in those with CFIDS and neurally mediated hypotension (NMH). Participants must be
18-50 years old and free of other significant medical and psychiatric illnesses. The study has a target of 100 patients. There is no cost to the patient. For more information, call Karen DeBusk, RN, at Johns Hopkins at (800) 624-4562.
25 Percent Group offers book of CFIDS/ME Cartoons
A book of cartoons entirely about CFIDS/ME entitled "It's Good To Laugh" has been published by a British group called the 25% M.E. Group.[Myalgic Encephalomyelitis (M.E.) is the British term for CFIDS which until recently was also used in the rest of the world.] The 25% Group was set up to support those PWC's who are most severely ill, that is, those that are housebound and even bedridden by the illness. The group wanted to raise funds for research into CFIDS but realized that they were too ill to throw bake sales or other traditional fund-raising events so they organized the book project instead. The book was put together by professional cartoonist Graham D. Kennedy whose wife is a member of the 25% Group. Proceeds from the sale of the book go to the Persistent Viral Disease Research Foundation. Although the group is British, they have established a U.S. contact to make ordering easier. To order your copy send $6.95 to:
Anchorage, AK 99502.
SOIJRCE: Simon Lawrence, Editor 25% Group M.E. Newsletter, 52 Downfield Street., Tollcross, Glasgow Scotland G32 8RT.
Canadians Don Scott and William Scott publish new book on neurodegenerative and systemic degenerative diseases
Donald W. Scott and William Scott, authors of The Extremelv Unfortunate Skull Valley Incident, have published a new book called The Brucellosis Triangle The new book takes up where Skull Valley leaves off, tracking CFIDS, M.E., FMS, MS, and other related diseases from the early 1940's to the present and demonstrating that these diseases will probably constitute the greatest medical challenge of the next millenium. The Scotts contend that the fundamental pathogenic component which has given rise to these neurodegenerative, systemic-degenerative diseases are the brucella species (including brucella melitensis, brucella abortus, and brucelia suis.) The Brucellosis Triangle is available through Chelmsford Publishers, Suite 405-190 Mountain Street, Sudbury, Ontario Canada 5B 402. [A limited number of Scott's book are available for $20 (a reduced cost for members of MPWC's). Send a check payable to MPWC's c/o, Anita Burgess, Box 8, Fairmont, MN 56031.]
Actress Helen Hunt is looking for a charity
Television and movie actress Helen Hunt of "Mad About You" is currently searching for a new "orphan" illness to sponsor. CFIDS would greatly benefit if Ms. Hunt chose this illness to support and champion. Please take a few minutes of your time and write Ms. Hunt or send her a postcard to let her know that we desperately need her help. Send your letters or postcards to:
9830 Wilshire Boulevard
Beverly Hills, CA 90212.
MPWC News is the newsletter of Medical Professionals/Persons with CFIDS Support And Advocacy Support Group. All articles in this newsletter are for informational purposes only. Patients should consult with their physicians before treatment Permission is hereby granted to reprint this document or articles contained herein in its/their entirety if the source is cited and information on membership to MPWC's is included. Permission is needed for edited or excerpted material or material copyrighted by persons other than MPWC's.