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CFS, Reeves, and the CDC: 
Rich History but Poor Past

Craig Maupin (


History relies on more than an account of the past.    History also relies on current perceptions and interpretations.   A historian's beliefs, experiences, and hopes form half of the story.

The history of this CFS (chronic fatigue syndrome) is as rich as its past has been poor.   It is a history worth protecting and honoring, and I have no doubt that someday it will offer lessons to future generations.    But recently, I have been concerned that myths are replacing our history, particularly in regard to the CDC (Centers for Disease Control and Prevention), and in particular, Dr. William Reeve's tenure at the CFS program.    What are those myths?


Myth 1.  Dr. William Reeves was, until recently, a bold innovator. His objectivity was lost in recent years, when he suddenly decided CFS was a stress disorder.


      First, William Reeves was extremely cautious with regard to his public statements about CFS.   Despite his tact, he freely offered his thoughts when asked by an advisory committee in 1995 what he thought caused CFS. He said that "the risk factor that we are finding most highly associated with chronic fatigue syndrome are multiple major lifetime stresses in the year before one becomes ill" (1).    This stress-predominant view toward CFS did not change throughout his tenure in the CDC's CFS program.

Secondly, evidence of Reeves' predilection toward CFS goes beyond his 1995 comment. Reeves (a) spent no money searching for a novel viruses, (b) he showed little interest in following up on distinct, previously published immune findings, including inflammatory cytokines.    By 2001, he began to invest the larger portion of his budget in the psychiatry department at Emory University. The precise targeting of those investments within the psychiatry department at Emory is even more important.  The psychiatrists with whom Reeve's chose to collaborate at Emory, such as Christine Heim and Andrew Miller, specialized in post-traumatic stress response and anxiety.  

Third, three of Reeves' most frequent collaborators (Andrew Lloyd, Wessely/Cleare at King's College, and James Jones) propose very similar models for the illness, models that emphasize a viral/lifestyle/emotional stress as the precipitating factor, with brain/behavior as the primary perpetuator.   Reeve's investments, his statements, his collaborators, and his choices say it all. 


 Myth 2. For years, sufferers have accused Reeves "of thinking ME/CFS was a psychological disorder but his open-ended attempt to merge gene expression, gene polymorphism and laboratory and clinical data suggested he was open, at least at that point, to various interpretations of the disease."


 This statement is based on a belief that biological research and genetic research belong to biomedical fields, not psychiatry.   While this belief is understandable from a layman's perspective, it is not accurate.   Current models of psychiatric disorders are multidimensional: stress trigger, genetic predisposition, lead to biological effects and behavioral perpetuation.   Today, depression, stress disorders, and anxiety disorders are researched with an emphasis on genetics, behavioral interventions, neuroendocrine imbalances, and mild immune alterations. (2).   That said, the biological emphasis of psychiatric research often differ from those of biomedical models.


Myth 3. The CDC's Dubbo Infections Outcomes contract with Dr. Andrew Lloyd, a virologist, shows openness to looking viral/immune models of causation.

 Lloyd and his collaborators were far more forthcoming with speculation about CFS than Reeves.   Long before Reeve's chose Lloyd as a collaborator, Lloyd's published work failed to reveal any signs of predilection toward a viral or immunological model for CFS.  Lloyd wrote:   "Current evidence suggests disruption of fundamental central nervous system mechanisms, such as the sleep-wake cycle and the hypothalamic-pituitary-adrenal axis, may underpin the clinical features of this disorder." (3)    In one of his most widely covered papers in 1994, he stated: "Psychological factors such as illness attitudes and coping style seem more important predictors of long term outcome than immunological or demographic variables" (4).     The list of Lloyd's fascination with the psychiatric (biopsychosocial) model goes on, and the list is long.

History will judge virologists involved in CFS (such as Andrew Lloyd, Stephen Strauss, William Reeves) NOT by how well those virologists were able to detect XMRV, Epstein-Barre, or any other virus.   Instead, history may judge them on how accurately they interpreted their own viral research and hypothesis on the brain.   History will also evaluate whether their  beliefs/attributions influenced their sample selection.   Even more importantly, the clinical beliefs and observations of the researcher are the foundation of their sample selection and conclusions for CFS.


 Myth 4. Regarding the 2006 CDC Press Conference on CFS, there are several stories floating around.   A common account goes something like this: "ME/CFS enjoys greatly increased credibility in the medical world and the CDC program played a large part in that.   The team’s innovative, cutting-edge techniques and its willingness to collaborate resulted in a signature event in ME/CFS history: the simultaneous publication of 14 papers in the Pharmacogenomics journal in 2006.   Coincident with that the head of the CDC proclaimed, at a national press conference, that ME/CFS is a serious and legitimate disorder.... Those events got the medical community to sit up and begin to pay attention."

Science Magazine has currently gained recognition for their publication on a possible link between XMRV and CFS. However, many forget that it was a Science article by Jocelyn Kaiser that raised serious concerns about the research methods, assumptions, and conclusions of the CDC's 2006 Pharmacogenomics study.   As of now, Science Magazine has published progressive articles on CFS more than once.   Twice. 

In Kaiser's article, the Pharmacogenomics study design was not only closely examined, but concerns from a wide array of scientists were voiced about the CDC's conclusions.   Concerns about the  small sample size and the lack of validation with PCR were aired.   Most importantly, the implication that the conclusions of the CDC team were significantly exaggerated was raised by a variety of researchers from diverse fields.

Furthermore, some severe flaws of the study were not included in the Science article, perhaps due to space constraints.   First, the study limited its results only to those genes involved in the HPA axis.   Even worse, the conclusion of the study's authors that three genes -- serotonin, glucocorticoid, and tryptophan - immediately extrapolate to an illness caused by an accumulation of lifetime stresses required, at minimum, an extremely robust imagination.    And the authors of the study never bothered to support such a large leap of faith with sources or citations.  

Despite these flaws, the leadership at the CDC, as well as the study's authors, decided that the study merited a shift in the conceptualization of the illness to a disorder of accumulated stress, and a press conference was called to proclaim that shift.  For many people who suffer from CFS, this decision was deeply discouraging and damaged the CDC's credibility as an objective research entity.

It is true that some of our most visible advocates, organizations, and clinicians participated in that press conference.   Researchers and clinicians such as Nancy Klimas and Anthony Komaroff hailed Reeves' findings.  Groups like the CFIDS Association of America joined in.   Understandably, this participation in disseminating Reeve's post-stress model damaged the CFS community's confidence in these researchers and advocacy groups.  That damage was intensified as Reeves unveiled more details of how the Pharmocogenomics study was to inform clinical guidelines of his five year plan.  

My concern is that many who participated in the CDC's efforts to shift the conceptualization of CFS believe that revising history -- particularly the history of William Reeves and his views toward CFS -- is a suitable way to recapture the CFS community's confidence.     The CFS community wants to move on.  It wants healing.  But it also wants its history to remain intact, truthful, and honest.  


In Conclusion  

The findings of the Whittemore-Peterson-Institute (WPI) research team stepped onto a field of discouragement in October, 2009.  The CFS community is well-aware that their preliminary findings may have one of many different conclusions and must be vetted by time and the scientific process.  And that is why a remembrance of our history our true history, is so important.

Perhaps advocacy groups or leaders make mistakes and associate themselves with powerful researchers, such as Reeves.  However, the best solution to past mistakes is to acknowledge those mistakes and show clear commitment to a new direction.  My concern is that many of those who are rewriting Reeves' history are not doing so in the best interest of the community they purport to serve.   






(1) Reeves, W. Presidential Advisory Committee on Gulf War Illnesses. November 7,1995.

(2) Several resources are available that are use for laypeople who want to become more informed about the types of genetics and biology that are emphasized in modern psychiatry.  Below are posted a few books with large previews available (Google books).  These texts can give anyone a general sense of what areas of biology are emphasized in PTSD. A brief skimming with the question "What areas of biology are emphasized?" is all that is required to become more educated on the subject. 

Vasterling and Brewin's 'Neuropsychology of PTSD: biological, cognitive, and clinical Perspectives' (2005) is an excellent place to skim.

The Psychobiology of Trauma and Resilience Across the Lifespan (2008) by Douglas Delanty explores genetic susceptibility and current genetic research.

(3) Hickie I, Lloyd A, Wakefield D, Ricci C (1996). Is there a post-infection fatigue syndrome? Aust Fam Physician Dec;25(12): pg. 1847-1852.

(4) Wilson A, Hickie I, Lloyd A, Hadzi-Pavlovic D, Boughton C, Dwyer J, Wakefield D. (1994) Longitudinal study of outcome of chronic fatigue syndrome. BMJ Mar 19;308(6931):756-759.

(5) Kaiser, J. Jocelyn Kaiser. Genes and Chronic Fatigue: How Strong Is the Evidence? Science 2006; 312: 669-671