| NCF Report: Breakthrough
"Hidden" Finding in the CDC's Gene Profiling Study by Alan Cocchetto Copyright © 2003 The Centers for Disease Control recently published the results of their study of CFS patients in work titled "Utility of the blood for gene expression profiling and biomarker discovery in chronic fatigue syndrome" [1]. One of the authors, Dr. William Reeves, heads up the CFS program at the CDC. Vitally important results, neither reported to the public by the CDC nor reported upon by other CFIDS advocacy groups, surfaced several weeks ago when the NCF finally received the publication from the medical journal Disease Markers. "It took several months to get a copy of the journal article because college libraries had difficulty in obtaining it for some reason!" exclaimed Gail Kansky, president of the NCF. In an interview in Smithsonian Magazine, Dr. Suzanne Vernon, head of the CDC's gene expression program for CFS and lead author for the study, stated that using gene expression profiling technology, the differences between CFS patients and controls could be seen. Furthermore, she predicted that its utilization would make it a diagnostic tool for CFS. However, the NCF's own medical advisors and scientific consultants felt that the CDC failed to adequately inform CFS patients, the public, and the news media about its most significant finding to date! Bluntly stated, the CDC ignored their own truths discovered by their own research team! When the CDC examined age matched controls with all CFS cases, the top gene being overexpressed was the Huntington's Disease protein, also known as the HD protein. Since this protein was not expressed in controls but was highly expressed in all CFS patients and this protein proved to have the greatest statistical significance, why then has the CDC ignored this scientific finding? Why hasn't the CDC raised the red flag? Why hasn't the CFS patient community or CFS researchers been told? Why hasn't Dr. William Reeves commented on this? Perhaps this is because of the following. The Huntington's Disease gene is used in the identification of Huntington's disease [2]. This gene and its identification with Huntington's Disease was first identified in 1993. Now, if CFS patients are expressing this gene in a statistically significant way, then these two diseases are linked together in some significant manner! This truth cannot be ignored nor can it be diluted no matter how hard you try! Furthermore, no "spin" on this will change these basic facts! Huntington's Disease (HD) is a devastating, degenerative brain disorder for which there is, at present, no effective treatment or cure. HD slowly diminishes the affected individual's ability to walk, think, talk and reason. Eventually, the person with HD becomes totally dependent upon others for his or her care. Huntington's Disease profoundly affects the lives of entire families, emotionally, socially and economically [3]. Early symptoms of Huntington's Disease may affect cognitive ability or mobility and include depression, mood swings, forgetfulness, clumsiness, involuntary twitching and lack of coordination. As the disease progresses, concentration and short-term memory diminish and involuntary movements of the head, trunk and limbs increase. Walking, speaking and swallowing abilities deteriorate. Eventually the person is unable to care for him or herself [3]. While Huntington's Disease is a genetically based disorder responsible for neurodegeneration, it is a disease associated with polyglutamine expansion. Huntington's Disease is one of approximately ten diseases identified thus far with a polyglutamine expansion component. The NCF believes that the CDC has purposefully downplayed this key scientific finding due to the fact that CFS patients may have a "new" disease associated with a polyglutamine expansion component that is responsible for neurologic as well as cognitive impairment that has already been identified with these types of disorders. Furthermore, the major implication here is that CFS patients would potentially have an "acquired" Huntington's disease-like process occurring that is no doubt due to a yet unidentified infectious agent. The NCF staffers and the scientists who we have contacted are excited by this very important finding because it fits the evolving CFS disease model that we have developed. We firmly believe this work is directly tied to the ciguatera epitope finding and that other work in-progress, via the NCF's Research Grant Program, should yield some major dividends in the near future. All of our research efforts are aimed at scientifically clarifying what we have put together and expediting appropriate medical treatments. The NCF is very committed in this regard and we will be reporting upon our other research efforts in the months ahead. Look for the CDC's article on our website at www.ncf-net.org. References: 1. Utility of the blood for gene expression profiling and biomarker discovery in chronic fatigue syndrome; SD Vernon, ER Unger, IM Dimulescu, M Rajeevan, WC Reeves; Disease Markers 18 (2002): 193-199 2. A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes. The Huntington's Disease Collaborative Research Group; Cell 1993 Mar 26; 72(6): 971-983 3. Huntington's Disease Society of America; www.hdsa.org |
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