New email bulletin on CFIDS and Huntington's disease--

Discussion in 'Fibromyalgia Main Forum' started by beckster, Aug 6, 2003.

  1. beckster

    beckster New Member

    Anyone else read this newly posted article????? Research done by the CDC (and slightly suppressed, not circulated)
    says that CFIDS may be an "acquired" new disease, similar to Huntington's Disease;we have a similar gene expression (which may actually be a biological marker of the disease)
    of an overexpressed HD protein. I don't know about you but this is disturbing to me. Funny that in the mid and late l980's the CDC tried to whitewash and underplay CFIDS as a non-existant disease (or neurosis or "merely" psychiatric), but then in the l990's "quietly" slipped CFIDS into the same category as AIDS and tuberculosis (that is microbial and infectious in nature), and now they are "quietly" slipping it out there as a chronic, neurodegenerative
    disease. Geeezzz. The good thing about the article is that the NCF (National CFIDS Foundation)is keeping on top of this, wants more press on it, they may be able to find a treatment, and NCF thinks it may be connected with the Ciguatera toxin problem. Still, it is kind of freaking me out, though, to tell you the truth, I already knew this from observing PWC further advanced in years and stage of the CFIDS disease.

    Feedback is bound to make me feel better. Any discussion????????

    Beckster
  2. Mikie

    Mikie Moderator

    Thanks for sharing this new info with us. I had read something about a possible gene marker for CFIDS, but I'd forgotten about it. The one I read did not mention Huntingtons or the fish toxin.

    Love, Mikie
  3. nayray

    nayray New Member

    Quite terrifying! I have a very good friend who's mom had huntington's and it was horrible. I'm sure I'm not making you feel any better. One thing that's slightly reassuring is that most people on this list really do have a syndrome, or group of problems. If you read the symptom list for Huntingtons', it's pretty specific and doesn't include a three page list of symptoms like some of us have. I think that's how a lot of people get diagnosed with CFS in the first place....symptoms are not specific enough for any one illness, hence the name Syndrome. I'm still scared...
  4. achy

    achy New Member

    When was this study done, and how long have they known about this?? And, um, when in the h### where they gonin to let "us" know??

    Once again our govenrment at it's finest!! Outrageous!!

    Warm fuzzies
    Achy
  5. adageek

    adageek New Member

    Vernon SD, Unger ER, Dimulescu IM, Rajeevan M, Reeves WC.
    Utility of the blood for gene expression profiling and biomarker discovery in chronic fatigue syndrome.
    Disease Markers 18: 193-199, 2002.

    Summary
    Gene expression profiling examines the activity (transcription) of genes by analyzing cell’s messenger RNA (mRNA). Gene expression is altered by many factors including cell differentiation, metabolic state, and disease status. By comparing expression of many genes simultaneously, gene expression profiles can be compared between persons (and populations) with and without disease and characteristic differences (or associations) can be identified. These differences, known as differential gene expression, can point to markers for diagnosis or altered physiologic pathways. Gene expression analysis is particularly suited to studying CFS because it examines RNA transcripts from thousands of genes at the same time, covering all from immune system proteins, neuroendocrine pathways, stress response proteins, metabolism, apoptosis, cell adhesion receptors, cell cycles and such data is essential for understanding biological pathways and processes. Most gene expression studies have focused on samples derived from cells or tissues with a known lesion, but CFS has no known to sample. We have hypothesized that peripheral blood mononuclear cells (PBMCs) reflect the systemic state, thus allowing for evaluation of multiple pathophysiological pathways. Some of these pathways should be affected by CFS.

    This paper is the first use of gene expression profiling as a biomarker to distinguish persons with CFS from healthy controls and for identifying genes that could serve as CFS biomarkers. The manuscript is intended as a “proof of concept” for use of gene expression profiling for an illness without a known lesion. This study measured gene expression profiles in peripheral blood cells from five persons with CFS and 17 non-fatigued controls identified during physician surveillance in Atlanta. Various other publications (Studies of Causes of CFS) also used these subjects. Both cluster analysis and multidimensional scaling analysis grouped and separated CFS from controls. The materials and methods section provides considerable detail as to the assays that CDC uses for measuring gene expression profiles. The materials and methods also provides detail as to analysis strategies.

    Abstract
    Chronic fatigue syndrome (CFS) is a debilitating illness lacking consistent anatomic lesions and eluding conventional laboratory diagnosis. Demonstration of the utility of the blood for gene expression profiling and biomarker discovery would have implications into the pathophysiology of CFS. The objective of this study was to determine if gene expression profiles of peripheral blood mononuclear cells (PBMCs) could distinguish between subjects with CFS and healthy controls. Total RNA from PBMCs of five CFS cases and seventeen controls was labeled and hybridized to 1764 genes on filter arrays. Gene intensity values were analyzed by various classification algorithms and nonparametric statistical methods. The classification algorithms grouped the majority of the CFS cases together, and distinguished them from the healthy controls. Eight genes were differentially expressed in both an age-matched case-control analysis and when comparing all CFS cases to all controls. Several of the differentially expressed genes are associated with immunologic functions (e.g., CMRF35 antigen, IL-8, HD protein) and implicate immune dysfunction in the pathophysiology of CFS. These results successfully demonstrate the utility of the blood for gene expression profiling to distinguish subjects with CFS from healthy controls and for identifying genes that could serve as CFS biomarkers.