From ME society and the "bad genes study"

Discussion in 'Fibromyalgia Main Forum' started by sues1, May 7, 2006.

  1. sues1

    sues1 New Member

    [Note: Abstracts of the CDC studies can be found
    at http://cfids-cab.org/MESA/pharmacogenomics.htm .]


    Science 5 May 2006:
    Vol. 312. no. 5774, pp. 669 - 671
    DOI: 10.1126/science.312.5774.669

    News of the Week
    BIOMEDICINE:
    Genes and Chronic Fatigue: How Strong Is the Evidence?
    Jocelyn Kaiser

    The U.S. Centers for Disease Control and Prevention (CDC) in Atlanta,
    Georgia, announced last month that it has cracked a medical mystery:

    Chronic fatigue syndrome (CFS) has a biological and genetic basis. CDC
    Director Julie Gerberding called the study "groundbreaking" and also
    hailed its novel methodology. These claims have attracted widespread
    media attention. But, like most aspects of CFS, the study and its
    findings are controversial.

    Some scientists think the agency is
    overstating the case for a link between the syndrome and genetic
    mutations.

    "Most complex-trait geneticists would interpret [these]
    findings more cautiously than the authors have," says Patrick
    Sullivan, a psychiatric geneticist at the University of North
    Carolina, Chapel Hill.

    CFS is defined as severe fatigue lasting more than 6 months,
    accompanied by symptoms such as muscle pain and memory problems. It is
    thought to afflict at least 1 million Americans, mostly women.

    The
    lack of specific diagnostic criteria since CFS was first defined 20
    years ago has led to debate over whether the cause could be an
    infectious agent, psychiatric, or something else--and made research
    funding for the disorder highly political. In 2000, a CDC division
    director lost his job after the agency diverted $12.9 million that
    Congress had instructed CDC to spend on CFS research to other
    infectious disease studies (Science, 7 January 2000, p. 22).

    The
    agency agreed to restore the money over 4 years and launch a major study.

    [Photo: Roots of fatigue. CDC Director Julie Gerberding applauds new
    study on chronic fatigue syndrome. One part divided 111 women into
    subgroups that correspond to different gene-expression patterns.]

    The new project, led by William Reeves, CDC's lead CFS researcher (who
    had blown the whistle on the diverted funds), took an unusual
    approach.

    Instead of recruiting patients already diagnosed with CFS,
    CDC surveyed one-quarter of the population of Wichita, Kansas, by
    phone to find people suffering from severe fatigue. Several thousand
    then underwent screening at a clinic for CFS.

    The population-based
    aspect is "a big plus" because it avoids the possible bias in tapping
    a pool of patients seeking treatment for their problems, says Simon
    Wessely, who studies CFS and a similar disorder, Gulf War illness, at
    King's College London.

    Out of this survey, 172 people, most of them white middle-aged women,
    were deemed to fit the criteria for CFS (58) or CFS-like illness
    (114).

    A total of 227 people, including 55 controls, then underwent an
    extensive 2-day battery of clinical measurements, including sleep
    studies, cognitive tests, biochemical analyses, and gene-expression
    studies on blood cells. This part of the study alone cost upward of $2
    million, says Reeves.

    In another unusual step, CDC's Suzanne Vernon then handed this massive
    data set to four teams of outside epidemiologists, mathematicians,
    physicists, and other experts.

    They spent 6 months examining
    statistical patterns in the data. For instance, one group analyzed
    patient characteristics such as obesity, sleep disturbance, and
    depression and grouped them into four to six distinct subtypes; they
    also looked for different gene-expression patterns in these
    categories.

    Some groups also looked for associations between CFS and
    43 common mutations in 11 genes involved in the
    hypothalamic-pituitary-adrenal axis, which controls the body's
    reaction to stress. The 14 papers were published last month in the
    journal Pharmacogenomics.

    The results, which include the finding that the patterns of expression
    of about two dozen genes involved in immune function, cell signaling,
    and other roles are different in CFS patients, provide what Harvard
    University CFS researcher Anthony Komaroff calls "solid evidence" for
    a biological basis of CFS.

    They dispel the notion that "this is a
    bunch of hysterical upper-class professional white women," says Reeves.

    Other scientists are much more cautious. The gene-expression results,
    says Jonathan Kerr of Imperial College London, are "meaningless"
    because they don't demonstrate conclusively, using the polymerase
    chain reaction, that the genes' RNA is indeed expressed.

    After this
    step, says Kerr, 30% to 40% of genes could drop out.

    The most controversial assertion, however, is that the Wichita study
    has tied CFS to particular mutations in three genes, including the
    glucocorticoid receptor and one affecting serotonin levels. Genetic
    epidemiologists are skeptical for two reasons. First, the team looked
    for associations with just 43 gene variants; some other set of genes
    might have correlated just as closely, notes Nancy Cox of the
    University of Chicago in Illinois.

    Second, the researchers studied no
    more than 100 or so individuals with fatigue. The results, although
    they meet the threshold for statistical significance, are "very likely
    not robust," says Sullivan. (Sullivan himself has co-authored twin
    studies finding a "modest" genetic component for CFS, although without
    pointing to a particular gene.)

    Reeves doesn't disagree: "One of our caveats is that it is a small
    study," he says. CDC researchers are now planning to repeat the study
    with 100 CFS patients.

    Vernon says her group is also validating the
    gene-expression results and will hold another computational exercise
    next month at Duke University in Durham, North Carolina, with a larger
    data set.

    Meanwhile, Gerberding has suggested that the same multipronged
    approach could be applied to seek genetic links to other complex
    diseases such as autism.

    That's already being done for many other
    diseases, from cancer to schizophrenia, notes Sullivan, although the
    studies use much larger samples and search the entire genome for
    disease markers.

    That scale may never be possible for relatively
    uncommon diseases such as CFS, he says. And he and other human
    geneticists warn that it's unclear whether any conclusions can be
    drawn from gene hunts carried out on such very small sample sizes.



  2. sues1

    sues1 New Member

    It is no wonder we walk around...confused! LOL.
    Blessings, Susan
  3. Marta608

    Marta608 Member

    "In 2000, a CDC division director lost his job after the agency diverted $12.9 million that Congress had instructed CDC to spend on CFS research to other infectious disease studies (Science, 7 January 2000, p. 22). "

    Am I awful for feeling glad?

    Also, I wonder how this theory jibes with Cheney's new cardiomyopathy theory.

    Marta
  4. findmind

    findmind New Member

    Yeah, i got this by email today....

    and Marta: Dr. Cheney says the low blood volume causes severe microcirculation problems to every part of the body, which prevents even the immune system from working properly...the proper nutrients, hormones, cell-signaling activities, et. don't work correctly.

    So Cheney feels the genes "change" as part of our adaptation to the illness, not that they cause it.

    findmind
  5. sues1

    sues1 New Member

    That was my "favorite part" and also the misuse of funds.......

    Shame shame..
  6. sues1

    sues1 New Member

  7. sues1

    sues1 New Member

  8. sues1

    sues1 New Member

    True, but so does everyone else. At least they are thinking (?) and researching. By pooling what we find ,we all learn more. None of us believe all we read. But we try to be informed.

    Sometimes some of it makes sense, or ties in with something you read later. Even my my fibro fog. Ha.

    Blessings Susan