Saturday, April 26, 2008

Chronic Obfuscation

  http://www.cfids-cab.org/MESA/reviews4.html

  Chronic Obfuscation

  Maryann Spurgin
  A Review of OSLER'S WEB: Inside the Labyrinth of the Chronic Fatigue
  Syndrome Epidemic

  By Hillary Johnson.
  Crown. 720 pp. $30.

  Circa 1984, around the time when San Francisco immunologist Jay Levy
  was investigating the cause of the "gay pneumonia," University of
  California medical school professor Carol Jessop began seeing women
  patients who presented a baffling array of signs and symptoms: fever,
  lymphadenopathy, sore throat, visual and other neurological
  disturbances, and paralytic muscle weakness. The worsening of these
  symptoms upon minor physical exertion formed a common denominator in
  all cases. But when Jessop began subjecting the patients to
  exhaustive tests to rule out autoimmune and other diseases, male
  colleagues scoffed, calling the tests "million dollar workups on
  neurotic women."
That derisive attitude set the tone for both medical
  and media discussions of an enigmatic illness for years to come. The
  problem was exacerbated by the 1988 Centers for Disease Control case
  definition -- set in stone in the Annals of Internal Medicine -- when
  the C.D.C.'s Gary Holmes labeled with the word "fatigue" a crippling
  disease of probable infectious etiology.

  "Chronic Fatigue Syndrome" (C.F.S.) is a name that reveals just how
  tenuous the connection between words and their referents can be. It
  is difficult to imagine clinical severity after hearing a name that
  denotes tiredness. In Osler's Web, Hillary Johnson provides a well-
  documented account of the politics behind that prejudicial choice of
  a name.
Written in the style of Randy Shilts's AIDS epic, And the
  Band Played On (and edited by that volume's editor, Michael Denneny),
  Johnson's book is a thorough medical and political history of this
  decades-old (and variously named) syndrome during the epidemic years
  of 1984-1994. Beginning with Jessop's experience, it reports on vast
  cluster outbreaks of C.F.S. in the eighties.

  But the most provocative portion of Johnson's discussion concerns the
  federal research establishment's attempt to manufacture a mental
  disorder out of a physical symptomatology. In meticulous detail,
  Johnson shows how bias in the choice of patients, value-laden
  selection of C.F.S.-related data and prejudicial allocation of
  research funds permitted government researchers to conclude that
  C.F.S. was a psychiatric condition, or rather, something more akin to
  a behavioral problem. If Johnson is correct, then the government's
  conclusion is a classic illustration of the Thomas Szasz thesis: The
  concept of mental illness is often a political tool with which
  society dismisses its inconvenient members.

  Johnson cites the voluminous evidence independent researchers have
  gathered in support of the claim that C.F.S. is a disease that
  attacks both the immune system and the brain -- including viral
  markers
that reveal a patient's inability to maintain latency of
  ubiquitous viruses (i.e., some viruses infect 95 percent of the
  population, but lie dormant prior to conditions of immune
  suppression) and brain abnormalities as evidenced on M.R.I. (shows
  structural defects) and SPECT (reveals functional defects). The brain
  abnormalities resemble those observed in AIDS.
The disease's clinical
  severity also emerges from the stories Johnson relates of formerly
  active men, women and children who, after contracting the malady,
  became homebound, suffered dementia or seizures, or faced confinement
  in nursing homes.

  Osler's Web juxtaposes evidence for the disease's gravity, prevalence   and contagion with an account of ongoing government efforts to   control the nature and availability of information about C.F.S.
  Representative of official bias was the C.D.C.'s tepid response to a
  1985 cluster outbreak in Incline Village, Nevada. Where clinician and
  C.F.S. researcher Paul Cheney had already identified over 150 cases,
  Holmes and Jon Kaplan of the C.D.C., working within the same patient
  population, claimed to have confirmed only fifteen cases. The
  discrepancy resulted from Holmes and Kaplan having selected out all
  patients displaying concomitant pathology, as though it were
  coincidental rather than a natural outcome of the disease process
  itself. For instance, patients with bacterial infections were
  excluded, even though infections might be expected under conditions
  of immune suppression. Selection bias characterized government
  research, surveillance and grant allocation from that point on.
  Cheney's partner, for instance, had observed an increase in lymphomas
  in his epidemic population. When he complained that Holmes was
  ignoring this evidence, Holmes wrote, "The identification
  of...lymphomas that occurred in your patients (and) MRI
  abnormalities...moves such patients out of the CFS category."

  But the central villain of Osler's Web is Stephen Straus, head of the
  medical virology section of the National Institute of Allergy and
  Infectious Diseases (NIAID). Johnson discovered that Straus, who was
  considered by his superiors to be an expert on the disease, omitted
  from consideration not only patients with post-C.F.S. lymphomas but
  those with such classic C.F.S. complications as seizures and, indeed,
  with any objective signs of disease. He then circularly concluded
  that C.F.S. is a subjective condition.

  Straus became the establishment's C.F.S. oracle. According to
  Johnson, he voted in favor of the C.D.C.'s obfuscatory name, "Chronic
  Fatigue Syndrome," peer reviewed prospective journal articles,
  supervised the dissemination of dubiously informational C.F.S.
  pamphlets to physicians and negatively influenced the allocation of
  federal research money. He thereby set the parameters for
  professional and lay discourse, insuring that it would be conducted
  only in terms of psychopathology. Moreover, Straus staunchly
  maintained this stance in spite of opposition to his conclusions from
  within the psychiatric community itself. In the end, the
  psychopathological paradigm of C.F.S. became an article of faith
  among those in mainstream and academic medicine -- physicians who
  disagreed were threatened with professional ostracism -- rather than
  an issue to be assessed in light of all available evidence.

  Evidence that C.F.S. was an illness didn't come from federal research
  money, since N.I.H. grants were dispersed according to the principle
  that C.F.S. was not a bona fide disease.
Promising grant proposals of
  dissenters from this clinical orthodoxy were passed over, and one
  casualty was that the cancer link with C.F.S. was never explored.
  Indeed, Johnson forcefully accuses both the N.I.H. and the C.D.C. of
  gross misuse of Congressionally appointed funds earmarked for C.F.S.
  Misappropriation of funds at the C.D.C. and biased selectivity in   grants at the N.I.H. went hand in hand -- no amount of money devoted to C.F.S. research seemed to prove helpful in understanding the disease, since the infrastructure was predisposed to dismiss it.
  Institutionalized intransigence became increasingly obvious as
  patients -- medical professionals among them -- sent written
  complaints to Anthony Fauci, head of NIAID and Straus's boss.
  According to Johnson, Fauci defended his subordinate's cavalier
  response to C.F.S. by citing studies by Connecticut psychiatrist
  Peter Manu, who, having failed to select his patients according to
  any known diagnostic criteria for C.F.S., concluded that C.F.S. was a
  somatization disorder -- a physical manifestation of a mental
  problem. And, in a move that strikingly illustrates Szasz's thesis,
  NIAID deputy director Jim Hill even suggested that those who
  criticized Straus were more likely to have a psychiatric component to
  their disease than those who agreed with him.

  One of Osler's Web's genuine strong points is its illustration of a
  propaganda system at work. Studies citing negative findings in C.F.S.
  were readily published, while studies reporting positive
  physiological findings were turned down
(e.g., by Lancet and The New
  England Journal of Medicine) or were published after being held to
  higher standards of verification than were papers on other diseases.
  Johnson illustrates how, in turn, this professional skepticism
  influenced the mainstream media and hence public perception. Time,
  The New York Times, The Washington Post and television networks
  seized upon the negative reports and on the pronouncements of
  government-paid scientists as those of unimpeachable authority.
  Insidiously, the patient organizations themselves were co-opted.
  According to Johnson, the largest of these organizations, the
  formerly ACT UPish C.F.I.D.S. Association, even came to permit
  government censorship of its journal in the name of "peer review."

  Johnson has worked from written documents, taped interviews and
  published journal articles, and she offers an impressive accumulation  of well-substantiated facts.
But her analyses are inadequate. She
  criticizes the new, 1994 case definition for its treatment of the
  disease as a subset of fatigue; criticizes the C.D.C. surveillance
  method of looking for the prevalence of fatigue in American society;
  criticizes Straus's intent to "define the disease... out of existence
  by embracing all who claimed fatigue under its umbrella"; but fails
  to state precisely what is wrong with these approaches. For the error
  here is fundamentally one of logic.

  Put most starkly, some members of the federal system take an
  accident, fatigue, as the disease's essence -- and from this a
  variety of unrelated diseases, linked by a shared symptom, are
  identified as one. Such was the error of Peter Manu, whom federal
  scientists frequently cite as an authority on the disease. From my
  own reading of Manu, it is apparent that he selected into his
  practice people with fatigue associated with depression. Since the
  usual prescription for fatigue is more exercise, many of Manu's
  patients, predictably, responded to a regimen of graded workouts.
  Manu went on to use this experience as the basis for patronizingly
  reassuring publications about C.F.S. -- a disease that, in fact,
  worsens with exercise. Manu's error was to identify two different
  diseases by a shared property, diseases so distinct that
  neuroendocrine studies have shown marked physiological contrasts

  between them. In other words, he committed the Fallacy of the
  Undistributed Middle. Such reasoning is only one of the damaging
  consequences of the name "Chronic Fatigue Syndrome." The conflation
  of C.F.S. and chronic fatigue permeates medical journals and federal  discussions of the disease and permits patients who fail to respond to standard fatigue therapies to be dismissed as malingerers and  somatizers.

  Fatigue is not a disease. It is a symptom of many diseases. Since
  there is no single underlying condition behind fatigue, by equating
  C.F.S. with unexplained fatigue, federal officials can say that there
  is no single underlying condition behind C.F.S. While there is
  nothing unreasonable about the claim that C.F.S. has multiple causes
  (exposure to toxins can trigger reactivation and hence chronicity of
  latent viruses, and it is probable that a number of viruses could
  cause the chronic postviral syndromes that are now classified as
  C.F.S.), what is unreasonable is the notion that C.F.S. is many
  unrelated diseases grouped by their shared symptom, fatigue. After
  excluding patients with the disease by excluding the whole complex of
  classic symptoms and complications that accompany C.F.S., federal
  officials went on to include those who don't have the disease via the
  symptom of fatigue. With the latter they "recognize" the disease
  without recognizing it: A truly effective system of repression is one
  that propagates the impression of its openness and fairness.

  Osler's Web harbors its own internal contradictions. Most striking,
  in light of Johnson's criticism of the "insidiously benign name," is
  the book's frequent use of the term "fatigue" to describe the
  disease's main component (relapsing of flu and neurological symptoms
  upon exertion, which leaves patients bedridden for days, weeks or
  years). Johnson fails to note that there is no necessary connection
  between a need for rest and tiredness: Rest might equally well serve
  to curb the exacerbation of pain and, speaking in more conceptually
  rigorous terms about C.F.S., of exertion-induced complications
. While
  Osler's Web thoroughly debunks the myth that any of these
  complications -- paralytic muscle weakness, blurred vision, dementia -
  - typify the habitual, volitional idleness that the term "chronic
  fatigue" suggests
, by adopting "fatigue," if only as a synthesizing
  placeholder, Johnson vitiates her own case against the name. Patients
  who criticize the name must take responsibility to eliminate the
  term, and doing so would be in keeping with the spirit of the
  namesake of Johnson's book: It was the Canadian clinician Sir William
  Osler (1849-1919) who championed research into disease phenomena, as
  opposed to the deductive approach of following out the logic of
  unthinkingly adopted concepts, which is among the tactics that have
  hindered meaningful research on C.F.S., so called.

  That federal officials ignored disease phenomena and rarely examined
  patients is Johnson's explanation of why they are resisting
  acknowledging the disease. Yet her explanation is inadequate, since
  the question of their motivation remains. The book presents strands
  of a cultural analysis (e.g., Straus's ill-concealed sexism) and
  hints of economic analyses (she names physicians who are more
  concerned with the potential insolvency of insurance companies than
  with patient well-being). And much of the story unwittingly
  illustrates Thomas Kuhn's characterization of normal science as
  inherently resistant to novelty. The thin line between normal science
  and propaganda is also evident from Johnson's account. But Osler's
  Web never quite achieves the synthetic grasp of concepts necessary to
  address properly the pervasive policy abuse it so convincingly
  exposes.

  Osler's Web also suffers stylistically from an accumulation of detail
  that, at times, serves no very evident purpose. Roughly one fourth of
  the book is devoted to the search for a retroviral cause of C.F.S.
  Since no such virus has yet been found, the book strikes an
  inconclusive note, rather like a postmodern novel. If Johnson is
  hinting that more money for viral studies should be allocated to
  independent researchers, she should have argued her case directly.

  In the end, Osler's Web is a kaleidoscope of tantalizing analytical
  fragments incompletely integrated. Yet too much theory might have
  overwhelmed a general reader, and this issue needs disclosure, not in
  some cloistered academic setting but in a public forum. Something
  appeared in the eighties that was more efficient at triggering the
  syndrome than any viral or toxic agent had been in the past, and
  C.F.S. is now a widespread, if still hidden, disease. At a time when
  the do-gooders at the C.F.I.D.S. Association are taking seriously
  books on spontaneous New Age recoveries in patients abducted by space
  aliens, Johnson has given us a fast-paced, highly readable political
  expose
, with a wealth of raw material for further constructive and
  penetrating critiques.

  ________________________________________

  Maryann Spurgin formerly taught philosophy.

  ________________________________________

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  _____________________________________________

  Maryann Spurgin did a very useful review, yet her assessment
  of "internal contradictions" in Osler's Web are somewhat
  poorly conceived.
  "Chronic Fatigue Syndrome" was the term the CDC deliberately applied
  to the illness, and we expected that people would understand this
  obviously referred to the ILLNESS rather than the definition itself -
  so we used the term, and Hillary Johnsons usage of the term occurs
  for that reason - and not out of personal choice or preference or a
  consideration that this was an accurate portrayal of the illness.

  The evidence of RNase-L activation calls for examination of an agent
  that can cause an antiviral response, until some viral agent or
  suitable explanation should be found, and the case for further
  research was directly made.

  Hillary did indeed note that there was no connection between the
  need for rest and the principal paralytic sensation of this
  phenonemon - even to the extent that bedrest sometimes had the
  uncanny effect of exacerbating the illness, so this topic was covered.

  The CDC's motivation for the creation of "Chronic Fatigue Syndrome"
  instead of recognizing ME was also adequately addressed in Osler's
  Web.

  Whatever failure of logic may have occurred were definitely not on
  Hillary Johnsons part.

  As Maryann Spurginn writes, the term CFS does reveal just how
  tenuous the connection between a word and its referents is.
  Despite the deliberately introduced inherent flaws in this
  appellation, we expected that people would still be willing to agree
  that the term "CFS" would refer to the illness under consideration at
  the time that term was invented for that very purpose.
  Unwillingness to even consider this possibility violates the
  fundamental tenets of the agreement by which language itself is
  constituted and facilitated.

  Whatever "confusion" might have occurred, whether by accident or
  by deliberate design, we believed would have been easily overcome by
  the purported basic desire of humans to "seek out the truth", who
  would therefore revisit the original source and obtain accurate
  information regarding these events.

  We counted on a trait has become notable by its absence.

  -Erik

Tests for CFS

I have put the list of tests that the CDC states patients with CFS should NOT have to compare with the list of tests that the Canadian Consensus Document SUGGESTS for ME/CFS patients (when appropriate) in two websites to make them both easy to download and compare side-by-side.  In the case of the CDC list, I took a paragraph and opened it up to bullet points so it would be easier for PWC/ME's to read.

The CDC list of tests NOT to give patients with CFS is here:
http://www.cfids-me.org/cdctests.html

The Canadian Consensus Document's list of tests FOR patients with ME/CFS is here:
http://www.cfids-me.org/consensustests.html

Mary Schweitzer

* * *

Like one of my doctors who refused to do appropriate tests, it becomes apparent that the point is to NOT see any evidence that would cause them to change their minds. 

As long as the only evidence of my symptoms was my say-so, the doctor could choose to ignore them, to claim I was exaggerating.  I suggested putting me in the hospital or a nursing home overnight for observation, and he refused.  Why?  Because if a nurse's notes backed up my story, he could no longer claim that there was "no objective evidence". 

Like CDC, he didn't want to see anything wrong.  He wanted to see a depressed woman, and objective evidence of physical illness would force him to change his opinion.  He had chosen to "interpret" my report of spending a great deal of time collapsed in bed because I no longer had enough energy to sit up as "excessive sleeping", a symptom of depression.  A nurse documenting that I was lying in bed but wide awake even at 3 AM would have forced him to admit that when I said I needed a sleeping pill, I was right, and that when he said I needed an anti-depressant, he was wrong. 

Doctors don't like to admit they're wrong.  So, they make all sorts of excuses, including lists of tests that would show physical abnormalities in CFS, which they say aren't necessary to be done, in order to avoid developing the evidence that would require them to change their minds.

Economic Impact of CFS (Excerpts)

Source: Dynamic Medicine Vol. 7, #6 Date: April 8, 2008

URL: http://www.dynamic-med.com/content/7/1/6

The Economic impact of ME/CFS: Individual and societal costs

Leonard A. Jason(1,*), Mary C. Benton(2), Lisa Valentine(3), Abra Johnson(1), Susan Torres-Harding(4)

1 Department of Psychology, Depaul University, Center for Community Research, Chicago, IL, USA

2 Department of Psychology, Wichita State University, Wichita, KS, USA

3 Department of Psychology, University of North Texas, Denton, TX, USA

4 Department of Psychology, Roosevelt University, Chicago, IL, USA

Email addresses: LAJ: ljason@depaul.edu ; MCB: mcbenton@wichita.edu ; LV: lvalentine@unt.edu ; AJ: ajohns25@depaul.edu ; STH: storresharding@roosevelt.edu

 * Corresponding author: Leonard A. Jason, Ph.D., Center for Community Research, DePaul University, 990 W. Fullerton Ave., Suite 3100, Chicago, Il. 60614 (email: Ljason@depaul.edu ).

Abstract

Background

ME/CFS is characterized by debilitating fatigue in addition to other physical and cognitive symptoms. It is estimated to affect over 800,000 adults in the U.S. ME/CFS often results in diminished functionality and increased economic impact. The economic impact of an illness is generally divided into two categories: direct and indirect costs. Despite high prevalence rates and the disabling nature of the illness, few studies have examined the costs of ME/CFS at the individual and societal level. In fact, of the four studies examining the economic impact of ME/ME/CFS only two used a U. S. sample.

The current study used community and tertiary samples to examine the direct costs of ME/CFS. Results For Study 1, the annual direct total cost per ME/CFS patient was estimated to be $2,342, with the total annual direct cost of ME/CFS to society being approximately $2 billion. In Study 2, the annual direct was estimated to be $8,675 per ME/CFS patient, with the total annual direct cost of ME/CFS to society being approximately $7 billion..

Conclusions

Using ME/CFS prevalence data of 0.42 and indirect costs estimates from Reynolds et al. (2004), the direct and indirect cost of ME/CFS to society was estimated to be $18,677,912,000 for the community sample and $23,972,300,000 for the tertiary sample. These findings indicate that whether or not individuals are recruited from a community or tertiary sample, ME/CFS imposes substantial economic costs.

Background

According to Jason et al. [1], chronic fatigue syndrome (CFS) affects over 800,000 adults in the United States. This illness is has more recently been referred to as ME/CFS (where ME stands for either Myalgic Encephalomyelitis or Myalgic Encephalopathy). The prognosis for severely afflicted patients with ME/CFS is poor [2-3]. The persistent and debilitating nature of ME/CFS often results in a reduction in work and family life activities, as well as an increase in health care costs [4]. Because it becomes difficult for patients with ME/CFS to continue employment at premorbid levels, many have little choice but to leave their jobs. Indeed, Jason et al. [1] found that participants with ME/CFS were more likely to be receiving disability income, be unemployed, or be working part-time than control participants. Similar findings of higher unemployment rates among patients with ME/CFS were found in Bombardier and Buchwald [5]; McCrone, Darbishire, Ridsdale, and Seed [6]; Reynolds, Vernon, Bouchery, and Reeves [7] and Tiersky, DeLuca, Dhar, Jonson, and Lange [8].

In addition to employment loss, patients with ME/CFS often experience escalating costs of health care due to the search for a more definitive diagnosis and treatment [9]. The economic impact of an illness is typically examined in terms of direct and indirect costs. The former refers to direct medical costs including hospital, ambulatory, prescription medications, over-the-counter medications, and medical laboratory testing. Indirect costs include transportation, work productivity losses, disability reimbursements, loss of leisure or duties at home, or services provided by family members, friends, or other informal care providers [10].

Four studies have examined the economic impact of ME/CFS, three of which use clinic-based, or tertiary samples, and only two of those samples are from the United States. McCrone et al. [6] examined both direct and indirect costs and found a higher proportion of medical service use and unemployment among the ME/CFS group, as well as higher lost employment costs and combined service costs for patients with ME/CFS in tertiary care settings in the United Kingdom.

Using an Australian tertiary sample, Lloyd and Pender [11] estimated an average cost of $9,436 per patient with ME/CFS, including about $2,000 per patient in direct medical costs. Extrapolating this figure to the population of Australia, Lloyd and Pender [11] estimated that ME/CFS cost the government in excess of $25 million and cost the Australian community approximately $59 million.

Bombardier and Buchwald [5] examined the direct cost of patients with ME/CFS in the United States using patients from a referral clinic. The estimated average annual expenditure was $1,013 per ME/CFS patient.

Reynolds et al. [7] used a community-based sample from Wichita, Kansas to estimate the indirect cost of ME/CFS. These authors estimated that the annual total value of lost productivity in the United States was $9.1 billion, or about $20,000 per individual with ME/CFS. The previous studies of the economic impact of ME/CFS provide evidence of the financial burden placed on individuals and their families, as well as on society as a whole, however, none of the previous studies have estimated these costs using both community-based and tertiary samples.

Direct medical costs

Medication usage and costs were assessed in the estimate of direct medical service use. Based on self-reported use and physician exam information, the mean number of prescription medications was 1.6 (SD=2.1) for participants with ME/CFS and .7 (SD=.9) for control participants, however these differences were not statistically significant, t(34)=1.56, p=.13. The mean number of over-the-counter medications was .4 (SD=.6) for participants with ME/CFS and .1 (SD=.4) for controls, and these differences were not significant, t(33)=1.57, p=.13. The total average annual cost of prescription and over-the-counter medications was significantly higher for participants with ME/CFS ($1,159; SD=1426) than for controls ($321; SD=415), t(25)=2.55, p=.02.

Based on medical record data, the mean number of office visits per year was 6.1 (SD=3.6) for participants with ME/CFS and 4.5 (SD=3.4) for control participants, but these differences were not statistically significant, t(34)=1.42, p=.17. Participants with ME/CFS spent an average of $470 (SD=274) on medical office visits, while control participants spent an average of $342 (SD=259). These cost were not statistically significant, t(34)=1.42, p=.17.

Although our data did not include salary variables and indirect costs could only be examined in terms of work status change and increased disability, we could apply the Reynolds [7] figure ($20,000) to our sample. For study 1, using estimates from Reynolds et al. [7], we could estimate that the annual indirect cost to society to be $16,720,000,000 (836,000 X $20,000) or almost $17 billion. Together the total indirect and direct costs to society could be estimated to be $18,677,912,000, or over 18 and a half billion dollars. For study 2, the estimated total annual indirect cost to society is 836,000 X $20,000=$16,720,000,000. Therefore, in study 2, together the total indirect and direct costs to society equals $23,972,300,000 or close to 24 billion dollars. For studies 1 and 2, the total direct and indirect costs due to ME/CFS were estimated to range from 17 to 24 billion dollars.

In conclusion, Jason et al. [1] estimates that more than 800,000 adults in the United States have ME/CFS. This figure combined with cost information reported in the current study suggests that ME/CFS has substantial economic costs, whether one uses samples recruited from the community or from a tertiary care clinic. These cost estimates in combination with high prevalence rates are some of the reasons that more research into the cause, effective diagnosis, and treatment are necessary.

References

1. Jason, L.A., Richman, J.A., Rademaker, A.W., Jordan, K.M, Plioplys, A.V., Taylor, R.R. (1999). A community-based study of chronic fatigue syndrome. Archives of Internal Medicine, 159, 2129-2137.

2. Hill, N.F., Tiersky, L.A., Scavalla, V.R., Lavietes, M., & Natelson, B.H. (1999). Natural history of severe chronic fatigue syndrome. Journal of Archives of Physical Medicine and Rehabilitation, 80, 1090-1094.

3. Reyes, M., Dobbins, J.G., Nisenbaum, R., Subedar, N.S., Randall, B. & Reeves, W.C. (1999). Chronic fatigue syndrome progression and self-definedrecovery: evidence from the CDC surveillance system. Journal of Chronic Fatigue Syndrome, 5, 17-27.

4. Jason, L.A., Fennell, P.A., & Taylor, R.R. (Eds.) (2003). The Handbook of chronic fatigue syndrome. New York: John Wiley & Sons, Inc.

5. Bombardier, C.H. & Buchwald, D. (1996). Chronic fatigue, chronic fatigue syndrome, and fibromyalgia: Disability and health care use. Medical Care, 34, 924-930.

6. McCrone, P., Darbishire, L., Ridsdale, L., & Seed, P. (2003). The economic cost of chronic fatigue and chronic fatigue syndrome in UK primary care. Psychological Medicine, 33, 253-261.

7. Reynolds, K.J., Vernon, S.D., Bouchery, E., Reeves, W.C. (2004). The economic impact of chronic fatigue syndrome. Cost Effectiveness and Resource Allocation, 4.

8. Tiersky, L.A., DeLuca, J., Hill, N., Dhar, S.K., Jonson, S.K., & Lange, G. (2001). Longitudinal assessment of neuropsychological functioning, psychiatric status, functional disability and employment status in chronic fatigue syndrome. Applied Neuropsychology, 8, 41-50.

9. Friedberg, F. & Jason, L.A. (1998). Understanding chronic fatigue syndrome: An empirical guide to assessment and treatment. Washington, DC: American Psychological Association

10. Robinson, R.L. & Jones, M.L. (2006). In search of pharmacoeconomic evaluations for fibromyalgia treatments: A review. Expert Opinion on Pharmacotherapy, 7, 1027-1039.

11. Lloyd, A.R. & Pender, H. (1992). The economic impact of chronic fatigue syndrome. The Medical Journal of Australia, 157, 599-601.

12. Fukuda, K, Straus, S.E., Hickie, I, Sharpe, M.C., Dobbins, K.G., & Komaroff, A. (1994). The chronic fatigue syndrome: a comprehensive approach to its definition and study. Annals of Internal Medicine, 121, 953-959.

13. Spitzer, R.L., Williams, J.B., Gibbon, M., & First, M.B. (1995). Structured Clinical Interview of DSM-IV-Non-Patient Edition (SCID-NP, Version 2.0). Washington DC: American Psychiatric Press.

14. Jason, L.A., Ropacki, M.T., & Santoro, N.B. (1997). A screening scale for chronic fatigue syndrome: Reliability and validity. Journal of Chronic Fatigue Syndrome, 3, 39-59.

15. Komaroff, A.L., Fagioli, L.R., Geiger, A.M. (1996). An examination of the working case definitions of chronic fatigue syndrome. American Journal of Medicine, 100, 56-64.

16. Chernin, T (Ed.). (2004). Physicians desk reference: Monthly prescribing guide September, 2004. Montvale, NJ: Thomson PDR.

17. Hogge, J. (Ed.). (2005). RedBook: Pharmacy's fundamental reference, February, 2005 Update. Montvale, NJ: Thomson PDR.

18. Gonzalez, M.L. & Zhang, P. (Eds.). (1998). Socioeconomic characteristics of medical practice 1997/1998. Chicago: American Medical Association.

19. Beecham, J, & Knapp, M.(2001). Costing psychiatric interventions. In G. Thornicroft (Ed.), Measuring mental health needs (pp. 200-224). London: Gaskell.

(c) 2008 BioMed Central Ltd.

* * *

$24 billion dollars.  TWENTY-FOUR BILLION DOLLARS.  Per year.  The total amount spent by the US government to research CFS over the past 25 years doesn't even amount to one year's income taxes on that.

Our grandmothers had a phrase for this "Penny wise and pound foolish".  The government would rather throw away 24B a year every year for the rest of our lives than to invest even 1B in finding a cure to get us back to work.  There's something wrong with this picture.

Etiology and Exercise (and Judith's Comments)

Reference:

Etiology of Chronic Fatigue Syndrome: Testing
Popular Hypotheses Using a National Birth Cohort
Study - see abstract, posted by Fred Springfield at
Co-Cure:
http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0804a&L=co-cure&T=0&P=1270

http://www.cfids.org/cfidslink/2008/040903.asp?tr=y&auid=3544493

Etiology, Exercise and CFS
~~~~~~~~~~~~~~~~
By Suzanne Vernon, Phd

Hot off the press from the journal Psychosomatic
Medicine is a paper by Samuel B. Harvey, Michael
Wadsworth, Simon Wessely and Matthew Hotopf
entitled "Etiology of Chronic Fatigue Syndrome:
Testing Popular Hypotheses Using a National Birth
Cohort Study."

Despite the psychological spin they put on the
results, the findings in this paper validate what
many in the patient community describe regarding
activity levels prior to the onset of illness: "I was a
runner. . . "; "I loved to hike. . . "; "until I got CFS."

This is an important publication because of that
validation. This paper also reminds us of the
importance and possible impact of events that
happen across the lifespan.

Let's first break down the title so that we understand
what the study attempts to do.

Etiology is the study of causation. Even though many
investigators have searched for the cause of CFS, it
has proven to be elusive. There have been many
explanations as to why scientists haven't pinned
down a cause, but the most likely one is that CFS is
a complex, chronic disease resulting from a
combination of gene-environment interactions.

Chronic diseases like CFS are tough to study let
alone to identify a cause because--as the name
chronic implies and the definition insists upon--the
disease occurs over time. The term birth cohort
refers to a group of people enrolled in a study from
birth and followed for a certain period to evaluate
any number of issues across the lifespan.

Three of this study's investigators are from the
Institute of Psychiatry at King's College London and
the other, Professor Michael Wadsworth, is the
retired director of the Department of Epidemiology
and Public Health at University College London. This
is the department that operated the National Survey
of Health and Development, a British national birth
cohort survey established in 1946, originally to
investigate how lifespan health matters might affect
fertility and obstetric issues.

In this study, the investigators aimed to test a set
of hypotheses about the cause of CFS. They
examined whether there were increased rates of
allergy and asthma (referred to as atopic illness),
decreased levels of physical exercise and/or
increased childhood illnesses in people with CFS.

Since this is a birth cohort, each hypothesis tapped
into information from various ages. For example,
childhood illness was evaluated between the ages of
6 to 15 years. A history of atopic illness was taken
when the study subjects were 36 and 43 years old.
Information on physical activity was gathered across
the lifespan up to 53 years of age.

While there is a great deal of data on this cohort,
only information relevant to the above hypotheses
was analyzed. (You can read more about this cohort
and the kinds of information collected at
http://ije.oxfordjournals.org/cgi/reprint/35/1/49.pdf .)

The first step was to determine how many people in
this cohort self-reported a diagnosis of CFS. Of 2,983
participants, 10 men and 24 women (1%) reported a
diagnosis of CFS with fatigue symptoms starting
between 41 and 53 years of age.

When investigators looked at rates of childhood
illnesses that resulted in school absence or
hospitalization in these 34 people with CFS, they
were no different from the rest. There were also no
differences in the rates of atopic illness. And rather
than finding decreased levels of physical exercise,
the authors were surprised to find that the 34 people
with CFS had higher than average levels of exercise
throughout childhood and a lower body mass index
prior to their CFS diagnosis.

Interestingly, these same folks reported continued
exercise even after they began to experience early
symptoms of fatigue.


So does this study identify the cause of CFS as being
exercise? No. However, it did a reasonable job of
decreasing the possible importance of atopic illness,
lifetime inactivity or exercise phobia as causes of
CFS.

The authors also did a good job of acknowledging
some of the strengths and weaknesses of the study.
But the greatest weakness of this study (which was
not acknowledged) is using a national birth cohort
that was designed to study something else.

Since this particular British national birth cohort was
designed to study fertility and obstetric issues, the
information collected is particularly relevant to these
two health questions.

So some potentially CFS-relevant information may be
missing. For example, the information on childhood
illness is limited, and there's no information on
illnesses--in particular infectious disease
episodes--after age 15.

The information that was not collected from this
national birth cohort isn't the fault of the authors.

But rather than interpreting that the drive to be
physically active is a personality trait that
predisposes people to CFS, what might these
researchers have found if they had the information
and inclination to approach their investigation from a
gene-environment perspective?

There is sufficient evidence in the literature that
points to genetic vulnerability for CFS. There's also
extensive evidence documenting environmental
events, such as infectious mononucleosis, that can
trigger CFS.

Now we see a possible connection to body mass and
lifetime activity. So what happens to active
individuals who get the "flu" and return to that same
lifestyle after they feel they've recovered? It's time
for investigators to step out of their comfort zone
and step up to the task of connecting these
tantalizing bits of disparate information to get to the
cause(s) of CFS.


(c) 2006, The CFIDS Association of America, Inc.

Judith opines:

I recently posted to CO-CURE a post that had as its purpose my concern  that
the basic canons of scientific methodology, logic, sound medical thinking  had
been badly violated in an article that had been announced on CO-CURE.   That
article appeared in a recent issue of PSYCHOSOMATIC MEDICINE.  It's  title
stated that it was a study of the most popular etiological factors (I am  not
sure what "popular" meant but certainly suggested "broadly accepted" or at  least
"broadly written about by worthy clinical and lab researchers.

What I objected to was not that there wasn't a shred of truth in the  article
or that there was nothing worthwhile. 

Now, Suzanne Vernon, who I know or knew knows what scientific methodology 
is, writes to defend the article because it used one of the most substantial 
cohorts.

And it mentioned some factors that most of us know are oft predisposing 
factors in the illness, like a history of atopy. But one of the central  (among so
many) bafflements about ME fall within the term "exercise  intolerance." 
Since a long flare after an increase in (I prefer to use)  muscle exertion/muscle
stress, even when it is "happy" and very longed for,  which in some studies
has been shown to correlate with changes in certain  metabolites, even when
that muscle exertion while it's happening is experienced  as pleasure and thus
maybe "causes" good neurochemicals to rise (popularly  referred to as
"endorphins") one hypothesis that cannot be dismissed is that  despite emotional and
physiological plusses being produced by muscle activity at  varying levels for
different people or the same people at different times in  their illness such an
experience would/could lead to increasing the inclination  to "exert their
muscles."

Unless they are masochists, I suppose.  But I don't think that  personality
problem has been sufficiently studied in even a small cohort.

To continue: Despite the size of the cohort and despite the correct mention 
of atopy as (I don't know what loading atopy has as a predisposing factor or
if  it's been studied both as a physiological characteristic and as a
psycho-social  one, including its role in early family development experiences that
shaped our  ME patient, which in some cases might have invited overprotective
parenting  and possibly the tendency to fear healthy activity though in
adolescence that  can be rejected and would have to be subjected to a long term, even
if  retrospective study) that article did nothing absolutely nothing to provide
a  sound differential diagnosis (exhaustive list of possible causal
hypotheses) for  "exercise intolerance."

Atopy does not.  Atopy does not ipso facto lead a person to fear  activity even though it can, rationally, lead to avoidance behavior.  But  that study did
not study how childhood atopy that might very well have "caused"  certain
avoidance behaviors that those who seem to have ME have  perpetuated in their
personality a tendency towards over-generalized  avoidance.

That is an hypthosis that is worthy of study though well designed and as I 
said above long-term not just large cohort.  And there would need to be a 
control group of those who were atopic and didn't develop ME so that the 
difference between the groups could then be studied if atopy were to be a  helpful
thing to know about the complex etiology of ME, if indeed ME is one  thing, which
it probably is not, and is a cluster of illnesses.

I do not comprehend, truly, how anyone with any medico-scientific 
credentials, knowledgeable about ME could possibly validate that study (Wesseley  among others was an author; there were several others) as throwing light on 
anything we don't already know about atopy and ME, even though it could be a  worthy
thing to study. 

The content and the logic, the substance of a small cohort study can often 
be far more useful to further getting to some of the central connunundrums  of
ME.  Not the size of the cohort.

I am starting to wonder if the model of thinking found affecting too much  US
governmental policy isn't a model for some of what we are seeing in the 
so-called ME scientific thinking.

But, then, I'm just sick and am rather sensitive to such sloppy reasoning 
about ME.  And I am one who feels that psychological factors and behavioral 
tendencies play their role in etiology, though I do not think there is ANY 
evidence that those factors are the ones that will lead us to major palliation  or
cure.

Judith Wisdom




Non-restorative sleep

The significance, assessment, and management of nonrestorative sleep
in fibromyalgia syndrome.

CNS Spectr. 2008 Mar;13(3 Suppl 5):22-6.

Moldofsky H.

Sleep Disorders Clinic of the Centre for Sleep and Chronobiology,
Toronto, Ontario, Canada. h.moldofsky@utoronto.ca

PMID: 18323770


People with fibromyalgia syndrome (FMS) experience unrefreshing
sleep, aches, hypersensitivity, and cognitive and emotional
difficulties. Although no specific causative factor or biological
agent is known to account for all of the features of FMS and these
related diagnoses, the generalized hypersensitivity of the body is
considered to be affected by disturbances in central nervous system
(CNS) functions.

Such CNS disturbances are intrinsic to the sleeping-waking brain,
where the common symptom elements in all these illnesses are poor
quality of sleep, nonspecific pain, fatigue, and psychological
distress in the absence of known disease pathology.

CFS/FMS and Cardiology

European Journal of Internal Medicine Vol. 19, #3, pp. 187-191, May 2008 URL: http://www.sciencedirect.com/science/journal/09536205

Electrocardiographic QT interval and cardiovascular reactivity in fibromyalgia differ from chronic fatigue syndrome

Jochanan E. Naschitz(a,*), Gleb Slobodin(a), Dauod Sharif(b), Madeline Fields(a), Hillel Isseroff(a), Edmond Sabo(a), Itzhak Rosner(c) a Departments of Internal Medicine A, Bnai Zion Medical Center and 'Rappaport Family' Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel b Heart Institute, Bnai Zion Medical Center and 'Rappaport Family' Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel c Rheumatology, Bnai Zion Medical Center and 'Rappaport Family' Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel * Corresponding author. Department of Internal Medicine A, Bnai Zion Medical Center, Haifa 31048, P.O. Box 4940, Israel. E-mail address: Naschitz@tx.technion.ac.il  (J.E. Naschitz).

Abstract

Background Fibromyalgia (FM) and chronic fatigue syndrome (CFS) frequently overlap clinically and have been considered variants of one common disorder. We have recently shown that CFS is associated with a short corrected electrocardio- graphic QT interval (QTc). In the present study, we evaluated whether FM and CFS can be distinguished by QTc.

Methods The study groups were comprised of women with FM (n=30) and with CFS (n=28). The patients were evaluated with a 10 min supine-30 min head-up tilt test. The electrocardiographic QT interval was corrected for heart rate (HR) according to Fridericia's equation (QTc). In addition, cardiovascular reactivity was assessed based on blood pressure and HR changes and was expressed as the 'hemodynamic instability score' (HIS).

Results The average supine QTc in FM was 417 ms (SD 25) versus 372 ms (SD 22) in CFS (p<0.0001); the supine QTc cut-off b385.7 ms was 79% sensitive and 87% specific for CFS vs. FM. The average QTc at the 10th minute of tilt was 409 ms (SD 18) in FM versus 367 ms (SD 21) in CFS (p<0.0001); the tilt QTc cut-off<383.3 ms was 71% sensitive and 91% specific for CFS vs. FM. The average HIS in FM patients was -3.52 (SD 1.96) versus +3.21 (SD 2.43) in CFS (p<0.0001).

Conclusion A relatively short QTc and positive HIS characterize CFS patients and distinguish them from FM patients. These data may support the contention that FM and CFS are separate disorders.

1. Introduction Fibromyalgia (FM) is a clinical syndrome characterized by widespread pain and abnormal sensitivity on palpation of specific tender points [1]. The pathogenesis of FM has been elusive, made difficult by the absence of distinctive biochemical or histological abnormalities. The very concept of FM has been challenged with suggestions that it represents an inappropriate extraction from the epidemiological continuum of subjective discomfort [2]. The clinical overlap of FM and chronic fatigue syndrome (CFS) reported to a variable extent has led to their frequent consideration as a single disorder [3-5]. On the other hand, support for FM as a distinct entity may be offered were a characteristic feature to be found which demarcates this group from the rest of the population [5]. Such evidence may be obtained from the study of the autonomic nervous system, which has been widely reported to be aberrant in FM [6-11].

In the clinical setting, autonomic nervous system activity is assessed by surrogate methods, chiefly cardiovascular reactivity (CVR). The fast response of the blood pressure (BP) and heart rate (HR) to acute stimuli is under autonomic nervous control. Therefore, BP and HR measurements during orthostatic challenge on head-up tilt testing (HUTT) can be used as one measure of cardiovascular autonomic activity, providing there is no evidence of organic heart disease, venous insufficiency or hypovolemia [12]. Classical pathological reactions to the HUTT are: vasodepressor reaction, cardioinhibitory reaction, orthostatic hypotension and postural tachycardia syndrome. In studies utilizing these outcome measures, evidence for abnormal cardiovascular reactivity was found in up to 60% FM patients [13]. However, these aberrations of CVR are considered to be nonspecific since the same reactions occur in a large variety of conditions associated with autonomic dysfunction [14]. Study of HR variability in FM patients has shown abnormalities consistent with sympathetic hyperactivity at rest and hyporeactivity to orthostatic stress [15-17] which is nonspecific, also occurring in a variety of other conditions associated with autonomic dysfunction [15,16]. By applying a novel method for the study of cardiovascular reactivity, an abnormal autonomic system functioning has been recognized in patients with CFS that differs from classic autonomic failure [6,7]. This method involves computing BP and HR changes during the course of a head-up tilt test with data processing by image analysis methods. These data receive numerical expression as the 'hemodynamic instability score' (HIS). HIS values >-0.98 are associated with CFS - sensitivity 84.5% and specificity 85% [7]. In contrast, by application of this methodology to FM, affected persons could not be distinguished from a normal population [6,8].

Changes in autonomic nervous activity also condition the repolarization kinetics of myocardial cells and, thereby, may modify the electrocardiographic QT interval [18-21]. In a recent study, a relatively short QT interval was found to be characteristic of CFS patients [22]. In the present study we examined whether QT intervals as well as cardiovascular reactivity differ in FM versus CFS.

2. Patients and methods

All participants gave informed consent and our institution's committee for human research approved the study. All patients were fully ambulatory at the time of the study. Technicians carrying out the HUTT were informed as to the patients' diagnosis but did not know of the intention to compare between the groups. Tilt test recordings of previously studied patients [23,24] were reevaluated. Consecutive female patients presenting either FM or CFS having completed 30 min of head-up tilt were selected for this analysis. Not included were subjects with comorbidities (such as obesity, diabetes mellitus) as well as those with overlapping FM and CFS. The FM patients (n=30) met the criteria of the American College of Rheumatology for FM [1]. The average number of tender points was 14.7 (SD 1.7). All patients had normal sedimentation rate, creatine kinase, and thyroid stimulating hormone levels and there was no evidence of any concomitant inflammatory rheumatic disorder. Their average age was 46.8 years (SD 7.1) and their average body mass index was 25.4.3 (SD 1.4). CFS patients (n=28) met the Centers of Disease Control and Prevention definition criteria of CFS [25]. Their average age was 35.8 years (SD 15.1) and their average body mass index was 25.1 (SD 1.4).

2.1. Head-up tilt test (HUTT)

The protocol of the HUTT was based on the 10-min supine-30 min head-up tilt test as previously described [6]. Testing was conducted from 8:00 a.m. to 11:00 a.m., in a quiet environment, and at a constant room temperature of 22-25 degC. The patients maintained a regular meal schedule, but were restricted from smoking and caffeine ingestion within 6 h of the examination. Intake of food products and medications with sympathomimetic activity prior to the study was prohibited. The patients lay in a supine position on the tilt table, secured to the table at the chest, hips and knees with adhesive girdles. Chest electrodes were placed on the right and left shoulders just below the clavicles and a third electrode was applied at the point where the left axillary line intersected the fifth intercostal space. The ECG was recorded on a Datex-Engstrom Cardiocap(TM) II instrument (Datex Instrumentation Corporation, Helsinki, Finland), connected to the Biopac MP 100 data acquisition system (Biopac, Santa Barbara, California). A sampling rate of 500 per second provided 1/500 Hz resolution. ECG tracings obtained corresponded to aVL, but when inappropriate measurements were obtained a chest modified lead V5 was utilized. Continuous ECG tracings were acquisitioned. The cuff of the BP recording device was attached to the left arm, which was supported at heart level at all times during the study. The stored data were later assessed by independent investigators who computed the hemodynamic instability score (HIS) and measured the QT and RR intervals.

2.2. Measurement of the QT interval

The ECG recordings were displayed on the computer screen at 50 mm/s speed with appropriate magnification for adequate identification of the T wave. The QT interval was measured from the beginning of the QRS complex to the point at which the T wave returned to the isoelectric line. When a U wave was present, the end point of the T wave was defined as the intersection of the steepest slope of the descending T wave and the isoelectric line [26]. The QT and RR intervals were measured by using the caliper of the Biopac computer program. Samples of 10 consecutive RR and QT intervals were measured a) at the end of 10 min of recumbence and b) at the end of 10 min of head-up tilt. The median value of each set of measurements represents the RR interval and the uncorrected QT interval, respectively. Coefficients of variation of the QT measurements have been previously established in two observers (MF and JEN): the intraobserver variation was 2.18% and 1.9%, respectively; the interobserver variation was 2.25% and 2.19%, respectively. Fridericia's equation performed the best to eliminate the effect of the HR on QT [22,27]. Fridericia's equation [28]: QTc = QT/RR^(1/3)

The best QTc cut-offs, separating CFS patients from a mixed control population (not including FM patients) were supine <385.7 ms and at the 10th minute of tilt <383.3 ms [22]. In the latter study, QTc values in healthy subjects were: supine average 396 ms (SD 26) and tilt 400 ms (SD 39). In the present study, the sensitivity of these cut-off values for CFS and their specificity vs. FM was reassessed.

The HIS was determined according to the protocol previously described [6] Several preliminary measurements were done, the first of them being calculation of the 'BP change' and 'HR change'. The BP and HR changes were also represented graphically in time-curves. The images were loaded in the computerized image analyzer Benoit Version 1.3 (Trusoft Int'l, Inc, 1999, St. Petersburg, Florida). The fractal dimension was automatically assessed by using the box counting method. Based on BP and HR changes and fractal dimension, an equation permitted to compute the 'hemodynamic instability score' (HIS).

HIS = 64.3303 + (SYST-FD.abs x -68.0135) + + (SYST-SD.cur x 111:3726)+HR-SD.cur x 60.4164)

The following independent predictors of the discriminant score were applied in this equation: the absolute value of systolic BP changes (SYST-FD.abs), the standard deviation of the current values of the systolic BP changes (SYST-SD.cur), and the standard deviation of the current values of the heart rate changes (HR-SD.cur). For reference, in 60 healthy subjects of whom 36 were women and the average age was 28.6 years (SD 8.3), HIS average was -3.14 (SD 2.9).

2.3. Statistical analysis

The difference between averages of two groups was assessed by unpaired Student's t test. Two-tailed p values of 0.05 or less were considered to be statistically significant.

3. Results

3.1. Supine QTc values

Supine QTc values had a normal distribution. The average supine QTc in FM patients was 417 ms (SD 25). The average supine QTc in CFS patients was 372 ms (SD 22). The difference between averages was 45 ms, the 95% CI 32-58, p<0.0001 (Fig. 1). The supine QTc cut-off <385.7 ms had 79% sensitivity for CFS and 87% specificity vs. FM.

3.2. Tilt QTc values

Tilt QTc values had a normal distribution. The average QTc in FM patients during the 10th minute of tilt was 409 ms (SD 18 ms). The average QTc in CFS patients at 10th minute tilt was 367 ms (SD 21). The difference between averages was 43 ms, the 95% CI 32-54, p<0.0001. The tilt QTc cut-off<383.3 ms had 71% sensitivity for CFS and 91% specificity vs. FM.

3.3. HIS values

The average HIS value in FM patients was -3.52 (SD1.96), with only one patient exceeding the -0.98 cut- off. The average HIS value in CFS patients was +3.21 (SD 2.43), being greater than -0.98 in all patients. The intergroup difference was statistically significant (p<0.0001).

4. Discussion

In this study, the QTc was within the normal range in the large majority of FM patients (average 417 ms supine and average 409 ms on tilt) while a relatively short QTc interval characterized CFS patients (average supine QTc 372 ms and average tilt QTc 367 ms).

The QT interval on the surface electrocardiogram (ECG) reflects depolarization and repolarization of myocardial cells. A variety of factors may influence the QT interval, including heart rate (HR), genetic abnormalities of the potassium channel, electrolyte disturbances, myocardial ischemia, drugs, and sympathetic and parasympathetic tone [19,21]. The HR influences the QT interval to a considerable extent, therefore, for common use, the QT is adjusted to HR (QTc). The methodology of QT correction utilized in this study is well established. The reproducibility of QT measurements was demonstrated by low intraobserver and interobserver variabilities and compared favorably with data published elsewhere [22,27-29]. In comparisons of 10 different QT correction formulas, Fridericia's correction was shown to provide the best results [29]. We tested various correction formulas in our patient population [22] and found, in fact, that Fridericia's correction performed the best and was, therefore, selected for the present investigation.

Usually QTc in the range of 0.400-0.440 s is considered to be normal [30]. While the upper limit of normal for the QTc is well defined and its prolongation has been used as an ECG marker to identify patients at risk for sudden arrhythmogenic death, there is no consensus on the lower limit of normal for the QTc or its clinical significance. Atropine causes QTc shortening [19]. Short QT intervals are encountered in hypercalcemia [31] and the recently described idiopathic rate-independent short QT syndrome [32]. A relatively short QTc is often noticed in patients with the chronic fatigue syndrome [22].

The mechanisms underlying the relatively short QTc in CFS have not been investigated. Prior studies in CFS, based on spectral analysis of HR and BP, showed that the vagal tone is reduced in these patients [33,34]. Decreased vagal tone may provide the mechanism for QTc shortening in CFS; however, it should be noted that not all studies have confirmed that vagal tone is diminished in CFS [35,36].

The HIS, which reflects autonomic nervous influences on the cardiovascular system, HIS differs significantly in FM versus CFS. In the present study, the average HIS in FM was -3.52 (SD 1.96) and the average HIS in CFS was +3.21 (SD 2.43) (p<0.0001). This data is consistent with previous results in female FM and CFS patients and compared to healthy controls. In one study [6], the HIS threshold -0.98 differentiated between CFS patients (HIS=average +2.02, SD 4.07) on one hand and healthy subjects (HIS=average -2.48, SD 4.07, p<0.0001) as well as FM (HIS average -3.27 p/m 2.63, p<0.0001) on the other hand. Subsequent studies confirmed these observations [7,8]. The overall specificity of the HIS for the diagnosis of CFS was 85% [23].

FM and CFS overlap has been repeatedly reported and raised the possibility that both conditions are variants of one common functional disorder [3-5]. Recent studies addressed the molecular basis of CFS. Data from the Wichita (KS, USA) CFS Surveillance Study identified 24 common genes in CFS patients, providing evidence for a biological basis of CFS [37]. A different possible genetic association has been reported in FM with a polymorphism in the serotonin transporter gene regulatory region [38]. Other scientists are skeptical with these results. Additional studies have suggested that CFS patients may be distinguished from those with FM by their cardiovascular reactivity pattern [24,39]. In the present study, the QTc and HIS were within the normal range in the large majority of FM patients. In contrast, a short QTc interval and increased HIS characterized CFS patients. Both HIS and QTc are influenced by autonomic nervous activity. Thus, an alteration in autonomic function which is operative in CFS but not in FM may explain the differences in QTc and HIS. A recent review article by Prins et al. [40] recapitulates the difficulties with the definition and understanding the pathophysiology of CFS. The authors suggest a framework for future studies by following two strategies: the aims at distinguishing CFS from other disorders; the other explores similarities and dissimilarities in functional somatic syndromes based on neurosciences. Applying the methodology of QTc and HIS in the study of autonomic functions in CFS and FM may be in line with those suggestions.

There are limitations to this study. Patients with FM and CFS were not of similar age; only milder cases of CFS were studied; patients with FM-CFS comorbidity were not included; and detailed assessment of autonomic nervous functions has not been performed. There are also limitations related to the methodology utilized. Only one monitor lead was used to measure the QT intervals and not the 12 lead electrocardiogram. This restriction was a function of the monitoring instrument used.

Combined evaluation of the cardiovascular reactivity and cardiac depolarization-repolarization may be of interest in research settings. Their applicability in clinical situations and their possible advantage as a diagnostic test remains to be investigated in prospective studies. In the future, electro-physiological studies and investigations of family members of CFS patients may be important to the understanding of the pathophysiology of shortened QTc in CFS and establish to what extent this phenomenon is inherited.

5. Learning points

* Fibromyalgia and chronic fatigue syndrome frequently overlap clinically and have been considered to be variants of one common disorder. Changes in autonomic nervous activity have been linked to the pathophysiology of both disorders.

* The present study showed that autonomic nervous functioning, indirectly evaluated via electrocardiographic QTc interval and cardiovascular reactivity, differs in fibromyalgia and chronic fatigue syndrome.

* This data may support the contention that fibromyalgia and chronic fatigue syndrome are separate disorders.

Figure caption

Fig. 1. QTc values in FM and CFS. FM_S=fibromyalgia patient measurements at the end of the supine phase, CFS_S=CFS patient measurements at the end of the supine phase; FM_T=FM patient measurements at 10 min of tilt; CFS_T=CFS patient measurements at 10 min of tilt. The boxes contain the 50% of values falling between the 25th and 75th percentiles; the horizontal line within the box represents the median value; the 'whiskers' are the lines that extend from the box to the highest and lowest values excluding the outliers.

CFS/FMS and Cardiology FOOTNOTES



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   Dysautonomia among patients with fibromyalgia: a noninvasive
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17 Martinez-Lavin M, Hermosillo AG, Rosas M, Soto ME. Circadian
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   and reproducibility. Clin Auton Res 1996;6:309-12.
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   variables from 24 hour electrocardiography and the two year risk of
   sudden death. Br Heart J 1993;70:43-8.
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   hypercalcemia. Am J Cardiol 1979;44:243-8.
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   Schoeps P, et al. Possible association of fibromyalgia with a
   polymorphism in the serotonin transporter gene regulatory region.
   Arthritis Rheum 1999;42:2482-8.
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   et al. Patterns of cardiovascular reactivity in disease diagnosis. QJM
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   Lancet 2006;367:346-55.

HPA Axis Abnormalities

URL:    http://www.newsrx.com/article.php?articleID=921018


Findings from Centers for Disease Control and Prevention broaden
understanding of central nervous system disorders genetics
----------------------------------------------------------------

Current study results from the report, 'Genetic evaluation of the serotonergic
system in chronic fatigue syndrome,' have been published. "Chronic fatigue
syndrome (CFS) is a debilitating disorder of unknown etiology with no known
lesions, diagnostic markers or therapeutic intervention. The pathophysiology
of CFS remains elusive, although abnormalities in the central nervous
system (CNS) have been implicated, particularly hyperactivity of the
serotonergic (5-hydroxytryptamine; 5-HT) system and hypoactivity of the
hypothalamic-pituitary-adrenal (HPA) axis," researchers in the United
States report.

--------
(c) 2008 NewsRx.com

National Scandal Exposed

Many thanks to Cindee Rice <cmarie3@cox.net>,
who drew my attention to this important broadcast

ME/CFS - A Hidden National Scandal Exposed
~~~~~~~~~~~~~~~~~~~~~~~~~~~~

This moving broadcast by Meridian TV (Meridian
Tonight) is a MUST for physicians, parliamentarians,
newspapers, tv stations, charities, lawyers,
teachers, patients, their family, friends, etc., etc.

It can be found at:
http://hk.youtube.com/watch?v=hkGq0BH6AHw


By opening *luminescentfeeling* on the right site,
you can find this excellent article:

Dr Kerr & the 'cure' that never was.
~~~~~~~~~~~~~~~~~~~~~~

Dr Kerr & the 'cure' that never was. No cure had been
made available. Not due to Dr Kerr - but due to the
blocking of funds to continue his work. (As has
happened to Dr Gow) - another genetic expert from
Scotland who is also finding things in this illness
that people don't want to hear.
I wonder why? Not
that they have anything to hide or anything, no......

This is an edited (for time) clip of a Meridian TV
news item that appeared on our screens over here in
England,UK in 2005.

Meridian TV should be applauded for having the
bravery to broadcast this - it was NOT broadcasted
nationally to protect the Government from shame
and being asked questions - obviously.
Consequently, only a few people saw it.

Even after this ground breaking genetic discovery
was broadcast the UK Government still continue to
block funding for research and a diagnostic test for
ME/CFS.

In 2008, not one ME/CFS clinic exists in the UK. All
money is still going to psychiatry and the 'Wessely
School' - despite M.E being recognised as a
neurological illness by the World Health Organisation
(W.H.O) since 1969.

This flow of money is blocked by the MRC (Medical
Research Council) who are influenced by the insurance
industry - who have too much to loose to open the
flood gates with 100,000's of thousands of patients
making disability claims. The truth on ME/CFS is thus
kept tightly shut. Doctors, civil servants and the
general public -still have no idea that ME can be
fatal.

All we hear about is 'recovered' CFS patients in the
newspaper - who 'recover' by taking anti-depressants
and deciding they weren't actually ill after all. As you
may know, the 'recovery' rate for ME is around 2%.
Meaning 98% of people do not recover. Despite this,
the british media rarely print articles on the severely
chronically sick and instead focus on the mentally ill.

These mentally ill people are 'volunteered' towards
the media by bogus CFS charities. These charities
are funded by the national lottery (Lotto) and extra
government funding - to push a psychiatric agenda.
The UK Government, and the BMA (British Medical
Association) are thus a disgrace - as are bogus CFS
patients, bogus CFS charities and the corrupt and
evil Psychiatrits who prey on desperately ill patients.

The NHS website in the UK claims 'most' people get
better, and that this illness may 'last for months'.
This is surely immoral? Promising people with viraly
induced brain stem/ cardiac damage/DNA damage a
cure with CBT/GE - graded exercise and behavioural
therapy!

For the TRUTH on what ME does to people, go to:
http://www.meresearch.org.uk/
http://www.investinme.org
http://www.cfsrf.com/
http://www.investinme.org
http://www.ahummingbirdsguide.com
http://phoenix-cfs.org
http://www.ahmf.org  (??)

````````````````````
Many other *ME/CFS-YouTube's* can be found at the
same address as above; some examples:
ME/CFS - Shortens lifespan by 25 years.
ME/CFS - Doctors disbelief kills young woman
Chronic Fatigue Syndrome CFS
ME/CFS - Doctors trained to neglect (part 2 of 4)
ME/CFS - The Possible Consequences Of Medical
Neglect
Why 'CFS' is a wastebasket diagnosis
ME/CFS - Doctors trained to neglect (part 1 of 4)
CFS 2006 awaresnes Campaign CDC
Sleepydust - About M.E. / Chronic Fatigue Syndrome
Missing my Life -deutsche Version-
A symptom list: Myalgic Encephalomyelitis
The Psychiatry Scandal
Japanese CFs
'CFS' harms everyone, not just M.E. sufferers
Problems with 'our' M.E. (and CFIDS, ME/CFS)
advocacy groups
Wessely wants "Chronic Fatigue Syndrome" - ITN
Gupta Programme for ME, CFS & Fibromyalgia
M.E. and Incapacity Benefit
A short CFS documentary
WHO's right? M.E. is neurological not psychiatric

~jvr


Still Paying for an Enjoyable Afternoon

I went to lunch the other day with an out-of-town friend. Since this was our only chance to see each other this year, I wasn't keeping close tabs on the time to avoid overdoing. Instead of coming home in 2 hours or less to avoid wearing myself out, I was out for about 3 1/2 hours. Most of it sitting down chatting -- typical office job behavior -- and four days later, I'm still feeling the effects of it. I'm exhausted, and falling asleep for 2-4 hours mid-afternoon.  There's your proof that I cannot hold a "real job" ... I would work one day and then would have to spend several days in bed.  And that's after not even a full 8 hour day away from home!

ADA-mandated accommodations do NOT include "work when able".  VocRehab won't help you if you can only work one day a week: they can't place someone who can't come in at least M/W/F.

Clearly, if I'd had the mandated Functional Capacity Evaluation, it would be obvious that I cannot work even one 8-hour day without collapsing, and therefore, I'm disabled.  The reason that my application for Disability benefits isn't approved is clearly that people "choose" to believe that a silly name equates to a minimal level of impairment, and they don't want to see any proof that there are demonstrable biological abnormalities (i.e., it's not just laziness).  The FCE hasn't been done, and I can assure you, it will never be done, because it would be more more piece of evidence that they don't want to see.  If they do only the tests that "should" be normal in CFS, they can continue to dispute my claim.

Tell Your Story -- Making the Invisible Visible

(Paul said this message could be re-posted)

Hi Everyone,

I have been making regular videos and putting them on YouTube for about a
year now. I started to do it mainly to keep a record for myself but also I
hoped that they may help others in at least knowing that they are not alone.
I
have been very surprised at the response that I have had, and my videos have
been watched over 13,000 times! This got me thinking....


I think that I am right in saying that May is ME awareness month. I have set
up a YouTube group for people to post videos about their experiences with
having ME. My hope is that this will help to raise awareness of the
condition.
Telling your story can be very powerful. It is easy for the public and
politicians to ignore facts and figures; it is far harder for them to ignore
real people, with real faces! All of the major political parties have
YouTube
accounts now as they have come to realise that it has huge potential to
raise
awareness of their policies. It wouldn't surprise me I some of their party
workers use it to find out the concerns of the public. I am speculating
here,
but it does seem reasonable.

The media is another group that often takes notice of things placed on
YouTube, so if enough people place their stories in this group, it may be
that
someone in the media will pick it up. But if none of this happens I still
think
that it would be a worthwhile project as it will encourage many people in
the
UK and worldwide who are suffering from ME. One way to get our videos the
most exposure is to get as many people to watch and rate them as possible. A
place near the top of YouTube's search engine, or if possible on their front
page, would create massive publicity.

So if you have a web cam, and would like to contribute please do. Don't
worry too much about the quality of the video. My videos not at all
professional.
I usually I have a rough idea what I am going to say and just speak! A
professional presentation is not important, what is important is you and
your
story. Your story counts. Someone has said that ME is an invisible disease,
let's
try and make it visible!

Here is the link: http://www.youtube.com/group/mecfsmystory

BW.

Paul

Sunday, April 20, 2008

"Tired" doesn't even come close

Reply to article which emphasises that M.E. is just not fatigue or tiredness
(link below my signature).

Now is your chance to say that people with M.E. know this and wish that
others did too.

letters to the Editor e-mail address is david.hart@haverhillecho.com

Cheers
John
drjohngreensmith@mefreeforall.org

Haverhill Echo Letters

Not only has Karen Steel bagged the best title for an article about
M.E. (*Tired just doesn't come close to ME, Haverhill Echo, 17 April 2008*), she has, in telling the story of M.E. sufferer, Chris Aldis, given the most accurate
account of this dreadfully disabling illness I have ever seen in a newspaper
for general readers, who may not have experienced it before.

Chris meets all the diagnostic criteria for M.E. (*Myalgic Encephalomyelitis*): an overwhelming feeling of lassitude, which does not present like
fatigue usually does and is not refreshed by any number of hours of sleep;
very slow recovery after quite minuscule effort ("post-exertional malaise");
cognitive problems, dizziness and he is prone to relapse if he overdoes
things when feeling a little better. Although Chris says he was depressed,
he was probably more likely, understandably, fed up by being unemployed,
discriminated against, possibly disbelieved and at the lack of social
contact due to the illness
, which seems to be have been fixed by a
sympathetic employer. M.E. sufferers, doctors and researchers will recognise
it and say this is exactly what M.E. is  and that it is not fatigue, nor a
psychiatric illness.

So, it would seem logical to publicly fund research, to understand the cause of what M.E is, with the aim of finding a cure and getting adults back to work and children back to school, thus saving on benefits and home tuition, rather than to waste money on what we already know M.E. is not.

Unfortunately, a report by NICE (National Institute for Health and Clinical
Excellence) published in August 2007, recommends the opposite approach. M.E.
sufferers are referred to one of a network of clinics, which cost £millions
to establish, for two treatments, one of which, Cognitive Behaviour Therapy
(CBT) - which was developed for psychiatric illnesses, such as anxiety and
depression - has no lasting benefit for people with M.E. and the other,
Graded Exercise treatment (GET), which leaves some irrecoverably worse after
it. Meanwhile, promising biomedical research projects are turned down by the
Medical Research Council (MRC) and have to rely on charity.

This policy, which leaves people with M.E. languishing ill and starves
research projects which may help them to get better, shows no signs of
changing.

Yours sincerely
drjohngreensmith@mefreeforall.org
Dr John H Greensmith
ME Free For All. org

http://www.haverhillecho.co.uk/news/Tired-just-doesn39t-come-close.3992758.jp

Tired just doesn't come close to ME
Haverhill Echo
Karen Steel, Deputy Editor
17 April 08

Imagine being so exhausted you sleep for 23 hours, only to wake up, make a
cup of tea and be so drained you need to go back to sleep again.

For some sufferers of ME (Myalgic Encephalomyelitis) or Chronic Fatigue
Syndrome that can be the reality, and as well as dealing with a debilitating
condition, they can face the stigma surrounding what has previously been
known as 'Yuppie flu'.

Now Haverhill man Chris Aldis is talking about his experience of the
condition in the hope it will raise awareness – and he's also hoping to
raise some money to support fellow sufferers by facing his phobia.

ME has traditionally attracted some controversy and confusion, because – as
yet – there is no single understanding of what causes or triggers it,
something backed up by Chris's own experience.

"It was around Christmas 2005, when I was working as a carer with the
elderly in Berkshire. I was really tired and run down, but I just assumed it
was the time of year.

"It got worse and, in February 2006, I collapsed at work and had to go into
hospital.

"I had a week off work, and after that, every time I tried to go back to
work, I relapsed."

Eventually he had to leave the job he loved, and it was at this time he was
sleeping up to 23 hours per day.

Simple actions such as making a cup of tea left him physically and mentally
exhausted,
but doctors were unable to shed any light on the condition, and
being forced to give up on what he had planned to be a long-term career left
him depressed.

As well as the exhaustion – which goes far beyond the average person's
experience of 'tiredness' – Chris suffers constant muscle pain, for which he
must take painkillers.

While even the slightest exertion can exacerbate the condition, Chris
learned to manage his symptoms and recognise his limits.

In March 2007, he decided a change in scenery might be needed, and moved to
Haverhill, with the hope of finding work again.

But some potential employers paled at the idea of taking on a person with
ME, who - they possibly imagined - would need to take a lot of time off
work.

He said: "So many people, as soon as they found out I had ME, my application
went in the bin."


One might think the demands of excitable, adventurous and physically active
small children might be beyond the realms of someone with chronic fatigue
syndrome, but Chris applied for a job with Dizzy's Day Nursery, in Hollands
Road, Haverhill, (although he admits he nearly didn't send the application
in) and the nursery was keen to employ him – in fact Chris cannot speak
highly enough of the support they have offered him.

Chris said: "It's a very demanding job, but I work with very understanding
people and they know I'm not the one who's going to be able to go out in the
garden with the children."

Liz Jones, manager of Dizzy's, said: "Chris is a great asset to the nursery,
so if we hadn't employed him, we would have lost out.

He's a great member of the team, and I really don't think he has more time
off than anyone else."

Chris, of Vetch Walk, admits to some resentment towards the ME, because he
is unable to go clubbing like many people his age, but has learned coping
strategies such as waking himself up an hour earlier than he needs to get
up.

There is a support network for young people with ME, called AYME
(Association for Young People with ME) and Chris now wants to raise money
for the organisation by facing his fear of snakes.

He hopes to first be in a room with, and later handle, a snake, being taken
to the nursery on May 13.

Anyone who wishes to sponsor him should contact the nursery on 01440 706246.