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Chronic Fatigue and Immune Dysfunction: Who Took the “ID” Out of CFIDS?

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Does anyone remember CFIDS, aka Chronic Fatigue and Immune Dysfunction Syndrome? Back in the 1990s this was the accepted term for what is now called CFS, or, if you are so inclined, ME/CFS. The “ID” was quietly dropped by researchers and doctors about 10 years ago in favor of Steven Straus’s infamous legacy: chronic fatigue syndrome. Everyone agrees that CFS is a confusing, misleading and utterly dismissive name for the illness. Not only does it harm the people who have CFS, it harms the people who don’t. In a recent study of patients newly diagnosed with MS, nearly one-third had been diagnosed with CFS (or with the even more vague, “fatigue”) for one to two years prior to being diagnosed with MS.

Imagine how many other patients with incipient cancer, heart disease, liver disease, diabetes (to name a few “fatiguing” illnesses) have had the catch-all diagnosis of CFS slapped on them simply because they were tired. The term CFS has been just as much a curse to those patients, whose correct diagnoses and treatments have been delayed by years, as it has been to patients with CFIDS.

Who did this? Who managed to drop the all-important feature of immune dysfunction from the name? After all, it is obvious that people with CFIDS have an immune dysfunction. Chronicity is, in fact, the product of an altered immune system. With a fully functioning immune system, the host recovers. Immune dysfunction is not just a feature of chronic disease, it is its definition.

What’s more, the furor over what to call the “Disease of a Thousand Names” has only intensified since the “ID” dropped out. Prior to its deletion, people who had been diagnosed with (depending on their geographic location) ME (myalgic encephalomyelitis) or CFIDS maintained a cordial relationship. Since the change, they are at each other’s throats. People with ME do not want to be diagnosed with an illness that not only reduces all their symptoms to the “f” word, but is doggedly lumped into some ill-defined category of mental illness.

Who did this? Who managed to divide what was once a unified community into squabbling sororities? The CFIDS community could, and did, accomplish so much when it spoke with one voice: national organizations, political lobbies, well-subscribed magazines. Now, it is factionalized, torn apart by the desire to achieve maximum distance from the stigma of “fatigue.”

An even more disturbing consequence of dropping the “ID” is that supposed friends, clinicians who once championed the cause, have not only slipped into the term CFS, but are adding insult to injury by dropping the S part and referring to an illness which not only destroys lives, but can eradicate them, simply as “chronic fatigue.” It’s bad enough when patients call their illness “chronic fatigue,” but Nancy Klimas, head of the Neuro Immune Institute and world-renowned CFIDS specialist, should know better.

Who did this? Who trivialized this illness among formerly committed researchers and clinicians? Who robbed CFIDS patients of their defenders?

Benjamin Natelson.

In 2002, Benjamin Natelson, noted CFIDS researcher, was given a grant by the NIH to do a meta-analysis of immune studies in CFIDS patients. Meta-analyses are not research studies, they are merely analyses of studies that have been performed in the past. Because meta-analyses basically serve as CliffsNotes for researchers who are too pressed for time to read the original work, their ultimate value to the research community has been questioned.

Natelson’s meta-analysis, entitled “Evidence for the Presence of Immune Dysfunction in Chronic Fatigue Syndrome,” examined 79 studies of immune function in CFIDS patients. Natelson found that that there was no consistent immune dysfunction. Some studies indicated that there were increased pro-inflammatory cytokines, others found increased anti-inflammatory cytokines.

Given the fact that one of the hallmarks of CFIDS is waxing and waning symptoms, this should not have come as a surprise. The immune dysfunction that characterizes CFIDS is that it both under- and over-responds. This is the ultimate outcome of the loss of homeostasis which lies at the heart of the illness.

Natelson ignored this aspect of immune dysfunction, just as he ignored the one consistent piece of data he found across these studies: low natural killer (NK) cell function. He concluded that “the available evidence does not support chronic fatigue syndrome as being due to any consistent immunological dysfunction […] we believe that the term “chronic fatigue syndrome” is preferable to the older “chronic fatigue and immune dysfunction syndrome.”

Aside from the damaging consequences of this conclusion, it turns out that Natelson was wrong.

In 2012, a group of Australian researchers headed by Ekua Brenu completed the first longitudinal study of immune function in patients with CFS/ME (CFIDS). This was the first time researchers had examined immune function over a long period of time, in this case, 12 months. The value of longitudinal studies to measure immune function is that the immune system is a moving target. It responds instantly to environmental input. Even the best short-term study of the immune system can’t give researchers more than a snapshot.

The Brenu study found that patients with CFIDS do indeed have an immune system dysfunction. It is the same immune dysfunction that most other immune studies have found over the past two decades: low NK function. The natural killer cells of CFIDS patients ignore invaders, tumor cells among them (which is perhaps why so many people diagnosed with CFIDS in the 1980s went on to develop lymphomas). The authors concluded that because cytotoxic activity was consistently decreased during the course of the 12-month study it “may be a suitable biomarker for diagnosing CFS/ME.”

Notwithstanding the tantalizing possibility that a biomarker may have finally been found, the real clincher came at the end of the discussion section, where the authors explained why previous short-term studies had been equivocal:

“Cytokine release in CFS/ME patients undergoes shifts during the course of the disease where patients may present with either an amplified or depressed anti-inflammatory or pro-inflammatory cytokine profile. These alterations in cytokine secretion may occur during the course of the disease and at different times causing either a shift towards a predominant Th1 or Th2 immune response in CFS/ME This makes it difficult to establish a unique CFS/ME-like inflammatory cytokine profile. The observed pattern of cytokine distribution among our CFS/ME patients is consistent with equivocal findings in the literature. In adolescents with CFS/ME, cytokine secretions have been observed to be correlated with seasonal variations. Therefore, CFS/ME may be associated with oscillations in pro and anti-inflammatory cytokines, supporting the heterogeneity and multifactorial nature of the disease and the diversity in symptom presentations.”

That paragraph alone should have heralded a new age in CFIDS research. It should have stimulated a lively discussion. It should have prompted a retraction of Natelson’s damning conclusion. It should have reinserted the ID.

But instead of doing any of those things, it was ignored, not just by the broader scientific community, but by CFIDS researchers, clinicians and, saddest of all, by those who would have benefitted the most – the patients. We are now lying in the bed that has been made for us.

And it is a hard one.

References:

Berger JR, Pocoski J, Preblick R, Boklage S. “Fatigue Heralding Multiple Sclerosis,” Mult Scler. 2013 Feb 25. [Epub ahead of print].

Natelson, Benjamin H., Mohammad H. Haghighi, and Nicholas M. Ponzio. “Evidence for the Presence of Immune Dysfunction in Chronic Fatigue Syndrome.” Clin Diagn Lab Immunol. 2002 July; 9(4): 747–752.

Ekua W Brenu, Mieke L van Driel, Donald R Staines, Kevin J Ashton, Sharni L Hardcastle, James Keane, Lotti Tajouri, Daniel Peterson, Sandra B Ramos, and Sonya M Marshall-Gradisnik. “Longitudinal investigation of natural killer cells and cytokines in chronic fatigue syndrome/myalgic encephalomyelitis.” J Transl Med 2012; 10: 88 doi: 10.1186/1479-5876-10-88.

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About Erica Verrillo

Erica Verrillo is the author of Chronic Fatigue Syndrome: A Treatment Guide, 2nd Edition. She has published three middle reader fantasies with Random House: Elissa's Quest, Elissa's Odyssey and World's End. Her short stories have appeared in Million Stories, Front Porch Review, 180 Split and Thema.
  • http://slightlyalive.blogspot.com Mary Schweitzer

    If you’ll look at the list of authors on the Australian study, you will find Dan Peterson of Incline Village, NV (where one of the best-known outbreaks took place in 1984-85), who has been collaborating with Staines. Peterson has used natural killer cell dysfunction as a biomarkers successfully for years, but NIH has consistently refused to fund any studies. He also uses the 37kDa Rnase-L defect; SPECT scans, fMRIs, spinal taps, and VO2 MAX stress tests. Those of us who fit the immune dysfunction/persistent viral infection subset of the patient population already have our biomarkers, if only CDC and NIH would pay attention. Most of Peterson’s patients have EBV involvement and/or persistent infections with beta herpesviruses: HHV-6A, cytomegalovirus (CMV or HHV-5), and/or HHV-7. He treats these with immune drugs and antivirals.

    As for the disappearance of the [ID] in CFIDS, it happened, IIRC, as a kind of an unspoken compromise for being willing to start using M.E., with a focus on the neurological category G93.3 in ICD-10.

    With all the information we have had for years (actually, decades) about beta herpesviruses and Coxsackie B (an enterovirus, of the polio family of viruses), it about drove me crazy to read all those headlines insisting there was “no evidence of viral involvement in CFS or M.E.” when the retrovirus research was squelched.

    Hopefully the successful publication of the Staines-Peterson collaboration is a harbinger of better news to come.

    Thanks for bringing this to everyone’s attention.

  • Erik Johnson

    I can answer that.
    “CFIDS” never was officially adopted or “officiated” into the medical literature by an authorized medical body, so it was never was anything more than a colloquialism.
    Seymour Grufferman suggested patients use CFIDS to impress doctors, but as this was not an official term, it has no “authoritative standing”
    “CFS” is, and remains the operative terminology.

  • http://slightlyalive.blogspot.com Mary Schweitzer

    If I can add another comment, one advantage to CFIDS, pronounced “See-fids” (aside from the reference to something medical!) was that it was easy to say. Neither “CFS” nor “chronic fatigue syndrome” is particularly easy to say, so instead of saying “Sea-fids,” we get “chronic fatigue” without “syndrome” attached, which is awful, but even our friends in the clinical and research world often drop “syndrome” when talking casually (and, unfortunatelely, that spills over into public use). But it is hard to push your doctor to say “Sea-Fids” when you’re already pushing for recognition of M.E. [I remember years ago my son said “Sea-fids? That sounds like something that’d get in my aquarium!”].

    So what do people think about that dilemma? How do you simultaneously encourage the use of CFIDS and recognition of M.E.? (FWIW, my own website, badly in need of updating, has been cfids-me.org for over fifteen years – but I can’t take credit fir that; it’s leftover from the short-lived organization WECAN (the Worldwide CFIDS-ME Action Network – the membership voted for the name), which was around from 1996 through 1999. Sigh.

  • Erik Johnson

    A name for anything automatically brings up the question, “To what was this name given?”

    If you ask what “CFIDS” was given to, it is “The Disease”, which leaves CFIDS wide open to being whatever the people who voted on the name happen to think “The Disease” is.

    “CFS” is a bit more restrictive.

    This was a term applied by the CDC’s Holmes committee to a database of evidence generated during an investigation into a particular illness outbreak…. and “speculatively” to other outbreaks, which may or may not have been the same.
    To be determined by further study into the matter.

    Change the name and you also change the people it was who gave it, and what the name was given to.

    Sometimes that changes everything.