“CFS” and Hope

"The Garden of Elisa" by jaci XIII



CFS/ME is Autoimmune Polyendocrine Syndrome:

An Original Hypothesis

- Cathi Carol, 2012



Updated March 2013

For thirty years, since 1982, I have had (what I was told was) CFS, aka ME in the UK.

My etiology, the onset of the disorder, and my symptoms are classic. I won’t list them; anyone with the disorder knows exactly what they are (also here and here), and what they are not (also here and here). (Also see the Resources page.)

I was and am a perfect example of someone with the disorder. I have no depression or other mental illness. I fit all of the physical and cognitive criteria for the diagnosis, expression, and outcome of the disease, even as different descriptions developed and have been put forth over the years by different research groups worldwide, starting with the CDC in the late 1980s to today’s International Consensus Criteria published in the Journal of Internal Medicine in 2011.

Except for some minor fiddling, especially with whether to include some psychosocial elements among the etiology and symptomologic effects (which was never appropriate but which causes much suffering among patients when it leads to them being accused of having a psychological disorder rather than a physical one or of malingering), the criteria for diagnosis hasn’t changed that much.

In fact, after the initial diagnosis, which fit me so well, I haven’t paid that much attention to the diagnostic criteria discussion among medical researchers or the dispute among some patients and patient advocates about what to “call” the disease; my personal interest, my literature research, and my own work (finding accurate physician clinical diagnosis of progressive organ failure and appropriate support, and my own record-keeping, self-testing, and scientific analysis) has remained focused on etiology, symptomology, and treatment.

My thirty years of research led me, this year, no longer to calling what I, and so many other thousands of people, have “CFS” or “ME”. I know, now, what it is.

It is Autoimmune Polyglandular Syndrome Type II (APS II), aka Polyglandular Autoimmune Syndrome Type 2 (PAS-2).

I believe that CFS/ME is either APS II or a variant of APS II.

Polyglandular Autoimmune Syndrome is caused by long-term autoimmune disease leading to advanced polyendocrine neuroautoimmune dysfunction.

Long-term autoimmune disease of unknown or any etiology, as far as is now known, attacks the organs and systems of the body until it breaks down into permanent disability.

The breakdown often occurs suddenly, over a few days to weeks, due to “a steep drop in production of several essential hormones by the glands that secrete these hormones”.

This steep drop in hormone production can be due to ongoing or to new, sudden, or overwhelming stress overtaxing already limited endocrine hormone output and/or tissue uptake. Therefore, the ability of the body to handle stress diminishes rapidly to near-zero or zero, and partial to full physical disability occurs.

The stress trigger can include inadequate sleep (even over just days or weeks), a debilitating infection such as the flu, surgery, or even a trip with friends.

To put it very simply, the body needs hormones to function, to do work, to warm itself, to operate its many systems, and to deal with stress. When physical demand is made and there are not enough hormones available to meet the demand, hypoxia may occur, cell damage accumulate, and broad systemic damage result.

If serum hormones, whether at subclinical, low, near-normal, or even normal levels, can’t get into the body’s tissues in adequate amounts, it’s possible that a vicious cycle of low intracellular hormone levels and cell damage caused by hypoxia may be set up.

Because APS II is thought to be a rare inherited disorder, the connection hasn’t yet been made to CFS/ME. I have just made it.

If CFS/ME is APS II then, obviously, APS II is not as rare as physicians now believe that it is.

But the illness is biophysical in origin, and to treat or cure it will require differential strategies of biophysical intervention.

What is confusing about this illness is that the cell damage caused by autoimmune disease accumulates very slowly and therefore is hard to diagnose and often a challenge to treat.

In each individual case there are varying levels of endocrine system, neurological, intramuscular, and other systemic damage that can take years to progress and finally to manifest clinically.

Extreme disorder and its effects, or “textbook” cases, are easier to spot; very low-level but chronic progressive disorder can easily be missed by physicians and may remain untreated, leading to advanced dysfunction, eventually, by what may be considered “idiopathic” means.

Many of the neurological and cellular/muscular symptoms of CFS/fibromyalgia are most likely due to chronic low-level cerebral and tissue hypoxia, not to chronically active infection.

Even subclinically-low levels of thyroid and adrenal hormones lead inexorably, over time, to tissue hypoxia and unsustainably low metabolic functioning, including a “hypothyroid heart”, which may not be diagnosable through heart imaging. Treatment with replacement hormones (liothyronine provides better tissue oxygen resaturation than levothyroxine and should be the first choice for treatment, but slower and more careful physical adaptation is required) should begin as soon as antibody titers and/or any level of internal tissue damage is suspected to prevent further tissue hypoxia; the careful interviewing of patients regarding symptomological progression may be more important than clinical signs during the early years of autoimmune disease progression.

Antibody titers may be present or not, or be high or low, depending on the etiology of the autoimmune disease, any remaining environmental triggering, and the timing of sample withdrawal as well as current levels of physical stress.

Measuring antibody titers should occur as early as autoimmune disease is suspected and may continue at intervals throughout life for research purposes, but reducing the antibody load seems not, necessarily, to slow or to heal the tissue destruction.

Currently, antibody titers seem to be a non-issue, in many ways, as the tissue damage that occurs with autoimmune disease, which takes years to decades to accumulate, depends on more than measured antibody load.

Oxygen, hormone, and nutrient tissue-uptake may be a more reliable indicator of tissue damage, subjective illness, and the need for mitigating treatment than blood titers of antibodies.

Doctors and patients who have tried hormone replacement therapy for “CFS” and seemingly have failed in alleviating symptoms may have failed because they didn’t persist in raising serum hormone levels to adequate tissue-uptake levels; this is critical.

Achieving optimal replacement hormone levels can take literally years of slow titration, physical adaptation, and adjustment. Short trials with low doses of replacement hormones generally do not, nor could, “work” to alleviate symptomology in many cases of long-term autoimmune disease.

As well, the “right” hormones must be chosen, tested iatrogenically, and the doses individualized for the patient through clinical analysis as well as patient feedback regarding symptom reduction. Patient persistence, endurance and self-adjustment through titration adaptive periods, careful record keeping, and reflective self-analysis is vital to the process of improvement, as it is with diabetes.

Self-trial and error with replacement hormones, such as a responsible diabetic must undertake, allowing time for titration and physical adaptation, may enable some patients to be successful at alleviating the symptoms of CFS / ME / APS II; supraphysiologic doses of liothyronine may be required in some cases.

Family and medical support, adequate rest and sleep, replacement hormones to provide adequate hormone uptake, avoiding oxygen desaturation of the tissues leading to slow hypoxia (slow cell death leading to heart muscle damage, ataxia, and brain and neurological damage including vestibular disturbances, vertigo, and cognitive issues) may all be critical to the improvement of the symptoms of autoimmune polyglandular disease.

At this point, understandably, the few people with “CFS” who have been cured experimentally have been with medically-administered courses of antivirals, antibiotics, antipathogens and/or other agents to reverse the effects of autoimmune disease.

Administering antivirals seems to improve or to cure the illness in early studies. Medical scientists may eventually find that it improves the illness in most “CFS” patients (as long as great care is taken to rule out depressives and others who do not have “CFS”).

More scientific research, such as that being carried out by Stanford’s Chronic Fatigue Initiative, which is looking into the infectious origins of autoimmune disease, may lead to more answers as to the cause and cure of “CFS”, or Autoimmune Polyendocrine Syndrome II.

In the meantime, treatment with adequate doses of replacement hormones in patients, carefully and slowly titrated to optimal levels, may provide relief from symptomology.

- Cathi Carol, 2012


Photo/Art Credit:

The Garden of Elisa
by jaci XIII


© 2013 Cathi Carol. All rights reserved. Please do not republish without permission.
Last Updated: March 30, 2013
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