Advances in Understanding the Pathophysiologyof Chronic Fatigue Syndrome (Komaroff, 2019)

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Its possible, but does not compute here. The hibernating bear is not experiencing Horrific Internal Poisoning. Bear may come to and feel hungry, or groggy, or have slow return of muscle function...all understandable.

Is the hibernating bear's gut biota sick? Doubt it. Is the permeability of gut and brain: increased in hibernating bear? Why would it be?

Its hard for me to identify any aspect of this body which is: functioning normally.

Last night I ignored the Sickness Response Messages. I went out anyway. The level of horrible I feel today is a type of POISONED.
I totally agree. We have to listen to our own bodies from minute to minute it seems. This illness is not normal and if anything it feels like a life sentence in jail. It’s difficult to be be very clear when writing about this stuff, brain fog and all.

We are not bears so shutting down is not normal. It’s an alarm going off. I’m saying there’s some general features of this illness that make sense in terms of how the body reacts. Over compensating happens as the body’s attempt to survive...like auto immune response. So, for instance, I think I intuitively did aggressive resting when I first got sick and I think it’s helped me in terms of making progress.

So there’s treating the symptoms and maybe a few of us will find a protocol that works. And there’s all that we come upon in our quest to get well. Discovering I have SIBO is ultimately a blessing in a way. Although I hate another thing I have to attend to. I’m counting on the herbal anti virals I now take will be another stepping stone to my recovery. And I have to say it’s good I’m not a workaholic anymore.

Tha shutting down of our bodies is a clue. It’s the body’s response to right the ship so to speak. I’m maybe 25% better, for the most part, because most of the time I listen and respect where my symptoms lead. And you all here at pr have been my guides.
 

Archie

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For me it`s hard to see Myalgic Encephalomyelitis and CFS as same . I dont have ME diagnosis but CFS , yet i dont particularly like how they are mentioned often as being same still.

I could copy paste a lot text about the issue, but it`s better to read them from Hummingbirds' Foundation for Myalgic Encephalomyelitis site

http://www.hfme.org/whatisme.htm


The creationg of CFS term look`s bit fishy , and there allready was full known medical definition for Myalgic Encephalomyelitis if i understand , so why all the sudden the need to hook up new " CFS " for ME .


Look`s like money is involved , as usual ...

Even in PR front page it says : " Myalgic Encephalomyelitis (ME) – also known as Chronic Fatigue Syndrome (CFS) "
 
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It's still so unclear what the disease is that i think it warrants a spread of defintions. Myalgic encephalomyeletis is one hell of a name to sayor read if youre only casually interested. CFs doesn't not convey the violence of the disease on the body and mind but neither does m.e.
To me it doesn't matter until things get more defined . We can worry about subgroups and definitions when the field gets more definite.
 

Gemini

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Gemini

Senior Member
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And the count keeps going up to 75,289 views as of today, seven weeks since publication.:thumbsup:
Here 2 1/2 weeks later, views are still rising, 76,317 as of today.

With number of views high, worldwide reach is wide [JAMA posted map & estimates]:

Komaroff JAMA article worlwide map 2019.PNG



Country frequency by order: US, UK, Canada, Australia, Spain, Netherlands, Norway, Sweden, other...
 
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Dear Members,
On July 17, 2019, I submitted the following comment to JAMA in response to Dr. Komaroff's article. Although my comment was not accepted for publication, it does express a valid opinion regarding the erroneous classification of CFS as a disease entity. Dr. Komoraff's article and much of the current research on CFS underplay the importance of epidemiological outbreaks as evidence for an infectious etiology of CFS. Kind regards, W. John Martin, MD, PhD.

To the Editor:
ME/CFS patients manifest highly variable combinations of symptoms, which can, however, vary markedly between different patients and even within individual patients over time. The ME/CFS diagnosis is being applied equally to patients who are still able to maintain fulltime employment and to patients who are bedbound and require skilled nursing care. A single diagnostic term is clearly inappropriate for an illness with such differing severity. Furthermore, with the arguable exception of post-exertional malaise, the symptoms described by ME/CFS patients are prominent features of many other illnesses.
Community outbreaks of ME/CFS-related illnesses have occurred both prior to and subsequent to the 1980’s when the term CFS was first introduced. Moreover, there are examples of complex neurological illnesses occurring among family members of ME/CFS patients, including the development of autism in children born to mothers affected by ME/CFS. A cell-damaging cytopathic virus was repeatedly isolated from a CFS patient in the early 1990s (1). This finding was not pursued by Public Health authorities when it became clear that the virus had arisen from the cytomegalovirus of African green monkeys (2). Cytomegalovirus infected monkeys were routinely used to produce live polio virus vaccines. It was soon realized that virtually all of the CFS patients tested by a specialized virus culturing technique were infected with atypical viruses, some of which were of monkey origin (3). The viruses differed from the viruses from which they were derived in not causing inflammation. This was likely due to the deletion or mutation of the genes coding for the relatively few virus components that are normally targeted by the cellular immune system; an immune evasion mechanism termed stealth adaptation.
A range of illnesses, including ME/CFS can be caused by stealth adapted viruses. These viruses can also induce illness in animals (4). Understanding ME/CFS from the larger perspective of a potentially contagious virus encephalopathy will help open new avenues for therapy, including boosting the alternative cellular energy (ACE) pathway as a non-immunological anti-virus defense mechanism (5).

W. John Martin, MD, PhD.

References:

1. Martin WJ et al. Cytomegalovirus‑related sequences in an atypical cytopathic virus repeatedly isolated from a patient with the chronic fatigue syndrome. Am. J. Path. 1994:145(2):441‑452. PMID: 8053501

2. Martin WJ et al. (1995) African green monkey origin of the atypical cytopathic 'stealth virus' isolated from a patient with chronic fatigue syndrome. Clin Diag Virol. 1995;4: 93‑103. doi.org/10.1016/0928-0197(95)00020-9.

3. Martin WJ. Severe stealth virus encephalopathy following chronic fatigue syndrome‑like illness: Clinical and histopathological features. Pathobiology 1996:64:1‑8. doi.org/10.1159/000163999

4. Martin WJ, Glass RT. Acute encephalopathy induced in cats with a stealth virus isolated from a patient with chronic fatigue syndrome. Pathobiology 1995:63:115‑118. doi.org/10.1159/000163942

5. Martin WJ (2016) The ACE pathway in comparison to the immune system in the defense against infectious diseases. J Human Virology & Retrovirology 2016;3: 00124. doi: 10.15406/jhvrv.2016.04.00124