The symptoms of chronic fatigue syndrome are related to abnormal ion channel function, 2000, Chaudhuri et al.

https://www.researchgate.net/public..._are_related_to_abnormal_ion_channel_function
Abstract
The pathogenesis of chronic fatigue syndrome (CFS) is unknown but one of the most characteristic features of the illness is fluctuation in symptoms which can be induced by physical and/or mental stress. Other conditions in which fluctuating fatigue occurs are caused by abnormal ion channels in the cell membrane. These include genetically determined channelopathies, e.g. hypokalemic periodic paralysis, episodic ataxia type 2 and acquired conditions such as neuromyotonia, myasthenic syndromes, multiple sclerosis and inflammatory demyelinating polyneuropathies. Our hypothesis is that abnormal ion channel function underlies the symptoms of CFS and this is supported also by the finding of abnormal cardiac-thallium201 SPECT scans in CFS, similar to that found in syndrome X, another disorder of ion channels. CFS and syndrome X can have identical clinical symptoms. CFS may begin after exposure to specific toxins which are known to produce abnormal sodium ion channels. Finally, in CFS, increased resting energy expenditure (REE) occurs, a state influenced by transmembrane ion transport. The hypothesis that ion channels are abnormal in CFS may help to explain the fluctuating fatigue and other symptoms.

 

Speculative and I think largely unsupported by any subsequent work, or at least not further explored:

Sci Hub link: https://sci-hub.se/10.1054/mehy.1998.0822

"INTRODUCTION
Chronic fatigue syndrome (CFS) is a common disorder characterized by fluctuating fatigue which is induced by stress, often related to infections and toxin exposure (1).
The mechanism of this fatigue, the hallmark of CFS, is poorly understood. Fatigue in CFS is distinct from the fatigue of neuromuscular disorders but it similar to that
found in multiple sclerosis, chronic inflammatory demye-linating polyneuropathy (CIDP) and endogenous depres-sion. Indeed, a poorly recognized but common and often
first symptom of CIDP is overwhelming, fluctuating fatigue. Other symptoms found in CFS include paroxysmal, usually nocturnal, sweating, myalgia, intermittent dyse-
quilibrium, mild myoclonus, angina-like chest pain and sleep disorder (1). Most patients complain of a migraine- like headache and may describe hemisensory symptoms.
A high incidence of irritable bowel disease and Gilbert’s disease is also present (2).

FATIGUE IN NEUROLOGICAL DISORDERS
Fatigue is a common symptom in many neurological diseases and may be the presenting symptom, as in myas-thenic syndromes, amyotrophic lateral sclerosis (ALS),
CIDP, post-polio syndrome and MS (3,4). Abnormal potassium ion channels have been postulated to be involved in MS (5), whilst immunologically mediated, voltage-gated, sodium channel abnormalities have been implicated in inflammatory demyelinating polyneuro-pathies (6). Fatigue also occurs in patients with acquired neuromyotonia where immune-mediated, voltage-gated,
potassium channel antibodies are present (7). Apathy and lethargy are common features in dystrophic myotonia (8), where the genetic abnormality (CTG trinucleotide repeats) leads to an abnormal serine threonine protein kinase function. Protein kinases play an important role in cellular signalling and ion channel functions, an abnor-mality of the latter being responsible for membrane
changes that cause clinical and electrical myotonia.

The well-characterized genetically determined channelopathy, i.e. periodic hypokalemic paralysis with calcium channel abnormality has fatigue as its prominent symptom (9). Fatigue is a feature of the genetically determined episodic ataxias (10) and occurs in the animal model of this disorder, the lethargic mouse (11). Antibodies against
voltage-gated calcium channels have been found in ALS (12) and in Lambert Eaton myasthenic syndrome (13). In acquired autoimmune myasthenia gravis, at least 50% of the patients have antibodies directed against their ryan-odine receptors (14). These receptors are involved in the modulation of L-type calcium channels of T-tubules and may influence the conspicuous and fluctuating fatigue characteristic of this disease. Familial hemiplegic migraine (FHM), a newly recognized calcium channelopathy, can be often precipitated by stress, exercise or following viral infections, the same precipitants as in CFS (1). The same or a closely related genetic locus is postulated to have a role in common migraine with or without aura (15). Migraine shares many features of CFS, e.g. headache, fatigue, sensitisation to foods and chemicals, photophobia, tran-sient anomia, confusion and serotonin sensitivity."

more at Sci-Hub

 

Depending on the language they were written in. It sounds like the author is claiming that poorly-defined kinda-sorta-similar symptoms are identical.

So, all PWME have been exposed to these specific toxins that cause serious health problems but haven't been regulated or have published health warnings about?

 

From what I could gather it was toxins poisons or viruses that were inactivating sodium channels leaving them open

 

From a quick check, it looks like sodium channel function can be measured with existing technology. There are radioactive sodium isotopes for PET scans, and dyes for microscopy, so his theories should be relatively easy to test.

To me it sounds like the researcher looked at some diseases that have some remotely similar symptoms and then jumped to the conclusion that CFS is due to the same mechanism. That's a huge, major jump, and thus requires huge, major supporting evidence.

 

I note that this is from 2000 so don't know what the state of the symptom list was completely there and whether there are any significant differences at all as to who has been dumped under that bucket up until now (it's probably worse now than then).

Given the bucket analogy I do think that looking at 'the same symptoms' and putting forward an issue that could explain this is an important flag for differential diagnosis purposes at least?

 

I agree the paper doesn't add up to much, but I'm not sure a type of channelopathy is necessarily a daft idea. There are dozens of them, and it's an expanding field that appears to have a long way to go.

Primary types are usually genetic conditions, and if this were the case DecodeME ought to pick up some signals. With acquired channelopathies, people don't necessarily need to have been exposed to some nefarious human-made chemical—it may be possible for them to develop as the result of various types of event, including infection.

Even if channelopathies are a long shot, I'd still want to leave them on the table to be ruled out.

 

2014 article here: https://www.s4me.info/threads/channelopathies-2014-june-bum-kim.30137/

 

Symptom similarities may not be as remote as you might think. But I agree, it's a jump.