Hypotheses and Research Directions for ME/CFS

[voner]

The problem here is that these are isolated findings over about half a century. People have tried to repeat Simpson's findings and nothing consistent has been reported as far as I know. In addition, we know the clinical presentation of conditions where red cells are stiff or misshapen and it isn't particularly like ME/CFS.

Slow flow in an artificial capillary system does not translate to low oxygenation in any direct way. Ron Davis has put a lot of energy into ME/CFS research but we have not seen any very organised studies over the last ten years and pretty much nothing in the way of formal replicated data.

A few people have noted metabolic shifts but not related to oxygen lack as far as I know - more to do with amino acid usage.

The underlying concern for me is that this 'particular vein of ore' is very much what a lay person without much idea of clinical physiology would go for as plausible. People have been attracted to it for decades. But those who are familiar with muscle physiology don't see it as very plausible after all because it does not add up, in the way I have described. And my old boss Richard Edwards (no relation) had a team of good people put on to muscle in ME/CFS in the 1980s and they found nothing.

I think it is hard for lay people to appreciate just how much medical research is reporting artefacts and irrelevances, particularly in the last 20 years. And if everyone continues to plough on studying these things that don't really add up the likelihood is that they won't scratch their heads and realise that something else might fit. I guess in a way that is what this forum is all about, scratching our heads to see if something else might fit, and keeping on wide-angled spectacles to pick up every bit of information that might just bear on that.

Jonathan,

I have long wondered about the validity of this research paper on Fibromyalgia from 2013. It discusses ischemia a bit. Are you familiar with it?

Excessive Peptidergic Sensory Innervation of Cutaneous Arteriole-Venule Shunts (AVS) in the Palmar Glabrous Skin of Fibromyalgia Patients: Implications for Widespread Deep Tissue Pain and Fatigue, May 2013, Pain Medicine, Albrecht, et al.

This is the only place I know on the Internet that has an open access copy:

https://www.humanempowerment.org/wp-content/uploads/2014/11/Albrecht2013.pdf

 

[Jonathan Edwards]

I have long wondered about the validity of this research paper on Fibromyalgia from 2013. It discuss as ischemia a bit. Are you familiar with it?

No, I had not seen that. It seems pretty speculative. Even if the differences in nerve density are reliable it is quite a long shot to suggest it is involved in causing pain. I have not heard of fibromyalgia pain suggesting ischaemia - i.e claudicating in pattern.

 

[Utsikt]

Jonathan,

I have long wondered about the validity of this research paper on Fibromyalgia from 2013. It discusses ischemia a bit. Are you familiar with it?

Excessive Peptidergic Sensory Innervation of Cutaneous Arteriole-Venule Shunts (AVS) in the Palmar Glabrous Skin of Fibromyalgia Patients: Implications for Widespread Deep Tissue Pain and Fatigue, May 2013, Pain Medicine, Albrecht, et al.

This is the only place I know on the Internet that has an open access copy:

https://www.humanempowerment.org/wp-content/uploads/2014/11/Albrecht2013.pdf

Created a thread:

https://www.s4me.info/threads/excessive-peptidergic-sensory-innervation-of-cutaneous-arteriole-venule-shunts-avs-in-the-palmar-glabrous-skin-of-fm-patients-2013-albrecht-et-al.47930/

 

[Creekside]

Regarding signs of reduced blood flow in capillaries, I occasionally get abcesses in the tissue at the sides of my nails (hands and feet). My theory is that tissue has poor capillary access, and so it's easy for tissue to die and become necrotic. If ME involved reduced blood flow, I should experience more of those abcesses, but instead I think I'm having fewer. So, counterevidence, for whatever it's worth.

I think it's very common--and very human--to notice evidence that supports a preferred theory, while ignoring counterevidence. So, seeing something like blood splinters under nails can make some people jump to the conclusion that it's proof that ME involves reduced microcirculation, while it really isn't (abundant other explanations for the phenomenon, and a lack of supporting phenomenon). The same applies to a lot of ME theories.

 

[bicentennial]

Maybe a varied PEM delay correlates to a varied stool transit time with an encyclopaedic, sequenced array of connections

A gut upset is not required in a working theory that some part of the encyclopaedic, sequential, digestive and metabolic process - is involved in the delay of PEM. But also, gut upsets mark something.

My food intolerances produce the same symptoms as PEM, so my theory is that there's a "PEM symptom-generating mechanism" that has multiple triggers, and is common but not a critical part of the ME mechanism.

In some cases food is tolerated, in other cases the type, quantity, frequency and even consistency of food can upset some part of the digestive tract, with or without a marked systemic impact.

The intestinal motility and permeability may vary from time to time and from person to person. There may be marked impacts on other organs and systems. Several combine to process meals.

Maybe what we all have in common is a more or less manageable or else unmanageable systemic disruption with some awry biochemistry in disarray for the duration, and this can be delayed, it can be triggered, some triggers can be food-related – and correlations indicating problems can differ.

There may be a pattern to the more or less variable delays. This might correlate to the more or less variable stool transit time which can vary in various circumstances

For example if the peristaltic muscle tone is slackened or tightened, eg 1-5 days for the passage of each meal. In some cases there is significant systemic and / or local relief once a stool is evacuated.

If stool transit time correlates to a PEM delay, but not all cases have the variably over-reactive gut upsets, what might that mean? There are so many factors and cascading processes involved.

A few of the organs locally involved can horribly upset the brain if malfunctioning. For some reason a mild malfunction might have a significantly escalated impact.

And when holistically considered as integrated, each of these specialised organs can obviously upset the others, so it can take a while to re-settle the whole combo (combinaton).