The CFS deconditioning hypothesis

Note from the moderators:
The discussion in this thread is focussed on the BPS theory of deconditioning. There is another thread for discussing the issue raised in this post: Muscle atrophy
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Hi Everyone

My recent muscle biopsy of my thigh has led to what seems like very relevant research findings that should be followed up urgently by researchers looking at muscle biopsies.

I am bed bound and had been for 5 months before the biopsy.

One of my results was: Severe Type II Muscle Atrophy

First I looked for other research and found this 1991 study: Mitochondrial abnormalities in the postviral fatigue syndrome* W. M. H. Behan1, I. A. R. More1, and P. O. Behan

In it they found that 39 of 50 patients that they classified as CFS has Type II muscle atrophy

But here's the thing...

In the most recent 2 papers that I could find that differentiated between the type of circumstances that result in specifically Type 1 or Type 2 muscle fibre atrophy...
Muscle type and fiber type specificity in muscle wasting☆
Author links open overlay panelStefanoCiciliota1Alberto C.Rossia12Kenneth A.DyaraBertBlaauwabStefanoSchiaffinoac

Muscle type and fiber type specificity in muscle wasting.
Ciciliot S1, Rossi AC, Dyar KA, Blaauw B, Schiaffino S.

They explain that disuse/inactivity results in such more Type 1 atrophy than Type II atrophy so one would expect to see a lot more Type 1 atrophy in Muscle Biopsies of ME patients. Yet on the limited evidence so far and certainly in my case where I hadn't used legs for 5 months that doesn't seem to be the case.

Interestingly, the 2nd paper generalises the group of conditions that cause Type II atrophy as Malnutrition and Inflammation which fits the Metabolic/Immune ME theories pretty well.

I am not a biomedical mind but they mention different pathways which may contribute to Type II atrophy including TGFb (for those of you who are scientific minds you might be interested in reading these papers as at least in my view they counter the deconditioning arguments nicely if research groups doing muscle biopsies find that we have Type II atrophy and might point towards factors that are contributing to this.

 

There is a certain irony in that the deconditioning theory was actually debunked by psych wackos from the Netherlands. Strong believers in CBT / GET who happen to be really good colleagues with wessely and co.

Basically they ran through their older CBT studies which had employed actometers, and saw that patients who had been given CBT which was supposed to increase activity, hadn't managed to increase the patients activity at all. Given how patients in the treatment group had still claimed to improve slightly with CBT, this was a problem.

Did this mean that patients given the treatment just reported that they were better, but did in fact not improve at all? I.E placebo?

No, of course not. The Dutch researchers came up with the most insane rationalization ever, but they at least had to concede that the deconditioning theory could not be correct, since patients ''improved'' without even increasing their levels of activity.

You can read the study here

https://www.researchgate.net/public...atigue_syndrome_The_role_of_physical_activity

Definitely one of the best studies into cognitive dissonance. Good for a laugh if you have a dark sense of humor.

 

Specially on people like me, I have a week in bed the next normal. I am relapsing remitting type, so deconditioning makes no sense. Note, I have POTs also, and I do get worst (my period drives the worst crashes).

 

There are none so blind as those who will not see......

It hasn't suited the BPS, insurers or DWP agenda so a great many people have spent much of the last 30 years trying to avoid looking at this kind of stuff.

 

There was a study posted recently in S4ME that concluded the results did not support the deconditioning theory - cannot recall which thread that was at the moment.

Edit: It was https://www.s4me.info/threads/eleva...ction-a-case-control-study-julia-newton.1745/

 

I know we all know that the deconditioning theory is ridiculous. But maybe I should have viewed this a different way.

The type II muscle atrophy study seems to me to be vital to follow up for those groups who are talking about doing muscle studies (I think Julia Newton, NIH)

If they can repeat these findings much more than debunking deconditioning again, its another piece to the puzzle which can lead towards finding the cause/causes of ME by looking at the pathways that can create this type II specific atrophy

 

One severe bedbound ME/CFS patient on Phoenix Rising (who also has Crohn's) used once weekly doses of corticosteroids like prednisolone to completely obliterate PEM, and by this approach he was able to visit the gym and engage in vigorous aerobic exercise once a week (but this only works if you do the exercise within around 4 hours of so of taking the prednisolone). See the bottom of this post.

This is quite amazing, because for the rest of the week he is bedbound. After a year of these weekly gym visits facilitated by prednisolone, and after slowly building up his cardiovascular fitness, he found that his POTS symptoms disappeared. But all that exercise had no effect on ME/CFS symptoms, he said.

So that anecdote would tend to argue against deconditioning playing a role in ME/CFS.

 

My POTS always gets worse after long periods of being bedbound, but my ME symptoms are usually reduced by the same.

 

"So it appears that while some patients are deconditioned - and those that are bedbound must surely be - many patients are not deconditioned yet still have CFS. This does rather rule out a primary role for deconditioning in perpetuating the illness."
[My bold]

Which is exactly the case for my wife I'm certain. As I've said before, I'm sure my wife is much fitter than your average couch potato. Her problem is not lack of fitness - it is lack of available energy supply to utilise the fitness that she has! If you were to take a top athlete, and in some way seriously obstruct of the flow of energy to their cells, then you would have a person at peak physical fitness, incapable of doing anything much ... because to do anything you need energy. It doesn't matter what the obstruction mechanism is - physical obstruction to the transport of energy, control (i.e. regulation) malfunction so less energy is made available than is needed, energy not converted fast enough in a form that is useful, whatever - if the energy is not supplied fast enough for what is needed, then the fittest person in the world will be floored. You can have the fastest most souped up car in the world, but if the fuel does not get to where it's needed fast enough, you end up with a very expensive door stop.

 

Some ME patients (me) have enough 'energy' to go out for a 30 minute run/workout and feel perfectly normal, but the next day PEM is almost deadly- PEM has nothing to do with deconditioning.

 

There was a thread earlier this year about a Vice article, which featured the journalist spending 70 days in bed for science

https://www.s4me.info/threads/how-i-felt-after-70-days-of-lying-in-bed-for-science-2015.3588/

https://www.vice.com/en_uk/article/jma83d/nasa-patient-8179-200

The article is oddly comforting. In showing that someone who didn't move at all for 70 days could return to absolute normal within 2 weeks, which honestly kind of surprised me. Whenever I fear I am starting to suffer from deconditioning, even though I still walk around the house, and move up and down the stairs multiple times every day with absolutely no effort. I always remind myself of this article, and that forcing myself to do all those unpleasant forced walks outside, which leave me feeling terrible, isn't a good use of my limited energy.

 

Whilst PACE etc premise that the mindset of PwME prevents them doing what is needed to recover for year upon year.

 

I've always thought the PACE study was actually a good study in ruling out deconditioning as the cause of ME/CFS. The 6-min walk test is a terrible test to show any improvement in a group of patients with a disease that is highly variable from day to day. Having someone walk for 6 minutes one day, then come in a year later and do it again is very unlikely to yield any useful information -- unless you didn't see any real improvement in their performance. Which, of course, is exactly what happened. If these patients were simply deconditioned, you would think after a year of graded exercise, they would be performing far better than they had originally. The fact that they didn't -- unless they all happened to be in PEM that day-- suggests deconditioning has nothing to do with this disease. I've never understood why we didn't hound that point into the ground.

 

Agreed about the six minute walk test. It’s really like spitting on the patients; what useful life activity can you do by walking for six minutes? Go out your door, go do ONE simple errand and come back. Can you do that in six minutes? It’s as if the test is designed to avoid touching on any of our landmine areas.

 

This really made me angry. The Mythbusters TV programme did a few shows that involved walking speeds and for each they did 10!!! tries and averaged them so they could get a more accurate result. A TV show, not a 5 million pound scientific trial published in the Lancet!!!

 

"Goldilocks theory" Haven't heard that before, its lovely!

 

I'm not sure. Perhaps @PhysiosforME can answer this one? If someone's sole problem genuinely is severe deconditioning, possibly left over from some other physical ailment that has subsequently recovered, is there a level of deconditioning severity that might require extreme effort (rather than just hard work) to get back to a point where just normal hard effort will continue to recondition them? Or is it the case that most people, if only deconditioned - nothing else - can recondition with normal hard work, no matter how deeply deconditioned they are?

Would be interesting and useful to know.

Agreed.