MeSci
ME/CFS since 1995; activity level 6?
- Messages
- 8,231
- Location
- Cornwall, UK
I take it you havn't tried CBT for it then? Works wonders apparently...so the nuts say anyway!
What - the peanuts?
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Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
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I take it you havn't tried CBT for it then? Works wonders apparently...so the nuts say anyway!
On PEM.
This is often presented as diagnostic for ME/CFS. I have always been concerned about its specificity.
Is the PEM of ME/CFS different from that which would be experienced in active incl chronic infection e.g. Lyme's, chronic lung probs, micronutrient deficiencies impacting on mitochondria etc?
Its the science that defines names, but when the science is not adequate the names are ambigous or have wiggle room.
I have not looked at the science on this yet, but there have been claims of successful graded peanut exposure:
http://en.wikipedia.org/wiki/Peanut_allergy#Treatments
biophile There is indeed research showing that repeated exposure to peanuts in very controlled amounts (much less than a single peanut) can lead to loss of the allergy. This is because food allergens also invoke a tolerance response. What they do, and I have not seen anything on this in years so my comment is purely from memory, is giving a dose small enough to not provoke an allergic response, but large enough to provoke a tolerance response. Its a dose in micrograms I think. Then they slowly increase the dose. So long as they keep it in the response window tolerance increases and an allergic response declines. This is not an easy process, and if they get the dose wrong the response will be a full allergic reaction. I also do not recall the success or failure rates.
On PEM.
This is often presented as diagnostic for ME/CFS. I have always been concerned about its specificity.
Is the PEM of ME/CFS different from that which would be experienced in active incl chronic infection e.g. Lyme's, chronic lung probs, micronutrient deficiencies impacting on mitochondria etc?
I have no idea why ... the URL itself is fine, it just seems to add some random characters to the end when hovering over it or clicking. Guess it has to be cut and pasted or clicked on then the last few characters (after ".pdf") deleted.Hi Val, FYI, the fist link appears to be broken.
I see what you mean. It's got a glitch. You could try editing your post, deleting the link, and reinserting it, if you feel like messing around with it.
The link seems to work if done afresh:
http://www.cfids-cab.org/rc/Wiborg.pdf
Yes.This issue always lurks in the background when markers for ME, CFS, FM are claimed. How was the ME, CFS, FM defined int he 1st place?
Sushi said: ↑
But in quoting Dr. De Meirleir to support your theory, you are distorting what he said
If you are talking about the YouTube clip then not at all, unless I missed something?- he wasn't exclusive in his comments re: sources of inflammation...
Oh aye? Do tellhe is much more specific about what he believes are the causes of inflammation--and they are not related to inactivity
The series of videos with English subtitles are at https://www.youtube.com/watch?v=X-uwSxoUqTY&list=PLsQ0FZQ_5JXQPVDLmt1EOgOlf2PAg6TFWOh aye? Do tell
My take on fear, inactivity, and pathophysiology:
as I believe neural hypersensitivity may lie at the heart of our illness and indirect/direct nerve mobilisation (which constitute activity) improves neural sensitisation, whereas relative inactivity only seems to worsen neuromuscular tension in those with the idiosyncratic structural profiles that put them at risk (I believe most PWME have these profiles e.g. dorsal defects/hypermobility)
- One may reasonably associate fear of PEM/PENE with (greater subsequent) inactivity in some cases
- Rowe associates inactivity with enhanced nerve sensitisation leading to enhanced central sensitisation and local inflammation
- Dr Meirleir associates mild inflammation with increased vit D 1,25
- Dr Meirleir associates increased vit D 1,25 with reactivation of herpesviridae
- Many experts associate ME/CFS (onset) with acute viral infection e.g. by herpesviridae
- Dr Meirleir observes higher than normal 'latent', but lower than acute infection, levels of herpesviridae activity in ME/CFS patients
Attempting exercise before neuromuscular and nerve detensioning has taken place and nerve glide is unimpeded and well tolerated is, however, clearly unwise if you subscribe to a theory like mine!
Ah cool, thanks - lots of interesting stuff there!The series of videos with English subtitles are at..
Sorry I do waffle on a bit some times! heheI am so confused reading this. Sorry
YesYou have a friend who avoids activities that will lead her to PEM. Is that right?
No. Avoidance is rationalAre you saying she doesn't really get PEM, ergo avoidance is irrational?
Yes, until she arrives at a point where she is in the right condition to tolerate increased activity on a sustainable basisOr are you saying she avoids activities that lead her to PEM in all it's horribleness and therefore what she is doing is perfectly sensible in order to get by?
It's not for me to say what she requires unless she asks me. Some of my friends with ME/CFS have asked for my advice, the one who has comorbid FM has not (we lost touch a few years ago)In which case she doesn't require therapy
Personally I wouldn't offer a full intervention myself, I am not a trained physician (medical or physical therapist), but as a starting point if I felt she could benefit from (physical) therapy I would encourage her to read my protocol and/or go through it (and the associated theory) with her, then see which parts she felt were worth pursuingWhat therapeutic intervention would you offer her - if you think she needs it?
It would be difficult to know without talking to her at length about the options in the context of her experiences and attitudes going forward. As Dr. Rowe suggests, however, CBT may be offered as an optional, supportive therapeutic tool (but I see no reason for it be applied in a blanket fashion - apart from anything else this is a waste of resources!)Do you think she needs counselling/CBT to help her get more active and just deal with PEM when it happens?
Absolutely notWhen it's really bad I have uncontrollable sleep where I simply fall asleep and am unrousable. I've even ended up in A&E. Would you want to risk that while caring for three young kids?
Indeed, although not all of us are so quick to learnI think that repeated malaise after activity is likely to reduce activity in almost all cases
I would love it if it could be shown that Rowe's theory relates to all PWME, but the sense I get from his article is that this may not be the case, and indeed the sense I get from the results of many studies suggests that there may well be distinct diseases at play, or at least distinct presentation of secondary disorders, in which case certain interventions found to be therapeutic for some will likely not be effective for all, and may, by extension, do more harm than goodWould you yourself apply what Rowe claims to all or only some patients?
In my humble, and untutored, estimation - it could well be something of a disease facilitating forceif this process is occurring in all of us at some point, how significant is it relative to other matters in your view?
I agree, although many of the issues you note, and their connection to my proposed 'core disease cascade', are explored (admittedly not in great detail and many of the associated mechanisms are not yet well understood) in my hypothesis articleI would be thinking of matters such as mitochondrial dysfunction, active infection, low cortisol etc. Supplementing with e.g. Mg might alleviate both some neurotensive probs and some mito dysfucntion at the same time, but there may be a great many factors in play, which a neurotension alleviating protocol will not address
Presumably a significant proportion of us or De Meirleir would not so confidently assert its significance in the reactivation picture (I'm afraid I have only just come across this link so I have yet to look into it further)On point three how many of us is this relavant to?
Without a detailed knowledge of 1,25, and having cast a cursory glance at the issue, given the symptomatology of excess 1,25 outside of the purported link with reactivation of latent herpesviridae on balance it seems probable to me that there is likely a degree of both inflammation-linked increased hydroxylation and enhanced systemic inflammation arising as a consequence of thisAnd is the inflammation driving the 1,25 or the other way round?
This is a question perhaps best put to De Meirleir - he mentions impaired TH1 immunity in the same video series so presumably he has considered, and discounted, any such apparently contradictory associationsHigh 1,25 is assocaited with some TH1 conditions, but many ME/CFS sufferers are TH2 dominant
That relative inactivity e.g. affecting nerve, and connected soft tissue, mobility may unfortunately complicate a core disease mechanism: Neural Hyper-Sensitivity (associated with neuromuscular/neuromechanical tension)What is you overall point?
I believe that they contribute to acute and chronic systemic inflammation respectively yes, and that efforts to reduce neuromuscular/neuromechanical tension may be viewed as a key, if not the key, target for therapeutic intervention in the context of rehabilitation and recovery from associated chronic health conditions (I believe ME/CFS is one such condition)Are you e.g. suggesting that a combination of PEN and overconversion of 25 to 1,25 vit D lies behind inflammation, and that exercise in sunlight (to replenish 25D) is the way to go after appropriate physio?
AgreedI personally think there is a good deal of heterogeneity among us, and this strategy might help some, but by no means all and by no means at every stage of their illness
Forming beliefs that all types of activity/exercise, at all stages of the illness, will necessarily lead to PEM/PENE, is what I find irrational. Of course this may actually be the case, and I may be mistaken in believing that most PWME can create the conditions in which activity may be better, and increasingly well, tolerated - however there is, at present, in my humble estimation and in so far as I know, no irrefutable evidence to suppose this is the case
Yes, until she arrives at a point where she is in the right condition to tolerate increased activity on a sustainable basis
When you see what this disease strips us of John, I really can't believe many patients go on to strip themselves of more.
We already know that many of us have been made far more disabled by forced exercise.
You see with a remitting relapsing disease the word "sustainable" isn't much use.