Dr. Enlander tackles a poor paper "Fear of movement and avoidance behaviour..."

[MeSci]

I take it you havn't tried CBT for it then? Works wonders apparently...so the nuts say anyway!

What - the peanuts?

 

[alex3619]

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?

In general discussion this is a real issue. However the work by Snell, Stevens et. al. and by the Lights may yet define it with respect to ME. In which case it will probably wind up with a new name. Its the science that defines names, but when the science is not adequate the names are ambigous or have wiggle room.

It is very clear that many disorders induce post exertional fatigue. It is not clear that many induce a constellation of post exertional symptoms like in ME. MS might be an exception - I have yet to see convincing evidence that post exertional issues in MS are different from ME. We need our exercise physiologist researchers to look at this. Yet if its the same, this raises a question. Is PEM not specific to ME, or are MS and ME two versions of the same disorder?

I don't have definitive answers on this, but I do have questions.

 

[Richie]

Its the science that defines names, but when the science is not adequate the names are ambigous or have wiggle room.

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?

 

[Bob]

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.

Yes, this is supposed to work, and I think that the NHS even recommends it for children in the UK.
After a long gradual process, I think the children end up eating one peanut a day, as a prescribed dose.

 

[Bob]

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 don't think there is enough research on it, because no one quite seems to know the answer.
I think that some experts says it is unique or almost unique. Others might disagree.
But I think it is the nature of PEM in ME that makes it very unusual, if not unique.
Firstly, it is post exertional 'malaise' and not 'fatigue'. (Involving a flare up of multiple symptoms.)
Secondly, it has, or can have, delayed onset.
Thirdly, it is a prolonged reaction that is not relieved by rest, or ordinary rest.

 

[Valentijn]

Hi Val, FYI, the fist link appears to be broken.

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.

 

[Undisclosed]

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

I have fixed the link in Val's post.

 

[alex3619]

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?

Yes Richie, and this falls afoul of a fallacy called "begging the question". First assume a cohort is right. The find a marker. Then prove the cohort was right using the marker. Thats a fallacy. Similar arguments apply to drug treatments.

Markers have to be robust (pervasive and well tested), and should not immediately be presumed definitive.

In machine learning these problems are well known. The data set can give rise to "robust" markers and rules, yet these fall apart under further scrutiny, particularly when applied to the real world.

We will be fairly sure we have good markers only when we really understand causation in ME.

In the meantime the FDA and researchers also want treatment markers, not just diagnostic markers. These do not have to be so definitive, just useful indicators of improvement, though that improvement does have to be established. Essentially what the marker does is define a subgroup, but it doesn't by itself tell you a lot about the whole group.

 

[Sushi]

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...

This is one of very many video interviews with Dr. De Meirleir. He has also written many, many research papers. In some of his other videos (which are easily accessible on this forum), he is much more specific about what he believes are the causes of inflammation--and they are not related to inactivity. I am also his patient so have more opportunity to learn about his theories.

Again, more reading of biomedical research would give you much better foundation for your theories.

Sushi

 

[John H Wolfe]

he is much more specific about what he believes are the causes of inflammation--and they are not related to inactivity

Oh aye? Do tell

 

[Valentijn]

Oh aye? Do tell

The series of videos with English subtitles are at https://www.youtube.com/watch?v=X-uwSxoUqTY&list=PLsQ0FZQ_5JXQPVDLmt1EOgOlf2PAg6TFW

His research can be found using http://scholar.google.com/ and doing a search for: author:"k de meirleir"

 

[Shell]

I am so confused reading this. Sorry.
John H Wolfe can I try and get something straight in my foggy little brain.

You have a friend who avoids activities that will lead her to PEM. Is that right?
Are you saying she doesn't really get PEM, ergo avoidance is irrational?
Or are you saying she does get PEM, but it's not so bad ergo her avoidance is not really based on reality?
Or 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? In which case she doesn't require therapy.
What therapeutic intervention would you offer her - if you think she needs it? Do you think she needs counselling/CBT to help her get more active and just deal with PEM when it happens?

I'm confused because, like your friend, I don't usually go about doing stuff that will make me crash. Serious PEM can last two or three days and I have kids so you can see that's not a great way to be. even if I didn't have responsibilities I can't see a rational reason for deliberately putting myself into a crash with all that pain, losing my vision and being unable to make my limbs move properly, vomiting and serious heart/BP and breathing problems. When 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?
My "fear" of PEM is as rational as my "fear" of mangos and my dh's "fear" of Brazil nuts.

If there was a way to cure PEM, wouldn't your friend and me just get on with life safe in the knowledge that a crash can be helped?

In the 16 years I worked in psychiatry I saw a lot of people with what might be labelled "irrational" fears. But I saw lots more people who had very rational fears. Obviously a therapeutic approach had to be different. depending on the root of the fear. The root fear of PEM is because PEM is bloody awful.

 

[Richie]

My take on fear, inactivity, and pathophysiology:

1. One may reasonably associate fear of PEM/PENE with (greater subsequent) inactivity in some cases
2. Rowe associates inactivity with enhanced nerve sensitisation leading to enhanced central sensitisation and local inflammation
3. Dr Meirleir associates mild inflammation with increased vit D 1,25
4. Dr Meirleir associates increased vit D 1,25 with reactivation of herpesviridae
5. Many experts associate ME/CFS (onset) with acute viral infection e.g. by herpesviridae
6. Dr Meirleir observes higher than normal 'latent', but lower than acute infection, levels of herpesviridae activity in ME/CFS patients

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)

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!

Hi John H
Your first point associates PEN with lowered activity in some cases. I think that repeated malaise after activity is likely to reduce activity in almost all cases. Since most/all? of us also suffer greater general baseline fatigu, our activity is likely to be lower anyway, of course.
Your second point quotes Rowe. Would you yourself apply what Rowe claims to all or only some patients? And if this process is occurring in all of us at some point, how significant is it relative to other matters in your view? (Perhaps you partially cover this point at the end of your post "Attempting........"), but I 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.
On point three how many of us is this relavant to? And is the inflammation driving the 1,25 or the other way round? High 1,25 is assocaited with some TH1 conditions , but many ME/CFS sufferers are TH2 dominant.

What is you overall point? 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?

I 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, but maybe I have misunderstood your ideas.

 

[Richie]

On the broader subject of depression in ME/CFS, I would characterise three types from my experience
1) Highly biological co-morbid depression - e.g. in my case arising from supplement use for no apparent reason and abating immediately on cessation. Depression arising from immune activation. Possibly incl a crisis cortisol output to decrease inflammation.
2) Ordinary "I've' lost my life" reactive depression, anxiety, which may mask each other.
3) Depression of vigourlessness. Brain hypo-function paralleling bodily hypofunction
4) Long term adaptive states - having to be hyper to survive/function undiagnosed, going into mental overdrive to compensate for 3) - and paying with an equivalent long term low, where 3) takes its revenge.

Sure all interact and interact closely with underlying biophysical factors.

 

[John H Wolfe]

The series of videos with English subtitles are at..

Ah cool, thanks - lots of interesting stuff there!

So far the more relevant things I've come across in his excellent coverage in that series relate to what could be behind:

POTS: "..it's a complex condition in which also the nervous system is involved; a number of abnormal reactions arise, caused by hidden inflammatory processes"*

Reduced tolerance to strain and (physical) stress: "a result of hormonal and neurological changes, which cause a patient to become more sensitive to stress" **

Sensory sensitivity: "..a result of a number of neurotoxic substances present in the body" ***

* I believe chronic (varying grade) neural hypersensitivity, affecting nervous system disorder through as yet not fully understood inflammatory mechanisms, is one such hidden inflammatory process

** I also believe that the net impact of the neurological disorders (including neuroendocrine [hormonal]) that relate to this neural sensitisation is enhanced sensitivity to stress thresholds across the board

*** In the discussion in my hypothesis article I link glutamate release associated with (central) sensitisation (which may be triggered by peripheral sensitising effects) to glutamic acid excitotoxicity (neurotoxicity), to which cerebral regions are apparently particularly vulnerable

Hence PART VII of my hypothesis article (and my protocol) centres on attempts to:

1) Reduce neuromuscular/neuromechanical tension (a vital aid in the reduction of neurogenic sensitisation)

2) Reduce systemic 'stress' by tackling as many areas that represent possible sources as I can currently conceive of

Sushi (and anyone else interested) if you know of any evidence (from Dr. De Meirleir or anyone else) that would nullify these relations/my theory then please do let me know the source(s) so I can look into it. Thanks

 

[John H Wolfe]

I am so confused reading this. Sorry

Sorry I do waffle on a bit some times! hehe

You have a friend who avoids activities that will lead her to PEM. Is that right?

Yes

Are you saying she doesn't really get PEM, ergo avoidance is irrational?

No. Avoidance is rational

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

Or 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?

Yes, until she arrives at a point where she is in the right condition to tolerate increased activity on a sustainable basis

In which case she doesn't require therapy

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)

What therapeutic intervention would you offer her - if you think she needs it?

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 pursuing

Additionally I might give her my take on how best they might be implemented (with reference to my own experience, the experience of others, and her particular presentation) with support, guidance and treatment from (a) professional(s) (there are plenty of hints as to how one might go about this in the general guidance provided in the protocol)

Do you think she needs counselling/CBT to help her get more active and just deal with PEM when it happens?

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!)

When 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?

Absolutely not

 

[John H Wolfe]

Hi Richard,

I think that repeated malaise after activity is likely to reduce activity in almost all cases

Indeed, although not all of us are so quick to learn

Would you yourself apply what Rowe claims to all or only some patients?

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 good

if this process is occurring in all of us at some point, how significant is it relative to other matters in your view?

In my humble, and untutored, estimation - it could well be something of a disease facilitating force

It does not necessarily follow that it could be the main route out but that's my best bet at present, and I suppose the reason Rowe is conducting a 2 year study is somewhat indicative of the fact that, has probably seen clinical indications that support this 'bet', at least for those who demonstrate obstructive PENE responses to other, more general efforts (that include physical rehabilitation)

I 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

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 article

It's also fair to say that my protocol incorporates a great deal besides neural de-tensioning and guidance designed specifically to be supportive of de-tensioning efforts

On point three how many of us is this relavant to?

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)

And is the inflammation driving the 1,25 or the other way round?

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 this

High 1,25 is assocaited with some TH1 conditions, but many ME/CFS sufferers are TH2 dominant

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 associations

What is you overall point?

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)

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?

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)

I know many PWME, including myself, find sunlight therapeutic (provided it's not too fierce and they take account of light sensitivity), and as you will no doubt be aware there are all manner of links between vitamin D deficiency (often associated with insufficient [seasonal/habitual] UV exposure) and poor health

Light also effects mood and bio rhythms (including circadian) so if one can combine mild exposure to sunshine with sensible supportive physio (catering adequately for OI/dehydration/mineral loss in perspiration) then that's got to be desirable yes!

I 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

Agreed

 

[Richie]

Thanks John
So much, I think, depends on order of intervention and addressing complicating factors.
Re TH1/25 Vit d Marshall, I think, made a claim that all CFS is TH1 driven but he is a big anti sunlight advocate as some on here will know.
Really is v important to know what is going on in any individual in order to work out a sensible protocol.

 

[Shell]

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

I wonder if there really is anyone who would say that all types of activity at all stages of ME will lead to PEM/PENE.
Are there any papers on this and how would it be measured I wonder?
Let's take having a shower.
Having a shower for a healthy person is no problem.
For someone as sick as me it leads to a mini-crash. For people much sicker than me, they can't even with a stool, manage a shower. Bedbound ME patients require bed baths. (Thank God I've never reached that point so far)
Now I have experience with both ends of this - ie I get what is mild PEM - just can't move much but pain and other stuff not so bad after a shower. I still shower.
Meanwhile I've experience of giving bedbaths. I have NEVER met any patient, no matter what their illness, who would rather a nurse wash him or her down than be able to get the bathroom. Even when I was assisting in the bathroom - the patient preferred that to a bed bath.
Some patients showed reluctance to make it from the bed to the bathroom - but those patients were in pain. Other patients were the opposite, putting themselves at risk because they longed for the ability.

I can't see how ME patients would be different?
In fact most PWME that I know would rather try something, like seeing a family member, and risk the consequences than avoid it.

The other issue those of us with ME face is some things might cause more problems one day than another. Some days I can get dressed with no problem. Other days it floors me. I can't always tell before hand what will happen.

I think it is almost impossible to work out an activity that a PWME is avoiding for a PEM that won't happen. You can't KNOW that and it's made more complicated by the waxing and waning and remitting relapsing nature of the disease.

Even less "life important" activities aren't avoided (at least by me) when I'm able. I used to play piano. Now I can't coordinate both hands (can't write either) so that skill is gone. But when I had a three day remission a few months ago I had a go at the piano and enjoyed playing again. Three days later I couldn't play any more.
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.

 

[lansbergen]

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.

Well said