[Blog] BACME, NHS ME/CFS clinics shift from deconditioning to dysregulation model of ME/CFS in anticipation of updated NICE Guideline

Whoever is interested.

An interesting point was made both by a health professional whose identity might be guessed and by a NICE committee representative at RT in response to the suggestion that ME/CFS needs to be dealt with by people properly trained in eg. rehabilitation. The response was that it didn't matter much what qualification letters people had as long as they knew what they were doing.

In science it does not tend to matter much who does the arguing. Very often you have to spend time learning skills in a new area yourself.

I am not necessarily suggesting that research is done in a BACME based clinic like YFC. Sue and Vikki say they are very busy with service provision anyway. But you need a clinical base. For RA that was centred around physician clinics. For ME at the moment it is centred around therapist-based clinics.

The thing is to think outside the box. So for instance, Caroline Kingdon is a nurse specialist who goes around visiting people with severe ME and liaising with GPs to collect samples from PWME. I think Julia Newton was hoping to make progress with physiological dysregulation in ME but she seems to have given up. I think maybe they went in looking for certain specific things that were not going to be there.

And the actimetry study I dream of may not need any clinic base. If the devices are clever enough they just get sent out to forty committed ME patients to wear for four months. They report back to a central hub via WIFI. Then all you need is a very clever person to interpret the data!

 

By talking to them?

 

Copying this from the pacing research thread where Mithriel was discussing a relaxation tape her Doctr gave her because i think its very relevant (maybe) to the Dysreg model.

I wish i could get scientists interested in the role of adrenaline. I've been banging on about it for 20yrs. The difference in me is noticeable to the point of spectacular.... Eg Unable to walk more than 10yrds, staggering, unsteady gait, poor coordination, disoriented cant speak properly or understand what's being said, in a lot of pain & dizzy very weak feel very faint on standing. Sunglasses on because light is so painful earplugs for sound.

Then something makes me frightened or angry, or both (more noticeable if its both). Suddenly my co ordination comes back on line, i can stand, walk straight 20yrds, cognitive & communication ability improves, i can turn the lights on and tolerate sound as long as it's not loud.

If i'm at my best when the scare/anger comes, i feel almost normal, can walk unaided, understand things that were beyond me before (ie all cognitive function comes back on line). Its glorious while it lasts, but if i behave according to how i feel, the PEM is horrendous, so the impact of the extra activity is as expected. It's like the adrenaline is a con.

Adrenaline is the reason a Dr has never ever seen me looking even remotely poorly. Seeing a Dr/health professional = anxiety = adrenaline = looks & feels almost 'well'.

I do hope this will factor in to any discussion of the dysregulation model @Jonathan Edwards because its a widespread experience for PwME & surely it must mean something, or at least be kept in mind because i'd have thought 'it cant be that because if it was that then adrenaline/anxiety wouldnt help', might be a thing. Sorry thats a very lay point of view i know, but its always seemed to me to be important but overlooked. I'd be interested in your pov on it.

 

"We sure do. From where is the question."
DecodeME - GWAS - actually something generated by MRC getting a panel together to identify promising research - @Jonathan Edwards was a member - DecodeME should e.g. indicate/settle the question of whether TRP receptors are relevant --- but also may indicate other potential underlying causes/predispositions --- and lead to research to understand the cause/treatments

Actimetry study was another thing Jonathan thought was promising i.e. last MRC "think tank" --- so an actimetry study would generate data.

EDIT - if adrenalin is relevant the DecodeME should indicate that @JemPD

 

Thank you for articulating my concerns so well.

From what I've seen from the BPSers, "HPA axis dysfunction" is the new "central sensitisation" (which, in turn, was the new "it's all in your head").

This is just a re-branding exercise because patients clearly weren't buying the old product. The hypothesised causes are still the same (ie, stress, childhood trauma) and the treatments are also the same (CBT, desensitisation, rehab, and other woo).

ETA: In my view, this is just the same old product with slicker marketing.

 

I've been thinking about this whilst trying to find the best way to record swim data, and it's clear that it's the app that makes most of the difference.

For instance, standard health apps aren't interested in whether someone is resting in a sitting or lying position, but that would be important for ME data collection. It might be possible to detect via changes in heart rate; most of the devices seem able to record that reasonably consistently.

Standard apps also don't separately record short periods of activity, such as going to the toilet. In terms of understanding how much capacity PWME have, it would be good to be able to distinguish between key non-negotiable activities and 'optional' ones. It must be possible to design an app to learn the consistent, repeated patterns of movement that almost everyone does multiple times a day to make a trip to the loo from their chair or their bed, even if at the beginning of the trial it has to ask patients to confirm Yes, that was a toilet trip.

 

That makes a lot of sense. I was thinking of the phenomenon of 'second wind' where agonising exhaustion at 8,000 metres in a 10,000 metre race can suddenly be replaced by a rhythm that will get you to the finishing line and even with a reasonable placing.

I think ME must have something to do with some down-forcing signal operating for no reason. It reminds me of our gas boiler that would fire up nicely when we open up house but switch off half an hour later, then fire then switch off ten minutes later and then keep switching off until it stayed off. It turned out to be an oversensitive water sensor. Now the house heats fine.

In terms of disease there might be a comparison with nephrotic syndrome where the liver actively reduces the plasma protein level, aggravating oedema already present due to capillary leakage. If you fill the plasma up with protein the liver just degrades it until the level is low again.

 

This model comes from the part-time RFH fatigue clinic part of the Infection and Immunity Service. An explanation of the pathology of CFS/ME also formed part of GET (that's how my hospital records read). During the explanation, I was presented with the above model and was told this is what was currently known to be the clinical picture of CFS/ME. I asked for the cause and was told they didn't know, but it seemed as though a "switch" had gone off and was stuck, and the model was what was currently understood to be wrong with patients based on current research (whose research - I don't know). Particular focus was placed on adrenaline and cortisol secretion dysregulation, autonomic dysregulation and cytokines.

I hope the explanation above answers your question. At the time, I wasn't told it was just a theory. It was the only understanding of ME I had until some time afterwards when a neurologist said it was a somatoform disorder.

RFH was also a dispensing clinic, so I've been told former patients who saw the consultant were often provided with drug management for symptoms and received referrals to secondary care for comorbid conditions such as POTS and other immune-deficiency conditions. I didn't receive any drugs as I never saw the consultant during my time there. I only learnt what other patients had been offered from local support groups.

I didn't do any increased activity tasks as part of GET, and wasn't told GET was a cure for ME - as there wasn't any cure, but it was to help reduce symptom severity and help regulate what had become dysregulated. Still, I think that was only supposed to form part of the treatment and the rest involved drugs to help stabilise the condition, which I think is referred to in the 2007 guideline.

 

This recording may explain more about it around 14.00.

https://www.youtube.com/watch?v=fU4JKeLdL9o

 

So if we are talking about “what’s going on with ME”, and throwing some ideas into a mixing pot, here are a few of mine: (There have been a few more posts as I was typing…. )

1. Adrenalin:

I can perform much better under adrenalin’s influence. As a biologist I recognise it as the “flight or fight” hormone. So basically it is about survival in the moment. Blood is diverted away from the gut, and towards the brain and muscles ready for action. Pain signals are also down-played, so the body is able to respond with less inhibition.

I won’t deny, I love a little adrenalin in my system.

However, as an ME patient, I find that once in my system, adrenalin leaves rather more slowly than I’d like.

A friend and I coined the phrase “dangerously okay” to describe the period when adrenalin fools you into believing you are better than you really are. This phase lingers even after an activity has drained the muscles of their energy. I KNOW I should be laying low, but I find it really difficult to appropriately rest in this state. It seems I don’t get PEM until after this phase passes.

2. Gut:

I have found I do active things better on an empty stomach. This may be because “doing stuff” involves adrenalin which diverts blood away from the gut, so of course it’s better if there isn’t a load of food in there. I regularly skip breakfast, and always on the days I’m going out to work my dogs.

3. Compression Wear:

So it seems if I want to do something a bit more active (eg my dog agility rounds which involve about 40 - 50 seconds of high concentration and co-ordination of my muscles - I’m just walking but none-the-less this is “active” effort). Lower body compression wear helps keep me on my feet for this, and means my brain able to keep thinking. This suggests to me that my peripheral blood vessels don’t respond correctly when I up my effort levels, because without compression wear, I quickly feel un-coordinated and sort of drunk (without the happy part).

4. PEM:

PEM feels like an immune reaction to something. This seems to tie in with its delayed response (48+ hrs after the event for me) and with PEM’s incapacitation. ‘Flu leaves you feeling sore all over, sensitive to light, sensitive to noise, without an appetite, and unable to get-up and go-on. As I understand it, these symptoms are down to the immune system fighting whatever virus is causing the ‘flu. PEM for me feels like this too. Whereas in the 24 hours after activity, I can feel like I’ve escaped the PEM reaction (no doubt the adrenalin), the “day after, the day after” brings home the truth.

5. If PEM is an immune response, to what is the immune response directed?

So here I’m feeling about in the dark.

A) Might it be that the gut gets “leaky” and our immune system fights some of those larger molecules that slip into the blood stream? This might connect with my observation that I “do better” on an empty stomach. Maybe if there’s less in the gut, then less leaks out of it? Who knows.

B) Might it be that the poor response of the peripheral blood vessels causes “something” to get flushed from the tissues to the lymphatic system, where an immune response is initiated to that particular molecule?

C) Might the fact that my muscles are highly fatiguable and the consequent anaerobic respiratory processes mean some weird respiratory by-product is produced at levels that sets off an immune response??? (Not sure on this one…).

D) Maybe the lack of production of ATP (cos anaerobic respiration can’t keep up) and the eventual conversion of ADP to AMP, could not only leave use drained of physical energy but also lead to other metabolic pathways that delay our ability to recover appropriately?

6. Energy Ceiling?

None of these things seem to account for the fact that each ME individual has an energy ceiling effect.

What factor accounts for its level? Why is it relatively consistent over time? Why does it occasionally change for the better or worse? If over exertion causes it to drop what is the mechanism for that drop? If an antiretroviral drug causes it to lift (as happened for me during 2016) why is that? What was the mechanism for the change?

What is it that sets the level for each person’s energy ceiling? What can we do to nudge the ceiling up again?

All we know now is that normal rehabilitation involving exercise is counter-productive. Why is that?

It also seems that rest, although essential for maintaining a current energy threshold, doesn’t necessarily help the threshold to re-adjust upwards. Though a waiting game of rest, may eventually mean that some natural change happens to restore a better energy level…. Or of course, it may not!

7. Boom and Bust ?

So here’s the thing, NO-ONE ever does the same amount each day! Not one person! We all go through cycles of doing a bit more, and then doing a bit less.

So if I choose to rest today and tomorrow, so I can do something a bit special the next day, and fully plan in my rest and recovery for the few days afterwards, then why should I not do that?

I have been doing exactly this for the past six years. In truth I have found it much more difficult to come back after a period of several days doing “just a tiny bit extra” than from a single day of “quite a bit extra”.

Understanding how these activity patterns work would also be useful, but I can’t seem to suggest a mechanism right now. It “feels” like there is something critical that gets depleted, and I just need to wait (and rest) until is gets restored.

****

Ooops… long post dumping a whole load of thoughts… hope it’s not too off topic. But maybe as the first of a load of “dumb ideas” it might make someone more knowledgeable than me think “Ah ha!”….

 

This would be the same Gabrielle Murphy who resigned from the NICE guideline committee because she couldn't support the finalised revised guidelines?

 

She also abruptly left the RFH fatigue service whilst developing the guideline.

 

The same. She resigned, but after signing up to the revised guidelines. Why she resigned nobody seems to know.

 

Your experience pretty much mirrors mine, although I can't use anything like compression wear due to my skin sensitivity (I've had this since a child, it's autism related).

So I would take issue with the new NICE guidelines which say that symptoms unpredictably fluctuate. They do to an extent, but the overall pattern is actually predictable if there's no additional things being thrown into the mix, such as an infection or unplanned life upheaval.

 

Your points 1-4 are an exact description of my experience @Keela Too

So the adrenaline perhaps turns off/nullifies the down-forcing signal?

But then why the PEM afterwards - which incidentally is so much like the flu/an infection that i cant tell the difference when i do get an actual infection. The only difference is that PEM comes with more symptoms on top like the much more pronounced cognitive impairment, strange gait, pins & needles & faulty proprioception etc, but all the 'immune' type symptoms like sore throat, swollen glands etc only come with PEM for me.

 

No one seems to know why she left the fatigue clinic at the time either........

 

My dealings with that particular consultant were bizarre...... We never met, but somehow I received an FS diagnosis even though her colleague's assessment said I had CFS/ME. She also emailed to say I should see Dr Weir.

 

But the mechanism she is describing though, is that chronic sympathetic nervous system activation provokes cytokine release = symptoms... but what I am saying, YELLING, is that when the sympathetic system is activated, i feel BETTER not worse. And if i ignore the feeling better, and maintain the activity level as normal (which is very hard - but occasionally possible) I do not get the PEM. So their theory as described on the video, is just, well, it doesnt fit with my experience at all. She spouts a lot about the immune system there (from 1bout 14.00 on the vid) @Jonathan Edwards... i'd be interested to hear what you think of what she's saying... ie is she talking twaddle or?? Mind you I'm sure you have better things to do with your time.

 

yup