United Kingdom: Learn about ME - webinar for GPs

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Learn about ME webinar for GPs: watch now
October 14, 2024

Dr Nina Muirhead and Dr Robin Kerr led a free Learn about ME webinar for GPs on Thursday 26 September.

Continues at:
https://www.actionforme.org.uk/news/learn-about-me-webinar-for-gps-watch-now/

 

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Looking at the transcript of the video it seems there is too high a level of credulity when it comes to some poor-quality biomedical research - no, we don't have "evidence in ME that it's endothelial dysfunction" or a sympathetic-parasympathetic imbalance or impaired oxygen extraction.

We were also wondering recently about AfME's clinical service - this paragraph may give some indication:

 

I'd like to know what questions came up in the Q&A

 

It's really frustrating. Some of it, especially where they talk about how patients describe their symptoms to doctors, could be really useful.

Do GPs need to hear all the theories about aetiology anyway? Surely they'd be most interested in what they can do. Given the base we're starting from, there's plenty: starting with accepting that ME/CFS is not due to aberrant thinking or deconditioning, then learning about how it presents, then getting a handle on useful questions to clarify the picture if they suspect it, then what they can do to support people if they diagnose it.

It doesn't need the hosts to talk about scantily-evidenced research in an attempt to make the material sound properly doctor-y.

 

It is very disappointing to see this.

This is exactly what I was trying to tell people to get away from in my Qeios article about feeding support.

For years the claim has been that patients are iller than they need be because they have unhelpful believes about having a disease called 'ME' - now always trotted out as a 'complex multi system, or neurological' disease. And yet these 'unhelpful' beliefs, if any of them are, are taught by one doctor to another in educational videos. It is the doctors who are generating these stories about endothelial inflammation and dying mitochondria (you thought Myhill had faded away but now it's official education).

This is about as counterproductive as you can get. Any sensible GP will see that this is not bona fide medical education based on reliable evidence and careful wording of practical advice - as you get in Bansal's 2016 article. It is propaganda and I worry seriously counterproductive.

It is what allows people like Maeve's coroner to believe that people with ME/CFS will die anyway from their disease even if fed.

The extraordinary thing is that now that the patient community have educated each other (and some of us medics) through a science forum it is the patients who are criticising the doctors for their unhelpful beliefs. I can well imagine a member seeing a GP who says 'well we now know you have a complex disease with endothelial inflammation' and the member politely tells them it is bullshit.

All the stuff about how many weeks you need to diagnose is nonsense too. Medicine doesn't work like that and most doctors realise that at junior registrar level. Almost all of the time you are dealing with probabilities and future possibilities about what is wrong and what might help. Diagnosis is a concept that patients believe in but doctors should realise is a shorthand for a much more subtle process of decision-making. And it isn't hard to talk in those terms. Amolak Bansal did it very well. Alastair Miller, bless his cotton socks, does it very well in a 2015 video. He just gets the aetiology and management wrong. ME/CFS is a syndrome, as he emphasises.

 

The doctor sounded like a blokey chef talking tasty winter stews.

We could really do without help like that.

 

Bansal's article is probably worthy of deeper discussion. I noticed he picks up on several aspects of the condition that are less frequently discussed e.g. alcohol intolerance, non-restorative sleep, cold extremities, hypersensitivity to certain medications (especially serotonergics) - all things I have experienced but which are often ignored. He has carefully considered how other conditions like depression present and mentions a variety of distinguishing features. There are a few aspects that I think are a little muddled or that I disagree with but overwhelmingly I get the impression of thoughtfulness, prolonged clinical experience & of genuinely listening to what patients have described over a long period of time. Imagine if we had a few dozen similar physicians, with clinical insights continually informing research. He would be a far better creator of teaching materials. He is retiring in December I think.

Some of the minor features of ME/CFS that he mentions are probably worthy of serious investigation as they may shed light on underlying pathophysiology. I have never seen any attempt at a serious mechanistic investigation of alcohol intolerance, for instance, although I can think of several investigative possibilities. It is a very curious feature.

 

Interesting one, isn't it? Maybe we should dig further into how it presents in those that have it. A few conversations suggest my experience (muscle pain and marked weakness, as well as nausea and headache, in response to a single unit of alcohol) isn't especially typical, but I'm not sure.

The other big one is sleep, and the apparent need of a significant proportion put aside time for recovering from it, the way we would from effort. And the vexed question this raises: does 'bad' sleep actually result in PEM, the way effort does?

 

you may already know this but I think Charles Shepherd sees alcohol intolerance as diagnostic. In fact for some while, at the beginning, i questioned my own dx because i dont have it.
I mean sure if i am in PEM already, alcohol makes it massively worse, but when well rested its actually rather pleasant, as long as i dont have more than a couple of units.

 

'why not fire them a couple of antihistamines for three months? Give it a try.'

Holy Moses.

 

My understanding is that Amolak withdrew from NHS ME/CFS practice a while back.
Yes, if we had just a dozen people with his interest, which we did forty years ago, things would be very different.

I have been reading Tronstad's paper with Fluge and Mella on pyruvate dehydrogenase activity and amino acid metabolism. It set me wondering about hepatic encephalopathy and brain fog. The amino acids themselves seem to be reduced in levels but I wonder if it is conceivable that there is a shift in something like ammonia or some ammonia scavenger or something along those lines in brain. Maybe something that competes with GABA or something. The PD shift would probably be a very epiphenomenal association with the real problem but the data do look quite convincing as a 'tell-tale' rather than as a direct mediator.

 

There are probably quite a lot of odd clinical clues around to ways in which unexpected molecules have profound signalling effects on brain and pain and nausea and all sort of similar generalised symptoms. I don't think we know why people with hepatitis suddenly cannot stand cigarettes for instance. Alcohol induced pain is a characteristic feature of Hodgkin's etc.

 

[

if we have hepatic encephalopathy and ammonia clearance issues, would lactulose clear our brain fog?
Edit: I meant “if we have issues similar to hepatic encephalopathy”

 

Yes, sorry - I meant retiring from private practice. A number of severe pwME have come to depend on a very small number of private physicians.

What I'd like to know first is if those of us who experience alcohol-related symptoms experience them similarly & over a similar time-course (its metabolism is relatively well understood). Plenty of possibilities for studying it - maybe looking at the activity of the dehydrogenase (ADH/ALDH) enzymes with PBMCs, maybe autonomic testing might tell us something, maybe MR spectroscopy could tell us about GABA activity, etc. Also wonder if any other vasodilators - or GABAergics - would produce similar adverse effects or if it's alcohol-specific.

I guess I should read Tronstad...

 

I don't understand why, but alcohol ingestion is a trigger for paralytic episodes in genetic hypokalaemic periodic paralysis. Not directly relevant, I only mention it because it's an odd effect, just as it is in ME/CFS.

 

My concern with the amino acid findings in Tronstad 2016 is that it doesn't seem to replicate very well. Amino acid differences are not really found in two of lipkin's metabolomics studies, either of two metabolomics studies by Hanson's group (at baseline), Naviaux's metabolomics study (some other urea cycle things and different amino acids from tronstadt's paper). I can remember I think three metabolomics paper's of Armstrong's (@MelbME ) and I don't think they see the same complement of amino acids as Tronstadt but do see reduced Glutamate/glutamine - which is kind of the heart of amino acid metabolism. The most well replicated baseline metabolites are to do with fats.

However I still think there could be something to it in an exercise dependent manner. Glutamate, amino acid and urea cycle metabolism becomes relevant only after exertion in Hanson's 2 day CPET metabolomics. There's also their small but striking accompanying post exercise urine metabolomics with a total lack of amino acid and nitrogen containing molecules in patients.

You can do tracer experiments with IV or orally ingested isotopically labelled amino acids. From this and the relative levels of non labelled metabolites you can work out the kinetics of metabolite catabolism. This would be a cool experiment I think to see if patients do preferentially use amino acids as substrates. Quite a logistically difficult and probably expensive experiment to do though.

 

I may be being dense @chillier , but reading the Tronstad paper puzzles me. The suggestion seems to be that pyruvate dehydrogenase activity is down in ME/CFS. If so I can see that group 1 amino acids might be unaffected if the rate limiting step in degradation was to pyruvate. But for the amino acids entering the cycle would we not expect the levels to be higher if they are not being consumed by a defective PD driven cycle?

Edit: I think I can see how it might be argued that amino acids that provide an alternative source of acetyl CoA might get used up, although I am not quite sure why that step would be increased by a lack of other supply of AcCoA but I am less clear why the group III AAs would be down.

 

Interesting that you have not found replication in the literature. The Tronstad data look very believable to me. Maybe it is something to do with Norwegian dietary practices!!