Preprint Management of Nutritional Failure in People with Severe ME/CFS: Review of the Case for Supplementing NICE Guideline NG206, 2024, Edwards (Qeios)

Yes there is an insidious creep that I have seen since I have retired. I see this as due to financial pressures within the system. Not a reasonable reason but governments and their policies are squeezing the health dollar more and more. It is so easy to dump their patients into the "psych" basket, or the "we can't help basket" and not willing to investigate further or upskill themselves. I find it amazing, in a bad way, that suddenly they are all experts in diagnosing psychiatric disorders. Often they are in for a surprise when psychiatry refuses to see them (and often point out their lack of medical work up). It's expedient for them, bordering on criminal (medicolegal) neglect for the patients.

Please share @bobbler your recent reading in a new post, if possible, that sounds interesting, I am presuming this is for the UK. I would like to say in NZ, liaison psychiatry or any specialty within psychiatry don't have enough time to "hawk through the wards or catch them in A&E". There is not enough CL psychiatrists or general psychiatrists/registrars to do such a thing. We don't have enough psychiatrists to see anything but moderate to high risk psychiatric disorders. It is also ethically unsound.
 
hibiscuswahine said:
Yes there is an insidious creep that I have seen since I have retired. I see this as due to financial pressures within the system. Not a reasonable reason but governments and their policies are squeezing the health dollar more and more. It is so easy to dump their patients into the "psych" basket, or the "we can't help basket" and not willing to investigate further or upskill themselves. I find it amazing, in a bad way, that suddenly they are all experts in diagnosing psychiatric disorders. Often they are in for a surprise when psychiatry refuses to see them (and often point out their lack of medical work up). It's expedient for them, bordering on criminal (medicolegal) neglect for the patients.

Please share @bobbler your recent reading in a new post, if possible, that sounds interesting, I am presuming this is for the UK. I would like to say in NZ, liaison psychiatry or any specialty within psychiatry don't have enough time to "hawk through the wards or catch them in A&E". There is not enough CL psychiatrists or general psychiatrists/registrars to do such a thing. We don't have enough psychiatrists to see anything but moderate to high risk psychiatric disorders. It is also ethically unsound.
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The most recent one I spotted I started talking about here:
Financial Outcome Measure

There are 3 posts (ie two after this)

I was intrigued by the middlesex situation and was googling a bit.

Anyway one example is from there - which relates to the A&E dept using an 'initiative' for 7 of their most frequent flyers and involved liaison psychiatry

Another one I've listed on this first post (referenced in the first paper) is: A PILOT PROJECT TARGETING FREQUENT ATTENDERS AT THE EMERGENCY DEPARTMENT WITH MEDICALLY UNEXPLAINED SYMPTOMS | Emergency Medicine Journal (bmj.com)

That I haven't looked into yet but I'll be intrigued to. I can only view the abstract sadly. I've finally found the date is Oct 2013, so it would be well-embedded as an initiative if it was taken on and kept up until now.

The exact wording in the conclusion of the abstract is insightful I think:

"Conclusion Providing a psychological intervention to this patient cohort is effective in reducing hospital costs by containing the most frequent attenders. CBT and care plans have reduced attendance to under once per month and subsequently reduced medical interventions and prescribing costs."

I don't know but highly suspect that whilst this starts of as claims of 'the frequent attenders' being the target, once they've suggested that 'these tend to be those with MUS' then it becomes 'stop them being attenders' and a focus on whatever they've decided 'indicates potential MUS'.

And the intro para of the abstract has a line I think is insightful :

"Indeed, despite frequent medical investigations/treatments, their symptoms persist, their problems are not resolved, they frequently complain and they keep coming back. "

So their 'crime' is to have a condition that won't improve with the 'whatever treatment it is that they actually gave them'. The inference is these people were well-investigated:

"The needs of these patients were not being met by a traditional dualistic approach in which people are seen in either physical or mental health settings."

So they were fished out of their database and put on a CBT course.
 
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Something that came up in today's testimony from Blackburn (the community dietician): he referenced a document he was familiar with about ME/CFS that had been produced by the British Dietetic Association.

I have been trying to find the source of this and I think this is it:

https://www.bda.uk.com/resourceLibrary/printPdf/?resource=chronic-fatigue-syndrome-diet

Haven't yet had the energy to read it fully so just mentioning this here as it might feed in to the discussions around a follow-up paper etc...
 
Thanks, @MSEsperanza, I have read the 4 reviews, all positive. Many thanks to the reviewers.

The peer approval note says:
Peer approval note
'Management of Nutritional Failure in People with Severe ME/CFS: Review of the Case for Supplementing NICE Guideline NG206' has been peer-approved following positive and detailed reviews. Reviewers commended its clear guidance on nutritional support for severe ME/CFS patients, practical recommendations for healthcare providers, and its foundation on NICE 2021 Guidelines. This paper provides critical insights into enhancing care for this vulnerable population.
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@Jonathan Edwards, will your proposed amendments to the article mean it has to go through peer review again, and if it passes peer review again will that mean a journal will publish it as already peer reviewed?
 
It is already published as peer reviewed in Qeios journal.
Qeios is an official journal as well as a preprint site.
But it also allows me to amend the article. The article version one remains a peer reviewed publication. Version 2 may get further reviews but as far as I know that doesn't impact the status of version 1.
 
I don't think these BSG guidelines on the management of adult patients with severe chronic small intestinal dysmotility have been posted here before; again, I wonder if these are contributing to the over-caution we are seeing in some very severely affected ME/CFS patients.

https://www.bsg.org.uk/getattachmen...5871f/gutjnl-2020-321631-full_.pdf?lang=en-US

In particular I'd note (a) the advice on fatigue management throughout, (b) the advice for FGIDs:
Significant caution should be exercised, however, to avoid escalating to more invasive forms of nutrition support in patients with functional symptoms, especially in pain predominant presentations, in the absence of objective features of biochemical disturbance or those who have a high or normal BMI. Such escalation of invasive intervention in these patients is subject to risks of iatrogenesis, and in clinical practice experience does not appear to improve global function, quality of life or symptoms.
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and (c) the commentary on hEDS:
Patients with hEDS and HSD represent a third of patients referred to a tertiary neurogastroenterology clinic and these patients tend to be young, female with a poorer quality of life. hEDS/HSD is associated with a range of gut disorders (acid reflux, abdominal pain (especially typical is pain after eating or when any food arrives in the gut even from an enteral feed) and constipation). There is often autonomic dysregulation, particularly PoTs, chronic urinary retention due to a failure of the urethral sphincter to relax (Fowler’s syndrome) and hypoglycaemia. Mast cell activation disorder is being increasingly reported (most commonly in those having PoTs).
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An increasing number of patients with joint hypermobility and gut dysmotility are being seen by nutrition support teams because of weight loss and malnutrition. This group seems especially sensitive to opioids and cyclizine, both of which can exacerbate all of their symptoms. It is currently unclear the degree to which the association of hEDS with gut symptoms encompasses specifically any greater degree of chronic small intestinal dysmotility, or whether there are any different treatment approaches to patients without hEDS who have the same functional symptoms. The same cautions therefore should apply when considering escalating invasiveness of nutrition support in this group as to that of functional gastrointestinal disorders in general, especially if there is a pain predominant presentation.
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Nightsong said:
I don't think these BSG guidelines on the management of adult patients with severe chronic small intestinal dysmotility have been posted here before; again, I wonder if these are contributing to the over-caution we are seeing in some very severely affected ME/CFS patients.
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Thanks very much for the pointer to that. It looks as if the same story as in the RCP advice is being spelled out in more detail here. It also demonstrates the complete confusion around 'hEDS', highlighting the problem that these people do not themselves have any understanding of the origin of false beliefs on the part of patients - i.e. from doctors.

The irony is that the people who are pushing back on things are themselves promulgating the memes that they are pushing back against. The whole thing is a complete mess.
 
Jonathan Edwards said:
Thanks very much for the pointer to that. It looks as if the same story as in the RCP advice is being spelled out in more detail here. It also demonstrates the complete confusion around 'hEDS', highlighting the problem that these people do not themselves have any understanding of the origin of false beliefs on the part of patients - i.e. from doctors.

The irony is that the people who are pushing back on things are themselves promulgating the memes that they are pushing back against. The whole thing is a complete mess.
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But you see the same with nutrition itself. I met a doctor at the NICU who told me milk allergy meant someone had to stay away from lactose/milk sugar (for those who don't know, milk allergy is to milk protein, typically the casein). I have no idea if this was a one-time mistake on the part of the doctor or if he regularly mixed up milk allergy (protein) to milk intolerance (typically used for lactose intolerance). There are doctors that tell their patients celiac disease or FODMAP intolerances are allergies, that meat allergy doesn't exist, that you can tell if someone is undernourished (ie. a patient that's not skin and bones cannot possibly be undernourished).

I always have to ask my patients what they have been told, as I never know if they have been given wrong information about their diet from someone else in healthcare (and I am more worried about this than if someone has read something on a blog as health care workers, especially doctors, get a lot of credit). And by "wrong" I mean "that word is used in a different manner to how I would use it". For example I understand perfectly if someone gets used to saying they have an allergy even if they know it's actually an intolerance - because others know what allergies are but an "intolerance" seem to be very hard to grasp. And it bugs me when health care professionals make fun of patients for using wrong terminology when the patients can in fact have been given the terminology by their doctor or someone else they trust in their health care team (f.ex. on foods to avoid, or an in-depth explanation of how different foods/supplements/diets may or may not influence their condition).
 
I am continuing to trawl the internet to help figure out what might be relevant to my son's difficulty maintaining weight, nausea & abdominal pain etc. Knowing that Gastroparesis has been mentioned as occurring in severe ME and aware as a T1D family that it is also a recognised comorbidity with that condition, I thought I'd search in relation to the latter. This paper had some useful information and the treatment recommendations are very clear. The obvious difference is that there is no doubt about the etiology of T1D. https://www.ncbi.nlm.nih.gov/books/NBK430794/
 
Deanne NZ said:
This paper had some useful information and the treatment recommendations are very clear.
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That is a clinical review by physicians with an interest in selling gastroparesis so I would treat it with caution. Sadly, medicine is now awash with these promotional reviews by people who don't necessarily have the scientific skills they seem to.

Uncontrolled diabetes is known to lead to autonomic system damage along with neuropathy and it would be plausible that this includes the gut but it may simply be someone joining dots in their head for most cases. As far as I know we have no indication of similar autonomic damage in ME/CFS. (Note that in postural tachycardia the autonomic feature is if anything in overdrive, not defective.)

I am still unclear on the relevance of and evidence for gastroparesis in ME/CFS but I am beginning to think that it may be a mistake to think of it as some extra abnormality rather than simply part and parcel of the intolerance response typical of ME/CFS. I am pretty sure that everyone has gastroparesis when they have 'flu'. It is not another disease, but, maybe like PoT, part of a normal response in an adverse situation.
 
Jonathan Edwards said:
I am still unclear on the relevance of and evidence for gastroparesis in ME/CFS but I am beginning to think that it may be a mistake to think of it as some extra abnormality rather than simply part and parcel of the intolerance response typical of ME/CFS. I am pretty sure that everyone has gastroparesis when they have 'flu'. It is not another disease, but, maybe like PoT, part of a normal response in an adverse situation.
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So part of the “Sickness Behaviour” response? That would make sense in my son’s case as these symptoms occur during significant & prolonged crashes (rolling PEM) but are not obvious when he is at a moderate level and having shorter & less severe PEM. Incidentally he also has bad breath when he has these GI symptoms despite maintaining oral hygiene.

There does not seem to be any controversy about a Gastroparesis diagnosis in T1D. It is not as common as Coeliac which is routinely tested for on an annual basis.
 
Deanne NZ said:
That would make sense in my son’s case as these symptoms occur during significant & prolonged crashes (rolling PEM) but are not obvious when he is at a moderate level and having shorter & less severe PEM. Incidentally he also has bad breath when he has these GI symptoms despite maintaining oral hygiene.
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I had just the same. When it was at its worst, the smell of my breath was so bad that people couldn't help recoiling.

The only thing that relieved it was not being deep in PEM. I was undiagnosed at the time and didn't understand that, so I had to put up with it for a large part of the 23 years it took to get a diagnosis.

It was investigated and I was told I was excreting food that was only partly digested, but no one knew why or what to do about it. I was prescribed digestive acids, but the tablets made me sick. I was very underweight (if I enter my height and weight at the time, a modern calculator gives a BMI of 15.5), but it was only because I couldn't get enough food through my system. My stomach wouldn't empty for eight or more hours after eating.

It eased for the first time after the really bad crash that led to my diagnosis. I'd been off work sick for eight months, had started to have a bit more function, and that made me realise the digestive problems were directly linked to the state of severe PEM I'd lived in since my teens. Since then I've been able to manage it better, and now I'm in my 60s and not working at all, it's infrequent and short term.
 
I don't think this has been mentioned here before but is perhaps relevant to both this and the Problems with POTS thread: there was a small-scale retrospective review in 2008 of patients sent to a paediatric referral centre who had undergone both gastric emptying and autonomic reflex tests (n=31 of which 21 POTS and 10 non-POTS; >=30 bpm on HUT was used as the threshold value). There was no difference between POTS and non-POTS groups in terms of symptoms and HUT δHR was not a predictor of abnormal gastric emptying. Among the authors' conclusions:
In summary, both GI symptoms and abnormal motility findings on GET [gastric emptying test] are not predicted by the extent of postural tachycardia. Furthermore, none of the common symptoms of orthostatic intolerance or GI symptoms were predictive of tachycardia on HUT.
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and on the 30 bpm threshold:
Although a heart rate change of 30 bpm or more has been described in the literature as a defining factor of POTS, in light of our review, a broader clinical approach that is less arbitrarily defined by heart rate change in the laboratory should be investigated. The traditionally accepted HUT change of 30 bpm or more does not seem to be sensitive or specific for confirming a clinical diagnosis of adolescent autonomic dysfunction, which we believe is different in presentation and course than adult POTS as classically reviewed in the medical literature.
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