Severe difficulties with eating in ME/CFS

[Hutan]

I do think trying to have a clearer and more consensus understanding of the main pathophysiological mechanisms (that we currently know)

What do we know?

 

[Hutan]

Some posts about specific people currently experiencing eating difficulties have been moved to
United Kingdom: Cases of people with ME/CFS with severe feeding problems, in the media
There is some content in those posts relevant to the wider questions being discussed here.

 

[hibiscuswahine]

What do we know?

I conceptualise things like this.

Severe difficulties of eating for ME/CFS is multifactorial and still much to be learnt and researched.

A) individual factors - preferences for that person, culture and their comorbid medical illnesses eg. Coeliac or perhaps other special diets that may cause malnutrition because pwME lack education on how to do these safely
B) environmental factors - ability to get nutrition and weight loss but also past treatments, alternative medicine but also the medical profession treatment including stigmatisation, positioning of patient, lack of access to a dietician, quality medical care for their M.E.
C) ME pathophysiology - still up in the air, - not researched or low evidence eg. something either locally in the GI tract, peripheral autonomic system, hormonal, (gut based and central mechanisms) eg. like hypothalamus (and perhaps that extends to pituitary, not sure) and other organ dysfunction (kidneys or liver) Immune factors, Gut biome, food sensitivities, sensory sensitivities, pain and discomfort from eating and digesting food.
D) the consequences on physiology from excessive weight loss and dehydration and effect on functioning on organs including musculature
E) other medical conditions, not yet diagnosed
E) unknown psychological factors (eg developmental) or undiagnosed psychiatric illness.
F) factors related to the primary care team, their knowledge, manner and expertise and their willingness to use parenteral nutrition or put in NG/ PEGS etc

 

[Jonathan Edwards]

Surely that's an understandable approach though, if you are trying to get specific investigations into physical problems, or when faced with people who don't believe in pandering to a patient with what they believe is a problem that could be fixed if the patient just (consciously) thought differently?

it is understandable. My point is that it is a red rag to the bull in charge of the poor patient and a distraction. We want research into problems, all of which are physical, including those to do with the mind. But encouraging patients to think that they should have unreliable tests and unproven treatments relating to half-baked ideas about gut problems simply fans the flames.

The people I described below are in charge. If they can be got to think sense great but until then maybe saving lives is more about not driving a wedge through the system.

If Weir and Speight pointed out that there is no evidence that talking therapy works that would be fine. But instead we have things couched in terms that patients and families will misinterpret.

'Eating disorder' means to virtually everyone who hears it 'could be fixed if the person thought differently about food'.

But it isn't as simple as that. Anorexia often cannot be fixed. Craniopharyngeoma obesity is regarded as a secondary eating disorder. What is 'thinking differently' and how might it be achieved? Medicine should and in my speciality does accept that everything is much more complicated. Eating disorder might sound 'psychological' to readers of the daily paper but the battle here is to alter thinking amongst physicians providing life-saving care. We cannot afford to be fussy.

I will probably come back for more but have been instructed to watch Inspector Morse.

 

[FMMM1]

I'm grateful for the above (although I haven't read all of the posts)- unfortunately this seems familiar to me both personally & re a family member ---
I'm with the Queen's physician/their translator ---
"
'we need to avoid Procrustean medicine'. In other words in 1977 the UK's top gastroenterologist actually understood the problem - we need to forget theories and get on with treatment."

I'm wondering if GWAS would turn up a signal but also whether e.g. there may be different (genetic) routes to get to the same/similar outcome?
(first hit on a Google search - "anorexia nervosa + gwas" - https://www.nature.com/articles/s41588-019-0439-2)

 

[Evergreen]

Pendergrast et al's table 4 reports percentages of housebound and non-housebound people with ME and CFS reporting bloating, stomach pain (under Pain subheading), "irritable bowel problems" and nausea (under Autonomic subheading), losing or gaining weight without trying and no appetite (under Neurendocrine) and "Sickened by smell, food, meds, chemicals" (under Immune). Despite the questionable categorisation, the data could be helpful: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5464362/

For me the nomenclature issue comes down to the fact that the term "eating disorder" is already a technical term, not just a plain English term, and it refers specifically to anorexia nervosa, bulimia and binge eating disorder, according to NICE https://www.nice.org.uk/guidance/ng69.

Since it is precisely those conditions, or more specifically anorexia nervosa (right?) that people with ME who run into real trouble with nutrition are often assumed to have, and parenteral feeding is sometimes withheld as a direct result of that misunderstanding, I think using the term eating disorder would make a bad situation worse for people with ME. Not to mention how traumatic it would be to receive the treatment for a condition you don't have, which would include, according to the guideline:

1.3.4For adults with anorexia nervosa, consider one of:

• individual eating-disorder-focused cognitive behavioural therapy (CBT‑ED)
• Maudsley Anorexia Nervosa Treatment for Adults (MANTRA)
• specialist supportive clinical management (SSCM).

If we start calling the nutrition challenges of people with ME "eating disorders", you can be sure that clinicians will just be directed to the existing eating disorder guideline.

I understand the frustration with the use of the terms physical and psychological/psychiatric, but I think what those using the terms are really saying is simply "this is not anorexia nervosa". Maybe it would be more helpful if those terms were avoided and instead the point was made that what is happening in ME does not seem to be an eating disorder like anorexia nervosa, but can be mistaken for it as oral intake can be low despite often normal GI test results. What is needed is supportive care, including dietitian input to optimise oral nutrition where that is possible and guide enteral and parenteral feeding when that is required, and gastroenterology to outrule treatable conditions, and, with the patient and dietitian, make decisions about enteral and parenteral feeding.

I think outruling an eating disorder is reasonable in some cases, but it would be helpful if when clinicians saw the patient's diagnosis of ME or CFS they thought, "Right, probably not anorexia nervosa, and tests may end up being normal, but might need more support than the average patient I see with what I consider functional disorders."

Where I worked, dietitians involved in a case would recommend parenteral nutrition if needed and not yet commenced by the medical team, but the decision lay with the physician. Often the team would decide to start NG feeding and would refer to dietetics then, as it was the dietitian who decided the details of the feed, and when and how it was to be given.

Unless the patient was under gastroenterology to begin with, gastro were only involved if the patient needed investigations or a PEG/similar.

Edited to change "parenteral" to "enteral and parenteral".

 

[Evergreen]

Eating disorder might sound 'psychological' to readers of the daily paper but the battle here is to alter thinking amongst physicians providing life-saving care. We cannot afford to be fussy.

I really understand the point you're making, but I think physicians are readers of the daily paper.

I think avoiding the whole "what is it" entirely and going straight to "Listen, people with ME who have difficulty getting adequate nutrition are not currently getting good care, let's lay out what good care for them would look like, so that we can improve things" is the way forward.

 

[AliceLily]

Could explain why I experience bowel movements slowing or stopping outright while in PEM.

Interesting, I am the opposite in PEM, loose bowels. Same mechanism but different expression?

Something I noticed in my very severe and severe years was every time I put on weight, the weight would trigger a bad PEM and I would lose the weight I had gained. The ME had made me underweight at the severe years and I could not get back to my original weight. It is only now that I am at moderate level that I am back to my original weight (65kg). But looking back on those earlier years my ME did not like my putting weight on. Could this be the vagus - hypothalamus causing it

 

[SNT Gatchaman]

Some recent articles relating to gastrointestinal motility —

2021
Novel understanding on genetic mechanisms of enteric neuropathies leading to severe gut dysmotility (Eur J Histochemistry)

2020
Understanding the Biology of Human Interstitial Cells of Cajal in Gastrointestinal Motility (Int J Molecular Science)

2019
Enteric neuroplasticity and dysmotility in inflammatory disease: key players and possible therapeutic targets (Gastrointestinal and Liver Physiology)
Advances in the physiology of gastric emptying (Neurogastroenterology & Motility)

2022 (Paywall)
Gastrointestinal Dysfunction in Parkinson's Disease (Drugs)

2021 (Paywall)
Diagnostic Evaluation of Gastric Motor and Sensory Disorders (Am J Gastroenterology)

2020 (Paywall)
An increasingly complex view of intestinal motility (Nature Reviews Gastroenterology and Hepatology) Edit: thread
Small Bowel Dysmotility, Pseudoobstruction, and Functional Correlation with Histopathology: Lessons Learned (Current Gastroenterology Reports) Edit: thread
Enteric nervous system: sensory transduction, neural circuits and gastrointestinal motility (Nature Reviews Gastroenterology and Hepatology)
Gender-Related Differences in Gastroparesis (Am J Medical Sciences)

2019 (Paywall)
Gastroparesis: a turning point in understanding and treatment (Gut)
Motilin: from gastric motility stimulation to hunger signalling (Nature Reviews Endocrinology)

2015 (Paywall)
Glutamine and intestinal barrier function (Amino Acids)

 

[josepdelafuente]

We want research into problems, all of which are physical, including those to do with the mind.

This obviously seems super sensible to me, it also seems unavoidably massive in implication - like wouldn't this imply basically scrapping the entire field of psychology? (I'm not a psychologist or doctor or scientist so I don't know what I'm talking about!)

 

[Binkie4]

Dr Weir is to be interviewed at 3.30pm today which will go out on Spotlight SW at 6.30pm, and probably 10.30pm.

Adam Broderick has agreed to record the interview with Dr Weir and upload it to utube and fb.

Edit: Interview with the BBC took place this afternoon. It is now not expected to go out till tomorrow.

 

[Midnattsol]

I think it might be helpful to compare with cystic fibrosis. When CF is advanced there are multiple body systems affected. Most people think about lung disease and bronchiectasis, but the GI tract is significantly affected. Tube feeding is well established in this scenario.

Apart from well known issues like inability to absorb and digest appropriately due epithelial transport impairment and pancreatic insufficiency, mechanical problems handling abnormal gut content, there can also be a significant higher workload of breathing that means eating competes with respiration. These patients are often on overnight continuous low-rate tube feeding to ensure they get adequate nutrition.

See eg —

Nutritional Care in Children with Cystic Fibrosis (2023, Nutrients)
Improving nutrition in cystic fibrosis: A systematic literature review (2022, Nutrition)

Related to the attitude "they will eat when they are hungry", it could perhaps also be useful to look at advice given when children with autism or ADHD are not eating enough. This is an attitude that has to be combatted so the child gets adequate help.

 

[CRG]

The part about weight loss is hardly insignificant:


The aim and net effect was to get the mention of weight loss removed from the guidelines.

And by saying weight loss is not part of CFS/ME, it increases the chances that it will be psychologicalised/blamed on a patient's maladaptive behaviour/similar

I don't know what White's aim was but the goal was an open one, and gives an object lesson in getting one's arguments straight before putting them in front of people who may not agree with those arguments or who have other agendas, which should probably be the main take away from that episode as it relates to the current concerns.

 

[Tom Kindlon]

As an aside/bit of background (though is in some ways related to main subject matter as bowel symptoms may affect diet, appetite, etc.), Peter White also argued other things weren’t part of ME/CFS when replying to the draft 2007 NICE guidelines
e.g.
(v) Bowel symptoms and CFS/ME:

Draft text:
6.4.5.5 Prescribing of gut anti-spasmodics (such as mebeverine,
alverine, and peppermint oil) should be considered for adults and
children with bowel symptoms, such as cramp or bloating.

SH St Bartholomew's Hospital Chronic Fatigue Services
85 FULL 229 6.4.5.5
"..gut anti-spasmodics.." are not
treatments of CFS/ME since bowel
symptoms are not part of CFS/ME. You
should make it explicit that this
treatment might be indicated for the
treatment of IBS, if present comorbidly.
Alternatively, and perhaps more wisely,
you could suggest that IBS, if present,
should be treated in the light of the best
available evidence, and refer readers to
appropriate guidance, which may or
may not include considering
antispasmodics as the treatment of
choice for "bloating", although we would
doubt it. You do mention IBS on page
233, line 12.

NICE:
We have revised this
recommendation and referred to the
NICE IBS guideline – currently in
development.

From:
https://listserv.nodak.edu/cgi-bin/...0mgmtii4AXYX898Azzv1g1NGgLd3mH04bWDtSTix0Erso

 

[Jonathan Edwards]

I think it might be helpful to compare with cystic fibrosis. When CF is advanced there are multiple body systems affected. Most people think about lung disease and bronchiectasis, but the GI tract is significantly affected. Tube feeding is well established in this scenario.

Cystic fibrosis may be an interesting comparison in that this is not the situation for ME, despite some 'experts' trying very hard to give that impression. There are no structural changes that would explain weight loss known to be part of ME.

In a way, this is what Peter White should have meant - nit that weight loss is not associated with ME but that the weight loss that is associated with ME cannot be put down to any specific 'ME lesion' known.

I agree that there is a downside to suggesting that difficulties with nutrition despite availability of food and carers in ME should be classified as an eating disorder. Nonetheless, I think it does fall within what an average physician would understand by the term used generally. (NICE guidelines are inevitably Procrustean so will tend to stick to AN and bulimia, despite at least some literature we have found indicating other patterns.) There really needs to be a term that has no baggage.

I wonder about something like 'nutritional intake intolerance'. That is clumsy but 'food intolerance' already has baggage and just nutritional intolerance might do. The idea would be to emphasise that some people with severe ME have a general intolerance of nutritional intake that needs to be treated on its own merits.

I am not getting any feedback from enquiries so far and I fear that this may be a topic that colleagues don't really want to broach. I will continue exploring.

 

[CRG]

I wonder about something like 'nutritional intake intolerance'. That is clumsy but 'food intolerance' already has baggage and just nutritional intolerance might do. The idea would be to emphasise that some people with severe ME have a general intolerance of nutritional intake that needs to be treated on its own merits.

I think there are two separate concepts that need to be communicated -

a) intolerance related to food sensitivities, something which may be addressed by dietary adjustment (FODMAP etc), but which in some individuals extends to an unmanageable range of foods leading to severe dietary restriction; and

b) intolerance related to the mechanisms of digestion - which may be affected by muscular and/or nervous system response. Nutritional intolerance encapsulates sense a) but not so clearly sense b). Motility disorder might be too precise a term but something comparable that allows communication of the sense that the muscle and nerve involvement in ME/CFS should be considered as potentially playing a role, is needed. I don't know if reference to the several papers on small fibre neuropathy might be applicable:

Complex syndromes of chronic pain, fatigue and cognitive impairment linked to autoimmune dysautonomia & small fiber neuropathy, 2020, Schoenfeld et al

https://www.s4me.info/threads/compl...fiber-neuropathy-2020-schoenfeld-et-al.14152/

Scientific Advances in and Clinical Approaches to Small-Fiber Polyneuropathy (2019) Oaklander et al

https://www.s4me.info/threads/scien...pathy-2019-oaklander-et-al.11225/#post-461004

Or a general reference to neuropathy and the GI tract: An update on autonomic neuropathy affecting the gastrointestinal tract SciHub: https://sci-hub.se/10.1007/s11892-006-0073-0

 

[Jonathan Edwards]

Nutritional intolerance encapsulates sense a) but not so clearly sense b). Motility disorder might be too precise a term but something comparable that allows communication of the sense that the muscle and nerve involvement in ME/CFS should be considered as potentially playing a role, is needed. I don't know if reference to the several papers on small fibre neuropathy might be applicable:

Yes, that was the reason for making it nutritional intake intolerance - emphasising that this is in the end of just getting nutrition in, not adverse symptoms for specific foods.

I think all specific motility mechanisms should be kept out of this at least until someone shows that they are real and what they contribute. The muscle and nerve involvement of not being able to eat with flu is just a general hypothalamic/vagal rejection reflex. I don't see that anything more than that has reliable evidence to date for ME.

Dysautonomia and small fibre neuropathy are easy to invoke but the odds are that they have nothing to do with this, so like mast cell activation they muddy the waters.

 

[Midnattsol]

Some foods are harder to digest than others, so could very well give a more adverse reaction if the problem is related to energy use in the gut and motility.

As a non-native English speaker I may be missing nuances here, but "nutritional intake" intead of "food" or "dietary" doesn't make much sense to me.

 

[hibiscuswahine]

yes, I prefer dietary (which as aligns with a dietician, a health professional in a pwME care team)

The "nutritional bit" may involve the potential for bowel absorption or motility problems (eg. on the purely mechanical front without causation, perhaps rapid transit or "irritable bowel type" symptoms fro some pwME or sits in stomach which becomes extended, doesn't empty properly and then etc then perhaps overwhelms small intestine causing more problems going through this and then large intestine etc)

or otherwise refers to the essential "nutritional" requirement's in the pwME's diet.

 

[Jonathan Edwards]

As a non-native English speaker I may be missing nuances here, but "nutritional intake" intead of "food" or "dietary" doesn't make much sense to me.

Partly to include fluids and electrolytes.
Also food and dietary intolerances tend to mean specific allergies or coeliac etc. which I don't think are the central issue. My understanding is that the people who at real risk cannot manage anything.