Severe difficulties with eating in ME/CFS

On this point:

I think it's important to distinguish between dietitians (who are also nutritionists) and nutritionists (who are not dietitians) - the ones we want here are dietitians - they're the ones who work in hospitals with sick people on NG tubes, PEGs, TPN etc, as well as everyone else on oral feeding.

This is an Irish document that outlines the differences.

https://www.indi.ie/2-news/public/494-how-can-a-dietitian-help-you-2.html

 

I tend to eat slowly, and in hospital I have previously lost weight due to food being taken away before I've finished it, e.g. when I have had to interrupt a meal to go to the loo. I ended up putting my unfinished food in a locker when leaving it, and finishing it when I came back.

On another occasion I missed a meal due to a long dialysis session. I was so hungry I was crying.

I lost a lot of weight in hospital. Had to eat a lot when I came out in order to get back to normal weight.

 

You may be right but I am not convinced that there are any 'associated comorbid conditions' of relevance. The idea that there is some link between ME and hypermobile states looks likely to be groundless. The problems that there is a group of fringe quasi-academic physicians with large private practices who like to diagnose all sorts of things and perpetuate myths about mechanisms that have never been validated.

 

I had much the same experience with trying to get a NJ tube. The hospital staff — and I was hospitalized at a nutrition department — said it would make my stomach lazy.

I would tend to think, too, that the problem of gastrointestinal motility probably extends beyond gastroparesis. I assume the latter is more prominent because the symptoms are more obvious and it can be tested for (with a gastric emptying scintigraphy), but it casts a shadow over other possible issues.

It seems to me, though, that slowed gastrointestinal motility is a symptom of severe ME/CFS rather than “pure” dysautonomia, in the sense that there may not be neuropathy but the body is somehow slowing or even shutting parts of the autonomous nervous system down to conserve energy, among which gastrointestinal motility (a significant source of energy expenditure that it would make sense to cut back on). In my experience, this is even aggravated during crashes / post-exertional malaise.

 

It makes no sense to impose malnutrition in order to avoid a ’lazy stomach’. The purpose of alternative feeding is to safely achieve adequate nutrition.

If it is possible to safely take some food orally, alternative feeding methods do not require the patient to be nil by mouth, so some food could be eaten normally. If it is not safe to take any food orally then worry about ‘lazy stomachs’ is totally irrelevant.

 

Do we have good documentation that gastroparesis is a problem in PWME that causes symptoms? This is where I think we lack essential data.

To my mind it might be better if we had research that said 'There is no gastroparesis in ME, and no mast cell activation, and no malabsorption and no SIBO but there is an intolerance of eating, that cannot be overcome, that has a mechanism we do not yet understand.

This would avoid conflicts between doctors and patients about what is causing things.

 

Yes, I was thinking about this some more after posting. In normal people the small bowel is always active and this would be additional energy demand. Presumably this background activity is good for bowel health and function, regardless of whether there's food currently passing through (you can see it on ultrasound even when people are starved for the procedure and hear it with a stethoscope). I wonder whether a similar lack of motility contributes to higher rate of gallbladder disease. It's common to see "gallbladder sludge" develop quite quickly in ICU patients and sometimes that goes on to forming stones, even in children and babies. Metabolic and microbiome changes could also be part of that picture.

Yes, I've done many of these, assessing safety of thin, thickened and solid liquids/foods with my speech-language therapist colleagues. Up until two years ago when I was last on-site, we probably did at least 6-8 week (as a national centre). We would try to reproduce the patient's usual feeding position, eg cerebral palsy in a supported wheelchair or younger child in a reclined chair, something like a car-seat. One test would be to see if sitting forward with supports improved swallow reliability.

I can't recall ever trying to assess lying flat in an older child/teenager. I'm not sure that would work well, but you could probably come up with an arrangement. (You couldn't fit the width of a hospital bed in between the machine for example).

Modern fluoroscopy units with sophisticated algorithms are able to run at quite low dose. Ultra-low dose settings and judicious use of the foot-pedal means that you can even place "well-behaved" nasojejunal or gastrojejunal tubes with trivial / unrecordable dose. When looking for laryngeal penetration/tracheal aspiration we would usually use a "moderate" radiation dose setting. However, it does require continuous or high frame rate to not miss subtleties, so overall it's one of the higher dose procedures. Having said that our local SLTs really appreciate this exam. They refer only after appropriate clinical assessment and they systematically review (usually in pairs) and they also publish related research.

Across all such diagnostic modalities, from radiographs to PET-CT, we accept the radiation penalty when the benefit is clearly in the patient's favour. That's usually a no-brainer when it comes to something like PET for confirmed lung cancer: how far has it spread? Recognising that such swallow tests are a snapshot in time and may miss variable change in function, I would consider the radiation burden appropriate in the relevant ME/CFS scenario.

 

I do not think so. There is Steinsvik’s recently published small study on a subset of patients from the RituxME trial who have functional dyspepsia, which significantly overlaps with gastroparesis in terms of symptoms, but according to the literature only about 30% of patients with FD exhibit delayed gastric emptying on a gastric emptying scintigraphy (the gold standard for diagnosing gastroparesis).

To my knowledge, gastroparesis has come to prominence in ME because of its relationship to dysautonomia and anecdotal accounts of very severe patients like Whitney Dafoe. I certainly agree that the mechanism of intolerance to eating in ME is unknown for now and we would be missing something by characterizing it otherwise.

 

As always - thank you.

Good to see thoughts turning to how this could be investigated.

I wonder if there any possibility of finding the cause using genetic studies?

 

IMO there are three approaches.
1. Increase awareness among healthcare workers that problems with eating and digestion are a consequence of ME.
2. Highlight the requirement to provide nutrition (whatever the cause of malnutrition) because it is a human right.
3. Call for research into the prevalence, pathogenesis, and characteristics of nutritional problems in ME patients, and investigation of monitoring for malnutrition and treatments.

 

I wonder if a letter to the BMJ might be in order.

This could point out:

· There is a lack of research into gastrointestinal symptoms in ME.

· There is a lack of clinical investigation into gastrointestinal symptoms in ME patients.

· There is a lack of knowledge among healthcare workers of GI symptoms in ME patients.

· Gastrointestinal symptoms are very common among ME patients, e. g. Retornaz et al reported 85% , Ghali et al reported 81% in all adult ME patients attending a clinic in Angers, France. Steinsvik et al reported 80% had meal-related gastrointestinal symptoms.

· GI symptoms were the third most common cause of attendance to emergency departments in ME patients (Timbol et al 2018) and 30% reported GI impairment as one of the most troublesome symptoms (Chang et al 2021). Gastric emptying is slow, with delays in liquid emptying more common than solid emptying (Burnet et al 2004). Epigastric pain, nausea and abdominal discomfort were the most common symptoms after a liquid meal (Steinsvik et al 2023)

· GI symptoms in ME patients cause malnutrition which can become life-threatening (Baxter et al 2021)

· Whatever the pathogenesis, it is clear that abnormal muscle fatigue is a key symptom of ME. The digestive system, from eating to emptying bowels involves muscular activity. Malnutrition in severe ME patients could result from severe muscle fatigue, resulting in difficulties chewing, swallowing, impaired gastric accommodation, and impaired progress through the gut. In very severe ME patients, muscle fatigue is extreme so it is not surprising they are unable to eat and digest food, and subsequently malnutrition may then contribute to the severity of the disease.

· To what extent malnutrition is a cause or consequence of severe ME needs investigation.

· The role of other conditions such as mast cell activation disease, POTS, and Ehler Danlos syndrome in malnutrition in ME patients needs to be investigated.

NB I have not done a systematic literature search (though I doubt there is much to find).

 

Wonder if it's worth highlighting to OMF - given Whitney's problems they may/should have considered + they'd probably welcome/support proposals to research this.

 

Unfortunately, I should point out that if a working group is to be set up, the representative(s) of the British Society of Gastroenterology is likely to be opposed to tube feeding in ME at all. @Jonathan Edwards

One author of the BSG’s guideline on functional dyspepsia, Dr Peter Paine (from the Salford Royal NHS Foundation Trust), wrote about ME/CFS as a central sensitization disorder that should require removal of tube feeding and rehab, in a BMJ Frontline Gastroenterology article entitled “Jejunal feeding: when is it the right thing to do?” (2019):

He has a more recent article on the BSG’s website, from 2022, which lists “somatoform disorder/central sensitivity disorder” as a reason not to escalate to tube feeding because of the lack of an “absolute objective marker” (see question 1 and Table 1). https://www.bsg.org.uk/web-educatio...three-underlying-questions-to-aid-management/

The guideline on functional dyspepsia also advocates for a psychological approach and “optimized oral nutrition” for patients presenting with weight loss or malnutrition rather than tube feeding (bolding mine; ARFID = avoidant/restrictive food intake disorder, DGBI = disorder of gut-brain interaction)

 

Thanks @cassava7. That seems to identify what we are up against!

From the quotes it looks like the usual unsubstantiated psychologisation with some interesting new pseudo-concepts like DGBI.

 

The BSG guideline on functional dyspepsia is a hoot - hard to believe really.
All the recommendations are strong or very strong and all the evidence is of low or very low quality. What a load of t........

 

Is prone versus supine a relevant question ? If the issue is Head of Bed elevation, then the recommendations for elevations seem comparable for both. Boullata et al are applying a relatavism so they are not saying there is no risk, only that risk is comparable when lying on front or back, they quote:

Administration of enteral nutrition to adult patients in the prone position
Dustin D. Linn, Robert D. Beckett, Kurtis Foellinger
Full at Scihub: https://sci-hub.se/10.1016/j.iccn.2014.07.002

from which, on one study reviewed:

"Within the prone position group, there were 30 episodes of vomiting during 218 6-hour periods of prone positioning compared to 26 episodes during 462 periods of supine positioning (RR [relative risk] 2.5; 95% confidence interval [CI] 1.5—4.0). EN was more likely to be discontinue in the prone group compared to the supine group (82% vs. 49%, p < 0.01). Incidence of VAP was similar between supine and prone groups (24% vs. 35%)."

and from the conclusion:

"Strategies to increase tolerance of EN for patients in the supine position, such as head-of-bed elevation, intestinal feeding and use of a prokinetic agent, may also increase EN tolerance for patients in
the prone position."

Prokinetic dugs can have unpleasant side effects including dystonic attacks which may not be well tolerated in PwME.

 

For patients with a single disease diagnosis of ME/CFS, the 2021 NICE guideline should provide some protection from psychologisation, it is those who have a collection of comorbids and alternatives that are especially vulnerable (the point I was trying to get at previously).

Jejunal feeding: when is it the right thing to do? is available on Scihub: https://sci-hub.se/10.1136/flgastro-2019-101181

 

Looking at those gastro articles I am not sure about that.

It looks as if we now have three categories clearly laid out:
1. structural/physical
2. psychiatric, as in psychosis or anorexia nervosa
3. 'functional'

The implication being that 'functional' cases, which seems to include my own GI problems, uniquely do not deserve rational evidence based care because they will respond to psychotherapy and anyway there is nothing wrong with them.

I don't see any protection for ME patients here if nutritional services are gastro led. The nutritional services will just reclassify patients as functional.

I need to look into this a bit more.

Again, it is not the psychological/physical divide the is the problem. It is this new divide between psychiatric and functional that harks back to judgmental approaches of the nineteenth century.

 

yes i have always felt much much more judged when i tell a HCP that i have ME/CFS than when i tell them (in the past about Depression dx or PTSD, nobody ever sneered or laughed at me or belittled my suffering), but plenty have over ME/CFS.
It sounds like the eating problems are where the distinction btwn functional & psychiatric is most extreme, to the serious detriment of patients

yes. I think the majority of Drs/specialties will have done by now. Particularly those covering conditions often labelled functional eg IBS, & Interstitial cystitis & pelvic pain in Gynaecology.