Severe difficulties with eating in ME/CFS

[Evergreen]

On this point:

I would like to see publications that include parenteral feeding experts, gastroenterologists and nutritionists

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

 

[MeSci]

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.

 

[Jonathan Edwards]

Perhaps there are two 'guidelines' needed - a general guidance on nutrition in ME/CFS concerned with obtaining the best outcomes in a challenging illness, and a supported nutrition guideline for GE units which covers severe ME/CFS and associated/comorbid conditions.

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.

 

[cassava7]

(my bolding of the quote)

The experience I had in hospital, (after I had come out of ICU & my initial NG tube had already been taken out, but then I had a setback and was vomiting continuously), is that doctors didn’t want me to have a tube again, not even an NJ tube which the dietician had recommended, because according to them, I would become “dependent” on it and my stomach would “get used to it” and “stop working”. This was despite the fact I was very unwell at the time and was losing weight, was vomiting up water too and wasn’t being given IVs either and had become very weak. The dietician was pushing for me to get extra support & was saying if the vomiting & severe nausea didn’t stop, then I needed more help and an NJ tube. Luckily, after 3 weeks the vomiting did suddenly stop & I didn’t need the feeding tube anymore. But it was a horrendous time because I was suffering a lot and not getting any help and yet the doctors kept saying that I should be discharged as vomiting wasn’t something that I needed to stay in hospital for.

But it made me realise what the attitudes were towards tube feeding, by doctors generally. All the doctors in the team were really unhelpful/unpleasant about this subject, and actually strongly were against tube feeding even when the dietician recommended it (I read it in her notes later). I don’t know why this was, except they seem to have this view that it makes people “reliant” on tube feeding and that we should work harder on eating by ourselves.
I think this isn’t only an ME thing, but the fact ME is thought to be psychological & so people can just “work harder” at trying to eat, will definitely be adding to doctors’ attitudes. I just remember thinking, what if I really had needed help in the long term, it would have been so horrendous to navigate it.

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.

This is a cine-MRI of what normal small bowel motility looks like, stepping from back to front through the abdomen. Judging from the aortic pulsation this is probably sped up x4, so go to the cogwheel settings button and reduce it to 0.25x to get more normal timing. You can see the small bowel has nice thin walls and is very dynamic, although apart from the odd gurgle we're not generally aware of this in daily life.



It is very striking when doing eg a real-time fluoroscopic study and you instead seeing the bowel static, with very slow progression to colon (hours and days, vs 20 minutes). I know gastroparesis (delayed stomach emptying) is generally discussed but I would have assumed that the problem in ME is more widespread through the gut and similar to some of these small bowel dysmotility conditions.

When I first got sick I couldn't tolerate normal meal sizes and had to try with small amounts more frequently (also no carbs) and protein supplements. The problem symptoms were principally horrible abdominal pain and nausea. I assumed this was dysmotility and thought it was most likely due to dysautonomia (eg reduced vagal inputs or increased inhibitory splanchnic sympathetic inputs) +/- smooth muscle impairment.

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.

 

[Peter T]

The hospital staff — and I was hospitalized at a nutrition department — said it would make my stomach lazy.

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.

 

[Jonathan Edwards]

I would tend to think, too, that the problem of gastrointestinal motility probably extends beyond gastroparesis.

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.

 

[SNT Gatchaman]

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

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.

It is possible to identify with X-ray videofluroscopy how well protected the airway is during swallowing, so I wonder if it is possible use it to identify if there is any pharyngeal regurgitation and if so how well individuals are able to protect their airway during enteral feeding when recumbent?

[added - this would probably have been impractical on the basis of the videofluroscopy I have witnessed, but this was getting on for thirty years ago and I am hoping it would be more flexible now.]

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).

Video-fluoroscopy has fallen out of failure because of radiation dosage. I don't think any test can guarantee that there isn't a risk.

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.

 

[cassava7]

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.

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.

 

[FMMM1]

I am wondering if a working party could be set up following the government research assessment group currently sitting.

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?

 

[Yvonne]

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.

 

[Yvonne]

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).

 

[FMMM1]

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 doMe 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.

 

[cassava7]

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):

Multi-system overlaps

It is increasingly common for patients with feeding intolerance to present with multiple functional symptom complexes including chronic fatigue syndrome/myalgic encephalomyelitis, fibromyalgia, postural orthostatic tachycardia syndromes, multiple chemical sensitivities, acoustic and photic sensitivities, hypermobile Ehlers-Danlos syndrome, functional bladder symptoms and functional neurological symptoms. There is considerable overlap between different functional conditions and somatoform disorder/somatic symptom disorder. However, these system functional disorders are often seen as discrete conditions and therefore are often managed within particular medical specialities that focus on those somatic symptoms. It is speculated that the core feature shared by all these symptom complexes is ‘central sensitisation’ of the central nervous system (so-called ‘central sensitivity syndromes’22), together with involvement of the central autonomic network and autonomic nervous system.

These patients are frequently young and may be transitioning from paediatric services. In more severe presentations, patients may develop fear avoidance, reduced function/deconditioning and maladaptive illness behaviour impacting their relationship with caregivers and health staff.

This group of patients appear to be particularly complex and vulnerable to escalating invasiveness of interventions without improvement in function or quality of life, and therefore it is essential that they are managed within a cohesive multidisciplinary team setting. It is also important to ensure that patient and carer expectations are managed from the outset. The fear avoidance model of pain is instructive in understanding factors which can determine a trajectory of either increasing disability or conversely one of rehabilitation and recovery (figure 1 23). A number of psychological approaches shown in figure 1 may be helpful in promoting recovery. Needless to say, de-escalating medicalisation of therapies, including jejunal feeding, and avoiding escalation in the first place is more likely to promote a recovery trajectory.

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)

The most challenging presentation of severe or refractory FD is when accompanied by substantial dietary restriction, weight loss or malnutrition. In tertiary care, weight loss in FD is strongly associated with early satiation, and also nausea and vomiting, but its predictive value for underlying organic disease is limited.281 Weight loss is more strongly associated with depression, a history of abuse, and somatisation than with gastric sensorimotor function, especially in viscerally hypersensitive patients,282 with more frequent physician visits and reduced quality of life,283and is more frequent in female patients with overlap of FD and IBS.114

In patients with FD and restricted diet or weight loss it is vital to screen for ARFID, and other eating or feeding disorders, to assist with behavioural management.179 252 ARFID is a feeding and eating disorder described recently in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders.284 There is a substantial overlap with DGBI, especially those with dyspepsia, nausea, vomiting, or abdominal pain components.285 Indeed, patients with FD frequently meet criteria for ARFID, irrespective of alterations in gastric emptying.179 This suggests that the restricted eating patterns reported by patients with FD may actually be driven primarily by ARFID. Unlike anorexia nervosa and bulimia, ARFID is not driven primarily by concerns about body shape or weight, but rather by other core motivations, of which fear avoidance of gastrointestinal symptoms is the most prevalent in DGBI.285 However, the precise relationship between DGBI and ARFID remains to be determined.285 These may be different names for the same presentation, separate comorbidities that frequently coexist, or else ARFID may develop secondary to a DGBI in some individuals.285 Caution has been advised regarding the risks of giving overly restrictive and avoidant dietary advice in DGBI,286 because ARFID may often go unrecognised. Moreover, nasogastric tube feeding may impair both nutritional rehabilitation and psychological recovery in ARFID.287 In contrast with some dietary approaches for FD, which avoid specific foods or reduce food volume, exposure-based CBT helps patients with ARFID re-build tolerance to specific foods and food volume systematically and gradually, decreasing fear and anxiety related to precipitating gastrointestinal sensations or symptoms, while regulating hunger satiety cues.179

Early dietitian involvement should, therefore, be considered to avoid over-restriction of diet in severe or refractory FD.288 Optimised oral nutrition is the best management option for most patients. If, and when, to escalate to clinically assisted nutrition or hydration support is a finely balanced risk versus benefit decision, which should be made in a multidisciplinary nutrition support team setting, and driven primarily by objective markers of malnutrition, rather than by severe symptoms alone.289 In terms of optimising weight, in a small RCT recruiting 34 patients with FD, without anxiety and depression and not on antidepressants, mirtazapine improved early satiation, quality of life, gastrointestinal-specific anxiety, nutrient tolerance and weight loss significantly, compared with placebo,225but this requires confirmation in larger studies before widespread adoption in clinical practice.290

 

[Jonathan Edwards]

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.

 

[Jonathan Edwards]

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........

 

[CRG]

This feels surreal to read to me as I found myself in the exact same situation just over a month ago. The hospital staff eventually let me try tube feeding at an angle of 15 degrees (though I lowered it to 10 when they were away), but I couldn’t continue as I didn’t tolerate nasogastric feeding due to gastroparesis.

When I looked at the evidence for the angle of 30 degrees, I found that it comes from studies on critically ill patients (mostly mechanically ventilated) who cannot protect their airways, so they are at risk of aspirating the feed into their lungs. There is, in fact, no evidence that it applies to patients who are not in the ICU, as per §6.3 to §6.6 of this 2017 review from the American Society for Parenteral and Enteral Nutrition on safe practices for enteral feeding (pp. 48-50, bolding mine):

"Question 6.4. Can [enteral nutrition] be administered safely in patients who require prone positioning?

Practice Recommendations

1. Assist the patient in clearing secretions as indicated and promote good oral hygiene.

2. Assess abdominal status every 4 hours and as indicated and monitor bowel status as a guide for GI motility status.

3. Consider short-term use of prokinetic agents if indicated clinically.

4. Consider transpyloric tube placement for patients who are at increased risk for aspiration or have persistently elevated [gastric residual volume]s.

Rationale

Evidence is limited, demonstrating the safety and tolerability of EN in the prone position, although the minimal available evidence does not suggest a substantial increase in complications compared to EN administered in a supine position. Strategies to increase enteral feeding tolerance in the supine position such as [head of bed] elevation, small bowel feeding, and use of prokinetic agents may increase EN tolerance for patients in the prone position. (…)"

Plus ça change…

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.

 

[CRG]

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.

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

 

[Jonathan Edwards]

For patients with a single disease diagnosis of ME/CFS, the 2021 NICE guideline should provide some protection from psychologisation,

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.

 

[Trish]

The psychosomatic classification of ME/CFS is the same problem as this FND classification. The BPS people class all these so called MUS, functional etc. conditions as neither physical nor psychiatric diseases, but a separate class where patients reported symptoms and physical difficulties with activities, eating, digesting are not believed to be real. We are not considered reliable reporters on our bodies. It sounds like it's not just neurologists who have bought into this misconception about ME/CFS, but gastroenterologists and other specialisms too.

 

[JemPD]

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

It sounds like it's not just neurologists who have bought into this misconception about ME/CFS, but gastroenterologists and other specialisms too.

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.