Severe difficulties with eating in ME/CFS

[Jonathan Edwards]

Various things associated with Dr Q Aziz ring the wrong bells for me - several of them, including his departure to the private sector.

If you want to contact a physician who is interested in ME, why not just contact Dr Weir and Dr Speight? They’ve been helping PwME in hospitals who’ve been tube-fed for a long time now.

I know Willie and Nigel well, and their views. The task is to discover what other views are and why there is such antagonism. I have not so far heard back from some enquiries and maybe the gastroenterologists prefer to keep ME off limits. That may be symptomatic of the problem.

What worries me is that the there is clearly a move in gastroenterology to identify patients with the sorts of labels that Dr Weir advocates as suitable for sending to psychologists rather than feeding. I think that situation needs sorting out. Whether I can be of use is another matter.

 

[AliceLily]

I may be mistaken, but one aspect of the problem we may have overlooked in this discussion is that sometimes, food itself is not the reason why some severe ME patients can’t eat. For example, when they overexert themselves doing another activity (such as cognitive activity, or maintaining personal hygiene), then they are unable to tolerate eating / feeding.

From my understanding, @Jonathan Edwards, you seem to want not to consider overexertion as a key mechanism of this intolerance to eating / feeding but it does feel like it is one.

Or perhaps what I wrote in the first paragraph is precisely the point you are trying to make (e.g. the analogy with the flu)?

I think from a post I read of JE is that it is something the patient cannot manage meaning it is involved in the PEM mechanism? I could have misunderstood though.

I agree with you though. What you described is how it felt to me. I have a few examples of the extreme PEM of very severe ME that I experiened. (I did not get to needing tube feeding though).

Examples of how very severe ME affects functioning:
1. I had non functioning sinuses to the point of a sore skull, toxic stuff coming out of my sinuses, burning my stomach and intestines. I needed antibiotics straight for nearly six months.

2. I could not sit in a chair for long. My neck and spine felt like jelly. I could not hold myself up.

Some people might thing I just had sinus problems from reading the above, but it wasn't it was a part of the whole PEM and rolling PEM that I was experiencing amidst a myriad of symptoms. The amount of symptoms in the very severe end of ME is shocking. Now at moderate level I don't experience that extreme anymore.

So, very severe ME does interrupt functioning and for me it felt like just as you described @cassava7 - the exertion induced PEM, and that is triggered even while just lying down in those years. It is even the body's metabolic process that causes PEM - the energy needed internally. Our intolerance for exertion has gotten to the point of metabolic processes inside the body triggering PEM alone.

 

[bobbler]

There are a number of standardised measurements of risk of undernutrition, MUST has already been mentioned in the thread. Others are NRS2002 and MST. There are also general guidelines on BMI and rate of weight loss for when someone is undernourished or not (f.ex. "BMI <18.5 or lost 5% of weight the last month").

Though difficult if someone has been ill for a while. I lost weight in a crash I had a few years ago, since then my weight has been more or less stable (I am fortifying my food with energy and eating easy digestible foods when necessary which likely plays into this, and I am lucky enough to have someone who can shop and cook for me when I am not able). My point is that weight loss may have occured and there may be problems with food intake that puts patients at risk of undernutrition, but presently weight is stable so this risk will not be picked up on unless BMI has become <18.5.

A survey of this kind is something it would be possible to apply for funding from say Dam Foundation in Norway if the Norwegian ME association is on board

Indeed, I think we need to think 'upswing/downswing' too ie if someone is 'stable' vs slowly getting better or slowly getting worse (sadly normally because we are in a situation where the exertion surrounding us is too much for our bodies, and that often means we can't 'call it' until we are then worse). Maybe that interacts with severity too, maybe also with other comorbidities or just the fact people have different bodies to begin with that will tend towards certain 'weaknesses' or issues.

But my gut is that those talking about PEM - and noting how impossible it can be for most the more severe you get to ever get out of that - and 'over-threshold' are more factors. But of course the more severe you are the more vulnerable to anything giving you PEM and the worse it is - except there are many different situations people can be in.

So someone going into a hospital after having been in the situation which has been trying to do what it can to keep PEM low is a vast vast difference in relation to this for someone with very severe ME.

And the whole thing would indeed be cumulative, it wouldn't just be those 2 issues made worse and those things getting worse would knock-on others etc. Over-exertion could also cause issues use more energy at the same time as it being less available etc?

But the crux: methodology is an issue because those who are so ill aren't going to be in the position to complete a survey. SO you skew the population. Without it being either a carefully identified representative sample (that you then work out the 'how' of) or just focus on the ones who do have issues - which is just as valid, just because some don't doesn't mean those who do don't exist so you study the phenomena itself - well there needs to be caution and not a rush.

And you certainly can't 'think pure' because whether these are comorbidities or something else or what at this stage it is 'people' and I think mapping in their 'entireity' as 'what happens' without getting bound up with not doing it 'because of explanations first'.

On a separate but related note I'm not sure most 'get it' on how exacerbating things they don't think are significant are and for how long, not that I know what might be the protocol (hospice type thing rather than hospital?) that can understand both issues, but for those with very severe ME/CFS these are 'gaps' that should be looked at because they exist and is the conundrum their life will revolve around for years (even if treatment became available that helped this conundrum would remain of who,where and how given limitations and them having to roll a dice on pros and cons of going to hospital I imagine).

 

[Hutan]

One contributing factor that I don't think we have mentioned is hypersomnia. If someone is asleep for, for example, 20 hours of the day, and not very alert for the remaining 4 hours, it is physically difficult for their carer to get enough food and water into them during that window. It also means that the carer has to be around, ready to jump into action to offer food and drink, all of the time.

 

[Hubris]

I have to say I'm not very surprised by these developments. Very few doctors want to discuss ME in good faith or believe the illness could make you housebound, let alone so sick that you need tube feeding. I've seen many dozens of doctors and I'm not sure a single one of them would have given me tube feeding if i needed it.

 

[Andy]

The anniversary of his death has reminded me what Bob went through towards the end, which seemed to be centered around issues with eating and digesting food. See here, Bob, where he describes his experience.

 

[cassava7]

Note that in the DSM-V, any abnormal change in eating / feeding behavior that does not match the criteria for characteristic eating disorders (namely: anorexia nervosa, bulimia nervosa, rumination disorder, pica and avoidant/restrictive food intake disorder) can be diagnosed as either “other specified or unspecified eating / feeding disorder”. https://bodymatters.com.au/wp-conte...V_Diagnostic_Critera_for_Eating_Disorders.pdf

Specified disorders are those that resemble characteristic ones but where the criteria are not fully met (e.g. anorexia where a healthy weight is maintained, or eating at night) while unspecified ones are left completely up to the clinician’s judgment.

People with ME who have severe difficulties with eating / feeding can therefore be diagnosed as having an unspecified eating disorder but this diagnosis is meant to be psychological in nature rather than secondary to a physical condition such as craniopharyngioma. While the DSM can evolve, this requires significant lobbying from well connected groups of psychiatrists, not ME charities. Therefore, I am not sure that it is helpful to frame difficulties with feeding in ME as a (behavioral) disorder; on the contrary, this can net patients a wrong and harmful diagnosis through which they can be sectioned.

 

[Michelle]

Calling the eating/feeding issues in ME/CFS an "eating disorder" strikes me as about the same as calling ME/CFS an "activity disorder."

 

[NelliePledge]

The anniversary of his death has reminded me what Bob went through towards the end, which seemed to be centered around issues with eating and digesting food. See here, Bob, where he describes his experience.

I think Forward ME need to be reminded about Bob

 

[It's M.E. Linda]

The anniversary of his death has reminded me what Bob went through towards the end, which seemed to be centered around issues with eating and digesting food. See here, Bob, where he describes his experience.

I remember reading of Bob’s experiences at the time.

Still furious, on his behalf, for what he was put through. Yet here we are again, years later, with 4 known cases (there will be many more), on Social Media, in England, where PwME are disbelieved, denigrated & still suffering

 

[Hutan]

A couple of threads on GDF15 - it would be so interesting to check the people with ME/CFS with severe nausea and vomiting for levels on GDF15:
Her Doctor Said Her Illness Was All in Her Head. This Scientist Was Determined to Find the Truth. NYT

Circulating levels of GDF15 in patients with myalgic encephalomyelitis/chronic fatigue syndrome, 2019, Melvin, Lacerda, Nacul et al

On a slightly different topic - I'm just listening to a discussion on the radio about anorexia nervosa and other eating disorders - there seems to be a strong metabolic basis, as so many of us expected. It was mentioned that people feel anxious, but, when they restrict food intake, they feel much calmer. And that the driver is metabolic.

 

[CRG]

Of possible relevance because it deals with altering approaches to feeding relative to the experience a) of women/girls b) people with autism

Christine McGuinness: Unmasking My Autism: BBC programme examining links between autism and eating disorders in young women: https://www.bbc.co.uk/iplayer/episode/m001k31t/christine-mcguinness-unmasking-my-autism

Article for parents on the Bitesize platform, based on the programme: https://www.bbc.co.uk/bitesize/articles/z4y4jfr

 

[SNT Gatchaman]

A more extreme mitochondrial disease that demonstrates severe gastrointestinal dysmotility (plus neurological symptoms) is MNGIE.

From NIH Gene Reviews: Mitochondrial Neurogastrointestinal Encephalopathy Disease (2005, PDF)

Mitochondrial neurogastrointestinal encephalopathy (MNGIE) disease is characterized by progressive gastrointestinal dysmotility (manifesting as early satiety, nausea, dysphagia, gastroesophageal reflux, postprandial emesis, episodic abdominal pain and/or distention, and diarrhea); cachexia; ptosis/ophthalmoplegia or ophthalmoparesis; leukoencephalopathy; and demyelinating peripheral neuropathy (manifesting as paresthesias (tingling, numbness, and pain) and symmetric and distal weakness more prominently affecting the lower extremities). The order in which manifestations appear is unpredictable. Onset is usually between the first and fifth decades; in about 60% of individuals, symptoms begin before age 20 years.

From Mitochondrial neurogastrointestinal encephalomyopathy (MNGIE): Position paper on diagnosis, prognosis, and treatment by the MNGIE International Network (2021, J Inherited Metabolic Disease, Paywall)

Mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) is a rare autosomal recessive disease caused by TYMP mutations and thymidine phosphorylase (TP) deficiency. Thymidine and deoxyuridine accumulate impairing the mitochondrial DNA maintenance and integrity. Clinically, patients show severe and progressive gastrointestinal and neurological manifestations. The onset typically occurs in the second decade of life and mean age at death is 37 years. Signs and symptoms of MNGIE are heterogeneous and confirmatory diagnostic tests are not routinely performed by most laboratories, accounting for common misdiagnosis.

From Case report: A patient with mitochondrial neurogastrointestinal encephalomyopathy and chronic intestinal failure (2022, Frontiers in Nutrition)

Despite poor initial prognosis, the patient is currently 43 years old and has been on home parenteral nutrition for more than 6 years with acceptable quality of life.

 

[Hoopoe]

Here is a study that I came across that investigated the genetics of eosinophilic esophagitis, which can cause severe difficulty eating. A feeding tube is sometimes required. One of the study participants later developed what seems to be ME/CFS although in the study it is suggested there was mild mitochondrial dysfunction. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5931135/

Genetic variants in OGDHL, a nuclear gene that encodes a predicted functional homolog of DHTKD1 (47), was identified independently in a 21-year-old patient with EoE and clinical presentation of chronic fatigue and exercise intolerance who was being evaluated in the Mitochondrial Disorders Program at CCHMC.

In brief, she experienced vomiting, stomach pain, and difficulty feeding as a child. A diagnosis of EoE was made at 12 years, and the patient was unsuccessfully treated with food trials but improved with prednisone. She eventually became dependent upon total parenteral nutrition, but her clinical symptoms progressed to include chronic fatigue, heat intolerance, and postural orthostatic tachycardia syndrome. She has an extensive work up for possible mitochondrial disease. She had complex IV deficiency as seen on muscle biopsy, but electron microscopy, mitochondrial DNA whole-genome sequencing, liver function, acylcarnitine level, organic acids, amino acid profiles, lactate/pyruvate levels, electromyogram, and brain MRI were all normal.

The patient also had pain but that is mentioned in a table.

The study also notes that

In addition to atopic disorders such as atopic dermatitis and asthma (19, 20), EoE has been observed in the presence of other comorbidities, including a spectrum of inherited connective tissue disorders (CTD) characterized by hypermobility syndrome, suggesting common disease pathways (21). For instance, TGF-β–mediated fibrotic responses have been implicated in both esophageal remodeling and dysmotility in EoE and the CTDs Marfan syndrome and Loeys-Dietz syndrome (21–25). Acquired mitochondrial dysfunction, often associated with coenzyme Q deficiency, has been noted in a cohort of patients with EoE (26). Mitochondriopathies can affect virtually all organ systems with various phenotypic manifestations. During allergic inflammatory responses, mast cell degranulation — which has been demonstrated to occur in the esophagus of patients with EoE — is dependent on mitochondrial translocation to sites of exocytosis; conversely, mast cells and eosinophils can also secrete mitochondrial components that, in turn, can induce mast cell degranulation and histamine release (27–30). Disrupted synthesis of mitochondria by haploinsufficiency of the intracellular phosphatidylcholine transport protein steroidogenic acute regulatory protein–related (StAR-related) lipid transfer domain protein 7 (StARD7) in epithelial cells results in spontaneous allergic responses in mice, highlighting the potential of mitochondrial dysfunction to induce inflammatory responses (29, 31). In addition, activated eosinophils can also release mitochondrial DNA traps into the extracellular space as an antibacterial defense mechanism (30). Despite these findings, however, no direct link between mitochondrial dysfunction and EoE has been reported.

It makes me wonder how common eosinophilic esophagitis is in ME/CFS patients.

My understanding is that similar eosinophilic diseases can also affect the stomach.

I also remember Bob saying that he cold not tolerate protein in foods (but I'm not sure what exactly he meant). Reacting to certain proteins in foods is a feature of eosinophilic esophagitis and elimination diets or meal replacement formulas where proteins have all been degraded into aminoacids are supposedly as effective as medications. Maybe what we need is a study to look into the immune system in the upper GI tract of people with ME/CFS that have symptoms consistent with that kind of problem.

 

[Evergreen]

What worries me is that the there is clearly a move in gastroenterology to identify patients with the sorts of labels that Dr Weir advocates as suitable for sending to psychologists rather than feeding.

Yep. I came across a table in a case study yesterday that may be relevant. The case study itself is on an 11 year old with nausea and vomiting (does not have ME, ends up being diagnosed with coeliac and Addison's). But figure 1 is interesting - the impression I get is that gastroenterologists really aren't interested in the "functional" category in that figure, considering those disorders to be someone else's turf or mild or harmless or just not somewhere they can add much value beyond perhaps trialling a few drugs (for some of them).

"Functional abdominal pain, irritable bowel syndrome, functional vomiting, and functional dyspepsia are rarely associated with weight loss."

Fasano A, Leonard MM, Mitchell DM, Eng G. Case 1-2020: An 11-Year-Old Boy with Vomiting and Weight Loss. N Engl J Med. 2020 Jan 9;382(2):180-189. doi: 10.1056/NEJMcpc1913469. PMID: 31914246; PMCID: PMC8176458.

In the Baxter et al case series they make the point that even if the ME patients did have eating disorders, there would still be an indication for tube feeding. So it may be that those with severe cases of disorders considered functional by gastroenterologists are not getting the enteral and parenteral feeding they require.

 

[JemPD]

says it all that they classify Munchausens in with 'functional' causes of vomiting doesnt it?

ie that they consider 'non organic' to be synonymous with psychiatric and or self induced -
that eating disorders & munchausens are included with eg gastroperesis & IBS, as if 'unknown' causes of vomiting were the same thing as self induced vomiting, is appalling

 

[SNT Gatchaman]

says it all that they classify Munchausens in with 'functional' causes of vomiting doesnt it?

I mostly just translate "functional" -> "idiopathic" these days.

That anatomical/surgical column is just a little brief: oesophageal stricture, food bolus impaction, achalasia, hiatus hernia, vascular ring, annular pancreas, complicated appendicitis, Meckel's diverticulum, segmental volvulus, Burkitt lymphoma. Intussusception at any age is not something that causes long term vomiting and weight loss and I've seen maybe 5 cases in 20 years over the age of 3 (lymphoma, Meckel's, gastric heterotopia, cystic fibrosis).

One year before the current presentation, he had had a Salter–Harris type 2 fracture of the left fifth finger. [...] The patient’s history of a Salter–Harris type 2 fracture of the left fifth finger (possible indirect evidence of osteoporosis — a potential complication of celiac disease)

Normal healthy 10 year olds get SH2 fractures of their fingers all the time (eg basketball, cricket, running into each other). I'd say there is basically zero chance that type of fracture could prospectively suggest osteoporosis. Vertebral compression fractures would be the go-to.

 

[JemPD]

I mostly just translate "functional" -> "idiopathic" these days.

But thats my point... munchausens vomiting & bulimia is intentionally self induced because of a psychiatric issue. whether you view psychiatric issues as biological or otherwise, sticking your fingers down your throat or taking something to make yourself vomit so it looks like you have organic illness, not 'idiopathic' vomiting.
And i think the fact that these gastros lump IBS, gastroperisis etc, in with them, is revealing... It suggests to me that in their thinking functional is shorthand not for idiopathic, but for psychogenic. Which will naturally make a big difference in how those problems are handled.

 

[Peter T]

But thats my point... munchausens vomiting & bulimia is intentionally self induced because of a psychiatric issue. whether you view psychiatric issues as biological or otherwise, sticking your fingers down your throat or taking something to make yourself vomit so it looks like you have organic illness, not 'idiopathic' vomiting.
And i think the fact that these gastros lump IBS, gastroperisis etc, in with them, is revealing... It suggests to me that in their thinking functional is shorthand not for idiopathic, but for psychogenic. Which will naturally make a big difference in how those problems are handled.

I agree the word functional is now very problematic, it is hard to know what the person using it intends and even if they are clear in their own understanding there is no guarantee that a significant percentage of readers will not misunderstand.

I wish if someone intends to convey ‘psychogenic’ they were up front and say ‘psychogenic’ and if they wish to be genuinely neutral about causes I agree with @SNT Gatchaman that ‘ideopathic’ is currently a better word. Though I guess it would not take long for ‘ideopathic [wink, wink]’ to become equally problematic, just as ‘somatic’ is increasingly short hand for ‘psychosomatic’.

 

[belbyr]

I have something strange to add. As stated before my worst symptoms are gastro issues that keep me house/bed bound and therapies/medications just doesn't work... I have also read some arguments about why patients vary so much in symptoms, even though emptying times don't seem to line up with symptom severity. It can come down to more about which areas of the GI tract are affected more or less, that drives symptom severity.

I was reading this about idiopathic gastroparesis and noticed the mention of macrophages. I recall Dr Nath has brought up macrophages multiple times in videos about his study into ME/CFS. Could there be a connection here?