Gastroparesis, post-prandial pain, eating difficulties

I don't usually like talking about this, but - as for my own brush with feeding problems the symptoms were entirely compatible with a disorder of motility: early satiety, delayed postprandial nausea & vomiting - notably worse with fatty meals - unrelieved by mebeverine, alverine, PPIs or H[2] antagonists but which seemed to respond well to a prokinetic (domperidone). In the absence of gastric-emptying scintigraphy - a hospital admission was and remains a very last resort for me under any circumstances - I can't say for certain that it was gastroparesis but it was at/near the top of the differential for me.

 

Once you have digested the meal, yes.

 

But if you get 9 times as many calories as you have to spend and everything is spread over many minutes there isn't going to be any realistic time point when you are down on energy. The symptom of being down on energy is hunger. That doesn't seem to be something people get immediately after eating.

 

Interesting question. I'm only moderately affected, but I still can't plan anything in the 90 or so minutes after a meal because my muscles feel as if they're made of lead. I struggle to cover the 12 metre walk to a bathroom, which was no problem before I ate and won't be again once I've recovered.

The severity partly depends on the meal. The higher the carb or salt content, the more unwilling my muscles are to work. But there's no food that doesn't have this effect at all, and if I need to keep going through the day I've no option but to skip lunch.

Recovery seems to coincide with the kidneys flushing out whatever it is. I can feel the muscles coming back to life over the course of a few minutes, after which I'm back to my version of normal. I'm not surprised people struggle to believe it; even after nearly half a century of it, it still sounds barmy to me.

 

Digestion is maybe exacerbating the already existing blood flow problems towards the muscles and extremities as more blood is directed towards the digestive system.

See this comment by Systrom on small fiber neuropathy

https://twitter.com/user/status/1817575873492799847

 

Sure, it takes 2 hours. But the point is that if you have two curves one going down and the other nine times as much up and you blur or overlap them by a spread of minutes you never get any time point with a serious down.

We know that there major autonomic signaling changes going on during and after eating. In fact they start even when you look at the food. Throughout the process the hypothalamus is accurately judging calories through a mass of different signals. It is easy enough to see how those signals might get distorted or rerouted.

What I cannot work out with an energy deficit model is which bit of you (organ) would be in deficit and why would that trigger symptoms. I just think the energy deficit model is based more on popular intuitions than on any coherent scientific story.

Moreover I can find no way of explaining the long term time course of ME/CFS with worsening after challenge on an energy deficit model. Signalling loops yes but energy shortage - i cannot see how stimulus makes that worse.

 

Apologies in advance if my terminology is wrong but could the symptoms of nausea, pain & fatigue be more akin to signalling in metabolic shifts in a similar way to Type 1 Diabetics experience hyperglycaemia and hypoglycemia? Both states cause significant and multiple symptoms (many similar to MECFS) that respond rapidly to carbohydrates or insulin. I am not suggesting this is caused by BGL in MECFS but perhaps some other metabolite, electrolyte imbalance or hormone (or something else) rather than a GI issue as such.

 

It’s the usual, then. ME causes these symptoms and we haven’t yet discovered why. Nevertheless, pwME report that eating can be difficult for them.

 

"Symptoms of late dumping syndrome usually occur between 1 and 3 h after a meal and are primarily the manifestations of hypoglycaemia, which mainly results from an incretin-driven hyperinsulinaemic response after carbohydrate ingestion. Hypoglycaemia-related symptoms are attributable to neuroglycopenia (which is indicated by fatigue, weakness, confusion, hunger and syncope) and to vagal and sympathetic activation (indicated by perspiration, palpitations, tremor and irritability)" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7351708/#Sec51title)

"Idiopathic forms of dumping have been described also. Similarly to gastroparesis, viral infections are a possible cause [50]. About 50% of patients with idiopathic dumping syndrome report a history of gastroenteritis symptoms [50]... a possible explanation for this is that these illnesses induced injury to duodenal receptors, namely fat and osmotic receptors which control gastric emptying. Another possibility is vagal nerve damage resulting in decreased fundic relaxation and accomodation, facilitating rapid emptying"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6723467

"Orthostatic intolerance, including postural tachycardia syndrome, is often associated with gastrointestinal symptoms. In the vast majority of the cases, the gastrointestinal symptoms are not secondary to the orthostatic disorder, but rather just a comorbid condition. This concept is critical, since treatment aimed at the orthostatic condition will not improve the gastrointestinal symptoms"
https://www.autonomicneuroscience.com/article/S1566-0702(18)30052-3/fulltext

 

I think it's possible that this is a component of the problem, though not the whole problem. I don't think gastroparesis can be dismissed out of hand because severe ME/CFS patients are usually too sick to undergo invasive investigations so research is done on the less severe.

I also think what's known colloquially as MCAS is linked to this eating intolerance. I was initially convinced it just had to do with histamine release, as per conventional wisdom peddled online, because the issue was somewhat responsive to H1 (but not H2) antagonists. However, as the severity progressed toward the more extreme end, even stuff like water and white rice started to trigger reactions. This to me suggests that it's not food per se that's the problem but rather any chewing/swallowing/peristalsis, like some sort of visceral hypersensitivity to ANYTHING going down. If the nervous system is abnormally reactive to everything in ME/CFS, including light, sounds, fragrances, exertion, stress etc., why not stuff moving down the digestive system?

Same here to all of the above. At one point I was down to just 3 (blended) foods and a few sips of water a day.

 

I assumed I had this so I got a 5-hour oral glucose tolerance test which turned out to be normal. I think the symptoms some people attribute to hypoglycaemia are actually due to abnormal autonomic response to feeding. Eating triggers POTS-like symptoms for me.

 

Speaking only for myself, the symptoms I (and the endocrinologist) attribute to suspected reactive hypoglycemia occur more when I've eaten more carbs, especially simple carbs, and are accompanied by relative drops in blood glucose (and are corrected by eating lots of sugar, and the rollercoaster continues) and largely avoided by avoiding simple carbs and whole portions of complex carbs in the first place.

That's just me though, it may be that I have dumping syndrome, I may not. Dumping syndrome may be common in ME, may not, the symptoms listed may be hypoglycemia, they may not...

Eta: I am quoting research I don't genuinely understand so hoping someone else can make some proper sense out of it all!

 

I am very curious about this as I appear to have issues with reactive hypoglycaemia.

I spoke to my GP about it 8 years ago but appear to not have been using the right words as they had no idea what was causing it. A sudden recent reoccurrance of it led me to do a quick Google and.. I found it described on Reddit.

Can you share where you found more about it please? Thanks.

 

"Rest and digest "

 

I messaged you

admins and mods, I don’t want to hijack this thread so will welcome any redirection

 

Thank you