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.
 
Midnattsol said:
Diet induced thermogenesis accounts for ~10% of energy requirement in energy requirement calculations.
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https://espen.org/documents/A174-02PaedPNGuidel_ESPGHANESPENPNGuidelines2Energy.pdf
Diet induced thermogenesis (DIT) reflects the amount of energy needed for food digestion, absorption and part of synthesis and can, therefore, be affected by the route of substrate administration (oral, enteral or parenteral). DIT usually accounts for about 10% of daily energy needs. In orally fed healthy adult subjects the time of food con- sumption may affect DIT (9). During PN, DIT and the respiratory quotient are affected by the mode of PN administration (continuously vs. cyclic) (10–12).
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Jonathan Edwards said:
Trouble is, disease physiology isn't simple. 10% of calories may be used to digest and transport and store but you are still 90% up on before the meal. So it isn't a problem of energy depletion.
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Certainly it isn't simple, but it looks as though digestion and associated processes is a significant consumption of energy. The suggestion here is that it is 10%, although it isn't clear if that is for both a healthy person and a bed-bound person who is scarcely moving. It seems to me there may well be a timing issue, in that the energy has to be expended first in order to release the energy in the calories.
 
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.
 
Jonathan Edwards said:
The onus is on the people who claim all these mechanisms to do some decent research and validate them.
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Yes, absolutely this.

Jonathan Edwards said:
If the stomach was starved of oxygen at least a few people with ME would be in the operating theater with ischaemia.
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But, I'm not sure that this needs to be true. There could be mechanisms that stop oxygen depletion becoming so severe that tissue dies. It looks as though it is possible to have significant intestinal ischaemia for 12 hours without significant tissue damage.

The pain and the need to lie down reduces energy use on things other than digesting. There is also the chronic diarrhoea that many people with ME/CFS get - the food intake is essentially rushed through the system, perhaps reducing the time that tissue is in oxygen/energy deficit. A shut down of gut motility might stop the process of digestion too.

All that might mean that it is important when giving assisted nutrition to people with ME/CFS to give food in a pulsed fashion, so the digestive system has a chance to rest.
 
Jonathan Edwards said:
The only reason I can think that using calories to digest might trigger symptoms is if some byproduct was signaling. But what?
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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.
 
Jonathan Edwards said:
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.
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I'm no expert of course, but I think the process of digestion which is noted above to include some molecule synthesis could in fact take more than some minutes. If you think about the post-Christmas dinner effect, people are not leaping about feeling full of energy immediately after consuming a big meal. The older people may have a nap. The usual instinct after a significant meal is to rest, rather than do physical activity. Babies tend to sleep after feeding.
 
Hutan said:
https://espen.org/documents/A174-02PaedPNGuidel_ESPGHANESPENPNGuidelines2Energy.pdf



Certainly it isn't simple, but it looks as though digestion and associated processes is a significant consumption of energy. The suggestion here is that it is 10%, although it isn't clear if that is for both a healthy person and a bed-bound person who is scarcely moving. It seems to me there may well be a timing issue, in that the energy has to be expended first in order to release the energy in the calories.
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Total energy expenditure is broken into three: basal metabolic rate (BMR, what is needed to maintain vital functions etc), diet induced thermogenesis (DIT) and physical activity. If the other two components are reduced the contribution from DIT on total energy expenditure could increase. Being bedbound means less physical activity so less energy expenditure there, but over time there would also be a reduction in lean muscle mass that cause a reduction in BMR as well. If it matters at all what the % contribution actually is I have no idea. But as others here digesting food can definitely be a PEM inducing exertion for me.
 
Hutan said:
I'm no expert of course, but I think the process of digestion which is noted above to include some molecule synthesis could in fact take more than some minutes. If you think about the post-Christmas dinner effect, people are not leaping about feeling full of energy immediately after consuming a big meal. The older people may have a nap. The usual instinct after a significant meal is to rest, rather than do physical activity. Babies tend to sleep after feeding.
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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.
 
Jonathan Edwards said:
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.
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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.
 
Deanne NZ said:
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.
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"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
 
Hutan said:
'Intolerability of eating' as an extension of intolerance of exertion and sensory stimuli doesn't really make sense to me.
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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?

Nightsong said:
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.
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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.
 
Haveyoutriedyoga said:
"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)
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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.
 
Sid said:
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.
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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!
 
Haveyoutriedyoga said:
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!
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Haveyoutriedyoga said:
suspected reactive hypoglycemia
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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.
 
Hutan said:
I'm no expert of course, but I think the process of digestion which is noted above to include some molecule synthesis could in fact take more than some minutes. If you think about the post-Christmas dinner effect, people are not leaping about feeling full of energy immediately after consuming a big meal. The older people may have a nap. The usual instinct after a significant meal is to rest, rather than do physical activity. Babies tend to sleep after feeding.
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"Rest and digest "
 
JellyBabyKid said:
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.
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I messaged you

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