Severe difficulties with eating in ME/CFS

This is an interesting case but it raises as many questions as answers, as SNTG says.

If gastroparesis is due to failure of stomach nerves then how come it improved? Autonomic nerve damage does occur in diabetes but that is a very different context.

The NHS information page says: Gastroparesis is thought to be a problem with the nerves and muscles in the stomach. It's not always known what causes it.

It seems people aren't even sure it is a problem with nerves. To me it is relevant that his sort of information will be written by the same gastroenterologists who are trying hard to justify not providing feeding support for such people, including people with ME/CFS. The people who Dr Roy was quoting in relation to Maeve Boothby O'Neil, saying feeding support was against guidelines.

We also recently saw a paper suggesting that tests for gastroparesis were unreliable and that the diagnosis made no difference to outcome and care.

My guess is that like ME/CFS this is a situation nobody actually understands. Gastroparesis is all very well as a diagnosis but if it comes under the 'functional' category, as it will, and we know what the implications of that are, I am not sure it is helpful.
 
This is an interesting case but it raises as many questions as answers, as SNTG says.

If gastroparesis is due to failure of stomach nerves then how come it improved? Autonomic nerve damage does occur in diabetes but that is a very different context.

The NHS information page says: Gastroparesis is thought to be a problem with the nerves and muscles in the stomach. It's not always known what causes it.

It seems people aren't even sure it is a problem with nerves. To me it is relevant that his sort of information will be written by the same gastroenterologists who are trying hard to justify not providing feeding support for such people, including people with ME/CFS. The people who Dr Roy was quoting in relation to Maeve Boothby O'Neil, saying feeding support was against guidelines.

We also recently saw a paper suggesting that tests for gastroparesis were unreliable and that the diagnosis made no difference to outcome and care.

My guess is that like ME/CFS this is a situation nobody actually understands. Gastroparesis is all very well as a diagnosis but if it comes under the 'functional' category, as it will, and we know what the implications of that are, I am not sure it is helpful.
Is it at all similar to what you get temporarily when you have a general anaesthetic ? And are warned not to go too overboard (even though you are often starving as you had to fast before op) eating too much for the next x hours?
 
Is it at all similar to what you get temporarily when you have a general anaesthetic ? And are warned not to go too overboard (even though you are often starving as you had to fast before op) eating too much for the next x hours?

I think that has more to do with the emetic effects of things like opiates, often used as part of anaesthesia. But maybe similar in that the problem is not in the gut nerves themselves.
 
If gastroparesis is due to failure of stomach nerves then how come it improved? Autonomic nerve damage does occur in diabetes but that is a very different context.

The NHS information page says: Gastroparesis is thought to be a problem with the nerves and muscles in the stomach. It's not always known what causes it.

It seems people aren't even sure it is a problem with nerves.

The answer may be in non-autonomic nerves, instead spinal sensory nerves in dorsal root ganglia, and involving innate immune cells. An interorgan neuroimmune circuit is identified, mediated via mast cells, though not classical IgE (in the case of the following paper, bladder / colon). An interorgan neuroimmune circuit promotes visceral hypersensitivity (2025, Preprint: Research Square)

Classically, internal sensations such hunger, satiety, and sickness are mediated by vagal sensory neurons that reside in the nodose ganglia. Beyond sensing somatic inputs, recent studies are shedding new light on the importance of spinal sensory neurons within the DRG in regulating a variety of visceral physiologies. However, the spectrum of symptoms and the mechanisms underlying noxious sensations from the viscera remain poorly understood. Here, we identify a unique subpopulation of DRG sensory neurons that respond to cues from two distinct organs and critically mediate the development of interorgan visceral hypersensitivity. The existence of polyorganic sensory neurons may explain what drives multiorgan visceral pain syndromes, and why visceral pain is so difficult to localize.

Mast cells are strategically situated at barrier surfaces challenged by both external and internal threats […] the identification of MRGPRX2 as a critical pathway in bladder-colon irritation reveals an alternative mechanism by which mast cells trigger nociception and host-protective behavior in deeper and caudally distributed pelvic organs. We speculate that while IgE is evolutionarily designed to react to potential threats in organs that continuously sample the environment, MRGPRX2 may have particularly unique roles in organs with primarily expulsive functions such as the bladder.

Our current findings reveal how the sensory arc coordinates interorgan reflexes that may bypass traditionally assumed pathways of sensorimotor regulation. Given that autonomic motor neurons exhibit highly selective projection and organ-specific physiology, we speculate that shared sensory networks establish a neuroanatomic basis for the timely coordination of visceral functions.
 
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