An article in The Canary (Nicola Jeffrey 2024) said: Dumping Syndrome may also be referrered to as reactive hypoglycemia, postprandial hypoglycemia, or rapid gastric emptying however some of those appear to be features of Dumping Syndrome rather than an alternative name. This article (Scarpellini et al 2020) explains Dumping Syndrome, including the difference between early and late Dumping Syndrome. Incidentally, this paper (Chelimsky 2018) says that Is Dumping Syndrome a common and underdiagnosed comorbidity in MECFS and if so, why? I followed this up because I have the symptoms of late dumping syndrome and have been recommended a trial of acarbose by the endocrinologist.
From Scarpellini (ref above) Dumping syndrome comprises a constellation of symptoms that can be subdivided into early and late dumping syndrome symptoms, which can occur jointly or separately1–8. Typically, symptoms of early dumping syndrome occur within the first hour after a meal and include gastrointestinal symptoms (abdominal pain, bloating, borborygmi, nausea and diarrhoea) and vasomotor symptoms (flushing, palpitations, perspiration, tachycardia, hypotension, fatigue, desire to lie down and, rarely, syncope)1,2. The underlying mechanisms might involve osmotic effects, peptide hormone release and autonomic neural responses1. 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)1,2. The literature has referred to late dumping syndrome as ‘reactive hypoglycaemia’ or, after bariatric surgery, as ‘postbariatric hypoglycaemia’. However, on the basis of a common pathophysiology of rapid exposure of the small intestine to nutrients, which is also seen in early dumping syndrome (see subsequent discussion), we refer to this phenomenon as ‘late dumping syndrome’.
I've no experience with late dumping syndrome, nor with acarbose, so not much help to you @Haveyoutriedyoga However, for a period of 2-3 years I had all the symptoms highly suggestive of early dumping syndrome. It started out of the blue, disappeared again by itself, and appeared unrelated to ME severity. I didn't pursue a diagnosis because a) I can't physically get myself to the nearest specialist b) even if I could have got there, I was 99% certain to be either disbelieved or psychologised since none of the widely accepted causal culprits applied to me (e.g. diabetes or gastric surgery) c) the symptoms went away when I followed the early dumping syndrome advice to separate intake of fluids and solid foods Every few months I tried something like minestrone as an experiment and it reliably resulted in the return of violent symptoms until one day it didn't and, fingers crossed, it hasn't returned Make of that what you will. It seems to suggest that for whatever reason the stomach nerves dealing with liquids and those dealing with solid foods got their wires crossed for a while, and then uncrossed again for equally unknown reasons I hope the drug trial works for you @Haveyoutriedyoga, or that you have a spontaneous recovery, too
I've experienced hypoglycaemia related to rapid gastric emptying before. It usually follows a very specific pattern that is quite rare for me now I live a more constrained life. But it used to go like this: 1. eat not very much for hours. 2. eat a massive quantity of carbs. 3. start to do some exercise. A classic example would be waking up on a Saturday, not eating til lunch time, eating a huge mountain of pasta, then jumping on my bike to go somewhere. And part of the way along getting trembles and dizziness and needing to lie down til it passed. It hasn't correlated with gut symptoms for me so I guess it's what they call "late gastric dumping"? You can see how this might cause the effect described in the paper above: "Rapid delivery of carbohydrates to the small intestine" - there's nothing blocking the way because I haven't eaten and then the exercise shakes it all down into the small intestine. As far as my mecfs symptoms go - if it is one at all - it's one of the least worrying. Manageable by eating sensible amounts at sensible times.
That's interesting, and really good that it is manageable - the paper suggests eating more frequent smaller meals, which the ME clinic actually told me to do when I was diagnosed. Unfortunately doesn't work for me, only eliminating almost all carbs does and that makes meal prep very complicated!
I’ve definitely had this a handful times when I’ve had a carb, particularly bread of the sliced white type binge during PEM. I thought it was possible wheat intolerance. I don’t get it with say jacket potato or rice. But possibly because I limit bread when I do get some I eat larger quantities than other carbs.
I often get this as part of PEM (severe/ v severe). The symptoms themselves are exhausting, so I have no choice but to stop eating until it goes away, and it goes away once my PEM remits. I imagine that if I ever develop unmanageable gastric problems it will be because I get stuck in a loop where the PEM doesn’t remit and I’m stuck with this full time.
I have been able to eat small portions of low glycemic index foods recently. I think I can attribute this to a long period of eating only very low GI, which might have helped me get off the high-low blood sugar rollercoaster Not drinking liquids within 30 minutes of a meal Taking digestive bitters 10 minutes before meals