How long after dinner was the late evening spike? What’d you eat?
A wrap with chicken, dairy-free sour cream, and lettuce. Not enough anything to shoot me up to 18 mmol/L. I really feel like maybe I had some sort of gastroparesis thing going on yesterday (though I don’t have that to my knowledge) where the reason I ran low all day is that all the food wasn’t digested until the evening, then it all hit at once when I lay down. That’s the only thing I can think of for why I’d lie down and shoot from my target range up to 18 (and I think I would’ve gone higher had I not taken a few units of Fiasp).
That happens to me when I eat a lot of high fat foods, particularly lately because I’ve been taking A PPI hopefully just short term
I take a PPI and have for years. I can’t say that the type of thing I saw yesterday is a normal occurance for me, though, at least not to the degree I saw last night.
I’m convinced it slows down the speed at which my food absorbs appreciably… makes a turkey sandwich act like pizza
If anything, I often feel like my food absorbs too quickly (insulin can’t keep up). I think PPIs are bad in general and I’ve tried to stop several times without success. The only time I was successful for about six months was when I was avoiding about 15 food triggers of my eosinophilic esophagitis, which was too much work to keep up long-term. I might give it another try since my goal is 2018 is to improve my health and to try to decrease the number of medicatios I’m taking. I may also ask my GI doctor if we can test for gastroparesis, as this isn’t the first time I’ve wondered if I might have some sort of mild and intermittent form (wouldn’t surprise me after 26 years of diabetes, either).
I sometimes wonder the same about my son. But I think possibly there are other hormonal processes at hand that are not obvious.
It seems, however, that food absorption is slower at night for him, while he is asleep.
My perceptions of gastroparesis is that the people who truly have it are absolutely positive something is very wrong with them and it is very unpleasant… and yet whenever a person with diabetes asks to be evaluated for it, they somehow discover “mild gastroparesis” virtually all the time even if there’s no symptoms at all—- but that in real world there’s hardly any such thing as a “mild form” that people don’t know they have… I could be wrong but that fits what I’ve observed on forums like these and in conversations with medical professionals
Probably the reason is that, whenever a phenomenon can be attributed to mild gastroparesis it is natural to think of that as a possible interpretation, since we all know of it.
But, imho, either everyone sometimes has such symptoms, or many other things can masquerade as that. But I could be wrong!
There’s definitely severe gastroparesis that people know they have. But it doesn’t make sense to me that there wouldn’t be a mild form. From what I’ve read of people who have it, in the beginning it can be inconsistent. People can have retinopathy, nephropathy, neuropathy without having it affect their daily life and without even knowing they have it at first, but when those conditions get to the more severe end of the spectrum then they definitely impact daily life. So why would gastroparesis and/or autonomic neuropathy be any different? It’s not like people just go from normal to severe symptoms with no stage in between.
And part of why I’m thinking about it is because I’ve had diabetes for 26 years. So it’s not beyond the realm of possibility that I have some nerve damage going on. It also just fits with several symptoms I’ve been having over the years (including ongoing stomach problems) that could be due to neuropathy but I’ve just never had them looked into, in part because I don’t want complications. So just something I was thinking about in combination with 2018 being my health-focused year.
Just because people’s stomachs empty at a range of different speeds without there necessarily being a “disorder” involved… and by the time that it becomes a disorder there are real symptoms… but when they go looking for something they can frequently find the “mild form” of it… whereas retinas and nephrons normally shouldn’t be bleeding and if they are it’s a sign something is wrong
When I was talking about my gallbladder a couple weekends ago and it turned out to be normal the general surgeon then insisted the only remaining possibility was gastroparesis (which I was certain it wasn’t because I have none of the relevant symptoms). My endo looked at that and said it was a ridiculous suggestion and I’d be completely certain if I had gastroparesis.
One thing I’m not clear about his if or how gastroparesis affects glucose metabolism? I know it makes people feel like crap because food just sits there raunching away in their stomach for way too long… but doesn’t glucose absorb at the same rate from the stomach whether it’s properly advancing its contents to the duodenum or not? I am not clear on that aspect…
See, this is key. I agree that if people have no symptoms it’s silly to go looking for a disorder. This seems to be WAY more common in the US, though. I have seen people post about getting reams and reams of tests done that just seems ridiculous to me. To my knowledge, in Canada you cannot get referred for tests unless you have specific symptoms that meet criteria for something being wrong. So in no way am I saying I’m going to go make an appointment and get tested… Things just don’t work that way here. I’m already seeing a gastroenterologist for my esophagus and stomach issues, so at most I’ll mention it to him as a possible cause of my stomach issues given some of the BG patterns I’ve seen. If he feels it warrants looking into, he’d refer me for testing. If not, it basically ends there unless I want to go looking for a second opinion, which is not always easy.
Glucose isn’t absorbed from the stomach, it’s absorbed from the small intestine. So if food sits in the stomach for hours, no glucose gets absorbed. The most common effect on blood sugar that I’ve read about is persistent lows after eating followed by unexplained extreme highs hours after the last meal. (Basically the insulin hits with no food which cuases a low, and then hours later the food hits with no insulin and causes a high.) I’ve also read that in general it just makes diabetes very difficult to control (it’s one of the causes of truly “brittle” diabetes).
Interesting… fatty foods in combination with significant carbs definitely have that effect on me… (not extreme, but definitely delayed spikes) but with anything approaching balanced meals I don’t see that at all— unless I’m taking PPIs, which I think it would make logical sense to assume theyd make it take longer to pass food into the small intestine…
I agree here in the USA diagnosis collecting is a very popular pastime for many… like baseball cards when I was a kid
FYI, PPIs = Proton Pump Inhibitors, partially block the production of stomach acid, and thereby slow down carb absorption—important side effect for PWDs.
I’ll have to read up more on PPIs and digestion. I didn’t think they slowed down digestion at all.
In the presence of a lot of fat, slower digestion is totally normal as fat slows down stomach emptying regardless. This is why people on pumps will use a six hour extended bolus to cover these types of foods.
My doc seems to kind of roll his eyes like I’m a moron when I explained that to him too but I’m pretty sure I’ve seen it… and more-so with the more powerful prescription strength ones than the over-the-counter varieties… so it makes sense to me
It’s a normal thing! If you read a medical encyclopaedia, you think you have half the diseases…
If you have a chance, read a lovely forgotten book by Jerome K Jerome called “Three men in a boat,” where there is a wonderful moment about reading such a medical book ($0.99 on Kindle!).
I’ve read the monograph that comes with my PPI, plus some information online when I first started taking it, and don’t recall any mention of slowed stomach emptying. And I didn’t even know PPIs were available over the counter. That must be different here, as the only OTC acid medications I know of are things like Zantac and TUMS, neither of which are PPIs. (I just googled and it seems we have one over-the-counter PPI medication available that came out in 2016, but all others are prescription-only.)
Omeprazole (Prilosec) lansoprazole (Prevacid) and esomeprazole (nexium) are all available in over-the counter strengths here as of a few years ago—- most are also made available in prescription only strengths… several others are prescription only
Interestingly, this study of PPIs suggests a possible positive effect in glycemic control for patients with Type 2 diabetes:
as does this one:
This discussion also mentions the same effect but in the context of diabetes being a factor for the failure of PPIs to work effectively, and points at PPIs slowing down gastric emptying :
Alternatively, delayed gastric emptying may lower HbA1c.
All studies mention PPIs’ effect on T2 diabetes as caused by stimulation in insulin secretion, which, likely, would not work for Type 1, leaving the delayed gastric emptying as a potential problem for Type 1s, since it would delay glucose absorption (as glucose is absorbed in the small intestine).