I think the answer should be yes, but it rarely works that way for me, I am not sure why.
Say you overdose a high by 1U. If your ICR is 1:12, should you eat 12 carbs to make that up?
I think it should work that way, because the process is the same: you eat carbs after using insulin (much later). For me, I always pre-bolus, so it is even more the same, since I eat my carbs 45 minutes (or more) after injecting.
But it rarely works that way. For instance, today I overdosed a 300 high on purpose to come down faster. Right now my CF for this type of high is about 1:20. I dosed altogether 13 (10 times 20, plus 3 units to come down fast, in three injections, while I was going up very fast: as I went up I injected more, all with a pen). My ICR is 1:12. I expected that I would need to eat about 36 carbs, less the amount of suspend time (I suspended 2 times 30 minutes on the way down, which took out 0.9U). So, in the end, I only had an extra 2.1U of insulin, which, for me, is about 25 carbs for my ICR. But I ended up having to eat almost 100 carbs to stop the low after that peak. This was a really bad example, but it never seems to work out as it should.
I know that ICR and CF are approximate. I keep track of them: I should not be very far off most of the time. Like right now for instance, my last morning hormone peak was a 1:20 peak, as were the last two weekdays before, so this one should be close to that also.
So I am wondering about whether carbs used for a low have a different ICR if you are trying to cancel out extra insulin. And, if they do, why?
@Kaelan I donāt think itās a simple ācancelling outā of insulin. There is a lot of stuff going on when you get low that is designed, I believe, to get your Bg back up. But it doesnāt work on PWDās.
Also, the insulin you took was probably at itās peak when you reached low and had a while before it petered out. And Iām sure insulin is more reactive when your Bg is low.
Iām sure someone can explain it better because after 3 glasses of juice Iām still low.
I thought you were going to say ābecause after 3 glasses of wine, I canāt.ā
I donāt know if you meant you were currently low after 3 glasses of juice, but Iām currently low and trying to read this. Also low after a bananaāwhich I felt like shouldāve brought me up. Im no help in here right now either so Iāll alsonstep aside and hang out to see if thereās a good explanationā¦
Which yours was, @docslotnickā¦ just waiting to see what else people come up with.
I am 5.2 (93) so I canāt use a low as an excuseā¦
I do not experience this. If I OD on insulin like you decribed I usually can just correct with carbs using my carb ratio.
Butā¦ If I have a way too high basal rate, I experience exactly what you describe. For example, if I have an ICR of 1:5 and my basal rate is 1U/hr too high you would think I just need to eat 5g of carbs per hour, but instead I need a lot more.
My theory is that having excess insulin causes your liver to reduce the amount of glucose being pumped out into your blood. So the extra carbs are covering the missing glucose from your liver.
Someone smarter than me can confirm my theory or could embaress me by exposing my stupidity.
Iām not, and Iāll do neither, but Iāll just throw in that I do believe that when our tried and true numbers donāt work out, itās usually because thereās something else at play. You mentioned a high basal rate, which I agree would also cause it, and I think of something like activity level or exercise. I guess Iām thinking backgroundā¦ if we could erase everything else that is contributing to our blood sugar, I would think this would line up well, but often weāre doing these corrections on the go, and there are more factors at play than what weāre calculating.
I didnāt accomplish it, but I was trying to sound smarter. If only I knew the answers to any of this, I couldāve done it.
I would be very interested to hear this is the case, as this is something Iāve been thinking about lately. When I have to correct a low, my ICR isnāt even a thought, because for me, I can eat 2-4g carbs and shoot up 20-40 points (my ICR is 1:15-1:30 depending on time of day/food eaten, by the way). Someone recently suggested that perhaps the reason Iām so sensitive to carbs when low is because I donāt have basal in the background.
I forgot to mention that I was on +30% temp basal earlier. But I turned off the temp basal 1.5 hour before I went low. Then I was low for more than 2 hours. I mean not always low when sugar took me up, but I would go low again. I did not mention the temp basal because I thought it was early enough that it would not affect my low.
Ok - I think this supports my hypothesis. What this is saying is that high levels of insulin suppress glucagon secretion from the Ī± cellls of the pancreas which in turn reduces the breakdown of glycogen in the liver, which reduces the glucose the liver is pumping out into the bloodstream.
āThese data indicate that an increase in insulin per se suppresses glucagon secretion and a decrease in insulin per se, in concert with a low glucose concentration, stimulates glucagon secretion. Thus, they document that insulin is a Ī²-cell secretory product that, in concert with glucose and among other signals, reciprocally regulates Ī±-cell glucagon secretion in humans.ā
All the tests were done on Type 1ās so they are pretty relevant.
@Aaron, this article was quite fascinating to me! This is a very well planned experiment, with 9 men and 8 women, all T1s, average 16 years post-diagnosis, well controlled (avg A1c 7.2), no significant complications. The conclusions seem pretty solid.
Here is something I found interesting in a discussion of the glucagon response to a decrease in insulin while in hypoglycemia:
The decrease in [ā¦] insulin did not restore a normal glucagon response to hypoglycemia in these patients with type 1 diabetes. [ā¦] Patients with type 1 diabetes have glucagon secretory responses to direct Ī±-cell stimuli [ā¦]. However, their maximum stimulated plasma glucagon concentrations are only ā¼20ā25% those of nondiabetic individuals [ā¦]. That finding was also documented in the present study. The peak glucagon response to intravenous arginine was ā¼25% of that in our earlier study of nondiabetic individuals.
This is very interesting because it probably means that, in closed-loop control systems such as Loop or Tandemās predictive suspend, we should see a stronger natural reaction to hypoglycemia in T1s: the glucagon response is lower (25%) than glucose normals but not inexistent. That would be true in closed loop systems only because this response requires a decrease in insulin, something that we would not see in a control system that is not closed-loop for T1s.
Another nugget was:
We have no clear explanation for the difference between our finding and that of Zhou et al. (17), who found no increase in glucagon secretion when insulin from which zinc had been removed was discontinued during hypoglycemia in diabetic rats. They studied rats, and we studied humans.
I think this is another example of the many promising results we often see of non-human trials, which too many times fizzle out when testing on real patientsā¦
In the process of checking this article out, I also ran into this 2015 article, which confirms that repeated administration of glucagon preserve the glycogen reserve in the liver, therefore confirming the possibility of a dual-substance pump (insulin and glucagon):
For reference, here is a solid summary 2011 article on what we know about glucagon and the liver:
@docslotnick the best is when dexcom just shows Low. Always good for a laff or a panic freak out or a heart attack or confirmation that the apocalypse is approachingā¦ Lol
