It’s all over the place… really the only correct answer for you is what works for you.
They use as a WAG formula kg weight*.6 for tdd with half basal half bolus but that’s just a starting point and doesn’t mean much in the real world…
But what is noteworthy is that on essentially every meal you eat you’re using more than your total daily basal… and you have a normal c pep… so it seems you’re dribbling almost enough insulin overnight… but not a drop more
The simple answer is “whatever their body requires.” It’s different for everyone, and it is not some fixed number, it varies over time. Here’s the scoop. The liver produces a “background” amount of glucose all the time, for instance to provide the energy that powers the activities of staying alive. So the body needs a corresponding amount of insulin to move the glucose from the bloodstream into the cells. To learn the “right amount” of basal, an individual can do “basal testing” which means watching what the BG does when not under the influence of food, exercise, stress, or other factors. If the BG has a tendency to rise all by itself, increase the basal by a small amount. If the BG has a tendency to fall all by itself, decrease the basal.
The Endo rechecked my c peptide. The latest number is 0.5. is there even any value to the c peptide? Why even check it? The BG at the time of blood draw was 75, fasting.
I think the c peptide can be invaluable in some cases. It can help distinguish a type 1 from a type 2.
A positive antibody test means type 1, but some people they have a negative result but still don’t make insulin. My DE is one of those, so she is still a type 1, but for unknown reasons. A c peptide tells them this person is not making insulin.
Plus it tells right up front, if you are high or high normal it’s a sign of type 2 and insulin resistance. But if you are low or low normal it’s a sign of type 1 and not making sufficient insulin. I have never heard of a type 1 testing high. But being an LADA you can still make insulin for a while 8 years or more. After the point of diagnosis for a LADA your C peptide can really vary on what socks you are wearing for the day. But usually you will be on the lower end and eventually at zero or almost zero.
Another reason it can be important for some if “type 1” was brought on by something else. Trauma to the pancreas, steroids. Sometimes over time these people can recover and start making some insulin eventually.
About 5+ years ago, the anti bodies results were, IIRC, below the detectable level. The Endo at the time, wanted to treat using sulfonylureas, which I was not enthusiastic about. He thought that I was most likely LADA. His first WAG of insulin dosage was too much. I “survived” on basal, and very little bolus based on eating reduced carb (not LCHF). When I say survived - I never fully got the hang of diabetes, carb counting, matching insulin, timing, pre bolusing…etc. I can pre bolus by about 15 minutes. I can try to eat my protein earlier in the meal and eat the carbs later in the meal.
what has changed? I would like to eat a little more carbs, a little more “normal”, not crazy bags of cookies and candies, just maybe 6-8 cookies, or a cider donut once a week? So it’s a new challenge - my wanting to eat more carbs.
Bg normal with artificial insulin… c pep a bit low, but why shouldn’t it be? There’s no demand for it. It’s like timing how long an elevator takes to arrive when nobody has pressed the button.
There’s very little value to it once you’re on insulin.
So does that mean you’re LADA/T1 but still potentially making some insulin/having some islet cell function, if it’s “a bit low”? I’ve never had any. C peptide testing done (nor has any longterm T1 since childhood person I’m guessing, because why), so I’m not super familiar with it, but wouldn’t you expect a full on T1 with no islet cell function to essentially have none?
It being “a bit low” with normal blood sugar means nothing… because your blood sugar was normal, so it was adequate to meet the demand (in this case with the help of long acting insulin) in that moment in time.
If it was absolutely zero—- which they’re actually discovering is pretty rare, it would mean absolutely zero islet cell function. This would be more in line with what we stereotypically think that long term childhood onset type 1 looks like… although we are learning it’s also not very accurate as more and more precise labs have been created to measure c peptide.
It’s quite common for LADA people to have some degree of endogenous “basal” function for many years, which can offset how much basal they require…
This gets mischaracterized as LADA being more “mild” diabetes sometimes though, unfairly. The system is still broken. It’s like an engine being seized in a car while people debate if there’s enough oil in it…
I mean, it wouldn’t be surprising to me that many LADA folks retain some islet cell function—I think it would explain why many of us with childhood T1 feel that oftentimes even LADA folks fully on insulin are dealing with a somewhat different disease. It also makes me wonder for instance, if that could be why you find Tresiba much, much more flexible than I and many other folks seem to in terms of adjusting to activity levels etc.
I don’t think it makes LADA not T1 diabetes, although I suspect it could at times make it a little easier to get very tight control (which is not saying it makes it easy—still hard work either way). So can many other factors though, like not having a menstrual cycle, not having co-morbid conditions with variable inflammation levels, and many many more.
Might be! But also my guess is I don’t make much at all, since within 8 hours of a missed Tresiba shot, I can see it in my blood sugar starting to steadily rise. If I do have functioning islet cells, they are real slackers. I do suspect based on my BG patterns that I somehow have some functioning alpha cells though, maybe because I never had truly severe lows, in the realm of needing medical intervention? Not sure if that’s what kills them off eventually for most T1s.
A little research on it brought up this interesting study, which suggests that while c-peptide preservation in longterm (think multiple decades) happens, it is uncommon (~10%) and those who have it tend to be in excellent control, as well as better metabolic health overall. Also the younger the age of onset, the less common extended duration of c-peptide is, though for anyone, the thinking should be years, not months (though I think for most of us, that tracks to our honeymoon phases). Based on their findings, I would indeed be surprised to have any c-peptide/islet cell functioning myself, since my diabetes doesn’t sound like that the folks who do have it.
It reminds me of the recent study suggesting qualitatively different diseases in juvenile onset vs adult onset T1, and it makes me wonder if it’s better characterized as islet cell destroying vs (severely) damaging diseases, the former of which is more common in juvenile onset and the latter in LADA, but exceptions occur.
If I understand correctly, based on my current insulin usage which is 7 units Tresiba for basal, and about 6-8+ units Novolog for a lunch (I need about 6-8+ units for dinner too) I don’t seem to fit the usual profile of a T1 diabetes. It is odd that I have to take so much insulin just for the meal time! My body does not seem capable of sending out the insulin for meals.
My understanding is that over the past few years, more recently than when that article was published, they have greatly refined their ability to measure in labs very low, but still existent levels of c peptide… which was a significant milestone in research because it meant that either islet cells still remain in most, or they are regenerating but still being destroyed
“Modern ultrasensitive c-peptide assays are able to detect c-peptide values as low as 0.0015–0.0025 nmol/l [6].”
I believe that article is using those types of assays, because they reference newer more sensitive ones, but could be wrong. The study you are citing is from the same exact research group and sample actually, as the study I cited, Mass Gen Hospital, same years, except your citation goes a little longer in terms of collecting f/u data. Both conclude that this is present in some T1s and a potentially useful metric in terms of control and complications; however, meaningful levels of c-peptides also still not that common by 3-4 decades in it seems…
I’ve seen references to the newfound knowledge of very low remaining c pep levels in quite a few places. In one of dr berensteins articles or podcasts or somewhere he even boasts about how he’s only seen 2 or three (something like that) patients with truly zero c peptide and he was one of them… not that he’s really any kind of researcher… but it’s been the topic of quite a bit of discussion over past few years
I think that’s less odd for LADA is the point, when people’s islet function may be intact enough to function some as steady basal, but less so for meals when a sudden robust increase in response is needed.