I think if you go by the self-reporting of frequent posters on online chat sessions, you're dealing with a self-selected group that is not really representative of the wider diabetic population. There's a very real tendency for folks in their 20's and 30's to be in these online groups more than older folks, and the ones most likely to be posting are the recently diagnosed LADA, who are likely more insulin sensitive (and maybe more prone to hypos) than you or me.
Number-of-severe-hypos-per-year (e.g. 911 call/glucagon/ER trip/whatever) varies a lot. From as often as several times a year, to as rare as never in decades.
I also think for young children, their parents/teachers might freak out at the sight of a 59 on a meter and sometimes call 911, when you and me (being adults with decades of experience with literally THOUSANDS of minor hypos) would just power through it. So again, a very uneven distribution between age groups. Of course, when you and me were young kids, there were no bg meters! At that age the by far most reliable indicator of a hypo was holding my hand out in front of me and seeing if it was shaking (adrenaline release from hypo). Urine tests, they do nothing! So you and me might have a different, maybe more self-reliant approach to hypos than many others.
My A1C mostly has bounced around between 5.5 and 6.5 over past 30+ years. You might think from this chart that I had a severe hypo every year or two, but no, I think I'm in the "lucky" category because I've only had 2 911 calls/ambulance rides/ER visits for hypos. Again, I attribute this to self-selection of those who visit the online bulletin boards (e.g. me, being a population of exaclty one, doesn't get much weight in statistics!!!).
It could also be that you are now under thighter control than you were on animal insulin, mainly cause you can test your bg more accurate and your bgs are more like 100 than before. That way you are not as aware of droppings than before. Cause with urine tests every bg under 200 was blue, which meant alright. I know somebody who participated in a studies wheter the more hypos were bc of the change of insulin or of the more accurate blood home tests.
I donĀ“t know if this can shed a light on the issue or not, but my story goes like this: IĀ“m type 1 for 31 years and never have had any trips to the ER because og severe hypo or really needed help from anyone to correct my lows either. In 2010 I had two islet cell transplants as part of a study here i Norway and I got off injecting insulin for a little more than a year. Point of telling all this is how I reacted when I got back to injecting insulin, - my first low was the worst IĀ“ve ever experienced and it wasnĀ“t even a bad low. (I had a CGM and could track the details and double checked with a meter; 65-70 mg/dl or 3,6-3,9 mmol/L). At first I didnĀ“t recognise it as a low and thougt I was having some kind of fit or stroke or whatever. It was just this horrible panicky feeling I never have felt before, my head was spinning, my stomach hurt and what was going on in my body felt like an earth quake or at least nothing I ever felt before. Later this has made me think maybe this was the way I felt every time I went low when I first started injecting insulin back in 1982, and that I just had been getting used to it, kind of "numbing" myself and just getting used to what it feels like when one inject insulin compared to producing the stuff myself. Because now that IĀ“ve been back to producing insulin myself I can tell itĀ“s a whole different ball game. For me, IĀ“ve noticed injecting insulin is accompanied with this ongoing almost not noticabel trembling at all times. Like beeing low without actually beeing low, and I think this is partly due to all the other hormones discussed here beeing in play because IĀ“m type 1. Also my islet cell transplant included the whole islet not just the beta cells itself, and thatĀ“s why most people experience more stable sugars after a tranplant even if they still need some injected insulin.
OK, long story and not sure how itĀ“s on topic,- but I think itsĀ“somehow related.
I agree, it's really quite amazing that we can survive at all. There are certain thresholds the body will just not tolerate and lead to self destruction (Kreb cycle for instance). SO much is mismatched in T1 but then desperately tries to work together; which can lead to a lot of horrible situations. Modern medicine and scientists have truly come a long way in understanding this so far! I'm sure it will continue to expand as well.
Oops, your right. Misread something somewhere about this, and it stuck in my mind that lack of insulin to suppress alpha cell secretion was what led to DKA.
After your post, I went back to school again (on the internet) and dug deeper. You are correct, alphas respond to BG levels.
The reason T1's are at risk for DKA is because the total lack of insulin fails to suppress glyconeogenesis in the liver; the functional betas a T2 has produce enough insulin to keep glyconeogenesis suppressed when BG levels are out of the hypo range.
T2's, like non-diabetics, shut off insulin production when BG gets in the hypo range. This lets glyconeogenesis to take off in the liver, leading to DKA.
yeah.. I'm not sure about all the causes that lead to dka in type two, that one sounds likely... I think there are other circumstances since it happens with infection also which can also happen in type 1. My fellow er patient had dka and kidney failure and he went to the icu before I did. I was in the er for 17 hours waiting for a bed there. someone on youtube said insulin resistance causes dka, not sure if he meant for type 2, but in a round about way once beta cells fail completely it could I guess.
I found statistics that said two thirds of yearly dka cases are type 1 and I guess the rest are type 2 and mody etc.
Glucagon is the insulin's twin from the Evil Superman universe.
We all know that Evil Superman does the opposite of Superman.
Glycogen is a dense collection of glucose molecules. It actually is a gigantic molecule itself, containing as many as 30,000 glucose molecules bound together. it is very much like starch. In fact, according Wikipedia, it is referred to "animal starch" in some circles.
Hmmm... my understanding is all non-animal derived insulins are produced using recombinant DNA (rDNA) technology, which, if my understanding is correct, uses bacteria as the medium for the DNA insertion and hormone production.
rDNA is more commonly known to the public as "genetic engineering".
Novolin as far as I could find uses rDNA for production. See these links:
T1s do suffer from a much higher incidence of DKA than T2s, though it's not unheard of in T2s, and from what can gather, the incidence among T2s seems to be going up.
dwallersv is right, the key is insulin production, which T2s have and T1s do not. DKA can happen at BG levels easily obtainable by T2s, though, so the inability to suppress glucagon release is not enough to explain the difference between T2s and T1s as far as DKA is concerned.
The overall misunderstanding, though, is that High BG causes DKA, but that is not the case. Ketone bodies produced normally from the breakdown of fats and proteins are acidic and will cause the pH of blood to drop. In the absence of insulin, the concentration of ketones can rise to dangerous levels in T1s, thus causing dangerously low and acidic conditions in the blood.
hi lotsofshots, amylin is produced in the beta cells like SC said, if you read the info I posted near the end of this whole thread it tells you the basics for all the cells in the pancreas, beta, alpha,delta and gamma, each doing different things.. pretty complex :)
I'm not thinking clearly at the moment as I need to go eat something but in dka for type 1, one of the things that keeps pushing the bg higher is glucagon production and something about alpha cells responding to low/high levels doesn't make sense. if they shut down production for higher levels, why don't they do that in dka.. I know the fact that our cells are not getting glucose in dka due to lack of insulin causes the liver to produce more glucagon etc. but bg levels are high in dka usually.
ok.. think I have an answer now, my brother says alpha cells are multi faceted and they do also respond to insulin levels, so when in type 1, glucose is high but insulin is also low they will respond by producing glucagon and that keeps causing bg levels to rise in dka.
so you were correct that they also respond to insulin levels :)
My bg wasn't super high, compared to what many people here have mentioned at least, when I was in dka, but it was climbing rapidly by the time I got to the hospital, and my acidosis was severe and it took a while to resolve.. I think that may also have been due to the way it was treated, I've read that it is better to keep your bg at 200 for a few hours with smaller fluid amount and lower insulin treatment and then the acidosis seems to resolve more quickly. I think most people understand that high bg alone will not cause dka and that you need fat burning & high ketones as well, most of the time due to low insulin, but it seems in type 2 what causes it is more complex because they don't usually have low insulin levels unless their beta cells have failed completely also.
It seems it is very complex. It's very hard to find statistics on all of this but since there are many more type 2 and they are somewhere around 1/3 of dka cases I would assume it is much less frequent. They are usually more at risk for hyperosmolar hyperglycemic event which I read about a while back but I've forgotten the process for that now and how often that happens.
