Their pancreases don’t miscalculate and over bolus. Their pancreases also have the ability to produce glucagon before they get to the point of major low.
It's been tested and is still on the table but two of the biggest issues I can think of are 1) you need two infusion sites and 2) glucagon hurts like a bitch and has a ton of side effects.
IIRC some of the first ever insulin pumps were dual hormone (insulin and glucagon) but the ones that were dual hormone didn't take off.
Plus, paired with a Dexcom.. the amount of time my Dexcom reads LOW because of a malfunction, I wouldn’t want it to be also followed by a glucagon injection automatically
Sometimes when I lay on my stomach (which is just how I sleep) my dexcom will read LOW. Doc told me that pressure on the site like that can make it read LOW. Also since I just sleep on my stomach it probably happens at least once a sensor.
It's not a malfunction, but a design problem. When you press on it, you block the flow.
AFAIK the Eversense, which is implanted, does not have this problem
You are super lucky! I have frequently gotten compression lows, but also just the sensor acting glitchy for no reason - like giving me a low reading right before it stops giving me readings at all.
Nah, it’s basically because there’s no stable, liquid glucagon.
Every company that makes an insulin pump has thought of, tried, and are probably are still trying trying to make dual-hormone pumps a thing, but until they have access to a stable form of liquid glucagon it’s just a non-starter. Unless you wanna change your glucagon infusion site multiple times a day.
That's Beta Bionics whole concept. Their iLet pump is just a MVP for them to start making money while they get through FDA clearance for the dual hormone pump.
Every pump company has looked into a dual-hormone system, but there’s *currently* no stable, liquid glucagon on the market. Virtually no one wants a system where they have to refill their pump and change their infusion site multiple times a day.
There’s research being done into this, and every pump company probably has a plan for if/when there’s stable liquid glucagon available.
There actually is this:
https://ogluo.info/
And this:
https://en.m.wikipedia.org/wiki/Dasiglucagon
Also in the Netherlands Inreda is quite far with their trails of fully automated pumps with insulin and glucagon (they use the cheap mits and replace glucagon daily afaik)
https://www.inredadiabetic.nl/
Okay, I looked at the first link, and I don’t see anything that says it’s a stable form of liquid glucagon suitable for a pump? Like it doesn’t really specify, it just says “it’s a kind of glucagon really good at treating hypoglycaemia.”
Like - glucagon pens have been around for decades, but they don’t have a stable, liquid, pump-suitable form of glucagon in them. I can’t speak to those examples specifically, but glucagon available in a pen and glucagon in a stable, liquid, pump-suitable form are two VERY different things.
Also, I am ONLY talking about glucagon that has completed clinical trials and has received regulatory approval. There’s a LOT of interesting research being done, but talking about promising research is just a little too speculative for my tastes.
Like, to the best of my knowledge, the Tandem Insulin Pump is called that because they were trying to develop stable, liquid, pump-suitable glucagon, and then market it as the “Tandem” pump because it would pump insulin and glucagon “in tandem” with each other. Clearly, that did not happen.
Yes but the main problem is glucagon is not stable in a liquid form. That’s why the glucagon injections come with it as a powder and the liquid separately.
I mean, is there any super compelling reason they can't use IV Dextrose instead of glucagon? It seems significantly more shelf stable, and figuring out 15g worth of sugar with a pump with IV dextrose doesn't seem too hard? (I mean, I don't play an endocrinologist or a pump manufacturer on TV, but that's what I'd be trying to do?)
Putting an IV in for dextrose is a lot more difficult than inserting subcutaneous cannula for insulin. And dextrose should not be administered subcutaneously or intramuscularly.
Dextrose in the intracellular space causes tissue necrosis, so you'd have to do IV infusions. Which are supposed to be changed frequently, have a higher risk of infection than subQ, and most importantly, require specialized training to place. I don't know if I could place an IV on myself, and placing IVs is literally my job.
FWIW, I do _really_ appreciate the comments in here, folks. I'm a well-read diabetic who has had the disease for 27 years, and I'm learning in this thread.
I know that some do and it is possible, but I feel like it’s in extremely rare circumstances? I’ve personally never met a non diabetic who has experienced a low, and often times when I try to explain that I’m having a low other non diabetics don’t really understand.
I work with a person who has a condition that causes lows. I don't remember what it's called or why it happens. Maybe overactive pancreas? In any case, she always has sugar available just like I do.
Diabetes is the cause of almost all hypoglycemia episodes - I believe the incidence is around 90% - always related to insulin use. There are other medical causes: metabolic diseases, tumors, sepsis, etc. A glucose of <70 is defined as hypoglycemia in an adult.
If your glucose always runs high, your ‘hypoglycemic blood glucose levels’ may be higher than 70 when you experience hypoglycemia. Your body will (or can) kind of reset your personal level at which you start feeling the effects of hypoglycemia.
I’ve read this three times - I’m not happy with the wording but hopefully the meaning got thru. I would get a grammarian to help - except I’m usually ‘that grammar bitch’ correcting everyone else 🤷♀️
I had easily HUNDREDS of extreme lows years before my diabetes diagnosis. My first severe low was in 2017 where I drove MYSELF to the ER telling them something was catastrophically wrong, but I didn't know what it was, and that they needed to figure it out RIGHT NOW. My glucose CMP came back at 19. (It was awesome, because then the doctor accused me of getting into someone's insulin for attention. Whee! I love medical gaslighting!) I had a CGM for years before being diagnosed, too. It wasn't until my first severe COVID infection that my numbers started getting higher and higher and they actually diagnosed me as T3c, and then a new endo did antibody testing and I came back positive for 2 of them late last year. I am actually THRILLED at the fact my numbers are creeping upward because I was going into the 30s and 40s on a several time a day basis for a while before! (And CATASTROPHICALLY FAST too. The fastest drop I've had recorded on xDrip is 60mg/dl in 5 min. KABOOM.)
I wasn't diagnosed until my late 20s. I would very occasionally experience mild low symptoms for at least 15 years prior. Mostly a sudden onset of a rubbery knee tired feeling that would occur during periods of activity. Eating something would always put it at bay. Looking back at this it was probably somehow tied to a faulty pancreas, a predictor of what lay ahead.
Officially find out? No. But I do have my pet theory. I'm a genetics junkie, so I've had my whole genome sequenced multiple times. I have a pathogenic variant on PYGL and a de novo homozygous delete over a portion of one of the promoter/enhancer regions on PYGL. I don't have a geneticist that I can pester to ask if that combo causes glycogen storage disease 6 or not, but given how catastrophically low I get often, that's my theory.
Depending on the specifics of the variants, you can try the OMIM database (entry 613741) and check on the UCSC genome browser where your variants are found specifically.
However, i am not sure if the whole region of the promotor/enhancer region is gone, but that *could* lead to either; lower expression of the gene, (including the pathogenic variant when it is even expressed at all) or no expression at all. The delete could also lead to nonsense mediated decay: RNA could be made, but the body recognizes it as nonsense. Eventually no protein will be translated and the RNA gets destroyed to prevent further damage.
I've checked OMIM, ClinVar, iobio, and this particular CNV doesn't appear to be listed on any of them. I really just need to find a geneticist at some point. Ha!
I had a classmate who was not diabetic but took lots of breaks to eat because he had hypoglycemia. Only one I’ve met before. But other people get low, that’s why hanger exists in generally everybody. In our case, we don’t have functioning endocrine systems to dump stored glucose all the time so it’s much more dangerous
"In our case, we don’t have functioning endocrine systems to dump stored glucose all the time"
This is my understanding as to why diabetics are susceptible to lows and non-diabetics are not. Not all Type 2 diabetics agree and will argue that low's don't.
I've had big people tell me they are having a low at which point I pull out a new lancet and have them check it. It was never low. I would tell them not to make an excuse if they want a Snickers then have one.
Old as in expired or reusing? I assume you are talking about cgm's but am not sure. If you are not a diabetic and are consistently in the 40's it is likely you would be having severe (grand Mal) reactions. There is also compression lows from cgm's. The completely normal human body is incredibly adept at staying alive. I've not found a single verifiable recorded case of a non-diabetic that low. I've been lower than that and after 35ish years I can maintain hindered cognitive and physical function at that level ( I literally have missing teeth from seizures.) I am honestly curious.
Only in the morning. And yes, cgm. He was switching from the g5, we had one left, and I wanted to experience what it was like to have that sort of attachment on my body to better understand what my son was going through. It was absolutely not from compression lows. I, of course, was very concerned at first. I'd shoot up relatively quickly after waking, though. My numbers stayed between 70-120 the remainder of the day.
My kid goes to the 40s quite easily, and he's fully functional (most of the time).
I'm wondering if it has to do with my pcos.
I literally DROVE MYSELF to the hospital and my CMP came back looking like this. I am DISGUSTINGLY functional at low numbers. Even when I run much higher now with the puttering out pancreas (do it FASTER dammit) I still usually don't even get SYMPTOMS til high 30's.
[https://imgur.com/a/k2Rl0hC](https://imgur.com/a/k2Rl0hC)
I do! I used my kids' leftover sensor from when he upgraded. I wore it for 2 weeks. Apparently, I tend to wake up in the 40s. It shoots up and stays stable relatively soon after.
They produce glucagon normally which brings them back up, also their livers are better at storing and releasing energy
Edit: that is a vast oversimplification and could very well be entirely wrong
Because insulin has a counterpart - glucagon - also made by the pancreas (alpha cells, actually). Without getting into some super crazy biochemistry, those two hormones balance each other out, and the body is capable of regulating that reaction whatever way it needs to to maintain blood sugar.
Normally, insulin and glucagon are secreted as necessary, in response to blood sugar, to adjust the level. So, glucose concentration is kept level constantly. Hypoglycemia is an occasional issue for normals, and hypers are a sign of insulin resistance/type 2 diabetes. But with a normally working, negative feedback system, the ideal range that’s very difficult for a diabetic on injected insulin to achieve, is simple for the body.
A lot of people are responding that it's to do with a lack of glucagon. While people with diabetes can have some issues with glucagon production, T1 (at least in its autoimmune form) is related to destruction of the beta cells in the pancreas, not the alpha cells, which produce glucagon. Many (most?) with T1 have no problem with glucagon production and release.
The big issue for us is that we inject fairly large quantities of insulin subcutaneously, from where it is absorbed gradually over several hours; even fast-acting insulin can take 8 hours or more to be fully absorbed. That means that we often have insulin still in our system, being absorbed, well after we require it any more or we might reduce our insulin needs after injecting by being physically active and we can't remove the insulin already injected.
A normally functioning pancreas, on the other hand, releases tiny amounts of insulin directly into the bloodstream, where it remains active for only a few minutes, not hours, and then releases further tiny amounts as required. If you engage in physical activity, you don't have hours worth of insulin already in your body that is no longer required and the pancreas won't keep releasing it if it's not required. It never (or rarely) allows for a build up of excess active insulin.
This should be the top comment! Thank you for your explanation, it makes sense
Edit: i googled the details and to correct a bit, the ultra-rapid fast acting insulins do not last active as long as 8 hours. "Like NovoRapid, Fiasp lasts for 4-5 hours, however, there will be slightly less active Fiasp left during the final 3-5 hours compared to NovoRapid."
I am aware of their claims as to duration but I'm also aware of independent testing done in the open-source looping community that shows that fast acting insulin has an effect on blood sugar levels for far longer than 4-5 hours. This is important to know so that the more agressive open-source looping algorithms don't stack too much insulin, which can happen if you set a duration of only 4-5 hours for the algorithm to work from. In my loop setup, I use a duration of 9 hours for either Humalog or Fiasp.
Commercial looping algorithms, like the Omnipod 5, Tandem's Control iQ and Medtronic's 780 can get by with setting a shorter duration because they are not as aggressive at bringing down above-target blood sugar levels.
It appears that the manufacturers use an arbitrary cutoff for activity at a level higher than 0% (I'm guessing around 5% but maybe it's lower) or their analytical method is less sensitive than a human body to end up with those shorter durations.
Thank you for your detailed responses. I’m a parent of a newly diagnosed child and trying to learn everything I can about this disease. Can you please provide some direction/resources on the open-source looping community? Thanks again.
Edit: I found OpenAPS which is super interesting. There are no commits in the last 2 years though. Is it so stable that it’s just in maintenance mode? There are still 72 open issues.
It's not true of all of them.
I was diagnosed with Chronic Hypoglycemia when I was 11 years old. I wasn't diagnosed with T1D until my mid-30's. it was explained to me that my pancreas over reacts to the presence of glucose in my body after eating, causing my BG to drop, but then doesn't properly respond to the drop by producing glucagon.
I've always wondered if my previous Chronic Hypoglycemia was a symptom that I would develope T1D. Also, I've wondered if it's the reason that I still deal with the seemingly unexplained hypoglemia that is very resistant to correction. I haven't been able to find any info online, so if anyone knows of a connection, I would appreciate a link.
I have read in several places that one of the early signs of diabetes (both in T1 and T2) is that first phase insulin release is borked. (That's a super technical term you can totally Google, I swear. ;) ) So what can happen is you go a bit higher than you ought to have since you didn't get first phase release, and when the lazy little ADHD pancreas wakes up and realizes it was supposed to do the insulin releasing thing but procrastinated, it says OH CRAP and like all the little ADHD things it tries too hard to do too well last minute and OVERDOES IT. Well, the liver is a teensy bit ADHD, too, and was sweatin to the oldies when it realized it forgot one of its primary functions and showed up late to the glycogen party. So ye old ADHD liver says CRAP and dumps the glycogen after already super low but at least you didn't die. :D
(This is seriously how I explained my hypoglycemia symptoms to lots of people until I got the T1 diagnosis!)
It's super interesting that you brought up ADHD in this way. GAD65 is one of the autoimmune tests they run for T1 which is essential for producing GABA. Some research has found that those with ADHD may have lower GABA levels/production, and it's also connected to sleep, stress, and anxiety. I was diagnosed with T1 [LADA] with low elevated GAD65, so its always been a question on my mind.
I wondered if there is a link between ADHD and T1 specifically with GABA. I myself was diagnosed and treated as a kid for ADHD and then was unmedicated until last year. I was diagnosed with T1 LADA 12 years later/14 years ago or so. Sadly, I left my science studies because of my diagnosis, so I've never really figured out if anything has been found to link them.
I should clarify that I understand that some non diabetics still have lows, or have conditions that cause lows. My question was more geared towards a majority of individuals who are non diabetic and don’t experience lows at all, and I was just wondering if their body does something differently
Sorry.
The pancreas also produces glucagon, so yes their bodies do it differently. Insulin to lower BG and glucagon to tell the liver to release glucose to raise it. A constant balancing act.
That's really interesting, thanks for sharing. I'm not T1D, my daughter is, but I have episodes at times that seem to mirror hypo symptoms and resolve with sugar. I haven't tested because I haven't had one since we've had the glucometer in the house (a month since her dx) but I have started to wonder if it's an indication for future issues.
I was also diagnosed with Hypoglycemia as a kid (16), long before I was diagnosed with t1 (33). The lows I felt were a lot different though. I mostly felt tired all the time and fainted easily. I'm just curious what your experience was. I've never met anyone else who's experienced both
I would get really tired and shaky,and felt faint. I don't remember actually fainting, but I do remember getting tunnel vision a few times. As a child, I remember that I was failing the class just before lunchtime because I couldn't concentrate. As an adult, I informed work that I had to have lunch at a consistent time or I would become very irritable and/or angry.
Edit to add: Within a few years of being diagnosed with T1D, I am now almost completely hypo-unaware.
My non diabetic son woke up pale and sweaty with a bgl of 3.1mmol.
I (not diabetic) have also experienced a weird phenomenon of waking covered in sweat and needing sugar like right fucken now. I was freezing cold for ages after. Got up and put all my wool thermals on.
Ae were both sick at the time and I assume the immune systems ketone purging went a little overboard.
We didn’t have the sense of doom and panic that my husband has tho.
3 reactive hypoglycemic peeps and me the t1d.
Their lows (husband and adult kids) look a lot like mine but they resolve faster. With theirs, I’ve seen them drop insanely fast and it seems to affect them because of the rate of change rather than how low they land.
In bicycling and other endurance sports, athletes talk about “bonking” or maybe “hitting the wall” which I have always assumed was hypoglycemia for non-diabetics. The cure is the same, rest and a Cliff Bar. One of the reasons I bicycle for exercise!
I’m not sure of the answer but I always assumed that insulin produced in the pancreas is instant and turns off instantly. So I wouldn’t imagine it stays active for up to 4 hours like my short acting insulin does. If a normal persons blood sugar is at a good level no insulin is produced, and if blood sugar is high, it creates insulin until levels are normal, and it stops immediately.
Again, that’s kinda just how I assume it works, I’ve done no research and am not a health professional.
Your short acting is actually active for 8 or more hours. There's not a lot of it left after 4 or so hours but it's still having an effect. Even ultra-fast insulins, like Lyumjev, can be affecting your blood sugar 9 hours after injecting.
Pretty certain I have some glucagon activity of some sort. When I have not had any recent endurance exercise days and have been eating fairly regularly and well balanced meals, I can ride out minor lows. After endurance exercise it takes DAYS before my BGs resume a regular pattern and I’m not constantly dropping rapidly and eating tons of food.
Generally speaking, it’s rare, but it can and does happen. As a kid, I remember my dad having low‘s a few times and my GF has, as well(she is a paramedic). And I would consider both athletes.
Well, the pancreas produces insulin. The liver produces glucose through a process called. glycogenolysis. So when the pancreas creates the insulin, it will give a certain amount if it’s too much then the liver will deliver glucose. It’s a counterbalance, If the pancreas gives too much insulin, then the liver will counteract with glucose. It’s like the body has a built-in BG meter. Too low, glucose is given to high insulin is given. If too much insulin is given then the liver will counteract with glucose..The beta cells are the cells that determines the glucose level in the body. A diabetic.Type 1 typically has issue with the beta cells. They also have problems with the. Islet cells. The Islet cells are clusters. They are basically the insulin producing cells, but they are part of a beta cell. The beta cell is approximately 50% along with other cells, including Islet insulin producing cells. The beta cells determine the blood glucose levels in the body, but the Islet cells are what produced the insulin. But don’t get me wrong. Beta cells do produce some glucose along with the liver so they both produce glucose not just one or the other.
So the answer is quite simply that the body stores glucose that is not needed as glycogen in the liver and muscles. When blood sugars are low through fasting, for example, glycogen gets broken down to glucose, which is then available to support bodily functioning. When your glycogen reserves are depleted, the body can convert amino acids/protein to glucose. In essence that’s why you don’t go low as a non diabetic. Gluconeogenesis is controlled via the interplay of insulin, glucagon and other hormones.
Their pancreases have a good ability to produce glucagon. The feedback loop in them has a very short response time too so their insulin is carefully titrated. They CAN experience a low though in extreme cases like running a marathon.
Weirdly enough, before I had diabetes I would occasionally get hypoglycemic after exercising. I didn’t know what it was I just knew that when it happens I need to eat everything and moving is a struggle. After getting diagnosed I can definitely confirm what I was experiencing was a hypo. Super weird as this only started a year or two prior to getting diagnosed with t1d. Doctor said it was strange as well but didn’t have any more insight on that.
I had the same thing before I was diagnosed! I was experiencing lows before I knew what lows even were. The thing is, when we were diagnosed, we were still diabetic before, we just didn’t know it yet. Your body slowly becomes diabetic as your insulin-producing cells die off. So likely your pancreas was still functioning somewhat but not effectively enough to prevent your blood sugar from going low. Kinda like how the honeymoon period works, your body still is making some insulin but not enough.
They create glucagon in the alpha cells of their pancreas. This gets transported to the liver via a direct vein. This triggers released stores of glycogen.
I’m sure there are other pathways to endogenous sugar production but this is the one often talked about
So do most people with T1.
T1 doesn't kill of our pancreas, in most cases, it just affects the beta cells.
It's the delayed effect of relatively large amounts of subcutaneous exogenous insulin (large in relation to the amounts of insulin released by a normally functioning pancreas) that probably is the biggest factor.
Their pancreases only release tiny amounts of insulin at a time directly into the blood stream and that insulin only remains active for a few minutes so they don't end up with an excess of insulin, unlike us, who inject relatively large quantities of insulin subcutaneously, from where it takes many hours to be absorbed into the blood stream, even when we no longer need it.
People who don't have T1 just very rarely have a large amount of active insulin circulating in their systems.
I do but it’s somewhat predictable. I can go without eating all day and be fine. But if I have cereal for breakfast and skip lunch I’ll go low around 4pm if I’m out and about.
I think it has something to do with my body having difficulty adjusting insulin production due to a high carb meal.
I borrowed my kids glucose meter one time and it showed me at 60. I had the classic symptoms. Shaking, sweating, feeling dizzy.
My father is not diabetic but has an auto immune disorder where if he doesn’t get enough protein he drops and he drops FAST. When I was still living at home I had to make him chocolate milk a few times because genuinely thought he was going to die
Perhaps I can answer this, based on my experience and talking to my son's endo. I'm a non diabetic. The pancreas produces glucagon, and the body will not want to have levels below 3.3 mmol/L, under extreme fasting. The insulin is regulated by the pancreas and so is the glucagon. There is enough glycogen to convert to sugar, and the muscles break down to convert to glucose, ketosis comes next.
For a diabetic, the insulin isn't regulated, it goes in and stays there which keeps doing its job.
I experimented with 0 calorie intake for 24 hours, and I was extremely hungry and angry at the same time. I checked my BG and it was at 4.1 mmol/L, I had 18 grams of carbs from dairy, and in 15 minutes I was over 5 mmol/L, but I was still too hungry and felt that way for close to an hour. When the hunger finally dissipated I decided to eat. That was my way of attempting to understand how trying to come out of a hypo feels.
Next time someone really wants to understand, ask them to take this challenge, 0 calories for 24 hours then 18 grams of carbs and not eat for the next 45 mins. They will understand this very well.
Very interesting topic. I’m aware of glucagon - have been an NICU practitioner (NNP) for 40 years. (for those who don’t know, that’s Neonatal/Newborn ICU, NNP is Neonatal Nurse Practitioner.) Newborns have lots of glucose issues, both high and low, and we used glucagon as a rescue injection.
But I’ve not thought of it as an infusion.
My dad sometimes drops low and has sugary foods/drinks to help him recover. He has the opposite problem - hypoglycemia, although he doesn't drop low too often.
I was staying in my parents the other week and my mams friend called over so no one ate much lunch. Later my dad was sweating, saying he felt unwell and weird so I checked his BG- 3.3! Checked my mam, 3.9 and I was 2.9! Very funny to me personally that we were all sitting there hypo!
10 minutes with a lot of fluff, but interesting case of hypoglycemia. (My bet would be hirata’s disease)
https://youtu.be/-7kP2rovbPw?si=NHJZqX9nvlTrUfvf
My husband is not T1 and he has had low BG episodes. He’s never been diagnosed with hypoglycemia, but once or twice a year, he has “the weakness,” as he call it and has to stuff food in his mouth. After my child was dx and we had a meter, we checked a couple times when he felt low. Once in the 50’s and once after jumping on trampoline with our kids he felt so low and told me to check….he was 39! I couldn’t believe it!
quickest vegetable silky escape seed pet frightening afterthought full entertain
*This post was mass deleted and anonymized with [Redact](https://redact.dev)*
Their pancreases don’t miscalculate and over bolus. Their pancreases also have the ability to produce glucagon before they get to the point of major low.
Do you or any others know if adding glucagon to pumps, along with insulin, is a potential for the future of diabetic management?
It's been tested and is still on the table but two of the biggest issues I can think of are 1) you need two infusion sites and 2) glucagon hurts like a bitch and has a ton of side effects. IIRC some of the first ever insulin pumps were dual hormone (insulin and glucagon) but the ones that were dual hormone didn't take off.
also glucagon isn’t as shelf stable
That’s actually THE reason there are no dual-hormone pumps available.
Plus, paired with a Dexcom.. the amount of time my Dexcom reads LOW because of a malfunction, I wouldn’t want it to be also followed by a glucagon injection automatically
Really? I’ve never had this happen due to a malfunction and I’ve been using Dexcom for 6/7 years
Sometimes when I lay on my stomach (which is just how I sleep) my dexcom will read LOW. Doc told me that pressure on the site like that can make it read LOW. Also since I just sleep on my stomach it probably happens at least once a sensor.
I get this too, I’ve heard them called ‘compression lows’
Oh okay! Interesting! There ya go, learn something everyday on Reddit!
That isn't a malfunction. It's a known issue.
So… it’s a malfunction… by definition.
It's not a malfunction, but a design problem. When you press on it, you block the flow. AFAIK the Eversense, which is implanted, does not have this problem
Well we call such things malfunctions, errors or flaws, interchangeably. But I mean also who gives a 💩! 😂
I never said it was or wasn't a malfunction, I was just sharing a time when my sensor reads low when I'm not actually low.
You are super lucky! I have frequently gotten compression lows, but also just the sensor acting glitchy for no reason - like giving me a low reading right before it stops giving me readings at all.
Nah, it’s basically because there’s no stable, liquid glucagon. Every company that makes an insulin pump has thought of, tried, and are probably are still trying trying to make dual-hormone pumps a thing, but until they have access to a stable form of liquid glucagon it’s just a non-starter. Unless you wanna change your glucagon infusion site multiple times a day.
That's Beta Bionics whole concept. Their iLet pump is just a MVP for them to start making money while they get through FDA clearance for the dual hormone pump.
Every pump company has looked into a dual-hormone system, but there’s *currently* no stable, liquid glucagon on the market. Virtually no one wants a system where they have to refill their pump and change their infusion site multiple times a day. There’s research being done into this, and every pump company probably has a plan for if/when there’s stable liquid glucagon available.
There actually is this: https://ogluo.info/ And this: https://en.m.wikipedia.org/wiki/Dasiglucagon Also in the Netherlands Inreda is quite far with their trails of fully automated pumps with insulin and glucagon (they use the cheap mits and replace glucagon daily afaik) https://www.inredadiabetic.nl/
Okay, I looked at the first link, and I don’t see anything that says it’s a stable form of liquid glucagon suitable for a pump? Like it doesn’t really specify, it just says “it’s a kind of glucagon really good at treating hypoglycaemia.” Like - glucagon pens have been around for decades, but they don’t have a stable, liquid, pump-suitable form of glucagon in them. I can’t speak to those examples specifically, but glucagon available in a pen and glucagon in a stable, liquid, pump-suitable form are two VERY different things. Also, I am ONLY talking about glucagon that has completed clinical trials and has received regulatory approval. There’s a LOT of interesting research being done, but talking about promising research is just a little too speculative for my tastes. Like, to the best of my knowledge, the Tandem Insulin Pump is called that because they were trying to develop stable, liquid, pump-suitable glucagon, and then market it as the “Tandem” pump because it would pump insulin and glucagon “in tandem” with each other. Clearly, that did not happen.
Yes but the main problem is glucagon is not stable in a liquid form. That’s why the glucagon injections come with it as a powder and the liquid separately.
I mean, is there any super compelling reason they can't use IV Dextrose instead of glucagon? It seems significantly more shelf stable, and figuring out 15g worth of sugar with a pump with IV dextrose doesn't seem too hard? (I mean, I don't play an endocrinologist or a pump manufacturer on TV, but that's what I'd be trying to do?)
Putting an IV in for dextrose is a lot more difficult than inserting subcutaneous cannula for insulin. And dextrose should not be administered subcutaneously or intramuscularly.
Dextrose in the intracellular space causes tissue necrosis, so you'd have to do IV infusions. Which are supposed to be changed frequently, have a higher risk of infection than subQ, and most importantly, require specialized training to place. I don't know if I could place an IV on myself, and placing IVs is literally my job.
FWIW, I do _really_ appreciate the comments in here, folks. I'm a well-read diabetic who has had the disease for 27 years, and I'm learning in this thread.
Some people do go hypoglycemic w/o diabetes, but also, liver dumps glucose, and ketosis also kicks in.
I know that some do and it is possible, but I feel like it’s in extremely rare circumstances? I’ve personally never met a non diabetic who has experienced a low, and often times when I try to explain that I’m having a low other non diabetics don’t really understand.
I work with a person who has a condition that causes lows. I don't remember what it's called or why it happens. Maybe overactive pancreas? In any case, she always has sugar available just like I do.
reactive hypoglycemia
Diabetes is the cause of almost all hypoglycemia episodes - I believe the incidence is around 90% - always related to insulin use. There are other medical causes: metabolic diseases, tumors, sepsis, etc. A glucose of <70 is defined as hypoglycemia in an adult. If your glucose always runs high, your ‘hypoglycemic blood glucose levels’ may be higher than 70 when you experience hypoglycemia. Your body will (or can) kind of reset your personal level at which you start feeling the effects of hypoglycemia. I’ve read this three times - I’m not happy with the wording but hopefully the meaning got thru. I would get a grammarian to help - except I’m usually ‘that grammar bitch’ correcting everyone else 🤷♀️
I had easily HUNDREDS of extreme lows years before my diabetes diagnosis. My first severe low was in 2017 where I drove MYSELF to the ER telling them something was catastrophically wrong, but I didn't know what it was, and that they needed to figure it out RIGHT NOW. My glucose CMP came back at 19. (It was awesome, because then the doctor accused me of getting into someone's insulin for attention. Whee! I love medical gaslighting!) I had a CGM for years before being diagnosed, too. It wasn't until my first severe COVID infection that my numbers started getting higher and higher and they actually diagnosed me as T3c, and then a new endo did antibody testing and I came back positive for 2 of them late last year. I am actually THRILLED at the fact my numbers are creeping upward because I was going into the 30s and 40s on a several time a day basis for a while before! (And CATASTROPHICALLY FAST too. The fastest drop I've had recorded on xDrip is 60mg/dl in 5 min. KABOOM.)
I wasn't diagnosed until my late 20s. I would very occasionally experience mild low symptoms for at least 15 years prior. Mostly a sudden onset of a rubbery knee tired feeling that would occur during periods of activity. Eating something would always put it at bay. Looking back at this it was probably somehow tied to a faulty pancreas, a predictor of what lay ahead.
What’s a T3c? And did they find out why you were having those lows without taking insulin?
Officially find out? No. But I do have my pet theory. I'm a genetics junkie, so I've had my whole genome sequenced multiple times. I have a pathogenic variant on PYGL and a de novo homozygous delete over a portion of one of the promoter/enhancer regions on PYGL. I don't have a geneticist that I can pester to ask if that combo causes glycogen storage disease 6 or not, but given how catastrophically low I get often, that's my theory.
Depending on the specifics of the variants, you can try the OMIM database (entry 613741) and check on the UCSC genome browser where your variants are found specifically. However, i am not sure if the whole region of the promotor/enhancer region is gone, but that *could* lead to either; lower expression of the gene, (including the pathogenic variant when it is even expressed at all) or no expression at all. The delete could also lead to nonsense mediated decay: RNA could be made, but the body recognizes it as nonsense. Eventually no protein will be translated and the RNA gets destroyed to prevent further damage.
I've checked OMIM, ClinVar, iobio, and this particular CNV doesn't appear to be listed on any of them. I really just need to find a geneticist at some point. Ha!
I had a classmate who was not diabetic but took lots of breaks to eat because he had hypoglycemia. Only one I’ve met before. But other people get low, that’s why hanger exists in generally everybody. In our case, we don’t have functioning endocrine systems to dump stored glucose all the time so it’s much more dangerous
"In our case, we don’t have functioning endocrine systems to dump stored glucose all the time" This is my understanding as to why diabetics are susceptible to lows and non-diabetics are not. Not all Type 2 diabetics agree and will argue that low's don't.
I've had big people tell me they are having a low at which point I pull out a new lancet and have them check it. It was never low. I would tell them not to make an excuse if they want a Snickers then have one.
I woke up in the 40s for about 2 weeks when I used my son's old sensor after an upgrade. The rest of the day was completely normal.
Old as in expired or reusing? I assume you are talking about cgm's but am not sure. If you are not a diabetic and are consistently in the 40's it is likely you would be having severe (grand Mal) reactions. There is also compression lows from cgm's. The completely normal human body is incredibly adept at staying alive. I've not found a single verifiable recorded case of a non-diabetic that low. I've been lower than that and after 35ish years I can maintain hindered cognitive and physical function at that level ( I literally have missing teeth from seizures.) I am honestly curious.
Only in the morning. And yes, cgm. He was switching from the g5, we had one left, and I wanted to experience what it was like to have that sort of attachment on my body to better understand what my son was going through. It was absolutely not from compression lows. I, of course, was very concerned at first. I'd shoot up relatively quickly after waking, though. My numbers stayed between 70-120 the remainder of the day. My kid goes to the 40s quite easily, and he's fully functional (most of the time). I'm wondering if it has to do with my pcos.
More likely than not PCOS i’ve heard a lot of people with PCOS have random lows. Dunno why though.
I would try a glucometer in the morning a few times. If you are both down to the 40's you may be a new breed of mutant. Find a professor x.
Lol, that's how I knew it wasn't a compression low. I probably am a mutant, though.
I literally DROVE MYSELF to the hospital and my CMP came back looking like this. I am DISGUSTINGLY functional at low numbers. Even when I run much higher now with the puttering out pancreas (do it FASTER dammit) I still usually don't even get SYMPTOMS til high 30's. [https://imgur.com/a/k2Rl0hC](https://imgur.com/a/k2Rl0hC)
I do! I used my kids' leftover sensor from when he upgraded. I wore it for 2 weeks. Apparently, I tend to wake up in the 40s. It shoots up and stays stable relatively soon after.
They produce glucagon normally which brings them back up, also their livers are better at storing and releasing energy Edit: that is a vast oversimplification and could very well be entirely wrong
Thank you for the explanation
Because insulin has a counterpart - glucagon - also made by the pancreas (alpha cells, actually). Without getting into some super crazy biochemistry, those two hormones balance each other out, and the body is capable of regulating that reaction whatever way it needs to to maintain blood sugar.
Hit us with that crazy biochemistry!
Also super interested in the biochemistry answer!
Normally, insulin and glucagon are secreted as necessary, in response to blood sugar, to adjust the level. So, glucose concentration is kept level constantly. Hypoglycemia is an occasional issue for normals, and hypers are a sign of insulin resistance/type 2 diabetes. But with a normally working, negative feedback system, the ideal range that’s very difficult for a diabetic on injected insulin to achieve, is simple for the body.
A lot of people are responding that it's to do with a lack of glucagon. While people with diabetes can have some issues with glucagon production, T1 (at least in its autoimmune form) is related to destruction of the beta cells in the pancreas, not the alpha cells, which produce glucagon. Many (most?) with T1 have no problem with glucagon production and release. The big issue for us is that we inject fairly large quantities of insulin subcutaneously, from where it is absorbed gradually over several hours; even fast-acting insulin can take 8 hours or more to be fully absorbed. That means that we often have insulin still in our system, being absorbed, well after we require it any more or we might reduce our insulin needs after injecting by being physically active and we can't remove the insulin already injected. A normally functioning pancreas, on the other hand, releases tiny amounts of insulin directly into the bloodstream, where it remains active for only a few minutes, not hours, and then releases further tiny amounts as required. If you engage in physical activity, you don't have hours worth of insulin already in your body that is no longer required and the pancreas won't keep releasing it if it's not required. It never (or rarely) allows for a build up of excess active insulin.
This should be the top comment! Thank you for your explanation, it makes sense Edit: i googled the details and to correct a bit, the ultra-rapid fast acting insulins do not last active as long as 8 hours. "Like NovoRapid, Fiasp lasts for 4-5 hours, however, there will be slightly less active Fiasp left during the final 3-5 hours compared to NovoRapid."
I am aware of their claims as to duration but I'm also aware of independent testing done in the open-source looping community that shows that fast acting insulin has an effect on blood sugar levels for far longer than 4-5 hours. This is important to know so that the more agressive open-source looping algorithms don't stack too much insulin, which can happen if you set a duration of only 4-5 hours for the algorithm to work from. In my loop setup, I use a duration of 9 hours for either Humalog or Fiasp. Commercial looping algorithms, like the Omnipod 5, Tandem's Control iQ and Medtronic's 780 can get by with setting a shorter duration because they are not as aggressive at bringing down above-target blood sugar levels. It appears that the manufacturers use an arbitrary cutoff for activity at a level higher than 0% (I'm guessing around 5% but maybe it's lower) or their analytical method is less sensitive than a human body to end up with those shorter durations.
Thank you for your detailed responses. I’m a parent of a newly diagnosed child and trying to learn everything I can about this disease. Can you please provide some direction/resources on the open-source looping community? Thanks again. Edit: I found OpenAPS which is super interesting. There are no commits in the last 2 years though. Is it so stable that it’s just in maintenance mode? There are still 72 open issues.
I don't know if many people use OpenAPS any more. AndroidAPS has largely superseded it. It's what I use. Google will take you to the docs.
It's not true of all of them. I was diagnosed with Chronic Hypoglycemia when I was 11 years old. I wasn't diagnosed with T1D until my mid-30's. it was explained to me that my pancreas over reacts to the presence of glucose in my body after eating, causing my BG to drop, but then doesn't properly respond to the drop by producing glucagon. I've always wondered if my previous Chronic Hypoglycemia was a symptom that I would develope T1D. Also, I've wondered if it's the reason that I still deal with the seemingly unexplained hypoglemia that is very resistant to correction. I haven't been able to find any info online, so if anyone knows of a connection, I would appreciate a link.
I have read in several places that one of the early signs of diabetes (both in T1 and T2) is that first phase insulin release is borked. (That's a super technical term you can totally Google, I swear. ;) ) So what can happen is you go a bit higher than you ought to have since you didn't get first phase release, and when the lazy little ADHD pancreas wakes up and realizes it was supposed to do the insulin releasing thing but procrastinated, it says OH CRAP and like all the little ADHD things it tries too hard to do too well last minute and OVERDOES IT. Well, the liver is a teensy bit ADHD, too, and was sweatin to the oldies when it realized it forgot one of its primary functions and showed up late to the glycogen party. So ye old ADHD liver says CRAP and dumps the glycogen after already super low but at least you didn't die. :D (This is seriously how I explained my hypoglycemia symptoms to lots of people until I got the T1 diagnosis!)
It's super interesting that you brought up ADHD in this way. GAD65 is one of the autoimmune tests they run for T1 which is essential for producing GABA. Some research has found that those with ADHD may have lower GABA levels/production, and it's also connected to sleep, stress, and anxiety. I was diagnosed with T1 [LADA] with low elevated GAD65, so its always been a question on my mind. I wondered if there is a link between ADHD and T1 specifically with GABA. I myself was diagnosed and treated as a kid for ADHD and then was unmedicated until last year. I was diagnosed with T1 LADA 12 years later/14 years ago or so. Sadly, I left my science studies because of my diagnosis, so I've never really figured out if anything has been found to link them.
I have no idea, either, but I'm painfully ADHD and my GAD65 is always OK. I'm pos for IAA and ZnT8.
I should clarify that I understand that some non diabetics still have lows, or have conditions that cause lows. My question was more geared towards a majority of individuals who are non diabetic and don’t experience lows at all, and I was just wondering if their body does something differently
Sorry. The pancreas also produces glucagon, so yes their bodies do it differently. Insulin to lower BG and glucagon to tell the liver to release glucose to raise it. A constant balancing act.
That's really interesting, thanks for sharing. I'm not T1D, my daughter is, but I have episodes at times that seem to mirror hypo symptoms and resolve with sugar. I haven't tested because I haven't had one since we've had the glucometer in the house (a month since her dx) but I have started to wonder if it's an indication for future issues.
I was also diagnosed with Hypoglycemia as a kid (16), long before I was diagnosed with t1 (33). The lows I felt were a lot different though. I mostly felt tired all the time and fainted easily. I'm just curious what your experience was. I've never met anyone else who's experienced both
I would get really tired and shaky,and felt faint. I don't remember actually fainting, but I do remember getting tunnel vision a few times. As a child, I remember that I was failing the class just before lunchtime because I couldn't concentrate. As an adult, I informed work that I had to have lunch at a consistent time or I would become very irritable and/or angry. Edit to add: Within a few years of being diagnosed with T1D, I am now almost completely hypo-unaware.
A normally functioning human body is pretty awesome.
Indeed. I wish I had one :(
My non diabetic son woke up pale and sweaty with a bgl of 3.1mmol. I (not diabetic) have also experienced a weird phenomenon of waking covered in sweat and needing sugar like right fucken now. I was freezing cold for ages after. Got up and put all my wool thermals on. Ae were both sick at the time and I assume the immune systems ketone purging went a little overboard. We didn’t have the sense of doom and panic that my husband has tho.
3 reactive hypoglycemic peeps and me the t1d. Their lows (husband and adult kids) look a lot like mine but they resolve faster. With theirs, I’ve seen them drop insanely fast and it seems to affect them because of the rate of change rather than how low they land.
In bicycling and other endurance sports, athletes talk about “bonking” or maybe “hitting the wall” which I have always assumed was hypoglycemia for non-diabetics. The cure is the same, rest and a Cliff Bar. One of the reasons I bicycle for exercise!
I’m not sure of the answer but I always assumed that insulin produced in the pancreas is instant and turns off instantly. So I wouldn’t imagine it stays active for up to 4 hours like my short acting insulin does. If a normal persons blood sugar is at a good level no insulin is produced, and if blood sugar is high, it creates insulin until levels are normal, and it stops immediately. Again, that’s kinda just how I assume it works, I’ve done no research and am not a health professional.
Your short acting is actually active for 8 or more hours. There's not a lot of it left after 4 or so hours but it's still having an effect. Even ultra-fast insulins, like Lyumjev, can be affecting your blood sugar 9 hours after injecting.
Excess insulin levels is less likely with a working pancreas than exogenous injections
It happens actually just not as frequently. My sister has reactive hypo.
Anyone else convinced their liver still pumps out glucagon? Pretty sure the lows I’ve had I should be dead 😂😂😂
Pretty certain I have some glucagon activity of some sort. When I have not had any recent endurance exercise days and have been eating fairly regularly and well balanced meals, I can ride out minor lows. After endurance exercise it takes DAYS before my BGs resume a regular pattern and I’m not constantly dropping rapidly and eating tons of food.
Generally speaking, it’s rare, but it can and does happen. As a kid, I remember my dad having low‘s a few times and my GF has, as well(she is a paramedic). And I would consider both athletes.
Well, the pancreas produces insulin. The liver produces glucose through a process called. glycogenolysis. So when the pancreas creates the insulin, it will give a certain amount if it’s too much then the liver will deliver glucose. It’s a counterbalance, If the pancreas gives too much insulin, then the liver will counteract with glucose. It’s like the body has a built-in BG meter. Too low, glucose is given to high insulin is given. If too much insulin is given then the liver will counteract with glucose..The beta cells are the cells that determines the glucose level in the body. A diabetic.Type 1 typically has issue with the beta cells. They also have problems with the. Islet cells. The Islet cells are clusters. They are basically the insulin producing cells, but they are part of a beta cell. The beta cell is approximately 50% along with other cells, including Islet insulin producing cells. The beta cells determine the blood glucose levels in the body, but the Islet cells are what produced the insulin. But don’t get me wrong. Beta cells do produce some glucose along with the liver so they both produce glucose not just one or the other.
So the answer is quite simply that the body stores glucose that is not needed as glycogen in the liver and muscles. When blood sugars are low through fasting, for example, glycogen gets broken down to glucose, which is then available to support bodily functioning. When your glycogen reserves are depleted, the body can convert amino acids/protein to glucose. In essence that’s why you don’t go low as a non diabetic. Gluconeogenesis is controlled via the interplay of insulin, glucagon and other hormones.
Their pancreases have a good ability to produce glucagon. The feedback loop in them has a very short response time too so their insulin is carefully titrated. They CAN experience a low though in extreme cases like running a marathon.
They have properly functioning alpha cells in their pancreas that signal to their liver when to release glucose/glucagon
Weirdly enough, before I had diabetes I would occasionally get hypoglycemic after exercising. I didn’t know what it was I just knew that when it happens I need to eat everything and moving is a struggle. After getting diagnosed I can definitely confirm what I was experiencing was a hypo. Super weird as this only started a year or two prior to getting diagnosed with t1d. Doctor said it was strange as well but didn’t have any more insight on that.
I had the same thing before I was diagnosed! I was experiencing lows before I knew what lows even were. The thing is, when we were diagnosed, we were still diabetic before, we just didn’t know it yet. Your body slowly becomes diabetic as your insulin-producing cells die off. So likely your pancreas was still functioning somewhat but not effectively enough to prevent your blood sugar from going low. Kinda like how the honeymoon period works, your body still is making some insulin but not enough.
They do but not to the same extremes.
But why is that? Do they also create something else that we don’t?
They are better at storing and releasing glycogen.
They create glucagon in the alpha cells of their pancreas. This gets transported to the liver via a direct vein. This triggers released stores of glycogen. I’m sure there are other pathways to endogenous sugar production but this is the one often talked about
So do most people with T1. T1 doesn't kill of our pancreas, in most cases, it just affects the beta cells. It's the delayed effect of relatively large amounts of subcutaneous exogenous insulin (large in relation to the amounts of insulin released by a normally functioning pancreas) that probably is the biggest factor.
Interesting. Never knew that, thank you
Their pancreases only release tiny amounts of insulin at a time directly into the blood stream and that insulin only remains active for a few minutes so they don't end up with an excess of insulin, unlike us, who inject relatively large quantities of insulin subcutaneously, from where it takes many hours to be absorbed into the blood stream, even when we no longer need it. People who don't have T1 just very rarely have a large amount of active insulin circulating in their systems.
I do but it’s somewhat predictable. I can go without eating all day and be fine. But if I have cereal for breakfast and skip lunch I’ll go low around 4pm if I’m out and about. I think it has something to do with my body having difficulty adjusting insulin production due to a high carb meal. I borrowed my kids glucose meter one time and it showed me at 60. I had the classic symptoms. Shaking, sweating, feeling dizzy.
My father is not diabetic but has an auto immune disorder where if he doesn’t get enough protein he drops and he drops FAST. When I was still living at home I had to make him chocolate milk a few times because genuinely thought he was going to die
Perhaps I can answer this, based on my experience and talking to my son's endo. I'm a non diabetic. The pancreas produces glucagon, and the body will not want to have levels below 3.3 mmol/L, under extreme fasting. The insulin is regulated by the pancreas and so is the glucagon. There is enough glycogen to convert to sugar, and the muscles break down to convert to glucose, ketosis comes next. For a diabetic, the insulin isn't regulated, it goes in and stays there which keeps doing its job. I experimented with 0 calorie intake for 24 hours, and I was extremely hungry and angry at the same time. I checked my BG and it was at 4.1 mmol/L, I had 18 grams of carbs from dairy, and in 15 minutes I was over 5 mmol/L, but I was still too hungry and felt that way for close to an hour. When the hunger finally dissipated I decided to eat. That was my way of attempting to understand how trying to come out of a hypo feels. Next time someone really wants to understand, ask them to take this challenge, 0 calories for 24 hours then 18 grams of carbs and not eat for the next 45 mins. They will understand this very well.
Very interesting topic. I’m aware of glucagon - have been an NICU practitioner (NNP) for 40 years. (for those who don’t know, that’s Neonatal/Newborn ICU, NNP is Neonatal Nurse Practitioner.) Newborns have lots of glucose issues, both high and low, and we used glucagon as a rescue injection. But I’ve not thought of it as an infusion.
My dad sometimes drops low and has sugary foods/drinks to help him recover. He has the opposite problem - hypoglycemia, although he doesn't drop low too often.
Because they have an intact glucose regulation system.
Glucagon does indeed hurt like a bitch. I always have WILD bruises when I need to use it.
Hi, I‘m a non diabetic and I can go as low as a 60 😅 my bf is a diabetic that‘s why I know. He gave me one if his libre sensors.
I was staying in my parents the other week and my mams friend called over so no one ate much lunch. Later my dad was sweating, saying he felt unwell and weird so I checked his BG- 3.3! Checked my mam, 3.9 and I was 2.9! Very funny to me personally that we were all sitting there hypo!
10 minutes with a lot of fluff, but interesting case of hypoglycemia. (My bet would be hirata’s disease) https://youtu.be/-7kP2rovbPw?si=NHJZqX9nvlTrUfvf
My husband is not T1 and he has had low BG episodes. He’s never been diagnosed with hypoglycemia, but once or twice a year, he has “the weakness,” as he call it and has to stuff food in his mouth. After my child was dx and we had a meter, we checked a couple times when he felt low. Once in the 50’s and once after jumping on trampoline with our kids he felt so low and told me to check….he was 39! I couldn’t believe it!
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I’m aware that non diabetics *could* experience low blood sugar, but it’s pretty rare and doesn’t happen nearly as much as diabetics.,
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I see, that makes sense
Some people get “hangry”- that’s probably pretty close to the experience of a diabetic’s low. (Except they can correct it much more easily with food)