Let’s get back to basics. We’re starting a new monthly series taking a look at the essential facts of diabetes. This week is insulin and this bonus episode includes the entire, much longer interview you might have heard excerpted in episode 207.

Endocrinologist Bryce Nelson takes us through what it does, how it works and the differences among brands.

Join the Diabetes Connections Facebook Group!

Basics of Insulin Info

More Info on Insulin Use

Use this link to get one free download and one free month of Audible, available to Diabetes Connections listeners!  —– Sign up for our newsletter here Get the App and listen to Diabetes Connections wherever you go!

Click here for iPhone

Click here for Android

Interview Transcription:

Stacey: Thanks so much for joining me. I’m so excited to start these educational segments and see what we can really learn. So thanks for making some time. I know you’re very busy.

Bryce: Well, thank you. This is quite an honor. I appreciate it Stacey that you’ve allowed me to be your first endocrinologist you’re talking to in this series.

Stacey: Well, sometimes that’s good. Sometimes you’re the guinea pig. So I’ll see you again at the end. We’ll see how it goes.

Bryce: Yeah as a researcher, you know, we that that’s okay.

Stacey: Before we get started talking about the basics of insulin. Let me just kind of let my listeners get to know you a little bit more. You’re a pediatric endocrinologist and we met several years ago at a conference. You really seem to go above and beyond for the families in your practice. Tell me a little bit about the camp you started. This is just a couple of years ago. Right?

Bryce: Right. We started Camp Buddy about three years ago and it was it was in response to a need. We didn’t have a day camp for young children. So this is a camp that for children ages 6 to 12 that they can come to for the day and really just gives them a chance to be around other kids with diabetes. At school or elsewhere sometimes kids can feel, you know, outside of the quote-unquote community and our camp is really a celebration of the community. The kids get to come together and learn that they can be a kid with diabetes and that’s an important theme of everything that I do in my practice and how I work with these children. They’re not “diabetics.” That is a word that I really, really don’t like. They are children who happen to have diabetes. They’re not defined by this disease and we want them to start learning in an early age. They can still do all of the things that children can do and be children and just but learn how to manage their diabetes through those things. I think that the earlier we start to do that where it just becomes second nature and it’s just part of how they live with the condition then the better off these children are long-term. That’s something that I maintain throughout all of my practice and something that at all ages I try to really really push. Because I think that’s what leads to success in life with this, learning how to live with this and learning you can still make your dreams. You can still set all your dreams. You can still set all your goals and achieve all of those. Just have to learn how to manage your condition and then the world is your oyster.

Stacey: You see a lot of patients who are tiny, you know who are six or under. I know you see toddlers as well, as a pediatric endocrinologist. But a lot of what we’ll talk about today is for people who are newer diagnosed, adults and older kids as well. I’ll be honest with you. I have a great endocrinologist and a great CDE and I still feel like I’m learning all the time. That’s one of the reasons why I wanted to get into this basic info. So let’s just dial down and get really basic Bryce. My first question, about insulin.

Bryce: Let’s do it.

Stacey: Yeah, let’s do it. My first question about insulin is why do people with type 1 diabetes need insulin?

Bryce: The reason that people with type 1 diabetes need insulin is really based on the disease process itself. We know that type 1 diabetes is what we call an autoimmune disease. We all have immune systems that are built to protect us from things outside of us. So things that could potentially harm us. The most common thing that we think about with that is infectious disease such as bacteria, viruses, those kind of things. The immune system is exquisitely designed to be able to help you with that. But because it is so well designed there can sometimes be hiccups in the system. So it’s like children can act up from time to time. Right? So it’s the immune system is acting up. It’s not supposed to attack us but in the case of type 1 diabetes the immune system got tricked and you know Stacey we still are just now understanding what are some of those triggers are and by what process the body starts to develop diabetes.

It all starts before people develop symptoms of diabetes, which we’ll talk about in a second. That autoimmune process gets triggered and so the immune system start to attack the part of the body that makes insulin and that part of the body is called the pancreas. The pancreas does several different things for the body. But in this case what we’re talking about is it makes a very important hormone called insulin. Insulin is the hormone that our body uses to lower blood sugar. As we all eat, that food is being broken down in our digestive system into different things and one of the things that’s being broken down into is a sugar called glucose. Our body uses glucose for energy.  We use it to move and to walk to do all the things that we do and we store excess energy in fat. Insulin is the hormone that tells the body to put the glucose where it’s supposed to be. So it’s that trigger. It’s what keeping our blood sugars, in addition to other hormones in check ,and where it’s supposed to be.

When that initial autoimmune process gets started, it’s killing off the cells of the pancreas that make insulin. And that’s a process that takes time. It doesn’t happen right away. So that’s why people can have that happen and never have any symptoms initially. It’s not till their body reaches a certain level of those cells that make insulin, once they’ve been destroyed to a certain level, the body can’t compensate anymore, it can’t keep up. As that happens, the insulin levels drop and blood sugar starts to go up because there’s not the hormone there to tell the body to put that sugar where it needs to be. And as those blood sugars go up, that’s when people develop the symptoms. That’s why people get thirsty because the bodies recognizing there’s too much sugar. The body is also trying to get rid of that sugar in any way it can so people start urinating more frequently because the kidneys are trying to get rid of that extra sugar. Because you’re urinating more frequently, that’s making you more thirsty. And because the sugar is not going into the skeletal muscle and to fat then the body thinks that you’re not getting energy. So that starts to make people hungry. So that’s why you get the three classic signs of people who have diabetes: increased thirst, increased urination, and increased hunger.

Stacey: I always thought the hunger was tied to the thirst. But that’s because your muscles aren’t getting what they need?

Bryce: Yes, your body’s thinking that it’s deprived. Your body thinks you’re starving. And that’s also why people start losing weight initially; insulin is a storage hormone. It tells fat to store energy for a rainy day. In the absence of insulin, you don’t have that signal anymore. So your body, because it thinks it’s starving, it’s tapping into its stores in fat and so people start breaking down their fat and that’s why they start losing some weight and as they’re breaking down the fat that starts to develop those dreaded ketones.

Stacey: I’m going to plan a future episode talking about ketones and illness and lots of things but let’s just touch on that briefly. So you said dreaded ketones. What are they? And why are they so bad?

Bryce: Ketones are actually intended to do a good thing. Your body is breaking down fat and it breaks it down into those things called ketones because your body can convert those ketones into blood sugar. So your liver can take those ketones and turn them into sugar. But the problem in diabetes is that you have excessive amounts of that breakdown and the ketones start to develop at too high of a level. It can change what we call your acid-base balance so it can make your blood acidic. It doesn’t literally turn your blood into battery acid, but that’s the concept. I use with my patients is that you know, as that becomes as your blood becomes more acidic, it becomes caustic and so your body doesn’t like that. Your liver doesn’t like that. Your kidneys don’t like that. Your gut doesn’t like that. It makes you sick to your stomach and makes you want to vomit. It gives you a headache. It can dehydrate you further. The ketones start out as a normal physiologic response – it’s what our body is supposed to do when we’re breaking down the fat. It makes us ketones so that your body can turn that into sugar for energy, quick energy. But in diabetes, without that insulin, your body is out of sync. So those ketones develop at too high of a rate and too much and it makes your body acidic.

Stacey: Okay dumb question. Can you define caustic? What does that mean?

Bryce: Yeah. So caustic, corrosive is what I mean. So when people think about that the concept that I use for teaching purposes with patients is, you know, imagine if you had battery acid on your finger it would cause a burn it wasn’t painful because it is corrosive. So it’s eating and burning down the skin tissue on your finger. When your blood stream gets acidic – remember your blood’s going to all parts of your body- imagine that same process happening to all parts of your body.

Stacey: Wow. It won’t surprise you that I know the definition of caustic as the second definition which is more, you know sarcasm and caustic in speaking.

Bryce: Yep. That’s right. Corrosive is a better word.

Stacey: That’s really interesting. Okay. So back to insulin, let’s talk about the different types of insulin. I don’t want to talk about brand names necessarily yet. But you know regular, long-acting, can you take us through. Let’s start with the older versions which are still around.

Bryce: What we do and why we treat with insulin is really a tenant of something that we all do in endocrinology which is hormone replacement. The medicines that we use, the insulin that we use, is trying to replace what is not there, because as type 1 diabetes it’s a insulin deficient state. This started back in the 1920s, obviously, with Banting and Best. They were able to isolate and find the hormone insulin and Lily was able to scale that up and market it as regular human insulin. But we can only give insulin as an injection, we have to bypass the digestive system because insulin is what we call a peptide and your stomach is very good at breaking down peptides. If you try to get insulin as a pill your stomach just breaks it down and deactivates it. It doesn’t work. Now who’s to say what’s going to happen down the road. I’m sure some very smart person will figure out how to do that. But we don’t have that capability right now. So that’s why insulin can only be given as an injection underneath the skin.

Most of us now practice using the two main different types of insulin. The concept is what we call basal / bolus insulin. This is really derived from us trying to be physiologic. The way that we get insulin is so that we can quote unquote think like a pancreas. Now that’s I am quoting that from Gary Scheiner. I don’t know if I can do that on your show.

Stacey: Oh yeah, Gary’s a pal. That’s a book, if you’re not familiar, as you listen, the book is called “Think Like A Pancreas.” It’s a terrific book and no, he would certainly not be upset at you mentioning it.

Bryce: Great. So basal/bolus is a tenant of what we try to teach. Because the way that our body makes insulin is it puts a little bit of insulin in our bloodstream all the time; it does all the background work of insulin. It’s what’s keeping the ketones in the right range they should be. It’s what’s telling the liver to deal with sugar as it should. It’s what’s telling muscle to deal with sugar as it should. And then when we all eat our our digestive system recognizes that big shot of sugar that we just got and it secretes insulin in response to that. And so you get what we call a bolus of insulin secretion from the body in response to a meal that has sugar in it. And so we try to mimic that in the clinical setting by giving injections of insulin.

And in order for us to do that. We have to use two different types now in the past, we’ve had several different ways that we had done this.

Initially, it was just with Regular insulin which starts to work in about an hour, peaks after four to six hours and has gone about six to eight hours. Not many of us use that as a as a go-to for how we treat patients anymore because that led to a lot of problems with how it doesn’t really match how people eat. It doesn’t match people’s daily lives. So it led to a lot of blood sugar variability. It led to into a lot of low blood sugars, high blood sugars, and it didn’t lead us to good control of the blood sugars. And so very smart people figured out that well one type of insulin is not going to be enough that we just can’t manage this and think like the pancreas because I have the the pancreas thinks with this so they developed other what we call basal insulins. These are insulins that do that background work that I was describing before. The basal just works in the background. They don’t adjust, they don’t change blood sugar very much, but they do a lot of background work.

One of the main ones that was used at the time several years ago was NPH. That was an insulin that started to work in about four to six hours and was gone by about 8 to 12 hours. So you had to give that insulin twice a day. And so initially people were doing a combination of the regular insulin and NPH doing two daily injections and they with that they had a lot of variability with their blood sugars from day to day. Also between different people, people absorb those insulins a little bit differently. Then some very smart people figured out well we can adjust the insulin molecule a little bit and make it more rapid acting and actually make it be sustained longer into the bloodstream if we mix it with certain chemicals. It will stay in the bloodstream for longer. So that’s where we’ve gotten to in our current treatment is where we have basal insulins that do the background work and that typically last about 24 to 36 hours. So they’re doing a lot of the background work and then when we all eat or if we have a high blood sugar, we use a rapid acting insulin that typically starts to work anywhere from about 12 to 15 minutes. It peaks in about an hour and then is gone within three or four hours. That makes it ideal for helping control a rise in blood sugar after a meal or if the blood sugar is high, to help bring it down.

Stacey: And you’ve mentioned this, but I was going to ask about onset, peak time, and duration because all these insulins have different timing. So when clinicians talk about those things like on set would be when it starts working, peak time is when it’s strongest and then duration, now as a lay person who’s been dealing with diabetes for more than a decade, it seems to me that peak time and duration is different person to person even with the same insulin. Is that true?

Bryce: Absolutely. It’s true. I mean, I see that clinically all the time because there are so many things that can affect how the body is dealing with that insulin you’re giving as an injection. It could depend on the different body site that you’re injecting into. It could depend on whether or not you have been injecting in the same site and developed scar tissue so that you’re not absorbing that insulin as well. And also I see some people who develop what we call an insulin resistance, so they are not as that, the insulin doesn’t work quite as well and is strongly in certain individuals or it might peak at a different time. And so clinically, after you see thousands of patients, you see that. You see that people have different responses and we know that through studies too.

People report these onset, peak time, duration, you have to remember that those are the averages and standard deviations based on a research study. So that means that 95% of people will have a rapid acting insulin that will start to work in about 15 minutes, will peak in about an hour, be gone three or four hours. But five percent of people won’t do that. There might be earlier onset. There might be a little bit later onset in terms of when it starts to work and that’s where that’s why one of the statements in the American Diabetes Association recommendations for clinical care is that care should be individualized because not everybody is going to react that same way. It can even vary from day to day. It can vary when people are sick and vary if they’ve had intensive exercise and it’s why diabetes is such a variable disease. You have to learn how to live with it and just recognize when you’re having the problems and know what to do about it and if things don’t react the way that you expect, well, you move on. You do your best and you move on for the next day and fight the next day.

Stacey: No doubt. And as you listen too, if you use an insulin pump or plan to, it’s good to talk to your educator or whoever helps you set it up and realize that things like duration are actually variables within the pump. You can tell the pump how long you think the insulin will last, that’s the insulin on board. Right Bryce? I don’t want to say anything out of turn here, but we have changed that over the years. It seems like insulin used to last longer when Benny was teeny tiny and you’re able to adjust that in almost every insulin pump.

Bryce: Yeah, and and so some of that is is I mean that that’s glad it’s that you recognize that because that is absolutely true Stacey. It can vary over time especially boys. When puberty hits wow, I’m sure you saw that.

Stacey: Oh my goodness.

Bryce: Puberty can be a boogerbear (note: this is a southern colloquialism. It means anything scary. The boogey man, etc)

Stacey: I have to interrupt because you see you gave me the funniest advice. I think when we met Benny was maybe 10 or 11 and we were talking about what was already starting to go on. And in addition to the physical changes and I’ve shared this on the show and Benny knows and is mortified, but he knows I talk about it. It’s the mental stuff too. And I think you said something like, “that’s a head in the bucket phase.”

Bryce: Yeah right, the head in the bucket. That’s a quote for my father. Head in the bucket. Tweens and teens can have a lot of trouble focusing!

Stacey: Let’s go through the brands of insulin if we could. Let’s start with Novolog. We’re start with the faster acting insulins. Novolog and Humalog have similar durations and peaks, right?

Bryce: They do. So Novolog and Humalog are similar in their reported onset, peak and duration. We use them interchangeably in practice and there’s really not much difference from patient to patient and within patients from day to day in terms of how those insulins work. Now the thing to point out in what you learn in clinical care when you see a lot of patients is that there can be some variability. I have some patients that prefer particular brands and they swear that they see differences when they are on different brands. And I support that. Because one – the patient is living with it every day and they’re seeing those things and you need to listen when they’re telling you those things. But the other thing is that if they’re perceiving it there or they feel like they’re having success with that, you know, we need to support that and continue to individualize that care. But when you look at the research studies, there’s really not that much difference in terms of how those two insulins act.

Stacey: We see that question very often in lots of parent Facebook groups and adult type one Facebook groups, “you know my insurance need wants to switch me from Novolog to Humalog or vice versa. Am I okay?” And I think you’ve answered that in that you should be but definitely talk to your Endo just in case.

Bryce: Right. Yeah, if you if you start noticing differences being switched to a different insulin that is definitely something you should let your endo know about. Your endocrinologist could then do something that’s called a prior authorization. The way that I view that is if we have to switch to say from Novolog to Humalog or from Humalog and Novolog because of an insurance change in preferred product, if that causes a rise in blood sugar’s that’s treatment failure. Because if we switch brands you can make the case with the insurer that the product has led to worsening care and they should be back on the non-preferred product. I rarely see that that, though, so I always urge my patients don’t be concerned if your insurance company is making a change in the brand name.

Virtually all of the rapid acting insulins work very similarly on paper. But we would just have to try and see what’s going to be the change and it would only take a week or so for you to know. If you start seeing higher blood sugars or lower blood sugars let your endocrinologist know so they can help you get that recognized as a treatment failure and get you back on the non-preferred or the product that was working better for you. Most insurance companies, do require that trial period. You’ve got to at least show them that that you had a problem with it. And they you know, they don’t want that either. They don’t want people to have worse care or have worsening problems with their diabetes care. So that’s why I haven’t really had a problem with, once we can demonstrate that they’ve had worsening blood sugars, that we can get them switched back to their preferred.

Stacey: That’s great. And it’s good advice. Thanks for fighting for us. Okay. The next insulin is another quicker onset, fast-acting, Apidra. What’s different about Apidra as compared to Novolog or Humalog?

Bryce: With Apidra, they changed the insulin molecule in a little bit of a different way than Novolog and Humalog. All three of those have a little bit of change in the insulin molecule that makes it more rapid acting and the change they made in Apidra made its onset of action a little bit faster. So it supposedly starts to work at about 10 to 12 minutes as opposed to 15 minutes. So it’s a little bit earlier onset of action. Me personally in clinical practice, I haven’t seen that much difference between Apidra, Novolog and Humalog. So clinically, because most people don’t really notice the blood sugar’s coming down a lot for about an hour after they eat, they all have pretty similar peak onsets. Now, there are some people for whom Apidra does work better. So if they’re having problems and they’re more of an insulin-resistant person or they’re having a problem rising pretty fast after a meal with their blood sugar. I’ll try Apidra to see if I can get a little bit better control for them. But it’s another one that I don’t see that much difference clinically in terms of how it’s helping me. I certainly hadn’t seen changes in A1C switching people from Novolog to Humalog and to Apidra.

Stacey: Apidra too is a little bit different in some insulin pumps. We use the Tandem and I believe it’s not indicated for that. Is that is there something with the makeup it doesn’t work well in an insulin pump?

Bryce: That’s correct and they’re not approved to use it in that pump.

Stacey: Okay, and then the other really new insulin is Fiasp. What is that? What you know, what makes that different is it really much more fast acting?

Bryce: It’s similar to Apidra. It’s onset of action is pretty similar to Apidra’s. Clinically it behaves similarly to Apidra. I have not found it personally to be that much of a difference. However, here in South Carolina, that’s not one of the preferred. So I don’t have much opportunity to use it, I don’t have that much clinical experience with that one yet. But the data is that it’s not that much different than Apidra.

Stacey: We’ll have to wait and see. But it is, it works the same if you were on Humalog or Novolog you could talk to your endocrinologist about Apidra or Fiasp. Let’s switch over to some of the longer acting insulins. When Benny was diagnosed we started on Lantus. Can you explain the differences Lantus and Levemir and we can talk about the other long-acting?

Bryce: Yeah. There’s been really an explosion of new basal insulins over the last couple of years. The one that really kind of revolutionized the basal/bolus and how we treat diabetes was Lantus or insulin glargine is the generic name of it. And it’s insulin that they have mixed with a certain chemical that will permit the body to slowly release it from the tissue underneath the skin. It was the first insulin that we really had that lasted a full, in most people, a full 24 hours. It was relatively what we call peakless. Meaning that it didn’t really rise much in the bloodstream. And so you saw that clinically most of the time. But when you really look at the how that insulin works, you do get a peak at about three hours. It’s a smaller peak compared to the rapid acting insulin. So it doesn’t drop blood sugars that much. It’s just doing background work. But some people had that peak so, like in very young children less than three, that particular insulin, I would give in the morning because I would want them to have that three hour peak during the day, not at night. That’s not based on any data Stacey, that’s just personal practice.  But that’s why in younger kids, I would tend to give that first thing in the morning as opposed to giving it at bedtime.

Stacey: I know a lot of people to split up their dose of long-acting. They’ll do half of it in the morning. Have of it in the evening. Does that make sense?

Bryce: Yeah, with Lantus that really is more of what we call a dose effect. So once you get to about more than 40 units of of Lantus a day, it really works with it better to split it up. And the reason is because the higher the dose of Lantus the more that peak is at three hours and the more the risk of hypoglycemia starts to creep in. You minimize that risk of low blood sugar by splitting the dose and some people feel like they get better steady control.

Another insulin, Levemir, is also a basal insulin. The generic for that is insulin detemir. It lasts about 24 hours. It tends to be a bit more variable and more people require that insulin twice a day as opposed to once a day. But again, it’s designed to last about 24 hours. So some of that is just trying to figure out how you know, whether you need that Levemir once or twice a day. An advantage of Lantus is it more consistently lasts 24 hours. But a disadvantage to Lantus is that it burns when you get it. So it’s one of the few insulins that we had that you actually feel when we give it. And in children that can be a big thing. That could be a barrier to care for some kids. So there are some that if they’re really having a problem with the burning with Lantus will switch to Levemir. And for a while those were really the two main basal insulins that we had on the market and and most of us were using Lantus as our main basal insulin.

Another, more recent insulin came on the market about two or so years ago. That’s Tresiba, the generic for that is insulin degludec. That’s actually approved for children down to age two. And it’s an insulin that lasts for 36 hours. And so what you can do because it last 36 hours is, it actually develops what we call a steady state. You get a much more flat insulin release from the tissue underneath the skin and so it is in some ways a much a little bit better basal insulin that you use. Some advantages we have in kids is that there’s actually information that there’s less low blood sugar overnight with Tresiba because there’s less of that peak. You have less peak in effect. It’s just doing the background work and in practice I’ve really liked to I’ve been switching several patients over to Tresiba. I’ve liked it as a basal insulin.

Stacey: I’ll be honest with you when I described Tresiba, because Benny has used it, I feel like I’m talking about whiskey. There’s no burn. It’s smooth. You know, it’s funny when you think about it like that, right?

Bryce: It’s great.

Stacey: It is a really interesting difference. My question for you is you mentioned it’s got a 36-hour, I’ve heard even a little bit longer duration, but you give it every 24 hours. But it doesn’t tank you. How does that work? Is it that steady state you were talking about it?

Bryce: It’s steady state. It’s the same principle we use for oral medications. In general, oral medications take you about four times to take it for your body to reach what we call steady state, where it’s in a consistent level in the blood stream. With Lantus, you don’t get that. So when you look at Lantus it never really develops a steady state because it starts to come up at about three hours and then by about 18 hours, the levels of Lantus in the bloodstream start to fall and it’s usually gone by about 24 hours. So between 18 to 24 hours people can see some differences in their blood sugars on Lantus. With Tresiba, it doesn’t stack, because you have that 36-hour you have a little bit of overlap. It doesn’t cause low blood sugars by giving the doses. It also gives you a little bit better variability with when you can dose it. So like in children, so I this is what I see as I’m a pediatric endocrinologist, using the concept quote-unquote bedtime. Bedtime can vary a lot for kids, especially for our teenagers, right Stacey?

Stacey: Oh yeah.

Bryce: Yeah, wait till you get to the summertime, you know, so bedtime might be three am. Bedtime might be 10 p.m. And Lantus, you really have to give within about an hour of the same time every night to maintain a better basal state. Tresiba, because it has that tail that goes 36 hours, you can get it at true bedtime. As long as they take it before bed, you don’t really see much difference in terms of how it acts and so that gives people a lot of better flexibility for how their dosing. Which is an advantage because that’s what life is right? Life is flexible, life is messy, life is variable. And so if we have an insulin that can better work in that situation, we’ve got a better chance for patients because people want to be able to live their lives. They want to be able to go to their son’s football game or their daughter’s baseball game or softball game, you know? And so that that tends to lend itself a little bit better to that. And it’s part of the reason I’ve really liked it as a go-to basal insulin.

Stacey: Before we move on, when we talked about Lantus did you say it’s also, is it Basaglar? Is that a brand name?

Bryce: Yes, Basaglar, is a brand name. It is what we call a “bioequivalent.” So, it is the same molecule as Lantus. It was just made by different companies. So it’s a generic Lantis, is how people can kind of think of it. It’s the same molecule that works the same as Lantus.  But if it, because it’s bioequivalent the FDA doesn’t require bioequivalence to go through quite the same rigorous study as say you had to go through with Lantus, but it’s insulin glargine. It’s the same thing.

Stacey: So if your insurance company puts you on Basaglar, it’s the same thing as Lantus as we’ve discussed?

Bryce: It’s the same thing correct.

Stacey: Ok, just checking.

Bryce: And I haven’t seen clinically honestly much difference switching people over. There can always be exceptions. That’s why you need to talk to your endocrinologist, to your provider if you’re noticing problems, but I haven’t seen any real problems if insurance companies are switching over. Because it’s because it’s a generic it’s cheaper.

Stacey: Got it. Yeah, I’ve heard it more and more in the last couple of months. Let’s move on and talk about the so called Walmart insulin. This is different from what we’ve discussed. This is the NPH we talked about a bit earlier, the older insulins.

Bryce: So, it’s NPH  and Regular is what they mostly prescribe. Those are cheaper and for some people without insurance, unfortunately, those are the ones that that we sometimes have to use. I don’t face that situation much in children because children are typically if they’re not covered under private insurance, they’re usually covered by Medicaid and so I don’t have that problem that often. It’s not till people, children become young adults and emerging adults and around 18 and 19 and are aging out of Medicaid and they don’t have insurance yet that that that we have to consider using some of those. But I rarely do that. It still can be effective but it’s an older way that we use insulin. So it’s you have to either mix those insulins together and it’s going back to doing to two injections a day.

Stacey: So definitely talk to your endocrinologist or an educator if you do need to do that because let’s face it, unfortunately people may have to and if you find yourself as you’re listening in that situation, it’s not interchangeable with these newer insulins. So please make sure to find out how to use it if you need to.

Bryce: Right. Yeah and you so you can’t mix those with the newer insulins. So those older insulins NPH and Regular you can mix those together, but with the newer insulins, you can’t mix them together. You can’t mix them with those and if you do have to switch over that you really need to let your, I agree with you on that Stacey, you need to let your endocrinologist, provider know. Because they’ll have to look at your total daily doses of insulin that you’re currently taking and figure out your new doses and work with you on that to get to the right dose. On those insulins you tend to have to be a little bit more strict with your diet in terms of the timing of when you eat and what you eat in and it can work quite well. If you’re pretty consistent and regimented with how you eat and making sure you get those insulins at specific times. It can still work well. Because it’s the hormone, it’s insulin, it’s going to bring your blood sugar down.

Stacey: I’m also seeing an insulin called Toujeo. This is a longer acting? What is this one explain it if you can?

Bryce: So, it is a concentrated glargine, so a concentrated Lantus. It’s not really more potent. It’s just there’s more insulin molecules per volume. And so what they have found is when you do, when you’re able to concentrate that insulin, it’s secreted a little bit more slowly and you actually get a reaction more like Tresiba. Now, it doesn’t work the same way as Tresiba, but the way the body handles it is similar. There’s less of a peak compared to Lantus.  Lantus is kind of the gold standard for basal insulin. So they all get compared to Lantus in terms of how they work. And this one is less of a peak at that first onset and you develop a closer steady state. Like I was saying with regular Lantus, it starts to decrease in the bloodstream around 18 to 24 hours. Toujeo stays a little stays more flat. And again, that’s one that I don’t have as much experience with because it’s not approved in children yet, but have used it in some older kids and it’s quite good., too, as an alternative to Lantus. Not all insurance companies cover that one yet so it’s not always a first line that we’re able to use it just based on what insurance coverage may be. But it it’s the same molecule as Lantus. It’s just more concentrated.

Stacey: These are all injectable insulins and we’re not going to go through the differences between syringes and pens and pumps. Maybe we’ll do that down the line in another episode but these are all injected as you mentioned at the very beginning. But there is an insulin that’s on the market. I know it’s not pediatric which is your specialty but let’s at least touch on Afrezza, the inhaled insulin. Can you just speak to what that is and how it works?

Bryce: The concept of inhaled insulin has been around for a while and part of that is people just don’t like to take injections. Looking at alternative ways that we can provide insulin and as I mentioned we have some barriers that we can’t get by the digestive system at this point to take it as a pill. So again, some very smart people, at Mannkind developed this molecule. It’s actually human insulin. So it’s like regular insulin, but they were able to develop a particle delivery system and take advantage of lung delivery. To explain, this is an inhaled insulin – this is something that you inhale like you would an inhaler for asthma treatment something like that.

The lungs have a lot of surface area and things can get into your bloodstream pretty quickly. Obviously, we want oxygen to get into our bloodstream very quickly and we want carbon dioxide to get out very quickly. The lung is specifically designed to do that. And so they took advantage of that saying well, why don’t we try to inhale insulin to get into the bloodstream faster to see if it works faster and to see if it mimics the way the insulin normally works. Because even our rapid acting insulins, Stacey, they don’t, while they’re great, they can peak in about 15 minutes. That’s a lot slower than the way human insulin works. When the pancreas is working, it can put out insulin, it can vary that peak, minute to minute. And that’s hard for us to mimic, even though we try to think like the pancreas, we still haven’t been able to do that yet. Afrezza gives us a way to possibly do that and by inhaling the insulin it gets into the bloodstream faster so they can actually detect insulin within about a minute of getting that when you inhale the insulin. You start to notice the onset within about 10 to 12 minutes which is a little bit earlier than the injectable insulins. And it’s typically gone within about two to three hours; the duration is a little bit shorter. On paper when you look at the graph of how that insulin is getting into the bloodstream, it looks more like a physiological insulin response compared to other insulins. So it’s a step towards trying to be more physiologic with how the insulin is working in the body. It’s still not perfect.

With Afrezza, the concept of how it’s dosed is a lot different than injectables. So that takes some people some time to really kind of get used to. There’s been less hypoglycemia with Afrezza. There has been improved A1C with Afrezza especially in type 2 diabetes. There’s been some really good data in type 2 in adults. Most of this is in adults, they’re still studying children, so I don’t have any information about children. But the other thing that I really like is, you know, we often don’t think about the role of the liver and how our body handles blood sugar. But the way the body does this when it makes insulin and puts insulin in the bloodstream, the first place it goes is the liver. A lot of how we regulate our blood sugar has to do with how insulin is working in the liver. Afrezza is delivered pretty quickly in this state and what happens is liver is what is making sugar for us and you want to turn that process off. So when you are eating sugar, you don’t want your body making more sugar. So you turn that process off in the body. And in people with diabetes that process is impaired. But if we have an insulin that gets to the liver quicker, that gives us another way that we can try to better control diabetes. It’s a theory that still has a lot to be tested and proven but I like the concept of that.

Another thing we know from animal studies, I got to get my research plugs in here, when you have mice that are genetically engineered to where they do not respond to insulin, you can genetically engineer them where they don’t respond to insulin in specific tissues. So I can block that in the liver, that can be blocked in skeletal muscle, so all the places where insulin works to do all those things that we talked about earlier in the show. When it is blocked in the liver, those animals develop diabetes, but when it’s blocked in muscle, which is where you would think they would develop diabetes because that’s what we think of is that you’re not able to bring sugar in because you can’t respond to insulin, those animals don’t develop diabetes.

Stacey: Wow.

Bryce: They develop in the liver knockout but they don’t in the skeletal muscle knockout. So the role of the liver in this I think is very important. So that’s why I’ve been intrigued by what Afrezza can do. The improvements in A1C and type 2 have been really pretty good. In type 1 it hasn’t been quite as good, and you know, some of that I think personally is that it’s there’s some dosing issues. Just trying to figure out how to titrate the dose. It takes some adjustment because you have cartridges. It’s an inhaler that you put a cartridge that contains insulin in that inhaler and then you put that inhaler to your mouth, and you take a deep breath to where it powder goes into your lung. And the cartridges come as 4, 8, and 12 units. We in Pediatrics are used to dosing things in half units and 1 unit.

Stacey: Right.

Bryce: So there’s a lot of yeah, there’s a lot of people that are like, ‘Wow, I can’t get as fine of control.’ But you still do, because what you have to take into account is that the four unit starts to work faster and is gone faster. So there’s less issue with stacking with that. So a lot of the Afrezza users – and there’s a lot of Afrezza lovers and if you look on Twitter –

Stacey: Oh yes.

Bryce: Yeah, they are there are a lot of Afrezza lovers out there and but it takes some time to figure out what you can use. But some people figure out what their meal dose is and then they might just take an extra cartridges that you just snack and they figure out what how much they need for the snack and so they can mix and match those cartridges. It takes a little bit more effort to fine-tune what you might need. But there’s less risk of low blood sugar because it’s acts so fast and it’s gone so fast. At least that’s what’s touted. Because it’s not approved in kids yet, I don’t have much practical experience with it. But just reading the data and the information about it, I think it’s exciting.

Stacey: People who – sorry go ahead.

Bryce: The other thing, it’s not an injection. That’s the other advantage is, you know, that that’s still a barrier to a lot of people, is having to give insulin as an injection.

Stacey: Yeah, the people who use Afrezza, as you say on social media, are quite passionate about it and we’ve done entire shows about it. I think it’s really exciting and interesting stuff. So thanks for touching on that. You mentioned stacking a couple of times. Let’s talk about that. When we mention insulin stacking, what do you mean and how do we avoid it?

Bryce: Insulin stacking is a concept that has developed really as we started to do more what we call basal/bolus insulin. It’s also become more of a problem as people have access to their blood sugar now every five minutes really. I mean, with continuous glucose monitoring people can see what their blood sugar is, but they can also see arrows are they going up, are they going down, are they going up fast, going down fast? Stacking has actually become a little bit more of a problem using those devices, continuous glucose monitoring, because it has to do with how long the insulin is working in your body. The duration of action, where you know, we’ve talked about previously. Peak action, when the insulin is working at its best. And then the duration of action, when most of that insulin is out of your body. Stacking has to do with the duration of action.

Insulin pumps have made it really easy for people to potentially stack. What that means is giving multiple insulin doses very close together that you don’t give time for the previous insulin dose to really work. So for instance, say Benny eats breakfast and you notice that an hour in or an hour and a half into his meal is blood sugar is 300 and he’s wearing his Dexcom G6 that I know he wears, and you’ve got two arrows still going up. You want to try to bring that down. But he’s an insulin resistant teenage boy and he had a big dose of insulin with his meal and it’s still kind of around his peak time of working. But you want to get that blood sugar down. So you give another correction dose based on the blood sugar and it’s so easy with the pump. But when you do that, you’re stacking that new dose on top of the dose that still working and that can lead to people dropping rapidly after that. So the problem with insulin stacking is the post-bolus low blood sugar. That can happen at varying times. Often insulin stacking happens because there may be a mismatch with what the basal rates for the pump may be or what the carb ratio may need to be. And some people will try to adjust that. The way the pump tries to handle insulin stacking is that famous active insulin time.

Stacey: Right.

Bryce: Right? And so the most people use an active insulin time of about three hours. But remember that that dose really lasts for about four hours. Some people might last a bit longer. Some people it might last less. So three hours may not work for everybody. But and when you use that this is the concept I worked with my patients about. That’s just a mathematical calculation. Okay, so the pump doesn’t really know how the insulin’s working your body. All it is is saying OK at this particular, so at one and a half hours, the pump will assume 50% of the previous bolus is gone. Does that make sense?

Stacey: Yep.

Bryce: Then, depending on how long it’s been since the last bolus and it says that at three hours none of that insulin is working anymore. So if you decrease the active time, if you say go from 3 hours of two and a half hours, you’re saying that all the insulin from the previous bolus is gone at two and a half hours not three hours. And that your peak time, for where 50% of it is gone, has now shifted from an hour and a half to you know, an hour and 15 minutes or something like that. You wind up stacking that way because you’re adjusting active insulin time when actually what probably just needs to be adjusted as either a basal rate or carb ratio. Insulin stacking is something that we need to be watching out for especially for people on pumps and on continuous glucose monitors. Because there is that tendency we want to try to get that blood sugar down and there are other special situations where your endocrinologist may say, ‘Ignore what the pump tells you I want you to go ahead and get that dose of insulin.’ Because they know that you’re insulin resistant or you’re sick and you need that full correction dose.  But in most situations, you generally want to wait two or three hours before you try to bring a blood sugar back down so that you can try to prevent that insulin stacking. If you are having problems with going up too high after a meal or you’re dropping too much after a correction dose, those are things to talk to your provider about to look at your settings to see if there’s something else that needs to be done.

Stacey: As someone who was very confused by stacking in the very early days. I had a 23-month-old and I thought my doctor said you can’t feed him in between the three hours of the dosing. That’s the most common bit of confusion I see among newly diagnosed families, parents of kids, and even adults. Which is the stacking refers to – and feel free to jump in and correct me if I’m wrong – the stacking refers to treating a blood sugar. It does not refer to dosing for food. Because by the time we figured it out, you’ve met Benny, he’s a hungry kid, that dude was up to like 8 to 10 shots a day because he was like, ‘I’m going to eat. Okay, I’ll have a shot. I’m gonna eat. Okay, I’ll have a shot.’ Now, that makes it more difficult to get an accurate blood sugar every couple of hours, I will give you that, especially at the beginning. You may want to talk to your doctor about planning that out a little bit more to get, you know, good blood sugar measurements. Because if you are grazing all day long that can be difficult. But that’s true right you can’t stack insulin if you’re giving insulin for food is my understanding?

Bryce: That that is the way that we teach correct. And because you’re needing that insulin to cover the carbohydrate that’s being consumed. And you’re taking in carbohydrate more the more problems with stacking you get and it can still happen Stacey. So even some of those people who are eating all the time, they might have, they might eat, you know, once an hour for five or six hours and then because they bolus throughout all of that. They might have a low later on. Because they’ve stack some of that. And part of that gets to the to the problem is that you know, as good as our insulins are, you know, we still can’t be the pancreas. All that we can do is think like the pancreas. And the pancreas can handle that grazing. That’s why you know medical nutrition therapy is so much a part of diabetes care, because it’s not just about the insulin about what you dose it. It’s about how you’re eating and what you’re eating. I tell people all the time grazing is something that’s tough for us to handle with our insulins. Because it does tend to lead to higher blood sugars. But in general no, the stacking doesn’t always happen with food, but it can if someone is a grazer.

Stacey: Keep in mind, my experience is with a toddler as well. It certainly got easier as Benny started eating at a more routine time. Although as you know, and I was so happy when you mentioned bedtime could be 3 a.m. I mean, you know over the summer there are times and hey listen, it’s you can criticize me as a parent I don’t care. But there are times where he’ll be playing video games and I go to bed and then you know, he’s been in the kitchen at midnight or 1 a.m. But he’s given insulin for it. So thank goodness for that.

Bryce: A good pediatric endocrinologist should recognize that. I know that I’m making changes. Once school gets done, and I’m not saying I’m a good pediatric endocrinologist,

Stacey: I’ll say that for you!

Bryce: You need to recognize how children’s schedules change when they go into the summer. You might have to make basal rate changes. You might have to make carb ratio changes because they are eating. While we can live in the great world of ‘no you shouldn’t eat in the middle of night,” I mean, they’re teenagers. This is real life and you have to know how to handle that. And so sometimes I have to adjust carb ratios in the middle of the night. I have to flip flop basal rates because they’re staying up all night and sleeping during the day. And so and again that gets to my main theme of how I care for our patients is, I want you to live life with this. I don’t want you to not be able to stay up with your friends and play video games. I still want them be able to have that experience and not let diabetes take that away from them. Because I can adjust their insulin doses. We can talk about how to eat better at that point. So that they can learn to do those things. Because I’m actually really happy that I mean Benny knows it. ‘Hey, if I go and eat, I got to check my blood sugar or I’ve got to look at by CGM and I gotta bolus for what I’m about to eat.’There’s some kids that won’t do that.

Stacey: Trust me, I knock wood all the time. We’re really very happy with that. One more concept before we start wrapping things up here. I do want to make sure to talk about pre-bolusing and why that is effective. We’ve mentioned the onset of insulin. It’s slower than food. Right? So, you know generally speaking it’s a good idea to bolus before a meal. Can you talk about that?

Bryce: That’s the main reason, Stacey, that we can’t be the pancreas we can only think like the pancreas. We have to wait about 15 minutes on average for those bolus insulins to start working and some of our more higher carb meals, so the higher the carb meal, the quicker your blood sugar starts to rise. So it becomes a mismatch. That’s also why liquid sugar beverages really are not a great part a regular diet. They’re not a great part of the regular diet anyway. But for people with diabetes it’s particularly problematic because those will make your blood sugar go up within a matter of a couple of minutes. But we got to wait 15 minutes before insulin starts to work.

We see this a lot at breakfast. I’m sure you’ve seen this with Benny. I mean it and it doesn’t matter how much whole grain he eats first thing in the morning, you know, it’s still tends to rise. And that could also be some hormone things as well. But you know, the there’s with those, our breakfasts in the United States tend to be pretty carb heavy in the morning. Breakfast cereal is notorious for this. Where you’ll have that that that blood sugar start to rise and not even that it’s peaking. It’s just it’s starting to go up and you’re having to wait for the insulin to work and then when you mismatch those, you have problems down the road later on in the day. And so pre-bolusing is an attempt to try to mitigate some of that. Or to prevent some of that. So if you give insulin of 15-minute head start, then it’s starting to work as you’re starting to eat so that you better match the insulin’s peak action with when your blood sugar is actually going up. And it’s very effective but it’s also very intense. So that’s always not the easiest thing for a teenager that wants to sleep in til the very last minute and roll up out of you know out of bed and just roll out to school and is eating a Nutrigrain bar on the bus or in the car. It doesn’t always lend itself easily to life. We certainly try to encourage that as much as we can because it does tend to just match it. It thinks like the pancreas better that way.

Stacey: I will get on teeny bit of a soapbox if I could and again, this is my opinion and my experience as a mom of a toddler. We didn’t have a CGM. I think Benny was diagnosed before Dexcom was even out, but we didn’t have a CGM when Benny was diagnosed. And we always dosed after the meal for a very long time because who knows what the two-year-old is gonna eat. I see a lot of stress of parents who will say, ‘Kids are so smart. My two-year-old has learned that if he doesn’t eat dinner, he will get ice cream anyway, or he will get a juice anyway, because we’ve dosed him.’ What do you tell parents of toddlers or any children who are struggling with the pre-bolus because they love to see that smooth line after a meal but dinner or lunch has become a battle.

Bryce:  I tell them not to fight that battle. I agree with you on this. Most of our toddlers, I’m bolusing after the meal. The way that I conceptualize that is, if we were in school and we were grading, how we did in terms of dosing insulin, the A answer is we want to pre-bolus. Does that make sense? But the B or B+ answer is you can bolus after the meal. It’s just not as effective as doing the pre-bolus but you know, and it also gets back to that tenant that it’s about individualizing care. I don’t want parents to have that battle and because I know toddlers will do that. I mean they’re that they operate under Pavlovian Theory. Can I say that?

Stacey: Yeah.

Bryce: Classically conditioned. Just like you said, you know, they learn pretty quickly with wow,  I’m going to get ice cream if I don’t eat my lunch. So I think it’s always safer in those kids and still effective to bolus after the meal. You might deal with more after meal rise, then otherwise, and the way that I try to handle that is is I tell parents, ‘Well, you have to have a timer. You give the child 15 minutes to eat and after 15 minutes, you count the carbs and that’s what you bolus for.’

Stacey: That makes sense.

Bryce: Try to mitigate that some ways. Because you know toddlers will also, they’ll sit there all day at the table just pick at their food. You just have to try to do the best to still be able to live life. Another thing is you really don’t want to have those frequent low blood sugars because while you might get a good A1C, those that those frequent low blood sugars can have, there are studies, and with very young children, less than three, there may be some cognitive effect of frequent hypoglycemia down the road that you’d be dealing with.  You wouldn’t see it until they’re older. So you’re putting the child at risk for a severe low blood sugar event. I try to avoid that if I can. I still do after bolus, I still bolus after meals in toddlers or people who don’t eat a consistent meal. If I can’t count on they’re going to eat what you put in front of them like in school because I don’t want them to have a little blood sugar at school. I want them to stay in class. I want them to do those things. Then I’ll take the B+ answer and I’ll bolus after, I’ll advise parents to bolus after the meal. There’s no data that I’ve ever seen that says, you know that bolusing after the meal is inferior. You might have to deal with some rise after the meal but you’re not dealing with the low blood sugar. And I don’t want to get to an A1C a seven a half or less, having twelve percent of your blood sugar’s less than 70. That’s not the way I want you to be there.

Stacey: Wow, a lot to take in. A lot of great education here. Before I let you go two more questions for you. You’ve given some terrific advice throughout this interview for newly diagnosed families and adults with type 1 about not letting diabetes rule their lives. That’s a great philosophy. I’d also like to ask you what excites you about the future of endocrinology and type 1. You know, what what gets you excited that’s happening?

Bryce: A lot of things get me excited about what’s happening with diabetes and I think you know really what’s been exciting over the last five years is just the explosion of technology that we’ve been able to use to help families live their lives with diabetes. I’m excited about the technology that’s here, the technology that’s coming. I’m also excited still about the cure. You know, I think that that still a viable option. I’m also excited about the research that’s going on with TrialNet that’s looking to try to prevent people from ever getting the disease. So, you know your listeners who are at places that help that participate in TrialNet which is the largest study for Type 1 diabetes, looking at understanding the natural history of the disease so that we can prevent people from ever getting it. And that’s just a good principle of pediatric care to me. We practice preventive medicine in Pediatrics. And so if I can ever prevent people from getting there, but I want to learn how to do that and there’s some wonderful researchers and very smart people, smarter than me, who are looking at those things.

The technology that I think has been the most exciting thing over the last five years and it’s exploded since really since Dexcom came on the market in pediatrics. I mean things have just dramatically changed,. We saw in another study there was about a 30% increase in CGM use in kids over a five-year period. I’ve seen that in my clinical practice and what I love about that is that it’s giving life back to people. Parents are now sleeping through the night. Parents are more comfortable sending their child to go spend the night at their friend’s house because they can see what their blood sugars are doing. And using technology like texting they can text their child say, ‘Hey, I see that you’re dropping you might want to eat a snack. Hey, you know, you’re going up you need to take a bolus? Did you eat?’ But it’s giving those children and parents back some freedom that I think is just remarkable because it ties into to my practice that I want them to learn how to live life with this.

The technology that’s coming out, I’m really excited about the Medtronic 670g pump. I know you’re going to deal with that in another show, but that having an automated insulin delivery system. Us having the artificial pancreas on the horizon. I think it’s great to where, you know, if we can use the technology to have people think less about their diabetes, wow what the future could be. We had a man named Bill Woods come talk at one of our diabetes days. Bill Woods, he was involved in one of the earlier Bionic Pancreas studies. (The Bionic Pancreas, also known as the iLet) uses both insulin and glucagon in the pump to manage diabetes. And he was in one of the home studies about that. And he said something about being that said that just strikes me is that he went to the zoo with his children and while he was wearing that bionic pancreas, and he said normally when he goes anywhere his first thought is, ‘Okay. What am I going to do if I have a low blood sugar? Where can I go? Where are my snacks? Where can I find, where are the refreshments if I need to get a drink? Or where are my things?’ It’s planning the the zoo trip around the diabetes. He said while I was on that, I went to the zoo. And for the first time in my life that I could remember I didn’t think about diabetes as the first thing. I just went to the zoo with the family. And that is powerful. We still got a long way to go, but the technology is here.

Just imagine the first cell phone that came out. That’s where we’re at. And I can’t wait till we get to the iPhone or the Galaxy 6 or whatever. I’m an iPhone guy, but I can’t wait to get to that point in the technology. And also, you know, we’re getting smarter about the data. Now that the data can go to the cloud and we have smart mathematicians that can you know, as this is going to the cloud, they can look at that big data and say okay if we know you’ve had this many steps per day, and you’ve eaten this, and your blood sugar’s have been running this, we can predict better how your blood sugar is going to respond to a certain insulin dose and we can tell you what insulin dose you need. So I think that the future is so bright you definitely gotta wear shades.

Stacey: I love what you have to say there! Let me just, if I could, step to the past before I let you go. Because you decided to become an endocrinologist for a reason that I think is worth talking about. Would you mind sharing that story? I know it may be difficult, but your uncle lived with type 1 and he was diagnosed a long time ago when care wasn’t what it is today, right?

Bryce: He did. So my uncle, Mitchell Dreiman, he was diagnosed when he was 12, and this was back in the early 60s. And as you know Stacey, it was a much different time. It, you know, the continuous glucose monitoring and insulin pumps in regular use now were just really a myth. They were science fiction at the time. We just didn’t really have access to that and my grandparents did the absolute best they could. He took Regular insulin and he didn’t have glucometers, you know?

Stacey: That’s amazing.

Bryce: It was a much different time and he did the best he could. My grandparents did the best they could with what they had. He really is who really showed me that you can live life with diabetes, but you fight it. Because he didn’t let diabetes stop him. He was always, you know, really the life of everybody that he was around. He was the light. When Mitchell walked in the room, you know, the place just came alive. I remember coming home to visit with family at Christmas and he was the one I was looking forward to get to meet. Because he always just loved hanging out with us and hanging around with the kids and making us feel special and that really started our friendship, and his mentorship to me, even if he didn’t know that. He didn’t know that he was showing me those things. When I was a kid, I didn’t know what diabetes was. I just knew that he had it. But we had an experience one Christmas where he had a pretty severe hypoglycemic event and had a very low blood sugar that I had to help him overcome. It was scary but that was when I started understanding more about what the disease is and I started understanding more and realize, man, this could really take my uncle and someone I love away from me. And I didn’t like that at all. You know, the fight was on.

We always stayed really close and he was with me when I graduated college. I had always had an interest in diabetes because of my uncle and I knew that’s what I wanted to work on. That’s what I wanted to be my life’s work. He knew that and was always supportive of me. Through college through medical school, he was there the day I graduated from medical school and graduate school. And he was actually the very first patient with diabetes that I examined. After I graduated from medical school, he came and just grabbed me and said, ‘Bryce grab your stethoscope.’ That’s what he told me. He said ‘I want to be the first patient that you ever examined who has diabetes.’ So it was an experience that I never forgot.

About that same time I was graduating medical school he was starting to have some of the complications of diabetes. He was having kidney failure. He was losing his eyesight. He was really fighting. He had a kidney transplant, but unfortunately that he was rejecting that kidney that was donated by his sister. And he then went to Duke and had a dual pancreas/kidney transplant. So for the last year of his life, he was diabetes free and was living a real wonderful life, but unfortunately the years of immunosuppression, he actually developed pancreatic cancer. And in my intern year of pediatric residency, I lost him. He died from pancreatic cancer. But you know, the thing that I always try to remember, while I love him and I miss my uncle more than I can say, the legacy that he left, I think is bigger than himself. And I think he understood that. You know that when I graduated medical school, he had told my mom that you know, if I have to live this fight so that Bryce can someday help other people, than this fight is worth it. You know, those are the kind of things that stick with you. And I knew that I wasn’t going to let my uncle down and I wasn’t going to let my future patients down. All the families that I work with now it’s all because of my Uncle Mitchell. What he did and the passion that he instilled in me. You now, even to this day, I hope that he’s proud of me.

Stacey: Bryce it’s amazing to think of what that means to you and the impact he had on you. And looking at all of the things that are coming, you know, I don’t want to get too cliche here, but you have to think about your uncle in terms of the difference he made in bringing you to medicine, the people that you help, and the advances that are being made. Do you must think about him all the time with that?

Bryce: I do. I think about him all the time and I you know, I think about the legacy that he started and the analogy I use is a tree. My uncle helped sow the seed in me and help this tree take root about helping improve the lives of children and family with diabetes. He sowed that seed. He helped that tree take root. Every family that I get to work with, we’re just adding new leaves to the tree. We’re adding new life to that tree. And it’s ever-growing. So whether I’m in Greenville or whether I’m somewhere else, that tree is is always growing. It’s growing, its thriving, and it’s adding new leaves every year. And so that that’s how I think about my uncle and the legacy that he had. And why it’s so much bigger than him, is that my love for him and my interaction with him is is what’s put me where I’m at and you know, help me be in the place that I feel like I need to be. That’s why taking care of families with diabetes is more than just adjusting insulin, it’s about improving their lives and helping them live their lives to the fullest.

Stacey: Bryce, thank you so much for joining me, for talking about insulin and so much more today. I really appreciate your time. This is extremely helpful. Thank you.

Bryce: Oh thank you Stacey. This has been quite an honor and I am so thankful that we have you in the fight and have you as an advocate and you’re such a strong voice in your shows, and your your presence is omnipresent. We’re really, I’m happy to have you as an ally and an advocate.

Stacey: Wow. Thank you.

 

This episode originally aired January 29, 2019

sponsors & partners


One Drop Logo
HypoPen Gvoke Logo
RealGood Foods Co. logo
dexcom logo