Anne L. Peters, MD

This transcript has been edited for clarity. 
 

I’m going to tell you the story of two patients with diabetes who had false-positive alcohol tests. 

The first patient is a patient of mine with type 1 diabetes. He was in a car accident. He hit the car in front of him that hit the car in front of them. Because the cars were quite damaged, the police were summoned. 

At the scene, he had a breathalyzer test. He flunked the breathalyzer test, and he was charged with a DUI. The woman in the middle car got out of her car and said her neck hurt. This then rose this to the level of a DUI with injury to one of the other people, and my patient was charged with a felony. He was taken to jail. 

He told them at the scene and at the jail that he had type 1 diabetes. The reason this is so important is because type 1 diabetes can cause a false-positive breathalyzer test. In particular, this patient of mine had not been eating all day long. He’d been getting his basal insulin through the pump, but he had not given any bolus doses of insulin. He was actually quite ketotic.

When he was put in jail, they took away his cell phone so he could no longer see his glucose levels, and they took away the controller for his Omnipod system. He basically had no way to give bolus doses of insulin. Fortunately, the Omnipod system lasted for a day and a half just by giving him basal. The jail physicians did not give him insulin until he’d been in jail for 3 days. 

This is someone with type 1 diabetes, and their protocol for insulin has something to do with high glucose levels and giving something like a sliding scale of insulin. They were not really prepared for managing somebody with type 1 diabetes who was on an automated insulin delivery system. 

I, along with my patient’s parents, worked very hard to get the jail doctors to finally give him Lantus. Inherent in all of this, it made me aware of a number of different issues. The first is that breathalyzer tests can be falsely positive in people with type 1 diabetes if they are ketotic; therefore, people with type 1 diabetes should ask for a blood test to test their alcohol levels if they think it could be a false positive. 

Second, we need to actually figure out a way to help people with type 1 diabetes who happen to be in jail or in prison because if they don’t have access to a smartphone, they’re not going to be able to run their devices. We need to make sure that devices have receivers that can be used, particularly continuous glucose monitors (CGMs), because CGM is the standard of care for patients and should be so for people who are incarcerated. 

The second case is much shorter and isn’t mine, but it was a letter in The New England Journal of Medicine about a man who was on probation, who was having urine tests to show that he had not been consuming alcohol. He was started on empagliflozin, which, interestingly, made his urine test become falsely positive. 

Why? Well, it’s thought it’s because it caused fermentation of the sugar with the bacteria that was in his urine because the people who were processing the sample hadn’t done it correctly, and they kept it out at room temperature for a prolonged period of time before testing it. The urine samples should be kept refrigerated to prevent this from happening. 

These are two people who had false-positive tests because they had diabetes. I think it’s important that we realize that this can happen, and we need to help our patients deal with these situations.

Dr. Peters is professor, Department of Clinical Medicine, Keck School of Medicine; Director, University of Southern California Westside Center for Diabetes, University of Southern California, Los Angeles. She reported conflicts of interest with Abbott Diabetes Care, Becton Dickinson, Boehringer Ingelheim, Eli Lilly, Lexicon Pharmaceuticals, Livongo, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, Zafgen, Dexcom, MannKind, and AstraZeneca.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity. 
 

I’m going to tell you the story of two patients with diabetes who had false-positive alcohol tests. 

The first patient is a patient of mine with type 1 diabetes. He was in a car accident. He hit the car in front of him that hit the car in front of them. Because the cars were quite damaged, the police were summoned. 

At the scene, he had a breathalyzer test. He flunked the breathalyzer test, and he was charged with a DUI. The woman in the middle car got out of her car and said her neck hurt. This then rose this to the level of a DUI with injury to one of the other people, and my patient was charged with a felony. He was taken to jail. 

He told them at the scene and at the jail that he had type 1 diabetes. The reason this is so important is because type 1 diabetes can cause a false-positive breathalyzer test. In particular, this patient of mine had not been eating all day long. He’d been getting his basal insulin through the pump, but he had not given any bolus doses of insulin. He was actually quite ketotic.

When he was put in jail, they took away his cell phone so he could no longer see his glucose levels, and they took away the controller for his Omnipod system. He basically had no way to give bolus doses of insulin. Fortunately, the Omnipod system lasted for a day and a half just by giving him basal. The jail physicians did not give him insulin until he’d been in jail for 3 days. 

This is someone with type 1 diabetes, and their protocol for insulin has something to do with high glucose levels and giving something like a sliding scale of insulin. They were not really prepared for managing somebody with type 1 diabetes who was on an automated insulin delivery system. 

I, along with my patient’s parents, worked very hard to get the jail doctors to finally give him Lantus. Inherent in all of this, it made me aware of a number of different issues. The first is that breathalyzer tests can be falsely positive in people with type 1 diabetes if they are ketotic; therefore, people with type 1 diabetes should ask for a blood test to test their alcohol levels if they think it could be a false positive. 

Second, we need to actually figure out a way to help people with type 1 diabetes who happen to be in jail or in prison because if they don’t have access to a smartphone, they’re not going to be able to run their devices. We need to make sure that devices have receivers that can be used, particularly continuous glucose monitors (CGMs), because CGM is the standard of care for patients and should be so for people who are incarcerated. 

The second case is much shorter and isn’t mine, but it was a letter in The New England Journal of Medicine about a man who was on probation, who was having urine tests to show that he had not been consuming alcohol. He was started on empagliflozin, which, interestingly, made his urine test become falsely positive. 

Why? Well, it’s thought it’s because it caused fermentation of the sugar with the bacteria that was in his urine because the people who were processing the sample hadn’t done it correctly, and they kept it out at room temperature for a prolonged period of time before testing it. The urine samples should be kept refrigerated to prevent this from happening. 

These are two people who had false-positive tests because they had diabetes. I think it’s important that we realize that this can happen, and we need to help our patients deal with these situations.

Dr. Peters is professor, Department of Clinical Medicine, Keck School of Medicine; Director, University of Southern California Westside Center for Diabetes, University of Southern California, Los Angeles. She reported conflicts of interest with Abbott Diabetes Care, Becton Dickinson, Boehringer Ingelheim, Eli Lilly, Lexicon Pharmaceuticals, Livongo, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, Zafgen, Dexcom, MannKind, and AstraZeneca.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity. 
 

I’m going to tell you the story of two patients with diabetes who had false-positive alcohol tests. 

The first patient is a patient of mine with type 1 diabetes. He was in a car accident. He hit the car in front of him that hit the car in front of them. Because the cars were quite damaged, the police were summoned. 

At the scene, he had a breathalyzer test. He flunked the breathalyzer test, and he was charged with a DUI. The woman in the middle car got out of her car and said her neck hurt. This then rose this to the level of a DUI with injury to one of the other people, and my patient was charged with a felony. He was taken to jail. 

He told them at the scene and at the jail that he had type 1 diabetes. The reason this is so important is because type 1 diabetes can cause a false-positive breathalyzer test. In particular, this patient of mine had not been eating all day long. He’d been getting his basal insulin through the pump, but he had not given any bolus doses of insulin. He was actually quite ketotic.

When he was put in jail, they took away his cell phone so he could no longer see his glucose levels, and they took away the controller for his Omnipod system. He basically had no way to give bolus doses of insulin. Fortunately, the Omnipod system lasted for a day and a half just by giving him basal. The jail physicians did not give him insulin until he’d been in jail for 3 days. 

This is someone with type 1 diabetes, and their protocol for insulin has something to do with high glucose levels and giving something like a sliding scale of insulin. They were not really prepared for managing somebody with type 1 diabetes who was on an automated insulin delivery system. 

I, along with my patient’s parents, worked very hard to get the jail doctors to finally give him Lantus. Inherent in all of this, it made me aware of a number of different issues. The first is that breathalyzer tests can be falsely positive in people with type 1 diabetes if they are ketotic; therefore, people with type 1 diabetes should ask for a blood test to test their alcohol levels if they think it could be a false positive. 

Second, we need to actually figure out a way to help people with type 1 diabetes who happen to be in jail or in prison because if they don’t have access to a smartphone, they’re not going to be able to run their devices. We need to make sure that devices have receivers that can be used, particularly continuous glucose monitors (CGMs), because CGM is the standard of care for patients and should be so for people who are incarcerated. 

The second case is much shorter and isn’t mine, but it was a letter in The New England Journal of Medicine about a man who was on probation, who was having urine tests to show that he had not been consuming alcohol. He was started on empagliflozin, which, interestingly, made his urine test become falsely positive. 

Why? Well, it’s thought it’s because it caused fermentation of the sugar with the bacteria that was in his urine because the people who were processing the sample hadn’t done it correctly, and they kept it out at room temperature for a prolonged period of time before testing it. The urine samples should be kept refrigerated to prevent this from happening. 

These are two people who had false-positive tests because they had diabetes. I think it’s important that we realize that this can happen, and we need to help our patients deal with these situations.

Dr. Peters is professor, Department of Clinical Medicine, Keck School of Medicine; Director, University of Southern California Westside Center for Diabetes, University of Southern California, Los Angeles. She reported conflicts of interest with Abbott Diabetes Care, Becton Dickinson, Boehringer Ingelheim, Eli Lilly, Lexicon Pharmaceuticals, Livongo, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, Zafgen, Dexcom, MannKind, and AstraZeneca.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Those of us in the field of diabetes have long wanted to cure type 1 diabetes, and there are little steps making me feel like this might be a possibility. One of those steps is that a company named Vertex – I’m actually on the steering committee for Vertex in terms of this project – has made beta cells from stem cells. Now, instead of waiting for a cadaveric donor, we can make little beta cells. They started giving them to people in human trials. The Food and Drug Administration has been cautious because it’s new, and I get that.

In the first part of these trials, we could only give half a dose of these beta cells. The doses were determined based on what we know from giving beta-cell transplants from cadaveric donors. We gave half a dose of these stem cell–derived beta cells to two people who were having episodes of severe hypoglycemia.

In patient 1, these beta cells worked incredibly well. He became insulin independent, and now after over a year, he’s basically free of his type 1 diabetes. Patient 2 received half a dose, and she did get some activity of the beta cells, but not enough to achieve insulin independence, so she got a second dose. Shortly after the second dose, she decided she didn’t want to participate in the trial anymore and she was lost to follow-up.

Patient 2 didn’t get the same response as patient 1, but then we moved on to four more patients who got a full dose to start with. Now, there’s a total of six patients. Of those additional four patients, one of them has now been followed for a year. Just like patient 1, he’s off insulin. It’s as though his body has normal beta cells and he’s doing great. For the next three patients, we don’t have enough follow-up data to tell you what’s going to happen to them at a year.

I can tell you that, in all six patients, the beta cells worked. They basically were producing insulin, they had positive C-peptide levels, and it showed that these beta cells work when given to human beings. Now the trial is going to start giving more patients these stem cell–derived beta cells.

One of the things that’s important to realize is that this is a very small sample size, at just six individuals. Even within those six individuals, there was variation in terms of the response to the treatment. Probably, just like with all things in medicine, there will be different doses, different ways in which people do respond, people who get off of insulin completely, and people who may require some ongoing insulin therapy. I have no idea what this is going to look like as we test this in more people.

Everybody did start making C-peptide, they were having an effect of these beta cells, and it was working. We’ll have to see how well it works, how well it works in whom, and how we’re going to be able to use these types of therapies in the future.

In terms of side effects, they were really related to immunosuppression. There were no real surprises, but again, this is a very small sample size.

In summary, I think this is really hopeful. I don’t like to give false hope, but each step of this development process has shown that these beta cells derived from stem cells do seem to work in human beings as native beta cells might. Hopefully, this portends a future of newer therapies in the treatment of people with type 1 diabetes. Thank you.
 

Dr. Peters is professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She has published more than 200 articles, reviews, and abstracts, and three books, on diabetes, and has been an investigator for more than 40 research studies. She has spoken internationally at over 400 programs and serves on many committees of several professional organizations She disclosed ties with Abbott Diabetes Care, AstraZeneca, Becton Dickinson, Boehringer Ingelheim Pharmaceuticals, Dexcom, Eli Lilly, Lexicon Pharmaceuticals, Livongo, MannKind Corporation, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, and Zafgen.

A version of this article originally appeared on Medscape.com.

This transcript has been edited for clarity.

Those of us in the field of diabetes have long wanted to cure type 1 diabetes, and there are little steps making me feel like this might be a possibility. One of those steps is that a company named Vertex – I’m actually on the steering committee for Vertex in terms of this project – has made beta cells from stem cells. Now, instead of waiting for a cadaveric donor, we can make little beta cells. They started giving them to people in human trials. The Food and Drug Administration has been cautious because it’s new, and I get that.

In the first part of these trials, we could only give half a dose of these beta cells. The doses were determined based on what we know from giving beta-cell transplants from cadaveric donors. We gave half a dose of these stem cell–derived beta cells to two people who were having episodes of severe hypoglycemia.

In patient 1, these beta cells worked incredibly well. He became insulin independent, and now after over a year, he’s basically free of his type 1 diabetes. Patient 2 received half a dose, and she did get some activity of the beta cells, but not enough to achieve insulin independence, so she got a second dose. Shortly after the second dose, she decided she didn’t want to participate in the trial anymore and she was lost to follow-up.

Patient 2 didn’t get the same response as patient 1, but then we moved on to four more patients who got a full dose to start with. Now, there’s a total of six patients. Of those additional four patients, one of them has now been followed for a year. Just like patient 1, he’s off insulin. It’s as though his body has normal beta cells and he’s doing great. For the next three patients, we don’t have enough follow-up data to tell you what’s going to happen to them at a year.

I can tell you that, in all six patients, the beta cells worked. They basically were producing insulin, they had positive C-peptide levels, and it showed that these beta cells work when given to human beings. Now the trial is going to start giving more patients these stem cell–derived beta cells.

One of the things that’s important to realize is that this is a very small sample size, at just six individuals. Even within those six individuals, there was variation in terms of the response to the treatment. Probably, just like with all things in medicine, there will be different doses, different ways in which people do respond, people who get off of insulin completely, and people who may require some ongoing insulin therapy. I have no idea what this is going to look like as we test this in more people.

Everybody did start making C-peptide, they were having an effect of these beta cells, and it was working. We’ll have to see how well it works, how well it works in whom, and how we’re going to be able to use these types of therapies in the future.

In terms of side effects, they were really related to immunosuppression. There were no real surprises, but again, this is a very small sample size.

In summary, I think this is really hopeful. I don’t like to give false hope, but each step of this development process has shown that these beta cells derived from stem cells do seem to work in human beings as native beta cells might. Hopefully, this portends a future of newer therapies in the treatment of people with type 1 diabetes. Thank you.
 

Dr. Peters is professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She has published more than 200 articles, reviews, and abstracts, and three books, on diabetes, and has been an investigator for more than 40 research studies. She has spoken internationally at over 400 programs and serves on many committees of several professional organizations She disclosed ties with Abbott Diabetes Care, AstraZeneca, Becton Dickinson, Boehringer Ingelheim Pharmaceuticals, Dexcom, Eli Lilly, Lexicon Pharmaceuticals, Livongo, MannKind Corporation, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, and Zafgen.

A version of this article originally appeared on Medscape.com.

This transcript has been edited for clarity.

Those of us in the field of diabetes have long wanted to cure type 1 diabetes, and there are little steps making me feel like this might be a possibility. One of those steps is that a company named Vertex – I’m actually on the steering committee for Vertex in terms of this project – has made beta cells from stem cells. Now, instead of waiting for a cadaveric donor, we can make little beta cells. They started giving them to people in human trials. The Food and Drug Administration has been cautious because it’s new, and I get that.

In the first part of these trials, we could only give half a dose of these beta cells. The doses were determined based on what we know from giving beta-cell transplants from cadaveric donors. We gave half a dose of these stem cell–derived beta cells to two people who were having episodes of severe hypoglycemia.

In patient 1, these beta cells worked incredibly well. He became insulin independent, and now after over a year, he’s basically free of his type 1 diabetes. Patient 2 received half a dose, and she did get some activity of the beta cells, but not enough to achieve insulin independence, so she got a second dose. Shortly after the second dose, she decided she didn’t want to participate in the trial anymore and she was lost to follow-up.

Patient 2 didn’t get the same response as patient 1, but then we moved on to four more patients who got a full dose to start with. Now, there’s a total of six patients. Of those additional four patients, one of them has now been followed for a year. Just like patient 1, he’s off insulin. It’s as though his body has normal beta cells and he’s doing great. For the next three patients, we don’t have enough follow-up data to tell you what’s going to happen to them at a year.

I can tell you that, in all six patients, the beta cells worked. They basically were producing insulin, they had positive C-peptide levels, and it showed that these beta cells work when given to human beings. Now the trial is going to start giving more patients these stem cell–derived beta cells.

One of the things that’s important to realize is that this is a very small sample size, at just six individuals. Even within those six individuals, there was variation in terms of the response to the treatment. Probably, just like with all things in medicine, there will be different doses, different ways in which people do respond, people who get off of insulin completely, and people who may require some ongoing insulin therapy. I have no idea what this is going to look like as we test this in more people.

Everybody did start making C-peptide, they were having an effect of these beta cells, and it was working. We’ll have to see how well it works, how well it works in whom, and how we’re going to be able to use these types of therapies in the future.

In terms of side effects, they were really related to immunosuppression. There were no real surprises, but again, this is a very small sample size.

In summary, I think this is really hopeful. I don’t like to give false hope, but each step of this development process has shown that these beta cells derived from stem cells do seem to work in human beings as native beta cells might. Hopefully, this portends a future of newer therapies in the treatment of people with type 1 diabetes. Thank you.
 

Dr. Peters is professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She has published more than 200 articles, reviews, and abstracts, and three books, on diabetes, and has been an investigator for more than 40 research studies. She has spoken internationally at over 400 programs and serves on many committees of several professional organizations She disclosed ties with Abbott Diabetes Care, AstraZeneca, Becton Dickinson, Boehringer Ingelheim Pharmaceuticals, Dexcom, Eli Lilly, Lexicon Pharmaceuticals, Livongo, MannKind Corporation, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, and Zafgen.

A version of this article originally appeared on Medscape.com.

This transcript has been edited for clarity.

There is wonderful news in the field of hybrid closed-loop pump technology because the Medtronic 780G system was just approved. I can’t tell you how happy this makes me because we’ve all been waiting for this seemingly forever and ever. This isn’t just a small upgrade from the 770G. It’s a quantum leap from the 770G to the 780G. The 780G has newer algorithms, a new sensor, and a longer-lasting infusion set.

USC Westside Center for Diabetes

It’s been used since 2020 in Europe, so we have good data on how well it works. Frankly, I think it works really well. We’ve seen nice improvements in [hemoglobin] A1c, time in range, other glycemic metrics, and patient satisfaction in studies done in Europe.

Now, I’ve never had the system to use in one of my patients. I always say I never know a system until I see it in use in my own patients, but let me tell you what I’ve read.

First, it has something called meal-detection technology with autocorrection boluses every 5 minutes. If this works, it can be a huge win for our patients because the problem my patients have is with mealtime dosing. They often dose late, or they may not dose enough insulin for the carbohydrates. That’s where the issues are.

All these hybrid closed-loop systems, this one included, show that the best improvements in glycemia are overnight. I’m hoping that this one shows some nice improvements in daytime glycemia as well. Stay tuned and I’ll let you know once I’ve been using it.

Next, it has adjustable targets down to 100. This is the lowest target for any hybrid closed-loop system. It has an extended-wear infusion set that lasts for 7 days. This infusion set is already available but works with this new system.

Finally, it has a new sensor. It looks like the old sensors, but it’s the Guardian 4, which requires much fewer finger sticks. Now, I’m not entirely sure about how often one has to do a finger stick. I know one has to do with finger sticking to initiate auto mode, or what they call SmartGuard, but I don’t know whether you ever have to do it again. I know for sure that you have to do it again if you fall out of the automated mode into manual mode. Once you’re in SmartGuard, I believe there are no further finger-stick calibrations required.

If people are already on the 770G system, this is just a software update that is presumably easy to upgrade to the 780G. Now, the physical pieces ... If someone doesn’t already have the Guardian 4 sensor or the extended-wear infusion set, they’ll have to get those. The software update to make the 770G increase to the 780G should just come through the cloud. I don’t know when that’s going to happen.

I do know that preorders for this system, if you want to buy the new physical system, start on May 15. The shipping of the new 780G system should occur in the United States toward the end of this summer.

I’m so excited. I think this is really going to benefit my patients. I can’t wait to start using it and letting patients see how these algorithms work and how they really help patients improve their glucose control.

Anne L. Peters, MD, is a professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She reported conflicts of interest with Abbott Diabetes Care, Becton Dickinson, Boehringer Ingelheim, Eli Lilly, Lexicon Pharmaceuticals, Livongo, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, Zafgen, Dexcom, MannKind, and AstraZeneca.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

There is wonderful news in the field of hybrid closed-loop pump technology because the Medtronic 780G system was just approved. I can’t tell you how happy this makes me because we’ve all been waiting for this seemingly forever and ever. This isn’t just a small upgrade from the 770G. It’s a quantum leap from the 770G to the 780G. The 780G has newer algorithms, a new sensor, and a longer-lasting infusion set.

USC Westside Center for Diabetes

It’s been used since 2020 in Europe, so we have good data on how well it works. Frankly, I think it works really well. We’ve seen nice improvements in [hemoglobin] A1c, time in range, other glycemic metrics, and patient satisfaction in studies done in Europe.

Now, I’ve never had the system to use in one of my patients. I always say I never know a system until I see it in use in my own patients, but let me tell you what I’ve read.

First, it has something called meal-detection technology with autocorrection boluses every 5 minutes. If this works, it can be a huge win for our patients because the problem my patients have is with mealtime dosing. They often dose late, or they may not dose enough insulin for the carbohydrates. That’s where the issues are.

All these hybrid closed-loop systems, this one included, show that the best improvements in glycemia are overnight. I’m hoping that this one shows some nice improvements in daytime glycemia as well. Stay tuned and I’ll let you know once I’ve been using it.

Next, it has adjustable targets down to 100. This is the lowest target for any hybrid closed-loop system. It has an extended-wear infusion set that lasts for 7 days. This infusion set is already available but works with this new system.

Finally, it has a new sensor. It looks like the old sensors, but it’s the Guardian 4, which requires much fewer finger sticks. Now, I’m not entirely sure about how often one has to do a finger stick. I know one has to do with finger sticking to initiate auto mode, or what they call SmartGuard, but I don’t know whether you ever have to do it again. I know for sure that you have to do it again if you fall out of the automated mode into manual mode. Once you’re in SmartGuard, I believe there are no further finger-stick calibrations required.

If people are already on the 770G system, this is just a software update that is presumably easy to upgrade to the 780G. Now, the physical pieces ... If someone doesn’t already have the Guardian 4 sensor or the extended-wear infusion set, they’ll have to get those. The software update to make the 770G increase to the 780G should just come through the cloud. I don’t know when that’s going to happen.

I do know that preorders for this system, if you want to buy the new physical system, start on May 15. The shipping of the new 780G system should occur in the United States toward the end of this summer.

I’m so excited. I think this is really going to benefit my patients. I can’t wait to start using it and letting patients see how these algorithms work and how they really help patients improve their glucose control.

Anne L. Peters, MD, is a professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She reported conflicts of interest with Abbott Diabetes Care, Becton Dickinson, Boehringer Ingelheim, Eli Lilly, Lexicon Pharmaceuticals, Livongo, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, Zafgen, Dexcom, MannKind, and AstraZeneca.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

There is wonderful news in the field of hybrid closed-loop pump technology because the Medtronic 780G system was just approved. I can’t tell you how happy this makes me because we’ve all been waiting for this seemingly forever and ever. This isn’t just a small upgrade from the 770G. It’s a quantum leap from the 770G to the 780G. The 780G has newer algorithms, a new sensor, and a longer-lasting infusion set.

USC Westside Center for Diabetes

It’s been used since 2020 in Europe, so we have good data on how well it works. Frankly, I think it works really well. We’ve seen nice improvements in [hemoglobin] A1c, time in range, other glycemic metrics, and patient satisfaction in studies done in Europe.

Now, I’ve never had the system to use in one of my patients. I always say I never know a system until I see it in use in my own patients, but let me tell you what I’ve read.

First, it has something called meal-detection technology with autocorrection boluses every 5 minutes. If this works, it can be a huge win for our patients because the problem my patients have is with mealtime dosing. They often dose late, or they may not dose enough insulin for the carbohydrates. That’s where the issues are.

All these hybrid closed-loop systems, this one included, show that the best improvements in glycemia are overnight. I’m hoping that this one shows some nice improvements in daytime glycemia as well. Stay tuned and I’ll let you know once I’ve been using it.

Next, it has adjustable targets down to 100. This is the lowest target for any hybrid closed-loop system. It has an extended-wear infusion set that lasts for 7 days. This infusion set is already available but works with this new system.

Finally, it has a new sensor. It looks like the old sensors, but it’s the Guardian 4, which requires much fewer finger sticks. Now, I’m not entirely sure about how often one has to do a finger stick. I know one has to do with finger sticking to initiate auto mode, or what they call SmartGuard, but I don’t know whether you ever have to do it again. I know for sure that you have to do it again if you fall out of the automated mode into manual mode. Once you’re in SmartGuard, I believe there are no further finger-stick calibrations required.

If people are already on the 770G system, this is just a software update that is presumably easy to upgrade to the 780G. Now, the physical pieces ... If someone doesn’t already have the Guardian 4 sensor or the extended-wear infusion set, they’ll have to get those. The software update to make the 770G increase to the 780G should just come through the cloud. I don’t know when that’s going to happen.

I do know that preorders for this system, if you want to buy the new physical system, start on May 15. The shipping of the new 780G system should occur in the United States toward the end of this summer.

I’m so excited. I think this is really going to benefit my patients. I can’t wait to start using it and letting patients see how these algorithms work and how they really help patients improve their glucose control.

Anne L. Peters, MD, is a professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She reported conflicts of interest with Abbott Diabetes Care, Becton Dickinson, Boehringer Ingelheim, Eli Lilly, Lexicon Pharmaceuticals, Livongo, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, Zafgen, Dexcom, MannKind, and AstraZeneca.

A version of this article first appeared on Medscape.com.

Up to half of patients with type 2 diabetes report poor adherence to their non-insulin medications. In this ReCAP, Dr Anne Peters, director of the University of Southern California Clinical Diabetes Programs in Los Angeles, California, offers clinicians suggestions on how to get their patients to "buy in" to these treatments, many of which do not make them feel any better. Research shows that quality of life, short- and long-term clinical outcomes, and side effects are important factors in treatment adherence. Dr Peters explains that adherence may be improved if patients understand why they need to take a medication, how it might make them feel, what to do about it, and how taking it will fit into their daily pattern. She also points out that access and affordability of the medication regimen are additional factors for which patients may need support to increase treatment adherence.

--

Anne L. Peters, MD, Professor, Department of Clinical Medicine, Clinical Scholar, Keck School of Medicine of the University of Southern California; Director, USC Clinical Diabetes Programs, University of Southern California Westside Center for Diabetes, Los Angeles, California

Anne L. Peters, MD, has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or a trustee for: Blue Circle Health; Vertex; Abbott Diabetes Care Received research grant from: Abbott Diabetes Care; Insulet Stock options from: Teladoc; Omada Health

Up to half of patients with type 2 diabetes report poor adherence to their non-insulin medications. In this ReCAP, Dr Anne Peters, director of the University of Southern California Clinical Diabetes Programs in Los Angeles, California, offers clinicians suggestions on how to get their patients to "buy in" to these treatments, many of which do not make them feel any better. Research shows that quality of life, short- and long-term clinical outcomes, and side effects are important factors in treatment adherence. Dr Peters explains that adherence may be improved if patients understand why they need to take a medication, how it might make them feel, what to do about it, and how taking it will fit into their daily pattern. She also points out that access and affordability of the medication regimen are additional factors for which patients may need support to increase treatment adherence.

--

Anne L. Peters, MD, Professor, Department of Clinical Medicine, Clinical Scholar, Keck School of Medicine of the University of Southern California; Director, USC Clinical Diabetes Programs, University of Southern California Westside Center for Diabetes, Los Angeles, California

Anne L. Peters, MD, has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or a trustee for: Blue Circle Health; Vertex; Abbott Diabetes Care Received research grant from: Abbott Diabetes Care; Insulet Stock options from: Teladoc; Omada Health

Up to half of patients with type 2 diabetes report poor adherence to their non-insulin medications. In this ReCAP, Dr Anne Peters, director of the University of Southern California Clinical Diabetes Programs in Los Angeles, California, offers clinicians suggestions on how to get their patients to "buy in" to these treatments, many of which do not make them feel any better. Research shows that quality of life, short- and long-term clinical outcomes, and side effects are important factors in treatment adherence. Dr Peters explains that adherence may be improved if patients understand why they need to take a medication, how it might make them feel, what to do about it, and how taking it will fit into their daily pattern. She also points out that access and affordability of the medication regimen are additional factors for which patients may need support to increase treatment adherence.

--

Anne L. Peters, MD, Professor, Department of Clinical Medicine, Clinical Scholar, Keck School of Medicine of the University of Southern California; Director, USC Clinical Diabetes Programs, University of Southern California Westside Center for Diabetes, Los Angeles, California

Anne L. Peters, MD, has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or a trustee for: Blue Circle Health; Vertex; Abbott Diabetes Care Received research grant from: Abbott Diabetes Care; Insulet Stock options from: Teladoc; Omada Health

This transcript has been edited for clarity.

Last week, a number of patients emailed me regarding their concerns about this phenomenon known as Ozempic face. I went on to read about what this meant. I live in Los Angeles, where most people appear to be on semaglutide (Ozempic). It’s the phenomenon where people lose weight relatively rapidly, making their faces thin out. Then what happens, apparently, is they look older because their face is more wrinkled and baggier. They might have to have further plastic surgery. I say that with slight sarcasm because of where I live.

I want to talk about what I think about this, living here where there’s a great pressure to prescribe semaglutide off label, and what I think about it for my patients with diabetes.

Historically, we haven’t had much in terms of effective medication for treating obesity, and frankly, now we do. We now have agents that are effective, that have relatively few side effects, and that have become part of what’s out there. People now want to use these agents, semaglutide, and there’s been a great need for these agents.

The problem, however, is twofold. One, as we all know, is that it has basically caused a shortage of medication for treating our patients who actually have type 2 diabetes and really need these medications to manage their disease. Then we have people who want these medications who can’t pay for them. Insurance doesn’t cover obesity medications, which is problematic and actually quite frustrating for people who, I think, really would benefit from using these medications.

What I tell people, frankly, is that until I have enough supply for my patients with type 2 diabetes, who need these agents to control their blood sugars, I want to keep this class of drugs available to them. I also hope we’re able to expand it more and more with improving insurance coverage – and that’s a big if, if you ask me – both for people who have prediabetes and for patients who are overweight and obese, because I think it’s really hard for people to lose weight.

It’s frustrating, and for many people, being overweight and obese causes all sorts of other health issues, not only diabetes. I believe that these drugs are both safe and effective and should be more available. I do think we need to be careful in terms of who we prescribe them to, at least at the moment. Hopefully, we’ll be able to expand their use.

Anything that can encourage our population to lose weight and maintain that weight loss is very important. We need to couple weight loss medications with lifestyle interventions. I think people can out-eat any medication; therefore, it’s very important to encourage our patients to eat better, to exercise more, and to do all the other things they need to do to reduce their risks for other comorbidities.

I am incredibly happy to have these newer agents on the market. I tell my patients – at least those who have diabetes – that they have to accept looking a little bit too thin for the benefits that we can see in using these medications.

Thank you.

Dr. Peters is professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She has published more than 200 articles, reviews, and abstracts, and three books, on diabetes, and has been an investigator for more than 40 research studies. She has spoken internationally at over 400 programs and serves on many committees of several professional organizations. She has ties with Abbott Diabetes Care, AstraZeneca Becton Dickinson, Boehringer Ingelheim Pharmaceuticals, Dexcom, Eli Lilly, Lexicon Pharmaceuticals, Livongo, MannKind Corporation, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, and Zafgen. A version of this article originally appeared on Medscape.com.

This transcript has been edited for clarity.

Last week, a number of patients emailed me regarding their concerns about this phenomenon known as Ozempic face. I went on to read about what this meant. I live in Los Angeles, where most people appear to be on semaglutide (Ozempic). It’s the phenomenon where people lose weight relatively rapidly, making their faces thin out. Then what happens, apparently, is they look older because their face is more wrinkled and baggier. They might have to have further plastic surgery. I say that with slight sarcasm because of where I live.

I want to talk about what I think about this, living here where there’s a great pressure to prescribe semaglutide off label, and what I think about it for my patients with diabetes.

Historically, we haven’t had much in terms of effective medication for treating obesity, and frankly, now we do. We now have agents that are effective, that have relatively few side effects, and that have become part of what’s out there. People now want to use these agents, semaglutide, and there’s been a great need for these agents.

The problem, however, is twofold. One, as we all know, is that it has basically caused a shortage of medication for treating our patients who actually have type 2 diabetes and really need these medications to manage their disease. Then we have people who want these medications who can’t pay for them. Insurance doesn’t cover obesity medications, which is problematic and actually quite frustrating for people who, I think, really would benefit from using these medications.

What I tell people, frankly, is that until I have enough supply for my patients with type 2 diabetes, who need these agents to control their blood sugars, I want to keep this class of drugs available to them. I also hope we’re able to expand it more and more with improving insurance coverage – and that’s a big if, if you ask me – both for people who have prediabetes and for patients who are overweight and obese, because I think it’s really hard for people to lose weight.

It’s frustrating, and for many people, being overweight and obese causes all sorts of other health issues, not only diabetes. I believe that these drugs are both safe and effective and should be more available. I do think we need to be careful in terms of who we prescribe them to, at least at the moment. Hopefully, we’ll be able to expand their use.

Anything that can encourage our population to lose weight and maintain that weight loss is very important. We need to couple weight loss medications with lifestyle interventions. I think people can out-eat any medication; therefore, it’s very important to encourage our patients to eat better, to exercise more, and to do all the other things they need to do to reduce their risks for other comorbidities.

I am incredibly happy to have these newer agents on the market. I tell my patients – at least those who have diabetes – that they have to accept looking a little bit too thin for the benefits that we can see in using these medications.

Thank you.

Dr. Peters is professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She has published more than 200 articles, reviews, and abstracts, and three books, on diabetes, and has been an investigator for more than 40 research studies. She has spoken internationally at over 400 programs and serves on many committees of several professional organizations. She has ties with Abbott Diabetes Care, AstraZeneca Becton Dickinson, Boehringer Ingelheim Pharmaceuticals, Dexcom, Eli Lilly, Lexicon Pharmaceuticals, Livongo, MannKind Corporation, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, and Zafgen. A version of this article originally appeared on Medscape.com.

This transcript has been edited for clarity.

Last week, a number of patients emailed me regarding their concerns about this phenomenon known as Ozempic face. I went on to read about what this meant. I live in Los Angeles, where most people appear to be on semaglutide (Ozempic). It’s the phenomenon where people lose weight relatively rapidly, making their faces thin out. Then what happens, apparently, is they look older because their face is more wrinkled and baggier. They might have to have further plastic surgery. I say that with slight sarcasm because of where I live.

I want to talk about what I think about this, living here where there’s a great pressure to prescribe semaglutide off label, and what I think about it for my patients with diabetes.

Historically, we haven’t had much in terms of effective medication for treating obesity, and frankly, now we do. We now have agents that are effective, that have relatively few side effects, and that have become part of what’s out there. People now want to use these agents, semaglutide, and there’s been a great need for these agents.

The problem, however, is twofold. One, as we all know, is that it has basically caused a shortage of medication for treating our patients who actually have type 2 diabetes and really need these medications to manage their disease. Then we have people who want these medications who can’t pay for them. Insurance doesn’t cover obesity medications, which is problematic and actually quite frustrating for people who, I think, really would benefit from using these medications.

What I tell people, frankly, is that until I have enough supply for my patients with type 2 diabetes, who need these agents to control their blood sugars, I want to keep this class of drugs available to them. I also hope we’re able to expand it more and more with improving insurance coverage – and that’s a big if, if you ask me – both for people who have prediabetes and for patients who are overweight and obese, because I think it’s really hard for people to lose weight.

It’s frustrating, and for many people, being overweight and obese causes all sorts of other health issues, not only diabetes. I believe that these drugs are both safe and effective and should be more available. I do think we need to be careful in terms of who we prescribe them to, at least at the moment. Hopefully, we’ll be able to expand their use.

Anything that can encourage our population to lose weight and maintain that weight loss is very important. We need to couple weight loss medications with lifestyle interventions. I think people can out-eat any medication; therefore, it’s very important to encourage our patients to eat better, to exercise more, and to do all the other things they need to do to reduce their risks for other comorbidities.

I am incredibly happy to have these newer agents on the market. I tell my patients – at least those who have diabetes – that they have to accept looking a little bit too thin for the benefits that we can see in using these medications.

Thank you.

Dr. Peters is professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She has published more than 200 articles, reviews, and abstracts, and three books, on diabetes, and has been an investigator for more than 40 research studies. She has spoken internationally at over 400 programs and serves on many committees of several professional organizations. She has ties with Abbott Diabetes Care, AstraZeneca Becton Dickinson, Boehringer Ingelheim Pharmaceuticals, Dexcom, Eli Lilly, Lexicon Pharmaceuticals, Livongo, MannKind Corporation, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, and Zafgen. A version of this article originally appeared on Medscape.com.

This transcript has been edited for clarity.

Recently, there have been a series of published studies in the realm of cardiovascular disease that have changed certain beliefs we’ve held in the past. I’m going to review a few of these.

The first is the TIME study. The TIME study looked at whether it matters if you give antihypertensive agents in the morning or the evening. This was a prospective, pragmatic, parallel-group study that was performed in the U.K. and published in The Lancet.

Their question was whether evening dosing of antihypertensives has benefit in cardiovascular outcomes in adults. They enrolled over 21,000 people with hypertension who were taking at least one antihypertensive medication. Patients were randomized to morning or evening dosing.

The primary outcome was death or hospitalization due to myocardial infarction or stroke. There was no difference. It doesn’t matter if you take your antihypertensive agent in the morning or the evening. I think this is important because, clinically, the simpler the regimen for the patient, the greater the adherence, leading to better outcomes.

I know I can safely ask a patient when they would rather take their medicine. For many people, that may be the morning because they’re brushing their teeth and they remember. If they want to take it in the evening, that’s fine, too. We’re no longer slave to telling a patient to take their antihypertensive medications in the evening.

At the meeting of the American Society of Nephrology, results from a study on the use of renin-angiotensin system (RAS) inhibitors in advanced CKD was presented, called the STOP ACEi trial. Again, another interesting trial asking a simple question. This was a randomized controlled trial (RCT) in patients who had an estimated glomerular filtration rate (eGFR) less than 30, and they were randomized to stop or continue therapy with their RAS inhibitors.

The primary outcome was the eGFR at 3 years. They enrolled 411 patients with a median baseline eGFR of 18. At 3 years, there was no difference in the eGFR between the groups. In the discontinuation group, the eGFR was 12.6 versus 13.3 in the continuation group. There were no differences in complications or anything else. Their conclusion was that among patients with advanced and progressive CKD, the discontinuation of a RAS inhibitor was not associated with a significant difference in the long-term rate of decrease in eGFR.

I think this is important because it changes our paradigm a bit. You can stop the RAS inhibitor; reduce the need for excessive medication in these patients; and, hopefully, focus on some newer medications that have been shown to prevent the decline in eGFR that are now available.

Next is from a letter published in JAMA, which asks the following question: Is diabetes itself an equivalent cardiovascular risk factor to those who have had a prior cardiovascular event?

We used to put having diabetes in that same high-risk category as people who’d already had a cardiovascular disease event. Well, have we made that any different? These authors are from Canada, and they did a retrospective population-based study looking at administrative health claims from Ontario, Canada, to assess the association of diabetes and prior cardiovascular disease with cardiovascular events from 1994 to 2014.

What I think is kind of cool, because I’m a diabetologist, is that over time the magnitude of the association between diabetes and cardiovascular event rates decreased. In somebody with diabetes, they don’t have the same high risk that a person who’s already had a cardiovascular event rate does. Diabetes is less of a risk factor for cardiovascular disease than having established cardiovascular disease, which means we’re treating diabetes better and reducing the risk for cardiovascular disease.

If you look at people with diabetes and a prior cardiovascular event, that’s still the very highest risk. The risk of people having another event who have established cardiovascular disease is pretty flat. Those people didn’t get better and the people with preexisting diabetes and cardiovascular events at baseline didn’t get much better, but those who had diabetes alone did improve in terms of looking at cardiovascular event rates.

I think this is good news because diabetes itself isn’t as high a cardiovascular risk factor as we once thought. It doesn’t mean that it isn’t a cardiovascular risk factor, but I think we’ve done better at mitigating the risk.

Finally, there is a relatively small study that was presented at the American Heart Association and published in the Journal of the American College of Cardiology, which asks whether supplements that are often used to lower LDL cholesterol are equivalent to a statin.

They compared six supplements with a placebo and with rosuvastatin, and looked to see what happened. This is not an outcome study, but a very short study, at 28 days, that used a placebo. They included 190 people with no history of cardiovascular disease but an increased 10-year risk for sclerotic cardiovascular disease.

The agents studied were rosuvastatin, placebo, fish oil, cinnamon, garlic, turmeric, plant sterols, and red yeast rice. Well, not surprisingly, rosuvastatin worked. It showed a 35% reduction in LDL cholesterol, and there was no significant impact on cholesterol levels with any of the other agents. The supplements yielded a similar response, as did the placebo. Side effects were similar, but they were most common with plant sterols and red yeast rice.

Clearly, a statin is better if you want to lower cholesterol levels. My approach, when patients want to take supplements, is to tell them what I know factually, which basically is that they don’t really cause much in the way of LDL cholesterol lowering. If I think the supplement isn’t going to hurt someone, I don’t tell them not to use it. I certainly tell them that they need to use agents that we know can actually reduce cardiovascular risk.

I think these studies really go through the gamut of asking questions. When can we stop an agent? What time of day do we need to give an agent? What, really, is the risk for type 2 diabetes with regard to cardiovascular events? What’s the value of supplements?

I think this is interesting, because I really encourage researchers to ask and answer these kinds of questions because it helps us clinically decide what’s best for treating our patients.

Thank you.

Dr. Peters is a professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She reported conflicts of interest with numerous pharmaceutical companies.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Recently, there have been a series of published studies in the realm of cardiovascular disease that have changed certain beliefs we’ve held in the past. I’m going to review a few of these.

The first is the TIME study. The TIME study looked at whether it matters if you give antihypertensive agents in the morning or the evening. This was a prospective, pragmatic, parallel-group study that was performed in the U.K. and published in The Lancet.

Their question was whether evening dosing of antihypertensives has benefit in cardiovascular outcomes in adults. They enrolled over 21,000 people with hypertension who were taking at least one antihypertensive medication. Patients were randomized to morning or evening dosing.

The primary outcome was death or hospitalization due to myocardial infarction or stroke. There was no difference. It doesn’t matter if you take your antihypertensive agent in the morning or the evening. I think this is important because, clinically, the simpler the regimen for the patient, the greater the adherence, leading to better outcomes.

I know I can safely ask a patient when they would rather take their medicine. For many people, that may be the morning because they’re brushing their teeth and they remember. If they want to take it in the evening, that’s fine, too. We’re no longer slave to telling a patient to take their antihypertensive medications in the evening.

At the meeting of the American Society of Nephrology, results from a study on the use of renin-angiotensin system (RAS) inhibitors in advanced CKD was presented, called the STOP ACEi trial. Again, another interesting trial asking a simple question. This was a randomized controlled trial (RCT) in patients who had an estimated glomerular filtration rate (eGFR) less than 30, and they were randomized to stop or continue therapy with their RAS inhibitors.

The primary outcome was the eGFR at 3 years. They enrolled 411 patients with a median baseline eGFR of 18. At 3 years, there was no difference in the eGFR between the groups. In the discontinuation group, the eGFR was 12.6 versus 13.3 in the continuation group. There were no differences in complications or anything else. Their conclusion was that among patients with advanced and progressive CKD, the discontinuation of a RAS inhibitor was not associated with a significant difference in the long-term rate of decrease in eGFR.

I think this is important because it changes our paradigm a bit. You can stop the RAS inhibitor; reduce the need for excessive medication in these patients; and, hopefully, focus on some newer medications that have been shown to prevent the decline in eGFR that are now available.

Next is from a letter published in JAMA, which asks the following question: Is diabetes itself an equivalent cardiovascular risk factor to those who have had a prior cardiovascular event?

We used to put having diabetes in that same high-risk category as people who’d already had a cardiovascular disease event. Well, have we made that any different? These authors are from Canada, and they did a retrospective population-based study looking at administrative health claims from Ontario, Canada, to assess the association of diabetes and prior cardiovascular disease with cardiovascular events from 1994 to 2014.

What I think is kind of cool, because I’m a diabetologist, is that over time the magnitude of the association between diabetes and cardiovascular event rates decreased. In somebody with diabetes, they don’t have the same high risk that a person who’s already had a cardiovascular event rate does. Diabetes is less of a risk factor for cardiovascular disease than having established cardiovascular disease, which means we’re treating diabetes better and reducing the risk for cardiovascular disease.

If you look at people with diabetes and a prior cardiovascular event, that’s still the very highest risk. The risk of people having another event who have established cardiovascular disease is pretty flat. Those people didn’t get better and the people with preexisting diabetes and cardiovascular events at baseline didn’t get much better, but those who had diabetes alone did improve in terms of looking at cardiovascular event rates.

I think this is good news because diabetes itself isn’t as high a cardiovascular risk factor as we once thought. It doesn’t mean that it isn’t a cardiovascular risk factor, but I think we’ve done better at mitigating the risk.

Finally, there is a relatively small study that was presented at the American Heart Association and published in the Journal of the American College of Cardiology, which asks whether supplements that are often used to lower LDL cholesterol are equivalent to a statin.

They compared six supplements with a placebo and with rosuvastatin, and looked to see what happened. This is not an outcome study, but a very short study, at 28 days, that used a placebo. They included 190 people with no history of cardiovascular disease but an increased 10-year risk for sclerotic cardiovascular disease.

The agents studied were rosuvastatin, placebo, fish oil, cinnamon, garlic, turmeric, plant sterols, and red yeast rice. Well, not surprisingly, rosuvastatin worked. It showed a 35% reduction in LDL cholesterol, and there was no significant impact on cholesterol levels with any of the other agents. The supplements yielded a similar response, as did the placebo. Side effects were similar, but they were most common with plant sterols and red yeast rice.

Clearly, a statin is better if you want to lower cholesterol levels. My approach, when patients want to take supplements, is to tell them what I know factually, which basically is that they don’t really cause much in the way of LDL cholesterol lowering. If I think the supplement isn’t going to hurt someone, I don’t tell them not to use it. I certainly tell them that they need to use agents that we know can actually reduce cardiovascular risk.

I think these studies really go through the gamut of asking questions. When can we stop an agent? What time of day do we need to give an agent? What, really, is the risk for type 2 diabetes with regard to cardiovascular events? What’s the value of supplements?

I think this is interesting, because I really encourage researchers to ask and answer these kinds of questions because it helps us clinically decide what’s best for treating our patients.

Thank you.

Dr. Peters is a professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She reported conflicts of interest with numerous pharmaceutical companies.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Recently, there have been a series of published studies in the realm of cardiovascular disease that have changed certain beliefs we’ve held in the past. I’m going to review a few of these.

The first is the TIME study. The TIME study looked at whether it matters if you give antihypertensive agents in the morning or the evening. This was a prospective, pragmatic, parallel-group study that was performed in the U.K. and published in The Lancet.

Their question was whether evening dosing of antihypertensives has benefit in cardiovascular outcomes in adults. They enrolled over 21,000 people with hypertension who were taking at least one antihypertensive medication. Patients were randomized to morning or evening dosing.

The primary outcome was death or hospitalization due to myocardial infarction or stroke. There was no difference. It doesn’t matter if you take your antihypertensive agent in the morning or the evening. I think this is important because, clinically, the simpler the regimen for the patient, the greater the adherence, leading to better outcomes.

I know I can safely ask a patient when they would rather take their medicine. For many people, that may be the morning because they’re brushing their teeth and they remember. If they want to take it in the evening, that’s fine, too. We’re no longer slave to telling a patient to take their antihypertensive medications in the evening.

At the meeting of the American Society of Nephrology, results from a study on the use of renin-angiotensin system (RAS) inhibitors in advanced CKD was presented, called the STOP ACEi trial. Again, another interesting trial asking a simple question. This was a randomized controlled trial (RCT) in patients who had an estimated glomerular filtration rate (eGFR) less than 30, and they were randomized to stop or continue therapy with their RAS inhibitors.

The primary outcome was the eGFR at 3 years. They enrolled 411 patients with a median baseline eGFR of 18. At 3 years, there was no difference in the eGFR between the groups. In the discontinuation group, the eGFR was 12.6 versus 13.3 in the continuation group. There were no differences in complications or anything else. Their conclusion was that among patients with advanced and progressive CKD, the discontinuation of a RAS inhibitor was not associated with a significant difference in the long-term rate of decrease in eGFR.

I think this is important because it changes our paradigm a bit. You can stop the RAS inhibitor; reduce the need for excessive medication in these patients; and, hopefully, focus on some newer medications that have been shown to prevent the decline in eGFR that are now available.

Next is from a letter published in JAMA, which asks the following question: Is diabetes itself an equivalent cardiovascular risk factor to those who have had a prior cardiovascular event?

We used to put having diabetes in that same high-risk category as people who’d already had a cardiovascular disease event. Well, have we made that any different? These authors are from Canada, and they did a retrospective population-based study looking at administrative health claims from Ontario, Canada, to assess the association of diabetes and prior cardiovascular disease with cardiovascular events from 1994 to 2014.

What I think is kind of cool, because I’m a diabetologist, is that over time the magnitude of the association between diabetes and cardiovascular event rates decreased. In somebody with diabetes, they don’t have the same high risk that a person who’s already had a cardiovascular event rate does. Diabetes is less of a risk factor for cardiovascular disease than having established cardiovascular disease, which means we’re treating diabetes better and reducing the risk for cardiovascular disease.

If you look at people with diabetes and a prior cardiovascular event, that’s still the very highest risk. The risk of people having another event who have established cardiovascular disease is pretty flat. Those people didn’t get better and the people with preexisting diabetes and cardiovascular events at baseline didn’t get much better, but those who had diabetes alone did improve in terms of looking at cardiovascular event rates.

I think this is good news because diabetes itself isn’t as high a cardiovascular risk factor as we once thought. It doesn’t mean that it isn’t a cardiovascular risk factor, but I think we’ve done better at mitigating the risk.

Finally, there is a relatively small study that was presented at the American Heart Association and published in the Journal of the American College of Cardiology, which asks whether supplements that are often used to lower LDL cholesterol are equivalent to a statin.

They compared six supplements with a placebo and with rosuvastatin, and looked to see what happened. This is not an outcome study, but a very short study, at 28 days, that used a placebo. They included 190 people with no history of cardiovascular disease but an increased 10-year risk for sclerotic cardiovascular disease.

The agents studied were rosuvastatin, placebo, fish oil, cinnamon, garlic, turmeric, plant sterols, and red yeast rice. Well, not surprisingly, rosuvastatin worked. It showed a 35% reduction in LDL cholesterol, and there was no significant impact on cholesterol levels with any of the other agents. The supplements yielded a similar response, as did the placebo. Side effects were similar, but they were most common with plant sterols and red yeast rice.

Clearly, a statin is better if you want to lower cholesterol levels. My approach, when patients want to take supplements, is to tell them what I know factually, which basically is that they don’t really cause much in the way of LDL cholesterol lowering. If I think the supplement isn’t going to hurt someone, I don’t tell them not to use it. I certainly tell them that they need to use agents that we know can actually reduce cardiovascular risk.

I think these studies really go through the gamut of asking questions. When can we stop an agent? What time of day do we need to give an agent? What, really, is the risk for type 2 diabetes with regard to cardiovascular events? What’s the value of supplements?

I think this is interesting, because I really encourage researchers to ask and answer these kinds of questions because it helps us clinically decide what’s best for treating our patients.

Thank you.

Dr. Peters is a professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She reported conflicts of interest with numerous pharmaceutical companies.

A version of this article first appeared on Medscape.com.

Dr Anne Peters, of the Keck School of Medicine of the University of Southern California, reports on the latest guidelines and updates in glycemic control for persons with type 2 diabetes, as presented at the 2022 European Association for the Study of Diabetes (EASD).  

Dr Peters opens by reporting on the eagerly awaited joint ADA/EASD guidelines on the management of hyperglycemia in type 2 diabetes. The updated guidelines emphasize weight goals and holistic person-centered care as essential components of comprehensive management.  

Next, Dr Peters comments on the report of the 44-year UK Prospective Diabetes Study (UKPDS), which demonstrated the benefits of early intensive blood glucose control over decades. The study began tracking volunteers in 1977 and continued until 2021.  

Finally, Dr Peters reports on a real-world data study examining gender disparities in the time to initiation of cardioprotective glucose-lowering drugs in patients with type 2 diabetes and cardiovascular disease. The study showed that although the therapeutic initiation rate for woman and men is comparable after stroke and peripheral arterial disease, men are prescribed cardioprotective glucose-lowering drugs faster than women when diagnosed with heart failure or ischemic heart disease.  

--

Anne L. Peters, MD, Professor, Department of Clinical Medicine, Clinical Scholar, Keck School of Medicine of the University of Southern California; Director, USC Clinical Diabetes Programs, University of Southern California Westside Center for Diabetes, Los Angeles, California 

Anne L. Peters, MD, has disclosed the following relevant financial relationships:  

Serve(d) as a director, officer, partner, employee, advisor, consultant, or a trustee for: AstraZeneca; Lilly; NovoNordisk; Abbott; Vertex; Zealand; ShouTi 

Received research grant from: Insulet; Dexcom; Abbott  

Received income in an amount equal to or greater than $250 from: AstraZeneca; Lilly; NovoNordisk; Abbott; Vertex; Zealand; ShouTi; Insulet; Dexcom 

Stock options from: Teladoc; Omada Health (not even close to 5% equity) 

Dr Anne Peters, of the Keck School of Medicine of the University of Southern California, reports on the latest guidelines and updates in glycemic control for persons with type 2 diabetes, as presented at the 2022 European Association for the Study of Diabetes (EASD).  

Dr Peters opens by reporting on the eagerly awaited joint ADA/EASD guidelines on the management of hyperglycemia in type 2 diabetes. The updated guidelines emphasize weight goals and holistic person-centered care as essential components of comprehensive management.  

Next, Dr Peters comments on the report of the 44-year UK Prospective Diabetes Study (UKPDS), which demonstrated the benefits of early intensive blood glucose control over decades. The study began tracking volunteers in 1977 and continued until 2021.  

Finally, Dr Peters reports on a real-world data study examining gender disparities in the time to initiation of cardioprotective glucose-lowering drugs in patients with type 2 diabetes and cardiovascular disease. The study showed that although the therapeutic initiation rate for woman and men is comparable after stroke and peripheral arterial disease, men are prescribed cardioprotective glucose-lowering drugs faster than women when diagnosed with heart failure or ischemic heart disease.  

--

Anne L. Peters, MD, Professor, Department of Clinical Medicine, Clinical Scholar, Keck School of Medicine of the University of Southern California; Director, USC Clinical Diabetes Programs, University of Southern California Westside Center for Diabetes, Los Angeles, California 

Anne L. Peters, MD, has disclosed the following relevant financial relationships:  

Serve(d) as a director, officer, partner, employee, advisor, consultant, or a trustee for: AstraZeneca; Lilly; NovoNordisk; Abbott; Vertex; Zealand; ShouTi 

Received research grant from: Insulet; Dexcom; Abbott  

Received income in an amount equal to or greater than $250 from: AstraZeneca; Lilly; NovoNordisk; Abbott; Vertex; Zealand; ShouTi; Insulet; Dexcom 

Stock options from: Teladoc; Omada Health (not even close to 5% equity) 

Dr Anne Peters, of the Keck School of Medicine of the University of Southern California, reports on the latest guidelines and updates in glycemic control for persons with type 2 diabetes, as presented at the 2022 European Association for the Study of Diabetes (EASD).  

Dr Peters opens by reporting on the eagerly awaited joint ADA/EASD guidelines on the management of hyperglycemia in type 2 diabetes. The updated guidelines emphasize weight goals and holistic person-centered care as essential components of comprehensive management.  

Next, Dr Peters comments on the report of the 44-year UK Prospective Diabetes Study (UKPDS), which demonstrated the benefits of early intensive blood glucose control over decades. The study began tracking volunteers in 1977 and continued until 2021.  

Finally, Dr Peters reports on a real-world data study examining gender disparities in the time to initiation of cardioprotective glucose-lowering drugs in patients with type 2 diabetes and cardiovascular disease. The study showed that although the therapeutic initiation rate for woman and men is comparable after stroke and peripheral arterial disease, men are prescribed cardioprotective glucose-lowering drugs faster than women when diagnosed with heart failure or ischemic heart disease.  

--

Anne L. Peters, MD, Professor, Department of Clinical Medicine, Clinical Scholar, Keck School of Medicine of the University of Southern California; Director, USC Clinical Diabetes Programs, University of Southern California Westside Center for Diabetes, Los Angeles, California 

Anne L. Peters, MD, has disclosed the following relevant financial relationships:  

Serve(d) as a director, officer, partner, employee, advisor, consultant, or a trustee for: AstraZeneca; Lilly; NovoNordisk; Abbott; Vertex; Zealand; ShouTi 

Received research grant from: Insulet; Dexcom; Abbott  

Received income in an amount equal to or greater than $250 from: AstraZeneca; Lilly; NovoNordisk; Abbott; Vertex; Zealand; ShouTi; Insulet; Dexcom 

Stock options from: Teladoc; Omada Health (not even close to 5% equity) 

Dr Anne Peters, of the Keck School of Medicine of the University of Southern California, reports on the latest research on insulin therapy in adults with type 2 diabetes, presented at the European Association for the Study of Diabetes (EASD). 

Dr Peters highlights a clinical study evaluating whether bedtime is optimal for the administration of neutral protamine Hagedorn (NPH) insulin, also known as isophane insulin. The results indicate that titration of NPH plays an important role in avoiding nocturnal hypoglycemia.

Next, Dr Peters discusses the ONWARDS 2 study, a phase 3a trial looking at once-weekly insulin icodec vs once-daily insulin degludec in basal insulin–treated type 2 diabetes. The trial found insulin icodec to be superior to insulin degludec in reducing A1c.

Dr Peters also examines the SoliMix trial, which compared iGlarLixi once daily to twice-daily premix BIAsp 30 in suboptimally controlled type 2 diabetes. The trial evaluated whether patients currently on a basal-bolus regimen would have an equal or more effective response to once-a-day combination therapy. Results showed that iGlarLixi provided better glycemic control and weight benefit than the twice-daily BlAsp 30.

Finally, Dr Peters evaluates a study that looked at switching from a basal-bolus insulin treatment to insulin degludec + liraglutide combination. The combination proved at least as effective as the basal-bolus approach. 

--

Anne L. Peters, MD, Professor, Department of Clinical Medicine, Clinical Scholar, Keck School of Medicine of the University of Southern California; Director, USC Clinical Diabetes Programs, University of Southern California Westside Center for Diabetes, Los Angeles, California

Anne L. Peters, MD, has disclosed the following relevant financial relationships:

Serve(d) as a director, officer, partner, employee, advisor, consultant, or a trustee for: AstraZeneca; Lilly; NovoNordisk; Abbott; Vertex; Zealand; ShouTi

Received research grant from: Insulet; Dexcom; Abbott

Received income in an amount equal to or greater than $250 from: AstraZeneca; Lilly; NovoNordisk; Abbott; Vertex; Zealand; ShouTi; Insulet; Dexcom

Stock options from: Teladoc; Omada Health (not even close to 5% equity)

Dr Anne Peters, of the Keck School of Medicine of the University of Southern California, reports on the latest research on insulin therapy in adults with type 2 diabetes, presented at the European Association for the Study of Diabetes (EASD). 

Dr Peters highlights a clinical study evaluating whether bedtime is optimal for the administration of neutral protamine Hagedorn (NPH) insulin, also known as isophane insulin. The results indicate that titration of NPH plays an important role in avoiding nocturnal hypoglycemia.

Next, Dr Peters discusses the ONWARDS 2 study, a phase 3a trial looking at once-weekly insulin icodec vs once-daily insulin degludec in basal insulin–treated type 2 diabetes. The trial found insulin icodec to be superior to insulin degludec in reducing A1c.

Dr Peters also examines the SoliMix trial, which compared iGlarLixi once daily to twice-daily premix BIAsp 30 in suboptimally controlled type 2 diabetes. The trial evaluated whether patients currently on a basal-bolus regimen would have an equal or more effective response to once-a-day combination therapy. Results showed that iGlarLixi provided better glycemic control and weight benefit than the twice-daily BlAsp 30.

Finally, Dr Peters evaluates a study that looked at switching from a basal-bolus insulin treatment to insulin degludec + liraglutide combination. The combination proved at least as effective as the basal-bolus approach. 

--

Anne L. Peters, MD, Professor, Department of Clinical Medicine, Clinical Scholar, Keck School of Medicine of the University of Southern California; Director, USC Clinical Diabetes Programs, University of Southern California Westside Center for Diabetes, Los Angeles, California

Anne L. Peters, MD, has disclosed the following relevant financial relationships:

Serve(d) as a director, officer, partner, employee, advisor, consultant, or a trustee for: AstraZeneca; Lilly; NovoNordisk; Abbott; Vertex; Zealand; ShouTi

Received research grant from: Insulet; Dexcom; Abbott

Received income in an amount equal to or greater than $250 from: AstraZeneca; Lilly; NovoNordisk; Abbott; Vertex; Zealand; ShouTi; Insulet; Dexcom

Stock options from: Teladoc; Omada Health (not even close to 5% equity)

Dr Anne Peters, of the Keck School of Medicine of the University of Southern California, reports on the latest research on insulin therapy in adults with type 2 diabetes, presented at the European Association for the Study of Diabetes (EASD). 

Dr Peters highlights a clinical study evaluating whether bedtime is optimal for the administration of neutral protamine Hagedorn (NPH) insulin, also known as isophane insulin. The results indicate that titration of NPH plays an important role in avoiding nocturnal hypoglycemia.

Next, Dr Peters discusses the ONWARDS 2 study, a phase 3a trial looking at once-weekly insulin icodec vs once-daily insulin degludec in basal insulin–treated type 2 diabetes. The trial found insulin icodec to be superior to insulin degludec in reducing A1c.

Dr Peters also examines the SoliMix trial, which compared iGlarLixi once daily to twice-daily premix BIAsp 30 in suboptimally controlled type 2 diabetes. The trial evaluated whether patients currently on a basal-bolus regimen would have an equal or more effective response to once-a-day combination therapy. Results showed that iGlarLixi provided better glycemic control and weight benefit than the twice-daily BlAsp 30.

Finally, Dr Peters evaluates a study that looked at switching from a basal-bolus insulin treatment to insulin degludec + liraglutide combination. The combination proved at least as effective as the basal-bolus approach. 

--

Anne L. Peters, MD, Professor, Department of Clinical Medicine, Clinical Scholar, Keck School of Medicine of the University of Southern California; Director, USC Clinical Diabetes Programs, University of Southern California Westside Center for Diabetes, Los Angeles, California

Anne L. Peters, MD, has disclosed the following relevant financial relationships:

Serve(d) as a director, officer, partner, employee, advisor, consultant, or a trustee for: AstraZeneca; Lilly; NovoNordisk; Abbott; Vertex; Zealand; ShouTi

Received research grant from: Insulet; Dexcom; Abbott

Received income in an amount equal to or greater than $250 from: AstraZeneca; Lilly; NovoNordisk; Abbott; Vertex; Zealand; ShouTi; Insulet; Dexcom

Stock options from: Teladoc; Omada Health (not even close to 5% equity)

This transcript has been edited for clarity.

Today, I’m going to discuss the results of a new automated insulin delivery system that I think can really help many people with type 1 diabetes.

Dr. Steven Russell presented the results at the Advanced Technologies & Treatments for Diabetes meeting. The study focused on the iLet system, which is made by Beta Bionics and has been under development for a while. This was the single-hormone study, so it just looked at their algorithm using insulin alone. Eventually they’re going to study this, looking at the use of insulin plus glucagon together to see if that further improves outcomes.

One of the main reasons I think this study was so cool is because it included over 25% minority individuals who aren’t routinely studied in these insulin device trials. The study also included people who had a wide range of hemoglobin A1c levels; there was no high cut-point here. Over 30% of participants had an A1c greater than 8%. They also studied both children and adults and combined the results together.

Before I talk about the results, let me tell you about the pump. This is a tubed pump that has a sensor that it communicates with – it’s the Dexcom sensor – and it has an algorithm so it does automated insulin delivery. Instead of having to enter all sorts of information into the system, this thing requires that you put in only the patient’s weight. That’s it. From there, the system begins to figure out what the patient needs in terms of automated insulin delivery.

There are several different target settings that can be entered, and they can differ by time of day. There’s basically the time of day that one is eating a meal, so breakfast, lunch, or dinner, and there is the meal size, basically small, medium, and large. The individual enters this in real time so the system knows they’re eating, but other than that, the system just works.

It does this in a way that doesn’t allow for the individual using the pump to fidget with it. They can’t override the system and they can’t put in other insulin doses. The system is just there to take care of their diabetes.

They compared this system with people on any other system, including other automated insulin delivery systems, and put them into this trial. People were randomized to this system vs. whatever they’d been on (that was the control group) and they followed them for 13 weeks, which is not all that long.

There was a 0.5% reduction in A1c between the two groups. There was also an increase in the time in range, and this improvement in time in range happened almost immediately – within the first day or two of people being on the system. In terms of actual numbers, the adult patients started out with a time in range of 56% and this increased to 69% by the end of the study. The biggest improvement was time in range overnight, as is seen with other automated insulin delivery systems.

There was no reduction in time below a glucose level of 54 and there was an increase in the number of episodes of severe hypoglycemia in the group treated with the iLet system, but this was not statistically significant between the two groups.

I think these results are hard to compare with other pivotal trials investigating automated insulin delivery systems. The Tandem pivotal trial was a randomized controlled trial similar to this one, but the Medtronic and Omnipod studies were single-arm trials where patients were compared before and after they used the device.

More than anything, I think what’s important about this system is that it may allow for greater use of automated insulin delivery systems. It may allow primary care providers to use these systems without needing all sorts of support, and patients may be able to use these devices more simply than a device where they have to do carb counting and adjusting in ways that I think tend to be pretty complicated and require higher numeracy and literacy skills.

I couldn’t be happier. I love what they’re doing at Beta Bionics, and I look forward to more results, and in particular, to see if these results improve further when they do a study of insulin and glucagon in their dual-hormone pump system.

Thank you very much. This has been Dr Anne Peters for Medscape.
 

Dr. Peters is professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She has published more than 200 articles, reviews, and abstracts, and three books, on diabetes, and has been an investigator for more than 40 research studies. She has spoken internationally at over 400 programs and serves on many committees of several professional organizations. She disclosed ties with Abbott Diabetes Care, AstraZeneca, Becton Dickinson, Boehringer Ingelheim Pharmaceuticals, Dexcom, Eli Lilly, Lexicon Pharmaceuticals, Livongo, MannKind Corporation, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, and Zafgen.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Today, I’m going to discuss the results of a new automated insulin delivery system that I think can really help many people with type 1 diabetes.

Dr. Steven Russell presented the results at the Advanced Technologies & Treatments for Diabetes meeting. The study focused on the iLet system, which is made by Beta Bionics and has been under development for a while. This was the single-hormone study, so it just looked at their algorithm using insulin alone. Eventually they’re going to study this, looking at the use of insulin plus glucagon together to see if that further improves outcomes.

One of the main reasons I think this study was so cool is because it included over 25% minority individuals who aren’t routinely studied in these insulin device trials. The study also included people who had a wide range of hemoglobin A1c levels; there was no high cut-point here. Over 30% of participants had an A1c greater than 8%. They also studied both children and adults and combined the results together.

Before I talk about the results, let me tell you about the pump. This is a tubed pump that has a sensor that it communicates with – it’s the Dexcom sensor – and it has an algorithm so it does automated insulin delivery. Instead of having to enter all sorts of information into the system, this thing requires that you put in only the patient’s weight. That’s it. From there, the system begins to figure out what the patient needs in terms of automated insulin delivery.

There are several different target settings that can be entered, and they can differ by time of day. There’s basically the time of day that one is eating a meal, so breakfast, lunch, or dinner, and there is the meal size, basically small, medium, and large. The individual enters this in real time so the system knows they’re eating, but other than that, the system just works.

It does this in a way that doesn’t allow for the individual using the pump to fidget with it. They can’t override the system and they can’t put in other insulin doses. The system is just there to take care of their diabetes.

They compared this system with people on any other system, including other automated insulin delivery systems, and put them into this trial. People were randomized to this system vs. whatever they’d been on (that was the control group) and they followed them for 13 weeks, which is not all that long.

There was a 0.5% reduction in A1c between the two groups. There was also an increase in the time in range, and this improvement in time in range happened almost immediately – within the first day or two of people being on the system. In terms of actual numbers, the adult patients started out with a time in range of 56% and this increased to 69% by the end of the study. The biggest improvement was time in range overnight, as is seen with other automated insulin delivery systems.

There was no reduction in time below a glucose level of 54 and there was an increase in the number of episodes of severe hypoglycemia in the group treated with the iLet system, but this was not statistically significant between the two groups.

I think these results are hard to compare with other pivotal trials investigating automated insulin delivery systems. The Tandem pivotal trial was a randomized controlled trial similar to this one, but the Medtronic and Omnipod studies were single-arm trials where patients were compared before and after they used the device.

More than anything, I think what’s important about this system is that it may allow for greater use of automated insulin delivery systems. It may allow primary care providers to use these systems without needing all sorts of support, and patients may be able to use these devices more simply than a device where they have to do carb counting and adjusting in ways that I think tend to be pretty complicated and require higher numeracy and literacy skills.

I couldn’t be happier. I love what they’re doing at Beta Bionics, and I look forward to more results, and in particular, to see if these results improve further when they do a study of insulin and glucagon in their dual-hormone pump system.

Thank you very much. This has been Dr Anne Peters for Medscape.
 

Dr. Peters is professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She has published more than 200 articles, reviews, and abstracts, and three books, on diabetes, and has been an investigator for more than 40 research studies. She has spoken internationally at over 400 programs and serves on many committees of several professional organizations. She disclosed ties with Abbott Diabetes Care, AstraZeneca, Becton Dickinson, Boehringer Ingelheim Pharmaceuticals, Dexcom, Eli Lilly, Lexicon Pharmaceuticals, Livongo, MannKind Corporation, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, and Zafgen.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Today, I’m going to discuss the results of a new automated insulin delivery system that I think can really help many people with type 1 diabetes.

Dr. Steven Russell presented the results at the Advanced Technologies & Treatments for Diabetes meeting. The study focused on the iLet system, which is made by Beta Bionics and has been under development for a while. This was the single-hormone study, so it just looked at their algorithm using insulin alone. Eventually they’re going to study this, looking at the use of insulin plus glucagon together to see if that further improves outcomes.

One of the main reasons I think this study was so cool is because it included over 25% minority individuals who aren’t routinely studied in these insulin device trials. The study also included people who had a wide range of hemoglobin A1c levels; there was no high cut-point here. Over 30% of participants had an A1c greater than 8%. They also studied both children and adults and combined the results together.

Before I talk about the results, let me tell you about the pump. This is a tubed pump that has a sensor that it communicates with – it’s the Dexcom sensor – and it has an algorithm so it does automated insulin delivery. Instead of having to enter all sorts of information into the system, this thing requires that you put in only the patient’s weight. That’s it. From there, the system begins to figure out what the patient needs in terms of automated insulin delivery.

There are several different target settings that can be entered, and they can differ by time of day. There’s basically the time of day that one is eating a meal, so breakfast, lunch, or dinner, and there is the meal size, basically small, medium, and large. The individual enters this in real time so the system knows they’re eating, but other than that, the system just works.

It does this in a way that doesn’t allow for the individual using the pump to fidget with it. They can’t override the system and they can’t put in other insulin doses. The system is just there to take care of their diabetes.

They compared this system with people on any other system, including other automated insulin delivery systems, and put them into this trial. People were randomized to this system vs. whatever they’d been on (that was the control group) and they followed them for 13 weeks, which is not all that long.

There was a 0.5% reduction in A1c between the two groups. There was also an increase in the time in range, and this improvement in time in range happened almost immediately – within the first day or two of people being on the system. In terms of actual numbers, the adult patients started out with a time in range of 56% and this increased to 69% by the end of the study. The biggest improvement was time in range overnight, as is seen with other automated insulin delivery systems.

There was no reduction in time below a glucose level of 54 and there was an increase in the number of episodes of severe hypoglycemia in the group treated with the iLet system, but this was not statistically significant between the two groups.

I think these results are hard to compare with other pivotal trials investigating automated insulin delivery systems. The Tandem pivotal trial was a randomized controlled trial similar to this one, but the Medtronic and Omnipod studies were single-arm trials where patients were compared before and after they used the device.

More than anything, I think what’s important about this system is that it may allow for greater use of automated insulin delivery systems. It may allow primary care providers to use these systems without needing all sorts of support, and patients may be able to use these devices more simply than a device where they have to do carb counting and adjusting in ways that I think tend to be pretty complicated and require higher numeracy and literacy skills.

I couldn’t be happier. I love what they’re doing at Beta Bionics, and I look forward to more results, and in particular, to see if these results improve further when they do a study of insulin and glucagon in their dual-hormone pump system.

Thank you very much. This has been Dr Anne Peters for Medscape.
 

Dr. Peters is professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She has published more than 200 articles, reviews, and abstracts, and three books, on diabetes, and has been an investigator for more than 40 research studies. She has spoken internationally at over 400 programs and serves on many committees of several professional organizations. She disclosed ties with Abbott Diabetes Care, AstraZeneca, Becton Dickinson, Boehringer Ingelheim Pharmaceuticals, Dexcom, Eli Lilly, Lexicon Pharmaceuticals, Livongo, MannKind Corporation, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, and Zafgen.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Does having had a COVID-19 infection increase your risk for the development of diabetes subsequently? Some data say yes and other data say no. No matter what, it’s obviously important to screen people for diabetes routinely, pandemic or not. Remember, screening should start at age 35.

For over a decade, we have known that SARS-type viruses bind to beta cells. This could cause either direct damage to the beta cell or in some way trigger beta cell autoimmunity. We also know that COVID-19 infection increases the levels of inflammatory mediators, which could cause damage to beta cells and potentially to insulin receptors. There is a potential that having had a COVID-19 infection could increase rates of developing type 1 and/or type 2 diabetes.

However, there are other possible causes for people to develop diabetes after having a COVID-19 infection. A COVID-19 infection could cause one to seek medical care, unmasking latent type 1 and/or type 2 diabetes by causing infection-related insulin resistance and worsening preexisting mild hypoglycemia. In addition, people could have sought more medical care in the years since the pandemic has been ebbing, which may make it look like cases have increased.

For example, during the worst of the pandemic, I had multiple referrals for “COVID-19–caused new-onset diabetes” only to find that the patient had an A1c level above 10% and a history of mildly elevated blood glucose levels. This suggests to me that COVID-19 did not cause the diabetes per se but rather worsened an underlying glucose abnormality.

Since the pandemic has improved, I have also seen people diagnosed with type 2 diabetes that I think is associated with pandemic-related weight gain and inactivity.

The bigger issue is what is happening to people after COVID-19 infection who lack risk factors. What about those who we didn’t think were at high risk to get diabetes to begin with and didn’t have prediabetes?

An article by Xie and Al-Aly in The Lancet Diabetes & Endocrinology showed an increase in rates of diabetes in a large VA cohort among those who had a COVID-19 infection compared with both a contemporaneous control who did not have COVID-19 and a historical control. The researchers looked at the patient data 1 year after they’d had COVID-19, so it wasn’t the immediate post–COVID-19 phase but several months later.

They found that the risk for incident type 2 diabetes development was increased by 40% after adjusting for many risk factors. This included individuals who didn’t have traditional risk factors before they developed type 2 diabetes.

What does this mean clinically? First, pandemic or not, people need screening for diabetes and encouragement to have a healthy lifestyle. There may be an increased risk for the diagnosis of type 2 diabetes after COVID-19 infection due to a variety of different mechanisms.

As for people with type 1 diabetes, we also don’t know if having a COVID-19 infection increases their risk. We do know that there was an increase in the severity of diabetic ketoacidosis presentation during the pandemic, so we need to be sure that we reinforce sick-day rules with our patients with type 1 diabetes and that all individuals with type 1 diabetes have the ability to test their ketone levels at home.

In people with new-onset diabetes, whether type 1 or type 2, caused by COVID-19 or not, we need to treat appropriately based on their clinical situation.

Data from registries started during the pandemic will provide more definitive answers and help us find out if there is a relationship between having had COVID-19 infection and developing diabetes.

Perhaps that can help us better understand the mechanisms behind the development of diabetes overall.

Dr. Peters is professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She disclosed ties with Abbott Diabetes Care, AstraZeneca, Becton Dickinson, Boehringer Ingelheim Pharmaceuticals, Dexcom, Eli Lilly, Lexicon Pharmaceuticals, Livongo, MannKind Corporation, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, and Zafgen. A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Does having had a COVID-19 infection increase your risk for the development of diabetes subsequently? Some data say yes and other data say no. No matter what, it’s obviously important to screen people for diabetes routinely, pandemic or not. Remember, screening should start at age 35.

For over a decade, we have known that SARS-type viruses bind to beta cells. This could cause either direct damage to the beta cell or in some way trigger beta cell autoimmunity. We also know that COVID-19 infection increases the levels of inflammatory mediators, which could cause damage to beta cells and potentially to insulin receptors. There is a potential that having had a COVID-19 infection could increase rates of developing type 1 and/or type 2 diabetes.

However, there are other possible causes for people to develop diabetes after having a COVID-19 infection. A COVID-19 infection could cause one to seek medical care, unmasking latent type 1 and/or type 2 diabetes by causing infection-related insulin resistance and worsening preexisting mild hypoglycemia. In addition, people could have sought more medical care in the years since the pandemic has been ebbing, which may make it look like cases have increased.

For example, during the worst of the pandemic, I had multiple referrals for “COVID-19–caused new-onset diabetes” only to find that the patient had an A1c level above 10% and a history of mildly elevated blood glucose levels. This suggests to me that COVID-19 did not cause the diabetes per se but rather worsened an underlying glucose abnormality.

Since the pandemic has improved, I have also seen people diagnosed with type 2 diabetes that I think is associated with pandemic-related weight gain and inactivity.

The bigger issue is what is happening to people after COVID-19 infection who lack risk factors. What about those who we didn’t think were at high risk to get diabetes to begin with and didn’t have prediabetes?

An article by Xie and Al-Aly in The Lancet Diabetes & Endocrinology showed an increase in rates of diabetes in a large VA cohort among those who had a COVID-19 infection compared with both a contemporaneous control who did not have COVID-19 and a historical control. The researchers looked at the patient data 1 year after they’d had COVID-19, so it wasn’t the immediate post–COVID-19 phase but several months later.

They found that the risk for incident type 2 diabetes development was increased by 40% after adjusting for many risk factors. This included individuals who didn’t have traditional risk factors before they developed type 2 diabetes.

What does this mean clinically? First, pandemic or not, people need screening for diabetes and encouragement to have a healthy lifestyle. There may be an increased risk for the diagnosis of type 2 diabetes after COVID-19 infection due to a variety of different mechanisms.

As for people with type 1 diabetes, we also don’t know if having a COVID-19 infection increases their risk. We do know that there was an increase in the severity of diabetic ketoacidosis presentation during the pandemic, so we need to be sure that we reinforce sick-day rules with our patients with type 1 diabetes and that all individuals with type 1 diabetes have the ability to test their ketone levels at home.

In people with new-onset diabetes, whether type 1 or type 2, caused by COVID-19 or not, we need to treat appropriately based on their clinical situation.

Data from registries started during the pandemic will provide more definitive answers and help us find out if there is a relationship between having had COVID-19 infection and developing diabetes.

Perhaps that can help us better understand the mechanisms behind the development of diabetes overall.

Dr. Peters is professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She disclosed ties with Abbott Diabetes Care, AstraZeneca, Becton Dickinson, Boehringer Ingelheim Pharmaceuticals, Dexcom, Eli Lilly, Lexicon Pharmaceuticals, Livongo, MannKind Corporation, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, and Zafgen. A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Does having had a COVID-19 infection increase your risk for the development of diabetes subsequently? Some data say yes and other data say no. No matter what, it’s obviously important to screen people for diabetes routinely, pandemic or not. Remember, screening should start at age 35.

For over a decade, we have known that SARS-type viruses bind to beta cells. This could cause either direct damage to the beta cell or in some way trigger beta cell autoimmunity. We also know that COVID-19 infection increases the levels of inflammatory mediators, which could cause damage to beta cells and potentially to insulin receptors. There is a potential that having had a COVID-19 infection could increase rates of developing type 1 and/or type 2 diabetes.

However, there are other possible causes for people to develop diabetes after having a COVID-19 infection. A COVID-19 infection could cause one to seek medical care, unmasking latent type 1 and/or type 2 diabetes by causing infection-related insulin resistance and worsening preexisting mild hypoglycemia. In addition, people could have sought more medical care in the years since the pandemic has been ebbing, which may make it look like cases have increased.

For example, during the worst of the pandemic, I had multiple referrals for “COVID-19–caused new-onset diabetes” only to find that the patient had an A1c level above 10% and a history of mildly elevated blood glucose levels. This suggests to me that COVID-19 did not cause the diabetes per se but rather worsened an underlying glucose abnormality.

Since the pandemic has improved, I have also seen people diagnosed with type 2 diabetes that I think is associated with pandemic-related weight gain and inactivity.

The bigger issue is what is happening to people after COVID-19 infection who lack risk factors. What about those who we didn’t think were at high risk to get diabetes to begin with and didn’t have prediabetes?

An article by Xie and Al-Aly in The Lancet Diabetes & Endocrinology showed an increase in rates of diabetes in a large VA cohort among those who had a COVID-19 infection compared with both a contemporaneous control who did not have COVID-19 and a historical control. The researchers looked at the patient data 1 year after they’d had COVID-19, so it wasn’t the immediate post–COVID-19 phase but several months later.

They found that the risk for incident type 2 diabetes development was increased by 40% after adjusting for many risk factors. This included individuals who didn’t have traditional risk factors before they developed type 2 diabetes.

What does this mean clinically? First, pandemic or not, people need screening for diabetes and encouragement to have a healthy lifestyle. There may be an increased risk for the diagnosis of type 2 diabetes after COVID-19 infection due to a variety of different mechanisms.

As for people with type 1 diabetes, we also don’t know if having a COVID-19 infection increases their risk. We do know that there was an increase in the severity of diabetic ketoacidosis presentation during the pandemic, so we need to be sure that we reinforce sick-day rules with our patients with type 1 diabetes and that all individuals with type 1 diabetes have the ability to test their ketone levels at home.

In people with new-onset diabetes, whether type 1 or type 2, caused by COVID-19 or not, we need to treat appropriately based on their clinical situation.

Data from registries started during the pandemic will provide more definitive answers and help us find out if there is a relationship between having had COVID-19 infection and developing diabetes.

Perhaps that can help us better understand the mechanisms behind the development of diabetes overall.

Dr. Peters is professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She disclosed ties with Abbott Diabetes Care, AstraZeneca, Becton Dickinson, Boehringer Ingelheim Pharmaceuticals, Dexcom, Eli Lilly, Lexicon Pharmaceuticals, Livongo, MannKind Corporation, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, and Zafgen. A version of this article first appeared on Medscape.com.