MDedge Endocrinology

Lauren is a 45-year-old corporate lawyer who managed to excel in every aspect of her life, including parenting her three children while working full-time as a corporate lawyer. A math major at Harvard, she loves data.

Suffice it to say, given that I was treating her for a thyroid condition rather than diabetes, I was a little surprised when she requested I prescribe her a FreeStyle Libre (Abbott) monitor. She explained she was struggling to lose 10 pounds, and she thought continuous glucose monitoring (CGM) would help her determine which foods were impeding her weight loss journey. 

While I didn’t see much downside to acquiescing, I felt she had probably been spending too much time on Reddit. What information could CGM give someone without diabetes that couldn’t be gleaned from a food label? Nevertheless, Lauren filled the prescription and began her foray into this relatively uncharted world. When she returned for a follow-up visit several months later, I was shocked to see that she had lost her intended weight. With my tail between my legs, I decided to review the theories and science behind the use of CGM in patients without insulin resistance. 

Although it’s not rocket science, CGM can help patients through a “carrot and stick” approach to dieting. Lean proteins, nonstarchy vegetables, and monounsaturated fats such as nuts and avocado all support weight loss and tend to keep blood glucose levels stable. In contrast, foods known to cause weight gain (eg, sugary foods, refined starches, and processed foods) cause sugar spikes in real time. Similarly, large portion sizes are more likely to result in sugar spikes, and pairing proteins with carbohydrates minimizes blood glucose excursions. 

Though all of this is basic common sense, the constant feedback from a CGM device holds patients accountable for their food choices and helps with behavioral change. And because blood glucose is influenced by myriad factors including stress, genetics and metabolism, CGM can also potentially help create personal guidance for food choices. 

In addition, CGM can reveal the effect of poor sleep and stress on blood glucose levels, thereby encouraging healthier lifestyle choices. The data collected also may provide information on how different modalities of physical activity affect blood glucose levels. A recent study compared the effect of high-intensity interval training (HIIT) and continuous moderate-intensity exercise on postmeal blood glucose in overweight individuals without diabetes. CGM revealed that HIIT is more advantageous for preventing postmeal spikes. 

Although CGM appears to be a sophisticated form of cognitive-behavioral therapy, I do worry that the incessant stream of information can lead to worsening anxiety, obsessive compulsive behaviors, or restrictive eating tendencies. Still, thanks to Lauren, I now believe that real-time CGM may lead to behavior modification in food selection and physical activity. 
 

Dr. Messer, Clinical Assistant Professor, Mount Sinai School of Medicine; Associate Professor, Hofstra School of Medicine, New York, NY, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Lauren is a 45-year-old corporate lawyer who managed to excel in every aspect of her life, including parenting her three children while working full-time as a corporate lawyer. A math major at Harvard, she loves data.

Suffice it to say, given that I was treating her for a thyroid condition rather than diabetes, I was a little surprised when she requested I prescribe her a FreeStyle Libre (Abbott) monitor. She explained she was struggling to lose 10 pounds, and she thought continuous glucose monitoring (CGM) would help her determine which foods were impeding her weight loss journey. 

While I didn’t see much downside to acquiescing, I felt she had probably been spending too much time on Reddit. What information could CGM give someone without diabetes that couldn’t be gleaned from a food label? Nevertheless, Lauren filled the prescription and began her foray into this relatively uncharted world. When she returned for a follow-up visit several months later, I was shocked to see that she had lost her intended weight. With my tail between my legs, I decided to review the theories and science behind the use of CGM in patients without insulin resistance. 

Although it’s not rocket science, CGM can help patients through a “carrot and stick” approach to dieting. Lean proteins, nonstarchy vegetables, and monounsaturated fats such as nuts and avocado all support weight loss and tend to keep blood glucose levels stable. In contrast, foods known to cause weight gain (eg, sugary foods, refined starches, and processed foods) cause sugar spikes in real time. Similarly, large portion sizes are more likely to result in sugar spikes, and pairing proteins with carbohydrates minimizes blood glucose excursions. 

Though all of this is basic common sense, the constant feedback from a CGM device holds patients accountable for their food choices and helps with behavioral change. And because blood glucose is influenced by myriad factors including stress, genetics and metabolism, CGM can also potentially help create personal guidance for food choices. 

In addition, CGM can reveal the effect of poor sleep and stress on blood glucose levels, thereby encouraging healthier lifestyle choices. The data collected also may provide information on how different modalities of physical activity affect blood glucose levels. A recent study compared the effect of high-intensity interval training (HIIT) and continuous moderate-intensity exercise on postmeal blood glucose in overweight individuals without diabetes. CGM revealed that HIIT is more advantageous for preventing postmeal spikes. 

Although CGM appears to be a sophisticated form of cognitive-behavioral therapy, I do worry that the incessant stream of information can lead to worsening anxiety, obsessive compulsive behaviors, or restrictive eating tendencies. Still, thanks to Lauren, I now believe that real-time CGM may lead to behavior modification in food selection and physical activity. 
 

Dr. Messer, Clinical Assistant Professor, Mount Sinai School of Medicine; Associate Professor, Hofstra School of Medicine, New York, NY, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Lauren is a 45-year-old corporate lawyer who managed to excel in every aspect of her life, including parenting her three children while working full-time as a corporate lawyer. A math major at Harvard, she loves data.

Suffice it to say, given that I was treating her for a thyroid condition rather than diabetes, I was a little surprised when she requested I prescribe her a FreeStyle Libre (Abbott) monitor. She explained she was struggling to lose 10 pounds, and she thought continuous glucose monitoring (CGM) would help her determine which foods were impeding her weight loss journey. 

While I didn’t see much downside to acquiescing, I felt she had probably been spending too much time on Reddit. What information could CGM give someone without diabetes that couldn’t be gleaned from a food label? Nevertheless, Lauren filled the prescription and began her foray into this relatively uncharted world. When she returned for a follow-up visit several months later, I was shocked to see that she had lost her intended weight. With my tail between my legs, I decided to review the theories and science behind the use of CGM in patients without insulin resistance. 

Although it’s not rocket science, CGM can help patients through a “carrot and stick” approach to dieting. Lean proteins, nonstarchy vegetables, and monounsaturated fats such as nuts and avocado all support weight loss and tend to keep blood glucose levels stable. In contrast, foods known to cause weight gain (eg, sugary foods, refined starches, and processed foods) cause sugar spikes in real time. Similarly, large portion sizes are more likely to result in sugar spikes, and pairing proteins with carbohydrates minimizes blood glucose excursions. 

Though all of this is basic common sense, the constant feedback from a CGM device holds patients accountable for their food choices and helps with behavioral change. And because blood glucose is influenced by myriad factors including stress, genetics and metabolism, CGM can also potentially help create personal guidance for food choices. 

In addition, CGM can reveal the effect of poor sleep and stress on blood glucose levels, thereby encouraging healthier lifestyle choices. The data collected also may provide information on how different modalities of physical activity affect blood glucose levels. A recent study compared the effect of high-intensity interval training (HIIT) and continuous moderate-intensity exercise on postmeal blood glucose in overweight individuals without diabetes. CGM revealed that HIIT is more advantageous for preventing postmeal spikes. 

Although CGM appears to be a sophisticated form of cognitive-behavioral therapy, I do worry that the incessant stream of information can lead to worsening anxiety, obsessive compulsive behaviors, or restrictive eating tendencies. Still, thanks to Lauren, I now believe that real-time CGM may lead to behavior modification in food selection and physical activity. 
 

Dr. Messer, Clinical Assistant Professor, Mount Sinai School of Medicine; Associate Professor, Hofstra School of Medicine, New York, NY, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

When prescribing glucagon-like peptide 1 (GLP-1) medications, many physicians prefer tirzepatide over the more well-known semaglutide due to its superior efficacy in weight loss and A1c reduction. Studies indicated that tirzepatide can lead to greater weight loss than semaglutide.

Factors like insurance coverage, drug availability, and side effects also influence physicians’ choices, with some patients benefiting from the broader dosing options that tirzepatide offers.

In this Q&A, Medscape Medical News explored how physicians can make the best decisions with their patients when choosing between GLP-1 medications tirzepatide and semaglutide for the treatment for type 2 diabetes and obesity.

We spoke to physicians who specialize in medical weight loss on things to consider when choosing between these two medications, such as patient profiles, drug access and availability, and financial considerations. We also discussed the side effect profiles of the medications based on current data in the literature.
 

Medscape Medical News: How are you deciding which of the two drugs to prescribe?

Caroline Messer, MD, endocrinologist at Lenox Hill Hospital, Northwell, New York City: To some degree, it’s based on insurance. But in general, I’m pushing most patients toward tirzepatide just because the data show that there’s more weight loss and more A1c reduction on tirzepatide. But the research shows that there are more side effects. But I think every practicing clinician who uses these medications knows that there are actually fewer side effects despite what the trial showed.

Sue Decotiis, MD, weight loss doctor, New York City: I think that many doctors that are prescribing these drugs are not really weight loss specialists. It’s just like one of many drugs that they prescribe. And semaglutide (Ozempic) is more well known. I think it’s because they don’t really know that it’s not as good as the other drugs. There are still massive shortages of these drugs. So that’s another reason why a doctor may choose one drug over another. Also, if a patient’s reliant on insurance to cover it, they may go with whatever the insurance company is willing to cover.

Kathleen Dungan, MD, professor of internal medicine, Division of Endocrinology, Diabetes and Metabolism, The Ohio State University Wexner Medical Center and College of Medicine: Some patients may have preferences with the delivery device. In the past year, in particular, availability of these drugs was limited and varied from time to time and geographically, and therefore, patients needed to substitute one drug for another in order to maintain treatment.

Maria Teresa Anton, MD, endocrinologist and educator, Pritikin Longevity Center, Miami: While I do not prescribe these medications, I do focus on integrating them into a comprehensive lifestyle program that empowers patients to make sustainable changes. By fostering an environment of education and support, we enhance their well-being and promote long-term health outcomes. In my practice, I’ve found that the most successful outcomes occur when these medications are combined with a comprehensive approach, including dietary changes, physical activity, and behavioral support.
 

Medscape Medical News: How do you make the decision of tirzepatide vs semaglutide?

Messer: There’s no guideline per se. Sometimes when I don’t want a patient to lose too much weight, I might consider Ozempic or Wegovy if you know they only have 5 lb to lose. If diabetes, then I might go for the Ozempic instead, just because the weight loss is so drastic with tirzepatide with any kind of appetite.

Decotiis: If somebody has a lot of weight to lose and they’re highly insulin resistant, as most people are when they start these drugs, I really prefer tirzepatide ... because I think patients are going to lose more weight, they’re going to lose more fat. I also see that patients have less side effects because before tirzepatide came out, I was prescribing mostly semaglutide, and there were a lot of side effects. But semaglutide is fine. I mean, it’s a good drug. Maybe it’s better for people that don’t have as much weight to lose. So I don’t have to worry about them hitting that wall after a certain period of time. But it’s a good drug. I mean, I certainly still use it.
 

Medscape Medical News: What of the data and the literature on the differences in the outcomes and the side effect profile?

Messer: In terms of outcomes, the weight loss is almost double [with tirzepatide]. It depends what trial you’re looking at, but we tend to see like about 15% of your body weight you lose with the semaglutide and 25%-30% with the tirzepatide. The big difference, I suppose…is semaglutide now has a cardiovascular indication and the tirzepatide doesn’t, but I’m very confident that tirzepatide is going to get the same indication.

Decotiis: When that first Lilly study came out in June of 2022, it really blew everybody away. I mean, some patients lost up to 25% of their weight on tirzepatide, whereas on Ozempic, it was really like 15%. Now, in my practice, I really monitor everyone with a body composition scale. I’m not just looking at somebody’s weight or body mass index, I am looking at how much body fat they have, how much muscle mass they have, how much water they have, and how much bone they have.

The golden rule here is make sure the patient loses fat, and you want to make sure they’re not losing muscle or too much water. The patient really needs to be adequately hydrated. So what I’m saying is a lot of people who have lost weight have not reached the promised land because they haven’t lost enough body fat to get them into that healthy zone. But once they reduce the body fat to a certain percentage, let’s say for a woman about 20%, or a man in the low teens, they’re less likely to regain that weight because they haven’t really lost fat. And that’s how we gain health.
 

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

When prescribing glucagon-like peptide 1 (GLP-1) medications, many physicians prefer tirzepatide over the more well-known semaglutide due to its superior efficacy in weight loss and A1c reduction. Studies indicated that tirzepatide can lead to greater weight loss than semaglutide.

Factors like insurance coverage, drug availability, and side effects also influence physicians’ choices, with some patients benefiting from the broader dosing options that tirzepatide offers.

In this Q&A, Medscape Medical News explored how physicians can make the best decisions with their patients when choosing between GLP-1 medications tirzepatide and semaglutide for the treatment for type 2 diabetes and obesity.

We spoke to physicians who specialize in medical weight loss on things to consider when choosing between these two medications, such as patient profiles, drug access and availability, and financial considerations. We also discussed the side effect profiles of the medications based on current data in the literature.
 

Medscape Medical News: How are you deciding which of the two drugs to prescribe?

Caroline Messer, MD, endocrinologist at Lenox Hill Hospital, Northwell, New York City: To some degree, it’s based on insurance. But in general, I’m pushing most patients toward tirzepatide just because the data show that there’s more weight loss and more A1c reduction on tirzepatide. But the research shows that there are more side effects. But I think every practicing clinician who uses these medications knows that there are actually fewer side effects despite what the trial showed.

Sue Decotiis, MD, weight loss doctor, New York City: I think that many doctors that are prescribing these drugs are not really weight loss specialists. It’s just like one of many drugs that they prescribe. And semaglutide (Ozempic) is more well known. I think it’s because they don’t really know that it’s not as good as the other drugs. There are still massive shortages of these drugs. So that’s another reason why a doctor may choose one drug over another. Also, if a patient’s reliant on insurance to cover it, they may go with whatever the insurance company is willing to cover.

Kathleen Dungan, MD, professor of internal medicine, Division of Endocrinology, Diabetes and Metabolism, The Ohio State University Wexner Medical Center and College of Medicine: Some patients may have preferences with the delivery device. In the past year, in particular, availability of these drugs was limited and varied from time to time and geographically, and therefore, patients needed to substitute one drug for another in order to maintain treatment.

Maria Teresa Anton, MD, endocrinologist and educator, Pritikin Longevity Center, Miami: While I do not prescribe these medications, I do focus on integrating them into a comprehensive lifestyle program that empowers patients to make sustainable changes. By fostering an environment of education and support, we enhance their well-being and promote long-term health outcomes. In my practice, I’ve found that the most successful outcomes occur when these medications are combined with a comprehensive approach, including dietary changes, physical activity, and behavioral support.
 

Medscape Medical News: How do you make the decision of tirzepatide vs semaglutide?

Messer: There’s no guideline per se. Sometimes when I don’t want a patient to lose too much weight, I might consider Ozempic or Wegovy if you know they only have 5 lb to lose. If diabetes, then I might go for the Ozempic instead, just because the weight loss is so drastic with tirzepatide with any kind of appetite.

Decotiis: If somebody has a lot of weight to lose and they’re highly insulin resistant, as most people are when they start these drugs, I really prefer tirzepatide ... because I think patients are going to lose more weight, they’re going to lose more fat. I also see that patients have less side effects because before tirzepatide came out, I was prescribing mostly semaglutide, and there were a lot of side effects. But semaglutide is fine. I mean, it’s a good drug. Maybe it’s better for people that don’t have as much weight to lose. So I don’t have to worry about them hitting that wall after a certain period of time. But it’s a good drug. I mean, I certainly still use it.
 

Medscape Medical News: What of the data and the literature on the differences in the outcomes and the side effect profile?

Messer: In terms of outcomes, the weight loss is almost double [with tirzepatide]. It depends what trial you’re looking at, but we tend to see like about 15% of your body weight you lose with the semaglutide and 25%-30% with the tirzepatide. The big difference, I suppose…is semaglutide now has a cardiovascular indication and the tirzepatide doesn’t, but I’m very confident that tirzepatide is going to get the same indication.

Decotiis: When that first Lilly study came out in June of 2022, it really blew everybody away. I mean, some patients lost up to 25% of their weight on tirzepatide, whereas on Ozempic, it was really like 15%. Now, in my practice, I really monitor everyone with a body composition scale. I’m not just looking at somebody’s weight or body mass index, I am looking at how much body fat they have, how much muscle mass they have, how much water they have, and how much bone they have.

The golden rule here is make sure the patient loses fat, and you want to make sure they’re not losing muscle or too much water. The patient really needs to be adequately hydrated. So what I’m saying is a lot of people who have lost weight have not reached the promised land because they haven’t lost enough body fat to get them into that healthy zone. But once they reduce the body fat to a certain percentage, let’s say for a woman about 20%, or a man in the low teens, they’re less likely to regain that weight because they haven’t really lost fat. And that’s how we gain health.
 

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

When prescribing glucagon-like peptide 1 (GLP-1) medications, many physicians prefer tirzepatide over the more well-known semaglutide due to its superior efficacy in weight loss and A1c reduction. Studies indicated that tirzepatide can lead to greater weight loss than semaglutide.

Factors like insurance coverage, drug availability, and side effects also influence physicians’ choices, with some patients benefiting from the broader dosing options that tirzepatide offers.

In this Q&A, Medscape Medical News explored how physicians can make the best decisions with their patients when choosing between GLP-1 medications tirzepatide and semaglutide for the treatment for type 2 diabetes and obesity.

We spoke to physicians who specialize in medical weight loss on things to consider when choosing between these two medications, such as patient profiles, drug access and availability, and financial considerations. We also discussed the side effect profiles of the medications based on current data in the literature.
 

Medscape Medical News: How are you deciding which of the two drugs to prescribe?

Caroline Messer, MD, endocrinologist at Lenox Hill Hospital, Northwell, New York City: To some degree, it’s based on insurance. But in general, I’m pushing most patients toward tirzepatide just because the data show that there’s more weight loss and more A1c reduction on tirzepatide. But the research shows that there are more side effects. But I think every practicing clinician who uses these medications knows that there are actually fewer side effects despite what the trial showed.

Sue Decotiis, MD, weight loss doctor, New York City: I think that many doctors that are prescribing these drugs are not really weight loss specialists. It’s just like one of many drugs that they prescribe. And semaglutide (Ozempic) is more well known. I think it’s because they don’t really know that it’s not as good as the other drugs. There are still massive shortages of these drugs. So that’s another reason why a doctor may choose one drug over another. Also, if a patient’s reliant on insurance to cover it, they may go with whatever the insurance company is willing to cover.

Kathleen Dungan, MD, professor of internal medicine, Division of Endocrinology, Diabetes and Metabolism, The Ohio State University Wexner Medical Center and College of Medicine: Some patients may have preferences with the delivery device. In the past year, in particular, availability of these drugs was limited and varied from time to time and geographically, and therefore, patients needed to substitute one drug for another in order to maintain treatment.

Maria Teresa Anton, MD, endocrinologist and educator, Pritikin Longevity Center, Miami: While I do not prescribe these medications, I do focus on integrating them into a comprehensive lifestyle program that empowers patients to make sustainable changes. By fostering an environment of education and support, we enhance their well-being and promote long-term health outcomes. In my practice, I’ve found that the most successful outcomes occur when these medications are combined with a comprehensive approach, including dietary changes, physical activity, and behavioral support.
 

Medscape Medical News: How do you make the decision of tirzepatide vs semaglutide?

Messer: There’s no guideline per se. Sometimes when I don’t want a patient to lose too much weight, I might consider Ozempic or Wegovy if you know they only have 5 lb to lose. If diabetes, then I might go for the Ozempic instead, just because the weight loss is so drastic with tirzepatide with any kind of appetite.

Decotiis: If somebody has a lot of weight to lose and they’re highly insulin resistant, as most people are when they start these drugs, I really prefer tirzepatide ... because I think patients are going to lose more weight, they’re going to lose more fat. I also see that patients have less side effects because before tirzepatide came out, I was prescribing mostly semaglutide, and there were a lot of side effects. But semaglutide is fine. I mean, it’s a good drug. Maybe it’s better for people that don’t have as much weight to lose. So I don’t have to worry about them hitting that wall after a certain period of time. But it’s a good drug. I mean, I certainly still use it.
 

Medscape Medical News: What of the data and the literature on the differences in the outcomes and the side effect profile?

Messer: In terms of outcomes, the weight loss is almost double [with tirzepatide]. It depends what trial you’re looking at, but we tend to see like about 15% of your body weight you lose with the semaglutide and 25%-30% with the tirzepatide. The big difference, I suppose…is semaglutide now has a cardiovascular indication and the tirzepatide doesn’t, but I’m very confident that tirzepatide is going to get the same indication.

Decotiis: When that first Lilly study came out in June of 2022, it really blew everybody away. I mean, some patients lost up to 25% of their weight on tirzepatide, whereas on Ozempic, it was really like 15%. Now, in my practice, I really monitor everyone with a body composition scale. I’m not just looking at somebody’s weight or body mass index, I am looking at how much body fat they have, how much muscle mass they have, how much water they have, and how much bone they have.

The golden rule here is make sure the patient loses fat, and you want to make sure they’re not losing muscle or too much water. The patient really needs to be adequately hydrated. So what I’m saying is a lot of people who have lost weight have not reached the promised land because they haven’t lost enough body fat to get them into that healthy zone. But once they reduce the body fat to a certain percentage, let’s say for a woman about 20%, or a man in the low teens, they’re less likely to regain that weight because they haven’t really lost fat. And that’s how we gain health.
 

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

This transcript has been edited for clarity.

Rachel S. Rubin, MD: I’m Dr. Rachel Rubin, a urologist and sexual medicine specialist in the Washington, DC, area. And I am so thrilled because my co-fellow, the brilliant and famous Dr. Ashley Winter, a board-certified urologist and a certified menopause practitioner, who sees patients in our practice from Los Angeles, is joining us today to talk about sex as a vital sign.

Ashley Winter, MD: To have the best sexual function, you need many different systems to work. You need your hormones to be in the right place. You need your blood vessels to dilate when you want them to. You need your nerves to connect to your genitalia to make them responsive. The way people say, “The eyes are the window into the soul” — well, the genitals are the window into the cardiovascular system, the peripheral nervous system, and the hormonal system. It’s so dynamic. Patients can understand how this reflects their health. We just need healthcare providers to hammer home how those things connect.

Rubin: If you’re a primary care doctor seeing a patient and you want to educate them on diabetes or high blood pressure, how can you “ ‘sell it with ‘sex”? How can you use sex to educate them about these important medical conditions?

Winter: I hate using it as a fear tactic, but sometimes you have to. Time and again, I’ve seen men with severe profound erectile dysfunction at a young age, with chronically uncontrolled diabetes.

Diabetes can impair the peripheral nerves, resulting in peripheral neuropathy. The same way that it can affect the fingers and toes, diabetes can affect the penis, even before those other areas. Diabetes can also lead to other conditions such as low testosterone, which also affects the function of the penis.

I’m being brutally honest when I tell patients that diabetes control is critical to having a wonderful sexspan — the duration of your life where you’re able to be sexually active and have great sex and do it in the way that you want.

Chronic conditions such as high cholesterol or hypertension can affect your ability to become erect or aroused whether you have a penis or a vulva, and even your ability to have an orgasm.

Rubin: None of my doctors has ever asked me about these issues. But we have to bring them up with patients because they›re not going to bring them up to us. I always say in the review of systems, we shouldn›t just ask, “Do you have any sexual problems?” (which nobody ever does) and move past the question about men, women or both. We should be asking, “Do you have any issues with libido? Do you want to talk about it? Any issues with erection, arousal, orgasm, or sexual pain?”

When you can talk about those things, you can treat the patient from a whole physiologic perspective. For example, how does their sciatica affect their sexual pain? How does their antidepressant cause a delayed orgasm? How does their low testosterone level affect their energy level, their libido, and their desire? 

We see so much shame and guilt in sexual health, to the extent that patients feel broken. We can help them understand the anatomy and physiology and explain that they aren’t broken. Instead, it’s “You need this medicine for your crippling anxiety, and that’s why your orgasm is delayed, and so can we augment it or add or subtract something to help you with it.”

Winter: In a primary care setting, where we are considering the patient›s overall health, we strive for medication compliance, but a huge part of medication noncompliance is sexual side effects, whether it›s antidepressants, beta-blockers, birth control, or this new world of GLP-1 agonists.

Rubin: I would add breast cancer treatments. Many patients go off their anastrozole or their tamoxifen because of the sexual side effects. 

Winter: This is where we get to the crux of this discussion about sex being a vital sign — something you need to check routinely. We need to become comfortable with it, because then we are unlocking the ability to treat every patient like a whole person, give them better outcomes, improve their compliance, and have a really powerful tool for education.

Rubin: We have a growing toolbox for all genders when it comes to sexual health. We have FDA- approved medications for low libido in women. We use testosterone in men in an evidence-based way to safely improve libido. We use medications to help with the genitourinary syndrome of menopause. Orgasm is a challenging one, but we have devices that can help with those reflexes. And working with people who specialize in sexual pain can be extremely helpful for patients.

Dr. Winter, having practiced in different settings, what would you tell the primary care doctors who don’t want to talk about libido or who minimize sexual complaints because they don’t know how to navigate them?

Winter: I do not envy the challenge of being a primary care provider in the healthcare world we are living in. I think it is the hardest job. The ultimate takeaway is to just normalize the conversation and be able to validate what is happening. Have a few basic tools, and then have referrals. It›s not that you have to have all the time in the world or you have to treat every condition, but you have to start the conversation, be comfortable with it, and then get patients hooked up with the right resources.

Rubin: Every doctor of every kind can connect with patients and try to understand what they care about. What are their goals? What do they want for their families, for their relationships, for their quality of life? And how can we work collaboratively as a team to help them with those things? 

Sex is a huge part of people’s lives. If we don’t ask about it; if we don’t look into it; and if we don’t admit that our physiology, our medications, and our surgeries can affect sexual health and functioning, how can we improve people’s lives? We can do so much as a team when we consider sex as a true vital sign.
 

Dr. Rubin, Assistant Clinical Professor, Department of Urology, Georgetown University, Washington, DC, has disclosed ties with Maternal Medical, Absorption Pharmaceuticals, GlaxoSmithKline, and Endo.

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

This transcript has been edited for clarity.

Rachel S. Rubin, MD: I’m Dr. Rachel Rubin, a urologist and sexual medicine specialist in the Washington, DC, area. And I am so thrilled because my co-fellow, the brilliant and famous Dr. Ashley Winter, a board-certified urologist and a certified menopause practitioner, who sees patients in our practice from Los Angeles, is joining us today to talk about sex as a vital sign.

Ashley Winter, MD: To have the best sexual function, you need many different systems to work. You need your hormones to be in the right place. You need your blood vessels to dilate when you want them to. You need your nerves to connect to your genitalia to make them responsive. The way people say, “The eyes are the window into the soul” — well, the genitals are the window into the cardiovascular system, the peripheral nervous system, and the hormonal system. It’s so dynamic. Patients can understand how this reflects their health. We just need healthcare providers to hammer home how those things connect.

Rubin: If you’re a primary care doctor seeing a patient and you want to educate them on diabetes or high blood pressure, how can you “ ‘sell it with ‘sex”? How can you use sex to educate them about these important medical conditions?

Winter: I hate using it as a fear tactic, but sometimes you have to. Time and again, I’ve seen men with severe profound erectile dysfunction at a young age, with chronically uncontrolled diabetes.

Diabetes can impair the peripheral nerves, resulting in peripheral neuropathy. The same way that it can affect the fingers and toes, diabetes can affect the penis, even before those other areas. Diabetes can also lead to other conditions such as low testosterone, which also affects the function of the penis.

I’m being brutally honest when I tell patients that diabetes control is critical to having a wonderful sexspan — the duration of your life where you’re able to be sexually active and have great sex and do it in the way that you want.

Chronic conditions such as high cholesterol or hypertension can affect your ability to become erect or aroused whether you have a penis or a vulva, and even your ability to have an orgasm.

Rubin: None of my doctors has ever asked me about these issues. But we have to bring them up with patients because they›re not going to bring them up to us. I always say in the review of systems, we shouldn›t just ask, “Do you have any sexual problems?” (which nobody ever does) and move past the question about men, women or both. We should be asking, “Do you have any issues with libido? Do you want to talk about it? Any issues with erection, arousal, orgasm, or sexual pain?”

When you can talk about those things, you can treat the patient from a whole physiologic perspective. For example, how does their sciatica affect their sexual pain? How does their antidepressant cause a delayed orgasm? How does their low testosterone level affect their energy level, their libido, and their desire? 

We see so much shame and guilt in sexual health, to the extent that patients feel broken. We can help them understand the anatomy and physiology and explain that they aren’t broken. Instead, it’s “You need this medicine for your crippling anxiety, and that’s why your orgasm is delayed, and so can we augment it or add or subtract something to help you with it.”

Winter: In a primary care setting, where we are considering the patient›s overall health, we strive for medication compliance, but a huge part of medication noncompliance is sexual side effects, whether it›s antidepressants, beta-blockers, birth control, or this new world of GLP-1 agonists.

Rubin: I would add breast cancer treatments. Many patients go off their anastrozole or their tamoxifen because of the sexual side effects. 

Winter: This is where we get to the crux of this discussion about sex being a vital sign — something you need to check routinely. We need to become comfortable with it, because then we are unlocking the ability to treat every patient like a whole person, give them better outcomes, improve their compliance, and have a really powerful tool for education.

Rubin: We have a growing toolbox for all genders when it comes to sexual health. We have FDA- approved medications for low libido in women. We use testosterone in men in an evidence-based way to safely improve libido. We use medications to help with the genitourinary syndrome of menopause. Orgasm is a challenging one, but we have devices that can help with those reflexes. And working with people who specialize in sexual pain can be extremely helpful for patients.

Dr. Winter, having practiced in different settings, what would you tell the primary care doctors who don’t want to talk about libido or who minimize sexual complaints because they don’t know how to navigate them?

Winter: I do not envy the challenge of being a primary care provider in the healthcare world we are living in. I think it is the hardest job. The ultimate takeaway is to just normalize the conversation and be able to validate what is happening. Have a few basic tools, and then have referrals. It›s not that you have to have all the time in the world or you have to treat every condition, but you have to start the conversation, be comfortable with it, and then get patients hooked up with the right resources.

Rubin: Every doctor of every kind can connect with patients and try to understand what they care about. What are their goals? What do they want for their families, for their relationships, for their quality of life? And how can we work collaboratively as a team to help them with those things? 

Sex is a huge part of people’s lives. If we don’t ask about it; if we don’t look into it; and if we don’t admit that our physiology, our medications, and our surgeries can affect sexual health and functioning, how can we improve people’s lives? We can do so much as a team when we consider sex as a true vital sign.
 

Dr. Rubin, Assistant Clinical Professor, Department of Urology, Georgetown University, Washington, DC, has disclosed ties with Maternal Medical, Absorption Pharmaceuticals, GlaxoSmithKline, and Endo.

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

This transcript has been edited for clarity.

Rachel S. Rubin, MD: I’m Dr. Rachel Rubin, a urologist and sexual medicine specialist in the Washington, DC, area. And I am so thrilled because my co-fellow, the brilliant and famous Dr. Ashley Winter, a board-certified urologist and a certified menopause practitioner, who sees patients in our practice from Los Angeles, is joining us today to talk about sex as a vital sign.

Ashley Winter, MD: To have the best sexual function, you need many different systems to work. You need your hormones to be in the right place. You need your blood vessels to dilate when you want them to. You need your nerves to connect to your genitalia to make them responsive. The way people say, “The eyes are the window into the soul” — well, the genitals are the window into the cardiovascular system, the peripheral nervous system, and the hormonal system. It’s so dynamic. Patients can understand how this reflects their health. We just need healthcare providers to hammer home how those things connect.

Rubin: If you’re a primary care doctor seeing a patient and you want to educate them on diabetes or high blood pressure, how can you “ ‘sell it with ‘sex”? How can you use sex to educate them about these important medical conditions?

Winter: I hate using it as a fear tactic, but sometimes you have to. Time and again, I’ve seen men with severe profound erectile dysfunction at a young age, with chronically uncontrolled diabetes.

Diabetes can impair the peripheral nerves, resulting in peripheral neuropathy. The same way that it can affect the fingers and toes, diabetes can affect the penis, even before those other areas. Diabetes can also lead to other conditions such as low testosterone, which also affects the function of the penis.

I’m being brutally honest when I tell patients that diabetes control is critical to having a wonderful sexspan — the duration of your life where you’re able to be sexually active and have great sex and do it in the way that you want.

Chronic conditions such as high cholesterol or hypertension can affect your ability to become erect or aroused whether you have a penis or a vulva, and even your ability to have an orgasm.

Rubin: None of my doctors has ever asked me about these issues. But we have to bring them up with patients because they›re not going to bring them up to us. I always say in the review of systems, we shouldn›t just ask, “Do you have any sexual problems?” (which nobody ever does) and move past the question about men, women or both. We should be asking, “Do you have any issues with libido? Do you want to talk about it? Any issues with erection, arousal, orgasm, or sexual pain?”

When you can talk about those things, you can treat the patient from a whole physiologic perspective. For example, how does their sciatica affect their sexual pain? How does their antidepressant cause a delayed orgasm? How does their low testosterone level affect their energy level, their libido, and their desire? 

We see so much shame and guilt in sexual health, to the extent that patients feel broken. We can help them understand the anatomy and physiology and explain that they aren’t broken. Instead, it’s “You need this medicine for your crippling anxiety, and that’s why your orgasm is delayed, and so can we augment it or add or subtract something to help you with it.”

Winter: In a primary care setting, where we are considering the patient›s overall health, we strive for medication compliance, but a huge part of medication noncompliance is sexual side effects, whether it›s antidepressants, beta-blockers, birth control, or this new world of GLP-1 agonists.

Rubin: I would add breast cancer treatments. Many patients go off their anastrozole or their tamoxifen because of the sexual side effects. 

Winter: This is where we get to the crux of this discussion about sex being a vital sign — something you need to check routinely. We need to become comfortable with it, because then we are unlocking the ability to treat every patient like a whole person, give them better outcomes, improve their compliance, and have a really powerful tool for education.

Rubin: We have a growing toolbox for all genders when it comes to sexual health. We have FDA- approved medications for low libido in women. We use testosterone in men in an evidence-based way to safely improve libido. We use medications to help with the genitourinary syndrome of menopause. Orgasm is a challenging one, but we have devices that can help with those reflexes. And working with people who specialize in sexual pain can be extremely helpful for patients.

Dr. Winter, having practiced in different settings, what would you tell the primary care doctors who don’t want to talk about libido or who minimize sexual complaints because they don’t know how to navigate them?

Winter: I do not envy the challenge of being a primary care provider in the healthcare world we are living in. I think it is the hardest job. The ultimate takeaway is to just normalize the conversation and be able to validate what is happening. Have a few basic tools, and then have referrals. It›s not that you have to have all the time in the world or you have to treat every condition, but you have to start the conversation, be comfortable with it, and then get patients hooked up with the right resources.

Rubin: Every doctor of every kind can connect with patients and try to understand what they care about. What are their goals? What do they want for their families, for their relationships, for their quality of life? And how can we work collaboratively as a team to help them with those things? 

Sex is a huge part of people’s lives. If we don’t ask about it; if we don’t look into it; and if we don’t admit that our physiology, our medications, and our surgeries can affect sexual health and functioning, how can we improve people’s lives? We can do so much as a team when we consider sex as a true vital sign.
 

Dr. Rubin, Assistant Clinical Professor, Department of Urology, Georgetown University, Washington, DC, has disclosed ties with Maternal Medical, Absorption Pharmaceuticals, GlaxoSmithKline, and Endo.

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

TOPLINE:

Adolescent girls with polycystic ovary syndrome (PCOS) have an increased risk for hypertension, according to a new study which underscores the importance of blood pressure surveillance in this population.

METHODOLOGY:

• The retrospective cohort study examined the association between PCOS and hypertension in adolescent girls within a diverse community-based US healthcare population.
• The researchers analyzed data from 224,418 adolescent girls (mean age at index visit, 14.9 years; 15.8% classified as having obesity) who had a well-child visit between 2013 and 2019, during which their systolic blood pressure and diastolic blood pressure were measured.
• Blood pressure in the hypertensive range was classified using the 2017 American Academy of Pediatrics Practice Guideline, with thresholds of 130/80 mm Hg or greater.

TAKEAWAY:

• The proportion of adolescent girls with high blood pressure was significantly greater among those with PCOS than among those without the condition (18.2% vs 7.1%; P < .001).
• Adolescent girls with PCOS had a 25% higher risk for hypertension than those without the disorder (adjusted odds ratio [aOR], 1.25; 95% CI, 1.10-1.42).
• Similarly, adolescent girls with obesity and PCOS had a 23% higher risk for high blood pressure than those without PCOS (aOR, 1.23; 95% CI, 1.06-1.42).

IN PRACTICE:

“The high prevalence of [hypertension] associated with PCOS emphasizes the key role of early [blood pressure] monitoring in this high-risk group,” the authors of the study wrote.

SOURCE:

The study was led by Sherry Zhang, MD, Kaiser Permanente Oakland Medical Center, Oakland, California, and was published online in the American Journal of Preventive Medicine.

LIMITATIONS:

The study relied on coded diagnoses of PCOS from clinical settings, which may have led to detection and referral biases. The findings may not be generalizable to an unselected population in which adolescent girls are systematically screened for both PCOS and hypertension.

DISCLOSURES:

This study was funded by the Cardiovascular and Metabolic Conditions Research Section and the Biostatistical Consulting Unit at the Division of Research, Kaiser Permanente Northern California and by the Kaiser Permanente Northern California Community Health Program. The authors declared having no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Adolescent girls with polycystic ovary syndrome (PCOS) have an increased risk for hypertension, according to a new study which underscores the importance of blood pressure surveillance in this population.

METHODOLOGY:

• The retrospective cohort study examined the association between PCOS and hypertension in adolescent girls within a diverse community-based US healthcare population.
• The researchers analyzed data from 224,418 adolescent girls (mean age at index visit, 14.9 years; 15.8% classified as having obesity) who had a well-child visit between 2013 and 2019, during which their systolic blood pressure and diastolic blood pressure were measured.
• Blood pressure in the hypertensive range was classified using the 2017 American Academy of Pediatrics Practice Guideline, with thresholds of 130/80 mm Hg or greater.

TAKEAWAY:

• The proportion of adolescent girls with high blood pressure was significantly greater among those with PCOS than among those without the condition (18.2% vs 7.1%; P < .001).
• Adolescent girls with PCOS had a 25% higher risk for hypertension than those without the disorder (adjusted odds ratio [aOR], 1.25; 95% CI, 1.10-1.42).
• Similarly, adolescent girls with obesity and PCOS had a 23% higher risk for high blood pressure than those without PCOS (aOR, 1.23; 95% CI, 1.06-1.42).

IN PRACTICE:

“The high prevalence of [hypertension] associated with PCOS emphasizes the key role of early [blood pressure] monitoring in this high-risk group,” the authors of the study wrote.

SOURCE:

The study was led by Sherry Zhang, MD, Kaiser Permanente Oakland Medical Center, Oakland, California, and was published online in the American Journal of Preventive Medicine.

LIMITATIONS:

The study relied on coded diagnoses of PCOS from clinical settings, which may have led to detection and referral biases. The findings may not be generalizable to an unselected population in which adolescent girls are systematically screened for both PCOS and hypertension.

DISCLOSURES:

This study was funded by the Cardiovascular and Metabolic Conditions Research Section and the Biostatistical Consulting Unit at the Division of Research, Kaiser Permanente Northern California and by the Kaiser Permanente Northern California Community Health Program. The authors declared having no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Adolescent girls with polycystic ovary syndrome (PCOS) have an increased risk for hypertension, according to a new study which underscores the importance of blood pressure surveillance in this population.

METHODOLOGY:

• The retrospective cohort study examined the association between PCOS and hypertension in adolescent girls within a diverse community-based US healthcare population.
• The researchers analyzed data from 224,418 adolescent girls (mean age at index visit, 14.9 years; 15.8% classified as having obesity) who had a well-child visit between 2013 and 2019, during which their systolic blood pressure and diastolic blood pressure were measured.
• Blood pressure in the hypertensive range was classified using the 2017 American Academy of Pediatrics Practice Guideline, with thresholds of 130/80 mm Hg or greater.

TAKEAWAY:

• The proportion of adolescent girls with high blood pressure was significantly greater among those with PCOS than among those without the condition (18.2% vs 7.1%; P < .001).
• Adolescent girls with PCOS had a 25% higher risk for hypertension than those without the disorder (adjusted odds ratio [aOR], 1.25; 95% CI, 1.10-1.42).
• Similarly, adolescent girls with obesity and PCOS had a 23% higher risk for high blood pressure than those without PCOS (aOR, 1.23; 95% CI, 1.06-1.42).

IN PRACTICE:

“The high prevalence of [hypertension] associated with PCOS emphasizes the key role of early [blood pressure] monitoring in this high-risk group,” the authors of the study wrote.

SOURCE:

The study was led by Sherry Zhang, MD, Kaiser Permanente Oakland Medical Center, Oakland, California, and was published online in the American Journal of Preventive Medicine.

LIMITATIONS:

The study relied on coded diagnoses of PCOS from clinical settings, which may have led to detection and referral biases. The findings may not be generalizable to an unselected population in which adolescent girls are systematically screened for both PCOS and hypertension.

DISCLOSURES:

This study was funded by the Cardiovascular and Metabolic Conditions Research Section and the Biostatistical Consulting Unit at the Division of Research, Kaiser Permanente Northern California and by the Kaiser Permanente Northern California Community Health Program. The authors declared having no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity. 

What do we do if we don’t like patients? We take the Hippocratic Oath as young students in Glasgow. We do that just before our graduation ceremony; we hold our hands up and repeat the Hippocratic Oath: “First, do no harm,” and so on.

What happens if we intensely dislike a patient? Is it possible to offer them the very best care? I was thinking back over a long career. I’ve been a cancer doctor for 40 years and I quite like saying that.

I can only think genuinely over a couple of times in which I’ve acted reflexively when a patient has done something awful. The couple of times it happened, it was just terrible racist comments to junior doctors who were with me. Extraordinarily dreadful things such as, “I don’t want to be touched by ...” or something of that sort.

Without really thinking about it, you react as a normal citizen and say, “That’s absolutely awful. Apologize immediately or leave the consultation room, and never ever come back again.” 

I remember that it happened once in Glasgow and once when I was a young professor in Birmingham, and it’s just an automatic gut reaction. The patient got a fright, and I immediately apologized and groveled around. In that relationship, we hold all the power, don’t we? Rather than being gentle about it, I was genuinely angry because of these ridiculous comments. 

Otherwise, I think most of the doctor-patient relationships are predicated on nonromantic love. I think patients want us to love them as one would a son, mother, father, or daughter, because if we do, then we will do better for them and we’ll pull out all the stops. “Placebo” means “I will please.” I think in the vast majority of cases, at least in our National Health Service (NHS), patients come with trust and a sense of wanting to build that relationship. That may be changing, but not for me. 

What about putting the boot on the other foot? What if the patients don’t like us rather than vice versa? As part of our accreditation appraisal process, from time to time we have to take patient surveys as to whether the patients felt that, after they had been seen in a consultation, they were treated with dignity, the quality of information given was appropriate, and they were treated with kindness. 

It’s an excellent exercise. Without bragging about it, patients objectively, according to these measures, appreciate the service that I give. It’s like getting five-star reviews on Trustpilot, or whatever these things are, that allow you to review car salesmen and so on. I have always had five-star reviews across the board. 

That, again, I thought was just a feature of that relationship, of patients wanting to please. These are patients who had been treated, who were in the outpatient department, who were in the midst of battle. Still, the scores are very high. I speak to my colleagues and that’s not uniformly the case. Patients actually do use these feedback forms, I think in a positive rather than negative way, reflecting back on the way that they were treated.

It has caused some of my colleagues to think quite hard about their personal style and approach to patients. That sense of feedback is important. 

What about losing trust? If that’s at the heart of everything that we do, then what would be an objective measure of losing trust? Again, in our healthcare system, it has been exceedingly unusual for a patient to request a second opinion. Now, that’s changing. The government is trying to change it. Leaders of the NHS are trying to change it so that patients feel assured that they can seek second opinions.

Again, in all the years I’ve been a cancer doctor, it has been incredibly infrequent that somebody has sought a second opinion after I’ve said something. That may be a measure of trust. Again, I’ve lived through an NHS in which seeking second opinions was something of a rarity. 

I’d be really interested to see what you think. In your own sphere of healthcare practice, is it possible for us to look after patients that we don’t like, or should we be honest and say, “I don’t like you. Our relationship has broken down. I want you to be seen by a colleague,” or “I want you to be nursed by somebody else”?

Has that happened? Is that something that you think is common or may become more common? What about when trust breaks down the other way? Can you think of instances in which the relationship, for whatever reason, just didn’t work and the patient had to move on because of that loss of trust and what underpinned it? I’d be really interested to know. 

I seek to be informed rather than the other way around. Can we truly look after patients that we don’t like or can we rise above it as Hippocrates might have done? 

Thanks for listening, as always. For the time being, over and out.

Dr. Kerr, Professor, Nuffield Department of Clinical Laboratory Science, University of Oxford; Professor of Cancer Medicine, Oxford Cancer Centre, Oxford, United Kingdom, disclosed ties with Celleron Therapeutics, Oxford Cancer Biomarkers, Afrox, GlaxoSmithKline, Bayer HealthCare Pharmaceuticals, Genomic Health, Merck Serono, and Roche.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

What do we do if we don’t like patients? We take the Hippocratic Oath as young students in Glasgow. We do that just before our graduation ceremony; we hold our hands up and repeat the Hippocratic Oath: “First, do no harm,” and so on.

What happens if we intensely dislike a patient? Is it possible to offer them the very best care? I was thinking back over a long career. I’ve been a cancer doctor for 40 years and I quite like saying that.

I can only think genuinely over a couple of times in which I’ve acted reflexively when a patient has done something awful. The couple of times it happened, it was just terrible racist comments to junior doctors who were with me. Extraordinarily dreadful things such as, “I don’t want to be touched by ...” or something of that sort.

Without really thinking about it, you react as a normal citizen and say, “That’s absolutely awful. Apologize immediately or leave the consultation room, and never ever come back again.” 

I remember that it happened once in Glasgow and once when I was a young professor in Birmingham, and it’s just an automatic gut reaction. The patient got a fright, and I immediately apologized and groveled around. In that relationship, we hold all the power, don’t we? Rather than being gentle about it, I was genuinely angry because of these ridiculous comments. 

Otherwise, I think most of the doctor-patient relationships are predicated on nonromantic love. I think patients want us to love them as one would a son, mother, father, or daughter, because if we do, then we will do better for them and we’ll pull out all the stops. “Placebo” means “I will please.” I think in the vast majority of cases, at least in our National Health Service (NHS), patients come with trust and a sense of wanting to build that relationship. That may be changing, but not for me. 

What about putting the boot on the other foot? What if the patients don’t like us rather than vice versa? As part of our accreditation appraisal process, from time to time we have to take patient surveys as to whether the patients felt that, after they had been seen in a consultation, they were treated with dignity, the quality of information given was appropriate, and they were treated with kindness. 

It’s an excellent exercise. Without bragging about it, patients objectively, according to these measures, appreciate the service that I give. It’s like getting five-star reviews on Trustpilot, or whatever these things are, that allow you to review car salesmen and so on. I have always had five-star reviews across the board. 

That, again, I thought was just a feature of that relationship, of patients wanting to please. These are patients who had been treated, who were in the outpatient department, who were in the midst of battle. Still, the scores are very high. I speak to my colleagues and that’s not uniformly the case. Patients actually do use these feedback forms, I think in a positive rather than negative way, reflecting back on the way that they were treated.

It has caused some of my colleagues to think quite hard about their personal style and approach to patients. That sense of feedback is important. 

What about losing trust? If that’s at the heart of everything that we do, then what would be an objective measure of losing trust? Again, in our healthcare system, it has been exceedingly unusual for a patient to request a second opinion. Now, that’s changing. The government is trying to change it. Leaders of the NHS are trying to change it so that patients feel assured that they can seek second opinions.

Again, in all the years I’ve been a cancer doctor, it has been incredibly infrequent that somebody has sought a second opinion after I’ve said something. That may be a measure of trust. Again, I’ve lived through an NHS in which seeking second opinions was something of a rarity. 

I’d be really interested to see what you think. In your own sphere of healthcare practice, is it possible for us to look after patients that we don’t like, or should we be honest and say, “I don’t like you. Our relationship has broken down. I want you to be seen by a colleague,” or “I want you to be nursed by somebody else”?

Has that happened? Is that something that you think is common or may become more common? What about when trust breaks down the other way? Can you think of instances in which the relationship, for whatever reason, just didn’t work and the patient had to move on because of that loss of trust and what underpinned it? I’d be really interested to know. 

I seek to be informed rather than the other way around. Can we truly look after patients that we don’t like or can we rise above it as Hippocrates might have done? 

Thanks for listening, as always. For the time being, over and out.

Dr. Kerr, Professor, Nuffield Department of Clinical Laboratory Science, University of Oxford; Professor of Cancer Medicine, Oxford Cancer Centre, Oxford, United Kingdom, disclosed ties with Celleron Therapeutics, Oxford Cancer Biomarkers, Afrox, GlaxoSmithKline, Bayer HealthCare Pharmaceuticals, Genomic Health, Merck Serono, and Roche.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

What do we do if we don’t like patients? We take the Hippocratic Oath as young students in Glasgow. We do that just before our graduation ceremony; we hold our hands up and repeat the Hippocratic Oath: “First, do no harm,” and so on.

What happens if we intensely dislike a patient? Is it possible to offer them the very best care? I was thinking back over a long career. I’ve been a cancer doctor for 40 years and I quite like saying that.

I can only think genuinely over a couple of times in which I’ve acted reflexively when a patient has done something awful. The couple of times it happened, it was just terrible racist comments to junior doctors who were with me. Extraordinarily dreadful things such as, “I don’t want to be touched by ...” or something of that sort.

Without really thinking about it, you react as a normal citizen and say, “That’s absolutely awful. Apologize immediately or leave the consultation room, and never ever come back again.” 

I remember that it happened once in Glasgow and once when I was a young professor in Birmingham, and it’s just an automatic gut reaction. The patient got a fright, and I immediately apologized and groveled around. In that relationship, we hold all the power, don’t we? Rather than being gentle about it, I was genuinely angry because of these ridiculous comments. 

Otherwise, I think most of the doctor-patient relationships are predicated on nonromantic love. I think patients want us to love them as one would a son, mother, father, or daughter, because if we do, then we will do better for them and we’ll pull out all the stops. “Placebo” means “I will please.” I think in the vast majority of cases, at least in our National Health Service (NHS), patients come with trust and a sense of wanting to build that relationship. That may be changing, but not for me. 

What about putting the boot on the other foot? What if the patients don’t like us rather than vice versa? As part of our accreditation appraisal process, from time to time we have to take patient surveys as to whether the patients felt that, after they had been seen in a consultation, they were treated with dignity, the quality of information given was appropriate, and they were treated with kindness. 

It’s an excellent exercise. Without bragging about it, patients objectively, according to these measures, appreciate the service that I give. It’s like getting five-star reviews on Trustpilot, or whatever these things are, that allow you to review car salesmen and so on. I have always had five-star reviews across the board. 

That, again, I thought was just a feature of that relationship, of patients wanting to please. These are patients who had been treated, who were in the outpatient department, who were in the midst of battle. Still, the scores are very high. I speak to my colleagues and that’s not uniformly the case. Patients actually do use these feedback forms, I think in a positive rather than negative way, reflecting back on the way that they were treated.

It has caused some of my colleagues to think quite hard about their personal style and approach to patients. That sense of feedback is important. 

What about losing trust? If that’s at the heart of everything that we do, then what would be an objective measure of losing trust? Again, in our healthcare system, it has been exceedingly unusual for a patient to request a second opinion. Now, that’s changing. The government is trying to change it. Leaders of the NHS are trying to change it so that patients feel assured that they can seek second opinions.

Again, in all the years I’ve been a cancer doctor, it has been incredibly infrequent that somebody has sought a second opinion after I’ve said something. That may be a measure of trust. Again, I’ve lived through an NHS in which seeking second opinions was something of a rarity. 

I’d be really interested to see what you think. In your own sphere of healthcare practice, is it possible for us to look after patients that we don’t like, or should we be honest and say, “I don’t like you. Our relationship has broken down. I want you to be seen by a colleague,” or “I want you to be nursed by somebody else”?

Has that happened? Is that something that you think is common or may become more common? What about when trust breaks down the other way? Can you think of instances in which the relationship, for whatever reason, just didn’t work and the patient had to move on because of that loss of trust and what underpinned it? I’d be really interested to know. 

I seek to be informed rather than the other way around. Can we truly look after patients that we don’t like or can we rise above it as Hippocrates might have done? 

Thanks for listening, as always. For the time being, over and out.

Dr. Kerr, Professor, Nuffield Department of Clinical Laboratory Science, University of Oxford; Professor of Cancer Medicine, Oxford Cancer Centre, Oxford, United Kingdom, disclosed ties with Celleron Therapeutics, Oxford Cancer Biomarkers, Afrox, GlaxoSmithKline, Bayer HealthCare Pharmaceuticals, Genomic Health, Merck Serono, and Roche.

A version of this article appeared on Medscape.com.

A new study provides more evidence that glucagon-like peptide 1 receptor agonists (GLP-1 RAs) used to treat diabetes and obesity could be repurposed for opioid use disorder (OUD) and alcohol use disorder (AUD).

Researchers found that patients with OUD or AUD who were taking semaglutide (Ozempic, Novo Nordisk) or similar medications for diabetes or weight-related conditions had a 40% lower rate of opioid overdose and a 50% lower rate of alcohol intoxication than their peers with OUD or AUD who were not taking these medications.

Their real-world study of more than 1 million adults with a history of OUD or AUD provide “foundational” estimates of the association between glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 RA prescriptions and opioid overdose/alcohol intoxication “and introduce the idea that GLP-1 RA and other related drugs should be investigated as a novel pharmacotherapy treatment option for individuals with OUD or AUD,” wrote the investigators, led by Fares Qeadan, PhD, Parkinson School of Health Sciences and Public Health, Loyola University Chicago, Maywood, Illinois.

The study was published online in the journal Addiction.
 

Protective Effect?

As previously reported by Medscape Medical News, earlier studies have pointed to a link between weight loss drugs and reduced overdose risk in people with OUD and decreased alcohol intake in people with AUD.

Until now, most studies on GLP-1 RAs and GIP agonists like tirzepatide (Mounjaro) to treat substance use disorders consisted of animal studies and small-scale clinical trials, investigators noted.

This new retrospective cohort study analyzed de-identified electronic health record data from the Oracle Health Real-World Data.

Participants, all aged 18 years or older, included 503,747 patients with a history of OUD, of whom 8103 had a GLP-1 RA or GIP prescription, and 817,309 patients with a history of AUD, of whom 5621 had a GLP-1 RA or GIP prescription.

Patients with OUD who were prescribed GLP-1 RAs had a 40% lower rate of opioid overdose than those without such prescriptions (adjusted incidence rate ratio [aIRR], 0.60; 95% CI, 0.43-0.83), the study team found.

In addition, patients with AUD and a GLP-1 RA prescription exhibited a 50% lower rate of alcohol intoxication (aIRR, 0.50; 95% CI, 0.40-0.63).

The protective effect of GLP-1 RA on opioid overdose and alcohol intoxication was maintained across patients with comorbid conditions, such as type 2 diabetes and obesity.

“Future research should focus on prospective clinical trials to validate these findings, explore the underlying mechanisms, and determine the long-term efficacy and safety of GIP/GLP-1 RA medications in diverse populations,” Qeadan and colleagues concluded.

“Additionally, the study highlights the importance of interdisciplinary research in understanding the neurobiological links between metabolic disorders and problematic substance use, potentially leading to more effective treatment strategies within healthcare systems,” they added.
 

Questions Remain

In a statement from the UK nonprofit Science Media Centre, Matt Field, DPhil, professor of psychology, The University of Sheffield, in England, noted that the findings “add to those from other studies, particularly animal research, which suggest that this and similar drugs might one day be prescribed to help people with addiction.”

However, “a note of caution is that the outcomes are very extreme instances of substance intoxication,” added Field, who wasn’t involved in the study.

“Those outcomes are very different from the outcomes used when researchers test new treatments for addiction, in which case we might look at whether the treatment helps people to stop taking the substance altogether (complete abstinence), or if it helps people to reduce the amount of substance they consume, or how often they consume it. Those things could not be measured in this study,” he continued.

“This leaves open the possibility that while Ozempic may — for reasons currently unknown — prevent people from taking so much alcohol or heroin that they overdose and end up in hospital, it may not actually help them to reduce their substance use, or to abstain altogether,” Field said.

The study had no specific funding. The study authors and Field declared no relevant conflicts of interest.
 

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

A new study provides more evidence that glucagon-like peptide 1 receptor agonists (GLP-1 RAs) used to treat diabetes and obesity could be repurposed for opioid use disorder (OUD) and alcohol use disorder (AUD).

Researchers found that patients with OUD or AUD who were taking semaglutide (Ozempic, Novo Nordisk) or similar medications for diabetes or weight-related conditions had a 40% lower rate of opioid overdose and a 50% lower rate of alcohol intoxication than their peers with OUD or AUD who were not taking these medications.

Their real-world study of more than 1 million adults with a history of OUD or AUD provide “foundational” estimates of the association between glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 RA prescriptions and opioid overdose/alcohol intoxication “and introduce the idea that GLP-1 RA and other related drugs should be investigated as a novel pharmacotherapy treatment option for individuals with OUD or AUD,” wrote the investigators, led by Fares Qeadan, PhD, Parkinson School of Health Sciences and Public Health, Loyola University Chicago, Maywood, Illinois.

The study was published online in the journal Addiction.
 

Protective Effect?

As previously reported by Medscape Medical News, earlier studies have pointed to a link between weight loss drugs and reduced overdose risk in people with OUD and decreased alcohol intake in people with AUD.

Until now, most studies on GLP-1 RAs and GIP agonists like tirzepatide (Mounjaro) to treat substance use disorders consisted of animal studies and small-scale clinical trials, investigators noted.

This new retrospective cohort study analyzed de-identified electronic health record data from the Oracle Health Real-World Data.

Participants, all aged 18 years or older, included 503,747 patients with a history of OUD, of whom 8103 had a GLP-1 RA or GIP prescription, and 817,309 patients with a history of AUD, of whom 5621 had a GLP-1 RA or GIP prescription.

Patients with OUD who were prescribed GLP-1 RAs had a 40% lower rate of opioid overdose than those without such prescriptions (adjusted incidence rate ratio [aIRR], 0.60; 95% CI, 0.43-0.83), the study team found.

In addition, patients with AUD and a GLP-1 RA prescription exhibited a 50% lower rate of alcohol intoxication (aIRR, 0.50; 95% CI, 0.40-0.63).

The protective effect of GLP-1 RA on opioid overdose and alcohol intoxication was maintained across patients with comorbid conditions, such as type 2 diabetes and obesity.

“Future research should focus on prospective clinical trials to validate these findings, explore the underlying mechanisms, and determine the long-term efficacy and safety of GIP/GLP-1 RA medications in diverse populations,” Qeadan and colleagues concluded.

“Additionally, the study highlights the importance of interdisciplinary research in understanding the neurobiological links between metabolic disorders and problematic substance use, potentially leading to more effective treatment strategies within healthcare systems,” they added.
 

Questions Remain

In a statement from the UK nonprofit Science Media Centre, Matt Field, DPhil, professor of psychology, The University of Sheffield, in England, noted that the findings “add to those from other studies, particularly animal research, which suggest that this and similar drugs might one day be prescribed to help people with addiction.”

However, “a note of caution is that the outcomes are very extreme instances of substance intoxication,” added Field, who wasn’t involved in the study.

“Those outcomes are very different from the outcomes used when researchers test new treatments for addiction, in which case we might look at whether the treatment helps people to stop taking the substance altogether (complete abstinence), or if it helps people to reduce the amount of substance they consume, or how often they consume it. Those things could not be measured in this study,” he continued.

“This leaves open the possibility that while Ozempic may — for reasons currently unknown — prevent people from taking so much alcohol or heroin that they overdose and end up in hospital, it may not actually help them to reduce their substance use, or to abstain altogether,” Field said.

The study had no specific funding. The study authors and Field declared no relevant conflicts of interest.
 

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

A new study provides more evidence that glucagon-like peptide 1 receptor agonists (GLP-1 RAs) used to treat diabetes and obesity could be repurposed for opioid use disorder (OUD) and alcohol use disorder (AUD).

Researchers found that patients with OUD or AUD who were taking semaglutide (Ozempic, Novo Nordisk) or similar medications for diabetes or weight-related conditions had a 40% lower rate of opioid overdose and a 50% lower rate of alcohol intoxication than their peers with OUD or AUD who were not taking these medications.

Their real-world study of more than 1 million adults with a history of OUD or AUD provide “foundational” estimates of the association between glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 RA prescriptions and opioid overdose/alcohol intoxication “and introduce the idea that GLP-1 RA and other related drugs should be investigated as a novel pharmacotherapy treatment option for individuals with OUD or AUD,” wrote the investigators, led by Fares Qeadan, PhD, Parkinson School of Health Sciences and Public Health, Loyola University Chicago, Maywood, Illinois.

The study was published online in the journal Addiction.
 

Protective Effect?

As previously reported by Medscape Medical News, earlier studies have pointed to a link between weight loss drugs and reduced overdose risk in people with OUD and decreased alcohol intake in people with AUD.

Until now, most studies on GLP-1 RAs and GIP agonists like tirzepatide (Mounjaro) to treat substance use disorders consisted of animal studies and small-scale clinical trials, investigators noted.

This new retrospective cohort study analyzed de-identified electronic health record data from the Oracle Health Real-World Data.

Participants, all aged 18 years or older, included 503,747 patients with a history of OUD, of whom 8103 had a GLP-1 RA or GIP prescription, and 817,309 patients with a history of AUD, of whom 5621 had a GLP-1 RA or GIP prescription.

Patients with OUD who were prescribed GLP-1 RAs had a 40% lower rate of opioid overdose than those without such prescriptions (adjusted incidence rate ratio [aIRR], 0.60; 95% CI, 0.43-0.83), the study team found.

In addition, patients with AUD and a GLP-1 RA prescription exhibited a 50% lower rate of alcohol intoxication (aIRR, 0.50; 95% CI, 0.40-0.63).

The protective effect of GLP-1 RA on opioid overdose and alcohol intoxication was maintained across patients with comorbid conditions, such as type 2 diabetes and obesity.

“Future research should focus on prospective clinical trials to validate these findings, explore the underlying mechanisms, and determine the long-term efficacy and safety of GIP/GLP-1 RA medications in diverse populations,” Qeadan and colleagues concluded.

“Additionally, the study highlights the importance of interdisciplinary research in understanding the neurobiological links between metabolic disorders and problematic substance use, potentially leading to more effective treatment strategies within healthcare systems,” they added.
 

Questions Remain

In a statement from the UK nonprofit Science Media Centre, Matt Field, DPhil, professor of psychology, The University of Sheffield, in England, noted that the findings “add to those from other studies, particularly animal research, which suggest that this and similar drugs might one day be prescribed to help people with addiction.”

However, “a note of caution is that the outcomes are very extreme instances of substance intoxication,” added Field, who wasn’t involved in the study.

“Those outcomes are very different from the outcomes used when researchers test new treatments for addiction, in which case we might look at whether the treatment helps people to stop taking the substance altogether (complete abstinence), or if it helps people to reduce the amount of substance they consume, or how often they consume it. Those things could not be measured in this study,” he continued.

“This leaves open the possibility that while Ozempic may — for reasons currently unknown — prevent people from taking so much alcohol or heroin that they overdose and end up in hospital, it may not actually help them to reduce their substance use, or to abstain altogether,” Field said.

The study had no specific funding. The study authors and Field declared no relevant conflicts of interest.
 

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

TOPLINE:

In healthy young adults, a single 30-minute bout of outdoor aerobic exercise significantly reduces fasting and 1-hour glucose levels during an oral glucose tolerance test (OGTT) the next day and improves insulin sensitivity.

METHODOLOGY:

• Recent studies have identified 1-hour post-load glucose concentration during an OGTT as a specific and early predictor of diabetes, and exercise has long been known for its metabolic benefits in people with and without diabetes.
• The researchers investigated the effect of a single bout of aerobic exercise on 1-hour post-load glucose levels during an OGTT in 32 young, healthy, normal-weight or marginally overweight individuals (mean age, 35 years; 14 women and 18 men) with a sedentary or moderately active lifestyle.
• The participants underwent an initial OGTT after at least 4 days of physical inactivity, followed by a second OGTT the day after a single 30-minute bout of aerobic exercise.
• The exercise session consisted of a light jog for 30 minutes, monitored using a metabolic holter to quantify energy expenditure and exercise intensity. The participants did not undertake any exercise outside the lab sessions.
• Blood glucose levels were measured, and insulin sensitivity and secretion were estimated using surrogate indices derived from OGTT glucose and insulin assays, including the Matsuda index, oral glucose insulin sensitivity (OGIS) index, and quantitative insulin sensitivity check index, as well as the homeostasis model assessment (HOMA) of insulin resistance and of beta-cell function (HOMA-B).

TAKEAWAY:

•  
• Postexercise insulin levels also were significantly lower 1 hour after glucose load, decreasing from 57.4 IU/mL at baseline to 43.5 IU/mL the day after exercise (P = .01).
• Insulin sensitivity improved significantly after exercise, as indicated by increases in the Matsuda index (P = .02) and OGIS index (P = .04), along with a reduction in insulin resistance (P = .04).
• The study found a trend toward increased beta-cell function the day after an exercise bout, as indicated by a nonsignificant increase in HOMA-B from 144.7 at baseline to 167.1 after exercise.

IN PRACTICE:

“Improvement in 1-hour post-load plasma glucose following a single session of aerobic physical activity suggests that exercise could have a direct effect on T2D [type 2 diabetes] risk and cardiovascular risk,” the authors wrote.

SOURCE:

The study was led by Simona Moffa, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, and Gian Pio Sorice, Università Degli Studi di Bari “Aldo Moro,” Bari, Italy. It was published online in the Journal of Endocrinological Investigation.

LIMITATIONS:

The study had a limited sample size, which may affect the generalizability of the findings. C-peptide levels, which could have provided additional insights into insulin secretion, were not assessed in the study.

DISCLOSURES:

The study was supported by grants from Università Cattolica del Sacro Cuore. The authors declared no conflicts of interest.
 

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

In healthy young adults, a single 30-minute bout of outdoor aerobic exercise significantly reduces fasting and 1-hour glucose levels during an oral glucose tolerance test (OGTT) the next day and improves insulin sensitivity.

METHODOLOGY:

• Recent studies have identified 1-hour post-load glucose concentration during an OGTT as a specific and early predictor of diabetes, and exercise has long been known for its metabolic benefits in people with and without diabetes.
• The researchers investigated the effect of a single bout of aerobic exercise on 1-hour post-load glucose levels during an OGTT in 32 young, healthy, normal-weight or marginally overweight individuals (mean age, 35 years; 14 women and 18 men) with a sedentary or moderately active lifestyle.
• The participants underwent an initial OGTT after at least 4 days of physical inactivity, followed by a second OGTT the day after a single 30-minute bout of aerobic exercise.
• The exercise session consisted of a light jog for 30 minutes, monitored using a metabolic holter to quantify energy expenditure and exercise intensity. The participants did not undertake any exercise outside the lab sessions.
• Blood glucose levels were measured, and insulin sensitivity and secretion were estimated using surrogate indices derived from OGTT glucose and insulin assays, including the Matsuda index, oral glucose insulin sensitivity (OGIS) index, and quantitative insulin sensitivity check index, as well as the homeostasis model assessment (HOMA) of insulin resistance and of beta-cell function (HOMA-B).

TAKEAWAY:

•  
• Postexercise insulin levels also were significantly lower 1 hour after glucose load, decreasing from 57.4 IU/mL at baseline to 43.5 IU/mL the day after exercise (P = .01).
• Insulin sensitivity improved significantly after exercise, as indicated by increases in the Matsuda index (P = .02) and OGIS index (P = .04), along with a reduction in insulin resistance (P = .04).
• The study found a trend toward increased beta-cell function the day after an exercise bout, as indicated by a nonsignificant increase in HOMA-B from 144.7 at baseline to 167.1 after exercise.

IN PRACTICE:

“Improvement in 1-hour post-load plasma glucose following a single session of aerobic physical activity suggests that exercise could have a direct effect on T2D [type 2 diabetes] risk and cardiovascular risk,” the authors wrote.

SOURCE:

The study was led by Simona Moffa, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, and Gian Pio Sorice, Università Degli Studi di Bari “Aldo Moro,” Bari, Italy. It was published online in the Journal of Endocrinological Investigation.

LIMITATIONS:

The study had a limited sample size, which may affect the generalizability of the findings. C-peptide levels, which could have provided additional insights into insulin secretion, were not assessed in the study.

DISCLOSURES:

The study was supported by grants from Università Cattolica del Sacro Cuore. The authors declared no conflicts of interest.
 

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

In healthy young adults, a single 30-minute bout of outdoor aerobic exercise significantly reduces fasting and 1-hour glucose levels during an oral glucose tolerance test (OGTT) the next day and improves insulin sensitivity.

METHODOLOGY:

• Recent studies have identified 1-hour post-load glucose concentration during an OGTT as a specific and early predictor of diabetes, and exercise has long been known for its metabolic benefits in people with and without diabetes.
• The researchers investigated the effect of a single bout of aerobic exercise on 1-hour post-load glucose levels during an OGTT in 32 young, healthy, normal-weight or marginally overweight individuals (mean age, 35 years; 14 women and 18 men) with a sedentary or moderately active lifestyle.
• The participants underwent an initial OGTT after at least 4 days of physical inactivity, followed by a second OGTT the day after a single 30-minute bout of aerobic exercise.
• The exercise session consisted of a light jog for 30 minutes, monitored using a metabolic holter to quantify energy expenditure and exercise intensity. The participants did not undertake any exercise outside the lab sessions.
• Blood glucose levels were measured, and insulin sensitivity and secretion were estimated using surrogate indices derived from OGTT glucose and insulin assays, including the Matsuda index, oral glucose insulin sensitivity (OGIS) index, and quantitative insulin sensitivity check index, as well as the homeostasis model assessment (HOMA) of insulin resistance and of beta-cell function (HOMA-B).

TAKEAWAY:

•  
• Postexercise insulin levels also were significantly lower 1 hour after glucose load, decreasing from 57.4 IU/mL at baseline to 43.5 IU/mL the day after exercise (P = .01).
• Insulin sensitivity improved significantly after exercise, as indicated by increases in the Matsuda index (P = .02) and OGIS index (P = .04), along with a reduction in insulin resistance (P = .04).
• The study found a trend toward increased beta-cell function the day after an exercise bout, as indicated by a nonsignificant increase in HOMA-B from 144.7 at baseline to 167.1 after exercise.

IN PRACTICE:

“Improvement in 1-hour post-load plasma glucose following a single session of aerobic physical activity suggests that exercise could have a direct effect on T2D [type 2 diabetes] risk and cardiovascular risk,” the authors wrote.

SOURCE:

The study was led by Simona Moffa, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, and Gian Pio Sorice, Università Degli Studi di Bari “Aldo Moro,” Bari, Italy. It was published online in the Journal of Endocrinological Investigation.

LIMITATIONS:

The study had a limited sample size, which may affect the generalizability of the findings. C-peptide levels, which could have provided additional insights into insulin secretion, were not assessed in the study.

DISCLOSURES:

The study was supported by grants from Università Cattolica del Sacro Cuore. The authors declared no conflicts of interest.
 

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Patients who achieved an A1c level < 6.5% after metabolic bariatric surgery (MBS) maintained this target in the short and long terms, regardless of whether they continued or discontinued metformin after the procedure.

METHODOLOGY:

• MBS is effective in individuals with type 2 diabetes (T2D) and obesity, but the recommendations for managing patients who achieve diabetes remission after bariatric surgery are not clear.
• Researchers conducted a retrospective cohort study using electronic health records from Clalit Health Services in Israel to assess the association between metformin continuation after MBS and the short- and long-term relapse of diabetes (2 and 5 years after surgery, respectively).
• They included 366 patients (aged ≥ 24 years; body mass index [BMI], ≥ 30) with obesity and T2D who received metformin and achieved A1c levels < 6.5% for up to 6 months after MBS.
• Patients who continued metformin (n = 122; ≥ 3 filled prescriptions; mean follow-up, 5.3 years) were matched and compared with those who discontinued it (n = 244; 0 prescriptions; mean follow-up, 5.8 years) after MBS.
• The primary outcome was the long-term relapse of diabetes, defined by an A1c level ≥ 6.5% during the follow-up period, and the secondary outcomes were short- and long-term A1c levels, changes in BMI, and all-cause mortality.

TAKEAWAY:

• After adjustment for patient variables, no significant association was found between metformin continuation after MBS and risk for relapse of diabetes (adjusted hazard ratio, 1.65).
• Patients in both groups maintained mean A1c levels < 6.5% during the short- and long-term follow-up periods, showing that discontinuing metformin did not impede glycemic control.
• No significant differences were noted between patients who continued or discontinued metformin in terms of weight loss.
• The mortality rate was low in both the groups, with no substantial difference noted between the groups that continued metformin (4.1%) or discontinued metformin (2.5%).

IN PRACTICE:

“The lack of a significant association of metformin continuation with A1c level observed in the current study supports the notion that metformin may not have an additional benefit after MBS,” the authors wrote.

SOURCE:

This study was led by Dror Dicker, MD, Internal Medicine Department D and Obesity Clinic, Hasharon Hospital, Rabin Medical Center, Petah Tikva, Israel, and published online in Diabetes, Obesity and Metabolism.

LIMITATIONS: 

The observational nature of the study and the lack of randomization may have introduced residual confounding. The small number of patients remaining in the final study population limited the generalizability of the findings. The follow-up period of approximately 5 years may not have been sufficient to observe the long-term effects of metformin continuation.

DISCLOSURES:

The study received funding from Ariel University. Two authors disclosed receiving grants, personal fees, or nonfinancial support from various sources unrelated to this study.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Patients who achieved an A1c level < 6.5% after metabolic bariatric surgery (MBS) maintained this target in the short and long terms, regardless of whether they continued or discontinued metformin after the procedure.

METHODOLOGY:

• MBS is effective in individuals with type 2 diabetes (T2D) and obesity, but the recommendations for managing patients who achieve diabetes remission after bariatric surgery are not clear.
• Researchers conducted a retrospective cohort study using electronic health records from Clalit Health Services in Israel to assess the association between metformin continuation after MBS and the short- and long-term relapse of diabetes (2 and 5 years after surgery, respectively).
• They included 366 patients (aged ≥ 24 years; body mass index [BMI], ≥ 30) with obesity and T2D who received metformin and achieved A1c levels < 6.5% for up to 6 months after MBS.
• Patients who continued metformin (n = 122; ≥ 3 filled prescriptions; mean follow-up, 5.3 years) were matched and compared with those who discontinued it (n = 244; 0 prescriptions; mean follow-up, 5.8 years) after MBS.
• The primary outcome was the long-term relapse of diabetes, defined by an A1c level ≥ 6.5% during the follow-up period, and the secondary outcomes were short- and long-term A1c levels, changes in BMI, and all-cause mortality.

TAKEAWAY:

• After adjustment for patient variables, no significant association was found between metformin continuation after MBS and risk for relapse of diabetes (adjusted hazard ratio, 1.65).
• Patients in both groups maintained mean A1c levels < 6.5% during the short- and long-term follow-up periods, showing that discontinuing metformin did not impede glycemic control.
• No significant differences were noted between patients who continued or discontinued metformin in terms of weight loss.
• The mortality rate was low in both the groups, with no substantial difference noted between the groups that continued metformin (4.1%) or discontinued metformin (2.5%).

IN PRACTICE:

“The lack of a significant association of metformin continuation with A1c level observed in the current study supports the notion that metformin may not have an additional benefit after MBS,” the authors wrote.

SOURCE:

This study was led by Dror Dicker, MD, Internal Medicine Department D and Obesity Clinic, Hasharon Hospital, Rabin Medical Center, Petah Tikva, Israel, and published online in Diabetes, Obesity and Metabolism.

LIMITATIONS: 

The observational nature of the study and the lack of randomization may have introduced residual confounding. The small number of patients remaining in the final study population limited the generalizability of the findings. The follow-up period of approximately 5 years may not have been sufficient to observe the long-term effects of metformin continuation.

DISCLOSURES:

The study received funding from Ariel University. Two authors disclosed receiving grants, personal fees, or nonfinancial support from various sources unrelated to this study.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Patients who achieved an A1c level < 6.5% after metabolic bariatric surgery (MBS) maintained this target in the short and long terms, regardless of whether they continued or discontinued metformin after the procedure.

METHODOLOGY:

• MBS is effective in individuals with type 2 diabetes (T2D) and obesity, but the recommendations for managing patients who achieve diabetes remission after bariatric surgery are not clear.
• Researchers conducted a retrospective cohort study using electronic health records from Clalit Health Services in Israel to assess the association between metformin continuation after MBS and the short- and long-term relapse of diabetes (2 and 5 years after surgery, respectively).
• They included 366 patients (aged ≥ 24 years; body mass index [BMI], ≥ 30) with obesity and T2D who received metformin and achieved A1c levels < 6.5% for up to 6 months after MBS.
• Patients who continued metformin (n = 122; ≥ 3 filled prescriptions; mean follow-up, 5.3 years) were matched and compared with those who discontinued it (n = 244; 0 prescriptions; mean follow-up, 5.8 years) after MBS.
• The primary outcome was the long-term relapse of diabetes, defined by an A1c level ≥ 6.5% during the follow-up period, and the secondary outcomes were short- and long-term A1c levels, changes in BMI, and all-cause mortality.

TAKEAWAY:

• After adjustment for patient variables, no significant association was found between metformin continuation after MBS and risk for relapse of diabetes (adjusted hazard ratio, 1.65).
• Patients in both groups maintained mean A1c levels < 6.5% during the short- and long-term follow-up periods, showing that discontinuing metformin did not impede glycemic control.
• No significant differences were noted between patients who continued or discontinued metformin in terms of weight loss.
• The mortality rate was low in both the groups, with no substantial difference noted between the groups that continued metformin (4.1%) or discontinued metformin (2.5%).

IN PRACTICE:

“The lack of a significant association of metformin continuation with A1c level observed in the current study supports the notion that metformin may not have an additional benefit after MBS,” the authors wrote.

SOURCE:

This study was led by Dror Dicker, MD, Internal Medicine Department D and Obesity Clinic, Hasharon Hospital, Rabin Medical Center, Petah Tikva, Israel, and published online in Diabetes, Obesity and Metabolism.

LIMITATIONS: 

The observational nature of the study and the lack of randomization may have introduced residual confounding. The small number of patients remaining in the final study population limited the generalizability of the findings. The follow-up period of approximately 5 years may not have been sufficient to observe the long-term effects of metformin continuation.

DISCLOSURES:

The study received funding from Ariel University. Two authors disclosed receiving grants, personal fees, or nonfinancial support from various sources unrelated to this study.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

The Fracture Risk Assessment Tool (FRAX), with bone mineral density, predicts the risk for major osteoporotic fractures and hip fractures in patients with cancer, but FRAX without bone mineral density slightly overestimates these risks, a new analysis found.

METHODOLOGY:

• Cancer-specific guidelines recommend using FRAX to assess fracture risk, but its applicability in patients with cancer remains unclear.
• This retrospective cohort study included 9877 patients with cancer (mean age, 67.1 years) and 45,875 matched control individuals without cancer (mean age, 66.2 years). All participants had dual-energy x-ray absorptiometry (DXA) scans.
• Researchers collected data on bone mineral density and fractures. The 10-year probabilities of major osteoporotic fractures and hip fractures were calculated using FRAX, and the observed 10-year probabilities of these fractures were compared with FRAX-derived probabilities.
• Compared with individuals without cancer, patients with cancer had a shorter mean follow-up duration (8.5 vs 7.6 years), a slightly higher mean body mass index, and a higher percentage of parental hip fractures (7.0% vs 8.2%); additionally, patients with cancer were more likely to have secondary causes of osteoporosis (10% vs 38.4%) and less likely to receive osteoporosis medication (9.9% vs 4.2%).

TAKEAWAY:

• Compared with individuals without cancer, patients with cancer had a significantly higher incidence rate of major fractures (12.9 vs 14.5 per 1000 person-years) and hip fractures (3.5 vs 4.2 per 1000 person-years).
• FRAX with bone mineral density exhibited excellent calibration for predicting major osteoporotic fractures (slope, 1.03) and hip fractures (0.97) in patients with cancer, regardless of the site of cancer diagnosis. FRAX without bone mineral density, however, underestimated the risk for both major (0.87) and hip fractures (0.72).
• In patients with cancer, FRAX with bone mineral density findings were associated with incident major osteoporotic fractures (hazard ratio [HR] per SD, 1.84) and hip fractures (HR per SD, 3.61).
• When models were adjusted for FRAX with bone mineral density, patients with cancer had an increased risk for both major osteoporotic fractures (HR, 1.17) and hip fractures (HR, 1.30). No difference was found in the risk for fracture between patients with and individuals without cancer when the models were adjusted for FRAX without bone mineral density, even when considering osteoporosis medication use.

IN PRACTICE:

“This retrospective cohort study demonstrates that individuals with cancer are at higher risk of fracture than individuals without cancer and that FRAX, particularly with BMD [bone mineral density], may accurately predict fracture risk in this population. These results, along with the known mortality risk of osteoporotic fractures among cancer survivors, further emphasize the clinical importance of closing the current osteoporosis care gap among cancer survivors,” the authors wrote.

SOURCE:

This study, led by Carrie Ye, MD, MPH, University of Alberta, Edmonton, Alberta, Canada, was published online in JAMA Oncology.

LIMITATIONS:

This study cohort included a selected group of cancer survivors who were referred for DXA scans and may not represent the general cancer population. The cohort consisted predominantly of women, limiting the generalizability to men with cancer. Given the heterogeneity of the population, the findings may not be applicable to all cancer subgroups. Information on cancer stage or the presence of bone metastases at the time of fracture risk assessment was lacking, which could have affected the findings.

DISCLOSURES:

This study was funded by the CancerCare Manitoba Foundation. Three authors reported having ties with various sources, including two who received grants from various organizations.
 

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

The Fracture Risk Assessment Tool (FRAX), with bone mineral density, predicts the risk for major osteoporotic fractures and hip fractures in patients with cancer, but FRAX without bone mineral density slightly overestimates these risks, a new analysis found.

METHODOLOGY:

• Cancer-specific guidelines recommend using FRAX to assess fracture risk, but its applicability in patients with cancer remains unclear.
• This retrospective cohort study included 9877 patients with cancer (mean age, 67.1 years) and 45,875 matched control individuals without cancer (mean age, 66.2 years). All participants had dual-energy x-ray absorptiometry (DXA) scans.
• Researchers collected data on bone mineral density and fractures. The 10-year probabilities of major osteoporotic fractures and hip fractures were calculated using FRAX, and the observed 10-year probabilities of these fractures were compared with FRAX-derived probabilities.
• Compared with individuals without cancer, patients with cancer had a shorter mean follow-up duration (8.5 vs 7.6 years), a slightly higher mean body mass index, and a higher percentage of parental hip fractures (7.0% vs 8.2%); additionally, patients with cancer were more likely to have secondary causes of osteoporosis (10% vs 38.4%) and less likely to receive osteoporosis medication (9.9% vs 4.2%).

TAKEAWAY:

• Compared with individuals without cancer, patients with cancer had a significantly higher incidence rate of major fractures (12.9 vs 14.5 per 1000 person-years) and hip fractures (3.5 vs 4.2 per 1000 person-years).
• FRAX with bone mineral density exhibited excellent calibration for predicting major osteoporotic fractures (slope, 1.03) and hip fractures (0.97) in patients with cancer, regardless of the site of cancer diagnosis. FRAX without bone mineral density, however, underestimated the risk for both major (0.87) and hip fractures (0.72).
• In patients with cancer, FRAX with bone mineral density findings were associated with incident major osteoporotic fractures (hazard ratio [HR] per SD, 1.84) and hip fractures (HR per SD, 3.61).
• When models were adjusted for FRAX with bone mineral density, patients with cancer had an increased risk for both major osteoporotic fractures (HR, 1.17) and hip fractures (HR, 1.30). No difference was found in the risk for fracture between patients with and individuals without cancer when the models were adjusted for FRAX without bone mineral density, even when considering osteoporosis medication use.

IN PRACTICE:

“This retrospective cohort study demonstrates that individuals with cancer are at higher risk of fracture than individuals without cancer and that FRAX, particularly with BMD [bone mineral density], may accurately predict fracture risk in this population. These results, along with the known mortality risk of osteoporotic fractures among cancer survivors, further emphasize the clinical importance of closing the current osteoporosis care gap among cancer survivors,” the authors wrote.

SOURCE:

This study, led by Carrie Ye, MD, MPH, University of Alberta, Edmonton, Alberta, Canada, was published online in JAMA Oncology.

LIMITATIONS:

This study cohort included a selected group of cancer survivors who were referred for DXA scans and may not represent the general cancer population. The cohort consisted predominantly of women, limiting the generalizability to men with cancer. Given the heterogeneity of the population, the findings may not be applicable to all cancer subgroups. Information on cancer stage or the presence of bone metastases at the time of fracture risk assessment was lacking, which could have affected the findings.

DISCLOSURES:

This study was funded by the CancerCare Manitoba Foundation. Three authors reported having ties with various sources, including two who received grants from various organizations.
 

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

The Fracture Risk Assessment Tool (FRAX), with bone mineral density, predicts the risk for major osteoporotic fractures and hip fractures in patients with cancer, but FRAX without bone mineral density slightly overestimates these risks, a new analysis found.

METHODOLOGY:

• Cancer-specific guidelines recommend using FRAX to assess fracture risk, but its applicability in patients with cancer remains unclear.
• This retrospective cohort study included 9877 patients with cancer (mean age, 67.1 years) and 45,875 matched control individuals without cancer (mean age, 66.2 years). All participants had dual-energy x-ray absorptiometry (DXA) scans.
• Researchers collected data on bone mineral density and fractures. The 10-year probabilities of major osteoporotic fractures and hip fractures were calculated using FRAX, and the observed 10-year probabilities of these fractures were compared with FRAX-derived probabilities.
• Compared with individuals without cancer, patients with cancer had a shorter mean follow-up duration (8.5 vs 7.6 years), a slightly higher mean body mass index, and a higher percentage of parental hip fractures (7.0% vs 8.2%); additionally, patients with cancer were more likely to have secondary causes of osteoporosis (10% vs 38.4%) and less likely to receive osteoporosis medication (9.9% vs 4.2%).

TAKEAWAY:

• Compared with individuals without cancer, patients with cancer had a significantly higher incidence rate of major fractures (12.9 vs 14.5 per 1000 person-years) and hip fractures (3.5 vs 4.2 per 1000 person-years).
• FRAX with bone mineral density exhibited excellent calibration for predicting major osteoporotic fractures (slope, 1.03) and hip fractures (0.97) in patients with cancer, regardless of the site of cancer diagnosis. FRAX without bone mineral density, however, underestimated the risk for both major (0.87) and hip fractures (0.72).
• In patients with cancer, FRAX with bone mineral density findings were associated with incident major osteoporotic fractures (hazard ratio [HR] per SD, 1.84) and hip fractures (HR per SD, 3.61).
• When models were adjusted for FRAX with bone mineral density, patients with cancer had an increased risk for both major osteoporotic fractures (HR, 1.17) and hip fractures (HR, 1.30). No difference was found in the risk for fracture between patients with and individuals without cancer when the models were adjusted for FRAX without bone mineral density, even when considering osteoporosis medication use.

IN PRACTICE:

“This retrospective cohort study demonstrates that individuals with cancer are at higher risk of fracture than individuals without cancer and that FRAX, particularly with BMD [bone mineral density], may accurately predict fracture risk in this population. These results, along with the known mortality risk of osteoporotic fractures among cancer survivors, further emphasize the clinical importance of closing the current osteoporosis care gap among cancer survivors,” the authors wrote.

SOURCE:

This study, led by Carrie Ye, MD, MPH, University of Alberta, Edmonton, Alberta, Canada, was published online in JAMA Oncology.

LIMITATIONS:

This study cohort included a selected group of cancer survivors who were referred for DXA scans and may not represent the general cancer population. The cohort consisted predominantly of women, limiting the generalizability to men with cancer. Given the heterogeneity of the population, the findings may not be applicable to all cancer subgroups. Information on cancer stage or the presence of bone metastases at the time of fracture risk assessment was lacking, which could have affected the findings.

DISCLOSURES:

This study was funded by the CancerCare Manitoba Foundation. Three authors reported having ties with various sources, including two who received grants from various organizations.
 

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Katie Sullivan, DNP, FNP-C, is publicizing her own challenge with updating an insulin pump as part of an effort to bring an end to the biannual seasonal clock changes in the United States.

On March 10, 2024, Sullivan, who works in the Endocrinology Clinic, Michigan State University, East Lansing, Michigan, mistakenly reversed the AM and PM settings while adjusting her own insulin pump. Sullivan, who has type 1 diabetes, noticed several hours later that her blood glucose levels had become higher than usual and was surprised to see her pump showed sleep mode during the day.

She was able to address this glitch before going to sleep and thus “escaped a potential occurrence of nocturnal hypoglycemia,” Sullivan and her colleague, Saleh Aldasouqi, MD, wrote in a September commentary in the journal Clinical Diabetes.

The risk of daylight saving time (DST) changes for people with insulin pumps is well known. Aldasouqi himself raised it in a 2014 article in the Journal of Diabetes Science and Technology.

Medtronic Inc., the leading maker of insulin pumps, told this news organization in an email that it intends for future devices to automate DST changes. The company did not provide any further details on when such changes would happen.

For now, Medtronic and other makers of insulin pumps join in twice-a-year efforts to remind people they need to update their devices to adjust for DST changes. They will need to gear up these outreach campaigns, which include social media posts, again ahead of the end of DST on November 3, when clocks shift back an hour. Diabetes clinics and hospitals also send notes to patients.

Even so, people will fail to make this change or to do it correctly.

“Despite our efforts to educate our patients about DST glitches, we have detected incorrect time settings in some of our patients’ insulin pumps after the DST changes in the fall and spring and occasional cases of incorrect insulin dosing, resulting in hyperglycemia or hypoglycemia,” Sullivan and Aldasouqi wrote in their article.

The US Food and Drug Administration (FDA) database of injuries and mishaps with devices contains many reports about patients not adjusting their insulin pumps for DST.

Known as Manufacturer and User Facility Device Experience (MAUDE), this database does not provide identifying details about the patients. Instead, the reports contain only a few lines describing what happened. In many cases, people were able to easily resolve their temporary glycemic issues and then set their devices to the correct time.

But some of the MAUDE reports tell of more severe consequences, with people ending up in emergency rooms because they did not adjust their insulin pumps for DST.

Among these is a report about a November 2022 incident, where a patient suffered due to what appeared to be inaccurate continuous glucose monitor readings, combined with the effects of an insulin pump that had not been updated for a DST change.

Although that patient’s mother was available to assist and the patient consumed three dextrose candies, the patient still reportedly lost consciousness and experienced tremors. That led to hospitalization, where the patient was treated with intravenous saline, intravenous insulin, saline fluids, and insulin fluids. The patient left the hospital with “the issue resolved and no permanent damage” but then switched to another method of insulin therapy, the MAUDE report said.

It’s unclear how often DST changes lead to problems with insulin pumps, reflecting difficulties in tracking flaws and glitches in medical devices, Madris Kinard, the chief executive officer and founder of Device Events, told this news organization.

The FDA relies heavily on passive surveillance, gathering MAUDE reports submitted by companies, clinicians, and patients. That means many cases likely are missed, said Kinard who earlier worked as an analyst at the FDA, updating processes and systems to help identify risky devices.

For example, Sullivan told this news organization she had not filed a report for her incident with the insulin pump.
 

Permanent Standard Time?

Many clinicians, including Aldasouqi and Sullivan, argue a better solution to these challenges would be to end DST.

In their Clinical Diabetes article, they also cited other health risks associated with clock changes such as fatigue, headache, and loss of attention and alertness that can result in injuries.

But a permanent time change is a “politically charged issue, and it continues to be debated nationally and at the state level,” they wrote.

At least 30 states also considered measures this year related to DST, according to the National Conference of State Legislatures. A pending Senate bill intended to make DST permanent has the support of 8 Democrats and 11 Republicans, including Sen. Tommy Tuberville (R-Ala).

“It’s amazing how many phone calls we get over this one topic. People across America agree that changing our clocks back and forth twice a year really makes no sense,” Tuberville said last year on the Senate floor. “People call and say they’re just sick of it.”

These federal and state efforts have stalled to date on the key question of whether to make either standard time or DST permanent, the National Conference of State Legislatures noted. A shift to permanent DST might have benefits for some agricultural and recreational industries, but many physicians say it would be bad for people’s health.

The American Academy of Sleep Medicine (AASM) argues strongly for moving to permanent standard time. In a position statement published in the Journal of Clinical Sleep Medicine, the group said the acute transitions from standard time to DST pose harms, citing research indicating increased risks for adverse cardiovascular events, mood disorders, and motor vehicle crashes.

The solution is to end shifts in time and opt for standard time, which best aligns with the human biological clock, AASM said.

AASM noted that there already was a failed experiment in the United States with a shift to permanent DST. Congress established this in response to the 1973 OPEC oil embargo, expecting that allowing more evening hours with light would lead to energy savings. That didn’t pay off in the expected reduction in energy and the policy was highly unpopular, especially in rural areas, AASM said.

“After a single winter, the policy was reversed by an overwhelming congressional majority,” wrote Muhammad Adeel Rishi, MD, and other authors of the statement. “The unpopularity of the act was likely because despite greater evening light, the policy resulted in a greater proportion of days that required waking up on dark mornings, particularly in the winter.”

Karin G. Johnson, MD, professor of neurology at the UMass Chan School of Medicine, Worcester, Massachusetts, told this news organization that a shift to permanent DST would rob many people of the signals their bodies need for sleep.

“Sunrises and sunsets are later and that creates a desire for our body to stay up later and have more trouble getting up in the morning,” Johnson said. “You’re all but making it impossible for certain segments of the population to get enough sleep” with permanent DST.

Johnson, Sullivan, and Aldasouqi had no relevant financial disclosures.

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

Katie Sullivan, DNP, FNP-C, is publicizing her own challenge with updating an insulin pump as part of an effort to bring an end to the biannual seasonal clock changes in the United States.

On March 10, 2024, Sullivan, who works in the Endocrinology Clinic, Michigan State University, East Lansing, Michigan, mistakenly reversed the AM and PM settings while adjusting her own insulin pump. Sullivan, who has type 1 diabetes, noticed several hours later that her blood glucose levels had become higher than usual and was surprised to see her pump showed sleep mode during the day.

She was able to address this glitch before going to sleep and thus “escaped a potential occurrence of nocturnal hypoglycemia,” Sullivan and her colleague, Saleh Aldasouqi, MD, wrote in a September commentary in the journal Clinical Diabetes.

The risk of daylight saving time (DST) changes for people with insulin pumps is well known. Aldasouqi himself raised it in a 2014 article in the Journal of Diabetes Science and Technology.

Medtronic Inc., the leading maker of insulin pumps, told this news organization in an email that it intends for future devices to automate DST changes. The company did not provide any further details on when such changes would happen.

For now, Medtronic and other makers of insulin pumps join in twice-a-year efforts to remind people they need to update their devices to adjust for DST changes. They will need to gear up these outreach campaigns, which include social media posts, again ahead of the end of DST on November 3, when clocks shift back an hour. Diabetes clinics and hospitals also send notes to patients.

Even so, people will fail to make this change or to do it correctly.

“Despite our efforts to educate our patients about DST glitches, we have detected incorrect time settings in some of our patients’ insulin pumps after the DST changes in the fall and spring and occasional cases of incorrect insulin dosing, resulting in hyperglycemia or hypoglycemia,” Sullivan and Aldasouqi wrote in their article.

The US Food and Drug Administration (FDA) database of injuries and mishaps with devices contains many reports about patients not adjusting their insulin pumps for DST.

Known as Manufacturer and User Facility Device Experience (MAUDE), this database does not provide identifying details about the patients. Instead, the reports contain only a few lines describing what happened. In many cases, people were able to easily resolve their temporary glycemic issues and then set their devices to the correct time.

But some of the MAUDE reports tell of more severe consequences, with people ending up in emergency rooms because they did not adjust their insulin pumps for DST.

Among these is a report about a November 2022 incident, where a patient suffered due to what appeared to be inaccurate continuous glucose monitor readings, combined with the effects of an insulin pump that had not been updated for a DST change.

Although that patient’s mother was available to assist and the patient consumed three dextrose candies, the patient still reportedly lost consciousness and experienced tremors. That led to hospitalization, where the patient was treated with intravenous saline, intravenous insulin, saline fluids, and insulin fluids. The patient left the hospital with “the issue resolved and no permanent damage” but then switched to another method of insulin therapy, the MAUDE report said.

It’s unclear how often DST changes lead to problems with insulin pumps, reflecting difficulties in tracking flaws and glitches in medical devices, Madris Kinard, the chief executive officer and founder of Device Events, told this news organization.

The FDA relies heavily on passive surveillance, gathering MAUDE reports submitted by companies, clinicians, and patients. That means many cases likely are missed, said Kinard who earlier worked as an analyst at the FDA, updating processes and systems to help identify risky devices.

For example, Sullivan told this news organization she had not filed a report for her incident with the insulin pump.
 

Permanent Standard Time?

Many clinicians, including Aldasouqi and Sullivan, argue a better solution to these challenges would be to end DST.

In their Clinical Diabetes article, they also cited other health risks associated with clock changes such as fatigue, headache, and loss of attention and alertness that can result in injuries.

But a permanent time change is a “politically charged issue, and it continues to be debated nationally and at the state level,” they wrote.

At least 30 states also considered measures this year related to DST, according to the National Conference of State Legislatures. A pending Senate bill intended to make DST permanent has the support of 8 Democrats and 11 Republicans, including Sen. Tommy Tuberville (R-Ala).

“It’s amazing how many phone calls we get over this one topic. People across America agree that changing our clocks back and forth twice a year really makes no sense,” Tuberville said last year on the Senate floor. “People call and say they’re just sick of it.”

These federal and state efforts have stalled to date on the key question of whether to make either standard time or DST permanent, the National Conference of State Legislatures noted. A shift to permanent DST might have benefits for some agricultural and recreational industries, but many physicians say it would be bad for people’s health.

The American Academy of Sleep Medicine (AASM) argues strongly for moving to permanent standard time. In a position statement published in the Journal of Clinical Sleep Medicine, the group said the acute transitions from standard time to DST pose harms, citing research indicating increased risks for adverse cardiovascular events, mood disorders, and motor vehicle crashes.

The solution is to end shifts in time and opt for standard time, which best aligns with the human biological clock, AASM said.

AASM noted that there already was a failed experiment in the United States with a shift to permanent DST. Congress established this in response to the 1973 OPEC oil embargo, expecting that allowing more evening hours with light would lead to energy savings. That didn’t pay off in the expected reduction in energy and the policy was highly unpopular, especially in rural areas, AASM said.

“After a single winter, the policy was reversed by an overwhelming congressional majority,” wrote Muhammad Adeel Rishi, MD, and other authors of the statement. “The unpopularity of the act was likely because despite greater evening light, the policy resulted in a greater proportion of days that required waking up on dark mornings, particularly in the winter.”

Karin G. Johnson, MD, professor of neurology at the UMass Chan School of Medicine, Worcester, Massachusetts, told this news organization that a shift to permanent DST would rob many people of the signals their bodies need for sleep.

“Sunrises and sunsets are later and that creates a desire for our body to stay up later and have more trouble getting up in the morning,” Johnson said. “You’re all but making it impossible for certain segments of the population to get enough sleep” with permanent DST.

Johnson, Sullivan, and Aldasouqi had no relevant financial disclosures.

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

Katie Sullivan, DNP, FNP-C, is publicizing her own challenge with updating an insulin pump as part of an effort to bring an end to the biannual seasonal clock changes in the United States.

On March 10, 2024, Sullivan, who works in the Endocrinology Clinic, Michigan State University, East Lansing, Michigan, mistakenly reversed the AM and PM settings while adjusting her own insulin pump. Sullivan, who has type 1 diabetes, noticed several hours later that her blood glucose levels had become higher than usual and was surprised to see her pump showed sleep mode during the day.

She was able to address this glitch before going to sleep and thus “escaped a potential occurrence of nocturnal hypoglycemia,” Sullivan and her colleague, Saleh Aldasouqi, MD, wrote in a September commentary in the journal Clinical Diabetes.

The risk of daylight saving time (DST) changes for people with insulin pumps is well known. Aldasouqi himself raised it in a 2014 article in the Journal of Diabetes Science and Technology.

Medtronic Inc., the leading maker of insulin pumps, told this news organization in an email that it intends for future devices to automate DST changes. The company did not provide any further details on when such changes would happen.

For now, Medtronic and other makers of insulin pumps join in twice-a-year efforts to remind people they need to update their devices to adjust for DST changes. They will need to gear up these outreach campaigns, which include social media posts, again ahead of the end of DST on November 3, when clocks shift back an hour. Diabetes clinics and hospitals also send notes to patients.

Even so, people will fail to make this change or to do it correctly.

“Despite our efforts to educate our patients about DST glitches, we have detected incorrect time settings in some of our patients’ insulin pumps after the DST changes in the fall and spring and occasional cases of incorrect insulin dosing, resulting in hyperglycemia or hypoglycemia,” Sullivan and Aldasouqi wrote in their article.

The US Food and Drug Administration (FDA) database of injuries and mishaps with devices contains many reports about patients not adjusting their insulin pumps for DST.

Known as Manufacturer and User Facility Device Experience (MAUDE), this database does not provide identifying details about the patients. Instead, the reports contain only a few lines describing what happened. In many cases, people were able to easily resolve their temporary glycemic issues and then set their devices to the correct time.

But some of the MAUDE reports tell of more severe consequences, with people ending up in emergency rooms because they did not adjust their insulin pumps for DST.

Among these is a report about a November 2022 incident, where a patient suffered due to what appeared to be inaccurate continuous glucose monitor readings, combined with the effects of an insulin pump that had not been updated for a DST change.

Although that patient’s mother was available to assist and the patient consumed three dextrose candies, the patient still reportedly lost consciousness and experienced tremors. That led to hospitalization, where the patient was treated with intravenous saline, intravenous insulin, saline fluids, and insulin fluids. The patient left the hospital with “the issue resolved and no permanent damage” but then switched to another method of insulin therapy, the MAUDE report said.

It’s unclear how often DST changes lead to problems with insulin pumps, reflecting difficulties in tracking flaws and glitches in medical devices, Madris Kinard, the chief executive officer and founder of Device Events, told this news organization.

The FDA relies heavily on passive surveillance, gathering MAUDE reports submitted by companies, clinicians, and patients. That means many cases likely are missed, said Kinard who earlier worked as an analyst at the FDA, updating processes and systems to help identify risky devices.

For example, Sullivan told this news organization she had not filed a report for her incident with the insulin pump.
 

Permanent Standard Time?

Many clinicians, including Aldasouqi and Sullivan, argue a better solution to these challenges would be to end DST.

In their Clinical Diabetes article, they also cited other health risks associated with clock changes such as fatigue, headache, and loss of attention and alertness that can result in injuries.

But a permanent time change is a “politically charged issue, and it continues to be debated nationally and at the state level,” they wrote.

At least 30 states also considered measures this year related to DST, according to the National Conference of State Legislatures. A pending Senate bill intended to make DST permanent has the support of 8 Democrats and 11 Republicans, including Sen. Tommy Tuberville (R-Ala).

“It’s amazing how many phone calls we get over this one topic. People across America agree that changing our clocks back and forth twice a year really makes no sense,” Tuberville said last year on the Senate floor. “People call and say they’re just sick of it.”

These federal and state efforts have stalled to date on the key question of whether to make either standard time or DST permanent, the National Conference of State Legislatures noted. A shift to permanent DST might have benefits for some agricultural and recreational industries, but many physicians say it would be bad for people’s health.

The American Academy of Sleep Medicine (AASM) argues strongly for moving to permanent standard time. In a position statement published in the Journal of Clinical Sleep Medicine, the group said the acute transitions from standard time to DST pose harms, citing research indicating increased risks for adverse cardiovascular events, mood disorders, and motor vehicle crashes.

The solution is to end shifts in time and opt for standard time, which best aligns with the human biological clock, AASM said.

AASM noted that there already was a failed experiment in the United States with a shift to permanent DST. Congress established this in response to the 1973 OPEC oil embargo, expecting that allowing more evening hours with light would lead to energy savings. That didn’t pay off in the expected reduction in energy and the policy was highly unpopular, especially in rural areas, AASM said.

“After a single winter, the policy was reversed by an overwhelming congressional majority,” wrote Muhammad Adeel Rishi, MD, and other authors of the statement. “The unpopularity of the act was likely because despite greater evening light, the policy resulted in a greater proportion of days that required waking up on dark mornings, particularly in the winter.”

Karin G. Johnson, MD, professor of neurology at the UMass Chan School of Medicine, Worcester, Massachusetts, told this news organization that a shift to permanent DST would rob many people of the signals their bodies need for sleep.

“Sunrises and sunsets are later and that creates a desire for our body to stay up later and have more trouble getting up in the morning,” Johnson said. “You’re all but making it impossible for certain segments of the population to get enough sleep” with permanent DST.

Johnson, Sullivan, and Aldasouqi had no relevant financial disclosures.

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