Clinical Endocrinology News

A low-carbohydrate diet can help preserve beta-cell function in people with mild type 2 diabetes (T2D), potentially allowing some to achieve target glucose levels without medication, new research suggests.

In the 12-week study of 57 people with T2D who were not using insulin, C-peptide levels were significantly higher among those randomized to receive a low-carbohydrate diet (~9% of total calories) vs a higher-carbohydrate diet (~55%). The results were published online on October 22, 2024, in The Journal of Clinical Endocrinology & Metabolism.

“While other studies have demonstrated metabolic health benefits of low-carb diets, our results are the first to show that dietary carbohydrate restriction can improve beta-cell function ... Furthermore, the carbohydrate-restricted diet improved insulin secretion in African American patients to a much greater extent than in Caucasian Americans,” study author Marian L. Yurchishin, MS, Department of Nutrition Sciences, The University of Alabama, Birmingham, Alabama, told Medscape Medical News.

Yurchishin added, “Our data suggests that a carbohydrate-restricted diet provides the opportunity to improve beta-cell function without the need for medication use or weight loss. This approach may be more appealing and effective for some persons with T2D, particularly in patients of African descent.”

At the same time, she clarified, “Our research should not be interpreted to mean that a carbohydrate-restricted diet can replace medical therapy in those who need it, especially patients at risk of cardiovascular disease, heart failure, or chronic kidney disease…or when medications are needed to achieve A1c targets.”

Asked to comment, Alison B. Evert, RDN, CDCES, former (now retired) manager of the Nutrition and Diabetes Education Programs at the University of Washington Medicine Primary Care, Kirkland, Washington, expressed some caveats about the findings, noting “I doubt this approach would be sustainable for the average person.” 

Evert also pointed out that the amount of fat in the carbohydrate-restricted diet — 65% of energy vs just 20% of energy with the higher-carbohydrate diet — was “extremely high ... essentially a keto diet,” and that in the real-world people might not receive education on heart-healthy fat intake. Moreover, she noted that the study’s use of grocery delivery to the participants with instructions for food preparation “is not a real-world situation either.”
 

Low-Carbohydrate Diet Increased C-Peptide Levels

The study participants were all either African American or European American. All had been diagnosed with T2D within the past 10 years, with average 4.9 years in the carbohydrate-restricted group vs 3.0 years in the higher-carbohydrate group. The two diets contained approximately the same number of calories.

All their medications were discontinued 1-2 weeks prior to baseline testing.

A hyperglycemic clamp was used to assess the acute (first-phase) and maximal (arginine-stimulated) C-peptide response to glucose at baseline and after 12 weeks of following the diets. First-phase beta-cell response to glucose was assessed at 30 minutes, insulin sensitivity was evaluated at 2 hours, and maximal beta-cell response to arginine was evaluated after another 30 minutes.

Oral glucose tolerance tests were also conducted at baseline and at 12 weeks to determine the disposition index (DI), a marker of beta-cell function that factors in both C-peptide and insulin sensitivity.

Of 65 participants enrolled, eight discontinued the study, most due to non-adherence. At 12 weeks, the acute C-peptide response from baseline was twice as high with the carbohydrate-restricted diet than with the higher-carbohydrate diet (P < .05). This difference was significant among the 37 African Americans (110% greater; P < .01) but not for the 20 European Americans.

Evert said that because people have typically lost at least 50% of their beta-cell function at the time of T2D diagnosis, “it is helpful to have return of first phase response, but long-term discontinuation of medications that also have cardioprotective function seems short sighted in this patient population.”

The overall maximal C-peptide response was 22% greater with the carbohydrate-restricted diet (P < .05), this time only significant in the European Americans (48%; P < .01) but not the African Americans.

In the combined group, the DI was 32% greater with the carbohydrate-restricted diet (P < .05) but only significantly so in the African American participants (48%; P < .01); however, no DI changes were seen with the higher-carbohydrate diet in the European American participants.

Regarding the racial differences, Yurchishin explained “Research supports the contention that the pathophysiology of T2D differs can differ among races based on genetic factors and environmental interactions that affect beta-cell function. For example, T2D onset in African Americans may be less related to obesity and insulin resistance than it is in European Americans and depend on alterations in beta-cell function to a larger degree. While sociocultural factors do influence T2D risk, other studies have also shown that there are inherent biological differences in the mechanisms that lead to beta-cell failure between races that warrant further investigation.” 

In their paper, Yurchishin and colleagues concluded, “With the caveat that carbohydrate restriction may be difficult for some patients, such a diet may allow patients with mild T2D to discontinue medication and enjoy eating meals and snacks that meet their energy needs while improving beta-cell function, an outcome that cannot be achieved with medication.” 

Evert commented, “I think it is a bit subjective to say that people following a 9% carb intake ‘will enjoy eating their meals and snacks that meet their energy needs.’ Guess they would enjoy as long as they choose very high fat, low carb foods.”

The research was supported by the National Institute of Diabetes and Digestive and Kidney Diseases, the UAB Nutrition Obesity Research Center, and the UAB Diabetes Research Center. Yurchishin was supported by the National Heart, Lung, and Blood Institute. Evert had no disclosures.
 

A version of this article appeared on Medscape.com.

A low-carbohydrate diet can help preserve beta-cell function in people with mild type 2 diabetes (T2D), potentially allowing some to achieve target glucose levels without medication, new research suggests.

In the 12-week study of 57 people with T2D who were not using insulin, C-peptide levels were significantly higher among those randomized to receive a low-carbohydrate diet (~9% of total calories) vs a higher-carbohydrate diet (~55%). The results were published online on October 22, 2024, in The Journal of Clinical Endocrinology & Metabolism.

“While other studies have demonstrated metabolic health benefits of low-carb diets, our results are the first to show that dietary carbohydrate restriction can improve beta-cell function ... Furthermore, the carbohydrate-restricted diet improved insulin secretion in African American patients to a much greater extent than in Caucasian Americans,” study author Marian L. Yurchishin, MS, Department of Nutrition Sciences, The University of Alabama, Birmingham, Alabama, told Medscape Medical News.

Yurchishin added, “Our data suggests that a carbohydrate-restricted diet provides the opportunity to improve beta-cell function without the need for medication use or weight loss. This approach may be more appealing and effective for some persons with T2D, particularly in patients of African descent.”

At the same time, she clarified, “Our research should not be interpreted to mean that a carbohydrate-restricted diet can replace medical therapy in those who need it, especially patients at risk of cardiovascular disease, heart failure, or chronic kidney disease…or when medications are needed to achieve A1c targets.”

Asked to comment, Alison B. Evert, RDN, CDCES, former (now retired) manager of the Nutrition and Diabetes Education Programs at the University of Washington Medicine Primary Care, Kirkland, Washington, expressed some caveats about the findings, noting “I doubt this approach would be sustainable for the average person.” 

Evert also pointed out that the amount of fat in the carbohydrate-restricted diet — 65% of energy vs just 20% of energy with the higher-carbohydrate diet — was “extremely high ... essentially a keto diet,” and that in the real-world people might not receive education on heart-healthy fat intake. Moreover, she noted that the study’s use of grocery delivery to the participants with instructions for food preparation “is not a real-world situation either.”
 

Low-Carbohydrate Diet Increased C-Peptide Levels

The study participants were all either African American or European American. All had been diagnosed with T2D within the past 10 years, with average 4.9 years in the carbohydrate-restricted group vs 3.0 years in the higher-carbohydrate group. The two diets contained approximately the same number of calories.

All their medications were discontinued 1-2 weeks prior to baseline testing.

A hyperglycemic clamp was used to assess the acute (first-phase) and maximal (arginine-stimulated) C-peptide response to glucose at baseline and after 12 weeks of following the diets. First-phase beta-cell response to glucose was assessed at 30 minutes, insulin sensitivity was evaluated at 2 hours, and maximal beta-cell response to arginine was evaluated after another 30 minutes.

Oral glucose tolerance tests were also conducted at baseline and at 12 weeks to determine the disposition index (DI), a marker of beta-cell function that factors in both C-peptide and insulin sensitivity.

Of 65 participants enrolled, eight discontinued the study, most due to non-adherence. At 12 weeks, the acute C-peptide response from baseline was twice as high with the carbohydrate-restricted diet than with the higher-carbohydrate diet (P < .05). This difference was significant among the 37 African Americans (110% greater; P < .01) but not for the 20 European Americans.

Evert said that because people have typically lost at least 50% of their beta-cell function at the time of T2D diagnosis, “it is helpful to have return of first phase response, but long-term discontinuation of medications that also have cardioprotective function seems short sighted in this patient population.”

The overall maximal C-peptide response was 22% greater with the carbohydrate-restricted diet (P < .05), this time only significant in the European Americans (48%; P < .01) but not the African Americans.

In the combined group, the DI was 32% greater with the carbohydrate-restricted diet (P < .05) but only significantly so in the African American participants (48%; P < .01); however, no DI changes were seen with the higher-carbohydrate diet in the European American participants.

Regarding the racial differences, Yurchishin explained “Research supports the contention that the pathophysiology of T2D differs can differ among races based on genetic factors and environmental interactions that affect beta-cell function. For example, T2D onset in African Americans may be less related to obesity and insulin resistance than it is in European Americans and depend on alterations in beta-cell function to a larger degree. While sociocultural factors do influence T2D risk, other studies have also shown that there are inherent biological differences in the mechanisms that lead to beta-cell failure between races that warrant further investigation.” 

In their paper, Yurchishin and colleagues concluded, “With the caveat that carbohydrate restriction may be difficult for some patients, such a diet may allow patients with mild T2D to discontinue medication and enjoy eating meals and snacks that meet their energy needs while improving beta-cell function, an outcome that cannot be achieved with medication.” 

Evert commented, “I think it is a bit subjective to say that people following a 9% carb intake ‘will enjoy eating their meals and snacks that meet their energy needs.’ Guess they would enjoy as long as they choose very high fat, low carb foods.”

The research was supported by the National Institute of Diabetes and Digestive and Kidney Diseases, the UAB Nutrition Obesity Research Center, and the UAB Diabetes Research Center. Yurchishin was supported by the National Heart, Lung, and Blood Institute. Evert had no disclosures.
 

A version of this article appeared on Medscape.com.

A low-carbohydrate diet can help preserve beta-cell function in people with mild type 2 diabetes (T2D), potentially allowing some to achieve target glucose levels without medication, new research suggests.

In the 12-week study of 57 people with T2D who were not using insulin, C-peptide levels were significantly higher among those randomized to receive a low-carbohydrate diet (~9% of total calories) vs a higher-carbohydrate diet (~55%). The results were published online on October 22, 2024, in The Journal of Clinical Endocrinology & Metabolism.

“While other studies have demonstrated metabolic health benefits of low-carb diets, our results are the first to show that dietary carbohydrate restriction can improve beta-cell function ... Furthermore, the carbohydrate-restricted diet improved insulin secretion in African American patients to a much greater extent than in Caucasian Americans,” study author Marian L. Yurchishin, MS, Department of Nutrition Sciences, The University of Alabama, Birmingham, Alabama, told Medscape Medical News.

Yurchishin added, “Our data suggests that a carbohydrate-restricted diet provides the opportunity to improve beta-cell function without the need for medication use or weight loss. This approach may be more appealing and effective for some persons with T2D, particularly in patients of African descent.”

At the same time, she clarified, “Our research should not be interpreted to mean that a carbohydrate-restricted diet can replace medical therapy in those who need it, especially patients at risk of cardiovascular disease, heart failure, or chronic kidney disease…or when medications are needed to achieve A1c targets.”

Asked to comment, Alison B. Evert, RDN, CDCES, former (now retired) manager of the Nutrition and Diabetes Education Programs at the University of Washington Medicine Primary Care, Kirkland, Washington, expressed some caveats about the findings, noting “I doubt this approach would be sustainable for the average person.” 

Evert also pointed out that the amount of fat in the carbohydrate-restricted diet — 65% of energy vs just 20% of energy with the higher-carbohydrate diet — was “extremely high ... essentially a keto diet,” and that in the real-world people might not receive education on heart-healthy fat intake. Moreover, she noted that the study’s use of grocery delivery to the participants with instructions for food preparation “is not a real-world situation either.”
 

Low-Carbohydrate Diet Increased C-Peptide Levels

The study participants were all either African American or European American. All had been diagnosed with T2D within the past 10 years, with average 4.9 years in the carbohydrate-restricted group vs 3.0 years in the higher-carbohydrate group. The two diets contained approximately the same number of calories.

All their medications were discontinued 1-2 weeks prior to baseline testing.

A hyperglycemic clamp was used to assess the acute (first-phase) and maximal (arginine-stimulated) C-peptide response to glucose at baseline and after 12 weeks of following the diets. First-phase beta-cell response to glucose was assessed at 30 minutes, insulin sensitivity was evaluated at 2 hours, and maximal beta-cell response to arginine was evaluated after another 30 minutes.

Oral glucose tolerance tests were also conducted at baseline and at 12 weeks to determine the disposition index (DI), a marker of beta-cell function that factors in both C-peptide and insulin sensitivity.

Of 65 participants enrolled, eight discontinued the study, most due to non-adherence. At 12 weeks, the acute C-peptide response from baseline was twice as high with the carbohydrate-restricted diet than with the higher-carbohydrate diet (P < .05). This difference was significant among the 37 African Americans (110% greater; P < .01) but not for the 20 European Americans.

Evert said that because people have typically lost at least 50% of their beta-cell function at the time of T2D diagnosis, “it is helpful to have return of first phase response, but long-term discontinuation of medications that also have cardioprotective function seems short sighted in this patient population.”

The overall maximal C-peptide response was 22% greater with the carbohydrate-restricted diet (P < .05), this time only significant in the European Americans (48%; P < .01) but not the African Americans.

In the combined group, the DI was 32% greater with the carbohydrate-restricted diet (P < .05) but only significantly so in the African American participants (48%; P < .01); however, no DI changes were seen with the higher-carbohydrate diet in the European American participants.

Regarding the racial differences, Yurchishin explained “Research supports the contention that the pathophysiology of T2D differs can differ among races based on genetic factors and environmental interactions that affect beta-cell function. For example, T2D onset in African Americans may be less related to obesity and insulin resistance than it is in European Americans and depend on alterations in beta-cell function to a larger degree. While sociocultural factors do influence T2D risk, other studies have also shown that there are inherent biological differences in the mechanisms that lead to beta-cell failure between races that warrant further investigation.” 

In their paper, Yurchishin and colleagues concluded, “With the caveat that carbohydrate restriction may be difficult for some patients, such a diet may allow patients with mild T2D to discontinue medication and enjoy eating meals and snacks that meet their energy needs while improving beta-cell function, an outcome that cannot be achieved with medication.” 

Evert commented, “I think it is a bit subjective to say that people following a 9% carb intake ‘will enjoy eating their meals and snacks that meet their energy needs.’ Guess they would enjoy as long as they choose very high fat, low carb foods.”

The research was supported by the National Institute of Diabetes and Digestive and Kidney Diseases, the UAB Nutrition Obesity Research Center, and the UAB Diabetes Research Center. Yurchishin was supported by the National Heart, Lung, and Blood Institute. Evert had no disclosures.
 

A version of this article appeared on Medscape.com.

Recent reports suggest diabetic retinopathy is more common in younger people than previously thought, leading to a call for more frequent screening for this condition and more attention to follow-up after diagnosis.

The increased incidence of diabetic retinopathy is “a potentially unappreciated public health catastrophe,” Julie Rosenthal, MD, MS, of the University of Michigan, Ann Arbor, Michigan, and her coauthors wrote in a recent viewpoint in JAMA Ophthalmology.

Rosenthal, an ophthalmologist, said she has been treating each year several young people with diabetes with symptoms of retinopathy that might have been prevented through earlier detection and treatment.

Some patients with retinopathy seek out eye specialists for issues such as seeing floaters, vision loss, or feeling of having cobwebs in their vision, which can be symptoms of bleeding. Other patients may have no symptoms with their retinopathy discovered only in screening.

“It would be wonderful to never need to treat any 20-year-olds with proliferative diabetic retinopathy who are losing vision,” Rosenthal said.

Diabetic retinopathy once was considered rare in young people, with earlier research suggesting an age-adjusted prevalence of 4%-13% in youths with type 2 diabetes, roughly in line with that for type 1 diabetes.

But an analysis of more recent data drawn from two major federally funded studies of diabetes in young people shows what Rosenthal and her colleagues called “alarming rates” of retinopathy. Data from these studies suggest more than half (52%) of youths with type 1 diabetes may have some retinopathy, and as many as 55% of those with youth-onset type 2 diabetes.

Other research suggests young people with type 2 diabetes may have almost twice the risk of developing retinopathy, develop it sooner after diabetes diagnosis, and are more likely to have vision-threatening retinopathy, Rosenthal and coauthors wrote.

Elizabeth Jensen, PhD, of Wake Forest University, Winston-Salem, North Carolina, the lead author of a 2023 study cited by Rosenthal and coauthors in their JAMA Ophthalmology viewpoint, told Medscape Medical News she also supports a call for more screening of young people.

“What many people don’t realize is that there is evidence of retinal changes consistent with development of diabetic retinopathy early in disease,” Jensen said.

The proportion of people with diabetic retinopathy varied according to a range of modifiable factors, including A1c levels and blood pressure, she added.

This fact underscores the need to not only screen for diabetic retinopathy early but also consider addressing those modifiable factors that may mitigate risk for the development and progression of diabetic retinopathy, Jensen said.

Rosenthal said some patients have the false impression of sight loss being inevitable with diabetes. Their primary care physicians can help make them aware that there are treatments for retinopathy in cases where it can’t be avoided.

These interventions include laser treatments and injecting medicines into the eye. “It sounds a lot scarier than it is,” Rosenthal said.

“We do know that keeping good control over not only glucose but also blood pressure, cholesterol, and lipids is all important for decreasing the risk. But even if those are under control, sometimes people can still get diabetes in their eyes,” Rosenthal said. “The longer you have diabetes, the higher your risk of having problems in your eye.”
 

‘Stagnant Guidelines’

Guidelines from major medical groups have “remained largely stagnant in the face of new evidence of increasing diabetes prevalence,” making it difficult to know when to screen younger people, according to Rosenthal and her colleagues.

Medical associations, including the American Diabetes Association (ADA) and the American Academy of Ophthalmology, now recommend ocular screening for youths with type 1 diabetes 3-5 years after diagnosis in those who are at least 11 years old or are experiencing puberty, and for youths with type 2 diabetes from the time of diagnosis.

Follow-up diabetic eye examinations can be performed every 2 years, with some groups advocating for even more infrequent follow-up examinations.

“These guidelines are rooted in evidence from prior studies showing that it is rare to have advanced retinopathy prior to this age,” Rosenthal and coauthors wrote. “However, these guidelines have remained largely stagnant in the face of new evidence of increasing diabetes prevalence.”

The American Academy of Ophthalmology told Medscape Medical News it has no immediate plans to update its recommendations. These include directing people with type 1 diabetes without known diabetic retinopathy to have annual dilated eye examinations beginning 5 years after the onset of diabetes. Individuals with type 2 diabetes without diabetic retinopathy should have annual dilated eye examinations to detect the onset of diabetic retinopathy.

The group also said clinicians should make sure patients understand that even if they may have good vision and no ocular symptoms, they may still have significant disease that needs treatment.
 

More Opportunities for Screening Tools

The current standards of care for retinopathy from the ADA note new products on the market are increasing the options for screening.

“Retinal photography with remote reading by experts has great potential to provide screening services in areas where qualified eye care professionals are not readily available,” according to standards.

“However, the benefits and optimal utilization of this type of screening have yet to be fully determined,” the group stated. “Results of all screening eye examinations should be documented and transmitted to the referring healthcare professionals.”

The approach has promise, despite some significant challenges, according to Rithwick Rajagopal, MD, PhD, an associate professor of ophthalmology and visual sciences at Washington University in St. Louis, St. Louis, Missouri.

Rajagopal and colleagues in 2022 published results of a test of retinopathy screening during appointments at the primary care medicine clinic of Barnes-Jewish Hospital in St. Louis, Missouri. They found the system used worked well in ruling out retinopathy and appeared to help more patients receive care for the condition. Among patients referred for follow-up eye exams, the adherence rate was 55.4% at 1-year compared with the historical adherence rate of 18.7%, Rajagopal and his colleagues reported.

In an email exchange with Medscape Medical News, Rajagopal highlighted several barriers to wider adoption of retinopathy screenings in primary care.

“First is unfamiliarity with eye anatomy and physiology, which is associated with low level of comfort in capturing the photographs and interpreting the results (even though the cameras are increasingly easy to use and that the AI software generates the diagnosis),” Rajagopal said.

In addition, questions about reimbursement and liability remain unresolved.

But Rajagopal said he still expects more use of products such as the EyeArt 2.0 automated DR screening software (Eyenuk, Inc.).

“Despite the above concerns, point-of-care screening offers a powerful solution to a long-standing problem: People with diabetes in this country are generally not adherent to recommended retinal screening guidelines,” Rajagopal told Medscape Medical News. “There are multiple causes of such poor adherence, but point-of-care screening solves several of them: No need to take time off for an additional medical visit, no additional co-pay for eye doctor visits, and no need for dilation in many cases.”

Aiding in the adoption of this service is likely the special Current Procedural Terminology (billing) code — 92229 — the American Medical Association introduced in 2021 for diabetic eye exams when ordered by a physician who is not an ophthalmologist. Many commercial health plans and many state Medicaid programs now cover this service, which is still off-label, Michael Abramoff, MD, PhD, of the University of Iowa, Iowa City, Iowa, and founder of Digital Diagnostics, maker of the AI-assisted LumineticsCore diagnostic system, told Medscape Medical News. A representative for Eyenuk also told Medscape Medical News many insurers now cover the screening service.

LumineticsCore has been used in a study done in conjunction with appointments for regular care at the Johns Hopkins Pediatric Diabetes Center in Baltimore.

Abramoff and coauthors, including Risa Wolf, MD, a pediatric endocrinologist at Johns Hopkins University School of Medicine in Baltimore, reported this year in Nature Communications that 100% of patients in the group offered the autonomous AI screening completed their eye exam that day, while only 22% of a comparison group followed through within 6 months to complete an eye exam with an optometrist or ophthalmologist.

Wolf, who is also a coauthor with Rosenthal of the commentary in JAMA Ophthalmology, said she agrees these tools have the potential to expand the pool of clinicians who can screen patients for retinopathy.
 

Make Screening Easier

The critical issue is to make it easier for young adults with diabetes to get checked for retinopathy, Wolf said. People in their late teens and early 20s face many challenges in getting needed medical screenings. They often are shifting away from living with parents, who likely managed their care for them in their childhood.

These young adults tend to be busy with college and the demands of starting out in careers while living on their own. And they may not want to address the potential consequences of diabetes, which can seem remote to people not feeling effects of the illness.

“It’s just not always a priority, especially when you’re in this time of life where you’re generally feeling very healthy,” Wolf said. “But we want to make sure that they are getting screened.”

Rosenthal reported receiving research grant support from MediBeacon, outside the submitted work. Other coauthors reported receiving grants from Breakthrough T1D, Physical Sciences, Novartis, Genentech/Roche, Novo Nordisk, and Boehringer Ingelheim, and receiving nonfinancial support from Optovue, Boston Micromachines, Novo Nordisk, Adaptive Sensory Technology, Genentech/Roche, Novartis, and Alcon outside the submitted work. Jensen reported no relevant financial disclosures.

Eyenuk Inc. provided the camera and automated screening software used in the study reported by Rajagopal and coauthors and was involved in the data collection and management, but otherwise had no role in the design or conduct of this research. Rajagopal had no personal financial disclosures.
 

A version of this article appeared on Medscape.com.

Recent reports suggest diabetic retinopathy is more common in younger people than previously thought, leading to a call for more frequent screening for this condition and more attention to follow-up after diagnosis.

The increased incidence of diabetic retinopathy is “a potentially unappreciated public health catastrophe,” Julie Rosenthal, MD, MS, of the University of Michigan, Ann Arbor, Michigan, and her coauthors wrote in a recent viewpoint in JAMA Ophthalmology.

Rosenthal, an ophthalmologist, said she has been treating each year several young people with diabetes with symptoms of retinopathy that might have been prevented through earlier detection and treatment.

Some patients with retinopathy seek out eye specialists for issues such as seeing floaters, vision loss, or feeling of having cobwebs in their vision, which can be symptoms of bleeding. Other patients may have no symptoms with their retinopathy discovered only in screening.

“It would be wonderful to never need to treat any 20-year-olds with proliferative diabetic retinopathy who are losing vision,” Rosenthal said.

Diabetic retinopathy once was considered rare in young people, with earlier research suggesting an age-adjusted prevalence of 4%-13% in youths with type 2 diabetes, roughly in line with that for type 1 diabetes.

But an analysis of more recent data drawn from two major federally funded studies of diabetes in young people shows what Rosenthal and her colleagues called “alarming rates” of retinopathy. Data from these studies suggest more than half (52%) of youths with type 1 diabetes may have some retinopathy, and as many as 55% of those with youth-onset type 2 diabetes.

Other research suggests young people with type 2 diabetes may have almost twice the risk of developing retinopathy, develop it sooner after diabetes diagnosis, and are more likely to have vision-threatening retinopathy, Rosenthal and coauthors wrote.

Elizabeth Jensen, PhD, of Wake Forest University, Winston-Salem, North Carolina, the lead author of a 2023 study cited by Rosenthal and coauthors in their JAMA Ophthalmology viewpoint, told Medscape Medical News she also supports a call for more screening of young people.

“What many people don’t realize is that there is evidence of retinal changes consistent with development of diabetic retinopathy early in disease,” Jensen said.

The proportion of people with diabetic retinopathy varied according to a range of modifiable factors, including A1c levels and blood pressure, she added.

This fact underscores the need to not only screen for diabetic retinopathy early but also consider addressing those modifiable factors that may mitigate risk for the development and progression of diabetic retinopathy, Jensen said.

Rosenthal said some patients have the false impression of sight loss being inevitable with diabetes. Their primary care physicians can help make them aware that there are treatments for retinopathy in cases where it can’t be avoided.

These interventions include laser treatments and injecting medicines into the eye. “It sounds a lot scarier than it is,” Rosenthal said.

“We do know that keeping good control over not only glucose but also blood pressure, cholesterol, and lipids is all important for decreasing the risk. But even if those are under control, sometimes people can still get diabetes in their eyes,” Rosenthal said. “The longer you have diabetes, the higher your risk of having problems in your eye.”
 

‘Stagnant Guidelines’

Guidelines from major medical groups have “remained largely stagnant in the face of new evidence of increasing diabetes prevalence,” making it difficult to know when to screen younger people, according to Rosenthal and her colleagues.

Medical associations, including the American Diabetes Association (ADA) and the American Academy of Ophthalmology, now recommend ocular screening for youths with type 1 diabetes 3-5 years after diagnosis in those who are at least 11 years old or are experiencing puberty, and for youths with type 2 diabetes from the time of diagnosis.

Follow-up diabetic eye examinations can be performed every 2 years, with some groups advocating for even more infrequent follow-up examinations.

“These guidelines are rooted in evidence from prior studies showing that it is rare to have advanced retinopathy prior to this age,” Rosenthal and coauthors wrote. “However, these guidelines have remained largely stagnant in the face of new evidence of increasing diabetes prevalence.”

The American Academy of Ophthalmology told Medscape Medical News it has no immediate plans to update its recommendations. These include directing people with type 1 diabetes without known diabetic retinopathy to have annual dilated eye examinations beginning 5 years after the onset of diabetes. Individuals with type 2 diabetes without diabetic retinopathy should have annual dilated eye examinations to detect the onset of diabetic retinopathy.

The group also said clinicians should make sure patients understand that even if they may have good vision and no ocular symptoms, they may still have significant disease that needs treatment.
 

More Opportunities for Screening Tools

The current standards of care for retinopathy from the ADA note new products on the market are increasing the options for screening.

“Retinal photography with remote reading by experts has great potential to provide screening services in areas where qualified eye care professionals are not readily available,” according to standards.

“However, the benefits and optimal utilization of this type of screening have yet to be fully determined,” the group stated. “Results of all screening eye examinations should be documented and transmitted to the referring healthcare professionals.”

The approach has promise, despite some significant challenges, according to Rithwick Rajagopal, MD, PhD, an associate professor of ophthalmology and visual sciences at Washington University in St. Louis, St. Louis, Missouri.

Rajagopal and colleagues in 2022 published results of a test of retinopathy screening during appointments at the primary care medicine clinic of Barnes-Jewish Hospital in St. Louis, Missouri. They found the system used worked well in ruling out retinopathy and appeared to help more patients receive care for the condition. Among patients referred for follow-up eye exams, the adherence rate was 55.4% at 1-year compared with the historical adherence rate of 18.7%, Rajagopal and his colleagues reported.

In an email exchange with Medscape Medical News, Rajagopal highlighted several barriers to wider adoption of retinopathy screenings in primary care.

“First is unfamiliarity with eye anatomy and physiology, which is associated with low level of comfort in capturing the photographs and interpreting the results (even though the cameras are increasingly easy to use and that the AI software generates the diagnosis),” Rajagopal said.

In addition, questions about reimbursement and liability remain unresolved.

But Rajagopal said he still expects more use of products such as the EyeArt 2.0 automated DR screening software (Eyenuk, Inc.).

“Despite the above concerns, point-of-care screening offers a powerful solution to a long-standing problem: People with diabetes in this country are generally not adherent to recommended retinal screening guidelines,” Rajagopal told Medscape Medical News. “There are multiple causes of such poor adherence, but point-of-care screening solves several of them: No need to take time off for an additional medical visit, no additional co-pay for eye doctor visits, and no need for dilation in many cases.”

Aiding in the adoption of this service is likely the special Current Procedural Terminology (billing) code — 92229 — the American Medical Association introduced in 2021 for diabetic eye exams when ordered by a physician who is not an ophthalmologist. Many commercial health plans and many state Medicaid programs now cover this service, which is still off-label, Michael Abramoff, MD, PhD, of the University of Iowa, Iowa City, Iowa, and founder of Digital Diagnostics, maker of the AI-assisted LumineticsCore diagnostic system, told Medscape Medical News. A representative for Eyenuk also told Medscape Medical News many insurers now cover the screening service.

LumineticsCore has been used in a study done in conjunction with appointments for regular care at the Johns Hopkins Pediatric Diabetes Center in Baltimore.

Abramoff and coauthors, including Risa Wolf, MD, a pediatric endocrinologist at Johns Hopkins University School of Medicine in Baltimore, reported this year in Nature Communications that 100% of patients in the group offered the autonomous AI screening completed their eye exam that day, while only 22% of a comparison group followed through within 6 months to complete an eye exam with an optometrist or ophthalmologist.

Wolf, who is also a coauthor with Rosenthal of the commentary in JAMA Ophthalmology, said she agrees these tools have the potential to expand the pool of clinicians who can screen patients for retinopathy.
 

Make Screening Easier

The critical issue is to make it easier for young adults with diabetes to get checked for retinopathy, Wolf said. People in their late teens and early 20s face many challenges in getting needed medical screenings. They often are shifting away from living with parents, who likely managed their care for them in their childhood.

These young adults tend to be busy with college and the demands of starting out in careers while living on their own. And they may not want to address the potential consequences of diabetes, which can seem remote to people not feeling effects of the illness.

“It’s just not always a priority, especially when you’re in this time of life where you’re generally feeling very healthy,” Wolf said. “But we want to make sure that they are getting screened.”

Rosenthal reported receiving research grant support from MediBeacon, outside the submitted work. Other coauthors reported receiving grants from Breakthrough T1D, Physical Sciences, Novartis, Genentech/Roche, Novo Nordisk, and Boehringer Ingelheim, and receiving nonfinancial support from Optovue, Boston Micromachines, Novo Nordisk, Adaptive Sensory Technology, Genentech/Roche, Novartis, and Alcon outside the submitted work. Jensen reported no relevant financial disclosures.

Eyenuk Inc. provided the camera and automated screening software used in the study reported by Rajagopal and coauthors and was involved in the data collection and management, but otherwise had no role in the design or conduct of this research. Rajagopal had no personal financial disclosures.
 

A version of this article appeared on Medscape.com.

Recent reports suggest diabetic retinopathy is more common in younger people than previously thought, leading to a call for more frequent screening for this condition and more attention to follow-up after diagnosis.

The increased incidence of diabetic retinopathy is “a potentially unappreciated public health catastrophe,” Julie Rosenthal, MD, MS, of the University of Michigan, Ann Arbor, Michigan, and her coauthors wrote in a recent viewpoint in JAMA Ophthalmology.

Rosenthal, an ophthalmologist, said she has been treating each year several young people with diabetes with symptoms of retinopathy that might have been prevented through earlier detection and treatment.

Some patients with retinopathy seek out eye specialists for issues such as seeing floaters, vision loss, or feeling of having cobwebs in their vision, which can be symptoms of bleeding. Other patients may have no symptoms with their retinopathy discovered only in screening.

“It would be wonderful to never need to treat any 20-year-olds with proliferative diabetic retinopathy who are losing vision,” Rosenthal said.

Diabetic retinopathy once was considered rare in young people, with earlier research suggesting an age-adjusted prevalence of 4%-13% in youths with type 2 diabetes, roughly in line with that for type 1 diabetes.

But an analysis of more recent data drawn from two major federally funded studies of diabetes in young people shows what Rosenthal and her colleagues called “alarming rates” of retinopathy. Data from these studies suggest more than half (52%) of youths with type 1 diabetes may have some retinopathy, and as many as 55% of those with youth-onset type 2 diabetes.

Other research suggests young people with type 2 diabetes may have almost twice the risk of developing retinopathy, develop it sooner after diabetes diagnosis, and are more likely to have vision-threatening retinopathy, Rosenthal and coauthors wrote.

Elizabeth Jensen, PhD, of Wake Forest University, Winston-Salem, North Carolina, the lead author of a 2023 study cited by Rosenthal and coauthors in their JAMA Ophthalmology viewpoint, told Medscape Medical News she also supports a call for more screening of young people.

“What many people don’t realize is that there is evidence of retinal changes consistent with development of diabetic retinopathy early in disease,” Jensen said.

The proportion of people with diabetic retinopathy varied according to a range of modifiable factors, including A1c levels and blood pressure, she added.

This fact underscores the need to not only screen for diabetic retinopathy early but also consider addressing those modifiable factors that may mitigate risk for the development and progression of diabetic retinopathy, Jensen said.

Rosenthal said some patients have the false impression of sight loss being inevitable with diabetes. Their primary care physicians can help make them aware that there are treatments for retinopathy in cases where it can’t be avoided.

These interventions include laser treatments and injecting medicines into the eye. “It sounds a lot scarier than it is,” Rosenthal said.

“We do know that keeping good control over not only glucose but also blood pressure, cholesterol, and lipids is all important for decreasing the risk. But even if those are under control, sometimes people can still get diabetes in their eyes,” Rosenthal said. “The longer you have diabetes, the higher your risk of having problems in your eye.”
 

‘Stagnant Guidelines’

Guidelines from major medical groups have “remained largely stagnant in the face of new evidence of increasing diabetes prevalence,” making it difficult to know when to screen younger people, according to Rosenthal and her colleagues.

Medical associations, including the American Diabetes Association (ADA) and the American Academy of Ophthalmology, now recommend ocular screening for youths with type 1 diabetes 3-5 years after diagnosis in those who are at least 11 years old or are experiencing puberty, and for youths with type 2 diabetes from the time of diagnosis.

Follow-up diabetic eye examinations can be performed every 2 years, with some groups advocating for even more infrequent follow-up examinations.

“These guidelines are rooted in evidence from prior studies showing that it is rare to have advanced retinopathy prior to this age,” Rosenthal and coauthors wrote. “However, these guidelines have remained largely stagnant in the face of new evidence of increasing diabetes prevalence.”

The American Academy of Ophthalmology told Medscape Medical News it has no immediate plans to update its recommendations. These include directing people with type 1 diabetes without known diabetic retinopathy to have annual dilated eye examinations beginning 5 years after the onset of diabetes. Individuals with type 2 diabetes without diabetic retinopathy should have annual dilated eye examinations to detect the onset of diabetic retinopathy.

The group also said clinicians should make sure patients understand that even if they may have good vision and no ocular symptoms, they may still have significant disease that needs treatment.
 

More Opportunities for Screening Tools

The current standards of care for retinopathy from the ADA note new products on the market are increasing the options for screening.

“Retinal photography with remote reading by experts has great potential to provide screening services in areas where qualified eye care professionals are not readily available,” according to standards.

“However, the benefits and optimal utilization of this type of screening have yet to be fully determined,” the group stated. “Results of all screening eye examinations should be documented and transmitted to the referring healthcare professionals.”

The approach has promise, despite some significant challenges, according to Rithwick Rajagopal, MD, PhD, an associate professor of ophthalmology and visual sciences at Washington University in St. Louis, St. Louis, Missouri.

Rajagopal and colleagues in 2022 published results of a test of retinopathy screening during appointments at the primary care medicine clinic of Barnes-Jewish Hospital in St. Louis, Missouri. They found the system used worked well in ruling out retinopathy and appeared to help more patients receive care for the condition. Among patients referred for follow-up eye exams, the adherence rate was 55.4% at 1-year compared with the historical adherence rate of 18.7%, Rajagopal and his colleagues reported.

In an email exchange with Medscape Medical News, Rajagopal highlighted several barriers to wider adoption of retinopathy screenings in primary care.

“First is unfamiliarity with eye anatomy and physiology, which is associated with low level of comfort in capturing the photographs and interpreting the results (even though the cameras are increasingly easy to use and that the AI software generates the diagnosis),” Rajagopal said.

In addition, questions about reimbursement and liability remain unresolved.

But Rajagopal said he still expects more use of products such as the EyeArt 2.0 automated DR screening software (Eyenuk, Inc.).

“Despite the above concerns, point-of-care screening offers a powerful solution to a long-standing problem: People with diabetes in this country are generally not adherent to recommended retinal screening guidelines,” Rajagopal told Medscape Medical News. “There are multiple causes of such poor adherence, but point-of-care screening solves several of them: No need to take time off for an additional medical visit, no additional co-pay for eye doctor visits, and no need for dilation in many cases.”

Aiding in the adoption of this service is likely the special Current Procedural Terminology (billing) code — 92229 — the American Medical Association introduced in 2021 for diabetic eye exams when ordered by a physician who is not an ophthalmologist. Many commercial health plans and many state Medicaid programs now cover this service, which is still off-label, Michael Abramoff, MD, PhD, of the University of Iowa, Iowa City, Iowa, and founder of Digital Diagnostics, maker of the AI-assisted LumineticsCore diagnostic system, told Medscape Medical News. A representative for Eyenuk also told Medscape Medical News many insurers now cover the screening service.

LumineticsCore has been used in a study done in conjunction with appointments for regular care at the Johns Hopkins Pediatric Diabetes Center in Baltimore.

Abramoff and coauthors, including Risa Wolf, MD, a pediatric endocrinologist at Johns Hopkins University School of Medicine in Baltimore, reported this year in Nature Communications that 100% of patients in the group offered the autonomous AI screening completed their eye exam that day, while only 22% of a comparison group followed through within 6 months to complete an eye exam with an optometrist or ophthalmologist.

Wolf, who is also a coauthor with Rosenthal of the commentary in JAMA Ophthalmology, said she agrees these tools have the potential to expand the pool of clinicians who can screen patients for retinopathy.
 

Make Screening Easier

The critical issue is to make it easier for young adults with diabetes to get checked for retinopathy, Wolf said. People in their late teens and early 20s face many challenges in getting needed medical screenings. They often are shifting away from living with parents, who likely managed their care for them in their childhood.

These young adults tend to be busy with college and the demands of starting out in careers while living on their own. And they may not want to address the potential consequences of diabetes, which can seem remote to people not feeling effects of the illness.

“It’s just not always a priority, especially when you’re in this time of life where you’re generally feeling very healthy,” Wolf said. “But we want to make sure that they are getting screened.”

Rosenthal reported receiving research grant support from MediBeacon, outside the submitted work. Other coauthors reported receiving grants from Breakthrough T1D, Physical Sciences, Novartis, Genentech/Roche, Novo Nordisk, and Boehringer Ingelheim, and receiving nonfinancial support from Optovue, Boston Micromachines, Novo Nordisk, Adaptive Sensory Technology, Genentech/Roche, Novartis, and Alcon outside the submitted work. Jensen reported no relevant financial disclosures.

Eyenuk Inc. provided the camera and automated screening software used in the study reported by Rajagopal and coauthors and was involved in the data collection and management, but otherwise had no role in the design or conduct of this research. Rajagopal had no personal financial disclosures.
 

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.

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.