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Diabetes Retinopathy Poses Threat to More Young People’s Sight
, 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.
, 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.
, 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.
Is CGM the New CBT?
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, . 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, . 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, . 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.
The Genitals Are a Window Into Health: Sex as a Vital Sign
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.
PCOS Linked to Hypertensive Blood Pressure in Teens
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.
Higher Doses of Vitamin D3 Do Not Reduce Cardiac Biomarkers in Older Adults
TOPLINE:
Higher doses of vitamin D3 supplementation did not significantly reduce cardiac biomarkers in older adults with low serum vitamin D levels. The STURDY trial found no significant differences in high-sensitivity cardiac troponin I (hs-cTnI) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) between low- and high-dose groups.
METHODOLOGY:
- A total of 688 participants aged 70 years or older with low serum 25-hydroxy vitamin D levels (10-29 ng/mL) were included in the STURDY trial.
- Participants were randomized to receive one of four doses of vitamin D3 supplementation: 200, 1000, 2000, or 4000 IU/d, with 200 IU/d as the reference dose.
- Cardiac biomarkers, including hs-cTnI and NT-proBNP, were measured at baseline, 3 months, 12 months, and 24 months.
- The trial was conducted at two community-based research institutions in the United States between July 2015 and March 2019.
- The effects of vitamin D3 dose on biomarkers were assessed via mixed-effects tobit models, with participants followed up to 24 months or until study termination.
TAKEAWAY:
- Higher doses of vitamin D3 supplementation did not significantly affect hs-cTnI levels compared with the low-dose group (1.6% difference; 95% CI, −5.3 to 8.9).
- No significant differences were observed in NT-proBNP levels between the high-dose and low-dose groups (−1.8% difference; 95% CI, −9.3 to 6.3).
- Both hs-cTnI and NT-proBNP levels increased in both low- and high-dose groups over time, with hs-cTnI increasing by 5.2% and 7.0%, respectively, and NT-proBNP increasing by 11.3% and 9.3%, respectively.
- The findings suggest that higher doses of vitamin D3 supplementation do not reduce markers of subclinical cardiovascular disease in older adults with low serum vitamin D levels.
IN PRACTICE:
“We can speculate that the systemic effects of vitamin D deficiency are more profound among the very old, and there may be an inverse relationship between supplementation and inflammation. It is also possible that serum vitamin D level is a risk marker but not a risk factor for CVD risk and related underlying mechanisms,” wrote the authors of the study.
SOURCE:
The study was led by Katharine W. Rainer, MD, Beth Israel Deaconess Medical Center in Boston. It was published online in the Journal of the American College of Cardiology.
LIMITATIONS:
The study’s community-based population may limit the generalizability of the findings to populations at higher risk for cardiovascular disease. Additionally, the baseline cardiac biomarkers were lower than those in some high-risk populations, which may affect the precision of the assay performance. The study may not have had adequate power for cross-sectional and subgroup analyses. Both groups received some vitamin D3 supplementation, making it difficult to determine the impact of lower-dose supplementation vs no supplementation.
DISCLOSURES:
The study was supported by grants from the National Institute on Aging, the Office of Dietary Supplements, the Mid-Atlantic Nutrition Obesity Research Center, and the Johns Hopkins Institute for Clinical and Translational Research. Rainer disclosed receiving grants from these organizations.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
Higher doses of vitamin D3 supplementation did not significantly reduce cardiac biomarkers in older adults with low serum vitamin D levels. The STURDY trial found no significant differences in high-sensitivity cardiac troponin I (hs-cTnI) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) between low- and high-dose groups.
METHODOLOGY:
- A total of 688 participants aged 70 years or older with low serum 25-hydroxy vitamin D levels (10-29 ng/mL) were included in the STURDY trial.
- Participants were randomized to receive one of four doses of vitamin D3 supplementation: 200, 1000, 2000, or 4000 IU/d, with 200 IU/d as the reference dose.
- Cardiac biomarkers, including hs-cTnI and NT-proBNP, were measured at baseline, 3 months, 12 months, and 24 months.
- The trial was conducted at two community-based research institutions in the United States between July 2015 and March 2019.
- The effects of vitamin D3 dose on biomarkers were assessed via mixed-effects tobit models, with participants followed up to 24 months or until study termination.
TAKEAWAY:
- Higher doses of vitamin D3 supplementation did not significantly affect hs-cTnI levels compared with the low-dose group (1.6% difference; 95% CI, −5.3 to 8.9).
- No significant differences were observed in NT-proBNP levels between the high-dose and low-dose groups (−1.8% difference; 95% CI, −9.3 to 6.3).
- Both hs-cTnI and NT-proBNP levels increased in both low- and high-dose groups over time, with hs-cTnI increasing by 5.2% and 7.0%, respectively, and NT-proBNP increasing by 11.3% and 9.3%, respectively.
- The findings suggest that higher doses of vitamin D3 supplementation do not reduce markers of subclinical cardiovascular disease in older adults with low serum vitamin D levels.
IN PRACTICE:
“We can speculate that the systemic effects of vitamin D deficiency are more profound among the very old, and there may be an inverse relationship between supplementation and inflammation. It is also possible that serum vitamin D level is a risk marker but not a risk factor for CVD risk and related underlying mechanisms,” wrote the authors of the study.
SOURCE:
The study was led by Katharine W. Rainer, MD, Beth Israel Deaconess Medical Center in Boston. It was published online in the Journal of the American College of Cardiology.
LIMITATIONS:
The study’s community-based population may limit the generalizability of the findings to populations at higher risk for cardiovascular disease. Additionally, the baseline cardiac biomarkers were lower than those in some high-risk populations, which may affect the precision of the assay performance. The study may not have had adequate power for cross-sectional and subgroup analyses. Both groups received some vitamin D3 supplementation, making it difficult to determine the impact of lower-dose supplementation vs no supplementation.
DISCLOSURES:
The study was supported by grants from the National Institute on Aging, the Office of Dietary Supplements, the Mid-Atlantic Nutrition Obesity Research Center, and the Johns Hopkins Institute for Clinical and Translational Research. Rainer disclosed receiving grants from these organizations.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
Higher doses of vitamin D3 supplementation did not significantly reduce cardiac biomarkers in older adults with low serum vitamin D levels. The STURDY trial found no significant differences in high-sensitivity cardiac troponin I (hs-cTnI) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) between low- and high-dose groups.
METHODOLOGY:
- A total of 688 participants aged 70 years or older with low serum 25-hydroxy vitamin D levels (10-29 ng/mL) were included in the STURDY trial.
- Participants were randomized to receive one of four doses of vitamin D3 supplementation: 200, 1000, 2000, or 4000 IU/d, with 200 IU/d as the reference dose.
- Cardiac biomarkers, including hs-cTnI and NT-proBNP, were measured at baseline, 3 months, 12 months, and 24 months.
- The trial was conducted at two community-based research institutions in the United States between July 2015 and March 2019.
- The effects of vitamin D3 dose on biomarkers were assessed via mixed-effects tobit models, with participants followed up to 24 months or until study termination.
TAKEAWAY:
- Higher doses of vitamin D3 supplementation did not significantly affect hs-cTnI levels compared with the low-dose group (1.6% difference; 95% CI, −5.3 to 8.9).
- No significant differences were observed in NT-proBNP levels between the high-dose and low-dose groups (−1.8% difference; 95% CI, −9.3 to 6.3).
- Both hs-cTnI and NT-proBNP levels increased in both low- and high-dose groups over time, with hs-cTnI increasing by 5.2% and 7.0%, respectively, and NT-proBNP increasing by 11.3% and 9.3%, respectively.
- The findings suggest that higher doses of vitamin D3 supplementation do not reduce markers of subclinical cardiovascular disease in older adults with low serum vitamin D levels.
IN PRACTICE:
“We can speculate that the systemic effects of vitamin D deficiency are more profound among the very old, and there may be an inverse relationship between supplementation and inflammation. It is also possible that serum vitamin D level is a risk marker but not a risk factor for CVD risk and related underlying mechanisms,” wrote the authors of the study.
SOURCE:
The study was led by Katharine W. Rainer, MD, Beth Israel Deaconess Medical Center in Boston. It was published online in the Journal of the American College of Cardiology.
LIMITATIONS:
The study’s community-based population may limit the generalizability of the findings to populations at higher risk for cardiovascular disease. Additionally, the baseline cardiac biomarkers were lower than those in some high-risk populations, which may affect the precision of the assay performance. The study may not have had adequate power for cross-sectional and subgroup analyses. Both groups received some vitamin D3 supplementation, making it difficult to determine the impact of lower-dose supplementation vs no supplementation.
DISCLOSURES:
The study was supported by grants from the National Institute on Aging, the Office of Dietary Supplements, the Mid-Atlantic Nutrition Obesity Research Center, and the Johns Hopkins Institute for Clinical and Translational Research. Rainer disclosed receiving grants from these organizations.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
Type 2 Diabetes: Insulin-Free for 24 Months After Novel Endoscopic Procedure
TOPLINE:
VIENNA, AUSTRIA —
METHODOLOGY:
- ReCET technology, manufactured by Endogenex, uses a specialized catheter that ablates the duodenal mucosa with electroporation, enhancing sensitivity to endogenous insulin.
- In the first-in-human study, a total of 14 participants (aged 28-75 years; body mass index, 24-40) underwent the ReCET procedure. They then followed a 2-week isocaloric liquid diet, after which they were initiated on semaglutide and gradually titrated up to 1 mg/wk.
- Patients were followed for a total of 24 months.
TAKEAWAY:
- Of the 14 participants, 12 (86%) no longer required insulin at the 6- and 12-month follow-ups.
- At the 24-month follow-up, 11 patients were still insulin-free while maintaining A1c levels below 7.5%. (One patient withdrew consent at 18 months.)
- Semaglutide at the maximum dose was well-tolerated by 93% of participants. One patient experienced nausea that limited titration to the maximum dose. There were no serious adverse events to the ReCET procedure.
- Researchers have started the EMINENT-2 trial that will compare the use of ReCET with a sham procedure. All patients will still receive semaglutide.
IN PRACTICE:
- “These findings are very encouraging, suggesting that ReCET is a safe and feasible procedure that, when combined with semaglutide, can effectively eliminate the need for insulin therapy,” said the study’s lead author.
- It’s a novel way of treating type 2 diabetes using a single endoscopic procedure instead of repeated insulin injections, Busch explained. “But we do need to consider whether repeat treatment will be necessary because I don’t believe this will be forever.”
SOURCE:
This study was led by Celine Busch, MBBS, a PhD candidate in gastroenterology at Amsterdam University Medical Center, Amsterdam, the Netherlands, and was presented (abstract OP049) at the United European Gastroenterology (UEG) Week 2024 in Vienna, Austria, on October 14, 2024.
LIMITATIONS:
Limitations included the small sample size, uncontrolled nature, and bias due to combination therapy.
DISCLOSURES:
This study received an unrestricted research grant from Endogenex. No other relevant disclosures were declared.
A version of this article first appeared on Medscape.com.
TOPLINE:
VIENNA, AUSTRIA —
METHODOLOGY:
- ReCET technology, manufactured by Endogenex, uses a specialized catheter that ablates the duodenal mucosa with electroporation, enhancing sensitivity to endogenous insulin.
- In the first-in-human study, a total of 14 participants (aged 28-75 years; body mass index, 24-40) underwent the ReCET procedure. They then followed a 2-week isocaloric liquid diet, after which they were initiated on semaglutide and gradually titrated up to 1 mg/wk.
- Patients were followed for a total of 24 months.
TAKEAWAY:
- Of the 14 participants, 12 (86%) no longer required insulin at the 6- and 12-month follow-ups.
- At the 24-month follow-up, 11 patients were still insulin-free while maintaining A1c levels below 7.5%. (One patient withdrew consent at 18 months.)
- Semaglutide at the maximum dose was well-tolerated by 93% of participants. One patient experienced nausea that limited titration to the maximum dose. There were no serious adverse events to the ReCET procedure.
- Researchers have started the EMINENT-2 trial that will compare the use of ReCET with a sham procedure. All patients will still receive semaglutide.
IN PRACTICE:
- “These findings are very encouraging, suggesting that ReCET is a safe and feasible procedure that, when combined with semaglutide, can effectively eliminate the need for insulin therapy,” said the study’s lead author.
- It’s a novel way of treating type 2 diabetes using a single endoscopic procedure instead of repeated insulin injections, Busch explained. “But we do need to consider whether repeat treatment will be necessary because I don’t believe this will be forever.”
SOURCE:
This study was led by Celine Busch, MBBS, a PhD candidate in gastroenterology at Amsterdam University Medical Center, Amsterdam, the Netherlands, and was presented (abstract OP049) at the United European Gastroenterology (UEG) Week 2024 in Vienna, Austria, on October 14, 2024.
LIMITATIONS:
Limitations included the small sample size, uncontrolled nature, and bias due to combination therapy.
DISCLOSURES:
This study received an unrestricted research grant from Endogenex. No other relevant disclosures were declared.
A version of this article first appeared on Medscape.com.
TOPLINE:
VIENNA, AUSTRIA —
METHODOLOGY:
- ReCET technology, manufactured by Endogenex, uses a specialized catheter that ablates the duodenal mucosa with electroporation, enhancing sensitivity to endogenous insulin.
- In the first-in-human study, a total of 14 participants (aged 28-75 years; body mass index, 24-40) underwent the ReCET procedure. They then followed a 2-week isocaloric liquid diet, after which they were initiated on semaglutide and gradually titrated up to 1 mg/wk.
- Patients were followed for a total of 24 months.
TAKEAWAY:
- Of the 14 participants, 12 (86%) no longer required insulin at the 6- and 12-month follow-ups.
- At the 24-month follow-up, 11 patients were still insulin-free while maintaining A1c levels below 7.5%. (One patient withdrew consent at 18 months.)
- Semaglutide at the maximum dose was well-tolerated by 93% of participants. One patient experienced nausea that limited titration to the maximum dose. There were no serious adverse events to the ReCET procedure.
- Researchers have started the EMINENT-2 trial that will compare the use of ReCET with a sham procedure. All patients will still receive semaglutide.
IN PRACTICE:
- “These findings are very encouraging, suggesting that ReCET is a safe and feasible procedure that, when combined with semaglutide, can effectively eliminate the need for insulin therapy,” said the study’s lead author.
- It’s a novel way of treating type 2 diabetes using a single endoscopic procedure instead of repeated insulin injections, Busch explained. “But we do need to consider whether repeat treatment will be necessary because I don’t believe this will be forever.”
SOURCE:
This study was led by Celine Busch, MBBS, a PhD candidate in gastroenterology at Amsterdam University Medical Center, Amsterdam, the Netherlands, and was presented (abstract OP049) at the United European Gastroenterology (UEG) Week 2024 in Vienna, Austria, on October 14, 2024.
LIMITATIONS:
Limitations included the small sample size, uncontrolled nature, and bias due to combination therapy.
DISCLOSURES:
This study received an unrestricted research grant from Endogenex. No other relevant disclosures were declared.
A version of this article first appeared on Medscape.com.
CGM With Geriatric Care Simplifies T1D Management in Seniors
TOPLINE:
METHODOLOGY:
- Researchers evaluated the effectiveness of CGM use enhanced by geriatric principles in adults aged ≥ 65 years with T1D and at least two episodes of hypoglycemia (blood glucose level, < 70 mg/dL for ≥ 20 minutes over 2 weeks), who were either CGM-naive or CGM users prior to the study.
- Participants were randomly assigned to an intervention group using CGM with geriatric principles (ie, adjusting goals based on overall health and simplifying regimens based on CGM patterns and clinical characteristics) or a control group receiving usual care by their endocrinologist.
- The primary outcome was the change in duration of hypoglycemia from baseline to 6 months.
- A cost-effectiveness analysis was also performed for the intervention using a healthcare sector perspective, considering the cost of CGM devices and the cost of medical staff time.
TAKEAWAY:
- Researchers included 131 participants (mean age, 71 years), of whom 68 were in the intervention group (35 CGM-naive) and 63 in the control group (23 CGM-naive).
- The intervention group showed a median reduction of 2.6% in the duration of hypoglycemia vs a 0.3% reduction in the control group (median difference, −2.3%; P < .001).
- This reduction was observed in both CGM users (median difference, −1.2%) and CGM-naive participants (median difference, −2.8%) in the intervention group.
- No significant difference in A1c levels was observed between the intervention and control groups, indicating that CGM enhanced with geriatric principles did not worsen glycemic control.
- The intervention was associated with an incremental cost-effectiveness ratio of $71,623 per quality-adjusted life-year and was cost-effective for CGM-naive participants but at a lower level owing to the high cost of the CGM device.
IN PRACTICE:
“Personalization of goals and simplification of complex regimens can be combined with CGM use to improve management of type 1 diabetes in older adults,” the study authors wrote.
SOURCE:
The study was led by Medha N. Munshi, MD, Joslin Diabetes Center, Boston. It was published online in Diabetes Care.
LIMITATIONS:
The study included a relatively small sample size and an ethnically homogeneous and highly educated cohort, which may have limited the generalizability of its findings. Additionally, the study did not measure adherence to individual simplification strategies, which may have hindered the quantification of behavioral changes.
DISCLOSURES:
This study was supported by the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health. Two authors declared serving as consultants for pharmaceutical companies.
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:
METHODOLOGY:
- Researchers evaluated the effectiveness of CGM use enhanced by geriatric principles in adults aged ≥ 65 years with T1D and at least two episodes of hypoglycemia (blood glucose level, < 70 mg/dL for ≥ 20 minutes over 2 weeks), who were either CGM-naive or CGM users prior to the study.
- Participants were randomly assigned to an intervention group using CGM with geriatric principles (ie, adjusting goals based on overall health and simplifying regimens based on CGM patterns and clinical characteristics) or a control group receiving usual care by their endocrinologist.
- The primary outcome was the change in duration of hypoglycemia from baseline to 6 months.
- A cost-effectiveness analysis was also performed for the intervention using a healthcare sector perspective, considering the cost of CGM devices and the cost of medical staff time.
TAKEAWAY:
- Researchers included 131 participants (mean age, 71 years), of whom 68 were in the intervention group (35 CGM-naive) and 63 in the control group (23 CGM-naive).
- The intervention group showed a median reduction of 2.6% in the duration of hypoglycemia vs a 0.3% reduction in the control group (median difference, −2.3%; P < .001).
- This reduction was observed in both CGM users (median difference, −1.2%) and CGM-naive participants (median difference, −2.8%) in the intervention group.
- No significant difference in A1c levels was observed between the intervention and control groups, indicating that CGM enhanced with geriatric principles did not worsen glycemic control.
- The intervention was associated with an incremental cost-effectiveness ratio of $71,623 per quality-adjusted life-year and was cost-effective for CGM-naive participants but at a lower level owing to the high cost of the CGM device.
IN PRACTICE:
“Personalization of goals and simplification of complex regimens can be combined with CGM use to improve management of type 1 diabetes in older adults,” the study authors wrote.
SOURCE:
The study was led by Medha N. Munshi, MD, Joslin Diabetes Center, Boston. It was published online in Diabetes Care.
LIMITATIONS:
The study included a relatively small sample size and an ethnically homogeneous and highly educated cohort, which may have limited the generalizability of its findings. Additionally, the study did not measure adherence to individual simplification strategies, which may have hindered the quantification of behavioral changes.
DISCLOSURES:
This study was supported by the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health. Two authors declared serving as consultants for pharmaceutical companies.
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:
METHODOLOGY:
- Researchers evaluated the effectiveness of CGM use enhanced by geriatric principles in adults aged ≥ 65 years with T1D and at least two episodes of hypoglycemia (blood glucose level, < 70 mg/dL for ≥ 20 minutes over 2 weeks), who were either CGM-naive or CGM users prior to the study.
- Participants were randomly assigned to an intervention group using CGM with geriatric principles (ie, adjusting goals based on overall health and simplifying regimens based on CGM patterns and clinical characteristics) or a control group receiving usual care by their endocrinologist.
- The primary outcome was the change in duration of hypoglycemia from baseline to 6 months.
- A cost-effectiveness analysis was also performed for the intervention using a healthcare sector perspective, considering the cost of CGM devices and the cost of medical staff time.
TAKEAWAY:
- Researchers included 131 participants (mean age, 71 years), of whom 68 were in the intervention group (35 CGM-naive) and 63 in the control group (23 CGM-naive).
- The intervention group showed a median reduction of 2.6% in the duration of hypoglycemia vs a 0.3% reduction in the control group (median difference, −2.3%; P < .001).
- This reduction was observed in both CGM users (median difference, −1.2%) and CGM-naive participants (median difference, −2.8%) in the intervention group.
- No significant difference in A1c levels was observed between the intervention and control groups, indicating that CGM enhanced with geriatric principles did not worsen glycemic control.
- The intervention was associated with an incremental cost-effectiveness ratio of $71,623 per quality-adjusted life-year and was cost-effective for CGM-naive participants but at a lower level owing to the high cost of the CGM device.
IN PRACTICE:
“Personalization of goals and simplification of complex regimens can be combined with CGM use to improve management of type 1 diabetes in older adults,” the study authors wrote.
SOURCE:
The study was led by Medha N. Munshi, MD, Joslin Diabetes Center, Boston. It was published online in Diabetes Care.
LIMITATIONS:
The study included a relatively small sample size and an ethnically homogeneous and highly educated cohort, which may have limited the generalizability of its findings. Additionally, the study did not measure adherence to individual simplification strategies, which may have hindered the quantification of behavioral changes.
DISCLOSURES:
This study was supported by the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health. Two authors declared serving as consultants for pharmaceutical companies.
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.
How to Treat Cancer While Preserving Fertility
Thanks to the continuously improving treatment options for cancer, the number of cancer survivors is increasing, and a large proportion of survivors is confronted with the long-term effects of cancer treatment. Especially for young patients, the question of the impact of therapy on fertility arises.
Dose adjustment or modification of the treatment regimen can achieve a lot. But experts at the congress of the European Society for Medical Oncology (ESMO) 2024 noted that knowledge about newer treatment options like immunotherapies is still insufficient.
Therapy Selection
The question of preserving fertility must be considered when deciding on the appropriate treatment, said Matteo Lambertini, MD, PhD, medical oncology consultant at the University of Genoa in Genoa, Italy.
“Preserving fertility is also an aim of cancer therapy,” he said.Lambertini, who is also a member of the ESMO Guideline Group on fertility preservation in cancer patients, referred to the 2020 ESMO guidelines, which list the gonadotoxicity of a substance depending on the treatment regimen and the patient’s age.
Isabelle Demeestere, MD, PhD, director of the research lab for human reproduction at the Erasmus Hospital of the Free University of Brussels in Brussels, Belgium, pointed out the limitations of general guidelines. “Therapies change over time, and a classification must be updated regularly.”
Knowledge gaps related to well-known therapies and many novel options persist. “For many FDA-approved medications, there are either no fertility data or only preclinical data available,” she added.
Chemotherapies and Immunotherapies
Chemotherapies with alkylating or platinum-containing substances are known for their effects on oocytes, follicle maturation, and spermatogenesis, said Demeestere.
Chemotherapy is gonadotoxic and leads to a temporary decrease in sperm quality or temporary azoospermia in men.
These effects, however, can lead to permanent azoospermia and endocrine disorders, depending on the dose, duration, or combination with radiation, said Demeestere.
Cryopreservation of sperm should always be performed before starting treatment. For high-risk patients who are prepubertal, samples of testicular tissue are taken.
In women, chemotherapy affects primordial follicles and follicle maturation through DNA damage. This process results in severe or temporary amenorrhea, a temporary or permanent decrease in egg reserve, and ultimately premature egg insufficiency.
Novel immunotherapies also influence fertility, presumably through interactions of the immune system with the reproductive organs. But insufficient data are available, according to Lambertini, who emphasized that “these data are urgently needed, especially for young patients with cancer.”
In a mouse model, immune checkpoint inhibitors affected ovarian function, and the inflammatory reaction in humans can affect fertility. No long-term data are available for women yet, however, explained Demeestere. The effects of other therapeutics such as PARP, CDK4/6, or tyrosine kinase inhibitors, as well as monoclonal antibodies like trastuzumab, are only seen sporadically.
In the PENELOPE-B phase 3 study, the CDK4/6 inhibitor palbociclib did not affect ovarian function, even though the cyclin-dependent kinases play an important role in mitotic arrest, said Demeestere.
Adjusting the Regimen
In a PET-guided approach, Demeestere’s research team investigated the effects of dose reduction or adjustment of the treatment regimen of procarbazine and cyclophosphamide on the fertility of patients younger than 45 years with advanced Hodgkin lymphoma.
By regularly controlling tumor growth with PET, the treatment could be adjusted so that the effect on egg reserve or spermatogenesis was significantly reduced and loss of fertility could be prevented.
During the 5-year follow-up period, the ovarian function of participating women was assessed by the serum concentration of follicle-stimulating hormone (FSH), estradiol, and anti-Müllerian hormone (AMH) to evaluate egg reserve. In men, testicular function was assessed at the beginning of the study. At the end of treatment, sperm analysis and FSH and testosterone levels were checked.
Demeestere and colleagues demonstrated that dose reduction or altering the treatment regimen for patients who responded early to treatment (determined by PET-guided monitoring) reduced the risk for gonadotoxicity from 46% to 14.5%. That is, the risk was reduced by more than half.
FSH and AMH correlated with the patient’s age and the dose of the alkylating agent. In men, sperm parameters recovered after dose or agent adjustment compared with the unchanged treatment regimen.
Newer results from the PHERGain study in women with early human epidermal growth factor receptor 2–positive breast cancer also provided hope, according to Demeestere. Under PET-guided control, chemotherapy could be reduced.
More Data Needed
The new treatment options pose a challenge to preserving fertility during cancer treatment, said Demeestere.
For new targeted therapies, uniform recommendations cannot be issued because of the lack of data and varying treatment durations. Still, the new therapies are safer than chemotherapy.
The need to collect data on fertility and long-term effects in cancer survivors in clinical studies is also reflected in the literature, according to Demeestere. “There are more review articles on this topic than clinical studies.”
This story was translated from the Medscape German edition 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.
Thanks to the continuously improving treatment options for cancer, the number of cancer survivors is increasing, and a large proportion of survivors is confronted with the long-term effects of cancer treatment. Especially for young patients, the question of the impact of therapy on fertility arises.
Dose adjustment or modification of the treatment regimen can achieve a lot. But experts at the congress of the European Society for Medical Oncology (ESMO) 2024 noted that knowledge about newer treatment options like immunotherapies is still insufficient.
Therapy Selection
The question of preserving fertility must be considered when deciding on the appropriate treatment, said Matteo Lambertini, MD, PhD, medical oncology consultant at the University of Genoa in Genoa, Italy.
“Preserving fertility is also an aim of cancer therapy,” he said.Lambertini, who is also a member of the ESMO Guideline Group on fertility preservation in cancer patients, referred to the 2020 ESMO guidelines, which list the gonadotoxicity of a substance depending on the treatment regimen and the patient’s age.
Isabelle Demeestere, MD, PhD, director of the research lab for human reproduction at the Erasmus Hospital of the Free University of Brussels in Brussels, Belgium, pointed out the limitations of general guidelines. “Therapies change over time, and a classification must be updated regularly.”
Knowledge gaps related to well-known therapies and many novel options persist. “For many FDA-approved medications, there are either no fertility data or only preclinical data available,” she added.
Chemotherapies and Immunotherapies
Chemotherapies with alkylating or platinum-containing substances are known for their effects on oocytes, follicle maturation, and spermatogenesis, said Demeestere.
Chemotherapy is gonadotoxic and leads to a temporary decrease in sperm quality or temporary azoospermia in men.
These effects, however, can lead to permanent azoospermia and endocrine disorders, depending on the dose, duration, or combination with radiation, said Demeestere.
Cryopreservation of sperm should always be performed before starting treatment. For high-risk patients who are prepubertal, samples of testicular tissue are taken.
In women, chemotherapy affects primordial follicles and follicle maturation through DNA damage. This process results in severe or temporary amenorrhea, a temporary or permanent decrease in egg reserve, and ultimately premature egg insufficiency.
Novel immunotherapies also influence fertility, presumably through interactions of the immune system with the reproductive organs. But insufficient data are available, according to Lambertini, who emphasized that “these data are urgently needed, especially for young patients with cancer.”
In a mouse model, immune checkpoint inhibitors affected ovarian function, and the inflammatory reaction in humans can affect fertility. No long-term data are available for women yet, however, explained Demeestere. The effects of other therapeutics such as PARP, CDK4/6, or tyrosine kinase inhibitors, as well as monoclonal antibodies like trastuzumab, are only seen sporadically.
In the PENELOPE-B phase 3 study, the CDK4/6 inhibitor palbociclib did not affect ovarian function, even though the cyclin-dependent kinases play an important role in mitotic arrest, said Demeestere.
Adjusting the Regimen
In a PET-guided approach, Demeestere’s research team investigated the effects of dose reduction or adjustment of the treatment regimen of procarbazine and cyclophosphamide on the fertility of patients younger than 45 years with advanced Hodgkin lymphoma.
By regularly controlling tumor growth with PET, the treatment could be adjusted so that the effect on egg reserve or spermatogenesis was significantly reduced and loss of fertility could be prevented.
During the 5-year follow-up period, the ovarian function of participating women was assessed by the serum concentration of follicle-stimulating hormone (FSH), estradiol, and anti-Müllerian hormone (AMH) to evaluate egg reserve. In men, testicular function was assessed at the beginning of the study. At the end of treatment, sperm analysis and FSH and testosterone levels were checked.
Demeestere and colleagues demonstrated that dose reduction or altering the treatment regimen for patients who responded early to treatment (determined by PET-guided monitoring) reduced the risk for gonadotoxicity from 46% to 14.5%. That is, the risk was reduced by more than half.
FSH and AMH correlated with the patient’s age and the dose of the alkylating agent. In men, sperm parameters recovered after dose or agent adjustment compared with the unchanged treatment regimen.
Newer results from the PHERGain study in women with early human epidermal growth factor receptor 2–positive breast cancer also provided hope, according to Demeestere. Under PET-guided control, chemotherapy could be reduced.
More Data Needed
The new treatment options pose a challenge to preserving fertility during cancer treatment, said Demeestere.
For new targeted therapies, uniform recommendations cannot be issued because of the lack of data and varying treatment durations. Still, the new therapies are safer than chemotherapy.
The need to collect data on fertility and long-term effects in cancer survivors in clinical studies is also reflected in the literature, according to Demeestere. “There are more review articles on this topic than clinical studies.”
This story was translated from the Medscape German edition 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.
Thanks to the continuously improving treatment options for cancer, the number of cancer survivors is increasing, and a large proportion of survivors is confronted with the long-term effects of cancer treatment. Especially for young patients, the question of the impact of therapy on fertility arises.
Dose adjustment or modification of the treatment regimen can achieve a lot. But experts at the congress of the European Society for Medical Oncology (ESMO) 2024 noted that knowledge about newer treatment options like immunotherapies is still insufficient.
Therapy Selection
The question of preserving fertility must be considered when deciding on the appropriate treatment, said Matteo Lambertini, MD, PhD, medical oncology consultant at the University of Genoa in Genoa, Italy.
“Preserving fertility is also an aim of cancer therapy,” he said.Lambertini, who is also a member of the ESMO Guideline Group on fertility preservation in cancer patients, referred to the 2020 ESMO guidelines, which list the gonadotoxicity of a substance depending on the treatment regimen and the patient’s age.
Isabelle Demeestere, MD, PhD, director of the research lab for human reproduction at the Erasmus Hospital of the Free University of Brussels in Brussels, Belgium, pointed out the limitations of general guidelines. “Therapies change over time, and a classification must be updated regularly.”
Knowledge gaps related to well-known therapies and many novel options persist. “For many FDA-approved medications, there are either no fertility data or only preclinical data available,” she added.
Chemotherapies and Immunotherapies
Chemotherapies with alkylating or platinum-containing substances are known for their effects on oocytes, follicle maturation, and spermatogenesis, said Demeestere.
Chemotherapy is gonadotoxic and leads to a temporary decrease in sperm quality or temporary azoospermia in men.
These effects, however, can lead to permanent azoospermia and endocrine disorders, depending on the dose, duration, or combination with radiation, said Demeestere.
Cryopreservation of sperm should always be performed before starting treatment. For high-risk patients who are prepubertal, samples of testicular tissue are taken.
In women, chemotherapy affects primordial follicles and follicle maturation through DNA damage. This process results in severe or temporary amenorrhea, a temporary or permanent decrease in egg reserve, and ultimately premature egg insufficiency.
Novel immunotherapies also influence fertility, presumably through interactions of the immune system with the reproductive organs. But insufficient data are available, according to Lambertini, who emphasized that “these data are urgently needed, especially for young patients with cancer.”
In a mouse model, immune checkpoint inhibitors affected ovarian function, and the inflammatory reaction in humans can affect fertility. No long-term data are available for women yet, however, explained Demeestere. The effects of other therapeutics such as PARP, CDK4/6, or tyrosine kinase inhibitors, as well as monoclonal antibodies like trastuzumab, are only seen sporadically.
In the PENELOPE-B phase 3 study, the CDK4/6 inhibitor palbociclib did not affect ovarian function, even though the cyclin-dependent kinases play an important role in mitotic arrest, said Demeestere.
Adjusting the Regimen
In a PET-guided approach, Demeestere’s research team investigated the effects of dose reduction or adjustment of the treatment regimen of procarbazine and cyclophosphamide on the fertility of patients younger than 45 years with advanced Hodgkin lymphoma.
By regularly controlling tumor growth with PET, the treatment could be adjusted so that the effect on egg reserve or spermatogenesis was significantly reduced and loss of fertility could be prevented.
During the 5-year follow-up period, the ovarian function of participating women was assessed by the serum concentration of follicle-stimulating hormone (FSH), estradiol, and anti-Müllerian hormone (AMH) to evaluate egg reserve. In men, testicular function was assessed at the beginning of the study. At the end of treatment, sperm analysis and FSH and testosterone levels were checked.
Demeestere and colleagues demonstrated that dose reduction or altering the treatment regimen for patients who responded early to treatment (determined by PET-guided monitoring) reduced the risk for gonadotoxicity from 46% to 14.5%. That is, the risk was reduced by more than half.
FSH and AMH correlated with the patient’s age and the dose of the alkylating agent. In men, sperm parameters recovered after dose or agent adjustment compared with the unchanged treatment regimen.
Newer results from the PHERGain study in women with early human epidermal growth factor receptor 2–positive breast cancer also provided hope, according to Demeestere. Under PET-guided control, chemotherapy could be reduced.
More Data Needed
The new treatment options pose a challenge to preserving fertility during cancer treatment, said Demeestere.
For new targeted therapies, uniform recommendations cannot be issued because of the lack of data and varying treatment durations. Still, the new therapies are safer than chemotherapy.
The need to collect data on fertility and long-term effects in cancer survivors in clinical studies is also reflected in the literature, according to Demeestere. “There are more review articles on this topic than clinical studies.”
This story was translated from the Medscape German edition 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.
Tirzepatide Shortage Resolved? FDA Says Yes, Compounders No
clarification aimed at compounders that Lilly said it can meet the “present and projected national demand” and that compounders are restricted from making the products.
The agency wrote in aNevertheless, patients and prescribers may still see “intermittent localized supply disruptions as the products move through the supply chain,” the FDA noted.
The Alliance for Pharmacy Compounding (APC) responded swiftly, alerting its members and the public to the resolved shortage and stating that compounders “must immediately cease preparing and dispensing compounded copies” of the two drugs.
However, APC CEO Scott Brunner added it often takes a long time for FDA-approved versions of the drug to become widely available to wholesalers, hospitals, and clinics. Even after Lilly announced greater availability for the drugs, including in a new vial format for low doses, “for most pharmacies, they’re lucky to get two or three boxes of Zepbound a day from their wholesaler — for a patient waiting list that can number in the hundreds.”
“We have already heard this morning from APC members that they are unable to fill orders for their patients,” he said.
Furthermore, he contended, “I suspect plenty of patients taking compounded tirzepatide are going to be caught flat-footed by this. They are being cut off cold turkey, their prescription no longer fillable. They’ll need to get in to see their provider to get a new prescription, and that will take some time. It’s possible that so many patients presently taking compounded GLP-1s [glucagon-like peptide 1] will be eventually switched to the FDA-approved versions — if they can afford them, of course — that it will push tirzepatide injection back into shortage.”
Commenting on the shortage resolution, endocrinologist Beverly Tchang, MD, DABOM, an assistant professor of clinical medicine at Weill Cornell Medicine in New York City told this news organization, “we are not yet experiencing relief from the shortages, but I hope this resolves at least one barrier to access for our patients.”
“I don’t think it will create confusion,” she said. “Fortunately or unfortunately, patients and clinicians are adept by now with therapeutic transitions because we’ve been forced to do so whenever insurance withdraws coverage or a shortage recurs or a coupon expires. It’s obviously not ideal but patients are motivated and clinicians don’t give up.”
This news organization has previously reported on the impact of the shortages and how endocrinologists and obesity medicine specialists were handling them, in light of concerns about compounding pharmacies that may or may not be well founded.
Dr. Tchang declared that she is an adviser to Novo Nordisk.
A version of this article appeared on Medscape.com.
clarification aimed at compounders that Lilly said it can meet the “present and projected national demand” and that compounders are restricted from making the products.
The agency wrote in aNevertheless, patients and prescribers may still see “intermittent localized supply disruptions as the products move through the supply chain,” the FDA noted.
The Alliance for Pharmacy Compounding (APC) responded swiftly, alerting its members and the public to the resolved shortage and stating that compounders “must immediately cease preparing and dispensing compounded copies” of the two drugs.
However, APC CEO Scott Brunner added it often takes a long time for FDA-approved versions of the drug to become widely available to wholesalers, hospitals, and clinics. Even after Lilly announced greater availability for the drugs, including in a new vial format for low doses, “for most pharmacies, they’re lucky to get two or three boxes of Zepbound a day from their wholesaler — for a patient waiting list that can number in the hundreds.”
“We have already heard this morning from APC members that they are unable to fill orders for their patients,” he said.
Furthermore, he contended, “I suspect plenty of patients taking compounded tirzepatide are going to be caught flat-footed by this. They are being cut off cold turkey, their prescription no longer fillable. They’ll need to get in to see their provider to get a new prescription, and that will take some time. It’s possible that so many patients presently taking compounded GLP-1s [glucagon-like peptide 1] will be eventually switched to the FDA-approved versions — if they can afford them, of course — that it will push tirzepatide injection back into shortage.”
Commenting on the shortage resolution, endocrinologist Beverly Tchang, MD, DABOM, an assistant professor of clinical medicine at Weill Cornell Medicine in New York City told this news organization, “we are not yet experiencing relief from the shortages, but I hope this resolves at least one barrier to access for our patients.”
“I don’t think it will create confusion,” she said. “Fortunately or unfortunately, patients and clinicians are adept by now with therapeutic transitions because we’ve been forced to do so whenever insurance withdraws coverage or a shortage recurs or a coupon expires. It’s obviously not ideal but patients are motivated and clinicians don’t give up.”
This news organization has previously reported on the impact of the shortages and how endocrinologists and obesity medicine specialists were handling them, in light of concerns about compounding pharmacies that may or may not be well founded.
Dr. Tchang declared that she is an adviser to Novo Nordisk.
A version of this article appeared on Medscape.com.
clarification aimed at compounders that Lilly said it can meet the “present and projected national demand” and that compounders are restricted from making the products.
The agency wrote in aNevertheless, patients and prescribers may still see “intermittent localized supply disruptions as the products move through the supply chain,” the FDA noted.
The Alliance for Pharmacy Compounding (APC) responded swiftly, alerting its members and the public to the resolved shortage and stating that compounders “must immediately cease preparing and dispensing compounded copies” of the two drugs.
However, APC CEO Scott Brunner added it often takes a long time for FDA-approved versions of the drug to become widely available to wholesalers, hospitals, and clinics. Even after Lilly announced greater availability for the drugs, including in a new vial format for low doses, “for most pharmacies, they’re lucky to get two or three boxes of Zepbound a day from their wholesaler — for a patient waiting list that can number in the hundreds.”
“We have already heard this morning from APC members that they are unable to fill orders for their patients,” he said.
Furthermore, he contended, “I suspect plenty of patients taking compounded tirzepatide are going to be caught flat-footed by this. They are being cut off cold turkey, their prescription no longer fillable. They’ll need to get in to see their provider to get a new prescription, and that will take some time. It’s possible that so many patients presently taking compounded GLP-1s [glucagon-like peptide 1] will be eventually switched to the FDA-approved versions — if they can afford them, of course — that it will push tirzepatide injection back into shortage.”
Commenting on the shortage resolution, endocrinologist Beverly Tchang, MD, DABOM, an assistant professor of clinical medicine at Weill Cornell Medicine in New York City told this news organization, “we are not yet experiencing relief from the shortages, but I hope this resolves at least one barrier to access for our patients.”
“I don’t think it will create confusion,” she said. “Fortunately or unfortunately, patients and clinicians are adept by now with therapeutic transitions because we’ve been forced to do so whenever insurance withdraws coverage or a shortage recurs or a coupon expires. It’s obviously not ideal but patients are motivated and clinicians don’t give up.”
This news organization has previously reported on the impact of the shortages and how endocrinologists and obesity medicine specialists were handling them, in light of concerns about compounding pharmacies that may or may not be well founded.
Dr. Tchang declared that she is an adviser to Novo Nordisk.
A version of this article appeared on Medscape.com.
Time-Restricted Eating Is Not a Metabolic Magic Bullet
This transcript has been edited for clarity.
One out of three American adults — about 100 million people in this country — have the metabolic syndrome. I’m showing you the official criteria here, but essentially this is a syndrome of insulin resistance and visceral adiposity that predisposes us to a host of chronic diseases such as diabetes, heart disease, and even dementia.
The metabolic syndrome is, fundamentally, a lifestyle disease. There is a direct line between our dietary habits and the wide availability of carbohydrate-rich, highly processed foods, and the rise in the syndrome in the population.
A saying I learned from one of my epidemiology teachers comes to mind: “Lifestyle diseases require lifestyle reinterventions.” But you know what? I’m not so sure anymore.
I’ve been around long enough to see multiple dietary fads come and go with varying efficacy. I grew up in the low-fat era, probably the most detrimental time to our national health as food manufacturers started replacing fats with carbohydrates, driving much of the problem we’re faced with today.
But I was also around for the Atkins diet and the low-carb craze — a healthier approach, all things being equal. And I’ve seen variants of these: the paleo diet (essentially a low-carb, high-protein diet based on minimally processed foods) and the Mediterranean diet, which sought to replace some percentage of fats with healthier fats.
And, of course, there is time-restricted eating.
Time-restricted eating, a variant of intermittent fasting, has the advantage of being very simple. No cookbooks, no recipes. Eat what you want — but limit it to certain hours in the day, ideally a window of less than 10 hours, such as 8 a.m. to 6 p.m.
When it comes to weight loss, the diets that work tend to work because they reduce calorie intake. I know, people will get angry about this, but thermodynamics is not just a good idea, it’s the law.
But weight loss is not the only reason we need to eat healthier. What we eat can impact our health in multiple ways; certain foods lead to more atherosclerosis, more inflammation, increased strain on the kidney and liver, and can affect our glucose homeostasis.
So I was really interested when I saw this article, “Time-Restricted Eating in Adults With Metabolic Syndrome,” appearing in Annals of Internal Medicine October 1, which examined the effect of time-restricted eating on the metabolic syndrome itself. Could this lifestyle intervention cure this lifestyle disease?
In the study, 108 individuals, all of whom had the metabolic syndrome but not full-blown diabetes, were randomized to usual care — basically, nutrition education — vs time-restricted eating. In that group, participants were instructed to reduce their window of eating by at least 4 hours to achieve an 8- to 10-hour eating window. The groups were followed for 3 months.
Now, before we get to the results, it’s important to remember that the success of a lifestyle intervention trial is quite dependent on how well people adhere to the lifestyle intervention. Time-restricted eating is not as easy as taking a pill once a day.
The researchers had participants log their consumption using a smartphone app to confirm whether they were adhering to that restricted eating window.
Broadly speaking, they did. At baseline, both groups had an eating window of about 14 hours a day — think 7 a.m. to 9 p.m. The intervention group reduced that to just under 10 hours, with 10% of days falling outside of the target window.
Lifestyle change achieved, the primary outcome was the change in hemoglobin A1c at 3 months. A1c integrates the serum glucose over time and is thus a good indicator of the success of the intervention in terms of insulin resistance. But the effect was, honestly, disappointing.
Technically, the time-restricted-eating group had a greater A1c change than the control group — by 0.1 percentage points. On average, they went from a baseline A1c of 5.87 to a 3-month A1c of 5.75.
Other metabolic syndrome markers were equally lackluster: no difference in fasting glucose, mean glucose, or fasting insulin.
There was some weight change. The control group, which got that dietary education, lost 1.5% of body weight over the 3 months. The time-restricted-eating group lost 3.3% — about 7 pounds, which is reasonable.
With that weight loss came statistically significant, albeit modest improvements in BMI, body fat percentage, and LDL cholesterol.
Of interest, despite the larger weight loss in the intermittent-fasting group, there was no difference in muscle mass loss, which is encouraging.
Taken together, we can say that, yes, it seems like time-restricted eating can help people lose some weight. This is essentially due to the fact that people eat fewer calories when they do time-restricted eating, as you can see here.
But, in the end, this trial examined whether this relatively straightforward lifestyle intervention would move the needle in terms of metabolic syndrome, and the data are not very compelling for that.
This graph shows how many of those five factors for metabolic syndrome the individuals in this trial had from the start to the end. You see that, over the 3 months, seven people in the time-restricted-eating group moved from having three criteria to two or one — being “cured” of metabolic syndrome, if you will. Nine people in the standard group were cured by that definition. Remember, they had to have at least three to have the syndrome and thus be eligible for the trial.
So If it just leads to weight loss by forcing people to consume less calories, then we need to acknowledge that we probably have better methods to achieve this same end. Ten years ago, I would have said that lifestyle change is the only way to end the epidemic of the metabolic syndrome in this country. Today, well, we live in a world of GLP-1 weight loss drugs. It is simply a different world now. Yes, they are expensive. Yes, they have side effects. But we need to evaluate them against the comparison. And so far, lifestyle changes alone are really no comparison.
Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
One out of three American adults — about 100 million people in this country — have the metabolic syndrome. I’m showing you the official criteria here, but essentially this is a syndrome of insulin resistance and visceral adiposity that predisposes us to a host of chronic diseases such as diabetes, heart disease, and even dementia.
The metabolic syndrome is, fundamentally, a lifestyle disease. There is a direct line between our dietary habits and the wide availability of carbohydrate-rich, highly processed foods, and the rise in the syndrome in the population.
A saying I learned from one of my epidemiology teachers comes to mind: “Lifestyle diseases require lifestyle reinterventions.” But you know what? I’m not so sure anymore.
I’ve been around long enough to see multiple dietary fads come and go with varying efficacy. I grew up in the low-fat era, probably the most detrimental time to our national health as food manufacturers started replacing fats with carbohydrates, driving much of the problem we’re faced with today.
But I was also around for the Atkins diet and the low-carb craze — a healthier approach, all things being equal. And I’ve seen variants of these: the paleo diet (essentially a low-carb, high-protein diet based on minimally processed foods) and the Mediterranean diet, which sought to replace some percentage of fats with healthier fats.
And, of course, there is time-restricted eating.
Time-restricted eating, a variant of intermittent fasting, has the advantage of being very simple. No cookbooks, no recipes. Eat what you want — but limit it to certain hours in the day, ideally a window of less than 10 hours, such as 8 a.m. to 6 p.m.
When it comes to weight loss, the diets that work tend to work because they reduce calorie intake. I know, people will get angry about this, but thermodynamics is not just a good idea, it’s the law.
But weight loss is not the only reason we need to eat healthier. What we eat can impact our health in multiple ways; certain foods lead to more atherosclerosis, more inflammation, increased strain on the kidney and liver, and can affect our glucose homeostasis.
So I was really interested when I saw this article, “Time-Restricted Eating in Adults With Metabolic Syndrome,” appearing in Annals of Internal Medicine October 1, which examined the effect of time-restricted eating on the metabolic syndrome itself. Could this lifestyle intervention cure this lifestyle disease?
In the study, 108 individuals, all of whom had the metabolic syndrome but not full-blown diabetes, were randomized to usual care — basically, nutrition education — vs time-restricted eating. In that group, participants were instructed to reduce their window of eating by at least 4 hours to achieve an 8- to 10-hour eating window. The groups were followed for 3 months.
Now, before we get to the results, it’s important to remember that the success of a lifestyle intervention trial is quite dependent on how well people adhere to the lifestyle intervention. Time-restricted eating is not as easy as taking a pill once a day.
The researchers had participants log their consumption using a smartphone app to confirm whether they were adhering to that restricted eating window.
Broadly speaking, they did. At baseline, both groups had an eating window of about 14 hours a day — think 7 a.m. to 9 p.m. The intervention group reduced that to just under 10 hours, with 10% of days falling outside of the target window.
Lifestyle change achieved, the primary outcome was the change in hemoglobin A1c at 3 months. A1c integrates the serum glucose over time and is thus a good indicator of the success of the intervention in terms of insulin resistance. But the effect was, honestly, disappointing.
Technically, the time-restricted-eating group had a greater A1c change than the control group — by 0.1 percentage points. On average, they went from a baseline A1c of 5.87 to a 3-month A1c of 5.75.
Other metabolic syndrome markers were equally lackluster: no difference in fasting glucose, mean glucose, or fasting insulin.
There was some weight change. The control group, which got that dietary education, lost 1.5% of body weight over the 3 months. The time-restricted-eating group lost 3.3% — about 7 pounds, which is reasonable.
With that weight loss came statistically significant, albeit modest improvements in BMI, body fat percentage, and LDL cholesterol.
Of interest, despite the larger weight loss in the intermittent-fasting group, there was no difference in muscle mass loss, which is encouraging.
Taken together, we can say that, yes, it seems like time-restricted eating can help people lose some weight. This is essentially due to the fact that people eat fewer calories when they do time-restricted eating, as you can see here.
But, in the end, this trial examined whether this relatively straightforward lifestyle intervention would move the needle in terms of metabolic syndrome, and the data are not very compelling for that.
This graph shows how many of those five factors for metabolic syndrome the individuals in this trial had from the start to the end. You see that, over the 3 months, seven people in the time-restricted-eating group moved from having three criteria to two or one — being “cured” of metabolic syndrome, if you will. Nine people in the standard group were cured by that definition. Remember, they had to have at least three to have the syndrome and thus be eligible for the trial.
So If it just leads to weight loss by forcing people to consume less calories, then we need to acknowledge that we probably have better methods to achieve this same end. Ten years ago, I would have said that lifestyle change is the only way to end the epidemic of the metabolic syndrome in this country. Today, well, we live in a world of GLP-1 weight loss drugs. It is simply a different world now. Yes, they are expensive. Yes, they have side effects. But we need to evaluate them against the comparison. And so far, lifestyle changes alone are really no comparison.
Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
One out of three American adults — about 100 million people in this country — have the metabolic syndrome. I’m showing you the official criteria here, but essentially this is a syndrome of insulin resistance and visceral adiposity that predisposes us to a host of chronic diseases such as diabetes, heart disease, and even dementia.
The metabolic syndrome is, fundamentally, a lifestyle disease. There is a direct line between our dietary habits and the wide availability of carbohydrate-rich, highly processed foods, and the rise in the syndrome in the population.
A saying I learned from one of my epidemiology teachers comes to mind: “Lifestyle diseases require lifestyle reinterventions.” But you know what? I’m not so sure anymore.
I’ve been around long enough to see multiple dietary fads come and go with varying efficacy. I grew up in the low-fat era, probably the most detrimental time to our national health as food manufacturers started replacing fats with carbohydrates, driving much of the problem we’re faced with today.
But I was also around for the Atkins diet and the low-carb craze — a healthier approach, all things being equal. And I’ve seen variants of these: the paleo diet (essentially a low-carb, high-protein diet based on minimally processed foods) and the Mediterranean diet, which sought to replace some percentage of fats with healthier fats.
And, of course, there is time-restricted eating.
Time-restricted eating, a variant of intermittent fasting, has the advantage of being very simple. No cookbooks, no recipes. Eat what you want — but limit it to certain hours in the day, ideally a window of less than 10 hours, such as 8 a.m. to 6 p.m.
When it comes to weight loss, the diets that work tend to work because they reduce calorie intake. I know, people will get angry about this, but thermodynamics is not just a good idea, it’s the law.
But weight loss is not the only reason we need to eat healthier. What we eat can impact our health in multiple ways; certain foods lead to more atherosclerosis, more inflammation, increased strain on the kidney and liver, and can affect our glucose homeostasis.
So I was really interested when I saw this article, “Time-Restricted Eating in Adults With Metabolic Syndrome,” appearing in Annals of Internal Medicine October 1, which examined the effect of time-restricted eating on the metabolic syndrome itself. Could this lifestyle intervention cure this lifestyle disease?
In the study, 108 individuals, all of whom had the metabolic syndrome but not full-blown diabetes, were randomized to usual care — basically, nutrition education — vs time-restricted eating. In that group, participants were instructed to reduce their window of eating by at least 4 hours to achieve an 8- to 10-hour eating window. The groups were followed for 3 months.
Now, before we get to the results, it’s important to remember that the success of a lifestyle intervention trial is quite dependent on how well people adhere to the lifestyle intervention. Time-restricted eating is not as easy as taking a pill once a day.
The researchers had participants log their consumption using a smartphone app to confirm whether they were adhering to that restricted eating window.
Broadly speaking, they did. At baseline, both groups had an eating window of about 14 hours a day — think 7 a.m. to 9 p.m. The intervention group reduced that to just under 10 hours, with 10% of days falling outside of the target window.
Lifestyle change achieved, the primary outcome was the change in hemoglobin A1c at 3 months. A1c integrates the serum glucose over time and is thus a good indicator of the success of the intervention in terms of insulin resistance. But the effect was, honestly, disappointing.
Technically, the time-restricted-eating group had a greater A1c change than the control group — by 0.1 percentage points. On average, they went from a baseline A1c of 5.87 to a 3-month A1c of 5.75.
Other metabolic syndrome markers were equally lackluster: no difference in fasting glucose, mean glucose, or fasting insulin.
There was some weight change. The control group, which got that dietary education, lost 1.5% of body weight over the 3 months. The time-restricted-eating group lost 3.3% — about 7 pounds, which is reasonable.
With that weight loss came statistically significant, albeit modest improvements in BMI, body fat percentage, and LDL cholesterol.
Of interest, despite the larger weight loss in the intermittent-fasting group, there was no difference in muscle mass loss, which is encouraging.
Taken together, we can say that, yes, it seems like time-restricted eating can help people lose some weight. This is essentially due to the fact that people eat fewer calories when they do time-restricted eating, as you can see here.
But, in the end, this trial examined whether this relatively straightforward lifestyle intervention would move the needle in terms of metabolic syndrome, and the data are not very compelling for that.
This graph shows how many of those five factors for metabolic syndrome the individuals in this trial had from the start to the end. You see that, over the 3 months, seven people in the time-restricted-eating group moved from having three criteria to two or one — being “cured” of metabolic syndrome, if you will. Nine people in the standard group were cured by that definition. Remember, they had to have at least three to have the syndrome and thus be eligible for the trial.
So If it just leads to weight loss by forcing people to consume less calories, then we need to acknowledge that we probably have better methods to achieve this same end. Ten years ago, I would have said that lifestyle change is the only way to end the epidemic of the metabolic syndrome in this country. Today, well, we live in a world of GLP-1 weight loss drugs. It is simply a different world now. Yes, they are expensive. Yes, they have side effects. But we need to evaluate them against the comparison. And so far, lifestyle changes alone are really no comparison.
Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.