Cardiology News

Artificial intelligence (AI) has identified two plant-based bioactive compounds with potential as glucagon-like-peptide-1 receptor (GLP-1R) agonists for weight loss as possible alternatives to pharmaceutical weight-loss drugs, but with potentially fewer side effects and oral administration.

Using AI, the work aimed to identify novel, natural-derived bioactive compounds that may activate the GLP-1R, which is the site of action of existing weight loss pharmaceutical drugs including semaglutide (Wegovy, Novo Nordisk) and dual agonist tirzepatide (Zepbound, Eli Lilly).

Presenter Elena Murcia, PhD, of the Structural Bioinformatics and High-Performance Computing Research Group & Eating Disorders Research Unit, Catholic University of Dr. Murcia, Dr. Murcia, Spain, will be sharing her work at the upcoming European Congress on Obesity (ECO 2024) in May.

Although GLP-1 agonists have shown effectiveness in trials, “there are some side effects associated with their use — gastrointestinal issues such as nausea and vomiting, as well as mental health changes like anxiety and irritability. Recent data has also confirmed that when patients stop treatment, they regain lost weight,” she said.

In addition, there is the issue of having to inject the drugs rather than taking them orally due to the peptide nature of existing GLP-1 agonists that risk degradation by stomach enzymes before they exert the required effect.

“Drugs that aren’t peptides may have fewer side effects and be easier to administer, meaning they could be given as pills rather than injections,” said Dr. Murcia.

Other recent research has highlighted two promising non-peptide compounds, TTOAD2 and orforglipron. “These are synthetic, and we were interested in finding natural alternatives,” she added.
 

Natural Versions of Compounds That Activate GLP-1Rs

Drawing on recent understanding around the TTOAD2 and orforglipron compounds, the present work focuses on using AI to identify new non-peptidic, natural-derived bioactive compounds to activate the GLP-1R, according to the researcher in her abstract and a preconference press release from ECO.

Using advanced AI techniques (an in silico approach that entails experimentation by computer), Dr. Murcia selected natural molecules as bioactive compounds with GLP-1R agonist activity in a stepwise process that initially used ligand and structure-based virtual screening of over 10,000 compounds, followed by additional visual analysis of the top 100 compounds with the highest similarity to determine their degree of interaction with amino acids on the GLP-1 receptors. Arriving at a shortlist of 65, the researchers synthesized these data to identify the compounds with the highest potential as GLP-1R agonists, and two of these, referred to as Compound A and Compound B — both plant-derived — were found to bind strongly to the key amino acids in a similar way to TTOAD2 and orforglipron.

“These compounds are currently being further investigated for their efficacy in obesity treatment through in vitro analysis,” wrote Dr. Murcia and her colleagues in their abstract.

Asked to comment on the work, Felix Wong, PhD, postdoctoral fellow at the Broad Institute of MIT and Harvard, Cambridge, Massachusetts, who recently discovered a new class of antibiotics with activity against methicillin-resistant Staphylococcus aureus using deep learning, told this news organization that, “The promise of AI for drug discovery has increasingly been realized, and just recently we have seen the discoveries of new antibiotics, senolytics, and anti-fibrotic compounds, among others.”

“This study, which is based on molecular docking, suggests that similar computational methods can be applied to popular therapeutic areas like GLP-1R agonist discovery,” he said, adding that “the study will need experimental validation given that computational predictions can lead to false positives and that natural products are often promiscuous.”

Dr. Murcia has declared no relevant conflicts. Dr. Wong has declared he is cofounder of Integrated Biosciences, an early-stage biotechnology company.

A version of this article appeared on Medscape.com.

Artificial intelligence (AI) has identified two plant-based bioactive compounds with potential as glucagon-like-peptide-1 receptor (GLP-1R) agonists for weight loss as possible alternatives to pharmaceutical weight-loss drugs, but with potentially fewer side effects and oral administration.

Using AI, the work aimed to identify novel, natural-derived bioactive compounds that may activate the GLP-1R, which is the site of action of existing weight loss pharmaceutical drugs including semaglutide (Wegovy, Novo Nordisk) and dual agonist tirzepatide (Zepbound, Eli Lilly).

Presenter Elena Murcia, PhD, of the Structural Bioinformatics and High-Performance Computing Research Group & Eating Disorders Research Unit, Catholic University of Dr. Murcia, Dr. Murcia, Spain, will be sharing her work at the upcoming European Congress on Obesity (ECO 2024) in May.

Although GLP-1 agonists have shown effectiveness in trials, “there are some side effects associated with their use — gastrointestinal issues such as nausea and vomiting, as well as mental health changes like anxiety and irritability. Recent data has also confirmed that when patients stop treatment, they regain lost weight,” she said.

In addition, there is the issue of having to inject the drugs rather than taking them orally due to the peptide nature of existing GLP-1 agonists that risk degradation by stomach enzymes before they exert the required effect.

“Drugs that aren’t peptides may have fewer side effects and be easier to administer, meaning they could be given as pills rather than injections,” said Dr. Murcia.

Other recent research has highlighted two promising non-peptide compounds, TTOAD2 and orforglipron. “These are synthetic, and we were interested in finding natural alternatives,” she added.
 

Natural Versions of Compounds That Activate GLP-1Rs

Drawing on recent understanding around the TTOAD2 and orforglipron compounds, the present work focuses on using AI to identify new non-peptidic, natural-derived bioactive compounds to activate the GLP-1R, according to the researcher in her abstract and a preconference press release from ECO.

Using advanced AI techniques (an in silico approach that entails experimentation by computer), Dr. Murcia selected natural molecules as bioactive compounds with GLP-1R agonist activity in a stepwise process that initially used ligand and structure-based virtual screening of over 10,000 compounds, followed by additional visual analysis of the top 100 compounds with the highest similarity to determine their degree of interaction with amino acids on the GLP-1 receptors. Arriving at a shortlist of 65, the researchers synthesized these data to identify the compounds with the highest potential as GLP-1R agonists, and two of these, referred to as Compound A and Compound B — both plant-derived — were found to bind strongly to the key amino acids in a similar way to TTOAD2 and orforglipron.

“These compounds are currently being further investigated for their efficacy in obesity treatment through in vitro analysis,” wrote Dr. Murcia and her colleagues in their abstract.

Asked to comment on the work, Felix Wong, PhD, postdoctoral fellow at the Broad Institute of MIT and Harvard, Cambridge, Massachusetts, who recently discovered a new class of antibiotics with activity against methicillin-resistant Staphylococcus aureus using deep learning, told this news organization that, “The promise of AI for drug discovery has increasingly been realized, and just recently we have seen the discoveries of new antibiotics, senolytics, and anti-fibrotic compounds, among others.”

“This study, which is based on molecular docking, suggests that similar computational methods can be applied to popular therapeutic areas like GLP-1R agonist discovery,” he said, adding that “the study will need experimental validation given that computational predictions can lead to false positives and that natural products are often promiscuous.”

Dr. Murcia has declared no relevant conflicts. Dr. Wong has declared he is cofounder of Integrated Biosciences, an early-stage biotechnology company.

A version of this article appeared on Medscape.com.

Artificial intelligence (AI) has identified two plant-based bioactive compounds with potential as glucagon-like-peptide-1 receptor (GLP-1R) agonists for weight loss as possible alternatives to pharmaceutical weight-loss drugs, but with potentially fewer side effects and oral administration.

Using AI, the work aimed to identify novel, natural-derived bioactive compounds that may activate the GLP-1R, which is the site of action of existing weight loss pharmaceutical drugs including semaglutide (Wegovy, Novo Nordisk) and dual agonist tirzepatide (Zepbound, Eli Lilly).

Presenter Elena Murcia, PhD, of the Structural Bioinformatics and High-Performance Computing Research Group & Eating Disorders Research Unit, Catholic University of Dr. Murcia, Dr. Murcia, Spain, will be sharing her work at the upcoming European Congress on Obesity (ECO 2024) in May.

Although GLP-1 agonists have shown effectiveness in trials, “there are some side effects associated with their use — gastrointestinal issues such as nausea and vomiting, as well as mental health changes like anxiety and irritability. Recent data has also confirmed that when patients stop treatment, they regain lost weight,” she said.

In addition, there is the issue of having to inject the drugs rather than taking them orally due to the peptide nature of existing GLP-1 agonists that risk degradation by stomach enzymes before they exert the required effect.

“Drugs that aren’t peptides may have fewer side effects and be easier to administer, meaning they could be given as pills rather than injections,” said Dr. Murcia.

Other recent research has highlighted two promising non-peptide compounds, TTOAD2 and orforglipron. “These are synthetic, and we were interested in finding natural alternatives,” she added.
 

Natural Versions of Compounds That Activate GLP-1Rs

Drawing on recent understanding around the TTOAD2 and orforglipron compounds, the present work focuses on using AI to identify new non-peptidic, natural-derived bioactive compounds to activate the GLP-1R, according to the researcher in her abstract and a preconference press release from ECO.

Using advanced AI techniques (an in silico approach that entails experimentation by computer), Dr. Murcia selected natural molecules as bioactive compounds with GLP-1R agonist activity in a stepwise process that initially used ligand and structure-based virtual screening of over 10,000 compounds, followed by additional visual analysis of the top 100 compounds with the highest similarity to determine their degree of interaction with amino acids on the GLP-1 receptors. Arriving at a shortlist of 65, the researchers synthesized these data to identify the compounds with the highest potential as GLP-1R agonists, and two of these, referred to as Compound A and Compound B — both plant-derived — were found to bind strongly to the key amino acids in a similar way to TTOAD2 and orforglipron.

“These compounds are currently being further investigated for their efficacy in obesity treatment through in vitro analysis,” wrote Dr. Murcia and her colleagues in their abstract.

Asked to comment on the work, Felix Wong, PhD, postdoctoral fellow at the Broad Institute of MIT and Harvard, Cambridge, Massachusetts, who recently discovered a new class of antibiotics with activity against methicillin-resistant Staphylococcus aureus using deep learning, told this news organization that, “The promise of AI for drug discovery has increasingly been realized, and just recently we have seen the discoveries of new antibiotics, senolytics, and anti-fibrotic compounds, among others.”

“This study, which is based on molecular docking, suggests that similar computational methods can be applied to popular therapeutic areas like GLP-1R agonist discovery,” he said, adding that “the study will need experimental validation given that computational predictions can lead to false positives and that natural products are often promiscuous.”

Dr. Murcia has declared no relevant conflicts. Dr. Wong has declared he is cofounder of Integrated Biosciences, an early-stage biotechnology company.

A version of this article appeared on Medscape.com.

As your patient’s scheduled bedtime is approaching, they begin to worry another restless night is looming. Could magnesium oil spray actually help them sleep? Some — even doctors — are sharing testimonials about how this simple tactic transformed their sleep quality. Experts suggest some sleep improvement is possible, though it does not negate the need for treatment, and should not be used in patients with cardiovascular disease.

Take Daniel Barrett, MD, a board-certified plastic surgeon and owner of Barrett Plastic Surgery in Beverly Hills, as an example. He decided to test whether magnesium oil could indeed give him a sleepy sensation and shared his experience. Dr. Barrett sprayed magnesium oil on his feet — until they felt “slippery and wet,” he said — and put his socks back on. (He said magnesium is absorbed more easily through the skin. Putting it on the skin helps this mineral get into the lymphatics and circulatory system, offering a way to get a higher concentration of magnesium in the bloodstream. The pores on the feet are also said to be the largest on the body, making them an ideal place for absorption.) 

“My central nervous system had calmed down a bit — it’s similar to what I feel when I take oral magnesium as well. It took about 15 minutes to feel the effect,” Dr. Barrett said.

Research shows that magnesium blocks N-methyl-D-aspartate (a receptor that can hinder sleep) and stimulates gamma-aminobutyric acid (a receptor that can promote good sleep), said Dennis Auckley, MD, director of MetroHealth’s Center for Sleep Medicine. And studies looking at the effects of oral magnesium have shown that taking it may be linked to better self-reported sleep quality and less daytime sleepiness, he said. But traditional magnesium supplements taken orally can sometimes come with side effects in your gut, so putting magnesium on the skin could help to avoid this. 

Magnesium oil on the feet could also help with certain sleep disturbances, such as nocturnal leg cramps and restless legs syndrome, said Sam Kashani, MD, a sleep medicine specialist and assistant clinical professor at UCLA Medical School. (Nocturnal leg cramps – one of the most common secondary factors of insomnia and sleep disturbances in older adults – includes sudden, painful contractions in the lower leg muscles while sleeping. Restless legs syndrome, on the other hand, is like nocturnal leg cramps, but minus the painful contractions, said Dr. Kashani.) 

“Magnesium is a mineral that does have some benefit with regard to reducing the muscle tightness and promoting a little bit more of relaxation of the muscles,” Dr. Kashani said. “This [magnesium oil on your soles] could be beneficial for these types of sleep problems.” 

Still, sleep medicine experts stressed that putting magnesium oil on your feet should not be viewed a cure-all for sleep troubles. 

“High-quality scientific evidence supporting magnesium as a sleep remedy is severely limited,” said Emerson Wickwire, PhD, an American Academy of Sleep Medicine spokesperson and section head of sleep medicine at the University of Maryland Medical School. “Certainly, magnesium is not supported as a treatment for sleep disorders.” 

If your patients plan to use magnesium oil on their feet to help them sleep, make sure they carefully follow the directions to make sure they are taking the proper dosage. Most importantly, patients with a history of cardiovascular complications, or issues with the heart and blood vessels should consult their doctor. 

“Magnesium is an electrolyte that has multiple roles and functions in the body, including within our cardiovascular system,” Dr. Kashani said. “So, if you are somebody who has heart troubles, you definitely want to talk to your primary doctor about any kind of supplements that you are taking, including magnesium.”
 

A version of this article appeared on WebMD.com.

As your patient’s scheduled bedtime is approaching, they begin to worry another restless night is looming. Could magnesium oil spray actually help them sleep? Some — even doctors — are sharing testimonials about how this simple tactic transformed their sleep quality. Experts suggest some sleep improvement is possible, though it does not negate the need for treatment, and should not be used in patients with cardiovascular disease.

Take Daniel Barrett, MD, a board-certified plastic surgeon and owner of Barrett Plastic Surgery in Beverly Hills, as an example. He decided to test whether magnesium oil could indeed give him a sleepy sensation and shared his experience. Dr. Barrett sprayed magnesium oil on his feet — until they felt “slippery and wet,” he said — and put his socks back on. (He said magnesium is absorbed more easily through the skin. Putting it on the skin helps this mineral get into the lymphatics and circulatory system, offering a way to get a higher concentration of magnesium in the bloodstream. The pores on the feet are also said to be the largest on the body, making them an ideal place for absorption.) 

“My central nervous system had calmed down a bit — it’s similar to what I feel when I take oral magnesium as well. It took about 15 minutes to feel the effect,” Dr. Barrett said.

Research shows that magnesium blocks N-methyl-D-aspartate (a receptor that can hinder sleep) and stimulates gamma-aminobutyric acid (a receptor that can promote good sleep), said Dennis Auckley, MD, director of MetroHealth’s Center for Sleep Medicine. And studies looking at the effects of oral magnesium have shown that taking it may be linked to better self-reported sleep quality and less daytime sleepiness, he said. But traditional magnesium supplements taken orally can sometimes come with side effects in your gut, so putting magnesium on the skin could help to avoid this. 

Magnesium oil on the feet could also help with certain sleep disturbances, such as nocturnal leg cramps and restless legs syndrome, said Sam Kashani, MD, a sleep medicine specialist and assistant clinical professor at UCLA Medical School. (Nocturnal leg cramps – one of the most common secondary factors of insomnia and sleep disturbances in older adults – includes sudden, painful contractions in the lower leg muscles while sleeping. Restless legs syndrome, on the other hand, is like nocturnal leg cramps, but minus the painful contractions, said Dr. Kashani.) 

“Magnesium is a mineral that does have some benefit with regard to reducing the muscle tightness and promoting a little bit more of relaxation of the muscles,” Dr. Kashani said. “This [magnesium oil on your soles] could be beneficial for these types of sleep problems.” 

Still, sleep medicine experts stressed that putting magnesium oil on your feet should not be viewed a cure-all for sleep troubles. 

“High-quality scientific evidence supporting magnesium as a sleep remedy is severely limited,” said Emerson Wickwire, PhD, an American Academy of Sleep Medicine spokesperson and section head of sleep medicine at the University of Maryland Medical School. “Certainly, magnesium is not supported as a treatment for sleep disorders.” 

If your patients plan to use magnesium oil on their feet to help them sleep, make sure they carefully follow the directions to make sure they are taking the proper dosage. Most importantly, patients with a history of cardiovascular complications, or issues with the heart and blood vessels should consult their doctor. 

“Magnesium is an electrolyte that has multiple roles and functions in the body, including within our cardiovascular system,” Dr. Kashani said. “So, if you are somebody who has heart troubles, you definitely want to talk to your primary doctor about any kind of supplements that you are taking, including magnesium.”
 

A version of this article appeared on WebMD.com.

As your patient’s scheduled bedtime is approaching, they begin to worry another restless night is looming. Could magnesium oil spray actually help them sleep? Some — even doctors — are sharing testimonials about how this simple tactic transformed their sleep quality. Experts suggest some sleep improvement is possible, though it does not negate the need for treatment, and should not be used in patients with cardiovascular disease.

Take Daniel Barrett, MD, a board-certified plastic surgeon and owner of Barrett Plastic Surgery in Beverly Hills, as an example. He decided to test whether magnesium oil could indeed give him a sleepy sensation and shared his experience. Dr. Barrett sprayed magnesium oil on his feet — until they felt “slippery and wet,” he said — and put his socks back on. (He said magnesium is absorbed more easily through the skin. Putting it on the skin helps this mineral get into the lymphatics and circulatory system, offering a way to get a higher concentration of magnesium in the bloodstream. The pores on the feet are also said to be the largest on the body, making them an ideal place for absorption.) 

“My central nervous system had calmed down a bit — it’s similar to what I feel when I take oral magnesium as well. It took about 15 minutes to feel the effect,” Dr. Barrett said.

Research shows that magnesium blocks N-methyl-D-aspartate (a receptor that can hinder sleep) and stimulates gamma-aminobutyric acid (a receptor that can promote good sleep), said Dennis Auckley, MD, director of MetroHealth’s Center for Sleep Medicine. And studies looking at the effects of oral magnesium have shown that taking it may be linked to better self-reported sleep quality and less daytime sleepiness, he said. But traditional magnesium supplements taken orally can sometimes come with side effects in your gut, so putting magnesium on the skin could help to avoid this. 

Magnesium oil on the feet could also help with certain sleep disturbances, such as nocturnal leg cramps and restless legs syndrome, said Sam Kashani, MD, a sleep medicine specialist and assistant clinical professor at UCLA Medical School. (Nocturnal leg cramps – one of the most common secondary factors of insomnia and sleep disturbances in older adults – includes sudden, painful contractions in the lower leg muscles while sleeping. Restless legs syndrome, on the other hand, is like nocturnal leg cramps, but minus the painful contractions, said Dr. Kashani.) 

“Magnesium is a mineral that does have some benefit with regard to reducing the muscle tightness and promoting a little bit more of relaxation of the muscles,” Dr. Kashani said. “This [magnesium oil on your soles] could be beneficial for these types of sleep problems.” 

Still, sleep medicine experts stressed that putting magnesium oil on your feet should not be viewed a cure-all for sleep troubles. 

“High-quality scientific evidence supporting magnesium as a sleep remedy is severely limited,” said Emerson Wickwire, PhD, an American Academy of Sleep Medicine spokesperson and section head of sleep medicine at the University of Maryland Medical School. “Certainly, magnesium is not supported as a treatment for sleep disorders.” 

If your patients plan to use magnesium oil on their feet to help them sleep, make sure they carefully follow the directions to make sure they are taking the proper dosage. Most importantly, patients with a history of cardiovascular complications, or issues with the heart and blood vessels should consult their doctor. 

“Magnesium is an electrolyte that has multiple roles and functions in the body, including within our cardiovascular system,” Dr. Kashani said. “So, if you are somebody who has heart troubles, you definitely want to talk to your primary doctor about any kind of supplements that you are taking, including magnesium.”
 

A version of this article appeared on WebMD.com.

TOPLINE:

Patients with sarcopenic obesity (SO) are at a greater risk for earlier death, but screening for muscle function could offer an opportunity for intervention.

METHODOLOGY:

• The proportion of older adults living with high body fat and/or low muscle function and mass has risen in recent years, but sarcopenia and SO are undiagnosed conditions.
• Researchers evaluated 5888 individuals who participated in a population-based cohort study in the Netherlands: Participants were largely of European descent (98%); the mean age of participants was 69.5 years, and 56.8% were female.
• Participants were included if they had available measurements of handgrip strength and had received a dual-energy x-ray absorptiometry scan.
• Sarcopenia was defined by researchers in JAMA Network Open as having low handgrip strength and was confirmed with a low appendicular skeletal muscle mass index; SO was defined as a body mass index (BMI) over 27, having low handgrip strength, a high fat percentage, and/or a low appendicular skeletal muscle index, which were defined as altered body composition (BC).

TAKEAWAY:

• Participants with probable and confirmed sarcopenia had a higher risk for all-cause mortality than those without during the 10-year follow-up period after adjusting for age, sex, and BMI (hazard ratios [HRs], 1.29, 1.93, respectively).
• Participants with SO and one BC component were at a higher risk for all-cause mortality (hazard ratio [HR], 1.94; 95% CI, 1.60-2.33).
• Participants with SO and both components of BC had almost three times the risk for mortality as those without (HR, 2.84; 95% CI, 1.97-4.11).

IN PRACTICE:

“These results suggest that screening for SO might be implemented in primary care. In addition, early nonpharmacologic interventions, such as nutrition and exercise training, should be included to delay the onset of and to treat sarcopenia, especially SO,” the researchers wrote.

SOURCE:

Yves Boirie, MD, PhD, of the Human Nutrition Unit at Université Clermont Auvergne in Clermont-Ferrand, France, is the corresponding author for this study. The study was funded by the Netherlands Organisation for Health Research and Development, the French National Research Agency, and the European Union’s Horizon 2020 research and innovation program, among others.

LIMITATIONS:

The researchers also did not consider specific causes of death. Because the most participants had European ancestry, the results cannot be generalized.

DISCLOSURES:

Various authors report receiving grants from the Agence Nationale de la Recherche and Agencia Estatal de Investigación. Other authors report being members of advisory board panels for Pfizer, Eli Lilly, Novo Nordisk, and Nutricia Research.

A version of this article appeared on Medscape.com.

TOPLINE:

Patients with sarcopenic obesity (SO) are at a greater risk for earlier death, but screening for muscle function could offer an opportunity for intervention.

METHODOLOGY:

• The proportion of older adults living with high body fat and/or low muscle function and mass has risen in recent years, but sarcopenia and SO are undiagnosed conditions.
• Researchers evaluated 5888 individuals who participated in a population-based cohort study in the Netherlands: Participants were largely of European descent (98%); the mean age of participants was 69.5 years, and 56.8% were female.
• Participants were included if they had available measurements of handgrip strength and had received a dual-energy x-ray absorptiometry scan.
• Sarcopenia was defined by researchers in JAMA Network Open as having low handgrip strength and was confirmed with a low appendicular skeletal muscle mass index; SO was defined as a body mass index (BMI) over 27, having low handgrip strength, a high fat percentage, and/or a low appendicular skeletal muscle index, which were defined as altered body composition (BC).

TAKEAWAY:

• Participants with probable and confirmed sarcopenia had a higher risk for all-cause mortality than those without during the 10-year follow-up period after adjusting for age, sex, and BMI (hazard ratios [HRs], 1.29, 1.93, respectively).
• Participants with SO and one BC component were at a higher risk for all-cause mortality (hazard ratio [HR], 1.94; 95% CI, 1.60-2.33).
• Participants with SO and both components of BC had almost three times the risk for mortality as those without (HR, 2.84; 95% CI, 1.97-4.11).

IN PRACTICE:

“These results suggest that screening for SO might be implemented in primary care. In addition, early nonpharmacologic interventions, such as nutrition and exercise training, should be included to delay the onset of and to treat sarcopenia, especially SO,” the researchers wrote.

SOURCE:

Yves Boirie, MD, PhD, of the Human Nutrition Unit at Université Clermont Auvergne in Clermont-Ferrand, France, is the corresponding author for this study. The study was funded by the Netherlands Organisation for Health Research and Development, the French National Research Agency, and the European Union’s Horizon 2020 research and innovation program, among others.

LIMITATIONS:

The researchers also did not consider specific causes of death. Because the most participants had European ancestry, the results cannot be generalized.

DISCLOSURES:

Various authors report receiving grants from the Agence Nationale de la Recherche and Agencia Estatal de Investigación. Other authors report being members of advisory board panels for Pfizer, Eli Lilly, Novo Nordisk, and Nutricia Research.

A version of this article appeared on Medscape.com.

TOPLINE:

Patients with sarcopenic obesity (SO) are at a greater risk for earlier death, but screening for muscle function could offer an opportunity for intervention.

METHODOLOGY:

• The proportion of older adults living with high body fat and/or low muscle function and mass has risen in recent years, but sarcopenia and SO are undiagnosed conditions.
• Researchers evaluated 5888 individuals who participated in a population-based cohort study in the Netherlands: Participants were largely of European descent (98%); the mean age of participants was 69.5 years, and 56.8% were female.
• Participants were included if they had available measurements of handgrip strength and had received a dual-energy x-ray absorptiometry scan.
• Sarcopenia was defined by researchers in JAMA Network Open as having low handgrip strength and was confirmed with a low appendicular skeletal muscle mass index; SO was defined as a body mass index (BMI) over 27, having low handgrip strength, a high fat percentage, and/or a low appendicular skeletal muscle index, which were defined as altered body composition (BC).

TAKEAWAY:

• Participants with probable and confirmed sarcopenia had a higher risk for all-cause mortality than those without during the 10-year follow-up period after adjusting for age, sex, and BMI (hazard ratios [HRs], 1.29, 1.93, respectively).
• Participants with SO and one BC component were at a higher risk for all-cause mortality (hazard ratio [HR], 1.94; 95% CI, 1.60-2.33).
• Participants with SO and both components of BC had almost three times the risk for mortality as those without (HR, 2.84; 95% CI, 1.97-4.11).

IN PRACTICE:

“These results suggest that screening for SO might be implemented in primary care. In addition, early nonpharmacologic interventions, such as nutrition and exercise training, should be included to delay the onset of and to treat sarcopenia, especially SO,” the researchers wrote.

SOURCE:

Yves Boirie, MD, PhD, of the Human Nutrition Unit at Université Clermont Auvergne in Clermont-Ferrand, France, is the corresponding author for this study. The study was funded by the Netherlands Organisation for Health Research and Development, the French National Research Agency, and the European Union’s Horizon 2020 research and innovation program, among others.

LIMITATIONS:

The researchers also did not consider specific causes of death. Because the most participants had European ancestry, the results cannot be generalized.

DISCLOSURES:

Various authors report receiving grants from the Agence Nationale de la Recherche and Agencia Estatal de Investigación. Other authors report being members of advisory board panels for Pfizer, Eli Lilly, Novo Nordisk, and Nutricia Research.

A version of this article appeared on Medscape.com.

TOPLINE:

Receipt of the bivalent COVID-19 vaccine was not associated with an increased stroke risk in the first 6 weeks after vaccination with either the Pfizer or Moderna vaccines, a new study of Medicare beneficiaries showed.

METHODOLOGY:

• The analysis included 5.4 million people age ≥ 65 years who received either the Pfizer-BioNTech COVID-19 bivalent vaccine or the Moderna bivalent vaccine, or the Pfizer vaccine and a high-dose or adjuvanted concomitant influenza vaccine (ie, administered on the same day).
• A total of 11,001 of the cohort experienced a stroke in the first 90 days after vaccination.
• The main outcome was stroke risk (nonhemorrhagic stroke, transient ischemic attack [TIA], or hemorrhagic stroke) during the 1- to 21-day or 22- to 42-day window after vaccination vs the 43- to 90-day control window.
• The mean age of participants was 74 years, and 56% were female.

TAKEAWAY:

• There was no statistically significant association with either brand of the COVID-19 bivalent vaccine or any of the stroke outcomes during the 1- to 21-day or 22- to 42-day risk window compared with the 43- to 90-day control window (incidence rate ratio [IRR] range, 0.72-1.12).
• Vaccination with COVID-19 bivalent vaccine plus a high-dose or adjuvanted influenza vaccine (n = 4596) was associated with a significantly greater risk for nonhemorrhagic stroke 22-42 days after vaccination with Pfizer-BioNTech (IRR, 1.20; risk difference/100,000 doses, 3.13) and an increase in TIA risk 1-21 days after vaccination with Moderna (IRR, 1.35; risk difference/100,000 doses, 3.33).
• There was a significant association between vaccination with a high-dose or adjuvanted influenza vaccine (n = 21,345) and nonhemorrhagic stroke 22-42 days after vaccination (IRR, 1.09; risk difference/100,000 doses, 1.65).

IN PRACTICE:

“The clinical significance of the risk of stroke after vaccination must be carefully considered together with the significant benefits of receiving an influenza vaccination,” the authors wrote. “Because the framework of the current self-controlled case series study does not compare the populations who were vaccinated vs those who were unvaccinated, it does not account for the reduced rate of severe influenza after vaccination. More studies are needed to better understand the association between high-dose or adjuvanted influenza vaccination and stroke.”

SOURCE:

Yun Lu, PhD, of the Center for Biologics Evaluation and Research, US Food and Drug Administration, Silver Spring, Maryland, was the lead and corresponding author of the study. It was published online on March 19 in JAMA.

LIMITATIONS:

Some stroke cases may have been missed or misclassified. The study included only vaccinated individuals — a population considered to have health-seeking behaviors — which may limit the generalizability of the findings. The study was conducted using COVID-19 bivalent vaccines, which are no longer available.

DISCLOSURES:

This work was funded by the US Food and Drug Administration through an interagency agreement with the Centers for Medicare & Medicaid Services. Dr. Lu reported no relevant financial relationships. The other authors’ disclosures are listed in the original paper.

A version of this article appeared on Medscape.com.

TOPLINE:

Receipt of the bivalent COVID-19 vaccine was not associated with an increased stroke risk in the first 6 weeks after vaccination with either the Pfizer or Moderna vaccines, a new study of Medicare beneficiaries showed.

METHODOLOGY:

• The analysis included 5.4 million people age ≥ 65 years who received either the Pfizer-BioNTech COVID-19 bivalent vaccine or the Moderna bivalent vaccine, or the Pfizer vaccine and a high-dose or adjuvanted concomitant influenza vaccine (ie, administered on the same day).
• A total of 11,001 of the cohort experienced a stroke in the first 90 days after vaccination.
• The main outcome was stroke risk (nonhemorrhagic stroke, transient ischemic attack [TIA], or hemorrhagic stroke) during the 1- to 21-day or 22- to 42-day window after vaccination vs the 43- to 90-day control window.
• The mean age of participants was 74 years, and 56% were female.

TAKEAWAY:

• There was no statistically significant association with either brand of the COVID-19 bivalent vaccine or any of the stroke outcomes during the 1- to 21-day or 22- to 42-day risk window compared with the 43- to 90-day control window (incidence rate ratio [IRR] range, 0.72-1.12).
• Vaccination with COVID-19 bivalent vaccine plus a high-dose or adjuvanted influenza vaccine (n = 4596) was associated with a significantly greater risk for nonhemorrhagic stroke 22-42 days after vaccination with Pfizer-BioNTech (IRR, 1.20; risk difference/100,000 doses, 3.13) and an increase in TIA risk 1-21 days after vaccination with Moderna (IRR, 1.35; risk difference/100,000 doses, 3.33).
• There was a significant association between vaccination with a high-dose or adjuvanted influenza vaccine (n = 21,345) and nonhemorrhagic stroke 22-42 days after vaccination (IRR, 1.09; risk difference/100,000 doses, 1.65).

IN PRACTICE:

“The clinical significance of the risk of stroke after vaccination must be carefully considered together with the significant benefits of receiving an influenza vaccination,” the authors wrote. “Because the framework of the current self-controlled case series study does not compare the populations who were vaccinated vs those who were unvaccinated, it does not account for the reduced rate of severe influenza after vaccination. More studies are needed to better understand the association between high-dose or adjuvanted influenza vaccination and stroke.”

SOURCE:

Yun Lu, PhD, of the Center for Biologics Evaluation and Research, US Food and Drug Administration, Silver Spring, Maryland, was the lead and corresponding author of the study. It was published online on March 19 in JAMA.

LIMITATIONS:

Some stroke cases may have been missed or misclassified. The study included only vaccinated individuals — a population considered to have health-seeking behaviors — which may limit the generalizability of the findings. The study was conducted using COVID-19 bivalent vaccines, which are no longer available.

DISCLOSURES:

This work was funded by the US Food and Drug Administration through an interagency agreement with the Centers for Medicare & Medicaid Services. Dr. Lu reported no relevant financial relationships. The other authors’ disclosures are listed in the original paper.

A version of this article appeared on Medscape.com.

TOPLINE:

Receipt of the bivalent COVID-19 vaccine was not associated with an increased stroke risk in the first 6 weeks after vaccination with either the Pfizer or Moderna vaccines, a new study of Medicare beneficiaries showed.

METHODOLOGY:

• The analysis included 5.4 million people age ≥ 65 years who received either the Pfizer-BioNTech COVID-19 bivalent vaccine or the Moderna bivalent vaccine, or the Pfizer vaccine and a high-dose or adjuvanted concomitant influenza vaccine (ie, administered on the same day).
• A total of 11,001 of the cohort experienced a stroke in the first 90 days after vaccination.
• The main outcome was stroke risk (nonhemorrhagic stroke, transient ischemic attack [TIA], or hemorrhagic stroke) during the 1- to 21-day or 22- to 42-day window after vaccination vs the 43- to 90-day control window.
• The mean age of participants was 74 years, and 56% were female.

TAKEAWAY:

• There was no statistically significant association with either brand of the COVID-19 bivalent vaccine or any of the stroke outcomes during the 1- to 21-day or 22- to 42-day risk window compared with the 43- to 90-day control window (incidence rate ratio [IRR] range, 0.72-1.12).
• Vaccination with COVID-19 bivalent vaccine plus a high-dose or adjuvanted influenza vaccine (n = 4596) was associated with a significantly greater risk for nonhemorrhagic stroke 22-42 days after vaccination with Pfizer-BioNTech (IRR, 1.20; risk difference/100,000 doses, 3.13) and an increase in TIA risk 1-21 days after vaccination with Moderna (IRR, 1.35; risk difference/100,000 doses, 3.33).
• There was a significant association between vaccination with a high-dose or adjuvanted influenza vaccine (n = 21,345) and nonhemorrhagic stroke 22-42 days after vaccination (IRR, 1.09; risk difference/100,000 doses, 1.65).

IN PRACTICE:

“The clinical significance of the risk of stroke after vaccination must be carefully considered together with the significant benefits of receiving an influenza vaccination,” the authors wrote. “Because the framework of the current self-controlled case series study does not compare the populations who were vaccinated vs those who were unvaccinated, it does not account for the reduced rate of severe influenza after vaccination. More studies are needed to better understand the association between high-dose or adjuvanted influenza vaccination and stroke.”

SOURCE:

Yun Lu, PhD, of the Center for Biologics Evaluation and Research, US Food and Drug Administration, Silver Spring, Maryland, was the lead and corresponding author of the study. It was published online on March 19 in JAMA.

LIMITATIONS:

Some stroke cases may have been missed or misclassified. The study included only vaccinated individuals — a population considered to have health-seeking behaviors — which may limit the generalizability of the findings. The study was conducted using COVID-19 bivalent vaccines, which are no longer available.

DISCLOSURES:

This work was funded by the US Food and Drug Administration through an interagency agreement with the Centers for Medicare & Medicaid Services. Dr. Lu reported no relevant financial relationships. The other authors’ disclosures are listed in the original paper.

A version of this article appeared on Medscape.com.

TOPLINE:

Long naps of an hour or more, naps in the morning, or regular siestas may increase blood glucose levels in older people with type 2 diabetes (T2D).

METHODOLOGY:

• Napping is common in China and other cultures and may play a role in cardiometabolic health, but previous studies on the relationship between napping and glycemic control in T2D have reported conflicting results.
• In a cross-sectional study, the researchers assessed 226 individuals with T2D (median age, 67 years; about half women; mostly retired) from two community healthcare centers in China between May 2023 and July 2023.
• Using questionnaires, the participants were evaluated for A1c levels, as well as frequency, duration (shorter or longer than 1 hour), timing, and type of napping behavior (restorative for lack of sleep vs appetitive by habit or for enjoyment).
• Multivariate analysis controlled for age, sex, body mass index, T2D treatment regimen, diabetes duration, cognitive impairment, depression, night sleep duration, and insomnia symptoms.

TAKEAWAY:

• Among 180 participants who reported napping, 61 (33.9%) took long naps of 60 minutes and more, 162 (90%) reported afternoon napping, and 131 (72.8%) displayed appetitive napping.
• Restorative napping was linked to lower A1c levels than appetitive napping (β, −0.176; P = 0.028).
• Napping frequency was not associated with A1c levels.

IN PRACTICE:

“In clinical practice, healthcare professionals may offer tips about napping, eg, taking a nap less than an hour, taking a nap in the afternoon instead of in the morning, avoiding appetitive napping,” the authors concluded.

SOURCE:

The study, from corresponding author Bingqian Zhu, PhD, of the Shanghai Jiao Tong University School of Nursing, Shanghai, was published in Frontiers in Endocrinology.

LIMITATIONS:

The participants were older individuals, mostly retired, who may have had less need for restorative napping and more time for appetitive napping, limiting generalizability. The sample size may have been too small to find a link to napping frequency. Self-reported data could introduce recall bias. Only A1c levels were used as a measure of glycemic control.

DISCLOSURES:

The study was supported by the National Natural Science Foundation of China and other sources. The authors declared no potential conflict of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

Long naps of an hour or more, naps in the morning, or regular siestas may increase blood glucose levels in older people with type 2 diabetes (T2D).

METHODOLOGY:

• Napping is common in China and other cultures and may play a role in cardiometabolic health, but previous studies on the relationship between napping and glycemic control in T2D have reported conflicting results.
• In a cross-sectional study, the researchers assessed 226 individuals with T2D (median age, 67 years; about half women; mostly retired) from two community healthcare centers in China between May 2023 and July 2023.
• Using questionnaires, the participants were evaluated for A1c levels, as well as frequency, duration (shorter or longer than 1 hour), timing, and type of napping behavior (restorative for lack of sleep vs appetitive by habit or for enjoyment).
• Multivariate analysis controlled for age, sex, body mass index, T2D treatment regimen, diabetes duration, cognitive impairment, depression, night sleep duration, and insomnia symptoms.

TAKEAWAY:

• Among 180 participants who reported napping, 61 (33.9%) took long naps of 60 minutes and more, 162 (90%) reported afternoon napping, and 131 (72.8%) displayed appetitive napping.
• Restorative napping was linked to lower A1c levels than appetitive napping (β, −0.176; P = 0.028).
• Napping frequency was not associated with A1c levels.

IN PRACTICE:

“In clinical practice, healthcare professionals may offer tips about napping, eg, taking a nap less than an hour, taking a nap in the afternoon instead of in the morning, avoiding appetitive napping,” the authors concluded.

SOURCE:

The study, from corresponding author Bingqian Zhu, PhD, of the Shanghai Jiao Tong University School of Nursing, Shanghai, was published in Frontiers in Endocrinology.

LIMITATIONS:

The participants were older individuals, mostly retired, who may have had less need for restorative napping and more time for appetitive napping, limiting generalizability. The sample size may have been too small to find a link to napping frequency. Self-reported data could introduce recall bias. Only A1c levels were used as a measure of glycemic control.

DISCLOSURES:

The study was supported by the National Natural Science Foundation of China and other sources. The authors declared no potential conflict of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

Long naps of an hour or more, naps in the morning, or regular siestas may increase blood glucose levels in older people with type 2 diabetes (T2D).

METHODOLOGY:

• Napping is common in China and other cultures and may play a role in cardiometabolic health, but previous studies on the relationship between napping and glycemic control in T2D have reported conflicting results.
• In a cross-sectional study, the researchers assessed 226 individuals with T2D (median age, 67 years; about half women; mostly retired) from two community healthcare centers in China between May 2023 and July 2023.
• Using questionnaires, the participants were evaluated for A1c levels, as well as frequency, duration (shorter or longer than 1 hour), timing, and type of napping behavior (restorative for lack of sleep vs appetitive by habit or for enjoyment).
• Multivariate analysis controlled for age, sex, body mass index, T2D treatment regimen, diabetes duration, cognitive impairment, depression, night sleep duration, and insomnia symptoms.

TAKEAWAY:

• Among 180 participants who reported napping, 61 (33.9%) took long naps of 60 minutes and more, 162 (90%) reported afternoon napping, and 131 (72.8%) displayed appetitive napping.
• Restorative napping was linked to lower A1c levels than appetitive napping (β, −0.176; P = 0.028).
• Napping frequency was not associated with A1c levels.

IN PRACTICE:

“In clinical practice, healthcare professionals may offer tips about napping, eg, taking a nap less than an hour, taking a nap in the afternoon instead of in the morning, avoiding appetitive napping,” the authors concluded.

SOURCE:

The study, from corresponding author Bingqian Zhu, PhD, of the Shanghai Jiao Tong University School of Nursing, Shanghai, was published in Frontiers in Endocrinology.

LIMITATIONS:

The participants were older individuals, mostly retired, who may have had less need for restorative napping and more time for appetitive napping, limiting generalizability. The sample size may have been too small to find a link to napping frequency. Self-reported data could introduce recall bias. Only A1c levels were used as a measure of glycemic control.

DISCLOSURES:

The study was supported by the National Natural Science Foundation of China and other sources. The authors declared no potential conflict of interest.

A version of this article appeared on Medscape.com.

The US Food and Drug Administration (FDA) has approved sotatercept (Winrevair, Merck), for the treatment of adults with pulmonary arterial hypertension (PAH), World Health Organization (WHO) Group 1, to increase exercise capacity, improve WHO functional class, and reduce the risk for clinical worsening events.

Sotatercept, which had breakthrough therapy designation, is a first-in-class activin signaling inhibitor that works by improving the balance between pro- and antiproliferative signaling to regulate the vascular cell proliferation that underlies PAH.

“Sotatercept added to background therapy has the potential to become a new standard-of-care option for patients with pulmonary arterial hypertension,” added coinvestigator Aaron B. Waxman, MD, PhD, executive director of the Center for Pulmonary Heart Diseases at Brigham and Women’s Hospital, Boston.

The approval was based on results of the phase 3 STELLAR study, a global, double-blind, placebo-controlled, multicenter, parallel-group clinical trial in which, 323 patients with PAH (WHO Group 1, functional class II or III) were randomly assigned 1:1 to add sotatercept or placebo to stable background therapy.

The results showed that sotatercept, administered subcutaneously every 3 weeks for 24 weeks, improved average 6-minute walk distance from baseline by a significant and clinically meaningful 40.8 meters compared with placebo for the trial’s primary efficacy endpoint (P < .001).

Sotatercept also led to significant improvement in multiple secondary outcome measures, including:

• Reduction in the risk for death from any cause or PAH clinical worsening events by 84% vs background therapy alone (number of events: 9 vs 42; hazard ratio [HR], 0.16; P < .001) 
• Improvement in FC from baseline at 24 weeks in 29% of patients compared with 14% of patients treated with placebo (P < .001) 
• Improvement in pulmonary vascular resistance (PVR), with an average 235 dyn/sec/cm⁵ reduction in PVR from baseline (P < .001) 
• Improvement from baseline in N-terminal pro–B-type natriuretic peptide (NT-proBNP) levels. The median treatment difference in NT-proBNP between sotatercept and placebo was -442 pg/mL (P < .001) 

The results were reported last year at the joint scientific sessions of the American College of Cardiology and the World Heart Federation, with simultaneous publication in The New England Journal of Medicine. 

Sotatercept injection may be administered by patients or caregivers with guidance, training, and follow-up from a healthcare provider. The recommended starting dose is 0.3 mg/kg. The recommended target dose is 0.7 mg/kg every 3 weeks.

Sotatercept may increase hemoglobin, may lead to erythrocytosis, and may decrease platelet count and lead to severe thrombocytopenia. Treatment should not be initiated if platelet count is < 50,000/mm³. 

Hemoglobin and platelets should be monitored before each dose of sotatercept for the first five doses, or longer if values are unstable, and periodically thereafter to determine if dose adjustments are required. 

Full prescribing information is available online. 

Merck estimates that sotatercept will be available for dispensing by select specialty pharmacies in the United States by the end of April 2024.

A version of this article appeared on Medscape.com.

The US Food and Drug Administration (FDA) has approved sotatercept (Winrevair, Merck), for the treatment of adults with pulmonary arterial hypertension (PAH), World Health Organization (WHO) Group 1, to increase exercise capacity, improve WHO functional class, and reduce the risk for clinical worsening events.

Sotatercept, which had breakthrough therapy designation, is a first-in-class activin signaling inhibitor that works by improving the balance between pro- and antiproliferative signaling to regulate the vascular cell proliferation that underlies PAH.

“Sotatercept added to background therapy has the potential to become a new standard-of-care option for patients with pulmonary arterial hypertension,” added coinvestigator Aaron B. Waxman, MD, PhD, executive director of the Center for Pulmonary Heart Diseases at Brigham and Women’s Hospital, Boston.

The approval was based on results of the phase 3 STELLAR study, a global, double-blind, placebo-controlled, multicenter, parallel-group clinical trial in which, 323 patients with PAH (WHO Group 1, functional class II or III) were randomly assigned 1:1 to add sotatercept or placebo to stable background therapy.

The results showed that sotatercept, administered subcutaneously every 3 weeks for 24 weeks, improved average 6-minute walk distance from baseline by a significant and clinically meaningful 40.8 meters compared with placebo for the trial’s primary efficacy endpoint (P < .001).

Sotatercept also led to significant improvement in multiple secondary outcome measures, including:

• Reduction in the risk for death from any cause or PAH clinical worsening events by 84% vs background therapy alone (number of events: 9 vs 42; hazard ratio [HR], 0.16; P < .001) 
• Improvement in FC from baseline at 24 weeks in 29% of patients compared with 14% of patients treated with placebo (P < .001) 
• Improvement in pulmonary vascular resistance (PVR), with an average 235 dyn/sec/cm⁵ reduction in PVR from baseline (P < .001) 
• Improvement from baseline in N-terminal pro–B-type natriuretic peptide (NT-proBNP) levels. The median treatment difference in NT-proBNP between sotatercept and placebo was -442 pg/mL (P < .001) 

The results were reported last year at the joint scientific sessions of the American College of Cardiology and the World Heart Federation, with simultaneous publication in The New England Journal of Medicine. 

Sotatercept injection may be administered by patients or caregivers with guidance, training, and follow-up from a healthcare provider. The recommended starting dose is 0.3 mg/kg. The recommended target dose is 0.7 mg/kg every 3 weeks.

Sotatercept may increase hemoglobin, may lead to erythrocytosis, and may decrease platelet count and lead to severe thrombocytopenia. Treatment should not be initiated if platelet count is < 50,000/mm³. 

Hemoglobin and platelets should be monitored before each dose of sotatercept for the first five doses, or longer if values are unstable, and periodically thereafter to determine if dose adjustments are required. 

Full prescribing information is available online. 

Merck estimates that sotatercept will be available for dispensing by select specialty pharmacies in the United States by the end of April 2024.

A version of this article appeared on Medscape.com.

The US Food and Drug Administration (FDA) has approved sotatercept (Winrevair, Merck), for the treatment of adults with pulmonary arterial hypertension (PAH), World Health Organization (WHO) Group 1, to increase exercise capacity, improve WHO functional class, and reduce the risk for clinical worsening events.

Sotatercept, which had breakthrough therapy designation, is a first-in-class activin signaling inhibitor that works by improving the balance between pro- and antiproliferative signaling to regulate the vascular cell proliferation that underlies PAH.

“Sotatercept added to background therapy has the potential to become a new standard-of-care option for patients with pulmonary arterial hypertension,” added coinvestigator Aaron B. Waxman, MD, PhD, executive director of the Center for Pulmonary Heart Diseases at Brigham and Women’s Hospital, Boston.

The approval was based on results of the phase 3 STELLAR study, a global, double-blind, placebo-controlled, multicenter, parallel-group clinical trial in which, 323 patients with PAH (WHO Group 1, functional class II or III) were randomly assigned 1:1 to add sotatercept or placebo to stable background therapy.

The results showed that sotatercept, administered subcutaneously every 3 weeks for 24 weeks, improved average 6-minute walk distance from baseline by a significant and clinically meaningful 40.8 meters compared with placebo for the trial’s primary efficacy endpoint (P < .001).

Sotatercept also led to significant improvement in multiple secondary outcome measures, including:

• Reduction in the risk for death from any cause or PAH clinical worsening events by 84% vs background therapy alone (number of events: 9 vs 42; hazard ratio [HR], 0.16; P < .001) 
• Improvement in FC from baseline at 24 weeks in 29% of patients compared with 14% of patients treated with placebo (P < .001) 
• Improvement in pulmonary vascular resistance (PVR), with an average 235 dyn/sec/cm⁵ reduction in PVR from baseline (P < .001) 
• Improvement from baseline in N-terminal pro–B-type natriuretic peptide (NT-proBNP) levels. The median treatment difference in NT-proBNP between sotatercept and placebo was -442 pg/mL (P < .001) 

The results were reported last year at the joint scientific sessions of the American College of Cardiology and the World Heart Federation, with simultaneous publication in The New England Journal of Medicine. 

Sotatercept injection may be administered by patients or caregivers with guidance, training, and follow-up from a healthcare provider. The recommended starting dose is 0.3 mg/kg. The recommended target dose is 0.7 mg/kg every 3 weeks.

Sotatercept may increase hemoglobin, may lead to erythrocytosis, and may decrease platelet count and lead to severe thrombocytopenia. Treatment should not be initiated if platelet count is < 50,000/mm³. 

Hemoglobin and platelets should be monitored before each dose of sotatercept for the first five doses, or longer if values are unstable, and periodically thereafter to determine if dose adjustments are required. 

Full prescribing information is available online. 

Merck estimates that sotatercept will be available for dispensing by select specialty pharmacies in the United States by the end of April 2024.

A version of this article appeared on Medscape.com.

TOPLINE:

The inclusion of sugar-substitute sweeteners and sweetness enhancers in a sugar-reduced maintenance diet following weight loss improves weight maintenance as well as well-being in adults, with no increases in type 2 diabetes or cardiovascular disease risk compared with a diet excluding the sweeteners, a randomized trial showed.

The study also showed that among overweight or obese children, greater reductions in uncontrolled eating were observed among those receiving the sweeteners.

The findings counter previous reports that raised concerns about the non-sugar sweeteners, including recent research from the World Health Organization suggesting no benefits in weight control and a possible increase in the risk for type 2 diabetes or cardiovascular disease with the sweeteners.

METHODOLOGY:

• The findings are from an exploratory analysis of the multicenter, randomized SWEET trial.
• The trial involved 341 adults with overweight or obesity (aged 18-65 years, 71% women, body mass index [BMI] ≥ 25) and 38 children with overweight (aged 6-12 years, 60% girls, BMI-for-age > 85th percentile), recruited in Denmark, Spain, Greece, and the Netherlands through webpages, social media, newspapers, and registries.
• For the first 2 months of the trial, adults were instructed to follow a low-energy diet (the Cambridge Weight Plan) with the goal of achieving at least 5% weight loss, while children received dietary advice to maintain body weight.
• In the subsequent 10 months, adults as well as children were randomized to healthy diets that either consisted of less than 10% of calories from added sugar but permitted foods and drinks with sweeteners and sweetness enhancers, or the same diet but not allowing the use of the sweeteners or sweetness enhancers.
• Participants had weight, BMI, anthropometry, and risk markers for type 2 diabetes and cardiovascular disease monitored at the trial’s baseline, as well as at 2, 6, and 12 months.
• In addition, participants completed food frequency questionnaires and provided urine samples to assess biomarkers of the sweeteners, fructose and sucrose, in order to measure compliance with the dietary instructions.

TAKEAWAY:

• While the sweetener and non-sweetener groups both had decreases in consumption of products high in sugar, the reduction was significantly higher in the group that allowed use of the sweeteners (P = .002).
• In the intention-to-treat analyses, adults (n = 277) permitted sweeteners showed a small but significantly greater weight loss maintenance after 1 year than the non-sweetener group (average weight loss, 7.2 kg vs 5.6 kg; P = .029).
• Among 203 participants who completed the trial, there were no differences between the groups in terms of markers for type 2 diabetes and cardiovascular disease.
• There were also no differences between the groups in terms of subjective appetite sensations and appetite hormones in a subgroup of 104 patients.
• In an analysis of 22 children who completed the study, there were no differences in BMI-for-age z scores between sweetener and non-sweetener groups.
• In terms of effects on eating behavior, adults in the sweetener group reported greater diet satisfaction when eating out (P = .03), increased positive mood (P = .013), and reduced craving for sweet food (P = .034) at 6 months than in the non-sweetener group.
• Conversely, those receiving no sweeteners had a greater liking bias for sweet vs savory foods at 6 months (P = .023) and 12 months (P = .005).
• There were no differences between the groups in reported physical activity or quality of life.
• However, among children with higher uncontrolled eating scores at baseline, the uncontrolled eating scores at 12 months were significantly lower among children who were allowed the sugar-substitute sweeteners vs the non-sweetener children (P = .021).

IN PRACTICE:

“Our findings suggest that the inclusion of low/no energy-sweetened products may benefit children who show high levels of uncontrolled eating,” said the study’s co-lead author, Clarissa Dakin, of the Appetite Control and Energy Balance Research Group at the University of Leeds, Leeds, England, in a press statement.

“Together, these findings provide important insights for the ongoing reevaluation of food additive sweeteners by the European Food Safety Authority and other health agencies worldwide,” she said.

Coauthor Jason Halford, head of the School of Psychology at the University of Leeds, added in the press statement that “the use of low-calorie sweeteners in weight management has been questioned, in part because of the link between their use and apparent weight gain in observational studies.”

“However, increasingly, it is becoming apparent that is not the case in long-term studies,” said a study co-author in a press statement.”

SOURCE:

The findings from the two abstracts will be presented in May at the European Association for the Study of Obesity. The study abstracts were issued in advance.

LIMITATIONS:

Some of the results, particularly in children’s subgroups, were limited by the relatively low number of children, underscoring the need for future studies on the issue, the authors noted.

DISCLOSURES:

Dr. Halford has received research funding from the American Beverage Association.

A version of this article appeared on Medscape.com.

TOPLINE:

The inclusion of sugar-substitute sweeteners and sweetness enhancers in a sugar-reduced maintenance diet following weight loss improves weight maintenance as well as well-being in adults, with no increases in type 2 diabetes or cardiovascular disease risk compared with a diet excluding the sweeteners, a randomized trial showed.

The study also showed that among overweight or obese children, greater reductions in uncontrolled eating were observed among those receiving the sweeteners.

The findings counter previous reports that raised concerns about the non-sugar sweeteners, including recent research from the World Health Organization suggesting no benefits in weight control and a possible increase in the risk for type 2 diabetes or cardiovascular disease with the sweeteners.

METHODOLOGY:

• The findings are from an exploratory analysis of the multicenter, randomized SWEET trial.
• The trial involved 341 adults with overweight or obesity (aged 18-65 years, 71% women, body mass index [BMI] ≥ 25) and 38 children with overweight (aged 6-12 years, 60% girls, BMI-for-age > 85th percentile), recruited in Denmark, Spain, Greece, and the Netherlands through webpages, social media, newspapers, and registries.
• For the first 2 months of the trial, adults were instructed to follow a low-energy diet (the Cambridge Weight Plan) with the goal of achieving at least 5% weight loss, while children received dietary advice to maintain body weight.
• In the subsequent 10 months, adults as well as children were randomized to healthy diets that either consisted of less than 10% of calories from added sugar but permitted foods and drinks with sweeteners and sweetness enhancers, or the same diet but not allowing the use of the sweeteners or sweetness enhancers.
• Participants had weight, BMI, anthropometry, and risk markers for type 2 diabetes and cardiovascular disease monitored at the trial’s baseline, as well as at 2, 6, and 12 months.
• In addition, participants completed food frequency questionnaires and provided urine samples to assess biomarkers of the sweeteners, fructose and sucrose, in order to measure compliance with the dietary instructions.

TAKEAWAY:

• While the sweetener and non-sweetener groups both had decreases in consumption of products high in sugar, the reduction was significantly higher in the group that allowed use of the sweeteners (P = .002).
• In the intention-to-treat analyses, adults (n = 277) permitted sweeteners showed a small but significantly greater weight loss maintenance after 1 year than the non-sweetener group (average weight loss, 7.2 kg vs 5.6 kg; P = .029).
• Among 203 participants who completed the trial, there were no differences between the groups in terms of markers for type 2 diabetes and cardiovascular disease.
• There were also no differences between the groups in terms of subjective appetite sensations and appetite hormones in a subgroup of 104 patients.
• In an analysis of 22 children who completed the study, there were no differences in BMI-for-age z scores between sweetener and non-sweetener groups.
• In terms of effects on eating behavior, adults in the sweetener group reported greater diet satisfaction when eating out (P = .03), increased positive mood (P = .013), and reduced craving for sweet food (P = .034) at 6 months than in the non-sweetener group.
• Conversely, those receiving no sweeteners had a greater liking bias for sweet vs savory foods at 6 months (P = .023) and 12 months (P = .005).
• There were no differences between the groups in reported physical activity or quality of life.
• However, among children with higher uncontrolled eating scores at baseline, the uncontrolled eating scores at 12 months were significantly lower among children who were allowed the sugar-substitute sweeteners vs the non-sweetener children (P = .021).

IN PRACTICE:

“Our findings suggest that the inclusion of low/no energy-sweetened products may benefit children who show high levels of uncontrolled eating,” said the study’s co-lead author, Clarissa Dakin, of the Appetite Control and Energy Balance Research Group at the University of Leeds, Leeds, England, in a press statement.

“Together, these findings provide important insights for the ongoing reevaluation of food additive sweeteners by the European Food Safety Authority and other health agencies worldwide,” she said.

Coauthor Jason Halford, head of the School of Psychology at the University of Leeds, added in the press statement that “the use of low-calorie sweeteners in weight management has been questioned, in part because of the link between their use and apparent weight gain in observational studies.”

“However, increasingly, it is becoming apparent that is not the case in long-term studies,” said a study co-author in a press statement.”

SOURCE:

The findings from the two abstracts will be presented in May at the European Association for the Study of Obesity. The study abstracts were issued in advance.

LIMITATIONS:

Some of the results, particularly in children’s subgroups, were limited by the relatively low number of children, underscoring the need for future studies on the issue, the authors noted.

DISCLOSURES:

Dr. Halford has received research funding from the American Beverage Association.

A version of this article appeared on Medscape.com.

TOPLINE:

The inclusion of sugar-substitute sweeteners and sweetness enhancers in a sugar-reduced maintenance diet following weight loss improves weight maintenance as well as well-being in adults, with no increases in type 2 diabetes or cardiovascular disease risk compared with a diet excluding the sweeteners, a randomized trial showed.

The study also showed that among overweight or obese children, greater reductions in uncontrolled eating were observed among those receiving the sweeteners.

The findings counter previous reports that raised concerns about the non-sugar sweeteners, including recent research from the World Health Organization suggesting no benefits in weight control and a possible increase in the risk for type 2 diabetes or cardiovascular disease with the sweeteners.

METHODOLOGY:

• The findings are from an exploratory analysis of the multicenter, randomized SWEET trial.
• The trial involved 341 adults with overweight or obesity (aged 18-65 years, 71% women, body mass index [BMI] ≥ 25) and 38 children with overweight (aged 6-12 years, 60% girls, BMI-for-age > 85th percentile), recruited in Denmark, Spain, Greece, and the Netherlands through webpages, social media, newspapers, and registries.
• For the first 2 months of the trial, adults were instructed to follow a low-energy diet (the Cambridge Weight Plan) with the goal of achieving at least 5% weight loss, while children received dietary advice to maintain body weight.
• In the subsequent 10 months, adults as well as children were randomized to healthy diets that either consisted of less than 10% of calories from added sugar but permitted foods and drinks with sweeteners and sweetness enhancers, or the same diet but not allowing the use of the sweeteners or sweetness enhancers.
• Participants had weight, BMI, anthropometry, and risk markers for type 2 diabetes and cardiovascular disease monitored at the trial’s baseline, as well as at 2, 6, and 12 months.
• In addition, participants completed food frequency questionnaires and provided urine samples to assess biomarkers of the sweeteners, fructose and sucrose, in order to measure compliance with the dietary instructions.

TAKEAWAY:

• While the sweetener and non-sweetener groups both had decreases in consumption of products high in sugar, the reduction was significantly higher in the group that allowed use of the sweeteners (P = .002).
• In the intention-to-treat analyses, adults (n = 277) permitted sweeteners showed a small but significantly greater weight loss maintenance after 1 year than the non-sweetener group (average weight loss, 7.2 kg vs 5.6 kg; P = .029).
• Among 203 participants who completed the trial, there were no differences between the groups in terms of markers for type 2 diabetes and cardiovascular disease.
• There were also no differences between the groups in terms of subjective appetite sensations and appetite hormones in a subgroup of 104 patients.
• In an analysis of 22 children who completed the study, there were no differences in BMI-for-age z scores between sweetener and non-sweetener groups.
• In terms of effects on eating behavior, adults in the sweetener group reported greater diet satisfaction when eating out (P = .03), increased positive mood (P = .013), and reduced craving for sweet food (P = .034) at 6 months than in the non-sweetener group.
• Conversely, those receiving no sweeteners had a greater liking bias for sweet vs savory foods at 6 months (P = .023) and 12 months (P = .005).
• There were no differences between the groups in reported physical activity or quality of life.
• However, among children with higher uncontrolled eating scores at baseline, the uncontrolled eating scores at 12 months were significantly lower among children who were allowed the sugar-substitute sweeteners vs the non-sweetener children (P = .021).

IN PRACTICE:

“Our findings suggest that the inclusion of low/no energy-sweetened products may benefit children who show high levels of uncontrolled eating,” said the study’s co-lead author, Clarissa Dakin, of the Appetite Control and Energy Balance Research Group at the University of Leeds, Leeds, England, in a press statement.

“Together, these findings provide important insights for the ongoing reevaluation of food additive sweeteners by the European Food Safety Authority and other health agencies worldwide,” she said.

Coauthor Jason Halford, head of the School of Psychology at the University of Leeds, added in the press statement that “the use of low-calorie sweeteners in weight management has been questioned, in part because of the link between their use and apparent weight gain in observational studies.”

“However, increasingly, it is becoming apparent that is not the case in long-term studies,” said a study co-author in a press statement.”

SOURCE:

The findings from the two abstracts will be presented in May at the European Association for the Study of Obesity. The study abstracts were issued in advance.

LIMITATIONS:

Some of the results, particularly in children’s subgroups, were limited by the relatively low number of children, underscoring the need for future studies on the issue, the authors noted.

DISCLOSURES:

Dr. Halford has received research funding from the American Beverage Association.

A version of this article appeared on Medscape.com.

Electronic health records (EHRs) make providing coordinated, efficient care easier and reduce medical errors and test duplications; research has also correlated EHR adoption with higher patient satisfaction and outcomes. However, for physicians, the benefits come at a cost.

Physicians spend significantly more time in healthcare portals, making notes, entering orders, reviewing clinical reports, and responding to patient messages.

“I spend at least the same amount of time in the portal that I do in scheduled clinical time with patients,” said Eve Rittenberg, MD, primary care physician at Brigham and Women’s Hospital and assistant professor at Harvard Medical School, Boston, Massachusetts. “So, if I have a 4-hour session of seeing patients, I spend at least another 4 or more hours in the patient portal.”

The latest data showed that primary care physicians logged a median of 36.2 minutes in the healthcare portal per patient visit, spending 58.9% more time on orders, 24.4% more time reading and responding to messages, and 13% more time on chart review compared to prepandemic portal use.

“EHRs can be very powerful tools,” said Ralph DeBiasi, MD, a clinical cardiac electrophysiologist at Yale New Haven Health. “We’re still working on how to best harness that power to make us better doctors and better care teams and to take better care of our patients because their use can take up a lot of time.”
 

Portal Time Isn’t Paid Time

Sharp increases in the amount of time spent in the EHR responding to messages or dispensing medical advice via the portal often aren’t linked to increases in compensation; most portal time is unpaid.

“There isn’t specific time allocated to working in the portal; it’s either done in the office while a patient is sitting in an exam room or in the mornings and evenings outside of traditional working hours,” Dr. DeBiasi said. “I think it’s reasonable to consider it being reimbursed because we’re taking our time and effort and making decisions to help the patient.”

Compensation for portal time affects all physicians, but the degree of impact depends on their specialties. Primary care physicians spent significantly more daily and after-hours time in the EHR, entering notes and orders, and doing clinical reviews compared to surgical and medical specialties.

In addition to the outsized impact on primary care, physician compensation for portal time is also an equity issue.

Dr. Rittenberg researched the issue and found a higher volume of communication from both patients and staff to female physicians than male physicians. As a result, female physicians spend 41.4 minutes more on the EHR than their male counterparts, which equates to more unpaid time. It’s likely no coincidence then that burnout rates are also higher among female physicians, who also leave the clinical workforce in higher numbers, especially in primary care.

“Finding ways to fairly compensate physicians for their work also will address some of the equity issues in workload and the consequences,” Dr. Rittenberg said.
 

Addressing the Issue

Some health systems have started charging patients who seek medical advice via patient portals, equating the communication to asynchronous acute care or an additional care touchpoint and billing based on the length and complexity of the messages. Patient fees for seeking medical advice via portals vary widely depending on their health system and insurance.

At University of California San Francisco Health, billing patients for EHR communication led to a sharp decrease in patient messages, which eased physician workload. At Cleveland Clinic, physicians receive “productivity credits” for the time spent in the EHR that can be used to reduce their clinic hours (but have no impact on their compensation).

Changes to the Medicare Physician Fee Schedule also allow physicians to bill for “digital evaluation and management” based on the time spent in an EHR responding to patient-initiated questions and requests.

However, more efforts are needed to ease burnout and reverse the number of physicians who are seeing fewer patients or leaving medical practice altogether as a direct result of spending increasing amounts of unpaid time in the EHR. Dr. Rittenberg, who spends an estimated 50% of her working hours in the portal, had to reduce her clinical workload by 25% due to such heavy portal requirements.

“The workload has become unsustainable,” she said. “The work has undergone a dramatic change over the past decade, and the compensation system has not kept up with that change.”
 

Prioritizing Patient and Physician Experiences

The ever-expanding use of EHR is a result of their value as a healthcare tool. Data showed that the electronic exchange of information between patients and physicians improves diagnostics, reduces medical errors, enhances communication, and leads to more patient-centered care — and physicians want their patients to use the portal to maximize their healthcare.

“[The EHR] is good for patients,” said Dr. DeBiasi. “Sometimes, patients have access issues with healthcare, whether that’s not knowing what number to call or getting the right message to the right person at the right office. If [the portal] is good for them and helps them get access to care, we should embrace that and figure out a way to work it into our day-to-day schedules.”

But maximizing the patient experience shouldn’t come at the physicians’ expense. Dr. Rittenberg advocates a model that compensates physicians for the time spent in the EHR and prioritizes a team approach to rebalance the EHR workload to ensure that physicians aren’t devoting too much time to administrative tasks and can, instead, focus their time on clinical tasks.

“The way in which we provide healthcare has fundamentally shifted, and compensation models need to reflect that new reality,” Dr. Rittenberg added.

A version of this article appeared on Medscape.com.

Electronic health records (EHRs) make providing coordinated, efficient care easier and reduce medical errors and test duplications; research has also correlated EHR adoption with higher patient satisfaction and outcomes. However, for physicians, the benefits come at a cost.

Physicians spend significantly more time in healthcare portals, making notes, entering orders, reviewing clinical reports, and responding to patient messages.

“I spend at least the same amount of time in the portal that I do in scheduled clinical time with patients,” said Eve Rittenberg, MD, primary care physician at Brigham and Women’s Hospital and assistant professor at Harvard Medical School, Boston, Massachusetts. “So, if I have a 4-hour session of seeing patients, I spend at least another 4 or more hours in the patient portal.”

The latest data showed that primary care physicians logged a median of 36.2 minutes in the healthcare portal per patient visit, spending 58.9% more time on orders, 24.4% more time reading and responding to messages, and 13% more time on chart review compared to prepandemic portal use.

“EHRs can be very powerful tools,” said Ralph DeBiasi, MD, a clinical cardiac electrophysiologist at Yale New Haven Health. “We’re still working on how to best harness that power to make us better doctors and better care teams and to take better care of our patients because their use can take up a lot of time.”
 

Portal Time Isn’t Paid Time

Sharp increases in the amount of time spent in the EHR responding to messages or dispensing medical advice via the portal often aren’t linked to increases in compensation; most portal time is unpaid.

“There isn’t specific time allocated to working in the portal; it’s either done in the office while a patient is sitting in an exam room or in the mornings and evenings outside of traditional working hours,” Dr. DeBiasi said. “I think it’s reasonable to consider it being reimbursed because we’re taking our time and effort and making decisions to help the patient.”

Compensation for portal time affects all physicians, but the degree of impact depends on their specialties. Primary care physicians spent significantly more daily and after-hours time in the EHR, entering notes and orders, and doing clinical reviews compared to surgical and medical specialties.

In addition to the outsized impact on primary care, physician compensation for portal time is also an equity issue.

Dr. Rittenberg researched the issue and found a higher volume of communication from both patients and staff to female physicians than male physicians. As a result, female physicians spend 41.4 minutes more on the EHR than their male counterparts, which equates to more unpaid time. It’s likely no coincidence then that burnout rates are also higher among female physicians, who also leave the clinical workforce in higher numbers, especially in primary care.

“Finding ways to fairly compensate physicians for their work also will address some of the equity issues in workload and the consequences,” Dr. Rittenberg said.
 

Addressing the Issue

Some health systems have started charging patients who seek medical advice via patient portals, equating the communication to asynchronous acute care or an additional care touchpoint and billing based on the length and complexity of the messages. Patient fees for seeking medical advice via portals vary widely depending on their health system and insurance.

At University of California San Francisco Health, billing patients for EHR communication led to a sharp decrease in patient messages, which eased physician workload. At Cleveland Clinic, physicians receive “productivity credits” for the time spent in the EHR that can be used to reduce their clinic hours (but have no impact on their compensation).

Changes to the Medicare Physician Fee Schedule also allow physicians to bill for “digital evaluation and management” based on the time spent in an EHR responding to patient-initiated questions and requests.

However, more efforts are needed to ease burnout and reverse the number of physicians who are seeing fewer patients or leaving medical practice altogether as a direct result of spending increasing amounts of unpaid time in the EHR. Dr. Rittenberg, who spends an estimated 50% of her working hours in the portal, had to reduce her clinical workload by 25% due to such heavy portal requirements.

“The workload has become unsustainable,” she said. “The work has undergone a dramatic change over the past decade, and the compensation system has not kept up with that change.”
 

Prioritizing Patient and Physician Experiences

The ever-expanding use of EHR is a result of their value as a healthcare tool. Data showed that the electronic exchange of information between patients and physicians improves diagnostics, reduces medical errors, enhances communication, and leads to more patient-centered care — and physicians want their patients to use the portal to maximize their healthcare.

“[The EHR] is good for patients,” said Dr. DeBiasi. “Sometimes, patients have access issues with healthcare, whether that’s not knowing what number to call or getting the right message to the right person at the right office. If [the portal] is good for them and helps them get access to care, we should embrace that and figure out a way to work it into our day-to-day schedules.”

But maximizing the patient experience shouldn’t come at the physicians’ expense. Dr. Rittenberg advocates a model that compensates physicians for the time spent in the EHR and prioritizes a team approach to rebalance the EHR workload to ensure that physicians aren’t devoting too much time to administrative tasks and can, instead, focus their time on clinical tasks.

“The way in which we provide healthcare has fundamentally shifted, and compensation models need to reflect that new reality,” Dr. Rittenberg added.

A version of this article appeared on Medscape.com.

Electronic health records (EHRs) make providing coordinated, efficient care easier and reduce medical errors and test duplications; research has also correlated EHR adoption with higher patient satisfaction and outcomes. However, for physicians, the benefits come at a cost.

Physicians spend significantly more time in healthcare portals, making notes, entering orders, reviewing clinical reports, and responding to patient messages.

“I spend at least the same amount of time in the portal that I do in scheduled clinical time with patients,” said Eve Rittenberg, MD, primary care physician at Brigham and Women’s Hospital and assistant professor at Harvard Medical School, Boston, Massachusetts. “So, if I have a 4-hour session of seeing patients, I spend at least another 4 or more hours in the patient portal.”

The latest data showed that primary care physicians logged a median of 36.2 minutes in the healthcare portal per patient visit, spending 58.9% more time on orders, 24.4% more time reading and responding to messages, and 13% more time on chart review compared to prepandemic portal use.

“EHRs can be very powerful tools,” said Ralph DeBiasi, MD, a clinical cardiac electrophysiologist at Yale New Haven Health. “We’re still working on how to best harness that power to make us better doctors and better care teams and to take better care of our patients because their use can take up a lot of time.”
 

Portal Time Isn’t Paid Time

Sharp increases in the amount of time spent in the EHR responding to messages or dispensing medical advice via the portal often aren’t linked to increases in compensation; most portal time is unpaid.

“There isn’t specific time allocated to working in the portal; it’s either done in the office while a patient is sitting in an exam room or in the mornings and evenings outside of traditional working hours,” Dr. DeBiasi said. “I think it’s reasonable to consider it being reimbursed because we’re taking our time and effort and making decisions to help the patient.”

Compensation for portal time affects all physicians, but the degree of impact depends on their specialties. Primary care physicians spent significantly more daily and after-hours time in the EHR, entering notes and orders, and doing clinical reviews compared to surgical and medical specialties.

In addition to the outsized impact on primary care, physician compensation for portal time is also an equity issue.

Dr. Rittenberg researched the issue and found a higher volume of communication from both patients and staff to female physicians than male physicians. As a result, female physicians spend 41.4 minutes more on the EHR than their male counterparts, which equates to more unpaid time. It’s likely no coincidence then that burnout rates are also higher among female physicians, who also leave the clinical workforce in higher numbers, especially in primary care.

“Finding ways to fairly compensate physicians for their work also will address some of the equity issues in workload and the consequences,” Dr. Rittenberg said.
 

Addressing the Issue

Some health systems have started charging patients who seek medical advice via patient portals, equating the communication to asynchronous acute care or an additional care touchpoint and billing based on the length and complexity of the messages. Patient fees for seeking medical advice via portals vary widely depending on their health system and insurance.

At University of California San Francisco Health, billing patients for EHR communication led to a sharp decrease in patient messages, which eased physician workload. At Cleveland Clinic, physicians receive “productivity credits” for the time spent in the EHR that can be used to reduce their clinic hours (but have no impact on their compensation).

Changes to the Medicare Physician Fee Schedule also allow physicians to bill for “digital evaluation and management” based on the time spent in an EHR responding to patient-initiated questions and requests.

However, more efforts are needed to ease burnout and reverse the number of physicians who are seeing fewer patients or leaving medical practice altogether as a direct result of spending increasing amounts of unpaid time in the EHR. Dr. Rittenberg, who spends an estimated 50% of her working hours in the portal, had to reduce her clinical workload by 25% due to such heavy portal requirements.

“The workload has become unsustainable,” she said. “The work has undergone a dramatic change over the past decade, and the compensation system has not kept up with that change.”
 

Prioritizing Patient and Physician Experiences

The ever-expanding use of EHR is a result of their value as a healthcare tool. Data showed that the electronic exchange of information between patients and physicians improves diagnostics, reduces medical errors, enhances communication, and leads to more patient-centered care — and physicians want their patients to use the portal to maximize their healthcare.

“[The EHR] is good for patients,” said Dr. DeBiasi. “Sometimes, patients have access issues with healthcare, whether that’s not knowing what number to call or getting the right message to the right person at the right office. If [the portal] is good for them and helps them get access to care, we should embrace that and figure out a way to work it into our day-to-day schedules.”

But maximizing the patient experience shouldn’t come at the physicians’ expense. Dr. Rittenberg advocates a model that compensates physicians for the time spent in the EHR and prioritizes a team approach to rebalance the EHR workload to ensure that physicians aren’t devoting too much time to administrative tasks and can, instead, focus their time on clinical tasks.

“The way in which we provide healthcare has fundamentally shifted, and compensation models need to reflect that new reality,” Dr. Rittenberg added.

A version of this article appeared on Medscape.com.

As a cardiologist specializing in obesity medicine, I often encounter patients who would greatly benefit from the new generation of weight loss drugs that work as glucagon-like peptide 1 (GLP-1) agonists. In the recently published SELECT trial results, for example, semaglutide (marketed by Novo Nordisk as Wegovy for weight loss and Ozempic for type 2 diabetes) demonstrated a 20% risk reduction of heart attacks and strokes in overweight and obese individuals without diabetes and with cardiovascular disease, establishing it as a cardiovascular disease–modifying medication in people without type 2 diabetes.

Unfortunately, the high demand for these new weight loss medications has resulted in a frustrating, long-lasting shortage. The manufacturers of the two FDA-approved drugs, Novo Nordisk and Eli Lilly (tirzepatide, marketed as Zepbound for weight loss and Mounjaro for type 2 diabetes), are struggling to meet the overwhelming need.

To ensure continuation of patient care, federal law allows compounding pharmacies to make “essentially a copy” of the medications that are listed as “currently in shortage” on the US Food and Drug Administration (FDA) drug shortage list. Both semaglutide and tirzepatide are on that list. For Americans who suffer from obesity and other weight-related diseases, these drugs could be a lifeline.

Despite this, the medical community has broadly criticized the utilization of compounded GLP-1 agonists, even those obtained from reputable and legitimate compounding pharmacies.

Yes, high demand has led to the emergence of unregulated companies and scammers producing substandard or counterfeit versions of these medications.

The FDA has found fraudulent products (masquerading as the weight loss drugs) and has issued warning letters to stop the distribution of illegally marketed semaglutide. “These drugs may be counterfeit, which means they could contain the wrong ingredients, contain too little, too much or no active ingredient at all, or contain other harmful ingredients,” it cautions. Some products use a similar-sounding semaglutide sodium salt, which has uncertain safety and efficacy, and had generated warnings from the FDA and state boards of pharmacy.

Many of these products are marketed directly to consumers online through websites and social media, with little to no medical oversight. This practice is a significant concern, as it may affect patient safety, and should be discouraged.

However, according to a statement from the Alliance for Pharmacy Compounding (APC), legitimate compounding pharmacies aren’t the ones selling these dubious products on the black market, particularly online. This illegal practice has garnered media attention and is sometimes incorrectly associated with legitimate pharmacy compounding.

In contrast, legal and certified versions of GLP-1 agonist medications can be obtained from well-regulated and reputable compounding pharmacies. These pharmacies must adhere to all federal and state regulations and dispense medications only with a valid prescription from a licensed physician.

Meanwhile, the APC statement notes, Novo Nordisk and Eli Lilly have sued compounding companies in several states, questioning, among other things, the purity and potency of some compounded products.

There are different designations for compounding pharmacies: 503A and 503B. 503As are state-licensed pharmacies and physicians, and 503B pharmacies are federally regulated outsourcing facilities that are strictly regulated by the FDA. This regulation, established following a 2012 fungal meningitis outbreak linked to a compounding pharmacy, ensures higher-quality control and oversight, especially for medications intended for intravenous or epidural use. These standards exceed those required for subcutaneous injections like GLP-1 analogs.

In the face of this Wild West climate, where compounded drugs may vary in their source, formulation, potency, and purity, The Obesity Society, the Obesity Medical Association, and the Obesity Action Coalition published a joint statement that advised against the use of compounded GLP-1 agonists, citing safety concerns and lack of regulatory oversight.

This stance, while aimed at ensuring patient safety, inadvertently raises a critical issue.

By completely dismissing compounded medications, experts may unintentionally bolster the black market and overlook the needs of patients who could benefit from these medications, contrary to the intentions of the exemption provided in federal law for compounding during a drug shortage. In fact, the presence of unreliable suppliers highlights the need to direct the public toward trustworthy sources, rather than imposing a total ban on medically appropriate alternatives.

The joint statement calls compounded GLP-1 agonists “counterfeit.” This inaccurate overgeneralization probably stems from a misunderstanding of the compounding process and its regulations. Legitimate and regulated pharmacies compound base GLP-1 agonists, which are “essentially a copy” of FDA-approved medications, not counterfeits. Recognizing this is crucial for maintaining trust in both compounding pharmacies and regulatory bodies.

It is correct that “the only FDA-approved manufacturers of these medications are the companies that created the active pharmaceutical ingredients — Novo Nordisk and Eli Lilly,” but the joint statement fails to mention the exemptions provided by law that allow compounding copies of the branded medications if they are on the shortage list.

Compounding pharmacies must obtain active pharmaceutical ingredients (APIs) from FDA-registered facilities, which are required to adhere to Current Good Manufacturing Practices (cGMP). This ensures the APIs’ quality, potency, and purity, crucial for the safety and efficacy of compounded medications.

Compounded drugs are not FDA approved, but they aren’t inherently unsafe. Compounded medications include critical drugs such as resuscitation medications and antibiotics, and are often used in healthcare settings, especially when there’s a shortage. This raises the question of why compounded GLP-1 agonists would be treated any differently in such scenarios.

And in the case of alternative drugs for individuals with obesity who have a higher risk for cardiovascular disease, the brand-name FDA-approved alternative may be of more concern than the compounded GLP-1 agonist. The obesity societies advise: “If you cannot find or get access to a GLP-1-based treatment now, there are other treatments available,” echoing experts. While the statement doesn’t specify the names of the alternatives, experts have advised using alternatives such as Qsymia and Contrave, despite their potential cardiovascular concerns. This recommendation to the public may not represent a responsible risk-benefit analysis.

Courtesy Dr. Einav

Possible Solutions

When prescribing GLP-1 agonists for obesity treatment, doctors should consider all of the following steps to ensure patient safety and effective treatment:

Preference for FDA-approved brands: FDA-approved branded GLP-1 agonist medications should be the primary choice because of their established safety and efficacy.

Risk-benefit analysis for non–FDA-approved products: In cases where FDA-approved options are not available, doctors may consider prescribing a non–FDA-approved copy of the branded medication. Prior to this, conduct a thorough risk-benefit analysis with the patient, ensuring that they are fully informed about the potential risks and benefits of using a non–FDA-approved product.

Choosing semaglutide copies for specific cases: In patients with obesity and cardiovascular disease, the benefits of using a compounded copy of semaglutide, with its cardiovascular disease–modifying properties, may outweigh the risks compared with other FDA-approved antiobesity drugs that might pose cardiovascular risks or compared with no antiobesity treatment at all.

Informed consent and monitoring: When prescribing a non–FDA-approved version of a GLP-1 agonist, obtaining informed consent from the patient is advised. They should be made aware of the differences between the FDA-approved and nonapproved versions.

Choosing between 503A and 503B pharmacies: Prescriptions for non–FDA-approved GLP-1 agonists can be directed to either 503A or 503B compounding pharmacies. However, it’s advisable to check whether the product can be compounded by a 503B pharmacy, which is subject to an additional layer of FDA regulation, offering greater quality assurance.

Clear prescription specifications: Ensure that the prescription explicitly states that the compounded GLP-1 agonist should be the base compound without additives.

Requesting a Certificate of Analysis: To further ensure safety, request a Certificate of Analysis from the compounding pharmacy. This provides detailed quality and composition information about the product.

Ongoing monitoring: Continuously monitor the patient’s response to the medication and adjust the treatment plan as necessary, maintaining regular follow-ups.

By adhering to these guidelines, doctors can navigate the complexities of prescribing GLP-1 agonists in a way that prioritizes patient well-being, particularly in scenarios where conventional treatment options are limited.
 

Dr. Einav is a board-certified cardiologist and a Diplomate of the American Board of Obesity Medicine. He is a fellow of the American College of Cardiology and a member of the Obesity Medicine Association. He serves as the medical director of cardiometabolic health in Guthrie Lourdes in Binghamton, New York, and is the founder of myW8/Cardiometabolic Health located in Beverly Hills, California. This article solely reflects the personal views of Dr. Einav and should not be considered as representing the official stance of Guthrie Lourdes. Dr. Einav served as a promotional speaker for Novo Nordisk in 2022. As of now, he has not prescribed any compounded GLP-1 agonist medications in his medical practice.

A version of this article appeared on Medscape.com.

As a cardiologist specializing in obesity medicine, I often encounter patients who would greatly benefit from the new generation of weight loss drugs that work as glucagon-like peptide 1 (GLP-1) agonists. In the recently published SELECT trial results, for example, semaglutide (marketed by Novo Nordisk as Wegovy for weight loss and Ozempic for type 2 diabetes) demonstrated a 20% risk reduction of heart attacks and strokes in overweight and obese individuals without diabetes and with cardiovascular disease, establishing it as a cardiovascular disease–modifying medication in people without type 2 diabetes.

Unfortunately, the high demand for these new weight loss medications has resulted in a frustrating, long-lasting shortage. The manufacturers of the two FDA-approved drugs, Novo Nordisk and Eli Lilly (tirzepatide, marketed as Zepbound for weight loss and Mounjaro for type 2 diabetes), are struggling to meet the overwhelming need.

To ensure continuation of patient care, federal law allows compounding pharmacies to make “essentially a copy” of the medications that are listed as “currently in shortage” on the US Food and Drug Administration (FDA) drug shortage list. Both semaglutide and tirzepatide are on that list. For Americans who suffer from obesity and other weight-related diseases, these drugs could be a lifeline.

Despite this, the medical community has broadly criticized the utilization of compounded GLP-1 agonists, even those obtained from reputable and legitimate compounding pharmacies.

Yes, high demand has led to the emergence of unregulated companies and scammers producing substandard or counterfeit versions of these medications.

The FDA has found fraudulent products (masquerading as the weight loss drugs) and has issued warning letters to stop the distribution of illegally marketed semaglutide. “These drugs may be counterfeit, which means they could contain the wrong ingredients, contain too little, too much or no active ingredient at all, or contain other harmful ingredients,” it cautions. Some products use a similar-sounding semaglutide sodium salt, which has uncertain safety and efficacy, and had generated warnings from the FDA and state boards of pharmacy.

Many of these products are marketed directly to consumers online through websites and social media, with little to no medical oversight. This practice is a significant concern, as it may affect patient safety, and should be discouraged.

However, according to a statement from the Alliance for Pharmacy Compounding (APC), legitimate compounding pharmacies aren’t the ones selling these dubious products on the black market, particularly online. This illegal practice has garnered media attention and is sometimes incorrectly associated with legitimate pharmacy compounding.

In contrast, legal and certified versions of GLP-1 agonist medications can be obtained from well-regulated and reputable compounding pharmacies. These pharmacies must adhere to all federal and state regulations and dispense medications only with a valid prescription from a licensed physician.

Meanwhile, the APC statement notes, Novo Nordisk and Eli Lilly have sued compounding companies in several states, questioning, among other things, the purity and potency of some compounded products.

There are different designations for compounding pharmacies: 503A and 503B. 503As are state-licensed pharmacies and physicians, and 503B pharmacies are federally regulated outsourcing facilities that are strictly regulated by the FDA. This regulation, established following a 2012 fungal meningitis outbreak linked to a compounding pharmacy, ensures higher-quality control and oversight, especially for medications intended for intravenous or epidural use. These standards exceed those required for subcutaneous injections like GLP-1 analogs.

In the face of this Wild West climate, where compounded drugs may vary in their source, formulation, potency, and purity, The Obesity Society, the Obesity Medical Association, and the Obesity Action Coalition published a joint statement that advised against the use of compounded GLP-1 agonists, citing safety concerns and lack of regulatory oversight.

This stance, while aimed at ensuring patient safety, inadvertently raises a critical issue.

By completely dismissing compounded medications, experts may unintentionally bolster the black market and overlook the needs of patients who could benefit from these medications, contrary to the intentions of the exemption provided in federal law for compounding during a drug shortage. In fact, the presence of unreliable suppliers highlights the need to direct the public toward trustworthy sources, rather than imposing a total ban on medically appropriate alternatives.

The joint statement calls compounded GLP-1 agonists “counterfeit.” This inaccurate overgeneralization probably stems from a misunderstanding of the compounding process and its regulations. Legitimate and regulated pharmacies compound base GLP-1 agonists, which are “essentially a copy” of FDA-approved medications, not counterfeits. Recognizing this is crucial for maintaining trust in both compounding pharmacies and regulatory bodies.

It is correct that “the only FDA-approved manufacturers of these medications are the companies that created the active pharmaceutical ingredients — Novo Nordisk and Eli Lilly,” but the joint statement fails to mention the exemptions provided by law that allow compounding copies of the branded medications if they are on the shortage list.

Compounding pharmacies must obtain active pharmaceutical ingredients (APIs) from FDA-registered facilities, which are required to adhere to Current Good Manufacturing Practices (cGMP). This ensures the APIs’ quality, potency, and purity, crucial for the safety and efficacy of compounded medications.

Compounded drugs are not FDA approved, but they aren’t inherently unsafe. Compounded medications include critical drugs such as resuscitation medications and antibiotics, and are often used in healthcare settings, especially when there’s a shortage. This raises the question of why compounded GLP-1 agonists would be treated any differently in such scenarios.

And in the case of alternative drugs for individuals with obesity who have a higher risk for cardiovascular disease, the brand-name FDA-approved alternative may be of more concern than the compounded GLP-1 agonist. The obesity societies advise: “If you cannot find or get access to a GLP-1-based treatment now, there are other treatments available,” echoing experts. While the statement doesn’t specify the names of the alternatives, experts have advised using alternatives such as Qsymia and Contrave, despite their potential cardiovascular concerns. This recommendation to the public may not represent a responsible risk-benefit analysis.

Courtesy Dr. Einav

Possible Solutions

When prescribing GLP-1 agonists for obesity treatment, doctors should consider all of the following steps to ensure patient safety and effective treatment:

Preference for FDA-approved brands: FDA-approved branded GLP-1 agonist medications should be the primary choice because of their established safety and efficacy.

Risk-benefit analysis for non–FDA-approved products: In cases where FDA-approved options are not available, doctors may consider prescribing a non–FDA-approved copy of the branded medication. Prior to this, conduct a thorough risk-benefit analysis with the patient, ensuring that they are fully informed about the potential risks and benefits of using a non–FDA-approved product.

Choosing semaglutide copies for specific cases: In patients with obesity and cardiovascular disease, the benefits of using a compounded copy of semaglutide, with its cardiovascular disease–modifying properties, may outweigh the risks compared with other FDA-approved antiobesity drugs that might pose cardiovascular risks or compared with no antiobesity treatment at all.

Informed consent and monitoring: When prescribing a non–FDA-approved version of a GLP-1 agonist, obtaining informed consent from the patient is advised. They should be made aware of the differences between the FDA-approved and nonapproved versions.

Choosing between 503A and 503B pharmacies: Prescriptions for non–FDA-approved GLP-1 agonists can be directed to either 503A or 503B compounding pharmacies. However, it’s advisable to check whether the product can be compounded by a 503B pharmacy, which is subject to an additional layer of FDA regulation, offering greater quality assurance.

Clear prescription specifications: Ensure that the prescription explicitly states that the compounded GLP-1 agonist should be the base compound without additives.

Requesting a Certificate of Analysis: To further ensure safety, request a Certificate of Analysis from the compounding pharmacy. This provides detailed quality and composition information about the product.

Ongoing monitoring: Continuously monitor the patient’s response to the medication and adjust the treatment plan as necessary, maintaining regular follow-ups.

By adhering to these guidelines, doctors can navigate the complexities of prescribing GLP-1 agonists in a way that prioritizes patient well-being, particularly in scenarios where conventional treatment options are limited.
 

Dr. Einav is a board-certified cardiologist and a Diplomate of the American Board of Obesity Medicine. He is a fellow of the American College of Cardiology and a member of the Obesity Medicine Association. He serves as the medical director of cardiometabolic health in Guthrie Lourdes in Binghamton, New York, and is the founder of myW8/Cardiometabolic Health located in Beverly Hills, California. This article solely reflects the personal views of Dr. Einav and should not be considered as representing the official stance of Guthrie Lourdes. Dr. Einav served as a promotional speaker for Novo Nordisk in 2022. As of now, he has not prescribed any compounded GLP-1 agonist medications in his medical practice.

A version of this article appeared on Medscape.com.

As a cardiologist specializing in obesity medicine, I often encounter patients who would greatly benefit from the new generation of weight loss drugs that work as glucagon-like peptide 1 (GLP-1) agonists. In the recently published SELECT trial results, for example, semaglutide (marketed by Novo Nordisk as Wegovy for weight loss and Ozempic for type 2 diabetes) demonstrated a 20% risk reduction of heart attacks and strokes in overweight and obese individuals without diabetes and with cardiovascular disease, establishing it as a cardiovascular disease–modifying medication in people without type 2 diabetes.

Unfortunately, the high demand for these new weight loss medications has resulted in a frustrating, long-lasting shortage. The manufacturers of the two FDA-approved drugs, Novo Nordisk and Eli Lilly (tirzepatide, marketed as Zepbound for weight loss and Mounjaro for type 2 diabetes), are struggling to meet the overwhelming need.

To ensure continuation of patient care, federal law allows compounding pharmacies to make “essentially a copy” of the medications that are listed as “currently in shortage” on the US Food and Drug Administration (FDA) drug shortage list. Both semaglutide and tirzepatide are on that list. For Americans who suffer from obesity and other weight-related diseases, these drugs could be a lifeline.

Despite this, the medical community has broadly criticized the utilization of compounded GLP-1 agonists, even those obtained from reputable and legitimate compounding pharmacies.

Yes, high demand has led to the emergence of unregulated companies and scammers producing substandard or counterfeit versions of these medications.

The FDA has found fraudulent products (masquerading as the weight loss drugs) and has issued warning letters to stop the distribution of illegally marketed semaglutide. “These drugs may be counterfeit, which means they could contain the wrong ingredients, contain too little, too much or no active ingredient at all, or contain other harmful ingredients,” it cautions. Some products use a similar-sounding semaglutide sodium salt, which has uncertain safety and efficacy, and had generated warnings from the FDA and state boards of pharmacy.

Many of these products are marketed directly to consumers online through websites and social media, with little to no medical oversight. This practice is a significant concern, as it may affect patient safety, and should be discouraged.

However, according to a statement from the Alliance for Pharmacy Compounding (APC), legitimate compounding pharmacies aren’t the ones selling these dubious products on the black market, particularly online. This illegal practice has garnered media attention and is sometimes incorrectly associated with legitimate pharmacy compounding.

In contrast, legal and certified versions of GLP-1 agonist medications can be obtained from well-regulated and reputable compounding pharmacies. These pharmacies must adhere to all federal and state regulations and dispense medications only with a valid prescription from a licensed physician.

Meanwhile, the APC statement notes, Novo Nordisk and Eli Lilly have sued compounding companies in several states, questioning, among other things, the purity and potency of some compounded products.

There are different designations for compounding pharmacies: 503A and 503B. 503As are state-licensed pharmacies and physicians, and 503B pharmacies are federally regulated outsourcing facilities that are strictly regulated by the FDA. This regulation, established following a 2012 fungal meningitis outbreak linked to a compounding pharmacy, ensures higher-quality control and oversight, especially for medications intended for intravenous or epidural use. These standards exceed those required for subcutaneous injections like GLP-1 analogs.

In the face of this Wild West climate, where compounded drugs may vary in their source, formulation, potency, and purity, The Obesity Society, the Obesity Medical Association, and the Obesity Action Coalition published a joint statement that advised against the use of compounded GLP-1 agonists, citing safety concerns and lack of regulatory oversight.

This stance, while aimed at ensuring patient safety, inadvertently raises a critical issue.

By completely dismissing compounded medications, experts may unintentionally bolster the black market and overlook the needs of patients who could benefit from these medications, contrary to the intentions of the exemption provided in federal law for compounding during a drug shortage. In fact, the presence of unreliable suppliers highlights the need to direct the public toward trustworthy sources, rather than imposing a total ban on medically appropriate alternatives.

The joint statement calls compounded GLP-1 agonists “counterfeit.” This inaccurate overgeneralization probably stems from a misunderstanding of the compounding process and its regulations. Legitimate and regulated pharmacies compound base GLP-1 agonists, which are “essentially a copy” of FDA-approved medications, not counterfeits. Recognizing this is crucial for maintaining trust in both compounding pharmacies and regulatory bodies.

It is correct that “the only FDA-approved manufacturers of these medications are the companies that created the active pharmaceutical ingredients — Novo Nordisk and Eli Lilly,” but the joint statement fails to mention the exemptions provided by law that allow compounding copies of the branded medications if they are on the shortage list.

Compounding pharmacies must obtain active pharmaceutical ingredients (APIs) from FDA-registered facilities, which are required to adhere to Current Good Manufacturing Practices (cGMP). This ensures the APIs’ quality, potency, and purity, crucial for the safety and efficacy of compounded medications.

Compounded drugs are not FDA approved, but they aren’t inherently unsafe. Compounded medications include critical drugs such as resuscitation medications and antibiotics, and are often used in healthcare settings, especially when there’s a shortage. This raises the question of why compounded GLP-1 agonists would be treated any differently in such scenarios.

And in the case of alternative drugs for individuals with obesity who have a higher risk for cardiovascular disease, the brand-name FDA-approved alternative may be of more concern than the compounded GLP-1 agonist. The obesity societies advise: “If you cannot find or get access to a GLP-1-based treatment now, there are other treatments available,” echoing experts. While the statement doesn’t specify the names of the alternatives, experts have advised using alternatives such as Qsymia and Contrave, despite their potential cardiovascular concerns. This recommendation to the public may not represent a responsible risk-benefit analysis.

Courtesy Dr. Einav

Possible Solutions

When prescribing GLP-1 agonists for obesity treatment, doctors should consider all of the following steps to ensure patient safety and effective treatment:

Preference for FDA-approved brands: FDA-approved branded GLP-1 agonist medications should be the primary choice because of their established safety and efficacy.

Risk-benefit analysis for non–FDA-approved products: In cases where FDA-approved options are not available, doctors may consider prescribing a non–FDA-approved copy of the branded medication. Prior to this, conduct a thorough risk-benefit analysis with the patient, ensuring that they are fully informed about the potential risks and benefits of using a non–FDA-approved product.

Choosing semaglutide copies for specific cases: In patients with obesity and cardiovascular disease, the benefits of using a compounded copy of semaglutide, with its cardiovascular disease–modifying properties, may outweigh the risks compared with other FDA-approved antiobesity drugs that might pose cardiovascular risks or compared with no antiobesity treatment at all.

Informed consent and monitoring: When prescribing a non–FDA-approved version of a GLP-1 agonist, obtaining informed consent from the patient is advised. They should be made aware of the differences between the FDA-approved and nonapproved versions.

Choosing between 503A and 503B pharmacies: Prescriptions for non–FDA-approved GLP-1 agonists can be directed to either 503A or 503B compounding pharmacies. However, it’s advisable to check whether the product can be compounded by a 503B pharmacy, which is subject to an additional layer of FDA regulation, offering greater quality assurance.

Clear prescription specifications: Ensure that the prescription explicitly states that the compounded GLP-1 agonist should be the base compound without additives.

Requesting a Certificate of Analysis: To further ensure safety, request a Certificate of Analysis from the compounding pharmacy. This provides detailed quality and composition information about the product.

Ongoing monitoring: Continuously monitor the patient’s response to the medication and adjust the treatment plan as necessary, maintaining regular follow-ups.

By adhering to these guidelines, doctors can navigate the complexities of prescribing GLP-1 agonists in a way that prioritizes patient well-being, particularly in scenarios where conventional treatment options are limited.
 

Dr. Einav is a board-certified cardiologist and a Diplomate of the American Board of Obesity Medicine. He is a fellow of the American College of Cardiology and a member of the Obesity Medicine Association. He serves as the medical director of cardiometabolic health in Guthrie Lourdes in Binghamton, New York, and is the founder of myW8/Cardiometabolic Health located in Beverly Hills, California. This article solely reflects the personal views of Dr. Einav and should not be considered as representing the official stance of Guthrie Lourdes. Dr. Einav served as a promotional speaker for Novo Nordisk in 2022. As of now, he has not prescribed any compounded GLP-1 agonist medications in his medical practice.

A version of this article appeared on Medscape.com.

I don’t recommend ice baths. Perhaps I should. On my podcast-filled commute, I am reminded for miles of the mental and physical benefits of this revolutionary wellness routine: Cold exposure causes a spike in adrenaline and raises your baseline dopamine, thereby giving you superhuman focus and energy. Goodbye procrastination! Eliminate your ADHD in one icy step! I’m trying to be the fashionable mustached-columnist here so maybe I should get on board.

In fact, a heavyset, similarly-mustached 32-year-old patient just asked if I do ice baths. It was meant as a compliment, I believe. Displaying poise wearing my Chief of Dermatology embroidered white coat in my toddler-art-adorned office, I could hear him thinking: “This doc is legit. On fleek.” (Note, this is an approximation and the patient’s actual thoughts may have varied). We were talking podcasts and he was curious about my daily routine.

Kaiser Permanente

Now, ice baths probably do have the benefits that Andrew Huberman, Joe Rogan, and the others have described, I don’t argue. And the experience is oft described as invigorating with a runner’s high-like euphoria that follows a good dunk. I’ve tried it. I would describe it as “very uncomfortable.” To boot, following icy-cold morning showers, I wasn’t any better able to stave off opening my New York Times app on a newsy day. No, cold water isn’t my jams. But then again, I don’t journal like Marcus Aurelius or sleep on a mattress that keeps my body a chill 97 degrees like an inverse sous vide. If I were asked by Huberman in an interview what I do to be mentally strong, I’d answer, “I clean the pool.”

“Here’s how I do it, Dr. Huberman,” I’d say. “First, open the pool cover. Then with a cup with pool water from about 12 inches down, fill these little beakers with water and add a few drops of chemical reagents. Then calculate the ounces of calcium hypochlorite, muriatic acid, and other chemicals to make your pools sparkle. After skimming, take your pool brush and brush the bottom and sides of your pool. Rack your equipment when done and close the cover back up. This exercise takes about 15 minutes.” It’s a mundane task, but ah, there’s the point. Like folding the laundry, weeding the garden, emptying the dishwasher, they can be oh, so gratifying. Each of these has a crisp beginning and end and offer a lovely spot to be present. Let the thoughts flow with each stroke of the brush. Watch the water ripple the surface as you slowly pull the long pole out, dripping 7.4 pH water as you glide it in for the next pass. This is the Benabio secret to success.

Dr. Benabio

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on X. Write to him at [email protected].

I don’t recommend ice baths. Perhaps I should. On my podcast-filled commute, I am reminded for miles of the mental and physical benefits of this revolutionary wellness routine: Cold exposure causes a spike in adrenaline and raises your baseline dopamine, thereby giving you superhuman focus and energy. Goodbye procrastination! Eliminate your ADHD in one icy step! I’m trying to be the fashionable mustached-columnist here so maybe I should get on board.

In fact, a heavyset, similarly-mustached 32-year-old patient just asked if I do ice baths. It was meant as a compliment, I believe. Displaying poise wearing my Chief of Dermatology embroidered white coat in my toddler-art-adorned office, I could hear him thinking: “This doc is legit. On fleek.” (Note, this is an approximation and the patient’s actual thoughts may have varied). We were talking podcasts and he was curious about my daily routine.

Kaiser Permanente

Now, ice baths probably do have the benefits that Andrew Huberman, Joe Rogan, and the others have described, I don’t argue. And the experience is oft described as invigorating with a runner’s high-like euphoria that follows a good dunk. I’ve tried it. I would describe it as “very uncomfortable.” To boot, following icy-cold morning showers, I wasn’t any better able to stave off opening my New York Times app on a newsy day. No, cold water isn’t my jams. But then again, I don’t journal like Marcus Aurelius or sleep on a mattress that keeps my body a chill 97 degrees like an inverse sous vide. If I were asked by Huberman in an interview what I do to be mentally strong, I’d answer, “I clean the pool.”

“Here’s how I do it, Dr. Huberman,” I’d say. “First, open the pool cover. Then with a cup with pool water from about 12 inches down, fill these little beakers with water and add a few drops of chemical reagents. Then calculate the ounces of calcium hypochlorite, muriatic acid, and other chemicals to make your pools sparkle. After skimming, take your pool brush and brush the bottom and sides of your pool. Rack your equipment when done and close the cover back up. This exercise takes about 15 minutes.” It’s a mundane task, but ah, there’s the point. Like folding the laundry, weeding the garden, emptying the dishwasher, they can be oh, so gratifying. Each of these has a crisp beginning and end and offer a lovely spot to be present. Let the thoughts flow with each stroke of the brush. Watch the water ripple the surface as you slowly pull the long pole out, dripping 7.4 pH water as you glide it in for the next pass. This is the Benabio secret to success.

Dr. Benabio

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on X. Write to him at [email protected].

I don’t recommend ice baths. Perhaps I should. On my podcast-filled commute, I am reminded for miles of the mental and physical benefits of this revolutionary wellness routine: Cold exposure causes a spike in adrenaline and raises your baseline dopamine, thereby giving you superhuman focus and energy. Goodbye procrastination! Eliminate your ADHD in one icy step! I’m trying to be the fashionable mustached-columnist here so maybe I should get on board.

In fact, a heavyset, similarly-mustached 32-year-old patient just asked if I do ice baths. It was meant as a compliment, I believe. Displaying poise wearing my Chief of Dermatology embroidered white coat in my toddler-art-adorned office, I could hear him thinking: “This doc is legit. On fleek.” (Note, this is an approximation and the patient’s actual thoughts may have varied). We were talking podcasts and he was curious about my daily routine.

Kaiser Permanente

Now, ice baths probably do have the benefits that Andrew Huberman, Joe Rogan, and the others have described, I don’t argue. And the experience is oft described as invigorating with a runner’s high-like euphoria that follows a good dunk. I’ve tried it. I would describe it as “very uncomfortable.” To boot, following icy-cold morning showers, I wasn’t any better able to stave off opening my New York Times app on a newsy day. No, cold water isn’t my jams. But then again, I don’t journal like Marcus Aurelius or sleep on a mattress that keeps my body a chill 97 degrees like an inverse sous vide. If I were asked by Huberman in an interview what I do to be mentally strong, I’d answer, “I clean the pool.”

“Here’s how I do it, Dr. Huberman,” I’d say. “First, open the pool cover. Then with a cup with pool water from about 12 inches down, fill these little beakers with water and add a few drops of chemical reagents. Then calculate the ounces of calcium hypochlorite, muriatic acid, and other chemicals to make your pools sparkle. After skimming, take your pool brush and brush the bottom and sides of your pool. Rack your equipment when done and close the cover back up. This exercise takes about 15 minutes.” It’s a mundane task, but ah, there’s the point. Like folding the laundry, weeding the garden, emptying the dishwasher, they can be oh, so gratifying. Each of these has a crisp beginning and end and offer a lovely spot to be present. Let the thoughts flow with each stroke of the brush. Watch the water ripple the surface as you slowly pull the long pole out, dripping 7.4 pH water as you glide it in for the next pass. This is the Benabio secret to success.

Dr. Benabio

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on X. Write to him at [email protected].