MDedge Endocrinology

BOSTON — Use of over-the-counter arthritis supplements containing undisclosed glucocorticoids can lead to iatrogenic adrenal dysfunction, Cushing syndrome, and/or adrenal insufficiency (AI). 

Patients who have been taking these supplements for prolonged periods must slowly taper off them with corticosteroid replacement, because abruptly stopping the supplement can precipitate AI, Kevin S. Wei, MD, said in a presentation of 12 cases — the largest such series to date of the phenomenon — at the annual meeting of the Endocrine Society.

The specific supplements used were Artri King in eight of the patients, Ardosons in two, and Ajo Rey in one. In April 2022, the US Food and Drug Administration issued a warning that Artri King contains diclofenac and dexamethasone not listed on the product label. In July 2023, the agency issued an expanded warning about that product and others including Ajo Rey.

The supplements are not believed to be sold in the United States, but they are available in Mexico and can be ordered online, said Dr. Wei, a second-year resident at the Keck School of Medicine at the University of California, Los Angeles.

“We found that quite a lot of patients after they’ve been on the Artri King or some other over the counter arthritis supplement, started developing these cushingoid features seen in the physical exam, such as rounded facial features or stretch marks of their abdomen,” he said.

And “when patients are abruptly taken off those supplements … sometimes this can cause them to go into signs or symptoms of adrenal insufficiency. That can occasionally be life-threatening if it’s not addressed in an inpatient setting,” Dr. Wei said.

In an interview, session moderator Sharon L. Wardlaw, MD, professor of medicine at Columbia University Irving Medical Center, New York, explained that when a person takes these drugs containing hidden glucocorticoids, “they won’t be picked up in a cortisol assay, but they’ll suppress the [adrenocorticotropic hormone] and the person’s own cortisol production. They look like they have Cushing, but when you measure their hormone levels, they’re undetectable. And then people wonder what’s going on. Well, their [hypothalamic-pituitary-adrenal] axis is suppressed.”

But if the product is suddenly stopped without cortisol replacement “If they get an infection they can die because they can’t mount a cortisol response.”

The takeaway message, she said, is “always ask patients to show you their supplements and look at them. In many cases, that’s why they work so well for pain relief because they have ingredients that people shouldn’t be taking.”

Twelve Patients Seen During 2022-2023

The 12 patients were seen during 2022-2023 at an endocrinology consult service in an urban safety net hospital. Their median age was 52 years, and one third were women. All had started using the supplements for joint pain, with a median of about 6 months of use prior to cessation.

Presenting symptoms included nausea/vomiting in 42%, fatigue in 42%, abdominal pain in 33%, and dizziness in 17%. Physical exam findings included moon facies in 66%, central adiposity in 66%, abdominal striae in 50%, dorsocervical fat pad in 33%, and bruising in 33%. Three required intensive care admission.

Cortisol testing was performed in 11 of the patients and was normal (≥ 16 mcg/dL) in just one. AI (≤ 3 mcg/dL) was found in three, while the rest had indeterminate results. Of those seven patients, subsequent cosyntropin-stimulation testing suggested AI (cortisol < 16 mcg/dL at 60 minutes post stimulation) in four patients, while the other two showed reduced but normal responses (cortisol 18.2-18.4 mcg/dL).

Ten of the 12 patients were prescribed glucocorticoid tapering replacements to avoid precipitating adrenal crisis, most commonly twice-daily hydrocortisone. Of those ten, eight continued to take the replacement steroids 1-2 years later, Dr. Wei said.

Dr. Wei and Dr. Wardlaw had no disclosures.

A version of this article appeared on Medscape.com.

BOSTON — Use of over-the-counter arthritis supplements containing undisclosed glucocorticoids can lead to iatrogenic adrenal dysfunction, Cushing syndrome, and/or adrenal insufficiency (AI). 

Patients who have been taking these supplements for prolonged periods must slowly taper off them with corticosteroid replacement, because abruptly stopping the supplement can precipitate AI, Kevin S. Wei, MD, said in a presentation of 12 cases — the largest such series to date of the phenomenon — at the annual meeting of the Endocrine Society.

The specific supplements used were Artri King in eight of the patients, Ardosons in two, and Ajo Rey in one. In April 2022, the US Food and Drug Administration issued a warning that Artri King contains diclofenac and dexamethasone not listed on the product label. In July 2023, the agency issued an expanded warning about that product and others including Ajo Rey.

The supplements are not believed to be sold in the United States, but they are available in Mexico and can be ordered online, said Dr. Wei, a second-year resident at the Keck School of Medicine at the University of California, Los Angeles.

“We found that quite a lot of patients after they’ve been on the Artri King or some other over the counter arthritis supplement, started developing these cushingoid features seen in the physical exam, such as rounded facial features or stretch marks of their abdomen,” he said.

And “when patients are abruptly taken off those supplements … sometimes this can cause them to go into signs or symptoms of adrenal insufficiency. That can occasionally be life-threatening if it’s not addressed in an inpatient setting,” Dr. Wei said.

In an interview, session moderator Sharon L. Wardlaw, MD, professor of medicine at Columbia University Irving Medical Center, New York, explained that when a person takes these drugs containing hidden glucocorticoids, “they won’t be picked up in a cortisol assay, but they’ll suppress the [adrenocorticotropic hormone] and the person’s own cortisol production. They look like they have Cushing, but when you measure their hormone levels, they’re undetectable. And then people wonder what’s going on. Well, their [hypothalamic-pituitary-adrenal] axis is suppressed.”

But if the product is suddenly stopped without cortisol replacement “If they get an infection they can die because they can’t mount a cortisol response.”

The takeaway message, she said, is “always ask patients to show you their supplements and look at them. In many cases, that’s why they work so well for pain relief because they have ingredients that people shouldn’t be taking.”

Twelve Patients Seen During 2022-2023

The 12 patients were seen during 2022-2023 at an endocrinology consult service in an urban safety net hospital. Their median age was 52 years, and one third were women. All had started using the supplements for joint pain, with a median of about 6 months of use prior to cessation.

Presenting symptoms included nausea/vomiting in 42%, fatigue in 42%, abdominal pain in 33%, and dizziness in 17%. Physical exam findings included moon facies in 66%, central adiposity in 66%, abdominal striae in 50%, dorsocervical fat pad in 33%, and bruising in 33%. Three required intensive care admission.

Cortisol testing was performed in 11 of the patients and was normal (≥ 16 mcg/dL) in just one. AI (≤ 3 mcg/dL) was found in three, while the rest had indeterminate results. Of those seven patients, subsequent cosyntropin-stimulation testing suggested AI (cortisol < 16 mcg/dL at 60 minutes post stimulation) in four patients, while the other two showed reduced but normal responses (cortisol 18.2-18.4 mcg/dL).

Ten of the 12 patients were prescribed glucocorticoid tapering replacements to avoid precipitating adrenal crisis, most commonly twice-daily hydrocortisone. Of those ten, eight continued to take the replacement steroids 1-2 years later, Dr. Wei said.

Dr. Wei and Dr. Wardlaw had no disclosures.

A version of this article appeared on Medscape.com.

BOSTON — Use of over-the-counter arthritis supplements containing undisclosed glucocorticoids can lead to iatrogenic adrenal dysfunction, Cushing syndrome, and/or adrenal insufficiency (AI). 

Patients who have been taking these supplements for prolonged periods must slowly taper off them with corticosteroid replacement, because abruptly stopping the supplement can precipitate AI, Kevin S. Wei, MD, said in a presentation of 12 cases — the largest such series to date of the phenomenon — at the annual meeting of the Endocrine Society.

The specific supplements used were Artri King in eight of the patients, Ardosons in two, and Ajo Rey in one. In April 2022, the US Food and Drug Administration issued a warning that Artri King contains diclofenac and dexamethasone not listed on the product label. In July 2023, the agency issued an expanded warning about that product and others including Ajo Rey.

The supplements are not believed to be sold in the United States, but they are available in Mexico and can be ordered online, said Dr. Wei, a second-year resident at the Keck School of Medicine at the University of California, Los Angeles.

“We found that quite a lot of patients after they’ve been on the Artri King or some other over the counter arthritis supplement, started developing these cushingoid features seen in the physical exam, such as rounded facial features or stretch marks of their abdomen,” he said.

And “when patients are abruptly taken off those supplements … sometimes this can cause them to go into signs or symptoms of adrenal insufficiency. That can occasionally be life-threatening if it’s not addressed in an inpatient setting,” Dr. Wei said.

In an interview, session moderator Sharon L. Wardlaw, MD, professor of medicine at Columbia University Irving Medical Center, New York, explained that when a person takes these drugs containing hidden glucocorticoids, “they won’t be picked up in a cortisol assay, but they’ll suppress the [adrenocorticotropic hormone] and the person’s own cortisol production. They look like they have Cushing, but when you measure their hormone levels, they’re undetectable. And then people wonder what’s going on. Well, their [hypothalamic-pituitary-adrenal] axis is suppressed.”

But if the product is suddenly stopped without cortisol replacement “If they get an infection they can die because they can’t mount a cortisol response.”

The takeaway message, she said, is “always ask patients to show you their supplements and look at them. In many cases, that’s why they work so well for pain relief because they have ingredients that people shouldn’t be taking.”

Twelve Patients Seen During 2022-2023

The 12 patients were seen during 2022-2023 at an endocrinology consult service in an urban safety net hospital. Their median age was 52 years, and one third were women. All had started using the supplements for joint pain, with a median of about 6 months of use prior to cessation.

Presenting symptoms included nausea/vomiting in 42%, fatigue in 42%, abdominal pain in 33%, and dizziness in 17%. Physical exam findings included moon facies in 66%, central adiposity in 66%, abdominal striae in 50%, dorsocervical fat pad in 33%, and bruising in 33%. Three required intensive care admission.

Cortisol testing was performed in 11 of the patients and was normal (≥ 16 mcg/dL) in just one. AI (≤ 3 mcg/dL) was found in three, while the rest had indeterminate results. Of those seven patients, subsequent cosyntropin-stimulation testing suggested AI (cortisol < 16 mcg/dL at 60 minutes post stimulation) in four patients, while the other two showed reduced but normal responses (cortisol 18.2-18.4 mcg/dL).

Ten of the 12 patients were prescribed glucocorticoid tapering replacements to avoid precipitating adrenal crisis, most commonly twice-daily hydrocortisone. Of those ten, eight continued to take the replacement steroids 1-2 years later, Dr. Wei said.

Dr. Wei and Dr. Wardlaw had no disclosures.

A version of this article appeared on Medscape.com.

I’d like to talk with you about a recent report in the British Medical Journal on the regular use of omega-3 fish oil supplements and the course of cardiovascular disease (CVD).

This is an observational study from the large-scale UK Biobank. The authors divided the participants into those with and those without CVD. In participants without CVD at baseline, those using fish oil supplements regularly had an increased incidence of both atrial fibrillation (AF) and stroke, whereas those with prevalent CVD had a reduction in the progression to major adverse cardiovascular events, which offset any increase in the risk for AF.

Observational studies of omega-3 supplements have potential limitations and confounding, and correlation in these studies does not prove causation. What do the randomized clinical trials of omega-3 supplements show? At least seven randomized trials have looked at AF. A meta-analysis published in Circulation in 2021 showed a dose-response relationship. In trials testing > 1 g/d of marine omega-3 fatty acids, there was close to a 50% overall increase in risk for AF. In studies testing lower doses, there was a very modest 12% increase and a significant dose-response gradient.

For the relationship between omega-3 supplements and major cardiovascular events, at least 15 individual randomized trials have been conducted. There actually have been more meta-analyses of these randomized trials than individual trials. The meta-analyses tend to show a significant reduction of coronary events with omega-3 supplementation, but no reduction in stroke. This is true in both primary and secondary prevention trials.

The one exception to this finding is the REDUCE-IT trial testing high-dose eicosapentaenoic acid (EPA) (4 g/day of icosapent ethyl), and there was a 25%-30% reduction in both cardiovascular events and stroke. But there has been some criticism of the mineral oil placebo used in the REDUCE-IT trial that it may have had adverse effects on biomarkers and might have interfered with the absorption of statins in the placebo group. So, it will be important to have a replication trial of the high-dose EPA, findings in a trial using an inert placebo such as corn oil.

What should be done in the meantime? It’s important to think about prescription omega-3s vs over-the-counter fish oil. The US Food and Drug Administration (FDA) has approved prescription omega-3 medications for several indications, including severely elevated triglyceride levels (> 500 mg/dL). In the REDUCE-IT trial, those who had moderate elevations of triglycerides (≥ 150 mg/dL) or prevalent CVD or diabetes, plus two additional risk factors, were also considered to have indications based on the FDA labeling for icosapent ethyl.

What about patients who don’t meet these criteria for prescription omega-3s? In the VITAL trial (the large-scale primary prevention trial), there was a similar reduction in coronary events but no effect on stroke. Those who seemed to benefit the most in terms of at least 40% reduction in coronary events were participants who had low fish consumption at baseline, had two or more risk factors for cardiovascular disease, or were African American. 

Someone who rarely or never eats fish and has multiple risk factors for CVD, but doesn’t meet criteria for prescription omega-3 medication, may want to discuss with their clinician the use of over-the-counter fish oil supplements. But fish oil and other dietary supplements will never be a substitute for healthy diet and healthy lifestyle. There is a national recommendation for one to two servings of fish per week. For those planning to take fish oil, it’s important to use reputable sources of the supplement, and check the bottle for a quality control seal. It’s also really important to avoid megadoses of fish oil, because high doses have been linked to an increased risk for AF and bleeding.

Dr. Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital, Boston, disclosed ties with Mars Symbioscience for the COSMOS trial.

A version of this article appeared on Medscape.com.

I’d like to talk with you about a recent report in the British Medical Journal on the regular use of omega-3 fish oil supplements and the course of cardiovascular disease (CVD).

This is an observational study from the large-scale UK Biobank. The authors divided the participants into those with and those without CVD. In participants without CVD at baseline, those using fish oil supplements regularly had an increased incidence of both atrial fibrillation (AF) and stroke, whereas those with prevalent CVD had a reduction in the progression to major adverse cardiovascular events, which offset any increase in the risk for AF.

Observational studies of omega-3 supplements have potential limitations and confounding, and correlation in these studies does not prove causation. What do the randomized clinical trials of omega-3 supplements show? At least seven randomized trials have looked at AF. A meta-analysis published in Circulation in 2021 showed a dose-response relationship. In trials testing > 1 g/d of marine omega-3 fatty acids, there was close to a 50% overall increase in risk for AF. In studies testing lower doses, there was a very modest 12% increase and a significant dose-response gradient.

For the relationship between omega-3 supplements and major cardiovascular events, at least 15 individual randomized trials have been conducted. There actually have been more meta-analyses of these randomized trials than individual trials. The meta-analyses tend to show a significant reduction of coronary events with omega-3 supplementation, but no reduction in stroke. This is true in both primary and secondary prevention trials.

The one exception to this finding is the REDUCE-IT trial testing high-dose eicosapentaenoic acid (EPA) (4 g/day of icosapent ethyl), and there was a 25%-30% reduction in both cardiovascular events and stroke. But there has been some criticism of the mineral oil placebo used in the REDUCE-IT trial that it may have had adverse effects on biomarkers and might have interfered with the absorption of statins in the placebo group. So, it will be important to have a replication trial of the high-dose EPA, findings in a trial using an inert placebo such as corn oil.

What should be done in the meantime? It’s important to think about prescription omega-3s vs over-the-counter fish oil. The US Food and Drug Administration (FDA) has approved prescription omega-3 medications for several indications, including severely elevated triglyceride levels (> 500 mg/dL). In the REDUCE-IT trial, those who had moderate elevations of triglycerides (≥ 150 mg/dL) or prevalent CVD or diabetes, plus two additional risk factors, were also considered to have indications based on the FDA labeling for icosapent ethyl.

What about patients who don’t meet these criteria for prescription omega-3s? In the VITAL trial (the large-scale primary prevention trial), there was a similar reduction in coronary events but no effect on stroke. Those who seemed to benefit the most in terms of at least 40% reduction in coronary events were participants who had low fish consumption at baseline, had two or more risk factors for cardiovascular disease, or were African American. 

Someone who rarely or never eats fish and has multiple risk factors for CVD, but doesn’t meet criteria for prescription omega-3 medication, may want to discuss with their clinician the use of over-the-counter fish oil supplements. But fish oil and other dietary supplements will never be a substitute for healthy diet and healthy lifestyle. There is a national recommendation for one to two servings of fish per week. For those planning to take fish oil, it’s important to use reputable sources of the supplement, and check the bottle for a quality control seal. It’s also really important to avoid megadoses of fish oil, because high doses have been linked to an increased risk for AF and bleeding.

Dr. Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital, Boston, disclosed ties with Mars Symbioscience for the COSMOS trial.

A version of this article appeared on Medscape.com.

I’d like to talk with you about a recent report in the British Medical Journal on the regular use of omega-3 fish oil supplements and the course of cardiovascular disease (CVD).

This is an observational study from the large-scale UK Biobank. The authors divided the participants into those with and those without CVD. In participants without CVD at baseline, those using fish oil supplements regularly had an increased incidence of both atrial fibrillation (AF) and stroke, whereas those with prevalent CVD had a reduction in the progression to major adverse cardiovascular events, which offset any increase in the risk for AF.

Observational studies of omega-3 supplements have potential limitations and confounding, and correlation in these studies does not prove causation. What do the randomized clinical trials of omega-3 supplements show? At least seven randomized trials have looked at AF. A meta-analysis published in Circulation in 2021 showed a dose-response relationship. In trials testing > 1 g/d of marine omega-3 fatty acids, there was close to a 50% overall increase in risk for AF. In studies testing lower doses, there was a very modest 12% increase and a significant dose-response gradient.

For the relationship between omega-3 supplements and major cardiovascular events, at least 15 individual randomized trials have been conducted. There actually have been more meta-analyses of these randomized trials than individual trials. The meta-analyses tend to show a significant reduction of coronary events with omega-3 supplementation, but no reduction in stroke. This is true in both primary and secondary prevention trials.

The one exception to this finding is the REDUCE-IT trial testing high-dose eicosapentaenoic acid (EPA) (4 g/day of icosapent ethyl), and there was a 25%-30% reduction in both cardiovascular events and stroke. But there has been some criticism of the mineral oil placebo used in the REDUCE-IT trial that it may have had adverse effects on biomarkers and might have interfered with the absorption of statins in the placebo group. So, it will be important to have a replication trial of the high-dose EPA, findings in a trial using an inert placebo such as corn oil.

What should be done in the meantime? It’s important to think about prescription omega-3s vs over-the-counter fish oil. The US Food and Drug Administration (FDA) has approved prescription omega-3 medications for several indications, including severely elevated triglyceride levels (> 500 mg/dL). In the REDUCE-IT trial, those who had moderate elevations of triglycerides (≥ 150 mg/dL) or prevalent CVD or diabetes, plus two additional risk factors, were also considered to have indications based on the FDA labeling for icosapent ethyl.

What about patients who don’t meet these criteria for prescription omega-3s? In the VITAL trial (the large-scale primary prevention trial), there was a similar reduction in coronary events but no effect on stroke. Those who seemed to benefit the most in terms of at least 40% reduction in coronary events were participants who had low fish consumption at baseline, had two or more risk factors for cardiovascular disease, or were African American. 

Someone who rarely or never eats fish and has multiple risk factors for CVD, but doesn’t meet criteria for prescription omega-3 medication, may want to discuss with their clinician the use of over-the-counter fish oil supplements. But fish oil and other dietary supplements will never be a substitute for healthy diet and healthy lifestyle. There is a national recommendation for one to two servings of fish per week. For those planning to take fish oil, it’s important to use reputable sources of the supplement, and check the bottle for a quality control seal. It’s also really important to avoid megadoses of fish oil, because high doses have been linked to an increased risk for AF and bleeding.

Dr. Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital, Boston, disclosed ties with Mars Symbioscience for the COSMOS trial.

A version of this article appeared on Medscape.com.

TOPLINE:

A study found that higher insulin sensitivity is associated with a decrease in lean mass loss during weight loss.

METHODOLOGY:

• Researchers conducted a 16-week controlled feeding study involving adults with overweight or obesity.
• The study included 57 participants with a baseline body mass index of 32.1 ± 3.8 kg/m² .
• Participants were assigned to either a standard (55% carbohydrate) or reduced carbohydrate diet (43% carbohydrate). Both groups consumed 18% protein.
• Body composition was assessed via dual-energy x-ray absorptiometry at baseline and at 16 weeks.
• Insulin sensitivity was measured using an intravenous glucose tolerance test, with multiple linear regression used to analyze the data.

TAKEAWAY:

• Lower baseline insulin was a predictor of greater lean muscle mass loss during weight loss.
• Identifying individuals with low insulin sensitivity prior to weight loss interventions could allow for personalized approaches to minimize lean mass loss.
• The study suggested that insulin sensitivity plays a significant role in determining the composition of weight lost during dieting.

IN PRACTICE:

“Identifying individuals with low insulin sensitivity prior to weight loss interventions may allow for a personalized approach aiming at minimizing lean mass loss,” wrote the authors of the study. This insight underscores the importance of considering insulin sensitivity in weight loss programs to preserve muscle mass. Individuals with low insulin sensitivity may benefit from increasing protein and incorporating resistance training during weight loss.

SOURCE:

The study was led by Ciera L. Bartholomew, Department of Nutrition Sciences, University of Alabama at Birmingham, Alabama. It was published online in Obesity (Silver Spring).

LIMITATIONS:

The study’s secondary analysis nature and its relatively small sample size limit the ability to establish relationships between insulin sensitivity and lean muscle loss. In addition, all food was provided, and participants all consumed the same protein level.

DISCLOSURES:

The study was supported by grants from the Comprehensive Diabetes Center, University of Alabama at Birmingham, and a National Institutes of Health Research Grant. The authors declared no conflicts of interest.

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

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

TOPLINE:

A study found that higher insulin sensitivity is associated with a decrease in lean mass loss during weight loss.

METHODOLOGY:

• Researchers conducted a 16-week controlled feeding study involving adults with overweight or obesity.
• The study included 57 participants with a baseline body mass index of 32.1 ± 3.8 kg/m² .
• Participants were assigned to either a standard (55% carbohydrate) or reduced carbohydrate diet (43% carbohydrate). Both groups consumed 18% protein.
• Body composition was assessed via dual-energy x-ray absorptiometry at baseline and at 16 weeks.
• Insulin sensitivity was measured using an intravenous glucose tolerance test, with multiple linear regression used to analyze the data.

TAKEAWAY:

• Lower baseline insulin was a predictor of greater lean muscle mass loss during weight loss.
• Identifying individuals with low insulin sensitivity prior to weight loss interventions could allow for personalized approaches to minimize lean mass loss.
• The study suggested that insulin sensitivity plays a significant role in determining the composition of weight lost during dieting.

IN PRACTICE:

“Identifying individuals with low insulin sensitivity prior to weight loss interventions may allow for a personalized approach aiming at minimizing lean mass loss,” wrote the authors of the study. This insight underscores the importance of considering insulin sensitivity in weight loss programs to preserve muscle mass. Individuals with low insulin sensitivity may benefit from increasing protein and incorporating resistance training during weight loss.

SOURCE:

The study was led by Ciera L. Bartholomew, Department of Nutrition Sciences, University of Alabama at Birmingham, Alabama. It was published online in Obesity (Silver Spring).

LIMITATIONS:

The study’s secondary analysis nature and its relatively small sample size limit the ability to establish relationships between insulin sensitivity and lean muscle loss. In addition, all food was provided, and participants all consumed the same protein level.

DISCLOSURES:

The study was supported by grants from the Comprehensive Diabetes Center, University of Alabama at Birmingham, and a National Institutes of Health Research Grant. The authors declared no conflicts of interest.

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

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

TOPLINE:

A study found that higher insulin sensitivity is associated with a decrease in lean mass loss during weight loss.

METHODOLOGY:

• Researchers conducted a 16-week controlled feeding study involving adults with overweight or obesity.
• The study included 57 participants with a baseline body mass index of 32.1 ± 3.8 kg/m² .
• Participants were assigned to either a standard (55% carbohydrate) or reduced carbohydrate diet (43% carbohydrate). Both groups consumed 18% protein.
• Body composition was assessed via dual-energy x-ray absorptiometry at baseline and at 16 weeks.
• Insulin sensitivity was measured using an intravenous glucose tolerance test, with multiple linear regression used to analyze the data.

TAKEAWAY:

• Lower baseline insulin was a predictor of greater lean muscle mass loss during weight loss.
• Identifying individuals with low insulin sensitivity prior to weight loss interventions could allow for personalized approaches to minimize lean mass loss.
• The study suggested that insulin sensitivity plays a significant role in determining the composition of weight lost during dieting.

IN PRACTICE:

“Identifying individuals with low insulin sensitivity prior to weight loss interventions may allow for a personalized approach aiming at minimizing lean mass loss,” wrote the authors of the study. This insight underscores the importance of considering insulin sensitivity in weight loss programs to preserve muscle mass. Individuals with low insulin sensitivity may benefit from increasing protein and incorporating resistance training during weight loss.

SOURCE:

The study was led by Ciera L. Bartholomew, Department of Nutrition Sciences, University of Alabama at Birmingham, Alabama. It was published online in Obesity (Silver Spring).

LIMITATIONS:

The study’s secondary analysis nature and its relatively small sample size limit the ability to establish relationships between insulin sensitivity and lean muscle loss. In addition, all food was provided, and participants all consumed the same protein level.

DISCLOSURES:

The study was supported by grants from the Comprehensive Diabetes Center, University of Alabama at Birmingham, and a National Institutes of Health Research Grant. The authors declared no conflicts of interest.

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

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

There has been much hyperbole since the presentation of results from the SELECT cardiovascular outcomes trial (CVOT) at this year’s European Congress on Obesity, which led many to herald semaglutide as the “new statin.”

In the SELECT CVOT, participants with overweight or obesity (body mass index [BMI] ≥ 27), established cardiovascular disease (CVD), and no history of type 2 diabetes were administered the injectable glucagon-like peptide 1 (GLP-1) receptor agonist semaglutide (Wegovy) at a 2.4-mg dose weekly. Treatment resulted in a significant 20% relative risk reduction in major adverse CV events (a composite endpoint comprising CV death, nonfatal myocardial infarction, or nonfatal stroke). Importantly, SELECT was a trial on secondary prevention of CVD. 

The CV benefits of semaglutide were notably independent of baseline weight or amount of weight lost. This suggests that the underlying driver of improved CV outcomes with semaglutide extends beyond simple reduction in obesity and perhaps indicates a direct effect on vasculature and reduction in atherosclerosis, although this remains unproven.
 

Not All Risk Reduction Is Equal 

Much of the sensationalist coverage in the lay press focused on the 20% relative risk reduction figure. This endpoint is often more impressive and headline-grabbing than the absolute risk reduction, which provides a clearer view of a treatment’s real-world impact.

In SELECT, the absolute risk reduction was 1.5 percentage points, which translated into a number needed to treat (NNT) of 67 over 34 months to prevent one primary outcome of a major adverse CV event.

Lower NNTs suggest more effective treatments because fewer people need to be treated to prevent one clinical event, such as the major adverse CV events used in SELECT.
 

Semaglutide vs Statins

How does the clinical effectiveness observed in the SELECT trial compare with that observed in statin trials when it comes to the secondary prevention of CVD?

The seminal 4S study published in 1994 explored the impact of simvastatin on all-cause mortality among people with previous myocardial infarction or angina and hyperlipidemia (mean baseline BMI, 26). After 5.4 years of follow-up, the trial was stopped early owing to a 3.3-percentage point absolute risk reduction in all-cause mortality (NNT, 30; relative risk reduction, 28%). The NNT to prevent one death from CV causes was 31, and the NNT to prevent one major coronary event was lower, at 15.

Other statin secondary prevention trials, such as the LIPID and MIRACL studies, demonstrated similarly low NNTs.

So, you can see that the NNTs for statins in secondary prevention are much lower than with semaglutide in SELECT. Furthermore, the benefits of semaglutide in preventing CVD in people living with overweight/obesity have yet to be elucidated. 

In contrast, we already have published evidence showing the benefits of statins in the primary prevention of CVD, albeit with higher and more variable NNTs than in the statin secondary prevention studies. 

The benefits of statins are also postulated to extend beyond their impact on lowering low-density lipoprotein cholesterol. Statins have been suggested to have anti-inflammatory and plaque-stabilizing effects, among other pleiotropic benefits.

We also currently lack evidence for the cost-effectiveness of semaglutide for CV risk reduction. Assessing economic viability and use in health care systems, such as the UK’s National Health Service, involves comparing the cost of semaglutide against the health care savings from prevented CV events. Health economic studies are vital to determine whether the benefits justify the expense. In contrast, the cost-effectiveness of statins is well established, particularly for high-risk individuals.
 

Advantages of GLP-1s Should Not Be Overlooked

Of course, statins don’t provide the significant weight loss benefits of semaglutide. 

Additional data from SELECT presented at the 2024 European Congress on Obesity demonstrated that participants lost a mean of 10.2% body weight and 7.7 cm from their waist circumference after 4 years. Moreover, after 2 years, 12% of individuals randomized to semaglutide had returned to a normal BMI, and nearly half were no longer living with obesity.

Although the CV benefits of semaglutide were independent of weight reduction, this level of weight loss is clinically meaningful and will reduce the risk of many other cardiometabolic conditions including type 2 diabetes, metabolic dysfunction–associated steatotic liver disease, and obstructive sleep apnea/hypopnea syndrome, as well as improve low mood, depression, and overall quality of life. Additionally, obesity is now a risk factor for 13 different types of cancer, including bowel, breast, and pancreatic cancer, so facilitating a return to a healthier body weight will also mitigate future risk for cancer.
 

Sticking With Our Cornerstone Therapy, For Now

In conclusion, I do not believe that semaglutide is the “new statin.” Statins are the cornerstone of primary and secondary prevention of CVD in a wide range of comorbidities, as evidenced in multiple large and high-quality trials dating back over 30 years.

However, there is no doubt that the GLP-1 receptor agonist class is the most significant therapeutic advance for the management of obesity and comorbidities to date. 

The SELECT CVOT data uniquely position semaglutide as a secondary CVD prevention agent on top of guideline-driven management for people living with overweight/obesity and established CVD. Additionally, the clinically meaningful weight loss achieved with semaglutide will impact the risk of developing many other cardiometabolic conditions, as well as improve mental health and overall quality of life.

Dr. Fernando, GP Partner, North Berwick Health Centre, North Berwick, Scotland, creates concise clinical aide-mémoire for primary and secondary care to make life easier for health care professionals and ultimately to improve the lives of patients. He is very active on social media (X handle @drkevinfernando), where he posts hot topics in type 2 diabetes and CVRM. He recently has forayed into YouTube (@DrKevinFernando) and TikTok (@drkevinfernando) with patient-facing video content. Dr. Fernando has been elected to Fellowship of the Royal College of General Practitioners, the Royal College of Physicians of Edinburgh, and the Academy of Medical Educators for his work in diabetes and medical education. He has disclosed the following relevant financial relationships: Serve(d) as a speaker or a member of a speakers bureau for AstraZeneca; Boehringer Ingelheim; Lilly; Menarini; Bayer; Dexcom; Novartis; Novo Nordisk; Amgen; and Daiichi Sankyo; received income in an amount equal to or greater than $250 from AstraZeneca; Boehringer Ingelheim; Lilly; Menarini; Bayer; Dexcom; Novartis; Novo Nordisk; Amgen; and Daiichi Sankyo.

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

There has been much hyperbole since the presentation of results from the SELECT cardiovascular outcomes trial (CVOT) at this year’s European Congress on Obesity, which led many to herald semaglutide as the “new statin.”

In the SELECT CVOT, participants with overweight or obesity (body mass index [BMI] ≥ 27), established cardiovascular disease (CVD), and no history of type 2 diabetes were administered the injectable glucagon-like peptide 1 (GLP-1) receptor agonist semaglutide (Wegovy) at a 2.4-mg dose weekly. Treatment resulted in a significant 20% relative risk reduction in major adverse CV events (a composite endpoint comprising CV death, nonfatal myocardial infarction, or nonfatal stroke). Importantly, SELECT was a trial on secondary prevention of CVD. 

The CV benefits of semaglutide were notably independent of baseline weight or amount of weight lost. This suggests that the underlying driver of improved CV outcomes with semaglutide extends beyond simple reduction in obesity and perhaps indicates a direct effect on vasculature and reduction in atherosclerosis, although this remains unproven.
 

Not All Risk Reduction Is Equal 

Much of the sensationalist coverage in the lay press focused on the 20% relative risk reduction figure. This endpoint is often more impressive and headline-grabbing than the absolute risk reduction, which provides a clearer view of a treatment’s real-world impact.

In SELECT, the absolute risk reduction was 1.5 percentage points, which translated into a number needed to treat (NNT) of 67 over 34 months to prevent one primary outcome of a major adverse CV event.

Lower NNTs suggest more effective treatments because fewer people need to be treated to prevent one clinical event, such as the major adverse CV events used in SELECT.
 

Semaglutide vs Statins

How does the clinical effectiveness observed in the SELECT trial compare with that observed in statin trials when it comes to the secondary prevention of CVD?

The seminal 4S study published in 1994 explored the impact of simvastatin on all-cause mortality among people with previous myocardial infarction or angina and hyperlipidemia (mean baseline BMI, 26). After 5.4 years of follow-up, the trial was stopped early owing to a 3.3-percentage point absolute risk reduction in all-cause mortality (NNT, 30; relative risk reduction, 28%). The NNT to prevent one death from CV causes was 31, and the NNT to prevent one major coronary event was lower, at 15.

Other statin secondary prevention trials, such as the LIPID and MIRACL studies, demonstrated similarly low NNTs.

So, you can see that the NNTs for statins in secondary prevention are much lower than with semaglutide in SELECT. Furthermore, the benefits of semaglutide in preventing CVD in people living with overweight/obesity have yet to be elucidated. 

In contrast, we already have published evidence showing the benefits of statins in the primary prevention of CVD, albeit with higher and more variable NNTs than in the statin secondary prevention studies. 

The benefits of statins are also postulated to extend beyond their impact on lowering low-density lipoprotein cholesterol. Statins have been suggested to have anti-inflammatory and plaque-stabilizing effects, among other pleiotropic benefits.

We also currently lack evidence for the cost-effectiveness of semaglutide for CV risk reduction. Assessing economic viability and use in health care systems, such as the UK’s National Health Service, involves comparing the cost of semaglutide against the health care savings from prevented CV events. Health economic studies are vital to determine whether the benefits justify the expense. In contrast, the cost-effectiveness of statins is well established, particularly for high-risk individuals.
 

Advantages of GLP-1s Should Not Be Overlooked

Of course, statins don’t provide the significant weight loss benefits of semaglutide. 

Additional data from SELECT presented at the 2024 European Congress on Obesity demonstrated that participants lost a mean of 10.2% body weight and 7.7 cm from their waist circumference after 4 years. Moreover, after 2 years, 12% of individuals randomized to semaglutide had returned to a normal BMI, and nearly half were no longer living with obesity.

Although the CV benefits of semaglutide were independent of weight reduction, this level of weight loss is clinically meaningful and will reduce the risk of many other cardiometabolic conditions including type 2 diabetes, metabolic dysfunction–associated steatotic liver disease, and obstructive sleep apnea/hypopnea syndrome, as well as improve low mood, depression, and overall quality of life. Additionally, obesity is now a risk factor for 13 different types of cancer, including bowel, breast, and pancreatic cancer, so facilitating a return to a healthier body weight will also mitigate future risk for cancer.
 

Sticking With Our Cornerstone Therapy, For Now

In conclusion, I do not believe that semaglutide is the “new statin.” Statins are the cornerstone of primary and secondary prevention of CVD in a wide range of comorbidities, as evidenced in multiple large and high-quality trials dating back over 30 years.

However, there is no doubt that the GLP-1 receptor agonist class is the most significant therapeutic advance for the management of obesity and comorbidities to date. 

The SELECT CVOT data uniquely position semaglutide as a secondary CVD prevention agent on top of guideline-driven management for people living with overweight/obesity and established CVD. Additionally, the clinically meaningful weight loss achieved with semaglutide will impact the risk of developing many other cardiometabolic conditions, as well as improve mental health and overall quality of life.

Dr. Fernando, GP Partner, North Berwick Health Centre, North Berwick, Scotland, creates concise clinical aide-mémoire for primary and secondary care to make life easier for health care professionals and ultimately to improve the lives of patients. He is very active on social media (X handle @drkevinfernando), where he posts hot topics in type 2 diabetes and CVRM. He recently has forayed into YouTube (@DrKevinFernando) and TikTok (@drkevinfernando) with patient-facing video content. Dr. Fernando has been elected to Fellowship of the Royal College of General Practitioners, the Royal College of Physicians of Edinburgh, and the Academy of Medical Educators for his work in diabetes and medical education. He has disclosed the following relevant financial relationships: Serve(d) as a speaker or a member of a speakers bureau for AstraZeneca; Boehringer Ingelheim; Lilly; Menarini; Bayer; Dexcom; Novartis; Novo Nordisk; Amgen; and Daiichi Sankyo; received income in an amount equal to or greater than $250 from AstraZeneca; Boehringer Ingelheim; Lilly; Menarini; Bayer; Dexcom; Novartis; Novo Nordisk; Amgen; and Daiichi Sankyo.

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

There has been much hyperbole since the presentation of results from the SELECT cardiovascular outcomes trial (CVOT) at this year’s European Congress on Obesity, which led many to herald semaglutide as the “new statin.”

In the SELECT CVOT, participants with overweight or obesity (body mass index [BMI] ≥ 27), established cardiovascular disease (CVD), and no history of type 2 diabetes were administered the injectable glucagon-like peptide 1 (GLP-1) receptor agonist semaglutide (Wegovy) at a 2.4-mg dose weekly. Treatment resulted in a significant 20% relative risk reduction in major adverse CV events (a composite endpoint comprising CV death, nonfatal myocardial infarction, or nonfatal stroke). Importantly, SELECT was a trial on secondary prevention of CVD. 

The CV benefits of semaglutide were notably independent of baseline weight or amount of weight lost. This suggests that the underlying driver of improved CV outcomes with semaglutide extends beyond simple reduction in obesity and perhaps indicates a direct effect on vasculature and reduction in atherosclerosis, although this remains unproven.
 

Not All Risk Reduction Is Equal 

Much of the sensationalist coverage in the lay press focused on the 20% relative risk reduction figure. This endpoint is often more impressive and headline-grabbing than the absolute risk reduction, which provides a clearer view of a treatment’s real-world impact.

In SELECT, the absolute risk reduction was 1.5 percentage points, which translated into a number needed to treat (NNT) of 67 over 34 months to prevent one primary outcome of a major adverse CV event.

Lower NNTs suggest more effective treatments because fewer people need to be treated to prevent one clinical event, such as the major adverse CV events used in SELECT.
 

Semaglutide vs Statins

How does the clinical effectiveness observed in the SELECT trial compare with that observed in statin trials when it comes to the secondary prevention of CVD?

The seminal 4S study published in 1994 explored the impact of simvastatin on all-cause mortality among people with previous myocardial infarction or angina and hyperlipidemia (mean baseline BMI, 26). After 5.4 years of follow-up, the trial was stopped early owing to a 3.3-percentage point absolute risk reduction in all-cause mortality (NNT, 30; relative risk reduction, 28%). The NNT to prevent one death from CV causes was 31, and the NNT to prevent one major coronary event was lower, at 15.

Other statin secondary prevention trials, such as the LIPID and MIRACL studies, demonstrated similarly low NNTs.

So, you can see that the NNTs for statins in secondary prevention are much lower than with semaglutide in SELECT. Furthermore, the benefits of semaglutide in preventing CVD in people living with overweight/obesity have yet to be elucidated. 

In contrast, we already have published evidence showing the benefits of statins in the primary prevention of CVD, albeit with higher and more variable NNTs than in the statin secondary prevention studies. 

The benefits of statins are also postulated to extend beyond their impact on lowering low-density lipoprotein cholesterol. Statins have been suggested to have anti-inflammatory and plaque-stabilizing effects, among other pleiotropic benefits.

We also currently lack evidence for the cost-effectiveness of semaglutide for CV risk reduction. Assessing economic viability and use in health care systems, such as the UK’s National Health Service, involves comparing the cost of semaglutide against the health care savings from prevented CV events. Health economic studies are vital to determine whether the benefits justify the expense. In contrast, the cost-effectiveness of statins is well established, particularly for high-risk individuals.
 

Advantages of GLP-1s Should Not Be Overlooked

Of course, statins don’t provide the significant weight loss benefits of semaglutide. 

Additional data from SELECT presented at the 2024 European Congress on Obesity demonstrated that participants lost a mean of 10.2% body weight and 7.7 cm from their waist circumference after 4 years. Moreover, after 2 years, 12% of individuals randomized to semaglutide had returned to a normal BMI, and nearly half were no longer living with obesity.

Although the CV benefits of semaglutide were independent of weight reduction, this level of weight loss is clinically meaningful and will reduce the risk of many other cardiometabolic conditions including type 2 diabetes, metabolic dysfunction–associated steatotic liver disease, and obstructive sleep apnea/hypopnea syndrome, as well as improve low mood, depression, and overall quality of life. Additionally, obesity is now a risk factor for 13 different types of cancer, including bowel, breast, and pancreatic cancer, so facilitating a return to a healthier body weight will also mitigate future risk for cancer.
 

Sticking With Our Cornerstone Therapy, For Now

In conclusion, I do not believe that semaglutide is the “new statin.” Statins are the cornerstone of primary and secondary prevention of CVD in a wide range of comorbidities, as evidenced in multiple large and high-quality trials dating back over 30 years.

However, there is no doubt that the GLP-1 receptor agonist class is the most significant therapeutic advance for the management of obesity and comorbidities to date. 

The SELECT CVOT data uniquely position semaglutide as a secondary CVD prevention agent on top of guideline-driven management for people living with overweight/obesity and established CVD. Additionally, the clinically meaningful weight loss achieved with semaglutide will impact the risk of developing many other cardiometabolic conditions, as well as improve mental health and overall quality of life.

Dr. Fernando, GP Partner, North Berwick Health Centre, North Berwick, Scotland, creates concise clinical aide-mémoire for primary and secondary care to make life easier for health care professionals and ultimately to improve the lives of patients. He is very active on social media (X handle @drkevinfernando), where he posts hot topics in type 2 diabetes and CVRM. He recently has forayed into YouTube (@DrKevinFernando) and TikTok (@drkevinfernando) with patient-facing video content. Dr. Fernando has been elected to Fellowship of the Royal College of General Practitioners, the Royal College of Physicians of Edinburgh, and the Academy of Medical Educators for his work in diabetes and medical education. He has disclosed the following relevant financial relationships: Serve(d) as a speaker or a member of a speakers bureau for AstraZeneca; Boehringer Ingelheim; Lilly; Menarini; Bayer; Dexcom; Novartis; Novo Nordisk; Amgen; and Daiichi Sankyo; received income in an amount equal to or greater than $250 from AstraZeneca; Boehringer Ingelheim; Lilly; Menarini; Bayer; Dexcom; Novartis; Novo Nordisk; Amgen; and Daiichi Sankyo.

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

Over a period of 5 years, the likelihood of major adverse cardiovascular events (MACE) in patients with psoriasis and dyslipidemia who were on statin therapy was 40% greater than that in non-psoriasis patients with dyslipidemia on statin therapy, even after adjusting for covariates, results from a large retrospective study showed.

“It is well-established that psoriasis is an independent risk factor for the development of MACE, with cardiometabolic risk factors being more prevalent and incident among patients with psoriasis,” the study’s first author Ana Ormaza Vera, MD, a dermatology research fellow at Eastern Virginia Medical School, Norfolk, said in an interview after the annual meeting of the Society for Investigational Dermatology, where the study was presented during a late-breaking abstract session.

Dr. Ormaza Vera

Current guidelines from the joint American Academy of Dermatology/National Psoriasis Foundation and the American Academy of Cardiology/American Heart Association Task Force recommend statins, a lipid-lowering and anti-inflammatory therapy, “for patients with psoriasis who have additional risk-enhancing factors, similar to recommendations made for the general population without psoriasis,” she noted. But how the incidence of MACE differs between patients with and without psoriasis while on statin therapy “has not been explored in real-world settings,” she added.

To address this question, the researchers used real-world data from the TriNetX health research network to identify individuals aged 18-90 years with a diagnosis of both psoriasis and lipid disorders who were undergoing treatment with statins. Those with a prior history of MACE were excluded from the analysis. Patients with lipid disorders on statin therapy, but without psoriatic disease, were matched 1:1 by age, sex, race, ethnicity, common risk factors for MACE, and medications shown to reduce MACE risk. The researchers then assessed the cohorts 5 years following their first statin prescription and used the TriNetX analytics tool to calculate the odds ratio (OR) with 95% CI to evaluate the likelihood of MACE in the presence of statin therapy.

Dr. Ormaza Vera and colleagues identified 20,660 patients with psoriasis and 2,768,429 patients without psoriasis who met the criteria for analysis. After propensity score matching, each cohort included 20,660 patients with a mean age of 60 years. During the 5-year observation period, 2725 patients in the psoriasis cohort experienced MACE compared with 2203 patients in the non-psoriasis cohort (OR, 1.40; 95% CI, 1.317-1.488).

“This was an unexpected outcome that challenges the current understanding and highlights the need for further research into tailored treatments for cardiovascular risk in psoriasis patients,” Dr. Ormaza Vera told this news organization.

She acknowledged certain limitations of the study, including its retrospective design, the inherent limitations of an observational study, and the use of electronic medical record data.

Lawrence J. Green, MD, clinical professor of dermatology, George Washington University, Washington, who was asked to comment on the study results, said that the findings imply that there is more than statin use alone to protect someone with psoriasis from having an increased risk for MACE. “This is not really surprising because statin use alone is only part of a prevention strategy in someone with psoriasis who usually has multiple comorbidities,” Dr. Green said. “On the other hand, the study only went out for 5 years and cardiovascular disease is a long accumulating process, so it could also be too early to demonstrate MACE prevention.”

The study was funded by a grant from the American Skin Association. Dr. Ormaza Vera and her coauthors reported having no relevant disclosures. Dr. Green disclosed that he is a speaker, consultant, or investigator for many pharmaceutical companies.

A version of this article appeared on Medscape.com .

Over a period of 5 years, the likelihood of major adverse cardiovascular events (MACE) in patients with psoriasis and dyslipidemia who were on statin therapy was 40% greater than that in non-psoriasis patients with dyslipidemia on statin therapy, even after adjusting for covariates, results from a large retrospective study showed.

“It is well-established that psoriasis is an independent risk factor for the development of MACE, with cardiometabolic risk factors being more prevalent and incident among patients with psoriasis,” the study’s first author Ana Ormaza Vera, MD, a dermatology research fellow at Eastern Virginia Medical School, Norfolk, said in an interview after the annual meeting of the Society for Investigational Dermatology, where the study was presented during a late-breaking abstract session.

Dr. Ormaza Vera

Current guidelines from the joint American Academy of Dermatology/National Psoriasis Foundation and the American Academy of Cardiology/American Heart Association Task Force recommend statins, a lipid-lowering and anti-inflammatory therapy, “for patients with psoriasis who have additional risk-enhancing factors, similar to recommendations made for the general population without psoriasis,” she noted. But how the incidence of MACE differs between patients with and without psoriasis while on statin therapy “has not been explored in real-world settings,” she added.

To address this question, the researchers used real-world data from the TriNetX health research network to identify individuals aged 18-90 years with a diagnosis of both psoriasis and lipid disorders who were undergoing treatment with statins. Those with a prior history of MACE were excluded from the analysis. Patients with lipid disorders on statin therapy, but without psoriatic disease, were matched 1:1 by age, sex, race, ethnicity, common risk factors for MACE, and medications shown to reduce MACE risk. The researchers then assessed the cohorts 5 years following their first statin prescription and used the TriNetX analytics tool to calculate the odds ratio (OR) with 95% CI to evaluate the likelihood of MACE in the presence of statin therapy.

Dr. Ormaza Vera and colleagues identified 20,660 patients with psoriasis and 2,768,429 patients without psoriasis who met the criteria for analysis. After propensity score matching, each cohort included 20,660 patients with a mean age of 60 years. During the 5-year observation period, 2725 patients in the psoriasis cohort experienced MACE compared with 2203 patients in the non-psoriasis cohort (OR, 1.40; 95% CI, 1.317-1.488).

“This was an unexpected outcome that challenges the current understanding and highlights the need for further research into tailored treatments for cardiovascular risk in psoriasis patients,” Dr. Ormaza Vera told this news organization.

She acknowledged certain limitations of the study, including its retrospective design, the inherent limitations of an observational study, and the use of electronic medical record data.

Lawrence J. Green, MD, clinical professor of dermatology, George Washington University, Washington, who was asked to comment on the study results, said that the findings imply that there is more than statin use alone to protect someone with psoriasis from having an increased risk for MACE. “This is not really surprising because statin use alone is only part of a prevention strategy in someone with psoriasis who usually has multiple comorbidities,” Dr. Green said. “On the other hand, the study only went out for 5 years and cardiovascular disease is a long accumulating process, so it could also be too early to demonstrate MACE prevention.”

The study was funded by a grant from the American Skin Association. Dr. Ormaza Vera and her coauthors reported having no relevant disclosures. Dr. Green disclosed that he is a speaker, consultant, or investigator for many pharmaceutical companies.

A version of this article appeared on Medscape.com .

Over a period of 5 years, the likelihood of major adverse cardiovascular events (MACE) in patients with psoriasis and dyslipidemia who were on statin therapy was 40% greater than that in non-psoriasis patients with dyslipidemia on statin therapy, even after adjusting for covariates, results from a large retrospective study showed.

“It is well-established that psoriasis is an independent risk factor for the development of MACE, with cardiometabolic risk factors being more prevalent and incident among patients with psoriasis,” the study’s first author Ana Ormaza Vera, MD, a dermatology research fellow at Eastern Virginia Medical School, Norfolk, said in an interview after the annual meeting of the Society for Investigational Dermatology, where the study was presented during a late-breaking abstract session.

Dr. Ormaza Vera

Current guidelines from the joint American Academy of Dermatology/National Psoriasis Foundation and the American Academy of Cardiology/American Heart Association Task Force recommend statins, a lipid-lowering and anti-inflammatory therapy, “for patients with psoriasis who have additional risk-enhancing factors, similar to recommendations made for the general population without psoriasis,” she noted. But how the incidence of MACE differs between patients with and without psoriasis while on statin therapy “has not been explored in real-world settings,” she added.

To address this question, the researchers used real-world data from the TriNetX health research network to identify individuals aged 18-90 years with a diagnosis of both psoriasis and lipid disorders who were undergoing treatment with statins. Those with a prior history of MACE were excluded from the analysis. Patients with lipid disorders on statin therapy, but without psoriatic disease, were matched 1:1 by age, sex, race, ethnicity, common risk factors for MACE, and medications shown to reduce MACE risk. The researchers then assessed the cohorts 5 years following their first statin prescription and used the TriNetX analytics tool to calculate the odds ratio (OR) with 95% CI to evaluate the likelihood of MACE in the presence of statin therapy.

Dr. Ormaza Vera and colleagues identified 20,660 patients with psoriasis and 2,768,429 patients without psoriasis who met the criteria for analysis. After propensity score matching, each cohort included 20,660 patients with a mean age of 60 years. During the 5-year observation period, 2725 patients in the psoriasis cohort experienced MACE compared with 2203 patients in the non-psoriasis cohort (OR, 1.40; 95% CI, 1.317-1.488).

“This was an unexpected outcome that challenges the current understanding and highlights the need for further research into tailored treatments for cardiovascular risk in psoriasis patients,” Dr. Ormaza Vera told this news organization.

She acknowledged certain limitations of the study, including its retrospective design, the inherent limitations of an observational study, and the use of electronic medical record data.

Lawrence J. Green, MD, clinical professor of dermatology, George Washington University, Washington, who was asked to comment on the study results, said that the findings imply that there is more than statin use alone to protect someone with psoriasis from having an increased risk for MACE. “This is not really surprising because statin use alone is only part of a prevention strategy in someone with psoriasis who usually has multiple comorbidities,” Dr. Green said. “On the other hand, the study only went out for 5 years and cardiovascular disease is a long accumulating process, so it could also be too early to demonstrate MACE prevention.”

The study was funded by a grant from the American Skin Association. Dr. Ormaza Vera and her coauthors reported having no relevant disclosures. Dr. Green disclosed that he is a speaker, consultant, or investigator for many pharmaceutical companies.

A version of this article appeared on Medscape.com .

BOSTON — New Endocrine Society guidelines call for limiting vitamin D supplementation beyond the daily recommended intake to specific risk groups and advises against routine 25-hydroxyvitamin D [25(OH)D] testing in healthy individuals. 

The evidence-based document was presented on June 3, 2024, at the Endocrine Society annual meeting, and simultaneously published in The Journal of Clinical Endocrinology and Metabolism. It advises that people who may benefit from vitamin D supplementation include: 

• Children aged 1-18 years to prevent rickets and to potentially lower the risk for respiratory tract infections
• Pregnant people to lower the risk for maternal and fetal or neonatal complications
• Adults older than 75 years to lower the risk for mortality
• Adults with prediabetes to lower the risk for type 2 diabetes

In those groups, the recommendation is for daily (rather than intermittent) empiric vitamin D supplementation of more than what was recommended in 2011 by the National Academy of Medicine (NAM), which was then called the Institute of Medicine (IOM): 600 IU/d for those aged 1-70 years and 800 IU/d for those older than 70 years. The document acknowledges that the optimal dose for these populations isn’t known, but it provides the dose ranges that were used in the trials cited as evidence for the recommendations. 

In contrast, the document advises against more vitamin D than the recommended daily intake for most healthier adults younger than 75 years and recommends against testing for blood vitamin D levels in the general population, including those with obesity or darker complexions. 

Guideline author Anastassios G. Pittas, MD, professor of medicine at Tufts University School of Medicine, Boston, told this news organization, “this guideline refers to people who are otherwise healthy, and there’s no clear indication for vitamin D, such as people with already established osteoporosis. This guideline is not relevant to them.”

Dr. Pittas also noted, “there’s no single question and single answer about the role of vitamin D in health and disease, which is what people often want to know. There are many questions, and we cannot answer all of them.”

Panel Chair Marie B. Demay, MD, professor of medicine at Harvard Medical School, Boston, told this news organization that indeed the panel was limited by lack of randomized clinical trial evidence to answer many important questions. “There is a paucity of data regarding definition of optimal levels and optimal intake of vitamin D for preventing specific diseases ... What we really need are large scale clinical trials and biomarkers so we can predict disease outcome before it happens.”

Overall, Dr. Demay said, “The recommendations are that populations adhere to the [NAM/IOM] dietary recommended intakes, and there are certain populations that will likely benefit from levels of intake above [those].” 

Asked to comment, session moderator Clifford J. Rosen, MD, director of Clinical and Translational Research and senior scientist at Maine Medical Center Research Institute, Scarborough, Maine, noted that screening for vitamin D is quite common in clinical practice, but the recommendation against doing so makes sense. 

“When clinicians measure vitamin D, then they’re forced to make a decision what to do about it. That’s where questions about the levels come in. And that’s a big problem. So what the panel’s saying is, don’t screen ... This really gets to the heart of the issue, because we have no data that there’s anything about screening that allows us to improve quality of life ... Screening is probably not worthwhile in any age group.”

Dr. Rosen, who was an author on the 2011 NAM/IOM dietary reference intakes, said that since then, new data have come out regarding the role of vitamin D in mortality in people older than 75 years, benefit in children with regard to respiratory illness, and the potential benefit of vitamin D in pregnancy. “Otherwise, I think we’re going over a lot of the same stuff that we’ve talked about since I was on the IOM panel 15 years ago ... But I think the level of evidence and rigor with which they did it is really impressive.”

However, Simeon I. Taylor, MD, professor of medicine at the University of Maryland, Baltimore, expressed disappointment that the document was limited to healthy people. “Although acknowledging challenges in managing vitamin D status in patients with several diseases, [such as] chronic kidney disease or inflammatory bowel disease, the new guidelines do not provide sufficient guidance for practicing physicians about how to manage these complex patients.”

In addition, Dr. Taylor said that the guidelines “do not explicitly consider the literature suggesting that alternative testing strategies may provide more relevant insights into vitamin D status. Just as variation in levels of thyroid-binding globulin have convinced endocrinologists not to rely on measurement of total thyroxine; interindividual variation in levels of vitamin D binding protein must be accounted for to interpret measurements of total levels of 25(OH)D. It would have been useful to explicitly consider the possible value of measuring vitamin D binding protein-independent indices of vitamin D status.”

Dr. Taylor also raised the same point as an audience member did during the Q&A period regarding patients with osteoporosis or osteopenia. “The value and utility of the new guidelines would be greatly strengthened by providing guidance for how to approach this important and very large group of individuals.”

Dr. Taylor did say that the document has “several strengths, including the fact that they acknowledge the major limitations of the quality of relevant evidence derived from clinical trials.” 

In an accompanying commentary, the guideline authors delve into the issues of skin pigmentation and race as they pertain to vitamin D metabolism, writing: 

The panel discovered that no randomized clinical trials have directly assessed vitamin D related patient-important outcomes based on participants’ skin pigmentation, although race and ethnicity often served as presumed proxies for skin pigmentation in the literature. In their deliberations, guideline panel members and selected Endocrine Society leaders underscored the critical need to distinguish between skin pigmentation as a biological variable and race and ethnicity as socially determined constructs. This differentiation is vital to maximize scientific rigor and, thus, the validity of resulting recommendations.

Dr. Pittas and Dr. Demay have no disclosures relevant to this clinical practice guideline. Dr. Rosen has no disclosures. Dr. Taylor serves as a consultant for Ionis Pharmaceuticals.
 

A version of this article appeared on Medscape.com.

BOSTON — New Endocrine Society guidelines call for limiting vitamin D supplementation beyond the daily recommended intake to specific risk groups and advises against routine 25-hydroxyvitamin D [25(OH)D] testing in healthy individuals. 

The evidence-based document was presented on June 3, 2024, at the Endocrine Society annual meeting, and simultaneously published in The Journal of Clinical Endocrinology and Metabolism. It advises that people who may benefit from vitamin D supplementation include: 

• Children aged 1-18 years to prevent rickets and to potentially lower the risk for respiratory tract infections
• Pregnant people to lower the risk for maternal and fetal or neonatal complications
• Adults older than 75 years to lower the risk for mortality
• Adults with prediabetes to lower the risk for type 2 diabetes

In those groups, the recommendation is for daily (rather than intermittent) empiric vitamin D supplementation of more than what was recommended in 2011 by the National Academy of Medicine (NAM), which was then called the Institute of Medicine (IOM): 600 IU/d for those aged 1-70 years and 800 IU/d for those older than 70 years. The document acknowledges that the optimal dose for these populations isn’t known, but it provides the dose ranges that were used in the trials cited as evidence for the recommendations. 

In contrast, the document advises against more vitamin D than the recommended daily intake for most healthier adults younger than 75 years and recommends against testing for blood vitamin D levels in the general population, including those with obesity or darker complexions. 

Guideline author Anastassios G. Pittas, MD, professor of medicine at Tufts University School of Medicine, Boston, told this news organization, “this guideline refers to people who are otherwise healthy, and there’s no clear indication for vitamin D, such as people with already established osteoporosis. This guideline is not relevant to them.”

Dr. Pittas also noted, “there’s no single question and single answer about the role of vitamin D in health and disease, which is what people often want to know. There are many questions, and we cannot answer all of them.”

Panel Chair Marie B. Demay, MD, professor of medicine at Harvard Medical School, Boston, told this news organization that indeed the panel was limited by lack of randomized clinical trial evidence to answer many important questions. “There is a paucity of data regarding definition of optimal levels and optimal intake of vitamin D for preventing specific diseases ... What we really need are large scale clinical trials and biomarkers so we can predict disease outcome before it happens.”

Overall, Dr. Demay said, “The recommendations are that populations adhere to the [NAM/IOM] dietary recommended intakes, and there are certain populations that will likely benefit from levels of intake above [those].” 

Asked to comment, session moderator Clifford J. Rosen, MD, director of Clinical and Translational Research and senior scientist at Maine Medical Center Research Institute, Scarborough, Maine, noted that screening for vitamin D is quite common in clinical practice, but the recommendation against doing so makes sense. 

“When clinicians measure vitamin D, then they’re forced to make a decision what to do about it. That’s where questions about the levels come in. And that’s a big problem. So what the panel’s saying is, don’t screen ... This really gets to the heart of the issue, because we have no data that there’s anything about screening that allows us to improve quality of life ... Screening is probably not worthwhile in any age group.”

Dr. Rosen, who was an author on the 2011 NAM/IOM dietary reference intakes, said that since then, new data have come out regarding the role of vitamin D in mortality in people older than 75 years, benefit in children with regard to respiratory illness, and the potential benefit of vitamin D in pregnancy. “Otherwise, I think we’re going over a lot of the same stuff that we’ve talked about since I was on the IOM panel 15 years ago ... But I think the level of evidence and rigor with which they did it is really impressive.”

However, Simeon I. Taylor, MD, professor of medicine at the University of Maryland, Baltimore, expressed disappointment that the document was limited to healthy people. “Although acknowledging challenges in managing vitamin D status in patients with several diseases, [such as] chronic kidney disease or inflammatory bowel disease, the new guidelines do not provide sufficient guidance for practicing physicians about how to manage these complex patients.”

In addition, Dr. Taylor said that the guidelines “do not explicitly consider the literature suggesting that alternative testing strategies may provide more relevant insights into vitamin D status. Just as variation in levels of thyroid-binding globulin have convinced endocrinologists not to rely on measurement of total thyroxine; interindividual variation in levels of vitamin D binding protein must be accounted for to interpret measurements of total levels of 25(OH)D. It would have been useful to explicitly consider the possible value of measuring vitamin D binding protein-independent indices of vitamin D status.”

Dr. Taylor also raised the same point as an audience member did during the Q&A period regarding patients with osteoporosis or osteopenia. “The value and utility of the new guidelines would be greatly strengthened by providing guidance for how to approach this important and very large group of individuals.”

Dr. Taylor did say that the document has “several strengths, including the fact that they acknowledge the major limitations of the quality of relevant evidence derived from clinical trials.” 

In an accompanying commentary, the guideline authors delve into the issues of skin pigmentation and race as they pertain to vitamin D metabolism, writing: 

The panel discovered that no randomized clinical trials have directly assessed vitamin D related patient-important outcomes based on participants’ skin pigmentation, although race and ethnicity often served as presumed proxies for skin pigmentation in the literature. In their deliberations, guideline panel members and selected Endocrine Society leaders underscored the critical need to distinguish between skin pigmentation as a biological variable and race and ethnicity as socially determined constructs. This differentiation is vital to maximize scientific rigor and, thus, the validity of resulting recommendations.

Dr. Pittas and Dr. Demay have no disclosures relevant to this clinical practice guideline. Dr. Rosen has no disclosures. Dr. Taylor serves as a consultant for Ionis Pharmaceuticals.
 

A version of this article appeared on Medscape.com.

BOSTON — New Endocrine Society guidelines call for limiting vitamin D supplementation beyond the daily recommended intake to specific risk groups and advises against routine 25-hydroxyvitamin D [25(OH)D] testing in healthy individuals. 

The evidence-based document was presented on June 3, 2024, at the Endocrine Society annual meeting, and simultaneously published in The Journal of Clinical Endocrinology and Metabolism. It advises that people who may benefit from vitamin D supplementation include: 

• Children aged 1-18 years to prevent rickets and to potentially lower the risk for respiratory tract infections
• Pregnant people to lower the risk for maternal and fetal or neonatal complications
• Adults older than 75 years to lower the risk for mortality
• Adults with prediabetes to lower the risk for type 2 diabetes

In those groups, the recommendation is for daily (rather than intermittent) empiric vitamin D supplementation of more than what was recommended in 2011 by the National Academy of Medicine (NAM), which was then called the Institute of Medicine (IOM): 600 IU/d for those aged 1-70 years and 800 IU/d for those older than 70 years. The document acknowledges that the optimal dose for these populations isn’t known, but it provides the dose ranges that were used in the trials cited as evidence for the recommendations. 

In contrast, the document advises against more vitamin D than the recommended daily intake for most healthier adults younger than 75 years and recommends against testing for blood vitamin D levels in the general population, including those with obesity or darker complexions. 

Guideline author Anastassios G. Pittas, MD, professor of medicine at Tufts University School of Medicine, Boston, told this news organization, “this guideline refers to people who are otherwise healthy, and there’s no clear indication for vitamin D, such as people with already established osteoporosis. This guideline is not relevant to them.”

Dr. Pittas also noted, “there’s no single question and single answer about the role of vitamin D in health and disease, which is what people often want to know. There are many questions, and we cannot answer all of them.”

Panel Chair Marie B. Demay, MD, professor of medicine at Harvard Medical School, Boston, told this news organization that indeed the panel was limited by lack of randomized clinical trial evidence to answer many important questions. “There is a paucity of data regarding definition of optimal levels and optimal intake of vitamin D for preventing specific diseases ... What we really need are large scale clinical trials and biomarkers so we can predict disease outcome before it happens.”

Overall, Dr. Demay said, “The recommendations are that populations adhere to the [NAM/IOM] dietary recommended intakes, and there are certain populations that will likely benefit from levels of intake above [those].” 

Asked to comment, session moderator Clifford J. Rosen, MD, director of Clinical and Translational Research and senior scientist at Maine Medical Center Research Institute, Scarborough, Maine, noted that screening for vitamin D is quite common in clinical practice, but the recommendation against doing so makes sense. 

“When clinicians measure vitamin D, then they’re forced to make a decision what to do about it. That’s where questions about the levels come in. And that’s a big problem. So what the panel’s saying is, don’t screen ... This really gets to the heart of the issue, because we have no data that there’s anything about screening that allows us to improve quality of life ... Screening is probably not worthwhile in any age group.”

Dr. Rosen, who was an author on the 2011 NAM/IOM dietary reference intakes, said that since then, new data have come out regarding the role of vitamin D in mortality in people older than 75 years, benefit in children with regard to respiratory illness, and the potential benefit of vitamin D in pregnancy. “Otherwise, I think we’re going over a lot of the same stuff that we’ve talked about since I was on the IOM panel 15 years ago ... But I think the level of evidence and rigor with which they did it is really impressive.”

However, Simeon I. Taylor, MD, professor of medicine at the University of Maryland, Baltimore, expressed disappointment that the document was limited to healthy people. “Although acknowledging challenges in managing vitamin D status in patients with several diseases, [such as] chronic kidney disease or inflammatory bowel disease, the new guidelines do not provide sufficient guidance for practicing physicians about how to manage these complex patients.”

In addition, Dr. Taylor said that the guidelines “do not explicitly consider the literature suggesting that alternative testing strategies may provide more relevant insights into vitamin D status. Just as variation in levels of thyroid-binding globulin have convinced endocrinologists not to rely on measurement of total thyroxine; interindividual variation in levels of vitamin D binding protein must be accounted for to interpret measurements of total levels of 25(OH)D. It would have been useful to explicitly consider the possible value of measuring vitamin D binding protein-independent indices of vitamin D status.”

Dr. Taylor also raised the same point as an audience member did during the Q&A period regarding patients with osteoporosis or osteopenia. “The value and utility of the new guidelines would be greatly strengthened by providing guidance for how to approach this important and very large group of individuals.”

Dr. Taylor did say that the document has “several strengths, including the fact that they acknowledge the major limitations of the quality of relevant evidence derived from clinical trials.” 

In an accompanying commentary, the guideline authors delve into the issues of skin pigmentation and race as they pertain to vitamin D metabolism, writing: 

The panel discovered that no randomized clinical trials have directly assessed vitamin D related patient-important outcomes based on participants’ skin pigmentation, although race and ethnicity often served as presumed proxies for skin pigmentation in the literature. In their deliberations, guideline panel members and selected Endocrine Society leaders underscored the critical need to distinguish between skin pigmentation as a biological variable and race and ethnicity as socially determined constructs. This differentiation is vital to maximize scientific rigor and, thus, the validity of resulting recommendations.

Dr. Pittas and Dr. Demay have no disclosures relevant to this clinical practice guideline. Dr. Rosen has no disclosures. Dr. Taylor serves as a consultant for Ionis Pharmaceuticals.
 

A version of this article appeared on Medscape.com.

The glucagon-like peptide-1 (GLP-1) receptor agonist semaglutide (Ozempic, Wegovy) enhances taste sensitivity, changes brain responses to sweet tastes and may even alter expression of genes in the tongue associated with taste bud development, according to new research presented at the annual meeting of the Endocrine Society, held in Boston. 

“Some studies have reported that individuals living with obesity often perceive tastes as less intense,” noted Mojca Jensterle Sever, PhD, of the University Medical Centre in Ljubljana, Slovenia, who presented the work. Research also suggests that “populations prone to obesity have an inherently elevated desire for sweet and energy-dense foods,” she continued. 

Studies in animal models have also previously shown that GLP-1 plays an important role in taste sensitivity, but it was not known if this hormone also influenced human taste perception. 

In this proof-of-concept study, researchers randomly assigned 30 women with polycystic ovary syndrome (PCOS) to either 1 mg of semaglutide, administered once a week, or placebo for 16 weeks. Participants were on average 34 years old with a body mass index (BMI) of 36.4. Participants with PCOS were selected with the “aim to reduce variability in taste perception across different phases of the menstrual cycle,” Dr. Sever said. 

Prior to the intervention, researchers tested participants’ taste sensitivity using 16 taste strips infused with four different concentrations of sweet, sour, salty, and bitter substances. Participants were asked to identify the taste of each strip. Every correct answer counted as one point, with a possible total of 16 points overall. Tongue biopsies were conducted for gene expression analysis. 

Researchers also used functional MRI (fMRI) to evaluate brain responses to a series of calorie-dense, low-calorie, and non-food visual cues as well as to sweet taste stimulus. A sweet solution was administered on the tongue 30 minutes before and after participants consumed a standardized meal: a high-protein enriched nutritional drink. 

These tests were repeated after 16 weeks. 

At the end of the study, the women taking semaglutide increased their taste sensitivity from 11.9 to 14.4 points; the estimated treatment difference from the control group was 2.5 points (95% CI, 1.7 - 3.3). 

The semaglutide group also exhibited decreased activation of the putamen (a structure in the brain involved with the brain’s reward system) on fMRI in response to calorie-dense cues. In response to sweet taste stimulus, those taking semaglutide showed increased activation of angular gyrus on MRI compared with the placebo group. The angular gyrus is part of the brain’s parietal lobe and is involved with language, memory, reasoning, and attention.

Lastly, researchers identified differential mRNA expression in the genes EYA, PRMT8, CRLF1, and CYP1B1, which are associated with taste bud development, renewal, and differentiation.

The findings are “fascinating, because we think about all of the factors that this new class of agents are able to improve, but taste is often not something that we look at, though there have been very strong associations,” said Gitanjali Srivastava, MD, of Vanderbilt University, Nashville, Tennessee, who moderated the session.

“Is it possible that another mechanism of action for this class of agents is perhaps indirectly altering our taste perception,” she posited, and, because of that, “we have an altered sense of satiety and hunger?”

Dr. Sever noted Dr. Several limitations to the study, including that only specific tastes were evaluated in a controlled study environment, “which may not reflect everyday experience,” she said. Taste perception can also vary widely from person to person, and changes in mRNA expression do not necessarily reflect changes in protein levels or activity.

“Our study should be seen and interpreted as a proof-of-concept study,” Dr. Sever added, with additional research needed to explore the relationship between semaglutide and taste perception.

Dr. Srivastava consults for Novo Nordisk, Eli Lilly, and Rhythm Pharmaceuticals. She has received research grant support from Eli Lilly. Dr. Sever reports no relevant financial relationships. 

A version of this article appeared on Medscape.com .

The glucagon-like peptide-1 (GLP-1) receptor agonist semaglutide (Ozempic, Wegovy) enhances taste sensitivity, changes brain responses to sweet tastes and may even alter expression of genes in the tongue associated with taste bud development, according to new research presented at the annual meeting of the Endocrine Society, held in Boston. 

“Some studies have reported that individuals living with obesity often perceive tastes as less intense,” noted Mojca Jensterle Sever, PhD, of the University Medical Centre in Ljubljana, Slovenia, who presented the work. Research also suggests that “populations prone to obesity have an inherently elevated desire for sweet and energy-dense foods,” she continued. 

Studies in animal models have also previously shown that GLP-1 plays an important role in taste sensitivity, but it was not known if this hormone also influenced human taste perception. 

In this proof-of-concept study, researchers randomly assigned 30 women with polycystic ovary syndrome (PCOS) to either 1 mg of semaglutide, administered once a week, or placebo for 16 weeks. Participants were on average 34 years old with a body mass index (BMI) of 36.4. Participants with PCOS were selected with the “aim to reduce variability in taste perception across different phases of the menstrual cycle,” Dr. Sever said. 

Prior to the intervention, researchers tested participants’ taste sensitivity using 16 taste strips infused with four different concentrations of sweet, sour, salty, and bitter substances. Participants were asked to identify the taste of each strip. Every correct answer counted as one point, with a possible total of 16 points overall. Tongue biopsies were conducted for gene expression analysis. 

Researchers also used functional MRI (fMRI) to evaluate brain responses to a series of calorie-dense, low-calorie, and non-food visual cues as well as to sweet taste stimulus. A sweet solution was administered on the tongue 30 minutes before and after participants consumed a standardized meal: a high-protein enriched nutritional drink. 

These tests were repeated after 16 weeks. 

At the end of the study, the women taking semaglutide increased their taste sensitivity from 11.9 to 14.4 points; the estimated treatment difference from the control group was 2.5 points (95% CI, 1.7 - 3.3). 

The semaglutide group also exhibited decreased activation of the putamen (a structure in the brain involved with the brain’s reward system) on fMRI in response to calorie-dense cues. In response to sweet taste stimulus, those taking semaglutide showed increased activation of angular gyrus on MRI compared with the placebo group. The angular gyrus is part of the brain’s parietal lobe and is involved with language, memory, reasoning, and attention.

Lastly, researchers identified differential mRNA expression in the genes EYA, PRMT8, CRLF1, and CYP1B1, which are associated with taste bud development, renewal, and differentiation.

The findings are “fascinating, because we think about all of the factors that this new class of agents are able to improve, but taste is often not something that we look at, though there have been very strong associations,” said Gitanjali Srivastava, MD, of Vanderbilt University, Nashville, Tennessee, who moderated the session.

“Is it possible that another mechanism of action for this class of agents is perhaps indirectly altering our taste perception,” she posited, and, because of that, “we have an altered sense of satiety and hunger?”

Dr. Sever noted Dr. Several limitations to the study, including that only specific tastes were evaluated in a controlled study environment, “which may not reflect everyday experience,” she said. Taste perception can also vary widely from person to person, and changes in mRNA expression do not necessarily reflect changes in protein levels or activity.

“Our study should be seen and interpreted as a proof-of-concept study,” Dr. Sever added, with additional research needed to explore the relationship between semaglutide and taste perception.

Dr. Srivastava consults for Novo Nordisk, Eli Lilly, and Rhythm Pharmaceuticals. She has received research grant support from Eli Lilly. Dr. Sever reports no relevant financial relationships. 

A version of this article appeared on Medscape.com .

The glucagon-like peptide-1 (GLP-1) receptor agonist semaglutide (Ozempic, Wegovy) enhances taste sensitivity, changes brain responses to sweet tastes and may even alter expression of genes in the tongue associated with taste bud development, according to new research presented at the annual meeting of the Endocrine Society, held in Boston. 

“Some studies have reported that individuals living with obesity often perceive tastes as less intense,” noted Mojca Jensterle Sever, PhD, of the University Medical Centre in Ljubljana, Slovenia, who presented the work. Research also suggests that “populations prone to obesity have an inherently elevated desire for sweet and energy-dense foods,” she continued. 

Studies in animal models have also previously shown that GLP-1 plays an important role in taste sensitivity, but it was not known if this hormone also influenced human taste perception. 

In this proof-of-concept study, researchers randomly assigned 30 women with polycystic ovary syndrome (PCOS) to either 1 mg of semaglutide, administered once a week, or placebo for 16 weeks. Participants were on average 34 years old with a body mass index (BMI) of 36.4. Participants with PCOS were selected with the “aim to reduce variability in taste perception across different phases of the menstrual cycle,” Dr. Sever said. 

Prior to the intervention, researchers tested participants’ taste sensitivity using 16 taste strips infused with four different concentrations of sweet, sour, salty, and bitter substances. Participants were asked to identify the taste of each strip. Every correct answer counted as one point, with a possible total of 16 points overall. Tongue biopsies were conducted for gene expression analysis. 

Researchers also used functional MRI (fMRI) to evaluate brain responses to a series of calorie-dense, low-calorie, and non-food visual cues as well as to sweet taste stimulus. A sweet solution was administered on the tongue 30 minutes before and after participants consumed a standardized meal: a high-protein enriched nutritional drink. 

These tests were repeated after 16 weeks. 

At the end of the study, the women taking semaglutide increased their taste sensitivity from 11.9 to 14.4 points; the estimated treatment difference from the control group was 2.5 points (95% CI, 1.7 - 3.3). 

The semaglutide group also exhibited decreased activation of the putamen (a structure in the brain involved with the brain’s reward system) on fMRI in response to calorie-dense cues. In response to sweet taste stimulus, those taking semaglutide showed increased activation of angular gyrus on MRI compared with the placebo group. The angular gyrus is part of the brain’s parietal lobe and is involved with language, memory, reasoning, and attention.

Lastly, researchers identified differential mRNA expression in the genes EYA, PRMT8, CRLF1, and CYP1B1, which are associated with taste bud development, renewal, and differentiation.

The findings are “fascinating, because we think about all of the factors that this new class of agents are able to improve, but taste is often not something that we look at, though there have been very strong associations,” said Gitanjali Srivastava, MD, of Vanderbilt University, Nashville, Tennessee, who moderated the session.

“Is it possible that another mechanism of action for this class of agents is perhaps indirectly altering our taste perception,” she posited, and, because of that, “we have an altered sense of satiety and hunger?”

Dr. Sever noted Dr. Several limitations to the study, including that only specific tastes were evaluated in a controlled study environment, “which may not reflect everyday experience,” she said. Taste perception can also vary widely from person to person, and changes in mRNA expression do not necessarily reflect changes in protein levels or activity.

“Our study should be seen and interpreted as a proof-of-concept study,” Dr. Sever added, with additional research needed to explore the relationship between semaglutide and taste perception.

Dr. Srivastava consults for Novo Nordisk, Eli Lilly, and Rhythm Pharmaceuticals. She has received research grant support from Eli Lilly. Dr. Sever reports no relevant financial relationships. 

A version of this article appeared on Medscape.com .

My crystal ball says that Big Food’s ongoing development and marketing of products designed for the reduced appetites of people taking anti-obesity medications will simultaneously be welcomed by their target market and scorned by self-righteous, healthy-living, just-try-harder, isn’t-this-just-feeding-the-problem hypocrites. 

For the privileged, self-righteous, healthy-living crowd, the right to enjoy dietary indulgences and conveniences is inversely proportional to your weight. Often, judgment isn’t cast on the less-than-perfect choices of those with so-called “normal” weight; that’s often not the case for those with obesity. 

Think you’re free from this paradigm? If you are, good for you. But I’d wager that there are plenty of readers who state that they’re free from bias, but when standing in supermarket checkout lines, they scrutinize and silently pass judgment on the contents of the grocery carts of people with obesity or, similarly, on the orders of people with obesity in fast-food restaurants.

Yet, there are bags of chips and cookies in most of our weekly carts, and who among us doesn’t, at times, grab some greasy comfort or convenience?

Unfortunately, the fuel for these sorts of judgments — implicit weight bias — is not only pervasive but also durable. A recent study of temporal changes to implicit biases demonstrated that unlike biases about race, skin tone, sexuality, age, and disability — between 2007 and 2016, tested levels of these implicit bias were seen to be in decline —biases about weight remain stable.

As to the products themselves, according to the recent article, they’ll be smaller, lower in calories, and high in protein and fat. To put it another way, compared with their nonshrunken counterparts, the food products will lead to the consumption of fewer calories while providing a potentially more-sating macronutrient distribution: a win-win. And no doubt, their sales won’t be restricted to those taking anti-obesity medications and, consequently, will provide everyone the ability to purchase and enjoy smaller dietary indulgences. 

With that said, I’d be remiss if I didn’t assert that the discussion of the merits or lack thereof of these sorts of offerings is misguided and pointless in that the food industry’s job is not one of social service provision or preventive healthcare. As I’ve written in the past, the food industry is neither friend, foe, nor partner. The food industry’s one job is to sell food, and if they see a market opportunity, they’ll take it. In this case, that turns out to be refreshing in a sense in that unlike moral-panic scolds, the food industry doesn’t judge its customers’ right to buy its products on the basis of how much their customers weigh. 

Whereas the food industry’s response to anti-obesity medications’ impact on appetite may be to embrace it, many others’, including in medicine, seem to involve some degree of judgment or scorn. Yes, our behavior has an impact on our weight, but intentional behavior change in the name of weight requires multiple layers of deep and perpetual privilege. And yes, our environment is indeed a tremendous contributor to the challenge of obesity, but the world is full of medical conditions influenced or caused by our environment. Yet, discussions around how medications fail to address obesity’s root cause are the only such root-cause discussions I ever see. 

Put more plainly, “how dare we develop medications for conditions influenced by our environment” is an odd stance to take in a world full of conditions influenced by our environments and where our environments’ primary change-driver is sales. Products that support the use of medications that improve life’s quality while markedly reducing the risk for an ever-growing number of conditions should be celebrated. 

Dr. Freedhoff has disclosed the following relevant financial relationships:

Serve(d) as a director, officer, partner, employee, adviser, consultant, or trustee for Bariatric Medical Institute and Constant Health; received research grant from Novo Nordisk; publicly shared opinions via Weighty Matters and social media.

A version of this article appeared on Medscape.com.

My crystal ball says that Big Food’s ongoing development and marketing of products designed for the reduced appetites of people taking anti-obesity medications will simultaneously be welcomed by their target market and scorned by self-righteous, healthy-living, just-try-harder, isn’t-this-just-feeding-the-problem hypocrites. 

For the privileged, self-righteous, healthy-living crowd, the right to enjoy dietary indulgences and conveniences is inversely proportional to your weight. Often, judgment isn’t cast on the less-than-perfect choices of those with so-called “normal” weight; that’s often not the case for those with obesity. 

Think you’re free from this paradigm? If you are, good for you. But I’d wager that there are plenty of readers who state that they’re free from bias, but when standing in supermarket checkout lines, they scrutinize and silently pass judgment on the contents of the grocery carts of people with obesity or, similarly, on the orders of people with obesity in fast-food restaurants.

Yet, there are bags of chips and cookies in most of our weekly carts, and who among us doesn’t, at times, grab some greasy comfort or convenience?

Unfortunately, the fuel for these sorts of judgments — implicit weight bias — is not only pervasive but also durable. A recent study of temporal changes to implicit biases demonstrated that unlike biases about race, skin tone, sexuality, age, and disability — between 2007 and 2016, tested levels of these implicit bias were seen to be in decline —biases about weight remain stable.

As to the products themselves, according to the recent article, they’ll be smaller, lower in calories, and high in protein and fat. To put it another way, compared with their nonshrunken counterparts, the food products will lead to the consumption of fewer calories while providing a potentially more-sating macronutrient distribution: a win-win. And no doubt, their sales won’t be restricted to those taking anti-obesity medications and, consequently, will provide everyone the ability to purchase and enjoy smaller dietary indulgences. 

With that said, I’d be remiss if I didn’t assert that the discussion of the merits or lack thereof of these sorts of offerings is misguided and pointless in that the food industry’s job is not one of social service provision or preventive healthcare. As I’ve written in the past, the food industry is neither friend, foe, nor partner. The food industry’s one job is to sell food, and if they see a market opportunity, they’ll take it. In this case, that turns out to be refreshing in a sense in that unlike moral-panic scolds, the food industry doesn’t judge its customers’ right to buy its products on the basis of how much their customers weigh. 

Whereas the food industry’s response to anti-obesity medications’ impact on appetite may be to embrace it, many others’, including in medicine, seem to involve some degree of judgment or scorn. Yes, our behavior has an impact on our weight, but intentional behavior change in the name of weight requires multiple layers of deep and perpetual privilege. And yes, our environment is indeed a tremendous contributor to the challenge of obesity, but the world is full of medical conditions influenced or caused by our environment. Yet, discussions around how medications fail to address obesity’s root cause are the only such root-cause discussions I ever see. 

Put more plainly, “how dare we develop medications for conditions influenced by our environment” is an odd stance to take in a world full of conditions influenced by our environments and where our environments’ primary change-driver is sales. Products that support the use of medications that improve life’s quality while markedly reducing the risk for an ever-growing number of conditions should be celebrated. 

Dr. Freedhoff has disclosed the following relevant financial relationships:

Serve(d) as a director, officer, partner, employee, adviser, consultant, or trustee for Bariatric Medical Institute and Constant Health; received research grant from Novo Nordisk; publicly shared opinions via Weighty Matters and social media.

A version of this article appeared on Medscape.com.

My crystal ball says that Big Food’s ongoing development and marketing of products designed for the reduced appetites of people taking anti-obesity medications will simultaneously be welcomed by their target market and scorned by self-righteous, healthy-living, just-try-harder, isn’t-this-just-feeding-the-problem hypocrites. 

For the privileged, self-righteous, healthy-living crowd, the right to enjoy dietary indulgences and conveniences is inversely proportional to your weight. Often, judgment isn’t cast on the less-than-perfect choices of those with so-called “normal” weight; that’s often not the case for those with obesity. 

Think you’re free from this paradigm? If you are, good for you. But I’d wager that there are plenty of readers who state that they’re free from bias, but when standing in supermarket checkout lines, they scrutinize and silently pass judgment on the contents of the grocery carts of people with obesity or, similarly, on the orders of people with obesity in fast-food restaurants.

Yet, there are bags of chips and cookies in most of our weekly carts, and who among us doesn’t, at times, grab some greasy comfort or convenience?

Unfortunately, the fuel for these sorts of judgments — implicit weight bias — is not only pervasive but also durable. A recent study of temporal changes to implicit biases demonstrated that unlike biases about race, skin tone, sexuality, age, and disability — between 2007 and 2016, tested levels of these implicit bias were seen to be in decline —biases about weight remain stable.

As to the products themselves, according to the recent article, they’ll be smaller, lower in calories, and high in protein and fat. To put it another way, compared with their nonshrunken counterparts, the food products will lead to the consumption of fewer calories while providing a potentially more-sating macronutrient distribution: a win-win. And no doubt, their sales won’t be restricted to those taking anti-obesity medications and, consequently, will provide everyone the ability to purchase and enjoy smaller dietary indulgences. 

With that said, I’d be remiss if I didn’t assert that the discussion of the merits or lack thereof of these sorts of offerings is misguided and pointless in that the food industry’s job is not one of social service provision or preventive healthcare. As I’ve written in the past, the food industry is neither friend, foe, nor partner. The food industry’s one job is to sell food, and if they see a market opportunity, they’ll take it. In this case, that turns out to be refreshing in a sense in that unlike moral-panic scolds, the food industry doesn’t judge its customers’ right to buy its products on the basis of how much their customers weigh. 

Whereas the food industry’s response to anti-obesity medications’ impact on appetite may be to embrace it, many others’, including in medicine, seem to involve some degree of judgment or scorn. Yes, our behavior has an impact on our weight, but intentional behavior change in the name of weight requires multiple layers of deep and perpetual privilege. And yes, our environment is indeed a tremendous contributor to the challenge of obesity, but the world is full of medical conditions influenced or caused by our environment. Yet, discussions around how medications fail to address obesity’s root cause are the only such root-cause discussions I ever see. 

Put more plainly, “how dare we develop medications for conditions influenced by our environment” is an odd stance to take in a world full of conditions influenced by our environments and where our environments’ primary change-driver is sales. Products that support the use of medications that improve life’s quality while markedly reducing the risk for an ever-growing number of conditions should be celebrated. 

Dr. Freedhoff has disclosed the following relevant financial relationships:

Serve(d) as a director, officer, partner, employee, adviser, consultant, or trustee for Bariatric Medical Institute and Constant Health; received research grant from Novo Nordisk; publicly shared opinions via Weighty Matters and social media.

A version of this article appeared on Medscape.com.

TOPLINE:

The cumulative effect of frequent corticosteroid injections (CSIs), a common treatment for musculoskeletal pain, does not appear to increase the risk for fractures.

METHODOLOGY:

• Researchers utilized an institutional electronic health record database to identify adults in Olmsted County, Minnesota, receiving corticosteroid injections from May 1, 2018, to July 1, 2022.
• Corticosteroid equivalents were calculated for medications injected, including methylprednisolone, triamcinolone, betamethasone, and dexamethasone.
• Patients were excluded if they had a prescription for oral prednisone equivalents greater than 2.5 mg/day for more than 30 days.
• Fracture events were identified using ICD-9 and ICD-10 codes and were included only if they occurred after the first corticosteroid injection.

TAKEAWAY:

• A total of 7197 patients were analyzed, with a mean age of 64.4 years, and of these patients, 346 (4.8%) had a new fracture in a mean time of 329 days from the first corticosteroid injection, including 149 (43.1%) in classic osteoporotic locations.
• The study reported no increased fracture risk associated with corticosteroid injections and no significant difference in fracture rates across cumulative corticosteroid injection dose quartiles, regardless of osteoporosis status.
• Factors such as previous fractures, age, and Charlson Comorbidity Index were associated with a higher risk for fractures, not corticosteroid injections.

IN PRACTICE:

“Clinicians should be reassured that frequent CSI is not associated with higher fracture risk and should not withhold these important pain treatments owing to concern for fracture,” wrote the authors of the study.

SOURCE:

The study was led by Terin T. Sytsma, MD, Division of Community Internal Medicine, Geriatrics, and Palliative Care, Mayo Clinic, Rochester, Minnesota. It was published online in JAMA Network Open.

LIMITATIONS:

The study’s retrospective cohort design and its focus on a predominantly White population in a single community may limit the generalizability of the findings. Confounding variables such as smoking status, alcohol intake, and physical activity were acknowledged as potential contributors to fracture risk. Only clinically apparent fractures were considered, excluding silent vertebral fractures, and differences in corticosteroid formulation were not delineated.

DISCLOSURES:

The study was supported by a Mayo Clinic Catalyst Award to Dr. Sytsma. The authors had no conflicts of interest to report.

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

A version of this article appeared on Medscape.com.

TOPLINE:

The cumulative effect of frequent corticosteroid injections (CSIs), a common treatment for musculoskeletal pain, does not appear to increase the risk for fractures.

METHODOLOGY:

• Researchers utilized an institutional electronic health record database to identify adults in Olmsted County, Minnesota, receiving corticosteroid injections from May 1, 2018, to July 1, 2022.
• Corticosteroid equivalents were calculated for medications injected, including methylprednisolone, triamcinolone, betamethasone, and dexamethasone.
• Patients were excluded if they had a prescription for oral prednisone equivalents greater than 2.5 mg/day for more than 30 days.
• Fracture events were identified using ICD-9 and ICD-10 codes and were included only if they occurred after the first corticosteroid injection.

TAKEAWAY:

• A total of 7197 patients were analyzed, with a mean age of 64.4 years, and of these patients, 346 (4.8%) had a new fracture in a mean time of 329 days from the first corticosteroid injection, including 149 (43.1%) in classic osteoporotic locations.
• The study reported no increased fracture risk associated with corticosteroid injections and no significant difference in fracture rates across cumulative corticosteroid injection dose quartiles, regardless of osteoporosis status.
• Factors such as previous fractures, age, and Charlson Comorbidity Index were associated with a higher risk for fractures, not corticosteroid injections.

IN PRACTICE:

“Clinicians should be reassured that frequent CSI is not associated with higher fracture risk and should not withhold these important pain treatments owing to concern for fracture,” wrote the authors of the study.

SOURCE:

The study was led by Terin T. Sytsma, MD, Division of Community Internal Medicine, Geriatrics, and Palliative Care, Mayo Clinic, Rochester, Minnesota. It was published online in JAMA Network Open.

LIMITATIONS:

The study’s retrospective cohort design and its focus on a predominantly White population in a single community may limit the generalizability of the findings. Confounding variables such as smoking status, alcohol intake, and physical activity were acknowledged as potential contributors to fracture risk. Only clinically apparent fractures were considered, excluding silent vertebral fractures, and differences in corticosteroid formulation were not delineated.

DISCLOSURES:

The study was supported by a Mayo Clinic Catalyst Award to Dr. Sytsma. The authors had no conflicts of interest to report.

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

A version of this article appeared on Medscape.com.

TOPLINE:

The cumulative effect of frequent corticosteroid injections (CSIs), a common treatment for musculoskeletal pain, does not appear to increase the risk for fractures.

METHODOLOGY:

• Researchers utilized an institutional electronic health record database to identify adults in Olmsted County, Minnesota, receiving corticosteroid injections from May 1, 2018, to July 1, 2022.
• Corticosteroid equivalents were calculated for medications injected, including methylprednisolone, triamcinolone, betamethasone, and dexamethasone.
• Patients were excluded if they had a prescription for oral prednisone equivalents greater than 2.5 mg/day for more than 30 days.
• Fracture events were identified using ICD-9 and ICD-10 codes and were included only if they occurred after the first corticosteroid injection.

TAKEAWAY:

• A total of 7197 patients were analyzed, with a mean age of 64.4 years, and of these patients, 346 (4.8%) had a new fracture in a mean time of 329 days from the first corticosteroid injection, including 149 (43.1%) in classic osteoporotic locations.
• The study reported no increased fracture risk associated with corticosteroid injections and no significant difference in fracture rates across cumulative corticosteroid injection dose quartiles, regardless of osteoporosis status.
• Factors such as previous fractures, age, and Charlson Comorbidity Index were associated with a higher risk for fractures, not corticosteroid injections.

IN PRACTICE:

“Clinicians should be reassured that frequent CSI is not associated with higher fracture risk and should not withhold these important pain treatments owing to concern for fracture,” wrote the authors of the study.

SOURCE:

The study was led by Terin T. Sytsma, MD, Division of Community Internal Medicine, Geriatrics, and Palliative Care, Mayo Clinic, Rochester, Minnesota. It was published online in JAMA Network Open.

LIMITATIONS:

The study’s retrospective cohort design and its focus on a predominantly White population in a single community may limit the generalizability of the findings. Confounding variables such as smoking status, alcohol intake, and physical activity were acknowledged as potential contributors to fracture risk. Only clinically apparent fractures were considered, excluding silent vertebral fractures, and differences in corticosteroid formulation were not delineated.

DISCLOSURES:

The study was supported by a Mayo Clinic Catalyst Award to Dr. Sytsma. The authors had no conflicts of interest to report.

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

A version of this article appeared on Medscape.com.

TOPLINE:

Women with low bone density are more likely to report their first fragility hip fracture in their 60s rather than at older ages.

METHODOLOGY:

• Researchers used hip fracture data from the National Health and Nutrition Examination Survey for 2009-2010, 2013-2014, and 2017-2018.
• They included women older than 60 years with a bone mineral density T score ≤ −1 at the femur neck, measured by dual-energy x-ray absorptiometry.
• Fragility fractures are defined as a self-reported hip fracture resulting from a fall from standing height or less.

TAKEAWAY:

• The number of women in their 60s who reported their first hip fracture grew by 50% from 2009 to 2018.
• The opposite was true for women in their 70s and 80s who reported fewer first hip fractures over the study period.
• Reported fragility hip fractures in women overall decreased by half from 2009 to 2018.
• The prevalence of women with osteoporosis (T score ≤ −2.5) grew from 18.1% to 21.3% over 10 years.

IN PRACTICE:

The decrease in fractures overall and in women older than 70 years “may be due to increasing awareness and utilization of measures to decrease falls such as exercise, nutrition, health education, and environmental modifications targeted toward the elderly population,” the authors wrote. The findings also underscore the importance of earlier bone health awareness in primary care to curb the rising trend in younger women, they added.

SOURCE:

The study was led by Avica Atri, MD, of Albert Einstein Medical Center in Philadelphia. She presented the findings at ENDO 2024: The Endocrine Society Annual Meeting.

LIMITATIONS:

The study was retrospective in nature and included self-reported health data.

DISCLOSURES:

The study received no commercial funding. The authors have reported no relevant financial relationships.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Women with low bone density are more likely to report their first fragility hip fracture in their 60s rather than at older ages.

METHODOLOGY:

• Researchers used hip fracture data from the National Health and Nutrition Examination Survey for 2009-2010, 2013-2014, and 2017-2018.
• They included women older than 60 years with a bone mineral density T score ≤ −1 at the femur neck, measured by dual-energy x-ray absorptiometry.
• Fragility fractures are defined as a self-reported hip fracture resulting from a fall from standing height or less.

TAKEAWAY:

• The number of women in their 60s who reported their first hip fracture grew by 50% from 2009 to 2018.
• The opposite was true for women in their 70s and 80s who reported fewer first hip fractures over the study period.
• Reported fragility hip fractures in women overall decreased by half from 2009 to 2018.
• The prevalence of women with osteoporosis (T score ≤ −2.5) grew from 18.1% to 21.3% over 10 years.

IN PRACTICE:

The decrease in fractures overall and in women older than 70 years “may be due to increasing awareness and utilization of measures to decrease falls such as exercise, nutrition, health education, and environmental modifications targeted toward the elderly population,” the authors wrote. The findings also underscore the importance of earlier bone health awareness in primary care to curb the rising trend in younger women, they added.

SOURCE:

The study was led by Avica Atri, MD, of Albert Einstein Medical Center in Philadelphia. She presented the findings at ENDO 2024: The Endocrine Society Annual Meeting.

LIMITATIONS:

The study was retrospective in nature and included self-reported health data.

DISCLOSURES:

The study received no commercial funding. The authors have reported no relevant financial relationships.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Women with low bone density are more likely to report their first fragility hip fracture in their 60s rather than at older ages.

METHODOLOGY:

• Researchers used hip fracture data from the National Health and Nutrition Examination Survey for 2009-2010, 2013-2014, and 2017-2018.
• They included women older than 60 years with a bone mineral density T score ≤ −1 at the femur neck, measured by dual-energy x-ray absorptiometry.
• Fragility fractures are defined as a self-reported hip fracture resulting from a fall from standing height or less.

TAKEAWAY:

• The number of women in their 60s who reported their first hip fracture grew by 50% from 2009 to 2018.
• The opposite was true for women in their 70s and 80s who reported fewer first hip fractures over the study period.
• Reported fragility hip fractures in women overall decreased by half from 2009 to 2018.
• The prevalence of women with osteoporosis (T score ≤ −2.5) grew from 18.1% to 21.3% over 10 years.

IN PRACTICE:

The decrease in fractures overall and in women older than 70 years “may be due to increasing awareness and utilization of measures to decrease falls such as exercise, nutrition, health education, and environmental modifications targeted toward the elderly population,” the authors wrote. The findings also underscore the importance of earlier bone health awareness in primary care to curb the rising trend in younger women, they added.

SOURCE:

The study was led by Avica Atri, MD, of Albert Einstein Medical Center in Philadelphia. She presented the findings at ENDO 2024: The Endocrine Society Annual Meeting.

LIMITATIONS:

The study was retrospective in nature and included self-reported health data.

DISCLOSURES:

The study received no commercial funding. The authors have reported no relevant financial relationships.
 

A version of this article appeared on Medscape.com.