Clinical Endocrinology News

TOPLINE:

Fragmented sleep — that is, increased wakefulness and reduced sleep efficiency — is a sign of metabolic dysfunction–associated steatotic liver disease (MASLD), a study using actigraphy showed.

METHODOLOGY:

• Researchers assessed sleep-wake rhythms in 35 patients with MASLD (median age, 58 years; 66% were men; 80% with metabolic syndrome) and 16 matched healthy controls (median age, 61 years; 50% were men) using data collected 24/7 via actigraphy for 4 weeks.
• Sub-analyses were conducted with MASLD comparator groups: 16 patients with MASH, 8 with MASH with cirrhosis, and 11 with non-MASH–related cirrhosis.
• All participants visited the clinic at baseline, week 2, and week 4 to undergo a clinical investigation and complete questionnaires about their sleep.
• A standardized sleep hygiene education session was conducted at week 2.

TAKEAWAY:

• Actigraphy data from patients with MASLD did not reveal significant differences in bedtime, sleep-onset latency, sleep duration, wake-up time, or time in bed compared with controls.
• However, compared with controls, those with MASLD woke 55% more often at night (8.5 vs 5.5), lay awake 113% longer after having first fallen asleep (45.4 minutes vs 21.3 minutes), and slept more often and longer during the day (decreased sleep efficiency).
• Subgroup analyses showed that actigraphy-measured sleep patterns and quality were similarly impaired in patients with MASH, MASH with cirrhosis, and non–MASH-related cirrhosis.
• Patients with MASLD self-reported their fragmented sleep as shorter sleep with a delayed onset. In sleep diaries, 32% of patients with MASLD reported sleep disturbances caused by psychological stress, compared with only 6.25% of controls and 9% of patients with cirrhosis.
• The sleep education session did not change the actigraphy measures or the sleep parameters assessed with sleep questionnaires at the end of the study.

IN PRACTICE:

“We concluded from our data that sleep fragmentation plays a role in the pathogenesis of human MASLD. Whether MASLD causes sleep disorders or vice versa remains unknown. The underlying mechanism presumably involves genetics, environmental factors, and the activation of immune responses — ultimately driven by obesity and metabolic syndrome,” said corresponding author.

SOURCE:

The study, led by Sofia Schaeffer, PhD, University of Basel, Switzerland, was published online in Frontiers in Network Physiology.

LIMITATIONS:

The study had several limitations. There was a significant difference in body mass index between patients with MASLD (median, 31) and controls (median, 23.5), representing a potential confounder that could explain the differences in sleep behavior. Undetected obstructive sleep apnea could also be a confounding factor. The small number of participants limited the interpretation and generalization of the data, especially in the MASLD subgroups.

DISCLOSURES:

This study was supported by a grant from the University of Basel. One coauthor received a research grant from the University Center for Gastrointestinal and Liver Diseases, Basel, Switzerland. Another coauthor was employed by NovoLytiX. Schaeffer and the remaining coauthors declared that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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

TOPLINE:

Fragmented sleep — that is, increased wakefulness and reduced sleep efficiency — is a sign of metabolic dysfunction–associated steatotic liver disease (MASLD), a study using actigraphy showed.

METHODOLOGY:

• Researchers assessed sleep-wake rhythms in 35 patients with MASLD (median age, 58 years; 66% were men; 80% with metabolic syndrome) and 16 matched healthy controls (median age, 61 years; 50% were men) using data collected 24/7 via actigraphy for 4 weeks.
• Sub-analyses were conducted with MASLD comparator groups: 16 patients with MASH, 8 with MASH with cirrhosis, and 11 with non-MASH–related cirrhosis.
• All participants visited the clinic at baseline, week 2, and week 4 to undergo a clinical investigation and complete questionnaires about their sleep.
• A standardized sleep hygiene education session was conducted at week 2.

TAKEAWAY:

• Actigraphy data from patients with MASLD did not reveal significant differences in bedtime, sleep-onset latency, sleep duration, wake-up time, or time in bed compared with controls.
• However, compared with controls, those with MASLD woke 55% more often at night (8.5 vs 5.5), lay awake 113% longer after having first fallen asleep (45.4 minutes vs 21.3 minutes), and slept more often and longer during the day (decreased sleep efficiency).
• Subgroup analyses showed that actigraphy-measured sleep patterns and quality were similarly impaired in patients with MASH, MASH with cirrhosis, and non–MASH-related cirrhosis.
• Patients with MASLD self-reported their fragmented sleep as shorter sleep with a delayed onset. In sleep diaries, 32% of patients with MASLD reported sleep disturbances caused by psychological stress, compared with only 6.25% of controls and 9% of patients with cirrhosis.
• The sleep education session did not change the actigraphy measures or the sleep parameters assessed with sleep questionnaires at the end of the study.

IN PRACTICE:

“We concluded from our data that sleep fragmentation plays a role in the pathogenesis of human MASLD. Whether MASLD causes sleep disorders or vice versa remains unknown. The underlying mechanism presumably involves genetics, environmental factors, and the activation of immune responses — ultimately driven by obesity and metabolic syndrome,” said corresponding author.

SOURCE:

The study, led by Sofia Schaeffer, PhD, University of Basel, Switzerland, was published online in Frontiers in Network Physiology.

LIMITATIONS:

The study had several limitations. There was a significant difference in body mass index between patients with MASLD (median, 31) and controls (median, 23.5), representing a potential confounder that could explain the differences in sleep behavior. Undetected obstructive sleep apnea could also be a confounding factor. The small number of participants limited the interpretation and generalization of the data, especially in the MASLD subgroups.

DISCLOSURES:

This study was supported by a grant from the University of Basel. One coauthor received a research grant from the University Center for Gastrointestinal and Liver Diseases, Basel, Switzerland. Another coauthor was employed by NovoLytiX. Schaeffer and the remaining coauthors declared that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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

TOPLINE:

Fragmented sleep — that is, increased wakefulness and reduced sleep efficiency — is a sign of metabolic dysfunction–associated steatotic liver disease (MASLD), a study using actigraphy showed.

METHODOLOGY:

• Researchers assessed sleep-wake rhythms in 35 patients with MASLD (median age, 58 years; 66% were men; 80% with metabolic syndrome) and 16 matched healthy controls (median age, 61 years; 50% were men) using data collected 24/7 via actigraphy for 4 weeks.
• Sub-analyses were conducted with MASLD comparator groups: 16 patients with MASH, 8 with MASH with cirrhosis, and 11 with non-MASH–related cirrhosis.
• All participants visited the clinic at baseline, week 2, and week 4 to undergo a clinical investigation and complete questionnaires about their sleep.
• A standardized sleep hygiene education session was conducted at week 2.

TAKEAWAY:

• Actigraphy data from patients with MASLD did not reveal significant differences in bedtime, sleep-onset latency, sleep duration, wake-up time, or time in bed compared with controls.
• However, compared with controls, those with MASLD woke 55% more often at night (8.5 vs 5.5), lay awake 113% longer after having first fallen asleep (45.4 minutes vs 21.3 minutes), and slept more often and longer during the day (decreased sleep efficiency).
• Subgroup analyses showed that actigraphy-measured sleep patterns and quality were similarly impaired in patients with MASH, MASH with cirrhosis, and non–MASH-related cirrhosis.
• Patients with MASLD self-reported their fragmented sleep as shorter sleep with a delayed onset. In sleep diaries, 32% of patients with MASLD reported sleep disturbances caused by psychological stress, compared with only 6.25% of controls and 9% of patients with cirrhosis.
• The sleep education session did not change the actigraphy measures or the sleep parameters assessed with sleep questionnaires at the end of the study.

IN PRACTICE:

“We concluded from our data that sleep fragmentation plays a role in the pathogenesis of human MASLD. Whether MASLD causes sleep disorders or vice versa remains unknown. The underlying mechanism presumably involves genetics, environmental factors, and the activation of immune responses — ultimately driven by obesity and metabolic syndrome,” said corresponding author.

SOURCE:

The study, led by Sofia Schaeffer, PhD, University of Basel, Switzerland, was published online in Frontiers in Network Physiology.

LIMITATIONS:

The study had several limitations. There was a significant difference in body mass index between patients with MASLD (median, 31) and controls (median, 23.5), representing a potential confounder that could explain the differences in sleep behavior. Undetected obstructive sleep apnea could also be a confounding factor. The small number of participants limited the interpretation and generalization of the data, especially in the MASLD subgroups.

DISCLOSURES:

This study was supported by a grant from the University of Basel. One coauthor received a research grant from the University Center for Gastrointestinal and Liver Diseases, Basel, Switzerland. Another coauthor was employed by NovoLytiX. Schaeffer and the remaining coauthors declared that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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

TOPLINE:

A program combining theoretical training with free disposal containers can effectively increase knowledge and improve sharps waste disposal practices among patients with diabetes.

METHODOLOGY:

• A significant number of patients with diabetes administer insulin at home. Unsafe waste disposal including insulin pens, syringes, and lancets increases the risk for needle-stick injuries, microbial infections, and plastic waste accumulation, highlighting the need for safe disposal practices.
• Researchers conducted an experimental study at El-Horraya Polyclinic in Alexandria, Egypt, between November 2022 and April 2023 to evaluate the effectiveness of an intervention program in improving knowledge and practices related to safe sharps disposal among patients with diabetes.
• Overall, 100 patients (median age, 61 years; 92% living in urban areas) with either type 1 or type 2 diabetes were recruited and divided into the educational intervention (n = 50) and nonintervention (n = 50) groups; majority (67%) had diabetes for more than 10 years.
• The intervention group received educational sessions addressing improper disposal risks and environmental impacts along with practical demonstrations of correct sharps disposal methods; they were also given free puncture-resistant containers to safely dispose of the sharp waste generated from diabetes management.
• Assessments were performed at baseline, 2 months, and 4 months postintervention, evaluating knowledge levels (poor: < 50%, fair: 50% to < 70%, good: 70%-100%) and practice scores (poor: 0-6, fair: 7-10, good: 11-14).

TAKEAWAY:

• Overall, 58% of the patients used insulin pens, and approximately 75% required two doses of insulin daily.
• The median monthly disposal was 10 syringes per patient among syringe users and eight pen needles per patient among pen users.
• At baseline, there were no differences in the knowledge scores between the intervention and nonintervention groups; however, at both 2 and 4 months, the intervention group showed a significantly higher median knowledge score than the nonintervention group (P < .001 for both).
• Likewise, practice scores also showed marked improvements in the intervention group, compared with the nonintervention group at the end of the program (P < .001).

IN PRACTICE:

“The success of the environmental education program underscores the need for targeted interventions to enhance patient knowledge and safe sharps disposal practices. By offering accessible disposal options and raising awareness, healthcare facilities can significantly contribute to preventing accidental needle-stick injuries and reducing the risk of infectious disease transmission,” the authors wrote.

SOURCE:

This study was led by Hossam Mohamed Hassan Soliman, High Institute of Public Health, Alexandria University, Egypt. It was published online in Scientific Reports.

LIMITATIONS:

Interview bias and self-reporting bias in data collection were major limitations of this study. The quasi-experimental design, lacking randomization, may have limited the strength of causal inferences.

DISCLOSURES:

No funding was received for this study, and the authors reported no relevant 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 program combining theoretical training with free disposal containers can effectively increase knowledge and improve sharps waste disposal practices among patients with diabetes.

METHODOLOGY:

• A significant number of patients with diabetes administer insulin at home. Unsafe waste disposal including insulin pens, syringes, and lancets increases the risk for needle-stick injuries, microbial infections, and plastic waste accumulation, highlighting the need for safe disposal practices.
• Researchers conducted an experimental study at El-Horraya Polyclinic in Alexandria, Egypt, between November 2022 and April 2023 to evaluate the effectiveness of an intervention program in improving knowledge and practices related to safe sharps disposal among patients with diabetes.
• Overall, 100 patients (median age, 61 years; 92% living in urban areas) with either type 1 or type 2 diabetes were recruited and divided into the educational intervention (n = 50) and nonintervention (n = 50) groups; majority (67%) had diabetes for more than 10 years.
• The intervention group received educational sessions addressing improper disposal risks and environmental impacts along with practical demonstrations of correct sharps disposal methods; they were also given free puncture-resistant containers to safely dispose of the sharp waste generated from diabetes management.
• Assessments were performed at baseline, 2 months, and 4 months postintervention, evaluating knowledge levels (poor: < 50%, fair: 50% to < 70%, good: 70%-100%) and practice scores (poor: 0-6, fair: 7-10, good: 11-14).

TAKEAWAY:

• Overall, 58% of the patients used insulin pens, and approximately 75% required two doses of insulin daily.
• The median monthly disposal was 10 syringes per patient among syringe users and eight pen needles per patient among pen users.
• At baseline, there were no differences in the knowledge scores between the intervention and nonintervention groups; however, at both 2 and 4 months, the intervention group showed a significantly higher median knowledge score than the nonintervention group (P < .001 for both).
• Likewise, practice scores also showed marked improvements in the intervention group, compared with the nonintervention group at the end of the program (P < .001).

IN PRACTICE:

“The success of the environmental education program underscores the need for targeted interventions to enhance patient knowledge and safe sharps disposal practices. By offering accessible disposal options and raising awareness, healthcare facilities can significantly contribute to preventing accidental needle-stick injuries and reducing the risk of infectious disease transmission,” the authors wrote.

SOURCE:

This study was led by Hossam Mohamed Hassan Soliman, High Institute of Public Health, Alexandria University, Egypt. It was published online in Scientific Reports.

LIMITATIONS:

Interview bias and self-reporting bias in data collection were major limitations of this study. The quasi-experimental design, lacking randomization, may have limited the strength of causal inferences.

DISCLOSURES:

No funding was received for this study, and the authors reported no relevant 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 program combining theoretical training with free disposal containers can effectively increase knowledge and improve sharps waste disposal practices among patients with diabetes.

METHODOLOGY:

• A significant number of patients with diabetes administer insulin at home. Unsafe waste disposal including insulin pens, syringes, and lancets increases the risk for needle-stick injuries, microbial infections, and plastic waste accumulation, highlighting the need for safe disposal practices.
• Researchers conducted an experimental study at El-Horraya Polyclinic in Alexandria, Egypt, between November 2022 and April 2023 to evaluate the effectiveness of an intervention program in improving knowledge and practices related to safe sharps disposal among patients with diabetes.
• Overall, 100 patients (median age, 61 years; 92% living in urban areas) with either type 1 or type 2 diabetes were recruited and divided into the educational intervention (n = 50) and nonintervention (n = 50) groups; majority (67%) had diabetes for more than 10 years.
• The intervention group received educational sessions addressing improper disposal risks and environmental impacts along with practical demonstrations of correct sharps disposal methods; they were also given free puncture-resistant containers to safely dispose of the sharp waste generated from diabetes management.
• Assessments were performed at baseline, 2 months, and 4 months postintervention, evaluating knowledge levels (poor: < 50%, fair: 50% to < 70%, good: 70%-100%) and practice scores (poor: 0-6, fair: 7-10, good: 11-14).

TAKEAWAY:

• Overall, 58% of the patients used insulin pens, and approximately 75% required two doses of insulin daily.
• The median monthly disposal was 10 syringes per patient among syringe users and eight pen needles per patient among pen users.
• At baseline, there were no differences in the knowledge scores between the intervention and nonintervention groups; however, at both 2 and 4 months, the intervention group showed a significantly higher median knowledge score than the nonintervention group (P < .001 for both).
• Likewise, practice scores also showed marked improvements in the intervention group, compared with the nonintervention group at the end of the program (P < .001).

IN PRACTICE:

“The success of the environmental education program underscores the need for targeted interventions to enhance patient knowledge and safe sharps disposal practices. By offering accessible disposal options and raising awareness, healthcare facilities can significantly contribute to preventing accidental needle-stick injuries and reducing the risk of infectious disease transmission,” the authors wrote.

SOURCE:

This study was led by Hossam Mohamed Hassan Soliman, High Institute of Public Health, Alexandria University, Egypt. It was published online in Scientific Reports.

LIMITATIONS:

Interview bias and self-reporting bias in data collection were major limitations of this study. The quasi-experimental design, lacking randomization, may have limited the strength of causal inferences.

DISCLOSURES:

No funding was received for this study, and the authors reported no relevant 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:

Combined exposure to dioxins and dioxin-like polychlorinated biphenyls (DL-PCBs) is significantly associated with an increased risk for obesity in adults, with 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin (HpCDD) showing the greatest contribution.

METHODOLOGY:

• Recent evidence has shown that environmental contaminants, particularly dioxins and dioxin-like polychlorinated biphenyls, may be linked to an increased risk for obesity as endocrine-disrupting chemicals.
• Researchers evaluated the relationship between mixed exposure to nine types of dioxins and DL-PCBs and obesity or obesity indices in 852 adults using data from the National Health and Nutrition Examination Survey from 2003 to 2004.
• They chose nine chemicals for analysis: 1,2,3,4,6,7,8-HpCDD; 1,2,3,4,6,7,8,9-octachlorodibenzo-p-dioxin (OCDD); 3,3’,4,4’,5-pentachlorodibenzofuran (PnCB); PCB28; PCB66; PCB74; PCB105; PCB118; and PCB156.
• General and abdominal obesity were present in 34% and 53.9% of participants, respectively.
• Multiple statistical approaches were employed to evaluate the association of exposures to dioxins and DL-PCBs with obesity. Mediation analysis was performed to assess the potential role of A1c in this association.

TAKEAWAY:

• Multivariable logistic regression analysis found that a single exposure to higher concentrations of 1,2,3,4,6,7,8-HpCDD; 1,2,3,4,6,7,8,9-OCDD; 3,3’,4,4’,5-PnCB; PCB74; PCB105; and PCB118 was associated with an increased risk for general and abdominal obesity (P for trend < .001 for all). A stratified analysis by sex found that except for PCB28, PCB66, PCB74, and PCB156, all chemicals were linked to increased general and abdominal obesity risk in both men and women.
• Combined exposure to dioxins and DL-PCBs was positively associated with the risk for obesity, with 1,2,3,4,6,7,8-HpCDD showing the greatest contribution.
• When considering obesity indices, 1,2,3,4,6,7,8,9-OCDD; 1,2,3,4,6,7,8-HpCDD; 3,3’,4,4’,5-PnCB; PCB74; PCB105; and PCB118 were significantly associated with body mass index and waist circumference.
• A1c levels significantly mediated the association between mixed exposure to dioxins and DL-PCBs and obesity (P < .05), with mediation proportions of 6.94% for general obesity and 5.21% for abdominal obesity.

IN PRACTICE:

“Our findings suggested that dioxins and DL-PCBs may be independent risk factors for obesity,” the authors wrote. “The hazards of dioxins on obesity should be emphasized, and additional studies are desirable to elucidate the potential mechanisms for dioxins on obesity in adults.”

SOURCE:

This study, led by Zhao-Xing Gao, Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University and Center for Big Data and Population Health of IHM, both in Hefei, China, was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

The cross-sectional nature of this study prevented the establishment of causal relationships between dioxins or DL-PCBs and obesity. This study relied on a small sample. Replacing chemical concentrations below the limit of detection with fixed values may have introduced bias.

DISCLOSURES:

This study was funded by grants from the National Natural Science Foundation of China, Research Fund of Anhui Institute of Translational Medicine, and Research Fund of Center for Big Data and Population Health of IHM. The authors declared no conflicts of interest.

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

TOPLINE:

Combined exposure to dioxins and dioxin-like polychlorinated biphenyls (DL-PCBs) is significantly associated with an increased risk for obesity in adults, with 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin (HpCDD) showing the greatest contribution.

METHODOLOGY:

• Recent evidence has shown that environmental contaminants, particularly dioxins and dioxin-like polychlorinated biphenyls, may be linked to an increased risk for obesity as endocrine-disrupting chemicals.
• Researchers evaluated the relationship between mixed exposure to nine types of dioxins and DL-PCBs and obesity or obesity indices in 852 adults using data from the National Health and Nutrition Examination Survey from 2003 to 2004.
• They chose nine chemicals for analysis: 1,2,3,4,6,7,8-HpCDD; 1,2,3,4,6,7,8,9-octachlorodibenzo-p-dioxin (OCDD); 3,3’,4,4’,5-pentachlorodibenzofuran (PnCB); PCB28; PCB66; PCB74; PCB105; PCB118; and PCB156.
• General and abdominal obesity were present in 34% and 53.9% of participants, respectively.
• Multiple statistical approaches were employed to evaluate the association of exposures to dioxins and DL-PCBs with obesity. Mediation analysis was performed to assess the potential role of A1c in this association.

TAKEAWAY:

• Multivariable logistic regression analysis found that a single exposure to higher concentrations of 1,2,3,4,6,7,8-HpCDD; 1,2,3,4,6,7,8,9-OCDD; 3,3’,4,4’,5-PnCB; PCB74; PCB105; and PCB118 was associated with an increased risk for general and abdominal obesity (P for trend < .001 for all). A stratified analysis by sex found that except for PCB28, PCB66, PCB74, and PCB156, all chemicals were linked to increased general and abdominal obesity risk in both men and women.
• Combined exposure to dioxins and DL-PCBs was positively associated with the risk for obesity, with 1,2,3,4,6,7,8-HpCDD showing the greatest contribution.
• When considering obesity indices, 1,2,3,4,6,7,8,9-OCDD; 1,2,3,4,6,7,8-HpCDD; 3,3’,4,4’,5-PnCB; PCB74; PCB105; and PCB118 were significantly associated with body mass index and waist circumference.
• A1c levels significantly mediated the association between mixed exposure to dioxins and DL-PCBs and obesity (P < .05), with mediation proportions of 6.94% for general obesity and 5.21% for abdominal obesity.

IN PRACTICE:

“Our findings suggested that dioxins and DL-PCBs may be independent risk factors for obesity,” the authors wrote. “The hazards of dioxins on obesity should be emphasized, and additional studies are desirable to elucidate the potential mechanisms for dioxins on obesity in adults.”

SOURCE:

This study, led by Zhao-Xing Gao, Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University and Center for Big Data and Population Health of IHM, both in Hefei, China, was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

The cross-sectional nature of this study prevented the establishment of causal relationships between dioxins or DL-PCBs and obesity. This study relied on a small sample. Replacing chemical concentrations below the limit of detection with fixed values may have introduced bias.

DISCLOSURES:

This study was funded by grants from the National Natural Science Foundation of China, Research Fund of Anhui Institute of Translational Medicine, and Research Fund of Center for Big Data and Population Health of IHM. The authors declared no conflicts of interest.

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

TOPLINE:

Combined exposure to dioxins and dioxin-like polychlorinated biphenyls (DL-PCBs) is significantly associated with an increased risk for obesity in adults, with 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin (HpCDD) showing the greatest contribution.

METHODOLOGY:

• Recent evidence has shown that environmental contaminants, particularly dioxins and dioxin-like polychlorinated biphenyls, may be linked to an increased risk for obesity as endocrine-disrupting chemicals.
• Researchers evaluated the relationship between mixed exposure to nine types of dioxins and DL-PCBs and obesity or obesity indices in 852 adults using data from the National Health and Nutrition Examination Survey from 2003 to 2004.
• They chose nine chemicals for analysis: 1,2,3,4,6,7,8-HpCDD; 1,2,3,4,6,7,8,9-octachlorodibenzo-p-dioxin (OCDD); 3,3’,4,4’,5-pentachlorodibenzofuran (PnCB); PCB28; PCB66; PCB74; PCB105; PCB118; and PCB156.
• General and abdominal obesity were present in 34% and 53.9% of participants, respectively.
• Multiple statistical approaches were employed to evaluate the association of exposures to dioxins and DL-PCBs with obesity. Mediation analysis was performed to assess the potential role of A1c in this association.

TAKEAWAY:

• Multivariable logistic regression analysis found that a single exposure to higher concentrations of 1,2,3,4,6,7,8-HpCDD; 1,2,3,4,6,7,8,9-OCDD; 3,3’,4,4’,5-PnCB; PCB74; PCB105; and PCB118 was associated with an increased risk for general and abdominal obesity (P for trend < .001 for all). A stratified analysis by sex found that except for PCB28, PCB66, PCB74, and PCB156, all chemicals were linked to increased general and abdominal obesity risk in both men and women.
• Combined exposure to dioxins and DL-PCBs was positively associated with the risk for obesity, with 1,2,3,4,6,7,8-HpCDD showing the greatest contribution.
• When considering obesity indices, 1,2,3,4,6,7,8,9-OCDD; 1,2,3,4,6,7,8-HpCDD; 3,3’,4,4’,5-PnCB; PCB74; PCB105; and PCB118 were significantly associated with body mass index and waist circumference.
• A1c levels significantly mediated the association between mixed exposure to dioxins and DL-PCBs and obesity (P < .05), with mediation proportions of 6.94% for general obesity and 5.21% for abdominal obesity.

IN PRACTICE:

“Our findings suggested that dioxins and DL-PCBs may be independent risk factors for obesity,” the authors wrote. “The hazards of dioxins on obesity should be emphasized, and additional studies are desirable to elucidate the potential mechanisms for dioxins on obesity in adults.”

SOURCE:

This study, led by Zhao-Xing Gao, Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University and Center for Big Data and Population Health of IHM, both in Hefei, China, was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

The cross-sectional nature of this study prevented the establishment of causal relationships between dioxins or DL-PCBs and obesity. This study relied on a small sample. Replacing chemical concentrations below the limit of detection with fixed values may have introduced bias.

DISCLOSURES:

This study was funded by grants from the National Natural Science Foundation of China, Research Fund of Anhui Institute of Translational Medicine, and Research Fund of Center for Big Data and Population Health of IHM. The authors declared no conflicts of interest.

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

December 31, 2024

This transcript has been edited for clarity. 

I’m Tamaan K. Osbourne-Roberts, family medicine physician and lifestyle medicine physician, here to discuss GLP-1 receptor agonist (RA) contraindications — the skinny on when not to prescribe. 

It can be hard not to think of GLP-1 RAs like Ozempic and Mounjaro as silver bullets, long-awaited miracle drugs that we should probably be putting in the water. And it’s true they have the potential to help a lot of people. 

However, there are definitely groups of patients who should not take these drugs or should take them with caution. They include the following: 

Patients with a family history of certain cancers. Given that GLP-1 RAs can increase the risk for thyroid cancer, patients with a personal or family history of medullary thyroid cancer or multiple endocrine neoplasia type 2 should not take these drugs.

Gut motility issues. Since one of the primary mechanisms of action for these drugs is to slow down the gut, patients with gastroparesis — diabetic or otherwise — or other gut motility issues should avoid these drugs. Patients with inflammatory bowel disease also should not use GLP-1 RAs. 

Pancreatitis. These medications can increase the risk for serious pancreatitis on their own, so use in patients who have had pancreatitis already is not recommended.

Renal impairment. An eGFR [estimated glomerular filtrationrate] below threshold, typically around 30 mL/min per 1.73 m², excludes GLP-1 RAs for some patients. Be certain to check the threshold for individual medications before prescribing. 

And finally, pregnancy. These drugs generally should not be used in pregnancy, and people of childbearing age with the ability to become pregnant should use contraception while taking these medications.

GLP-1 RAs are great medications and have the potential to revolutionize obesity medicine, but like all drugs, it’s important to use them safely. Knowing when not to prescribe them is an important step in ensuring patient safety and will help ensure they are available for those who need them.

Tamaan K. Osbourne-Roberts, MD, MBA, Denver, Colorado, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

December 31, 2024

This transcript has been edited for clarity. 

I’m Tamaan K. Osbourne-Roberts, family medicine physician and lifestyle medicine physician, here to discuss GLP-1 receptor agonist (RA) contraindications — the skinny on when not to prescribe. 

It can be hard not to think of GLP-1 RAs like Ozempic and Mounjaro as silver bullets, long-awaited miracle drugs that we should probably be putting in the water. And it’s true they have the potential to help a lot of people. 

However, there are definitely groups of patients who should not take these drugs or should take them with caution. They include the following: 

Patients with a family history of certain cancers. Given that GLP-1 RAs can increase the risk for thyroid cancer, patients with a personal or family history of medullary thyroid cancer or multiple endocrine neoplasia type 2 should not take these drugs.

Gut motility issues. Since one of the primary mechanisms of action for these drugs is to slow down the gut, patients with gastroparesis — diabetic or otherwise — or other gut motility issues should avoid these drugs. Patients with inflammatory bowel disease also should not use GLP-1 RAs. 

Pancreatitis. These medications can increase the risk for serious pancreatitis on their own, so use in patients who have had pancreatitis already is not recommended.

Renal impairment. An eGFR [estimated glomerular filtrationrate] below threshold, typically around 30 mL/min per 1.73 m², excludes GLP-1 RAs for some patients. Be certain to check the threshold for individual medications before prescribing. 

And finally, pregnancy. These drugs generally should not be used in pregnancy, and people of childbearing age with the ability to become pregnant should use contraception while taking these medications.

GLP-1 RAs are great medications and have the potential to revolutionize obesity medicine, but like all drugs, it’s important to use them safely. Knowing when not to prescribe them is an important step in ensuring patient safety and will help ensure they are available for those who need them.

Tamaan K. Osbourne-Roberts, MD, MBA, Denver, Colorado, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

December 31, 2024

This transcript has been edited for clarity. 

I’m Tamaan K. Osbourne-Roberts, family medicine physician and lifestyle medicine physician, here to discuss GLP-1 receptor agonist (RA) contraindications — the skinny on when not to prescribe. 

It can be hard not to think of GLP-1 RAs like Ozempic and Mounjaro as silver bullets, long-awaited miracle drugs that we should probably be putting in the water. And it’s true they have the potential to help a lot of people. 

However, there are definitely groups of patients who should not take these drugs or should take them with caution. They include the following: 

Patients with a family history of certain cancers. Given that GLP-1 RAs can increase the risk for thyroid cancer, patients with a personal or family history of medullary thyroid cancer or multiple endocrine neoplasia type 2 should not take these drugs.

Gut motility issues. Since one of the primary mechanisms of action for these drugs is to slow down the gut, patients with gastroparesis — diabetic or otherwise — or other gut motility issues should avoid these drugs. Patients with inflammatory bowel disease also should not use GLP-1 RAs. 

Pancreatitis. These medications can increase the risk for serious pancreatitis on their own, so use in patients who have had pancreatitis already is not recommended.

Renal impairment. An eGFR [estimated glomerular filtrationrate] below threshold, typically around 30 mL/min per 1.73 m², excludes GLP-1 RAs for some patients. Be certain to check the threshold for individual medications before prescribing. 

And finally, pregnancy. These drugs generally should not be used in pregnancy, and people of childbearing age with the ability to become pregnant should use contraception while taking these medications.

GLP-1 RAs are great medications and have the potential to revolutionize obesity medicine, but like all drugs, it’s important to use them safely. Knowing when not to prescribe them is an important step in ensuring patient safety and will help ensure they are available for those who need them.

Tamaan K. Osbourne-Roberts, MD, MBA, Denver, Colorado, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

More than two thirds of American counties don’t have an endocrinologist, according to a new analysis by GoodRx, a company that provides discount coupons for medications.

A total of 50 million people who live in the 2168 counties without a practicing endocrinologist are at a higher risk for poor health outcomes, according to the analysis. 

The author reported that individuals who live in endocrinology “deserts” are 12% more likely to die from endocrine-related conditions and have higher rates of diabetes, obesity, and stroke than those who live in counties where there are endocrinologists.

GoodRx’s finely detailed maps show that endocrinologists are clustered on the coasts and around major cities. Many counties have just a single endocrinologist and no pediatric endocrinologists.

Endocrinologists are not flocking to areas with a high type 2 diabetes prevalence — such as southern states, many parts of Texas, and counties with high concentrations of Native Americans or Alaskan Natives.

The maps speak volumes about disparities. In Sabine Parish, Louisiana, which shares a border with east Texas, the adult diabetes prevalence is 14%. The age-adjusted diabetes death rate is 52.6 per 100,000, in a population of 16,936 adults. There are no endocrinologists in that parish and one in a bordering parish.

In the entire state of Alaska, there are a total of two adult endocrinologists — one in Anchorage County and one in Fairbanks County — and two pediatric endocrinologists, both in Anchorage.

Buffalo County, South Dakota, which has no endocrinologists and is dominated by the Crow Creek Reservation, has a diabetes prevalence of 16.6% and a diabetes death rate of 143.3 per 100,000.

Connecticut’s Hartford County, however, has 69 adult endocrinologists and 9 pediatric endocrinologists. The adult diabetes prevalence is 0%, and the death rate is 26.3 per 100,000, in a population of 896,854.

To come up with its maps, GoodRx used population estimates from the 2024 Centers for Disease Control and Prevention (CDC) Places dataset and calculated adult diabetes rates and age-adjusted diabetes-related death rates per 100,000 using the 2024 CDC Places and CDC Wonder datasets. Data on the number of practicing endocrinologists came from HealthLink Dimensions, a company that provides databases for marketing purposes.

Robert Lash, MD, chief medical officer for The Endocrine Society, said that the GoodRx data are not especially new. Endocrinology “deserts” have existed for a decade or more, Lash said.

The GoodRx analysis concluded that a lack of endocrinologists in the “desert” counties directly led to higher death rates in those areas. “This is much more an association that it is causation,” countered Lash, noting that the deserts tend to align with healthcare professional shortage areas.

GoodRx also acknowledged the overlap and said that it could mean less access to primary care. In turn, “many patients may not even receive a diagnosis for endocrine-related conditions, let alone the specialized care they need,” wrote the analyst. “Preventable conditions like diabetes spiral into severe complications.”

Lash said seeking out a primary care doctor is one option for those without access to an endocrinologist. Telemedicine has also helped expand access, said Lash, adding that endocrinologists have been among the more frequent users.

Even so, the shortage of endocrinologists is an ongoing problem, he said. Only about 5000-6000 endocrinologists are actively practicing, estimates The Endocrine Society.

Fewer medical school graduates are choosing endocrinology, in part because of the lack of compensation, said Lash.

The society has begun a push to interest more students. Starting in 2024, The Society awarded grants to 10 medical schools to start endocrinology interest groups. The Medical School Engagement Program also sponsors two students for a VIP-type experience at the annual scientific meeting.

The hope is to boost interest in fellowships, which come after 3 years of internal medicine residency. Currently, there are only about 11 applicants for every 10 fellowship spots, said Lash.

It may be a while before the society’s experiment bears fruit. Those entering medical school in 2024 would not be eligible for fellowship until 2031, noted Lash.

“We’re in this for the long haul,” he said. “We know that this problem is not going to get solved overnight.”

A version of this article appeared on Medscape.com.

More than two thirds of American counties don’t have an endocrinologist, according to a new analysis by GoodRx, a company that provides discount coupons for medications.

A total of 50 million people who live in the 2168 counties without a practicing endocrinologist are at a higher risk for poor health outcomes, according to the analysis. 

The author reported that individuals who live in endocrinology “deserts” are 12% more likely to die from endocrine-related conditions and have higher rates of diabetes, obesity, and stroke than those who live in counties where there are endocrinologists.

GoodRx’s finely detailed maps show that endocrinologists are clustered on the coasts and around major cities. Many counties have just a single endocrinologist and no pediatric endocrinologists.

Endocrinologists are not flocking to areas with a high type 2 diabetes prevalence — such as southern states, many parts of Texas, and counties with high concentrations of Native Americans or Alaskan Natives.

The maps speak volumes about disparities. In Sabine Parish, Louisiana, which shares a border with east Texas, the adult diabetes prevalence is 14%. The age-adjusted diabetes death rate is 52.6 per 100,000, in a population of 16,936 adults. There are no endocrinologists in that parish and one in a bordering parish.

In the entire state of Alaska, there are a total of two adult endocrinologists — one in Anchorage County and one in Fairbanks County — and two pediatric endocrinologists, both in Anchorage.

Buffalo County, South Dakota, which has no endocrinologists and is dominated by the Crow Creek Reservation, has a diabetes prevalence of 16.6% and a diabetes death rate of 143.3 per 100,000.

Connecticut’s Hartford County, however, has 69 adult endocrinologists and 9 pediatric endocrinologists. The adult diabetes prevalence is 0%, and the death rate is 26.3 per 100,000, in a population of 896,854.

To come up with its maps, GoodRx used population estimates from the 2024 Centers for Disease Control and Prevention (CDC) Places dataset and calculated adult diabetes rates and age-adjusted diabetes-related death rates per 100,000 using the 2024 CDC Places and CDC Wonder datasets. Data on the number of practicing endocrinologists came from HealthLink Dimensions, a company that provides databases for marketing purposes.

Robert Lash, MD, chief medical officer for The Endocrine Society, said that the GoodRx data are not especially new. Endocrinology “deserts” have existed for a decade or more, Lash said.

The GoodRx analysis concluded that a lack of endocrinologists in the “desert” counties directly led to higher death rates in those areas. “This is much more an association that it is causation,” countered Lash, noting that the deserts tend to align with healthcare professional shortage areas.

GoodRx also acknowledged the overlap and said that it could mean less access to primary care. In turn, “many patients may not even receive a diagnosis for endocrine-related conditions, let alone the specialized care they need,” wrote the analyst. “Preventable conditions like diabetes spiral into severe complications.”

Lash said seeking out a primary care doctor is one option for those without access to an endocrinologist. Telemedicine has also helped expand access, said Lash, adding that endocrinologists have been among the more frequent users.

Even so, the shortage of endocrinologists is an ongoing problem, he said. Only about 5000-6000 endocrinologists are actively practicing, estimates The Endocrine Society.

Fewer medical school graduates are choosing endocrinology, in part because of the lack of compensation, said Lash.

The society has begun a push to interest more students. Starting in 2024, The Society awarded grants to 10 medical schools to start endocrinology interest groups. The Medical School Engagement Program also sponsors two students for a VIP-type experience at the annual scientific meeting.

The hope is to boost interest in fellowships, which come after 3 years of internal medicine residency. Currently, there are only about 11 applicants for every 10 fellowship spots, said Lash.

It may be a while before the society’s experiment bears fruit. Those entering medical school in 2024 would not be eligible for fellowship until 2031, noted Lash.

“We’re in this for the long haul,” he said. “We know that this problem is not going to get solved overnight.”

A version of this article appeared on Medscape.com.

More than two thirds of American counties don’t have an endocrinologist, according to a new analysis by GoodRx, a company that provides discount coupons for medications.

A total of 50 million people who live in the 2168 counties without a practicing endocrinologist are at a higher risk for poor health outcomes, according to the analysis. 

The author reported that individuals who live in endocrinology “deserts” are 12% more likely to die from endocrine-related conditions and have higher rates of diabetes, obesity, and stroke than those who live in counties where there are endocrinologists.

GoodRx’s finely detailed maps show that endocrinologists are clustered on the coasts and around major cities. Many counties have just a single endocrinologist and no pediatric endocrinologists.

Endocrinologists are not flocking to areas with a high type 2 diabetes prevalence — such as southern states, many parts of Texas, and counties with high concentrations of Native Americans or Alaskan Natives.

The maps speak volumes about disparities. In Sabine Parish, Louisiana, which shares a border with east Texas, the adult diabetes prevalence is 14%. The age-adjusted diabetes death rate is 52.6 per 100,000, in a population of 16,936 adults. There are no endocrinologists in that parish and one in a bordering parish.

In the entire state of Alaska, there are a total of two adult endocrinologists — one in Anchorage County and one in Fairbanks County — and two pediatric endocrinologists, both in Anchorage.

Buffalo County, South Dakota, which has no endocrinologists and is dominated by the Crow Creek Reservation, has a diabetes prevalence of 16.6% and a diabetes death rate of 143.3 per 100,000.

Connecticut’s Hartford County, however, has 69 adult endocrinologists and 9 pediatric endocrinologists. The adult diabetes prevalence is 0%, and the death rate is 26.3 per 100,000, in a population of 896,854.

To come up with its maps, GoodRx used population estimates from the 2024 Centers for Disease Control and Prevention (CDC) Places dataset and calculated adult diabetes rates and age-adjusted diabetes-related death rates per 100,000 using the 2024 CDC Places and CDC Wonder datasets. Data on the number of practicing endocrinologists came from HealthLink Dimensions, a company that provides databases for marketing purposes.

Robert Lash, MD, chief medical officer for The Endocrine Society, said that the GoodRx data are not especially new. Endocrinology “deserts” have existed for a decade or more, Lash said.

The GoodRx analysis concluded that a lack of endocrinologists in the “desert” counties directly led to higher death rates in those areas. “This is much more an association that it is causation,” countered Lash, noting that the deserts tend to align with healthcare professional shortage areas.

GoodRx also acknowledged the overlap and said that it could mean less access to primary care. In turn, “many patients may not even receive a diagnosis for endocrine-related conditions, let alone the specialized care they need,” wrote the analyst. “Preventable conditions like diabetes spiral into severe complications.”

Lash said seeking out a primary care doctor is one option for those without access to an endocrinologist. Telemedicine has also helped expand access, said Lash, adding that endocrinologists have been among the more frequent users.

Even so, the shortage of endocrinologists is an ongoing problem, he said. Only about 5000-6000 endocrinologists are actively practicing, estimates The Endocrine Society.

Fewer medical school graduates are choosing endocrinology, in part because of the lack of compensation, said Lash.

The society has begun a push to interest more students. Starting in 2024, The Society awarded grants to 10 medical schools to start endocrinology interest groups. The Medical School Engagement Program also sponsors two students for a VIP-type experience at the annual scientific meeting.

The hope is to boost interest in fellowships, which come after 3 years of internal medicine residency. Currently, there are only about 11 applicants for every 10 fellowship spots, said Lash.

It may be a while before the society’s experiment bears fruit. Those entering medical school in 2024 would not be eligible for fellowship until 2031, noted Lash.

“We’re in this for the long haul,” he said. “We know that this problem is not going to get solved overnight.”

A version of this article appeared on Medscape.com.

TOPLINE:

COVID-19 survivors show a more pronounced decline in kidney function than those who recover from pneumonia caused by other infections. This decline in kidney function, measured by the estimated glomerular filtration rate (eGFR), is particularly steep among individuals who require hospitalization for COVID-19.

METHODOLOGY:

• SARS-CoV-2, the virus that causes COVID-19, has been associated with acute kidney injury, but its potential impact on long-term kidney function remains unclear.
• Researchers investigated the decline in kidney function after COVID-19 vs pneumonia by including all hospitalized and nonhospitalized adults from the Stockholm Creatinine Measurements Project who had at least one eGFR measurement in the 2 years before a positive COVID-19 test result or pneumonia diagnosis.
• Overall, 134,565 individuals (median age, 51 years; 55.6% women) who had their first SARS-CoV-2 infection between February 2020 and January 2022 were included, of whom 13.3% required hospitalization within 28 days of their first positive COVID-19 test result.
• They were compared with 35,987 patients (median age, 71 years; 53.8% women) who were diagnosed with pneumonia between February 2018 and January 2020; 46.5% of them required hospitalization.
• The primary outcome measure focused on the mean annual change in eGFR slopes before and after each infection; the secondary outcome assessed was the annual change in postinfection eGFR slopes between COVID-19 and pneumonia cases.

TAKEAWAY:

• Before COVID-19, eGFR changes were minimal, but after the infection, the average decline increased to 4.1 (95% CI, 3.8-4.4) mL/min/1.73 m²; however, in the pneumonia cohort, a decline in eGFR was noted both before and after the infection.
• After COVID-19, the mean annual decline in eGFR was 3.4% (95% CI, 3.2%-3.5%), increasing to 5.4% (95% CI, 5.2%-5.6%) for those who were hospitalized.
• In contrast, the pneumonia group experienced an average annual decline of 2.3% (95% CI, 2.1%-2.5%) after the infection, which remained unchanged when analyzing only patients who were hospitalized.
• The risk for a 25% reduction in eGFR was higher in patients with COVID-19 than in those with pneumonia (hazard ratio [HR], 1.19; 95% CI, 1.07-1.34), with the risk being even higher among those who required hospitalization (HR, 1.42; 95% CI, 1.22-1.64).

IN PRACTICE:

“These findings help inform decisions regarding the need to monitor kidney function in survivors of COVID-19 and could have implications for policymakers regarding future healthcare planning and kidney service provision,” the authors wrote.

SOURCE:

This study was led by Viyaasan Mahalingasivam, MPhil, London School of Hygiene & Tropical Medicine, London, England. It was published online in JAMA Network Open.

LIMITATIONS:

This study lacked information on important confounders such as ethnicity and body mass index. The follow-up period was not long enough to fully evaluate the long-term association of COVID-19 with kidney function. Some individuals may have been misclassified as nonhospitalized if their first infection was mild and a subsequent infection required hospitalization.

DISCLOSURES:

This study was supported by grants from the National Institute for Health and Care Research, Njurfonden, Stig and Gunborg Westman Foundation, and the Swedish Research Council. One author reported receiving a Career Development Award from the National Institute for Health and Care Research, and another author reported receiving grants from Njurfonden, Stig and Gunborg Westman Foundation, Swedish Research Council, Swedish Heart Lung Foundation, and Region Stockholm during the conduct of the study.

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

TOPLINE:

COVID-19 survivors show a more pronounced decline in kidney function than those who recover from pneumonia caused by other infections. This decline in kidney function, measured by the estimated glomerular filtration rate (eGFR), is particularly steep among individuals who require hospitalization for COVID-19.

METHODOLOGY:

• SARS-CoV-2, the virus that causes COVID-19, has been associated with acute kidney injury, but its potential impact on long-term kidney function remains unclear.
• Researchers investigated the decline in kidney function after COVID-19 vs pneumonia by including all hospitalized and nonhospitalized adults from the Stockholm Creatinine Measurements Project who had at least one eGFR measurement in the 2 years before a positive COVID-19 test result or pneumonia diagnosis.
• Overall, 134,565 individuals (median age, 51 years; 55.6% women) who had their first SARS-CoV-2 infection between February 2020 and January 2022 were included, of whom 13.3% required hospitalization within 28 days of their first positive COVID-19 test result.
• They were compared with 35,987 patients (median age, 71 years; 53.8% women) who were diagnosed with pneumonia between February 2018 and January 2020; 46.5% of them required hospitalization.
• The primary outcome measure focused on the mean annual change in eGFR slopes before and after each infection; the secondary outcome assessed was the annual change in postinfection eGFR slopes between COVID-19 and pneumonia cases.

TAKEAWAY:

• Before COVID-19, eGFR changes were minimal, but after the infection, the average decline increased to 4.1 (95% CI, 3.8-4.4) mL/min/1.73 m²; however, in the pneumonia cohort, a decline in eGFR was noted both before and after the infection.
• After COVID-19, the mean annual decline in eGFR was 3.4% (95% CI, 3.2%-3.5%), increasing to 5.4% (95% CI, 5.2%-5.6%) for those who were hospitalized.
• In contrast, the pneumonia group experienced an average annual decline of 2.3% (95% CI, 2.1%-2.5%) after the infection, which remained unchanged when analyzing only patients who were hospitalized.
• The risk for a 25% reduction in eGFR was higher in patients with COVID-19 than in those with pneumonia (hazard ratio [HR], 1.19; 95% CI, 1.07-1.34), with the risk being even higher among those who required hospitalization (HR, 1.42; 95% CI, 1.22-1.64).

IN PRACTICE:

“These findings help inform decisions regarding the need to monitor kidney function in survivors of COVID-19 and could have implications for policymakers regarding future healthcare planning and kidney service provision,” the authors wrote.

SOURCE:

This study was led by Viyaasan Mahalingasivam, MPhil, London School of Hygiene & Tropical Medicine, London, England. It was published online in JAMA Network Open.

LIMITATIONS:

This study lacked information on important confounders such as ethnicity and body mass index. The follow-up period was not long enough to fully evaluate the long-term association of COVID-19 with kidney function. Some individuals may have been misclassified as nonhospitalized if their first infection was mild and a subsequent infection required hospitalization.

DISCLOSURES:

This study was supported by grants from the National Institute for Health and Care Research, Njurfonden, Stig and Gunborg Westman Foundation, and the Swedish Research Council. One author reported receiving a Career Development Award from the National Institute for Health and Care Research, and another author reported receiving grants from Njurfonden, Stig and Gunborg Westman Foundation, Swedish Research Council, Swedish Heart Lung Foundation, and Region Stockholm during the conduct of the study.

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

TOPLINE:

COVID-19 survivors show a more pronounced decline in kidney function than those who recover from pneumonia caused by other infections. This decline in kidney function, measured by the estimated glomerular filtration rate (eGFR), is particularly steep among individuals who require hospitalization for COVID-19.

METHODOLOGY:

• SARS-CoV-2, the virus that causes COVID-19, has been associated with acute kidney injury, but its potential impact on long-term kidney function remains unclear.
• Researchers investigated the decline in kidney function after COVID-19 vs pneumonia by including all hospitalized and nonhospitalized adults from the Stockholm Creatinine Measurements Project who had at least one eGFR measurement in the 2 years before a positive COVID-19 test result or pneumonia diagnosis.
• Overall, 134,565 individuals (median age, 51 years; 55.6% women) who had their first SARS-CoV-2 infection between February 2020 and January 2022 were included, of whom 13.3% required hospitalization within 28 days of their first positive COVID-19 test result.
• They were compared with 35,987 patients (median age, 71 years; 53.8% women) who were diagnosed with pneumonia between February 2018 and January 2020; 46.5% of them required hospitalization.
• The primary outcome measure focused on the mean annual change in eGFR slopes before and after each infection; the secondary outcome assessed was the annual change in postinfection eGFR slopes between COVID-19 and pneumonia cases.

TAKEAWAY:

• Before COVID-19, eGFR changes were minimal, but after the infection, the average decline increased to 4.1 (95% CI, 3.8-4.4) mL/min/1.73 m²; however, in the pneumonia cohort, a decline in eGFR was noted both before and after the infection.
• After COVID-19, the mean annual decline in eGFR was 3.4% (95% CI, 3.2%-3.5%), increasing to 5.4% (95% CI, 5.2%-5.6%) for those who were hospitalized.
• In contrast, the pneumonia group experienced an average annual decline of 2.3% (95% CI, 2.1%-2.5%) after the infection, which remained unchanged when analyzing only patients who were hospitalized.
• The risk for a 25% reduction in eGFR was higher in patients with COVID-19 than in those with pneumonia (hazard ratio [HR], 1.19; 95% CI, 1.07-1.34), with the risk being even higher among those who required hospitalization (HR, 1.42; 95% CI, 1.22-1.64).

IN PRACTICE:

“These findings help inform decisions regarding the need to monitor kidney function in survivors of COVID-19 and could have implications for policymakers regarding future healthcare planning and kidney service provision,” the authors wrote.

SOURCE:

This study was led by Viyaasan Mahalingasivam, MPhil, London School of Hygiene & Tropical Medicine, London, England. It was published online in JAMA Network Open.

LIMITATIONS:

This study lacked information on important confounders such as ethnicity and body mass index. The follow-up period was not long enough to fully evaluate the long-term association of COVID-19 with kidney function. Some individuals may have been misclassified as nonhospitalized if their first infection was mild and a subsequent infection required hospitalization.

DISCLOSURES:

This study was supported by grants from the National Institute for Health and Care Research, Njurfonden, Stig and Gunborg Westman Foundation, and the Swedish Research Council. One author reported receiving a Career Development Award from the National Institute for Health and Care Research, and another author reported receiving grants from Njurfonden, Stig and Gunborg Westman Foundation, Swedish Research Council, Swedish Heart Lung Foundation, and Region Stockholm during the conduct of the study.

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

The Food and Drug Administration (FDA) has approved the obesity treatment tirzepatide (Zepbound, Eli Lilly) for treating moderate to severe obstructive sleep apnea (OSA) in adults with obesity.

The new indication is for use in combination with reduced-calorie diet and increased physical activity. The once-weekly injectable is the first-ever drug treatment for OSA. Until now, OSA treatment has focused on mechanical support during sleep in the form of positive airway pressure (PAP) therapy. 

“Today’s approval marks the first drug treatment option for certain patients with obstructive sleep apnea,” said Sally Seymour, MD, director of the Division of Pulmonology, Allergy, and Critical Care in the FDA’s Center for Drug Evaluation and Research. “This is a major step forward for patients with obstructive sleep apnea.”

Excess weight is a major risk factor for OSA, in which the upper airways become blocked multiple times during sleep and obstruct breathing. The condition causes loud snoring, recurrent awakenings, and daytime sleepiness. It is also associated with cardiovascular disease.

Tirzepatide, a dual glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide receptor agonist, was initially approved with brand name Mounjaro in May 2022 for the treatment of type 2 diabetes, and as Zepbound for weight loss in November 2023.

The new OSA approval was based on two phase 3, double-blind randomized controlled trials, SURMOUNT-OSA, in patients with obesity and moderate to severe OSA, conducted at 60 sites in nine countries. Results from both were presented in June 2024 at the annual Scientific Sessions of the American Diabetes Association and were simultaneously published in The New England Journal of Medicine.

The first trial enrolled 469 participants who were unable or unwilling to use PAP therapy, while the second included 234 who had been using PAP for at least 3 months and planned to continue during the trial. In both, the participants randomly received either 10 mg or 15 mg of tirzepatide or placebo once weekly for 52 weeks.

At baseline, 65%-70% of participants had severe OSA, with more than 30 events/h on the apnea-hypopnea index (AHI) and a mean of 51.5 events/h. By 52 weeks, those randomized to tirzepatide had 27-30 fewer events/h, compared with 4-6 fewer events/h for those taking placebo. In addition, significantly more of those on tirzepatide achieved OSA remission or severity reduction to mild.

Those randomized to tirzepatide also averaged up to 20% weight loss, significantly more than with placebo. “The improvement in AHI in participants with OSA is likely related to body weight reduction with Zepbound,” according to an FDA statement.

Side effects of tirzepatide include nausea, diarrhea, vomiting, constipation, abdominal discomfort and pain, injection site reactions, fatigue, hypersensitivity reactions (typically fever and rash), burping, hair loss, and gastroesophageal reflux disease.

In an editorial accompanying The New England Journal of Medicine publication of the SURMOUNT-OSA results, Sanjay R. Patel, MD, wrote: “The potential incorporation of tirzepatide into treatment algorithms for obstructive sleep apnea should include consideration of the challenges of adherence to treatment and the imperative to address racial disparities in medical care.”

Patel, who is professor of medicine and epidemiology at the University of Pittsburgh in Pennsylvania, and medical director of the University of Pittsburgh Medical Center’s Comprehensive Sleep Disorders program, pointed out that suboptimal adherence to continuous PAP therapy has been a major limitation, but that adherence to the GLP-1 drug class has also been suboptimal.

“Although adherence to tirzepatide therapy in the SURMOUNT-OSA trial was high, real-world evidence suggests that nearly 50% of patients who begin treatment with a GLP-1 receptor agonist for obesity discontinue therapy within 12 months. Thus, it is likely that any incorporation of tirzepatide into treatment pathways for obstructive sleep apnea will not diminish the importance of long-term strategies to optimize adherence to treatment.”

Moreover, Patel noted, “racial disparities in the use of GLP-1 receptor agonists among patients with diabetes arouse concern that the addition of tirzepatide as a treatment option for obstructive sleep apnea without directly addressing policies relative to coverage of care will only further exacerbate already pervasive disparities in clinical care for obstructive sleep apnea.”

Patel reported consulting for Apnimed, Bayer Pharmaceuticals, Lilly USA, NovaResp Technologies, Philips Respironics, and Powell Mansfield. He is a fiduciary officer of BreathPA.

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

The Food and Drug Administration (FDA) has approved the obesity treatment tirzepatide (Zepbound, Eli Lilly) for treating moderate to severe obstructive sleep apnea (OSA) in adults with obesity.

The new indication is for use in combination with reduced-calorie diet and increased physical activity. The once-weekly injectable is the first-ever drug treatment for OSA. Until now, OSA treatment has focused on mechanical support during sleep in the form of positive airway pressure (PAP) therapy. 

“Today’s approval marks the first drug treatment option for certain patients with obstructive sleep apnea,” said Sally Seymour, MD, director of the Division of Pulmonology, Allergy, and Critical Care in the FDA’s Center for Drug Evaluation and Research. “This is a major step forward for patients with obstructive sleep apnea.”

Excess weight is a major risk factor for OSA, in which the upper airways become blocked multiple times during sleep and obstruct breathing. The condition causes loud snoring, recurrent awakenings, and daytime sleepiness. It is also associated with cardiovascular disease.

Tirzepatide, a dual glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide receptor agonist, was initially approved with brand name Mounjaro in May 2022 for the treatment of type 2 diabetes, and as Zepbound for weight loss in November 2023.

The new OSA approval was based on two phase 3, double-blind randomized controlled trials, SURMOUNT-OSA, in patients with obesity and moderate to severe OSA, conducted at 60 sites in nine countries. Results from both were presented in June 2024 at the annual Scientific Sessions of the American Diabetes Association and were simultaneously published in The New England Journal of Medicine.

The first trial enrolled 469 participants who were unable or unwilling to use PAP therapy, while the second included 234 who had been using PAP for at least 3 months and planned to continue during the trial. In both, the participants randomly received either 10 mg or 15 mg of tirzepatide or placebo once weekly for 52 weeks.

At baseline, 65%-70% of participants had severe OSA, with more than 30 events/h on the apnea-hypopnea index (AHI) and a mean of 51.5 events/h. By 52 weeks, those randomized to tirzepatide had 27-30 fewer events/h, compared with 4-6 fewer events/h for those taking placebo. In addition, significantly more of those on tirzepatide achieved OSA remission or severity reduction to mild.

Those randomized to tirzepatide also averaged up to 20% weight loss, significantly more than with placebo. “The improvement in AHI in participants with OSA is likely related to body weight reduction with Zepbound,” according to an FDA statement.

Side effects of tirzepatide include nausea, diarrhea, vomiting, constipation, abdominal discomfort and pain, injection site reactions, fatigue, hypersensitivity reactions (typically fever and rash), burping, hair loss, and gastroesophageal reflux disease.

In an editorial accompanying The New England Journal of Medicine publication of the SURMOUNT-OSA results, Sanjay R. Patel, MD, wrote: “The potential incorporation of tirzepatide into treatment algorithms for obstructive sleep apnea should include consideration of the challenges of adherence to treatment and the imperative to address racial disparities in medical care.”

Patel, who is professor of medicine and epidemiology at the University of Pittsburgh in Pennsylvania, and medical director of the University of Pittsburgh Medical Center’s Comprehensive Sleep Disorders program, pointed out that suboptimal adherence to continuous PAP therapy has been a major limitation, but that adherence to the GLP-1 drug class has also been suboptimal.

“Although adherence to tirzepatide therapy in the SURMOUNT-OSA trial was high, real-world evidence suggests that nearly 50% of patients who begin treatment with a GLP-1 receptor agonist for obesity discontinue therapy within 12 months. Thus, it is likely that any incorporation of tirzepatide into treatment pathways for obstructive sleep apnea will not diminish the importance of long-term strategies to optimize adherence to treatment.”

Moreover, Patel noted, “racial disparities in the use of GLP-1 receptor agonists among patients with diabetes arouse concern that the addition of tirzepatide as a treatment option for obstructive sleep apnea without directly addressing policies relative to coverage of care will only further exacerbate already pervasive disparities in clinical care for obstructive sleep apnea.”

Patel reported consulting for Apnimed, Bayer Pharmaceuticals, Lilly USA, NovaResp Technologies, Philips Respironics, and Powell Mansfield. He is a fiduciary officer of BreathPA.

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

The Food and Drug Administration (FDA) has approved the obesity treatment tirzepatide (Zepbound, Eli Lilly) for treating moderate to severe obstructive sleep apnea (OSA) in adults with obesity.

The new indication is for use in combination with reduced-calorie diet and increased physical activity. The once-weekly injectable is the first-ever drug treatment for OSA. Until now, OSA treatment has focused on mechanical support during sleep in the form of positive airway pressure (PAP) therapy. 

“Today’s approval marks the first drug treatment option for certain patients with obstructive sleep apnea,” said Sally Seymour, MD, director of the Division of Pulmonology, Allergy, and Critical Care in the FDA’s Center for Drug Evaluation and Research. “This is a major step forward for patients with obstructive sleep apnea.”

Excess weight is a major risk factor for OSA, in which the upper airways become blocked multiple times during sleep and obstruct breathing. The condition causes loud snoring, recurrent awakenings, and daytime sleepiness. It is also associated with cardiovascular disease.

Tirzepatide, a dual glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide receptor agonist, was initially approved with brand name Mounjaro in May 2022 for the treatment of type 2 diabetes, and as Zepbound for weight loss in November 2023.

The new OSA approval was based on two phase 3, double-blind randomized controlled trials, SURMOUNT-OSA, in patients with obesity and moderate to severe OSA, conducted at 60 sites in nine countries. Results from both were presented in June 2024 at the annual Scientific Sessions of the American Diabetes Association and were simultaneously published in The New England Journal of Medicine.

The first trial enrolled 469 participants who were unable or unwilling to use PAP therapy, while the second included 234 who had been using PAP for at least 3 months and planned to continue during the trial. In both, the participants randomly received either 10 mg or 15 mg of tirzepatide or placebo once weekly for 52 weeks.

At baseline, 65%-70% of participants had severe OSA, with more than 30 events/h on the apnea-hypopnea index (AHI) and a mean of 51.5 events/h. By 52 weeks, those randomized to tirzepatide had 27-30 fewer events/h, compared with 4-6 fewer events/h for those taking placebo. In addition, significantly more of those on tirzepatide achieved OSA remission or severity reduction to mild.

Those randomized to tirzepatide also averaged up to 20% weight loss, significantly more than with placebo. “The improvement in AHI in participants with OSA is likely related to body weight reduction with Zepbound,” according to an FDA statement.

Side effects of tirzepatide include nausea, diarrhea, vomiting, constipation, abdominal discomfort and pain, injection site reactions, fatigue, hypersensitivity reactions (typically fever and rash), burping, hair loss, and gastroesophageal reflux disease.

In an editorial accompanying The New England Journal of Medicine publication of the SURMOUNT-OSA results, Sanjay R. Patel, MD, wrote: “The potential incorporation of tirzepatide into treatment algorithms for obstructive sleep apnea should include consideration of the challenges of adherence to treatment and the imperative to address racial disparities in medical care.”

Patel, who is professor of medicine and epidemiology at the University of Pittsburgh in Pennsylvania, and medical director of the University of Pittsburgh Medical Center’s Comprehensive Sleep Disorders program, pointed out that suboptimal adherence to continuous PAP therapy has been a major limitation, but that adherence to the GLP-1 drug class has also been suboptimal.

“Although adherence to tirzepatide therapy in the SURMOUNT-OSA trial was high, real-world evidence suggests that nearly 50% of patients who begin treatment with a GLP-1 receptor agonist for obesity discontinue therapy within 12 months. Thus, it is likely that any incorporation of tirzepatide into treatment pathways for obstructive sleep apnea will not diminish the importance of long-term strategies to optimize adherence to treatment.”

Moreover, Patel noted, “racial disparities in the use of GLP-1 receptor agonists among patients with diabetes arouse concern that the addition of tirzepatide as a treatment option for obstructive sleep apnea without directly addressing policies relative to coverage of care will only further exacerbate already pervasive disparities in clinical care for obstructive sleep apnea.”

Patel reported consulting for Apnimed, Bayer Pharmaceuticals, Lilly USA, NovaResp Technologies, Philips Respironics, and Powell Mansfield. He is a fiduciary officer of BreathPA.

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

TOPLINE:

Long-term daily supplementation with moderate (1600 international units [IU]) or high (3200 IU) doses of vitamin D3 doesn’t reduce the risk for type 2 diabetes (T2D) among generally healthy older adults who have serum vitamin D levels sufficient for bone health.

 

METHODOLOGY:

• Observational studies have consistently linked low vitamin D levels with an increased risk for T2D, and short-term randomized trials have shown a protective effect of vitamin D supplementation for those with impaired glucose metabolism but not in populations of average risk-taking low doses.
• The Finnish Vitamin D Trial, conducted from 2012 to 2018 in generally healthy men (≥ 60 years) and women (≥ 65 years) without a history of cardiovascular disease or cancer, assessed the effects of 5 years of moderate and high vitamin D3 supplementation on the incidence of major chronic diseases.
• This analysis of T2D incidence included 2271 older participants (mean age, 68.2 years; 43.9% women) without self-reported use of diabetes medications at baseline.
• Participants were randomly assigned to receive placebo (n = 760), 1600 IU/d of vitamin D3 (n = 744), or 3200 IU/d of vitamin D3 (n = 767) and followed for a mean duration of 4.2 years, with T2D incidence assessed by diagnostic code from health registries.
• A representative subcohort of 505 participants underwent detailed investigations including blood sampling at months 0, 6, 12, and 24 for serum 25-hydroxyvitamin D3 [25(OH)D3], plasma glucose, and insulin concentrations.

TAKEAWAY:

• No significant difference in T2D incidence was observed between groups: Placebo (5.0%; 38 people), 1600 IU/d (4.2%; 31 people), and 3200 IU/d (4.7%; 36 people; P = .731 for trend), with no appreciable sex differences.
• When stratified by body mass index (BMI), a lower incidence of T2D with vitamin D supplementation was observed among those with a BMI < 25 (with wide CIs), but not among those with a higher BMI.
• In the subcohort, no significant differences in changes in plasma glucose, insulin concentrations, BMI, or waist circumference with vitamin D3 were observed between the three treatment groups during the 24-month follow-up (P ≥ .19).
• In an analysis excluding T2D from the first 2 years, researchers observed a potentially increased risk for T2D with increasing vitamin D dose (with wide CIs).

IN PRACTICE:

“Our findings do not suggest benefits of long-term moderate- or high-dose vitamin D3 supplementation for incidence of type 2 diabetes or glucose metabolism or body size among generally healthy older vitamin D–sufficient men and women who were not at high risk for type 2 diabetes,” the authors wrote.

SOURCE:

The study was led by Jyrki K. Virtanen, University of Eastern Finland, Institute of Public Health and Clinical Nutrition, Kuopio, and was published online in Diabetologia.

LIMITATIONS:

The study relied on national health registries to collect data on incident T2D events, which may have led to some T2D cases being missed. Data on serum 25(OH)D3 concentrations were available for the subcohort only, which prevented the investigation of whether vitamin D–deficient participants would have benefited from supplementation. The study was not specifically designed or powered for diabetes prevention, and information on participants’ diabetes history at baseline was not available. Wide CIs suggest uncertainty around some of the findings. Study participants were White and older, so caution is needed in generalizing results to groups of other ages, races and ethnicities, and different vitamin D levels.

DISCLOSURES:

The study received funding from the Academy of Finland, University of Eastern Finland, Juho Vainio Foundation, and other sources. Some authors reported receiving grants or travel support from pharmaceutical companies and certain institutions.

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:

Long-term daily supplementation with moderate (1600 international units [IU]) or high (3200 IU) doses of vitamin D3 doesn’t reduce the risk for type 2 diabetes (T2D) among generally healthy older adults who have serum vitamin D levels sufficient for bone health.

 

METHODOLOGY:

• Observational studies have consistently linked low vitamin D levels with an increased risk for T2D, and short-term randomized trials have shown a protective effect of vitamin D supplementation for those with impaired glucose metabolism but not in populations of average risk-taking low doses.
• The Finnish Vitamin D Trial, conducted from 2012 to 2018 in generally healthy men (≥ 60 years) and women (≥ 65 years) without a history of cardiovascular disease or cancer, assessed the effects of 5 years of moderate and high vitamin D3 supplementation on the incidence of major chronic diseases.
• This analysis of T2D incidence included 2271 older participants (mean age, 68.2 years; 43.9% women) without self-reported use of diabetes medications at baseline.
• Participants were randomly assigned to receive placebo (n = 760), 1600 IU/d of vitamin D3 (n = 744), or 3200 IU/d of vitamin D3 (n = 767) and followed for a mean duration of 4.2 years, with T2D incidence assessed by diagnostic code from health registries.
• A representative subcohort of 505 participants underwent detailed investigations including blood sampling at months 0, 6, 12, and 24 for serum 25-hydroxyvitamin D3 [25(OH)D3], plasma glucose, and insulin concentrations.

TAKEAWAY:

• No significant difference in T2D incidence was observed between groups: Placebo (5.0%; 38 people), 1600 IU/d (4.2%; 31 people), and 3200 IU/d (4.7%; 36 people; P = .731 for trend), with no appreciable sex differences.
• When stratified by body mass index (BMI), a lower incidence of T2D with vitamin D supplementation was observed among those with a BMI < 25 (with wide CIs), but not among those with a higher BMI.
• In the subcohort, no significant differences in changes in plasma glucose, insulin concentrations, BMI, or waist circumference with vitamin D3 were observed between the three treatment groups during the 24-month follow-up (P ≥ .19).
• In an analysis excluding T2D from the first 2 years, researchers observed a potentially increased risk for T2D with increasing vitamin D dose (with wide CIs).

IN PRACTICE:

“Our findings do not suggest benefits of long-term moderate- or high-dose vitamin D3 supplementation for incidence of type 2 diabetes or glucose metabolism or body size among generally healthy older vitamin D–sufficient men and women who were not at high risk for type 2 diabetes,” the authors wrote.

SOURCE:

The study was led by Jyrki K. Virtanen, University of Eastern Finland, Institute of Public Health and Clinical Nutrition, Kuopio, and was published online in Diabetologia.

LIMITATIONS:

The study relied on national health registries to collect data on incident T2D events, which may have led to some T2D cases being missed. Data on serum 25(OH)D3 concentrations were available for the subcohort only, which prevented the investigation of whether vitamin D–deficient participants would have benefited from supplementation. The study was not specifically designed or powered for diabetes prevention, and information on participants’ diabetes history at baseline was not available. Wide CIs suggest uncertainty around some of the findings. Study participants were White and older, so caution is needed in generalizing results to groups of other ages, races and ethnicities, and different vitamin D levels.

DISCLOSURES:

The study received funding from the Academy of Finland, University of Eastern Finland, Juho Vainio Foundation, and other sources. Some authors reported receiving grants or travel support from pharmaceutical companies and certain institutions.

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:

Long-term daily supplementation with moderate (1600 international units [IU]) or high (3200 IU) doses of vitamin D3 doesn’t reduce the risk for type 2 diabetes (T2D) among generally healthy older adults who have serum vitamin D levels sufficient for bone health.

 

METHODOLOGY:

• Observational studies have consistently linked low vitamin D levels with an increased risk for T2D, and short-term randomized trials have shown a protective effect of vitamin D supplementation for those with impaired glucose metabolism but not in populations of average risk-taking low doses.
• The Finnish Vitamin D Trial, conducted from 2012 to 2018 in generally healthy men (≥ 60 years) and women (≥ 65 years) without a history of cardiovascular disease or cancer, assessed the effects of 5 years of moderate and high vitamin D3 supplementation on the incidence of major chronic diseases.
• This analysis of T2D incidence included 2271 older participants (mean age, 68.2 years; 43.9% women) without self-reported use of diabetes medications at baseline.
• Participants were randomly assigned to receive placebo (n = 760), 1600 IU/d of vitamin D3 (n = 744), or 3200 IU/d of vitamin D3 (n = 767) and followed for a mean duration of 4.2 years, with T2D incidence assessed by diagnostic code from health registries.
• A representative subcohort of 505 participants underwent detailed investigations including blood sampling at months 0, 6, 12, and 24 for serum 25-hydroxyvitamin D3 [25(OH)D3], plasma glucose, and insulin concentrations.

TAKEAWAY:

• No significant difference in T2D incidence was observed between groups: Placebo (5.0%; 38 people), 1600 IU/d (4.2%; 31 people), and 3200 IU/d (4.7%; 36 people; P = .731 for trend), with no appreciable sex differences.
• When stratified by body mass index (BMI), a lower incidence of T2D with vitamin D supplementation was observed among those with a BMI < 25 (with wide CIs), but not among those with a higher BMI.
• In the subcohort, no significant differences in changes in plasma glucose, insulin concentrations, BMI, or waist circumference with vitamin D3 were observed between the three treatment groups during the 24-month follow-up (P ≥ .19).
• In an analysis excluding T2D from the first 2 years, researchers observed a potentially increased risk for T2D with increasing vitamin D dose (with wide CIs).

IN PRACTICE:

“Our findings do not suggest benefits of long-term moderate- or high-dose vitamin D3 supplementation for incidence of type 2 diabetes or glucose metabolism or body size among generally healthy older vitamin D–sufficient men and women who were not at high risk for type 2 diabetes,” the authors wrote.

SOURCE:

The study was led by Jyrki K. Virtanen, University of Eastern Finland, Institute of Public Health and Clinical Nutrition, Kuopio, and was published online in Diabetologia.

LIMITATIONS:

The study relied on national health registries to collect data on incident T2D events, which may have led to some T2D cases being missed. Data on serum 25(OH)D3 concentrations were available for the subcohort only, which prevented the investigation of whether vitamin D–deficient participants would have benefited from supplementation. The study was not specifically designed or powered for diabetes prevention, and information on participants’ diabetes history at baseline was not available. Wide CIs suggest uncertainty around some of the findings. Study participants were White and older, so caution is needed in generalizing results to groups of other ages, races and ethnicities, and different vitamin D levels.

DISCLOSURES:

The study received funding from the Academy of Finland, University of Eastern Finland, Juho Vainio Foundation, and other sources. Some authors reported receiving grants or travel support from pharmaceutical companies and certain institutions.

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.

Estimation of cardiovascular risk (CVR) in individuals living with type 1 diabetes (T1D) was a key topic presented by Sophie Borot, MD, from Besançon University Hospital, Besançon, France, at the 40th congress of the French Society of Endocrinology. Borot highlighted the complexities of this subject, outlining several factors that contribute to its challenges.

A Heterogeneous Disease

T1D is a highly heterogeneous condition, and the patients included in studies reflect this diversity:

• The impact of blood glucose levels on CVR changes depending on diabetes duration, its history, the frequency of hypoglycemic episodes, average A1c levels over several years, and the patient’s age at diagnosis.
• A T1D diagnosis from the 1980s involved different management strategies compared with a diagnosis today.
• Patient profiles also vary based on complications such as nephropathy or cardiac autonomic neuropathy.
• Diffuse and distal arterial damage in T1D leads to more subtle and delayed pathologic events than in type 2 diabetes (T2D).
• Most clinical studies assess CVR over 10 years, but a 20- or 30-year evaluation would be more relevant.
• Patients may share CVR factors with the general population (eg, family history, smoking, sedentary lifestyle, obesity, hypertension, or elevated low-density lipoprotein [LDL] levels), raising questions about possible overlap with metabolic syndrome.
• Study criteria differ, with a focus on outcomes such as cardiovascular death, major adverse cardiovascular events like myocardial infarction and stroke, or other endpoints.
• CVR is measured using either absolute or relative values, with varying units of measurement.

A Recent Awareness

The concept of CVR in T1D is relatively new. Until the publication of the prospective Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications study in 2005, it was believed that T1D control had no impact on CVR. However, follow-up results from the same cohort of 50,000 patients, published in 2022 after 30 years of observation, revealed that CVR was 20% higher in patients who received conventional hyperglycemia-targeted treatment than those undergoing intensive treatment. The CVR increases in conjunction with diabetes duration. The study also showed that even well-controlled glycemia in T1D carries CVR (primarily due to microangiopathy), and that the most critical factor for CVR is not A1c control but rather LDL cholesterol levels.

These findings were corroborated by a Danish prospective study, which demonstrated that while CVR increased in conjunction with the number of risk factors, it was 82% higher in patients with T1D than in a control group — even in the absence of risk factors.
 

Key Takeaways

At diagnosis, a fundamental difference exists between T1D and T2D in terms of the urgency to address CVR. In T2D, diabetes may have progressed for years before diagnosis, necessitating immediate CVR reduction efforts. In contrast, T1D is often diagnosed in younger patients with initially low CVR, raising questions about the optimal timing for interventions such as statin prescriptions.

Recommendations

The American Diabetes Association/European Association for the Study of Diabetes guidelines (2024) include the following recommendations:

For adults with T1D, treatment should mirror that for T2D:

• Between ages 20 and 40, statins are recommended if at least one CVR factor is present.
• For children 10 years of age or older with T1D, the LDL target is < 1.0 g/L. Statins are prescribed if LDL exceeds 1.6 g/L without CVR factors or 1.3 g/L with at least one CVR factor.

The European Society of Cardiology guidelines (2023) include the following:

• For the first time, a dedicated chapter addresses T1D. Like the American guidelines, routine statin use after age 40 is recommended.
• Before age 40, statins are prescribed if there is at least one CVR factor (microangiopathy) or a 10-year CVR ≥ 10% (based on a CVR calculator).

The International Society for Pediatric and Adolescent Diabetes guidelines (2022) recommend:

• For children 10 years of age or older, the LDL target is < 1.0 g/L. Statins are recommended if LDL exceeds 1.3 g/L.

CAC Score in High CVR

The French Society of Cardiology and the French-speaking Society of Diabetology recommend incorporating the coronary artery calcium (CAC) score to refine CVR classification in high-risk patients. For those without prior cardiovascular events, LDL targets vary based on CAC and age. For example:

• High-risk patients with a CAC of 0-10 are reclassified as moderate risk, with an LDL target of < 1 g/L.
• A CAC ≥ 400 indicates very high risk, warranting coronary exploration.
• Patients under 50 years of age with a CAC of 11-100 remain high risk, with an LDL target of 0.7 g/L.

Conclusion

CVR in patients with T1D remains challenging to define. However, it is essential to consider long-term outcomes, planning for 30 or 40 years into the future. This involves educating patients about the importance of prevention, even when reassuring numbers are seen in their youth.

This story was translated from Univadis France 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.

Estimation of cardiovascular risk (CVR) in individuals living with type 1 diabetes (T1D) was a key topic presented by Sophie Borot, MD, from Besançon University Hospital, Besançon, France, at the 40th congress of the French Society of Endocrinology. Borot highlighted the complexities of this subject, outlining several factors that contribute to its challenges.

A Heterogeneous Disease

T1D is a highly heterogeneous condition, and the patients included in studies reflect this diversity:

• The impact of blood glucose levels on CVR changes depending on diabetes duration, its history, the frequency of hypoglycemic episodes, average A1c levels over several years, and the patient’s age at diagnosis.
• A T1D diagnosis from the 1980s involved different management strategies compared with a diagnosis today.
• Patient profiles also vary based on complications such as nephropathy or cardiac autonomic neuropathy.
• Diffuse and distal arterial damage in T1D leads to more subtle and delayed pathologic events than in type 2 diabetes (T2D).
• Most clinical studies assess CVR over 10 years, but a 20- or 30-year evaluation would be more relevant.
• Patients may share CVR factors with the general population (eg, family history, smoking, sedentary lifestyle, obesity, hypertension, or elevated low-density lipoprotein [LDL] levels), raising questions about possible overlap with metabolic syndrome.
• Study criteria differ, with a focus on outcomes such as cardiovascular death, major adverse cardiovascular events like myocardial infarction and stroke, or other endpoints.
• CVR is measured using either absolute or relative values, with varying units of measurement.

A Recent Awareness

The concept of CVR in T1D is relatively new. Until the publication of the prospective Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications study in 2005, it was believed that T1D control had no impact on CVR. However, follow-up results from the same cohort of 50,000 patients, published in 2022 after 30 years of observation, revealed that CVR was 20% higher in patients who received conventional hyperglycemia-targeted treatment than those undergoing intensive treatment. The CVR increases in conjunction with diabetes duration. The study also showed that even well-controlled glycemia in T1D carries CVR (primarily due to microangiopathy), and that the most critical factor for CVR is not A1c control but rather LDL cholesterol levels.

These findings were corroborated by a Danish prospective study, which demonstrated that while CVR increased in conjunction with the number of risk factors, it was 82% higher in patients with T1D than in a control group — even in the absence of risk factors.
 

Key Takeaways

At diagnosis, a fundamental difference exists between T1D and T2D in terms of the urgency to address CVR. In T2D, diabetes may have progressed for years before diagnosis, necessitating immediate CVR reduction efforts. In contrast, T1D is often diagnosed in younger patients with initially low CVR, raising questions about the optimal timing for interventions such as statin prescriptions.

Recommendations

The American Diabetes Association/European Association for the Study of Diabetes guidelines (2024) include the following recommendations:

For adults with T1D, treatment should mirror that for T2D:

• Between ages 20 and 40, statins are recommended if at least one CVR factor is present.
• For children 10 years of age or older with T1D, the LDL target is < 1.0 g/L. Statins are prescribed if LDL exceeds 1.6 g/L without CVR factors or 1.3 g/L with at least one CVR factor.

The European Society of Cardiology guidelines (2023) include the following:

• For the first time, a dedicated chapter addresses T1D. Like the American guidelines, routine statin use after age 40 is recommended.
• Before age 40, statins are prescribed if there is at least one CVR factor (microangiopathy) or a 10-year CVR ≥ 10% (based on a CVR calculator).

The International Society for Pediatric and Adolescent Diabetes guidelines (2022) recommend:

• For children 10 years of age or older, the LDL target is < 1.0 g/L. Statins are recommended if LDL exceeds 1.3 g/L.

CAC Score in High CVR

The French Society of Cardiology and the French-speaking Society of Diabetology recommend incorporating the coronary artery calcium (CAC) score to refine CVR classification in high-risk patients. For those without prior cardiovascular events, LDL targets vary based on CAC and age. For example:

• High-risk patients with a CAC of 0-10 are reclassified as moderate risk, with an LDL target of < 1 g/L.
• A CAC ≥ 400 indicates very high risk, warranting coronary exploration.
• Patients under 50 years of age with a CAC of 11-100 remain high risk, with an LDL target of 0.7 g/L.

Conclusion

CVR in patients with T1D remains challenging to define. However, it is essential to consider long-term outcomes, planning for 30 or 40 years into the future. This involves educating patients about the importance of prevention, even when reassuring numbers are seen in their youth.

This story was translated from Univadis France 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.

Estimation of cardiovascular risk (CVR) in individuals living with type 1 diabetes (T1D) was a key topic presented by Sophie Borot, MD, from Besançon University Hospital, Besançon, France, at the 40th congress of the French Society of Endocrinology. Borot highlighted the complexities of this subject, outlining several factors that contribute to its challenges.

A Heterogeneous Disease

T1D is a highly heterogeneous condition, and the patients included in studies reflect this diversity:

• The impact of blood glucose levels on CVR changes depending on diabetes duration, its history, the frequency of hypoglycemic episodes, average A1c levels over several years, and the patient’s age at diagnosis.
• A T1D diagnosis from the 1980s involved different management strategies compared with a diagnosis today.
• Patient profiles also vary based on complications such as nephropathy or cardiac autonomic neuropathy.
• Diffuse and distal arterial damage in T1D leads to more subtle and delayed pathologic events than in type 2 diabetes (T2D).
• Most clinical studies assess CVR over 10 years, but a 20- or 30-year evaluation would be more relevant.
• Patients may share CVR factors with the general population (eg, family history, smoking, sedentary lifestyle, obesity, hypertension, or elevated low-density lipoprotein [LDL] levels), raising questions about possible overlap with metabolic syndrome.
• Study criteria differ, with a focus on outcomes such as cardiovascular death, major adverse cardiovascular events like myocardial infarction and stroke, or other endpoints.
• CVR is measured using either absolute or relative values, with varying units of measurement.

A Recent Awareness

The concept of CVR in T1D is relatively new. Until the publication of the prospective Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications study in 2005, it was believed that T1D control had no impact on CVR. However, follow-up results from the same cohort of 50,000 patients, published in 2022 after 30 years of observation, revealed that CVR was 20% higher in patients who received conventional hyperglycemia-targeted treatment than those undergoing intensive treatment. The CVR increases in conjunction with diabetes duration. The study also showed that even well-controlled glycemia in T1D carries CVR (primarily due to microangiopathy), and that the most critical factor for CVR is not A1c control but rather LDL cholesterol levels.

These findings were corroborated by a Danish prospective study, which demonstrated that while CVR increased in conjunction with the number of risk factors, it was 82% higher in patients with T1D than in a control group — even in the absence of risk factors.
 

Key Takeaways

At diagnosis, a fundamental difference exists between T1D and T2D in terms of the urgency to address CVR. In T2D, diabetes may have progressed for years before diagnosis, necessitating immediate CVR reduction efforts. In contrast, T1D is often diagnosed in younger patients with initially low CVR, raising questions about the optimal timing for interventions such as statin prescriptions.

Recommendations

The American Diabetes Association/European Association for the Study of Diabetes guidelines (2024) include the following recommendations:

For adults with T1D, treatment should mirror that for T2D:

• Between ages 20 and 40, statins are recommended if at least one CVR factor is present.
• For children 10 years of age or older with T1D, the LDL target is < 1.0 g/L. Statins are prescribed if LDL exceeds 1.6 g/L without CVR factors or 1.3 g/L with at least one CVR factor.

The European Society of Cardiology guidelines (2023) include the following:

• For the first time, a dedicated chapter addresses T1D. Like the American guidelines, routine statin use after age 40 is recommended.
• Before age 40, statins are prescribed if there is at least one CVR factor (microangiopathy) or a 10-year CVR ≥ 10% (based on a CVR calculator).

The International Society for Pediatric and Adolescent Diabetes guidelines (2022) recommend:

• For children 10 years of age or older, the LDL target is < 1.0 g/L. Statins are recommended if LDL exceeds 1.3 g/L.

CAC Score in High CVR

The French Society of Cardiology and the French-speaking Society of Diabetology recommend incorporating the coronary artery calcium (CAC) score to refine CVR classification in high-risk patients. For those without prior cardiovascular events, LDL targets vary based on CAC and age. For example:

• High-risk patients with a CAC of 0-10 are reclassified as moderate risk, with an LDL target of < 1 g/L.
• A CAC ≥ 400 indicates very high risk, warranting coronary exploration.
• Patients under 50 years of age with a CAC of 11-100 remain high risk, with an LDL target of 0.7 g/L.

Conclusion

CVR in patients with T1D remains challenging to define. However, it is essential to consider long-term outcomes, planning for 30 or 40 years into the future. This involves educating patients about the importance of prevention, even when reassuring numbers are seen in their youth.

This story was translated from Univadis France 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.

A new evidence-based guideline recommends prescribing metformin when initiating antipsychotic treatment to help mitigate weight gain in certain instances.

There is “good evidence” that metformin can prevent weight gain caused by antipsychotics, first author Aoife Carolan, MPharm, with Saint John of God Hospital and the Royal College of Surgeons, Dublin, Ireland, said in an interview.

“While there have been some general recommendations to use metformin for this purpose, until now, clear guidance on how to prevent this side effect of treatment has been lacking,” Carolan said. “At present, it is likely that metformin is underused and when used, it is likely to be started after the weight gain occurs. Therefore, this guideline will reflect a new practice for most clinicians.” 

The guideline was published online on December 9 in Schizophrenia Bulletin.

It offers three key recommendations:

• Initiate metformin when prescribing a high-risk weight-inducing antipsychotic, such as olanzapine or clozapine.
• Initiate metformin with a medium-risk antipsychotic (quetiapine, paliperidone, or risperidone) in patients with one or more cardiometabolic risk factors; in patients aged 10-25 years; or in patients with a body mass index (BMI) between 25 and 30.
• Initiate metformin with any antipsychotic if > 3% increase in baseline body weight is observed during the first 12 months of treatment.

The guideline authors noted that a recent Cochrane review of pharmacological interventions for the prevention of antipsychotic-induced weight gain showed that metformin is the only pharmacological agent that may be effective for preventing weight gain.

The review showed that starting metformin with antipsychotic medicines can reduce the extent of weight gain by 4.03 kg, compared with controls.

In terms of dose, the guideline recommends escalating from 500 mg daily to 500 mg twice daily over 2 weeks, followed by biweekly increases of 500 mg as tolerated up to 1 g twice daily at week 6.

Metformin should be discontinued if risks for lactic acidosis are present, or the condition is suspected; if BMI falls below 20; or if the antipsychotic medicine is discontinued. Metformin should be avoided where there is harmful use of alcohol.

While the guideline focused on metformin, it also recommends that, if available, glucagon-like peptide 1 (GLP-1) agonists, should be considered for patients with a BMI > 30, certain cardiometabolic diseases, or obstructive sleep apnea.

“At present, there is insufficient evidence for the risk benefit calculation for GLP-1 agonists as a preventative agent, but we will continue to monitor the evidence and update the guideline if it is needed,” Carolan said.

 

Experts Weigh In

This news organization asked several psychiatrists not involved in the guideline development for their thoughts on it.

Ipsit Vahia, MD, McLean Hospital, Belmont, and Harvard Medical School, Boston, both in Massachusetts, said: “There is an urgent need for evidence to guide treatments that can mitigate the metabolic side effects of antipsychotics.”

While metformin has shown some potential based on preliminary studies, this paper offers more substantial evidence to guide clinicians in using these medications and marks a significant step forward in clinical psychiatry, Vahia said.

Lynn DeLisi, MD, also with Harvard Medical School, emphasized that decisions about the use of metformin in patients taking antipsychotics should be made on an individual basis.

“It should not be used routinely with all antipsychotics, as metformin has its own set of side effects,” said DeLisi.

Xiaoduo Fan, MD, MPH, with UMass Chan Medical School, Worcester, Massachusetts, director of UMass MIND, noted that the evidence regarding metformin’s benefits to prevent or mitigate antipsychotic-induced weight gain and other metabolic disturbances is clear.

“It was somewhat controversial when psychiatrists started to prescribe metformin 15-20 years ago, but now many psychiatrists feel comfortable doing so. In many clinical settings, especially in academically affiliated hospitals, using metformin to address antipsychotic-associated metabolic concerns has become part of the routine practice,” said Fan.

“The guideline recommendations are generally consistent with what we have been doing clinically. The publication of the guideline may help promote wider use of metformin in the patient population we serve,” Fan added.

Fan also noted that a growing body of the literature has demonstrated the weight loss effect and other metabolic benefits of GLP-1 agonists. “Compared with metformin, GLP-1 agonists are more effective in inducing weight loss and mitigating cardiometabolic risks,” he said.

Fan said his group has completed a double-blind, placebo-controlled trial of 6-month weekly injection of the GLP-1 receptor agonist exenatide, as an adjunctive treatment in 70 patients with schizophrenia. “Preliminary data analysis suggests positive metabolic benefits,” he reported.

This research had no commercial funding. Carolan had no relevant disclosures. A complete list of disclosures for the guideline authors is available with the original article. DeLisi had no relevant disclosures. Fan had received research support from Alkermes, Eli Lilly, Janssen, Otsuka Pharmaceutical, Roche, Lundbeck, Boehringer Ingelheim, Neurocrine Biosciences, Intra-Cellular Therapies, Teva, and Bristol-Myers Squibb. He served on the BMJ Best Practice’s US Advisory Panel and as the contributor for the BMJ Best Practice — Schizophrenia Topic. Vahia had served as a consultant for Otsuka.

A version of this article appeared on Medscape.com.

A new evidence-based guideline recommends prescribing metformin when initiating antipsychotic treatment to help mitigate weight gain in certain instances.

There is “good evidence” that metformin can prevent weight gain caused by antipsychotics, first author Aoife Carolan, MPharm, with Saint John of God Hospital and the Royal College of Surgeons, Dublin, Ireland, said in an interview.

“While there have been some general recommendations to use metformin for this purpose, until now, clear guidance on how to prevent this side effect of treatment has been lacking,” Carolan said. “At present, it is likely that metformin is underused and when used, it is likely to be started after the weight gain occurs. Therefore, this guideline will reflect a new practice for most clinicians.” 

The guideline was published online on December 9 in Schizophrenia Bulletin.

It offers three key recommendations:

• Initiate metformin when prescribing a high-risk weight-inducing antipsychotic, such as olanzapine or clozapine.
• Initiate metformin with a medium-risk antipsychotic (quetiapine, paliperidone, or risperidone) in patients with one or more cardiometabolic risk factors; in patients aged 10-25 years; or in patients with a body mass index (BMI) between 25 and 30.
• Initiate metformin with any antipsychotic if > 3% increase in baseline body weight is observed during the first 12 months of treatment.

The guideline authors noted that a recent Cochrane review of pharmacological interventions for the prevention of antipsychotic-induced weight gain showed that metformin is the only pharmacological agent that may be effective for preventing weight gain.

The review showed that starting metformin with antipsychotic medicines can reduce the extent of weight gain by 4.03 kg, compared with controls.

In terms of dose, the guideline recommends escalating from 500 mg daily to 500 mg twice daily over 2 weeks, followed by biweekly increases of 500 mg as tolerated up to 1 g twice daily at week 6.

Metformin should be discontinued if risks for lactic acidosis are present, or the condition is suspected; if BMI falls below 20; or if the antipsychotic medicine is discontinued. Metformin should be avoided where there is harmful use of alcohol.

While the guideline focused on metformin, it also recommends that, if available, glucagon-like peptide 1 (GLP-1) agonists, should be considered for patients with a BMI > 30, certain cardiometabolic diseases, or obstructive sleep apnea.

“At present, there is insufficient evidence for the risk benefit calculation for GLP-1 agonists as a preventative agent, but we will continue to monitor the evidence and update the guideline if it is needed,” Carolan said.

 

Experts Weigh In

This news organization asked several psychiatrists not involved in the guideline development for their thoughts on it.

Ipsit Vahia, MD, McLean Hospital, Belmont, and Harvard Medical School, Boston, both in Massachusetts, said: “There is an urgent need for evidence to guide treatments that can mitigate the metabolic side effects of antipsychotics.”

While metformin has shown some potential based on preliminary studies, this paper offers more substantial evidence to guide clinicians in using these medications and marks a significant step forward in clinical psychiatry, Vahia said.

Lynn DeLisi, MD, also with Harvard Medical School, emphasized that decisions about the use of metformin in patients taking antipsychotics should be made on an individual basis.

“It should not be used routinely with all antipsychotics, as metformin has its own set of side effects,” said DeLisi.

Xiaoduo Fan, MD, MPH, with UMass Chan Medical School, Worcester, Massachusetts, director of UMass MIND, noted that the evidence regarding metformin’s benefits to prevent or mitigate antipsychotic-induced weight gain and other metabolic disturbances is clear.

“It was somewhat controversial when psychiatrists started to prescribe metformin 15-20 years ago, but now many psychiatrists feel comfortable doing so. In many clinical settings, especially in academically affiliated hospitals, using metformin to address antipsychotic-associated metabolic concerns has become part of the routine practice,” said Fan.

“The guideline recommendations are generally consistent with what we have been doing clinically. The publication of the guideline may help promote wider use of metformin in the patient population we serve,” Fan added.

Fan also noted that a growing body of the literature has demonstrated the weight loss effect and other metabolic benefits of GLP-1 agonists. “Compared with metformin, GLP-1 agonists are more effective in inducing weight loss and mitigating cardiometabolic risks,” he said.

Fan said his group has completed a double-blind, placebo-controlled trial of 6-month weekly injection of the GLP-1 receptor agonist exenatide, as an adjunctive treatment in 70 patients with schizophrenia. “Preliminary data analysis suggests positive metabolic benefits,” he reported.

This research had no commercial funding. Carolan had no relevant disclosures. A complete list of disclosures for the guideline authors is available with the original article. DeLisi had no relevant disclosures. Fan had received research support from Alkermes, Eli Lilly, Janssen, Otsuka Pharmaceutical, Roche, Lundbeck, Boehringer Ingelheim, Neurocrine Biosciences, Intra-Cellular Therapies, Teva, and Bristol-Myers Squibb. He served on the BMJ Best Practice’s US Advisory Panel and as the contributor for the BMJ Best Practice — Schizophrenia Topic. Vahia had served as a consultant for Otsuka.

A version of this article appeared on Medscape.com.

A new evidence-based guideline recommends prescribing metformin when initiating antipsychotic treatment to help mitigate weight gain in certain instances.

There is “good evidence” that metformin can prevent weight gain caused by antipsychotics, first author Aoife Carolan, MPharm, with Saint John of God Hospital and the Royal College of Surgeons, Dublin, Ireland, said in an interview.

“While there have been some general recommendations to use metformin for this purpose, until now, clear guidance on how to prevent this side effect of treatment has been lacking,” Carolan said. “At present, it is likely that metformin is underused and when used, it is likely to be started after the weight gain occurs. Therefore, this guideline will reflect a new practice for most clinicians.” 

The guideline was published online on December 9 in Schizophrenia Bulletin.

It offers three key recommendations:

• Initiate metformin when prescribing a high-risk weight-inducing antipsychotic, such as olanzapine or clozapine.
• Initiate metformin with a medium-risk antipsychotic (quetiapine, paliperidone, or risperidone) in patients with one or more cardiometabolic risk factors; in patients aged 10-25 years; or in patients with a body mass index (BMI) between 25 and 30.
• Initiate metformin with any antipsychotic if > 3% increase in baseline body weight is observed during the first 12 months of treatment.

The guideline authors noted that a recent Cochrane review of pharmacological interventions for the prevention of antipsychotic-induced weight gain showed that metformin is the only pharmacological agent that may be effective for preventing weight gain.

The review showed that starting metformin with antipsychotic medicines can reduce the extent of weight gain by 4.03 kg, compared with controls.

In terms of dose, the guideline recommends escalating from 500 mg daily to 500 mg twice daily over 2 weeks, followed by biweekly increases of 500 mg as tolerated up to 1 g twice daily at week 6.

Metformin should be discontinued if risks for lactic acidosis are present, or the condition is suspected; if BMI falls below 20; or if the antipsychotic medicine is discontinued. Metformin should be avoided where there is harmful use of alcohol.

While the guideline focused on metformin, it also recommends that, if available, glucagon-like peptide 1 (GLP-1) agonists, should be considered for patients with a BMI > 30, certain cardiometabolic diseases, or obstructive sleep apnea.

“At present, there is insufficient evidence for the risk benefit calculation for GLP-1 agonists as a preventative agent, but we will continue to monitor the evidence and update the guideline if it is needed,” Carolan said.

 

Experts Weigh In

This news organization asked several psychiatrists not involved in the guideline development for their thoughts on it.

Ipsit Vahia, MD, McLean Hospital, Belmont, and Harvard Medical School, Boston, both in Massachusetts, said: “There is an urgent need for evidence to guide treatments that can mitigate the metabolic side effects of antipsychotics.”

While metformin has shown some potential based on preliminary studies, this paper offers more substantial evidence to guide clinicians in using these medications and marks a significant step forward in clinical psychiatry, Vahia said.

Lynn DeLisi, MD, also with Harvard Medical School, emphasized that decisions about the use of metformin in patients taking antipsychotics should be made on an individual basis.

“It should not be used routinely with all antipsychotics, as metformin has its own set of side effects,” said DeLisi.

Xiaoduo Fan, MD, MPH, with UMass Chan Medical School, Worcester, Massachusetts, director of UMass MIND, noted that the evidence regarding metformin’s benefits to prevent or mitigate antipsychotic-induced weight gain and other metabolic disturbances is clear.

“It was somewhat controversial when psychiatrists started to prescribe metformin 15-20 years ago, but now many psychiatrists feel comfortable doing so. In many clinical settings, especially in academically affiliated hospitals, using metformin to address antipsychotic-associated metabolic concerns has become part of the routine practice,” said Fan.

“The guideline recommendations are generally consistent with what we have been doing clinically. The publication of the guideline may help promote wider use of metformin in the patient population we serve,” Fan added.

Fan also noted that a growing body of the literature has demonstrated the weight loss effect and other metabolic benefits of GLP-1 agonists. “Compared with metformin, GLP-1 agonists are more effective in inducing weight loss and mitigating cardiometabolic risks,” he said.

Fan said his group has completed a double-blind, placebo-controlled trial of 6-month weekly injection of the GLP-1 receptor agonist exenatide, as an adjunctive treatment in 70 patients with schizophrenia. “Preliminary data analysis suggests positive metabolic benefits,” he reported.

This research had no commercial funding. Carolan had no relevant disclosures. A complete list of disclosures for the guideline authors is available with the original article. DeLisi had no relevant disclosures. Fan had received research support from Alkermes, Eli Lilly, Janssen, Otsuka Pharmaceutical, Roche, Lundbeck, Boehringer Ingelheim, Neurocrine Biosciences, Intra-Cellular Therapies, Teva, and Bristol-Myers Squibb. He served on the BMJ Best Practice’s US Advisory Panel and as the contributor for the BMJ Best Practice — Schizophrenia Topic. Vahia had served as a consultant for Otsuka.

A version of this article appeared on Medscape.com.