Miriam E. Tucker

TOPLINE:

No significant association was found between the use of glucagon-like peptide 1 receptor agonists (GLP-1 RAs) and thyroid cancer over nearly 4 years.

METHODOLOGY:

• A cohort study using data from nationwide registers in Denmark, Norway, and Sweden between 2007 and 2021 included 145,410 patients who initiated GLP-1 RAs and 291,667 propensity score-matched patients initiating dipeptidyl peptidase 4 (DPP4) inhibitors as active comparators.
• Additional analysis included 111,744 who initiated GLP-1 RAs and 148,179 patients initiating sodium-glucose cotransporter 2 (SGLT2) inhibitors.
• Overall, mean follow-up time was 3.9 years, with 25% followed for more than 6 years.

TAKEAWAY:

• The most common individual GLP-1 RAs were liraglutide (57.3%) and semaglutide (32.9%).
• During follow-up, there were 76 incident thyroid cancer cases among GLP-1 RA users and 184 cases in DPP4 inhibitor users, giving incidence rates per 10,000 of 1.33 and 1.46, respectively, a nonsignificant difference (hazard ratio [HR], 0.93; 95% CI, 0.66-1.31).
• Papillary thyroid cancer was the most common thyroid cancer subtype, followed by follicular and medullary, with no significant increases in risk with GLP-1 RAs by cancer type, although the numbers were small.
• In the SGLT2 inhibitor comparison, there was also no significantly increased thyroid cancer risk for GLP-1 RAs (HR, 1.16; 95% CI, 0.65-2.05).

IN PRACTICE:

“Given the upper limit of the confidence interval, the findings are incompatible with more than a 31% increased relative risk of thyroid cancer. In absolute terms, this translates to no more than 0.36 excess cases per 10 000 person-years, a figure that should be interpreted against the background incidence of 1.46 per 10,000 person-years among the comparator group in the study populations.”

SOURCE:

This study was conducted by Björn Pasternak, MD, PhD, of the Karolinska Institutet, Stockholm, and colleagues. It was published online on April 10, 2024, in The BMJ.

LIMITATIONS:

Relatively short follow-up for cancer risk. Risk by individual GLP-1 RA not analyzed. Small event numbers. Observational, with potential for residual confounding and time-release bias.

DISCLOSURES:

The study was supported by grants from the Swedish Cancer Society and the Swedish Research Council. Dr. Pasternak was supported by a consolidator investigator grant from Karolinska Institutet. Some of the coauthors had industry disclosures.

A version of this article appeared on Medscape.com.

TOPLINE:

No significant association was found between the use of glucagon-like peptide 1 receptor agonists (GLP-1 RAs) and thyroid cancer over nearly 4 years.

METHODOLOGY:

• A cohort study using data from nationwide registers in Denmark, Norway, and Sweden between 2007 and 2021 included 145,410 patients who initiated GLP-1 RAs and 291,667 propensity score-matched patients initiating dipeptidyl peptidase 4 (DPP4) inhibitors as active comparators.
• Additional analysis included 111,744 who initiated GLP-1 RAs and 148,179 patients initiating sodium-glucose cotransporter 2 (SGLT2) inhibitors.
• Overall, mean follow-up time was 3.9 years, with 25% followed for more than 6 years.

TAKEAWAY:

• The most common individual GLP-1 RAs were liraglutide (57.3%) and semaglutide (32.9%).
• During follow-up, there were 76 incident thyroid cancer cases among GLP-1 RA users and 184 cases in DPP4 inhibitor users, giving incidence rates per 10,000 of 1.33 and 1.46, respectively, a nonsignificant difference (hazard ratio [HR], 0.93; 95% CI, 0.66-1.31).
• Papillary thyroid cancer was the most common thyroid cancer subtype, followed by follicular and medullary, with no significant increases in risk with GLP-1 RAs by cancer type, although the numbers were small.
• In the SGLT2 inhibitor comparison, there was also no significantly increased thyroid cancer risk for GLP-1 RAs (HR, 1.16; 95% CI, 0.65-2.05).

IN PRACTICE:

“Given the upper limit of the confidence interval, the findings are incompatible with more than a 31% increased relative risk of thyroid cancer. In absolute terms, this translates to no more than 0.36 excess cases per 10 000 person-years, a figure that should be interpreted against the background incidence of 1.46 per 10,000 person-years among the comparator group in the study populations.”

SOURCE:

This study was conducted by Björn Pasternak, MD, PhD, of the Karolinska Institutet, Stockholm, and colleagues. It was published online on April 10, 2024, in The BMJ.

LIMITATIONS:

Relatively short follow-up for cancer risk. Risk by individual GLP-1 RA not analyzed. Small event numbers. Observational, with potential for residual confounding and time-release bias.

DISCLOSURES:

The study was supported by grants from the Swedish Cancer Society and the Swedish Research Council. Dr. Pasternak was supported by a consolidator investigator grant from Karolinska Institutet. Some of the coauthors had industry disclosures.

A version of this article appeared on Medscape.com.

TOPLINE:

No significant association was found between the use of glucagon-like peptide 1 receptor agonists (GLP-1 RAs) and thyroid cancer over nearly 4 years.

METHODOLOGY:

• A cohort study using data from nationwide registers in Denmark, Norway, and Sweden between 2007 and 2021 included 145,410 patients who initiated GLP-1 RAs and 291,667 propensity score-matched patients initiating dipeptidyl peptidase 4 (DPP4) inhibitors as active comparators.
• Additional analysis included 111,744 who initiated GLP-1 RAs and 148,179 patients initiating sodium-glucose cotransporter 2 (SGLT2) inhibitors.
• Overall, mean follow-up time was 3.9 years, with 25% followed for more than 6 years.

TAKEAWAY:

• The most common individual GLP-1 RAs were liraglutide (57.3%) and semaglutide (32.9%).
• During follow-up, there were 76 incident thyroid cancer cases among GLP-1 RA users and 184 cases in DPP4 inhibitor users, giving incidence rates per 10,000 of 1.33 and 1.46, respectively, a nonsignificant difference (hazard ratio [HR], 0.93; 95% CI, 0.66-1.31).
• Papillary thyroid cancer was the most common thyroid cancer subtype, followed by follicular and medullary, with no significant increases in risk with GLP-1 RAs by cancer type, although the numbers were small.
• In the SGLT2 inhibitor comparison, there was also no significantly increased thyroid cancer risk for GLP-1 RAs (HR, 1.16; 95% CI, 0.65-2.05).

IN PRACTICE:

“Given the upper limit of the confidence interval, the findings are incompatible with more than a 31% increased relative risk of thyroid cancer. In absolute terms, this translates to no more than 0.36 excess cases per 10 000 person-years, a figure that should be interpreted against the background incidence of 1.46 per 10,000 person-years among the comparator group in the study populations.”

SOURCE:

This study was conducted by Björn Pasternak, MD, PhD, of the Karolinska Institutet, Stockholm, and colleagues. It was published online on April 10, 2024, in The BMJ.

LIMITATIONS:

Relatively short follow-up for cancer risk. Risk by individual GLP-1 RA not analyzed. Small event numbers. Observational, with potential for residual confounding and time-release bias.

DISCLOSURES:

The study was supported by grants from the Swedish Cancer Society and the Swedish Research Council. Dr. Pasternak was supported by a consolidator investigator grant from Karolinska Institutet. Some of the coauthors had industry disclosures.

A version of this article appeared on Medscape.com.

TOPLINE:

Trimethylamine N-oxide (TMAO) is a gut microbiota-derived metabolite generated by metabolism of dietary L-carnitine, primarily from red meat, and choline, from a variety of animal source foods. TMAO has been shown to cause kidney injury and tubulointerstitial fibrosis in experimental models.

In this study, TMAO was independently associated with higher risks for incident chronic kidney disease (CKD) and faster kidney function decline in humans.

The findings suggest that TMAO may be a novel risk factor and intervention target for CKD prevention and treatment.

METHODOLOGY:

• Study population was 10,564 participants from two community-based, prospective cohorts without baseline CKD (estimated glomerular filtration rate [eGFR] ≥ 60 mL/min/1.73 m²).
• Incident CKD was defined as eGFR decline ≥ 30% from baseline, resulting in eGFR < 60 mL/min/1.73 m².

TAKEAWAY:

• During a median 9.4 years, 979 incident CKD events occurred.
• Correlation between baseline TMAO and total meat intake was small but statistically significant (P = .08).
• After adjustments for sociodemographic, lifestyle, diet, and cardiovascular risk factors, higher plasma TMAO was associated with more than doubled CKD incidence (hazard ratio, 2.24 for top vs bottom quintile).
• Higher TMAO levels were also associated with greater annual eGFR decline (top vs bottom quintile eGFR change = −0.43 mL/min/1.73 m² per year.
• Compared with other major CKD risk factors, the association for the top vs bottom TMAO quintile (−0.43 mL/min/1.73 m² per year) was similar to that seen per 10 years of older age (−0.43) and presence of diabetes (−0.51), and larger than that seen comparing Black vs non-Black race (−0.28) and per 10 mm Hg systolic blood pressure (−0.16).

IN PRACTICE:

“TMAO levels are highly modifiable by both lifestyle-like diet and pharmacologic interventions. Besides using novel drugs to lower TMAO in patients, using dietary interventions to lower TMAO in the general population could be a cost-efficient and low-risk preventive strategy for chronic kidney disease development. ... These findings support future studies to investigate whether lifestyle and pharmacologic interventions to lower TMAO may prevent CKD development and progression.”

SOURCE:

The study was conducted by Meng Wang, PhD, of Tufts University, Boston, and colleagues and published online in the Journal of the American Society of Nephrology.

LIMITATIONS:

Observational design, can’t exclude residual confounding.

Inter-assay variability.

Use of International Classification of Diseases codes for hospitalization-based CKD, subject to reporting errors.

DISCLOSURES:

The study was supported by grants from the National Institutes of Health and an American Heart Association Postdoctoral Fellowship. Dr. Wang had no disclosures but several coauthors have patents on various diagnostics and/or industry disclosures.

A version of this article appeared on Medscape.com.

TOPLINE:

Trimethylamine N-oxide (TMAO) is a gut microbiota-derived metabolite generated by metabolism of dietary L-carnitine, primarily from red meat, and choline, from a variety of animal source foods. TMAO has been shown to cause kidney injury and tubulointerstitial fibrosis in experimental models.

In this study, TMAO was independently associated with higher risks for incident chronic kidney disease (CKD) and faster kidney function decline in humans.

The findings suggest that TMAO may be a novel risk factor and intervention target for CKD prevention and treatment.

METHODOLOGY:

• Study population was 10,564 participants from two community-based, prospective cohorts without baseline CKD (estimated glomerular filtration rate [eGFR] ≥ 60 mL/min/1.73 m²).
• Incident CKD was defined as eGFR decline ≥ 30% from baseline, resulting in eGFR < 60 mL/min/1.73 m².

TAKEAWAY:

• During a median 9.4 years, 979 incident CKD events occurred.
• Correlation between baseline TMAO and total meat intake was small but statistically significant (P = .08).
• After adjustments for sociodemographic, lifestyle, diet, and cardiovascular risk factors, higher plasma TMAO was associated with more than doubled CKD incidence (hazard ratio, 2.24 for top vs bottom quintile).
• Higher TMAO levels were also associated with greater annual eGFR decline (top vs bottom quintile eGFR change = −0.43 mL/min/1.73 m² per year.
• Compared with other major CKD risk factors, the association for the top vs bottom TMAO quintile (−0.43 mL/min/1.73 m² per year) was similar to that seen per 10 years of older age (−0.43) and presence of diabetes (−0.51), and larger than that seen comparing Black vs non-Black race (−0.28) and per 10 mm Hg systolic blood pressure (−0.16).

IN PRACTICE:

“TMAO levels are highly modifiable by both lifestyle-like diet and pharmacologic interventions. Besides using novel drugs to lower TMAO in patients, using dietary interventions to lower TMAO in the general population could be a cost-efficient and low-risk preventive strategy for chronic kidney disease development. ... These findings support future studies to investigate whether lifestyle and pharmacologic interventions to lower TMAO may prevent CKD development and progression.”

SOURCE:

The study was conducted by Meng Wang, PhD, of Tufts University, Boston, and colleagues and published online in the Journal of the American Society of Nephrology.

LIMITATIONS:

Observational design, can’t exclude residual confounding.

Inter-assay variability.

Use of International Classification of Diseases codes for hospitalization-based CKD, subject to reporting errors.

DISCLOSURES:

The study was supported by grants from the National Institutes of Health and an American Heart Association Postdoctoral Fellowship. Dr. Wang had no disclosures but several coauthors have patents on various diagnostics and/or industry disclosures.

A version of this article appeared on Medscape.com.

TOPLINE:

Trimethylamine N-oxide (TMAO) is a gut microbiota-derived metabolite generated by metabolism of dietary L-carnitine, primarily from red meat, and choline, from a variety of animal source foods. TMAO has been shown to cause kidney injury and tubulointerstitial fibrosis in experimental models.

In this study, TMAO was independently associated with higher risks for incident chronic kidney disease (CKD) and faster kidney function decline in humans.

The findings suggest that TMAO may be a novel risk factor and intervention target for CKD prevention and treatment.

METHODOLOGY:

• Study population was 10,564 participants from two community-based, prospective cohorts without baseline CKD (estimated glomerular filtration rate [eGFR] ≥ 60 mL/min/1.73 m²).
• Incident CKD was defined as eGFR decline ≥ 30% from baseline, resulting in eGFR < 60 mL/min/1.73 m².

TAKEAWAY:

• During a median 9.4 years, 979 incident CKD events occurred.
• Correlation between baseline TMAO and total meat intake was small but statistically significant (P = .08).
• After adjustments for sociodemographic, lifestyle, diet, and cardiovascular risk factors, higher plasma TMAO was associated with more than doubled CKD incidence (hazard ratio, 2.24 for top vs bottom quintile).
• Higher TMAO levels were also associated with greater annual eGFR decline (top vs bottom quintile eGFR change = −0.43 mL/min/1.73 m² per year.
• Compared with other major CKD risk factors, the association for the top vs bottom TMAO quintile (−0.43 mL/min/1.73 m² per year) was similar to that seen per 10 years of older age (−0.43) and presence of diabetes (−0.51), and larger than that seen comparing Black vs non-Black race (−0.28) and per 10 mm Hg systolic blood pressure (−0.16).

IN PRACTICE:

“TMAO levels are highly modifiable by both lifestyle-like diet and pharmacologic interventions. Besides using novel drugs to lower TMAO in patients, using dietary interventions to lower TMAO in the general population could be a cost-efficient and low-risk preventive strategy for chronic kidney disease development. ... These findings support future studies to investigate whether lifestyle and pharmacologic interventions to lower TMAO may prevent CKD development and progression.”

SOURCE:

The study was conducted by Meng Wang, PhD, of Tufts University, Boston, and colleagues and published online in the Journal of the American Society of Nephrology.

LIMITATIONS:

Observational design, can’t exclude residual confounding.

Inter-assay variability.

Use of International Classification of Diseases codes for hospitalization-based CKD, subject to reporting errors.

DISCLOSURES:

The study was supported by grants from the National Institutes of Health and an American Heart Association Postdoctoral Fellowship. Dr. Wang had no disclosures but several coauthors have patents on various diagnostics and/or industry disclosures.

A version of this article appeared on Medscape.com.

Statins raise the risks for increased glucose levels and the development of type 2 diabetes among people who don’t have it at baseline, but those risks are outweighed by the cardiovascular benefit, new data suggested.

The findings come from an analysis of individual participant data from a total of 23 randomized trials of statin therapy involving 154,664 individuals. In people without diabetes at baseline, statin therapy produces a dose-dependent increase in the risk for diabetes diagnosis, particularly among those whose glycemia marker levels are already at the diagnostic threshold.

Statins also tend to raise glucose levels in people who already have diabetes, but “the diabetes-related risks arising from the small changes in glycemia resulting from statin therapy are greatly outweighed by the benefits of statins on major vascular events when the direct clinical consequences of these outcomes are taken into consideration,” wrote the authors of the Cholesterol Treatment Trialists’ (CTT) Collaboration in their paper, published online in The Lancet Diabetes & Endocrinology.

Moreover, they say, “since the effect of statin therapy on measures of glycemia within an individual is small, there is likely to be little clinical benefit in measuring glucose concentrations and A1c values routinely after starting statin therapy with the aim of making comparisons to values taken before the initiation of a statin. However, people should continue to be screened for diabetes and associated risk factors and have their glycemic control monitored in accordance with current clinical guidelines.”

The CTT is co-led by Christina Reith, MBChB, PhD, and David Preiss, PhD, FRCPath, MRCP, both of the Nuffield Department of Population Health, University of Oxford, England.

In an accompanying editorial, Hertzel C. Gerstein, MD, and Marie Pigeyre, MD, PhD, both of McMaster University and Hamilton Health Sciences, Hamilton, Ontario, Canada, noted that the decreased absolute annual incidence of life-threatening cardiovascular outcomes with statins in people at high risk for type 2 diabetes “clearly exceeds the 0.1%-1.3% per year increased absolute incidence of type 2 diabetes.”

Dr. Gerstein and Dr. Pigeyre also said “these findings emphasize the importance of holistic care. As people at risk for cardiovascular outcomes are also at risk for type 2 diabetes, any prescription of a statin should be accompanied by promoting proven strategies to prevent or delay diabetes, such as modest weight reduction and increased physical activity. Finally, these findings emphasize the importance of always being alert for harmful adverse effects, even with the most beneficial and successful preventive therapies.”
 

Statins Raise Diabetes Risk, Glucose Levels Slightly

The meta-analysis of trials in the CTT Collaboration included individual participant data from 19 double-blind randomized, controlled trials with a median follow-up of 4.3 years comparing statins with placebo in a total of 123,940 participants, including 18% who had known type 2 diabetes at randomization. Also analyzed were another four double-blind trials of lower- vs higher-intensity statins involving a total of 30,724 participants followed for a median of 4.9 years, with 15% having diabetes at baseline.

In the 19 trials of low- or moderate-intensity statins vs placebo, statins resulted in a significant 10% increase in new-onset diabetes compared with placebo (rate ratio, 1.10), while high-intensity statins raised the risk by an also significant 36% (1.36). This translated to a mean absolute excess of 0.12% per year of treatment.

Compared with less intensive statin therapy, more intensive statin therapy resulted in a significant 10% proportional increase in new-onset diabetes (1.10), giving an absolute annual excess of 0.22%.

In the statin vs placebo trials, differences in A1c values from placebo were 0.06 percentage points higher for low- or moderate-intensity statins and 0.08 points greater for high-intensity statins.

Nearly two thirds (62%) of the excess cases of new-onset diabetes occurred among participants in the highest quarter of the baseline glycemia distribution for both low-intensity or moderate-intensity and high-intensity statin therapy.

And among participants who already had diabetes at baseline, there was a significant 10% relative increase in worsening glycemia (defined by adverse glycemic event, A1c increase of ≥ 0.5 percentage points, or medication escalation) with low- or moderate-intensity statins compared with placebo and a 24% relative increase in the high-intensity trials.

The Nuffield Department of Population Health has an explicit policy of not accepting any personal honoraria payments directly or indirectly from the pharmaceutical and food industries. It seeks reimbursement to the University of Oxford for the costs of travel and accommodation to participate in scientific meetings. Dr. Reith reported receiving funding to the University of Oxford from the UK National Institute for Health and Care Research Health Technology Assessment Programme and holding unpaid roles on the Clinical Data Interchange Standards Consortium as a board member and WHO as a scientific advisor. Dr. Preiss reported receiving funding to his research institution (but no personal funding) from Novartis for the ORION 4 trial of inclisiran, Novo Nordisk for the ASCEND PLUS trial of semaglutide, and Boehringer Ingelheim and Eli Lilly for the EMPA-KIDNEY trial and being a committee member for a National Institute for Health and Care Excellence guideline.

Dr. Gerstein holds the McMaster-Sanofi Population Health Institute Chair in Diabetes Research and Care. He reported research grants from Eli Lilly, AstraZeneca, Novo Nordisk, Hanmi, and Merck; continuing medical education grants to McMaster University from Eli Lilly, Abbott, Sanofi, Novo Nordisk, and Boehringer Ingelheim; honoraria for speaking from AstraZeneca, Eli Lilly, Novo Nordisk, DKSH, Zuellig Pharma, Sanofi, and Jiangsu Hanson; and consulting fees from Abbott, Eli Lilly, Novo Nordisk, Pfizer, Carbon Brand, Sanofi, Kowa, and Hanmi. Pigeyre had no disclosures.
 

A version of this article appeared on Medscape.com.

Statins raise the risks for increased glucose levels and the development of type 2 diabetes among people who don’t have it at baseline, but those risks are outweighed by the cardiovascular benefit, new data suggested.

The findings come from an analysis of individual participant data from a total of 23 randomized trials of statin therapy involving 154,664 individuals. In people without diabetes at baseline, statin therapy produces a dose-dependent increase in the risk for diabetes diagnosis, particularly among those whose glycemia marker levels are already at the diagnostic threshold.

Statins also tend to raise glucose levels in people who already have diabetes, but “the diabetes-related risks arising from the small changes in glycemia resulting from statin therapy are greatly outweighed by the benefits of statins on major vascular events when the direct clinical consequences of these outcomes are taken into consideration,” wrote the authors of the Cholesterol Treatment Trialists’ (CTT) Collaboration in their paper, published online in The Lancet Diabetes & Endocrinology.

Moreover, they say, “since the effect of statin therapy on measures of glycemia within an individual is small, there is likely to be little clinical benefit in measuring glucose concentrations and A1c values routinely after starting statin therapy with the aim of making comparisons to values taken before the initiation of a statin. However, people should continue to be screened for diabetes and associated risk factors and have their glycemic control monitored in accordance with current clinical guidelines.”

The CTT is co-led by Christina Reith, MBChB, PhD, and David Preiss, PhD, FRCPath, MRCP, both of the Nuffield Department of Population Health, University of Oxford, England.

In an accompanying editorial, Hertzel C. Gerstein, MD, and Marie Pigeyre, MD, PhD, both of McMaster University and Hamilton Health Sciences, Hamilton, Ontario, Canada, noted that the decreased absolute annual incidence of life-threatening cardiovascular outcomes with statins in people at high risk for type 2 diabetes “clearly exceeds the 0.1%-1.3% per year increased absolute incidence of type 2 diabetes.”

Dr. Gerstein and Dr. Pigeyre also said “these findings emphasize the importance of holistic care. As people at risk for cardiovascular outcomes are also at risk for type 2 diabetes, any prescription of a statin should be accompanied by promoting proven strategies to prevent or delay diabetes, such as modest weight reduction and increased physical activity. Finally, these findings emphasize the importance of always being alert for harmful adverse effects, even with the most beneficial and successful preventive therapies.”
 

Statins Raise Diabetes Risk, Glucose Levels Slightly

The meta-analysis of trials in the CTT Collaboration included individual participant data from 19 double-blind randomized, controlled trials with a median follow-up of 4.3 years comparing statins with placebo in a total of 123,940 participants, including 18% who had known type 2 diabetes at randomization. Also analyzed were another four double-blind trials of lower- vs higher-intensity statins involving a total of 30,724 participants followed for a median of 4.9 years, with 15% having diabetes at baseline.

In the 19 trials of low- or moderate-intensity statins vs placebo, statins resulted in a significant 10% increase in new-onset diabetes compared with placebo (rate ratio, 1.10), while high-intensity statins raised the risk by an also significant 36% (1.36). This translated to a mean absolute excess of 0.12% per year of treatment.

Compared with less intensive statin therapy, more intensive statin therapy resulted in a significant 10% proportional increase in new-onset diabetes (1.10), giving an absolute annual excess of 0.22%.

In the statin vs placebo trials, differences in A1c values from placebo were 0.06 percentage points higher for low- or moderate-intensity statins and 0.08 points greater for high-intensity statins.

Nearly two thirds (62%) of the excess cases of new-onset diabetes occurred among participants in the highest quarter of the baseline glycemia distribution for both low-intensity or moderate-intensity and high-intensity statin therapy.

And among participants who already had diabetes at baseline, there was a significant 10% relative increase in worsening glycemia (defined by adverse glycemic event, A1c increase of ≥ 0.5 percentage points, or medication escalation) with low- or moderate-intensity statins compared with placebo and a 24% relative increase in the high-intensity trials.

The Nuffield Department of Population Health has an explicit policy of not accepting any personal honoraria payments directly or indirectly from the pharmaceutical and food industries. It seeks reimbursement to the University of Oxford for the costs of travel and accommodation to participate in scientific meetings. Dr. Reith reported receiving funding to the University of Oxford from the UK National Institute for Health and Care Research Health Technology Assessment Programme and holding unpaid roles on the Clinical Data Interchange Standards Consortium as a board member and WHO as a scientific advisor. Dr. Preiss reported receiving funding to his research institution (but no personal funding) from Novartis for the ORION 4 trial of inclisiran, Novo Nordisk for the ASCEND PLUS trial of semaglutide, and Boehringer Ingelheim and Eli Lilly for the EMPA-KIDNEY trial and being a committee member for a National Institute for Health and Care Excellence guideline.

Dr. Gerstein holds the McMaster-Sanofi Population Health Institute Chair in Diabetes Research and Care. He reported research grants from Eli Lilly, AstraZeneca, Novo Nordisk, Hanmi, and Merck; continuing medical education grants to McMaster University from Eli Lilly, Abbott, Sanofi, Novo Nordisk, and Boehringer Ingelheim; honoraria for speaking from AstraZeneca, Eli Lilly, Novo Nordisk, DKSH, Zuellig Pharma, Sanofi, and Jiangsu Hanson; and consulting fees from Abbott, Eli Lilly, Novo Nordisk, Pfizer, Carbon Brand, Sanofi, Kowa, and Hanmi. Pigeyre had no disclosures.
 

A version of this article appeared on Medscape.com.

Statins raise the risks for increased glucose levels and the development of type 2 diabetes among people who don’t have it at baseline, but those risks are outweighed by the cardiovascular benefit, new data suggested.

The findings come from an analysis of individual participant data from a total of 23 randomized trials of statin therapy involving 154,664 individuals. In people without diabetes at baseline, statin therapy produces a dose-dependent increase in the risk for diabetes diagnosis, particularly among those whose glycemia marker levels are already at the diagnostic threshold.

Statins also tend to raise glucose levels in people who already have diabetes, but “the diabetes-related risks arising from the small changes in glycemia resulting from statin therapy are greatly outweighed by the benefits of statins on major vascular events when the direct clinical consequences of these outcomes are taken into consideration,” wrote the authors of the Cholesterol Treatment Trialists’ (CTT) Collaboration in their paper, published online in The Lancet Diabetes & Endocrinology.

Moreover, they say, “since the effect of statin therapy on measures of glycemia within an individual is small, there is likely to be little clinical benefit in measuring glucose concentrations and A1c values routinely after starting statin therapy with the aim of making comparisons to values taken before the initiation of a statin. However, people should continue to be screened for diabetes and associated risk factors and have their glycemic control monitored in accordance with current clinical guidelines.”

The CTT is co-led by Christina Reith, MBChB, PhD, and David Preiss, PhD, FRCPath, MRCP, both of the Nuffield Department of Population Health, University of Oxford, England.

In an accompanying editorial, Hertzel C. Gerstein, MD, and Marie Pigeyre, MD, PhD, both of McMaster University and Hamilton Health Sciences, Hamilton, Ontario, Canada, noted that the decreased absolute annual incidence of life-threatening cardiovascular outcomes with statins in people at high risk for type 2 diabetes “clearly exceeds the 0.1%-1.3% per year increased absolute incidence of type 2 diabetes.”

Dr. Gerstein and Dr. Pigeyre also said “these findings emphasize the importance of holistic care. As people at risk for cardiovascular outcomes are also at risk for type 2 diabetes, any prescription of a statin should be accompanied by promoting proven strategies to prevent or delay diabetes, such as modest weight reduction and increased physical activity. Finally, these findings emphasize the importance of always being alert for harmful adverse effects, even with the most beneficial and successful preventive therapies.”
 

Statins Raise Diabetes Risk, Glucose Levels Slightly

The meta-analysis of trials in the CTT Collaboration included individual participant data from 19 double-blind randomized, controlled trials with a median follow-up of 4.3 years comparing statins with placebo in a total of 123,940 participants, including 18% who had known type 2 diabetes at randomization. Also analyzed were another four double-blind trials of lower- vs higher-intensity statins involving a total of 30,724 participants followed for a median of 4.9 years, with 15% having diabetes at baseline.

In the 19 trials of low- or moderate-intensity statins vs placebo, statins resulted in a significant 10% increase in new-onset diabetes compared with placebo (rate ratio, 1.10), while high-intensity statins raised the risk by an also significant 36% (1.36). This translated to a mean absolute excess of 0.12% per year of treatment.

Compared with less intensive statin therapy, more intensive statin therapy resulted in a significant 10% proportional increase in new-onset diabetes (1.10), giving an absolute annual excess of 0.22%.

In the statin vs placebo trials, differences in A1c values from placebo were 0.06 percentage points higher for low- or moderate-intensity statins and 0.08 points greater for high-intensity statins.

Nearly two thirds (62%) of the excess cases of new-onset diabetes occurred among participants in the highest quarter of the baseline glycemia distribution for both low-intensity or moderate-intensity and high-intensity statin therapy.

And among participants who already had diabetes at baseline, there was a significant 10% relative increase in worsening glycemia (defined by adverse glycemic event, A1c increase of ≥ 0.5 percentage points, or medication escalation) with low- or moderate-intensity statins compared with placebo and a 24% relative increase in the high-intensity trials.

The Nuffield Department of Population Health has an explicit policy of not accepting any personal honoraria payments directly or indirectly from the pharmaceutical and food industries. It seeks reimbursement to the University of Oxford for the costs of travel and accommodation to participate in scientific meetings. Dr. Reith reported receiving funding to the University of Oxford from the UK National Institute for Health and Care Research Health Technology Assessment Programme and holding unpaid roles on the Clinical Data Interchange Standards Consortium as a board member and WHO as a scientific advisor. Dr. Preiss reported receiving funding to his research institution (but no personal funding) from Novartis for the ORION 4 trial of inclisiran, Novo Nordisk for the ASCEND PLUS trial of semaglutide, and Boehringer Ingelheim and Eli Lilly for the EMPA-KIDNEY trial and being a committee member for a National Institute for Health and Care Excellence guideline.

Dr. Gerstein holds the McMaster-Sanofi Population Health Institute Chair in Diabetes Research and Care. He reported research grants from Eli Lilly, AstraZeneca, Novo Nordisk, Hanmi, and Merck; continuing medical education grants to McMaster University from Eli Lilly, Abbott, Sanofi, Novo Nordisk, and Boehringer Ingelheim; honoraria for speaking from AstraZeneca, Eli Lilly, Novo Nordisk, DKSH, Zuellig Pharma, Sanofi, and Jiangsu Hanson; and consulting fees from Abbott, Eli Lilly, Novo Nordisk, Pfizer, Carbon Brand, Sanofi, Kowa, and Hanmi. Pigeyre had no disclosures.
 

A version of this article appeared on Medscape.com.

Among adults with type 2 diabetes (T2D) older than 65 years, a body mass index (BMI) in the moderate overweight category (26-28) appears to offer better protection from cardiovascular death than does a BMI in the “normal” range, new data suggested.

On the other hand, the study findings also suggest that the “normal” range of 23-25 is optimal for middle-aged adults with T2D.

The findings reflect a previously demonstrated phenomenon called the “obesity paradox,” in which older people with overweight may have better outcomes than leaner people due to factors such as bone loss, frailty, and nutritional deficits, study lead author Shaoyong Xu, of Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, China, told this news organization.

“In this era of population growth and aging, the question arises as to whether obesity or overweight can be beneficial in improving survival rates for older individuals with diabetes. This topic holds significant relevance due to the potential implications it has on weight management strategies for older adults. If overweight does not pose an increased risk of cardiovascular mortality, it may suggest that older individuals are not necessarily required to strive for weight loss to achieve so-called normal values.”

Moreover, Dr. Xu added, “inappropriate weight loss and being underweight could potentially elevate the risk of cardiovascular events, myocardial infarction, cerebral infarction, and all-cause mortality.”

Thus, he said, “while there are general guidelines recommending a BMI below 25, our findings suggest that personalized BMI targets may be more beneficial, particularly for different age groups and individuals with specific health conditions.”

Asked to comment, Ian J. Neeland, MD, director of cardiovascular prevention, University Hospitals Harrington Heart & Vascular Institute, Case Western Reserve University, Cleveland, Ohio, pointed out that older people who are underweight or in lower weight categories may be more likely to smoke or have undiagnosed cancer, or that “their BMI is not so much reflective of fat mass as of low muscle mass, or sarcopenia, and that is definitely a risk factor for adverse outcomes and risks. ... And those who have slightly higher BMIs may be maintaining muscle mass, even though they’re older, and therefore they have less risk.”

However, Dr. Neeland disagreed with the authors’ conclusions regarding “optimal” BMI. “Just because you have different risk categories based on BMI doesn’t mean that’s ‘optimal’ BMI. The way I would interpret this paper is that there’s an association of mildly overweight with better outcomes in adults who are over 65 with type 2 diabetes. We need to try to understand the mechanisms underlying that observation.”

Dr. Neeland advised that for an older person with T2D who has low muscle mass and frailty, “I wouldn’t recommend necessarily targeted weight loss in that person. But I would potentially recommend weight loss in addition to resistance training, muscle building, and endurance training, and therefore reducing fat mass. The goal would be not so much weight loss but reduction of body fat and maintaining and improving muscle health.”
 

U-Shaped Relationship Found Between Age, BMI, and Cardiovascular Disease (CVD) Risk

The data come from the UK Biobank, a population-based prospective cohort study of adults in the United Kingdom. A total of 22,874 participants with baseline T2D were included in the current study. Baseline surveys were conducted between 2006 and 2010, and follow-up was a median of 12.52 years. During that time, 891 people died of CVD.

Hazard ratios were adjusted for baseline variables including age, sex, smoking history, alcohol consumption, level of physical exercise, and history of CVDs.

Compared with people with BMI a < 25 in the group who were aged 65 years or younger, those with a BMI of 25.0-29.9 had a 13% higher risk for cardiovascular death. However, among those older than 65 years, a BMI between 25.0 and 29.9 was associated with an 18% lower risk.

A U-shaped relationship was found between BMI and the risk for cardiovascular death, with an optimal BMI cutoff of 24.0 in the under-65 group and a 27.0 cutoff in the older group. Ranges of 23.0-25.0 in the under-65 group and 26.0-28 in the older group were associated with the lowest cardiovascular risk.

In contrast, there was a linear relationship between both waist circumference and waist-to-height ratio and the risk for cardiovascular death, making those more direct measures of adiposity, Dr. Xu told this news organization.

“For clinicians, our data underscores the importance of considering age when assessing BMI targets for cardiovascular health. Personalized treatment plans that account for age-specific BMI cutoffs and other risk factors may enhance patient outcomes and reduce CVD mortality,” Dr. Xu said.

However, he added, “while these findings suggest an optimal BMI range, it is crucial to acknowledge that these cutoff points may vary based on gender, race, and other factors. Our future studies will validate these findings in different populations and attempt to explain the mechanism by which the optimal nodal values exist in people with diabetes at different ages.”

Dr. Neeland cautioned, “I think more work needs to be done in terms of not just identifying the risk differences but understanding why and how to better risk stratify individuals and do personalized medicine. I think that’s important, but you have to have good data to support the strategies you’re going to use. These data are observational, and they’re a good start, but they wouldn’t directly impact practice at this point.”

The data will be presented at the European Congress on Obesity taking place May 12-15 in Venice, Italy.

The authors declared no competing interests. Study funding came from several sources, including the Young Talents Project of Hubei Provincial Health Commission, China, Hubei Provincial Natural Science Foundation of China, the Science and Technology Research Key Project of the Education Department of Hubei Province China, and the Sanuo Diabetes Charity Foundation, China, and the Xiangyang Science and Technology Plan Project, China. Dr. Neeland is a speaker and/or consultant for Boehringer Ingelheim, Novo Nordisk, Bayer, and Eli Lilly and Company.
 

A version of this article appeared on Medscape.com.

Among adults with type 2 diabetes (T2D) older than 65 years, a body mass index (BMI) in the moderate overweight category (26-28) appears to offer better protection from cardiovascular death than does a BMI in the “normal” range, new data suggested.

On the other hand, the study findings also suggest that the “normal” range of 23-25 is optimal for middle-aged adults with T2D.

The findings reflect a previously demonstrated phenomenon called the “obesity paradox,” in which older people with overweight may have better outcomes than leaner people due to factors such as bone loss, frailty, and nutritional deficits, study lead author Shaoyong Xu, of Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, China, told this news organization.

“In this era of population growth and aging, the question arises as to whether obesity or overweight can be beneficial in improving survival rates for older individuals with diabetes. This topic holds significant relevance due to the potential implications it has on weight management strategies for older adults. If overweight does not pose an increased risk of cardiovascular mortality, it may suggest that older individuals are not necessarily required to strive for weight loss to achieve so-called normal values.”

Moreover, Dr. Xu added, “inappropriate weight loss and being underweight could potentially elevate the risk of cardiovascular events, myocardial infarction, cerebral infarction, and all-cause mortality.”

Thus, he said, “while there are general guidelines recommending a BMI below 25, our findings suggest that personalized BMI targets may be more beneficial, particularly for different age groups and individuals with specific health conditions.”

Asked to comment, Ian J. Neeland, MD, director of cardiovascular prevention, University Hospitals Harrington Heart & Vascular Institute, Case Western Reserve University, Cleveland, Ohio, pointed out that older people who are underweight or in lower weight categories may be more likely to smoke or have undiagnosed cancer, or that “their BMI is not so much reflective of fat mass as of low muscle mass, or sarcopenia, and that is definitely a risk factor for adverse outcomes and risks. ... And those who have slightly higher BMIs may be maintaining muscle mass, even though they’re older, and therefore they have less risk.”

However, Dr. Neeland disagreed with the authors’ conclusions regarding “optimal” BMI. “Just because you have different risk categories based on BMI doesn’t mean that’s ‘optimal’ BMI. The way I would interpret this paper is that there’s an association of mildly overweight with better outcomes in adults who are over 65 with type 2 diabetes. We need to try to understand the mechanisms underlying that observation.”

Dr. Neeland advised that for an older person with T2D who has low muscle mass and frailty, “I wouldn’t recommend necessarily targeted weight loss in that person. But I would potentially recommend weight loss in addition to resistance training, muscle building, and endurance training, and therefore reducing fat mass. The goal would be not so much weight loss but reduction of body fat and maintaining and improving muscle health.”
 

U-Shaped Relationship Found Between Age, BMI, and Cardiovascular Disease (CVD) Risk

The data come from the UK Biobank, a population-based prospective cohort study of adults in the United Kingdom. A total of 22,874 participants with baseline T2D were included in the current study. Baseline surveys were conducted between 2006 and 2010, and follow-up was a median of 12.52 years. During that time, 891 people died of CVD.

Hazard ratios were adjusted for baseline variables including age, sex, smoking history, alcohol consumption, level of physical exercise, and history of CVDs.

Compared with people with BMI a < 25 in the group who were aged 65 years or younger, those with a BMI of 25.0-29.9 had a 13% higher risk for cardiovascular death. However, among those older than 65 years, a BMI between 25.0 and 29.9 was associated with an 18% lower risk.

A U-shaped relationship was found between BMI and the risk for cardiovascular death, with an optimal BMI cutoff of 24.0 in the under-65 group and a 27.0 cutoff in the older group. Ranges of 23.0-25.0 in the under-65 group and 26.0-28 in the older group were associated with the lowest cardiovascular risk.

In contrast, there was a linear relationship between both waist circumference and waist-to-height ratio and the risk for cardiovascular death, making those more direct measures of adiposity, Dr. Xu told this news organization.

“For clinicians, our data underscores the importance of considering age when assessing BMI targets for cardiovascular health. Personalized treatment plans that account for age-specific BMI cutoffs and other risk factors may enhance patient outcomes and reduce CVD mortality,” Dr. Xu said.

However, he added, “while these findings suggest an optimal BMI range, it is crucial to acknowledge that these cutoff points may vary based on gender, race, and other factors. Our future studies will validate these findings in different populations and attempt to explain the mechanism by which the optimal nodal values exist in people with diabetes at different ages.”

Dr. Neeland cautioned, “I think more work needs to be done in terms of not just identifying the risk differences but understanding why and how to better risk stratify individuals and do personalized medicine. I think that’s important, but you have to have good data to support the strategies you’re going to use. These data are observational, and they’re a good start, but they wouldn’t directly impact practice at this point.”

The data will be presented at the European Congress on Obesity taking place May 12-15 in Venice, Italy.

The authors declared no competing interests. Study funding came from several sources, including the Young Talents Project of Hubei Provincial Health Commission, China, Hubei Provincial Natural Science Foundation of China, the Science and Technology Research Key Project of the Education Department of Hubei Province China, and the Sanuo Diabetes Charity Foundation, China, and the Xiangyang Science and Technology Plan Project, China. Dr. Neeland is a speaker and/or consultant for Boehringer Ingelheim, Novo Nordisk, Bayer, and Eli Lilly and Company.
 

A version of this article appeared on Medscape.com.

Among adults with type 2 diabetes (T2D) older than 65 years, a body mass index (BMI) in the moderate overweight category (26-28) appears to offer better protection from cardiovascular death than does a BMI in the “normal” range, new data suggested.

On the other hand, the study findings also suggest that the “normal” range of 23-25 is optimal for middle-aged adults with T2D.

The findings reflect a previously demonstrated phenomenon called the “obesity paradox,” in which older people with overweight may have better outcomes than leaner people due to factors such as bone loss, frailty, and nutritional deficits, study lead author Shaoyong Xu, of Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, China, told this news organization.

“In this era of population growth and aging, the question arises as to whether obesity or overweight can be beneficial in improving survival rates for older individuals with diabetes. This topic holds significant relevance due to the potential implications it has on weight management strategies for older adults. If overweight does not pose an increased risk of cardiovascular mortality, it may suggest that older individuals are not necessarily required to strive for weight loss to achieve so-called normal values.”

Moreover, Dr. Xu added, “inappropriate weight loss and being underweight could potentially elevate the risk of cardiovascular events, myocardial infarction, cerebral infarction, and all-cause mortality.”

Thus, he said, “while there are general guidelines recommending a BMI below 25, our findings suggest that personalized BMI targets may be more beneficial, particularly for different age groups and individuals with specific health conditions.”

Asked to comment, Ian J. Neeland, MD, director of cardiovascular prevention, University Hospitals Harrington Heart & Vascular Institute, Case Western Reserve University, Cleveland, Ohio, pointed out that older people who are underweight or in lower weight categories may be more likely to smoke or have undiagnosed cancer, or that “their BMI is not so much reflective of fat mass as of low muscle mass, or sarcopenia, and that is definitely a risk factor for adverse outcomes and risks. ... And those who have slightly higher BMIs may be maintaining muscle mass, even though they’re older, and therefore they have less risk.”

However, Dr. Neeland disagreed with the authors’ conclusions regarding “optimal” BMI. “Just because you have different risk categories based on BMI doesn’t mean that’s ‘optimal’ BMI. The way I would interpret this paper is that there’s an association of mildly overweight with better outcomes in adults who are over 65 with type 2 diabetes. We need to try to understand the mechanisms underlying that observation.”

Dr. Neeland advised that for an older person with T2D who has low muscle mass and frailty, “I wouldn’t recommend necessarily targeted weight loss in that person. But I would potentially recommend weight loss in addition to resistance training, muscle building, and endurance training, and therefore reducing fat mass. The goal would be not so much weight loss but reduction of body fat and maintaining and improving muscle health.”
 

U-Shaped Relationship Found Between Age, BMI, and Cardiovascular Disease (CVD) Risk

The data come from the UK Biobank, a population-based prospective cohort study of adults in the United Kingdom. A total of 22,874 participants with baseline T2D were included in the current study. Baseline surveys were conducted between 2006 and 2010, and follow-up was a median of 12.52 years. During that time, 891 people died of CVD.

Hazard ratios were adjusted for baseline variables including age, sex, smoking history, alcohol consumption, level of physical exercise, and history of CVDs.

Compared with people with BMI a < 25 in the group who were aged 65 years or younger, those with a BMI of 25.0-29.9 had a 13% higher risk for cardiovascular death. However, among those older than 65 years, a BMI between 25.0 and 29.9 was associated with an 18% lower risk.

A U-shaped relationship was found between BMI and the risk for cardiovascular death, with an optimal BMI cutoff of 24.0 in the under-65 group and a 27.0 cutoff in the older group. Ranges of 23.0-25.0 in the under-65 group and 26.0-28 in the older group were associated with the lowest cardiovascular risk.

In contrast, there was a linear relationship between both waist circumference and waist-to-height ratio and the risk for cardiovascular death, making those more direct measures of adiposity, Dr. Xu told this news organization.

“For clinicians, our data underscores the importance of considering age when assessing BMI targets for cardiovascular health. Personalized treatment plans that account for age-specific BMI cutoffs and other risk factors may enhance patient outcomes and reduce CVD mortality,” Dr. Xu said.

However, he added, “while these findings suggest an optimal BMI range, it is crucial to acknowledge that these cutoff points may vary based on gender, race, and other factors. Our future studies will validate these findings in different populations and attempt to explain the mechanism by which the optimal nodal values exist in people with diabetes at different ages.”

Dr. Neeland cautioned, “I think more work needs to be done in terms of not just identifying the risk differences but understanding why and how to better risk stratify individuals and do personalized medicine. I think that’s important, but you have to have good data to support the strategies you’re going to use. These data are observational, and they’re a good start, but they wouldn’t directly impact practice at this point.”

The data will be presented at the European Congress on Obesity taking place May 12-15 in Venice, Italy.

The authors declared no competing interests. Study funding came from several sources, including the Young Talents Project of Hubei Provincial Health Commission, China, Hubei Provincial Natural Science Foundation of China, the Science and Technology Research Key Project of the Education Department of Hubei Province China, and the Sanuo Diabetes Charity Foundation, China, and the Xiangyang Science and Technology Plan Project, China. Dr. Neeland is a speaker and/or consultant for Boehringer Ingelheim, Novo Nordisk, Bayer, and Eli Lilly and Company.
 

A version of this article appeared on Medscape.com.

Data derived from continuous glucose monitoring (CGM) devices can help guide nutrition management and insulin dosing in people with type 2 diabetes (T2D) in primary care settings.

At the Advanced Technologies & Treatments for Diabetes meeting, two experts from the International Diabetes Center – HealthPartners Institute, Minneapolis, offered advice for clinicians. Tara Ettestad, RN, LD, CDCES, program manager for care transformation and training at the center, shared tips for helping patients change their diet based on CGM readings. The center’s medical director Thomas Martens, MD, provided a systematic approach to using CGM to guide adjustment of insulin doses and other medications for insulin-treated patients with T2D.
 

CGM-Guided Nutrition: Focus on Sustainable Changes

With CGM, people with diabetes get real-time feedback about the impact of foods on their glucose levels. This can help them learn not just what they can’t eat but what they can eat, Ms. Ettestad pointed out.

“People want to know what to eat. This is the number-one question that people who are newly diagnosed with diabetes ask, and unfortunately, they typically hear what not to eat. No carbohydrates, no sugar, no white foods, no sweets. This can be really disheartening and confusing for many. We should be focusing on sustainable changes to help improve diets,” she said.

She added, “Not everyone can see a dietitian, but all clinicians can help provide evidence-based nutrition guidance.”

When guiding patients, it’s important to focus on the four “core concepts” outlined in the American Diabetes Association’s nutrition consensus report:

• Emphasize nonstarchy vegetables
• Minimize added sugars and refined grains
• Eat more whole foods, less highly processed foods
• Replace sugar-sweetened beverages with water as often as possible

With CGM, patients can see the differences in response to refined carbs (wheat, rice, and potato), sugars (sucrose, fructose, and glucose), and resistant starches (whole grains, fruits, and legumes). Typically, glucose responses are steeper and higher for the first two compared to resistant starches.

CGM can also show the effects of eating fat and protein, in that they can delay glucose responses to meals even with the same carbohydrate content, Ms. Ettestad said.

It’s important to remind patients that although one goal of using CGM is to reduce post-meal glucose spikes, eating a lot of high-saturated fat, high-calorie foods isn’t the healthful way to do it. “What’s really important when we’re using CGM to help guide nutrition is remembering nutrition quality and what can be good for glucose is not always good for our overall health,” Ms. Ettestad stressed.

She provided these further tips:

• Pick one meal at a time to focus on. Collaborate with patients to see what changes they are able and willing to make. For example, rather than entirely giving up rice or noodles at dinner, try eating less of those and adding more vegetables.
• Suggest that patients keep a food log or use a tracking app so that the source of specific glucose patterns can be identified and addressed.
• Show patients how to check their time in range (TIR) on their mobile device or reader each week so they can see big-picture results of their changes. “This can be really motivating for people to see,” she said.
• Remind people that glucose rises with meals. This seems obvious but may not be to those newly diagnosed, she pointed out.
• Educate patients on glucose targets and explain that other factors such as stress and activity can influence glucose levels.
• Focus on the positive. “What have you been learning about how your meals and beverages affect your glucose?”
• Help guide patients toward better diet quality, even when TIR is a goal, using the four core concepts.
• Encourage curiosity, such as by experimenting with portions, timing, or food order. “What if you try eating nonstarchy foods first?”
• Before adjusting a medication dose, consider asking if the patient is willing to make a nutrition change. “Every visit is an opportunity!”

Adjusting Insulin With the Help of CGM: Focus on Four Patient Subgroups

Dr. Martens noted that about a quarter of people with T2D will require insulin treatment, despite increasing use of sodium-glucose cotransporter 2 (SGLT2) inhibitors and glucagon-like peptide 1 (GLP-1) receptor agonists. And even when insulin is used as a “salvage therapy” in T2D, about two thirds of those individuals still struggle to achieve an A1c below 7% with or without other glucose-lowering medications, he noted.

“So, we have this huge population with type 2 diabetes who have limited access to endocrinology, and advanced insulin delivery devices are not yet available for them. Can better use of CGM drive improvements in care?”

He pointed to MOBILE, a randomized clinical trial, which showed that CGM use resulted in significantly improved A1c at 8 months compared with fingerstick monitoring among adults with T2D taking long-acting insulin alone without premeal insulin. However, TIR was still just 59% (vs 43% with fingerstick testing), suggesting room for improvement.

“This could have been much, much better…Rapid interpretation isn’t really enough. We need to move from interpretation into action,” Dr. Martens said.

His team recently developed a program called “CGM Clinician Guided Management (CCGM)” aimed at primary care that encourages the following principles:

• Appropriate movement toward the safer “high value” noninsulin therapies, that is, GLP-1 agonists and SGLT2 inhibitors.
• Appropriate insulin titration.
• Appropriate cycle time in titration, that is, accelerating more rapidly when one dose isn’t working. “That’s the Achilles heel of primary care,” he noted.
• Quick identification of when the limits of basal insulin therapy have been reached.
• Team-based management for difficult situations and for individuals on multiple daily injections and mealtime insulin regimens. “This is a group that really struggles…in primary care settings,” he noted.

The following three steps are based on published T2D management guidelines:

• Step 1: If the patient has atherosclerotic cardiovascular disease, start with either an SGLT2 inhibitor or GLP-1 agonist. For those with congestive heart failure and/or chronic kidney disease, SGLT2 inhibitors are indicated.
• Step 2: Is the patient on sulfonylurea? Consider eliminating it before moving to CGM-based insulin titration.
• Step 3: Was there a change in therapy based on steps 1 or 2? If not, move to CGM-guided insulin titration. If yes, wait 2-4 weeks to see the impact of therapy change before moving on.

The program categorizes patients into one of four groups based on CGM data, with respective management approaches:

• Category 1: TIR > 70%, time below range (TBR) < 3%: Doing well, keep on going!
• Category 2: TIR > 70%, TBR ≥ 3%: Too much hypoglycemia, need to decrease therapy. Stop sulfonylureas, and if TBR > 10%, also decrease basal insulin dose.
• Category 3: TIR < 70%, TBR < 3%: Too much hyperglycemia — increase therapy.
• Category 4: TIR < 70%, TBR ≥ 3%: This is the toughest category. Fix or advance therapy. These patients should be either referred to a diabetes care and education specialist (formerly known as “diabetes educators”) to troubleshoot their regimens or have their therapy advanced to multiple daily injections. The hypoglycemia should be addressed first for safety, then the hyperglycemia.

“We hope that CCGM is going to be the translation of CGM data into action in primary care, where we struggle with action and inaction,” Dr. Martens said. It’s expected to be posted on the IDC website soon.

Ms. Ettestad’s employer received educational grant funds from Abbott Diabetes Care and Sanofi-Aventis Groupe. She also worked as a product trainer with Tandem Diabetes Care. She is employed by nonprofit International Diabetes Center – HealthPartners Institute and received no personal income or honoraria from these activities. Dr. Martens’ employer received funds on his behalf for research and speaking support from Dexcom, Abbott Diabetes Care, Medtronic, Insulet, Tandem, Sanofi, Lilly, and Novo Nordisk and for consulting from Sanofi and Lilly. He is employed by nonprofit HealthPartners Institute – International Diabetes Center and received no personal income or honoraria from these activities.

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

Data derived from continuous glucose monitoring (CGM) devices can help guide nutrition management and insulin dosing in people with type 2 diabetes (T2D) in primary care settings.

At the Advanced Technologies & Treatments for Diabetes meeting, two experts from the International Diabetes Center – HealthPartners Institute, Minneapolis, offered advice for clinicians. Tara Ettestad, RN, LD, CDCES, program manager for care transformation and training at the center, shared tips for helping patients change their diet based on CGM readings. The center’s medical director Thomas Martens, MD, provided a systematic approach to using CGM to guide adjustment of insulin doses and other medications for insulin-treated patients with T2D.
 

CGM-Guided Nutrition: Focus on Sustainable Changes

With CGM, people with diabetes get real-time feedback about the impact of foods on their glucose levels. This can help them learn not just what they can’t eat but what they can eat, Ms. Ettestad pointed out.

“People want to know what to eat. This is the number-one question that people who are newly diagnosed with diabetes ask, and unfortunately, they typically hear what not to eat. No carbohydrates, no sugar, no white foods, no sweets. This can be really disheartening and confusing for many. We should be focusing on sustainable changes to help improve diets,” she said.

She added, “Not everyone can see a dietitian, but all clinicians can help provide evidence-based nutrition guidance.”

When guiding patients, it’s important to focus on the four “core concepts” outlined in the American Diabetes Association’s nutrition consensus report:

• Emphasize nonstarchy vegetables
• Minimize added sugars and refined grains
• Eat more whole foods, less highly processed foods
• Replace sugar-sweetened beverages with water as often as possible

With CGM, patients can see the differences in response to refined carbs (wheat, rice, and potato), sugars (sucrose, fructose, and glucose), and resistant starches (whole grains, fruits, and legumes). Typically, glucose responses are steeper and higher for the first two compared to resistant starches.

CGM can also show the effects of eating fat and protein, in that they can delay glucose responses to meals even with the same carbohydrate content, Ms. Ettestad said.

It’s important to remind patients that although one goal of using CGM is to reduce post-meal glucose spikes, eating a lot of high-saturated fat, high-calorie foods isn’t the healthful way to do it. “What’s really important when we’re using CGM to help guide nutrition is remembering nutrition quality and what can be good for glucose is not always good for our overall health,” Ms. Ettestad stressed.

She provided these further tips:

• Pick one meal at a time to focus on. Collaborate with patients to see what changes they are able and willing to make. For example, rather than entirely giving up rice or noodles at dinner, try eating less of those and adding more vegetables.
• Suggest that patients keep a food log or use a tracking app so that the source of specific glucose patterns can be identified and addressed.
• Show patients how to check their time in range (TIR) on their mobile device or reader each week so they can see big-picture results of their changes. “This can be really motivating for people to see,” she said.
• Remind people that glucose rises with meals. This seems obvious but may not be to those newly diagnosed, she pointed out.
• Educate patients on glucose targets and explain that other factors such as stress and activity can influence glucose levels.
• Focus on the positive. “What have you been learning about how your meals and beverages affect your glucose?”
• Help guide patients toward better diet quality, even when TIR is a goal, using the four core concepts.
• Encourage curiosity, such as by experimenting with portions, timing, or food order. “What if you try eating nonstarchy foods first?”
• Before adjusting a medication dose, consider asking if the patient is willing to make a nutrition change. “Every visit is an opportunity!”

Adjusting Insulin With the Help of CGM: Focus on Four Patient Subgroups

Dr. Martens noted that about a quarter of people with T2D will require insulin treatment, despite increasing use of sodium-glucose cotransporter 2 (SGLT2) inhibitors and glucagon-like peptide 1 (GLP-1) receptor agonists. And even when insulin is used as a “salvage therapy” in T2D, about two thirds of those individuals still struggle to achieve an A1c below 7% with or without other glucose-lowering medications, he noted.

“So, we have this huge population with type 2 diabetes who have limited access to endocrinology, and advanced insulin delivery devices are not yet available for them. Can better use of CGM drive improvements in care?”

He pointed to MOBILE, a randomized clinical trial, which showed that CGM use resulted in significantly improved A1c at 8 months compared with fingerstick monitoring among adults with T2D taking long-acting insulin alone without premeal insulin. However, TIR was still just 59% (vs 43% with fingerstick testing), suggesting room for improvement.

“This could have been much, much better…Rapid interpretation isn’t really enough. We need to move from interpretation into action,” Dr. Martens said.

His team recently developed a program called “CGM Clinician Guided Management (CCGM)” aimed at primary care that encourages the following principles:

• Appropriate movement toward the safer “high value” noninsulin therapies, that is, GLP-1 agonists and SGLT2 inhibitors.
• Appropriate insulin titration.
• Appropriate cycle time in titration, that is, accelerating more rapidly when one dose isn’t working. “That’s the Achilles heel of primary care,” he noted.
• Quick identification of when the limits of basal insulin therapy have been reached.
• Team-based management for difficult situations and for individuals on multiple daily injections and mealtime insulin regimens. “This is a group that really struggles…in primary care settings,” he noted.

The following three steps are based on published T2D management guidelines:

• Step 1: If the patient has atherosclerotic cardiovascular disease, start with either an SGLT2 inhibitor or GLP-1 agonist. For those with congestive heart failure and/or chronic kidney disease, SGLT2 inhibitors are indicated.
• Step 2: Is the patient on sulfonylurea? Consider eliminating it before moving to CGM-based insulin titration.
• Step 3: Was there a change in therapy based on steps 1 or 2? If not, move to CGM-guided insulin titration. If yes, wait 2-4 weeks to see the impact of therapy change before moving on.

The program categorizes patients into one of four groups based on CGM data, with respective management approaches:

• Category 1: TIR > 70%, time below range (TBR) < 3%: Doing well, keep on going!
• Category 2: TIR > 70%, TBR ≥ 3%: Too much hypoglycemia, need to decrease therapy. Stop sulfonylureas, and if TBR > 10%, also decrease basal insulin dose.
• Category 3: TIR < 70%, TBR < 3%: Too much hyperglycemia — increase therapy.
• Category 4: TIR < 70%, TBR ≥ 3%: This is the toughest category. Fix or advance therapy. These patients should be either referred to a diabetes care and education specialist (formerly known as “diabetes educators”) to troubleshoot their regimens or have their therapy advanced to multiple daily injections. The hypoglycemia should be addressed first for safety, then the hyperglycemia.

“We hope that CCGM is going to be the translation of CGM data into action in primary care, where we struggle with action and inaction,” Dr. Martens said. It’s expected to be posted on the IDC website soon.

Ms. Ettestad’s employer received educational grant funds from Abbott Diabetes Care and Sanofi-Aventis Groupe. She also worked as a product trainer with Tandem Diabetes Care. She is employed by nonprofit International Diabetes Center – HealthPartners Institute and received no personal income or honoraria from these activities. Dr. Martens’ employer received funds on his behalf for research and speaking support from Dexcom, Abbott Diabetes Care, Medtronic, Insulet, Tandem, Sanofi, Lilly, and Novo Nordisk and for consulting from Sanofi and Lilly. He is employed by nonprofit HealthPartners Institute – International Diabetes Center and received no personal income or honoraria from these activities.

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

Data derived from continuous glucose monitoring (CGM) devices can help guide nutrition management and insulin dosing in people with type 2 diabetes (T2D) in primary care settings.

At the Advanced Technologies & Treatments for Diabetes meeting, two experts from the International Diabetes Center – HealthPartners Institute, Minneapolis, offered advice for clinicians. Tara Ettestad, RN, LD, CDCES, program manager for care transformation and training at the center, shared tips for helping patients change their diet based on CGM readings. The center’s medical director Thomas Martens, MD, provided a systematic approach to using CGM to guide adjustment of insulin doses and other medications for insulin-treated patients with T2D.
 

CGM-Guided Nutrition: Focus on Sustainable Changes

With CGM, people with diabetes get real-time feedback about the impact of foods on their glucose levels. This can help them learn not just what they can’t eat but what they can eat, Ms. Ettestad pointed out.

“People want to know what to eat. This is the number-one question that people who are newly diagnosed with diabetes ask, and unfortunately, they typically hear what not to eat. No carbohydrates, no sugar, no white foods, no sweets. This can be really disheartening and confusing for many. We should be focusing on sustainable changes to help improve diets,” she said.

She added, “Not everyone can see a dietitian, but all clinicians can help provide evidence-based nutrition guidance.”

When guiding patients, it’s important to focus on the four “core concepts” outlined in the American Diabetes Association’s nutrition consensus report:

• Emphasize nonstarchy vegetables
• Minimize added sugars and refined grains
• Eat more whole foods, less highly processed foods
• Replace sugar-sweetened beverages with water as often as possible

With CGM, patients can see the differences in response to refined carbs (wheat, rice, and potato), sugars (sucrose, fructose, and glucose), and resistant starches (whole grains, fruits, and legumes). Typically, glucose responses are steeper and higher for the first two compared to resistant starches.

CGM can also show the effects of eating fat and protein, in that they can delay glucose responses to meals even with the same carbohydrate content, Ms. Ettestad said.

It’s important to remind patients that although one goal of using CGM is to reduce post-meal glucose spikes, eating a lot of high-saturated fat, high-calorie foods isn’t the healthful way to do it. “What’s really important when we’re using CGM to help guide nutrition is remembering nutrition quality and what can be good for glucose is not always good for our overall health,” Ms. Ettestad stressed.

She provided these further tips:

• Pick one meal at a time to focus on. Collaborate with patients to see what changes they are able and willing to make. For example, rather than entirely giving up rice or noodles at dinner, try eating less of those and adding more vegetables.
• Suggest that patients keep a food log or use a tracking app so that the source of specific glucose patterns can be identified and addressed.
• Show patients how to check their time in range (TIR) on their mobile device or reader each week so they can see big-picture results of their changes. “This can be really motivating for people to see,” she said.
• Remind people that glucose rises with meals. This seems obvious but may not be to those newly diagnosed, she pointed out.
• Educate patients on glucose targets and explain that other factors such as stress and activity can influence glucose levels.
• Focus on the positive. “What have you been learning about how your meals and beverages affect your glucose?”
• Help guide patients toward better diet quality, even when TIR is a goal, using the four core concepts.
• Encourage curiosity, such as by experimenting with portions, timing, or food order. “What if you try eating nonstarchy foods first?”
• Before adjusting a medication dose, consider asking if the patient is willing to make a nutrition change. “Every visit is an opportunity!”

Adjusting Insulin With the Help of CGM: Focus on Four Patient Subgroups

Dr. Martens noted that about a quarter of people with T2D will require insulin treatment, despite increasing use of sodium-glucose cotransporter 2 (SGLT2) inhibitors and glucagon-like peptide 1 (GLP-1) receptor agonists. And even when insulin is used as a “salvage therapy” in T2D, about two thirds of those individuals still struggle to achieve an A1c below 7% with or without other glucose-lowering medications, he noted.

“So, we have this huge population with type 2 diabetes who have limited access to endocrinology, and advanced insulin delivery devices are not yet available for them. Can better use of CGM drive improvements in care?”

He pointed to MOBILE, a randomized clinical trial, which showed that CGM use resulted in significantly improved A1c at 8 months compared with fingerstick monitoring among adults with T2D taking long-acting insulin alone without premeal insulin. However, TIR was still just 59% (vs 43% with fingerstick testing), suggesting room for improvement.

“This could have been much, much better…Rapid interpretation isn’t really enough. We need to move from interpretation into action,” Dr. Martens said.

His team recently developed a program called “CGM Clinician Guided Management (CCGM)” aimed at primary care that encourages the following principles:

• Appropriate movement toward the safer “high value” noninsulin therapies, that is, GLP-1 agonists and SGLT2 inhibitors.
• Appropriate insulin titration.
• Appropriate cycle time in titration, that is, accelerating more rapidly when one dose isn’t working. “That’s the Achilles heel of primary care,” he noted.
• Quick identification of when the limits of basal insulin therapy have been reached.
• Team-based management for difficult situations and for individuals on multiple daily injections and mealtime insulin regimens. “This is a group that really struggles…in primary care settings,” he noted.

The following three steps are based on published T2D management guidelines:

• Step 1: If the patient has atherosclerotic cardiovascular disease, start with either an SGLT2 inhibitor or GLP-1 agonist. For those with congestive heart failure and/or chronic kidney disease, SGLT2 inhibitors are indicated.
• Step 2: Is the patient on sulfonylurea? Consider eliminating it before moving to CGM-based insulin titration.
• Step 3: Was there a change in therapy based on steps 1 or 2? If not, move to CGM-guided insulin titration. If yes, wait 2-4 weeks to see the impact of therapy change before moving on.

The program categorizes patients into one of four groups based on CGM data, with respective management approaches:

• Category 1: TIR > 70%, time below range (TBR) < 3%: Doing well, keep on going!
• Category 2: TIR > 70%, TBR ≥ 3%: Too much hypoglycemia, need to decrease therapy. Stop sulfonylureas, and if TBR > 10%, also decrease basal insulin dose.
• Category 3: TIR < 70%, TBR < 3%: Too much hyperglycemia — increase therapy.
• Category 4: TIR < 70%, TBR ≥ 3%: This is the toughest category. Fix or advance therapy. These patients should be either referred to a diabetes care and education specialist (formerly known as “diabetes educators”) to troubleshoot their regimens or have their therapy advanced to multiple daily injections. The hypoglycemia should be addressed first for safety, then the hyperglycemia.

“We hope that CCGM is going to be the translation of CGM data into action in primary care, where we struggle with action and inaction,” Dr. Martens said. It’s expected to be posted on the IDC website soon.

Ms. Ettestad’s employer received educational grant funds from Abbott Diabetes Care and Sanofi-Aventis Groupe. She also worked as a product trainer with Tandem Diabetes Care. She is employed by nonprofit International Diabetes Center – HealthPartners Institute and received no personal income or honoraria from these activities. Dr. Martens’ employer received funds on his behalf for research and speaking support from Dexcom, Abbott Diabetes Care, Medtronic, Insulet, Tandem, Sanofi, Lilly, and Novo Nordisk and for consulting from Sanofi and Lilly. He is employed by nonprofit HealthPartners Institute – International Diabetes Center and received no personal income or honoraria from these activities.

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

Amid rising concern about the potential long-term costs of using glucagon-like peptide 1 (GLP-1) agonists to treat obesity, some insurers are making access to bariatric surgery easier.

While the relationship may not be entirely causal, data do suggest that at least for now, these new agents for treating obesity including semaglutide (Wegovy) and tirzepatide (Zepbound) are not cost-effective, whereas the surgery is.

According to GoodRx, Wegovy (semaglutide) has a list price of about $1350 for a 28-day supply. And the American Society for Metabolic and Bariatric Surgery (ASMBS) said that the average cost of bariatric surgery ranges between $17,000 and $26,000. But ASMBS added that third-party payers will recover those costs within 2-4 years due to reduction or elimination of obesity-related conditions and associated treatment costs, with an approximate 29% healthcare cost reduction at 5 years.

Recently, for example, Geisinger Health of Pennsylvania and Blue Cross/Blue Shield of Massachusetts expanded body mass index (BMI) eligibility for bariatric surgery procedures, while Blue Cross Blue Shield of Michigan dropped prior authorization requirements for several services, including bariatric surgery.

While most major health insurers cover Wegovy for obesity treatment, they typically require prior authorization and/or trials of other therapies first. Recently, some employers have denied coverage for the medications for treating obesity. Medicare does not cover these drugs. Coverage varies across state Medicaid plans.

“For years, insurers…have played games with the surgery, making people jump through hoops, hoping that they would just give up and go away. And now that health plans are getting concerned about [the cost of] drugs for obesity, and they’re getting so much attention, they’re thinking oh, maybe we shouldn’t be playing these games anymore,” obesity policy expert Ted Kyle, RPh, founder of ConscienHealth, told this news organization.

However, Christopher Doubet Still, DO, director of Nutrition and Weight Management at Geisinger Medical Center, Danville, Pennsylvania, told this news organization that Geisinger Health Plan’s change in May 2023 to lower the BMI surgery eligibility cutoff from 35 kg/m2 to 30 kg/m2 for people with comorbidities was not related to the cost of GLP-1 drugs.

“To date, bariatric surgery remains the most effective, enduring treatment of obesity, and most importantly, its comorbid medical problems. So that was really the reasoning. The weight loss is secondary to the profound medical benefits of bariatric surgery. I think that was the impetus of that change, not having really anything to do at the time with GLP-1s,” Dr. Still said.

The Geisinger Health Plan does not currently cover antiobesity medications, although Geisinger Health Plan Family, a state Medicaid plan, does because Pennsylvania is now one of a handful of states that cover the medications through Medicaid.
 

The Equation Keeps Changing

Health economist James Chambers, PhD, of Tufts University, Boston, Massachusetts, told this news organizations, “when you think about the value of a treatment, you don’t look at it in isolation. You’re looking at the difference in cost and benefits. So now that you have these expensive drugs, it’s not that surgeries become less expensive, but it does make you interpret the cost differently. When diet and exercise and counseling were the only real options, surgeries seemed like a much more expensive intervention. But with the advent of the GLP-1s, then, maybe plans consider the costs of surgery a little bit differently.”

And that equation is likely to change further, Dr. Still noted.

“I just think we’re dealing with a short-term financial problem because there’s basically only two main medications so the prices are high, but as more medications come on the market, the prices will come down,” he said.

Cristy Ms. Gallagher, MPAff, research project director of the STOP Obesity Alliance at the Milken Institute School of Public Health at George Washington University, Washington, DC, agreed.

“We have a lot of data on obesity treatment coverage from before 2023. But then this [GLP-1] explosion happened in 2023…The health payers are out there trying to figure out coverage, and they’re trying to figure out what this is going to look like for them,” Ms. Gallagher said.

However, she pointed out, “there is no treatment that fits everyone. The GLP-1s won’t work for every person because of the different stages of obesity, the side effects, and then because of the coverage. I think that you will not see a decrease in bariatric surgery in the near term, by any means.”

Ms. Gallagher also noted that although the data now suggest people will have to keep taking the drugs for life, there may be other future approaches.

“Once a person hits their goal weight, maybe then they could be transferred to a different pill form that might be cheaper, something that’s sort of more of a maintenance drug. I think that is a huge unknown right now,” she said.

And Mr. Kyle said that while bariatric surgery does provide the most durable benefit, “weight regain after surgery is a fact of life. People are still healthier 5 years later, but they do have some weight regain. And in those cases, you might want to follow-up with medicines…It’s not necessarily an either/or proposition any more than surgical treatment of cancer, surgical oncology is an either/or with medical oncology.”
 

A New View of Obesity

According to Mr. Kyle, all this attention on the new medications “is prompting people to rethink or think differently about obesity and consider it more carefully as a chronic medical condition and not a condition of appearance and behavior. And that’s all good, whether you’re thinking about it from the standpoint of bariatric surgery or from the standpoint of medical treatment of obesity because then people start considering options more rationally.”

This shifting view of obesity has meant that bariatric surgeons and medical obesity specialists are starting to work more collaboratively, he said.

“There is a trend that I detect toward more integrated approaches to obesity,” Mr. Kyle said.

He added, “We now have more tools. And we’re in the messy middle of figuring out how, as a practical matter, to use them.”

And as far as insurance coverage, “people are going to make mistakes. They are making mistakes. But I have been the eternal optimist, and I have faith that people are also figuring it out. It would be hard to do worse.”

For now, any initiatives to increase bariatric surgery rates in the GLP-1 era haven’t yet had an impact, American Society for Metabolic and Bariatric Surgery President Marina S. Kurian, MD, told this news organization in a statement.

“While we have heard of some insurers possibly changing their requirements for bariatric surgery, we have not seen a significant rise in procedures related to changes in insurance coverage for either antiobesity medications or metabolic and bariatric surgery,” Dr. Kurian said.

Mr. Kyle had accepted speaking or professional fees from Novo Nordisk, Behringer Ingelheim, Nutrisystem, Roman Health, and Emerald Lake Safety. Dr. Still was on the speaker’s bureau and did clinical trials for Eli Lilly and Novo Nordisk. Dr. Chambers and Gallagher had no disclosures.

A version of this article appeared on Medscape.com.

Amid rising concern about the potential long-term costs of using glucagon-like peptide 1 (GLP-1) agonists to treat obesity, some insurers are making access to bariatric surgery easier.

While the relationship may not be entirely causal, data do suggest that at least for now, these new agents for treating obesity including semaglutide (Wegovy) and tirzepatide (Zepbound) are not cost-effective, whereas the surgery is.

According to GoodRx, Wegovy (semaglutide) has a list price of about $1350 for a 28-day supply. And the American Society for Metabolic and Bariatric Surgery (ASMBS) said that the average cost of bariatric surgery ranges between $17,000 and $26,000. But ASMBS added that third-party payers will recover those costs within 2-4 years due to reduction or elimination of obesity-related conditions and associated treatment costs, with an approximate 29% healthcare cost reduction at 5 years.

Recently, for example, Geisinger Health of Pennsylvania and Blue Cross/Blue Shield of Massachusetts expanded body mass index (BMI) eligibility for bariatric surgery procedures, while Blue Cross Blue Shield of Michigan dropped prior authorization requirements for several services, including bariatric surgery.

While most major health insurers cover Wegovy for obesity treatment, they typically require prior authorization and/or trials of other therapies first. Recently, some employers have denied coverage for the medications for treating obesity. Medicare does not cover these drugs. Coverage varies across state Medicaid plans.

“For years, insurers…have played games with the surgery, making people jump through hoops, hoping that they would just give up and go away. And now that health plans are getting concerned about [the cost of] drugs for obesity, and they’re getting so much attention, they’re thinking oh, maybe we shouldn’t be playing these games anymore,” obesity policy expert Ted Kyle, RPh, founder of ConscienHealth, told this news organization.

However, Christopher Doubet Still, DO, director of Nutrition and Weight Management at Geisinger Medical Center, Danville, Pennsylvania, told this news organization that Geisinger Health Plan’s change in May 2023 to lower the BMI surgery eligibility cutoff from 35 kg/m2 to 30 kg/m2 for people with comorbidities was not related to the cost of GLP-1 drugs.

“To date, bariatric surgery remains the most effective, enduring treatment of obesity, and most importantly, its comorbid medical problems. So that was really the reasoning. The weight loss is secondary to the profound medical benefits of bariatric surgery. I think that was the impetus of that change, not having really anything to do at the time with GLP-1s,” Dr. Still said.

The Geisinger Health Plan does not currently cover antiobesity medications, although Geisinger Health Plan Family, a state Medicaid plan, does because Pennsylvania is now one of a handful of states that cover the medications through Medicaid.
 

The Equation Keeps Changing

Health economist James Chambers, PhD, of Tufts University, Boston, Massachusetts, told this news organizations, “when you think about the value of a treatment, you don’t look at it in isolation. You’re looking at the difference in cost and benefits. So now that you have these expensive drugs, it’s not that surgeries become less expensive, but it does make you interpret the cost differently. When diet and exercise and counseling were the only real options, surgeries seemed like a much more expensive intervention. But with the advent of the GLP-1s, then, maybe plans consider the costs of surgery a little bit differently.”

And that equation is likely to change further, Dr. Still noted.

“I just think we’re dealing with a short-term financial problem because there’s basically only two main medications so the prices are high, but as more medications come on the market, the prices will come down,” he said.

Cristy Ms. Gallagher, MPAff, research project director of the STOP Obesity Alliance at the Milken Institute School of Public Health at George Washington University, Washington, DC, agreed.

“We have a lot of data on obesity treatment coverage from before 2023. But then this [GLP-1] explosion happened in 2023…The health payers are out there trying to figure out coverage, and they’re trying to figure out what this is going to look like for them,” Ms. Gallagher said.

However, she pointed out, “there is no treatment that fits everyone. The GLP-1s won’t work for every person because of the different stages of obesity, the side effects, and then because of the coverage. I think that you will not see a decrease in bariatric surgery in the near term, by any means.”

Ms. Gallagher also noted that although the data now suggest people will have to keep taking the drugs for life, there may be other future approaches.

“Once a person hits their goal weight, maybe then they could be transferred to a different pill form that might be cheaper, something that’s sort of more of a maintenance drug. I think that is a huge unknown right now,” she said.

And Mr. Kyle said that while bariatric surgery does provide the most durable benefit, “weight regain after surgery is a fact of life. People are still healthier 5 years later, but they do have some weight regain. And in those cases, you might want to follow-up with medicines…It’s not necessarily an either/or proposition any more than surgical treatment of cancer, surgical oncology is an either/or with medical oncology.”
 

A New View of Obesity

According to Mr. Kyle, all this attention on the new medications “is prompting people to rethink or think differently about obesity and consider it more carefully as a chronic medical condition and not a condition of appearance and behavior. And that’s all good, whether you’re thinking about it from the standpoint of bariatric surgery or from the standpoint of medical treatment of obesity because then people start considering options more rationally.”

This shifting view of obesity has meant that bariatric surgeons and medical obesity specialists are starting to work more collaboratively, he said.

“There is a trend that I detect toward more integrated approaches to obesity,” Mr. Kyle said.

He added, “We now have more tools. And we’re in the messy middle of figuring out how, as a practical matter, to use them.”

And as far as insurance coverage, “people are going to make mistakes. They are making mistakes. But I have been the eternal optimist, and I have faith that people are also figuring it out. It would be hard to do worse.”

For now, any initiatives to increase bariatric surgery rates in the GLP-1 era haven’t yet had an impact, American Society for Metabolic and Bariatric Surgery President Marina S. Kurian, MD, told this news organization in a statement.

“While we have heard of some insurers possibly changing their requirements for bariatric surgery, we have not seen a significant rise in procedures related to changes in insurance coverage for either antiobesity medications or metabolic and bariatric surgery,” Dr. Kurian said.

Mr. Kyle had accepted speaking or professional fees from Novo Nordisk, Behringer Ingelheim, Nutrisystem, Roman Health, and Emerald Lake Safety. Dr. Still was on the speaker’s bureau and did clinical trials for Eli Lilly and Novo Nordisk. Dr. Chambers and Gallagher had no disclosures.

A version of this article appeared on Medscape.com.

Amid rising concern about the potential long-term costs of using glucagon-like peptide 1 (GLP-1) agonists to treat obesity, some insurers are making access to bariatric surgery easier.

While the relationship may not be entirely causal, data do suggest that at least for now, these new agents for treating obesity including semaglutide (Wegovy) and tirzepatide (Zepbound) are not cost-effective, whereas the surgery is.

According to GoodRx, Wegovy (semaglutide) has a list price of about $1350 for a 28-day supply. And the American Society for Metabolic and Bariatric Surgery (ASMBS) said that the average cost of bariatric surgery ranges between $17,000 and $26,000. But ASMBS added that third-party payers will recover those costs within 2-4 years due to reduction or elimination of obesity-related conditions and associated treatment costs, with an approximate 29% healthcare cost reduction at 5 years.

Recently, for example, Geisinger Health of Pennsylvania and Blue Cross/Blue Shield of Massachusetts expanded body mass index (BMI) eligibility for bariatric surgery procedures, while Blue Cross Blue Shield of Michigan dropped prior authorization requirements for several services, including bariatric surgery.

While most major health insurers cover Wegovy for obesity treatment, they typically require prior authorization and/or trials of other therapies first. Recently, some employers have denied coverage for the medications for treating obesity. Medicare does not cover these drugs. Coverage varies across state Medicaid plans.

“For years, insurers…have played games with the surgery, making people jump through hoops, hoping that they would just give up and go away. And now that health plans are getting concerned about [the cost of] drugs for obesity, and they’re getting so much attention, they’re thinking oh, maybe we shouldn’t be playing these games anymore,” obesity policy expert Ted Kyle, RPh, founder of ConscienHealth, told this news organization.

However, Christopher Doubet Still, DO, director of Nutrition and Weight Management at Geisinger Medical Center, Danville, Pennsylvania, told this news organization that Geisinger Health Plan’s change in May 2023 to lower the BMI surgery eligibility cutoff from 35 kg/m2 to 30 kg/m2 for people with comorbidities was not related to the cost of GLP-1 drugs.

“To date, bariatric surgery remains the most effective, enduring treatment of obesity, and most importantly, its comorbid medical problems. So that was really the reasoning. The weight loss is secondary to the profound medical benefits of bariatric surgery. I think that was the impetus of that change, not having really anything to do at the time with GLP-1s,” Dr. Still said.

The Geisinger Health Plan does not currently cover antiobesity medications, although Geisinger Health Plan Family, a state Medicaid plan, does because Pennsylvania is now one of a handful of states that cover the medications through Medicaid.
 

The Equation Keeps Changing

Health economist James Chambers, PhD, of Tufts University, Boston, Massachusetts, told this news organizations, “when you think about the value of a treatment, you don’t look at it in isolation. You’re looking at the difference in cost and benefits. So now that you have these expensive drugs, it’s not that surgeries become less expensive, but it does make you interpret the cost differently. When diet and exercise and counseling were the only real options, surgeries seemed like a much more expensive intervention. But with the advent of the GLP-1s, then, maybe plans consider the costs of surgery a little bit differently.”

And that equation is likely to change further, Dr. Still noted.

“I just think we’re dealing with a short-term financial problem because there’s basically only two main medications so the prices are high, but as more medications come on the market, the prices will come down,” he said.

Cristy Ms. Gallagher, MPAff, research project director of the STOP Obesity Alliance at the Milken Institute School of Public Health at George Washington University, Washington, DC, agreed.

“We have a lot of data on obesity treatment coverage from before 2023. But then this [GLP-1] explosion happened in 2023…The health payers are out there trying to figure out coverage, and they’re trying to figure out what this is going to look like for them,” Ms. Gallagher said.

However, she pointed out, “there is no treatment that fits everyone. The GLP-1s won’t work for every person because of the different stages of obesity, the side effects, and then because of the coverage. I think that you will not see a decrease in bariatric surgery in the near term, by any means.”

Ms. Gallagher also noted that although the data now suggest people will have to keep taking the drugs for life, there may be other future approaches.

“Once a person hits their goal weight, maybe then they could be transferred to a different pill form that might be cheaper, something that’s sort of more of a maintenance drug. I think that is a huge unknown right now,” she said.

And Mr. Kyle said that while bariatric surgery does provide the most durable benefit, “weight regain after surgery is a fact of life. People are still healthier 5 years later, but they do have some weight regain. And in those cases, you might want to follow-up with medicines…It’s not necessarily an either/or proposition any more than surgical treatment of cancer, surgical oncology is an either/or with medical oncology.”
 

A New View of Obesity

According to Mr. Kyle, all this attention on the new medications “is prompting people to rethink or think differently about obesity and consider it more carefully as a chronic medical condition and not a condition of appearance and behavior. And that’s all good, whether you’re thinking about it from the standpoint of bariatric surgery or from the standpoint of medical treatment of obesity because then people start considering options more rationally.”

This shifting view of obesity has meant that bariatric surgeons and medical obesity specialists are starting to work more collaboratively, he said.

“There is a trend that I detect toward more integrated approaches to obesity,” Mr. Kyle said.

He added, “We now have more tools. And we’re in the messy middle of figuring out how, as a practical matter, to use them.”

And as far as insurance coverage, “people are going to make mistakes. They are making mistakes. But I have been the eternal optimist, and I have faith that people are also figuring it out. It would be hard to do worse.”

For now, any initiatives to increase bariatric surgery rates in the GLP-1 era haven’t yet had an impact, American Society for Metabolic and Bariatric Surgery President Marina S. Kurian, MD, told this news organization in a statement.

“While we have heard of some insurers possibly changing their requirements for bariatric surgery, we have not seen a significant rise in procedures related to changes in insurance coverage for either antiobesity medications or metabolic and bariatric surgery,” Dr. Kurian said.

Mr. Kyle had accepted speaking or professional fees from Novo Nordisk, Behringer Ingelheim, Nutrisystem, Roman Health, and Emerald Lake Safety. Dr. Still was on the speaker’s bureau and did clinical trials for Eli Lilly and Novo Nordisk. Dr. Chambers and Gallagher had no disclosures.

A version of this article appeared on Medscape.com.

TOPLINE:

Sodium-glucose cotransporter 2 inhibitor (SGLT2i)-associated diabetes ketoacidosis (DKA) in people with type 2 diabetes (T2D) is associated with lower degrees of hyperglycemia over the first 24 hours of treatment than seen in type 1 diabetes (T1D)-associated DKA, potentially leading to hypo- or hyperglycemia if the same insulin infusion protocols are used.

METHODOLOGY:

• Retrospective cohort study comparing natural history and response to treatment for 37 episodes of SGLT2i-associated DKA (n = 27) or ketosis (n = 10) in people with T2D vs 19 episodes of T1D-associated DKA in people of the same age range as the T2D group, identified from endocrine consultation requests in two South Australian tertiary hospitals.

TAKEAWAY:

• Patients with T2D and SGLT2i-associated DKA had milder DKA than T1D-associated DKA (median ketone peak, 5.3 vs 6.5 mmol/L; P = .02).
• The SGLT2i group had delayed resolution compared with the T1D group (median time, 36 vs 18 h; P = .002).
• Weight was higher in the T2D SGLT2i group than the T1D group (81.8 vs 67.7 kg; P = .04) yet patients with SGLT2i DKA received significantly less insulin (intravenous and subcutaneous) in the first 24 hours of treatment compared with the T1D DKA group (median dose, 44.0 vs 87.0 units; P = .01).
• In SGLT2i DKA, changes in ketone levels over the first 24 hours were significantly associated with baseline insulin therapy (P = .002), lower bicarbonate nadir (P = .02), and higher admission plasma glucose (P = .24).

IN PRACTICE:

“T1D DKA is driven by absolute insulin deficiency, leading to ketosis and hyperglycemia. In contrast, SGLT2i DKA occurs due to a reduction in plasma glucose from urinary glucose losses, which reduces insulin secretion and stimulates glucagon secretion, leading to ketosis. Accordingly, plasma glucose levels in SGLT2i DKA are often normal or mildly elevated.” “Despite these differences, the American Association of Clinical Endocrinologists and American College of Endocrinology recommend treatment with the same protocols for both types. This may result in hypoglycemia when patients receive fixed-dose insulin infusion or inadequate insulin dosing and reduced ketone clearance when patients receive dynamic insulin infusions.” “It would be reasonable, based on the evidence and the safety profile of intravenous dextrose, to increase dextrose infusion rates and concentration to allow increased insulin administration and suppression of ketosis.”

SOURCE:

Conducted by Mahesh M. Umapathysivam, DPhil, of Southern Adelaide Diabetes and Endocrine Services, Flinders Medical Centre, Adelaide, South Australia, and colleagues. The study was published online in JAMA Network Open.

LIMITATIONS:

The study was retrospective, and the sample size was small.

DISCLOSURES:

This work has been supported by a Diabetes South Australia (SA) investigator grant and support from the Hospital Research Foundation. Umapathysivam reported receiving grants from Diabetes SA during the conduct of the study and grants from the Australian Diabetes Society funded by AstraZeneca outside the submitted work.

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

TOPLINE:

Sodium-glucose cotransporter 2 inhibitor (SGLT2i)-associated diabetes ketoacidosis (DKA) in people with type 2 diabetes (T2D) is associated with lower degrees of hyperglycemia over the first 24 hours of treatment than seen in type 1 diabetes (T1D)-associated DKA, potentially leading to hypo- or hyperglycemia if the same insulin infusion protocols are used.

METHODOLOGY:

• Retrospective cohort study comparing natural history and response to treatment for 37 episodes of SGLT2i-associated DKA (n = 27) or ketosis (n = 10) in people with T2D vs 19 episodes of T1D-associated DKA in people of the same age range as the T2D group, identified from endocrine consultation requests in two South Australian tertiary hospitals.

TAKEAWAY:

• Patients with T2D and SGLT2i-associated DKA had milder DKA than T1D-associated DKA (median ketone peak, 5.3 vs 6.5 mmol/L; P = .02).
• The SGLT2i group had delayed resolution compared with the T1D group (median time, 36 vs 18 h; P = .002).
• Weight was higher in the T2D SGLT2i group than the T1D group (81.8 vs 67.7 kg; P = .04) yet patients with SGLT2i DKA received significantly less insulin (intravenous and subcutaneous) in the first 24 hours of treatment compared with the T1D DKA group (median dose, 44.0 vs 87.0 units; P = .01).
• In SGLT2i DKA, changes in ketone levels over the first 24 hours were significantly associated with baseline insulin therapy (P = .002), lower bicarbonate nadir (P = .02), and higher admission plasma glucose (P = .24).

IN PRACTICE:

“T1D DKA is driven by absolute insulin deficiency, leading to ketosis and hyperglycemia. In contrast, SGLT2i DKA occurs due to a reduction in plasma glucose from urinary glucose losses, which reduces insulin secretion and stimulates glucagon secretion, leading to ketosis. Accordingly, plasma glucose levels in SGLT2i DKA are often normal or mildly elevated.” “Despite these differences, the American Association of Clinical Endocrinologists and American College of Endocrinology recommend treatment with the same protocols for both types. This may result in hypoglycemia when patients receive fixed-dose insulin infusion or inadequate insulin dosing and reduced ketone clearance when patients receive dynamic insulin infusions.” “It would be reasonable, based on the evidence and the safety profile of intravenous dextrose, to increase dextrose infusion rates and concentration to allow increased insulin administration and suppression of ketosis.”

SOURCE:

Conducted by Mahesh M. Umapathysivam, DPhil, of Southern Adelaide Diabetes and Endocrine Services, Flinders Medical Centre, Adelaide, South Australia, and colleagues. The study was published online in JAMA Network Open.

LIMITATIONS:

The study was retrospective, and the sample size was small.

DISCLOSURES:

This work has been supported by a Diabetes South Australia (SA) investigator grant and support from the Hospital Research Foundation. Umapathysivam reported receiving grants from Diabetes SA during the conduct of the study and grants from the Australian Diabetes Society funded by AstraZeneca outside the submitted work.

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

TOPLINE:

Sodium-glucose cotransporter 2 inhibitor (SGLT2i)-associated diabetes ketoacidosis (DKA) in people with type 2 diabetes (T2D) is associated with lower degrees of hyperglycemia over the first 24 hours of treatment than seen in type 1 diabetes (T1D)-associated DKA, potentially leading to hypo- or hyperglycemia if the same insulin infusion protocols are used.

METHODOLOGY:

• Retrospective cohort study comparing natural history and response to treatment for 37 episodes of SGLT2i-associated DKA (n = 27) or ketosis (n = 10) in people with T2D vs 19 episodes of T1D-associated DKA in people of the same age range as the T2D group, identified from endocrine consultation requests in two South Australian tertiary hospitals.

TAKEAWAY:

• Patients with T2D and SGLT2i-associated DKA had milder DKA than T1D-associated DKA (median ketone peak, 5.3 vs 6.5 mmol/L; P = .02).
• The SGLT2i group had delayed resolution compared with the T1D group (median time, 36 vs 18 h; P = .002).
• Weight was higher in the T2D SGLT2i group than the T1D group (81.8 vs 67.7 kg; P = .04) yet patients with SGLT2i DKA received significantly less insulin (intravenous and subcutaneous) in the first 24 hours of treatment compared with the T1D DKA group (median dose, 44.0 vs 87.0 units; P = .01).
• In SGLT2i DKA, changes in ketone levels over the first 24 hours were significantly associated with baseline insulin therapy (P = .002), lower bicarbonate nadir (P = .02), and higher admission plasma glucose (P = .24).

IN PRACTICE:

“T1D DKA is driven by absolute insulin deficiency, leading to ketosis and hyperglycemia. In contrast, SGLT2i DKA occurs due to a reduction in plasma glucose from urinary glucose losses, which reduces insulin secretion and stimulates glucagon secretion, leading to ketosis. Accordingly, plasma glucose levels in SGLT2i DKA are often normal or mildly elevated.” “Despite these differences, the American Association of Clinical Endocrinologists and American College of Endocrinology recommend treatment with the same protocols for both types. This may result in hypoglycemia when patients receive fixed-dose insulin infusion or inadequate insulin dosing and reduced ketone clearance when patients receive dynamic insulin infusions.” “It would be reasonable, based on the evidence and the safety profile of intravenous dextrose, to increase dextrose infusion rates and concentration to allow increased insulin administration and suppression of ketosis.”

SOURCE:

Conducted by Mahesh M. Umapathysivam, DPhil, of Southern Adelaide Diabetes and Endocrine Services, Flinders Medical Centre, Adelaide, South Australia, and colleagues. The study was published online in JAMA Network Open.

LIMITATIONS:

The study was retrospective, and the sample size was small.

DISCLOSURES:

This work has been supported by a Diabetes South Australia (SA) investigator grant and support from the Hospital Research Foundation. Umapathysivam reported receiving grants from Diabetes SA during the conduct of the study and grants from the Australian Diabetes Society funded by AstraZeneca outside the submitted work.

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

A new position statement from the International Diabetes Federation advises using a 1-hour 75-g oral glucose tolerance test (OGTT) to improve identification of people at risk of developing type 2 diabetes.

“There are many, many people who may appear ‘normal’ if you use A1c or fasting glucose, but if you do a glucose tolerance test, they may have an abnormality after a glucose load. …The 1-hour plasma glucose has been found to be a more sensitive biomarker for the earlier identification of these high-risk individuals,” lead author Michael Bergman, MD, professor of medicine and population health at New York University Grossman School of Medicine, New York City, told this news organization in an interview.

Dr. Bergman presented the document, written by a 22-member international expert panel, on March 6, 2024, at the annual Advanced Technologies & Treatments for Diabetes meeting. It was simultaneously published in Diabetes Research and Clinical Practice.

This is the International Diabetes Federation’s (IDF’s) proposed screening algorithm for “intermediate hyperglycemia” and type 2 diabetes:

• At-risk high-risk individuals are first screened with a validated questionnaire such as the FINDRISK or the American Diabetes Association’s (ADA’s) risk screening tool.
• People identified as high risk should undergo laboratory screening with a 1-hour 75-g OGTT (although a 2-hour OGTT, fasting glucose, or A1c, as currently recommended by several organizations, is still considered acceptable).
• People with a 1-hour plasma glucose value at or above 155 mg (8.6 mmol/L) are considered to have intermediate hyperglycemia and should be prescribed lifestyle intervention and referred to a diabetes prevention program.
• Those with a 1-hour value greater than or equal to 209 mg/dL (11.6 mmol/L) are considered to have type 2 diabetes and should have a repeat test to confirm the diagnosis, with referral for further evaluation and treatment.

The new guidance is based on increasing evidence that the 1-hour test is a better predictor than other tests, including the 2-hour OGTT, of progression to type 2 diabetes and its associated complications, in a variety of populations. The document cites data showing that a plasma glucose of 155 mg/dl or greater on the 1-hour post-75-g test can identify people with undiagnosed type 2 diabetes or who are at increased risk but who have “normal” glucose tolerance as defined by an A1c < 5.7% (38.8 mmol/mol), a fasting plasma glucose < 100 mg/dL (5.6 mmol/L), or a 2-hour value below 140 mg/dL (7.8 mmol/L).

However, even though a 1-hour test may be more convenient than the traditional 2-hour test, incorporating OGTT into busy clinical practice may still pose logistical problems and may not improve ultimate outcomes, Elizabeth Selvin, PhD, MPH, of the Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, told this news organization. “I worry that emphasizing a burdensome test is not going to improve diabetes screening or diabetes prevention. Doing more 1-hour glucose screening is not going to get more people into diabetes prevention programs.”

When an audience member raised the logistics concern during the session Q&A, Dr. Bergman replied, “It’s no different than recommending colonoscopy or a mammogram. … I tell patients that we want to learn more about what is going on before we make a firm diagnosis. … I’ve done more than a hundred 1-hour glucose tolerance tests and have not seen one patient who refused because of inconvenience. Everything depends on the way we discuss things with patients.”
 

Recommendation Based on Emerging Evidence

“Intermediate hyperglycemia” is the World Health Organization’s term to refer to either impaired fasting glucose (IFG) or impaired glucose tolerance (IGT). These conditions are often called “prediabetes,” especially in the United States, but that term has been controversial because not everyone with IFG and IGT will go on to develop type 2 diabetes, said Dr. Bergman, who is also director of the NYU Langone Diabetes Prevention Program.

“With ‘prediabetes’ you’re labeling someone with a disease they may not develop. It’s not normal, but it’s not diabetes, so it’s an intermediate state,” he explained.

The statement provides a detailed summary of the data from 19 studies supporting use of a 1-hour plasma glucose of ≥ 155 mg/dL (8.6 mmol/L) to diagnose intermediate hyperglycemia and type 2 diabetes, including links between that level of glycemia and worsened metabolic and atherogenic profiles, risk for microvascular and macrovascular complications and mortality, and identification of risks for obstructive sleep apnea, cystic fibrosis-related diabetes mellitus, fatty liver disease, and premature mortality.

One major problem with current testing, Dr. Bergman said, is that “there is a huge disconnect between A1c and glucose values. … Only about 30% of individuals with an abnormal A1c will have an abnormal fasting glucose, and the inverse is also true. There’s a big mismatch between the two.”

Current guidelines suggest using both A1c and fasting glucose, but Dr. Bergman said that even then “you’re still missing about 20-30% who have IGT. … Part of the problem is that the criteria we use for defining abnormal fasting and 2-hour levels are too high. … 140 [mg/dL] for the 2-hour is too high and 100 [mg/dL] fasting is too high. … And that’s one of the reasons why many people progress to type 2 diabetes, because we’re using screening thresholds that are nonphysiologic.”

But Dr. Selvin disagrees, pointing to her own work showing that “using a combination of fasting glucose and A1c for screening does an excellent job at identifying high-risk individuals.”

She’s also unconvinced by other data cited in the paper. “I am deeply skeptical about 1-hour glucose being more prognostic than all other glycemic tests. … Associations of glucose tests with incident diabetes are inherently a circular analysis since diabetes is defined by elevations in those same tests. It is helpful to look at progression of diabetes, but these analyses are not simple and doing them well, especially with head-to-head comparisons against different glycemic tests, is hard,” she said.

In her view, “lifestyle interventions and weight loss should be recommended in at-risk individuals, including those with overweight and obesity, hypertension, metabolic syndrome, etc., regardless of 1-hour glucose test results.”

She added, “If we want to prevent diabetes, we need to focus on preventing weight gain and obesity and managing cardiometabolic risk factors. Lifestyle interventions are not effective unless they are intensive and patients are highly adherent. We need to make lifestyle interventions available and affordable for patients. That is the big barrier. I don’t think more screening with 1-hour glucose is going to help.”

Dr. Bergman pointed out that the International Diabetes Federation represents more than 100 countries, including many that are middle- and low-income. “They need a simple, cost-effective tool for screening effectively. A1c is more expensive, and fasting glucose alone will underestimate disease prevalence. So, the IDF felt, after doing a fairly comprehensive due diligence, that the data warranted recommendation of the 1-hour glucose.”

He’s hoping other organizations like the ADA and the World Health Organization will sign on to bring this guidance into the primary care arena. This news organization reached out to ADA for comment, but their representative hadn’t responded by press time.

Dr. Bergman had no disclosures. Dr. Selvin was supported by the National Institutes of Health.

A version of this article appeared on Medscape.com.

A new position statement from the International Diabetes Federation advises using a 1-hour 75-g oral glucose tolerance test (OGTT) to improve identification of people at risk of developing type 2 diabetes.

“There are many, many people who may appear ‘normal’ if you use A1c or fasting glucose, but if you do a glucose tolerance test, they may have an abnormality after a glucose load. …The 1-hour plasma glucose has been found to be a more sensitive biomarker for the earlier identification of these high-risk individuals,” lead author Michael Bergman, MD, professor of medicine and population health at New York University Grossman School of Medicine, New York City, told this news organization in an interview.

Dr. Bergman presented the document, written by a 22-member international expert panel, on March 6, 2024, at the annual Advanced Technologies & Treatments for Diabetes meeting. It was simultaneously published in Diabetes Research and Clinical Practice.

This is the International Diabetes Federation’s (IDF’s) proposed screening algorithm for “intermediate hyperglycemia” and type 2 diabetes:

• At-risk high-risk individuals are first screened with a validated questionnaire such as the FINDRISK or the American Diabetes Association’s (ADA’s) risk screening tool.
• People identified as high risk should undergo laboratory screening with a 1-hour 75-g OGTT (although a 2-hour OGTT, fasting glucose, or A1c, as currently recommended by several organizations, is still considered acceptable).
• People with a 1-hour plasma glucose value at or above 155 mg (8.6 mmol/L) are considered to have intermediate hyperglycemia and should be prescribed lifestyle intervention and referred to a diabetes prevention program.
• Those with a 1-hour value greater than or equal to 209 mg/dL (11.6 mmol/L) are considered to have type 2 diabetes and should have a repeat test to confirm the diagnosis, with referral for further evaluation and treatment.

The new guidance is based on increasing evidence that the 1-hour test is a better predictor than other tests, including the 2-hour OGTT, of progression to type 2 diabetes and its associated complications, in a variety of populations. The document cites data showing that a plasma glucose of 155 mg/dl or greater on the 1-hour post-75-g test can identify people with undiagnosed type 2 diabetes or who are at increased risk but who have “normal” glucose tolerance as defined by an A1c < 5.7% (38.8 mmol/mol), a fasting plasma glucose < 100 mg/dL (5.6 mmol/L), or a 2-hour value below 140 mg/dL (7.8 mmol/L).

However, even though a 1-hour test may be more convenient than the traditional 2-hour test, incorporating OGTT into busy clinical practice may still pose logistical problems and may not improve ultimate outcomes, Elizabeth Selvin, PhD, MPH, of the Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, told this news organization. “I worry that emphasizing a burdensome test is not going to improve diabetes screening or diabetes prevention. Doing more 1-hour glucose screening is not going to get more people into diabetes prevention programs.”

When an audience member raised the logistics concern during the session Q&A, Dr. Bergman replied, “It’s no different than recommending colonoscopy or a mammogram. … I tell patients that we want to learn more about what is going on before we make a firm diagnosis. … I’ve done more than a hundred 1-hour glucose tolerance tests and have not seen one patient who refused because of inconvenience. Everything depends on the way we discuss things with patients.”
 

Recommendation Based on Emerging Evidence

“Intermediate hyperglycemia” is the World Health Organization’s term to refer to either impaired fasting glucose (IFG) or impaired glucose tolerance (IGT). These conditions are often called “prediabetes,” especially in the United States, but that term has been controversial because not everyone with IFG and IGT will go on to develop type 2 diabetes, said Dr. Bergman, who is also director of the NYU Langone Diabetes Prevention Program.

“With ‘prediabetes’ you’re labeling someone with a disease they may not develop. It’s not normal, but it’s not diabetes, so it’s an intermediate state,” he explained.

The statement provides a detailed summary of the data from 19 studies supporting use of a 1-hour plasma glucose of ≥ 155 mg/dL (8.6 mmol/L) to diagnose intermediate hyperglycemia and type 2 diabetes, including links between that level of glycemia and worsened metabolic and atherogenic profiles, risk for microvascular and macrovascular complications and mortality, and identification of risks for obstructive sleep apnea, cystic fibrosis-related diabetes mellitus, fatty liver disease, and premature mortality.

One major problem with current testing, Dr. Bergman said, is that “there is a huge disconnect between A1c and glucose values. … Only about 30% of individuals with an abnormal A1c will have an abnormal fasting glucose, and the inverse is also true. There’s a big mismatch between the two.”

Current guidelines suggest using both A1c and fasting glucose, but Dr. Bergman said that even then “you’re still missing about 20-30% who have IGT. … Part of the problem is that the criteria we use for defining abnormal fasting and 2-hour levels are too high. … 140 [mg/dL] for the 2-hour is too high and 100 [mg/dL] fasting is too high. … And that’s one of the reasons why many people progress to type 2 diabetes, because we’re using screening thresholds that are nonphysiologic.”

But Dr. Selvin disagrees, pointing to her own work showing that “using a combination of fasting glucose and A1c for screening does an excellent job at identifying high-risk individuals.”

She’s also unconvinced by other data cited in the paper. “I am deeply skeptical about 1-hour glucose being more prognostic than all other glycemic tests. … Associations of glucose tests with incident diabetes are inherently a circular analysis since diabetes is defined by elevations in those same tests. It is helpful to look at progression of diabetes, but these analyses are not simple and doing them well, especially with head-to-head comparisons against different glycemic tests, is hard,” she said.

In her view, “lifestyle interventions and weight loss should be recommended in at-risk individuals, including those with overweight and obesity, hypertension, metabolic syndrome, etc., regardless of 1-hour glucose test results.”

She added, “If we want to prevent diabetes, we need to focus on preventing weight gain and obesity and managing cardiometabolic risk factors. Lifestyle interventions are not effective unless they are intensive and patients are highly adherent. We need to make lifestyle interventions available and affordable for patients. That is the big barrier. I don’t think more screening with 1-hour glucose is going to help.”

Dr. Bergman pointed out that the International Diabetes Federation represents more than 100 countries, including many that are middle- and low-income. “They need a simple, cost-effective tool for screening effectively. A1c is more expensive, and fasting glucose alone will underestimate disease prevalence. So, the IDF felt, after doing a fairly comprehensive due diligence, that the data warranted recommendation of the 1-hour glucose.”

He’s hoping other organizations like the ADA and the World Health Organization will sign on to bring this guidance into the primary care arena. This news organization reached out to ADA for comment, but their representative hadn’t responded by press time.

Dr. Bergman had no disclosures. Dr. Selvin was supported by the National Institutes of Health.

A version of this article appeared on Medscape.com.

A new position statement from the International Diabetes Federation advises using a 1-hour 75-g oral glucose tolerance test (OGTT) to improve identification of people at risk of developing type 2 diabetes.

“There are many, many people who may appear ‘normal’ if you use A1c or fasting glucose, but if you do a glucose tolerance test, they may have an abnormality after a glucose load. …The 1-hour plasma glucose has been found to be a more sensitive biomarker for the earlier identification of these high-risk individuals,” lead author Michael Bergman, MD, professor of medicine and population health at New York University Grossman School of Medicine, New York City, told this news organization in an interview.

Dr. Bergman presented the document, written by a 22-member international expert panel, on March 6, 2024, at the annual Advanced Technologies & Treatments for Diabetes meeting. It was simultaneously published in Diabetes Research and Clinical Practice.

This is the International Diabetes Federation’s (IDF’s) proposed screening algorithm for “intermediate hyperglycemia” and type 2 diabetes:

• At-risk high-risk individuals are first screened with a validated questionnaire such as the FINDRISK or the American Diabetes Association’s (ADA’s) risk screening tool.
• People identified as high risk should undergo laboratory screening with a 1-hour 75-g OGTT (although a 2-hour OGTT, fasting glucose, or A1c, as currently recommended by several organizations, is still considered acceptable).
• People with a 1-hour plasma glucose value at or above 155 mg (8.6 mmol/L) are considered to have intermediate hyperglycemia and should be prescribed lifestyle intervention and referred to a diabetes prevention program.
• Those with a 1-hour value greater than or equal to 209 mg/dL (11.6 mmol/L) are considered to have type 2 diabetes and should have a repeat test to confirm the diagnosis, with referral for further evaluation and treatment.

The new guidance is based on increasing evidence that the 1-hour test is a better predictor than other tests, including the 2-hour OGTT, of progression to type 2 diabetes and its associated complications, in a variety of populations. The document cites data showing that a plasma glucose of 155 mg/dl or greater on the 1-hour post-75-g test can identify people with undiagnosed type 2 diabetes or who are at increased risk but who have “normal” glucose tolerance as defined by an A1c < 5.7% (38.8 mmol/mol), a fasting plasma glucose < 100 mg/dL (5.6 mmol/L), or a 2-hour value below 140 mg/dL (7.8 mmol/L).

However, even though a 1-hour test may be more convenient than the traditional 2-hour test, incorporating OGTT into busy clinical practice may still pose logistical problems and may not improve ultimate outcomes, Elizabeth Selvin, PhD, MPH, of the Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, told this news organization. “I worry that emphasizing a burdensome test is not going to improve diabetes screening or diabetes prevention. Doing more 1-hour glucose screening is not going to get more people into diabetes prevention programs.”

When an audience member raised the logistics concern during the session Q&A, Dr. Bergman replied, “It’s no different than recommending colonoscopy or a mammogram. … I tell patients that we want to learn more about what is going on before we make a firm diagnosis. … I’ve done more than a hundred 1-hour glucose tolerance tests and have not seen one patient who refused because of inconvenience. Everything depends on the way we discuss things with patients.”
 

Recommendation Based on Emerging Evidence

“Intermediate hyperglycemia” is the World Health Organization’s term to refer to either impaired fasting glucose (IFG) or impaired glucose tolerance (IGT). These conditions are often called “prediabetes,” especially in the United States, but that term has been controversial because not everyone with IFG and IGT will go on to develop type 2 diabetes, said Dr. Bergman, who is also director of the NYU Langone Diabetes Prevention Program.

“With ‘prediabetes’ you’re labeling someone with a disease they may not develop. It’s not normal, but it’s not diabetes, so it’s an intermediate state,” he explained.

The statement provides a detailed summary of the data from 19 studies supporting use of a 1-hour plasma glucose of ≥ 155 mg/dL (8.6 mmol/L) to diagnose intermediate hyperglycemia and type 2 diabetes, including links between that level of glycemia and worsened metabolic and atherogenic profiles, risk for microvascular and macrovascular complications and mortality, and identification of risks for obstructive sleep apnea, cystic fibrosis-related diabetes mellitus, fatty liver disease, and premature mortality.

One major problem with current testing, Dr. Bergman said, is that “there is a huge disconnect between A1c and glucose values. … Only about 30% of individuals with an abnormal A1c will have an abnormal fasting glucose, and the inverse is also true. There’s a big mismatch between the two.”

Current guidelines suggest using both A1c and fasting glucose, but Dr. Bergman said that even then “you’re still missing about 20-30% who have IGT. … Part of the problem is that the criteria we use for defining abnormal fasting and 2-hour levels are too high. … 140 [mg/dL] for the 2-hour is too high and 100 [mg/dL] fasting is too high. … And that’s one of the reasons why many people progress to type 2 diabetes, because we’re using screening thresholds that are nonphysiologic.”

But Dr. Selvin disagrees, pointing to her own work showing that “using a combination of fasting glucose and A1c for screening does an excellent job at identifying high-risk individuals.”

She’s also unconvinced by other data cited in the paper. “I am deeply skeptical about 1-hour glucose being more prognostic than all other glycemic tests. … Associations of glucose tests with incident diabetes are inherently a circular analysis since diabetes is defined by elevations in those same tests. It is helpful to look at progression of diabetes, but these analyses are not simple and doing them well, especially with head-to-head comparisons against different glycemic tests, is hard,” she said.

In her view, “lifestyle interventions and weight loss should be recommended in at-risk individuals, including those with overweight and obesity, hypertension, metabolic syndrome, etc., regardless of 1-hour glucose test results.”

She added, “If we want to prevent diabetes, we need to focus on preventing weight gain and obesity and managing cardiometabolic risk factors. Lifestyle interventions are not effective unless they are intensive and patients are highly adherent. We need to make lifestyle interventions available and affordable for patients. That is the big barrier. I don’t think more screening with 1-hour glucose is going to help.”

Dr. Bergman pointed out that the International Diabetes Federation represents more than 100 countries, including many that are middle- and low-income. “They need a simple, cost-effective tool for screening effectively. A1c is more expensive, and fasting glucose alone will underestimate disease prevalence. So, the IDF felt, after doing a fairly comprehensive due diligence, that the data warranted recommendation of the 1-hour glucose.”

He’s hoping other organizations like the ADA and the World Health Organization will sign on to bring this guidance into the primary care arena. This news organization reached out to ADA for comment, but their representative hadn’t responded by press time.

Dr. Bergman had no disclosures. Dr. Selvin was supported by the National Institutes of Health.

A version of this article appeared on Medscape.com.

TOPLINE:

People with diabetes who live in small towns in the United States experience higher rates of complications than those living in cities and remote areas.

METHODOLOGY:

Retrospective cohort study using the OptumLabs Data Warehouse used a deidentified data set of US commercial and Medicare Advantage beneficiaries including 2,901,563 adults with diabetes between 2012 and 2021.

Overall, 2.6% lived in remote areas (population < 2500), 14.1% in small towns (2500-50,000), and 83.3% in cities (> 50,000).

Multivariable analysis adjusted for age, sex, health plan type, index year, diabetes type, baseline comorbidities, and medication use.

TAKEAWAY:

Relative to people living in cities, people in remote areas had significantly greater risks for myocardial infarction (hazard ratio, 1.06) and revascularization (1.04) but lower risks for hypoglycemia (0.90) and stroke (0.91).

Compared with cities, people living in small towns had significantly more hyperglycemia (1.06), hypoglycemia (1.15), end-stage kidney disease (1.04), myocardial infarction (1.10), heart failure (1.05), amputation (1.05), other lower-extremity complications (1.02), and revascularization (1.05), but a lower risk for stroke (0.95).

Compared with small towns, people living in remote areas had lower risks for hyperglycemia (0.85), hypoglycemia (0.92), and heart failure (0.94).

No geographic differences were found for retinopathy or atrial fibrillation/flutter.

The results didn’t differ significantly when the 2.5% overall with type 1 diabetes were removed from the dataset.

IN PRACTICE:

“While more research is needed to better understand the underlying causes of disparate diabetes outcomes along the rural-urban continuum, this study establishes the foundational differences to guide improvement efforts and helps to identify complications with the greatest disparities to which policy interventions may be targeted.”

SOURCE:

The study was conducted by Kyle Steiger, MD, Internal Medicine Residency, Mayo Clinic, Rochester, Minnesota, and colleagues, and published February 22 in Diabetes Care.

LIMITATIONS:

Claims data were from a single national health insurance provider that administers multiple private and Medicare Advantage health plans with disproportionate representation of urban populations and without people who have Medicaid or traditional Medicare fee-for-service or who are without insurance (and would be expected to have higher complication rates). There were no data on race/ethnicity. Potential for residual confounding.

DISCLOSURES:

This study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases. Dr. Steiger had no disclosures.
 

A version of this article appeared on Medscape.com.

TOPLINE:

People with diabetes who live in small towns in the United States experience higher rates of complications than those living in cities and remote areas.

METHODOLOGY:

Retrospective cohort study using the OptumLabs Data Warehouse used a deidentified data set of US commercial and Medicare Advantage beneficiaries including 2,901,563 adults with diabetes between 2012 and 2021.

Overall, 2.6% lived in remote areas (population < 2500), 14.1% in small towns (2500-50,000), and 83.3% in cities (> 50,000).

Multivariable analysis adjusted for age, sex, health plan type, index year, diabetes type, baseline comorbidities, and medication use.

TAKEAWAY:

Relative to people living in cities, people in remote areas had significantly greater risks for myocardial infarction (hazard ratio, 1.06) and revascularization (1.04) but lower risks for hypoglycemia (0.90) and stroke (0.91).

Compared with cities, people living in small towns had significantly more hyperglycemia (1.06), hypoglycemia (1.15), end-stage kidney disease (1.04), myocardial infarction (1.10), heart failure (1.05), amputation (1.05), other lower-extremity complications (1.02), and revascularization (1.05), but a lower risk for stroke (0.95).

Compared with small towns, people living in remote areas had lower risks for hyperglycemia (0.85), hypoglycemia (0.92), and heart failure (0.94).

No geographic differences were found for retinopathy or atrial fibrillation/flutter.

The results didn’t differ significantly when the 2.5% overall with type 1 diabetes were removed from the dataset.

IN PRACTICE:

“While more research is needed to better understand the underlying causes of disparate diabetes outcomes along the rural-urban continuum, this study establishes the foundational differences to guide improvement efforts and helps to identify complications with the greatest disparities to which policy interventions may be targeted.”

SOURCE:

The study was conducted by Kyle Steiger, MD, Internal Medicine Residency, Mayo Clinic, Rochester, Minnesota, and colleagues, and published February 22 in Diabetes Care.

LIMITATIONS:

Claims data were from a single national health insurance provider that administers multiple private and Medicare Advantage health plans with disproportionate representation of urban populations and without people who have Medicaid or traditional Medicare fee-for-service or who are without insurance (and would be expected to have higher complication rates). There were no data on race/ethnicity. Potential for residual confounding.

DISCLOSURES:

This study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases. Dr. Steiger had no disclosures.
 

A version of this article appeared on Medscape.com.

TOPLINE:

People with diabetes who live in small towns in the United States experience higher rates of complications than those living in cities and remote areas.

METHODOLOGY:

Retrospective cohort study using the OptumLabs Data Warehouse used a deidentified data set of US commercial and Medicare Advantage beneficiaries including 2,901,563 adults with diabetes between 2012 and 2021.

Overall, 2.6% lived in remote areas (population < 2500), 14.1% in small towns (2500-50,000), and 83.3% in cities (> 50,000).

Multivariable analysis adjusted for age, sex, health plan type, index year, diabetes type, baseline comorbidities, and medication use.

TAKEAWAY:

Relative to people living in cities, people in remote areas had significantly greater risks for myocardial infarction (hazard ratio, 1.06) and revascularization (1.04) but lower risks for hypoglycemia (0.90) and stroke (0.91).

Compared with cities, people living in small towns had significantly more hyperglycemia (1.06), hypoglycemia (1.15), end-stage kidney disease (1.04), myocardial infarction (1.10), heart failure (1.05), amputation (1.05), other lower-extremity complications (1.02), and revascularization (1.05), but a lower risk for stroke (0.95).

Compared with small towns, people living in remote areas had lower risks for hyperglycemia (0.85), hypoglycemia (0.92), and heart failure (0.94).

No geographic differences were found for retinopathy or atrial fibrillation/flutter.

The results didn’t differ significantly when the 2.5% overall with type 1 diabetes were removed from the dataset.

IN PRACTICE:

“While more research is needed to better understand the underlying causes of disparate diabetes outcomes along the rural-urban continuum, this study establishes the foundational differences to guide improvement efforts and helps to identify complications with the greatest disparities to which policy interventions may be targeted.”

SOURCE:

The study was conducted by Kyle Steiger, MD, Internal Medicine Residency, Mayo Clinic, Rochester, Minnesota, and colleagues, and published February 22 in Diabetes Care.

LIMITATIONS:

Claims data were from a single national health insurance provider that administers multiple private and Medicare Advantage health plans with disproportionate representation of urban populations and without people who have Medicaid or traditional Medicare fee-for-service or who are without insurance (and would be expected to have higher complication rates). There were no data on race/ethnicity. Potential for residual confounding.

DISCLOSURES:

This study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases. Dr. Steiger had no disclosures.
 

A version of this article appeared on Medscape.com.

The US Food and Drug Administration (FDA) announced the removal of the endocrine-disrupting chemicals (EDCs) per- and polyfluoroalkyl substances (PFAS) from food packaging.

Issued on February 28, 2024, “this means the major source of dietary exposure to PFAS from food packaging like fast-food wrappers, microwave popcorn bags, take-out paperboard containers, and pet food bags is being eliminated,” the FDA said in a statement.

In 2020, the FDA had secured commitments from manufacturers to stop selling products containing PFAS used in the food packaging for grease-proofing. “Today’s announcement marks the fulfillment of these voluntary commitments,” according to the agency.

PFAS, a class of thousands of chemicals also called “forever chemicals” are widely used in consumer and industrial products. People may be exposed via contaminated food packaging (although perhaps no longer in the United States) or occupationally. Studies have found that some PFAS disrupt hormones including estrogen and testosterone, whereas others may impair thyroid function.
 

Endocrine Society Report Sounds the Alarm About PFAS and Others

The FDA’s announcement came just 2 days after the Endocrine Society issued a new alarm about the human health dangers from environmental EDCs including PFAS in a report covering the latest science.

“Endocrine disrupting chemicals” are individual substances or mixtures that can interfere with natural hormonal function, leading to disease or even death. Many are ubiquitous in the modern environment and contribute to a wide range of human diseases.

The new report Endocrine Disrupting Chemicals: Threats to Human Health was issued jointly with the International Pollutants Elimination Network (IPEN), a global advocacy organization. It’s an update to the Endocrine Society’s 2015 report, providing new data on the endocrine-disrupting substances previously covered and adding four EDCs not discussed in that document: Pesticides, plastics, PFAS, and children’s products containing arsenic.

At a briefing held during the United Nations Environment Assembly meeting in Nairobi, Kenya, last week, the new report’s lead author Andrea C. Gore, PhD, of the University of Texas at Austin, noted, “A well-established body of scientific research indicates that endocrine-disrupting chemicals that are part of our daily lives are making us more susceptible to reproductive disorders, cancer, diabetes, obesity, heart disease, and other serious health conditions.”

Added Dr. Gore, who is also a member of the Endocrine Society’s Board of Directors, “These chemicals pose particularly serious risks to pregnant women and children. Now is the time for the UN Environment Assembly and other global policymakers to take action to address this threat to public health.”

While the science has been emerging rapidly, global and national chemical control policies haven’t kept up, the authors said. Of particular concern is that EDCs behave differently from other chemicals in many ways, including that even very low-dose exposures can pose health threats, but policies thus far haven’t dealt with that aspect.

Moreover, “the effects of low doses cannot be predicted by the effects observed at high doses. This means there may be no safe dose for exposure to EDCs,” according to the report.

Exposures can come from household products, including furniture, toys, and food packages, as well as electronics building materials and cosmetics. These chemicals are also in the outdoor environment, via pesticides, air pollution, and industrial waste.

“IPEN and the Endocrine Society call for chemical regulations based on the most modern scientific understanding of how hormones act and how EDCs can perturb these actions. We work to educate policy makers in global, regional, and national government assemblies and help ensure that regulations correlate with current scientific understanding,” they said in the report.
 

New Data on Four Classes of EDCs

Chapters of the report summarized the latest information about the science of EDCs and their links to endocrine disease and real-world exposure. It included a special section about “EDCs throughout the plastics life cycle” and a summary of the links between EDCs and climate change.

The report reviewed three pesticides, including the world’s most heavily applied herbicide, glycophosphate. Exposures can occur directly from the air, water, dust, and food residues. Recent data linked glycophosphate to adverse reproductive health outcomes.

Two toxic plastic chemicals, phthalates and bisphenols, are present in personal care products, among others. Emerging evidence links them with impaired neurodevelopment, leading to impaired cognitive function, learning, attention, and impulsivity.

Arsenic has long been linked to human health conditions including cancer, but more recent evidence finds it can disrupt multiple endocrine systems and lead to metabolic conditions including diabetes, reproductive dysfunction, and cardiovascular and neurocognitive conditions.

The special section about plastics noted that they are made from fossil fuels and chemicals, including many toxic substances that are known or suspected EDCs. People who live near plastic production facilities or waste dumps may be at greatest risk, but anyone can be exposed using any plastic product. Plastic waste disposal is increasingly problematic and often foisted on lower- and middle-income countries.
 

‘Additional Education and Awareness-Raising Among Stakeholders Remain Necessary’

Policies aimed at reducing human health risks from EDCs have included the 2022 Plastics Treaty, a resolution adopted by 175 countries at the United Nations Environmental Assembly that “may be a significant step toward global control of plastics and elimination of threats from exposures to EDCs in plastics,” the report said.

The authors added, “While significant progress has been made in recent years connecting scientific advances on EDCs with health-protective policies, additional education and awareness-raising among stakeholders remain necessary to achieve a safer and more sustainable environment that minimizes exposure to these harmful chemicals.”

The document was produced with financial contributions from the Government of Sweden, the Tides Foundation, Passport Foundation, and other donors.

A version of this article appeared on Medscape.com.

The US Food and Drug Administration (FDA) announced the removal of the endocrine-disrupting chemicals (EDCs) per- and polyfluoroalkyl substances (PFAS) from food packaging.

Issued on February 28, 2024, “this means the major source of dietary exposure to PFAS from food packaging like fast-food wrappers, microwave popcorn bags, take-out paperboard containers, and pet food bags is being eliminated,” the FDA said in a statement.

In 2020, the FDA had secured commitments from manufacturers to stop selling products containing PFAS used in the food packaging for grease-proofing. “Today’s announcement marks the fulfillment of these voluntary commitments,” according to the agency.

PFAS, a class of thousands of chemicals also called “forever chemicals” are widely used in consumer and industrial products. People may be exposed via contaminated food packaging (although perhaps no longer in the United States) or occupationally. Studies have found that some PFAS disrupt hormones including estrogen and testosterone, whereas others may impair thyroid function.
 

Endocrine Society Report Sounds the Alarm About PFAS and Others

The FDA’s announcement came just 2 days after the Endocrine Society issued a new alarm about the human health dangers from environmental EDCs including PFAS in a report covering the latest science.

“Endocrine disrupting chemicals” are individual substances or mixtures that can interfere with natural hormonal function, leading to disease or even death. Many are ubiquitous in the modern environment and contribute to a wide range of human diseases.

The new report Endocrine Disrupting Chemicals: Threats to Human Health was issued jointly with the International Pollutants Elimination Network (IPEN), a global advocacy organization. It’s an update to the Endocrine Society’s 2015 report, providing new data on the endocrine-disrupting substances previously covered and adding four EDCs not discussed in that document: Pesticides, plastics, PFAS, and children’s products containing arsenic.

At a briefing held during the United Nations Environment Assembly meeting in Nairobi, Kenya, last week, the new report’s lead author Andrea C. Gore, PhD, of the University of Texas at Austin, noted, “A well-established body of scientific research indicates that endocrine-disrupting chemicals that are part of our daily lives are making us more susceptible to reproductive disorders, cancer, diabetes, obesity, heart disease, and other serious health conditions.”

Added Dr. Gore, who is also a member of the Endocrine Society’s Board of Directors, “These chemicals pose particularly serious risks to pregnant women and children. Now is the time for the UN Environment Assembly and other global policymakers to take action to address this threat to public health.”

While the science has been emerging rapidly, global and national chemical control policies haven’t kept up, the authors said. Of particular concern is that EDCs behave differently from other chemicals in many ways, including that even very low-dose exposures can pose health threats, but policies thus far haven’t dealt with that aspect.

Moreover, “the effects of low doses cannot be predicted by the effects observed at high doses. This means there may be no safe dose for exposure to EDCs,” according to the report.

Exposures can come from household products, including furniture, toys, and food packages, as well as electronics building materials and cosmetics. These chemicals are also in the outdoor environment, via pesticides, air pollution, and industrial waste.

“IPEN and the Endocrine Society call for chemical regulations based on the most modern scientific understanding of how hormones act and how EDCs can perturb these actions. We work to educate policy makers in global, regional, and national government assemblies and help ensure that regulations correlate with current scientific understanding,” they said in the report.
 

New Data on Four Classes of EDCs

Chapters of the report summarized the latest information about the science of EDCs and their links to endocrine disease and real-world exposure. It included a special section about “EDCs throughout the plastics life cycle” and a summary of the links between EDCs and climate change.

The report reviewed three pesticides, including the world’s most heavily applied herbicide, glycophosphate. Exposures can occur directly from the air, water, dust, and food residues. Recent data linked glycophosphate to adverse reproductive health outcomes.

Two toxic plastic chemicals, phthalates and bisphenols, are present in personal care products, among others. Emerging evidence links them with impaired neurodevelopment, leading to impaired cognitive function, learning, attention, and impulsivity.

Arsenic has long been linked to human health conditions including cancer, but more recent evidence finds it can disrupt multiple endocrine systems and lead to metabolic conditions including diabetes, reproductive dysfunction, and cardiovascular and neurocognitive conditions.

The special section about plastics noted that they are made from fossil fuels and chemicals, including many toxic substances that are known or suspected EDCs. People who live near plastic production facilities or waste dumps may be at greatest risk, but anyone can be exposed using any plastic product. Plastic waste disposal is increasingly problematic and often foisted on lower- and middle-income countries.
 

‘Additional Education and Awareness-Raising Among Stakeholders Remain Necessary’

Policies aimed at reducing human health risks from EDCs have included the 2022 Plastics Treaty, a resolution adopted by 175 countries at the United Nations Environmental Assembly that “may be a significant step toward global control of plastics and elimination of threats from exposures to EDCs in plastics,” the report said.

The authors added, “While significant progress has been made in recent years connecting scientific advances on EDCs with health-protective policies, additional education and awareness-raising among stakeholders remain necessary to achieve a safer and more sustainable environment that minimizes exposure to these harmful chemicals.”

The document was produced with financial contributions from the Government of Sweden, the Tides Foundation, Passport Foundation, and other donors.

A version of this article appeared on Medscape.com.

The US Food and Drug Administration (FDA) announced the removal of the endocrine-disrupting chemicals (EDCs) per- and polyfluoroalkyl substances (PFAS) from food packaging.

Issued on February 28, 2024, “this means the major source of dietary exposure to PFAS from food packaging like fast-food wrappers, microwave popcorn bags, take-out paperboard containers, and pet food bags is being eliminated,” the FDA said in a statement.

In 2020, the FDA had secured commitments from manufacturers to stop selling products containing PFAS used in the food packaging for grease-proofing. “Today’s announcement marks the fulfillment of these voluntary commitments,” according to the agency.

PFAS, a class of thousands of chemicals also called “forever chemicals” are widely used in consumer and industrial products. People may be exposed via contaminated food packaging (although perhaps no longer in the United States) or occupationally. Studies have found that some PFAS disrupt hormones including estrogen and testosterone, whereas others may impair thyroid function.
 

Endocrine Society Report Sounds the Alarm About PFAS and Others

The FDA’s announcement came just 2 days after the Endocrine Society issued a new alarm about the human health dangers from environmental EDCs including PFAS in a report covering the latest science.

“Endocrine disrupting chemicals” are individual substances or mixtures that can interfere with natural hormonal function, leading to disease or even death. Many are ubiquitous in the modern environment and contribute to a wide range of human diseases.

The new report Endocrine Disrupting Chemicals: Threats to Human Health was issued jointly with the International Pollutants Elimination Network (IPEN), a global advocacy organization. It’s an update to the Endocrine Society’s 2015 report, providing new data on the endocrine-disrupting substances previously covered and adding four EDCs not discussed in that document: Pesticides, plastics, PFAS, and children’s products containing arsenic.

At a briefing held during the United Nations Environment Assembly meeting in Nairobi, Kenya, last week, the new report’s lead author Andrea C. Gore, PhD, of the University of Texas at Austin, noted, “A well-established body of scientific research indicates that endocrine-disrupting chemicals that are part of our daily lives are making us more susceptible to reproductive disorders, cancer, diabetes, obesity, heart disease, and other serious health conditions.”

Added Dr. Gore, who is also a member of the Endocrine Society’s Board of Directors, “These chemicals pose particularly serious risks to pregnant women and children. Now is the time for the UN Environment Assembly and other global policymakers to take action to address this threat to public health.”

While the science has been emerging rapidly, global and national chemical control policies haven’t kept up, the authors said. Of particular concern is that EDCs behave differently from other chemicals in many ways, including that even very low-dose exposures can pose health threats, but policies thus far haven’t dealt with that aspect.

Moreover, “the effects of low doses cannot be predicted by the effects observed at high doses. This means there may be no safe dose for exposure to EDCs,” according to the report.

Exposures can come from household products, including furniture, toys, and food packages, as well as electronics building materials and cosmetics. These chemicals are also in the outdoor environment, via pesticides, air pollution, and industrial waste.

“IPEN and the Endocrine Society call for chemical regulations based on the most modern scientific understanding of how hormones act and how EDCs can perturb these actions. We work to educate policy makers in global, regional, and national government assemblies and help ensure that regulations correlate with current scientific understanding,” they said in the report.
 

New Data on Four Classes of EDCs

Chapters of the report summarized the latest information about the science of EDCs and their links to endocrine disease and real-world exposure. It included a special section about “EDCs throughout the plastics life cycle” and a summary of the links between EDCs and climate change.

The report reviewed three pesticides, including the world’s most heavily applied herbicide, glycophosphate. Exposures can occur directly from the air, water, dust, and food residues. Recent data linked glycophosphate to adverse reproductive health outcomes.

Two toxic plastic chemicals, phthalates and bisphenols, are present in personal care products, among others. Emerging evidence links them with impaired neurodevelopment, leading to impaired cognitive function, learning, attention, and impulsivity.

Arsenic has long been linked to human health conditions including cancer, but more recent evidence finds it can disrupt multiple endocrine systems and lead to metabolic conditions including diabetes, reproductive dysfunction, and cardiovascular and neurocognitive conditions.

The special section about plastics noted that they are made from fossil fuels and chemicals, including many toxic substances that are known or suspected EDCs. People who live near plastic production facilities or waste dumps may be at greatest risk, but anyone can be exposed using any plastic product. Plastic waste disposal is increasingly problematic and often foisted on lower- and middle-income countries.
 

‘Additional Education and Awareness-Raising Among Stakeholders Remain Necessary’

Policies aimed at reducing human health risks from EDCs have included the 2022 Plastics Treaty, a resolution adopted by 175 countries at the United Nations Environmental Assembly that “may be a significant step toward global control of plastics and elimination of threats from exposures to EDCs in plastics,” the report said.

The authors added, “While significant progress has been made in recent years connecting scientific advances on EDCs with health-protective policies, additional education and awareness-raising among stakeholders remain necessary to achieve a safer and more sustainable environment that minimizes exposure to these harmful chemicals.”

The document was produced with financial contributions from the Government of Sweden, the Tides Foundation, Passport Foundation, and other donors.

A version of this article appeared on Medscape.com.