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Diabetes Drugs and Eye Disease: These Protect, These Don’t
TOPLINE:
METHODOLOGY:
- Researchers conducted a retrospective analysis of electronic medical records from the TriNetX health research network to evaluate how systemic medications, such as GLP-1 RAs, fenofibrates, thiazolidinediones, and calcium channel blockers, influence the risk of developing DME in patients with type 2 diabetes.
- They included patients with a 5-year history of type 2 diabetes and an absence of DME at baseline.
- The treatment group included patients who initiated treatment with calcium channel blockers (n = 107,193), GLP-1 RAs (n = 76,583), thiazolidinediones (n = 25,657), or fenofibrates (n = 18,606) after a diagnosis of diabetes. The control group received none of these medications within 1 year of being diagnosed with the condition.
- The researchers used propensity score matching to balance baseline characteristics and comorbidities between both groups.
- The primary outcome was the incidence of diagnoses of DME within a 2-year follow-up period after the initiation of systemic medications.
TAKEAWAY:
- Patients treated with calcium channel blockers showed an increased risk for incident DME (hazard ratio [HR], 1.66; 95% CI, 1.54-1.78) compared with control individuals.
- Treatment with GLP-1 RAs was associated with a reduced risk for DME (HR, 0.77; 95% CI, 0.70-0.85), as was treatment with fenofibrates (HR, 0.83; 95% CI, 0.68-0.98).
- No significant difference in risk for DME was observed between patients taking thiazolidinediones and control individuals.
IN PRACTICE:
“We found a possible protective effect for GLP-1 RA medications and fenofibrate for DME and an adverse effect for calcium channel blockers with regard to the development of DME in patients” with type 2 diabetes, the authors wrote.
“Our preliminary data suggests a protective effect with regard to GLP-1 RA drugs and the development of DME. Clinical studies examining a potential therapeutic effect of GLP-1 RA drugs on DME do seem warranted. A single orally administered drug could conceivably lower blood sugar, reduce weight, offer cardiovascular protection, and treat DME” in patients with type 2 diabetes, they added.
SOURCE:
The study was led by Jawad Muayad, BS, of the School of Medicine at Texas A&M University, in Houston. It was published online on December 5, 2024, in Ophthalmology Retina.
LIMITATIONS:
The study was retrospective in nature. It relied on electronic medical records for the diagnosis of DME instead of directly assessing retinal images or measuring retinal thickness. Moreover, patients on certain medications may have been monitored more closely, potentially influencing the likelihood of a diagnosis of DME being recorded.
DISCLOSURES:
The study did not receive any funding support. One author disclosed receiving consulting fees from various institutions and pharmaceutical companies. The other authors reported no relevant conflicts of interest.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- Researchers conducted a retrospective analysis of electronic medical records from the TriNetX health research network to evaluate how systemic medications, such as GLP-1 RAs, fenofibrates, thiazolidinediones, and calcium channel blockers, influence the risk of developing DME in patients with type 2 diabetes.
- They included patients with a 5-year history of type 2 diabetes and an absence of DME at baseline.
- The treatment group included patients who initiated treatment with calcium channel blockers (n = 107,193), GLP-1 RAs (n = 76,583), thiazolidinediones (n = 25,657), or fenofibrates (n = 18,606) after a diagnosis of diabetes. The control group received none of these medications within 1 year of being diagnosed with the condition.
- The researchers used propensity score matching to balance baseline characteristics and comorbidities between both groups.
- The primary outcome was the incidence of diagnoses of DME within a 2-year follow-up period after the initiation of systemic medications.
TAKEAWAY:
- Patients treated with calcium channel blockers showed an increased risk for incident DME (hazard ratio [HR], 1.66; 95% CI, 1.54-1.78) compared with control individuals.
- Treatment with GLP-1 RAs was associated with a reduced risk for DME (HR, 0.77; 95% CI, 0.70-0.85), as was treatment with fenofibrates (HR, 0.83; 95% CI, 0.68-0.98).
- No significant difference in risk for DME was observed between patients taking thiazolidinediones and control individuals.
IN PRACTICE:
“We found a possible protective effect for GLP-1 RA medications and fenofibrate for DME and an adverse effect for calcium channel blockers with regard to the development of DME in patients” with type 2 diabetes, the authors wrote.
“Our preliminary data suggests a protective effect with regard to GLP-1 RA drugs and the development of DME. Clinical studies examining a potential therapeutic effect of GLP-1 RA drugs on DME do seem warranted. A single orally administered drug could conceivably lower blood sugar, reduce weight, offer cardiovascular protection, and treat DME” in patients with type 2 diabetes, they added.
SOURCE:
The study was led by Jawad Muayad, BS, of the School of Medicine at Texas A&M University, in Houston. It was published online on December 5, 2024, in Ophthalmology Retina.
LIMITATIONS:
The study was retrospective in nature. It relied on electronic medical records for the diagnosis of DME instead of directly assessing retinal images or measuring retinal thickness. Moreover, patients on certain medications may have been monitored more closely, potentially influencing the likelihood of a diagnosis of DME being recorded.
DISCLOSURES:
The study did not receive any funding support. One author disclosed receiving consulting fees from various institutions and pharmaceutical companies. The other authors reported no relevant conflicts of interest.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- Researchers conducted a retrospective analysis of electronic medical records from the TriNetX health research network to evaluate how systemic medications, such as GLP-1 RAs, fenofibrates, thiazolidinediones, and calcium channel blockers, influence the risk of developing DME in patients with type 2 diabetes.
- They included patients with a 5-year history of type 2 diabetes and an absence of DME at baseline.
- The treatment group included patients who initiated treatment with calcium channel blockers (n = 107,193), GLP-1 RAs (n = 76,583), thiazolidinediones (n = 25,657), or fenofibrates (n = 18,606) after a diagnosis of diabetes. The control group received none of these medications within 1 year of being diagnosed with the condition.
- The researchers used propensity score matching to balance baseline characteristics and comorbidities between both groups.
- The primary outcome was the incidence of diagnoses of DME within a 2-year follow-up period after the initiation of systemic medications.
TAKEAWAY:
- Patients treated with calcium channel blockers showed an increased risk for incident DME (hazard ratio [HR], 1.66; 95% CI, 1.54-1.78) compared with control individuals.
- Treatment with GLP-1 RAs was associated with a reduced risk for DME (HR, 0.77; 95% CI, 0.70-0.85), as was treatment with fenofibrates (HR, 0.83; 95% CI, 0.68-0.98).
- No significant difference in risk for DME was observed between patients taking thiazolidinediones and control individuals.
IN PRACTICE:
“We found a possible protective effect for GLP-1 RA medications and fenofibrate for DME and an adverse effect for calcium channel blockers with regard to the development of DME in patients” with type 2 diabetes, the authors wrote.
“Our preliminary data suggests a protective effect with regard to GLP-1 RA drugs and the development of DME. Clinical studies examining a potential therapeutic effect of GLP-1 RA drugs on DME do seem warranted. A single orally administered drug could conceivably lower blood sugar, reduce weight, offer cardiovascular protection, and treat DME” in patients with type 2 diabetes, they added.
SOURCE:
The study was led by Jawad Muayad, BS, of the School of Medicine at Texas A&M University, in Houston. It was published online on December 5, 2024, in Ophthalmology Retina.
LIMITATIONS:
The study was retrospective in nature. It relied on electronic medical records for the diagnosis of DME instead of directly assessing retinal images or measuring retinal thickness. Moreover, patients on certain medications may have been monitored more closely, potentially influencing the likelihood of a diagnosis of DME being recorded.
DISCLOSURES:
The study did not receive any funding support. One author disclosed receiving consulting fees from various institutions and pharmaceutical companies. The other authors reported no relevant conflicts of interest.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
Do GLP-1s Lower VTE Risk in People With Type 2 Diabetes?
Overall, GLP-1 agonist use was associated with a 20% reduction in VTE, compared with DPP-4 inhibitor use, in those with type 2 diabetes, and this benefit held regardless of people’s obesity status, said study investigator Cho-Han Chiang, MD, a medical resident at Mount Auburn Hospital, Cambridge, Massachusetts, who presented the findings at the American Society of Hematology (ASH) 2024 Annual Meeting.
The incidence of VTE has increased by 20% over the past 10 years, and obesity is a risk factor for VTE, Chiang explained. A growing body of evidence demonstrated that GLP-1s provide a variety of cardiovascular benefits in people with type 2 diabetes, but data on VTE benefits remain more limited.
In the retrospective study, the researchers combed electronic health records from the TriNetX global database, which includes more than 250 million patients, and identified adults with type 2 diabetes who were taking a GLP-1 agonist or a DPP-4 inhibitor.
After excluding anyone with prior VTE or atrial fibrillation as well as those treated with both drugs or with oral anticoagulants, patients on GLP-1s were matched with those on DPP-4 inhibitors based on predetermined variables, including age, sex, race, body mass index (BMI), hemoglobin A1c, use of other antidiabetic agents, and underlying comorbidities. VTE was a composite of pulmonary embolism and deep vein thrombosis.
The researchers also performed a subgroup analysis that stratified patients by obesity status, defined as a BMI ≥ 30.
Within 1 year of GLP-1 or DPP-4 prescription, VTE occurred at a rate of 6.5 cases/1000 person-years in the GLP-1 group vs 7.9 cases/1000 person years in the DPP-4 inhibitor group (hazard ratio [HR], 0.80; P < .001).
The 20% risk reduction in VTE held across various subgroups of BMI, including among those with obesity, Chiang reported.
Among patients with the highest BMI (≥ 40), VTE occurred at a rate of 7.2 cases/1000 person years in the GLP-1 group vs 9.6 cases/1000 person years in the DPP-4 inhibitor group (HR, 0.74). Among patients with the next highest BMI (30-34.9), VTE occurred at a rate of 4.8 cases/1000 person years in the GLP-1 group vs 7.9 cases/1000 person years in the DPP-4 inhibitor group (HR, 0.60). Among those with the lowest BMI (18.5-24.9), VTE occurred significantly less frequently among those in the GLP-1 group — 4.7 cases/1000 person years vs 7.4 cases/1000 person years in the DPP-4 inhibitor group (HR, 0.61).
The lower risk for VTE associated with GLP-1s also held across the individual components of the composite VTE. Pulmonary embolism occurred at a rate of 3.1 cases/1000 person years in the GLP-1 group vs 3.9 cases/1000 person years in the DPP-4 inhibitor group (HR, 0.78), and deep vein thrombosis occurred in 4.2 cases/1000 person years in the GLP-1 group vs 5.0 cases/1000 person years in the DPP-4 inhibitor group (HR, 0.82).
Interestingly, the GLP-1 and DPP-4 curves started diverging within the first 30 days of the index prescription date, said Chiang.
Session moderator Ghadeer Dawwas, PhD, said in an interview that patients with type 2 diabetes are increasingly using GLP-1 agonists because of the cardiovascular benefits associated with the agents, which include lower risks for stroke and heart failure, but the antithrombotic benefits are still debated.
“The current study indicates that GLP-1 agonists may help lower the risk of VTE in patients with type 2 diabetes, irrespective of their baseline body weight,” said Dawwas, a pharmacoepidemiologist and assistant professor of medicine at Vanderbilt University Medical Center in Nashville, Tennessee. “However, given the current landscape of evidence and the existence of conflicting data on VTE risk, clinicians should proceed with caution and await further studies to validate these findings before making clinical decisions.”
This study was funded by the National Blood Clot Alliance and Conquer Cancer Foundation. Chiang and Dawwas had no disclosures.
A version of this article appeared on Medscape.com.
Overall, GLP-1 agonist use was associated with a 20% reduction in VTE, compared with DPP-4 inhibitor use, in those with type 2 diabetes, and this benefit held regardless of people’s obesity status, said study investigator Cho-Han Chiang, MD, a medical resident at Mount Auburn Hospital, Cambridge, Massachusetts, who presented the findings at the American Society of Hematology (ASH) 2024 Annual Meeting.
The incidence of VTE has increased by 20% over the past 10 years, and obesity is a risk factor for VTE, Chiang explained. A growing body of evidence demonstrated that GLP-1s provide a variety of cardiovascular benefits in people with type 2 diabetes, but data on VTE benefits remain more limited.
In the retrospective study, the researchers combed electronic health records from the TriNetX global database, which includes more than 250 million patients, and identified adults with type 2 diabetes who were taking a GLP-1 agonist or a DPP-4 inhibitor.
After excluding anyone with prior VTE or atrial fibrillation as well as those treated with both drugs or with oral anticoagulants, patients on GLP-1s were matched with those on DPP-4 inhibitors based on predetermined variables, including age, sex, race, body mass index (BMI), hemoglobin A1c, use of other antidiabetic agents, and underlying comorbidities. VTE was a composite of pulmonary embolism and deep vein thrombosis.
The researchers also performed a subgroup analysis that stratified patients by obesity status, defined as a BMI ≥ 30.
Within 1 year of GLP-1 or DPP-4 prescription, VTE occurred at a rate of 6.5 cases/1000 person-years in the GLP-1 group vs 7.9 cases/1000 person years in the DPP-4 inhibitor group (hazard ratio [HR], 0.80; P < .001).
The 20% risk reduction in VTE held across various subgroups of BMI, including among those with obesity, Chiang reported.
Among patients with the highest BMI (≥ 40), VTE occurred at a rate of 7.2 cases/1000 person years in the GLP-1 group vs 9.6 cases/1000 person years in the DPP-4 inhibitor group (HR, 0.74). Among patients with the next highest BMI (30-34.9), VTE occurred at a rate of 4.8 cases/1000 person years in the GLP-1 group vs 7.9 cases/1000 person years in the DPP-4 inhibitor group (HR, 0.60). Among those with the lowest BMI (18.5-24.9), VTE occurred significantly less frequently among those in the GLP-1 group — 4.7 cases/1000 person years vs 7.4 cases/1000 person years in the DPP-4 inhibitor group (HR, 0.61).
The lower risk for VTE associated with GLP-1s also held across the individual components of the composite VTE. Pulmonary embolism occurred at a rate of 3.1 cases/1000 person years in the GLP-1 group vs 3.9 cases/1000 person years in the DPP-4 inhibitor group (HR, 0.78), and deep vein thrombosis occurred in 4.2 cases/1000 person years in the GLP-1 group vs 5.0 cases/1000 person years in the DPP-4 inhibitor group (HR, 0.82).
Interestingly, the GLP-1 and DPP-4 curves started diverging within the first 30 days of the index prescription date, said Chiang.
Session moderator Ghadeer Dawwas, PhD, said in an interview that patients with type 2 diabetes are increasingly using GLP-1 agonists because of the cardiovascular benefits associated with the agents, which include lower risks for stroke and heart failure, but the antithrombotic benefits are still debated.
“The current study indicates that GLP-1 agonists may help lower the risk of VTE in patients with type 2 diabetes, irrespective of their baseline body weight,” said Dawwas, a pharmacoepidemiologist and assistant professor of medicine at Vanderbilt University Medical Center in Nashville, Tennessee. “However, given the current landscape of evidence and the existence of conflicting data on VTE risk, clinicians should proceed with caution and await further studies to validate these findings before making clinical decisions.”
This study was funded by the National Blood Clot Alliance and Conquer Cancer Foundation. Chiang and Dawwas had no disclosures.
A version of this article appeared on Medscape.com.
Overall, GLP-1 agonist use was associated with a 20% reduction in VTE, compared with DPP-4 inhibitor use, in those with type 2 diabetes, and this benefit held regardless of people’s obesity status, said study investigator Cho-Han Chiang, MD, a medical resident at Mount Auburn Hospital, Cambridge, Massachusetts, who presented the findings at the American Society of Hematology (ASH) 2024 Annual Meeting.
The incidence of VTE has increased by 20% over the past 10 years, and obesity is a risk factor for VTE, Chiang explained. A growing body of evidence demonstrated that GLP-1s provide a variety of cardiovascular benefits in people with type 2 diabetes, but data on VTE benefits remain more limited.
In the retrospective study, the researchers combed electronic health records from the TriNetX global database, which includes more than 250 million patients, and identified adults with type 2 diabetes who were taking a GLP-1 agonist or a DPP-4 inhibitor.
After excluding anyone with prior VTE or atrial fibrillation as well as those treated with both drugs or with oral anticoagulants, patients on GLP-1s were matched with those on DPP-4 inhibitors based on predetermined variables, including age, sex, race, body mass index (BMI), hemoglobin A1c, use of other antidiabetic agents, and underlying comorbidities. VTE was a composite of pulmonary embolism and deep vein thrombosis.
The researchers also performed a subgroup analysis that stratified patients by obesity status, defined as a BMI ≥ 30.
Within 1 year of GLP-1 or DPP-4 prescription, VTE occurred at a rate of 6.5 cases/1000 person-years in the GLP-1 group vs 7.9 cases/1000 person years in the DPP-4 inhibitor group (hazard ratio [HR], 0.80; P < .001).
The 20% risk reduction in VTE held across various subgroups of BMI, including among those with obesity, Chiang reported.
Among patients with the highest BMI (≥ 40), VTE occurred at a rate of 7.2 cases/1000 person years in the GLP-1 group vs 9.6 cases/1000 person years in the DPP-4 inhibitor group (HR, 0.74). Among patients with the next highest BMI (30-34.9), VTE occurred at a rate of 4.8 cases/1000 person years in the GLP-1 group vs 7.9 cases/1000 person years in the DPP-4 inhibitor group (HR, 0.60). Among those with the lowest BMI (18.5-24.9), VTE occurred significantly less frequently among those in the GLP-1 group — 4.7 cases/1000 person years vs 7.4 cases/1000 person years in the DPP-4 inhibitor group (HR, 0.61).
The lower risk for VTE associated with GLP-1s also held across the individual components of the composite VTE. Pulmonary embolism occurred at a rate of 3.1 cases/1000 person years in the GLP-1 group vs 3.9 cases/1000 person years in the DPP-4 inhibitor group (HR, 0.78), and deep vein thrombosis occurred in 4.2 cases/1000 person years in the GLP-1 group vs 5.0 cases/1000 person years in the DPP-4 inhibitor group (HR, 0.82).
Interestingly, the GLP-1 and DPP-4 curves started diverging within the first 30 days of the index prescription date, said Chiang.
Session moderator Ghadeer Dawwas, PhD, said in an interview that patients with type 2 diabetes are increasingly using GLP-1 agonists because of the cardiovascular benefits associated with the agents, which include lower risks for stroke and heart failure, but the antithrombotic benefits are still debated.
“The current study indicates that GLP-1 agonists may help lower the risk of VTE in patients with type 2 diabetes, irrespective of their baseline body weight,” said Dawwas, a pharmacoepidemiologist and assistant professor of medicine at Vanderbilt University Medical Center in Nashville, Tennessee. “However, given the current landscape of evidence and the existence of conflicting data on VTE risk, clinicians should proceed with caution and await further studies to validate these findings before making clinical decisions.”
This study was funded by the National Blood Clot Alliance and Conquer Cancer Foundation. Chiang and Dawwas had no disclosures.
A version of this article appeared on Medscape.com.
FROM ASH 2024
CGM Use, GLP-1s, Drinking Water Key of 2025 ADA Standards
plus a strong endorsement for drinking water and much more.
The Standards of Care — 2025 were published December 9 as a supplement to Diabetes Care. The standards “incorporate the latest information from clinical trial data and knowledge of diabetes management into a comprehensive guidelines document that will assist physicians in managing patients with diabetes in their practices,” said Mandeep Bajaj, MBBS, ADA’s President, Medicine & Science.
In an interview, Bajaj highlighted some of the most important of the clinical updates in 2024, including the following:
- Consideration of the use of continuous glucose monitoring devices in adults with type 2 diabetes (T2D) who don’t use insulin. Medicare and many other payers currently only cover CGM for people who use insulin or are otherwise at risk for hypoglycemia. However, some CGMs are now available over the counter, Bajaj pointed out.
- Actions to be taken in the event of medication shortages. The ADA published guidance for this in the case of GLP-1 RAs on December 2. Essentially ADA advised substituting a different GLP-1 RA if possible. Nonapproved products aren’t recommended, but guidance is provided for people who choose to use them.
- Use of GLP-1 RAs for heart and kidney health. Recommendations were revised to explicitly advise on choice of pharmacotherapy for individuals with T2D, based on new data on those with established or high risk for atherosclerotic cardiovascular disease, heart failure with preserved ejection fraction, and chronic kidney disease.
- Treatment of MAFLD with moderate or advanced liver fibrosis. A new recommendation for use of a thyroid hormone receptor–beta agonist is based on trial data for resmetirom. Moreover, Bajaj noted, “we’ve adopted the new nomenclature, which was previously NAFLD and NASH, and now is MAFLD and MASH [metabolic-associated steatohepatitis].”
- Advice to continue weight management therapy beyond achieving weight loss goals. This is based on a large amount of evidence that “stopping these therapies are associated with weight regain and increased cardiovascular risk,” Bajaj said, adding that this recommendation was made in collaboration with the Obesity Society.
- Antibody-based screening for presymptomatic T1D in family members of people with T2D and others who may be at risk. “Individuals who test autoantibody positive should be provided with or referred for counseling about the risk of developing diabetes, diabetes symptoms, and [diabetic ketoacidosis] prevention and should be given consideration for referral to a specialized center for further evaluation and/or consideration of a clinical trial or approved therapy to potentially delay development of clinical diabetes,” the document says.
- Screen for psychosocial issues. People with diabetes should be screened for concerns including diabetes distress, depression, anxiety, fear of hypoglycemia, and disordered eating behaviors. “People on insulin or sulfonylureas may have fear of hypoglycemia, but diabetes distress can happen to anyone with diabetes,” Bajaj pointed out. Caregivers and family members should be screened as well, the document advises.
- Drink water, not soda. In the nutrition section, a new recommendation strongly advises drinking water instead of nutritive or nonnutritive sweetened beverages. “This is an important recommendation. So, when patients ask what’s the best thing to drink, our answer is drink water rather than Coca Cola or Diet Coke,” Bajaj said. But, what about people with diabetes who can’t quit their diet soda habit? “We’ve said that the nonnutritive sweetener is preferred over sugar sweetener, provided it’s in moderation and short term ... but the best is water.”
Bajaj has received grant support from ADA. He had no further disclosures.
A version of this article first appeared on Medscape.com.
plus a strong endorsement for drinking water and much more.
The Standards of Care — 2025 were published December 9 as a supplement to Diabetes Care. The standards “incorporate the latest information from clinical trial data and knowledge of diabetes management into a comprehensive guidelines document that will assist physicians in managing patients with diabetes in their practices,” said Mandeep Bajaj, MBBS, ADA’s President, Medicine & Science.
In an interview, Bajaj highlighted some of the most important of the clinical updates in 2024, including the following:
- Consideration of the use of continuous glucose monitoring devices in adults with type 2 diabetes (T2D) who don’t use insulin. Medicare and many other payers currently only cover CGM for people who use insulin or are otherwise at risk for hypoglycemia. However, some CGMs are now available over the counter, Bajaj pointed out.
- Actions to be taken in the event of medication shortages. The ADA published guidance for this in the case of GLP-1 RAs on December 2. Essentially ADA advised substituting a different GLP-1 RA if possible. Nonapproved products aren’t recommended, but guidance is provided for people who choose to use them.
- Use of GLP-1 RAs for heart and kidney health. Recommendations were revised to explicitly advise on choice of pharmacotherapy for individuals with T2D, based on new data on those with established or high risk for atherosclerotic cardiovascular disease, heart failure with preserved ejection fraction, and chronic kidney disease.
- Treatment of MAFLD with moderate or advanced liver fibrosis. A new recommendation for use of a thyroid hormone receptor–beta agonist is based on trial data for resmetirom. Moreover, Bajaj noted, “we’ve adopted the new nomenclature, which was previously NAFLD and NASH, and now is MAFLD and MASH [metabolic-associated steatohepatitis].”
- Advice to continue weight management therapy beyond achieving weight loss goals. This is based on a large amount of evidence that “stopping these therapies are associated with weight regain and increased cardiovascular risk,” Bajaj said, adding that this recommendation was made in collaboration with the Obesity Society.
- Antibody-based screening for presymptomatic T1D in family members of people with T2D and others who may be at risk. “Individuals who test autoantibody positive should be provided with or referred for counseling about the risk of developing diabetes, diabetes symptoms, and [diabetic ketoacidosis] prevention and should be given consideration for referral to a specialized center for further evaluation and/or consideration of a clinical trial or approved therapy to potentially delay development of clinical diabetes,” the document says.
- Screen for psychosocial issues. People with diabetes should be screened for concerns including diabetes distress, depression, anxiety, fear of hypoglycemia, and disordered eating behaviors. “People on insulin or sulfonylureas may have fear of hypoglycemia, but diabetes distress can happen to anyone with diabetes,” Bajaj pointed out. Caregivers and family members should be screened as well, the document advises.
- Drink water, not soda. In the nutrition section, a new recommendation strongly advises drinking water instead of nutritive or nonnutritive sweetened beverages. “This is an important recommendation. So, when patients ask what’s the best thing to drink, our answer is drink water rather than Coca Cola or Diet Coke,” Bajaj said. But, what about people with diabetes who can’t quit their diet soda habit? “We’ve said that the nonnutritive sweetener is preferred over sugar sweetener, provided it’s in moderation and short term ... but the best is water.”
Bajaj has received grant support from ADA. He had no further disclosures.
A version of this article first appeared on Medscape.com.
plus a strong endorsement for drinking water and much more.
The Standards of Care — 2025 were published December 9 as a supplement to Diabetes Care. The standards “incorporate the latest information from clinical trial data and knowledge of diabetes management into a comprehensive guidelines document that will assist physicians in managing patients with diabetes in their practices,” said Mandeep Bajaj, MBBS, ADA’s President, Medicine & Science.
In an interview, Bajaj highlighted some of the most important of the clinical updates in 2024, including the following:
- Consideration of the use of continuous glucose monitoring devices in adults with type 2 diabetes (T2D) who don’t use insulin. Medicare and many other payers currently only cover CGM for people who use insulin or are otherwise at risk for hypoglycemia. However, some CGMs are now available over the counter, Bajaj pointed out.
- Actions to be taken in the event of medication shortages. The ADA published guidance for this in the case of GLP-1 RAs on December 2. Essentially ADA advised substituting a different GLP-1 RA if possible. Nonapproved products aren’t recommended, but guidance is provided for people who choose to use them.
- Use of GLP-1 RAs for heart and kidney health. Recommendations were revised to explicitly advise on choice of pharmacotherapy for individuals with T2D, based on new data on those with established or high risk for atherosclerotic cardiovascular disease, heart failure with preserved ejection fraction, and chronic kidney disease.
- Treatment of MAFLD with moderate or advanced liver fibrosis. A new recommendation for use of a thyroid hormone receptor–beta agonist is based on trial data for resmetirom. Moreover, Bajaj noted, “we’ve adopted the new nomenclature, which was previously NAFLD and NASH, and now is MAFLD and MASH [metabolic-associated steatohepatitis].”
- Advice to continue weight management therapy beyond achieving weight loss goals. This is based on a large amount of evidence that “stopping these therapies are associated with weight regain and increased cardiovascular risk,” Bajaj said, adding that this recommendation was made in collaboration with the Obesity Society.
- Antibody-based screening for presymptomatic T1D in family members of people with T2D and others who may be at risk. “Individuals who test autoantibody positive should be provided with or referred for counseling about the risk of developing diabetes, diabetes symptoms, and [diabetic ketoacidosis] prevention and should be given consideration for referral to a specialized center for further evaluation and/or consideration of a clinical trial or approved therapy to potentially delay development of clinical diabetes,” the document says.
- Screen for psychosocial issues. People with diabetes should be screened for concerns including diabetes distress, depression, anxiety, fear of hypoglycemia, and disordered eating behaviors. “People on insulin or sulfonylureas may have fear of hypoglycemia, but diabetes distress can happen to anyone with diabetes,” Bajaj pointed out. Caregivers and family members should be screened as well, the document advises.
- Drink water, not soda. In the nutrition section, a new recommendation strongly advises drinking water instead of nutritive or nonnutritive sweetened beverages. “This is an important recommendation. So, when patients ask what’s the best thing to drink, our answer is drink water rather than Coca Cola or Diet Coke,” Bajaj said. But, what about people with diabetes who can’t quit their diet soda habit? “We’ve said that the nonnutritive sweetener is preferred over sugar sweetener, provided it’s in moderation and short term ... but the best is water.”
Bajaj has received grant support from ADA. He had no further disclosures.
A version of this article first appeared on Medscape.com.
Skin Stress Biomarker May Predict Nerve Damage in Early T2D
TOPLINE:
Increased cutaneous carbonyl stress is linked to slower nerve conduction in patients with metabolically well-controlled, recent-onset type 2 diabetes (T2D) and can predict the development of neuropathic deficits over 5 years.
METHODOLOGY:
- Accumulation of advanced glycation end products (AGEs), which results from endogenous carbonyl stress, may be a potential target for preventing and treating the diabetic sensorimotor polyneuropathy (DSPN) that is a common complication of T2D.
- Researchers investigated novel cutaneous biomarkers for the development and progression of DSPN in 160 individuals with recent-onset T2D (diagnosed within 12 months or less) and 144 individuals with normal glucose tolerance, all recruited consecutively from the German Diabetes Study baseline cohort.
- Peripheral nerve function was assessed through nerve conduction studies, quantitative sensory testing, and clinical neuropathy scores.
- Skin biopsies were used to analyze intraepidermal nerve fiber density, endothelial integrity, cutaneous oxidative stress markers, and cutaneous carbonyl stress markers, including AGE autofluorescence and argpyrimidine area.
- Skin autofluorescence was measured noninvasively using an AGE reader device.
- A subgroup of 80 patients with T2D were reassessed after 5 years to evaluate the progression of neurophysiological deficits.
TAKEAWAY:
- Patients with recent-onset T2D had greater AGE autofluorescence and argpyrimidine area (P ≤ .05 for both) and lower nerve fiber density (P ≤ .05) than individuals with normal glucose tolerance.
- In patients with T2D, AGE autofluorescence was inversely associated with nerve conduction (P = .0002, P = .002, and P = .001 for peroneal motor, median motor, and sural sensory nerve conduction velocity, respectively) and positively associated with AGE reader measurements (P < .05); no such associations were observed in those with normal glucose tolerance.
- In the prospective T2D cohort, associations were noted between cutaneous markers for AGEs and endothelial cells at baseline and changes in nerve function indices over a 5-year period.
IN PRACTICE:
“Prospective analyses revealed some predictive value of cutaneous AGEs and lower endothelial integrity for declining nerve function, supporting the role of carbonyl stress in the development and progression of DSPN, representing a potential therapeutic target,” the authors wrote.
SOURCE:
The study was led by Gidon J. Bönhof, Department of Endocrinology and Diabetology, Medical Faculty, University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. It was published online in Diabetes Care.
LIMITATIONS:
The observational design of the study limited the ability to draw causal conclusions. The groups were not matched for age or body mass index. Various mechanisms related to DSPN were analyzed; however, specific pathways of AGEs were not studied in detail. The relatively low number of individuals with clinically manifested DSPN limited the exploration of different stages of the condition.
DISCLOSURES:
The study was supported by a German Center for Diabetes Research grant. The German Diabetes Study was supported by the German Diabetes Center funded by the German Federal Ministry of Health (Berlin), the Ministry of Innovation, Science, Research and Technology of North Rhine-Westphalia (Düsseldorf, Germany), and grants from the German Federal Ministry of Education and Research to the German Center for Diabetes Research e.V. No relevant conflicts of interest were reported.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
A version of this article first appeared on Medscape.com.
TOPLINE:
Increased cutaneous carbonyl stress is linked to slower nerve conduction in patients with metabolically well-controlled, recent-onset type 2 diabetes (T2D) and can predict the development of neuropathic deficits over 5 years.
METHODOLOGY:
- Accumulation of advanced glycation end products (AGEs), which results from endogenous carbonyl stress, may be a potential target for preventing and treating the diabetic sensorimotor polyneuropathy (DSPN) that is a common complication of T2D.
- Researchers investigated novel cutaneous biomarkers for the development and progression of DSPN in 160 individuals with recent-onset T2D (diagnosed within 12 months or less) and 144 individuals with normal glucose tolerance, all recruited consecutively from the German Diabetes Study baseline cohort.
- Peripheral nerve function was assessed through nerve conduction studies, quantitative sensory testing, and clinical neuropathy scores.
- Skin biopsies were used to analyze intraepidermal nerve fiber density, endothelial integrity, cutaneous oxidative stress markers, and cutaneous carbonyl stress markers, including AGE autofluorescence and argpyrimidine area.
- Skin autofluorescence was measured noninvasively using an AGE reader device.
- A subgroup of 80 patients with T2D were reassessed after 5 years to evaluate the progression of neurophysiological deficits.
TAKEAWAY:
- Patients with recent-onset T2D had greater AGE autofluorescence and argpyrimidine area (P ≤ .05 for both) and lower nerve fiber density (P ≤ .05) than individuals with normal glucose tolerance.
- In patients with T2D, AGE autofluorescence was inversely associated with nerve conduction (P = .0002, P = .002, and P = .001 for peroneal motor, median motor, and sural sensory nerve conduction velocity, respectively) and positively associated with AGE reader measurements (P < .05); no such associations were observed in those with normal glucose tolerance.
- In the prospective T2D cohort, associations were noted between cutaneous markers for AGEs and endothelial cells at baseline and changes in nerve function indices over a 5-year period.
IN PRACTICE:
“Prospective analyses revealed some predictive value of cutaneous AGEs and lower endothelial integrity for declining nerve function, supporting the role of carbonyl stress in the development and progression of DSPN, representing a potential therapeutic target,” the authors wrote.
SOURCE:
The study was led by Gidon J. Bönhof, Department of Endocrinology and Diabetology, Medical Faculty, University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. It was published online in Diabetes Care.
LIMITATIONS:
The observational design of the study limited the ability to draw causal conclusions. The groups were not matched for age or body mass index. Various mechanisms related to DSPN were analyzed; however, specific pathways of AGEs were not studied in detail. The relatively low number of individuals with clinically manifested DSPN limited the exploration of different stages of the condition.
DISCLOSURES:
The study was supported by a German Center for Diabetes Research grant. The German Diabetes Study was supported by the German Diabetes Center funded by the German Federal Ministry of Health (Berlin), the Ministry of Innovation, Science, Research and Technology of North Rhine-Westphalia (Düsseldorf, Germany), and grants from the German Federal Ministry of Education and Research to the German Center for Diabetes Research e.V. No relevant conflicts of interest were reported.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
A version of this article first appeared on Medscape.com.
TOPLINE:
Increased cutaneous carbonyl stress is linked to slower nerve conduction in patients with metabolically well-controlled, recent-onset type 2 diabetes (T2D) and can predict the development of neuropathic deficits over 5 years.
METHODOLOGY:
- Accumulation of advanced glycation end products (AGEs), which results from endogenous carbonyl stress, may be a potential target for preventing and treating the diabetic sensorimotor polyneuropathy (DSPN) that is a common complication of T2D.
- Researchers investigated novel cutaneous biomarkers for the development and progression of DSPN in 160 individuals with recent-onset T2D (diagnosed within 12 months or less) and 144 individuals with normal glucose tolerance, all recruited consecutively from the German Diabetes Study baseline cohort.
- Peripheral nerve function was assessed through nerve conduction studies, quantitative sensory testing, and clinical neuropathy scores.
- Skin biopsies were used to analyze intraepidermal nerve fiber density, endothelial integrity, cutaneous oxidative stress markers, and cutaneous carbonyl stress markers, including AGE autofluorescence and argpyrimidine area.
- Skin autofluorescence was measured noninvasively using an AGE reader device.
- A subgroup of 80 patients with T2D were reassessed after 5 years to evaluate the progression of neurophysiological deficits.
TAKEAWAY:
- Patients with recent-onset T2D had greater AGE autofluorescence and argpyrimidine area (P ≤ .05 for both) and lower nerve fiber density (P ≤ .05) than individuals with normal glucose tolerance.
- In patients with T2D, AGE autofluorescence was inversely associated with nerve conduction (P = .0002, P = .002, and P = .001 for peroneal motor, median motor, and sural sensory nerve conduction velocity, respectively) and positively associated with AGE reader measurements (P < .05); no such associations were observed in those with normal glucose tolerance.
- In the prospective T2D cohort, associations were noted between cutaneous markers for AGEs and endothelial cells at baseline and changes in nerve function indices over a 5-year period.
IN PRACTICE:
“Prospective analyses revealed some predictive value of cutaneous AGEs and lower endothelial integrity for declining nerve function, supporting the role of carbonyl stress in the development and progression of DSPN, representing a potential therapeutic target,” the authors wrote.
SOURCE:
The study was led by Gidon J. Bönhof, Department of Endocrinology and Diabetology, Medical Faculty, University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, Düsseldorf, Germany. It was published online in Diabetes Care.
LIMITATIONS:
The observational design of the study limited the ability to draw causal conclusions. The groups were not matched for age or body mass index. Various mechanisms related to DSPN were analyzed; however, specific pathways of AGEs were not studied in detail. The relatively low number of individuals with clinically manifested DSPN limited the exploration of different stages of the condition.
DISCLOSURES:
The study was supported by a German Center for Diabetes Research grant. The German Diabetes Study was supported by the German Diabetes Center funded by the German Federal Ministry of Health (Berlin), the Ministry of Innovation, Science, Research and Technology of North Rhine-Westphalia (Düsseldorf, Germany), and grants from the German Federal Ministry of Education and Research to the German Center for Diabetes Research e.V. No relevant conflicts of interest were reported.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
A version of this article first appeared on Medscape.com.
No, Diet and Exercise Are Not Better Than Drugs for Obesity
They’re literally not better. Idealistically, sure, but literally not. And there’s really no debate. Meaning there’s never been a reproducible diet and exercise intervention that has led to anywhere near the average weight lost by those taking obesity medications. Furthermore, when it comes to the durability of weight lost, the gulf between outcomes with diet and exercise vs obesity medications is even more dramatic.
Looking to the literature, one of the most trotted out studies on lifestyle’s impact on weight over time is the Look AHEAD trial. Before useful obesity medications came on the scene, I trotted it out myself. Why? Because it was heartening when faced with the societal refrain that diet and exercise never worked to be able to show that yes, in fact they do. But how well?
Looking to Look AHEAD’s 4-year data (Obesity [Silver Spring]. 2011 Oct;19[10]:1987-1998), those randomized to the intensive lifestyle initiative arm averaged a 4.7% total body weight loss – an amount that remained the same at 8 years. But I chose 4 years because that’s a better comparison with the semaglutide SELECT trial that revealed at 4 years, the average sustained weight lost was more than double that of Look AHEAD’s, at 10.2%. Meanwhile the recently released SURMOUNT-4 study on tirzepatide reported that at 88 weeks, the average weight lost by participants was a near bariatric surgery level of 25.3% with no signs suggestive of pending regains.
Now maybe you want to cling to the notion that if you just try hard enough, your diet and exercise regime can beat our new meds. Well, it’s difficult to think of a more miserable, often actual vomit-inducing intervention, than the spectacle that used to air weekly on prime time called The Biggest Loser, where participants lived on a ranch and were berated and exercised all day long for the chance to lose the most and win a quarter of a million dollars. But even there, the meds prove to be superior. Although the short-term Biggest Loser data do look markedly better than meds (and than bariatric surgery), whereby the average participant lost 48.8% of their body weight during the grueling 7-month long, 24/7 competition, by postcompetition year 6, the average weight lost dropped to 12.7%.
Yet on November 26, when word came out that Medicare is likely to extend coverage to obesity medications for far more Americans, one of the most common refrains was something along the lines of yes, lifestyle modification is the best choice for dealing with obesity but it’s good that there will be medication options for those where that’s insufficient.
What?
The message is that people simply aren’t trying hard enough. This despite our comfort in knowing that medications have more of an impact than lifestyle on pretty much every other chronic disease. Nor can I recall any other circumstance when coverage of a remarkably effective drug was qualified by the suggestion that known-to-be-inferior interventions are still the best or favored choice.
At this point, obesity medications are plainly the first-line choice of treatment. They provide not only dramatically greater and more durable weight loss than lifestyle interventions, they have also been shown to very significantly reduce the risk for an ever-growing list of other medical concerns including heart attacks, strokes, type 2 diabetes, hypertension, sleep apnea, fatty liver disease, and more, while carrying minimal risk.
Let it also be said that improvements to diet and exercise are worth striving for at any weight, though one should not lose sight of the fact that perpetual, dramatic, intentional, behavior change in the name of health requires vast amounts of wide-ranging privilege to enact — amounts far beyond the average person’s abilities or physiologies (as demonstrated with obesity by decades of disappointing long-term lifestyle outcome data).
Let it also be said that some people will indeed find success solely through lifestyle and that not every person who meets the medical criteria for any medication’s prescription, including obesity medications, is required or encouraged to take it. The clinician’s job, however, at its most basic, is to inform patients who meet medical use criteria of their options, and if a medication is indicated, to inform them of that medication’s risks and benefits and expected outcomes, to help their patients come to their own treatment decisions.
It’s not a bad thing that we have medications that deliver better outcomes than lifestyle — in fact, it’s terrific, and thankfully that they do is true for pretty much every medical condition for which we have medication. That’s in fact why we have medications! And so this constant refrain of golly-gee wouldn’t it be better if we could just manage obesity with lifestyle changes needs to be put to rest — we literally know it wouldn’t be better, and it’s only weight bias that would lead this evidence-based statement to seem off-putting.
Dr. Freedhoff is Associate Professor, Department of Family Medicine, University of Ottawa, and Medical Director, Bariatric Medical Institute, Ottawa, Ontario, Canada. He reported conflicts of interest with the Bariatric Medical Institute, Constant Health, Novo Nordisk, and Weighty Matters.
A version of this article first appeared on Medscape.com.
They’re literally not better. Idealistically, sure, but literally not. And there’s really no debate. Meaning there’s never been a reproducible diet and exercise intervention that has led to anywhere near the average weight lost by those taking obesity medications. Furthermore, when it comes to the durability of weight lost, the gulf between outcomes with diet and exercise vs obesity medications is even more dramatic.
Looking to the literature, one of the most trotted out studies on lifestyle’s impact on weight over time is the Look AHEAD trial. Before useful obesity medications came on the scene, I trotted it out myself. Why? Because it was heartening when faced with the societal refrain that diet and exercise never worked to be able to show that yes, in fact they do. But how well?
Looking to Look AHEAD’s 4-year data (Obesity [Silver Spring]. 2011 Oct;19[10]:1987-1998), those randomized to the intensive lifestyle initiative arm averaged a 4.7% total body weight loss – an amount that remained the same at 8 years. But I chose 4 years because that’s a better comparison with the semaglutide SELECT trial that revealed at 4 years, the average sustained weight lost was more than double that of Look AHEAD’s, at 10.2%. Meanwhile the recently released SURMOUNT-4 study on tirzepatide reported that at 88 weeks, the average weight lost by participants was a near bariatric surgery level of 25.3% with no signs suggestive of pending regains.
Now maybe you want to cling to the notion that if you just try hard enough, your diet and exercise regime can beat our new meds. Well, it’s difficult to think of a more miserable, often actual vomit-inducing intervention, than the spectacle that used to air weekly on prime time called The Biggest Loser, where participants lived on a ranch and were berated and exercised all day long for the chance to lose the most and win a quarter of a million dollars. But even there, the meds prove to be superior. Although the short-term Biggest Loser data do look markedly better than meds (and than bariatric surgery), whereby the average participant lost 48.8% of their body weight during the grueling 7-month long, 24/7 competition, by postcompetition year 6, the average weight lost dropped to 12.7%.
Yet on November 26, when word came out that Medicare is likely to extend coverage to obesity medications for far more Americans, one of the most common refrains was something along the lines of yes, lifestyle modification is the best choice for dealing with obesity but it’s good that there will be medication options for those where that’s insufficient.
What?
The message is that people simply aren’t trying hard enough. This despite our comfort in knowing that medications have more of an impact than lifestyle on pretty much every other chronic disease. Nor can I recall any other circumstance when coverage of a remarkably effective drug was qualified by the suggestion that known-to-be-inferior interventions are still the best or favored choice.
At this point, obesity medications are plainly the first-line choice of treatment. They provide not only dramatically greater and more durable weight loss than lifestyle interventions, they have also been shown to very significantly reduce the risk for an ever-growing list of other medical concerns including heart attacks, strokes, type 2 diabetes, hypertension, sleep apnea, fatty liver disease, and more, while carrying minimal risk.
Let it also be said that improvements to diet and exercise are worth striving for at any weight, though one should not lose sight of the fact that perpetual, dramatic, intentional, behavior change in the name of health requires vast amounts of wide-ranging privilege to enact — amounts far beyond the average person’s abilities or physiologies (as demonstrated with obesity by decades of disappointing long-term lifestyle outcome data).
Let it also be said that some people will indeed find success solely through lifestyle and that not every person who meets the medical criteria for any medication’s prescription, including obesity medications, is required or encouraged to take it. The clinician’s job, however, at its most basic, is to inform patients who meet medical use criteria of their options, and if a medication is indicated, to inform them of that medication’s risks and benefits and expected outcomes, to help their patients come to their own treatment decisions.
It’s not a bad thing that we have medications that deliver better outcomes than lifestyle — in fact, it’s terrific, and thankfully that they do is true for pretty much every medical condition for which we have medication. That’s in fact why we have medications! And so this constant refrain of golly-gee wouldn’t it be better if we could just manage obesity with lifestyle changes needs to be put to rest — we literally know it wouldn’t be better, and it’s only weight bias that would lead this evidence-based statement to seem off-putting.
Dr. Freedhoff is Associate Professor, Department of Family Medicine, University of Ottawa, and Medical Director, Bariatric Medical Institute, Ottawa, Ontario, Canada. He reported conflicts of interest with the Bariatric Medical Institute, Constant Health, Novo Nordisk, and Weighty Matters.
A version of this article first appeared on Medscape.com.
They’re literally not better. Idealistically, sure, but literally not. And there’s really no debate. Meaning there’s never been a reproducible diet and exercise intervention that has led to anywhere near the average weight lost by those taking obesity medications. Furthermore, when it comes to the durability of weight lost, the gulf between outcomes with diet and exercise vs obesity medications is even more dramatic.
Looking to the literature, one of the most trotted out studies on lifestyle’s impact on weight over time is the Look AHEAD trial. Before useful obesity medications came on the scene, I trotted it out myself. Why? Because it was heartening when faced with the societal refrain that diet and exercise never worked to be able to show that yes, in fact they do. But how well?
Looking to Look AHEAD’s 4-year data (Obesity [Silver Spring]. 2011 Oct;19[10]:1987-1998), those randomized to the intensive lifestyle initiative arm averaged a 4.7% total body weight loss – an amount that remained the same at 8 years. But I chose 4 years because that’s a better comparison with the semaglutide SELECT trial that revealed at 4 years, the average sustained weight lost was more than double that of Look AHEAD’s, at 10.2%. Meanwhile the recently released SURMOUNT-4 study on tirzepatide reported that at 88 weeks, the average weight lost by participants was a near bariatric surgery level of 25.3% with no signs suggestive of pending regains.
Now maybe you want to cling to the notion that if you just try hard enough, your diet and exercise regime can beat our new meds. Well, it’s difficult to think of a more miserable, often actual vomit-inducing intervention, than the spectacle that used to air weekly on prime time called The Biggest Loser, where participants lived on a ranch and were berated and exercised all day long for the chance to lose the most and win a quarter of a million dollars. But even there, the meds prove to be superior. Although the short-term Biggest Loser data do look markedly better than meds (and than bariatric surgery), whereby the average participant lost 48.8% of their body weight during the grueling 7-month long, 24/7 competition, by postcompetition year 6, the average weight lost dropped to 12.7%.
Yet on November 26, when word came out that Medicare is likely to extend coverage to obesity medications for far more Americans, one of the most common refrains was something along the lines of yes, lifestyle modification is the best choice for dealing with obesity but it’s good that there will be medication options for those where that’s insufficient.
What?
The message is that people simply aren’t trying hard enough. This despite our comfort in knowing that medications have more of an impact than lifestyle on pretty much every other chronic disease. Nor can I recall any other circumstance when coverage of a remarkably effective drug was qualified by the suggestion that known-to-be-inferior interventions are still the best or favored choice.
At this point, obesity medications are plainly the first-line choice of treatment. They provide not only dramatically greater and more durable weight loss than lifestyle interventions, they have also been shown to very significantly reduce the risk for an ever-growing list of other medical concerns including heart attacks, strokes, type 2 diabetes, hypertension, sleep apnea, fatty liver disease, and more, while carrying minimal risk.
Let it also be said that improvements to diet and exercise are worth striving for at any weight, though one should not lose sight of the fact that perpetual, dramatic, intentional, behavior change in the name of health requires vast amounts of wide-ranging privilege to enact — amounts far beyond the average person’s abilities or physiologies (as demonstrated with obesity by decades of disappointing long-term lifestyle outcome data).
Let it also be said that some people will indeed find success solely through lifestyle and that not every person who meets the medical criteria for any medication’s prescription, including obesity medications, is required or encouraged to take it. The clinician’s job, however, at its most basic, is to inform patients who meet medical use criteria of their options, and if a medication is indicated, to inform them of that medication’s risks and benefits and expected outcomes, to help their patients come to their own treatment decisions.
It’s not a bad thing that we have medications that deliver better outcomes than lifestyle — in fact, it’s terrific, and thankfully that they do is true for pretty much every medical condition for which we have medication. That’s in fact why we have medications! And so this constant refrain of golly-gee wouldn’t it be better if we could just manage obesity with lifestyle changes needs to be put to rest — we literally know it wouldn’t be better, and it’s only weight bias that would lead this evidence-based statement to seem off-putting.
Dr. Freedhoff is Associate Professor, Department of Family Medicine, University of Ottawa, and Medical Director, Bariatric Medical Institute, Ottawa, Ontario, Canada. He reported conflicts of interest with the Bariatric Medical Institute, Constant Health, Novo Nordisk, and Weighty Matters.
A version of this article first appeared on Medscape.com.
Dark Chocolate: A Bittersweet Remedy for Diabetes Risk
TOPLINE:
Consuming five or more servings per week of dark chocolate is associated with a lower risk for type 2 diabetes (T2D), compared with infrequent or no consumption. Conversely, a higher consumption of milk chocolate does not significantly affect the risk for diabetes and may contribute to greater weight gain.
METHODOLOGY:
- Chocolate is rich in flavanols, natural compounds known to support heart health and lower the risk for T2D. However, the link between chocolate consumption and the risk for T2D is uncertain, with inconsistent research findings that don’t distinguish between dark or milk chocolate.
- Researchers conducted a prospective cohort study to investigate the associations between dark, milk, and total chocolate consumption and the risk for T2D in three long-term US studies of female nurses and male healthcare professionals with no history of diabetes, cardiovascular disease, or cancer at baseline.
- The relationship between total chocolate consumption and the risk for diabetes was investigated in 192,208 individuals who reported their chocolate consumption using validated food frequency questionnaires every 4 years from 1986 onward.
- Information on chocolate subtypes was assessed from 2006/2007 onward in 111,654 participants.
- Participants self-reported T2D through biennial questionnaires, which was confirmed via supplementary questionnaires collecting data on glucose levels, hemoglobin A1c concentration, symptoms, and treatments; they also self-reported their body weight at baseline and during follow-ups.
TAKEAWAY:
- During 4,829,175 person-years of follow-up, researchers identified 18,862 individuals with incident T2D in the total chocolate analysis cohort.
- In the chocolate subtype cohort, 4771 incident T2D cases were identified during 1,270,348 person-years of follow-up. Having at least five servings per week of dark chocolate was associated with a 21% lower risk for T2D (adjusted hazard ratio, 0.79; P for trend = .006), while milk chocolate consumption showed no significant link (P for trend = .75).
- The risk for T2D decreased by 3% for each additional serving of dark chocolate consumed weekly, indicating a dose-response effect.
- Compared with individuals who did not change their chocolate intake, those who had an increased milk chocolate intake had greater weight gain over 4-year periods (mean difference, 0.35 kg; 95% CI, 0.27-0.43); dark chocolate showed no significant association with weight change.
IN PRACTICE:
“Even though dark and milk chocolate have similar levels of calories and saturated fat, it appears that the rich polyphenols in dark chocolate might offset the effects of saturated fat and sugar on weight gain and diabetes. It’s an intriguing difference that’s worth exploring more,” corresponding author Qi Sun from the Departments of Nutrition and Epidemiology, Harvard TH Chan School of Public Health, Boston, Massachusetts, said in a press release.
SOURCE:
This study was led by Binkai Liu, Harvard TH Chan School of Public Health. It was published online in The BMJ.
LIMITATIONS:
The relatively limited number of participants in the higher chocolate consumption groups may have reduced the statistical power for detecting modest associations between dark chocolate consumption and the risk for T2D. Additionally, the study population primarily consisted of non-Hispanic White adults older than 50 years at baseline, which, along with their professional backgrounds, may have limited the generalizability of the study findings to other populations with different socioeconomic or personal characteristics. Chocolate consumption in this study was lower than the national average of three servings per week, which may have limited the ability to assess the dose-response relationship at higher intake levels.
DISCLOSURES:
This study was supported by grants from the National Institutes of Health. Some authors reported receiving investigator-initiated grants, being on scientific advisory boards, and receiving research funding from certain institutions.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
TOPLINE:
Consuming five or more servings per week of dark chocolate is associated with a lower risk for type 2 diabetes (T2D), compared with infrequent or no consumption. Conversely, a higher consumption of milk chocolate does not significantly affect the risk for diabetes and may contribute to greater weight gain.
METHODOLOGY:
- Chocolate is rich in flavanols, natural compounds known to support heart health and lower the risk for T2D. However, the link between chocolate consumption and the risk for T2D is uncertain, with inconsistent research findings that don’t distinguish between dark or milk chocolate.
- Researchers conducted a prospective cohort study to investigate the associations between dark, milk, and total chocolate consumption and the risk for T2D in three long-term US studies of female nurses and male healthcare professionals with no history of diabetes, cardiovascular disease, or cancer at baseline.
- The relationship between total chocolate consumption and the risk for diabetes was investigated in 192,208 individuals who reported their chocolate consumption using validated food frequency questionnaires every 4 years from 1986 onward.
- Information on chocolate subtypes was assessed from 2006/2007 onward in 111,654 participants.
- Participants self-reported T2D through biennial questionnaires, which was confirmed via supplementary questionnaires collecting data on glucose levels, hemoglobin A1c concentration, symptoms, and treatments; they also self-reported their body weight at baseline and during follow-ups.
TAKEAWAY:
- During 4,829,175 person-years of follow-up, researchers identified 18,862 individuals with incident T2D in the total chocolate analysis cohort.
- In the chocolate subtype cohort, 4771 incident T2D cases were identified during 1,270,348 person-years of follow-up. Having at least five servings per week of dark chocolate was associated with a 21% lower risk for T2D (adjusted hazard ratio, 0.79; P for trend = .006), while milk chocolate consumption showed no significant link (P for trend = .75).
- The risk for T2D decreased by 3% for each additional serving of dark chocolate consumed weekly, indicating a dose-response effect.
- Compared with individuals who did not change their chocolate intake, those who had an increased milk chocolate intake had greater weight gain over 4-year periods (mean difference, 0.35 kg; 95% CI, 0.27-0.43); dark chocolate showed no significant association with weight change.
IN PRACTICE:
“Even though dark and milk chocolate have similar levels of calories and saturated fat, it appears that the rich polyphenols in dark chocolate might offset the effects of saturated fat and sugar on weight gain and diabetes. It’s an intriguing difference that’s worth exploring more,” corresponding author Qi Sun from the Departments of Nutrition and Epidemiology, Harvard TH Chan School of Public Health, Boston, Massachusetts, said in a press release.
SOURCE:
This study was led by Binkai Liu, Harvard TH Chan School of Public Health. It was published online in The BMJ.
LIMITATIONS:
The relatively limited number of participants in the higher chocolate consumption groups may have reduced the statistical power for detecting modest associations between dark chocolate consumption and the risk for T2D. Additionally, the study population primarily consisted of non-Hispanic White adults older than 50 years at baseline, which, along with their professional backgrounds, may have limited the generalizability of the study findings to other populations with different socioeconomic or personal characteristics. Chocolate consumption in this study was lower than the national average of three servings per week, which may have limited the ability to assess the dose-response relationship at higher intake levels.
DISCLOSURES:
This study was supported by grants from the National Institutes of Health. Some authors reported receiving investigator-initiated grants, being on scientific advisory boards, and receiving research funding from certain institutions.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
TOPLINE:
Consuming five or more servings per week of dark chocolate is associated with a lower risk for type 2 diabetes (T2D), compared with infrequent or no consumption. Conversely, a higher consumption of milk chocolate does not significantly affect the risk for diabetes and may contribute to greater weight gain.
METHODOLOGY:
- Chocolate is rich in flavanols, natural compounds known to support heart health and lower the risk for T2D. However, the link between chocolate consumption and the risk for T2D is uncertain, with inconsistent research findings that don’t distinguish between dark or milk chocolate.
- Researchers conducted a prospective cohort study to investigate the associations between dark, milk, and total chocolate consumption and the risk for T2D in three long-term US studies of female nurses and male healthcare professionals with no history of diabetes, cardiovascular disease, or cancer at baseline.
- The relationship between total chocolate consumption and the risk for diabetes was investigated in 192,208 individuals who reported their chocolate consumption using validated food frequency questionnaires every 4 years from 1986 onward.
- Information on chocolate subtypes was assessed from 2006/2007 onward in 111,654 participants.
- Participants self-reported T2D through biennial questionnaires, which was confirmed via supplementary questionnaires collecting data on glucose levels, hemoglobin A1c concentration, symptoms, and treatments; they also self-reported their body weight at baseline and during follow-ups.
TAKEAWAY:
- During 4,829,175 person-years of follow-up, researchers identified 18,862 individuals with incident T2D in the total chocolate analysis cohort.
- In the chocolate subtype cohort, 4771 incident T2D cases were identified during 1,270,348 person-years of follow-up. Having at least five servings per week of dark chocolate was associated with a 21% lower risk for T2D (adjusted hazard ratio, 0.79; P for trend = .006), while milk chocolate consumption showed no significant link (P for trend = .75).
- The risk for T2D decreased by 3% for each additional serving of dark chocolate consumed weekly, indicating a dose-response effect.
- Compared with individuals who did not change their chocolate intake, those who had an increased milk chocolate intake had greater weight gain over 4-year periods (mean difference, 0.35 kg; 95% CI, 0.27-0.43); dark chocolate showed no significant association with weight change.
IN PRACTICE:
“Even though dark and milk chocolate have similar levels of calories and saturated fat, it appears that the rich polyphenols in dark chocolate might offset the effects of saturated fat and sugar on weight gain and diabetes. It’s an intriguing difference that’s worth exploring more,” corresponding author Qi Sun from the Departments of Nutrition and Epidemiology, Harvard TH Chan School of Public Health, Boston, Massachusetts, said in a press release.
SOURCE:
This study was led by Binkai Liu, Harvard TH Chan School of Public Health. It was published online in The BMJ.
LIMITATIONS:
The relatively limited number of participants in the higher chocolate consumption groups may have reduced the statistical power for detecting modest associations between dark chocolate consumption and the risk for T2D. Additionally, the study population primarily consisted of non-Hispanic White adults older than 50 years at baseline, which, along with their professional backgrounds, may have limited the generalizability of the study findings to other populations with different socioeconomic or personal characteristics. Chocolate consumption in this study was lower than the national average of three servings per week, which may have limited the ability to assess the dose-response relationship at higher intake levels.
DISCLOSURES:
This study was supported by grants from the National Institutes of Health. Some authors reported receiving investigator-initiated grants, being on scientific advisory boards, and receiving research funding from certain institutions.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
ADA Advises Against Using Compounded GLP-1 RA Medications
In a new statement, the American Diabetes Association (ADA) has advised against the use of compounded glucagon-like peptide 1 receptor agonist (GLP-1 RA) and dual glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 RA medication classes.
The ADA recommends GLP-1 RA and GIP/GLP-1 RA medications approved by the Food and Drug Administration (FDA) for the treatment of type 2 diabetes, cardiovascular and kidney disease risk reduction, and weight management. The new ADA statement pertains to the unapproved, unregulated versions that have emerged as the demand for these medications for weight loss increases. These are often marketed directly to consumers.
“Compounded GLP-1 RA and dual GIP/GLP-1 RA products have been associated with clinically important dosing errors and adverse events. More concerning to individuals’ safety are counterfeit products that have made their way into the US drug supply chain and those advertised online and by unregulated sources,” the ADA said in the statement, published online on December 2, 2024, in Diabetes Care.
The statement, authored by Joshua J. Neumiller, PharmD, CDCES, of the Department of Pharmacotherapy, Washington State University, Spokane, and colleagues, states the following:
- Non–FDA-approved compounded incretin products are not recommended for use due to uncertainty about their content and resulting concerns about safety, quality, and effectiveness.
- If an incretin medication is unavailable (eg, in shortage), switching to a different FDA-approved medication is recommended as clinically appropriate to achieve and maintain individualized glucose-lowering, weight management, and/or cardiovascular and kidney risk reduction goals.
- Upon resolution of incretin product unavailability, reassess the appropriateness of resuming the original FDA-approved incretin medication.
The document points out that compounded products are not identical to the FDA-approved versions, may be distributed in nonstandard dosing devices, and may not provide sufficient user instructions.
However, “the ADA also recognizes that individuals and clinicians may still elect to use or recommend compounded products for financial or other reasons,” and therefore offers additional advice for the public, including the following:
- Discuss product use with their usual healthcare providers.
- Only use products that include dosing guidance.
- Verify that the compounding pharmacy is registered with FDA.
In addition, report any adverse events or medication errors to the FDA’s Medwatch.
A version of this article appeared on Medscape.com.
In a new statement, the American Diabetes Association (ADA) has advised against the use of compounded glucagon-like peptide 1 receptor agonist (GLP-1 RA) and dual glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 RA medication classes.
The ADA recommends GLP-1 RA and GIP/GLP-1 RA medications approved by the Food and Drug Administration (FDA) for the treatment of type 2 diabetes, cardiovascular and kidney disease risk reduction, and weight management. The new ADA statement pertains to the unapproved, unregulated versions that have emerged as the demand for these medications for weight loss increases. These are often marketed directly to consumers.
“Compounded GLP-1 RA and dual GIP/GLP-1 RA products have been associated with clinically important dosing errors and adverse events. More concerning to individuals’ safety are counterfeit products that have made their way into the US drug supply chain and those advertised online and by unregulated sources,” the ADA said in the statement, published online on December 2, 2024, in Diabetes Care.
The statement, authored by Joshua J. Neumiller, PharmD, CDCES, of the Department of Pharmacotherapy, Washington State University, Spokane, and colleagues, states the following:
- Non–FDA-approved compounded incretin products are not recommended for use due to uncertainty about their content and resulting concerns about safety, quality, and effectiveness.
- If an incretin medication is unavailable (eg, in shortage), switching to a different FDA-approved medication is recommended as clinically appropriate to achieve and maintain individualized glucose-lowering, weight management, and/or cardiovascular and kidney risk reduction goals.
- Upon resolution of incretin product unavailability, reassess the appropriateness of resuming the original FDA-approved incretin medication.
The document points out that compounded products are not identical to the FDA-approved versions, may be distributed in nonstandard dosing devices, and may not provide sufficient user instructions.
However, “the ADA also recognizes that individuals and clinicians may still elect to use or recommend compounded products for financial or other reasons,” and therefore offers additional advice for the public, including the following:
- Discuss product use with their usual healthcare providers.
- Only use products that include dosing guidance.
- Verify that the compounding pharmacy is registered with FDA.
In addition, report any adverse events or medication errors to the FDA’s Medwatch.
A version of this article appeared on Medscape.com.
In a new statement, the American Diabetes Association (ADA) has advised against the use of compounded glucagon-like peptide 1 receptor agonist (GLP-1 RA) and dual glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 RA medication classes.
The ADA recommends GLP-1 RA and GIP/GLP-1 RA medications approved by the Food and Drug Administration (FDA) for the treatment of type 2 diabetes, cardiovascular and kidney disease risk reduction, and weight management. The new ADA statement pertains to the unapproved, unregulated versions that have emerged as the demand for these medications for weight loss increases. These are often marketed directly to consumers.
“Compounded GLP-1 RA and dual GIP/GLP-1 RA products have been associated with clinically important dosing errors and adverse events. More concerning to individuals’ safety are counterfeit products that have made their way into the US drug supply chain and those advertised online and by unregulated sources,” the ADA said in the statement, published online on December 2, 2024, in Diabetes Care.
The statement, authored by Joshua J. Neumiller, PharmD, CDCES, of the Department of Pharmacotherapy, Washington State University, Spokane, and colleagues, states the following:
- Non–FDA-approved compounded incretin products are not recommended for use due to uncertainty about their content and resulting concerns about safety, quality, and effectiveness.
- If an incretin medication is unavailable (eg, in shortage), switching to a different FDA-approved medication is recommended as clinically appropriate to achieve and maintain individualized glucose-lowering, weight management, and/or cardiovascular and kidney risk reduction goals.
- Upon resolution of incretin product unavailability, reassess the appropriateness of resuming the original FDA-approved incretin medication.
The document points out that compounded products are not identical to the FDA-approved versions, may be distributed in nonstandard dosing devices, and may not provide sufficient user instructions.
However, “the ADA also recognizes that individuals and clinicians may still elect to use or recommend compounded products for financial or other reasons,” and therefore offers additional advice for the public, including the following:
- Discuss product use with their usual healthcare providers.
- Only use products that include dosing guidance.
- Verify that the compounding pharmacy is registered with FDA.
In addition, report any adverse events or medication errors to the FDA’s Medwatch.
A version of this article appeared on Medscape.com.
Focus on Nutrient Density Instead of Limiting Certain Foods
The word “malnutrition” probably brings to mind images of very thin patients with catabolic illness. But it really just means “poor nutrition,” which can — and often does — apply to patients with overweight or obesity.
That’s because malnutrition doesn’t occur simply because of a lack of calories, but rather because there is a gap in the nutrition the body requires and the nutrition it receives.
Each day, clinicians see patients with chronic conditions related to malnutrition. That list includes diabetes and hypertension, which can be promoted by excess intake of certain nutrients (carbohydrates and sodium) or inadequate intake of others (fiber, protein, potassium, magnesium, and calcium).
Diet Education Is Vital in Chronic Disease Management
Diet education is without a doubt a core pillar of chronic disease management. Nutrition therapy is recommended in treatment guidelines for the management of some of the most commonly seen chronic conditions such as hypertension, diabetes, and kidney disease. But in one study, only 58% of physicians, nurses and other health professionals surveyed had received formal nutrition education and only 40% were confident in their ability to provide nutrition education to patients.
As a registered dietitian, I welcome referrals for both prevention and management of chronic diseases with open arms. But medical nutrition therapy with a registered dietitian may not be realistic for all patients owing to financial, geographic, or other constraints. So, their best option may be the few minutes that a physician or physician extender has to spare at the end of their appointment.
But time constraints may result in clinicians turning to short, easy-to-remember messages such as “Don’t eat anything white” or “Only shop the edges of the grocery store.” Although catchy, this type of advice can inadvertently encourage patients to skip over foods that are actually very nutrient dense. For example, white foods such as onions, turnips, mushrooms, cauliflower, and even popcorn are low in calories and high in nutritional value. The center aisles of the grocery store may harbor high-carbohydrate breakfast cereals and potato chips, but they are also home to legumes, nuts, and canned and frozen fruits and vegetables.
What may be more effective is educating the patient on the importance of focusing on the nutrient density of foods, rather than simply limiting certain food groups or colors.
How to Work Nutrient Density into the Conversation
Nutrient density is a concept that refers to the proportion of nutrients to calories in a food item: essentially, a food’s qualitative nutritional value. It provides more depth than simply referring to foods as being high or low in calories, healthy or unhealthy, or good or bad.
Educating patients about nutrition density and encouraging a focus on foods that are low in calories and high in vitamins and minerals can help address micronutrient deficiencies, which may be more common than previously thought and linked to the chronic diseases that we see daily. It is worth noting that some foods that are not low in calories are still nutrient dense. Avocados, liver, and nuts come to mind as foods that are high in calories, but they have additional nutrients such as fiber, potassium, antioxidants, vitamin A, iron, and selenium that can still make them an excellent choice if they are part of a well-balanced diet.
I fear that we often underestimate our patients. We worry that not providing them with a list of acceptable foods will set them up for failure. But, in my experience, that list of “good” and “bad” foods may be useful for a week or so but will eventually become lost on the fridge under children’s artwork and save-the-dates.
Patients know that potato chips offer little more than fat, carbs, and salt and that they’re a poor choice for long-term health. What they might not know is that cocktail peanuts can also satisfy the craving for a salty snack, with more than four times the protein, twice the fiber, and just over half of the sodium found in the same serving size of regular salted potato chips. Peanuts have the added bonus of being high in heart-healthy monounsaturated fatty acids.
The best thing that clinicians can do with just a few minutes of time for diet education is to talk to patients about the nutrient density of whole foods and caution patients against highly processed foods, because processing can decrease nutritional content. Our most effective option is to explain why a varied diet with focus on fruits, vegetables, lean protein, nuts, legumes, and healthy fats is beneficial for cardiovascular and metabolic health. After that, all that is left is to trust the patient to make the right choices for their health.
Brandy Winfree Root, a renal dietitian in private practice in Mary Esther, Florida, has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
The word “malnutrition” probably brings to mind images of very thin patients with catabolic illness. But it really just means “poor nutrition,” which can — and often does — apply to patients with overweight or obesity.
That’s because malnutrition doesn’t occur simply because of a lack of calories, but rather because there is a gap in the nutrition the body requires and the nutrition it receives.
Each day, clinicians see patients with chronic conditions related to malnutrition. That list includes diabetes and hypertension, which can be promoted by excess intake of certain nutrients (carbohydrates and sodium) or inadequate intake of others (fiber, protein, potassium, magnesium, and calcium).
Diet Education Is Vital in Chronic Disease Management
Diet education is without a doubt a core pillar of chronic disease management. Nutrition therapy is recommended in treatment guidelines for the management of some of the most commonly seen chronic conditions such as hypertension, diabetes, and kidney disease. But in one study, only 58% of physicians, nurses and other health professionals surveyed had received formal nutrition education and only 40% were confident in their ability to provide nutrition education to patients.
As a registered dietitian, I welcome referrals for both prevention and management of chronic diseases with open arms. But medical nutrition therapy with a registered dietitian may not be realistic for all patients owing to financial, geographic, or other constraints. So, their best option may be the few minutes that a physician or physician extender has to spare at the end of their appointment.
But time constraints may result in clinicians turning to short, easy-to-remember messages such as “Don’t eat anything white” or “Only shop the edges of the grocery store.” Although catchy, this type of advice can inadvertently encourage patients to skip over foods that are actually very nutrient dense. For example, white foods such as onions, turnips, mushrooms, cauliflower, and even popcorn are low in calories and high in nutritional value. The center aisles of the grocery store may harbor high-carbohydrate breakfast cereals and potato chips, but they are also home to legumes, nuts, and canned and frozen fruits and vegetables.
What may be more effective is educating the patient on the importance of focusing on the nutrient density of foods, rather than simply limiting certain food groups or colors.
How to Work Nutrient Density into the Conversation
Nutrient density is a concept that refers to the proportion of nutrients to calories in a food item: essentially, a food’s qualitative nutritional value. It provides more depth than simply referring to foods as being high or low in calories, healthy or unhealthy, or good or bad.
Educating patients about nutrition density and encouraging a focus on foods that are low in calories and high in vitamins and minerals can help address micronutrient deficiencies, which may be more common than previously thought and linked to the chronic diseases that we see daily. It is worth noting that some foods that are not low in calories are still nutrient dense. Avocados, liver, and nuts come to mind as foods that are high in calories, but they have additional nutrients such as fiber, potassium, antioxidants, vitamin A, iron, and selenium that can still make them an excellent choice if they are part of a well-balanced diet.
I fear that we often underestimate our patients. We worry that not providing them with a list of acceptable foods will set them up for failure. But, in my experience, that list of “good” and “bad” foods may be useful for a week or so but will eventually become lost on the fridge under children’s artwork and save-the-dates.
Patients know that potato chips offer little more than fat, carbs, and salt and that they’re a poor choice for long-term health. What they might not know is that cocktail peanuts can also satisfy the craving for a salty snack, with more than four times the protein, twice the fiber, and just over half of the sodium found in the same serving size of regular salted potato chips. Peanuts have the added bonus of being high in heart-healthy monounsaturated fatty acids.
The best thing that clinicians can do with just a few minutes of time for diet education is to talk to patients about the nutrient density of whole foods and caution patients against highly processed foods, because processing can decrease nutritional content. Our most effective option is to explain why a varied diet with focus on fruits, vegetables, lean protein, nuts, legumes, and healthy fats is beneficial for cardiovascular and metabolic health. After that, all that is left is to trust the patient to make the right choices for their health.
Brandy Winfree Root, a renal dietitian in private practice in Mary Esther, Florida, has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
The word “malnutrition” probably brings to mind images of very thin patients with catabolic illness. But it really just means “poor nutrition,” which can — and often does — apply to patients with overweight or obesity.
That’s because malnutrition doesn’t occur simply because of a lack of calories, but rather because there is a gap in the nutrition the body requires and the nutrition it receives.
Each day, clinicians see patients with chronic conditions related to malnutrition. That list includes diabetes and hypertension, which can be promoted by excess intake of certain nutrients (carbohydrates and sodium) or inadequate intake of others (fiber, protein, potassium, magnesium, and calcium).
Diet Education Is Vital in Chronic Disease Management
Diet education is without a doubt a core pillar of chronic disease management. Nutrition therapy is recommended in treatment guidelines for the management of some of the most commonly seen chronic conditions such as hypertension, diabetes, and kidney disease. But in one study, only 58% of physicians, nurses and other health professionals surveyed had received formal nutrition education and only 40% were confident in their ability to provide nutrition education to patients.
As a registered dietitian, I welcome referrals for both prevention and management of chronic diseases with open arms. But medical nutrition therapy with a registered dietitian may not be realistic for all patients owing to financial, geographic, or other constraints. So, their best option may be the few minutes that a physician or physician extender has to spare at the end of their appointment.
But time constraints may result in clinicians turning to short, easy-to-remember messages such as “Don’t eat anything white” or “Only shop the edges of the grocery store.” Although catchy, this type of advice can inadvertently encourage patients to skip over foods that are actually very nutrient dense. For example, white foods such as onions, turnips, mushrooms, cauliflower, and even popcorn are low in calories and high in nutritional value. The center aisles of the grocery store may harbor high-carbohydrate breakfast cereals and potato chips, but they are also home to legumes, nuts, and canned and frozen fruits and vegetables.
What may be more effective is educating the patient on the importance of focusing on the nutrient density of foods, rather than simply limiting certain food groups or colors.
How to Work Nutrient Density into the Conversation
Nutrient density is a concept that refers to the proportion of nutrients to calories in a food item: essentially, a food’s qualitative nutritional value. It provides more depth than simply referring to foods as being high or low in calories, healthy or unhealthy, or good or bad.
Educating patients about nutrition density and encouraging a focus on foods that are low in calories and high in vitamins and minerals can help address micronutrient deficiencies, which may be more common than previously thought and linked to the chronic diseases that we see daily. It is worth noting that some foods that are not low in calories are still nutrient dense. Avocados, liver, and nuts come to mind as foods that are high in calories, but they have additional nutrients such as fiber, potassium, antioxidants, vitamin A, iron, and selenium that can still make them an excellent choice if they are part of a well-balanced diet.
I fear that we often underestimate our patients. We worry that not providing them with a list of acceptable foods will set them up for failure. But, in my experience, that list of “good” and “bad” foods may be useful for a week or so but will eventually become lost on the fridge under children’s artwork and save-the-dates.
Patients know that potato chips offer little more than fat, carbs, and salt and that they’re a poor choice for long-term health. What they might not know is that cocktail peanuts can also satisfy the craving for a salty snack, with more than four times the protein, twice the fiber, and just over half of the sodium found in the same serving size of regular salted potato chips. Peanuts have the added bonus of being high in heart-healthy monounsaturated fatty acids.
The best thing that clinicians can do with just a few minutes of time for diet education is to talk to patients about the nutrient density of whole foods and caution patients against highly processed foods, because processing can decrease nutritional content. Our most effective option is to explain why a varied diet with focus on fruits, vegetables, lean protein, nuts, legumes, and healthy fats is beneficial for cardiovascular and metabolic health. After that, all that is left is to trust the patient to make the right choices for their health.
Brandy Winfree Root, a renal dietitian in private practice in Mary Esther, Florida, has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
New ‘Touchless’ Blood Pressure Screening Tech: How It Works
When a patient signs on to a telehealth portal, there’s little more a provider can do than ask questions. But a new artificial intelligence (AI) technology could allow providers to get feedback about the patient’s blood pressure and diabetes risk just from a video call or a smartphone app.
Researchers at the University of Tokyo in Japan are using AI to determine whether people might have high blood pressure or diabetes based on video data collected with a special sensor.
The technology relies on photoplethysmography (PPG), which measures changes in blood volume by detecting the amount of light absorbed by blood just below the skin.
Wearable devices like Apple Watches and Fitbits also use PPG technologies to detect heart rate and atrial fibrillation.
“If we could detect and accurately measure your blood pressure, heart rate, and oxygen saturation non-invasively that would be fantastic,” said Eugene Yang, MD, professor of medicine in the division of cardiology at the University of Washington School of Medicine in Seattle who was not involved in the study.
How Does PPG Work — and Is This New Tech Accurate?
Using PPG, “you’re detecting these small, little blood vessels that sit underneath the surface of your skin,” explained Yang.
“Since both hypertension and diabetes are diseases that damage blood vessels, we thought these diseases might affect blood flow and pulse wave transit times,” said Ryoko Uchida, a project researcher in the cardiology department at the University of Tokyo and one of the leaders of the study.
PPG devices primarily use green light to detect blood flow, as hemoglobin, the oxygen-carrying molecule in blood, absorbs green light most effectively, Yang said. “So, if you extract and remove all the other channels of light and only focus on the green channel, then that’s when you’ll be able to potentially see blood flow and pulsatile blood flow activity,” he noted.
The University of Tokyo researchers used remote or contactless PPG, which requires a short video recording of someone’s face and palms, as the person holds as still as possible. A special sensor collects the video and detects only certain wavelengths of light. Then the researchers developed an AI algorithm to extract data from participants’ skin, such as changes in pulse transit time — the time it takes for the pulse to travel from the palm to the face.
To correlate the video algorithm to blood pressure and diabetes risk, the researchers measured blood participants’ pressure with a continuous sphygmomanometer (an automatic blood pressure cuff) at the same time as they collected the video. They also did a blood A1c test to detect diabetes.
So far, they’ve tested their video algorithm on 215 people. The algorithm applied to a 30-second video was 86% accurate in detecting if blood pressure was above normal, and a 5-second video was 81% accurate in detecting higher blood pressure.
Compared with using hemoglobin A1c blood test results to screen for diabetes, the video algorithm was 75% accurate in identifying people who had subtle blood changes that correlated to diabetes.
“Most of this focus has been on wearable devices, patches, rings, wrist devices,” Yang said, “the facial video stuff is great because you can imagine that there are other ways of applying it.”
Yang, who is also doing research on facial video processing, pointed out it could be helpful not only in telehealth visits, but also for patients in the hospital with highly contagious diseases who need to be in isolation, or just for people using their smartphones.
“People are tied to their smartphones, so you could imagine that that would be great as a way for people to have awareness about their blood pressure or their diabetes status,” Yang noted.
More Work to Do
The study has a few caveats. The special sensor they used in this study isn’t yet integrated into smartphone cameras or other common video recording devices. But Uchida is hopeful that it could be mass-produced and inexpensive to someday add.
Also, the study was done in a Japanese population, and lighter skin may be easier to capture changes in blood flow, Uchida noted. Pulse oximeters, which use the same technology, tend to overestimate blood oxygen in people with darker skin tones.
“It is necessary to test whether the same results are obtained in a variety of subjects other than Japanese and Asians,” Uchida said, in addition to validating the tool with more participants.
The study has also not yet undergone peer review.
And Yang pointed out that this new AI technology provides more of a screening tool to predict who is at high risk for high blood pressure or diabetes, rather than precise measurements for either disease.
There are already some devices that claim to measure blood pressure using PPG technology, like blood pressure monitoring watches. But Yang warns that these kinds of devices aren’t validated, meaning we don’t really know how well they work.
One difficulty in getting any kind of PPG blood pressure monitoring device to market is that the organizations involved in setting medical device standards (like the International Organization for Standards) doesn’t yet have a validation standard for this technology, Yang said, so there’s really no way to consistently verify the technology’s accuracy.
“I am optimistic that we are capable of figuring out how to validate these things. I just think we have so many things we have to iron out before that happens,” Yang explained, noting that it will be at least 3 years before a remote blood monitoring system is widely available.
A version of this article first appeared on Medscape.com.
When a patient signs on to a telehealth portal, there’s little more a provider can do than ask questions. But a new artificial intelligence (AI) technology could allow providers to get feedback about the patient’s blood pressure and diabetes risk just from a video call or a smartphone app.
Researchers at the University of Tokyo in Japan are using AI to determine whether people might have high blood pressure or diabetes based on video data collected with a special sensor.
The technology relies on photoplethysmography (PPG), which measures changes in blood volume by detecting the amount of light absorbed by blood just below the skin.
Wearable devices like Apple Watches and Fitbits also use PPG technologies to detect heart rate and atrial fibrillation.
“If we could detect and accurately measure your blood pressure, heart rate, and oxygen saturation non-invasively that would be fantastic,” said Eugene Yang, MD, professor of medicine in the division of cardiology at the University of Washington School of Medicine in Seattle who was not involved in the study.
How Does PPG Work — and Is This New Tech Accurate?
Using PPG, “you’re detecting these small, little blood vessels that sit underneath the surface of your skin,” explained Yang.
“Since both hypertension and diabetes are diseases that damage blood vessels, we thought these diseases might affect blood flow and pulse wave transit times,” said Ryoko Uchida, a project researcher in the cardiology department at the University of Tokyo and one of the leaders of the study.
PPG devices primarily use green light to detect blood flow, as hemoglobin, the oxygen-carrying molecule in blood, absorbs green light most effectively, Yang said. “So, if you extract and remove all the other channels of light and only focus on the green channel, then that’s when you’ll be able to potentially see blood flow and pulsatile blood flow activity,” he noted.
The University of Tokyo researchers used remote or contactless PPG, which requires a short video recording of someone’s face and palms, as the person holds as still as possible. A special sensor collects the video and detects only certain wavelengths of light. Then the researchers developed an AI algorithm to extract data from participants’ skin, such as changes in pulse transit time — the time it takes for the pulse to travel from the palm to the face.
To correlate the video algorithm to blood pressure and diabetes risk, the researchers measured blood participants’ pressure with a continuous sphygmomanometer (an automatic blood pressure cuff) at the same time as they collected the video. They also did a blood A1c test to detect diabetes.
So far, they’ve tested their video algorithm on 215 people. The algorithm applied to a 30-second video was 86% accurate in detecting if blood pressure was above normal, and a 5-second video was 81% accurate in detecting higher blood pressure.
Compared with using hemoglobin A1c blood test results to screen for diabetes, the video algorithm was 75% accurate in identifying people who had subtle blood changes that correlated to diabetes.
“Most of this focus has been on wearable devices, patches, rings, wrist devices,” Yang said, “the facial video stuff is great because you can imagine that there are other ways of applying it.”
Yang, who is also doing research on facial video processing, pointed out it could be helpful not only in telehealth visits, but also for patients in the hospital with highly contagious diseases who need to be in isolation, or just for people using their smartphones.
“People are tied to their smartphones, so you could imagine that that would be great as a way for people to have awareness about their blood pressure or their diabetes status,” Yang noted.
More Work to Do
The study has a few caveats. The special sensor they used in this study isn’t yet integrated into smartphone cameras or other common video recording devices. But Uchida is hopeful that it could be mass-produced and inexpensive to someday add.
Also, the study was done in a Japanese population, and lighter skin may be easier to capture changes in blood flow, Uchida noted. Pulse oximeters, which use the same technology, tend to overestimate blood oxygen in people with darker skin tones.
“It is necessary to test whether the same results are obtained in a variety of subjects other than Japanese and Asians,” Uchida said, in addition to validating the tool with more participants.
The study has also not yet undergone peer review.
And Yang pointed out that this new AI technology provides more of a screening tool to predict who is at high risk for high blood pressure or diabetes, rather than precise measurements for either disease.
There are already some devices that claim to measure blood pressure using PPG technology, like blood pressure monitoring watches. But Yang warns that these kinds of devices aren’t validated, meaning we don’t really know how well they work.
One difficulty in getting any kind of PPG blood pressure monitoring device to market is that the organizations involved in setting medical device standards (like the International Organization for Standards) doesn’t yet have a validation standard for this technology, Yang said, so there’s really no way to consistently verify the technology’s accuracy.
“I am optimistic that we are capable of figuring out how to validate these things. I just think we have so many things we have to iron out before that happens,” Yang explained, noting that it will be at least 3 years before a remote blood monitoring system is widely available.
A version of this article first appeared on Medscape.com.
When a patient signs on to a telehealth portal, there’s little more a provider can do than ask questions. But a new artificial intelligence (AI) technology could allow providers to get feedback about the patient’s blood pressure and diabetes risk just from a video call or a smartphone app.
Researchers at the University of Tokyo in Japan are using AI to determine whether people might have high blood pressure or diabetes based on video data collected with a special sensor.
The technology relies on photoplethysmography (PPG), which measures changes in blood volume by detecting the amount of light absorbed by blood just below the skin.
Wearable devices like Apple Watches and Fitbits also use PPG technologies to detect heart rate and atrial fibrillation.
“If we could detect and accurately measure your blood pressure, heart rate, and oxygen saturation non-invasively that would be fantastic,” said Eugene Yang, MD, professor of medicine in the division of cardiology at the University of Washington School of Medicine in Seattle who was not involved in the study.
How Does PPG Work — and Is This New Tech Accurate?
Using PPG, “you’re detecting these small, little blood vessels that sit underneath the surface of your skin,” explained Yang.
“Since both hypertension and diabetes are diseases that damage blood vessels, we thought these diseases might affect blood flow and pulse wave transit times,” said Ryoko Uchida, a project researcher in the cardiology department at the University of Tokyo and one of the leaders of the study.
PPG devices primarily use green light to detect blood flow, as hemoglobin, the oxygen-carrying molecule in blood, absorbs green light most effectively, Yang said. “So, if you extract and remove all the other channels of light and only focus on the green channel, then that’s when you’ll be able to potentially see blood flow and pulsatile blood flow activity,” he noted.
The University of Tokyo researchers used remote or contactless PPG, which requires a short video recording of someone’s face and palms, as the person holds as still as possible. A special sensor collects the video and detects only certain wavelengths of light. Then the researchers developed an AI algorithm to extract data from participants’ skin, such as changes in pulse transit time — the time it takes for the pulse to travel from the palm to the face.
To correlate the video algorithm to blood pressure and diabetes risk, the researchers measured blood participants’ pressure with a continuous sphygmomanometer (an automatic blood pressure cuff) at the same time as they collected the video. They also did a blood A1c test to detect diabetes.
So far, they’ve tested their video algorithm on 215 people. The algorithm applied to a 30-second video was 86% accurate in detecting if blood pressure was above normal, and a 5-second video was 81% accurate in detecting higher blood pressure.
Compared with using hemoglobin A1c blood test results to screen for diabetes, the video algorithm was 75% accurate in identifying people who had subtle blood changes that correlated to diabetes.
“Most of this focus has been on wearable devices, patches, rings, wrist devices,” Yang said, “the facial video stuff is great because you can imagine that there are other ways of applying it.”
Yang, who is also doing research on facial video processing, pointed out it could be helpful not only in telehealth visits, but also for patients in the hospital with highly contagious diseases who need to be in isolation, or just for people using their smartphones.
“People are tied to their smartphones, so you could imagine that that would be great as a way for people to have awareness about their blood pressure or their diabetes status,” Yang noted.
More Work to Do
The study has a few caveats. The special sensor they used in this study isn’t yet integrated into smartphone cameras or other common video recording devices. But Uchida is hopeful that it could be mass-produced and inexpensive to someday add.
Also, the study was done in a Japanese population, and lighter skin may be easier to capture changes in blood flow, Uchida noted. Pulse oximeters, which use the same technology, tend to overestimate blood oxygen in people with darker skin tones.
“It is necessary to test whether the same results are obtained in a variety of subjects other than Japanese and Asians,” Uchida said, in addition to validating the tool with more participants.
The study has also not yet undergone peer review.
And Yang pointed out that this new AI technology provides more of a screening tool to predict who is at high risk for high blood pressure or diabetes, rather than precise measurements for either disease.
There are already some devices that claim to measure blood pressure using PPG technology, like blood pressure monitoring watches. But Yang warns that these kinds of devices aren’t validated, meaning we don’t really know how well they work.
One difficulty in getting any kind of PPG blood pressure monitoring device to market is that the organizations involved in setting medical device standards (like the International Organization for Standards) doesn’t yet have a validation standard for this technology, Yang said, so there’s really no way to consistently verify the technology’s accuracy.
“I am optimistic that we are capable of figuring out how to validate these things. I just think we have so many things we have to iron out before that happens,” Yang explained, noting that it will be at least 3 years before a remote blood monitoring system is widely available.
A version of this article first appeared on Medscape.com.
Diabetes Drugs Promising for Alcohol Use Disorder
TOPLINE:
Use of the glucagon-like peptide 1 (GLP-1) receptor agonists semaglutide and liraglutide is linked to a lower risk for alcohol use disorder (AUD)–related hospitalizations, compared with traditional AUD medications, a new study suggested.
METHODOLOGY:
- Researchers conducted a nationwide cohort study from 2006 to 2023 in Sweden that included more than 220,000 individuals with AUD (mean age, 40 years; 64% men).
- Data were obtained from registers of inpatient and specialized outpatient care, sickness absence, and disability pension, with a median follow-up period of 8.8 years.
- The primary exposure measured was the use of individual GLP-1 receptor agonists — commonly used to treat type 2 diabetes and obesity — compared with nonuse.
- The secondary exposure examined was the use of medications indicated for AUD.
- The primary outcome was AUD-related hospitalization; secondary outcomes included hospitalization due to substance use disorder (SUD), somatic hospitalization, and suicide attempts.
TAKEAWAY:
- About 59% of participants experienced AUD-related hospitalization.
- Semaglutide users (n = 4321) had the lowest risk for hospitalization related to AUD (adjusted hazard ratio [aHR], 0.64; 95% CI, 0.50-0.83) and to any SUD (aHR, 0.68; 95% CI, 0.54-0.85).
- Liraglutide users (n = 2509) had the second lowest risk for both AUD-related (aHR, 0.72; 95% CI, 0.57-0.92) and SUD-related (aHR, 0.78; 95% CI, 0.64-0.97) hospitalizations.
- The use of both semaglutide (aHR, 0.78; 95% CI, 0.68-0.90) and liraglutide (aHR, 0.79; 95% CI, 0.69-0.91) was linked to a reduced risk for hospitalization because of somatic reasons but was not associated with the risk of suicide attempts.
- Traditional AUD medications showed modest effectiveness with a slightly decreased but nonsignificant risk for AUD-related hospitalization (aHR, 0.98).
IN PRACTICE:
“AUDs and SUDs are undertreated pharmacologically, despite the availability of effective treatments. However, novel treatments are also needed because existing treatments may not be suitable for all patients. Semaglutide and liraglutide may be effective in the treatment of AUD, and clinical trials are urgently needed to confirm these findings,” the investigators wrote.
SOURCE:
This study was led by Markku Lähteenvuo, MD, PhD, University of Eastern Finland, Niuvanniemi Hospital, Kuopio. It was published online on November 13 in JAMA Psychiatry.
LIMITATIONS:
The observational nature of this study limited causal inferences.
DISCLOSURES:
The data used in this study were obtained from the REWHARD consortium, supported by the Swedish Research Council. Four of the six authors reported receiving grants or personal fees from various sources outside the submitted work, which are fully listed in the original article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
Use of the glucagon-like peptide 1 (GLP-1) receptor agonists semaglutide and liraglutide is linked to a lower risk for alcohol use disorder (AUD)–related hospitalizations, compared with traditional AUD medications, a new study suggested.
METHODOLOGY:
- Researchers conducted a nationwide cohort study from 2006 to 2023 in Sweden that included more than 220,000 individuals with AUD (mean age, 40 years; 64% men).
- Data were obtained from registers of inpatient and specialized outpatient care, sickness absence, and disability pension, with a median follow-up period of 8.8 years.
- The primary exposure measured was the use of individual GLP-1 receptor agonists — commonly used to treat type 2 diabetes and obesity — compared with nonuse.
- The secondary exposure examined was the use of medications indicated for AUD.
- The primary outcome was AUD-related hospitalization; secondary outcomes included hospitalization due to substance use disorder (SUD), somatic hospitalization, and suicide attempts.
TAKEAWAY:
- About 59% of participants experienced AUD-related hospitalization.
- Semaglutide users (n = 4321) had the lowest risk for hospitalization related to AUD (adjusted hazard ratio [aHR], 0.64; 95% CI, 0.50-0.83) and to any SUD (aHR, 0.68; 95% CI, 0.54-0.85).
- Liraglutide users (n = 2509) had the second lowest risk for both AUD-related (aHR, 0.72; 95% CI, 0.57-0.92) and SUD-related (aHR, 0.78; 95% CI, 0.64-0.97) hospitalizations.
- The use of both semaglutide (aHR, 0.78; 95% CI, 0.68-0.90) and liraglutide (aHR, 0.79; 95% CI, 0.69-0.91) was linked to a reduced risk for hospitalization because of somatic reasons but was not associated with the risk of suicide attempts.
- Traditional AUD medications showed modest effectiveness with a slightly decreased but nonsignificant risk for AUD-related hospitalization (aHR, 0.98).
IN PRACTICE:
“AUDs and SUDs are undertreated pharmacologically, despite the availability of effective treatments. However, novel treatments are also needed because existing treatments may not be suitable for all patients. Semaglutide and liraglutide may be effective in the treatment of AUD, and clinical trials are urgently needed to confirm these findings,” the investigators wrote.
SOURCE:
This study was led by Markku Lähteenvuo, MD, PhD, University of Eastern Finland, Niuvanniemi Hospital, Kuopio. It was published online on November 13 in JAMA Psychiatry.
LIMITATIONS:
The observational nature of this study limited causal inferences.
DISCLOSURES:
The data used in this study were obtained from the REWHARD consortium, supported by the Swedish Research Council. Four of the six authors reported receiving grants or personal fees from various sources outside the submitted work, which are fully listed in the original article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
Use of the glucagon-like peptide 1 (GLP-1) receptor agonists semaglutide and liraglutide is linked to a lower risk for alcohol use disorder (AUD)–related hospitalizations, compared with traditional AUD medications, a new study suggested.
METHODOLOGY:
- Researchers conducted a nationwide cohort study from 2006 to 2023 in Sweden that included more than 220,000 individuals with AUD (mean age, 40 years; 64% men).
- Data were obtained from registers of inpatient and specialized outpatient care, sickness absence, and disability pension, with a median follow-up period of 8.8 years.
- The primary exposure measured was the use of individual GLP-1 receptor agonists — commonly used to treat type 2 diabetes and obesity — compared with nonuse.
- The secondary exposure examined was the use of medications indicated for AUD.
- The primary outcome was AUD-related hospitalization; secondary outcomes included hospitalization due to substance use disorder (SUD), somatic hospitalization, and suicide attempts.
TAKEAWAY:
- About 59% of participants experienced AUD-related hospitalization.
- Semaglutide users (n = 4321) had the lowest risk for hospitalization related to AUD (adjusted hazard ratio [aHR], 0.64; 95% CI, 0.50-0.83) and to any SUD (aHR, 0.68; 95% CI, 0.54-0.85).
- Liraglutide users (n = 2509) had the second lowest risk for both AUD-related (aHR, 0.72; 95% CI, 0.57-0.92) and SUD-related (aHR, 0.78; 95% CI, 0.64-0.97) hospitalizations.
- The use of both semaglutide (aHR, 0.78; 95% CI, 0.68-0.90) and liraglutide (aHR, 0.79; 95% CI, 0.69-0.91) was linked to a reduced risk for hospitalization because of somatic reasons but was not associated with the risk of suicide attempts.
- Traditional AUD medications showed modest effectiveness with a slightly decreased but nonsignificant risk for AUD-related hospitalization (aHR, 0.98).
IN PRACTICE:
“AUDs and SUDs are undertreated pharmacologically, despite the availability of effective treatments. However, novel treatments are also needed because existing treatments may not be suitable for all patients. Semaglutide and liraglutide may be effective in the treatment of AUD, and clinical trials are urgently needed to confirm these findings,” the investigators wrote.
SOURCE:
This study was led by Markku Lähteenvuo, MD, PhD, University of Eastern Finland, Niuvanniemi Hospital, Kuopio. It was published online on November 13 in JAMA Psychiatry.
LIMITATIONS:
The observational nature of this study limited causal inferences.
DISCLOSURES:
The data used in this study were obtained from the REWHARD consortium, supported by the Swedish Research Council. Four of the six authors reported receiving grants or personal fees from various sources outside the submitted work, which are fully listed in the original article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.