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Synchronizing refills saves money, improves outcomes
NATIONAL HARBOR, MD. – according to research presented at the annual meeting of the Academy of Managed Care Pharmacy.
Investigators with Pharmacy Quality Alliance (PQA) used data from Truven MarketScan Research Databases to conduct a retrospective cohort study of more than 20,000 patients eligible for inclusion in PQA’s diabetes medication adherence measure. To be included, patients needed to have two or more prescriptions for diabetes medications (excluding insulin), statins, or renin-angiotensin system antagonists. About 80% of patients were commercially insured and 20% came from Medicare supplement insurance (Medigap) plans.
Commercially insured patients whose medication refills were synchronized had better medication adherence than did matched controls (67.7% vs. 57.4%) and lower median health care expenditures ($3,687 vs. $7,480).
The same was true for patients with Medicare supplemental insurance. Synchronized patients in this group also had better medication adherence than controls, at 86.5% vs. 70.4% and lower median health care expenditures ($7,353 vs. $10,592).
Based on their findings in diabetes patients, “I think we should synchronize refills,” Matthew K. Pickering, PharmD, senior director of research and quality strategies at PQA, said. “However, there are populations that were not represented in this, like COPD [chronic obstructive pulmonary disease]. That’s another high-comorbidity, high-cost population that should be studied.”
Session moderator Laura Happe, PharmD, editor in chief of the Journal of Managed Care and Specialty Pharmacy, questioned Dr. Pickering about the barriers to medication synchronization.
In previous research, “we discovered that some patients were resistant to synchronizing their medication refills because of the copays – having all of their copays at one time, rather than spreading them out over the month,” Dr. Happe said.
“Certainly, patients may not be able to afford all their copays at one time, so that can be a barrier,” Dr. Pickering said. “With medication synchronization programs, there’s a lot of variation across the board. Patients can choose which medication to synchronize in some programs. Others only synchronize the three-star medication, etc. But there are real barriers and they should be explored.”
Pharmacy Quality Alliance is a nonprofit public-private partnership that develops pharmacy quality measures in collaboration with the Centers for Medicare & Medicaid Services.
Dr. Pickering disclosed no relevant conflicts of interest.
NATIONAL HARBOR, MD. – according to research presented at the annual meeting of the Academy of Managed Care Pharmacy.
Investigators with Pharmacy Quality Alliance (PQA) used data from Truven MarketScan Research Databases to conduct a retrospective cohort study of more than 20,000 patients eligible for inclusion in PQA’s diabetes medication adherence measure. To be included, patients needed to have two or more prescriptions for diabetes medications (excluding insulin), statins, or renin-angiotensin system antagonists. About 80% of patients were commercially insured and 20% came from Medicare supplement insurance (Medigap) plans.
Commercially insured patients whose medication refills were synchronized had better medication adherence than did matched controls (67.7% vs. 57.4%) and lower median health care expenditures ($3,687 vs. $7,480).
The same was true for patients with Medicare supplemental insurance. Synchronized patients in this group also had better medication adherence than controls, at 86.5% vs. 70.4% and lower median health care expenditures ($7,353 vs. $10,592).
Based on their findings in diabetes patients, “I think we should synchronize refills,” Matthew K. Pickering, PharmD, senior director of research and quality strategies at PQA, said. “However, there are populations that were not represented in this, like COPD [chronic obstructive pulmonary disease]. That’s another high-comorbidity, high-cost population that should be studied.”
Session moderator Laura Happe, PharmD, editor in chief of the Journal of Managed Care and Specialty Pharmacy, questioned Dr. Pickering about the barriers to medication synchronization.
In previous research, “we discovered that some patients were resistant to synchronizing their medication refills because of the copays – having all of their copays at one time, rather than spreading them out over the month,” Dr. Happe said.
“Certainly, patients may not be able to afford all their copays at one time, so that can be a barrier,” Dr. Pickering said. “With medication synchronization programs, there’s a lot of variation across the board. Patients can choose which medication to synchronize in some programs. Others only synchronize the three-star medication, etc. But there are real barriers and they should be explored.”
Pharmacy Quality Alliance is a nonprofit public-private partnership that develops pharmacy quality measures in collaboration with the Centers for Medicare & Medicaid Services.
Dr. Pickering disclosed no relevant conflicts of interest.
NATIONAL HARBOR, MD. – according to research presented at the annual meeting of the Academy of Managed Care Pharmacy.
Investigators with Pharmacy Quality Alliance (PQA) used data from Truven MarketScan Research Databases to conduct a retrospective cohort study of more than 20,000 patients eligible for inclusion in PQA’s diabetes medication adherence measure. To be included, patients needed to have two or more prescriptions for diabetes medications (excluding insulin), statins, or renin-angiotensin system antagonists. About 80% of patients were commercially insured and 20% came from Medicare supplement insurance (Medigap) plans.
Commercially insured patients whose medication refills were synchronized had better medication adherence than did matched controls (67.7% vs. 57.4%) and lower median health care expenditures ($3,687 vs. $7,480).
The same was true for patients with Medicare supplemental insurance. Synchronized patients in this group also had better medication adherence than controls, at 86.5% vs. 70.4% and lower median health care expenditures ($7,353 vs. $10,592).
Based on their findings in diabetes patients, “I think we should synchronize refills,” Matthew K. Pickering, PharmD, senior director of research and quality strategies at PQA, said. “However, there are populations that were not represented in this, like COPD [chronic obstructive pulmonary disease]. That’s another high-comorbidity, high-cost population that should be studied.”
Session moderator Laura Happe, PharmD, editor in chief of the Journal of Managed Care and Specialty Pharmacy, questioned Dr. Pickering about the barriers to medication synchronization.
In previous research, “we discovered that some patients were resistant to synchronizing their medication refills because of the copays – having all of their copays at one time, rather than spreading them out over the month,” Dr. Happe said.
“Certainly, patients may not be able to afford all their copays at one time, so that can be a barrier,” Dr. Pickering said. “With medication synchronization programs, there’s a lot of variation across the board. Patients can choose which medication to synchronize in some programs. Others only synchronize the three-star medication, etc. But there are real barriers and they should be explored.”
Pharmacy Quality Alliance is a nonprofit public-private partnership that develops pharmacy quality measures in collaboration with the Centers for Medicare & Medicaid Services.
Dr. Pickering disclosed no relevant conflicts of interest.
REPORTING FROM AMCP NEXUS 2019
Net prices of drugs rising four-times faster than inflation
NATIONAL HARBOR, MD. – The net prices of drugs are increasing four times faster than the rate of inflation, despite being offset 43% from list prices.
List prices increased by 232% from 2007 to 2018 (12% per year) and net prices increased 133% during that same time period. For Medicaid, the gross-to-net discount increased from 40% in 2007 to 68% in 2018. For all other payers, the increase was 22%-50% during that same period, Inmaculada Hernandez, PharmD, and colleagues reported at annual meeting of the Academy of Managed Care Pharmacy.
The investigators also found a wide variation on discounts across therapeutic classes. For example, list price for drugs in the multiple sclerosis category increased 407% over the study period while net price increased 221%. Insulins came in second in terms of gross price increases (337%) but saw only net prices increases by 83% due to increasing discounts, according to Dr. Hernandez, assistant professor of pharmacy and therapeutics at the University of Pittsburgh.
List prices for noninsulin diabetes treatments tripled during the observation period, but net prices went up only 24%. List price increases were lowest in the antineoplastic class, averaging 135%, though there were only 34% in rebates to offset the list price, resulting in an average net price increase of 89%.
Research was based on pricing data supplied by investment firm SSR Health for branded products and U.S. sales reported by publicly traded companies. The National Heart, Lung, and Blood Institute sponsored the study.
SOURCE: Hernandez I et a. AMCP Nexus, poster U2.
NATIONAL HARBOR, MD. – The net prices of drugs are increasing four times faster than the rate of inflation, despite being offset 43% from list prices.
List prices increased by 232% from 2007 to 2018 (12% per year) and net prices increased 133% during that same time period. For Medicaid, the gross-to-net discount increased from 40% in 2007 to 68% in 2018. For all other payers, the increase was 22%-50% during that same period, Inmaculada Hernandez, PharmD, and colleagues reported at annual meeting of the Academy of Managed Care Pharmacy.
The investigators also found a wide variation on discounts across therapeutic classes. For example, list price for drugs in the multiple sclerosis category increased 407% over the study period while net price increased 221%. Insulins came in second in terms of gross price increases (337%) but saw only net prices increases by 83% due to increasing discounts, according to Dr. Hernandez, assistant professor of pharmacy and therapeutics at the University of Pittsburgh.
List prices for noninsulin diabetes treatments tripled during the observation period, but net prices went up only 24%. List price increases were lowest in the antineoplastic class, averaging 135%, though there were only 34% in rebates to offset the list price, resulting in an average net price increase of 89%.
Research was based on pricing data supplied by investment firm SSR Health for branded products and U.S. sales reported by publicly traded companies. The National Heart, Lung, and Blood Institute sponsored the study.
SOURCE: Hernandez I et a. AMCP Nexus, poster U2.
NATIONAL HARBOR, MD. – The net prices of drugs are increasing four times faster than the rate of inflation, despite being offset 43% from list prices.
List prices increased by 232% from 2007 to 2018 (12% per year) and net prices increased 133% during that same time period. For Medicaid, the gross-to-net discount increased from 40% in 2007 to 68% in 2018. For all other payers, the increase was 22%-50% during that same period, Inmaculada Hernandez, PharmD, and colleagues reported at annual meeting of the Academy of Managed Care Pharmacy.
The investigators also found a wide variation on discounts across therapeutic classes. For example, list price for drugs in the multiple sclerosis category increased 407% over the study period while net price increased 221%. Insulins came in second in terms of gross price increases (337%) but saw only net prices increases by 83% due to increasing discounts, according to Dr. Hernandez, assistant professor of pharmacy and therapeutics at the University of Pittsburgh.
List prices for noninsulin diabetes treatments tripled during the observation period, but net prices went up only 24%. List price increases were lowest in the antineoplastic class, averaging 135%, though there were only 34% in rebates to offset the list price, resulting in an average net price increase of 89%.
Research was based on pricing data supplied by investment firm SSR Health for branded products and U.S. sales reported by publicly traded companies. The National Heart, Lung, and Blood Institute sponsored the study.
SOURCE: Hernandez I et a. AMCP Nexus, poster U2.
REPORTING FROM AMCP NEXUS 2019
GABA falls short for type 1 diabetes prevention in children
BARCELONA – Gamma aminobutyric acid (GABA) alone or given in combination with glutamic acid decarboxylase (GAD) had little to no effect on the progression of type 1 diabetes in children, according to early data presented at the annual meeting of the European Association for the Study of Diabetes.
There was no difference between the two active treatment groups and placebo for the primary outcome measure, which was the effect on meal-stimulated C-peptide secretion before and after 1 year of treatment, study investigator Kenneth L. McCormick, MD, reported, nor was there any difference in glycemic control, based on hemoglobin A1c (HbA1c) and insulin dose, between the children who received GABA alone (n = 39) or combined with GAD (n = 22), and those who received placebo (n = 30).
“However, the GABA–GAD combination tended to have greater efficacy [than placebo] in terms of the daily insulin dose and the fasting C-peptide–to–glucagon ratio,” said Dr. McCormick, a pediatric endocrinologist at the University of Alabama at Birmingham.
“At 12 months, fasting glucagon was reduced [P less than .013] in the GABA–GAD group, compared with placebo,” he said. This was a “novel observation,” because stimulated glucagon was also reduced in this cohort. “This could be a potential salutatory metabolic effect in diabetes.”
The data were the first to be reported from the trial, and results of the immunologic analyses should be available by the end of the year and might reveal more positive effects of GABA and GAD, Dr. McCormick suggested. Data from a “proinsulin analysis” will also be available later.
The inspiration for the trial was a study performed in mice showing that GABA exerted a protective and regenerative effect on the islet beta cells and “reversed diabetes” (Proc Natl Acad Sci USA. 2011;108:11692-7). It took almost 4 years from the publication of that study to enroll the first patient for the current study.
“GABA was intriguing ... first of all, it is available in health food stores and in supermarkets in the United States,” said Dr. McCormick. “It has a strong safety profile, it’s tasteless, and can be given orally – what better could you ask for in a trial of children with type 1 diabetes?”
GABA is thought to have multiple effects in the pancreas, from increasing insulin secretion and suppressing glucagon secretion, to altering inflammation and T-cell populations. “That’s what’s so important to emphasize, besides its metabolic effects, this compound also has immunosuppressant action,” Dr. McCormick noted.
The study hypothesis was that treatment with oral GABA, or a combination of GABA–GAD, would hinder the progression of new-onset type 1 diabetes. The double-blind trial was designed to run for 1 year (Contemp Clin Trials. 2019;82:93-100) and recruited 97 children with newly diagnosed type 1 diabetes, aged 4-18 years, who were randomized to the three study groups. They were evaluated at baseline and months 1, 5, 8, and 12.
The trial had several limitations, however, which might explain the findings. A key limitation was that the researchers used a low dose of GABA – 1 to 1.5 g/m2 a day, given as a twice-daily oral dose, as mandated by the Food and Drug Administration. “For the GABA dose and the response, we are at the threshold. I don’t believe we are overdosing these kids,” Dr. McCormick said, noting that this is the first study done with GABA in humans.
In fact, GABA has a short half-life of around 2.5-5 hours, so the dose may need to be much higher to show an effect and perhaps administered three times a day, he said.
Another limitation was compliance with the twice-daily medication, especially because 35% of the patients were teenagers, and that it was a young population, with about a third of the patients aged younger that 8 years.
GABA and GABA–GAD should still be studied further, Dr. McCormick concluded, but “additional studies with a higher dose of GABA [given] three times a day, and not twice, are warranted.” Such studies also need to have more participants in each group.
The University of Alabama at Birmingham sponsored the study. Collaborators included Diamyd, NOW Foods, Janssen, and the Juvenile Diabetes Research Foundation. Dr. McCormick did not have any disclosures.
SOURCE: McCormick KL et al. EASD 2019, Abstract S05.1.
BARCELONA – Gamma aminobutyric acid (GABA) alone or given in combination with glutamic acid decarboxylase (GAD) had little to no effect on the progression of type 1 diabetes in children, according to early data presented at the annual meeting of the European Association for the Study of Diabetes.
There was no difference between the two active treatment groups and placebo for the primary outcome measure, which was the effect on meal-stimulated C-peptide secretion before and after 1 year of treatment, study investigator Kenneth L. McCormick, MD, reported, nor was there any difference in glycemic control, based on hemoglobin A1c (HbA1c) and insulin dose, between the children who received GABA alone (n = 39) or combined with GAD (n = 22), and those who received placebo (n = 30).
“However, the GABA–GAD combination tended to have greater efficacy [than placebo] in terms of the daily insulin dose and the fasting C-peptide–to–glucagon ratio,” said Dr. McCormick, a pediatric endocrinologist at the University of Alabama at Birmingham.
“At 12 months, fasting glucagon was reduced [P less than .013] in the GABA–GAD group, compared with placebo,” he said. This was a “novel observation,” because stimulated glucagon was also reduced in this cohort. “This could be a potential salutatory metabolic effect in diabetes.”
The data were the first to be reported from the trial, and results of the immunologic analyses should be available by the end of the year and might reveal more positive effects of GABA and GAD, Dr. McCormick suggested. Data from a “proinsulin analysis” will also be available later.
The inspiration for the trial was a study performed in mice showing that GABA exerted a protective and regenerative effect on the islet beta cells and “reversed diabetes” (Proc Natl Acad Sci USA. 2011;108:11692-7). It took almost 4 years from the publication of that study to enroll the first patient for the current study.
“GABA was intriguing ... first of all, it is available in health food stores and in supermarkets in the United States,” said Dr. McCormick. “It has a strong safety profile, it’s tasteless, and can be given orally – what better could you ask for in a trial of children with type 1 diabetes?”
GABA is thought to have multiple effects in the pancreas, from increasing insulin secretion and suppressing glucagon secretion, to altering inflammation and T-cell populations. “That’s what’s so important to emphasize, besides its metabolic effects, this compound also has immunosuppressant action,” Dr. McCormick noted.
The study hypothesis was that treatment with oral GABA, or a combination of GABA–GAD, would hinder the progression of new-onset type 1 diabetes. The double-blind trial was designed to run for 1 year (Contemp Clin Trials. 2019;82:93-100) and recruited 97 children with newly diagnosed type 1 diabetes, aged 4-18 years, who were randomized to the three study groups. They were evaluated at baseline and months 1, 5, 8, and 12.
The trial had several limitations, however, which might explain the findings. A key limitation was that the researchers used a low dose of GABA – 1 to 1.5 g/m2 a day, given as a twice-daily oral dose, as mandated by the Food and Drug Administration. “For the GABA dose and the response, we are at the threshold. I don’t believe we are overdosing these kids,” Dr. McCormick said, noting that this is the first study done with GABA in humans.
In fact, GABA has a short half-life of around 2.5-5 hours, so the dose may need to be much higher to show an effect and perhaps administered three times a day, he said.
Another limitation was compliance with the twice-daily medication, especially because 35% of the patients were teenagers, and that it was a young population, with about a third of the patients aged younger that 8 years.
GABA and GABA–GAD should still be studied further, Dr. McCormick concluded, but “additional studies with a higher dose of GABA [given] three times a day, and not twice, are warranted.” Such studies also need to have more participants in each group.
The University of Alabama at Birmingham sponsored the study. Collaborators included Diamyd, NOW Foods, Janssen, and the Juvenile Diabetes Research Foundation. Dr. McCormick did not have any disclosures.
SOURCE: McCormick KL et al. EASD 2019, Abstract S05.1.
BARCELONA – Gamma aminobutyric acid (GABA) alone or given in combination with glutamic acid decarboxylase (GAD) had little to no effect on the progression of type 1 diabetes in children, according to early data presented at the annual meeting of the European Association for the Study of Diabetes.
There was no difference between the two active treatment groups and placebo for the primary outcome measure, which was the effect on meal-stimulated C-peptide secretion before and after 1 year of treatment, study investigator Kenneth L. McCormick, MD, reported, nor was there any difference in glycemic control, based on hemoglobin A1c (HbA1c) and insulin dose, between the children who received GABA alone (n = 39) or combined with GAD (n = 22), and those who received placebo (n = 30).
“However, the GABA–GAD combination tended to have greater efficacy [than placebo] in terms of the daily insulin dose and the fasting C-peptide–to–glucagon ratio,” said Dr. McCormick, a pediatric endocrinologist at the University of Alabama at Birmingham.
“At 12 months, fasting glucagon was reduced [P less than .013] in the GABA–GAD group, compared with placebo,” he said. This was a “novel observation,” because stimulated glucagon was also reduced in this cohort. “This could be a potential salutatory metabolic effect in diabetes.”
The data were the first to be reported from the trial, and results of the immunologic analyses should be available by the end of the year and might reveal more positive effects of GABA and GAD, Dr. McCormick suggested. Data from a “proinsulin analysis” will also be available later.
The inspiration for the trial was a study performed in mice showing that GABA exerted a protective and regenerative effect on the islet beta cells and “reversed diabetes” (Proc Natl Acad Sci USA. 2011;108:11692-7). It took almost 4 years from the publication of that study to enroll the first patient for the current study.
“GABA was intriguing ... first of all, it is available in health food stores and in supermarkets in the United States,” said Dr. McCormick. “It has a strong safety profile, it’s tasteless, and can be given orally – what better could you ask for in a trial of children with type 1 diabetes?”
GABA is thought to have multiple effects in the pancreas, from increasing insulin secretion and suppressing glucagon secretion, to altering inflammation and T-cell populations. “That’s what’s so important to emphasize, besides its metabolic effects, this compound also has immunosuppressant action,” Dr. McCormick noted.
The study hypothesis was that treatment with oral GABA, or a combination of GABA–GAD, would hinder the progression of new-onset type 1 diabetes. The double-blind trial was designed to run for 1 year (Contemp Clin Trials. 2019;82:93-100) and recruited 97 children with newly diagnosed type 1 diabetes, aged 4-18 years, who were randomized to the three study groups. They were evaluated at baseline and months 1, 5, 8, and 12.
The trial had several limitations, however, which might explain the findings. A key limitation was that the researchers used a low dose of GABA – 1 to 1.5 g/m2 a day, given as a twice-daily oral dose, as mandated by the Food and Drug Administration. “For the GABA dose and the response, we are at the threshold. I don’t believe we are overdosing these kids,” Dr. McCormick said, noting that this is the first study done with GABA in humans.
In fact, GABA has a short half-life of around 2.5-5 hours, so the dose may need to be much higher to show an effect and perhaps administered three times a day, he said.
Another limitation was compliance with the twice-daily medication, especially because 35% of the patients were teenagers, and that it was a young population, with about a third of the patients aged younger that 8 years.
GABA and GABA–GAD should still be studied further, Dr. McCormick concluded, but “additional studies with a higher dose of GABA [given] three times a day, and not twice, are warranted.” Such studies also need to have more participants in each group.
The University of Alabama at Birmingham sponsored the study. Collaborators included Diamyd, NOW Foods, Janssen, and the Juvenile Diabetes Research Foundation. Dr. McCormick did not have any disclosures.
SOURCE: McCormick KL et al. EASD 2019, Abstract S05.1.
REPORTING FROM EASD 2019
SUSTAIN 10: Weight loss, glycemic control better with semaglutide than liraglutide
BARCELONA – Patients with type 2 diabetes who were treated with semaglutide achieved greater reductions in glycated hemoglobin (HbA1c) levels and body weight, compared with those receiving liraglutide, according to results presented at the annual meeting of the European Association for the Study of Diabetes.
In the phase 3b SUSTAIN 10 trial, conducted in 11 European countries, mean glycated hemoglobin at 30 weeks decreased by 1.7% with once-weekly semaglutide and 1.0% for once-daily liraglutide, from the overall baseline level of 8.2%. The estimated treatment difference (ETD) between the two treatments was –0.69 percentage points (95% confidence interval, –0.82 to –0.56; P less than .0001).
Mean body weight decreased during the same period by 5.8 kg with semaglutide and 1.9 kg with liraglutide, from a baseline of 96.9 kg. The ETD was 3.83 kg (95% CI, –4.57 to –3.09; P less than .0001).
The doses of semaglutide and liraglutide used in the study were 1.0 mg and 1.2 mg, respectively, the latter being the dose that is used most commonly in clinical practice, study investigator Matthew Capehorn, MB, CAB, explained in an interview at the meeting.
“We know that at a dose of 1.8 mg, liraglutide is more effective than 1.2 mg, but it’s about whether it is deemed more cost effective,” said Dr. Capehorn, who is clinical manager at Rotherham (England) Institute for Obesity, Clifton Medical Centre. “Certainly, in the United Kingdom, we’re encouraged to use the 1.2-mg dose” according to guidance from the National Institute for Heath and Care Excellence, and “other European countries are the same.”
Dr. Capehorn noted that studies are being done with a higher dose of semaglutide to see if it has potential as a weight loss drug in its own right in patients who do not have type 2 diabetes. “I care as much about obesity and cardiovascular disease as I do about chasing the HbA1c level and getting that reduced, so I would rather pick an agent that covers all three [components], than just looking at the HbA1c,” he said.
In SUSTAIN 10,577 adults with type 2 diabetes and an HbA1c level of between 7.0% and 11.0% who were on stable doses of one to three oral antidiabetic drugs were randomized to receive semaglutide (n = 290) or liraglutide (n = 287) for 30 weeks.
The primary endpoint was the change in HbA1c from baseline to week 30, and the secondary confirmatory endpoint was change in body weight over the same period.
In presenting the findings, which were simultaneously published in Diabetes & Metabolism, Dr. Capehorn noted that the efficacy results were consistent with those of other SUSTAIN trials that compared semaglutide with other glucagonlike peptide–1 receptor antagonists, notably SUSTAIN 3 (with exenatide extended release) and SUSTAIN 7 (with dulaglutide).
Other efficacy findings from SUSTAIN 10 were that semaglutide produced greater mean changes than did liraglutide in both fasting plasma glucose and in a 7-point, self-monitoring of blood glucose profile.
A greater percentage of people treated with semaglutide, compared with liraglutide, also achieved their glycemic targets of less than 7.0% (80% vs. 46%, respectively) and of 6.5% or less (58% vs. 25%), and their weight loss targets of 5% or more (56% vs. 18%) and 10% or more (19% vs. 4%).
In addition, more semaglutide- than liraglutide-treated patients achieved an HbA1c target of less than 7.0% without severe or blood glucose–confirmed symptomatic hypoglycemia, with or without weight gain (76% vs. 37%; P less than .0001). There were also more semaglutide patients who achieved an HbA1c reduction of 1% or more and a weight loss reduction of 10% or more (17% vs. 4% for liraglutide, P less than .0001).
The safety profiles were similar for semaglutide and liraglutide, Dr. Capehorn noted, but gastrointestinal adverse events were more prevalent in patients receiving semaglutide, compared with liraglutide (43.9% vs. 38.3%), and more patients receiving semaglutide discontinued treatment prematurely because of those adverse events (11.4% vs. 6.6% for liraglutide).
Novo Nordisk sponsored the study. Dr. Capehorn reported receiving research funding from, providing advisory board support to, and speaker fees from Novo Nordisk and from several other companies.
SOURCE: Capehorn M et al. EASD 2019, Oral Presentation 53; Capehorn M et al. Diabetes Metab. 2019 Sep 17. doi: 10.1016/j.diabet.2019.101117.
BARCELONA – Patients with type 2 diabetes who were treated with semaglutide achieved greater reductions in glycated hemoglobin (HbA1c) levels and body weight, compared with those receiving liraglutide, according to results presented at the annual meeting of the European Association for the Study of Diabetes.
In the phase 3b SUSTAIN 10 trial, conducted in 11 European countries, mean glycated hemoglobin at 30 weeks decreased by 1.7% with once-weekly semaglutide and 1.0% for once-daily liraglutide, from the overall baseline level of 8.2%. The estimated treatment difference (ETD) between the two treatments was –0.69 percentage points (95% confidence interval, –0.82 to –0.56; P less than .0001).
Mean body weight decreased during the same period by 5.8 kg with semaglutide and 1.9 kg with liraglutide, from a baseline of 96.9 kg. The ETD was 3.83 kg (95% CI, –4.57 to –3.09; P less than .0001).
The doses of semaglutide and liraglutide used in the study were 1.0 mg and 1.2 mg, respectively, the latter being the dose that is used most commonly in clinical practice, study investigator Matthew Capehorn, MB, CAB, explained in an interview at the meeting.
“We know that at a dose of 1.8 mg, liraglutide is more effective than 1.2 mg, but it’s about whether it is deemed more cost effective,” said Dr. Capehorn, who is clinical manager at Rotherham (England) Institute for Obesity, Clifton Medical Centre. “Certainly, in the United Kingdom, we’re encouraged to use the 1.2-mg dose” according to guidance from the National Institute for Heath and Care Excellence, and “other European countries are the same.”
Dr. Capehorn noted that studies are being done with a higher dose of semaglutide to see if it has potential as a weight loss drug in its own right in patients who do not have type 2 diabetes. “I care as much about obesity and cardiovascular disease as I do about chasing the HbA1c level and getting that reduced, so I would rather pick an agent that covers all three [components], than just looking at the HbA1c,” he said.
In SUSTAIN 10,577 adults with type 2 diabetes and an HbA1c level of between 7.0% and 11.0% who were on stable doses of one to three oral antidiabetic drugs were randomized to receive semaglutide (n = 290) or liraglutide (n = 287) for 30 weeks.
The primary endpoint was the change in HbA1c from baseline to week 30, and the secondary confirmatory endpoint was change in body weight over the same period.
In presenting the findings, which were simultaneously published in Diabetes & Metabolism, Dr. Capehorn noted that the efficacy results were consistent with those of other SUSTAIN trials that compared semaglutide with other glucagonlike peptide–1 receptor antagonists, notably SUSTAIN 3 (with exenatide extended release) and SUSTAIN 7 (with dulaglutide).
Other efficacy findings from SUSTAIN 10 were that semaglutide produced greater mean changes than did liraglutide in both fasting plasma glucose and in a 7-point, self-monitoring of blood glucose profile.
A greater percentage of people treated with semaglutide, compared with liraglutide, also achieved their glycemic targets of less than 7.0% (80% vs. 46%, respectively) and of 6.5% or less (58% vs. 25%), and their weight loss targets of 5% or more (56% vs. 18%) and 10% or more (19% vs. 4%).
In addition, more semaglutide- than liraglutide-treated patients achieved an HbA1c target of less than 7.0% without severe or blood glucose–confirmed symptomatic hypoglycemia, with or without weight gain (76% vs. 37%; P less than .0001). There were also more semaglutide patients who achieved an HbA1c reduction of 1% or more and a weight loss reduction of 10% or more (17% vs. 4% for liraglutide, P less than .0001).
The safety profiles were similar for semaglutide and liraglutide, Dr. Capehorn noted, but gastrointestinal adverse events were more prevalent in patients receiving semaglutide, compared with liraglutide (43.9% vs. 38.3%), and more patients receiving semaglutide discontinued treatment prematurely because of those adverse events (11.4% vs. 6.6% for liraglutide).
Novo Nordisk sponsored the study. Dr. Capehorn reported receiving research funding from, providing advisory board support to, and speaker fees from Novo Nordisk and from several other companies.
SOURCE: Capehorn M et al. EASD 2019, Oral Presentation 53; Capehorn M et al. Diabetes Metab. 2019 Sep 17. doi: 10.1016/j.diabet.2019.101117.
BARCELONA – Patients with type 2 diabetes who were treated with semaglutide achieved greater reductions in glycated hemoglobin (HbA1c) levels and body weight, compared with those receiving liraglutide, according to results presented at the annual meeting of the European Association for the Study of Diabetes.
In the phase 3b SUSTAIN 10 trial, conducted in 11 European countries, mean glycated hemoglobin at 30 weeks decreased by 1.7% with once-weekly semaglutide and 1.0% for once-daily liraglutide, from the overall baseline level of 8.2%. The estimated treatment difference (ETD) between the two treatments was –0.69 percentage points (95% confidence interval, –0.82 to –0.56; P less than .0001).
Mean body weight decreased during the same period by 5.8 kg with semaglutide and 1.9 kg with liraglutide, from a baseline of 96.9 kg. The ETD was 3.83 kg (95% CI, –4.57 to –3.09; P less than .0001).
The doses of semaglutide and liraglutide used in the study were 1.0 mg and 1.2 mg, respectively, the latter being the dose that is used most commonly in clinical practice, study investigator Matthew Capehorn, MB, CAB, explained in an interview at the meeting.
“We know that at a dose of 1.8 mg, liraglutide is more effective than 1.2 mg, but it’s about whether it is deemed more cost effective,” said Dr. Capehorn, who is clinical manager at Rotherham (England) Institute for Obesity, Clifton Medical Centre. “Certainly, in the United Kingdom, we’re encouraged to use the 1.2-mg dose” according to guidance from the National Institute for Heath and Care Excellence, and “other European countries are the same.”
Dr. Capehorn noted that studies are being done with a higher dose of semaglutide to see if it has potential as a weight loss drug in its own right in patients who do not have type 2 diabetes. “I care as much about obesity and cardiovascular disease as I do about chasing the HbA1c level and getting that reduced, so I would rather pick an agent that covers all three [components], than just looking at the HbA1c,” he said.
In SUSTAIN 10,577 adults with type 2 diabetes and an HbA1c level of between 7.0% and 11.0% who were on stable doses of one to three oral antidiabetic drugs were randomized to receive semaglutide (n = 290) or liraglutide (n = 287) for 30 weeks.
The primary endpoint was the change in HbA1c from baseline to week 30, and the secondary confirmatory endpoint was change in body weight over the same period.
In presenting the findings, which were simultaneously published in Diabetes & Metabolism, Dr. Capehorn noted that the efficacy results were consistent with those of other SUSTAIN trials that compared semaglutide with other glucagonlike peptide–1 receptor antagonists, notably SUSTAIN 3 (with exenatide extended release) and SUSTAIN 7 (with dulaglutide).
Other efficacy findings from SUSTAIN 10 were that semaglutide produced greater mean changes than did liraglutide in both fasting plasma glucose and in a 7-point, self-monitoring of blood glucose profile.
A greater percentage of people treated with semaglutide, compared with liraglutide, also achieved their glycemic targets of less than 7.0% (80% vs. 46%, respectively) and of 6.5% or less (58% vs. 25%), and their weight loss targets of 5% or more (56% vs. 18%) and 10% or more (19% vs. 4%).
In addition, more semaglutide- than liraglutide-treated patients achieved an HbA1c target of less than 7.0% without severe or blood glucose–confirmed symptomatic hypoglycemia, with or without weight gain (76% vs. 37%; P less than .0001). There were also more semaglutide patients who achieved an HbA1c reduction of 1% or more and a weight loss reduction of 10% or more (17% vs. 4% for liraglutide, P less than .0001).
The safety profiles were similar for semaglutide and liraglutide, Dr. Capehorn noted, but gastrointestinal adverse events were more prevalent in patients receiving semaglutide, compared with liraglutide (43.9% vs. 38.3%), and more patients receiving semaglutide discontinued treatment prematurely because of those adverse events (11.4% vs. 6.6% for liraglutide).
Novo Nordisk sponsored the study. Dr. Capehorn reported receiving research funding from, providing advisory board support to, and speaker fees from Novo Nordisk and from several other companies.
SOURCE: Capehorn M et al. EASD 2019, Oral Presentation 53; Capehorn M et al. Diabetes Metab. 2019 Sep 17. doi: 10.1016/j.diabet.2019.101117.
REPORTING FROM EASD 2019
Severe hypoglycemia, poor glycemic control fuels fracture risk in older diabetic patients
Patients with type 2 diabetes and poor glycemic control or severe hypoglycemia may be at greater risk for fracture, according to recent research from a Japanese cohort of older men and postmenopausal women.
“The impacts of severe hypoglycemia and poor glycemic control on fractures appeared to be independent,” noted Yuji Komorita, MD, PhD, of the department of medicine and clinical science, Graduate School of Medical Sciences at Kyushu University, and colleagues. “This study suggests that the glycemic target to prevent fractures may be HbA1c <75 mmol/mol, which is far higher than that used to prevent microvascular complications, and higher than that for older adults with type 2 diabetes.”
Dr. Komorita and colleagues performed a prospective analysis of fracture incidence for 2,755 men and 1,951 postmenopausal women with type 2 diabetes in the Fukuoka Diabetes Registry who were mean 66 years old between April 2008 and October 2010. At the start of the study, the researchers assessed patient diabetes duration, previous fracture history, physical activity, alcohol and smoking status, whether patients were treated for diabetic retinopathy with laser photocoagulation, and their history of coronary artery disease or stroke. Patients were followed for a median 5.3 years, during which fractures were assessed through an annual self-administered questionnaire, with the results stratified by glycemic control and hypoglycemia.
Overall, there were 249 men and 413 women who experienced fractures during the study period, with a follow-up rate of 97.6%. In a multivariate analysis, patients with a higher risk of fracture included those with two or more episodes of severe hypoglycemia (hazard ratio, 2.25; 95% confidence interval, 1.57-3.22) and one episode of severe hypoglycemia (HR, 1.57; 95% CI, 1.11-2.20). In patients without severe hypoglycemic episodes, there was an increased risk of fracture in those with baseline hemoglobin A1c (HbA1c) level of 53 to less than 64 mmol/mol (7% to less than 8%; HR, 1.14; 0.94-1.39), 64 to less than 75 mmol/mol (8% to less than 9%; HR, 1.11; 95% CI, 0.86-1.43), and at least 75 mmol/mol (at least 9%; HR, 1.45; 95% CI, 1.06-1.98).
Compared with postmenopausal women, the unadjusted risk of fracture was higher in men with multiple severe hypoglycemic episodes (HR, 3.46; 95% CI, 2.05-5.85) and one episode of hypoglycemia (HR, 2.81; 95% CI, 1.74-4.56). These higher risks in older men persisted after adjustment for age, multivariate factors, and HbA1c.
“The association between severe hypoglycemia, poor glycemic control, and fracture risk at any anatomic site seems to be stronger in men than in postmenopausal women, although the interaction between men and postmenopausal women for fracture risk was not significant,” the researchers said. “The higher incidence rate of fractures in postmenopausal women, compared with men, was attributed to drastic changes in sex hormones after menopause, which may reduce the apparent impacts of hyperglycemia and severe hypoglycemia on postmenopausal women.”
Researchers said they did not consider potential external factors for fracture incidence, nor did they measure incident falls or other markers of bone health, such as bone mineral density and 25-hydroxyvitamin D levels. They also noted among the limitations of the study the self-reported nature of fracture reporting, and the lack of generalizability of the results.
This study was funded in part by grants from The Japan Society for the Promotion of Science KAKENHI from the Ministry of Education, Culture, Sports, Science and Technology of Japan; the Junior Scientist Development Grant supported by the Japan Diabetes Society; and the Lilly Research Grant Program for Bone & Mineral Research. The authors reported no relevant conflicts of interest.
SOURCE: Komorita Y et al. Diabet Med. 2019 Sep 25. doi: 10.1111/dme.14142.
Patients with type 2 diabetes and poor glycemic control or severe hypoglycemia may be at greater risk for fracture, according to recent research from a Japanese cohort of older men and postmenopausal women.
“The impacts of severe hypoglycemia and poor glycemic control on fractures appeared to be independent,” noted Yuji Komorita, MD, PhD, of the department of medicine and clinical science, Graduate School of Medical Sciences at Kyushu University, and colleagues. “This study suggests that the glycemic target to prevent fractures may be HbA1c <75 mmol/mol, which is far higher than that used to prevent microvascular complications, and higher than that for older adults with type 2 diabetes.”
Dr. Komorita and colleagues performed a prospective analysis of fracture incidence for 2,755 men and 1,951 postmenopausal women with type 2 diabetes in the Fukuoka Diabetes Registry who were mean 66 years old between April 2008 and October 2010. At the start of the study, the researchers assessed patient diabetes duration, previous fracture history, physical activity, alcohol and smoking status, whether patients were treated for diabetic retinopathy with laser photocoagulation, and their history of coronary artery disease or stroke. Patients were followed for a median 5.3 years, during which fractures were assessed through an annual self-administered questionnaire, with the results stratified by glycemic control and hypoglycemia.
Overall, there were 249 men and 413 women who experienced fractures during the study period, with a follow-up rate of 97.6%. In a multivariate analysis, patients with a higher risk of fracture included those with two or more episodes of severe hypoglycemia (hazard ratio, 2.25; 95% confidence interval, 1.57-3.22) and one episode of severe hypoglycemia (HR, 1.57; 95% CI, 1.11-2.20). In patients without severe hypoglycemic episodes, there was an increased risk of fracture in those with baseline hemoglobin A1c (HbA1c) level of 53 to less than 64 mmol/mol (7% to less than 8%; HR, 1.14; 0.94-1.39), 64 to less than 75 mmol/mol (8% to less than 9%; HR, 1.11; 95% CI, 0.86-1.43), and at least 75 mmol/mol (at least 9%; HR, 1.45; 95% CI, 1.06-1.98).
Compared with postmenopausal women, the unadjusted risk of fracture was higher in men with multiple severe hypoglycemic episodes (HR, 3.46; 95% CI, 2.05-5.85) and one episode of hypoglycemia (HR, 2.81; 95% CI, 1.74-4.56). These higher risks in older men persisted after adjustment for age, multivariate factors, and HbA1c.
“The association between severe hypoglycemia, poor glycemic control, and fracture risk at any anatomic site seems to be stronger in men than in postmenopausal women, although the interaction between men and postmenopausal women for fracture risk was not significant,” the researchers said. “The higher incidence rate of fractures in postmenopausal women, compared with men, was attributed to drastic changes in sex hormones after menopause, which may reduce the apparent impacts of hyperglycemia and severe hypoglycemia on postmenopausal women.”
Researchers said they did not consider potential external factors for fracture incidence, nor did they measure incident falls or other markers of bone health, such as bone mineral density and 25-hydroxyvitamin D levels. They also noted among the limitations of the study the self-reported nature of fracture reporting, and the lack of generalizability of the results.
This study was funded in part by grants from The Japan Society for the Promotion of Science KAKENHI from the Ministry of Education, Culture, Sports, Science and Technology of Japan; the Junior Scientist Development Grant supported by the Japan Diabetes Society; and the Lilly Research Grant Program for Bone & Mineral Research. The authors reported no relevant conflicts of interest.
SOURCE: Komorita Y et al. Diabet Med. 2019 Sep 25. doi: 10.1111/dme.14142.
Patients with type 2 diabetes and poor glycemic control or severe hypoglycemia may be at greater risk for fracture, according to recent research from a Japanese cohort of older men and postmenopausal women.
“The impacts of severe hypoglycemia and poor glycemic control on fractures appeared to be independent,” noted Yuji Komorita, MD, PhD, of the department of medicine and clinical science, Graduate School of Medical Sciences at Kyushu University, and colleagues. “This study suggests that the glycemic target to prevent fractures may be HbA1c <75 mmol/mol, which is far higher than that used to prevent microvascular complications, and higher than that for older adults with type 2 diabetes.”
Dr. Komorita and colleagues performed a prospective analysis of fracture incidence for 2,755 men and 1,951 postmenopausal women with type 2 diabetes in the Fukuoka Diabetes Registry who were mean 66 years old between April 2008 and October 2010. At the start of the study, the researchers assessed patient diabetes duration, previous fracture history, physical activity, alcohol and smoking status, whether patients were treated for diabetic retinopathy with laser photocoagulation, and their history of coronary artery disease or stroke. Patients were followed for a median 5.3 years, during which fractures were assessed through an annual self-administered questionnaire, with the results stratified by glycemic control and hypoglycemia.
Overall, there were 249 men and 413 women who experienced fractures during the study period, with a follow-up rate of 97.6%. In a multivariate analysis, patients with a higher risk of fracture included those with two or more episodes of severe hypoglycemia (hazard ratio, 2.25; 95% confidence interval, 1.57-3.22) and one episode of severe hypoglycemia (HR, 1.57; 95% CI, 1.11-2.20). In patients without severe hypoglycemic episodes, there was an increased risk of fracture in those with baseline hemoglobin A1c (HbA1c) level of 53 to less than 64 mmol/mol (7% to less than 8%; HR, 1.14; 0.94-1.39), 64 to less than 75 mmol/mol (8% to less than 9%; HR, 1.11; 95% CI, 0.86-1.43), and at least 75 mmol/mol (at least 9%; HR, 1.45; 95% CI, 1.06-1.98).
Compared with postmenopausal women, the unadjusted risk of fracture was higher in men with multiple severe hypoglycemic episodes (HR, 3.46; 95% CI, 2.05-5.85) and one episode of hypoglycemia (HR, 2.81; 95% CI, 1.74-4.56). These higher risks in older men persisted after adjustment for age, multivariate factors, and HbA1c.
“The association between severe hypoglycemia, poor glycemic control, and fracture risk at any anatomic site seems to be stronger in men than in postmenopausal women, although the interaction between men and postmenopausal women for fracture risk was not significant,” the researchers said. “The higher incidence rate of fractures in postmenopausal women, compared with men, was attributed to drastic changes in sex hormones after menopause, which may reduce the apparent impacts of hyperglycemia and severe hypoglycemia on postmenopausal women.”
Researchers said they did not consider potential external factors for fracture incidence, nor did they measure incident falls or other markers of bone health, such as bone mineral density and 25-hydroxyvitamin D levels. They also noted among the limitations of the study the self-reported nature of fracture reporting, and the lack of generalizability of the results.
This study was funded in part by grants from The Japan Society for the Promotion of Science KAKENHI from the Ministry of Education, Culture, Sports, Science and Technology of Japan; the Junior Scientist Development Grant supported by the Japan Diabetes Society; and the Lilly Research Grant Program for Bone & Mineral Research. The authors reported no relevant conflicts of interest.
SOURCE: Komorita Y et al. Diabet Med. 2019 Sep 25. doi: 10.1111/dme.14142.
FROM DIABETIC MEDICINE
Dapagliflozin approved for reducing HF hospitalization in diabetes
The Food And Drug Administration has approved the sodium-glucose cotransporter 2 (SGLT2) inhibitor dapagliflozin (Farxiga) for reducing the risk of hospitalization for heart failure in adults with type 2 diabetes and established cardiovascular disease or multiple cardiovascular risk factors, according to a statement from AstraZeneca.
The approval was based on results from the DECLARE-TIMI 58 cardiovascular outcomes trial, which evaluated dapagliflozin in more than 17,000 patients with type 2 diabetes and cardiovascular risk factors or cardiovascular disease. They showed that dapagliflozin significantly reduced the risk of the primary composite endpoint of hospitalization for heart failure by 27%, compared with placebo (2.5% vs. 3.3%; HR, 0.73; 95% confidence interval, 0.61-0.88).
The drug is an oral, once-daily SGLT2 inhibitor initially approved as a monotherapy or combination therapy for glycemic control in adults with type 2 diabetes. It has additional benefits of weight loss and reduction in blood pressure in concert with diet and exercise in the same population.
“,” Ruud Dobber, PhD, executive vice president of the company’s biopharmaceuticals business unit, said in the statement. “This is promising news for the 30 million people living with type 2 diabetes in the U.S., as heart failure is one of the earliest cardiovascular complications for them, before heart attack or stroke. [Dapagliflozin] now offers the opportunity for physicians to act sooner and reduce the risk of hospitalization for heart failure.”
In September, the agency granted dapagliflozin a Fast Track designation to reduce the risk of cardiovascular death, or the worsening of heart failure in adults with heart failure with reduced ejection fraction or preserved ejection fraction, based on the phase 3 DAPA-HF and DELIVER trials. It also gave the drug Fast Track designation to delay the progression of renal failure and prevent CV and renal death in patients with chronic kidney disease based on the phase 3 DAPA-CKD trial, the statement noted.
The Food And Drug Administration has approved the sodium-glucose cotransporter 2 (SGLT2) inhibitor dapagliflozin (Farxiga) for reducing the risk of hospitalization for heart failure in adults with type 2 diabetes and established cardiovascular disease or multiple cardiovascular risk factors, according to a statement from AstraZeneca.
The approval was based on results from the DECLARE-TIMI 58 cardiovascular outcomes trial, which evaluated dapagliflozin in more than 17,000 patients with type 2 diabetes and cardiovascular risk factors or cardiovascular disease. They showed that dapagliflozin significantly reduced the risk of the primary composite endpoint of hospitalization for heart failure by 27%, compared with placebo (2.5% vs. 3.3%; HR, 0.73; 95% confidence interval, 0.61-0.88).
The drug is an oral, once-daily SGLT2 inhibitor initially approved as a monotherapy or combination therapy for glycemic control in adults with type 2 diabetes. It has additional benefits of weight loss and reduction in blood pressure in concert with diet and exercise in the same population.
“,” Ruud Dobber, PhD, executive vice president of the company’s biopharmaceuticals business unit, said in the statement. “This is promising news for the 30 million people living with type 2 diabetes in the U.S., as heart failure is one of the earliest cardiovascular complications for them, before heart attack or stroke. [Dapagliflozin] now offers the opportunity for physicians to act sooner and reduce the risk of hospitalization for heart failure.”
In September, the agency granted dapagliflozin a Fast Track designation to reduce the risk of cardiovascular death, or the worsening of heart failure in adults with heart failure with reduced ejection fraction or preserved ejection fraction, based on the phase 3 DAPA-HF and DELIVER trials. It also gave the drug Fast Track designation to delay the progression of renal failure and prevent CV and renal death in patients with chronic kidney disease based on the phase 3 DAPA-CKD trial, the statement noted.
The Food And Drug Administration has approved the sodium-glucose cotransporter 2 (SGLT2) inhibitor dapagliflozin (Farxiga) for reducing the risk of hospitalization for heart failure in adults with type 2 diabetes and established cardiovascular disease or multiple cardiovascular risk factors, according to a statement from AstraZeneca.
The approval was based on results from the DECLARE-TIMI 58 cardiovascular outcomes trial, which evaluated dapagliflozin in more than 17,000 patients with type 2 diabetes and cardiovascular risk factors or cardiovascular disease. They showed that dapagliflozin significantly reduced the risk of the primary composite endpoint of hospitalization for heart failure by 27%, compared with placebo (2.5% vs. 3.3%; HR, 0.73; 95% confidence interval, 0.61-0.88).
The drug is an oral, once-daily SGLT2 inhibitor initially approved as a monotherapy or combination therapy for glycemic control in adults with type 2 diabetes. It has additional benefits of weight loss and reduction in blood pressure in concert with diet and exercise in the same population.
“,” Ruud Dobber, PhD, executive vice president of the company’s biopharmaceuticals business unit, said in the statement. “This is promising news for the 30 million people living with type 2 diabetes in the U.S., as heart failure is one of the earliest cardiovascular complications for them, before heart attack or stroke. [Dapagliflozin] now offers the opportunity for physicians to act sooner and reduce the risk of hospitalization for heart failure.”
In September, the agency granted dapagliflozin a Fast Track designation to reduce the risk of cardiovascular death, or the worsening of heart failure in adults with heart failure with reduced ejection fraction or preserved ejection fraction, based on the phase 3 DAPA-HF and DELIVER trials. It also gave the drug Fast Track designation to delay the progression of renal failure and prevent CV and renal death in patients with chronic kidney disease based on the phase 3 DAPA-CKD trial, the statement noted.
Certain diabetes drugs may thwart dementia
COPENHAGEN – Selected antidiabetes medications appear to blunt the increased risk of dementia associated with type 2 diabetes, according to a Danish national case control registry study.
This benefit applies to the newer antidiabetic agents – specifically, the dipeptidyl peptidase 4 (DPP4) inhibitors, the glucagon-like peptide 1 (GLP1) analogs, and the sodium-glucose transport protein 2 (SGLT2) inhibitors – and metformin as well, Merete Osler, MD, PhD, reported at the annual congress of the European College of Neuropsychopharmacology.
In contrast, neither insulin nor the sulfonylureas showed any signal of a protective effect against development of dementia. In fact, the use of sulfonylureas was associated with a small but statistically significant 7% increased risk, added Dr. Osler, of the University of Copenhagen.
Elsewhere at the meeting, investigators tapped a Swedish national registry to demonstrate that individuals with type 1 diabetes have a sharply reduced risk of developing schizophrenia.
Type 2 diabetes medications and dementia
Dr. Osler and colleagues are among several groups of investigators who have previously shown that patients with type 2 diabetes have an increased risk of dementia.
“This has raised the question of the role of dysregulated glucose metabolism in the development of this neurodegenerative disorder, and the possible effect of antidiabetic medications,” she noted.
To further explore this issue, which links two great ongoing global epidemics, Dr. Osler and coinvestigators conducted a nested case-control study including all 176,250 patients with type 2 diabetes in the comprehensive Danish National Diabetes Register for 1995-2012. The 11,619 patients with type 2 diabetes who received a dementia diagnosis were matched with 46,476 type 2 diabetes patients without dementia. The objective was to determine associations between dementia and ever-use and cumulative dose of antidiabetes drugs, alone and in combination, in logistic regression analyses adjusted for demographics, comorbid conditions, marital status, diabetic complications, and year of dementia diagnosis.
Patients who had ever used metformin had an adjusted 6% reduction in the likelihood of dementia compared with metformin nonusers, a modest but statistically significant difference. Those on a DPP4 inhibitor had a 20% reduction in risk. The GLP1 analogs were associated with a 42% decrease in risk. So were the SGLT2 inhibitors. A dose-response relationship was evident: The higher the cumulative exposure to these agents, the lower the odds of dementia.
Combination therapy is common in type 2 diabetes, so the investigators scrutinized the impact of a variety of multidrug combinations. Combinations including a DPP4 inhibitor or GLP1 analog were also associated with significantly reduced dementia risk.
Records of glycemic control in the form of hemoglobin A1c values were available on only 1,446 type 2 diabetic dementia patients and 4,003 matched controls. An analysis that incorporated this variable showed that the observed anti-dementia effect of selected diabetes drugs was independent of glycemic control, according to Dr. Osler.
The protective effect appeared to extend to both Alzheimer’s disease and vascular dementias, although firm conclusions can’t be drawn on this score because the study was insufficiently powered to address that issue.
Dr. Osler noted that the Danish study confirms a recent Taiwanese study showing an apparent protective effect against dementia for metformin in patients with type 2 diabetes (Aging Dis. 2019 Feb 1;10(1):37-48).
“Ours is the first study on the newer diabetic drugs, so our results need to be confirmed,” she pointed out.
If confirmed, however, it would warrant exploration of these drugs more generally as potential interventions to prevent dementia. That could open a whole new chapter in the remarkable story of the SGLT2 inhibitors, a class of drugs originally developed for treatment of type 2 diabetes but which in major randomized clinical trials later proved to be so effective in the treatment of heart failure that they are now considered cardiology drugs first.
Asked if she thinks these antidiabetes agents have a general neuroprotective effect or, instead, that the observed reduced risk of dementia is a function of patients being treated better early on with modern drugs, the psychiatrist replied, “I think it might be a combination of both, especially because we find different risk estimates between the drugs.”
Dr. Osler reported having no financial conflicts of interest regarding the study, which was funded by the Danish Diabetes Foundation, the Danish Medical Association, and several other foundations.
The full study details were published online shortly before her presentation at ECNP 2019 (Eur J Endocrinol. 2019 Aug 1. pii: EJE-19-0259.R1. doi: 10.1530/EJE-19-0259).
Type 1 diabetes and schizophrenia risk
Kristina Melkersson, MD, PhD, presented a cohort study that utilized Swedish national registries to examine the relationship between type 1 diabetes and schizophrenia. The study comprised 1,745,977 individuals, of whom 10,117 had type 1 diabetes, who were followed for a median of 9.7 and maximum of 18 years from their 13th birthday. During follow-up, 1,280 individuals were diagnosed with schizophrenia and 649 others with schizoaffective disorder. The adjusted risk of schizophrenia was 70% lower in patients with type 1 diabetes. However, there was no difference in the risk of schizoaffective disorder in the type 1 diabetic versus nondiabetic subjects.
The Swedish data confirm the findings of an earlier Finnish national study showing that the risk of schizophrenia is reduced in patients with type 1 diabetes (Arch Gen Psychiatry. 2007 Aug;64(8):894-9). These findings raise the intriguing possibility that autoimmunity somehow figures into the etiology of the psychiatric disorder. Other investigators have previously reported a reduced prevalence of rheumatoid arthritis in patients with schizophrenia, noted Dr. Melkersson of the Karolinska Institute in Stockholm.
She reported having no financial conflicts regarding her study.
SOURCE: Osler M. ECNP Abstract P180. Melkersson K. Abstract 81.
COPENHAGEN – Selected antidiabetes medications appear to blunt the increased risk of dementia associated with type 2 diabetes, according to a Danish national case control registry study.
This benefit applies to the newer antidiabetic agents – specifically, the dipeptidyl peptidase 4 (DPP4) inhibitors, the glucagon-like peptide 1 (GLP1) analogs, and the sodium-glucose transport protein 2 (SGLT2) inhibitors – and metformin as well, Merete Osler, MD, PhD, reported at the annual congress of the European College of Neuropsychopharmacology.
In contrast, neither insulin nor the sulfonylureas showed any signal of a protective effect against development of dementia. In fact, the use of sulfonylureas was associated with a small but statistically significant 7% increased risk, added Dr. Osler, of the University of Copenhagen.
Elsewhere at the meeting, investigators tapped a Swedish national registry to demonstrate that individuals with type 1 diabetes have a sharply reduced risk of developing schizophrenia.
Type 2 diabetes medications and dementia
Dr. Osler and colleagues are among several groups of investigators who have previously shown that patients with type 2 diabetes have an increased risk of dementia.
“This has raised the question of the role of dysregulated glucose metabolism in the development of this neurodegenerative disorder, and the possible effect of antidiabetic medications,” she noted.
To further explore this issue, which links two great ongoing global epidemics, Dr. Osler and coinvestigators conducted a nested case-control study including all 176,250 patients with type 2 diabetes in the comprehensive Danish National Diabetes Register for 1995-2012. The 11,619 patients with type 2 diabetes who received a dementia diagnosis were matched with 46,476 type 2 diabetes patients without dementia. The objective was to determine associations between dementia and ever-use and cumulative dose of antidiabetes drugs, alone and in combination, in logistic regression analyses adjusted for demographics, comorbid conditions, marital status, diabetic complications, and year of dementia diagnosis.
Patients who had ever used metformin had an adjusted 6% reduction in the likelihood of dementia compared with metformin nonusers, a modest but statistically significant difference. Those on a DPP4 inhibitor had a 20% reduction in risk. The GLP1 analogs were associated with a 42% decrease in risk. So were the SGLT2 inhibitors. A dose-response relationship was evident: The higher the cumulative exposure to these agents, the lower the odds of dementia.
Combination therapy is common in type 2 diabetes, so the investigators scrutinized the impact of a variety of multidrug combinations. Combinations including a DPP4 inhibitor or GLP1 analog were also associated with significantly reduced dementia risk.
Records of glycemic control in the form of hemoglobin A1c values were available on only 1,446 type 2 diabetic dementia patients and 4,003 matched controls. An analysis that incorporated this variable showed that the observed anti-dementia effect of selected diabetes drugs was independent of glycemic control, according to Dr. Osler.
The protective effect appeared to extend to both Alzheimer’s disease and vascular dementias, although firm conclusions can’t be drawn on this score because the study was insufficiently powered to address that issue.
Dr. Osler noted that the Danish study confirms a recent Taiwanese study showing an apparent protective effect against dementia for metformin in patients with type 2 diabetes (Aging Dis. 2019 Feb 1;10(1):37-48).
“Ours is the first study on the newer diabetic drugs, so our results need to be confirmed,” she pointed out.
If confirmed, however, it would warrant exploration of these drugs more generally as potential interventions to prevent dementia. That could open a whole new chapter in the remarkable story of the SGLT2 inhibitors, a class of drugs originally developed for treatment of type 2 diabetes but which in major randomized clinical trials later proved to be so effective in the treatment of heart failure that they are now considered cardiology drugs first.
Asked if she thinks these antidiabetes agents have a general neuroprotective effect or, instead, that the observed reduced risk of dementia is a function of patients being treated better early on with modern drugs, the psychiatrist replied, “I think it might be a combination of both, especially because we find different risk estimates between the drugs.”
Dr. Osler reported having no financial conflicts of interest regarding the study, which was funded by the Danish Diabetes Foundation, the Danish Medical Association, and several other foundations.
The full study details were published online shortly before her presentation at ECNP 2019 (Eur J Endocrinol. 2019 Aug 1. pii: EJE-19-0259.R1. doi: 10.1530/EJE-19-0259).
Type 1 diabetes and schizophrenia risk
Kristina Melkersson, MD, PhD, presented a cohort study that utilized Swedish national registries to examine the relationship between type 1 diabetes and schizophrenia. The study comprised 1,745,977 individuals, of whom 10,117 had type 1 diabetes, who were followed for a median of 9.7 and maximum of 18 years from their 13th birthday. During follow-up, 1,280 individuals were diagnosed with schizophrenia and 649 others with schizoaffective disorder. The adjusted risk of schizophrenia was 70% lower in patients with type 1 diabetes. However, there was no difference in the risk of schizoaffective disorder in the type 1 diabetic versus nondiabetic subjects.
The Swedish data confirm the findings of an earlier Finnish national study showing that the risk of schizophrenia is reduced in patients with type 1 diabetes (Arch Gen Psychiatry. 2007 Aug;64(8):894-9). These findings raise the intriguing possibility that autoimmunity somehow figures into the etiology of the psychiatric disorder. Other investigators have previously reported a reduced prevalence of rheumatoid arthritis in patients with schizophrenia, noted Dr. Melkersson of the Karolinska Institute in Stockholm.
She reported having no financial conflicts regarding her study.
SOURCE: Osler M. ECNP Abstract P180. Melkersson K. Abstract 81.
COPENHAGEN – Selected antidiabetes medications appear to blunt the increased risk of dementia associated with type 2 diabetes, according to a Danish national case control registry study.
This benefit applies to the newer antidiabetic agents – specifically, the dipeptidyl peptidase 4 (DPP4) inhibitors, the glucagon-like peptide 1 (GLP1) analogs, and the sodium-glucose transport protein 2 (SGLT2) inhibitors – and metformin as well, Merete Osler, MD, PhD, reported at the annual congress of the European College of Neuropsychopharmacology.
In contrast, neither insulin nor the sulfonylureas showed any signal of a protective effect against development of dementia. In fact, the use of sulfonylureas was associated with a small but statistically significant 7% increased risk, added Dr. Osler, of the University of Copenhagen.
Elsewhere at the meeting, investigators tapped a Swedish national registry to demonstrate that individuals with type 1 diabetes have a sharply reduced risk of developing schizophrenia.
Type 2 diabetes medications and dementia
Dr. Osler and colleagues are among several groups of investigators who have previously shown that patients with type 2 diabetes have an increased risk of dementia.
“This has raised the question of the role of dysregulated glucose metabolism in the development of this neurodegenerative disorder, and the possible effect of antidiabetic medications,” she noted.
To further explore this issue, which links two great ongoing global epidemics, Dr. Osler and coinvestigators conducted a nested case-control study including all 176,250 patients with type 2 diabetes in the comprehensive Danish National Diabetes Register for 1995-2012. The 11,619 patients with type 2 diabetes who received a dementia diagnosis were matched with 46,476 type 2 diabetes patients without dementia. The objective was to determine associations between dementia and ever-use and cumulative dose of antidiabetes drugs, alone and in combination, in logistic regression analyses adjusted for demographics, comorbid conditions, marital status, diabetic complications, and year of dementia diagnosis.
Patients who had ever used metformin had an adjusted 6% reduction in the likelihood of dementia compared with metformin nonusers, a modest but statistically significant difference. Those on a DPP4 inhibitor had a 20% reduction in risk. The GLP1 analogs were associated with a 42% decrease in risk. So were the SGLT2 inhibitors. A dose-response relationship was evident: The higher the cumulative exposure to these agents, the lower the odds of dementia.
Combination therapy is common in type 2 diabetes, so the investigators scrutinized the impact of a variety of multidrug combinations. Combinations including a DPP4 inhibitor or GLP1 analog were also associated with significantly reduced dementia risk.
Records of glycemic control in the form of hemoglobin A1c values were available on only 1,446 type 2 diabetic dementia patients and 4,003 matched controls. An analysis that incorporated this variable showed that the observed anti-dementia effect of selected diabetes drugs was independent of glycemic control, according to Dr. Osler.
The protective effect appeared to extend to both Alzheimer’s disease and vascular dementias, although firm conclusions can’t be drawn on this score because the study was insufficiently powered to address that issue.
Dr. Osler noted that the Danish study confirms a recent Taiwanese study showing an apparent protective effect against dementia for metformin in patients with type 2 diabetes (Aging Dis. 2019 Feb 1;10(1):37-48).
“Ours is the first study on the newer diabetic drugs, so our results need to be confirmed,” she pointed out.
If confirmed, however, it would warrant exploration of these drugs more generally as potential interventions to prevent dementia. That could open a whole new chapter in the remarkable story of the SGLT2 inhibitors, a class of drugs originally developed for treatment of type 2 diabetes but which in major randomized clinical trials later proved to be so effective in the treatment of heart failure that they are now considered cardiology drugs first.
Asked if she thinks these antidiabetes agents have a general neuroprotective effect or, instead, that the observed reduced risk of dementia is a function of patients being treated better early on with modern drugs, the psychiatrist replied, “I think it might be a combination of both, especially because we find different risk estimates between the drugs.”
Dr. Osler reported having no financial conflicts of interest regarding the study, which was funded by the Danish Diabetes Foundation, the Danish Medical Association, and several other foundations.
The full study details were published online shortly before her presentation at ECNP 2019 (Eur J Endocrinol. 2019 Aug 1. pii: EJE-19-0259.R1. doi: 10.1530/EJE-19-0259).
Type 1 diabetes and schizophrenia risk
Kristina Melkersson, MD, PhD, presented a cohort study that utilized Swedish national registries to examine the relationship between type 1 diabetes and schizophrenia. The study comprised 1,745,977 individuals, of whom 10,117 had type 1 diabetes, who were followed for a median of 9.7 and maximum of 18 years from their 13th birthday. During follow-up, 1,280 individuals were diagnosed with schizophrenia and 649 others with schizoaffective disorder. The adjusted risk of schizophrenia was 70% lower in patients with type 1 diabetes. However, there was no difference in the risk of schizoaffective disorder in the type 1 diabetic versus nondiabetic subjects.
The Swedish data confirm the findings of an earlier Finnish national study showing that the risk of schizophrenia is reduced in patients with type 1 diabetes (Arch Gen Psychiatry. 2007 Aug;64(8):894-9). These findings raise the intriguing possibility that autoimmunity somehow figures into the etiology of the psychiatric disorder. Other investigators have previously reported a reduced prevalence of rheumatoid arthritis in patients with schizophrenia, noted Dr. Melkersson of the Karolinska Institute in Stockholm.
She reported having no financial conflicts regarding her study.
SOURCE: Osler M. ECNP Abstract P180. Melkersson K. Abstract 81.
REPORTING FROM ECNP 2019
Eating disorders may add to poor type 2 control, but BMI confounds the issue
Type 2 diabetes patients with binge-eating psychopathology had worse glycemic control than did type 2 diabetes patients without eating disorders, but weight may be a modifying factor, according to a study of 70 outpatients with type 2 diabetes.
“Although the comorbidity of an ED [eating disorder] and T2DM [type 2 diabetes mellitus] has been observed across studies, the impact of this association on the clinical control of diabetes has been less consistent,” wrote Marcello Papelbaum, MD, of the State Institute of Diabetes and Endocrinology, Rio de Janeiro and colleagues.
In an exploratory study published in the Journal of Eating Disorders, the researchers assessed consecutive diabetes patients at a single center. The patients were aged 18-65 years, 77% were women, and 50% were obese. Glycemic control of diabetes was assessed measuring the levels of fasting blood glucose (FBG) and hemoglobin A1c. A total of 14 patients had an eating disorder, and 7 of them had binge eating disorder (BED). The BED patients were combined with three bulimic patients and four patients with subclinical BED and classified as binge-eating related ED.
Although FBG and HbA1c were significantly worse in patients with an eating disorder, compared with patients with normal eating patterns, the significance disappeared when body mass index (BMI) was added to the regression model. “Specifically, normal-BMI individuals exhibited a rate of ED of 8%, contrasted with a 26% prevalence of ED in obese patients,” the authors stated.
The findings were limited by the exploratory study design, small sample size, and lack of controlling for multiple variables, the researchers noted.
However, “although the objective negative clinical impact of an ED on type 2 diabetes control is yet to be confirmed, is possible to speculate that the remission of binge episodes could play a major role in diabetes treatment,” they said.
The researchers had no financial conflicts to disclose.
SOURCE: Papelbaum M et al. J Eat Disord. 2019 Sep 6. doi: 10.1186/s40337-019-0260-4.
Type 2 diabetes patients with binge-eating psychopathology had worse glycemic control than did type 2 diabetes patients without eating disorders, but weight may be a modifying factor, according to a study of 70 outpatients with type 2 diabetes.
“Although the comorbidity of an ED [eating disorder] and T2DM [type 2 diabetes mellitus] has been observed across studies, the impact of this association on the clinical control of diabetes has been less consistent,” wrote Marcello Papelbaum, MD, of the State Institute of Diabetes and Endocrinology, Rio de Janeiro and colleagues.
In an exploratory study published in the Journal of Eating Disorders, the researchers assessed consecutive diabetes patients at a single center. The patients were aged 18-65 years, 77% were women, and 50% were obese. Glycemic control of diabetes was assessed measuring the levels of fasting blood glucose (FBG) and hemoglobin A1c. A total of 14 patients had an eating disorder, and 7 of them had binge eating disorder (BED). The BED patients were combined with three bulimic patients and four patients with subclinical BED and classified as binge-eating related ED.
Although FBG and HbA1c were significantly worse in patients with an eating disorder, compared with patients with normal eating patterns, the significance disappeared when body mass index (BMI) was added to the regression model. “Specifically, normal-BMI individuals exhibited a rate of ED of 8%, contrasted with a 26% prevalence of ED in obese patients,” the authors stated.
The findings were limited by the exploratory study design, small sample size, and lack of controlling for multiple variables, the researchers noted.
However, “although the objective negative clinical impact of an ED on type 2 diabetes control is yet to be confirmed, is possible to speculate that the remission of binge episodes could play a major role in diabetes treatment,” they said.
The researchers had no financial conflicts to disclose.
SOURCE: Papelbaum M et al. J Eat Disord. 2019 Sep 6. doi: 10.1186/s40337-019-0260-4.
Type 2 diabetes patients with binge-eating psychopathology had worse glycemic control than did type 2 diabetes patients without eating disorders, but weight may be a modifying factor, according to a study of 70 outpatients with type 2 diabetes.
“Although the comorbidity of an ED [eating disorder] and T2DM [type 2 diabetes mellitus] has been observed across studies, the impact of this association on the clinical control of diabetes has been less consistent,” wrote Marcello Papelbaum, MD, of the State Institute of Diabetes and Endocrinology, Rio de Janeiro and colleagues.
In an exploratory study published in the Journal of Eating Disorders, the researchers assessed consecutive diabetes patients at a single center. The patients were aged 18-65 years, 77% were women, and 50% were obese. Glycemic control of diabetes was assessed measuring the levels of fasting blood glucose (FBG) and hemoglobin A1c. A total of 14 patients had an eating disorder, and 7 of them had binge eating disorder (BED). The BED patients were combined with three bulimic patients and four patients with subclinical BED and classified as binge-eating related ED.
Although FBG and HbA1c were significantly worse in patients with an eating disorder, compared with patients with normal eating patterns, the significance disappeared when body mass index (BMI) was added to the regression model. “Specifically, normal-BMI individuals exhibited a rate of ED of 8%, contrasted with a 26% prevalence of ED in obese patients,” the authors stated.
The findings were limited by the exploratory study design, small sample size, and lack of controlling for multiple variables, the researchers noted.
However, “although the objective negative clinical impact of an ED on type 2 diabetes control is yet to be confirmed, is possible to speculate that the remission of binge episodes could play a major role in diabetes treatment,” they said.
The researchers had no financial conflicts to disclose.
SOURCE: Papelbaum M et al. J Eat Disord. 2019 Sep 6. doi: 10.1186/s40337-019-0260-4.
FROM THE JOURNAL OF EATING DISORDERS
Duloxetine ‘sprinkle’ launches for patients with difficulty swallowing
Drizalma Sprinkle (duloxetine delayed-release capsule) has launched for the treatment of various neuropsychiatric and pain disorders in patients with difficulty swallowing, according to a release from Sun Pharma. It can be swallowed whole, sprinkled on applesauce, or administered via nasogastric tube.
Difficulty swallowing affects approximately 30%-35% of long-term care residents, but the main alternative – crushing tablets – introduces risks of its own to the administration process.
This sprinkle is indicated for the treatment of major depressive disorder in adults, generalized anxiety disorder in patients aged 7 years and older, diabetic peripheral neuropathic pain in adults, and chronic musculoskeletal pain in adults. It was approved by the Food and Drug Administration for these indications July 19, 2019.
It carries a boxed warning for suicidal thoughts and behaviors. The most common adverse reactions (5% or more of treated participants and twice the incidence with placebo) were nausea, dry mouth, somnolence, constipation, decreased appetite, and hyperhidrosis. The full prescribing information can be found on the FDA website.
[email protected]
Drizalma Sprinkle (duloxetine delayed-release capsule) has launched for the treatment of various neuropsychiatric and pain disorders in patients with difficulty swallowing, according to a release from Sun Pharma. It can be swallowed whole, sprinkled on applesauce, or administered via nasogastric tube.
Difficulty swallowing affects approximately 30%-35% of long-term care residents, but the main alternative – crushing tablets – introduces risks of its own to the administration process.
This sprinkle is indicated for the treatment of major depressive disorder in adults, generalized anxiety disorder in patients aged 7 years and older, diabetic peripheral neuropathic pain in adults, and chronic musculoskeletal pain in adults. It was approved by the Food and Drug Administration for these indications July 19, 2019.
It carries a boxed warning for suicidal thoughts and behaviors. The most common adverse reactions (5% or more of treated participants and twice the incidence with placebo) were nausea, dry mouth, somnolence, constipation, decreased appetite, and hyperhidrosis. The full prescribing information can be found on the FDA website.
[email protected]
Drizalma Sprinkle (duloxetine delayed-release capsule) has launched for the treatment of various neuropsychiatric and pain disorders in patients with difficulty swallowing, according to a release from Sun Pharma. It can be swallowed whole, sprinkled on applesauce, or administered via nasogastric tube.
Difficulty swallowing affects approximately 30%-35% of long-term care residents, but the main alternative – crushing tablets – introduces risks of its own to the administration process.
This sprinkle is indicated for the treatment of major depressive disorder in adults, generalized anxiety disorder in patients aged 7 years and older, diabetic peripheral neuropathic pain in adults, and chronic musculoskeletal pain in adults. It was approved by the Food and Drug Administration for these indications July 19, 2019.
It carries a boxed warning for suicidal thoughts and behaviors. The most common adverse reactions (5% or more of treated participants and twice the incidence with placebo) were nausea, dry mouth, somnolence, constipation, decreased appetite, and hyperhidrosis. The full prescribing information can be found on the FDA website.
[email protected]
Obesity ups type 2 diabetes risk far more than lifestyle, genetics
BARCELONA – Obesity, more so than having a poor lifestyle, significantly raised the odds of developing type 2 diabetes, independent of individuals’ genetic susceptibility, according to data from a Danish population-based, case-cohort study.
In fact, having a body mass index (BMI) of more than 30 kg/m2 was linked with a 480% risk of incident type 2 diabetes, compared with being of normal weight (BMI, 18.5-24.9 kg/m2). The 95% confidence interval was 5.16-6.55. Being overweight (BMI, 25-29.9 kg/m2) also carried a 100% increased risk of type 2 diabetes (hazard ratio, 2.37; 95% CI, 2.15-2.62).
Having an unfavorable lifestyle – which was defined as having no or only one of several healthy-living characteristics, from not smoking and moderating alcohol use to eating a well-balanced, nutritious diet and exercising regularly – increased the risk of diabetes by 18%, compared with having a favorable lifestyle (HR, 1.18; 95% CI, 1.06-1.30).
Individuals with a high genetic risk score (GRS) had a 100% increased risk of developing the disease versus those with a low GRS (HR, 2.0; 95% CI, 1.1-1.3).
“High genetic risk, obesity, and [an] unfavorable lifestyle increase the individual-level risk of incident type 2 diabetes,” Hermina Jakupovic and associates reported in a poster presentation at the annual meeting of the European Association for the Study of Diabetes. Their results suggest that “the effect of obesity on type 2 diabetes risk is dominant over other risk factors, highlighting the importance of weight management in type 2 diabetes prevention.”
Ms. Jakupovic, a PhD student at the Novo Nordisk Foundation Center for Basic Metabolic Research at the University of Copenhagen, and coauthors examined data on 9,555 participants of the Diet, Cancer, and Health cohort, a large, prospective study that has been running since the early 1990s.
Around half of the study sample were women and the mean age was 52 years. Just over one-fifth (22.8%) were obese, 43% were overweight, and the remaining 35.2% were of normal weight. A quarter (25.4%) had an unfavorable lifestyle, 40% a favorable lifestyle, and the remainder an “intermediate” lifestyle. Over a follow-up of almost 15 years, nearly half (49.5%) developed type 2 diabetes.
Genetic risk was assessed by a GRS comprising 193 genetic variants known to be strongly associated with type 2 diabetes, Ms. Jakupovic explained, adding that, using the GRS, patients were categorized into being at low (the lowest 20%), intermediate (middle 60%) and high risk (top 20%) of type 2 diabetes.
Considering individuals’ GRS and lifestyle score together showed an increasing risk of developing type 2 diabetes from the low GRS/favorable-lifestyle category (HR, 1.0; reference) upward to the high GRS/unfavorable lifestyle (HR, 2.22; 95% CI, 1.76-2.81).
The Diet, Cancer, and Health cohort is supported by the Danish Cancer Society. The Novo Nordisk Foundation Center for Basic Metabolic Research is an independent research center at the University of Copenhagen partially funded by an unrestricted donation from the Novo Nordisk Foundation. Ms. Jakupovic and associates are funded either directly or indirectly by the Novo Nordisk Foundation.
SOURCE: Jakupovic H et al. EASD 2019, Abstract 376.
BARCELONA – Obesity, more so than having a poor lifestyle, significantly raised the odds of developing type 2 diabetes, independent of individuals’ genetic susceptibility, according to data from a Danish population-based, case-cohort study.
In fact, having a body mass index (BMI) of more than 30 kg/m2 was linked with a 480% risk of incident type 2 diabetes, compared with being of normal weight (BMI, 18.5-24.9 kg/m2). The 95% confidence interval was 5.16-6.55. Being overweight (BMI, 25-29.9 kg/m2) also carried a 100% increased risk of type 2 diabetes (hazard ratio, 2.37; 95% CI, 2.15-2.62).
Having an unfavorable lifestyle – which was defined as having no or only one of several healthy-living characteristics, from not smoking and moderating alcohol use to eating a well-balanced, nutritious diet and exercising regularly – increased the risk of diabetes by 18%, compared with having a favorable lifestyle (HR, 1.18; 95% CI, 1.06-1.30).
Individuals with a high genetic risk score (GRS) had a 100% increased risk of developing the disease versus those with a low GRS (HR, 2.0; 95% CI, 1.1-1.3).
“High genetic risk, obesity, and [an] unfavorable lifestyle increase the individual-level risk of incident type 2 diabetes,” Hermina Jakupovic and associates reported in a poster presentation at the annual meeting of the European Association for the Study of Diabetes. Their results suggest that “the effect of obesity on type 2 diabetes risk is dominant over other risk factors, highlighting the importance of weight management in type 2 diabetes prevention.”
Ms. Jakupovic, a PhD student at the Novo Nordisk Foundation Center for Basic Metabolic Research at the University of Copenhagen, and coauthors examined data on 9,555 participants of the Diet, Cancer, and Health cohort, a large, prospective study that has been running since the early 1990s.
Around half of the study sample were women and the mean age was 52 years. Just over one-fifth (22.8%) were obese, 43% were overweight, and the remaining 35.2% were of normal weight. A quarter (25.4%) had an unfavorable lifestyle, 40% a favorable lifestyle, and the remainder an “intermediate” lifestyle. Over a follow-up of almost 15 years, nearly half (49.5%) developed type 2 diabetes.
Genetic risk was assessed by a GRS comprising 193 genetic variants known to be strongly associated with type 2 diabetes, Ms. Jakupovic explained, adding that, using the GRS, patients were categorized into being at low (the lowest 20%), intermediate (middle 60%) and high risk (top 20%) of type 2 diabetes.
Considering individuals’ GRS and lifestyle score together showed an increasing risk of developing type 2 diabetes from the low GRS/favorable-lifestyle category (HR, 1.0; reference) upward to the high GRS/unfavorable lifestyle (HR, 2.22; 95% CI, 1.76-2.81).
The Diet, Cancer, and Health cohort is supported by the Danish Cancer Society. The Novo Nordisk Foundation Center for Basic Metabolic Research is an independent research center at the University of Copenhagen partially funded by an unrestricted donation from the Novo Nordisk Foundation. Ms. Jakupovic and associates are funded either directly or indirectly by the Novo Nordisk Foundation.
SOURCE: Jakupovic H et al. EASD 2019, Abstract 376.
BARCELONA – Obesity, more so than having a poor lifestyle, significantly raised the odds of developing type 2 diabetes, independent of individuals’ genetic susceptibility, according to data from a Danish population-based, case-cohort study.
In fact, having a body mass index (BMI) of more than 30 kg/m2 was linked with a 480% risk of incident type 2 diabetes, compared with being of normal weight (BMI, 18.5-24.9 kg/m2). The 95% confidence interval was 5.16-6.55. Being overweight (BMI, 25-29.9 kg/m2) also carried a 100% increased risk of type 2 diabetes (hazard ratio, 2.37; 95% CI, 2.15-2.62).
Having an unfavorable lifestyle – which was defined as having no or only one of several healthy-living characteristics, from not smoking and moderating alcohol use to eating a well-balanced, nutritious diet and exercising regularly – increased the risk of diabetes by 18%, compared with having a favorable lifestyle (HR, 1.18; 95% CI, 1.06-1.30).
Individuals with a high genetic risk score (GRS) had a 100% increased risk of developing the disease versus those with a low GRS (HR, 2.0; 95% CI, 1.1-1.3).
“High genetic risk, obesity, and [an] unfavorable lifestyle increase the individual-level risk of incident type 2 diabetes,” Hermina Jakupovic and associates reported in a poster presentation at the annual meeting of the European Association for the Study of Diabetes. Their results suggest that “the effect of obesity on type 2 diabetes risk is dominant over other risk factors, highlighting the importance of weight management in type 2 diabetes prevention.”
Ms. Jakupovic, a PhD student at the Novo Nordisk Foundation Center for Basic Metabolic Research at the University of Copenhagen, and coauthors examined data on 9,555 participants of the Diet, Cancer, and Health cohort, a large, prospective study that has been running since the early 1990s.
Around half of the study sample were women and the mean age was 52 years. Just over one-fifth (22.8%) were obese, 43% were overweight, and the remaining 35.2% were of normal weight. A quarter (25.4%) had an unfavorable lifestyle, 40% a favorable lifestyle, and the remainder an “intermediate” lifestyle. Over a follow-up of almost 15 years, nearly half (49.5%) developed type 2 diabetes.
Genetic risk was assessed by a GRS comprising 193 genetic variants known to be strongly associated with type 2 diabetes, Ms. Jakupovic explained, adding that, using the GRS, patients were categorized into being at low (the lowest 20%), intermediate (middle 60%) and high risk (top 20%) of type 2 diabetes.
Considering individuals’ GRS and lifestyle score together showed an increasing risk of developing type 2 diabetes from the low GRS/favorable-lifestyle category (HR, 1.0; reference) upward to the high GRS/unfavorable lifestyle (HR, 2.22; 95% CI, 1.76-2.81).
The Diet, Cancer, and Health cohort is supported by the Danish Cancer Society. The Novo Nordisk Foundation Center for Basic Metabolic Research is an independent research center at the University of Copenhagen partially funded by an unrestricted donation from the Novo Nordisk Foundation. Ms. Jakupovic and associates are funded either directly or indirectly by the Novo Nordisk Foundation.
SOURCE: Jakupovic H et al. EASD 2019, Abstract 376.
REPORTING FROM EASD 2019