Diabetes Hub

The scientific evidence does not support tight glycemic control as a means to prevent the complications of type 2 diabetes, even though most clinical practice guidelines, quality-of-care measures, quality improvement interventions, and academic and clinical statements unequivocally endorse tight glycemic control for that purpose, according to a report published online Aug. 23 in Circulation: Cardiovascular Quality and Outcomes.

There is an enormous disconnect between the widespread consensus that tight glycemic control is essential on the one hand, and the overwhelming data demonstrating that it doesn’t prevent 10 of the 11 micro- and macrovascular complications that matter most to patients on the other hand. “This consensus and its downstream consequences to practice, policy, and research” must be recalibrated, said Rene Rodriguez-Gutierrez, MD, and Victor M. Montori, MD, both of the Knowledge and Evaluation Research Unit, Division of Endocrinology, Mayo Clinic, Rochester, Minn.

©CDC

They systematically reviewed the current evidence regarding tight glycemic control (achieving hemoglobin A_1c under 7%) published in the five “most impactful” general medical journals (the New England Journal of Medicine, the Lancet, JAMA, the British Medical Journal, and Annals of Internal Medicine) and the two most impactful specialty journals (Diabetes Care and the Journal of the American College of Cardiology) between 2006 and 2015. This included 328 research articles, 16 sets of treatment guidelines, 11 meta-analyses, and five large, randomized clinical trials and their extension studies, as well as relevant letters, commentaries, and editorials. They also reviewed national guidelines and standards of care published in all languages during the study period.

The investigators focused on the effect of tight glycemic control, as opposed to looser control, on 11 outcomes most important to patients: end-stage renal disease or the need for dialysis, renal death, blindness, clinical neuropathy, microalbuminuria, retinal photocoagulation, all-cause mortality, cardiovascular mortality, nonfatal MI, fatal and nonfatal stroke, and peripheral vascular events or amputations.

Regarding the microvascular complications, good evidence shows that tight glycemic control has no significant impact on the risk of end-stage renal disease, renal death, blindness, or clinical neuropathy, and that there is no threshold HbA1_c effect on risk. Moreover, the incidence of such complications is very low (less than 6%). Nevertheless, “practice guidelines and published statements offer a consistent and confident consensus, with 100% of the guidelines and 77%-100% of academic and clinical statements in favor of tight glycemic control to prevent microvascular complications,” according to Dr. Rodriguez-Gutierrez and Dr. Montori (Circ Cardiovasc Qual Outcomes. 2016 Aug 23;9:00-00. doi: 10.1161/CIRCOUTCOMES.116.002901).

Regarding the macrovascular complications, the evidence consistently shows that tight glycemic control exerts no significant effect on all-cause or cardiovascular mortality or on fatal or nonfatal stroke. The putative protective effect reported on amputations is “imprecise,” as it is based on very few such events. The only protective effect of tight glycemic control in this category of complications is that it reduces the risk of nonfatal MI by 15%.

Since the publication of the ACCORD trial, which clearly questioned the ability of tight glycemic control to prevent macrovascular complications, the consensus on this point has “withered.” At present, 64%-79% of published statements now express “uncertainty and skepticism” that tight glycemic control is essential. Yet two sets of guidelines – the American Diabetes Association standards published in 2003 and 2004 – did so.

The study findings indicate that despite good evidence to the contrary, the unsupported “consensus” on tight glycemic control drives most guidelines and quality-of-care interventions. It also underlies “the Food and Drug Administration policy to approve diabetes mellitus drugs only on the basis of their antihyperglycemic effect, without requiring evidence of reduction in the risk of complications,” the investigators said.

“This consensus is also driving studies such as the National Institutes of Health–funded GRADE trial comparing antihyperglycemic drugs on their ability to reduce HbA_1c, rather than to reduce the risk of diabetes complications,” they added.

The narrow focus on tight glycemic control has undercut research on other possible interventions to prevent these complications. There are zero trials currently under way assessing treatment possibilities other than drugs that reduce hyperglycemia, and there are zero evidence-based therapies either mentioned in guidelines or routinely prescribed to patients for preventing these complications, Dr. Rodriguez-Gutierrez and Dr. Montori wrote.

“A careful and thoughtful recalibration” is needed. “Today, patients with type 2 diabetes, at least in some parts of the world, seem to live longer lives with fewer complications. The evidence summarized here requires us to explore factors other than tight glycemic control to explain this improvement and better address the diabetes epidemic,” they noted.

This study was supported by the National Center for Advancing Translational Sciences, a component of the National Institutes of Health. Dr. Rodriguez-Gutierrez and Dr. Montori reported having no relevant financial disclosures.

The scientific evidence does not support tight glycemic control as a means to prevent the complications of type 2 diabetes, even though most clinical practice guidelines, quality-of-care measures, quality improvement interventions, and academic and clinical statements unequivocally endorse tight glycemic control for that purpose, according to a report published online Aug. 23 in Circulation: Cardiovascular Quality and Outcomes.

There is an enormous disconnect between the widespread consensus that tight glycemic control is essential on the one hand, and the overwhelming data demonstrating that it doesn’t prevent 10 of the 11 micro- and macrovascular complications that matter most to patients on the other hand. “This consensus and its downstream consequences to practice, policy, and research” must be recalibrated, said Rene Rodriguez-Gutierrez, MD, and Victor M. Montori, MD, both of the Knowledge and Evaluation Research Unit, Division of Endocrinology, Mayo Clinic, Rochester, Minn.

©CDC

They systematically reviewed the current evidence regarding tight glycemic control (achieving hemoglobin A_1c under 7%) published in the five “most impactful” general medical journals (the New England Journal of Medicine, the Lancet, JAMA, the British Medical Journal, and Annals of Internal Medicine) and the two most impactful specialty journals (Diabetes Care and the Journal of the American College of Cardiology) between 2006 and 2015. This included 328 research articles, 16 sets of treatment guidelines, 11 meta-analyses, and five large, randomized clinical trials and their extension studies, as well as relevant letters, commentaries, and editorials. They also reviewed national guidelines and standards of care published in all languages during the study period.

The investigators focused on the effect of tight glycemic control, as opposed to looser control, on 11 outcomes most important to patients: end-stage renal disease or the need for dialysis, renal death, blindness, clinical neuropathy, microalbuminuria, retinal photocoagulation, all-cause mortality, cardiovascular mortality, nonfatal MI, fatal and nonfatal stroke, and peripheral vascular events or amputations.

Regarding the microvascular complications, good evidence shows that tight glycemic control has no significant impact on the risk of end-stage renal disease, renal death, blindness, or clinical neuropathy, and that there is no threshold HbA1_c effect on risk. Moreover, the incidence of such complications is very low (less than 6%). Nevertheless, “practice guidelines and published statements offer a consistent and confident consensus, with 100% of the guidelines and 77%-100% of academic and clinical statements in favor of tight glycemic control to prevent microvascular complications,” according to Dr. Rodriguez-Gutierrez and Dr. Montori (Circ Cardiovasc Qual Outcomes. 2016 Aug 23;9:00-00. doi: 10.1161/CIRCOUTCOMES.116.002901).

Regarding the macrovascular complications, the evidence consistently shows that tight glycemic control exerts no significant effect on all-cause or cardiovascular mortality or on fatal or nonfatal stroke. The putative protective effect reported on amputations is “imprecise,” as it is based on very few such events. The only protective effect of tight glycemic control in this category of complications is that it reduces the risk of nonfatal MI by 15%.

Since the publication of the ACCORD trial, which clearly questioned the ability of tight glycemic control to prevent macrovascular complications, the consensus on this point has “withered.” At present, 64%-79% of published statements now express “uncertainty and skepticism” that tight glycemic control is essential. Yet two sets of guidelines – the American Diabetes Association standards published in 2003 and 2004 – did so.

The study findings indicate that despite good evidence to the contrary, the unsupported “consensus” on tight glycemic control drives most guidelines and quality-of-care interventions. It also underlies “the Food and Drug Administration policy to approve diabetes mellitus drugs only on the basis of their antihyperglycemic effect, without requiring evidence of reduction in the risk of complications,” the investigators said.

“This consensus is also driving studies such as the National Institutes of Health–funded GRADE trial comparing antihyperglycemic drugs on their ability to reduce HbA_1c, rather than to reduce the risk of diabetes complications,” they added.

The narrow focus on tight glycemic control has undercut research on other possible interventions to prevent these complications. There are zero trials currently under way assessing treatment possibilities other than drugs that reduce hyperglycemia, and there are zero evidence-based therapies either mentioned in guidelines or routinely prescribed to patients for preventing these complications, Dr. Rodriguez-Gutierrez and Dr. Montori wrote.

“A careful and thoughtful recalibration” is needed. “Today, patients with type 2 diabetes, at least in some parts of the world, seem to live longer lives with fewer complications. The evidence summarized here requires us to explore factors other than tight glycemic control to explain this improvement and better address the diabetes epidemic,” they noted.

This study was supported by the National Center for Advancing Translational Sciences, a component of the National Institutes of Health. Dr. Rodriguez-Gutierrez and Dr. Montori reported having no relevant financial disclosures.

The scientific evidence does not support tight glycemic control as a means to prevent the complications of type 2 diabetes, even though most clinical practice guidelines, quality-of-care measures, quality improvement interventions, and academic and clinical statements unequivocally endorse tight glycemic control for that purpose, according to a report published online Aug. 23 in Circulation: Cardiovascular Quality and Outcomes.

There is an enormous disconnect between the widespread consensus that tight glycemic control is essential on the one hand, and the overwhelming data demonstrating that it doesn’t prevent 10 of the 11 micro- and macrovascular complications that matter most to patients on the other hand. “This consensus and its downstream consequences to practice, policy, and research” must be recalibrated, said Rene Rodriguez-Gutierrez, MD, and Victor M. Montori, MD, both of the Knowledge and Evaluation Research Unit, Division of Endocrinology, Mayo Clinic, Rochester, Minn.

©CDC

They systematically reviewed the current evidence regarding tight glycemic control (achieving hemoglobin A_1c under 7%) published in the five “most impactful” general medical journals (the New England Journal of Medicine, the Lancet, JAMA, the British Medical Journal, and Annals of Internal Medicine) and the two most impactful specialty journals (Diabetes Care and the Journal of the American College of Cardiology) between 2006 and 2015. This included 328 research articles, 16 sets of treatment guidelines, 11 meta-analyses, and five large, randomized clinical trials and their extension studies, as well as relevant letters, commentaries, and editorials. They also reviewed national guidelines and standards of care published in all languages during the study period.

The investigators focused on the effect of tight glycemic control, as opposed to looser control, on 11 outcomes most important to patients: end-stage renal disease or the need for dialysis, renal death, blindness, clinical neuropathy, microalbuminuria, retinal photocoagulation, all-cause mortality, cardiovascular mortality, nonfatal MI, fatal and nonfatal stroke, and peripheral vascular events or amputations.

Regarding the microvascular complications, good evidence shows that tight glycemic control has no significant impact on the risk of end-stage renal disease, renal death, blindness, or clinical neuropathy, and that there is no threshold HbA1_c effect on risk. Moreover, the incidence of such complications is very low (less than 6%). Nevertheless, “practice guidelines and published statements offer a consistent and confident consensus, with 100% of the guidelines and 77%-100% of academic and clinical statements in favor of tight glycemic control to prevent microvascular complications,” according to Dr. Rodriguez-Gutierrez and Dr. Montori (Circ Cardiovasc Qual Outcomes. 2016 Aug 23;9:00-00. doi: 10.1161/CIRCOUTCOMES.116.002901).

Regarding the macrovascular complications, the evidence consistently shows that tight glycemic control exerts no significant effect on all-cause or cardiovascular mortality or on fatal or nonfatal stroke. The putative protective effect reported on amputations is “imprecise,” as it is based on very few such events. The only protective effect of tight glycemic control in this category of complications is that it reduces the risk of nonfatal MI by 15%.

Since the publication of the ACCORD trial, which clearly questioned the ability of tight glycemic control to prevent macrovascular complications, the consensus on this point has “withered.” At present, 64%-79% of published statements now express “uncertainty and skepticism” that tight glycemic control is essential. Yet two sets of guidelines – the American Diabetes Association standards published in 2003 and 2004 – did so.

The study findings indicate that despite good evidence to the contrary, the unsupported “consensus” on tight glycemic control drives most guidelines and quality-of-care interventions. It also underlies “the Food and Drug Administration policy to approve diabetes mellitus drugs only on the basis of their antihyperglycemic effect, without requiring evidence of reduction in the risk of complications,” the investigators said.

“This consensus is also driving studies such as the National Institutes of Health–funded GRADE trial comparing antihyperglycemic drugs on their ability to reduce HbA_1c, rather than to reduce the risk of diabetes complications,” they added.

The narrow focus on tight glycemic control has undercut research on other possible interventions to prevent these complications. There are zero trials currently under way assessing treatment possibilities other than drugs that reduce hyperglycemia, and there are zero evidence-based therapies either mentioned in guidelines or routinely prescribed to patients for preventing these complications, Dr. Rodriguez-Gutierrez and Dr. Montori wrote.

“A careful and thoughtful recalibration” is needed. “Today, patients with type 2 diabetes, at least in some parts of the world, seem to live longer lives with fewer complications. The evidence summarized here requires us to explore factors other than tight glycemic control to explain this improvement and better address the diabetes epidemic,” they noted.

This study was supported by the National Center for Advancing Translational Sciences, a component of the National Institutes of Health. Dr. Rodriguez-Gutierrez and Dr. Montori reported having no relevant financial disclosures.

Avoid weight-based language, use motivational interviewing techniques, and promote healthy family-based lifestyle modifications to prevent and manage obesity without predisposing adolescents to eating disorders, according to new recommendations in an American Academy of Pediatrics clinical report.

Obesity and eating disorders are becoming increasingly prevalent in adolescents. In 2012, 20.5% of 12- to 19-year-olds met sex-specific body mass index (BMI) criteria for obesity, according to data from the National Health and Nutrition Examination survey. From 1999 to 2006, there was a 119% increase in hospitalizations due to eating disorders among children younger than 12 years, according to a 2011 study by the Agency for Healthcare Research and Quality.

©moodboard/thinkstockphotos.com

Most adolescents who develop eating disorders are not obese, lead coauthor Neville H. Golden, MD, of Stanford (Calif.) University and his associates noted in the report by the AAP Committee on Nutrition, the Committee on Adolescence, and the Section on Obesity (Pediatrics. 2016 Aug. doi: 10.1542/peds.2016-1649).

However, in some adolescents, obesity prevention or management and initial attempts to lose weight can spiral into the development of an eating disorder, they said. “In one study in adolescents seeking treatment of an [eating disorder], 36.7% had a previous weight greater than the 85th percentile for age and sex.”

Cross-sectional and longitudinal observational studies identified dieting, body dissatisfaction, and talking about or teasing a child about his or her weight as risk factors for obesity and eating disorders. Conversely, family meals have been associated with improved dietary quality and a reduction in eating disorders among adolescent girls.

As pediatricians are often the first professional consulted by a parent when eating disorders or obesity are a concern, the investigators recommended the following office-based, evidence-informed tools to provide guidance about obesity and eating disorders:

• Discourage dieting, skipping of meals, or the use of diet pills.

• Encourage healthy eating and physical activity.

• Promote a positive body image; do not focus on body dissatisfaction as a reason for dieting.

• Encourage family meals.

• Encourage families not to talk about weight, but rather to talk about healthy eating and being active to stay healthy.

• Inquire about a history of mistreatment or bullying in overweight and obese teenagers and address this issue with patients and their families.

• Monitor weight loss in adolescents who need to lose weight.

The American Academy of Pediatrics supported this clinical report. The authors had no relevant disclosures to report.

[email protected]

On Twitter @jessnicolecraig

Avoid weight-based language, use motivational interviewing techniques, and promote healthy family-based lifestyle modifications to prevent and manage obesity without predisposing adolescents to eating disorders, according to new recommendations in an American Academy of Pediatrics clinical report.

Obesity and eating disorders are becoming increasingly prevalent in adolescents. In 2012, 20.5% of 12- to 19-year-olds met sex-specific body mass index (BMI) criteria for obesity, according to data from the National Health and Nutrition Examination survey. From 1999 to 2006, there was a 119% increase in hospitalizations due to eating disorders among children younger than 12 years, according to a 2011 study by the Agency for Healthcare Research and Quality.

©moodboard/thinkstockphotos.com

Most adolescents who develop eating disorders are not obese, lead coauthor Neville H. Golden, MD, of Stanford (Calif.) University and his associates noted in the report by the AAP Committee on Nutrition, the Committee on Adolescence, and the Section on Obesity (Pediatrics. 2016 Aug. doi: 10.1542/peds.2016-1649).

However, in some adolescents, obesity prevention or management and initial attempts to lose weight can spiral into the development of an eating disorder, they said. “In one study in adolescents seeking treatment of an [eating disorder], 36.7% had a previous weight greater than the 85th percentile for age and sex.”

Cross-sectional and longitudinal observational studies identified dieting, body dissatisfaction, and talking about or teasing a child about his or her weight as risk factors for obesity and eating disorders. Conversely, family meals have been associated with improved dietary quality and a reduction in eating disorders among adolescent girls.

As pediatricians are often the first professional consulted by a parent when eating disorders or obesity are a concern, the investigators recommended the following office-based, evidence-informed tools to provide guidance about obesity and eating disorders:

• Discourage dieting, skipping of meals, or the use of diet pills.

• Encourage healthy eating and physical activity.

• Promote a positive body image; do not focus on body dissatisfaction as a reason for dieting.

• Encourage family meals.

• Encourage families not to talk about weight, but rather to talk about healthy eating and being active to stay healthy.

• Inquire about a history of mistreatment or bullying in overweight and obese teenagers and address this issue with patients and their families.

• Monitor weight loss in adolescents who need to lose weight.

The American Academy of Pediatrics supported this clinical report. The authors had no relevant disclosures to report.

[email protected]

On Twitter @jessnicolecraig

Avoid weight-based language, use motivational interviewing techniques, and promote healthy family-based lifestyle modifications to prevent and manage obesity without predisposing adolescents to eating disorders, according to new recommendations in an American Academy of Pediatrics clinical report.

Obesity and eating disorders are becoming increasingly prevalent in adolescents. In 2012, 20.5% of 12- to 19-year-olds met sex-specific body mass index (BMI) criteria for obesity, according to data from the National Health and Nutrition Examination survey. From 1999 to 2006, there was a 119% increase in hospitalizations due to eating disorders among children younger than 12 years, according to a 2011 study by the Agency for Healthcare Research and Quality.

©moodboard/thinkstockphotos.com

Most adolescents who develop eating disorders are not obese, lead coauthor Neville H. Golden, MD, of Stanford (Calif.) University and his associates noted in the report by the AAP Committee on Nutrition, the Committee on Adolescence, and the Section on Obesity (Pediatrics. 2016 Aug. doi: 10.1542/peds.2016-1649).

However, in some adolescents, obesity prevention or management and initial attempts to lose weight can spiral into the development of an eating disorder, they said. “In one study in adolescents seeking treatment of an [eating disorder], 36.7% had a previous weight greater than the 85th percentile for age and sex.”

Cross-sectional and longitudinal observational studies identified dieting, body dissatisfaction, and talking about or teasing a child about his or her weight as risk factors for obesity and eating disorders. Conversely, family meals have been associated with improved dietary quality and a reduction in eating disorders among adolescent girls.

As pediatricians are often the first professional consulted by a parent when eating disorders or obesity are a concern, the investigators recommended the following office-based, evidence-informed tools to provide guidance about obesity and eating disorders:

• Discourage dieting, skipping of meals, or the use of diet pills.

• Encourage healthy eating and physical activity.

• Promote a positive body image; do not focus on body dissatisfaction as a reason for dieting.

• Encourage family meals.

• Encourage families not to talk about weight, but rather to talk about healthy eating and being active to stay healthy.

• Inquire about a history of mistreatment or bullying in overweight and obese teenagers and address this issue with patients and their families.

• Monitor weight loss in adolescents who need to lose weight.

The American Academy of Pediatrics supported this clinical report. The authors had no relevant disclosures to report.

[email protected]

On Twitter @jessnicolecraig

SAN DIEGO – A sleep specialist told an audience of diabetes educators that quality sleep is “profoundly important” to the health of their patients, and regularly sleeping fewer than 7 hours a night can wreak havoc on glucose levels and insulin resistance.

There’s even evidence of a link between lack of sleep, diabetes, and heart disease, according to Terese C. Hammond, MD, medical director of the Keck Hospital of the University of Southern California Sleep Disorders Center in Los Angeles. “We don’t know which way the cause goes, but we know there’s a connection,” she said.

© YinYang/iStockphoto.com

Dr. Hammond, who spoke at the annual meeting of the American Association of Diabetes Educators, noted that the vast majority of adults need 7-9 hours of sleep a night.

If you repeatedly don’t reach 7 hours, “there is ample evidence that some metabolic and biologic things happen to your body. Glucose goes up and insulin is secreted. Leptin decreases – the protein that tells us when we’re sated, when our hunger is satisfied. It’s a pretty potent combination, and this is associated with increases in weight and carbohydrate intake,” Dr. Hammond said.

Indeed, findings from one small study suggest a link between chronic insufficient sleep to consumption of more calories, mostly carbohydrates. The study authors speculated this may be because people eat extra food to account for being awake more but take in more than they need (Proc Natl Acad Sci USA. 2013 Apr;110[14]:5695-700).

It is possible for people to pay off a “sleep debt” by catching up on sleep, Dr. Hammond said, but only if the sleep is lost temporarily, as during a heavy medical rotation or after a personal tragedy. When sleep loss is chronic, she said, “it’s becoming apparent that the end-organ consequences are not fully recoverable.”

In regard to diabetes specifically, she said, research has linked insufficient sleep to higher rates of central obesity, higher rates of diabetes in blacks and whites, impaired glucose tolerance, decreased insulin, metabolic syndrome, and high lipids. Too much sleep has also been linked to poor health outcomes.

How can medical professionals help patients improve sleep? “The most important thing to remember about sleep is that it’s a very primitive process,” according to Dr. Hammond. “You can’t think yourself into better sleep. You have to act yourself into better sleep through light, temperature, sound, and repetitive behaviors.”

Controversial research has linked sleeping pills to higher mortality rates, she says.“I try to avoid them long term for insomnia, and not only because there’s probably an increased risk. They stop working eventually.”

Another approach, cognitive behavioral therapy (CBT), is “the most potent way to change behavior,” she said.

“CBT improves sleep efficiency in a vast majority of chronic medical diseases,” she said. “It does just as well as drugs and better than most sleeping pills.”

According to Dr. Hammond, CBT focuses on several strategies:

• Education about sleep hygiene, such as limiting the bedroom to nighttime sleep and intimacy, going to bed at the same time every night, and focusing on a dark, cool, quiet environment.

• Increasing the “sleep drive” through temporary sleep deprivation.

• Relaxation training through techniques like guided imagery, biofeedback, progressive muscle relaxation, and self-hypnosis.

Dr. Hammond reported having no relevant financial disclosures.

SAN DIEGO – A sleep specialist told an audience of diabetes educators that quality sleep is “profoundly important” to the health of their patients, and regularly sleeping fewer than 7 hours a night can wreak havoc on glucose levels and insulin resistance.

There’s even evidence of a link between lack of sleep, diabetes, and heart disease, according to Terese C. Hammond, MD, medical director of the Keck Hospital of the University of Southern California Sleep Disorders Center in Los Angeles. “We don’t know which way the cause goes, but we know there’s a connection,” she said.

© YinYang/iStockphoto.com

Dr. Hammond, who spoke at the annual meeting of the American Association of Diabetes Educators, noted that the vast majority of adults need 7-9 hours of sleep a night.

If you repeatedly don’t reach 7 hours, “there is ample evidence that some metabolic and biologic things happen to your body. Glucose goes up and insulin is secreted. Leptin decreases – the protein that tells us when we’re sated, when our hunger is satisfied. It’s a pretty potent combination, and this is associated with increases in weight and carbohydrate intake,” Dr. Hammond said.

Indeed, findings from one small study suggest a link between chronic insufficient sleep to consumption of more calories, mostly carbohydrates. The study authors speculated this may be because people eat extra food to account for being awake more but take in more than they need (Proc Natl Acad Sci USA. 2013 Apr;110[14]:5695-700).

It is possible for people to pay off a “sleep debt” by catching up on sleep, Dr. Hammond said, but only if the sleep is lost temporarily, as during a heavy medical rotation or after a personal tragedy. When sleep loss is chronic, she said, “it’s becoming apparent that the end-organ consequences are not fully recoverable.”

In regard to diabetes specifically, she said, research has linked insufficient sleep to higher rates of central obesity, higher rates of diabetes in blacks and whites, impaired glucose tolerance, decreased insulin, metabolic syndrome, and high lipids. Too much sleep has also been linked to poor health outcomes.

How can medical professionals help patients improve sleep? “The most important thing to remember about sleep is that it’s a very primitive process,” according to Dr. Hammond. “You can’t think yourself into better sleep. You have to act yourself into better sleep through light, temperature, sound, and repetitive behaviors.”

Controversial research has linked sleeping pills to higher mortality rates, she says.“I try to avoid them long term for insomnia, and not only because there’s probably an increased risk. They stop working eventually.”

Another approach, cognitive behavioral therapy (CBT), is “the most potent way to change behavior,” she said.

“CBT improves sleep efficiency in a vast majority of chronic medical diseases,” she said. “It does just as well as drugs and better than most sleeping pills.”

According to Dr. Hammond, CBT focuses on several strategies:

• Education about sleep hygiene, such as limiting the bedroom to nighttime sleep and intimacy, going to bed at the same time every night, and focusing on a dark, cool, quiet environment.

• Increasing the “sleep drive” through temporary sleep deprivation.

• Relaxation training through techniques like guided imagery, biofeedback, progressive muscle relaxation, and self-hypnosis.

Dr. Hammond reported having no relevant financial disclosures.

SAN DIEGO – A sleep specialist told an audience of diabetes educators that quality sleep is “profoundly important” to the health of their patients, and regularly sleeping fewer than 7 hours a night can wreak havoc on glucose levels and insulin resistance.

There’s even evidence of a link between lack of sleep, diabetes, and heart disease, according to Terese C. Hammond, MD, medical director of the Keck Hospital of the University of Southern California Sleep Disorders Center in Los Angeles. “We don’t know which way the cause goes, but we know there’s a connection,” she said.

© YinYang/iStockphoto.com

Dr. Hammond, who spoke at the annual meeting of the American Association of Diabetes Educators, noted that the vast majority of adults need 7-9 hours of sleep a night.

If you repeatedly don’t reach 7 hours, “there is ample evidence that some metabolic and biologic things happen to your body. Glucose goes up and insulin is secreted. Leptin decreases – the protein that tells us when we’re sated, when our hunger is satisfied. It’s a pretty potent combination, and this is associated with increases in weight and carbohydrate intake,” Dr. Hammond said.

Indeed, findings from one small study suggest a link between chronic insufficient sleep to consumption of more calories, mostly carbohydrates. The study authors speculated this may be because people eat extra food to account for being awake more but take in more than they need (Proc Natl Acad Sci USA. 2013 Apr;110[14]:5695-700).

It is possible for people to pay off a “sleep debt” by catching up on sleep, Dr. Hammond said, but only if the sleep is lost temporarily, as during a heavy medical rotation or after a personal tragedy. When sleep loss is chronic, she said, “it’s becoming apparent that the end-organ consequences are not fully recoverable.”

In regard to diabetes specifically, she said, research has linked insufficient sleep to higher rates of central obesity, higher rates of diabetes in blacks and whites, impaired glucose tolerance, decreased insulin, metabolic syndrome, and high lipids. Too much sleep has also been linked to poor health outcomes.

How can medical professionals help patients improve sleep? “The most important thing to remember about sleep is that it’s a very primitive process,” according to Dr. Hammond. “You can’t think yourself into better sleep. You have to act yourself into better sleep through light, temperature, sound, and repetitive behaviors.”

Controversial research has linked sleeping pills to higher mortality rates, she says.“I try to avoid them long term for insomnia, and not only because there’s probably an increased risk. They stop working eventually.”

Another approach, cognitive behavioral therapy (CBT), is “the most potent way to change behavior,” she said.

“CBT improves sleep efficiency in a vast majority of chronic medical diseases,” she said. “It does just as well as drugs and better than most sleeping pills.”

According to Dr. Hammond, CBT focuses on several strategies:

• Education about sleep hygiene, such as limiting the bedroom to nighttime sleep and intimacy, going to bed at the same time every night, and focusing on a dark, cool, quiet environment.

• Increasing the “sleep drive” through temporary sleep deprivation.

• Relaxation training through techniques like guided imagery, biofeedback, progressive muscle relaxation, and self-hypnosis.

Dr. Hammond reported having no relevant financial disclosures.

SAN DIEGO – A top endocrinologist cautioned diabetes educators that research is linking nighttime hypoglycemia to a variety of ills, and technology isn’t providing much hope – yet.

Patients with nocturnal low blood sugar “say this is the hardest thing they have to deal with. It upsets their whole day and they feel terrible,” said Anthony L. McCall, MD, PhD, James M. Moss Professor of Diabetes at the University of Virginia, Charlottesville, and vice president of clinical science with the Endocrine Society.

Dr. McCall told an audience at the annual meeting of the American Association of Diabetes Educators that half of hypoglycemia is nocturnal and unrecognized despite its dangers. According to him, hypoglycemia represents a blood glucose level of at or under 70 mg/dL (3.9 mmol/L). This is higher than the threshold for hypoglycemia in nondiabetics and those with well controlled diabetes.

Even as few as two values in a week in the range of the 60s (mg/dL) can go unrecognized and lead to full-blown hypoglycemia-associated autonomic failure, he said. There are other possible risks: “impaired sleep quality, daytime drowsiness, mood changes, risk for nocturnal falls,” he said.

Cognitive dysfunction is possible, especially in children, he added. “Neurological dysfunction may be temporary, but those who can answer simple questions may not be OK.”

There’s a potential for a vicious cycle here, he said, because people with diabetes can also develop impaired hypoglycemia awareness, making it less likely they’ll notice the low blood sugar levels that contribute to autonomic failure.

Dr. McCall reported that nighttime hypoglycemia may also:

• Trigger neurologic symptoms like those of strokes or temporary ischemic attacks. “Someone’s got check to their blood sugar,” he says.

• Lengthen the QT interval and boost the risk of irregular heartbeats.

• Contribute to “dead in bed” syndrome in which young people with type 1 diabetes are discovered dead despite not having any complications or showing signs of convulsion.

What can be done to help these patients? One approach is to combat impaired hypoglycemia awareness. Bedtime snacks, caffeine, and uncooked cornstarch are among the many nutrition supplements (and medications) that have shown inconsistent results at best on this front, Dr. McCall said. If they work, he said, they often lead to hyperglycemia.

Another strategy is to look for factors that raise the risk of nighttime hypoglycemia, such as basal insulin overtreatment, long periods between meals, delayed effects of exercise, and higher insulin sensitivity overnight.

Insulin pumps may be helpful, he said, and he generally favors their use. However, he cautioned that it’s hard to show that they reduce hypoglycemia, and some patients don’t use them properly.

Data have been mixed until recently regarding real-time continuous glucose monitoring, he said, and the devices must be worn 75%-85% of the time to show benefit. As for sensor-augmented insulin pumps, he said they’ve shown mixed results.

Dr. McCall said the artificial pancreas, once it makes it to market, could mark the beginning of a new era. “This was around the corner 40 years ago. But it’s closer now,” he said. “I have great hope that we’re going to do better.”

Dr. McCall reported being a consultant to Sanofi regarding new insulin studies and serving on the advisory board of DexCom/Google regarding the use of continuous glucose monitoring.

SAN DIEGO – A top endocrinologist cautioned diabetes educators that research is linking nighttime hypoglycemia to a variety of ills, and technology isn’t providing much hope – yet.

Patients with nocturnal low blood sugar “say this is the hardest thing they have to deal with. It upsets their whole day and they feel terrible,” said Anthony L. McCall, MD, PhD, James M. Moss Professor of Diabetes at the University of Virginia, Charlottesville, and vice president of clinical science with the Endocrine Society.

Dr. McCall told an audience at the annual meeting of the American Association of Diabetes Educators that half of hypoglycemia is nocturnal and unrecognized despite its dangers. According to him, hypoglycemia represents a blood glucose level of at or under 70 mg/dL (3.9 mmol/L). This is higher than the threshold for hypoglycemia in nondiabetics and those with well controlled diabetes.

Even as few as two values in a week in the range of the 60s (mg/dL) can go unrecognized and lead to full-blown hypoglycemia-associated autonomic failure, he said. There are other possible risks: “impaired sleep quality, daytime drowsiness, mood changes, risk for nocturnal falls,” he said.

Cognitive dysfunction is possible, especially in children, he added. “Neurological dysfunction may be temporary, but those who can answer simple questions may not be OK.”

There’s a potential for a vicious cycle here, he said, because people with diabetes can also develop impaired hypoglycemia awareness, making it less likely they’ll notice the low blood sugar levels that contribute to autonomic failure.

Dr. McCall reported that nighttime hypoglycemia may also:

• Trigger neurologic symptoms like those of strokes or temporary ischemic attacks. “Someone’s got check to their blood sugar,” he says.

• Lengthen the QT interval and boost the risk of irregular heartbeats.

• Contribute to “dead in bed” syndrome in which young people with type 1 diabetes are discovered dead despite not having any complications or showing signs of convulsion.

What can be done to help these patients? One approach is to combat impaired hypoglycemia awareness. Bedtime snacks, caffeine, and uncooked cornstarch are among the many nutrition supplements (and medications) that have shown inconsistent results at best on this front, Dr. McCall said. If they work, he said, they often lead to hyperglycemia.

Another strategy is to look for factors that raise the risk of nighttime hypoglycemia, such as basal insulin overtreatment, long periods between meals, delayed effects of exercise, and higher insulin sensitivity overnight.

Insulin pumps may be helpful, he said, and he generally favors their use. However, he cautioned that it’s hard to show that they reduce hypoglycemia, and some patients don’t use them properly.

Data have been mixed until recently regarding real-time continuous glucose monitoring, he said, and the devices must be worn 75%-85% of the time to show benefit. As for sensor-augmented insulin pumps, he said they’ve shown mixed results.

Dr. McCall said the artificial pancreas, once it makes it to market, could mark the beginning of a new era. “This was around the corner 40 years ago. But it’s closer now,” he said. “I have great hope that we’re going to do better.”

Dr. McCall reported being a consultant to Sanofi regarding new insulin studies and serving on the advisory board of DexCom/Google regarding the use of continuous glucose monitoring.

SAN DIEGO – A top endocrinologist cautioned diabetes educators that research is linking nighttime hypoglycemia to a variety of ills, and technology isn’t providing much hope – yet.

Patients with nocturnal low blood sugar “say this is the hardest thing they have to deal with. It upsets their whole day and they feel terrible,” said Anthony L. McCall, MD, PhD, James M. Moss Professor of Diabetes at the University of Virginia, Charlottesville, and vice president of clinical science with the Endocrine Society.

Dr. McCall told an audience at the annual meeting of the American Association of Diabetes Educators that half of hypoglycemia is nocturnal and unrecognized despite its dangers. According to him, hypoglycemia represents a blood glucose level of at or under 70 mg/dL (3.9 mmol/L). This is higher than the threshold for hypoglycemia in nondiabetics and those with well controlled diabetes.

Even as few as two values in a week in the range of the 60s (mg/dL) can go unrecognized and lead to full-blown hypoglycemia-associated autonomic failure, he said. There are other possible risks: “impaired sleep quality, daytime drowsiness, mood changes, risk for nocturnal falls,” he said.

Cognitive dysfunction is possible, especially in children, he added. “Neurological dysfunction may be temporary, but those who can answer simple questions may not be OK.”

There’s a potential for a vicious cycle here, he said, because people with diabetes can also develop impaired hypoglycemia awareness, making it less likely they’ll notice the low blood sugar levels that contribute to autonomic failure.

Dr. McCall reported that nighttime hypoglycemia may also:

• Trigger neurologic symptoms like those of strokes or temporary ischemic attacks. “Someone’s got check to their blood sugar,” he says.

• Lengthen the QT interval and boost the risk of irregular heartbeats.

• Contribute to “dead in bed” syndrome in which young people with type 1 diabetes are discovered dead despite not having any complications or showing signs of convulsion.

What can be done to help these patients? One approach is to combat impaired hypoglycemia awareness. Bedtime snacks, caffeine, and uncooked cornstarch are among the many nutrition supplements (and medications) that have shown inconsistent results at best on this front, Dr. McCall said. If they work, he said, they often lead to hyperglycemia.

Another strategy is to look for factors that raise the risk of nighttime hypoglycemia, such as basal insulin overtreatment, long periods between meals, delayed effects of exercise, and higher insulin sensitivity overnight.

Insulin pumps may be helpful, he said, and he generally favors their use. However, he cautioned that it’s hard to show that they reduce hypoglycemia, and some patients don’t use them properly.

Data have been mixed until recently regarding real-time continuous glucose monitoring, he said, and the devices must be worn 75%-85% of the time to show benefit. As for sensor-augmented insulin pumps, he said they’ve shown mixed results.

Dr. McCall said the artificial pancreas, once it makes it to market, could mark the beginning of a new era. “This was around the corner 40 years ago. But it’s closer now,” he said. “I have great hope that we’re going to do better.”

Dr. McCall reported being a consultant to Sanofi regarding new insulin studies and serving on the advisory board of DexCom/Google regarding the use of continuous glucose monitoring.

SAN DIEGO – A Food and Drug Administration official told diabetes educators that her agency is carefully monitoring the growth of an unusual development in diabetes care: the do-it-yourself artificial pancreas.

While the homemade insulin pumps are serving a need that has been unmet by manufacturers, the unregulated devices can be dangerous, according to Courtney Lias, PhD, director of the FDA’s Division of Chemistry and Toxicology Devices, who spoke at the annual meeting of the American Association of Diabetes Educators. “As they go toward a larger community, we see that the risk is raised.”

Still, “people are doing this because they feel this is the best way for them to help themselves or their children. We understand why people are doing it, but we want to make sure they do it safely,” Dr. Lias said.

At issue: The need for a “closed loop” artificial pancreas that needs little or no human intervention to measure blood sugar levels and deliver insulin as needed.

While current insulin pumps can deliver basal insulin continuously, users must program them to deliver an insulin bolus after meals or to address high blood sugar. Manufacturers are trying to develop a closed-loop artificial pancreas (also known as a bionic pancreas) that will simplify the process.

On their own, computer experts have been experimenting with jury-rigged homemade do-it-yourself (DIY) systems. “We recognize that for many PWDs [people with diabetes] the available help is not yet enough, so we are not waiting,” according to Dana Lewis and Scott Leibrand, two bloggers on a site called DIYPS.org.

In May 2016, The Wall Street Journal profiled a San Diego third-grader who uses a homemade “robotic pancreas” designed by his software engineer father. “More than 50 people have soldered, tinkered, and written software to make such devices for themselves or their children,” according to the Wall Street Journal report.

In her talk at the American Association of Diabetes Educators meeting, Dr. Lias noted that “there are a lot of questions about whether this is something that should be done.”

The algorithm behind a homemade device is one of area of concern, she said. “Who developed it and who’s responsible for having developed it? You may not understand how the algorithm is developed and what information is behind it. If something goes wrong, there’s no recourse.”

There are also questions about quality control, she noted: “Is there a responsible party for understanding things, for collecting information and making corrections?”

Dr. Lias said physicians should ask these questions if patients say they are using a DIY artificial pancreas: Do you understand exactly what algorithm is being used? Is it right for you? Have you checked the code to ensure it implements the algorithm correctly? Have you double-checked? When new, modified versions of code are shared, have you re-validated your entire system before implementing it?

It’s also important, she said, to note that these devices have not been determined to be safe and effective.

As the FDA monitors these DIY devices, Dr. Lias said, it’s also working to be ready to consider the work of manufacturers who are trying to develop the first commercial artificial pancreas device.

“Artificial pancreas devices do not have to be perfect with zero risk to be beneficial,” she says. “The approval decision is a benefit/risk decision. We make this decision in the context of the high risks that people with diabetes face every day.”

For now, she says, one focus is to make it easier for companies to work together to create the components of an artificial pancreas device.

The FDA is also concerned about what newly diagnosed people with diabetes will do if their devices break down, and they don’t know how to give themselves an insulin injection. “That’s a scenario that we will need to work out,” she said. “We’re talking with manufacturers about how they plan to work with that.”

SAN DIEGO – A Food and Drug Administration official told diabetes educators that her agency is carefully monitoring the growth of an unusual development in diabetes care: the do-it-yourself artificial pancreas.

While the homemade insulin pumps are serving a need that has been unmet by manufacturers, the unregulated devices can be dangerous, according to Courtney Lias, PhD, director of the FDA’s Division of Chemistry and Toxicology Devices, who spoke at the annual meeting of the American Association of Diabetes Educators. “As they go toward a larger community, we see that the risk is raised.”

Still, “people are doing this because they feel this is the best way for them to help themselves or their children. We understand why people are doing it, but we want to make sure they do it safely,” Dr. Lias said.

At issue: The need for a “closed loop” artificial pancreas that needs little or no human intervention to measure blood sugar levels and deliver insulin as needed.

While current insulin pumps can deliver basal insulin continuously, users must program them to deliver an insulin bolus after meals or to address high blood sugar. Manufacturers are trying to develop a closed-loop artificial pancreas (also known as a bionic pancreas) that will simplify the process.

On their own, computer experts have been experimenting with jury-rigged homemade do-it-yourself (DIY) systems. “We recognize that for many PWDs [people with diabetes] the available help is not yet enough, so we are not waiting,” according to Dana Lewis and Scott Leibrand, two bloggers on a site called DIYPS.org.

In May 2016, The Wall Street Journal profiled a San Diego third-grader who uses a homemade “robotic pancreas” designed by his software engineer father. “More than 50 people have soldered, tinkered, and written software to make such devices for themselves or their children,” according to the Wall Street Journal report.

In her talk at the American Association of Diabetes Educators meeting, Dr. Lias noted that “there are a lot of questions about whether this is something that should be done.”

The algorithm behind a homemade device is one of area of concern, she said. “Who developed it and who’s responsible for having developed it? You may not understand how the algorithm is developed and what information is behind it. If something goes wrong, there’s no recourse.”

There are also questions about quality control, she noted: “Is there a responsible party for understanding things, for collecting information and making corrections?”

Dr. Lias said physicians should ask these questions if patients say they are using a DIY artificial pancreas: Do you understand exactly what algorithm is being used? Is it right for you? Have you checked the code to ensure it implements the algorithm correctly? Have you double-checked? When new, modified versions of code are shared, have you re-validated your entire system before implementing it?

It’s also important, she said, to note that these devices have not been determined to be safe and effective.

As the FDA monitors these DIY devices, Dr. Lias said, it’s also working to be ready to consider the work of manufacturers who are trying to develop the first commercial artificial pancreas device.

“Artificial pancreas devices do not have to be perfect with zero risk to be beneficial,” she says. “The approval decision is a benefit/risk decision. We make this decision in the context of the high risks that people with diabetes face every day.”

For now, she says, one focus is to make it easier for companies to work together to create the components of an artificial pancreas device.

The FDA is also concerned about what newly diagnosed people with diabetes will do if their devices break down, and they don’t know how to give themselves an insulin injection. “That’s a scenario that we will need to work out,” she said. “We’re talking with manufacturers about how they plan to work with that.”

SAN DIEGO – A Food and Drug Administration official told diabetes educators that her agency is carefully monitoring the growth of an unusual development in diabetes care: the do-it-yourself artificial pancreas.

While the homemade insulin pumps are serving a need that has been unmet by manufacturers, the unregulated devices can be dangerous, according to Courtney Lias, PhD, director of the FDA’s Division of Chemistry and Toxicology Devices, who spoke at the annual meeting of the American Association of Diabetes Educators. “As they go toward a larger community, we see that the risk is raised.”

Still, “people are doing this because they feel this is the best way for them to help themselves or their children. We understand why people are doing it, but we want to make sure they do it safely,” Dr. Lias said.

At issue: The need for a “closed loop” artificial pancreas that needs little or no human intervention to measure blood sugar levels and deliver insulin as needed.

While current insulin pumps can deliver basal insulin continuously, users must program them to deliver an insulin bolus after meals or to address high blood sugar. Manufacturers are trying to develop a closed-loop artificial pancreas (also known as a bionic pancreas) that will simplify the process.

On their own, computer experts have been experimenting with jury-rigged homemade do-it-yourself (DIY) systems. “We recognize that for many PWDs [people with diabetes] the available help is not yet enough, so we are not waiting,” according to Dana Lewis and Scott Leibrand, two bloggers on a site called DIYPS.org.

In May 2016, The Wall Street Journal profiled a San Diego third-grader who uses a homemade “robotic pancreas” designed by his software engineer father. “More than 50 people have soldered, tinkered, and written software to make such devices for themselves or their children,” according to the Wall Street Journal report.

In her talk at the American Association of Diabetes Educators meeting, Dr. Lias noted that “there are a lot of questions about whether this is something that should be done.”

The algorithm behind a homemade device is one of area of concern, she said. “Who developed it and who’s responsible for having developed it? You may not understand how the algorithm is developed and what information is behind it. If something goes wrong, there’s no recourse.”

There are also questions about quality control, she noted: “Is there a responsible party for understanding things, for collecting information and making corrections?”

Dr. Lias said physicians should ask these questions if patients say they are using a DIY artificial pancreas: Do you understand exactly what algorithm is being used? Is it right for you? Have you checked the code to ensure it implements the algorithm correctly? Have you double-checked? When new, modified versions of code are shared, have you re-validated your entire system before implementing it?

It’s also important, she said, to note that these devices have not been determined to be safe and effective.

As the FDA monitors these DIY devices, Dr. Lias said, it’s also working to be ready to consider the work of manufacturers who are trying to develop the first commercial artificial pancreas device.

“Artificial pancreas devices do not have to be perfect with zero risk to be beneficial,” she says. “The approval decision is a benefit/risk decision. We make this decision in the context of the high risks that people with diabetes face every day.”

For now, she says, one focus is to make it easier for companies to work together to create the components of an artificial pancreas device.

The FDA is also concerned about what newly diagnosed people with diabetes will do if their devices break down, and they don’t know how to give themselves an insulin injection. “That’s a scenario that we will need to work out,” she said. “We’re talking with manufacturers about how they plan to work with that.”

At current prices, PCSK9 inhibitors are not cost-effective for patients with heterozygous familial hypercholesterolemia or atherosclerotic cardiovascular disease, according to an analysis published Aug. 16 in JAMA.

The costs of the cholesterol-lowering drugs would have to be reduced by at least two-thirds to reach cost-effectiveness, on the basis of data from the simulation model of atherosclerotic cardiovascular disease in the United States and the 2015 annual PCSK9 inhibitor costs of $14,350.

The high cost of PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibition remains a challenge because it is meant for lifelong use, and “the potential increase in health care expenditures at current or even moderately discounted prices could be staggering,” wrote Kirsten Bibbins-Domingo, MD, PhD, of the University of California, San Francisco, and her colleagues (JAMA 2016 Aug 16;316[7]:743-53).

The researchers used the Cardiovascular Disease Policy Model, which included adults aged 35-94 years and compared the cost-effectiveness of PCSK9 inhibitors and ezetimibe in treating two of the three indications for the drugs, heterozygous familial hypercholesterolemia (FH) or atherosclerotic cardiovascular disease (ASCVD). Homozygous FH was not included in the analysis.

The researchers assumed that statins, ezetimibe, and the two approved PCSK9 inhibitors (evolocumab and alirocumab) each would reduce the risk of cardiovascular events by an identical amount per mg/dL of LDL cholesterol reduction.

They found that, for PCSK9 inhibitors to be cost-effective at less than $100,000 per quality-adjusted life-year (QALY), the annual cost would need to drop from its current cost of roughly $14,000 per patient to $4,536 or less per patient, the researchers said.

Overall, the model showed that adding PCSK9 to statins for patients with heterozygous FH or ASCVD prevented 316,300 major adverse cardiovascular events (defined as cardiovascular death, nonfatal MI, or stroke), compared with adding ezetimibe; the cost was $503,000 per QALY. Adding PCSK9 inhibitors to statins for patients with ASCVD prevented about 4.3 million major cardiac adverse events, compared with adding ezetimibe; the cost was $414,000 per QALY.

In addition, the researchers found that PCSK9 inhibitor use would cut cardiovascular care costs by $29 billion over 5 years. However, the model projected an increase of about $592 in annual drug costs from 2015, as well as a 4% annual increase in U.S. health care costs overall.

The results were limited by several factors including the lack of long-term data on outcomes in patients taking PCSK9 inhibitors, the researchers noted. However, the findings suggest that the best way to improve the value of PCSK9 is to cut the price, they added.

In the meantime, “payers must consider the potential trade-off between paying for new drug treatments like PCSK9 inhibitors and investing in interventions known to improve access, physician prescription rates, and patient adherence to statin therapy among those at high ASCVD risk,” they said.

Dr. Bibbins-Domingo is the chair of the U.S. Preventive Services Task Force, but the study does not represent a recommendation from the USPSTF. She had no personal financial conflicts to disclose. The study was funded in part by the New England Comparative Effectiveness Public Advisory Council, which receives grants from several nonprofit organizations.

At current prices, PCSK9 inhibitors are not cost-effective for patients with heterozygous familial hypercholesterolemia or atherosclerotic cardiovascular disease, according to an analysis published Aug. 16 in JAMA.

The costs of the cholesterol-lowering drugs would have to be reduced by at least two-thirds to reach cost-effectiveness, on the basis of data from the simulation model of atherosclerotic cardiovascular disease in the United States and the 2015 annual PCSK9 inhibitor costs of $14,350.

The high cost of PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibition remains a challenge because it is meant for lifelong use, and “the potential increase in health care expenditures at current or even moderately discounted prices could be staggering,” wrote Kirsten Bibbins-Domingo, MD, PhD, of the University of California, San Francisco, and her colleagues (JAMA 2016 Aug 16;316[7]:743-53).

The researchers used the Cardiovascular Disease Policy Model, which included adults aged 35-94 years and compared the cost-effectiveness of PCSK9 inhibitors and ezetimibe in treating two of the three indications for the drugs, heterozygous familial hypercholesterolemia (FH) or atherosclerotic cardiovascular disease (ASCVD). Homozygous FH was not included in the analysis.

The researchers assumed that statins, ezetimibe, and the two approved PCSK9 inhibitors (evolocumab and alirocumab) each would reduce the risk of cardiovascular events by an identical amount per mg/dL of LDL cholesterol reduction.

They found that, for PCSK9 inhibitors to be cost-effective at less than $100,000 per quality-adjusted life-year (QALY), the annual cost would need to drop from its current cost of roughly $14,000 per patient to $4,536 or less per patient, the researchers said.

Overall, the model showed that adding PCSK9 to statins for patients with heterozygous FH or ASCVD prevented 316,300 major adverse cardiovascular events (defined as cardiovascular death, nonfatal MI, or stroke), compared with adding ezetimibe; the cost was $503,000 per QALY. Adding PCSK9 inhibitors to statins for patients with ASCVD prevented about 4.3 million major cardiac adverse events, compared with adding ezetimibe; the cost was $414,000 per QALY.

In addition, the researchers found that PCSK9 inhibitor use would cut cardiovascular care costs by $29 billion over 5 years. However, the model projected an increase of about $592 in annual drug costs from 2015, as well as a 4% annual increase in U.S. health care costs overall.

The results were limited by several factors including the lack of long-term data on outcomes in patients taking PCSK9 inhibitors, the researchers noted. However, the findings suggest that the best way to improve the value of PCSK9 is to cut the price, they added.

In the meantime, “payers must consider the potential trade-off between paying for new drug treatments like PCSK9 inhibitors and investing in interventions known to improve access, physician prescription rates, and patient adherence to statin therapy among those at high ASCVD risk,” they said.

Dr. Bibbins-Domingo is the chair of the U.S. Preventive Services Task Force, but the study does not represent a recommendation from the USPSTF. She had no personal financial conflicts to disclose. The study was funded in part by the New England Comparative Effectiveness Public Advisory Council, which receives grants from several nonprofit organizations.

At current prices, PCSK9 inhibitors are not cost-effective for patients with heterozygous familial hypercholesterolemia or atherosclerotic cardiovascular disease, according to an analysis published Aug. 16 in JAMA.

The costs of the cholesterol-lowering drugs would have to be reduced by at least two-thirds to reach cost-effectiveness, on the basis of data from the simulation model of atherosclerotic cardiovascular disease in the United States and the 2015 annual PCSK9 inhibitor costs of $14,350.

The high cost of PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibition remains a challenge because it is meant for lifelong use, and “the potential increase in health care expenditures at current or even moderately discounted prices could be staggering,” wrote Kirsten Bibbins-Domingo, MD, PhD, of the University of California, San Francisco, and her colleagues (JAMA 2016 Aug 16;316[7]:743-53).

The researchers used the Cardiovascular Disease Policy Model, which included adults aged 35-94 years and compared the cost-effectiveness of PCSK9 inhibitors and ezetimibe in treating two of the three indications for the drugs, heterozygous familial hypercholesterolemia (FH) or atherosclerotic cardiovascular disease (ASCVD). Homozygous FH was not included in the analysis.

The researchers assumed that statins, ezetimibe, and the two approved PCSK9 inhibitors (evolocumab and alirocumab) each would reduce the risk of cardiovascular events by an identical amount per mg/dL of LDL cholesterol reduction.

They found that, for PCSK9 inhibitors to be cost-effective at less than $100,000 per quality-adjusted life-year (QALY), the annual cost would need to drop from its current cost of roughly $14,000 per patient to $4,536 or less per patient, the researchers said.

Overall, the model showed that adding PCSK9 to statins for patients with heterozygous FH or ASCVD prevented 316,300 major adverse cardiovascular events (defined as cardiovascular death, nonfatal MI, or stroke), compared with adding ezetimibe; the cost was $503,000 per QALY. Adding PCSK9 inhibitors to statins for patients with ASCVD prevented about 4.3 million major cardiac adverse events, compared with adding ezetimibe; the cost was $414,000 per QALY.

In addition, the researchers found that PCSK9 inhibitor use would cut cardiovascular care costs by $29 billion over 5 years. However, the model projected an increase of about $592 in annual drug costs from 2015, as well as a 4% annual increase in U.S. health care costs overall.

The results were limited by several factors including the lack of long-term data on outcomes in patients taking PCSK9 inhibitors, the researchers noted. However, the findings suggest that the best way to improve the value of PCSK9 is to cut the price, they added.

In the meantime, “payers must consider the potential trade-off between paying for new drug treatments like PCSK9 inhibitors and investing in interventions known to improve access, physician prescription rates, and patient adherence to statin therapy among those at high ASCVD risk,” they said.

Dr. Bibbins-Domingo is the chair of the U.S. Preventive Services Task Force, but the study does not represent a recommendation from the USPSTF. She had no personal financial conflicts to disclose. The study was funded in part by the New England Comparative Effectiveness Public Advisory Council, which receives grants from several nonprofit organizations.

Higher levels of LDL cholesterol, HDL cholesterol, and triglycerides over a lifetime are protective against type 2 diabetes, a Mendelian randomization study has shown.

The study also bolstered established evidence that LDL cholesterol and triglycerides boost the risk of coronary artery disease (CAD) but showed no contribution of HDL cholesterol to that risk.

©Kativ/iStockphoto

Investigators sought to shed light on the role of the most commonly measured lipid fractions – LDL cholesterol, HDL cholesterol, and triglycerides – in the development of CAD and diabetes, particularly the observed link between statin therapy and an increased risk of diabetes.

Because genotype is not modifiable by disease, a genetic instrument can be used as an model for an exposure, and “Mendelian randomization generates unbiased, unconfounded effect estimates that are sometimes taken as evidence of a causal role,” Jon White, PhD, of University College London and his coinvestigators explained.

They used data from three genome-wide association studies involving 188,577 persons with blood lipid measures, 63,158 CAD cases, and 34,840 diabetes cases. All involved only people of European ancestry. Summary-level data for lipids were from the Global Lipids Genetics Consortium (Nat Genet. 2013;45[11]:1274-83), diabetes data came from the Diabetes Genetics Replication and Meta-analysis (Nat Genet. 2012;44[9]:981-90), and CAD data were from the Coronary Artery Disease Genome-wide Replication and Meta-analysis plus Coronary Artery Disease Genetics (Nat Genet. 2013;45[1]:25-33). From these, the investigators constructed genetic instruments comprised of single-nucleotide polymorphisms (SNPs) and conducted Mendelian randomizations designed to adjust for the SNPs’ possible associations with other traits, or pleiotropy.

The results showed that two lipid fractions were associated with reduced risk for type 2 diabetes and one had no discernible effect. LDL cholesterol showed the strongest association: An increase of 1 standard deviation, equivalent to 38 mg/dL, was tied to a 21% reduction in risk (odds ratio, 0.79) of diabetes. For HDL, a 1-SD rise of 16 mg/DL in HDL was associated with a 17% lower risk (OR, 0.83). A 1-SD rise of triglycerides, 89 mg/dL, also reduced risk by 17% (OR, 0.83), but there were statistical inconsistencies between analyses.

The associations between 1-SD increases and CAD were consistent with conventional wisdom: For LDL cholesterol, CAD risk rose by 68%; for triglycerides, the increase was 28%; and for HDL cholesterol, the risk was slightly reduced by 5% but was not statistically significant (JAMA Cardiol. 2016 Aug 3. doi: 10.1001/jamacardio.2016.1884).

These results can help to identify the potential effects of lipid-modifying drugs, yet “although all three lipids were associated with reduced risk of diabetes, it does not necessarily follow that lowering of LDL cholesterol or triglyceride levels through use of drugs that target specific proteins (eg, PCSK9) will alter the risk of diabetes,” Dr. White and his colleagues wrote. Large-scale genetic and clinical trials are needed to determine such dysglycemic associations.

This study was conducted by the Clinical Trial Service Unit of the University of Oxford through a grant by Merck Sharp & Dohme, with additional funding from numerous academic and research institutions. The funding sources had no role in the design or conduct of the study. Two of the investigators had ties to pharmaceutical companies.

[email protected]

Higher levels of LDL cholesterol, HDL cholesterol, and triglycerides over a lifetime are protective against type 2 diabetes, a Mendelian randomization study has shown.

The study also bolstered established evidence that LDL cholesterol and triglycerides boost the risk of coronary artery disease (CAD) but showed no contribution of HDL cholesterol to that risk.

©Kativ/iStockphoto

Investigators sought to shed light on the role of the most commonly measured lipid fractions – LDL cholesterol, HDL cholesterol, and triglycerides – in the development of CAD and diabetes, particularly the observed link between statin therapy and an increased risk of diabetes.

Because genotype is not modifiable by disease, a genetic instrument can be used as an model for an exposure, and “Mendelian randomization generates unbiased, unconfounded effect estimates that are sometimes taken as evidence of a causal role,” Jon White, PhD, of University College London and his coinvestigators explained.

They used data from three genome-wide association studies involving 188,577 persons with blood lipid measures, 63,158 CAD cases, and 34,840 diabetes cases. All involved only people of European ancestry. Summary-level data for lipids were from the Global Lipids Genetics Consortium (Nat Genet. 2013;45[11]:1274-83), diabetes data came from the Diabetes Genetics Replication and Meta-analysis (Nat Genet. 2012;44[9]:981-90), and CAD data were from the Coronary Artery Disease Genome-wide Replication and Meta-analysis plus Coronary Artery Disease Genetics (Nat Genet. 2013;45[1]:25-33). From these, the investigators constructed genetic instruments comprised of single-nucleotide polymorphisms (SNPs) and conducted Mendelian randomizations designed to adjust for the SNPs’ possible associations with other traits, or pleiotropy.

The results showed that two lipid fractions were associated with reduced risk for type 2 diabetes and one had no discernible effect. LDL cholesterol showed the strongest association: An increase of 1 standard deviation, equivalent to 38 mg/dL, was tied to a 21% reduction in risk (odds ratio, 0.79) of diabetes. For HDL, a 1-SD rise of 16 mg/DL in HDL was associated with a 17% lower risk (OR, 0.83). A 1-SD rise of triglycerides, 89 mg/dL, also reduced risk by 17% (OR, 0.83), but there were statistical inconsistencies between analyses.

The associations between 1-SD increases and CAD were consistent with conventional wisdom: For LDL cholesterol, CAD risk rose by 68%; for triglycerides, the increase was 28%; and for HDL cholesterol, the risk was slightly reduced by 5% but was not statistically significant (JAMA Cardiol. 2016 Aug 3. doi: 10.1001/jamacardio.2016.1884).

These results can help to identify the potential effects of lipid-modifying drugs, yet “although all three lipids were associated with reduced risk of diabetes, it does not necessarily follow that lowering of LDL cholesterol or triglyceride levels through use of drugs that target specific proteins (eg, PCSK9) will alter the risk of diabetes,” Dr. White and his colleagues wrote. Large-scale genetic and clinical trials are needed to determine such dysglycemic associations.

This study was conducted by the Clinical Trial Service Unit of the University of Oxford through a grant by Merck Sharp & Dohme, with additional funding from numerous academic and research institutions. The funding sources had no role in the design or conduct of the study. Two of the investigators had ties to pharmaceutical companies.

[email protected]

Higher levels of LDL cholesterol, HDL cholesterol, and triglycerides over a lifetime are protective against type 2 diabetes, a Mendelian randomization study has shown.

The study also bolstered established evidence that LDL cholesterol and triglycerides boost the risk of coronary artery disease (CAD) but showed no contribution of HDL cholesterol to that risk.

©Kativ/iStockphoto

Investigators sought to shed light on the role of the most commonly measured lipid fractions – LDL cholesterol, HDL cholesterol, and triglycerides – in the development of CAD and diabetes, particularly the observed link between statin therapy and an increased risk of diabetes.

Because genotype is not modifiable by disease, a genetic instrument can be used as an model for an exposure, and “Mendelian randomization generates unbiased, unconfounded effect estimates that are sometimes taken as evidence of a causal role,” Jon White, PhD, of University College London and his coinvestigators explained.

They used data from three genome-wide association studies involving 188,577 persons with blood lipid measures, 63,158 CAD cases, and 34,840 diabetes cases. All involved only people of European ancestry. Summary-level data for lipids were from the Global Lipids Genetics Consortium (Nat Genet. 2013;45[11]:1274-83), diabetes data came from the Diabetes Genetics Replication and Meta-analysis (Nat Genet. 2012;44[9]:981-90), and CAD data were from the Coronary Artery Disease Genome-wide Replication and Meta-analysis plus Coronary Artery Disease Genetics (Nat Genet. 2013;45[1]:25-33). From these, the investigators constructed genetic instruments comprised of single-nucleotide polymorphisms (SNPs) and conducted Mendelian randomizations designed to adjust for the SNPs’ possible associations with other traits, or pleiotropy.

The results showed that two lipid fractions were associated with reduced risk for type 2 diabetes and one had no discernible effect. LDL cholesterol showed the strongest association: An increase of 1 standard deviation, equivalent to 38 mg/dL, was tied to a 21% reduction in risk (odds ratio, 0.79) of diabetes. For HDL, a 1-SD rise of 16 mg/DL in HDL was associated with a 17% lower risk (OR, 0.83). A 1-SD rise of triglycerides, 89 mg/dL, also reduced risk by 17% (OR, 0.83), but there were statistical inconsistencies between analyses.

The associations between 1-SD increases and CAD were consistent with conventional wisdom: For LDL cholesterol, CAD risk rose by 68%; for triglycerides, the increase was 28%; and for HDL cholesterol, the risk was slightly reduced by 5% but was not statistically significant (JAMA Cardiol. 2016 Aug 3. doi: 10.1001/jamacardio.2016.1884).

These results can help to identify the potential effects of lipid-modifying drugs, yet “although all three lipids were associated with reduced risk of diabetes, it does not necessarily follow that lowering of LDL cholesterol or triglyceride levels through use of drugs that target specific proteins (eg, PCSK9) will alter the risk of diabetes,” Dr. White and his colleagues wrote. Large-scale genetic and clinical trials are needed to determine such dysglycemic associations.

This study was conducted by the Clinical Trial Service Unit of the University of Oxford through a grant by Merck Sharp & Dohme, with additional funding from numerous academic and research institutions. The funding sources had no role in the design or conduct of the study. Two of the investigators had ties to pharmaceutical companies.

[email protected]

The rate of diabetes-related emergency department visits was 464.5 per 100,000 U.S. population among Americans under age 30 in 2012, with young adults heading to the ED far more often than children, according to the Agency for Healthcare Research and Quality.

Young adults aged 18-29 years made diabetes-related ED visits at a rate of 905 per 100,000 in 2012, compared with 149 per 100,000 for children 17 and under. Narrowing down the age groups shows even greater differences: The rate was 47 per 100,000 for children aged 5 years and under, 95 for children aged 6-9, 193 for 10- to 13-year-olds, 316.5 for those aged 14-17, 607 for 18- to 21-year-olds, 889 for 22- to 25-year-olds, and 1,236 for those aged 26-29 years, the AHRQ reported.

Patients aged 5 years and under were, however, the most likely to be admitted to the hospital in 2012: 29% of their diabetes-related ED visits resulted in admission, compared with 26% for those aged 26-29. Those aged 22-25 years were the least likely to be admitted, with 18% staying after their ED visit, and the overall admission rate for those aged 0-29 years was 23.5%, the report noted.

The ED visit rate for diabetes was higher for females than for males aged 0-29 years – 569 per 100,000 vs. 355 – but males were more likely to be admitted – 27% vs. 21% for females, according to data from the Nationwide Emergency Department Sample.

[email protected]

The rate of diabetes-related emergency department visits was 464.5 per 100,000 U.S. population among Americans under age 30 in 2012, with young adults heading to the ED far more often than children, according to the Agency for Healthcare Research and Quality.

Young adults aged 18-29 years made diabetes-related ED visits at a rate of 905 per 100,000 in 2012, compared with 149 per 100,000 for children 17 and under. Narrowing down the age groups shows even greater differences: The rate was 47 per 100,000 for children aged 5 years and under, 95 for children aged 6-9, 193 for 10- to 13-year-olds, 316.5 for those aged 14-17, 607 for 18- to 21-year-olds, 889 for 22- to 25-year-olds, and 1,236 for those aged 26-29 years, the AHRQ reported.

Patients aged 5 years and under were, however, the most likely to be admitted to the hospital in 2012: 29% of their diabetes-related ED visits resulted in admission, compared with 26% for those aged 26-29. Those aged 22-25 years were the least likely to be admitted, with 18% staying after their ED visit, and the overall admission rate for those aged 0-29 years was 23.5%, the report noted.

The ED visit rate for diabetes was higher for females than for males aged 0-29 years – 569 per 100,000 vs. 355 – but males were more likely to be admitted – 27% vs. 21% for females, according to data from the Nationwide Emergency Department Sample.

[email protected]

The rate of diabetes-related emergency department visits was 464.5 per 100,000 U.S. population among Americans under age 30 in 2012, with young adults heading to the ED far more often than children, according to the Agency for Healthcare Research and Quality.

Young adults aged 18-29 years made diabetes-related ED visits at a rate of 905 per 100,000 in 2012, compared with 149 per 100,000 for children 17 and under. Narrowing down the age groups shows even greater differences: The rate was 47 per 100,000 for children aged 5 years and under, 95 for children aged 6-9, 193 for 10- to 13-year-olds, 316.5 for those aged 14-17, 607 for 18- to 21-year-olds, 889 for 22- to 25-year-olds, and 1,236 for those aged 26-29 years, the AHRQ reported.

Patients aged 5 years and under were, however, the most likely to be admitted to the hospital in 2012: 29% of their diabetes-related ED visits resulted in admission, compared with 26% for those aged 26-29. Those aged 22-25 years were the least likely to be admitted, with 18% staying after their ED visit, and the overall admission rate for those aged 0-29 years was 23.5%, the report noted.

The ED visit rate for diabetes was higher for females than for males aged 0-29 years – 569 per 100,000 vs. 355 – but males were more likely to be admitted – 27% vs. 21% for females, according to data from the Nationwide Emergency Department Sample.

[email protected]

The Food and Drug Administration has approved the once-daily injectable lixisenatide, a glucagonlike peptide-1 (GLP-1) receptor agonist, as an adjunct to diet and exercise for improved glycemic control in adults with type 2 diabetes.

The safety and effectiveness of lixisenatide (Adlyxin, Sanofi) were evaluated either as a standalone therapy or in combination with other FDA-approved treatments in a series of clinical trials that enrolled 5,400 adults with poorly controlled type 2 diabetes. The combinations tested in the GetGoal Duo2 studies included lixisenatide with metformin, sulfonylureas, pioglitazone, or basal insulin. Lixisenatide successfully met the primary endpoint of improved hemoglobin A_1c levels.

Sanofi, the drug’s manufacturer, withdrew its original 2013 application for lixisenatide’s approval pending evaluation of its cardiovascular safety profile using data from the randomized, controlled Evaluation of Lixisenatide in Acute Coronary Syndrome ELIXA trial. In that study of more than 6,000 adults with type 2 diabetes at risk for atherosclerotic cardiovascular disease, lixisenatide did not increase the risk of cardiovascular adverse events, which occurred in 13.2% of placebo patients and 13.4% of treatment group patients (N Engl J Med. 2015;373:2247-57).

The drug’s most common side effects are nausea, vomiting, headache, diarrhea, dizziness, and hypoglycemia. Severe hypersensitivity reactions, including anaphylaxis, also were reported in the clinical trials.

Lixisenatide should not be used to treat people with type 1 diabetes or patients with diabetic ketoacidosis.

The drug will be marketed in disposable, 20-mcg single-dose pens to be injected postprandially, once daily, following initial treatment with a once-daily dose of 10 mcg for 14 days.

Lixisenatide is approved in more than 60 countries and marketed as Lyxumia in over 40, according to information on the manufacturer’s website.

Postmarketing studies for lixisenatide will be required to evaluate dosing, efficacy, and safety in pediatric patients, and to evaluate the drug’s immunogenicity, according to an FDA statement.

“The FDA continues to support the development of new drug therapies for diabetes management,” said Mary Thanh Hai Parks, MD, deputy director, Office of Drug Evaluation II in the FDA’s Center for Drug Evaluation and Research. “Adlyxin will add to the available treatment options to control blood sugar levels for those with type 2.”

[email protected]

On Twitter @whitneymcknight

The Food and Drug Administration has approved the once-daily injectable lixisenatide, a glucagonlike peptide-1 (GLP-1) receptor agonist, as an adjunct to diet and exercise for improved glycemic control in adults with type 2 diabetes.

The safety and effectiveness of lixisenatide (Adlyxin, Sanofi) were evaluated either as a standalone therapy or in combination with other FDA-approved treatments in a series of clinical trials that enrolled 5,400 adults with poorly controlled type 2 diabetes. The combinations tested in the GetGoal Duo2 studies included lixisenatide with metformin, sulfonylureas, pioglitazone, or basal insulin. Lixisenatide successfully met the primary endpoint of improved hemoglobin A_1c levels.

Sanofi, the drug’s manufacturer, withdrew its original 2013 application for lixisenatide’s approval pending evaluation of its cardiovascular safety profile using data from the randomized, controlled Evaluation of Lixisenatide in Acute Coronary Syndrome ELIXA trial. In that study of more than 6,000 adults with type 2 diabetes at risk for atherosclerotic cardiovascular disease, lixisenatide did not increase the risk of cardiovascular adverse events, which occurred in 13.2% of placebo patients and 13.4% of treatment group patients (N Engl J Med. 2015;373:2247-57).

The drug’s most common side effects are nausea, vomiting, headache, diarrhea, dizziness, and hypoglycemia. Severe hypersensitivity reactions, including anaphylaxis, also were reported in the clinical trials.

Lixisenatide should not be used to treat people with type 1 diabetes or patients with diabetic ketoacidosis.

The drug will be marketed in disposable, 20-mcg single-dose pens to be injected postprandially, once daily, following initial treatment with a once-daily dose of 10 mcg for 14 days.

Lixisenatide is approved in more than 60 countries and marketed as Lyxumia in over 40, according to information on the manufacturer’s website.

Postmarketing studies for lixisenatide will be required to evaluate dosing, efficacy, and safety in pediatric patients, and to evaluate the drug’s immunogenicity, according to an FDA statement.

“The FDA continues to support the development of new drug therapies for diabetes management,” said Mary Thanh Hai Parks, MD, deputy director, Office of Drug Evaluation II in the FDA’s Center for Drug Evaluation and Research. “Adlyxin will add to the available treatment options to control blood sugar levels for those with type 2.”

[email protected]

On Twitter @whitneymcknight

The Food and Drug Administration has approved the once-daily injectable lixisenatide, a glucagonlike peptide-1 (GLP-1) receptor agonist, as an adjunct to diet and exercise for improved glycemic control in adults with type 2 diabetes.

The safety and effectiveness of lixisenatide (Adlyxin, Sanofi) were evaluated either as a standalone therapy or in combination with other FDA-approved treatments in a series of clinical trials that enrolled 5,400 adults with poorly controlled type 2 diabetes. The combinations tested in the GetGoal Duo2 studies included lixisenatide with metformin, sulfonylureas, pioglitazone, or basal insulin. Lixisenatide successfully met the primary endpoint of improved hemoglobin A_1c levels.

Sanofi, the drug’s manufacturer, withdrew its original 2013 application for lixisenatide’s approval pending evaluation of its cardiovascular safety profile using data from the randomized, controlled Evaluation of Lixisenatide in Acute Coronary Syndrome ELIXA trial. In that study of more than 6,000 adults with type 2 diabetes at risk for atherosclerotic cardiovascular disease, lixisenatide did not increase the risk of cardiovascular adverse events, which occurred in 13.2% of placebo patients and 13.4% of treatment group patients (N Engl J Med. 2015;373:2247-57).

The drug’s most common side effects are nausea, vomiting, headache, diarrhea, dizziness, and hypoglycemia. Severe hypersensitivity reactions, including anaphylaxis, also were reported in the clinical trials.

Lixisenatide should not be used to treat people with type 1 diabetes or patients with diabetic ketoacidosis.

The drug will be marketed in disposable, 20-mcg single-dose pens to be injected postprandially, once daily, following initial treatment with a once-daily dose of 10 mcg for 14 days.

Lixisenatide is approved in more than 60 countries and marketed as Lyxumia in over 40, according to information on the manufacturer’s website.

Postmarketing studies for lixisenatide will be required to evaluate dosing, efficacy, and safety in pediatric patients, and to evaluate the drug’s immunogenicity, according to an FDA statement.

“The FDA continues to support the development of new drug therapies for diabetes management,” said Mary Thanh Hai Parks, MD, deputy director, Office of Drug Evaluation II in the FDA’s Center for Drug Evaluation and Research. “Adlyxin will add to the available treatment options to control blood sugar levels for those with type 2.”

[email protected]

On Twitter @whitneymcknight

From 1997 to 2014, cancer survivors had a significantly faster increase in obesity prevalence compared with adults without a history of cancer, investigators found.

Furthermore, the elevated annual increase in rates of obesity was more pronounced in women, in breast and colorectal cancer survivors, and in non-Hispanic blacks.

©SandraMatic/Thinkstock

Cancer patients may be at an increased risk for weight gain caused by specific cancer treatments such as chemotherapy, steroid modifications, and various hormone therapies, especially in “hormonally and metabolically driven cancers such as breast and colorectal cancer,” wrote Heather Greenlee, ND, PhD, of Columbia University, New York, and her associates (J Clin Oncol. 2016 July 25. doi: 10.1200/JCO.2016.66.4391). “To better inform future research on obesity and cancer survival and to inform the planning and implementation of weight loss interventions in cancer survivors, we compared trends from 1997 to 2014 in obesity prevalence in U.S. adults with and without a history of cancer,” the researchers explained.

Obesity prevalence and trends were evaluated through the National Health Interview Survey, an ongoing cross-sectional survey of the health status, health care access, and behaviors of the U.S. civilian population conducted by the National Center for Health Statistics.

For the current study, surveys from a total of 538,969 adults aged 18-85 years with (n = 32,447) or without (n = 506,522) a history of cancer were analyzed. Participants provided self-reported height and weight measures from which body mass index was calculated. Obesity was defined as a BMI of 30 kg/m² or higher for non-Asians and 27.5 kg/m² or higher for Asians. Participants also self-reported sex, race, and cancer history.

Overall, the prevalence of obesity consistently increased from 1997 to 2014. Among cancer survivors, the prevalence of obesity increased from 22.4% to 31.7% while in adults without a history of cancer, prevalence increased from 20.9% to 29.5%.

The annual increase in the rate of obesity was significantly greater in both women and men with a history of cancer (2.9% and 2.8% respectively) compared with those without a history of cancer (2.3% and 2.4%, P less than .001 for all).

The elevated annual increase in rates of obesity was even higher in colorectal (3.1% in women and 3.7% in men) and breast (3.0%) cancer survivors compared with adults without a history of cancer, but was lower in prostate cancer survivors (2.1%; P = .001 for all).

“These findings call for public health planning of effective and scalable weight management and control programs for cancer survivors, especially for breast and colorectal cancer survivors and for non-Hispanic blacks,” the investigators concluded.

The National Cancer Institute funded the study. Dr. Greenlee and one other investigator reported serving in advisory roles for EHE International.

[email protected]

On Twitter @jessnicolecraig

From 1997 to 2014, cancer survivors had a significantly faster increase in obesity prevalence compared with adults without a history of cancer, investigators found.

Furthermore, the elevated annual increase in rates of obesity was more pronounced in women, in breast and colorectal cancer survivors, and in non-Hispanic blacks.

©SandraMatic/Thinkstock

Cancer patients may be at an increased risk for weight gain caused by specific cancer treatments such as chemotherapy, steroid modifications, and various hormone therapies, especially in “hormonally and metabolically driven cancers such as breast and colorectal cancer,” wrote Heather Greenlee, ND, PhD, of Columbia University, New York, and her associates (J Clin Oncol. 2016 July 25. doi: 10.1200/JCO.2016.66.4391). “To better inform future research on obesity and cancer survival and to inform the planning and implementation of weight loss interventions in cancer survivors, we compared trends from 1997 to 2014 in obesity prevalence in U.S. adults with and without a history of cancer,” the researchers explained.

Obesity prevalence and trends were evaluated through the National Health Interview Survey, an ongoing cross-sectional survey of the health status, health care access, and behaviors of the U.S. civilian population conducted by the National Center for Health Statistics.

For the current study, surveys from a total of 538,969 adults aged 18-85 years with (n = 32,447) or without (n = 506,522) a history of cancer were analyzed. Participants provided self-reported height and weight measures from which body mass index was calculated. Obesity was defined as a BMI of 30 kg/m² or higher for non-Asians and 27.5 kg/m² or higher for Asians. Participants also self-reported sex, race, and cancer history.

Overall, the prevalence of obesity consistently increased from 1997 to 2014. Among cancer survivors, the prevalence of obesity increased from 22.4% to 31.7% while in adults without a history of cancer, prevalence increased from 20.9% to 29.5%.

The annual increase in the rate of obesity was significantly greater in both women and men with a history of cancer (2.9% and 2.8% respectively) compared with those without a history of cancer (2.3% and 2.4%, P less than .001 for all).

The elevated annual increase in rates of obesity was even higher in colorectal (3.1% in women and 3.7% in men) and breast (3.0%) cancer survivors compared with adults without a history of cancer, but was lower in prostate cancer survivors (2.1%; P = .001 for all).

“These findings call for public health planning of effective and scalable weight management and control programs for cancer survivors, especially for breast and colorectal cancer survivors and for non-Hispanic blacks,” the investigators concluded.

The National Cancer Institute funded the study. Dr. Greenlee and one other investigator reported serving in advisory roles for EHE International.

[email protected]

On Twitter @jessnicolecraig

From 1997 to 2014, cancer survivors had a significantly faster increase in obesity prevalence compared with adults without a history of cancer, investigators found.

Furthermore, the elevated annual increase in rates of obesity was more pronounced in women, in breast and colorectal cancer survivors, and in non-Hispanic blacks.

©SandraMatic/Thinkstock

Cancer patients may be at an increased risk for weight gain caused by specific cancer treatments such as chemotherapy, steroid modifications, and various hormone therapies, especially in “hormonally and metabolically driven cancers such as breast and colorectal cancer,” wrote Heather Greenlee, ND, PhD, of Columbia University, New York, and her associates (J Clin Oncol. 2016 July 25. doi: 10.1200/JCO.2016.66.4391). “To better inform future research on obesity and cancer survival and to inform the planning and implementation of weight loss interventions in cancer survivors, we compared trends from 1997 to 2014 in obesity prevalence in U.S. adults with and without a history of cancer,” the researchers explained.

Obesity prevalence and trends were evaluated through the National Health Interview Survey, an ongoing cross-sectional survey of the health status, health care access, and behaviors of the U.S. civilian population conducted by the National Center for Health Statistics.

For the current study, surveys from a total of 538,969 adults aged 18-85 years with (n = 32,447) or without (n = 506,522) a history of cancer were analyzed. Participants provided self-reported height and weight measures from which body mass index was calculated. Obesity was defined as a BMI of 30 kg/m² or higher for non-Asians and 27.5 kg/m² or higher for Asians. Participants also self-reported sex, race, and cancer history.

Overall, the prevalence of obesity consistently increased from 1997 to 2014. Among cancer survivors, the prevalence of obesity increased from 22.4% to 31.7% while in adults without a history of cancer, prevalence increased from 20.9% to 29.5%.

The annual increase in the rate of obesity was significantly greater in both women and men with a history of cancer (2.9% and 2.8% respectively) compared with those without a history of cancer (2.3% and 2.4%, P less than .001 for all).

The elevated annual increase in rates of obesity was even higher in colorectal (3.1% in women and 3.7% in men) and breast (3.0%) cancer survivors compared with adults without a history of cancer, but was lower in prostate cancer survivors (2.1%; P = .001 for all).

“These findings call for public health planning of effective and scalable weight management and control programs for cancer survivors, especially for breast and colorectal cancer survivors and for non-Hispanic blacks,” the investigators concluded.

The National Cancer Institute funded the study. Dr. Greenlee and one other investigator reported serving in advisory roles for EHE International.

[email protected]

On Twitter @jessnicolecraig