Diabetes Hub

SAN DIEGO – In adults with obesity, lowering intake of dietary fat may lead to greater body fat loss than lowering intake of dietary carbohydrates, results from a small federally funded study showed.

“A lot of focus has been placed on the idea of the competing importance of dietary carbohydrate versus dietary fat in the treatment and prevention of obesity,” lead study author Kevin D. Hall, Ph.D., said during a press briefing at the meeting of the Endocrine Society. “The fashion of which is the evil macronutrient of choice at one time or another is vacillating back and forth. More recently I would say that dietary carbohydrate has been the one demonized, with sugars and refined carbohydrates being the main culprit.”

Doug Brunk/Frontline Medical News

Dr. Hall, a senior investigator at the National Institute of Diabetes and Digestive and Kidney Diseases, went on to note that at the level of the whole body, “you can think of fat balance as a balance between the intake of fat and how much fat is being burned. So if you’re eating a certain amount of fat and burning that same amount of fat, your body fat will be stable. The only way to perturb that fat balance at the whole-body level is to induce an imbalance between intake of fat and the amount of fat that is being burned.” The low carbohydrate advocates will suggest that an obese adult should decrease carbohydrate intake in the diet, thereby lowering insulin. This in turn has the effect of releasing fat from the fat cells, thereby leading to an imbalance that will eventually rebalance at a lower level of body fat. Alternatively, another way an obese adult could potentially achieve the same results is to cut dietary fat. The resulting state of fat imbalance would promote loss of body fat, according to Dr. Hall.

In an effort to investigate the whole-body energy expenditure and metabolic fat balance from selective restriction of dietary carbohydrate versus dietary fat, the researchers enrolled 19 nondiabetic volunteers with a mean age of 34 years and a mean body mass index of 36 mg/m². Of the 19 volunteers, 10 were men. The volunteers were housed in a metabolic ward at the National Institutes of Health for a pair of 2-week inpatient visits. For 5 days, everyone was fed a eucaloric baseline diet of 50% carbohydrate, 35% fat, and 15% protein that was designed to provide them with the number of calories they needed to maintain their body weight. Next, the volunteers were randomized to one of two groups where they received a 30% reduced energy diet by restriction of their intake of either fat or carbohydrate. “We provided all of their food; they had no choice in what they ate,” Dr. Hall said.

After a 2-4-week washout period the volunteers returned to the ward and received the alternative diet after the same 5-day baseline run-in phase. “The idea here was [that] we knew exactly how much they ate, and during the time they spent in metabolic chambers we could measure how much fat they burned,” he explained. “So we could calculate how fat oxidation changed as well as the fat imbalance in the body. The low-carb diet selectively reduced carbohydrates, keeping fat and protein at the constant levels, whereas the low-fat diet selectively reduced fat, keeping carbohydrate and protein at baseline levels.”

During the 6-day diet phase the researchers cut 30% of participants’ calories, selectively from either carbohydrates or fat. This translated into about 800 calories per day being cut from both diets.

Dr. Hall reported that reduction of dietary carbohydrates led to a significant increase in whole-body 24-hour fat oxidation (P< .0001), while isocaloric reduction of dietary fat in the same subjects had no significant effect on 24-hour fat oxidation (P = .15). However, the cumulative metabolic fat balance (adding up the daily imbalance between intake and expenditure of fat) indicated that the reduced fat diet resulted in about 80% greater body fat loss, compared with the reduced carbohydrate diet (P = .0003).

Dr. Hall acknowledged certain limitations of the study, including the fact that it did not address the long-term efficacy of low-carbohydrate or low-fat diets. One remaining key unanswered question is whether “the low fat diet continue to outpace the low carbohydrate diet with respect to body fat?” he asked. “This is a short-term study, a small number of people with obesity under metabolic ward conditions. We can’t extrapolate about what might happen to their health with respect to these diets, if they were able to adhere to them for long periods of time.”

The study was funded by the Intramural Research Program of the NIDDK. Dr. Hall reported having no relevant financial conflicts.

[email protected]

On Twitter @dougbrunk

SAN DIEGO – In adults with obesity, lowering intake of dietary fat may lead to greater body fat loss than lowering intake of dietary carbohydrates, results from a small federally funded study showed.

“A lot of focus has been placed on the idea of the competing importance of dietary carbohydrate versus dietary fat in the treatment and prevention of obesity,” lead study author Kevin D. Hall, Ph.D., said during a press briefing at the meeting of the Endocrine Society. “The fashion of which is the evil macronutrient of choice at one time or another is vacillating back and forth. More recently I would say that dietary carbohydrate has been the one demonized, with sugars and refined carbohydrates being the main culprit.”

Doug Brunk/Frontline Medical News

Dr. Hall, a senior investigator at the National Institute of Diabetes and Digestive and Kidney Diseases, went on to note that at the level of the whole body, “you can think of fat balance as a balance between the intake of fat and how much fat is being burned. So if you’re eating a certain amount of fat and burning that same amount of fat, your body fat will be stable. The only way to perturb that fat balance at the whole-body level is to induce an imbalance between intake of fat and the amount of fat that is being burned.” The low carbohydrate advocates will suggest that an obese adult should decrease carbohydrate intake in the diet, thereby lowering insulin. This in turn has the effect of releasing fat from the fat cells, thereby leading to an imbalance that will eventually rebalance at a lower level of body fat. Alternatively, another way an obese adult could potentially achieve the same results is to cut dietary fat. The resulting state of fat imbalance would promote loss of body fat, according to Dr. Hall.

In an effort to investigate the whole-body energy expenditure and metabolic fat balance from selective restriction of dietary carbohydrate versus dietary fat, the researchers enrolled 19 nondiabetic volunteers with a mean age of 34 years and a mean body mass index of 36 mg/m². Of the 19 volunteers, 10 were men. The volunteers were housed in a metabolic ward at the National Institutes of Health for a pair of 2-week inpatient visits. For 5 days, everyone was fed a eucaloric baseline diet of 50% carbohydrate, 35% fat, and 15% protein that was designed to provide them with the number of calories they needed to maintain their body weight. Next, the volunteers were randomized to one of two groups where they received a 30% reduced energy diet by restriction of their intake of either fat or carbohydrate. “We provided all of their food; they had no choice in what they ate,” Dr. Hall said.

After a 2-4-week washout period the volunteers returned to the ward and received the alternative diet after the same 5-day baseline run-in phase. “The idea here was [that] we knew exactly how much they ate, and during the time they spent in metabolic chambers we could measure how much fat they burned,” he explained. “So we could calculate how fat oxidation changed as well as the fat imbalance in the body. The low-carb diet selectively reduced carbohydrates, keeping fat and protein at the constant levels, whereas the low-fat diet selectively reduced fat, keeping carbohydrate and protein at baseline levels.”

During the 6-day diet phase the researchers cut 30% of participants’ calories, selectively from either carbohydrates or fat. This translated into about 800 calories per day being cut from both diets.

Dr. Hall reported that reduction of dietary carbohydrates led to a significant increase in whole-body 24-hour fat oxidation (P< .0001), while isocaloric reduction of dietary fat in the same subjects had no significant effect on 24-hour fat oxidation (P = .15). However, the cumulative metabolic fat balance (adding up the daily imbalance between intake and expenditure of fat) indicated that the reduced fat diet resulted in about 80% greater body fat loss, compared with the reduced carbohydrate diet (P = .0003).

Dr. Hall acknowledged certain limitations of the study, including the fact that it did not address the long-term efficacy of low-carbohydrate or low-fat diets. One remaining key unanswered question is whether “the low fat diet continue to outpace the low carbohydrate diet with respect to body fat?” he asked. “This is a short-term study, a small number of people with obesity under metabolic ward conditions. We can’t extrapolate about what might happen to their health with respect to these diets, if they were able to adhere to them for long periods of time.”

The study was funded by the Intramural Research Program of the NIDDK. Dr. Hall reported having no relevant financial conflicts.

[email protected]

On Twitter @dougbrunk

SAN DIEGO – In adults with obesity, lowering intake of dietary fat may lead to greater body fat loss than lowering intake of dietary carbohydrates, results from a small federally funded study showed.

“A lot of focus has been placed on the idea of the competing importance of dietary carbohydrate versus dietary fat in the treatment and prevention of obesity,” lead study author Kevin D. Hall, Ph.D., said during a press briefing at the meeting of the Endocrine Society. “The fashion of which is the evil macronutrient of choice at one time or another is vacillating back and forth. More recently I would say that dietary carbohydrate has been the one demonized, with sugars and refined carbohydrates being the main culprit.”

Doug Brunk/Frontline Medical News

Dr. Hall, a senior investigator at the National Institute of Diabetes and Digestive and Kidney Diseases, went on to note that at the level of the whole body, “you can think of fat balance as a balance between the intake of fat and how much fat is being burned. So if you’re eating a certain amount of fat and burning that same amount of fat, your body fat will be stable. The only way to perturb that fat balance at the whole-body level is to induce an imbalance between intake of fat and the amount of fat that is being burned.” The low carbohydrate advocates will suggest that an obese adult should decrease carbohydrate intake in the diet, thereby lowering insulin. This in turn has the effect of releasing fat from the fat cells, thereby leading to an imbalance that will eventually rebalance at a lower level of body fat. Alternatively, another way an obese adult could potentially achieve the same results is to cut dietary fat. The resulting state of fat imbalance would promote loss of body fat, according to Dr. Hall.

In an effort to investigate the whole-body energy expenditure and metabolic fat balance from selective restriction of dietary carbohydrate versus dietary fat, the researchers enrolled 19 nondiabetic volunteers with a mean age of 34 years and a mean body mass index of 36 mg/m². Of the 19 volunteers, 10 were men. The volunteers were housed in a metabolic ward at the National Institutes of Health for a pair of 2-week inpatient visits. For 5 days, everyone was fed a eucaloric baseline diet of 50% carbohydrate, 35% fat, and 15% protein that was designed to provide them with the number of calories they needed to maintain their body weight. Next, the volunteers were randomized to one of two groups where they received a 30% reduced energy diet by restriction of their intake of either fat or carbohydrate. “We provided all of their food; they had no choice in what they ate,” Dr. Hall said.

After a 2-4-week washout period the volunteers returned to the ward and received the alternative diet after the same 5-day baseline run-in phase. “The idea here was [that] we knew exactly how much they ate, and during the time they spent in metabolic chambers we could measure how much fat they burned,” he explained. “So we could calculate how fat oxidation changed as well as the fat imbalance in the body. The low-carb diet selectively reduced carbohydrates, keeping fat and protein at the constant levels, whereas the low-fat diet selectively reduced fat, keeping carbohydrate and protein at baseline levels.”

During the 6-day diet phase the researchers cut 30% of participants’ calories, selectively from either carbohydrates or fat. This translated into about 800 calories per day being cut from both diets.

Dr. Hall reported that reduction of dietary carbohydrates led to a significant increase in whole-body 24-hour fat oxidation (P< .0001), while isocaloric reduction of dietary fat in the same subjects had no significant effect on 24-hour fat oxidation (P = .15). However, the cumulative metabolic fat balance (adding up the daily imbalance between intake and expenditure of fat) indicated that the reduced fat diet resulted in about 80% greater body fat loss, compared with the reduced carbohydrate diet (P = .0003).

Dr. Hall acknowledged certain limitations of the study, including the fact that it did not address the long-term efficacy of low-carbohydrate or low-fat diets. One remaining key unanswered question is whether “the low fat diet continue to outpace the low carbohydrate diet with respect to body fat?” he asked. “This is a short-term study, a small number of people with obesity under metabolic ward conditions. We can’t extrapolate about what might happen to their health with respect to these diets, if they were able to adhere to them for long periods of time.”

The study was funded by the Intramural Research Program of the NIDDK. Dr. Hall reported having no relevant financial conflicts.

[email protected]

On Twitter @dougbrunk

Metformin showed superior glycemic durability compared with sulfonylurea and meglitinide in a nationwide observational study in Sweden, according to a report published online in BMJ Open Diabetes Research & Care.

To study glycemic durability in real-world patients, researchers analyzed data from five Swedish national registries of diabetes care, prescribed drugs, causes of death, hospital discharges, and health insurance. They examined the medical records of 69,667 adults who had heretofore untreated type 2 diabetes and were initially prescribed metformin, sulfonylurea, or meglitinide during a 4-year period. They also analyzed medication use in a subset of propensity-matched patients who were well balanced for numerous covariates that can impact diabetes progression, such as age, gender, hemoglobin A_1c level, eGFR, and CVD history.

Each medication’s glycemic durability was judged according to whether these patients continued using their initial diabetes drug, switched to a different drug, or added a second drug during 5.5 years of follow-up, said Dr. Nils Ekstrom of the University of Gothenburg (Sweden) and his associates.

Mean patient age was 71 years, mean duration of diabetes was 5 years, and mean body mass index was 28 kg/m². Overall, almost half of these patients discontinued their initial medication, switched to a different medication, or required a second diabetes drug be added to their regimen during follow-up.

Compared with metformin, sulfonylurea and meglitinide showed a significantly increased risk of monotherapy failure (hazard ratio, 1.74). Sulfonylurea and meglitinide had an even greater risk of requiring a switch to a new agent (HR, 2.81) and of requiring an add-on agent (HR, 3.14). These results from the main analyses were confirmed in two sensitivity analyses involving approximately 60,000 participants, the investigators said (BMJ Open Diab. Res. Care 2015 [doi:10.1136/bmjdrc-2014-000059]).

Patients who continued on their initial monotherapy throughout follow-up showed improved HbA_1c levels of approximately 10%, regardless of which medication they used. This group represents treatment responders. In contrast, patients who discontinued, switched, or added a new agent to their initial medication showed stable or slightly increasing HbA_1c levels over time, which represented deteriorating glycemic control.

“These results strengthen the current evidence of a superior durability with metformin compared with sulfonylureas” in the real-world setting, and suggest that the same is true regarding meglitinide, Dr. Ekstrom and his associates said.

Metformin showed superior glycemic durability compared with sulfonylurea and meglitinide in a nationwide observational study in Sweden, according to a report published online in BMJ Open Diabetes Research & Care.

To study glycemic durability in real-world patients, researchers analyzed data from five Swedish national registries of diabetes care, prescribed drugs, causes of death, hospital discharges, and health insurance. They examined the medical records of 69,667 adults who had heretofore untreated type 2 diabetes and were initially prescribed metformin, sulfonylurea, or meglitinide during a 4-year period. They also analyzed medication use in a subset of propensity-matched patients who were well balanced for numerous covariates that can impact diabetes progression, such as age, gender, hemoglobin A_1c level, eGFR, and CVD history.

Each medication’s glycemic durability was judged according to whether these patients continued using their initial diabetes drug, switched to a different drug, or added a second drug during 5.5 years of follow-up, said Dr. Nils Ekstrom of the University of Gothenburg (Sweden) and his associates.

Mean patient age was 71 years, mean duration of diabetes was 5 years, and mean body mass index was 28 kg/m². Overall, almost half of these patients discontinued their initial medication, switched to a different medication, or required a second diabetes drug be added to their regimen during follow-up.

Compared with metformin, sulfonylurea and meglitinide showed a significantly increased risk of monotherapy failure (hazard ratio, 1.74). Sulfonylurea and meglitinide had an even greater risk of requiring a switch to a new agent (HR, 2.81) and of requiring an add-on agent (HR, 3.14). These results from the main analyses were confirmed in two sensitivity analyses involving approximately 60,000 participants, the investigators said (BMJ Open Diab. Res. Care 2015 [doi:10.1136/bmjdrc-2014-000059]).

Patients who continued on their initial monotherapy throughout follow-up showed improved HbA_1c levels of approximately 10%, regardless of which medication they used. This group represents treatment responders. In contrast, patients who discontinued, switched, or added a new agent to their initial medication showed stable or slightly increasing HbA_1c levels over time, which represented deteriorating glycemic control.

“These results strengthen the current evidence of a superior durability with metformin compared with sulfonylureas” in the real-world setting, and suggest that the same is true regarding meglitinide, Dr. Ekstrom and his associates said.

Metformin showed superior glycemic durability compared with sulfonylurea and meglitinide in a nationwide observational study in Sweden, according to a report published online in BMJ Open Diabetes Research & Care.

To study glycemic durability in real-world patients, researchers analyzed data from five Swedish national registries of diabetes care, prescribed drugs, causes of death, hospital discharges, and health insurance. They examined the medical records of 69,667 adults who had heretofore untreated type 2 diabetes and were initially prescribed metformin, sulfonylurea, or meglitinide during a 4-year period. They also analyzed medication use in a subset of propensity-matched patients who were well balanced for numerous covariates that can impact diabetes progression, such as age, gender, hemoglobin A_1c level, eGFR, and CVD history.

Each medication’s glycemic durability was judged according to whether these patients continued using their initial diabetes drug, switched to a different drug, or added a second drug during 5.5 years of follow-up, said Dr. Nils Ekstrom of the University of Gothenburg (Sweden) and his associates.

Mean patient age was 71 years, mean duration of diabetes was 5 years, and mean body mass index was 28 kg/m². Overall, almost half of these patients discontinued their initial medication, switched to a different medication, or required a second diabetes drug be added to their regimen during follow-up.

Compared with metformin, sulfonylurea and meglitinide showed a significantly increased risk of monotherapy failure (hazard ratio, 1.74). Sulfonylurea and meglitinide had an even greater risk of requiring a switch to a new agent (HR, 2.81) and of requiring an add-on agent (HR, 3.14). These results from the main analyses were confirmed in two sensitivity analyses involving approximately 60,000 participants, the investigators said (BMJ Open Diab. Res. Care 2015 [doi:10.1136/bmjdrc-2014-000059]).

Patients who continued on their initial monotherapy throughout follow-up showed improved HbA_1c levels of approximately 10%, regardless of which medication they used. This group represents treatment responders. In contrast, patients who discontinued, switched, or added a new agent to their initial medication showed stable or slightly increasing HbA_1c levels over time, which represented deteriorating glycemic control.

“These results strengthen the current evidence of a superior durability with metformin compared with sulfonylureas” in the real-world setting, and suggest that the same is true regarding meglitinide, Dr. Ekstrom and his associates said.

Aflibercept, a vascular endothelial growth factor (VEGF) inhibitor administered by intravitreal injection, is now approved for treating diabetic retinopathy in patients with diabetic macular edema (DME), the Food and Drug Administration announced on March 25.

Aflibercept was previously approved for treating wet (neovascular) age-related macular degeneration, and for treating DME and macular edema secondary to retinal vein occlusions, “both of which cause fluid to leak into the macula resulting in blurred vision,” according to the FDA statement announcing approval. The first five injections of aflibercept are administered once a month, followed by one injection every 2 months. Aflibercept is marketed as Eylea by Regeneron Pharmaceuticals; it was initially approved in 2011.

“Today’s approval gives patients with diabetic retinopathy and diabetic macular edema another therapy to treat this vision-impairing complication,” Dr. Edward Cox, director of the office of antimicrobial products in the FDA’s Center for Drug Evaluation and Research, said in the statement. In February, the FDA approved ranibizumab (Lucentis), another VEGF inhibitor, for the same indication.

Approval of aflibercept was based on two phase III studies of 679 patients with diabetic retinopathy and DME, who were randomized to treatment with aflibercept or macular laser photocoagulation. At 2 years, those treated with aflibercept “showed significant improvement in the severity of their diabetic retinopathy, compared to patients who did not receive Eylea,” according to the FDA statement. Conjunctival hemorrhage, eye pain, cataracts, vitreous floaters, increased intraocular pressure, and vitreous detachment were among the most common adverse events (reported by at least 5% of treated patients) associated with treatment. Endophthalmitis and retinal detachments were among the serious adverse events associated with treatment.

The two studies are the VISTA-DME and VIVID-DME trials, according to the Regeneron statement announcing approval.

Adverse events associated with aflibercept should be reported to the FDA’s MedWatch program at 800-332-1088 or www.fda.gov/medwatch.

[email protected]

Aflibercept, a vascular endothelial growth factor (VEGF) inhibitor administered by intravitreal injection, is now approved for treating diabetic retinopathy in patients with diabetic macular edema (DME), the Food and Drug Administration announced on March 25.

Aflibercept was previously approved for treating wet (neovascular) age-related macular degeneration, and for treating DME and macular edema secondary to retinal vein occlusions, “both of which cause fluid to leak into the macula resulting in blurred vision,” according to the FDA statement announcing approval. The first five injections of aflibercept are administered once a month, followed by one injection every 2 months. Aflibercept is marketed as Eylea by Regeneron Pharmaceuticals; it was initially approved in 2011.

“Today’s approval gives patients with diabetic retinopathy and diabetic macular edema another therapy to treat this vision-impairing complication,” Dr. Edward Cox, director of the office of antimicrobial products in the FDA’s Center for Drug Evaluation and Research, said in the statement. In February, the FDA approved ranibizumab (Lucentis), another VEGF inhibitor, for the same indication.

Approval of aflibercept was based on two phase III studies of 679 patients with diabetic retinopathy and DME, who were randomized to treatment with aflibercept or macular laser photocoagulation. At 2 years, those treated with aflibercept “showed significant improvement in the severity of their diabetic retinopathy, compared to patients who did not receive Eylea,” according to the FDA statement. Conjunctival hemorrhage, eye pain, cataracts, vitreous floaters, increased intraocular pressure, and vitreous detachment were among the most common adverse events (reported by at least 5% of treated patients) associated with treatment. Endophthalmitis and retinal detachments were among the serious adverse events associated with treatment.

The two studies are the VISTA-DME and VIVID-DME trials, according to the Regeneron statement announcing approval.

Adverse events associated with aflibercept should be reported to the FDA’s MedWatch program at 800-332-1088 or www.fda.gov/medwatch.

[email protected]

Aflibercept, a vascular endothelial growth factor (VEGF) inhibitor administered by intravitreal injection, is now approved for treating diabetic retinopathy in patients with diabetic macular edema (DME), the Food and Drug Administration announced on March 25.

Aflibercept was previously approved for treating wet (neovascular) age-related macular degeneration, and for treating DME and macular edema secondary to retinal vein occlusions, “both of which cause fluid to leak into the macula resulting in blurred vision,” according to the FDA statement announcing approval. The first five injections of aflibercept are administered once a month, followed by one injection every 2 months. Aflibercept is marketed as Eylea by Regeneron Pharmaceuticals; it was initially approved in 2011.

“Today’s approval gives patients with diabetic retinopathy and diabetic macular edema another therapy to treat this vision-impairing complication,” Dr. Edward Cox, director of the office of antimicrobial products in the FDA’s Center for Drug Evaluation and Research, said in the statement. In February, the FDA approved ranibizumab (Lucentis), another VEGF inhibitor, for the same indication.

Approval of aflibercept was based on two phase III studies of 679 patients with diabetic retinopathy and DME, who were randomized to treatment with aflibercept or macular laser photocoagulation. At 2 years, those treated with aflibercept “showed significant improvement in the severity of their diabetic retinopathy, compared to patients who did not receive Eylea,” according to the FDA statement. Conjunctival hemorrhage, eye pain, cataracts, vitreous floaters, increased intraocular pressure, and vitreous detachment were among the most common adverse events (reported by at least 5% of treated patients) associated with treatment. Endophthalmitis and retinal detachments were among the serious adverse events associated with treatment.

The two studies are the VISTA-DME and VIVID-DME trials, according to the Regeneron statement announcing approval.

Adverse events associated with aflibercept should be reported to the FDA’s MedWatch program at 800-332-1088 or www.fda.gov/medwatch.

[email protected]

More new diabetes patients are being diagnosed in states that have expanded their Medicaid programs under the Affordable Care Act, compared with states that chose not to expand, according to a study published online March 23 in Diabetes Care.

Dr. Harvey Kaufman, senior medical director at Quest Diagnostics, and his colleagues analyzed data from Quest Diagnostics’ corporate database of clinical laboratory services for the first 6 months of 2013 and the same period in 2014, identifying 215,398 with a new diagnosis of diabetes in 2013 and 218,890 in 2014. A total of 26,237 were enrolled in Medicaid in 2013 vs. 29,673 in 2014 – a 13% increase in overall new diagnoses of diabetes.

©Tashatuvango/Thinkstockphotos.com

The increase was greater – 23% – in the 26 states and the District of Columbia that had expanded their Medicaid programs. In states that had not expanded, the increase in newly diagnosed patients was 0.4% (Diabetes Care 2015 March 23 [doi: 10.2337/dc14-2334]).

“It is likely that changes in access to health care for patients with Medicaid contributed to testing for diabetes at an earlier stage of disease,” Dr. Kaufman wrote .

Access to health care also identified patients at earlier stages of diabetes, as evidenced by diagnosis at a lower mean hemoglobin A_1c level. In states with expanded Medicaid programs, mean HbA_1c was 7.96 at diagnosis, compared to 8.14 in states without expanded Medicaid programs.

“These Medicaid patients with newly identified diabetes will experience better management of their diabetes than if diagnosis had been made later,” Dr.Kaufman wrote. “This could be anticipated to lead to fewer long-term complications.”

[email protected]

More new diabetes patients are being diagnosed in states that have expanded their Medicaid programs under the Affordable Care Act, compared with states that chose not to expand, according to a study published online March 23 in Diabetes Care.

Dr. Harvey Kaufman, senior medical director at Quest Diagnostics, and his colleagues analyzed data from Quest Diagnostics’ corporate database of clinical laboratory services for the first 6 months of 2013 and the same period in 2014, identifying 215,398 with a new diagnosis of diabetes in 2013 and 218,890 in 2014. A total of 26,237 were enrolled in Medicaid in 2013 vs. 29,673 in 2014 – a 13% increase in overall new diagnoses of diabetes.

©Tashatuvango/Thinkstockphotos.com

The increase was greater – 23% – in the 26 states and the District of Columbia that had expanded their Medicaid programs. In states that had not expanded, the increase in newly diagnosed patients was 0.4% (Diabetes Care 2015 March 23 [doi: 10.2337/dc14-2334]).

“It is likely that changes in access to health care for patients with Medicaid contributed to testing for diabetes at an earlier stage of disease,” Dr. Kaufman wrote .

Access to health care also identified patients at earlier stages of diabetes, as evidenced by diagnosis at a lower mean hemoglobin A_1c level. In states with expanded Medicaid programs, mean HbA_1c was 7.96 at diagnosis, compared to 8.14 in states without expanded Medicaid programs.

“These Medicaid patients with newly identified diabetes will experience better management of their diabetes than if diagnosis had been made later,” Dr.Kaufman wrote. “This could be anticipated to lead to fewer long-term complications.”

[email protected]

More new diabetes patients are being diagnosed in states that have expanded their Medicaid programs under the Affordable Care Act, compared with states that chose not to expand, according to a study published online March 23 in Diabetes Care.

Dr. Harvey Kaufman, senior medical director at Quest Diagnostics, and his colleagues analyzed data from Quest Diagnostics’ corporate database of clinical laboratory services for the first 6 months of 2013 and the same period in 2014, identifying 215,398 with a new diagnosis of diabetes in 2013 and 218,890 in 2014. A total of 26,237 were enrolled in Medicaid in 2013 vs. 29,673 in 2014 – a 13% increase in overall new diagnoses of diabetes.

©Tashatuvango/Thinkstockphotos.com

The increase was greater – 23% – in the 26 states and the District of Columbia that had expanded their Medicaid programs. In states that had not expanded, the increase in newly diagnosed patients was 0.4% (Diabetes Care 2015 March 23 [doi: 10.2337/dc14-2334]).

“It is likely that changes in access to health care for patients with Medicaid contributed to testing for diabetes at an earlier stage of disease,” Dr. Kaufman wrote .

Access to health care also identified patients at earlier stages of diabetes, as evidenced by diagnosis at a lower mean hemoglobin A_1c level. In states with expanded Medicaid programs, mean HbA_1c was 7.96 at diagnosis, compared to 8.14 in states without expanded Medicaid programs.

“These Medicaid patients with newly identified diabetes will experience better management of their diabetes than if diagnosis had been made later,” Dr.Kaufman wrote. “This could be anticipated to lead to fewer long-term complications.”

[email protected]

In these days of struggles over obesity, it may be hard to remember that being too thin may be a bigger health threat than being too fat. Anorexia nervosa is a very serious but hidden disorder in which the person has a relentless pursuit of thinness, is unwilling to maintain a healthy weight, has distorted body image and intense fear of gaining weight, disturbed eating behavior, and, in girls, amenorrhea.

Anorexia nervosa is actually the third-leading chronic illness in adolescent females and has a mortality rate as high as 20% – one-third by suicide. Boys are not only not immune, but also are even more difficult to suspect and detect. While most affected children improve with behavioral treatment, anorexia nervosa severe enough to warrant hospitalization can result in permanent damage to bones, heart, and brain.

I refer to these patients as “children” here, but you may rightly associate anorexia with adolescents: 43% of those affected had onset at 16-20 years and 86% by 20 years. But listen to this disturbing statistic: 42% of 1st-3rd grade girls report that they want to be thinner and 81% of 10-year-olds are “afraid” of being fat. Over half of teen girls and one-third of boys skip meals, fast, smoke cigarettes, vomit, or take laxatives to control weight – ineffective practices that can lead to eating disorders. Healthy foods and exercise may seem too slow or difficult ways to control weight.

Even with a prevalence of 0.5% you may be wondering, “Gee, I haven’t seen anyone with that for years!” But you probably have been seeing children with the most common presentations of anorexia, which are concerns over complications rather than a request for help with excess weight loss. These are usually complaints about abdominal pain, bloating, or constipation, but may be about headaches, amenorrhea, or feeling faint. You may see them for the first time after an intercurrent illness such as viral gastroenteritis or mononucleosis that sends their emaciated bodies over the edge. Do those patients sound more familiar?

Anorexia nervosa works its damage from starvation and purging behaviors. Any system of the body can be affected from starvation, ranging from suppression of bone marrow with anemia, low white count, and low platelets; endocrine suppression with low TSH and T4 and amenorrhea; cardiomyopathy with resulting mitral valve prolapse, arrhythmias, and syncope; or even seizures and brain atrophy. Depression and anxiety are pretty inevitable when one is starving but, while comorbid, their primacy or severity really can’t be assessed until the starvation state is resolved.

Why aren’t the affected children worried about these serious complications? Actually, they may be worried when they find out about them, but their first fear is about getting fat. Characteristic of anorexia is a distorted body image that nags at them incessantly to lose weight. In U.S. culture, weight loss and fitness ads are all around us, making this concern seem quite normal or even more urgent. They may even panic and get angry if their excessive exercise routine is interrupted. The missing link is that they can’t see that they are not overweight, instead fearing being fat.

Many children with anorexia have tried to stop their dieting but failed. They may be ashamed, embarrassed, or worried about being stigmatized if they are found out. But they often feel that they are on the right path for themselves. At best they are ambivalent about being detected and pushed into treatment. So they get really good at hiding their condition, sometimes getting new ideas online. Common strategies to evade detection include eating apart from the family, saying they are “not hungry now” or even cooking for others but not eating themselves. They wear baggy clothes to hide their emaciation. They often exercise to an extreme, in any weather, whether sick or well. When it is time to be weighed they may drink quarts of water and fill pockets with stones so their true weight loss is not evident.

Actions children take for weight control or loss create much of the morbidity. Most common are use of laxatives and diuretics that can result in fatal electrolyte imbalances and arrhythmias. Purging in anorexia and also in bulimia nervosa can result in gastroesophageal reflux disease, esophageal tears, and bleeding. Self-induced vomiting also destroys tooth enamel, fosters cavities, and can cause scars of palate or knuckles from forcing their hand down their throat. Hypoglycemia from severe restriction can even result in seizures.

When your patients have those metabolic and physical signs, you are not likely to be tricked into thinking all is well. But those athletes in your practice, of whom you and the parents are so proud, can sneak up on you. Those participating in individual “aesthetic” sports such as dance, figure skating, and gymnastics are especially vulnerable to (and rewarded by) extreme thinness. They have been coached to be slim. But to make it worse, the most elite athletes also often have personalities that make extreme weight control possible including perfectionism, competitiveness, compulsiveness, drive, and high activity level.

Parents of children with anorexia may be ambivalent, also, as they see their child eating healthy foods and exercising as they have encouraged them to do. It is not so clear when they have gone too far. But 35% of “normal dieters” go on to pathological dieting and, of those, 20%-25% develop eating disorders of varying degree.

As with most disorders, earlier detection of anorexia symptoms can allow for an easier treatment course and fewer long-term complications. So, when should you be thinking and asking about abnormal eating? Certainly, it is time to ask questions when a child is not gaining weight appropriately, is losing weight to below 15% of appropriate weight for height, or has 3 or more months of amenorrhea. But also consider it when you hear complaints of abdominal pain, headache, or feeling faint that you can’t explain. Ask directly “What would you like to weigh?” A desired weight that would give a body mass index (BMI) of <19 kg/m² is nearly diagnostic. Also ask them to, “Tell me what you eat at each meal on a typical day,” looking for extremely low-calorie bizarre choices such as all lettuce, and “How much exercise do you do daily?” Be specific in collecting information about dieting, binging, self-induced vomiting, and use of laxatives, diuretics, or diet pills for weight control. Asking family members what they have observed about the child’s exercise, dieting, and statements about body image gives even more objective information that the child may try to obscure.

Specific screening self report tools such as the SCOFF questionnaire and Patient Health Questionnaire – Adolescents (PHQ-A) used for all teens or those with signs of weight loss are both a way to get more accurate information and a valuable point of conversation.

When you detect signs and symptoms, the initial work up should include complete blood count, electrolytes, liver function, thyroid-stimulating hormone, and urinalysis, but most importantly an accurate height, weight, and BMI measured in underwear in a gown. Amenorrhea may require endocrine tests as well. While malignancy, endocrine and gastrointestinal disorders are in the differential, characteristic history, physical exam, and lab results will point to the diagnosis. If there is bradycardia or low potassium, chloride, or sodium, an electrocardiogram and hospitalization are urgent as these are the harbingers of life-threatening arrhythmias that are the most common cause of death.

So when you suspect anorexia, you may be facing a difficult-to-detect, life-threatening condition with resistant patients and even reluctant parents. While you may be able to make a contract for biweekly weigh-ins and coaching for subclinical anorexia not otherwise specified, a team will be needed in most full-blown cases. Eating disorder programs are often part of departments of psychiatry, but adolescent specialists also may have assembled needed teams.

Dr. Howard is assistant professor of pediatrics at the Johns Hopkins University School of Medicine, Baltimore, and creator of CHADIS. She has no other relevant disclosures. Dr. Howard’s contribution to this publication was as a paid expert to Frontline. E-mail her at [email protected].

In these days of struggles over obesity, it may be hard to remember that being too thin may be a bigger health threat than being too fat. Anorexia nervosa is a very serious but hidden disorder in which the person has a relentless pursuit of thinness, is unwilling to maintain a healthy weight, has distorted body image and intense fear of gaining weight, disturbed eating behavior, and, in girls, amenorrhea.

Anorexia nervosa is actually the third-leading chronic illness in adolescent females and has a mortality rate as high as 20% – one-third by suicide. Boys are not only not immune, but also are even more difficult to suspect and detect. While most affected children improve with behavioral treatment, anorexia nervosa severe enough to warrant hospitalization can result in permanent damage to bones, heart, and brain.

I refer to these patients as “children” here, but you may rightly associate anorexia with adolescents: 43% of those affected had onset at 16-20 years and 86% by 20 years. But listen to this disturbing statistic: 42% of 1st-3rd grade girls report that they want to be thinner and 81% of 10-year-olds are “afraid” of being fat. Over half of teen girls and one-third of boys skip meals, fast, smoke cigarettes, vomit, or take laxatives to control weight – ineffective practices that can lead to eating disorders. Healthy foods and exercise may seem too slow or difficult ways to control weight.

Even with a prevalence of 0.5% you may be wondering, “Gee, I haven’t seen anyone with that for years!” But you probably have been seeing children with the most common presentations of anorexia, which are concerns over complications rather than a request for help with excess weight loss. These are usually complaints about abdominal pain, bloating, or constipation, but may be about headaches, amenorrhea, or feeling faint. You may see them for the first time after an intercurrent illness such as viral gastroenteritis or mononucleosis that sends their emaciated bodies over the edge. Do those patients sound more familiar?

Anorexia nervosa works its damage from starvation and purging behaviors. Any system of the body can be affected from starvation, ranging from suppression of bone marrow with anemia, low white count, and low platelets; endocrine suppression with low TSH and T4 and amenorrhea; cardiomyopathy with resulting mitral valve prolapse, arrhythmias, and syncope; or even seizures and brain atrophy. Depression and anxiety are pretty inevitable when one is starving but, while comorbid, their primacy or severity really can’t be assessed until the starvation state is resolved.

Why aren’t the affected children worried about these serious complications? Actually, they may be worried when they find out about them, but their first fear is about getting fat. Characteristic of anorexia is a distorted body image that nags at them incessantly to lose weight. In U.S. culture, weight loss and fitness ads are all around us, making this concern seem quite normal or even more urgent. They may even panic and get angry if their excessive exercise routine is interrupted. The missing link is that they can’t see that they are not overweight, instead fearing being fat.

Many children with anorexia have tried to stop their dieting but failed. They may be ashamed, embarrassed, or worried about being stigmatized if they are found out. But they often feel that they are on the right path for themselves. At best they are ambivalent about being detected and pushed into treatment. So they get really good at hiding their condition, sometimes getting new ideas online. Common strategies to evade detection include eating apart from the family, saying they are “not hungry now” or even cooking for others but not eating themselves. They wear baggy clothes to hide their emaciation. They often exercise to an extreme, in any weather, whether sick or well. When it is time to be weighed they may drink quarts of water and fill pockets with stones so their true weight loss is not evident.

Actions children take for weight control or loss create much of the morbidity. Most common are use of laxatives and diuretics that can result in fatal electrolyte imbalances and arrhythmias. Purging in anorexia and also in bulimia nervosa can result in gastroesophageal reflux disease, esophageal tears, and bleeding. Self-induced vomiting also destroys tooth enamel, fosters cavities, and can cause scars of palate or knuckles from forcing their hand down their throat. Hypoglycemia from severe restriction can even result in seizures.

When your patients have those metabolic and physical signs, you are not likely to be tricked into thinking all is well. But those athletes in your practice, of whom you and the parents are so proud, can sneak up on you. Those participating in individual “aesthetic” sports such as dance, figure skating, and gymnastics are especially vulnerable to (and rewarded by) extreme thinness. They have been coached to be slim. But to make it worse, the most elite athletes also often have personalities that make extreme weight control possible including perfectionism, competitiveness, compulsiveness, drive, and high activity level.

Parents of children with anorexia may be ambivalent, also, as they see their child eating healthy foods and exercising as they have encouraged them to do. It is not so clear when they have gone too far. But 35% of “normal dieters” go on to pathological dieting and, of those, 20%-25% develop eating disorders of varying degree.

As with most disorders, earlier detection of anorexia symptoms can allow for an easier treatment course and fewer long-term complications. So, when should you be thinking and asking about abnormal eating? Certainly, it is time to ask questions when a child is not gaining weight appropriately, is losing weight to below 15% of appropriate weight for height, or has 3 or more months of amenorrhea. But also consider it when you hear complaints of abdominal pain, headache, or feeling faint that you can’t explain. Ask directly “What would you like to weigh?” A desired weight that would give a body mass index (BMI) of <19 kg/m² is nearly diagnostic. Also ask them to, “Tell me what you eat at each meal on a typical day,” looking for extremely low-calorie bizarre choices such as all lettuce, and “How much exercise do you do daily?” Be specific in collecting information about dieting, binging, self-induced vomiting, and use of laxatives, diuretics, or diet pills for weight control. Asking family members what they have observed about the child’s exercise, dieting, and statements about body image gives even more objective information that the child may try to obscure.

Specific screening self report tools such as the SCOFF questionnaire and Patient Health Questionnaire – Adolescents (PHQ-A) used for all teens or those with signs of weight loss are both a way to get more accurate information and a valuable point of conversation.

When you detect signs and symptoms, the initial work up should include complete blood count, electrolytes, liver function, thyroid-stimulating hormone, and urinalysis, but most importantly an accurate height, weight, and BMI measured in underwear in a gown. Amenorrhea may require endocrine tests as well. While malignancy, endocrine and gastrointestinal disorders are in the differential, characteristic history, physical exam, and lab results will point to the diagnosis. If there is bradycardia or low potassium, chloride, or sodium, an electrocardiogram and hospitalization are urgent as these are the harbingers of life-threatening arrhythmias that are the most common cause of death.

So when you suspect anorexia, you may be facing a difficult-to-detect, life-threatening condition with resistant patients and even reluctant parents. While you may be able to make a contract for biweekly weigh-ins and coaching for subclinical anorexia not otherwise specified, a team will be needed in most full-blown cases. Eating disorder programs are often part of departments of psychiatry, but adolescent specialists also may have assembled needed teams.

Dr. Howard is assistant professor of pediatrics at the Johns Hopkins University School of Medicine, Baltimore, and creator of CHADIS. She has no other relevant disclosures. Dr. Howard’s contribution to this publication was as a paid expert to Frontline. E-mail her at [email protected].

In these days of struggles over obesity, it may be hard to remember that being too thin may be a bigger health threat than being too fat. Anorexia nervosa is a very serious but hidden disorder in which the person has a relentless pursuit of thinness, is unwilling to maintain a healthy weight, has distorted body image and intense fear of gaining weight, disturbed eating behavior, and, in girls, amenorrhea.

Anorexia nervosa is actually the third-leading chronic illness in adolescent females and has a mortality rate as high as 20% – one-third by suicide. Boys are not only not immune, but also are even more difficult to suspect and detect. While most affected children improve with behavioral treatment, anorexia nervosa severe enough to warrant hospitalization can result in permanent damage to bones, heart, and brain.

I refer to these patients as “children” here, but you may rightly associate anorexia with adolescents: 43% of those affected had onset at 16-20 years and 86% by 20 years. But listen to this disturbing statistic: 42% of 1st-3rd grade girls report that they want to be thinner and 81% of 10-year-olds are “afraid” of being fat. Over half of teen girls and one-third of boys skip meals, fast, smoke cigarettes, vomit, or take laxatives to control weight – ineffective practices that can lead to eating disorders. Healthy foods and exercise may seem too slow or difficult ways to control weight.

Even with a prevalence of 0.5% you may be wondering, “Gee, I haven’t seen anyone with that for years!” But you probably have been seeing children with the most common presentations of anorexia, which are concerns over complications rather than a request for help with excess weight loss. These are usually complaints about abdominal pain, bloating, or constipation, but may be about headaches, amenorrhea, or feeling faint. You may see them for the first time after an intercurrent illness such as viral gastroenteritis or mononucleosis that sends their emaciated bodies over the edge. Do those patients sound more familiar?

Anorexia nervosa works its damage from starvation and purging behaviors. Any system of the body can be affected from starvation, ranging from suppression of bone marrow with anemia, low white count, and low platelets; endocrine suppression with low TSH and T4 and amenorrhea; cardiomyopathy with resulting mitral valve prolapse, arrhythmias, and syncope; or even seizures and brain atrophy. Depression and anxiety are pretty inevitable when one is starving but, while comorbid, their primacy or severity really can’t be assessed until the starvation state is resolved.

Why aren’t the affected children worried about these serious complications? Actually, they may be worried when they find out about them, but their first fear is about getting fat. Characteristic of anorexia is a distorted body image that nags at them incessantly to lose weight. In U.S. culture, weight loss and fitness ads are all around us, making this concern seem quite normal or even more urgent. They may even panic and get angry if their excessive exercise routine is interrupted. The missing link is that they can’t see that they are not overweight, instead fearing being fat.

Many children with anorexia have tried to stop their dieting but failed. They may be ashamed, embarrassed, or worried about being stigmatized if they are found out. But they often feel that they are on the right path for themselves. At best they are ambivalent about being detected and pushed into treatment. So they get really good at hiding their condition, sometimes getting new ideas online. Common strategies to evade detection include eating apart from the family, saying they are “not hungry now” or even cooking for others but not eating themselves. They wear baggy clothes to hide their emaciation. They often exercise to an extreme, in any weather, whether sick or well. When it is time to be weighed they may drink quarts of water and fill pockets with stones so their true weight loss is not evident.

Actions children take for weight control or loss create much of the morbidity. Most common are use of laxatives and diuretics that can result in fatal electrolyte imbalances and arrhythmias. Purging in anorexia and also in bulimia nervosa can result in gastroesophageal reflux disease, esophageal tears, and bleeding. Self-induced vomiting also destroys tooth enamel, fosters cavities, and can cause scars of palate or knuckles from forcing their hand down their throat. Hypoglycemia from severe restriction can even result in seizures.

When your patients have those metabolic and physical signs, you are not likely to be tricked into thinking all is well. But those athletes in your practice, of whom you and the parents are so proud, can sneak up on you. Those participating in individual “aesthetic” sports such as dance, figure skating, and gymnastics are especially vulnerable to (and rewarded by) extreme thinness. They have been coached to be slim. But to make it worse, the most elite athletes also often have personalities that make extreme weight control possible including perfectionism, competitiveness, compulsiveness, drive, and high activity level.

Parents of children with anorexia may be ambivalent, also, as they see their child eating healthy foods and exercising as they have encouraged them to do. It is not so clear when they have gone too far. But 35% of “normal dieters” go on to pathological dieting and, of those, 20%-25% develop eating disorders of varying degree.

As with most disorders, earlier detection of anorexia symptoms can allow for an easier treatment course and fewer long-term complications. So, when should you be thinking and asking about abnormal eating? Certainly, it is time to ask questions when a child is not gaining weight appropriately, is losing weight to below 15% of appropriate weight for height, or has 3 or more months of amenorrhea. But also consider it when you hear complaints of abdominal pain, headache, or feeling faint that you can’t explain. Ask directly “What would you like to weigh?” A desired weight that would give a body mass index (BMI) of <19 kg/m² is nearly diagnostic. Also ask them to, “Tell me what you eat at each meal on a typical day,” looking for extremely low-calorie bizarre choices such as all lettuce, and “How much exercise do you do daily?” Be specific in collecting information about dieting, binging, self-induced vomiting, and use of laxatives, diuretics, or diet pills for weight control. Asking family members what they have observed about the child’s exercise, dieting, and statements about body image gives even more objective information that the child may try to obscure.

Specific screening self report tools such as the SCOFF questionnaire and Patient Health Questionnaire – Adolescents (PHQ-A) used for all teens or those with signs of weight loss are both a way to get more accurate information and a valuable point of conversation.

When you detect signs and symptoms, the initial work up should include complete blood count, electrolytes, liver function, thyroid-stimulating hormone, and urinalysis, but most importantly an accurate height, weight, and BMI measured in underwear in a gown. Amenorrhea may require endocrine tests as well. While malignancy, endocrine and gastrointestinal disorders are in the differential, characteristic history, physical exam, and lab results will point to the diagnosis. If there is bradycardia or low potassium, chloride, or sodium, an electrocardiogram and hospitalization are urgent as these are the harbingers of life-threatening arrhythmias that are the most common cause of death.

So when you suspect anorexia, you may be facing a difficult-to-detect, life-threatening condition with resistant patients and even reluctant parents. While you may be able to make a contract for biweekly weigh-ins and coaching for subclinical anorexia not otherwise specified, a team will be needed in most full-blown cases. Eating disorder programs are often part of departments of psychiatry, but adolescent specialists also may have assembled needed teams.

Dr. Howard is assistant professor of pediatrics at the Johns Hopkins University School of Medicine, Baltimore, and creator of CHADIS. She has no other relevant disclosures. Dr. Howard’s contribution to this publication was as a paid expert to Frontline. E-mail her at [email protected].

Humans can host up to 6 pounds of microbes in our gut alone. We comprise about 10 trillion human cells – they comprise 100 trillion bacterial cells. Their genetic material outstrips us even more impressively – we are the product of 20,000 human genes. But inside our gut, we carry up to 2 million microbial genes.

Emerging research suggests that these complex communities – which interact fluidly not only with their human host, but also with each other – play important roles in health and disease. They appear to confer both protection from and risk for many chronic illnesses, from asthma and allergies to obesity and diabetes.

And what we don’t know about them dwarfs what we do know, according to Dr. Robert Ratner, the chief medical officer of the American Diabetes Association.

“We’re literally at the forefront of an unknown universe,” Dr. Ratner said at the annual advanced postgraduate course held by the ADA. “Research into the microbiome and how it interacts with human health is one of our most intriguing investigations.”

The microbiome is as vastly individual as every person who carries it. The differences are myriad, in the amount and variety of species, and in the sheer numbers of microbes that make up each community. Each region of the gut, from mouth to rectum, hosts a completely different population.

Two main phyla populate the gut: Bacteroidetes, which are involved in protein and carbohydrate breakdown, and Firmicutes, which promote the absorption of fat. The ratios of these communities, however, has changed over the last 30 years, diverging along a path that mirrors global spikes in obesity, diabetes, and allergic and inflammatory disorders.

“We have seen dramatic increases worldwide in these disorders,” Dr. Ratner said. “We’ve also seen decreased diversity of the microbiome, with a progressive change in density from Bacteroidetes to Firmicutes. These are associations – not causations – but I think the time has come to ask ‘What are we doing to change these bacteria?’ ”

The rampant use of antibiotics is the first place suspicion falls – and it’s no wonder, since the epidemiologic changes Dr. Ratner described began to appear shortly after World War II. Antibiotics could exert their flora-changing effects a couple of ways, he noted.

They directly alter the composition of communities in the person who consumes the drug, even if just in the short-term. There is someevidence that early-life antibiotics, though changing the microbiome only temporarily, can change fat metabolism for the entire lifespan (Cell 2014;158:705-21).

The associations between an altered gut microbiome and long-term health is unproven. But a picture does seem to emerge when viewed in light of the exponential increases in obesity and its attendant rise in diabetes.

The Type 1 Diabetes Prediction and Prevention Project (DIPP) is an effort to predict and search for means to delay or prevent type 1 diabetes. Launched in 1994, it’s following a cohort of children who had genetic risk factors for type 1 diabetes. Data have consistently shown that those who develop the disease have significantly lower diversity in their gut flora, Dr. Ratner said. Certain species of Bacteroides increased the risk of autoimmunity by up to 20 times.

Again, he said, this is association, not causation. But some very new evidence suggests that these are functional, not just observational, links. “It does now appear that our microbes are actually controlling our metabolism,” he said. “Some of these species liberate lipopolysaccharides, which function as endotoxins. These cross the mucosal barrier in the intestine, enter the interstitial space, and set up an inflammation that impacts the liver and adipocytes, potentially decreasing insulin sensitivity.”

Unpublished data from the laboratory of Dr. Martin J. Blaser at New York University show for the first time that a specific bacterium can cause diabetes, and removing it cures the disease. The bacterium in question, Ralstonia, is a gram-negative pathogen that contaminates drinking water. Mice engineered as a model of prediabetes gained much more weight when they consumed live Ralstonia than when they got a heat-inactivated version. They also developed insulin resistance and hyperglycemia in the presence of the live version. But when the same mice were given a Ralstonia antibody, they lost weight and their glycemic profile normalized.

“This is the first direct evidence we have of causality,” Dr. Ratner said.

Strong evidence of causation is also emerging in the surgical realm. Roux-en-Y gastric bypass seems to change the microbiome in a way that facilitates weight loss, beyond caloric intake.Randy Seeley, Ph.D., of the University of Michigan, Ann Arbor, has been studying how weight-loss surgery affects the microbiome. He theorizes that the physical manipulation of the gut induces what he calls “enteroplasticity” – a fluid adaptation of both the gut’s structure and its bacterial communities to the altered physical and chemical environment. “There’s more going on during postsurgical weight loss than just food restriction and malabsorption,” Dr. Seeley said in an interview. “It’s logical to think that when you do this kind of surgery, the microbes in the intestine will change.”

Roseburia intestinalis is a Firmicute that typically increases after bariatric surgery. It’s also found to be deficient in people who have diabetes. Dr. Seeley coauthored an article showing that Roseburia and other beneficial firmicutes increased significantly in mice that underwent vertical sleeve gastrectomy (Nature 2014;509:183-8). These mice lost weight after surgery, as would be expected, but then showed a preference for the high-protein and carbohydrate-rich foods that Firmicutes need. Their microbiome also showed decreases in the concentration of fat-loving Bacteroides species.

But interestingly, weight loss and microbiome improvement happened only in mice that had a normal bile acid–signaling system. Immediately after surgery, mice engineered to lack bile acid receptors did eat less and lose weight. But a week later, their appetites came back full force, and they actually seemed driven to eat fat. They quickly returned to their presurgical weight. Their microbiome didn’t show the same improvement as their cousins with normal signaling pathways, suggesting that a complex interaction between bacteria and the gut’s physical alteration may be driving weight loss.

“Is weight-loss surgery, then, fixing this ‘broken’ component of the microbiome?” Dr. Seeley asked. “Is Roseburia the causal agent of improvement? Or is it a marker of improvement in an entire community? I would say it’s probably the entire community changing, and changing its interaction with its host organism.”

Dr. Seeley disclosed that he has received financial support from Johnson & Johnson, Novo Nordisk, and Eisai.

[email protected]

On Twitter @alz_gal

Humans can host up to 6 pounds of microbes in our gut alone. We comprise about 10 trillion human cells – they comprise 100 trillion bacterial cells. Their genetic material outstrips us even more impressively – we are the product of 20,000 human genes. But inside our gut, we carry up to 2 million microbial genes.

Emerging research suggests that these complex communities – which interact fluidly not only with their human host, but also with each other – play important roles in health and disease. They appear to confer both protection from and risk for many chronic illnesses, from asthma and allergies to obesity and diabetes.

And what we don’t know about them dwarfs what we do know, according to Dr. Robert Ratner, the chief medical officer of the American Diabetes Association.

“We’re literally at the forefront of an unknown universe,” Dr. Ratner said at the annual advanced postgraduate course held by the ADA. “Research into the microbiome and how it interacts with human health is one of our most intriguing investigations.”

The microbiome is as vastly individual as every person who carries it. The differences are myriad, in the amount and variety of species, and in the sheer numbers of microbes that make up each community. Each region of the gut, from mouth to rectum, hosts a completely different population.

Two main phyla populate the gut: Bacteroidetes, which are involved in protein and carbohydrate breakdown, and Firmicutes, which promote the absorption of fat. The ratios of these communities, however, has changed over the last 30 years, diverging along a path that mirrors global spikes in obesity, diabetes, and allergic and inflammatory disorders.

“We have seen dramatic increases worldwide in these disorders,” Dr. Ratner said. “We’ve also seen decreased diversity of the microbiome, with a progressive change in density from Bacteroidetes to Firmicutes. These are associations – not causations – but I think the time has come to ask ‘What are we doing to change these bacteria?’ ”

The rampant use of antibiotics is the first place suspicion falls – and it’s no wonder, since the epidemiologic changes Dr. Ratner described began to appear shortly after World War II. Antibiotics could exert their flora-changing effects a couple of ways, he noted.

They directly alter the composition of communities in the person who consumes the drug, even if just in the short-term. There is someevidence that early-life antibiotics, though changing the microbiome only temporarily, can change fat metabolism for the entire lifespan (Cell 2014;158:705-21).

The associations between an altered gut microbiome and long-term health is unproven. But a picture does seem to emerge when viewed in light of the exponential increases in obesity and its attendant rise in diabetes.

The Type 1 Diabetes Prediction and Prevention Project (DIPP) is an effort to predict and search for means to delay or prevent type 1 diabetes. Launched in 1994, it’s following a cohort of children who had genetic risk factors for type 1 diabetes. Data have consistently shown that those who develop the disease have significantly lower diversity in their gut flora, Dr. Ratner said. Certain species of Bacteroides increased the risk of autoimmunity by up to 20 times.

Again, he said, this is association, not causation. But some very new evidence suggests that these are functional, not just observational, links. “It does now appear that our microbes are actually controlling our metabolism,” he said. “Some of these species liberate lipopolysaccharides, which function as endotoxins. These cross the mucosal barrier in the intestine, enter the interstitial space, and set up an inflammation that impacts the liver and adipocytes, potentially decreasing insulin sensitivity.”

Unpublished data from the laboratory of Dr. Martin J. Blaser at New York University show for the first time that a specific bacterium can cause diabetes, and removing it cures the disease. The bacterium in question, Ralstonia, is a gram-negative pathogen that contaminates drinking water. Mice engineered as a model of prediabetes gained much more weight when they consumed live Ralstonia than when they got a heat-inactivated version. They also developed insulin resistance and hyperglycemia in the presence of the live version. But when the same mice were given a Ralstonia antibody, they lost weight and their glycemic profile normalized.

“This is the first direct evidence we have of causality,” Dr. Ratner said.

Strong evidence of causation is also emerging in the surgical realm. Roux-en-Y gastric bypass seems to change the microbiome in a way that facilitates weight loss, beyond caloric intake.Randy Seeley, Ph.D., of the University of Michigan, Ann Arbor, has been studying how weight-loss surgery affects the microbiome. He theorizes that the physical manipulation of the gut induces what he calls “enteroplasticity” – a fluid adaptation of both the gut’s structure and its bacterial communities to the altered physical and chemical environment. “There’s more going on during postsurgical weight loss than just food restriction and malabsorption,” Dr. Seeley said in an interview. “It’s logical to think that when you do this kind of surgery, the microbes in the intestine will change.”

Roseburia intestinalis is a Firmicute that typically increases after bariatric surgery. It’s also found to be deficient in people who have diabetes. Dr. Seeley coauthored an article showing that Roseburia and other beneficial firmicutes increased significantly in mice that underwent vertical sleeve gastrectomy (Nature 2014;509:183-8). These mice lost weight after surgery, as would be expected, but then showed a preference for the high-protein and carbohydrate-rich foods that Firmicutes need. Their microbiome also showed decreases in the concentration of fat-loving Bacteroides species.

But interestingly, weight loss and microbiome improvement happened only in mice that had a normal bile acid–signaling system. Immediately after surgery, mice engineered to lack bile acid receptors did eat less and lose weight. But a week later, their appetites came back full force, and they actually seemed driven to eat fat. They quickly returned to their presurgical weight. Their microbiome didn’t show the same improvement as their cousins with normal signaling pathways, suggesting that a complex interaction between bacteria and the gut’s physical alteration may be driving weight loss.

“Is weight-loss surgery, then, fixing this ‘broken’ component of the microbiome?” Dr. Seeley asked. “Is Roseburia the causal agent of improvement? Or is it a marker of improvement in an entire community? I would say it’s probably the entire community changing, and changing its interaction with its host organism.”

Dr. Seeley disclosed that he has received financial support from Johnson & Johnson, Novo Nordisk, and Eisai.

[email protected]

On Twitter @alz_gal

Humans can host up to 6 pounds of microbes in our gut alone. We comprise about 10 trillion human cells – they comprise 100 trillion bacterial cells. Their genetic material outstrips us even more impressively – we are the product of 20,000 human genes. But inside our gut, we carry up to 2 million microbial genes.

Emerging research suggests that these complex communities – which interact fluidly not only with their human host, but also with each other – play important roles in health and disease. They appear to confer both protection from and risk for many chronic illnesses, from asthma and allergies to obesity and diabetes.

And what we don’t know about them dwarfs what we do know, according to Dr. Robert Ratner, the chief medical officer of the American Diabetes Association.

“We’re literally at the forefront of an unknown universe,” Dr. Ratner said at the annual advanced postgraduate course held by the ADA. “Research into the microbiome and how it interacts with human health is one of our most intriguing investigations.”

The microbiome is as vastly individual as every person who carries it. The differences are myriad, in the amount and variety of species, and in the sheer numbers of microbes that make up each community. Each region of the gut, from mouth to rectum, hosts a completely different population.

Two main phyla populate the gut: Bacteroidetes, which are involved in protein and carbohydrate breakdown, and Firmicutes, which promote the absorption of fat. The ratios of these communities, however, has changed over the last 30 years, diverging along a path that mirrors global spikes in obesity, diabetes, and allergic and inflammatory disorders.

“We have seen dramatic increases worldwide in these disorders,” Dr. Ratner said. “We’ve also seen decreased diversity of the microbiome, with a progressive change in density from Bacteroidetes to Firmicutes. These are associations – not causations – but I think the time has come to ask ‘What are we doing to change these bacteria?’ ”

The rampant use of antibiotics is the first place suspicion falls – and it’s no wonder, since the epidemiologic changes Dr. Ratner described began to appear shortly after World War II. Antibiotics could exert their flora-changing effects a couple of ways, he noted.

They directly alter the composition of communities in the person who consumes the drug, even if just in the short-term. There is someevidence that early-life antibiotics, though changing the microbiome only temporarily, can change fat metabolism for the entire lifespan (Cell 2014;158:705-21).

The associations between an altered gut microbiome and long-term health is unproven. But a picture does seem to emerge when viewed in light of the exponential increases in obesity and its attendant rise in diabetes.

The Type 1 Diabetes Prediction and Prevention Project (DIPP) is an effort to predict and search for means to delay or prevent type 1 diabetes. Launched in 1994, it’s following a cohort of children who had genetic risk factors for type 1 diabetes. Data have consistently shown that those who develop the disease have significantly lower diversity in their gut flora, Dr. Ratner said. Certain species of Bacteroides increased the risk of autoimmunity by up to 20 times.

Again, he said, this is association, not causation. But some very new evidence suggests that these are functional, not just observational, links. “It does now appear that our microbes are actually controlling our metabolism,” he said. “Some of these species liberate lipopolysaccharides, which function as endotoxins. These cross the mucosal barrier in the intestine, enter the interstitial space, and set up an inflammation that impacts the liver and adipocytes, potentially decreasing insulin sensitivity.”

Unpublished data from the laboratory of Dr. Martin J. Blaser at New York University show for the first time that a specific bacterium can cause diabetes, and removing it cures the disease. The bacterium in question, Ralstonia, is a gram-negative pathogen that contaminates drinking water. Mice engineered as a model of prediabetes gained much more weight when they consumed live Ralstonia than when they got a heat-inactivated version. They also developed insulin resistance and hyperglycemia in the presence of the live version. But when the same mice were given a Ralstonia antibody, they lost weight and their glycemic profile normalized.

“This is the first direct evidence we have of causality,” Dr. Ratner said.

Strong evidence of causation is also emerging in the surgical realm. Roux-en-Y gastric bypass seems to change the microbiome in a way that facilitates weight loss, beyond caloric intake.Randy Seeley, Ph.D., of the University of Michigan, Ann Arbor, has been studying how weight-loss surgery affects the microbiome. He theorizes that the physical manipulation of the gut induces what he calls “enteroplasticity” – a fluid adaptation of both the gut’s structure and its bacterial communities to the altered physical and chemical environment. “There’s more going on during postsurgical weight loss than just food restriction and malabsorption,” Dr. Seeley said in an interview. “It’s logical to think that when you do this kind of surgery, the microbes in the intestine will change.”

Roseburia intestinalis is a Firmicute that typically increases after bariatric surgery. It’s also found to be deficient in people who have diabetes. Dr. Seeley coauthored an article showing that Roseburia and other beneficial firmicutes increased significantly in mice that underwent vertical sleeve gastrectomy (Nature 2014;509:183-8). These mice lost weight after surgery, as would be expected, but then showed a preference for the high-protein and carbohydrate-rich foods that Firmicutes need. Their microbiome also showed decreases in the concentration of fat-loving Bacteroides species.

But interestingly, weight loss and microbiome improvement happened only in mice that had a normal bile acid–signaling system. Immediately after surgery, mice engineered to lack bile acid receptors did eat less and lose weight. But a week later, their appetites came back full force, and they actually seemed driven to eat fat. They quickly returned to their presurgical weight. Their microbiome didn’t show the same improvement as their cousins with normal signaling pathways, suggesting that a complex interaction between bacteria and the gut’s physical alteration may be driving weight loss.

“Is weight-loss surgery, then, fixing this ‘broken’ component of the microbiome?” Dr. Seeley asked. “Is Roseburia the causal agent of improvement? Or is it a marker of improvement in an entire community? I would say it’s probably the entire community changing, and changing its interaction with its host organism.”

Dr. Seeley disclosed that he has received financial support from Johnson & Johnson, Novo Nordisk, and Eisai.

[email protected]

On Twitter @alz_gal

SAN DIEGO – Patients taking calcium supplementation after gastric bypass surgery had higher rates of kidney stone growth, compared with those who received no calcium supplementation, results from a single-center retrospective study showed.

In addition, the majority of stones in patients taking calcium supplementation were comprised of calcium oxalate monohydrate, which is less amenable to extracorporeal shockwave therapy. “You need more invasive procedures to break up these kinds of stones,” lead author Christopher Loftus said in an interview at the meeting of the Endocrine Society, where the study was presented during a late-breaking abstract session.

Doug Brunk/Frontline Medical News

Though it has been demonstrated that bariatric surgery is associated with an increased risk of kidney stone formation (Kidney Int. 2014 [doi:10.1038/ki.2014.352]), Mr. Loftus, a fourth-year medical student at Cleveland Clinic Lerner College of Medicine, and his associates set out to determine whether calcium supplementation increases the risk of nephrolithiasis in 60 stone-forming patients after gastric bypass surgery performed at the Cleveland Clinic. For each patient, two unenhanced CT scans at least 1 month apart and less than 2 years apart were selected at the start of the supplementation date and after the gastric bypass surgery date. The researchers calculated the rate of stone growth by the change in consecutive stone burden (the sum of maximum diameters of stones) divided by the elapsed time between scans.

Of the 60 patients, 31 received postoperative calcium supplementation (an average of 500 mg/day) and 29 did not. Compared with patients who did not take calcium supplementation, those who did were younger (a mean of 53 years vs. 58 years, respectively), more likely to be female (81% vs. 69%), and had a higher body mass index (34.5 kg/m² vs. 32.7 kg/m²). In addition, a greater proportion of patients taking calcium supplements underwent Roux-en-Y bypass (83% vs. 64%; P = .19), had stones comprised of calcium oxalate (81% vs. 67%; P = .56), and a higher rate of stone growth (more than 10 mm/year vs. less than 5 mm/year; P = .0004). “We weren’t expecting such a pronounced effect,” Mr. Loftus said.

In their abstract, the researchers said that further studies are required to elucidate the exact role of calcium supplementation on stone disease in this patient population.

The study was funded in part by a grant from the American Society of Nephrology. Mr. Loftus reported having no relevant financial conflicts.

[email protected]

On Twitter @dougbrunk

SAN DIEGO – Patients taking calcium supplementation after gastric bypass surgery had higher rates of kidney stone growth, compared with those who received no calcium supplementation, results from a single-center retrospective study showed.

In addition, the majority of stones in patients taking calcium supplementation were comprised of calcium oxalate monohydrate, which is less amenable to extracorporeal shockwave therapy. “You need more invasive procedures to break up these kinds of stones,” lead author Christopher Loftus said in an interview at the meeting of the Endocrine Society, where the study was presented during a late-breaking abstract session.

Doug Brunk/Frontline Medical News

Though it has been demonstrated that bariatric surgery is associated with an increased risk of kidney stone formation (Kidney Int. 2014 [doi:10.1038/ki.2014.352]), Mr. Loftus, a fourth-year medical student at Cleveland Clinic Lerner College of Medicine, and his associates set out to determine whether calcium supplementation increases the risk of nephrolithiasis in 60 stone-forming patients after gastric bypass surgery performed at the Cleveland Clinic. For each patient, two unenhanced CT scans at least 1 month apart and less than 2 years apart were selected at the start of the supplementation date and after the gastric bypass surgery date. The researchers calculated the rate of stone growth by the change in consecutive stone burden (the sum of maximum diameters of stones) divided by the elapsed time between scans.

Of the 60 patients, 31 received postoperative calcium supplementation (an average of 500 mg/day) and 29 did not. Compared with patients who did not take calcium supplementation, those who did were younger (a mean of 53 years vs. 58 years, respectively), more likely to be female (81% vs. 69%), and had a higher body mass index (34.5 kg/m² vs. 32.7 kg/m²). In addition, a greater proportion of patients taking calcium supplements underwent Roux-en-Y bypass (83% vs. 64%; P = .19), had stones comprised of calcium oxalate (81% vs. 67%; P = .56), and a higher rate of stone growth (more than 10 mm/year vs. less than 5 mm/year; P = .0004). “We weren’t expecting such a pronounced effect,” Mr. Loftus said.

In their abstract, the researchers said that further studies are required to elucidate the exact role of calcium supplementation on stone disease in this patient population.

The study was funded in part by a grant from the American Society of Nephrology. Mr. Loftus reported having no relevant financial conflicts.

[email protected]

On Twitter @dougbrunk

SAN DIEGO – Patients taking calcium supplementation after gastric bypass surgery had higher rates of kidney stone growth, compared with those who received no calcium supplementation, results from a single-center retrospective study showed.

In addition, the majority of stones in patients taking calcium supplementation were comprised of calcium oxalate monohydrate, which is less amenable to extracorporeal shockwave therapy. “You need more invasive procedures to break up these kinds of stones,” lead author Christopher Loftus said in an interview at the meeting of the Endocrine Society, where the study was presented during a late-breaking abstract session.

Doug Brunk/Frontline Medical News

Though it has been demonstrated that bariatric surgery is associated with an increased risk of kidney stone formation (Kidney Int. 2014 [doi:10.1038/ki.2014.352]), Mr. Loftus, a fourth-year medical student at Cleveland Clinic Lerner College of Medicine, and his associates set out to determine whether calcium supplementation increases the risk of nephrolithiasis in 60 stone-forming patients after gastric bypass surgery performed at the Cleveland Clinic. For each patient, two unenhanced CT scans at least 1 month apart and less than 2 years apart were selected at the start of the supplementation date and after the gastric bypass surgery date. The researchers calculated the rate of stone growth by the change in consecutive stone burden (the sum of maximum diameters of stones) divided by the elapsed time between scans.

Of the 60 patients, 31 received postoperative calcium supplementation (an average of 500 mg/day) and 29 did not. Compared with patients who did not take calcium supplementation, those who did were younger (a mean of 53 years vs. 58 years, respectively), more likely to be female (81% vs. 69%), and had a higher body mass index (34.5 kg/m² vs. 32.7 kg/m²). In addition, a greater proportion of patients taking calcium supplements underwent Roux-en-Y bypass (83% vs. 64%; P = .19), had stones comprised of calcium oxalate (81% vs. 67%; P = .56), and a higher rate of stone growth (more than 10 mm/year vs. less than 5 mm/year; P = .0004). “We weren’t expecting such a pronounced effect,” Mr. Loftus said.

In their abstract, the researchers said that further studies are required to elucidate the exact role of calcium supplementation on stone disease in this patient population.

The study was funded in part by a grant from the American Society of Nephrology. Mr. Loftus reported having no relevant financial conflicts.

[email protected]

On Twitter @dougbrunk

Improved reporting of adverse events associated with insulin pumps and increased funding of registries and clinical studies that evaluate the safety of these devices are among the recommendations included in a statement by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD).

Insulin pumps “appear to provide clinically important and increasing benefits for people with diabetes,” leading to their acceptance by the international diabetes community. However, “there are associated challenges, including potential risks to users,” according to the diabetes technology working group of the ADA and the EASD.

The two organizations reviewed the current approach to the evaluation of the clinical safety of insulin pumps, with the aim of considering “how health care professionals, pump manufacturers, regulatory authorities, and policymakers can best ensure the safety of new and long-standing users of insulin pumps, as the technology continues to develop,” according to the statement, which is in the April issue of Diabetes Care (2015;38:1-7 [doi:10.2337/dc15-0168).

While the rapidly evolving technology in diabetes treatment is “certainly a good thing, we don’t have very good postmarketing surveillance for devices such as insulin pumps, particularly in Europe where manufacturers often introduce products prior to releasing them in the United States,” Dr. Anne Peters, director of the University of Southern California Clinical Diabetes Program, Los Angeles, and one of the statement’s authors, said in a press release issued by the ADA. “We need to make sure we have sufficient data about how the devices are working once they hit the market, so that we can support patients by helping them understand how to prevent errors in using them.”

The working group reviewed evidence from published studies, regulatory authorities, manufacturers of pumps, and other sources. Among the conclusions is that there is a need for a more “standardized and transparent approach to identifying, reporting, and cataloging” adverse event reports, which would help patients and health care providers understand the risks of insulin pump therapy more clearly.

The statement refers to limitations of the postmarketing adverse event reporting systems for devices in the United States and in Europe, MAUDE (Manufacturer and User Facility Device Experience) and EUDAMED (European Databank on Medical Devices). For example, EUDAMED data are not accessible to the public and the MAUDE database is difficult to search.

The statement recommends specific actions that should be undertaken by five groups: regulators, pump manufacturers, professional societies, research funding bodies, and health care teams. For their part, health care teams should “encourage and support pump users under their care to report all” adverse events, and should provide structured training and regular updates for their patients who use pumps, based on standards set by national and international guidelines,

Professional societies should “provide updated evidence-based guidelines on indications for insulin pump therapy,” and “set standards for levels of staffing and skills” for health care teams.

Patient registries have collected information on metabolic control of patients. They should expand their scope to include more data on adverse events associated with insulin pumps and other information, according to the statement. More funding should be provided for trials that evaluate clinically relevant issues, and manufacturer-funded trials should be conducted by “independent investigators to minimize bias and credibility.”

The authors estimated that there could be 750,000 to 1 million pump users worldwide and that most pump users have type 1 diabetes. But a more accurate estimate would be useful to more reliably calculate the rates of malfunctioning pumps and human errors, they added.

Members of the working group did not receive honoraria for writing the manuscript or attending related meetings; their travel costs were paid by the EASD and ADA. Most of the members work with industry, and disclosures included having served as advisers or consultants to companies that manufacture diagnostic or therapeutic products for diabetes. Dr. Peters disclosed having served as a consultant for Medtronic/MiniMed, and having served as a consultant and/or speaker for non–device-related companies.

[email protected]

Improved reporting of adverse events associated with insulin pumps and increased funding of registries and clinical studies that evaluate the safety of these devices are among the recommendations included in a statement by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD).

Insulin pumps “appear to provide clinically important and increasing benefits for people with diabetes,” leading to their acceptance by the international diabetes community. However, “there are associated challenges, including potential risks to users,” according to the diabetes technology working group of the ADA and the EASD.

The two organizations reviewed the current approach to the evaluation of the clinical safety of insulin pumps, with the aim of considering “how health care professionals, pump manufacturers, regulatory authorities, and policymakers can best ensure the safety of new and long-standing users of insulin pumps, as the technology continues to develop,” according to the statement, which is in the April issue of Diabetes Care (2015;38:1-7 [doi:10.2337/dc15-0168).

While the rapidly evolving technology in diabetes treatment is “certainly a good thing, we don’t have very good postmarketing surveillance for devices such as insulin pumps, particularly in Europe where manufacturers often introduce products prior to releasing them in the United States,” Dr. Anne Peters, director of the University of Southern California Clinical Diabetes Program, Los Angeles, and one of the statement’s authors, said in a press release issued by the ADA. “We need to make sure we have sufficient data about how the devices are working once they hit the market, so that we can support patients by helping them understand how to prevent errors in using them.”

The working group reviewed evidence from published studies, regulatory authorities, manufacturers of pumps, and other sources. Among the conclusions is that there is a need for a more “standardized and transparent approach to identifying, reporting, and cataloging” adverse event reports, which would help patients and health care providers understand the risks of insulin pump therapy more clearly.

The statement refers to limitations of the postmarketing adverse event reporting systems for devices in the United States and in Europe, MAUDE (Manufacturer and User Facility Device Experience) and EUDAMED (European Databank on Medical Devices). For example, EUDAMED data are not accessible to the public and the MAUDE database is difficult to search.

The statement recommends specific actions that should be undertaken by five groups: regulators, pump manufacturers, professional societies, research funding bodies, and health care teams. For their part, health care teams should “encourage and support pump users under their care to report all” adverse events, and should provide structured training and regular updates for their patients who use pumps, based on standards set by national and international guidelines,

Professional societies should “provide updated evidence-based guidelines on indications for insulin pump therapy,” and “set standards for levels of staffing and skills” for health care teams.

Patient registries have collected information on metabolic control of patients. They should expand their scope to include more data on adverse events associated with insulin pumps and other information, according to the statement. More funding should be provided for trials that evaluate clinically relevant issues, and manufacturer-funded trials should be conducted by “independent investigators to minimize bias and credibility.”

The authors estimated that there could be 750,000 to 1 million pump users worldwide and that most pump users have type 1 diabetes. But a more accurate estimate would be useful to more reliably calculate the rates of malfunctioning pumps and human errors, they added.

Members of the working group did not receive honoraria for writing the manuscript or attending related meetings; their travel costs were paid by the EASD and ADA. Most of the members work with industry, and disclosures included having served as advisers or consultants to companies that manufacture diagnostic or therapeutic products for diabetes. Dr. Peters disclosed having served as a consultant for Medtronic/MiniMed, and having served as a consultant and/or speaker for non–device-related companies.

[email protected]

Improved reporting of adverse events associated with insulin pumps and increased funding of registries and clinical studies that evaluate the safety of these devices are among the recommendations included in a statement by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD).

Insulin pumps “appear to provide clinically important and increasing benefits for people with diabetes,” leading to their acceptance by the international diabetes community. However, “there are associated challenges, including potential risks to users,” according to the diabetes technology working group of the ADA and the EASD.

The two organizations reviewed the current approach to the evaluation of the clinical safety of insulin pumps, with the aim of considering “how health care professionals, pump manufacturers, regulatory authorities, and policymakers can best ensure the safety of new and long-standing users of insulin pumps, as the technology continues to develop,” according to the statement, which is in the April issue of Diabetes Care (2015;38:1-7 [doi:10.2337/dc15-0168).

While the rapidly evolving technology in diabetes treatment is “certainly a good thing, we don’t have very good postmarketing surveillance for devices such as insulin pumps, particularly in Europe where manufacturers often introduce products prior to releasing them in the United States,” Dr. Anne Peters, director of the University of Southern California Clinical Diabetes Program, Los Angeles, and one of the statement’s authors, said in a press release issued by the ADA. “We need to make sure we have sufficient data about how the devices are working once they hit the market, so that we can support patients by helping them understand how to prevent errors in using them.”

The working group reviewed evidence from published studies, regulatory authorities, manufacturers of pumps, and other sources. Among the conclusions is that there is a need for a more “standardized and transparent approach to identifying, reporting, and cataloging” adverse event reports, which would help patients and health care providers understand the risks of insulin pump therapy more clearly.

The statement refers to limitations of the postmarketing adverse event reporting systems for devices in the United States and in Europe, MAUDE (Manufacturer and User Facility Device Experience) and EUDAMED (European Databank on Medical Devices). For example, EUDAMED data are not accessible to the public and the MAUDE database is difficult to search.

The statement recommends specific actions that should be undertaken by five groups: regulators, pump manufacturers, professional societies, research funding bodies, and health care teams. For their part, health care teams should “encourage and support pump users under their care to report all” adverse events, and should provide structured training and regular updates for their patients who use pumps, based on standards set by national and international guidelines,

Professional societies should “provide updated evidence-based guidelines on indications for insulin pump therapy,” and “set standards for levels of staffing and skills” for health care teams.

Patient registries have collected information on metabolic control of patients. They should expand their scope to include more data on adverse events associated with insulin pumps and other information, according to the statement. More funding should be provided for trials that evaluate clinically relevant issues, and manufacturer-funded trials should be conducted by “independent investigators to minimize bias and credibility.”

The authors estimated that there could be 750,000 to 1 million pump users worldwide and that most pump users have type 1 diabetes. But a more accurate estimate would be useful to more reliably calculate the rates of malfunctioning pumps and human errors, they added.

Members of the working group did not receive honoraria for writing the manuscript or attending related meetings; their travel costs were paid by the EASD and ADA. Most of the members work with industry, and disclosures included having served as advisers or consultants to companies that manufacture diagnostic or therapeutic products for diabetes. Dr. Peters disclosed having served as a consultant for Medtronic/MiniMed, and having served as a consultant and/or speaker for non–device-related companies.

[email protected]