Diabetes Hub

The phenomenon of “healthy obesity”– having a body mass index over 30 kg/m² but without significant metabolic risk factors – is most often a transitive phase toward unhealthiness, and not a stable physiological stage, a new report suggests.

“Healthy obese” adults were nearly eight times more likely to progress to an unhealthy obese state after 20 years than were healthy nonobese adults. After 20 years, roughly 50% of healthy obese adults were unhealthy obese, and 10% were healthy nonobese, lead author Joshua A. Bell wrote in a research letter published Jan. 5 in the Journal of the American College of Cardiology (doi: /10.1016/j.jacc.2014.09.077).

© kikkerdirk/Thinkstockphotos.com

Mr. Bell and his colleagues from the department of epidemiology and public health at University College London examined data from 2,521 British government workers between the ages of 39 and 62 years. Each participant’s body mass index, cholesterol, blood pressure, fasting plasma glucose and insulin resistance was measured over 5 years, 10 years, and 20 years. Three-quarters of the participants were male.

The sample included 66 “healthy obese” adults at baseline, or about a third of all obese participants. Of these subjects, 21 (32%) were unhealthy obese after 5 years, and 27 (41%), 23 (35%), and 34 (52%) were unhealthy obese after 10, 15, and 20 years, respectively.

“Our results, which were obtained with a longer, more detailed follow-up than any previous study, suggest that long-term stability is the exception, not the norm. The natural course of healthy obesity is progression to metabolic deterioration,” the authors wrote.

There were no relevant disclosures to report.

[email protected]

The phenomenon of “healthy obesity”– having a body mass index over 30 kg/m² but without significant metabolic risk factors – is most often a transitive phase toward unhealthiness, and not a stable physiological stage, a new report suggests.

“Healthy obese” adults were nearly eight times more likely to progress to an unhealthy obese state after 20 years than were healthy nonobese adults. After 20 years, roughly 50% of healthy obese adults were unhealthy obese, and 10% were healthy nonobese, lead author Joshua A. Bell wrote in a research letter published Jan. 5 in the Journal of the American College of Cardiology (doi: /10.1016/j.jacc.2014.09.077).

© kikkerdirk/Thinkstockphotos.com

Mr. Bell and his colleagues from the department of epidemiology and public health at University College London examined data from 2,521 British government workers between the ages of 39 and 62 years. Each participant’s body mass index, cholesterol, blood pressure, fasting plasma glucose and insulin resistance was measured over 5 years, 10 years, and 20 years. Three-quarters of the participants were male.

The sample included 66 “healthy obese” adults at baseline, or about a third of all obese participants. Of these subjects, 21 (32%) were unhealthy obese after 5 years, and 27 (41%), 23 (35%), and 34 (52%) were unhealthy obese after 10, 15, and 20 years, respectively.

“Our results, which were obtained with a longer, more detailed follow-up than any previous study, suggest that long-term stability is the exception, not the norm. The natural course of healthy obesity is progression to metabolic deterioration,” the authors wrote.

There were no relevant disclosures to report.

[email protected]

The phenomenon of “healthy obesity”– having a body mass index over 30 kg/m² but without significant metabolic risk factors – is most often a transitive phase toward unhealthiness, and not a stable physiological stage, a new report suggests.

“Healthy obese” adults were nearly eight times more likely to progress to an unhealthy obese state after 20 years than were healthy nonobese adults. After 20 years, roughly 50% of healthy obese adults were unhealthy obese, and 10% were healthy nonobese, lead author Joshua A. Bell wrote in a research letter published Jan. 5 in the Journal of the American College of Cardiology (doi: /10.1016/j.jacc.2014.09.077).

© kikkerdirk/Thinkstockphotos.com

Mr. Bell and his colleagues from the department of epidemiology and public health at University College London examined data from 2,521 British government workers between the ages of 39 and 62 years. Each participant’s body mass index, cholesterol, blood pressure, fasting plasma glucose and insulin resistance was measured over 5 years, 10 years, and 20 years. Three-quarters of the participants were male.

The sample included 66 “healthy obese” adults at baseline, or about a third of all obese participants. Of these subjects, 21 (32%) were unhealthy obese after 5 years, and 27 (41%), 23 (35%), and 34 (52%) were unhealthy obese after 10, 15, and 20 years, respectively.

“Our results, which were obtained with a longer, more detailed follow-up than any previous study, suggest that long-term stability is the exception, not the norm. The natural course of healthy obesity is progression to metabolic deterioration,” the authors wrote.

There were no relevant disclosures to report.

[email protected]

Many patients with type 2 diabetes have “material need insecurities” – trouble paying for food, medications, housing, or utilities – which greatly impact control of the disease and their use of health care resources, according to a report published online Dec. 29 in JAMA Internal Medicine.

If these pressing but nonmedical needs aren’t identified and addressed, increasing access to health care and diabetes treatments will likely be futile, said Dr. Seth A. Berkowitz of Massachusetts General Hospital and Harvard Medical School, Boston, and his associates.

© Tashatuvango/Thinkstockphotos.com

Most previous research into such material needs have focused on a single need in isolation. In their study, Dr. Berkowitz and his colleagues assessed several material needs simultaneously, to obtain a more accurate picture of the real-world experience of diabetes patients at the lower end of the socioeconomic scale. They surveyed 411 patients attending two community health centers, an academic internal medicine practice, or a diabetes specialty clinic in the Boston area during a 1-year period. The mean patient age was 62 years; 48% were women, and 79% were of non-Hispanic white ethnicity. Health insurance coverage was very high, since Massachusetts has near-universal coverage; only 4% of the study participants were uninsured or self-pay clients, and less than 35 lacked coverage of prescription medication.

Eighty respondents reported having a limited or uncertain availability of food due to its cost. This likely included many who relied on cheap, calorie-dense, highly processed foods because of the inaccessibility of healthier alternatives recommended for glycemic control. A total of 104 respondents reported that they underused medications because of costs; 44 reported housing instability, including homelessness, evictions, frequent moves, or residing with friends or relatives to share living expenses; and 72 reported that they couldn’t consistently afford household heating or cooling.

Diabetes patients who had food, medication, housing, or utility insecurities were significantly more likely than others to have poor diabetes control, poor lipid profiles, poor control of hypertension, and to require more outpatient and emergency department/inpatient visits. Moreover, every additional material need insecurity raised the odds of poor diabetes control by 39%, the odds of outpatient visits by 9%, and the odds of emergency department/inpatient visits by 22%, Dr. Berkowitz and his associates said (JAMA Intern. Med. 2014 Dec. 29 [doi:10.1001/jamainternmed.2014.6888]). These findings indicate that to achieve diabetes control, many patients need not just standard medications but comprehensive interventions that also address access to food, medication, and stable housing. Programs that link patients to government and community resources would be beneficial, as would direct supplementation of healthy foods and “bundling” of low-cost (generic) medications such as metformin, statins, and ACE inhibitors, the investigators said.

This study was supported by the Institutional National Research Service, the Ryoichi Sasakawa Fellowship Fund, the division of general internal medicine at Massachusetts General Hospital, and the National Institutes of Health. Dr. Berkowitz and his associates reported having no relevant financial conflicts of interest.

Many patients with type 2 diabetes have “material need insecurities” – trouble paying for food, medications, housing, or utilities – which greatly impact control of the disease and their use of health care resources, according to a report published online Dec. 29 in JAMA Internal Medicine.

If these pressing but nonmedical needs aren’t identified and addressed, increasing access to health care and diabetes treatments will likely be futile, said Dr. Seth A. Berkowitz of Massachusetts General Hospital and Harvard Medical School, Boston, and his associates.

© Tashatuvango/Thinkstockphotos.com

Most previous research into such material needs have focused on a single need in isolation. In their study, Dr. Berkowitz and his colleagues assessed several material needs simultaneously, to obtain a more accurate picture of the real-world experience of diabetes patients at the lower end of the socioeconomic scale. They surveyed 411 patients attending two community health centers, an academic internal medicine practice, or a diabetes specialty clinic in the Boston area during a 1-year period. The mean patient age was 62 years; 48% were women, and 79% were of non-Hispanic white ethnicity. Health insurance coverage was very high, since Massachusetts has near-universal coverage; only 4% of the study participants were uninsured or self-pay clients, and less than 35 lacked coverage of prescription medication.

Eighty respondents reported having a limited or uncertain availability of food due to its cost. This likely included many who relied on cheap, calorie-dense, highly processed foods because of the inaccessibility of healthier alternatives recommended for glycemic control. A total of 104 respondents reported that they underused medications because of costs; 44 reported housing instability, including homelessness, evictions, frequent moves, or residing with friends or relatives to share living expenses; and 72 reported that they couldn’t consistently afford household heating or cooling.

Diabetes patients who had food, medication, housing, or utility insecurities were significantly more likely than others to have poor diabetes control, poor lipid profiles, poor control of hypertension, and to require more outpatient and emergency department/inpatient visits. Moreover, every additional material need insecurity raised the odds of poor diabetes control by 39%, the odds of outpatient visits by 9%, and the odds of emergency department/inpatient visits by 22%, Dr. Berkowitz and his associates said (JAMA Intern. Med. 2014 Dec. 29 [doi:10.1001/jamainternmed.2014.6888]). These findings indicate that to achieve diabetes control, many patients need not just standard medications but comprehensive interventions that also address access to food, medication, and stable housing. Programs that link patients to government and community resources would be beneficial, as would direct supplementation of healthy foods and “bundling” of low-cost (generic) medications such as metformin, statins, and ACE inhibitors, the investigators said.

This study was supported by the Institutional National Research Service, the Ryoichi Sasakawa Fellowship Fund, the division of general internal medicine at Massachusetts General Hospital, and the National Institutes of Health. Dr. Berkowitz and his associates reported having no relevant financial conflicts of interest.

Many patients with type 2 diabetes have “material need insecurities” – trouble paying for food, medications, housing, or utilities – which greatly impact control of the disease and their use of health care resources, according to a report published online Dec. 29 in JAMA Internal Medicine.

If these pressing but nonmedical needs aren’t identified and addressed, increasing access to health care and diabetes treatments will likely be futile, said Dr. Seth A. Berkowitz of Massachusetts General Hospital and Harvard Medical School, Boston, and his associates.

© Tashatuvango/Thinkstockphotos.com

Most previous research into such material needs have focused on a single need in isolation. In their study, Dr. Berkowitz and his colleagues assessed several material needs simultaneously, to obtain a more accurate picture of the real-world experience of diabetes patients at the lower end of the socioeconomic scale. They surveyed 411 patients attending two community health centers, an academic internal medicine practice, or a diabetes specialty clinic in the Boston area during a 1-year period. The mean patient age was 62 years; 48% were women, and 79% were of non-Hispanic white ethnicity. Health insurance coverage was very high, since Massachusetts has near-universal coverage; only 4% of the study participants were uninsured or self-pay clients, and less than 35 lacked coverage of prescription medication.

Eighty respondents reported having a limited or uncertain availability of food due to its cost. This likely included many who relied on cheap, calorie-dense, highly processed foods because of the inaccessibility of healthier alternatives recommended for glycemic control. A total of 104 respondents reported that they underused medications because of costs; 44 reported housing instability, including homelessness, evictions, frequent moves, or residing with friends or relatives to share living expenses; and 72 reported that they couldn’t consistently afford household heating or cooling.

Diabetes patients who had food, medication, housing, or utility insecurities were significantly more likely than others to have poor diabetes control, poor lipid profiles, poor control of hypertension, and to require more outpatient and emergency department/inpatient visits. Moreover, every additional material need insecurity raised the odds of poor diabetes control by 39%, the odds of outpatient visits by 9%, and the odds of emergency department/inpatient visits by 22%, Dr. Berkowitz and his associates said (JAMA Intern. Med. 2014 Dec. 29 [doi:10.1001/jamainternmed.2014.6888]). These findings indicate that to achieve diabetes control, many patients need not just standard medications but comprehensive interventions that also address access to food, medication, and stable housing. Programs that link patients to government and community resources would be beneficial, as would direct supplementation of healthy foods and “bundling” of low-cost (generic) medications such as metformin, statins, and ACE inhibitors, the investigators said.

This study was supported by the Institutional National Research Service, the Ryoichi Sasakawa Fellowship Fund, the division of general internal medicine at Massachusetts General Hospital, and the National Institutes of Health. Dr. Berkowitz and his associates reported having no relevant financial conflicts of interest.

The American Diabetes Association has issued a new recommendation stating that all Asian American adults who present with a body mass index of at least 23 kg/m² should be tested for type 2 diabetes.

In its latest position statement, the ADA cites increasing evidence that body mass index (BMI) is more indicative than just body weight for determining a patient’s likelihood of developing type 2 diabetes, along with data on the higher predisposition for diabetes among Asian Americans, as the main reasons for lowering the cut point from 25 kg/m², which is the established BMI at which all adults should be tested for diabetes (Diabetes Care 2015;38:1-9 [doi:10.2337/dc14-2391]).

“Given that established BMI cut points indicating elevated diabetes risk are inappropriate for Asian Americans, establishing a specific BMI cut point to identify Asian Americans with or at risk for future diabetes would be beneficial to the potential health of millions of Asian American individuals,” the ADA said in the statement.

© Tashatuvango/Thinkstockphotos.com

According to the ADA, Asian Americans – who currently make up the fastest-growing ethnic group in the United States – are prone to developing diabetes at a lower BMI because, instead of gathering in the thighs, their weight gains tend to accumulate around the waist, an area that is known for being the most harmful from the standpoint of adiposity and disease. The ADA also highlights lifestyle and dietary habits inherent to Asian cultures as reasons for why Asian Americans are more predisposed to the disease.

“Clinicians have known this intuitively for quite some time,” said Dr. William C. Hsu, lead author of the position statement. “They can see that Asian Americans are being diagnosed with diabetes when they do not appear to be overweight or obese according to general standards. But if you use the previous association standard for diabetes screening of being age 45 or older with a BMI of 25 kg/m² or above, you will miss many Asian Americans who are at risk,” said Dr. Hsu of Harvard Medical School in Boston, who is vice president of international programs at Joslin Diabetes Center.

According to the ADA, most studies tend to group Asian Americans along with Native Hawaiian and Pacific Islander demographics, although the groups differ significantly in terms of physiology and body composition. By focusing more on Asian American populations specifically, the ADA aims to have more reliable data that can lead to earlier and more accurate diagnosis of type 2 diabetes within the demographic.

“This paper is a significant step in the right direction of widely recognizing the diabetes disparity that exists in our populations and communities,” said Dr. Ho Luong Tran, president of the National Council of Asian Pacific Islander Physicians and lead coordinator of the Asian American Native Hawaiian and Pacific Islanders Diabetes Coalition. “The next steps are to increase the amount of clinical research and data on this diverse population, while simultaneously pushing for policy change that will positively impact health outcomes.”

[email protected]

The American Diabetes Association has issued a new recommendation stating that all Asian American adults who present with a body mass index of at least 23 kg/m² should be tested for type 2 diabetes.

In its latest position statement, the ADA cites increasing evidence that body mass index (BMI) is more indicative than just body weight for determining a patient’s likelihood of developing type 2 diabetes, along with data on the higher predisposition for diabetes among Asian Americans, as the main reasons for lowering the cut point from 25 kg/m², which is the established BMI at which all adults should be tested for diabetes (Diabetes Care 2015;38:1-9 [doi:10.2337/dc14-2391]).

“Given that established BMI cut points indicating elevated diabetes risk are inappropriate for Asian Americans, establishing a specific BMI cut point to identify Asian Americans with or at risk for future diabetes would be beneficial to the potential health of millions of Asian American individuals,” the ADA said in the statement.

© Tashatuvango/Thinkstockphotos.com

According to the ADA, Asian Americans – who currently make up the fastest-growing ethnic group in the United States – are prone to developing diabetes at a lower BMI because, instead of gathering in the thighs, their weight gains tend to accumulate around the waist, an area that is known for being the most harmful from the standpoint of adiposity and disease. The ADA also highlights lifestyle and dietary habits inherent to Asian cultures as reasons for why Asian Americans are more predisposed to the disease.

“Clinicians have known this intuitively for quite some time,” said Dr. William C. Hsu, lead author of the position statement. “They can see that Asian Americans are being diagnosed with diabetes when they do not appear to be overweight or obese according to general standards. But if you use the previous association standard for diabetes screening of being age 45 or older with a BMI of 25 kg/m² or above, you will miss many Asian Americans who are at risk,” said Dr. Hsu of Harvard Medical School in Boston, who is vice president of international programs at Joslin Diabetes Center.

According to the ADA, most studies tend to group Asian Americans along with Native Hawaiian and Pacific Islander demographics, although the groups differ significantly in terms of physiology and body composition. By focusing more on Asian American populations specifically, the ADA aims to have more reliable data that can lead to earlier and more accurate diagnosis of type 2 diabetes within the demographic.

“This paper is a significant step in the right direction of widely recognizing the diabetes disparity that exists in our populations and communities,” said Dr. Ho Luong Tran, president of the National Council of Asian Pacific Islander Physicians and lead coordinator of the Asian American Native Hawaiian and Pacific Islanders Diabetes Coalition. “The next steps are to increase the amount of clinical research and data on this diverse population, while simultaneously pushing for policy change that will positively impact health outcomes.”

[email protected]

The American Diabetes Association has issued a new recommendation stating that all Asian American adults who present with a body mass index of at least 23 kg/m² should be tested for type 2 diabetes.

In its latest position statement, the ADA cites increasing evidence that body mass index (BMI) is more indicative than just body weight for determining a patient’s likelihood of developing type 2 diabetes, along with data on the higher predisposition for diabetes among Asian Americans, as the main reasons for lowering the cut point from 25 kg/m², which is the established BMI at which all adults should be tested for diabetes (Diabetes Care 2015;38:1-9 [doi:10.2337/dc14-2391]).

“Given that established BMI cut points indicating elevated diabetes risk are inappropriate for Asian Americans, establishing a specific BMI cut point to identify Asian Americans with or at risk for future diabetes would be beneficial to the potential health of millions of Asian American individuals,” the ADA said in the statement.

© Tashatuvango/Thinkstockphotos.com

According to the ADA, Asian Americans – who currently make up the fastest-growing ethnic group in the United States – are prone to developing diabetes at a lower BMI because, instead of gathering in the thighs, their weight gains tend to accumulate around the waist, an area that is known for being the most harmful from the standpoint of adiposity and disease. The ADA also highlights lifestyle and dietary habits inherent to Asian cultures as reasons for why Asian Americans are more predisposed to the disease.

“Clinicians have known this intuitively for quite some time,” said Dr. William C. Hsu, lead author of the position statement. “They can see that Asian Americans are being diagnosed with diabetes when they do not appear to be overweight or obese according to general standards. But if you use the previous association standard for diabetes screening of being age 45 or older with a BMI of 25 kg/m² or above, you will miss many Asian Americans who are at risk,” said Dr. Hsu of Harvard Medical School in Boston, who is vice president of international programs at Joslin Diabetes Center.

According to the ADA, most studies tend to group Asian Americans along with Native Hawaiian and Pacific Islander demographics, although the groups differ significantly in terms of physiology and body composition. By focusing more on Asian American populations specifically, the ADA aims to have more reliable data that can lead to earlier and more accurate diagnosis of type 2 diabetes within the demographic.

“This paper is a significant step in the right direction of widely recognizing the diabetes disparity that exists in our populations and communities,” said Dr. Ho Luong Tran, president of the National Council of Asian Pacific Islander Physicians and lead coordinator of the Asian American Native Hawaiian and Pacific Islanders Diabetes Coalition. “The next steps are to increase the amount of clinical research and data on this diverse population, while simultaneously pushing for policy change that will positively impact health outcomes.”

[email protected]

A healthy diet that was modified to have a low glycemic index did not improve insulin sensitivity, lipid levels, or blood pressure in overweight and obese adults, compared with one with a high glycemic index, according to a report published online Dec. 16 in JAMA.

This unexpected finding indicates that, against a background diet that is already healthy, “using glycemic index to select specific foods may not improve cardiovascular risk factors or insulin resistance,” said Dr. Frank M. Sacks of the department of nutrition, Harvard School of Public Health, Boston, and his associates.

The investigators performed a randomized, crossover feeding study in which 163 people aged at least 30 years were randomly assigned to one of four study diets for 5 weeks, then switched to a different diet for a further 5 weeks, after a 2-week washout period.

“We studied diets that had a large contrast in glycemic index, while at the same time we controlled intake of total carbohydrates and other key nutrients such as fatty acids, potassium, and sodium and maintained body weight. The background diets in which we manipulated glycemic index were healthful dietary patterns established in the Dietary Approaches to Stop Hypertension (DASH) and Optimal Macronutrient Intake to Prevent Heart Disease (OmniHeart) studies that are being recommended in dietary guidelines to prevent CVD,” they noted. About half of the study population were female and half were black, and there were high prevalences of obesity (56%), hypertension (26%), high cholesterol (68%), and impaired fasting glucose (30%). All meals, snacks, and beverages were provided on site. Adherence, which was closely monitored, was high: All study foods and no nonstudy foods were consumed on 96% of person-days on each diet.

Contrary to expectations, the two low-glycemic-index diets failed to improve insulin sensitivity, cholesterol levels, or blood pressure when compared with the two high-glycemic-index diets. “Composing a DASH-type diet with low-glycemic-index foods ... does not improve CVD risk factors and may in fact reduce insulin sensitivity and increase LDL cholesterol,” Dr. Sacks and his associates wrote (JAMA 2014 Dec. 16 [doi:10.1001/jama.2014.16658]).

They noted that these findings are especially important given that some nutrition policies advocate replacing high-glycemic-index with low-glycemic-index foods. Even though some experts go so far as to promote that all foods be labeled with their glycemic-index values, “the benefits of glycemic index are uncertain, especially with persons are already consuming a healthful diet rich in whole grains, vegetables, and fruits.”

The investigators emphasized that none of the study participants had type 2 diabetes, so these findings do not apply to patients with that disease.

A healthy diet that was modified to have a low glycemic index did not improve insulin sensitivity, lipid levels, or blood pressure in overweight and obese adults, compared with one with a high glycemic index, according to a report published online Dec. 16 in JAMA.

This unexpected finding indicates that, against a background diet that is already healthy, “using glycemic index to select specific foods may not improve cardiovascular risk factors or insulin resistance,” said Dr. Frank M. Sacks of the department of nutrition, Harvard School of Public Health, Boston, and his associates.

The investigators performed a randomized, crossover feeding study in which 163 people aged at least 30 years were randomly assigned to one of four study diets for 5 weeks, then switched to a different diet for a further 5 weeks, after a 2-week washout period.

“We studied diets that had a large contrast in glycemic index, while at the same time we controlled intake of total carbohydrates and other key nutrients such as fatty acids, potassium, and sodium and maintained body weight. The background diets in which we manipulated glycemic index were healthful dietary patterns established in the Dietary Approaches to Stop Hypertension (DASH) and Optimal Macronutrient Intake to Prevent Heart Disease (OmniHeart) studies that are being recommended in dietary guidelines to prevent CVD,” they noted. About half of the study population were female and half were black, and there were high prevalences of obesity (56%), hypertension (26%), high cholesterol (68%), and impaired fasting glucose (30%). All meals, snacks, and beverages were provided on site. Adherence, which was closely monitored, was high: All study foods and no nonstudy foods were consumed on 96% of person-days on each diet.

Contrary to expectations, the two low-glycemic-index diets failed to improve insulin sensitivity, cholesterol levels, or blood pressure when compared with the two high-glycemic-index diets. “Composing a DASH-type diet with low-glycemic-index foods ... does not improve CVD risk factors and may in fact reduce insulin sensitivity and increase LDL cholesterol,” Dr. Sacks and his associates wrote (JAMA 2014 Dec. 16 [doi:10.1001/jama.2014.16658]).

They noted that these findings are especially important given that some nutrition policies advocate replacing high-glycemic-index with low-glycemic-index foods. Even though some experts go so far as to promote that all foods be labeled with their glycemic-index values, “the benefits of glycemic index are uncertain, especially with persons are already consuming a healthful diet rich in whole grains, vegetables, and fruits.”

The investigators emphasized that none of the study participants had type 2 diabetes, so these findings do not apply to patients with that disease.

A healthy diet that was modified to have a low glycemic index did not improve insulin sensitivity, lipid levels, or blood pressure in overweight and obese adults, compared with one with a high glycemic index, according to a report published online Dec. 16 in JAMA.

This unexpected finding indicates that, against a background diet that is already healthy, “using glycemic index to select specific foods may not improve cardiovascular risk factors or insulin resistance,” said Dr. Frank M. Sacks of the department of nutrition, Harvard School of Public Health, Boston, and his associates.

The investigators performed a randomized, crossover feeding study in which 163 people aged at least 30 years were randomly assigned to one of four study diets for 5 weeks, then switched to a different diet for a further 5 weeks, after a 2-week washout period.

“We studied diets that had a large contrast in glycemic index, while at the same time we controlled intake of total carbohydrates and other key nutrients such as fatty acids, potassium, and sodium and maintained body weight. The background diets in which we manipulated glycemic index were healthful dietary patterns established in the Dietary Approaches to Stop Hypertension (DASH) and Optimal Macronutrient Intake to Prevent Heart Disease (OmniHeart) studies that are being recommended in dietary guidelines to prevent CVD,” they noted. About half of the study population were female and half were black, and there were high prevalences of obesity (56%), hypertension (26%), high cholesterol (68%), and impaired fasting glucose (30%). All meals, snacks, and beverages were provided on site. Adherence, which was closely monitored, was high: All study foods and no nonstudy foods were consumed on 96% of person-days on each diet.

Contrary to expectations, the two low-glycemic-index diets failed to improve insulin sensitivity, cholesterol levels, or blood pressure when compared with the two high-glycemic-index diets. “Composing a DASH-type diet with low-glycemic-index foods ... does not improve CVD risk factors and may in fact reduce insulin sensitivity and increase LDL cholesterol,” Dr. Sacks and his associates wrote (JAMA 2014 Dec. 16 [doi:10.1001/jama.2014.16658]).

They noted that these findings are especially important given that some nutrition policies advocate replacing high-glycemic-index with low-glycemic-index foods. Even though some experts go so far as to promote that all foods be labeled with their glycemic-index values, “the benefits of glycemic index are uncertain, especially with persons are already consuming a healthful diet rich in whole grains, vegetables, and fruits.”

The investigators emphasized that none of the study participants had type 2 diabetes, so these findings do not apply to patients with that disease.

PHILADELPHIA– Anti-TGF-beta 1 therapy was safe and well-tolerated, but failed to slow disease progression in patients with advanced diabetic nephropathy in a randomized, double-masked, phase 2 dose-ranging study.

In fact, the trial was terminated 4 months early for efficacy futility, Dr. James R. Voelker reported at Kidney Week 2014.

In 416 patients with type 1 or type 2 diabetes and a likelihood of rapid disease progression who were randomized to receive subcutaneous treatment with either placebo or various doses of a beta-1-specific humanized monoclonal neutralizing antibody known as LY2382770 (LY).

Treatment at any dose was not significantly more effective than placebo with respect to the primary outcome measure of mean change in serum creatinine. Mean serum creatinine increased from 2.22 to 2.48 mg/dl in the placebo group, and in the treatment groups it increased from 2.15 to 2.49 mg/dl (2 mg/month group), from 2.13 to 2.49 mg/dl (10 mg/month group), and from 2.15 to 2.50 mg/dl (50 mg/month group), Dr. Voelker of Eli Lilly and Co., Indianapolis, said at the meeting, which was sponsored by the American Society of Nephrology.

Patients in the study were adults aged 25 years or older (mean 62.2 years ) with serum creatinine of 1.3 to 3.3 mg/dl for women, and 1.5 to 3.5 mg/dl for men, or estimated glomerular filtration rate of 20 to 60 ml/min/1.73 m², and they had a 24-hour urine protein/creatinine ratio of at least 800 mg/g. The groups were similar with respect to demographics and baseline characteristic, and most (75%) were men with type 2 diabetes (90%). All patient were receiving stable renin-angiotensin-system inhibition (RASi) therapy.

The intent was to select a population with a likelihood of fairly rapid disease progression during the course of the study to enable detection of a treatment effect, Dr. Voelker explained.

“Diabetic nephropathy is a disease of significant unmet medical need, as it is the leading cause of end-stage renal disease in much of the world. Thus. it is incumbent upon the nephrology community to identify new and more effective treatments than are currently available,” Dr. Voelker said.

TGF-beta over-activity has been implicated as a key pathogenic factor in diabetic neuropathy, and it was previously demonstrated that a TGF-beta 1-specific humanized monoclonal antibody was as effective as an antibody against all three TGF-beta isoforms, he said.

“We also had demonstrated that beta 1-specific inhibition in preclinical animal toxicology testing was far more tolerated than when you inhibit all 3 TGF-beta isoforms, which I should mention are all differentially expressed and regulated, but all signal through the same receptor complex,” he added, noting that based on these and other data, it was hypothesized that modulating excessive beta 1 activity with LY would safely slow renal progression in patients with diabetes on background RASi therapy.

The study was overseen by an independent data safety monitoring committee that reviewed unblinded safety data at periodic intervals. No safety issues emerged, but in the later stages of the study the committee did recommend that an unscheduled utility analysis be performed. Based on the results of that analysis, the decision was made to prematurely terminate the study about 4 months before its scheduled completion.

“Unfortunately there was no evidence in any of the study arms of a slowing of the rate of (serum creatinine increase),” Dr. Voelker said, adding that there also was no evidence of a benefit in numerous subgroup analyses, including analyses based on diabetes type.

Dr. Voelker is an employee of Eli Lilly and Co, which sponsored this study.

PHILADELPHIA– Anti-TGF-beta 1 therapy was safe and well-tolerated, but failed to slow disease progression in patients with advanced diabetic nephropathy in a randomized, double-masked, phase 2 dose-ranging study.

In fact, the trial was terminated 4 months early for efficacy futility, Dr. James R. Voelker reported at Kidney Week 2014.

In 416 patients with type 1 or type 2 diabetes and a likelihood of rapid disease progression who were randomized to receive subcutaneous treatment with either placebo or various doses of a beta-1-specific humanized monoclonal neutralizing antibody known as LY2382770 (LY).

Treatment at any dose was not significantly more effective than placebo with respect to the primary outcome measure of mean change in serum creatinine. Mean serum creatinine increased from 2.22 to 2.48 mg/dl in the placebo group, and in the treatment groups it increased from 2.15 to 2.49 mg/dl (2 mg/month group), from 2.13 to 2.49 mg/dl (10 mg/month group), and from 2.15 to 2.50 mg/dl (50 mg/month group), Dr. Voelker of Eli Lilly and Co., Indianapolis, said at the meeting, which was sponsored by the American Society of Nephrology.

Patients in the study were adults aged 25 years or older (mean 62.2 years ) with serum creatinine of 1.3 to 3.3 mg/dl for women, and 1.5 to 3.5 mg/dl for men, or estimated glomerular filtration rate of 20 to 60 ml/min/1.73 m², and they had a 24-hour urine protein/creatinine ratio of at least 800 mg/g. The groups were similar with respect to demographics and baseline characteristic, and most (75%) were men with type 2 diabetes (90%). All patient were receiving stable renin-angiotensin-system inhibition (RASi) therapy.

The intent was to select a population with a likelihood of fairly rapid disease progression during the course of the study to enable detection of a treatment effect, Dr. Voelker explained.

“Diabetic nephropathy is a disease of significant unmet medical need, as it is the leading cause of end-stage renal disease in much of the world. Thus. it is incumbent upon the nephrology community to identify new and more effective treatments than are currently available,” Dr. Voelker said.

TGF-beta over-activity has been implicated as a key pathogenic factor in diabetic neuropathy, and it was previously demonstrated that a TGF-beta 1-specific humanized monoclonal antibody was as effective as an antibody against all three TGF-beta isoforms, he said.

“We also had demonstrated that beta 1-specific inhibition in preclinical animal toxicology testing was far more tolerated than when you inhibit all 3 TGF-beta isoforms, which I should mention are all differentially expressed and regulated, but all signal through the same receptor complex,” he added, noting that based on these and other data, it was hypothesized that modulating excessive beta 1 activity with LY would safely slow renal progression in patients with diabetes on background RASi therapy.

The study was overseen by an independent data safety monitoring committee that reviewed unblinded safety data at periodic intervals. No safety issues emerged, but in the later stages of the study the committee did recommend that an unscheduled utility analysis be performed. Based on the results of that analysis, the decision was made to prematurely terminate the study about 4 months before its scheduled completion.

“Unfortunately there was no evidence in any of the study arms of a slowing of the rate of (serum creatinine increase),” Dr. Voelker said, adding that there also was no evidence of a benefit in numerous subgroup analyses, including analyses based on diabetes type.

Dr. Voelker is an employee of Eli Lilly and Co, which sponsored this study.

PHILADELPHIA– Anti-TGF-beta 1 therapy was safe and well-tolerated, but failed to slow disease progression in patients with advanced diabetic nephropathy in a randomized, double-masked, phase 2 dose-ranging study.

In fact, the trial was terminated 4 months early for efficacy futility, Dr. James R. Voelker reported at Kidney Week 2014.

In 416 patients with type 1 or type 2 diabetes and a likelihood of rapid disease progression who were randomized to receive subcutaneous treatment with either placebo or various doses of a beta-1-specific humanized monoclonal neutralizing antibody known as LY2382770 (LY).

Treatment at any dose was not significantly more effective than placebo with respect to the primary outcome measure of mean change in serum creatinine. Mean serum creatinine increased from 2.22 to 2.48 mg/dl in the placebo group, and in the treatment groups it increased from 2.15 to 2.49 mg/dl (2 mg/month group), from 2.13 to 2.49 mg/dl (10 mg/month group), and from 2.15 to 2.50 mg/dl (50 mg/month group), Dr. Voelker of Eli Lilly and Co., Indianapolis, said at the meeting, which was sponsored by the American Society of Nephrology.

Patients in the study were adults aged 25 years or older (mean 62.2 years ) with serum creatinine of 1.3 to 3.3 mg/dl for women, and 1.5 to 3.5 mg/dl for men, or estimated glomerular filtration rate of 20 to 60 ml/min/1.73 m², and they had a 24-hour urine protein/creatinine ratio of at least 800 mg/g. The groups were similar with respect to demographics and baseline characteristic, and most (75%) were men with type 2 diabetes (90%). All patient were receiving stable renin-angiotensin-system inhibition (RASi) therapy.

The intent was to select a population with a likelihood of fairly rapid disease progression during the course of the study to enable detection of a treatment effect, Dr. Voelker explained.

“Diabetic nephropathy is a disease of significant unmet medical need, as it is the leading cause of end-stage renal disease in much of the world. Thus. it is incumbent upon the nephrology community to identify new and more effective treatments than are currently available,” Dr. Voelker said.

TGF-beta over-activity has been implicated as a key pathogenic factor in diabetic neuropathy, and it was previously demonstrated that a TGF-beta 1-specific humanized monoclonal antibody was as effective as an antibody against all three TGF-beta isoforms, he said.

“We also had demonstrated that beta 1-specific inhibition in preclinical animal toxicology testing was far more tolerated than when you inhibit all 3 TGF-beta isoforms, which I should mention are all differentially expressed and regulated, but all signal through the same receptor complex,” he added, noting that based on these and other data, it was hypothesized that modulating excessive beta 1 activity with LY would safely slow renal progression in patients with diabetes on background RASi therapy.

The study was overseen by an independent data safety monitoring committee that reviewed unblinded safety data at periodic intervals. No safety issues emerged, but in the later stages of the study the committee did recommend that an unscheduled utility analysis be performed. Based on the results of that analysis, the decision was made to prematurely terminate the study about 4 months before its scheduled completion.

“Unfortunately there was no evidence in any of the study arms of a slowing of the rate of (serum creatinine increase),” Dr. Voelker said, adding that there also was no evidence of a benefit in numerous subgroup analyses, including analyses based on diabetes type.

Dr. Voelker is an employee of Eli Lilly and Co, which sponsored this study.

PHILADELPHIA – Patients with type 2 diabetes, chronic kidney disease, and a high risk of obstructive sleep apnea have more rapid loss of kidney function than do similar patients with a low risk of sleep apnea, findings from a retrospective cohort study suggest.

Of 56 patients with diabetic nephropathy who underwent screening for obstructive sleep apnea, 34 (61%) were at high risk. Compared with 22 patients with a low risk score, the high-risk patients had a significantly greater loss of estimated glomerular filtration rate over time (median loss of -3.4 vs. 1.5 ml/min/1.73 m² per year for the high- vs. low-risk patients, respectively), Dr. Roberto Pisoni reported in a poster at the annual meeting of the American Society of Nephrology.

This finding was despite comparable blood pressure for the high- and low-risk groups (systolic: 141.7 and 143.7 mm Hg; diastolic: 72.0 and 72.4 mm Hg, respectively), proteinuria upon admission to a chronic kidney disease clinic (urinary protein/creatinine ratio, 1.9 and 1.6 g/g, respectively), and time spent in clinic (1.9 vs. 2.1 years, respectively), said Dr. Pisoni of the Medical University of South Carolina, Charleston.

Patients in the high- and low-risk groups also had similar baseline gender, body mass index, use of renin-angiotensin-aldosterone system blockers, eGFR, and co-morbidities, he noted.

Data used for this study were from the University of Alabama at Birmingham Chronic Kidney Disease Database. Patients had completed the Berlin questionnaire to assess for sleep apnea during a 9-month study period.

Obstructive sleep apnea is common in patients with type 2 diabetes and is also associated with glomerular hyperfiltration and proteinuria in patients with normal renal function, which raised the question of whether it might be related to chronic kidney disease progression, Dr. Pisoni explained. He noted that the association between obstructive sleep apnea and diabetic nephropathy has not been fully investigated.

The study demonstrated that the “simple approach” of assessing obstructive sleep apnea risk identifies patients who are also at increased risk of CKD progression, he said, adding that the findings require replication in a prospective cohort.

Dr. Pisoni reported having no disclosures.

PHILADELPHIA – Patients with type 2 diabetes, chronic kidney disease, and a high risk of obstructive sleep apnea have more rapid loss of kidney function than do similar patients with a low risk of sleep apnea, findings from a retrospective cohort study suggest.

Of 56 patients with diabetic nephropathy who underwent screening for obstructive sleep apnea, 34 (61%) were at high risk. Compared with 22 patients with a low risk score, the high-risk patients had a significantly greater loss of estimated glomerular filtration rate over time (median loss of -3.4 vs. 1.5 ml/min/1.73 m² per year for the high- vs. low-risk patients, respectively), Dr. Roberto Pisoni reported in a poster at the annual meeting of the American Society of Nephrology.

This finding was despite comparable blood pressure for the high- and low-risk groups (systolic: 141.7 and 143.7 mm Hg; diastolic: 72.0 and 72.4 mm Hg, respectively), proteinuria upon admission to a chronic kidney disease clinic (urinary protein/creatinine ratio, 1.9 and 1.6 g/g, respectively), and time spent in clinic (1.9 vs. 2.1 years, respectively), said Dr. Pisoni of the Medical University of South Carolina, Charleston.

Patients in the high- and low-risk groups also had similar baseline gender, body mass index, use of renin-angiotensin-aldosterone system blockers, eGFR, and co-morbidities, he noted.

Data used for this study were from the University of Alabama at Birmingham Chronic Kidney Disease Database. Patients had completed the Berlin questionnaire to assess for sleep apnea during a 9-month study period.

Obstructive sleep apnea is common in patients with type 2 diabetes and is also associated with glomerular hyperfiltration and proteinuria in patients with normal renal function, which raised the question of whether it might be related to chronic kidney disease progression, Dr. Pisoni explained. He noted that the association between obstructive sleep apnea and diabetic nephropathy has not been fully investigated.

The study demonstrated that the “simple approach” of assessing obstructive sleep apnea risk identifies patients who are also at increased risk of CKD progression, he said, adding that the findings require replication in a prospective cohort.

Dr. Pisoni reported having no disclosures.

PHILADELPHIA – Patients with type 2 diabetes, chronic kidney disease, and a high risk of obstructive sleep apnea have more rapid loss of kidney function than do similar patients with a low risk of sleep apnea, findings from a retrospective cohort study suggest.

Of 56 patients with diabetic nephropathy who underwent screening for obstructive sleep apnea, 34 (61%) were at high risk. Compared with 22 patients with a low risk score, the high-risk patients had a significantly greater loss of estimated glomerular filtration rate over time (median loss of -3.4 vs. 1.5 ml/min/1.73 m² per year for the high- vs. low-risk patients, respectively), Dr. Roberto Pisoni reported in a poster at the annual meeting of the American Society of Nephrology.

This finding was despite comparable blood pressure for the high- and low-risk groups (systolic: 141.7 and 143.7 mm Hg; diastolic: 72.0 and 72.4 mm Hg, respectively), proteinuria upon admission to a chronic kidney disease clinic (urinary protein/creatinine ratio, 1.9 and 1.6 g/g, respectively), and time spent in clinic (1.9 vs. 2.1 years, respectively), said Dr. Pisoni of the Medical University of South Carolina, Charleston.

Patients in the high- and low-risk groups also had similar baseline gender, body mass index, use of renin-angiotensin-aldosterone system blockers, eGFR, and co-morbidities, he noted.

Data used for this study were from the University of Alabama at Birmingham Chronic Kidney Disease Database. Patients had completed the Berlin questionnaire to assess for sleep apnea during a 9-month study period.

Obstructive sleep apnea is common in patients with type 2 diabetes and is also associated with glomerular hyperfiltration and proteinuria in patients with normal renal function, which raised the question of whether it might be related to chronic kidney disease progression, Dr. Pisoni explained. He noted that the association between obstructive sleep apnea and diabetic nephropathy has not been fully investigated.

The study demonstrated that the “simple approach” of assessing obstructive sleep apnea risk identifies patients who are also at increased risk of CKD progression, he said, adding that the findings require replication in a prospective cohort.

Dr. Pisoni reported having no disclosures.