Type 2 Diabetes ICYMI

Ongoing follow-up and lifestyle interventions are needed in lean patients with nonalcoholic fatty liver disease (NAFLD), suggests a panel of experts in a recent review.

They also urge screening for NAFLD in individuals who are older than 40 years with type 2 diabetes, even if they are not overweight.

NAFLD is a leading cause of chronic liver disease that affects more than 25% of the United States and worldwide populations, note lead author Michelle T. Long, MD, Boston Medical Center, Boston University, and colleagues.

Evidence-based approaches

The 15 best practice advice statements covered a wide range of clinical areas, first defining lean as a body mass index (BMI) less than 25 in non-Asian persons and less than 23 in Asian persons.

The authors go on to stipulate, for example, that lean individuals in the general population should not be screened for NAFLD but that screening should be considered for individuals older than 40 years with type 2 diabetes.

More broadly, they write that the condition should be considered in lean individuals with metabolic diseases, such as type 2 diabetes, dyslipidemia, and hypertension, as well as elevated values on liver biochemical tests or incidentally noted hepatic steatosis.

After other causes of liver diseases are ruled out, the authors note that clinicians should consider liver biopsy as the reference test if uncertainties remain about liver injury causes and/or liver fibrosis staging.

They also write that the NAFLD fibrosis score and Fibrosis-4 score, along with imaging techniques, may be used as alternatives to biopsy for staging and during follow-up.

The authors, who provide a diagnosis and management algorithm to aid clinicians, suggest that lean patients with NAFLD follow lifestyle interventions, such as exercise, diet modification, and avoidance of fructose- and sugar-sweetened drinks, to achieve weight loss of 3%-5%.

Vitamin E may be considered, they continue, in patients with biopsy-confirmed nonalcoholic steatohepatitis but without type 2 diabetes or cirrhosis. Additionally, oral pioglitazone may be considered in lean persons with biopsy-confirmed nonalcoholic steatohepatitis without cirrhosis.

In contrast, they write that the role of glucagonlike peptide 1 agonists and sodium-glucose cotransporter 2 inhibitors requires further investigation.

The advice also says that lean patients with NAFLD should be routinely evaluated for comorbid conditions, such as type 2 diabetes, dyslipidemia, and hypertension, and risk-stratified for hepatic fibrosis to identify those with advanced fibrosis or cirrhosis.

For lean patients with NAFLD and clinical markers compatible with liver cirrhosis, twice-yearly surveillance for hepatocellular carcinoma is also advised.

Fatty liver disease in lean people with metabolic conditions

Approached for comment, Liyun Yuan, MD, PhD, assistant professor of clinical medicine, University of Southern California, Los Angeles, said it is very important to have uniform guidelines for general practitioners and other specialties on NAFLD in lean individuals.

Dr. Yuan, who was not involved in the review, told this news organization that it is crucial to raise awareness of NAFLD, just like awareness of breast cancer screening among women of a certain age was increased, so that individuals are screened for metabolic conditions regardless of whether they have obesity or overweight.

Zobair Younossi, MD, MPH, professor of medicine, Virginia Commonwealth University, Inova Campus, Falls Church, Va., added that there is a lack of awareness that NAFLD occurs in lean individuals, especially in those who have diabetes.

He said in an interview that although it is accurate to define individuals as being lean in terms of their BMI, the best way is to look not only at BMI but also at waist circumference.

Dr. Younossi said that he and his colleagues have shown that when BMI is combined with waist circumference, the prediction of mortality risk in NAFLD is affected, such that lean individuals with an obese waist circumference have a higher risk for all-cause mortality.

Dr. Long is supported in part by the National Institute of Diabetes and Digestive and Kidney Diseases, Doris Duke Charitable Foundation, Gilead Sciences Research Scholars Award, Boston University School of Medicine Department of Medicine Career Investment Award, and Boston University Clinical Translational Science Institute. Dr. Long declares relationships with Novo Nordisk, Echosens Corporation, and Gilead Sciences. Dr. Yuan declares relationships with Genfit, Intercept, and Gilead Sciences. Dr. Younossi declares no relevant relationships.

A version of this article first appeared on Medscape.com.

*This article was updated on July 27, 2022.

Ongoing follow-up and lifestyle interventions are needed in lean patients with nonalcoholic fatty liver disease (NAFLD), suggests a panel of experts in a recent review.

They also urge screening for NAFLD in individuals who are older than 40 years with type 2 diabetes, even if they are not overweight.

NAFLD is a leading cause of chronic liver disease that affects more than 25% of the United States and worldwide populations, note lead author Michelle T. Long, MD, Boston Medical Center, Boston University, and colleagues.

Evidence-based approaches

The 15 best practice advice statements covered a wide range of clinical areas, first defining lean as a body mass index (BMI) less than 25 in non-Asian persons and less than 23 in Asian persons.

The authors go on to stipulate, for example, that lean individuals in the general population should not be screened for NAFLD but that screening should be considered for individuals older than 40 years with type 2 diabetes.

More broadly, they write that the condition should be considered in lean individuals with metabolic diseases, such as type 2 diabetes, dyslipidemia, and hypertension, as well as elevated values on liver biochemical tests or incidentally noted hepatic steatosis.

After other causes of liver diseases are ruled out, the authors note that clinicians should consider liver biopsy as the reference test if uncertainties remain about liver injury causes and/or liver fibrosis staging.

They also write that the NAFLD fibrosis score and Fibrosis-4 score, along with imaging techniques, may be used as alternatives to biopsy for staging and during follow-up.

The authors, who provide a diagnosis and management algorithm to aid clinicians, suggest that lean patients with NAFLD follow lifestyle interventions, such as exercise, diet modification, and avoidance of fructose- and sugar-sweetened drinks, to achieve weight loss of 3%-5%.

Vitamin E may be considered, they continue, in patients with biopsy-confirmed nonalcoholic steatohepatitis but without type 2 diabetes or cirrhosis. Additionally, oral pioglitazone may be considered in lean persons with biopsy-confirmed nonalcoholic steatohepatitis without cirrhosis.

In contrast, they write that the role of glucagonlike peptide 1 agonists and sodium-glucose cotransporter 2 inhibitors requires further investigation.

The advice also says that lean patients with NAFLD should be routinely evaluated for comorbid conditions, such as type 2 diabetes, dyslipidemia, and hypertension, and risk-stratified for hepatic fibrosis to identify those with advanced fibrosis or cirrhosis.

For lean patients with NAFLD and clinical markers compatible with liver cirrhosis, twice-yearly surveillance for hepatocellular carcinoma is also advised.

Fatty liver disease in lean people with metabolic conditions

Approached for comment, Liyun Yuan, MD, PhD, assistant professor of clinical medicine, University of Southern California, Los Angeles, said it is very important to have uniform guidelines for general practitioners and other specialties on NAFLD in lean individuals.

Dr. Yuan, who was not involved in the review, told this news organization that it is crucial to raise awareness of NAFLD, just like awareness of breast cancer screening among women of a certain age was increased, so that individuals are screened for metabolic conditions regardless of whether they have obesity or overweight.

Zobair Younossi, MD, MPH, professor of medicine, Virginia Commonwealth University, Inova Campus, Falls Church, Va., added that there is a lack of awareness that NAFLD occurs in lean individuals, especially in those who have diabetes.

He said in an interview that although it is accurate to define individuals as being lean in terms of their BMI, the best way is to look not only at BMI but also at waist circumference.

Dr. Younossi said that he and his colleagues have shown that when BMI is combined with waist circumference, the prediction of mortality risk in NAFLD is affected, such that lean individuals with an obese waist circumference have a higher risk for all-cause mortality.

Dr. Long is supported in part by the National Institute of Diabetes and Digestive and Kidney Diseases, Doris Duke Charitable Foundation, Gilead Sciences Research Scholars Award, Boston University School of Medicine Department of Medicine Career Investment Award, and Boston University Clinical Translational Science Institute. Dr. Long declares relationships with Novo Nordisk, Echosens Corporation, and Gilead Sciences. Dr. Yuan declares relationships with Genfit, Intercept, and Gilead Sciences. Dr. Younossi declares no relevant relationships.

A version of this article first appeared on Medscape.com.

*This article was updated on July 27, 2022.

Ongoing follow-up and lifestyle interventions are needed in lean patients with nonalcoholic fatty liver disease (NAFLD), suggests a panel of experts in a recent review.

They also urge screening for NAFLD in individuals who are older than 40 years with type 2 diabetes, even if they are not overweight.

NAFLD is a leading cause of chronic liver disease that affects more than 25% of the United States and worldwide populations, note lead author Michelle T. Long, MD, Boston Medical Center, Boston University, and colleagues.

Evidence-based approaches

The 15 best practice advice statements covered a wide range of clinical areas, first defining lean as a body mass index (BMI) less than 25 in non-Asian persons and less than 23 in Asian persons.

The authors go on to stipulate, for example, that lean individuals in the general population should not be screened for NAFLD but that screening should be considered for individuals older than 40 years with type 2 diabetes.

More broadly, they write that the condition should be considered in lean individuals with metabolic diseases, such as type 2 diabetes, dyslipidemia, and hypertension, as well as elevated values on liver biochemical tests or incidentally noted hepatic steatosis.

After other causes of liver diseases are ruled out, the authors note that clinicians should consider liver biopsy as the reference test if uncertainties remain about liver injury causes and/or liver fibrosis staging.

They also write that the NAFLD fibrosis score and Fibrosis-4 score, along with imaging techniques, may be used as alternatives to biopsy for staging and during follow-up.

The authors, who provide a diagnosis and management algorithm to aid clinicians, suggest that lean patients with NAFLD follow lifestyle interventions, such as exercise, diet modification, and avoidance of fructose- and sugar-sweetened drinks, to achieve weight loss of 3%-5%.

Vitamin E may be considered, they continue, in patients with biopsy-confirmed nonalcoholic steatohepatitis but without type 2 diabetes or cirrhosis. Additionally, oral pioglitazone may be considered in lean persons with biopsy-confirmed nonalcoholic steatohepatitis without cirrhosis.

In contrast, they write that the role of glucagonlike peptide 1 agonists and sodium-glucose cotransporter 2 inhibitors requires further investigation.

The advice also says that lean patients with NAFLD should be routinely evaluated for comorbid conditions, such as type 2 diabetes, dyslipidemia, and hypertension, and risk-stratified for hepatic fibrosis to identify those with advanced fibrosis or cirrhosis.

For lean patients with NAFLD and clinical markers compatible with liver cirrhosis, twice-yearly surveillance for hepatocellular carcinoma is also advised.

Fatty liver disease in lean people with metabolic conditions

Approached for comment, Liyun Yuan, MD, PhD, assistant professor of clinical medicine, University of Southern California, Los Angeles, said it is very important to have uniform guidelines for general practitioners and other specialties on NAFLD in lean individuals.

Dr. Yuan, who was not involved in the review, told this news organization that it is crucial to raise awareness of NAFLD, just like awareness of breast cancer screening among women of a certain age was increased, so that individuals are screened for metabolic conditions regardless of whether they have obesity or overweight.

Zobair Younossi, MD, MPH, professor of medicine, Virginia Commonwealth University, Inova Campus, Falls Church, Va., added that there is a lack of awareness that NAFLD occurs in lean individuals, especially in those who have diabetes.

He said in an interview that although it is accurate to define individuals as being lean in terms of their BMI, the best way is to look not only at BMI but also at waist circumference.

Dr. Younossi said that he and his colleagues have shown that when BMI is combined with waist circumference, the prediction of mortality risk in NAFLD is affected, such that lean individuals with an obese waist circumference have a higher risk for all-cause mortality.

Dr. Long is supported in part by the National Institute of Diabetes and Digestive and Kidney Diseases, Doris Duke Charitable Foundation, Gilead Sciences Research Scholars Award, Boston University School of Medicine Department of Medicine Career Investment Award, and Boston University Clinical Translational Science Institute. Dr. Long declares relationships with Novo Nordisk, Echosens Corporation, and Gilead Sciences. Dr. Yuan declares relationships with Genfit, Intercept, and Gilead Sciences. Dr. Younossi declares no relevant relationships.

A version of this article first appeared on Medscape.com.

*This article was updated on July 27, 2022.

Those of us who treat patients with type 2 diabetes (T2D) daily have long recognized a disturbing irony: diabetes is a disease whose management requires consistency in approach and constancy in delivery, but it is most prevalent among those whose lives often allow little to no time for either. 

In our clinic, many patients with diabetes are struggling, in some way, to incorporate diabetes management into their daily lives. They are juggling multiple jobs and family responsibilities; they are working jobs with inconsistent access to food or refrigeration (such as farming, service industry work, and others); and many—even those with insurance—are struggling to afford their insulin and non insulin medications, insulin administration supplies, and glucose testing equipment.

Studies show how stress deleteriously affects this disease. The body does not deal well with these frequent and persistent stressors; higher cortisol levels result in higher blood glucose levels, increased systemic inflammation, and other drivers of both diabetes and its complications; all have been extensively documented. 

What has been frustrating for our clinical community is knowing that since the early 2000s, new diabetes medications and technologies have been available that can make a difference in our patients’ lives, but for various reasons, they have not been well adopted, particularly among patients most likely to benefit from them. Consequently, we have not consistently seen meaningfully reduced glycated hemoglobin (A1c) levels or reduced rates of acute or chronic diabetes complications. Therapeutic inertia exists at the patient, systemic, and physician levels. 

Many of the new glucose-lowering medications can also improve cardiovascular and kidney disease outcomes with low risk for hypoglycemia and weight gain. Diabetes technologies like insulin pumps and continuous glucose monitors (CGM) have been demonstrated in clinical trials to improve A1c and reduce hypoglycemia risk. But the reality is that clinicians are seeing an increasing number of patients with high A1c, with hypoglycemia, with severe hyperglycemia, and with long-term diabetes complications. 

If these advancements are supposed to improve health outcomes, why are patient, community, and population health not improving? Why are some patients not receiving the care they need, while others get extra services that do not improve their health and may even harm them?

These advancements also create new questions for clinicians. At what point in the disease course should existing medications be ramped up, ramped down, or changed? Which patient characteristics or comorbidities allow or do not allow these changes?  When should we use technologies or when does their burden outweigh their potential benefits? What resources and support systems do our patients need to live well with their disease and how can these be procured?

Herein lies the problem: Diabetes is a dynamic disease that needs to be handled in a dynamic way, and that has not universally—or even frequently—occurred. Management must be a team endeavor, meaning that both patient and clinician must be proactive in diabetes management. It has been our experience, demonstrated in our work and in other studies, that success relies on a robust and comprehensive primary care system whose team members—physicians, advanced practice providers, nurses, pharmacists, certified diabetes care and education specialists, social workers, nurses, pharmacists, and dietitians—are all resilient and motivated to tackle one of the most complex, multifaceted, and multidimensional chronic health conditions in our practice.

Proactivity also includes consistent monitoring, learning from successes and failures, and public reporting. For the patient, proactive involvement generally means self-care multiple times a day.    

Let us now discuss the evidence that prompted our team’s proactive approach to caring for people living with diabetes.

Gauges and perspective

The prevalence of T2D in this country stands at 11.3% within the adult population. Between 2015 and 2020, death from diabetes increased by 27%.

For years, the research community has documented the wide range of socioeconomic factors that increase the risk for developing T2D and that, once developed, make it more difficult for patients to manage their disease and achieve optimal health outcomes that are possible with available medications and technologies. 

In 2019, Kazemian et al published work that examined the indicators of diabetes management progress (eg, A1c levels, cholesterol levels) of 1742 individuals, from 2005 to 2016. Just 23% to 25% of these patients achieved all goals, even though, during the study period, numerous medications were approved to manage disease better. Arguably, these should have improved the all-goal findings in the study. 

The first injectable glucagon-like peptide 1 receptor agonist (GLP-1 RA) was approved in 2005; between 2013 and 2016, the FDA also approved 4 sodium-glucose cotransporter 2 (SGLT2) inhibitors. Both medication classes can safely and effectively lower A1c with no weight gain and low risk for hypoglycemia. Over the past 4 years, a robust body of evidence has emerged to show that GLP-1 RAs and SGLT2 inhibitors not only lower A1c, but also reduce the likelihood of death from cardiovascular and kidney diseases. SGLT2 inhibitors are better at saving lives from hypertensive heart failure while the GLP-1 RAs are more protective from atherosclerotic cardiovascular events like myocardial infarction and stroke, as compared with placebo. Yet, these medications have not been, and continue not to be, regularly prescribed. In 1 study, the authors found that the rate of use for SGLT2 inhibitors was 3.8% in 2015 and 11.9% in 2019.

But there are several other reasons that patients do not receive these medicines.

Insurance

We conducted a retrospective cohort study of  382,574 adults between 58 and 66 years of age, insured by either a Medicare Advantage plan or commercial insurance, and compared treatment initiation of the 3 most common brand-name, second-line diabetes medications (as opposed to generic sulfonylureas), between 2016 and 2019. The rate of initiation was universally lower for Medicare Advantage members vs commercially insured individuals. 

While the rates of initiation of GLP-1 RAs, SGLT2 inhibitors, and dipeptidyl peptidase 4 (DPP-4) inhibitors increased between 2016 and 2019, rates were significantly higher among patients with commercial insurance. Specifically, GLP-1 RA initiation increased from 2.1% to 20.0% among commercial insurance beneficiaries and from 1.5% to 11.4% among Medicare Advantage beneficiaries. SGLT2 inhibitor initiation increased from 2.7% to 18.2% with commercial insurance and from 1.57% to 8.51% with Medicare Advantage. DPP-4 inhibitor initiation increased from 3.3% to 11.7% with commercial insurance and from 2.44% to 7.68% with Medicare Advantage. Within each calendar year, the odds of initiating one of these 3 medications with Medicare Advantage as compared with commercial insurance ranged from 0.28 to 0.70 for GLP-1 RAs; from 0.21 to 0.57 for SGLT2 inhibitors; and from 0.37 to 0.73 for DPP-4 inhibitors. 

We also looked at the initiation of these medications in individuals with cardiorenal comorbidities. In many cases, a drug was prescribed indiscriminately. A patient who would benefit from a GLP-1 RA because of cardiovascular, cerebrovascular, or kidney disease was less likely to be prescribed a GLP-1 RA than a medication like a DPP-4 inhibitor, which usually has the same formulary tier/class but does not have any of the cardiovascular or kidney benefits. Likewise, in those with heart failure or kidney disease, an SGLT2 inhibitor would have been the appropriate choice, but these patients were too often started on a DPP-4 inhibitor, which is not advised for those with heart failure and does provide kidney benefits. 

Last year, Tummalapalli et al, in their evaluation of 4135 US health plans, including commercial- or employer-based, Medicare, Medicaid, and other public health plans, identified multiple barriers to accessing SGLT2 inhibitor medications. While all plans included at least 1 SGLT2 inhibitor on their formularies, they restricted access in other ways. Prior authorizations were required by nearly half of Medicaid plans and nearly 40% of other public plans such as the Veterans Health Administration. Medicare and other public plans commonly imposed quantity limits on fills. Commercial plans frequently (up to 40%) required step therapy (use or failure of a generic diabetes medication) before approval. Copayments were also high in commercial plans, Medicare, and others. 

The need for prior authorizations dominates attempts to prescribe. Centene Corporation, for example, which manages plans for private and public payers, will not approve use of an SGLT2 inhibitor until the patient fails for 3 consecutive months on a prior treatment, has established cardiovascular disease or diabetic nephropathy, or has multiple cardiovascular risk factors. These comorbidities must be documented and verified, and the prior authorizations must be completed, often resulting in substantial administrative burden to clinicians. No wonder many, especially in primary care, may be wary of prescribing drugs that come with a paperwork trail and hours spent on documentation and insurance appeals, rather than on patient care.

The same can be said for prescribing a GLP-1 RA. United Healthcare’s Oxford Benefit Management requires that clinicians show a “history of suboptimal response, contraindication, or intolerance to metformin” before prescribing any of the 8 GLP-1 RAs. 

The average retail cost of 30 empagliflozin tablets, a once-daily medication, is $752. During the pandemic, 24% of the 5000 patients surveyed in an American Diabetes Association (ADA) poll used their stimulus check, relied on loans, or spent savings to pay for diabetes care. GLP-1 RA medications are even more expensive.  Depending on the patient’s pharmacy benefits, they may have to pay a substantial coinsurance out of pocket even after the annual deductible is met, creating financial barriers to starting and continuing recommended, evidence-based medications. Even if patients do get the recommended medications, they may be forced to ration other aspects of their lives, including other medications, food, and other necessities.

There are other important barriers to optimal utilization of evidence-based therapies, stemming from the fundamental social determinants of health: low income, low education level, and living in a socioeconomically deprived neighborhood.  

Social Determinants of Health

Diabetes prevalence is higher in patients experiencing socioeconomic and other structural barriers to health and health care. Fundamentally, 1 study showed that prevalence of diabetes was 1.4 times higher among people living on less than $15,000 a year, as opposed to those earning at least $50,000 a year. 

The risk of diabetes complications is also higher in individuals experiencing food or housing insecurity, those who have low income or education level, and residents in rural and socioeconomically deprived neighborhoods. Importantly, the same patient populations are also less likely to receive timely evidence-based care, contributing to and worsening health disparities. Despite their prevalence and importance, social determinants of health (SDoH) are not routinely recognized or discussed during clinical encounters, such that improving diabetes care and health outcomes is predicated on developing a system to screen for, recognize, and address the wide range of barriers faced by our patients. If a patient cannot afford a new medication or get to the clinic on a regular basis, lacks access to healthy food, or does not have time for diabetes self-management education or to focus on their health, then their well-being will suffer.

Many of these SDoH disproportionately affect racial and ethnic minority populations as the direct result of longstanding and deeply embedded systems, policies, and laws that underlie disparities in diabetes incidence, prevalence, management, and outcomes. As such, structural racism is increasingly recognized as a root cause of health disparities in diabetes and other chronic health conditions.

Proactive strategies

Since reactive care has not and cannot provide patients with the help they need and deserve, many in the diabetes care community have turned to proactive, team-based care. The Chronic Care Model, established in the 1990s, stresses decision-making support, strong team organization and delivery system design, and the wherewithal to monitor progress continually. Research has shown that the best results for patients stem from a multidisciplinary, data-driven, and proactive approach to identifying and meeting the totality of patient care needs. 

The ADA stresses the importance of comprehensive, team-based care for successful management of diabetes. This includes expanding the role of teams to implement evidence-based diabetes care, using electronic health record tools to support timely and guideline-recommended delivery of services, empowering and educating patients and caregivers, eliciting and addressing financial and psychosocial barriers to care, and identifying, developing, and engaging community resources to support better health and well-being.

Recognizing the centrality of team-based care to diabetes management, our team has developed and implemented an enhanced primary care diabetes (EPCD) model across the internal medicine and family medicine practices of Mayo Clinic, first in Rochester, Minnesota and then across multiple rural and small urban sites in southeast Minnesota. This model is centered around the primary care team nurse, who partners with clinicians to oversee, enforce, and coordinate the diabetes management of patients paneled to those clinicians. Nurses proactively identify patients, engage other members of the healthcare team (eg, pharmacists, social workers, certified diabetes care and education specialists) as needed, and maintain a continuous relationship with each patient to help them achieve and maintain their goals. This model was not only effective at improving glycemic control and other indicators of diabetes care quality, but also improved nursing and clinician satisfaction. 

It is important to recognize that comprehensive diabetes care comprises both medical and nonmedical interventions that address the totality of the patient’s care needs and the circumstances that hinder optimal health. Increasingly, robust data are emerging in support of nonmedical interventions that target SDoH, including structural racism as a root cause of racial and ethnic disparities in diabetes care and outcomes, with demonstrated evidence of improved health outcomes and narrowed health disparities.

It takes work, effort, and commitment to manage diabetes. But a team-based approach allows players on all sides to win. 

Those of us who treat patients with type 2 diabetes (T2D) daily have long recognized a disturbing irony: diabetes is a disease whose management requires consistency in approach and constancy in delivery, but it is most prevalent among those whose lives often allow little to no time for either. 

In our clinic, many patients with diabetes are struggling, in some way, to incorporate diabetes management into their daily lives. They are juggling multiple jobs and family responsibilities; they are working jobs with inconsistent access to food or refrigeration (such as farming, service industry work, and others); and many—even those with insurance—are struggling to afford their insulin and non insulin medications, insulin administration supplies, and glucose testing equipment.

Studies show how stress deleteriously affects this disease. The body does not deal well with these frequent and persistent stressors; higher cortisol levels result in higher blood glucose levels, increased systemic inflammation, and other drivers of both diabetes and its complications; all have been extensively documented. 

What has been frustrating for our clinical community is knowing that since the early 2000s, new diabetes medications and technologies have been available that can make a difference in our patients’ lives, but for various reasons, they have not been well adopted, particularly among patients most likely to benefit from them. Consequently, we have not consistently seen meaningfully reduced glycated hemoglobin (A1c) levels or reduced rates of acute or chronic diabetes complications. Therapeutic inertia exists at the patient, systemic, and physician levels. 

Many of the new glucose-lowering medications can also improve cardiovascular and kidney disease outcomes with low risk for hypoglycemia and weight gain. Diabetes technologies like insulin pumps and continuous glucose monitors (CGM) have been demonstrated in clinical trials to improve A1c and reduce hypoglycemia risk. But the reality is that clinicians are seeing an increasing number of patients with high A1c, with hypoglycemia, with severe hyperglycemia, and with long-term diabetes complications. 

If these advancements are supposed to improve health outcomes, why are patient, community, and population health not improving? Why are some patients not receiving the care they need, while others get extra services that do not improve their health and may even harm them?

These advancements also create new questions for clinicians. At what point in the disease course should existing medications be ramped up, ramped down, or changed? Which patient characteristics or comorbidities allow or do not allow these changes?  When should we use technologies or when does their burden outweigh their potential benefits? What resources and support systems do our patients need to live well with their disease and how can these be procured?

Herein lies the problem: Diabetes is a dynamic disease that needs to be handled in a dynamic way, and that has not universally—or even frequently—occurred. Management must be a team endeavor, meaning that both patient and clinician must be proactive in diabetes management. It has been our experience, demonstrated in our work and in other studies, that success relies on a robust and comprehensive primary care system whose team members—physicians, advanced practice providers, nurses, pharmacists, certified diabetes care and education specialists, social workers, nurses, pharmacists, and dietitians—are all resilient and motivated to tackle one of the most complex, multifaceted, and multidimensional chronic health conditions in our practice.

Proactivity also includes consistent monitoring, learning from successes and failures, and public reporting. For the patient, proactive involvement generally means self-care multiple times a day.    

Let us now discuss the evidence that prompted our team’s proactive approach to caring for people living with diabetes.

Gauges and perspective

The prevalence of T2D in this country stands at 11.3% within the adult population. Between 2015 and 2020, death from diabetes increased by 27%.

For years, the research community has documented the wide range of socioeconomic factors that increase the risk for developing T2D and that, once developed, make it more difficult for patients to manage their disease and achieve optimal health outcomes that are possible with available medications and technologies. 

In 2019, Kazemian et al published work that examined the indicators of diabetes management progress (eg, A1c levels, cholesterol levels) of 1742 individuals, from 2005 to 2016. Just 23% to 25% of these patients achieved all goals, even though, during the study period, numerous medications were approved to manage disease better. Arguably, these should have improved the all-goal findings in the study. 

The first injectable glucagon-like peptide 1 receptor agonist (GLP-1 RA) was approved in 2005; between 2013 and 2016, the FDA also approved 4 sodium-glucose cotransporter 2 (SGLT2) inhibitors. Both medication classes can safely and effectively lower A1c with no weight gain and low risk for hypoglycemia. Over the past 4 years, a robust body of evidence has emerged to show that GLP-1 RAs and SGLT2 inhibitors not only lower A1c, but also reduce the likelihood of death from cardiovascular and kidney diseases. SGLT2 inhibitors are better at saving lives from hypertensive heart failure while the GLP-1 RAs are more protective from atherosclerotic cardiovascular events like myocardial infarction and stroke, as compared with placebo. Yet, these medications have not been, and continue not to be, regularly prescribed. In 1 study, the authors found that the rate of use for SGLT2 inhibitors was 3.8% in 2015 and 11.9% in 2019.

But there are several other reasons that patients do not receive these medicines.

Insurance

We conducted a retrospective cohort study of  382,574 adults between 58 and 66 years of age, insured by either a Medicare Advantage plan or commercial insurance, and compared treatment initiation of the 3 most common brand-name, second-line diabetes medications (as opposed to generic sulfonylureas), between 2016 and 2019. The rate of initiation was universally lower for Medicare Advantage members vs commercially insured individuals. 

While the rates of initiation of GLP-1 RAs, SGLT2 inhibitors, and dipeptidyl peptidase 4 (DPP-4) inhibitors increased between 2016 and 2019, rates were significantly higher among patients with commercial insurance. Specifically, GLP-1 RA initiation increased from 2.1% to 20.0% among commercial insurance beneficiaries and from 1.5% to 11.4% among Medicare Advantage beneficiaries. SGLT2 inhibitor initiation increased from 2.7% to 18.2% with commercial insurance and from 1.57% to 8.51% with Medicare Advantage. DPP-4 inhibitor initiation increased from 3.3% to 11.7% with commercial insurance and from 2.44% to 7.68% with Medicare Advantage. Within each calendar year, the odds of initiating one of these 3 medications with Medicare Advantage as compared with commercial insurance ranged from 0.28 to 0.70 for GLP-1 RAs; from 0.21 to 0.57 for SGLT2 inhibitors; and from 0.37 to 0.73 for DPP-4 inhibitors. 

We also looked at the initiation of these medications in individuals with cardiorenal comorbidities. In many cases, a drug was prescribed indiscriminately. A patient who would benefit from a GLP-1 RA because of cardiovascular, cerebrovascular, or kidney disease was less likely to be prescribed a GLP-1 RA than a medication like a DPP-4 inhibitor, which usually has the same formulary tier/class but does not have any of the cardiovascular or kidney benefits. Likewise, in those with heart failure or kidney disease, an SGLT2 inhibitor would have been the appropriate choice, but these patients were too often started on a DPP-4 inhibitor, which is not advised for those with heart failure and does provide kidney benefits. 

Last year, Tummalapalli et al, in their evaluation of 4135 US health plans, including commercial- or employer-based, Medicare, Medicaid, and other public health plans, identified multiple barriers to accessing SGLT2 inhibitor medications. While all plans included at least 1 SGLT2 inhibitor on their formularies, they restricted access in other ways. Prior authorizations were required by nearly half of Medicaid plans and nearly 40% of other public plans such as the Veterans Health Administration. Medicare and other public plans commonly imposed quantity limits on fills. Commercial plans frequently (up to 40%) required step therapy (use or failure of a generic diabetes medication) before approval. Copayments were also high in commercial plans, Medicare, and others. 

The need for prior authorizations dominates attempts to prescribe. Centene Corporation, for example, which manages plans for private and public payers, will not approve use of an SGLT2 inhibitor until the patient fails for 3 consecutive months on a prior treatment, has established cardiovascular disease or diabetic nephropathy, or has multiple cardiovascular risk factors. These comorbidities must be documented and verified, and the prior authorizations must be completed, often resulting in substantial administrative burden to clinicians. No wonder many, especially in primary care, may be wary of prescribing drugs that come with a paperwork trail and hours spent on documentation and insurance appeals, rather than on patient care.

The same can be said for prescribing a GLP-1 RA. United Healthcare’s Oxford Benefit Management requires that clinicians show a “history of suboptimal response, contraindication, or intolerance to metformin” before prescribing any of the 8 GLP-1 RAs. 

The average retail cost of 30 empagliflozin tablets, a once-daily medication, is $752. During the pandemic, 24% of the 5000 patients surveyed in an American Diabetes Association (ADA) poll used their stimulus check, relied on loans, or spent savings to pay for diabetes care. GLP-1 RA medications are even more expensive.  Depending on the patient’s pharmacy benefits, they may have to pay a substantial coinsurance out of pocket even after the annual deductible is met, creating financial barriers to starting and continuing recommended, evidence-based medications. Even if patients do get the recommended medications, they may be forced to ration other aspects of their lives, including other medications, food, and other necessities.

There are other important barriers to optimal utilization of evidence-based therapies, stemming from the fundamental social determinants of health: low income, low education level, and living in a socioeconomically deprived neighborhood.  

Social Determinants of Health

Diabetes prevalence is higher in patients experiencing socioeconomic and other structural barriers to health and health care. Fundamentally, 1 study showed that prevalence of diabetes was 1.4 times higher among people living on less than $15,000 a year, as opposed to those earning at least $50,000 a year. 

The risk of diabetes complications is also higher in individuals experiencing food or housing insecurity, those who have low income or education level, and residents in rural and socioeconomically deprived neighborhoods. Importantly, the same patient populations are also less likely to receive timely evidence-based care, contributing to and worsening health disparities. Despite their prevalence and importance, social determinants of health (SDoH) are not routinely recognized or discussed during clinical encounters, such that improving diabetes care and health outcomes is predicated on developing a system to screen for, recognize, and address the wide range of barriers faced by our patients. If a patient cannot afford a new medication or get to the clinic on a regular basis, lacks access to healthy food, or does not have time for diabetes self-management education or to focus on their health, then their well-being will suffer.

Many of these SDoH disproportionately affect racial and ethnic minority populations as the direct result of longstanding and deeply embedded systems, policies, and laws that underlie disparities in diabetes incidence, prevalence, management, and outcomes. As such, structural racism is increasingly recognized as a root cause of health disparities in diabetes and other chronic health conditions.

Proactive strategies

Since reactive care has not and cannot provide patients with the help they need and deserve, many in the diabetes care community have turned to proactive, team-based care. The Chronic Care Model, established in the 1990s, stresses decision-making support, strong team organization and delivery system design, and the wherewithal to monitor progress continually. Research has shown that the best results for patients stem from a multidisciplinary, data-driven, and proactive approach to identifying and meeting the totality of patient care needs. 

The ADA stresses the importance of comprehensive, team-based care for successful management of diabetes. This includes expanding the role of teams to implement evidence-based diabetes care, using electronic health record tools to support timely and guideline-recommended delivery of services, empowering and educating patients and caregivers, eliciting and addressing financial and psychosocial barriers to care, and identifying, developing, and engaging community resources to support better health and well-being.

Recognizing the centrality of team-based care to diabetes management, our team has developed and implemented an enhanced primary care diabetes (EPCD) model across the internal medicine and family medicine practices of Mayo Clinic, first in Rochester, Minnesota and then across multiple rural and small urban sites in southeast Minnesota. This model is centered around the primary care team nurse, who partners with clinicians to oversee, enforce, and coordinate the diabetes management of patients paneled to those clinicians. Nurses proactively identify patients, engage other members of the healthcare team (eg, pharmacists, social workers, certified diabetes care and education specialists) as needed, and maintain a continuous relationship with each patient to help them achieve and maintain their goals. This model was not only effective at improving glycemic control and other indicators of diabetes care quality, but also improved nursing and clinician satisfaction. 

It is important to recognize that comprehensive diabetes care comprises both medical and nonmedical interventions that address the totality of the patient’s care needs and the circumstances that hinder optimal health. Increasingly, robust data are emerging in support of nonmedical interventions that target SDoH, including structural racism as a root cause of racial and ethnic disparities in diabetes care and outcomes, with demonstrated evidence of improved health outcomes and narrowed health disparities.

It takes work, effort, and commitment to manage diabetes. But a team-based approach allows players on all sides to win. 

Those of us who treat patients with type 2 diabetes (T2D) daily have long recognized a disturbing irony: diabetes is a disease whose management requires consistency in approach and constancy in delivery, but it is most prevalent among those whose lives often allow little to no time for either. 

In our clinic, many patients with diabetes are struggling, in some way, to incorporate diabetes management into their daily lives. They are juggling multiple jobs and family responsibilities; they are working jobs with inconsistent access to food or refrigeration (such as farming, service industry work, and others); and many—even those with insurance—are struggling to afford their insulin and non insulin medications, insulin administration supplies, and glucose testing equipment.

Studies show how stress deleteriously affects this disease. The body does not deal well with these frequent and persistent stressors; higher cortisol levels result in higher blood glucose levels, increased systemic inflammation, and other drivers of both diabetes and its complications; all have been extensively documented. 

What has been frustrating for our clinical community is knowing that since the early 2000s, new diabetes medications and technologies have been available that can make a difference in our patients’ lives, but for various reasons, they have not been well adopted, particularly among patients most likely to benefit from them. Consequently, we have not consistently seen meaningfully reduced glycated hemoglobin (A1c) levels or reduced rates of acute or chronic diabetes complications. Therapeutic inertia exists at the patient, systemic, and physician levels. 

Many of the new glucose-lowering medications can also improve cardiovascular and kidney disease outcomes with low risk for hypoglycemia and weight gain. Diabetes technologies like insulin pumps and continuous glucose monitors (CGM) have been demonstrated in clinical trials to improve A1c and reduce hypoglycemia risk. But the reality is that clinicians are seeing an increasing number of patients with high A1c, with hypoglycemia, with severe hyperglycemia, and with long-term diabetes complications. 

If these advancements are supposed to improve health outcomes, why are patient, community, and population health not improving? Why are some patients not receiving the care they need, while others get extra services that do not improve their health and may even harm them?

These advancements also create new questions for clinicians. At what point in the disease course should existing medications be ramped up, ramped down, or changed? Which patient characteristics or comorbidities allow or do not allow these changes?  When should we use technologies or when does their burden outweigh their potential benefits? What resources and support systems do our patients need to live well with their disease and how can these be procured?

Herein lies the problem: Diabetes is a dynamic disease that needs to be handled in a dynamic way, and that has not universally—or even frequently—occurred. Management must be a team endeavor, meaning that both patient and clinician must be proactive in diabetes management. It has been our experience, demonstrated in our work and in other studies, that success relies on a robust and comprehensive primary care system whose team members—physicians, advanced practice providers, nurses, pharmacists, certified diabetes care and education specialists, social workers, nurses, pharmacists, and dietitians—are all resilient and motivated to tackle one of the most complex, multifaceted, and multidimensional chronic health conditions in our practice.

Proactivity also includes consistent monitoring, learning from successes and failures, and public reporting. For the patient, proactive involvement generally means self-care multiple times a day.    

Let us now discuss the evidence that prompted our team’s proactive approach to caring for people living with diabetes.

Gauges and perspective

The prevalence of T2D in this country stands at 11.3% within the adult population. Between 2015 and 2020, death from diabetes increased by 27%.

For years, the research community has documented the wide range of socioeconomic factors that increase the risk for developing T2D and that, once developed, make it more difficult for patients to manage their disease and achieve optimal health outcomes that are possible with available medications and technologies. 

In 2019, Kazemian et al published work that examined the indicators of diabetes management progress (eg, A1c levels, cholesterol levels) of 1742 individuals, from 2005 to 2016. Just 23% to 25% of these patients achieved all goals, even though, during the study period, numerous medications were approved to manage disease better. Arguably, these should have improved the all-goal findings in the study. 

The first injectable glucagon-like peptide 1 receptor agonist (GLP-1 RA) was approved in 2005; between 2013 and 2016, the FDA also approved 4 sodium-glucose cotransporter 2 (SGLT2) inhibitors. Both medication classes can safely and effectively lower A1c with no weight gain and low risk for hypoglycemia. Over the past 4 years, a robust body of evidence has emerged to show that GLP-1 RAs and SGLT2 inhibitors not only lower A1c, but also reduce the likelihood of death from cardiovascular and kidney diseases. SGLT2 inhibitors are better at saving lives from hypertensive heart failure while the GLP-1 RAs are more protective from atherosclerotic cardiovascular events like myocardial infarction and stroke, as compared with placebo. Yet, these medications have not been, and continue not to be, regularly prescribed. In 1 study, the authors found that the rate of use for SGLT2 inhibitors was 3.8% in 2015 and 11.9% in 2019.

But there are several other reasons that patients do not receive these medicines.

Insurance

We conducted a retrospective cohort study of  382,574 adults between 58 and 66 years of age, insured by either a Medicare Advantage plan or commercial insurance, and compared treatment initiation of the 3 most common brand-name, second-line diabetes medications (as opposed to generic sulfonylureas), between 2016 and 2019. The rate of initiation was universally lower for Medicare Advantage members vs commercially insured individuals. 

While the rates of initiation of GLP-1 RAs, SGLT2 inhibitors, and dipeptidyl peptidase 4 (DPP-4) inhibitors increased between 2016 and 2019, rates were significantly higher among patients with commercial insurance. Specifically, GLP-1 RA initiation increased from 2.1% to 20.0% among commercial insurance beneficiaries and from 1.5% to 11.4% among Medicare Advantage beneficiaries. SGLT2 inhibitor initiation increased from 2.7% to 18.2% with commercial insurance and from 1.57% to 8.51% with Medicare Advantage. DPP-4 inhibitor initiation increased from 3.3% to 11.7% with commercial insurance and from 2.44% to 7.68% with Medicare Advantage. Within each calendar year, the odds of initiating one of these 3 medications with Medicare Advantage as compared with commercial insurance ranged from 0.28 to 0.70 for GLP-1 RAs; from 0.21 to 0.57 for SGLT2 inhibitors; and from 0.37 to 0.73 for DPP-4 inhibitors. 

We also looked at the initiation of these medications in individuals with cardiorenal comorbidities. In many cases, a drug was prescribed indiscriminately. A patient who would benefit from a GLP-1 RA because of cardiovascular, cerebrovascular, or kidney disease was less likely to be prescribed a GLP-1 RA than a medication like a DPP-4 inhibitor, which usually has the same formulary tier/class but does not have any of the cardiovascular or kidney benefits. Likewise, in those with heart failure or kidney disease, an SGLT2 inhibitor would have been the appropriate choice, but these patients were too often started on a DPP-4 inhibitor, which is not advised for those with heart failure and does provide kidney benefits. 

Last year, Tummalapalli et al, in their evaluation of 4135 US health plans, including commercial- or employer-based, Medicare, Medicaid, and other public health plans, identified multiple barriers to accessing SGLT2 inhibitor medications. While all plans included at least 1 SGLT2 inhibitor on their formularies, they restricted access in other ways. Prior authorizations were required by nearly half of Medicaid plans and nearly 40% of other public plans such as the Veterans Health Administration. Medicare and other public plans commonly imposed quantity limits on fills. Commercial plans frequently (up to 40%) required step therapy (use or failure of a generic diabetes medication) before approval. Copayments were also high in commercial plans, Medicare, and others. 

The need for prior authorizations dominates attempts to prescribe. Centene Corporation, for example, which manages plans for private and public payers, will not approve use of an SGLT2 inhibitor until the patient fails for 3 consecutive months on a prior treatment, has established cardiovascular disease or diabetic nephropathy, or has multiple cardiovascular risk factors. These comorbidities must be documented and verified, and the prior authorizations must be completed, often resulting in substantial administrative burden to clinicians. No wonder many, especially in primary care, may be wary of prescribing drugs that come with a paperwork trail and hours spent on documentation and insurance appeals, rather than on patient care.

The same can be said for prescribing a GLP-1 RA. United Healthcare’s Oxford Benefit Management requires that clinicians show a “history of suboptimal response, contraindication, or intolerance to metformin” before prescribing any of the 8 GLP-1 RAs. 

The average retail cost of 30 empagliflozin tablets, a once-daily medication, is $752. During the pandemic, 24% of the 5000 patients surveyed in an American Diabetes Association (ADA) poll used their stimulus check, relied on loans, or spent savings to pay for diabetes care. GLP-1 RA medications are even more expensive.  Depending on the patient’s pharmacy benefits, they may have to pay a substantial coinsurance out of pocket even after the annual deductible is met, creating financial barriers to starting and continuing recommended, evidence-based medications. Even if patients do get the recommended medications, they may be forced to ration other aspects of their lives, including other medications, food, and other necessities.

There are other important barriers to optimal utilization of evidence-based therapies, stemming from the fundamental social determinants of health: low income, low education level, and living in a socioeconomically deprived neighborhood.  

Social Determinants of Health

Diabetes prevalence is higher in patients experiencing socioeconomic and other structural barriers to health and health care. Fundamentally, 1 study showed that prevalence of diabetes was 1.4 times higher among people living on less than $15,000 a year, as opposed to those earning at least $50,000 a year. 

The risk of diabetes complications is also higher in individuals experiencing food or housing insecurity, those who have low income or education level, and residents in rural and socioeconomically deprived neighborhoods. Importantly, the same patient populations are also less likely to receive timely evidence-based care, contributing to and worsening health disparities. Despite their prevalence and importance, social determinants of health (SDoH) are not routinely recognized or discussed during clinical encounters, such that improving diabetes care and health outcomes is predicated on developing a system to screen for, recognize, and address the wide range of barriers faced by our patients. If a patient cannot afford a new medication or get to the clinic on a regular basis, lacks access to healthy food, or does not have time for diabetes self-management education or to focus on their health, then their well-being will suffer.

Many of these SDoH disproportionately affect racial and ethnic minority populations as the direct result of longstanding and deeply embedded systems, policies, and laws that underlie disparities in diabetes incidence, prevalence, management, and outcomes. As such, structural racism is increasingly recognized as a root cause of health disparities in diabetes and other chronic health conditions.

Proactive strategies

Since reactive care has not and cannot provide patients with the help they need and deserve, many in the diabetes care community have turned to proactive, team-based care. The Chronic Care Model, established in the 1990s, stresses decision-making support, strong team organization and delivery system design, and the wherewithal to monitor progress continually. Research has shown that the best results for patients stem from a multidisciplinary, data-driven, and proactive approach to identifying and meeting the totality of patient care needs. 

The ADA stresses the importance of comprehensive, team-based care for successful management of diabetes. This includes expanding the role of teams to implement evidence-based diabetes care, using electronic health record tools to support timely and guideline-recommended delivery of services, empowering and educating patients and caregivers, eliciting and addressing financial and psychosocial barriers to care, and identifying, developing, and engaging community resources to support better health and well-being.

Recognizing the centrality of team-based care to diabetes management, our team has developed and implemented an enhanced primary care diabetes (EPCD) model across the internal medicine and family medicine practices of Mayo Clinic, first in Rochester, Minnesota and then across multiple rural and small urban sites in southeast Minnesota. This model is centered around the primary care team nurse, who partners with clinicians to oversee, enforce, and coordinate the diabetes management of patients paneled to those clinicians. Nurses proactively identify patients, engage other members of the healthcare team (eg, pharmacists, social workers, certified diabetes care and education specialists) as needed, and maintain a continuous relationship with each patient to help them achieve and maintain their goals. This model was not only effective at improving glycemic control and other indicators of diabetes care quality, but also improved nursing and clinician satisfaction. 

It is important to recognize that comprehensive diabetes care comprises both medical and nonmedical interventions that address the totality of the patient’s care needs and the circumstances that hinder optimal health. Increasingly, robust data are emerging in support of nonmedical interventions that target SDoH, including structural racism as a root cause of racial and ethnic disparities in diabetes care and outcomes, with demonstrated evidence of improved health outcomes and narrowed health disparities.

It takes work, effort, and commitment to manage diabetes. But a team-based approach allows players on all sides to win. 

Walking 10,000 steps per day may reduce the risk of death for those who have trouble regulating their blood sugar, according to the findings from a study of almost 1,700 American adults with prediabetes or diabetes.

Researchers from the University of Seville, Spain, evaluated U.S. adults with prediabetes and diabetes using data from the Centers for Disease Control and Prevention’s National Health and Nutrition Examination Survey, collected between 2005 and 2006.

The findings were published this month in Diabetes Care.

Ariel Skelley/Getty Images

Of the total, 1,194 adults had prediabetes, and 493 had diabetes. People with diabetes in the study were diagnosed by a doctor or had a fasting blood glucose level higher than 126 mg/dL. People with prediabetes in the study were also diagnosed by a doctor or had a fasting glucose level from 100 to 125 mg/dL.

Over half (56%) of prediabetic adults were male (average age 55 years), and they took an average of 8,500 steps per day. Half (51%) of the diabetic adults were also male (average age 61 years), and they took fewer steps per day – about 6,300.

The people in the study wore an accelerometer on their waist to count their steps for 7 consecutive days. The researchers adjusted for age, sex, ethnicity, smoking, alcohol use, diet, and use of diabetes medications.

Over 9 years, 200 people with prediabetes and 138 with diabetes died. Based on those who survived after follow-up, walking nearly 10,000 steps per day was best for reducing the risk of death from any cause for people with prediabetes and diabetes.

But about 20% of people in the study were removed from the analysis because they had invalid accelerometry data. Adults who are healthy enough to walk 10,000 steps may have different rates of death from those who aren’t, according to the study authors, who called for more research to compare these two groups.

If 10,000 steps seem like a daunting task, talking to a doctor about finding a routine that works for your physical ability could be helpful, the study authors suggest.

A version of this article first appeared on Medscape.com.

Walking 10,000 steps per day may reduce the risk of death for those who have trouble regulating their blood sugar, according to the findings from a study of almost 1,700 American adults with prediabetes or diabetes.

Researchers from the University of Seville, Spain, evaluated U.S. adults with prediabetes and diabetes using data from the Centers for Disease Control and Prevention’s National Health and Nutrition Examination Survey, collected between 2005 and 2006.

The findings were published this month in Diabetes Care.

Ariel Skelley/Getty Images

Of the total, 1,194 adults had prediabetes, and 493 had diabetes. People with diabetes in the study were diagnosed by a doctor or had a fasting blood glucose level higher than 126 mg/dL. People with prediabetes in the study were also diagnosed by a doctor or had a fasting glucose level from 100 to 125 mg/dL.

Over half (56%) of prediabetic adults were male (average age 55 years), and they took an average of 8,500 steps per day. Half (51%) of the diabetic adults were also male (average age 61 years), and they took fewer steps per day – about 6,300.

The people in the study wore an accelerometer on their waist to count their steps for 7 consecutive days. The researchers adjusted for age, sex, ethnicity, smoking, alcohol use, diet, and use of diabetes medications.

Over 9 years, 200 people with prediabetes and 138 with diabetes died. Based on those who survived after follow-up, walking nearly 10,000 steps per day was best for reducing the risk of death from any cause for people with prediabetes and diabetes.

But about 20% of people in the study were removed from the analysis because they had invalid accelerometry data. Adults who are healthy enough to walk 10,000 steps may have different rates of death from those who aren’t, according to the study authors, who called for more research to compare these two groups.

If 10,000 steps seem like a daunting task, talking to a doctor about finding a routine that works for your physical ability could be helpful, the study authors suggest.

A version of this article first appeared on Medscape.com.

Walking 10,000 steps per day may reduce the risk of death for those who have trouble regulating their blood sugar, according to the findings from a study of almost 1,700 American adults with prediabetes or diabetes.

Researchers from the University of Seville, Spain, evaluated U.S. adults with prediabetes and diabetes using data from the Centers for Disease Control and Prevention’s National Health and Nutrition Examination Survey, collected between 2005 and 2006.

The findings were published this month in Diabetes Care.

Ariel Skelley/Getty Images

Of the total, 1,194 adults had prediabetes, and 493 had diabetes. People with diabetes in the study were diagnosed by a doctor or had a fasting blood glucose level higher than 126 mg/dL. People with prediabetes in the study were also diagnosed by a doctor or had a fasting glucose level from 100 to 125 mg/dL.

Over half (56%) of prediabetic adults were male (average age 55 years), and they took an average of 8,500 steps per day. Half (51%) of the diabetic adults were also male (average age 61 years), and they took fewer steps per day – about 6,300.

The people in the study wore an accelerometer on their waist to count their steps for 7 consecutive days. The researchers adjusted for age, sex, ethnicity, smoking, alcohol use, diet, and use of diabetes medications.

Over 9 years, 200 people with prediabetes and 138 with diabetes died. Based on those who survived after follow-up, walking nearly 10,000 steps per day was best for reducing the risk of death from any cause for people with prediabetes and diabetes.

But about 20% of people in the study were removed from the analysis because they had invalid accelerometry data. Adults who are healthy enough to walk 10,000 steps may have different rates of death from those who aren’t, according to the study authors, who called for more research to compare these two groups.

If 10,000 steps seem like a daunting task, talking to a doctor about finding a routine that works for your physical ability could be helpful, the study authors suggest.

A version of this article first appeared on Medscape.com.

Research continues to demonstrate the benefits of glucagon-like peptide-1 receptor (GLP-1R) agonists or co-agonists for type 2 diabetes (T2D). Arslanian and the AWARD-PEDS investigators have published the results of a randomized controlled trial comparing once-weekly dulaglutide vs.placebo in youths between 10 and17 years of age with T2D. A1c was reduced by 1.2% with 0.75 mg dulaglutide and by 1.5% with a 1.5 mg dose, compared with placebo. Of note, there was no significant weight difference between dulaglutide and placebo, similar to what has been found with liraglutide and extended-release exenatide in similar populations. This is also contrary to the weight loss that is found with GLP-1R agonists in adult studies. While the GLP-1R agonist class provides a nice glycemic benefit in youth with T2D, it remains perplexing as to why weight loss has not been demonstrated in clinical trials.

In the SURPASS trials of the GLP-1/gastric inhibitory polypeptide (GIP) receptor co-agonist tirzepatide, there was robust A1c lowering and weight loss among individuals with T2D. A meta-analysis published by Karagiannis and colleagues of seven tirzepatide trials has shown dose-dependent superiority for A1c and weight compared withplacebo, GLP-1R agonists, and basal insulin. Gastrointestinal side effects were similar to what we have come to expect with GLP-1R agonist–based therapies. Tirzepatide, recently approved by the US Food and Drug Administration (FDA) for the treatment of T2D, is a welcome addition to the pharmacotherapy toolkit.

In the SURPASS-2 study, all doses of tirzepatide were superior to 1 mg semaglutide for both A1c and body weight reduction. Following the recent approval of 2 mg semaglutide by the FDA for the management of T2D, Vadher and colleagues explored how tirzepatide compares with 2 mg semaglutide via an indirect treatment comparison. Using data from the SUSTAIN-FORTE and SURPASS-2 trials, these authors found that A1c and weight reductions were significantly greater for 10 and 15 mg tirzepatide vs 2 mg semaglutide and similar for 5 mg tirzepatide vs 2 mg semaglutide. In the absence of a head-to-head trial, this analysis suggests greater efficacy with tirzepatide compared with high-dose semaglutide in T2D.

Continuous glucose monitoring (CGM) provides information about glycemia that is not available with A1c and capillary glucose monitoring. The coefficient of variation (CV) calculated from CGM is a good measure of glycemic variability, with a goal of ≤36%. There are inconsistent data for the association of CV with microvascular or macrovascular complications and very little study of the relationship between CV and long-term mortality. Mo and colleagues investigated the association between short-term glycemic variability measured by CV and all-cause mortality in a prospective study of 1839 individuals with T2D and a well-controlled glucose profile monitored by CGM. After about 7 years of follow-up, a greater baseline CV was associated with an increased risk for all-cause mortality, with a greater than twofold risk fo rmortality with a baseline CV of >35% compared witha baseline CV of ≤20%. This study suggests that clinicians should pay attention when CV is high, even with otherwise good glycemic control. With the expanding use of CGM, long-term intervention studies are needed to determine the role of glycemic variability(CV) in the development of complications and hard outcomes.

Research continues to demonstrate the benefits of glucagon-like peptide-1 receptor (GLP-1R) agonists or co-agonists for type 2 diabetes (T2D). Arslanian and the AWARD-PEDS investigators have published the results of a randomized controlled trial comparing once-weekly dulaglutide vs.placebo in youths between 10 and17 years of age with T2D. A1c was reduced by 1.2% with 0.75 mg dulaglutide and by 1.5% with a 1.5 mg dose, compared with placebo. Of note, there was no significant weight difference between dulaglutide and placebo, similar to what has been found with liraglutide and extended-release exenatide in similar populations. This is also contrary to the weight loss that is found with GLP-1R agonists in adult studies. While the GLP-1R agonist class provides a nice glycemic benefit in youth with T2D, it remains perplexing as to why weight loss has not been demonstrated in clinical trials.

In the SURPASS trials of the GLP-1/gastric inhibitory polypeptide (GIP) receptor co-agonist tirzepatide, there was robust A1c lowering and weight loss among individuals with T2D. A meta-analysis published by Karagiannis and colleagues of seven tirzepatide trials has shown dose-dependent superiority for A1c and weight compared withplacebo, GLP-1R agonists, and basal insulin. Gastrointestinal side effects were similar to what we have come to expect with GLP-1R agonist–based therapies. Tirzepatide, recently approved by the US Food and Drug Administration (FDA) for the treatment of T2D, is a welcome addition to the pharmacotherapy toolkit.

In the SURPASS-2 study, all doses of tirzepatide were superior to 1 mg semaglutide for both A1c and body weight reduction. Following the recent approval of 2 mg semaglutide by the FDA for the management of T2D, Vadher and colleagues explored how tirzepatide compares with 2 mg semaglutide via an indirect treatment comparison. Using data from the SUSTAIN-FORTE and SURPASS-2 trials, these authors found that A1c and weight reductions were significantly greater for 10 and 15 mg tirzepatide vs 2 mg semaglutide and similar for 5 mg tirzepatide vs 2 mg semaglutide. In the absence of a head-to-head trial, this analysis suggests greater efficacy with tirzepatide compared with high-dose semaglutide in T2D.

Continuous glucose monitoring (CGM) provides information about glycemia that is not available with A1c and capillary glucose monitoring. The coefficient of variation (CV) calculated from CGM is a good measure of glycemic variability, with a goal of ≤36%. There are inconsistent data for the association of CV with microvascular or macrovascular complications and very little study of the relationship between CV and long-term mortality. Mo and colleagues investigated the association between short-term glycemic variability measured by CV and all-cause mortality in a prospective study of 1839 individuals with T2D and a well-controlled glucose profile monitored by CGM. After about 7 years of follow-up, a greater baseline CV was associated with an increased risk for all-cause mortality, with a greater than twofold risk fo rmortality with a baseline CV of >35% compared witha baseline CV of ≤20%. This study suggests that clinicians should pay attention when CV is high, even with otherwise good glycemic control. With the expanding use of CGM, long-term intervention studies are needed to determine the role of glycemic variability(CV) in the development of complications and hard outcomes.

Research continues to demonstrate the benefits of glucagon-like peptide-1 receptor (GLP-1R) agonists or co-agonists for type 2 diabetes (T2D). Arslanian and the AWARD-PEDS investigators have published the results of a randomized controlled trial comparing once-weekly dulaglutide vs.placebo in youths between 10 and17 years of age with T2D. A1c was reduced by 1.2% with 0.75 mg dulaglutide and by 1.5% with a 1.5 mg dose, compared with placebo. Of note, there was no significant weight difference between dulaglutide and placebo, similar to what has been found with liraglutide and extended-release exenatide in similar populations. This is also contrary to the weight loss that is found with GLP-1R agonists in adult studies. While the GLP-1R agonist class provides a nice glycemic benefit in youth with T2D, it remains perplexing as to why weight loss has not been demonstrated in clinical trials.

In the SURPASS trials of the GLP-1/gastric inhibitory polypeptide (GIP) receptor co-agonist tirzepatide, there was robust A1c lowering and weight loss among individuals with T2D. A meta-analysis published by Karagiannis and colleagues of seven tirzepatide trials has shown dose-dependent superiority for A1c and weight compared withplacebo, GLP-1R agonists, and basal insulin. Gastrointestinal side effects were similar to what we have come to expect with GLP-1R agonist–based therapies. Tirzepatide, recently approved by the US Food and Drug Administration (FDA) for the treatment of T2D, is a welcome addition to the pharmacotherapy toolkit.

In the SURPASS-2 study, all doses of tirzepatide were superior to 1 mg semaglutide for both A1c and body weight reduction. Following the recent approval of 2 mg semaglutide by the FDA for the management of T2D, Vadher and colleagues explored how tirzepatide compares with 2 mg semaglutide via an indirect treatment comparison. Using data from the SUSTAIN-FORTE and SURPASS-2 trials, these authors found that A1c and weight reductions were significantly greater for 10 and 15 mg tirzepatide vs 2 mg semaglutide and similar for 5 mg tirzepatide vs 2 mg semaglutide. In the absence of a head-to-head trial, this analysis suggests greater efficacy with tirzepatide compared with high-dose semaglutide in T2D.

Continuous glucose monitoring (CGM) provides information about glycemia that is not available with A1c and capillary glucose monitoring. The coefficient of variation (CV) calculated from CGM is a good measure of glycemic variability, with a goal of ≤36%. There are inconsistent data for the association of CV with microvascular or macrovascular complications and very little study of the relationship between CV and long-term mortality. Mo and colleagues investigated the association between short-term glycemic variability measured by CV and all-cause mortality in a prospective study of 1839 individuals with T2D and a well-controlled glucose profile monitored by CGM. After about 7 years of follow-up, a greater baseline CV was associated with an increased risk for all-cause mortality, with a greater than twofold risk fo rmortality with a baseline CV of >35% compared witha baseline CV of ≤20%. This study suggests that clinicians should pay attention when CV is high, even with otherwise good glycemic control. With the expanding use of CGM, long-term intervention studies are needed to determine the role of glycemic variability(CV) in the development of complications and hard outcomes.

Wireless devices, like smart phones and tablets, appear to induce compulsive or even addictive use in many individuals, leading to adverse health consequences that are likely to be curtailed only through often difficult behavior modification, according to a pediatric endocrinologist’s take on the problem.

While the summary was based in part on the analysis of 234 published papers drawn from the medical literature, the lead author, Nidhi Gupta, MD, said the data reinforce her own clinical experience.

Lisa Nainggolin/MDedge News

“As a pediatric endocrinologist, the trend in smartphone-associated health disorders, such as obesity, sleep, and behavior issues, worries me,” Dr. Gupta, director of KAP Pediatric Endocrinology, Nashville, Tenn., said at the annual meeting of the Endocrine Society.

Based on her search of the medical literature, the available data raise concern. In one study she cited, for example, each hour per day of screen time was found to translate into a body mass index increase of 0.5 to 0.7 kg/m² (P < .001).

With this type of progressive rise in BMI comes prediabetes, dyslipidemia, and other metabolic disorders associated with major health risks, including cardiovascular disease. And there are others. Dr. Gupta cited data suggesting screen time before bed disturbs sleep, which has its own set of health risks.

“When I say health, it includes physical health, mental health, and emotional health,” said Dr. Gupta.

In the U.S. and other countries with a growing obesity epidemic, lack of physical activity and unhealthy eating are widely considered the major culprits. Excessive screen time contributes to both.

“When we are engaged with our devices, we are often snacking subconsciously and not very mindful that we are making unhealthy choices,” Dr. Gupta said.

The problem is that there is a vicious circle. Compulsive use of devices follows the same loop as other types of addictive behaviors, according to Dr. Gupta. She traced overuse of wireless devices to the dopaminergic system, which is a powerful neuroendocrine-mediated process of craving, response, and reward.

Like fat, sugar, and salt, which provoke a neuroendocrine reward signal, the chimes and buzzes of a cell phone provide their own cues for reward in the form of a dopamine surge. As a result, these become the “triggers of an irresistible and irrational urge to check our device that makes the dopamine go high in our brain,” Dr. Gupta explained.

Although the vicious cycle can be thwarted by turning off the device, Dr. Gupta characterized this as “impractical” when smartphones are so vital to daily communication. Rather, Dr. Gupta advocated a program of moderation, reserving the phone for useful tasks without succumbing to the siren song of apps that waste time.

The most conspicuous culprit is social media, which Dr. Gupta considers to be among the most Pavlovian triggers of cell phone addiction. However, she acknowledged that participation in social media has its justifications.

“I, myself, use social media for my own branding and marketing,” Dr. Gupta said.

The problem that users have is distinguishing between screen time that does and does not have value, according to Dr. Gupta. She indicated that many of those overusing their smart devices are being driven by the dopaminergic reward system, which is generally divorced from the real goals of life, such as personal satisfaction and activity that is rewarding monetarily or in other ways.

“I am not asking for these devices to be thrown out the window. I am advocating for moderation, balance, and real-life engagement,” Dr. Gupta said at the meeting, held in Atlanta and virtually.

She outlined a long list of practical suggestions, including turning off the alarms, chimes, and messages that engage the user into the vicious dopaminergic-reward system loop. She suggested mindfulness so that the user can distinguish between valuable device use and activity that is simply procrastination.

“The devices are designed to be addictive. They are designed to manipulate our brain,” she said. “Eliminate the reward. Let’s try to make our devices boring, unappealing, or enticing so that they only work as tools.”

The medical literature is filled with data that support the potential harms of excessive screen use, leading many others to make some of the same points. In 2017, Thomas N. Robinson, MD, professor of child health at Stanford (Calif.) University, reviewed data showing an association between screen media exposure and obesity in children and adolescents.

“This is an area crying out for more research,” Dr. Robinson said in an interview. The problem of screen time, sedentary behavior, and weight gain has been an issue since the television was invented, which was the point he made in his 2017 paper, but he agreed that the problem is only getting worse.

“Digital technology has become ubiquitous, touching nearly every aspect of people’s lives,” he said. Yet, as evidence grows that overuse of this technology can be harmful, it is creating a problem without a clear solution.

“There are few data about the efficacy of specific strategies to reduce harmful impacts of digital screen use,” he said.

While some of the solutions that Dr. Gupta described make sense, they are more easily described than executed. The dopaminergic reward system is strong and largely experienced subconsciously. Recruiting patients to recognize that dopaminergic rewards are not rewards in any true sense is already a challenge. Enlisting patients to take the difficult steps to avoid the behavioral cues might be even more difficult.

Dr. Gupta and Dr. Robinson report no potential conflicts of interest.

Wireless devices, like smart phones and tablets, appear to induce compulsive or even addictive use in many individuals, leading to adverse health consequences that are likely to be curtailed only through often difficult behavior modification, according to a pediatric endocrinologist’s take on the problem.

While the summary was based in part on the analysis of 234 published papers drawn from the medical literature, the lead author, Nidhi Gupta, MD, said the data reinforce her own clinical experience.

Lisa Nainggolin/MDedge News

“As a pediatric endocrinologist, the trend in smartphone-associated health disorders, such as obesity, sleep, and behavior issues, worries me,” Dr. Gupta, director of KAP Pediatric Endocrinology, Nashville, Tenn., said at the annual meeting of the Endocrine Society.

Based on her search of the medical literature, the available data raise concern. In one study she cited, for example, each hour per day of screen time was found to translate into a body mass index increase of 0.5 to 0.7 kg/m² (P < .001).

With this type of progressive rise in BMI comes prediabetes, dyslipidemia, and other metabolic disorders associated with major health risks, including cardiovascular disease. And there are others. Dr. Gupta cited data suggesting screen time before bed disturbs sleep, which has its own set of health risks.

“When I say health, it includes physical health, mental health, and emotional health,” said Dr. Gupta.

In the U.S. and other countries with a growing obesity epidemic, lack of physical activity and unhealthy eating are widely considered the major culprits. Excessive screen time contributes to both.

“When we are engaged with our devices, we are often snacking subconsciously and not very mindful that we are making unhealthy choices,” Dr. Gupta said.

The problem is that there is a vicious circle. Compulsive use of devices follows the same loop as other types of addictive behaviors, according to Dr. Gupta. She traced overuse of wireless devices to the dopaminergic system, which is a powerful neuroendocrine-mediated process of craving, response, and reward.

Like fat, sugar, and salt, which provoke a neuroendocrine reward signal, the chimes and buzzes of a cell phone provide their own cues for reward in the form of a dopamine surge. As a result, these become the “triggers of an irresistible and irrational urge to check our device that makes the dopamine go high in our brain,” Dr. Gupta explained.

Although the vicious cycle can be thwarted by turning off the device, Dr. Gupta characterized this as “impractical” when smartphones are so vital to daily communication. Rather, Dr. Gupta advocated a program of moderation, reserving the phone for useful tasks without succumbing to the siren song of apps that waste time.

The most conspicuous culprit is social media, which Dr. Gupta considers to be among the most Pavlovian triggers of cell phone addiction. However, she acknowledged that participation in social media has its justifications.

“I, myself, use social media for my own branding and marketing,” Dr. Gupta said.

The problem that users have is distinguishing between screen time that does and does not have value, according to Dr. Gupta. She indicated that many of those overusing their smart devices are being driven by the dopaminergic reward system, which is generally divorced from the real goals of life, such as personal satisfaction and activity that is rewarding monetarily or in other ways.

“I am not asking for these devices to be thrown out the window. I am advocating for moderation, balance, and real-life engagement,” Dr. Gupta said at the meeting, held in Atlanta and virtually.

She outlined a long list of practical suggestions, including turning off the alarms, chimes, and messages that engage the user into the vicious dopaminergic-reward system loop. She suggested mindfulness so that the user can distinguish between valuable device use and activity that is simply procrastination.

“The devices are designed to be addictive. They are designed to manipulate our brain,” she said. “Eliminate the reward. Let’s try to make our devices boring, unappealing, or enticing so that they only work as tools.”

The medical literature is filled with data that support the potential harms of excessive screen use, leading many others to make some of the same points. In 2017, Thomas N. Robinson, MD, professor of child health at Stanford (Calif.) University, reviewed data showing an association between screen media exposure and obesity in children and adolescents.

“This is an area crying out for more research,” Dr. Robinson said in an interview. The problem of screen time, sedentary behavior, and weight gain has been an issue since the television was invented, which was the point he made in his 2017 paper, but he agreed that the problem is only getting worse.

“Digital technology has become ubiquitous, touching nearly every aspect of people’s lives,” he said. Yet, as evidence grows that overuse of this technology can be harmful, it is creating a problem without a clear solution.

“There are few data about the efficacy of specific strategies to reduce harmful impacts of digital screen use,” he said.

While some of the solutions that Dr. Gupta described make sense, they are more easily described than executed. The dopaminergic reward system is strong and largely experienced subconsciously. Recruiting patients to recognize that dopaminergic rewards are not rewards in any true sense is already a challenge. Enlisting patients to take the difficult steps to avoid the behavioral cues might be even more difficult.

Dr. Gupta and Dr. Robinson report no potential conflicts of interest.

Wireless devices, like smart phones and tablets, appear to induce compulsive or even addictive use in many individuals, leading to adverse health consequences that are likely to be curtailed only through often difficult behavior modification, according to a pediatric endocrinologist’s take on the problem.

While the summary was based in part on the analysis of 234 published papers drawn from the medical literature, the lead author, Nidhi Gupta, MD, said the data reinforce her own clinical experience.

Lisa Nainggolin/MDedge News

“As a pediatric endocrinologist, the trend in smartphone-associated health disorders, such as obesity, sleep, and behavior issues, worries me,” Dr. Gupta, director of KAP Pediatric Endocrinology, Nashville, Tenn., said at the annual meeting of the Endocrine Society.

Based on her search of the medical literature, the available data raise concern. In one study she cited, for example, each hour per day of screen time was found to translate into a body mass index increase of 0.5 to 0.7 kg/m² (P < .001).

With this type of progressive rise in BMI comes prediabetes, dyslipidemia, and other metabolic disorders associated with major health risks, including cardiovascular disease. And there are others. Dr. Gupta cited data suggesting screen time before bed disturbs sleep, which has its own set of health risks.

“When I say health, it includes physical health, mental health, and emotional health,” said Dr. Gupta.

In the U.S. and other countries with a growing obesity epidemic, lack of physical activity and unhealthy eating are widely considered the major culprits. Excessive screen time contributes to both.

“When we are engaged with our devices, we are often snacking subconsciously and not very mindful that we are making unhealthy choices,” Dr. Gupta said.

The problem is that there is a vicious circle. Compulsive use of devices follows the same loop as other types of addictive behaviors, according to Dr. Gupta. She traced overuse of wireless devices to the dopaminergic system, which is a powerful neuroendocrine-mediated process of craving, response, and reward.

Like fat, sugar, and salt, which provoke a neuroendocrine reward signal, the chimes and buzzes of a cell phone provide their own cues for reward in the form of a dopamine surge. As a result, these become the “triggers of an irresistible and irrational urge to check our device that makes the dopamine go high in our brain,” Dr. Gupta explained.

Although the vicious cycle can be thwarted by turning off the device, Dr. Gupta characterized this as “impractical” when smartphones are so vital to daily communication. Rather, Dr. Gupta advocated a program of moderation, reserving the phone for useful tasks without succumbing to the siren song of apps that waste time.

The most conspicuous culprit is social media, which Dr. Gupta considers to be among the most Pavlovian triggers of cell phone addiction. However, she acknowledged that participation in social media has its justifications.

“I, myself, use social media for my own branding and marketing,” Dr. Gupta said.

The problem that users have is distinguishing between screen time that does and does not have value, according to Dr. Gupta. She indicated that many of those overusing their smart devices are being driven by the dopaminergic reward system, which is generally divorced from the real goals of life, such as personal satisfaction and activity that is rewarding monetarily or in other ways.

“I am not asking for these devices to be thrown out the window. I am advocating for moderation, balance, and real-life engagement,” Dr. Gupta said at the meeting, held in Atlanta and virtually.

She outlined a long list of practical suggestions, including turning off the alarms, chimes, and messages that engage the user into the vicious dopaminergic-reward system loop. She suggested mindfulness so that the user can distinguish between valuable device use and activity that is simply procrastination.

“The devices are designed to be addictive. They are designed to manipulate our brain,” she said. “Eliminate the reward. Let’s try to make our devices boring, unappealing, or enticing so that they only work as tools.”

The medical literature is filled with data that support the potential harms of excessive screen use, leading many others to make some of the same points. In 2017, Thomas N. Robinson, MD, professor of child health at Stanford (Calif.) University, reviewed data showing an association between screen media exposure and obesity in children and adolescents.

“This is an area crying out for more research,” Dr. Robinson said in an interview. The problem of screen time, sedentary behavior, and weight gain has been an issue since the television was invented, which was the point he made in his 2017 paper, but he agreed that the problem is only getting worse.

“Digital technology has become ubiquitous, touching nearly every aspect of people’s lives,” he said. Yet, as evidence grows that overuse of this technology can be harmful, it is creating a problem without a clear solution.

“There are few data about the efficacy of specific strategies to reduce harmful impacts of digital screen use,” he said.

While some of the solutions that Dr. Gupta described make sense, they are more easily described than executed. The dopaminergic reward system is strong and largely experienced subconsciously. Recruiting patients to recognize that dopaminergic rewards are not rewards in any true sense is already a challenge. Enlisting patients to take the difficult steps to avoid the behavioral cues might be even more difficult.

Dr. Gupta and Dr. Robinson report no potential conflicts of interest.

People with diabetes who had a poor-quality diet and food insecurity were significantly more likely to have poor glycemic and cholesterol control than were those with a healthier diet and food security, based on data from a national study of more than 2,000 individuals.

The American Diabetes Association recommends a high-quality diet for people with diabetes (PWD) to achieve treatment goals; however, roughly 18% of PWD in the United States are food insecure and/or have a poor-quality diet, Sarah S. Casagrande, PhD, of DLH Corporation, Silver Spring, Md., and colleagues wrote in a poster presented at the annual scientific sessions of the ADA in New Orleans.

To examine the impact of food insecurity and diet quality on diabetes and lipid management, the researchers reviewed data from 2,075 adults with self-reported diabetes who completed the National Health and Nutrition Examination Surveys between 2013 and 2018.

Diet quality was divided into quartiles based on the 2015 Healthy Eating Index. Food insecurity was assessed using a standard 10-item questionnaire including questions about running out of food and not being able to afford more, reducing meal sizes, eating less or not at all, and going hungry because of lack of money for food.

The logistic regression analysis controlled for factors including sociodemographics, health care use, smoking, diabetes medications, blood pressure medication use, cholesterol medication use, and body mass index.

Overall, 17.6% of the participants were food insecure and had a low-quality diet, 14.2% were food insecure with a high-quality diet, 33.1% were food secure with a low-quality diet, and 35.2% were food secure with a high-quality diet.

PWD in the food insecure/low-quality diet group were significantly more likely to be younger, non-Hispanic black or Hispanic, and uninsured compared to those in the food secure/high-quality diet group (P < .001 for all).

When the researchers examined glycemic control, they found that PWD in the food insecurity/low-quality diet groups were significantly more likely than were those with food security/high-quality diets to have hemoglobin A1c of at least 7.0% (adjusted odds ratio, 1.85), A1c of at least 8.0% (aOR, 1.79), low HDL cholesterol (aOR, 1.69), and high triglycerides (aOR, 3.26).

PWD with food insecurity but a high-quality diet also were significantly more likely than were those with food security and a high quality diet to have A1c of at least 7.0% (aOR, 1.69), A1c of at least 8.0% (aOR, 1.83), and high triglycerides (aOR, 2.44). PWD with food security but a low-quality diet were significantly more likely than was the food security/high-quality diet group to have A1c of at least 7% (aOR, 1.55).

The study findings were limited by several factors including the cross-sectional design, reliance on self-reports, and inability to distinguish between type 1 and type 2 diabetes, the researchers wrote.

However, the results were strengthened by the large, nationally representative sample and the inclusion of multiple clinical outcomes in the patient assessment, they said.

The results suggest that food insecurity had a significant impact on both glycemic control and cholesterol management independent of diet quality, the researchers noted. Based on these findings, health care providers treating PWD may wish to assess their patients’ food security status, and “interventions could address disparities in food security,” they concluded.
 

Food insecurity a growing problem

“With more communities being pushed into state of war, drought, and famine globally, it is important to track impact of food insecurity and low quality food on common medical conditions like diabetes in our vulnerable communities,” Romesh K. Khardori, MD, professor of medicine: endocrinology, and metabolism at Eastern Virginia Medical School, Norfolk, said in an interview.

Dr. Khardori, who was not involved in the study, said he was not surprised by the current study findings.

“Type of food, amount of food, and quality of food have been stressed in diabetes management for more than 100 years,” he said. “Organizations charged with recommendations, such as the ADA and American Dietetic Association, have regularly updated their recommendations,” he noted. “It was not surprising, therefore, to find food insecurity and low quality tied to poor glycemic control.”

The take-home message for clinicians is to consider the availability and quality of food that their patients are exposed to when evaluating barriers to proper glycemic control, Dr. Khardori emphasized.

However, additional research is needed to explore whether the prescription of a sufficient amount of good quality food would alleviate the adverse impact seen in the current study, he said.

The study was supported by the National Institute of Diabetes and Digestive and Kidney Diseases. The researchers and Dr. Khardori had no financial conflicts to disclose.

People with diabetes who had a poor-quality diet and food insecurity were significantly more likely to have poor glycemic and cholesterol control than were those with a healthier diet and food security, based on data from a national study of more than 2,000 individuals.

The American Diabetes Association recommends a high-quality diet for people with diabetes (PWD) to achieve treatment goals; however, roughly 18% of PWD in the United States are food insecure and/or have a poor-quality diet, Sarah S. Casagrande, PhD, of DLH Corporation, Silver Spring, Md., and colleagues wrote in a poster presented at the annual scientific sessions of the ADA in New Orleans.

To examine the impact of food insecurity and diet quality on diabetes and lipid management, the researchers reviewed data from 2,075 adults with self-reported diabetes who completed the National Health and Nutrition Examination Surveys between 2013 and 2018.

Diet quality was divided into quartiles based on the 2015 Healthy Eating Index. Food insecurity was assessed using a standard 10-item questionnaire including questions about running out of food and not being able to afford more, reducing meal sizes, eating less or not at all, and going hungry because of lack of money for food.

The logistic regression analysis controlled for factors including sociodemographics, health care use, smoking, diabetes medications, blood pressure medication use, cholesterol medication use, and body mass index.

Overall, 17.6% of the participants were food insecure and had a low-quality diet, 14.2% were food insecure with a high-quality diet, 33.1% were food secure with a low-quality diet, and 35.2% were food secure with a high-quality diet.

PWD in the food insecure/low-quality diet group were significantly more likely to be younger, non-Hispanic black or Hispanic, and uninsured compared to those in the food secure/high-quality diet group (P < .001 for all).

When the researchers examined glycemic control, they found that PWD in the food insecurity/low-quality diet groups were significantly more likely than were those with food security/high-quality diets to have hemoglobin A1c of at least 7.0% (adjusted odds ratio, 1.85), A1c of at least 8.0% (aOR, 1.79), low HDL cholesterol (aOR, 1.69), and high triglycerides (aOR, 3.26).

PWD with food insecurity but a high-quality diet also were significantly more likely than were those with food security and a high quality diet to have A1c of at least 7.0% (aOR, 1.69), A1c of at least 8.0% (aOR, 1.83), and high triglycerides (aOR, 2.44). PWD with food security but a low-quality diet were significantly more likely than was the food security/high-quality diet group to have A1c of at least 7% (aOR, 1.55).

The study findings were limited by several factors including the cross-sectional design, reliance on self-reports, and inability to distinguish between type 1 and type 2 diabetes, the researchers wrote.

However, the results were strengthened by the large, nationally representative sample and the inclusion of multiple clinical outcomes in the patient assessment, they said.

The results suggest that food insecurity had a significant impact on both glycemic control and cholesterol management independent of diet quality, the researchers noted. Based on these findings, health care providers treating PWD may wish to assess their patients’ food security status, and “interventions could address disparities in food security,” they concluded.
 

Food insecurity a growing problem

“With more communities being pushed into state of war, drought, and famine globally, it is important to track impact of food insecurity and low quality food on common medical conditions like diabetes in our vulnerable communities,” Romesh K. Khardori, MD, professor of medicine: endocrinology, and metabolism at Eastern Virginia Medical School, Norfolk, said in an interview.

Dr. Khardori, who was not involved in the study, said he was not surprised by the current study findings.

“Type of food, amount of food, and quality of food have been stressed in diabetes management for more than 100 years,” he said. “Organizations charged with recommendations, such as the ADA and American Dietetic Association, have regularly updated their recommendations,” he noted. “It was not surprising, therefore, to find food insecurity and low quality tied to poor glycemic control.”

The take-home message for clinicians is to consider the availability and quality of food that their patients are exposed to when evaluating barriers to proper glycemic control, Dr. Khardori emphasized.

However, additional research is needed to explore whether the prescription of a sufficient amount of good quality food would alleviate the adverse impact seen in the current study, he said.

The study was supported by the National Institute of Diabetes and Digestive and Kidney Diseases. The researchers and Dr. Khardori had no financial conflicts to disclose.

People with diabetes who had a poor-quality diet and food insecurity were significantly more likely to have poor glycemic and cholesterol control than were those with a healthier diet and food security, based on data from a national study of more than 2,000 individuals.

The American Diabetes Association recommends a high-quality diet for people with diabetes (PWD) to achieve treatment goals; however, roughly 18% of PWD in the United States are food insecure and/or have a poor-quality diet, Sarah S. Casagrande, PhD, of DLH Corporation, Silver Spring, Md., and colleagues wrote in a poster presented at the annual scientific sessions of the ADA in New Orleans.

To examine the impact of food insecurity and diet quality on diabetes and lipid management, the researchers reviewed data from 2,075 adults with self-reported diabetes who completed the National Health and Nutrition Examination Surveys between 2013 and 2018.

Diet quality was divided into quartiles based on the 2015 Healthy Eating Index. Food insecurity was assessed using a standard 10-item questionnaire including questions about running out of food and not being able to afford more, reducing meal sizes, eating less or not at all, and going hungry because of lack of money for food.

The logistic regression analysis controlled for factors including sociodemographics, health care use, smoking, diabetes medications, blood pressure medication use, cholesterol medication use, and body mass index.

Overall, 17.6% of the participants were food insecure and had a low-quality diet, 14.2% were food insecure with a high-quality diet, 33.1% were food secure with a low-quality diet, and 35.2% were food secure with a high-quality diet.

PWD in the food insecure/low-quality diet group were significantly more likely to be younger, non-Hispanic black or Hispanic, and uninsured compared to those in the food secure/high-quality diet group (P < .001 for all).

When the researchers examined glycemic control, they found that PWD in the food insecurity/low-quality diet groups were significantly more likely than were those with food security/high-quality diets to have hemoglobin A1c of at least 7.0% (adjusted odds ratio, 1.85), A1c of at least 8.0% (aOR, 1.79), low HDL cholesterol (aOR, 1.69), and high triglycerides (aOR, 3.26).

PWD with food insecurity but a high-quality diet also were significantly more likely than were those with food security and a high quality diet to have A1c of at least 7.0% (aOR, 1.69), A1c of at least 8.0% (aOR, 1.83), and high triglycerides (aOR, 2.44). PWD with food security but a low-quality diet were significantly more likely than was the food security/high-quality diet group to have A1c of at least 7% (aOR, 1.55).

The study findings were limited by several factors including the cross-sectional design, reliance on self-reports, and inability to distinguish between type 1 and type 2 diabetes, the researchers wrote.

However, the results were strengthened by the large, nationally representative sample and the inclusion of multiple clinical outcomes in the patient assessment, they said.

The results suggest that food insecurity had a significant impact on both glycemic control and cholesterol management independent of diet quality, the researchers noted. Based on these findings, health care providers treating PWD may wish to assess their patients’ food security status, and “interventions could address disparities in food security,” they concluded.
 

Food insecurity a growing problem

“With more communities being pushed into state of war, drought, and famine globally, it is important to track impact of food insecurity and low quality food on common medical conditions like diabetes in our vulnerable communities,” Romesh K. Khardori, MD, professor of medicine: endocrinology, and metabolism at Eastern Virginia Medical School, Norfolk, said in an interview.

Dr. Khardori, who was not involved in the study, said he was not surprised by the current study findings.

“Type of food, amount of food, and quality of food have been stressed in diabetes management for more than 100 years,” he said. “Organizations charged with recommendations, such as the ADA and American Dietetic Association, have regularly updated their recommendations,” he noted. “It was not surprising, therefore, to find food insecurity and low quality tied to poor glycemic control.”

The take-home message for clinicians is to consider the availability and quality of food that their patients are exposed to when evaluating barriers to proper glycemic control, Dr. Khardori emphasized.

However, additional research is needed to explore whether the prescription of a sufficient amount of good quality food would alleviate the adverse impact seen in the current study, he said.

The study was supported by the National Institute of Diabetes and Digestive and Kidney Diseases. The researchers and Dr. Khardori had no financial conflicts to disclose.

Key clinical point: Greater glycemic variability measured as the coefficient of variation for glucose (%CV) level was associated with a higher risk for all-cause mortality in patients with type 2 diabetes (T2D) and a well-controlled glucose status.

Major finding: Compared with patients with a %CV level of ≤20%, those with a %CV level of 20%-25% (adjusted HR [aHR] 1.16; 95% CI 0.78-1.73), 25%-30% (aHR 1.38; 95% CI 0.89-2.15), 30%-35% (aHR 1.33; 95% CI 0.77-2.29), and >35% (aHR 2.26; 95% CI 1.13-4.52) had a higher risk for all-cause mortality.

Study details: This study was a part of the INDIGO study including 1839 patients with T2D who reached continuous glucose monitoring glycemic targets and were classified into five groups by %CV level.

Disclosures: This study was supported by the National Key R&D Program of China, the National Natural Science Foundation of China, and others. The authors declared no conflicts of interest.

Source: Mo Y et al. Impact of short-term glycemic variability on risk of all-cause mortality in type 2 diabetes patients with well-controlled glucose profile by continuous glucose monitoring: A prospective cohort study. Diabetes Res Clin Pract. 2022;189:109940 (Jun 1). Doi: 10.1016/j.diabres.2022.109940

Key clinical point: Greater glycemic variability measured as the coefficient of variation for glucose (%CV) level was associated with a higher risk for all-cause mortality in patients with type 2 diabetes (T2D) and a well-controlled glucose status.

Major finding: Compared with patients with a %CV level of ≤20%, those with a %CV level of 20%-25% (adjusted HR [aHR] 1.16; 95% CI 0.78-1.73), 25%-30% (aHR 1.38; 95% CI 0.89-2.15), 30%-35% (aHR 1.33; 95% CI 0.77-2.29), and >35% (aHR 2.26; 95% CI 1.13-4.52) had a higher risk for all-cause mortality.

Study details: This study was a part of the INDIGO study including 1839 patients with T2D who reached continuous glucose monitoring glycemic targets and were classified into five groups by %CV level.

Disclosures: This study was supported by the National Key R&D Program of China, the National Natural Science Foundation of China, and others. The authors declared no conflicts of interest.

Source: Mo Y et al. Impact of short-term glycemic variability on risk of all-cause mortality in type 2 diabetes patients with well-controlled glucose profile by continuous glucose monitoring: A prospective cohort study. Diabetes Res Clin Pract. 2022;189:109940 (Jun 1). Doi: 10.1016/j.diabres.2022.109940

Key clinical point: Greater glycemic variability measured as the coefficient of variation for glucose (%CV) level was associated with a higher risk for all-cause mortality in patients with type 2 diabetes (T2D) and a well-controlled glucose status.

Major finding: Compared with patients with a %CV level of ≤20%, those with a %CV level of 20%-25% (adjusted HR [aHR] 1.16; 95% CI 0.78-1.73), 25%-30% (aHR 1.38; 95% CI 0.89-2.15), 30%-35% (aHR 1.33; 95% CI 0.77-2.29), and >35% (aHR 2.26; 95% CI 1.13-4.52) had a higher risk for all-cause mortality.

Study details: This study was a part of the INDIGO study including 1839 patients with T2D who reached continuous glucose monitoring glycemic targets and were classified into five groups by %CV level.

Disclosures: This study was supported by the National Key R&D Program of China, the National Natural Science Foundation of China, and others. The authors declared no conflicts of interest.

Source: Mo Y et al. Impact of short-term glycemic variability on risk of all-cause mortality in type 2 diabetes patients with well-controlled glucose profile by continuous glucose monitoring: A prospective cohort study. Diabetes Res Clin Pract. 2022;189:109940 (Jun 1). Doi: 10.1016/j.diabres.2022.109940

Key clinical point: Monocyte-lymphocyte ratio (MLR) was significantly associated with proliferative diabetic retinopathy (PDR) in patients with type 2 diabetes (T2D).

Major finding: Each 0.1 unit increase in MLR increased the risk for PDR by 46% (adjusted odds ratio 1.46; P = .014), with the effects being stable across different subgroups stratified by age, sex, hemoglobin, and glycated hemoglobin categories.

Study details: Findings are from a cross-sectional study of 367 patients with T2D and diabetic retinopathy, of which 27% were diagnosed with PDR.

Disclosures: This study did not receive any funding. The authors declared no conflicts of interest.

Source: Wang H et al. Association of monocyte-lymphocyte ratio and proliferative diabetic retinopathy in the U.S. population with type 2 diabetes. J Transl Med. 2022;20:219 (May 13). Doi: 10.1186/s12967-022-03425-4

Key clinical point: Monocyte-lymphocyte ratio (MLR) was significantly associated with proliferative diabetic retinopathy (PDR) in patients with type 2 diabetes (T2D).

Major finding: Each 0.1 unit increase in MLR increased the risk for PDR by 46% (adjusted odds ratio 1.46; P = .014), with the effects being stable across different subgroups stratified by age, sex, hemoglobin, and glycated hemoglobin categories.

Study details: Findings are from a cross-sectional study of 367 patients with T2D and diabetic retinopathy, of which 27% were diagnosed with PDR.

Disclosures: This study did not receive any funding. The authors declared no conflicts of interest.

Source: Wang H et al. Association of monocyte-lymphocyte ratio and proliferative diabetic retinopathy in the U.S. population with type 2 diabetes. J Transl Med. 2022;20:219 (May 13). Doi: 10.1186/s12967-022-03425-4

Key clinical point: Monocyte-lymphocyte ratio (MLR) was significantly associated with proliferative diabetic retinopathy (PDR) in patients with type 2 diabetes (T2D).

Major finding: Each 0.1 unit increase in MLR increased the risk for PDR by 46% (adjusted odds ratio 1.46; P = .014), with the effects being stable across different subgroups stratified by age, sex, hemoglobin, and glycated hemoglobin categories.

Study details: Findings are from a cross-sectional study of 367 patients with T2D and diabetic retinopathy, of which 27% were diagnosed with PDR.

Disclosures: This study did not receive any funding. The authors declared no conflicts of interest.

Source: Wang H et al. Association of monocyte-lymphocyte ratio and proliferative diabetic retinopathy in the U.S. population with type 2 diabetes. J Transl Med. 2022;20:219 (May 13). Doi: 10.1186/s12967-022-03425-4

Key clinical point: Greater glycemic variability measured as the coefficient of variation for glucose (%CV) level was associated with a higher risk for all-cause mortality in patients with type 2 diabetes (T2D) and a well-controlled glucose status.

Major finding: Compared with patients with a %CV level of ≤20%, those with a %CV level of 20%-25% (adjusted HR [aHR] 1.16; 95% CI 0.78-1.73), 25%-30% (aHR 1.38; 95% CI 0.89-2.15), 30%-35% (aHR 1.33; 95% CI 0.77-2.29), and >35% (aHR 2.26; 95% CI 1.13-4.52) had a higher risk for all-cause mortality.

Study details: This study was a part of the INDIGO study including 1839 patients with T2D who reached continuous glucose monitoring glycemic targets and were classified into five groups by %CV level.

Disclosures: This study was supported by the National Key R&D Program of China, the National Natural Science Foundation of China, and others. The authors declared no conflicts of interest.

Source: Mo Y et al. Impact of short-term glycemic variability on risk of all-cause mortality in type 2 diabetes patients with well-controlled glucose profile by continuous glucose monitoring: A prospective cohort study. Diabetes Res Clin Pract. 2022;189:109940 (Jun 1). Doi: 10.1016/j.diabres.2022.109940

Key clinical point: Greater glycemic variability measured as the coefficient of variation for glucose (%CV) level was associated with a higher risk for all-cause mortality in patients with type 2 diabetes (T2D) and a well-controlled glucose status.

Major finding: Compared with patients with a %CV level of ≤20%, those with a %CV level of 20%-25% (adjusted HR [aHR] 1.16; 95% CI 0.78-1.73), 25%-30% (aHR 1.38; 95% CI 0.89-2.15), 30%-35% (aHR 1.33; 95% CI 0.77-2.29), and >35% (aHR 2.26; 95% CI 1.13-4.52) had a higher risk for all-cause mortality.

Study details: This study was a part of the INDIGO study including 1839 patients with T2D who reached continuous glucose monitoring glycemic targets and were classified into five groups by %CV level.

Disclosures: This study was supported by the National Key R&D Program of China, the National Natural Science Foundation of China, and others. The authors declared no conflicts of interest.

Source: Mo Y et al. Impact of short-term glycemic variability on risk of all-cause mortality in type 2 diabetes patients with well-controlled glucose profile by continuous glucose monitoring: A prospective cohort study. Diabetes Res Clin Pract. 2022;189:109940 (Jun 1). Doi: 10.1016/j.diabres.2022.109940

Key clinical point: Greater glycemic variability measured as the coefficient of variation for glucose (%CV) level was associated with a higher risk for all-cause mortality in patients with type 2 diabetes (T2D) and a well-controlled glucose status.

Major finding: Compared with patients with a %CV level of ≤20%, those with a %CV level of 20%-25% (adjusted HR [aHR] 1.16; 95% CI 0.78-1.73), 25%-30% (aHR 1.38; 95% CI 0.89-2.15), 30%-35% (aHR 1.33; 95% CI 0.77-2.29), and >35% (aHR 2.26; 95% CI 1.13-4.52) had a higher risk for all-cause mortality.

Study details: This study was a part of the INDIGO study including 1839 patients with T2D who reached continuous glucose monitoring glycemic targets and were classified into five groups by %CV level.

Disclosures: This study was supported by the National Key R&D Program of China, the National Natural Science Foundation of China, and others. The authors declared no conflicts of interest.

Source: Mo Y et al. Impact of short-term glycemic variability on risk of all-cause mortality in type 2 diabetes patients with well-controlled glucose profile by continuous glucose monitoring: A prospective cohort study. Diabetes Res Clin Pract. 2022;189:109940 (Jun 1). Doi: 10.1016/j.diabres.2022.109940

Key clinical point: Addition of low-dose (0.25 mg/day) vs. standard-dose (0.5 mg/day) lobeglitazone to metformin plus dipeptidyl peptidase 4 inhibitor (DPP4i) therapy led to noninferior glucose lowering effects and fewer adverse outcomes in patients with type 2 diabetes mellitus (T2D).

Major finding: At week 24, the mean glycated hemoglobin level in the low-dose vs. standard-dose lobeglitazone group was 6.87% ± 0.54% vs. 6.68% ±0 .46%, respectively, with a between-group difference of 0.18% (95% Cl 0.017%-0.345%) showing noninferiority of the low-dose to standard-dose treatment. Treatment-emergent adverse events were more frequent in the standard-dose vs. low-dose group.

Study details: This was a phase 4 study including 134 patients with T2D inadequately controlled on metformin plus DPP4i therapy who were randomly assigned to receive low-dose (n = 67) or standard-dose (n = 67) lobeglitazone.

Disclosures: This study was supported by a research grant from Chong Kun Dang Pharmaceutical

Corporation, Seoul, Republic of Korea.

Source: Ryang S et al. A double-blind, Randomized controlled trial on glucose-lowering EFfects and safety of adding 0.25 or 0.5 mg lobeglitazone in type 2 diabetes patients with INadequate control on metformin and dipeptidyl peptidase-4 inhibitor therapy: REFIND study. Diabetes Obes Metab. 2022 (May 17). Doi: 10.1111/dom.14766.

Key clinical point: Addition of low-dose (0.25 mg/day) vs. standard-dose (0.5 mg/day) lobeglitazone to metformin plus dipeptidyl peptidase 4 inhibitor (DPP4i) therapy led to noninferior glucose lowering effects and fewer adverse outcomes in patients with type 2 diabetes mellitus (T2D).

Major finding: At week 24, the mean glycated hemoglobin level in the low-dose vs. standard-dose lobeglitazone group was 6.87% ± 0.54% vs. 6.68% ±0 .46%, respectively, with a between-group difference of 0.18% (95% Cl 0.017%-0.345%) showing noninferiority of the low-dose to standard-dose treatment. Treatment-emergent adverse events were more frequent in the standard-dose vs. low-dose group.

Study details: This was a phase 4 study including 134 patients with T2D inadequately controlled on metformin plus DPP4i therapy who were randomly assigned to receive low-dose (n = 67) or standard-dose (n = 67) lobeglitazone.

Disclosures: This study was supported by a research grant from Chong Kun Dang Pharmaceutical

Corporation, Seoul, Republic of Korea.

Source: Ryang S et al. A double-blind, Randomized controlled trial on glucose-lowering EFfects and safety of adding 0.25 or 0.5 mg lobeglitazone in type 2 diabetes patients with INadequate control on metformin and dipeptidyl peptidase-4 inhibitor therapy: REFIND study. Diabetes Obes Metab. 2022 (May 17). Doi: 10.1111/dom.14766.

Key clinical point: Addition of low-dose (0.25 mg/day) vs. standard-dose (0.5 mg/day) lobeglitazone to metformin plus dipeptidyl peptidase 4 inhibitor (DPP4i) therapy led to noninferior glucose lowering effects and fewer adverse outcomes in patients with type 2 diabetes mellitus (T2D).

Major finding: At week 24, the mean glycated hemoglobin level in the low-dose vs. standard-dose lobeglitazone group was 6.87% ± 0.54% vs. 6.68% ±0 .46%, respectively, with a between-group difference of 0.18% (95% Cl 0.017%-0.345%) showing noninferiority of the low-dose to standard-dose treatment. Treatment-emergent adverse events were more frequent in the standard-dose vs. low-dose group.

Study details: This was a phase 4 study including 134 patients with T2D inadequately controlled on metformin plus DPP4i therapy who were randomly assigned to receive low-dose (n = 67) or standard-dose (n = 67) lobeglitazone.

Disclosures: This study was supported by a research grant from Chong Kun Dang Pharmaceutical

Corporation, Seoul, Republic of Korea.

Source: Ryang S et al. A double-blind, Randomized controlled trial on glucose-lowering EFfects and safety of adding 0.25 or 0.5 mg lobeglitazone in type 2 diabetes patients with INadequate control on metformin and dipeptidyl peptidase-4 inhibitor therapy: REFIND study. Diabetes Obes Metab. 2022 (May 17). Doi: 10.1111/dom.14766.