NY CERC Clinical Connections



Activity Overview

The 2017 NY CERC delivers state-of-the-art clinical updates and strategies aimed directly at the intersection of metabolic and cardiovascular (CV) disease prevention. This activity will present highlights for binge eating disorder (BED) and cardiovascular outcomes in type 2 diabetes (T2D). The activities will address clinically relevant topics in cardiometabolic health, including CV disease prevention, dyslipidemia, diabetes, obesity management, hypertension, and/or other cardiometabolic risk factors. This clinical connection conference will offer cardiometabolic health care professionals (HCPs) the opportunity to advance their understanding and knowledge of chronic cardiometabolic diseases and associated comorbidities.

Acknowledgement of Commercial Support

This activity is supported by educational grants from Shire, and Boehringer Ingelheim Pharmaceuticals, Inc., Lilly USA, LLC, and Novo Nordisk Inc.

Instructions for This Activity and Receiving Credit

  • You will need to login to participate in the activity.
  • Each presentation may contain an interactive question(s). You may move forward through the presentation; however, you may not go back to change answers or review videos/content until you finish the presentation.
  • At the end of the activity, “educational content/video files” will be available for your reference.
  • In order to receive a CME/CE certificate, participants must complete the activity.
  • Complete the posttest and pass with a score of 70% or higher, complete the evaluation and then click on request for credit. Participants may immediately download a CME/CE certificate upon completion of these steps.

Target Audience

This educational activity is directed toward cardiologists, endocrinologists, specialty nurse practitioners, specialty physician assistants, certified diabetes educators, other specialty allied health professionals, and other HCPs interested in the treatment of cardiometabolic disorders.

Learning Objectives

After completing this educational activity, you should be able to:

  • Discuss the association of BED with a multitude of cardiometabolic comorbidities.
  • Interpret clinical evidence from various CV outcomes trials related to glucose-lowering agents used in the management of persons with T2D.
  • Asses the practical implications of this evidence for use in clinical practice.

Faculty, Staff, and Planners' Disclosures

Carlos M. Grilo, PhD
Professor of Psychiatry, Yale School of Medicine
Professor of Psychology, Yale University
Director, Program for Obesity Weight and Eating Research (POWER), Yale School of Medicine
New Haven, Connecticut

Disclosure: Research funding: National Institutes of Health; Consultant: Shire, Sunovion; Book royalties (academic books): Guilford Press, Taylor & Francis Publishing
Silvio E. Inzucchi, MD
Professor of Medicine
Clinical Director, Section of Endocrinology
Medical Director, Yale Diabetes Center
Director, Endocrinology & Metabolism Fellowship
Director, Yale Affiliated Hospitals Program
New Haven, Connecticut

Disclosure: Research funding: National Institute of Diabetes and Digestive and Kidney Diseases; Consultant: Boehringer Ingelheim, AstraZeneca, Novo Nordisk, VTV Pharmaceuticals, Janssen, Sanofi/Lexicon, Eisai

The staff of PER® have no relevant financial relationships with commercial interests to disclose.

The following contributors have no relevant financial relationships with commercial interests to disclose. 

Physicians’ Education Resource®, LLC (PER®
Planning Staff—David Heckard; Maryjo Dixon, RPh; and Kate Bowen.

Global Education Group 
Lindsay Borvansky; Andrea Funk; and Liddy Knight

Accreditation/Designation of Credit

This activity is jointly provided by Global Education Group and Physicians’ Education Resource®, LLC. AMA PRA Category 1 Credit™ is provided by Global Education Group.
This activity has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of Global Education Group and Physicians’ Education Resource®, LLC. Global Education Group is accredited by the ACCME to provide continuing medical education for physicians.

Global Education Group designates this live activity for a maximum of 1.0 AMA PRA Category 1 Credit™. Physicians should claim only the credit commensurate with the extent of their participation
in the activity.

Disclosure Policy and Resolution of Conflicts Of Interest (Coi)

Global Education Group (Global) requires instructors, planners, managers and other individuals and their spouse/life partner who are in a position to control the content of this activity to disclose any real or apparent conflict of interest they may have as related to the content of this activity. All identified conflicts of interest are thoroughly vetted by Global for fair balance, scientific objectivity of studies mentioned in the materials or used as the basis for content, and appropriateness of patient care recommendations.

Off-Label Disclosure and Disclaimer

This CME/CE activity may or may not discuss investigational, unapproved, or off-label uses of drugs. Participants are advised to consult prescribing information for any products discussed. The information provided in this CME/CE activity is for continuing medical and nursing education purposes only and is not meant to substitute for the independent clinical judgment of a physician or nurse relative to the diagnostic, treatment, and management options for a specific patient’s medical condition.

The opinions expressed in the content are solely those of the individual faculty members and do not reflect those of Physicians’ Education Resource®, LLC, or any of the companies that provided commercial support for this activity.

Improving the Identification and Management of Binge Eating Disorder in the Cardiometabolic Setting


Individuals with binge eating disorder (BED) experience recurrent episodes of binge eating (defined as eating unusually large quantities of food while experiencing a subjective sense of lack of control), but without inappropriate compensatory behaviors to prevent weight gain (eg, self-induced vomiting or laxative abuse). The episodes of binge eating typically involve at least 3 of the following characteristics: eating more quickly than usual, eating until physically uncomfortable, overeating despite not being hungry, eating alone due to embarrassment, and feeling disgust and shame afterward. The BED diagnosis requires marked distress about binge eating, that binge eating occur at least weekly for at least 3 months, and that the person does not meet criteria for either bulimia nervosa or anorexia nervosa. BED is now considered the most prevalent eating disorder in the United States,1 affecting 1% to 5% of the general population, and is recognized as a distinct cause of obesity.2-5

BED is associated strongly with obesity and with heightened risk for other psychiatric and medical comorbidities. The heightened medical comorbidities associated with BED appear largely due to the excess weight in many persons with BED. Medical comorbidities associated with BED include cardiometabolic conditions such as hypertension, hypercholesterolemia, heart disease, and type 2 diabetes.2 Metabolic syndrome is present in more than 40% of obese patients with BED and comprises a constellation of symptoms, including elevated triglycerides, abdominal obesity, hypertension, low HDL cholesterol, and type 2 diabetes.6Thus, BED is considered a major public health issue that presents both medical and psychiatric issues that impair patients’ quality of life. As of 2013, BED was included in the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition,7 as a specific, formal eating disorder with a corresponding diagnosis code.
HCPs should be aware of the diagnosis criteria for BED and be prepared to discuss BED with patients at risk for or suspected of having the disorder. Interacting with patients in a nonjudgmental, compassionate manner and discussing available treatment options is vital. Most patients are embarrassed or secretive about BED symptoms because they have likely encountered stigma or shaming from family members or health care providers about their weight. Being willing to discuss binge-eating symptoms with patients and speak to them without bias is critical. This will help patients feel understood and be more receptive to recommendations, which will allow the provider to outline the range of available nonpharmacologic and pharmacologic treatment options.

  1. Iacovino JM, Gredysa DM, Altman M, Wilfley DE. Psychological treatments for binge eating disorder. Curr Psychiatry Rep. 2012;14:432-446.
  2. National Eating Disorders Association. Binge eating disorder. Nationaleatingdisorders.org. www.nationaleatingdisorders.org/binge-eating-disorder. Accessed April 25, 2017.
  3. Kessler RC, Berglund PA, Chiu WT, et al. The prevalence and correlates of binge eating disorder in the World health Organization World Mental Health Surveys. Biol Psychiatry. 2013;73:904-914.
  4. Swanson SA, Crow SJ, Le Grange D, Swendsen J, Merikangas KR. Prevalence and correlates of eating disorders in adolescents. Results from the national comorbidity survey replication adolescent supplement. Arch Gen Psychiatr. 2011;68:714-723.
  5. Gonzalez-Campoy JM. Vyvanse approved for binge-eating disorder in adults. EndocrineWeb.com. www.endocrineweb.com/news/obesity/14136-vyvanse-approved-binge-eating-disorder-adults. Accessed April 25, 2017.
  6. Hudson JI, Lalonde JK, Coit CE, et al. Longitudinal study of the diagnosis of components of the metabolic syndrome in individuals with binge eating disorder. Am J Clin Nutr. 2010;91:1568-1573.
  7. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Washington, DC: American Psychiatric Association; 2013.

Cardiovascular Outcomes in Type 2 Diabetes:

Examining Cutting-Edge Data and Clinical Implications for Patient Care


The aims of managing patients with type 2 diabetes (T2D) are to avoid acute osmotic symptoms of hyperglycemia, avoid instability in blood glucose over time, and prevent/delay the development of diabetes complications without adversely affecting quality of life.1-3 Individuals with uncontrolled diabetes commonly develop macrovascular and microvascular complications. Reducing macrovascular complications is essential because persons with diabetes are 2 to 4 times more likely than those without diabetes to die from a cardiovascular (CV) disease, which accounts for 65% of deaths in persons with diabetes.4 For individuals with diabetes, poor glycemic control and CV risk factors (dyslipidemia, being overweight/obese, and/or hypertension), the risk of having a CV event (myocardial infarction [MI], stroke, and/or death) is increased.5Thus, glycemic control and management of one or more CV risk factors are essential to reduce the risk of a CV event in these individuals.
In 2008, the FDA required assessment of CV safety for all antidiabetic drugs to be licensed in the future.6 So far, several drug classes that have been studied in large, randomized clinical trials meet this mandate, including basal insulin, sodium glucose cotransporter-2 (SGLT2) inhibitors, and glucagonlike peptide-1 (GLP-1) receptor agonists. The following are summaries of those trials:

  • DEVOTE (Insulin Degludec versus Insulin Glargine in Patients with Type 2 Diabetes at High Risk of Cardiovascular Events), a randomized, double-blind, parallel-group, event-driven trial, was conducted to confirm the CV safety of insulin degludec compared with insulin glargine U100 for persons with T2D at high risk of CV disease.7 The primary composite outcome was the first occurrence of an adjudicated major CV event (death from CV causes, nonfatal MI, or nonfatal stroke) with a prespecified non-inferiority margin of 1.3. Results showed the primary outcome occurred in 8.5% of participants randomized to degludec versus 9.3% of participants randomized to glargine (<.001 for non-inferiority).
  • The EMPA-REG OUTCOME trial examined the effects of empagliflozin, an SGLT2 inhibitor, versus standard of care on CV morbidity and mortality in persons with T2D at high risk for CV events.8 The primary composite outcome was death from CV causes, nonfatal MI, or nonfatal stroke. Results revealed the primary outcome occurred in 10.5% of participants randomized to empagliflozin versus 12.1% of those randomized to placebo (<.001 for non-inferiority; = .04 for superiority). Although there were no significant differences between groups in the rates of MI or stroke, those randomized to empagliflozin experienced significantly lower rates of death from CV causes (<.001), hospitalization for heart failure (<.002), and death from any cause (<.001).
  • The CANVAS (Canagliflozin Cardiovascular Assessment Study) Program integrated data from 2 trials involving persons with T2D and high CV risk, who were randomized to either canagliflozin, an SGLT2 inhibitor, or placebo.9 The primary outcome was a composite of death from cardiovascular causes, nonfatal MI, or nonfatal stroke. Results showed the rate of the primary outcome was lower with canagliflozin than with placebo (<.001 for non-inferiority; = .02 for superiority).
  • The LEADER study (Liraglutide Effect and Action in Diabetes: Evaluation of Cardiovascular Outcome Results) was a randomized, double-blind trial that assessed the effect of liraglutide, a GLP-1 receptor agonist, versus placebo and standard of care on CV outcomes in patients with T2D at high risk for, or with, CV disease.10 Results showed that after a median follow-up of 3.8 years, the composite primary outcome (MI, stroke, or CV death) occurred in 13.0% of those randomized to liraglutide versus 14.9% of those randomized to placebo (<.001 for non-inferiority; = .01 for superiority). 

Within the next several years, results from other large-scale clinical outcomes studies evaluating various drug classes will be available, which will allow clinicians to decide which drug is best for the overall management of persons with T2D who have a high–CV-risk profile.

  1. Inzucchi SE, Bergenstal RM, Buse JB, et al. Management of hyperglycemia in type 2 diabetes, 2015: a patient-centered approach: update to a position statement of the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care. 2015;38:140-149.
  2. American Diabetes Association. Standards of medical care in diabetes – 2017. Diabetes Care. 2017;40(suppl 1):S1-S135.
  3. Garber AJ, Abrahamson MJ, Barzilay JI, et al. Consensus statement by the American Association of Clinical Endocrinologists and American College of Endocrinology on the comprehensive type 2 diabetes management algorithm – 2017 executive summary. Endocr Pract. 2017;23:207-238.
  4. Benjamin EJ, Blaha MJ, Chiuve SE, et al; American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics – 2017 update: a report from the American Heart Association. Circulation. 2017;135:e146-e603.
  5. Imperatore G, Cadwell BL, Geiss LS, Saaddine JB, Williams DE, Ford ES. Thirty-year trends in cardiovascular risk factor levels among U.S. adults with diabetes. Am J Epidemiol. 2004;160:531-539.
  6. US Food and Drug Administration. Guidance for industry – diabetes mellitus: developing drugs and therapeutic biologics for treatment and prevention, 2008. FDA.gov. www.fda.gov/downloads/Drugs/Guidances/ucm071624.pdf. Accessed September 2, 2017.
  7. Marso SP, McGuire DK, Zinman B, et al; DEVOTE Study Group. Efficacy and safety of degludec versus glargine in type 2 diabetes. N Engl J Med. 2017;377:723-732.
  8. Zinman B, Wanner C, Lachin JM, et al; EMPA-REG OUTCOME Investigators. Empagliflozin, cardiovascular outcomes, and mortality in type 2 diabetes. N Engl J Med. 2015;373:2117-2128.
  9. Neal B, Perkovic V, Mahaffey KW, et al; CANVAS Program Collaborative Group. Canagliflozin and cardiovascular and renal events in type 2 diabetes. N Engl J Med. 2017;377:644-657.
  10. Marso SP, Daniels GH, Brown-Frandsen K, et al; LEADER Steering Committee; LEADER Trial Investigators. Liraglutide and cardiovascular outcomes in type 2 diabetes. N Engl J Med. 2016;375:311-322.

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