Dr. Garvey: My name Dr. W. Timothy Garvey, M.D. FACE. I’m the professor and chair of the department of Nutrition Sciences at the University of Alabama at Birmingham, UAB. I’m also director of our NIH funded Diabetes Research Center and a staff position and investigator at the Birmingham VA Medical Center. I’m an endocrinologist and I’ve studied insulin resistance most of my career. In recent years I’ve become passionate about obesity as a disease and establishing rational care patterns for patients with obesity.
Steve Freed: What are the reasons for you to be here at AACE? And by the way this is AACE 2016 the American Association of Clinical Endocrinologists.
Dr. Garvey: Well I’ve become active in AACE over the past five years really. I think these meetings are really outstanding meetings for clinical endocrinologists. It provides some basic research information as well, really targeted to the clinical endocrinologist. No other meeting really does it as well as this meeting does. I’m on the board of directors with AACE. I think working with this organization has been rewarding to me. It has also given me a platform for working on positions statements and in guidelines, such as the diabetes guidelines, and the new comprehensive clinical practice guidelines for the medical care of patients with obesity, which were just published online yesterday. I was the chair of the task force that drafted those guidelines.
Steve Freed: Maybe go over some of those guidelines for obesity for our people that are watching as far as medical professionals.
Dr. Garvey: There are a number of guidelines that professional societies have put out. I think that they’ve created some confusion among primary care health care professionals. Some of them only address questions for which randomized clinical trials were available, which certainly aren’t all of the questions that health care professionals have to face when they’re taking care of a patient with obesity. I think what we really needed was an evidenced based, comprehensive guideline that address all aspects of patient care, beginning with screening, diagnosis, evaluation, treatment decisions, disease staging, goals of therapy, follow-up. We generated questions in each of those areas and reviewed the literature, the evidence base that addresses each of those questions and came up with 123 evidence based recommendations that address all aspects of obesity care. These recommendations were then the basis of what were translated into an algorithm. Algorithmic materials to inform rational care for patients with obesity, as well as a chronic care model, the outlines of a chronic care model that involves an activated patient and a prepared practice that can use these guidelines to optimal benefit. That process has to sit within our larger health care system and our society actually. If we’re really going to get serious about treating obesity as a disease, reducing the morbidity in patient suffering, and decreasing the social cost of obesity.
Steve Freed: So what is your definition? You sit on the board, you help generate the guidelines. What is your definition of obesity?
Dr. Garvey: We think that at least the diagnostic criteria or components for obesity are two-fold. One you need an anthropometric component to the diagnosis, which is an indication of whether you have excess adipose tissue mass, excess adiposity. We use BMI for that. We’re recommending that we continue to use BMI for the anthropometric component of the diagnosis. Although it’s important to realize that edema or a high degree of muscularity, or sarcopenia, all of these things can affect BMI which interrelates height and weight of course, independent of adipose tissue mass. The BMI is a number that needs to be clinically evaluated. You need to make sure that a high BMI represents increased adipose tissue mass in your patient. The second component of the diagnosis is an assessment of the degree to which that excess adiposity impacts the health of the patient, adversely impacts the health of the patient, which we define as the risk presence and severity of weight related complications. Any treatment of a patient with obesity has to involve both assessment for excess adiposity and an evaluation for a key set of weight related complications which include prediabetes and metabolic syndrome, type 2 diabetes, hypertension, dyslipidemia, non-alcoholic fatty liver disease, the cardiometabolic nexus of complications, as well as biomechanical complications that arise just through carrying around a heavier body mass. These are important as well and include obstructive sleep apnea, osteoarthritis, GERD, urinary stress incontinence, and depression as well. Really what we emphasize in the medical treatment of obesity as a disease is the therapy is designed to improve the health of the patient. That’s the goal, not necessarily to get X amount of pounds off. With different complications, there’s a dose responsibility between how much weight loss you need to achieve to improve or reverse certain complications. The idea is to achieve sufficient weight loss for that purpose. We’re treating a medical disease here. Some patients are overweight or obese and have no complications. So called metabolically healthy obese. That’s important to know, I think they still need therapy, more along the lines of secondary prevention, prevent progressive weight gain, prevent the emergence of complications. Once you have these complications, that tells you that that degree of adiposity is adversely affecting health. You need to enter a more tertiary phase of disease intervention, really prevent further deterioration, get some weight off, and prevent or reverse the complications that exist.
Steve Freed: When you talk about obesity and diabetes, it is obviously interrelated. But sometimes people can weigh 400 pounds and never get diabetes, it’s not in their genes, their genetic makeup. But if you look at obesity by itself, we see a lot of the same comorbidities: hypertension, hypolipidemia, cardiovascular disease. So they’re really very closely related.
Dr. Garvey: I think it’s insulin resistance which is the common link there. Your degree of insulin sensitivity or resistance is a trait that is expressed very early in life, even perhaps in utero. There’s a big individual variation in insulin sensitivity in adult populations, five-fold, independent of BMI. The way I put this together is if you have progressive weight gain on an insulin sensitive background, yes, you’ll become obese, you won’t be at risk or be at much reduced risk of the cardiometabolic complications that include diabetes and include premature vascular disease as well. You may still be at risk of the biomechanical complications, sleep apnea, and osteoarthritis. But on the other hand if you have progressive weight gain on an insulin resistant background, you have abnormal, dysfunctional fat tissue that doesn’t store lipid as well. Some of that lipid goes to liver cells and muscle cells and worsens insulin resistance. If you also start getting some impaired insulin secretory responses, you’re going to get type 2 diabetes, as well as other cardiometabolic manifestations, like fatty liver or cardiovascular disease, hypertension, and dyslipidemia. The insulin sensitivity versus resistance background that’s important. You add increased adiposity on top of that, the people that are more on the insulin resistant side of the spectrum are the ones that are going to get cardiometabolic disease and are at more risk of type 2 diabetes. Because not all obese patients are the same. Overweight and obesity constitute 2/3rds of America. We can’t put 2/3rds of America on highly structured intensive lifestyle interventions, weight loss medications or bariatric surgery. So is there a way to identify which of those patients with overweight or obesity are at greater risk of progressing to type 2 diabetes. If we could risk stratify them, we could then target our preventative therapy to those in the higher risk strata. We’ve published some papers using a tool we call cardiometabolic disease staging (CMDS). This utilizes information, data, that’s readily available to the clinician. We have four stages of risk. Stage 0: there’s no metabolic syndrome traits, blood pressure, lipids, fasting glucose, waist circumference, all normal, that’s stage 0, that’s the metabolically healthy obese. The stage 1 is if there’s one or two metabolic syndrome traits. Stage 2 is basically if you meet criteria for metabolic syndrome or prediabetes but not both and stage 3 is if you meet criteria for both prediabetes and metabolic syndrome, and if you validate that risk stratification approach, in large cohort studies such as Cardia and Eric, you see that over a 12 to 20 year period of follow-up, you can stratify risk for development of type 2 diabetes forty-fold. So the stage 0 without metabolic syndrome traits, those are the insulin sensitive obese individuals, they really have very low rates of incident diabetes, and do much better with cardiovascular mortality and cardiovascular disease events. The highest risk, if you have both metabolic syndrome and prediabetes, much higher rates of incident diabetes. So you could target your more aggressive weight loss interventions to those individuals and of course, you get 10% weight loss, you can effectively prevent 80% of patients from developing diabetes.
Steve Freed: That’s interesting because that’s one of the few diseases that you can have a huge impact on in preventing comorbidities that people hear about whether it be kidney failure, blindness, limb amputation. All of those things are just waiting for people not to follow the guidelines as like a punishment. We told you and now it’s here. I know it’s very difficult to get people to change lifestyles. How much time do you physically actually get with a patient. Some physicians have a huge staff and three CDEs and they got all these medical people and it’s a no-brainer. But a lot of physicians, they don’t have that luxury. So what do you do when you get 15 maybe 30 minutes.
Dr. Garvey: That’s an excellent question. At UAB, Weight-Loss Medicine we call our weight management clinic, we have a number of patients with diabetes in there. We do have a multidisciplinary team. Physician-driven programs that include nurse educators, dietitians, exercise therapists, a clinical psychologist, which we find to be an important member of the team. But I tell you, an informed physician working together with a dietitian, and I’m not saying any dietitian, but a dietitian who’s been trained in the principals of weight-loss, you can do a lot of good. I think that’s the essence, you can’t do it yourself. You’ve got 15 minutes to be with the patient, you got 10 people out in the waiting room, and you don’t have to do everything at the first visit. You can take care of some objectives at the first visit and then subsequent visits. The greater the degree to which you prescribe a lifestyle intervention to which the patient can comply, the more likely you are going to be successful. What do I mean by that, we have various healthy meal plans, low-carb, low-fat, dash diet, Mediterranean diet, vegetarian diet, we have a very low calorie diet option as well. We try to pick a healthy meal plan that is compatible with the personal and cultural preferences of the patient. We want them to adhere to the diet so we want to give them food they like to eat, deliver that in a reduced calorie format. The physical activity component, we don’t like to use the word exercise, we use physical activity, something they like to do, something they are capable of doing, something that they have access to. So you really have to individualize, and behavioral interventions are also important. They are really designed to enhance adherence to reduced calorie meal plan and increased physical activity. Those are very important. Many patients after a year or two years will start to regain weight, it’s not their fault. They have a disease. There are all kinds of pathophysiological mechanisms that are driving that weight regain. Hormones like Ghrelin in the stomach that make you eat more go up. Hormones like GLP-1, CCK, and PYY from the intestines, they make you eat less, and they go down. The amount of energy your body expends just at rest goes down, which favors increased weight accretion. Even your psychological preferences for foods get oriented to a more calorie dense diet with a higher fat and sugar content. So all of these factors that are part of the pathophysiology of the disease are driving this weight regain. That’s what patients have to fight against. Which is why we need weight-loss medications in some patients because they really act, at least the pre-clinical data, indicate that they act at the level of the hypothalamus. The satiety mechanisms that these hormones that I mentioned control appetite, they act to suppress appetite and really enable patients to adhere to a lifestyle intervention program. Help your patients out, you’ve got these weight loss medicines with proven efficacy and safety, FDA-approved. I think we are really at a new era of obesity medicine. Actually obesity medicine is an evolving subspecialty, using some of these tools and individualizing care to the best benefit risk-ratio for a patient.