Well, hello everyone, and welcome to today's webinar. This session is the fifth installment in the Hands-On Tips to Improve Diabetes Care webinar series for 2023-24. Today our panel will share their expertise and insight on weight management in type 2 diabetes. We're very glad you're here. I am the moderator, Dr. Eden Miller. I will be going through and introducing today's program. Let me share a little bit about myself. My personal mission and adage for care is that I only succeed as a healthcare provider if I turn patients into experts on their own disease. I believe a physiologic patient individualized approach to health intervention is crucial for our success. If our nation is to triumph over the ravages of obesity and diabetes, we need a collaborative effort unhindered by fear of personal scrutiny and barriers for effective treatment. Those all need to be removed. So let me switch today to the agenda. So we'll go to the next slide for the agenda, please. We will spend the next hour together by following the agenda on the screen. We'll be using interactive features today. So we will go through our announcement, our presentation of case studies, and make sure to do the question and answer down in that box down there. There's questions in there we want to make sure and get to. That's one of my favorite parts of that. But we will be sending you some important links, so you need to stay informed throughout our session. So you got to look at the chat box, okay? We're going to be using Zoom question and answer. And if you think of a question as we go, it's okay if you put it in there, because I will at the very end, we're going to be going through those questions. So now if we go to the next slide, we're also going to be using a really cool interactive tool called Kahoot during our webinar. It's a very fun interactive game-like platform that allows us to ask these knowledge-based questions and open-ended questions and collect those answers in real time. So how do you connect to Kahoot? If you have a mobile phone or tablet nearby, it's often the easiest and best way to do it. So if you have something like that, a secondary piece of technology, you can go and click that link for Kahoot in that chat feature. Now, if you don't have anything else nearby, you can also use whatever device you're currently doing. You just need to open another window, you know, go up in there, open another window, click on that Kahoot link, and then you will get connected with us. You'll open that browser, type Kahoot.com in it if you're opening up a secondary link, and you enter that pin, today's pin, okay? I'm going to give everybody about 15 seconds or so to do that. So again, if you have a different device, you can click on the link that was put in the chat. You can go to Kahoot.com to try and connect and interface with us. Make sure that you're putting that link in there and that code so you can join into our discussion. It's Kahoot.com, Kahoot.com, so just open up another window, Kahoot.com, and you can then put in the pin that we had, and if we could, Kahoot.it, I apologize, here, I'm leading you astray from the very beginning, and I'm the moderator leading you astray, Kahoot.it, and if we can give us the pin in the chat as well, you can see you can just enter that into the corner. A couple more seconds to get everybody going. Now remember, we also have additional insights hands-on webinar. We're having one coming up. Join us March 12th, 2024, for the next installment in the hands-on webinar series, Current Insights into Screening and Prevention in Type 1 Diabetes, and this webinar's speakers, Jason Galia and Lauren Jacobson, will discuss the latest development and best practices for screening and prevention. Click the link in your chat box to register today for that lovely hands-on webinar that's coming up Tuesday, March 12th, Tuesday, March 12th. To register for the Innovations and Latest Development in Type 1 webinar, click that link in your Zoom box, because we want to make sure that you have that continuing educational credit. You can see that what this one is particularly provides you in terms of the hours of credit, and it's really intended for all of those who interface with those individuals in Team Diabetes, especially in Type 1 Diabetes. So with that, let's get to our panelists, because that's why we're all here. It is just my distinct pleasure to introduce Dr. Robert Kushner. He is a professor of medicine and medical education at Northwestern University Feinberg School of Medicine and director of the Center for Lifestyle Medicine in Chicago, Illinois. After finishing a residency in internal medicine at Northwestern University, he went on to complete a postgraduate fellowship in clinical nutrition and earned a master's degree in clinical nutrition and nutritional biology from the University of Chicago. Dr. Kushner is the past president of the Obesity Society, the American Society of Parenteral and Enteral Nutrition, and the American Board of Physicians Nutritional Specialists, as well as a founder and first chair of the American Board of Obesity Medicine. Dr. Kushner has authored over 250 original articles, reviews, books and books chapters covering medical nutrition, medical nutrition education, and obesity, and is definitely an internationally recognized expert in the care of persons with overweight and obesity issues. I'd also like to invite Mary Lou Perry. She is an MSRDN, CDCES registered dietitian educator out there in the trenches working in collaborative diabetes cardiometabolic practice at the University of Virginia. She has over 35 years of clinical experience working in the field of diabesity. Mary Lou has been active in the Academy of Nutrition and Dietetics Diabetes Practice Group and the Weight Management Practice Group. She has seen the field evolve over the last three decades with particular emphasis on the chronicity of overweight and obesity, that complexity of dietology, and the treatment and more recent focus on working internationally on our own sense of bias and stigma. Mary Lou's biggest professional thrill was serving on the ADA Professional Practice Committee and also working with Dr. Langvey and Dr. Kushner on Chapter 8 of the Standards of Care. She just finished her two-year term. Mary Lou and her husband, Mark, are empty nesters or what I like to call open nesters ready for that next adventure, what is ever to come. And so with that, I'm going to show the disclosures for our esteemed faculty today. And at this time, I'd like the panelists to introduce themselves and take it from here. Thank you, Dr. Miller. I am Bob Kushner. You've already did a very nice introduction for me. So thank you. And I'm very happy to be here and provide this presentation. And my name is Mary Lou Perry. I have no, well, I have a disclosure, LifeScan Diabetes Institute. So I'm also looking forward to presenting. Wonderful. And I am going to be going first. So the title of my presentation is Weight Management in Type 2 Diabetes. Everyone on this webinar sees, who sees patients with Type 2 diabetes, chances are they also have accompanying obesity. And I'm going to be focusing on treatment of both of them at the same time. My learning objectives are to explain the association between obesity and diabetes. The pathophysiology underlines this link, and to discuss pharmacologic treatment options and outcomes. Ozempic and Wegovy and Zepound are sweeping the nation. I think more people know the word ozempic than who's running for president. It is really an incredibly exciting time. I want to start off with one slide on epidemiology, and what you're seeing is the change in the population prevalence between diabetes, which is the bottom line, which has gone up about four percentage points over the past 20, over the past 18 years, this ends in 2018, and you also see a similar trend, but even more dramatic for obesity, which went up 12 percentage points over the same period of time. If we now look at the combination of the two, I think it's going to be very clear why we want to focus on obesity. If I've changed the bar graph a little bit here, the orange lines on the bottom is the same data I showed you for diabetes, goes from 9.8% in 2000 up to 14% in 2018, but the blue bars or purple bars are a little bit different. What I'm showing you here is what percent of individuals with diabetes have concomitant obesity. What you see from this epidemiologic data is that 60% to 80% of people living with diabetes have a body mass index of 30 or greater, and if you add overweight and obesity, combine those two, overweight meaning over BMI 25, you're now upwards to probably 90% to 95%, so clearly you see individuals that are suffering or living with both these conditions. In fact, these conditions occur so commonly together, we have given the name syndemic. That may be a new word in your vocabulary list that you can write down if you haven't heard of it. A syndemic or a synergistic epidemic involves the clustering of two or more diseases within a population, the biological, social and psychological interaction of those diseases in the large-scale social forces that precipitate disease clustering in the first place. I couldn't have said it better myself, and that is the definition of syndemic, and the syndemic we're talking about is diabetes, another new word for you perhaps, and that's the combination of obesity and diabetes together. What this slide shows is the individual in your clinic who is suffering from obesity who is most likely to have a risk of having type 2 diabetes and complications, and this is a phenotypic presentation that you're looking for, and this is someone with this upper body fat distribution we call central and visceral adiposity, right, the abdomen is large, increased waist circumference and so forth, and that's the individual who is likely to have the cardiometabolic risk factors and the cardiovascular outcomes that occur from the combination of obesity and diabetes. So what's the underlying pathophysiology? The obesity gives way to diabetes. It's not that diabetes gives way to obesity. So the underpinnings of the diabetes epidemic is obesity, and from that you then have more likely to have insulin resistance and diabetes. There are multiple pathological mechanisms. I just list three of the probably most common ones here just as a quick review for you. We know that increased fat mass leads to prolonged dilation of free fatty acids in the blood, which themselves result in whole body insulin resistance. The second bullet point is that increased levels of pro-inflammatory cytokines, which you often call adipokines as well, examples would be tumor necrosis factor alpha, nanolucan-6, suppress insulin action, and you also have a reduction in protective adipokines, adiponectin would be the example there. And lastly, when you talk about this upper body fat phenotype, when you have increased deposition of fat in extra adipose tissue, such as the pancreas, the liver, the heart, other areas, it's known as ectopic fat. Ectopic is it shouldn't be there, but it starts to infiltrate organs. Fat in the liver directly affects insulin resistance sensitivity, whereas exposure of beta cells to triglycerides and free fatty acids decreases our ability to respond to an acute increase in glucose levels. So it's the, the lipotoxicity, the spread of fat throughout the body, as well as into the blood and pro-inflammatory adipokines that gives way to the insulin resistance. Now the good news is, which gets to the heart of an obesity-centric approach, is that there is a large body of knowledge that weight loss improves obesity-related metabolic dysfunction, and that's what's shown in these images here. It often begins with a reduction in liver triglycerides, which then increases liver sensitivity, will improve beta cell function as you, as you start releasing fat from the pancreas as well. We know that abdominal adipose tissue goes down, inflammatory markers, C-reactive protein would probably be the most clinically relevant inflammatory marker, but you also have improvement in muscle insulin sensitivity and adipose insulin sensitivity of three different organs. We know from other studies that insulin sensitivity and adipose sensitivity improve at a lower level of body weight, and it kind of then stop, but muscle insulin sensitivity continues to improve with greater weight loss, as well as using your muscle, and Mary Lou is a little bit later going to be talking about the action of not only diet, but physical activity and healthy lifestyle, which improve muscle sensitivity. Very nice article came out two years ago by Ildi Linvey, which Dr. Miller mentioned early, who is our lead on chapter eight in the 88 guidelines on obesity, in which he, she called for her and her coauthors called for a shift from a glucocentric to an adipocentric approach. And it's a nice way to summarize what I've been saying so far is to shift from a reactive treatment of hyperglycemia to sustained weight loss. We want to target adipose tissue as an underlying driver of type two diabetes. We now know from multiple studies, the studies in Europe and others, that a 15% weight loss just may result in diabetes remission, not just control, but remission, meaning off of all medication with the hemoglobin A1C below 6.5, but it's often seen in individuals with more recent development of diabetes, and the bottom right is now shifting to treatment. As an addition to a foundation of lifestyle management, consider pharmacotherapy and bariatric surgery as very effective treatments, depending upon the patient's presentation. So I'm showing you here is a treatment pyramid that we have used for decades now in the obesity world, which summarizes the treatments that we have. I like showing it as a pyramid or a triangle is because the foundation of treatment is at the bottom of this triangle. It's healthy eating pattern, being more physically active, all round up in behavioral modification. So that's foundation, whether you escalate or become more aggressive in your care, it's still a foundation of how one lives their life. But if one needs a more aggressive treatment, then you go up to either medications or surgery. And I put a red line around medications because that's particularly what I want to focus for you. So what I'm showing you here are all of the currently available anti-obesity medications approved by the FDA in the United States. They're not all available around the world, but this is what we have in the United States. What you see in the first column is the agents. The second column is mechanism of action, the effect, and then the approval date. I won't go through all the mechanisms action with you, but you can see the drugs here. A few things I want to point out, though, in the third column, which says effect, the target of treatment currently for all the medications approved, except oralistat, which blocks dietary fat absorption, all the other medications have the same action, and that's appetite regulation. So if you put someone on any of these medications, the way one loses weight is they're eating less food, less caloric intake below what they need, and they burn body fat, and that's how they lose weight. We have yet to arrive at other safe targets for obesity, so appetite regulation is how they work. The other thing I want to point out is the loraclitide, semaglutide, and terzapatide. You're all familiar with these drugs because prior to approval for diabetes, excuse me, prior to approval of obesity, the three of them have already been approved for diabetes because you all know GLP-1 receptor agonists have an effect on glucose-dependent insulin secretion, but at higher doses generally for all of them, they have an independent effect on appetite regulation. So those are the three drugs that are really changing the entire landscape when it comes to obesity care. What I'm showing you here is lining up all of these medications along with the key pivotal trials on the bottom, and I'm showing you mean percent body weight loss. Now, these drugs have not been studied back-to-back within one trial. I took the liberty of putting all of them on one slide, but what I'm showing you in the dark purple are individuals who are randomized to drug over approximately a year, and in the light purple are those randomized to placebo. So you can see very quickly as you go through all of these drugs from left to right is that the deep purple bar is taller than the light purple bar, which means the drugs work. But the other thing that you see, and I'm putting in a dashed line here at 10 percent weight loss, because that has been the golden ring for those of us involved in obesity care for decades. Why 10 percent? Patients can start to feel it, a provider feels more rewarded, and probably most importantly, you start seeing more significant clinical benefits when you have a 10 percent weight loss or greater when it comes to cardiovascular benefit, diabetes benefit, hyperlipidemia, hypertension, urinary incontinence, arthritis, and the list goes on to 200 problems. But what you're seeing here by putting in the dashed line is something very clear, is that when we have the approval and release of semaglutide 2.4 milligrams and then terzapatide, you see how all of a sudden they are surpassing that 10 percent weight loss routinely, whereas terzapatide is even greater than semaglutide. These newer drugs, there's a new term for you as well, these are called second generation NUSH-based therapeutics. NUSH stands for nutrient-stimulated hormone, that's what NUSH is, nutrient-stimulated hormone-based therapeutics. Most people call them GLP-1s, but you don't want to get trapped in that because there's dual and triagonists coming along the line. So GLP-1 is not the only treatment. I want to show you just data from two studies to make a point. This is from the STEP2 semaglutide trial. Individuals with overweight, obesity, and type 2 diabetes were randomized to semaglutide 1 milligram, so that'd be approved for diabetes. Semaglutide 2.4 milligrams approved for obesity and placebo. Towards the left, what you see is the mean reduction hemoglobin A1C. They started off at 8.1%, and what you see for placebo is they had a reduction in hemoglobin A1C of 0.4%. For the two doses of semaglutide, both of them were reduced approximately about the same, either 1.5 or 1.6 reduction. The higher dose of semaglutide did not have a profound increased reduction in hemoglobin A1C, but if you look to the right, which is the weight change, the higher dose of semaglutide does indeed cause a greater weight loss than the 1 milligram dose. So instead of 7% weight loss with semaglutide 1 milligram, it goes down to almost 10% weight loss with the 2.4. Those are for all patients. Now, what I put there also, another very important teaching point, is that if you take individuals living with obesity or diabetes who do not have diabetes, the average weight loss is 15%, but if you add diabetes in mix, they lose less weight, and that's something we have seen with every pharmacologic trial, including weight loss trials. Individuals with diabetes do not lose the same amount of body weight as individuals without diabetes, but still a significant weight loss, and they're very effective for diabetes. That's why they're also approved for diabetes under a different trade name. This is the only other study I'm gonna show you, and this comes from the SEMANT2 study with terzepatide. Same scenario. On the left is a reduction in hemoglobin A1C. On the right is the reduction in body weight. So they look very similar, except for just a few differences. Towards the left, you have a more profound reduction in hemoglobin A1C of about roughly 2% reduction versus the 1.5 with semaglutide, and you're looking at two different doses of terzepatide, 10 and 15. Towards the right, now you're looking at loss of body weight. Greater amount of loss of body weight, 13 to almost 15% weight loss, but the mean weight loss in individuals without diabetes from a different study was 21%. Again, reaffirming with two different drugs, same kind of study design, that individuals lose less weight if they have diabetes, but still the reduction in hemoglobin A1C is really quite profound. When we look at the latest guidelines, because of the data I showed you with weight loss and improvement in hemoglobin A1C, both semaglutide and terzepatide have been listed as very highly efficacious and listed as suggested use for individuals with type 2 diabetes where you also have independent weight loss goals, although other GLP-1 medications like galactitides and loraglutide are also recommended. One question just about approaching patient obesity, and I'm gonna shortly turn it over to Mary Lou, is when you see a patient with obesity and diabetes, obesity is a little bit different than diabetes. There's a whole area of stigmatization and stereotyping and discrimination and shame and frustration and being picked on and so forth throughout their whole life, not so much with diabetes. So you have to have a more sensitivity. You have to be more aware that even though we're suggesting treating both of them, obesity is a little bit different because of the social psychological impact. You always wanna be patient centered, but please be empathetic and unbiased when you see them. Also use people first language, and I've been doing it throughout my presentation. I've been purposely saying a person, and Dr. Mill would do it as well, a person or a patient with obesity or with diabetes instead of I have an obese diabetic patient. Very different if you heard the difference when I'm talking to the patient. Take home points. Diabetes and obesity commonly coexist. We give the name diabetes. The visceral and ectopic fat release inflammatory dipakines increases insulin resistance. The newer medications, somacotitin and trucepatide that are approved for diabetes and obesity are effective in improving both conditions. Now it is time for a quiz. Why is there a shift in type two diabetes management to an obesity centric approach? Adipose tissue has a direct effect on the release of incretin hormones. Adipose centric approach improves multiple complications beyond diabetes. Glucose focused treatments have a higher side effect rates. Adipose centric treatments are more cost effective. And the answer is the yellow one, nine. Adipose centric approach improves multiple complications. The fuller was adipose tissue has a direct effect on the release of incretin hormone. Incretin hormones are released from the gut. GLP-1 and GIP and amylin, they're from the gut. They're not from the adipose tissue. I am gonna go to the next one and there's the scoreboard and I'm gonna turn it over to Mary Lou. Thank you, Bob. So I've been in weight management and diabetes for about 40 years. And I think we found the Holy grail of weight management. And I echo what Dr. Kushner has said. There's a place for these medicines in diabetes management. That's not really the question. The question is, where does lifestyle fit in? And if it fits in at all. I mean, diet, exercise and behavioral therapy are the foundation of diabetes management. But given the adipocentric model, is there a new cornerstone in the foundation? So when ozempic and subsequently trazepatide started to be used in our practice and I work in an academic medical center, I was on board recognizing the adipocentric approach. But I began to see patients not show for nutrition appointments or assure their provider when it came time to set the appointment with a registered dietician. They said, been there and done that. And, or I've got this. I know what I'm doing with behavior. I don't really need to see her. So this begs the question, where does lifestyle fit in? So I wanna turn to landmark interventions that we know lifestyle works. Clearly we know that it works. We know from look ahead, DPP and real health. I'm gonna talk a little bit about those, but let me talk specifically about the National Weight Control Registry, because these are a specific set of behaviors that we can relate to our patients. And a little bit about the National Weight Control Registry. It's been around since 1994. It was started by Rena Wing and James Hill. And this is the largest prospective group of individuals that are successful weight maintainers. The average weight that they've been able to maintain is about 66 pounds and for about five years. And so in looking at or surveying these individuals, 98% say that they've changed what they're eating and 94% say that they've changed how they're moving. In addition to that, they've also found some other commonalities amongst weight maintainers. Here's what you see with weight maintainers. And I think we're gonna see some of these behaviors consistent across the board. 78% eat breakfast every day. 62% watch less than 10 hours of TV each day. 90% on average walk about one hour daily and about 75% weigh themselves at least once a week. We also know that there is a weight control registry outside the US. In fact, several weight control registries, although not as robust in the US as in the US, but they're finding very similar things. Some of the things that these places have shown is that they are, if I have my notes here, that these folks, there are four domains that seem to be consistent in these weight control registries again, it's a Portugal, Germany, Finland, and Greece. Four domains include things that are different, dietary choices. In other words, those individuals have typically eat breakfast and increase their vegetable and fiber intake. Secondly, they have regulation restrictions that's limiting the intake of certain foods. So they decrease sugary foods. There's a sense of also planning, planning to have healthy food available and limiting food that are trigger foods that come into the home. And then finally, energy compensation. So what we see is that weight maintainers, again, this is survey perspective data, weight maintainers do things differently than weight regainers. And I will talk just really briefly about the other landmark studies, which include the DPP look ahead and the real health study. And DPP has been shown, which is weight control management study looking at diabetes prevention. And they found that lifestyle outperformed metformin and outperformed metformin by a significant amount. We also found this same thing in the look ahead trial. When look ahead looked at, although it was looking particularly not only at weight loss, but cardiovascular benefit, this was one of the largest and longest weight control trials. And they looked at intensive lifestyle interventions and found over time that intensive lifestyle as opposed to placebo or control worked. In fact, with intensive lifestyle in the first year, the first two years with intensive lifestyle, there was an 8.2% weight loss. And in subsequent years, they were able to maintain that weight loss. With less intervention or less behavioral intervention, but nevertheless, we're able to maintain that weight loss at the four year mark and even at the weight year mark of about 4% weight loss. In the real health diabetes randomized clinical trial, less rigorous study than look ahead, but nevertheless, very real world analysis where they took the look ahead protocol and adapted it to community health centers and compare that to medical nutrition therapy and looked at intensive weight management and found very similar results. And so, and in fact, those individuals, I'll show that to you in just a minute, those individuals... Sorry, trying to get to the other slide. Thank you. Thank you. I appreciate that. So again, this is the result of a two-year lifestyle intervention for type 2 diabetes called the Reach Ahead for Lifestyle. And again, what I just wanna bring to your attention is that weight loss and what they did was explore intensive lifestyle therapy by way of telephone and in-person, which showed very similar results at year one and even at year, at 12 months. There was very little difference at 24 and 36 weeks, 36 months between the two groups, between MNT as well as lifestyle intervention. So we know that it works. And if we look at, and I'll show you in a minute, categorical weight losses in those, in the Look Ahead trial, we see that those categorical weight losses were about 30% in the remote and in the intensive lifestyle, and those that lost more than 5%, a little over 10. And as you see, those individuals that lost at least 10% was significantly lower. I'll show you in a minute, some of those other trials in comparison to what semilacotide and trazepatide show. So here, what I'm showing is categorical weight losses. And this is a way to understand weight losses beyond the mean weight loss. And so this is a way to look at weight losses for individuals. So you're looking at those individuals that were able to lose, percent of individuals able to lose 5, 10, 15, or 20%. Here, you see those two landmark studies that I had mentioned earlier, the DPP and the Look Ahead. And you're seeing that 20% were very few, individuals were able to lose that 20% body weight. If we compare that to the step trials in semaglutide in the Step 1 and Step 5 trial, you'll find that 32 and respectively 36% of individuals were able to lose at least 20% weight loss. And you see that even higher with trazepatide. So although these studies with the Step 1, Step 5 and the Surmount trial, these studies did have lifestyle intervention, but it was slightly watered down. So this was the result of lifestyle and drug for losing that weight loss. So, and what I want to, this is what Bob talked about when we talk about the obesity-centric model, we want to talk very differently to our patients with obesity and function on, and focus on shared decision-making. So in short, we know that lifestyle works or lifestyle interventions work, but here's the rub. They work, but maybe not to the extent that we'd like to see them work. We know that the first generation medicines along with lifestyle, as Bob showed earlier in his slide, things like Phentylamine and Topiramate probably give a little bit more than 10% weight loss. But what we're seeing with some of those nutrient-stimulated therapies or a second generation obesity drugs, we're seeing greater weight losses. 15, 20, and even up to 25% with those second generation medications. Again, I just want to talk a little bit about why we move from a glucose-centric to an adipocentric model, and talk about really what we're doing is shifting that framework from reactive treatment of hyperglycemia to looking at sustained weight loss as the primary treatment goal. And we're really looking at targeting the adipose tissue as the driver for the underlying disease process. And looking at, in order to get meaningful weight loss, we want to get weight losses above 15%, and consider pharmacotherapy and bariatric surgery one of the best ways to do that. So Bob showed this slide, and this is what most of us think about when we think about components of an effective obesity management program. We think about physical activity, behavior modification, and healthy eating with medications. But I'm kind of thinking them slightly different with this model, where it's not necessarily a hierarchical model, but we may move medications concurrent with some of those lifestyle treatments. So medications occur concurrently with behavior modification, with physical activity, and with healthy eating pattern. This is the new treatment paradigm for diabetes. So I read this quote from Dr. Wadden in a recent review when he was comparing or looking at what place do the anti-obesity medicines have, and what place does lifestyle modification have? And I think this quote was very useful, and I think it really represents what we're seeing even in our own practice. When used with the new AOMs of the anti-obesity medicines, the focus of lifestyle modification is likely to change from inducing weight loss to facilitating patient's adoption of dietary and activity patterns that promote optimal changes in body composition and overall health. What you see here is, and I wanna show this, this is a slide from the Obesity Society, and it's in revision now, and obviously being revised. But what I want you to see is, these are the contributors to obesity. And so in the paradigm that we're talking about, we're trying to go after all of these contributors that we can. And so on the left-hand side are those contributors inside the person, on the right-hand side are those contributors outside the person. Top third is those contributors that lead to increased intake, and the bottom third looked at those contributors that lead to reduced expenditure. Most of our lifestyle interventions are gonna hit the outside the person with lifestyle intervention and maybe with emotional coping inside the person, but also our lifestyle interventions are gonna hit decreasing sedentary time and hit physical activity. But what the obesity, second-generation obesity drugs are gonna do are target that obesity tissue. That's really gonna be the change agent. And the way that these medications work is through the appetite regulation. So what we see in this study is, when looking at individuals that, this was a parallel crossover design, looking at individuals that were on for 20 weeks semaglutide, and asked them questions around hunger, fullness, satiety, even looked at their eating consumption and their appetite suppression scores. And they found those individuals on semaglutide had lower hunger, had higher fullness level, had greater satiety, had fewer cravings for sweet foods, for savory foods, even had lower caloric composition with their ad libitum lunch, 35% lower. So clearly individuals that are using these drugs work by reducing intake through the appetite regulation mechanism. And this is how these new medications work for the gut brain access and communicate the GLP-1s and the GIPs communicate with the brain to signal the brain in the appetite centers to decrease hunger, to increase fullness and control cravings. So what would we do? I mean, we know that lifestyle is effective, but we know that there may be limitations. And we also know that the addition of the second generation anti-obesity medicines with some lifestyle mixed in probably has definite benefit or accelerated benefit. But as a dietician, what would be the things that I'd wanna bring into the mix when I'm talking with patients that are starting on anti-obesity medications? And so the things that I would probably do is still focus on nutrition. But if we're bringing anti-obesity medicines into the mix, I'm gonna focus on ensuring that the individual is getting adequate amounts of protein, at least 60 grams of protein. I also wanna look at the nutrient quality of the diet. So we're not just looking at reducing calories, but we're looking at improving the nutrient quality so that their nutrient quality has a benefit in their cardiometabolic health. That comes through hydration, it comes through increasing fruits and vegetables. We also wanna look at meal spacing for these individuals so that their meal spacing occurs more evenly throughout the day. The role also could be mitigating some of these side effects because we know nausea, constipation, vomiting can be a side effect that occurs. And so the dietician or the clinician can help the patient mitigate some of those side effects and then assess the need for self-monitoring and behavioral strategies. Also, we would help the individual to look at what would that lifestyle focus be with the anti-obesity medication? That lifestyle focus would be encouraging them to have at least 150 minutes a week of physical activity. Strength training really does need to be part of that two days a week to protect the loss of lean tissue. For some patients, we might need to consider referral to a clinical exercise physiologist. Decrease sedentary time. And clearly we know that sleep makes a big impact not only on diabetes management but also on weight and weight management. So talking to our patients about sleep hygiene and getting enough sleep. So those things become also the focus with anti-obesity medicines. So as a dietician or as a clinician, what we wanna do is get the right drug at the right time to the right patient. And so one of the ways that we would do that is through the shared decision-making through these second generation anti-obesity medicines. And we would do that. And I found these three bucket approaches through this review article by Tom Wadden. And he says, looking at lifestyle assessment, looking at the three buckets of lifestyle assessment, physical activity, and psychological assessment. So this is what you're doing as you're talking with your patient about starting an anti-obesity medication. So you're looking at their lifestyle, physical activity, and doing the psychological assessment. That's determining that, or that's going into that decision about when to start or if to start with an anti-obesity medicine. But also it goes into determining what would lifestyle look like during their course of treatment. If you're looking at that lifestyle assessment bucket, physical activity bucket, and psychosocial assessment bucket, how are you going to adjust those through treatment when you're dealing with patients? So just quickly, I just wanna give you a quick rundown of what that might look like for clinicians. So say you've got, that you've decided to introduce lifestyle as well as anti-obesity medicines into the mix. What would that first visit look like? And what would you talk about? You would talk about the lifestyle change has to be part of that discussion. That lifestyle change has to be part of that, part of with medication. That you'd also talk about long-term medication use because these medicines will have to be used long-term. Talking about obesity as a chronic disease, how these medicines work. Obviously, if we're working with patients with diabetes, if there's a potential for hypoglycemia, we can discuss dose administration, dose escalation, the medication timing side effects, and patient expectations. Eating slowly, limiting high fat foods, and limiting spicy foods. Now that is a boatload to talk about at that first visit. And so it may be through the course of one or two visits, but these are the things to talk about during that first visit as you're looking at starting these obesity medicines. And as you're asking patients to titrate or escalate dose. At the second visit, you might wanna check in, check in with side effects, how their eating strategies are doing, and a discussion of their weight history. I've heard Bob often talk about this, he uses a weight history graph, and I found this to be very useful in our own practice. And it gives story or it gives voice to the patient's weight loss experience. So you just have them track what their weight loss journey has been like. And in doing so, they're able to make connections between lifestyle and between things that maybe have occurred within their life or life events, and use that information in the future in determining what needs to happen with their weight maintenance. So that can be very helpful. Another idea might be at visit three, there may be dose escalation, discussion of physical activity, meal pattern, what their protein intake looks like, the side effects, discuss any changes in mood, or psychosocial functions, look at the sleep pattern. So obviously these are gonna be adjusted to the individual, but these are the things that you'd wanna cover. Visit four may also be some very similar things, the dose escalation, the discussion of physical activity, the meal pattern, the protein intake, if there's been any changes in mood, the psychosocial function, checking in with that, the sleep patterns, the blood glucose patterns, and also looking at setting behavioral goals, long-term for physical activity, for sleep, nutritional quality, and their meal patterns. And then finally, looking at visit five and even beyond. So we're looking at seeing these patients, maybe not as frequently, but still seeing them, to talk about what's going on with behavior, talk about what's going on with dose adjustment, talk about what's going on with physical activity and sleep. And then ideally, obviously, discussing some of those long-term behavioral issues. How do you build new food relationships? How do you create healthy habits? Navigating inter and interpersonal influence, and internalized stressors, and self-regulations. Those are all components that are important parts of behavioral management of overweight and obesity. So in the absence of evidence-based clinical recommendations, these are the things that I would say as a dietician, but also as a clinician in delivering person-centered care, as Bob spoke about eloquently, using person-centered language and shared decision-making. That diabetes is a chronic disease that may require treatment changes over time, that utilize the entire team to support medication management and long-term lifestyle change, and recognize societal, structural, and systemic drivers of care, and seek to change them in your sphere of influence and beyond. So let's come to a quiz. And the quiz question is, which of these behaviors was not observed in a majority of members studied in the National Weight Control Registry? They consume breakfast every day, weighed themselves at least weekly, exercised on average about an hour daily, or use digital apps for tracking behaviors. Which one was not observed in those individuals? So go ahead and cast your vote. And that is correct. All of those were behaviors that were used in Weight Control Registry. So other than using digital apps, there were various ways that they kept up with that, but they consumed breakfast, they weighed themselves on a regular basis, and interestingly, exercised an hour a day, at least six, on average, six days a week. So let me turn this over to, I guess, five key tips, or five takeaway messages. And I guess I'll go through. Bob, I'll let you take over, because you talked about the first, at least the first three. Do you want to give the five key tips and takeaways? Sure. Visceral and ectopic fat releases inflammatory adipokines that increase insulin resistance. I covered that with you. The newer medications, somagotide, trisepatide, approved for diabetes and obesity, are effective in improving both conditions. And they were originally approved for diabetes, and then at higher doses subsequently approved for obesity. Second generation AOM should be considered as part of an adipocentric model in diabetes management. And even with AOMs, lifestyle change and education are important for long-term sustainability. The frequency and intensity should be individualized. And finally, empathic, judgment-free, patient-centered care focusing on health rather than weight should always be used no matter what treatment option is proposed. And so with that, I'm going to turn it over to Dr. Miller. Oh, you guys, that was amazing. You know, every time I get the opportunity to get together, to see that top-down approach to intervention with the obesity and diabetes, it's great. And I'd like to thank you so much for that content. If you already haven't put your questions in, I've seen that we have a few coming in. We're going to get right to you with those questions, and I'm going to dole those out in the last few remaining minutes that we have. I'm going to start with one that I thought was quite good, and that is kind of to briefly comment, Mary Lou, if you can, about the relationship of diabesity as we age, that there was some questions regarding that. As you have an individual getting older, is there any more, how shall I say, higher result of that? Or what are some of the factors that come into play with aging and diabetes? Well, I think as this relates to second-generation anti-obesity medicines, you're looking at probably faster weight loss. So you have to be very careful about losing lean tissue. So, and you might even increase the protein content, maybe 1.5 grams per kilogram body weight, especially for older individuals. I don't know, Bob, do you do that in your practice? Well, let me answer the question just a little bit different way, is that the relationship I showed you, which was BMI and diabetes, falls apart with aging, because now you're entering sarcopenia. So even though someone who's elderly may not have the same BMI, in fact, BMI drops as you age, but body fat may not drop. It's a lean mass that drops down. So the relationship between excess adiposity and diabetes continues to exist, maybe harder to pick up though in practice because of the changing body composition. No, those are great. Hey, we have a couple of questions that are real similar, and so I'm gonna lump them together for both of you to respond. There's this discussion about what we call remission, remission of diabetes, remission in bariatric surgery. One question was with, you know, we see this remission of diabetes shortly after bariatric surgery, yet we haven't seen any weight loss. And then that second follow-up question, I'd like to get your thoughts on it, is what is that kind of A1C that we all kind of think is possibly a remissive state or like I like to term as maybe a slowing down of the progressive state? Yeah, I can go first. So we do see that in bariatric surgery. It happens very quickly. Reduction in caloric intake, a increase in the incretin hormone response, bile acids, and so forth. But what we now know is early remission in diabetes, and you're more likely to achieve a remission if you've had a shorter duration of diabetes and you're not on insulin when you go into surgery, which means you have healthier beta cell mass. But we know now if you follow individuals up long enough to have bariatric surgery, they recur. There's a recurrence, not only of body weight, but also of diabetes. You have to follow people up long-term. When it comes to diet alone, I'm pulling mostly from data from the DIRECT study, which was done in Europe, in which individuals could not have diabetes more than, I think, six years, were not on insulin. The goal is to lose 15% body weight, and about 84% of those who lost that weight went into remission. And the definition they used is what a lot of people accept now, which means the hemoglobin A1C under 6.5% off all of medications at least for three to four months. So that's a definition they used in the DIRECT study. Yeah, and looking at that diabetes remission, again, one thing I think that is clear is that if you're off of treatment, that's considered remission. But then one would also suggest, can you slow the progression or remission in terms of with pharmacology too? So don't neglect that. Even if you were on pharmacology and you got in a remissive state, that still would be an ideal goal. We're not trying to necessarily get off all our meds. Right. So I have another question here to you, Mary Lou. It talks about, it's maybe that one of the possibilities that we tend to lose less weight for those clients, that those individuals, the persons who have diabetes as well as obesity-related conditions, is it possible that maybe some of that is because they're on other agents that tend to cause weight gainers, such as sulfonylureas and insulin? Well, yes. And I think what has been demonstrated in these studies is that the weight loss, when you look at people with diabetes and those without comorbid conditions, so those individuals with just overweight and obesity, you're gonna see a better response without diabetes. And part of it is gonna be the additional, maybe weight addition of the medications. But this, Bob, you talked about that. Is it related to the physiology? What's the reason behind the, I mean, good weight loss, but not as robust as we might see somebody without diabetes? The last Dr. Miller comes to the rescue, it's a big black box. I've talked to a lot of people, and it could be the change from catabolic to anabolic state. You're not losing sugar through the urine if you're out of control. Weight gaining and glucose-lowering medications. But it's kind of a big black box. I don't really know, I'm not sure anyone really knows why individuals with diabetes fully do not lose as much weight. Eden, do you have anything? Yeah, I would agree that we have our own thoughts. And I think my thought is I always think of diabetes as starvation in the land of plenty. 50% of the glycemic load in person with diabetes is gluconeogenesis. And so when you have an individual who maybe doesn't express diabetes, they're not in that constantly producing food state. And so glucagon being a paramount hormone over insulin, yes, our increting classes do inhibit glucagon. But remember, even though you're losing weight, you still have that underlying broken physiology, that dysfunctional metabolic state. And so I would think that it's probably related to the fact that if we looked at it as a singularity of those without diabetes, those with diabetes and concomitant obesity, we see more weight loss in the non-diabetic related individuals because the individuals, they have two disease states that are competing with each other. Even though, yeah, we always want to see the same type of things, but we do tend to see different. But I don't think we have an exact realm, but I do think we know that it's because of that dysfunctional glycemia. So I think I have one more time for a question. I want you guys to comment on this because I see it quite a bit. And that is what about, what kind of lean body mass versus fat body mass are we losing and are we worried about that with some of these agents? Yeah, I'll jump in there first. First thing, any weight loss intervention, you have a loss of lean mass and body fat mass. So it doesn't matter what it is, whether it's diet, pharmacotherapy, bariatric surgery, low carb diet, very low calorie diet, you're going to lose both. And that is a concern we need to watch our patients carefully, particularly older individuals for development of sarcopenia. With the second generation NUSH therapy, so I like saying that a lot, with profound weight loss for many patients, 20 to 25% body weight. You take someone who's 60 years old losing 25% body weight, I am going to be very, very concerned about losing too much lean body mass. That is why I slow them down, watch them carefully, emphasize physical activity, resistance training, good protein intake in the diet. We need more investigations about how much weight loss is occurring. We have some data, but it's very small. And more importantly, how to preserve our muscle mass. So stay tuned for the next generation of studies that will be coming out. Yeah, great answer. I mean, absolutely. That's wonderful. So thank you so much for joining us. We do have some post-webinar discussion here. Make sure that you complete the post-test and claim your CE credit. That will be sent out via email. In addition, check for the webinar recording for the ADA's Institute of Learning Library. And we so thank you for your participation. And we just want you to go out there and take all of this knowledge and put it into practice. We want to thank both of our panelists today for the amazing content that they gave to us. And with that, make sure you stay tuned for other webinars in the future for the ADA. And we conclude this session and have a great afternoon. Thank you. Awesome.

webinar

obesity

type 2 diabetes

weight management

adipocentric approach

pharmacotherapy

lifestyle interventions

individualized treatment plans

patient-centered care

healthcare professionals