Weight Loss Can't Cure Obesity, So What Can?

Carolyn Jasik, MD:

Thank you and welcome to today's Employer Benefits News webinar and what we lovingly call at Omada our Grand Rounds series on clinical topics that are relevant in employee health as it relates to what Omada focuses on. So today, I couldn't be more excited to welcome all of you because we have an exciting topic with amazing speakers. The topic today is Weight Loss Can't Cure Obesity, So What Can? Now obviously, this topic comes at an amazing time in history. We have some really fascinating and interesting new treatment options within obesity, but it's also bringing up an important question. When the weight does come off for a patient, does that mean that their condition or their disease is cured? And so we're going to have a great discussion today about that.

I wanted to remind everybody that we do have questions at the end. So as you hear the speakers and if something comes across your mind, please do put those questions in the interface and we will answer them at the end. So by way of a bit of introductions, I'm Carolyn Jasick. I'm Chief Medical Officer at Omada Health. I couldn't be more excited to be here with two amazing women who are going to speak with us today. So first, we have Dr. Fatima Cody Stanford. Dr. Stanford is an Associate Professor of Medicine in Pediatrics at Massachusetts General Hospital and Harvard Medical School. She's a pioneering obesity medicine physician with over 200 peer-reviewed publications.

She's recognized for her leadership and contributions to public health and has received numerous awards, including the AMA Inspirational Physician Award and the MMS Award for Women's Health. Her extensive training includes an obesity, medicine and nutrition fellowship at Mass General and serving as a health communications fellow at the CDC. Recently, she was named to the 2025 Dietary Guidelines Advisory Committee by the US Department of Health and Human Services and Agriculture. And on a personal note, it's my feeling that if a good conversation about obesity is happening in the media or in academic circles, you can usually find Dr. Fatima Cody Stanford. So really, really excited to have her here.

Also excited to share with all of you my amazing colleague, Bola Bukoye, who is a public health expert and certified quality improvement professional who works at Omada as our lead on Quality and Health Equity. She's experienced in leading health equity projects around the world. She received her BS in biological sciences at the Mississippi University for Women and earned her MSPH degree in global health at the Harvard School of Public Health with a major in epidemiology and infectious disease. I'll find it in myself to forgive both of you for being affiliated with Harvard. I've never had that pleasure, but hear about it frequently from my brother who works there. So Bola has spent her career driving innovation and health system transformation at various institutions like Beth Israel Deaconess Medical Center, Boston Children's Hospital and Adriadne Labs. She's a passionate advocate for creating healthcare systems that deliver equitable outcomes for all communities.

Okay, and so now we're going to go into a little bit of an introduction today on today's topics. So we're going to start with a look back at obesity over time. Then we're going to talk about obesity as a chronic disease, external risk factors and have a panel of discussion. At various times, our speakers will come in and out with their thoughts and their expertise. So a little bit of a look back on obesity over time. Now, I don't need to tell everybody here that obesity has been increasing over time or that currently 42% of US adults are living with obesity. What I do want to highlight is that for pediatricians like myself and Dr. Cody Stanford and experts like Bola, we have been working in this field for, in my case, a couple of decades and we have never seen a new treatment like GLP. The last major treatment that came into play was bariatric surgery.

And what's interesting about GLP as an innovation, there's many things, but to my mind, they have brought to the forefront for the first time a very smart and appropriate conversation about obesity as a disease versus obesity as a choice and a personal responsibility. It's also important for me to emphasize and we'll be discussing this even more later, the major disparities in obesity by sex and race and Hispanic origin. And this is important to emphasize, because as we talk about important treatments like GLP and we talk about this point of view on personal responsibility, it brings up this question of, "Who has access to treatments and what do we think about different communities and their access and what are the biases and impressions that people have in the community about communities? And are we bringing everyone forward when we're bringing in these important new treatments?"

So what is a disease? A disease is an abnormal condition that affects the structure or function of part or all of the body and is usually associated with specific signs and symptoms. Why do I need to even define that for this group? Well, it's interesting because according to many, many people in the medical field, obesity isn't a disease. Now, Dr. Cody Stanford can confirm this. I was in practice for many years before I joined Omada, I couldn't even code for obesity as a clinical diagnosis and get reimbursed for insurance because it wasn't considered a disease, again going back to this bias and impression that it's a matter of personal responsibility.

So is it a disease or a personal responsibility? In 2013, the AMA recognized obesity as a disease state with multiple pathophysiological aspects requiring a range of interventions to advance obesity treatment and prevention. This was done as a call-out, specifically attempt to drive reimbursement for important evidence-based treatments. In 2016, we were seeing news coverage that was covering obesity with language like Americans blame obesity on willpower despite evidence that it's genetic. By 2023, we are seeing a change in the public discourse with promise and unrealized potential 10 years of the American Medical Association classifying obesity as a disease. Have we made progress during that time? Are we seeing an improvement in how people think about this disease?

The answer was really no. The AMA came out with this statement. It didn't change reimbursement, it didn't change broad cultural opinions about obesity as a disease and so many people who worked in the obesity community were still hacking our way through reimbursement and through care. Now enters GLPs. So in 2021, obviously GLPs have been around for a while with relation to diabetes care, but really starting in 2021, the public started to talk about GLP as a covered medication for obesity and this was driven by the manufacturers who found a new indication for diabetes medication in the area of obesity. And what was interesting about this is, as this medication got approved by the FDA for use in obesity and as an indication, it started to shift the public consciousness and the discourse, and frankly I would say, within the medical community to talk about obesity more as a disease because now we have a medication that has an FDA indication to cover it.

And this brings up a topic that we're going to talk about today. So if, and I believe it is, obesity is a disease and it has physiologic underpinnings and it has important treatments that we should indicate, what are the considerations that opens up and what is the knowledge that we need to understand obesity as a disease? So to summarize, obesity is a chronic disease that requires long-term treatment. So what we're going to learn today is that there are important physiological drivers of obesity that are fixed for individuals. They can improve somewhat and be ameliorated by weight loss, but these predispositions, whether they are socioeconomic or part of a social driver of health or whether they're physiologic, they do not stop with the treatment of obesity, and so therefore, individuals, regardless of their current weight status, should be and need to be eligible for support and treatment for as long as is needed and that treatment should be reimbursed.

So now with that said, hopefully, you've had enough of me and we're going to go into our first speaker, Dr. Stanford. Thank you so much for joining us.

 

Fatima Cody Stanford, MD, MPH, MPA:

And it's a delight to be here to talk about obesity as a chronic disease. I think that was a wonderful primer and introduction to this really complex chronic multifactorial disease that is obesity. And I really want to just jump right into this conversation of looking at obesity as a chronic disease. And that is why I'm going to talk about why it is important to understand obesity, its interest and the need for treatment now. And so I want to talk about what obesity is and what it isn't. And so this is really going to be important for us to look at as we think about this as a chronic disease and a chronic multifactorial disease process.

So let's look at what we're talking about. And I want to define a myth for you. A calorie is a calorie is a calorie. And so we've thought about it this way that just a calorie is a calorie is a calorie and this is indeed a myth. And why am I saying that? And I'm going to set you up for this by looking at our next slide and that is, "All calories are not created equal." In my introduction, we talked about me being a member of the US Dietary Guidelines Committee and so let's look at this particular slide. So on the left slide, we're looking at a slice of pepperoni pizza, right? So many of you might like pepperoni. It's actually not something I actually enjoy at all. And you might think I'm a little strange and that is okay. I'm okay with that, but let's look at the quality of what's being presented here. This is a slice of pepperoni pizza on the order of approximately 350 kcals for this particular slice of pizza.

And now on the right side of the screen, we have a dinner plate, quinoas, chickpeas, carrots, tabbouleh probably closer to about 700 kcals. Now I do ask my patients, because I do pull up this slide for them, "Which one should they eat?" And most will adequately point out the right side and say that this is probably what they should eat. And I ask them, "Why should they choose this when this is indeed more calories?" And they might adequately or correctly point out that, "Well, it's probably healthier for me. There's something about this being better and it's about the processing of one's food." We want our food to look like it looks in the environment. The less processing the better for us.

But just because it looks like this doesn't mean we will defend a lean body type or less adiposity. What do I mean by adipose? Adipose is this tissue or organ we call fat. And we presume that just because we're eating like this that we will defend a lean setpoint. All calories are not created equal and so we have to be aware of this. And so we have been marching by this mantra that it's all about calories in and calories out. All we have to do is pay attention to our food and beverage intake and our bodily functions and physical activity. So we need to just eat less and exercise more, right? This is what we tell people to do all about sweat equity, "A lot of people just need to just do this and be just like me. I got up, I did my workout, I ate this. It's all about me and what I did and because I was born with this lean phenotype and this is what I do to defend this," but we weren't all given the same milieu.

And so this idea, this mantra that we have been supporting is indeed what has gotten us into this state of where we are. We are not all created equal. We do not all have the same milieu. We do not all have the same body chemistry that supports a lean phenotype. And this era that we are in that was pointed to in our introduction helps us to understand that the brain and the way it communicates with our gut, the idea the rise of GLP-1 or glucagon-like peptide-1 receptor agonist has pointed to this physiology that differs in all of us. And what is really important for us to know is that when we're looking at GLP-1s, we must be aware of the fact that GLP-1s are already housed within our bodies. Just some of us have more of it than others. GLP-1s are housed in all of our bodies, but for those of us that have more of it inherently within us, we don't need to administer it to ourselves because we have that inherently within us to govern our brain function and it tells us that we are going to defend a lean set point at baseline.

So this myth of us controlling how much we eat is indeed a myth. What we do know is that we have our brain regulating how much we eat, particularly a key portion of the brain called the hypothalamus that is getting signals from our diet quality. Now our diet quality, we want it to be lean proteins, whole grains, fruits and vegetables. But we already talked about that just because we eat like that doesn't mean we will defend a lean phenotype. There are different mechanisms that are going on within our body and our genetics environment, etcetera, that are controlling how our body defends our body's weight.

Now, physical activity is also an important component and we want our bodies to be active. I got up very early before flying in to give this talk to you today, but I want you to think about your favorite sport. Maybe it's basketball. Think about your favorite athlete in that sport. Maybe it's LeBron James, maybe it's Steph Curry, whoever it might be. And I want you to think about them playing that sport over and over in basketball and I want you to ask yourself a very important question. And that important question is, do you see them losing weight between game to game? Basketball is an aggressive sport. They go up and down the court, up and down the court, play, so many games you can't keep up, but are they losing weight between games or are they maintaining their weight?

And so when we look at weight and weight regulation, what we do know about exercise is that it helps us to maintain our weight, but doesn't typically contribute to significant weight loss. Now, sleep quality and duration plays a large role in how the body regulates weight and this is something that's often overlooked in this equation of weight and weight regulation. So this is something that I have to ask patients, whether they're my pediatric or adult patients. And this is a major and critical thing that we have to look at from childhood all the way into adulthood. I like to say I take care of patients from twinkle to wrinkle. My patients do range in age from two to 90+ and this is a really important consideration.

Now, medications that we do prescribe for other conditions may dysregulate how the brain sees weight. What are these types of medications? Medications like lithium, Depakote, Tegretol, Celexa, Cymbalta, Effexor, Paxil, Prozac, Ambien, trazodone, Lunesta, gabapentin, Glyburide, glipizide, glimepiride, metoprolol, atenolol, propranolol, long-term insulin, long-term prednisone. Just to say the ones I wanted to say very quickly before I gave out a breath right there. It just says that we have medications that are weight-promoting medications that dysregulate the pathways that regulate weight within the body.

These medications can contribute up to 200+ pounds of weight gain and we don't recognize that these are medications that do cause weight dysregulation. Now it looks like I'd made a mistake on this slide and I'm presenting another sleeping person and indeed this person is sleeping. But what you might not notice here is that this person is sleeping during the daytime. This is circadian rhythm disruption. And when we have circadian rhythm disruption, we are disrupting the normal patterns of the body with when we're supposed to be asleep.

So as humans, we are supposed to sleep on a cycle or we're asleep during the nighttime and we're awake during the daytime, but some of us have jobs that aren't conducive to that. Maybe we're nightshift workers. Maybe we're doctors that work during the nighttime. Maybe we're food service workers that work during the night shift. Whatever it might be, when we disrupt that natural rhythm of things, our bodies go into a storage mechanism or mode and defends the storage of adipose or fat, that organ that I keep alluding to, and that causes us to retain more weight than it should. And then finally, thermogenesis, which is just how much the body stores or burns at baseline. A lot of this is genetically determined. So you can see that these are different components that regulate weight within our body.

So there is a key myth here and you can see that this myth is that obesity is a choice, that those that have obesity have just chosen to be that way. Maybe because we have these biases that those that happen to carry extra weight are just that because they didn't do something well enough. Maybe they didn't eat little enough, maybe they didn't exercise enough because we have chosen to assume that they are just there because they didn't do something well enough. And why do we make these assumptions? Because unlike other disease processes, obesity is a disease that you wear.

Other disease processes are typically internal, right? It's even in the medicine that I practice, it's internal medicine. Obesity is external medicine, right? We actually see this disease process and we make judgments associated with that. So I want to change it into the reality that obesity is a disease, a multifactorial disease and there are actually over a hundred plus contributors to obesity both inside and outside of a person. If you don't actually believe me, I'm actually going to show that to you on this next slide. And so this slide is one of the busiest slides you'll probably ever see in life and this is intentionally busy because I want to show you these from The Obesity Society and this slide is circa 2015. But I wanted you to see that on the left side of the slide are factors that are inside of a person that contribute to weight gain.

Now on the right side of the screen are factors that are outside of an individual that contribute to weight gain. Now in this top row, these things increase one's intake. They increase how much someone weighs, right? And these things decrease how much someone's able to burn, okay? And in the middle here, these things affect how much you take in or how much you burn where there's this little word that you might not be able to see on your screen or maybe you do if you have a really large screen, it says, "You're unknown." We are still figuring out this complex thing that's called the human body. But what you can see is that there's a lot going on here.

And this next slide I'm going to show you that there are several big categories that were represented there. There are biological or medical reasons why someone may struggle with weight, food and beverage, behavior and environment, maternal and developmental, social, psychological, economic or environmental pressures on physical activity that may affect someone's weight. So I'm not going to go over all of those things or we'd be here until tomorrow, but let's go over a few key elements that may affect someone's weight struggles, okay? And so we're going to talk about a few factors that are inside of a person. What are some things that may contribute to one's intake? What about hyperreactivity to environmental food cues? What in the heck does that mean?

There's someone that may walk past a food place like maybe a pizza store, since we were talking about pizza earlier today, they noticed that pizza shop a mile away. They're like, "Oh my gosh, I smell the pizza." I might not even notice the pizza place and I've walked past it for five weeks. I pass by it on the way to work. Don't even notice it's there. That hyperreactivity will obviously increase one's likelihood in taking that food. Delayed satiety, it takes a long time to feel full. We talk about GLP-1 agonists. We know that these things promote satiety, for example. Remember we have GLP-1, so all of us have it in our body, some of us that have a lot of it in our body, we get full quicker than those that don't have as much housed within our body. Disordered eating. If we have some disordered eating, that's going to increase our intake.

What about things that decrease how much we're able to burn? Did you know that the gut microbiota, which means the bacteria in the gut differs in those that are lean versus those that have obesity? So much so that at Mass General we're doing studies, taking the gut microbiota out of those that are lean, placing it into those that have obesity and seeing weight shifts with no other changes. The gut microbiota does matter. Thermogenesis, we talked about this, "How much do you burn at rest and with activity?" Just me here sitting there, you just looking at me, you might be burning more. Those things, those differences can have significant effects when weight and weight impacts. If you are not able-bodied, there's some disability you have, you can imagine, you burn less.

What are things that affect intake and expenditure, increased intake and decreased expenditure, genetic and epigenetics? We cannot disregard that genetics and epigenetics play a large role in weight and weight dysregulation. Age-related changes, hugely germane to women's lives. Three major times in women's lives where we see major weight shifts. The onset of menarche. What is that fancy word I just used? When women get their menstrual cycles as adolescents. We see major weight shifts often for individuals there. Pregnancy and also desired, and I say that facetiously, menopause. There are major weight shifts and actually the number one person that will seek care for weight management, not only here in the US but around the world, is usually a peri- or postmenopausal woman. That's where we see a shift in weight going from a gynoid distribution of weight, which is where women will carry weight in their hip, buttock and thigh region to an android.

And for those of you who chose to buy android phones, I feel sorry for you, but android means male-like or central distribution of fat and that is an android distribution of that which happens in the menopausal transition. Mood disturbances, which means depression, anxiety. These things increase intake and decrease expenditure. Things that are outside of the person that lead to weight shifts. These things are environmental and chemical toxins, pervasive food advertising or large portion sizes. Things that decrease in expenditure are things like the built environment. Is your environment conducive to movement or sedentary time? Maybe some of you are on your Pelotons in the middle of this and so maybe you're not actually just sitting there looking at me. That would be a little strange if I did that during the middle of the presentation.

Labor-saving devices, your dishwashers, washing machines, things of that sort, things that increase intake and decrease expenditure. Believe it or not, weight bias and stigma actually leads to weight gain, meaning, do you actually speak negatively to those that carry excess weight? That leads to actual weight gain over time. Weight cycling, what does that mean? You go on this diet, come off of it, you lose weight, you gain more than you started with. You go on the next diet, you lose weight, you weight gain. That's weight cycling. And then if you have parents that have obesity and that maternal obesity does increase intake and decrease expenditure.

So we've talked about obesity being a disease and that's really important. We do know that obesity is a multifactorial disorder where genetics, environment development and behavior all play a role, and if you want to see the complexity of it, I want to show you this slide. It's not as simple as calories in, calories out. What I want you to see here if you're looking at this is that there is energy demands and drive to eat and we have appetite-stimulating hormones. The key hormone that's stimulating our drive and desire to eat are things like ghrelin, but we also have things that are inhibiting us from eating such as leptin and other adipokines.

And look here, remember I told you, we have hormones like CCK, which is cholecystokinin, peptide YY, and in all of our bodies, GLP-1s that are inhibiting our desire to eat. Some of us have more of these things. Those of us that have more of us, we have leaner bodies, right? So that's important for us to know. The regulation of food intake happening in this one little area of the brain, the hypothalamus, the key area of the body where things are happening, getting signals from our fat tissue, our small intestine, our large intestine, our pancreas and our stomach, sending signals to our brain to tell us not only how much to eat but also how much to store.

And I want you guys to just see this. I'm not going to spend a lot of time here, but there are key parts of our body where these things are happening and they have relevant effect on feeding the key hormone, I told you, that's really telling us to eat more, that's orexigenic in our brain, stimulating our appetite. It's in our stomach, but it's also in our brain. And then we have these other hormones that are anorexigenic. So orexigenic, stimulating our desire to eat. Anorexigenic promoting satiety. What are those hormones? Insulin, leptin, CCK, peptide YY and then also things like GLP-1.

So then I want to show you guys something very, very important as we look at this. I'm going to show you guys leptin. I want you to remember this before we go to the next slide. Leptin is a key hormone that's produced in the short term in the stomach and in the long term in the fat cells. Its relevant effect on feeding is that it is anorexigenic, which means it promotes satiety. I want to show you this because this is really important for you to understand why obesity is a disease. When leptin signals down this pathway of the brain, it stimulates a neuron called a POMC neuron in the brain.

You don't have to remember that, I do, but what I want you to remember is that if you travel down this pathway of the brain, you receive an anorexigenic signal. When you hear anorexigenic, it decreases your food intake. So people that travel down this pathway produce something called BDNF. And when you have high levels of BDNF, you have a lean expression of body type, right? These are lean people. But if you don't signal so well down that pathway, you signal down another pathway where a different neuron fires in the brain called the AGRP neuron. And if you signal down this pathway, you receive an orexigenic signal which increases food intake. And when you do that, you express adiposity, which means you express fat, meaning storage of adipose. This is where my patients typically signal. So this is not something that you can choose. This is not a choice. This is an actual disease process. And so this is very, very important.

Now I want to show you something about the historical landscape before I conclude my part and hand it over to my dear colleague. And I want to show you that we did not just begin developing medications to treat this disease yesterday. This started over a hundred years ago. And you guys are going to be shocked, but back in 1933, the FDA approved this first medication to treat obesity. In case you were unsure of what year we were in, about close to a hundred years ago, we started to do this. DNP was approved for the treatment of obesity back in 1933, so not quite a hundred years ago, more like 90 years ago.

Then I want you to see that that was withdrawn because it caused issues like hypothermia, tachycardia that means overheating, heartbeat, and death. That was a problem. We don't want people to die, but I want you guys to see something else that got approved. Methamphetamine. In case you don't know that fancy word, it means meth got approved for the treatment of obesity in 1947 here in the United States of America. Then moving ahead, we can see phenmetrazine got approved. Then we had a lot of medications, some of which are still available in 1959, phendimetrazine, diethylpropion, that was approved. Phentermine, which we still use.

Then rainbow pills because this is the '60s, "Why not? Let's go and approve those." Then rainbow pills were withdrawn in the 1960s. Then we approved fenfluramine. Then meth finally was withdrawn in 1979. You guys, look at how long meth was approved for the treatment of obesity. Let's move over here. Dexfenfluramine was approved, then sibutramine, then Orlistat which is still available over-the-counter for the treatment of obesity. And then we move over into 2012, so we can start to see lorcaserin, phentermine topiramate. We see our first GLP-1 approved in 2014, liraglutide, that's that once-daily injection. Bupropion-naltrexone. We don't see semaglutide approved for the treatment of obesity until 2021.

So we've had some rocky things, a lot of things withdrawn from the market and just wanted to show you that history. But I want to leave you with this. I want you to recognize that obesity is a disease. I want you to know that obesity is no one's fault and I also want you to know that a doctor can offer help in treatment. And I want to hand it over to my dear colleague, so that she can take it over. So I'm going to hand it over to Bola.

 

Carolyn Jasik, MD:

Great. So just briefly, I'll just say thank you so much for those remarks before we get to Bola and just highlight a couple things that I heard that I thought were amazing. First of all, obesity is not a choice, it's a disease. I think the more that we think about that, the more that we can continue to divorce ourselves from this feeling that it's a personal responsibility and stop the blame that has been so rampant. And then the second is I want to leave people with another reflection I took from your remarks, which is that the factors that predispose us to obesity are fixed and these factors are fixed in an individual regardless of what their current weight status is. And so the risk for regain persists even after a person has achieved weight loss, either through one of the medications that you went through or some other mechanism. So thank you. And now-

 

Fatima Cody Stanford, MD, MPH, MPA:

Absolutely.

 

Carolyn Jasik, MD:

Great. And so now we will hand it over to Bola who's going to go over another component of fixed risk for obesity, which is the social drivers and the environmental aspects of what predisposes folks to obesity. So on to Bola.

 

Bola Bukoye, MPH:

Thank you so much. So now we will talk a little bit about the external factors. We heard a lot about the physiology and let's discuss more to understand what the contributors are of social drivers of health to obesity. So first, I'd like to really help us make the connection between social drivers of health and health equity. We learned a little bit earlier that there are existing disparities with respect to obesity and these are due to race, ethnicity. It could be language or even socioeconomic status. And the reality is that a lot of these disparities are not fully explained by health behaviors alone, which leads us to really consider the impact of social drivers in helping to tackle these disparities.

I don't want to assume that everyone understands what I mean when I talk about health equity. So I want to share with you a definition that we've adopted here at Omada and it is one by the CDC. It defines health equity as the state in which everyone has a fair and just opportunity to attain their best health outcomes. Now, there are two terms that are often conflated where equity is concerned and that's equality and equity and I'm hoping that I can help you better understand what the differences are because I think it's really critical in this conversation.

Equality, as depicted by the picture on the left, implies sameness. And you can see that with the height of this platform that each individual is standing on, regardless of the unique circumstances that each of this individual is facing, the solution that is preferred to them is exactly the same. Equity on the other hand is different in the sense that it takes into consideration the unique needs, the unique barriers that each of these individuals is facing and ensures that the solution that is preferred to them addresses those needs. So equity takes action and the approach is a one-size-fit-one rather than a one-size-fit-all approach. And I think that's really critical as we continue this conversation to better understand the disparities that exist in obesity management.

So where there is equity, there is inequity. And in particular, I want to highlight structural inequities. And this is a term that describes the systematic disadvantage that one social group has compared to others. These are rooted in years of social practices, laws or regulations, government policies and politics. If I were to poll this audience to ask you, of the communities that you see, of the two communities on the screen, which one you might choose to live in? I can assure you that a good amount of us will select the more vibrant community on the left side with green spaces, potential, easier access to healthy food options compared to the community that you see on the right side, which is more depleted. You don't see the access to green spaces.

And a lot of this is real for patients where obesity is concerned and you can imagine the ways in which it impacts their access to physical activity, which is an important factor where obesity is concerned as well as nutrition. So access to healthy food options will be limited for that community versus the other community. So you can begin to see the ways in which we can see different health outcomes for people depending on the communities that they live in. So with that, I really want to emphasize the impact of social drivers of health. And this term has become so much more ubiquitous in the last several years because we are building our understanding of really how much they influence health outcomes.

Now simply put, social drivers are the nonmedical factors that impact health outcomes. And a datapoint that I think is so critical to highlight here is that they represent up to 80% of the modifiable factors that impact health outcomes. I'll say that again, 80%. That number is significant. So if we want to be able to really make a change and begin to close these disparities as it relates to obesity care, it is imperative that we understand that addressing social drivers of health is a viable approach to be able to see sustainable and equitable outcomes for individuals as well as communities.

And when I say social drivers of health, I'm referring to a number of different things, including socioeconomic factors like economic stability, educational levels as well as neighborhood and physical environment where people live, where they work, where they play and the community and social context. And finally, access relative to food, healthy food options and the healthcare system. So these are all of the factors that contribute immensely to the health outcomes that we see related to obesity. I'll also note that as a digital health technology company, an additional layer that we have to think about is related to digital drivers of health.

A lot of us I'm sure have experienced technology as it relates to our healthcare and this is also the same for people in different communities. Now the heart of the matter is that a lot of digital technology is not created with health equity in mind and what ends up happening is that, rather than addressing disparities, we end up worsening disparities. So when we talk about digital drivers, we're referring to technology access. We're talking about the relationships that patients and even their clinicians might have with technology, the healthcare infrastructure that supports the use of technology and also policies. So federal policies, for instance, that can influence adoption of healthcare technology in different neighborhoods. These are all really critical and I think really highlights the importance of addressing obesity, utilizing a multi-model approach, considering just the complexity of all of the factors that influence the outcomes that we see.

And finally, what I want to leave you with when we talk about social drivers is to really double click on that social context as well as the community piece as well. And that's the reality that, for a lot of people, especially black and brown communities and those of lower socioeconomic status, we cannot overemphasize the importance of social support and community belonging in helping them to make healthier choices and to see better health outcomes as it relates to management of obesity as a disease.

 

Carolyn Jasik, MD:

Thank you so much. That was really interesting. As always, I'm super grateful to have you in my orbit, Bola, as a colleague and just really important points to share. Some of you may be wondering why did we spend half of the webinar talking about physiology and epidemiology and the medical piece of obesity and why did we spend the second half talking about health equity and external factors? Well, the reality is in obesity, they are both important and they're both equally important and they're both factors that are with a person for the duration of their life. They live in their community and they also carry their physiology with them.

And so as we talk about obesity as a lifelong disease, you can't talk about one without talking about the other because, just because you do an injection, that doesn't mean that you have erased some of the barriers and the pieces of your community that drive your obesity and your access to that medication is also highly influenced by where you live and what you have access to. So thank you Bola so much. In the interest of time and because of the lively discussion that we've had on the audience Q&A, we're going to skip right to the audience Q&A portion of the webinar and we're going to start with the first question and I'm going to give Bola a break and let Dr. Stanford answer it.

So, Dr. Stanford, "How do we move away from obesity being seen as a moral failure from a treatment perspective? The amount of prior auth requirements for bariatric surgery or GLP-1s is stricter than most other procedures for other diseases. How do we move past this?"

 

Fatima Cody Stanford, MD, MPH, MPA:

Well, first of all, whoever asked that question, I feel your pain. The amount of work that I have to put in and my staff and all of those surrounding me have to put in for prior authorization for bariatric surgery, for GLP-1s and for continuation of GLP-1s once patients achieve a certain "weight status", and I put that in air quotes because there are these cutoffs that, "Oh, they've lost enough weight. Now let's pull them off of therapy," is absurd and I'm going to use absurd because I think it's absurd. There's no other disease process that is thought of this way and I think it's me doing work like this, my colleagues doing work like this to help people understand the physiology and going back exactly that was just stated.

The reason we talked about physiology is to get people to understand that this is very complex. It's not just a magic, "I give you a surgery. Everything's done." "I give you medication. We solve the problem." It's not just, "You've lost the weight, the disease has gone away." Let's think about this like we think about any other disease. If I treat your hypertension with an antihypertensive, hypertension didn't magically disappear. If I treat you with a cholesterol medicine, a statin for example, your cholesterol is not magically gone when I stop giving you the medication. If I treat you with a medication to treat diabetes, diabetes doesn’t magically disappear. And so when we begin to change our framing or thinking surrounding obesity as a disease like we do other disease processes, then we can begin to stop thinking about this as a moral failure and thinking about it like we do other chronic disease processes.

But we have been glacial in our thinking, the glacial in our pace of thinking about this as a disease process. And with that glacial thinking, our pace of thinking, we run into these multiple barriers that are burdensome on us as physicians and other healthcare providers and our support staff that make it such that, even the turnover that we experience, we're processing in our office close to 300,000 prior authorizations a year. I'm going to just say that, for our office alone, 300,000+ prior authorizations a year for the medications for our patients alone. That is absurd. It makes no sense. That's bewildering.

Who can handle that? Do you think that our team likes to stay? Do you think that the turnover of our team is high? Absolutely. It's absolutely bizarre. And a patient texted me. How she got my number, I have no idea. I was on the plane to give a talk at the NIH yesterday. I get a text message as I'm walking on the plane. She needed prior authorization for a medicine that day. First of all, I don't run the prior auths, as the doc, number one. Number two, how am I going to get that accomplished? Number three, as you mentioned, there's so many barriers to get that done. Number four, the minimum amount of time that it takes to get prior authorizations through, even with the best resources at Mass General Hospital its an average of four weeks. It is absurd. And so I understand, I agree, but it takes advocacy, it takes work and it takes grit and determination to change the minds. So I know I said a lot, but that's the reality.

 

Carolyn Jasik, MD:

Yeah, I sure do remember those days, I'm not in practice now, of the second shift, I called it, after the clinic was done and you spent the rest of the evening doing the charts and the prior authorizations and the other things. And so my hope working in technology is that technology will help us in some way facilitate those prior authorizations and make it lighten the load a little bit on the providers. I think the other thing that we desperately need is price relief on these medications, obviously. Once we have that, which I believe will come hopefully in short order with the amount of agents that are in the pipeline and the amount of competition that will come along, we will have some relief on pricing. And that will help our colleagues who are watching, who are trying to figure out how to pay the bill do this in a reasonable way because it is such a challenge.

Okay, so our next question is, "What about the research that shows that post-obesity people are very likely to regain the weight? Can you speak to that?" So I was thinking we might have Bola, maybe you can give us your thoughts about why it's so hard for patients to maintain the weight loss after they have achieved it. Let's say in this scenario: they've done it with lifestyle change or medications and maybe they go off the medications or they don't. What are the factors that make that regain happen?

 

Bola Bukoye, MPH:

Very important question, and I believe it goes back to what we just discussed in terms of other social drivers of health, which are often not thought about when we just prescribe the medication and expect that that will solve the disease for patients, but it can ... Other factors to think about are, "Are they engaged in physical activity and do they have the level of support that is needed to sustain this new lifestyle?" That's another really critical aspect to this. And I think the other big piece to you here is, again just this cost, the cost of the medication like you mentioned earlier, Dr. Jasik, that for a lot of people is just unaffordable in the event that this is something that they have to be on for a long period of time. Even in the event that this is covered by insurance, the co-pays still tend to be very costly for a lot of people. 

And we see this being less sustainable again for people and communities that are medically underserved. So I think that the outcomes that we see for different communities tend to differ based on those factors.

 

Carolyn Jasik, MD:

Super helpful.

 

Fatima Cody Stanford, MD, MPH, MPA:

May I speak to that? May I speak to that one also?

 

Carolyn Jasik, MD:

Yeah, I was going to say. Yes, please do.

 

Fatima Cody Stanford, MD, MPH, MPA:

Yeah, I'd love to speak to the biology. So there actually is biology to why people regain weight. So when we look at these hormones, and I'll use bariatric surgery as a key case in point, when we initially go to bariatric surgery, and I always explain this to my patients because I've done a lot of studies on this, there is a honeymoon period that happens in the post-bariatric surgery patient. When we do let's say a sleeve gastrectomy, which is the number one surgery performed in the US and around the world, we cut out ghrelin. Ghrelin is housed in the fundus region of the stomach. When we do a sleeve hysterectomy, we cut out ghrelin in the fundus region. And so in that immediate postoperative course, and I would say in that first usually three to six months, ghrelin goes down in that region, but ghrelin is still housed, if you remember, in the neurons in the hypothalamus.

So immediately, the patient's like, "Oh, wow, I'm not hungry. I don't even understand. Wow, it's amazing, I'm loving this. This is great. This is what people feel all the time? I never knew what this felt like." But the brain is smart. Not only is it smart, meaning, "I know that to recall that I have a phone here or I'm looking at a laptop," it's smart in that the neurons in the hypothalamus pick back up, ghrelin rises once again. Not only did ghrelin come back up, GLP-1 after surgery initially decided it to come up. So you're filling in full very, very quickly. You're like, "Wow, I had one spoonful. Wow, I'm full amazingly," but GLP-1 levels start to decline.

So bariatric surgery is just one case in point, but even after immediate weight loss from restrictive eating, et cetera, these things happen, but over time, very quickly, these hormones that were initially changed start to reemerge. And so that weight cycling piece that I talked about, this is what we're going against the hormones that are in the body. And so these things are reemerging and so we're fighting what's going on internally. And so that regain that's happening is actually due to those hormones, ghrelin, GLP-1, cholecystokinin, GIP, all of these hormones.

And so the reason why if you pull someone off of let's say a GLP-1 they're going to regain is because we haven't fixed what's inside the body, we're just treating what's inside the body. And so when you pull back something that was treating it, the body is going to go back up. Much like if you pull back an antihypertensive, you haven't fixed what's going on, you're treating what's going on. So I just want to say it's actually the physiology that's still dysfunctional. We are treating it. When we pull that therapy back, we're no longer treating the actual dysfunction and the physiology.

 

Carolyn Jasik, MD:

So fascinating. Thank you so much. And I didn't know that about ghrelin and bariatric surgery actually, so it's super helpful. I'm reminded of a conversation we had a few months ago in one of these webinars about how little education there is for patients about their physiology and understanding what's going on in their body, both post-bariatric surgery and if they make the choice to discontinue GLPs, how important it's for patients to know what they're up against in terms of fighting that metabolism as you spoke to. So thank you. I love the next question. It's one of my favorite questions, so I always would like to hear people's answer. I will not answer it because I'm facilitating, not answering today, but maybe Dr. Stanford, "Can you speak to BMI and why this is a flawed metric used in obesity care?"

And maybe I'll even push you a little bit to say, if you agree that it's a flawed metric, what does good look like for us to be able to look at people's health as it relates to their weight and body chem position?

 

Fatima Cody Stanford, MD, MPH, MPA:

I'm absolutely happy to explain this. So BMI actually was based off of the work of Adolphe Quetelet or Adolphe Quetelet, depending upon how you want to pronounce his name. He's a Belgian statistician in the 1800s who decided to determine what was considered to be normal for Belgium soldiers in terms of weight in the 1800s. As you might know and I don't know how many Belgian people are watching the webinar today, how many Belgian soldiers are watching today, but probably not many and probably not a lot of Belgian white male soldiers, I don't know. But if you are there, you can feel free to type in the chat.

And so this became the basis for eugenics. It was espoused by Hitler as the framework or basis for eugenics actually in a more serious fashion. And so this also then became the Quetelet Index. Fast forward to the 1930s and 1940s, the Metropolitan Life Insurance Company decided to determine what was considered to be the likelihood of dying based upon your weight status, hence the term morbid as it relates to obesity. What was your insurability based upon your weight if you were a white man or a woman insured by the Metropolitan Life Insurance Company? Because if you looked like me or Bola, you weren't insured by the Metropolitan Life Insurance Company. And so the term morbid as it relates to obesity based upon weight status was born out of actuarial tables in the 1930s and '40s.

Then we are going to fast forward to the 1970s where Keys decided, "Oh, let's just look at height and weight. That has to be simple enough. And let's just come up with something called BMI." This was then espoused to be a metric that will determine weight status used by then statisticians at the time, hence the term BMI. Now if you'll listen to the chronology of events from statisticians to actuarial tables, you'll notice that I never ... And once in that chronology of events ever brought up medicine or science, yet it is what we use today to determine what health looks like.

And so there are some problems in this in terms of determining health as a metric of BMI, yet it is what we use universally to determine what weight looks like. I will tell you the Lancet Commission, of which I am one of the commissioners, will deviate from this being the solo metric. The AMA has already mentioned that BMI alone is not a great solo metric, and we do need to combine, if we're going to use BMI, with other metrics like waist circumference, looking at central adiposity, which I mentioned in my talk and looking at other factors.

Because for example, if you get admitted to the hospital and let's say you have heart failure and I take fluid off of you, meaning I diurese you, I pull fluid off of you and you lose 20 pounds very quickly, did your health really improve or did you just that pulled water off of you? Your health didn't improve, you still have heart failure, your BMI looks better, doesn't tell me about your health. So it's not really a health metric, it's just a number and it just tells us your height and your weight. So I think that it's problematic by itself and there are some things that are dysfunctional using this metric alone to determine whether or not you're healthy. So that's my thoughts and I gave you the whole history. There you go.

 

Carolyn Jasik, MD:

I am delighted to have that history. I was absolutely transfixed because I had not heard it go quite back that far. Bola, I don't want to entirely put you on the spot, but could you comment on BMI from a health equity standpoint in terms of Dr. Stanford hinted a little bit about how it is inadequate, but do you have any thoughts about how we use BMI in different patient populations based on their background?

 

Bola Bukoye, MPH:

Yes, of course. I think in addition to Dr. Stanford's really important comments, there are different physiologies across different communities too. And I think historically what we've done is we've assumed that there is a defined healthy weight regardless of who you are, regardless of your individual situation. And that ends up worsening disparities in the sense of us categorizing people as obese who otherwise are at a healthy weight. So I think it's really important again, that we think about what it means to have a one-size-fit-one approach and that's not the easy thing. So I think that's part of why this is so hard because it does demand that we're listening to our patients and that we are making sure that the solutions that we're putting forward really does take into consideration this bigger picture, which highlights BMI as just a piece of this bigger picture in terms of what influences someone's healthy weight.

 

Carolyn Jasik, MD:

I couldn't agree more. I'm so looking forward to the day, waist circumference, body composition using other tools, having some advances in technology to allow us to understand someone's risk at a much more personal level. I agree with you. Well, as usual, the time flies when you're talking about something important and interesting. I'd like to give each of you a chance to give some parting words on your thoughts about the topic today. We can start with Dr. Stanford.

 

Fatima Cody Stanford, MD, MPH, MPA:

Absolutely. Well, first of all, it has been a delight being here with you and I hope that, if you leave with nothing else, you number one leave with recognizing obesity as a complex multifactorial disease and recognizing that this is a disease that impacts us across the lifespan. It's one that affects pediatric patients, affects us everywhere around the world. And it's one that we need to really check our biases at the door. Unfortunately, this is a disease that we wear and we need to recognize that we need to treat patients that have obesity with dignity and respect like we do any other disease process. It starts with our language. Let's eliminate the words obese. "Obesity is a disease. People have the disease of obesity and they aren't obese people." Let's eliminate the word morbid as it relates to obesity, "They have severe obesity." And let's, like I said, treat them with dignity, kindness, respect and let's get rid of our biases.

Let's work towards advocacy. This is the most prevalent chronic disease in human history. And if we treat obesity, we treat the 230+ chronic diseases that come along with it. And those are my parting words. Thanks so much for having me.

 

Carolyn Jasik, MD:

Thank you. Bola?

 

Bola Bukoye, MPH:

I couldn't put it any better, but I will echo the same thought just in the sense of us putting the patient's back in the center of this conversation where they belong. I think that's the biggest advocacy tool that we have to really make sure that we recognize the lived experience that patients have with this disease and the recognition that it is real. These are people. This is their lives and we have to make sure that, when we are thinking about how this disease is managed, that we consider what works for individuals and that we consider what works for different communities because it will be different. So our approach has to keep that in mind.

 

Carolyn Jasik, MD:

Wonderful, ladies. Thank you so much. And I guess the only thing I'll leave everyone with is, first of all, gratitude to both of you for attending and then just asking our audience, let's not let price and our biases hold us back from helping, what is it, frankly, the majority of humans on this Earth. So let's make a commitment together to give people what they need and treat them with respect. So thank you, everyone, and we look forward to seeing you on the next Omada Grand Rounds.