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Hollywood’s New Weight-Loss Drug and the Obesity Epidemic


In this video, Jeremy Faust, MD, editor-in-chief of MedPage Today, sits down with Fatima Stanford, MD, MPH, MPA, and Karl Nadolsky, DO, to talk about Hollywood’s newest weight-loss drug semaglutide (sold under the trade name Wegovy for weight loss and Ozempic for diabetes). Stanford and Nadolsky also discuss the failures in medical education and continuing stigma against obesity that results in only 3% of Americans receiving the care they need.

The following is a transcript of their remarks:

Faust: We’re talking today about weight-loss drugs, especially this new class of weight-[loss drug] — well, it’s a new application of a drug we’ve had. I want to get your opinion on it. It’s kind of big in Hollywood; people are talking about it as a big fad.

But the question is, is it really different? Is this “the one”? Because I think we’ve had so many fixes for weight-loss drugs or ideas, whether it’s a drug or whether it’s bariatric surgery, over the years. The data on this one look a little different.

So, let me just start with Dr. Stanford. Can you tell us a little bit about what Ozempic and Wegovy (semaglutide) is? Tell us what that is and how they work and, in your opinion, are they working for weight loss?

Stanford: Yeah. This is semaglutide. I just want people to know, because people will say, “I don’t want to be on Ozempic, I want to be on Wegovy,” and, “I don’t want to be on Wegovy, I want to be on Ozempic.” This is the same thing. They’re the same exact drug made by the same exact company under two different trade name labels.

Ozempic is the label used for patients with type 2 diabetes and Wegovy is the label used for persons with obesity, but it’s the exact same drug and does the exact same thing because it is the same drug. There’s no difference, it’s just two different labels. It’s like if you were to go buy a black car versus a red car, but they’re the same brand, same make, and model. It’s the exact same thing. OK, I just wanted to first throw that out there.

This type of medication is what we call a GLP-1 agonist or glucagon-like peptide 1 agonist. This works in the body in four different ways, but I have to teach you a little bit about obesity to understand the first way.

There are two pathways by which our brain regulates weight. There’s the POMC or the proopiomelanocortin pathway — say that five times fast — that’s the pathway that tells us to eat less and store less. Then we have another pathway to the brain, which is the AgRP pathway or the agouti-related peptide pathway, which tells us to eat more and store more.

With this medication, the first way it works is by upregulating that POMC pathway, which is beneficial and the pathway we want to go down, and inhibiting the pathway that’s not as desirable. It slows gastric emptying, which means as food moves through the GI tract, it moves slowly so you stay full longer. It increases your insulin secretion, how much your pancreas actually puts out. Then the fourth thing that it does which a lot of people are unaware of is that it actually helps to brown your white fat tissue. So when your fat tissue is more brown in color, much like my skin, you burn more at rest and with activity than if not. Those are the four ways of how it works on the body.

This class of medication, when we look at the data from GLP-1 that is approved, which is Wegovy, we’re looking at on average a total body weight loss of about 15.5%. There is another medication coming down the pike which will have a GLP but it’ll also have a GIP in it, which is a combo-type medicine that has been shown, as tirzepatide is known to show, on average cause 22.5% total body weight loss.

Now, I’m a huge fan of using all of the anti-obesity medications because not everything works for every person. So, just because I just gave you these large numbers, it does not mean that each person will respond. It’s an average. Like if you take a test in a class, some people are going to do really, really well and some people are not going to do as well.

It’s about finding the right tool for the person, and so I do use the full spectrum of medications, not just these medications. Some people that don’t do well on these medications may do well on some of the more traditional therapies. I’ve seen with some of the more traditional therapies 50% total body weight loss or something very, very dramatic because that was the right drug for that patient.

So, the key thing I would say when using these medications for weight regulation is that when you commit to it, just like with any other chronic disease, it is a long-term commitment. This is not something you go on and then come off of, because as soon as you come off of it, you’re going to regain whatever you lost while using the medication. That’s really important to know.

Faust: That is a masterclass on how it works. Also, the fact that it’s not just a one-size-fits-all approach, I think that obviously comes from experience.

Dr. Nadolsky, a lot of people are asking me about this even though I’m the opposite of an endocrinologist. I’m an emergency physician, I don’t ever prescribe these medications. But they’re asking me, “Can I get on this even though it’s just for a little bit of weight loss, not necessarily obesity or diabetes?” Can people who don’t have substantial obesity or type 2 diabetes use these drugs without risking any kind of hard side effects?

Nadolsky: Well, I would say the good news is that these types of medications have a very good track record for benefits outweighing risks.

This class of medication that she just went over greatly has been around for awhile, since exenatide was approved back in 2006 or something. I was a med student when exenatide, or Byetta by trade name, was being used twice a day for type 2 diabetes and had the benefits that she mentioned for weight loss and really treating part of the underlying issue of obesity driving type 2 diabetes.

Since then, there was developed liraglutide [Victoza], which is from the company that makes semaglutide or Ozempic/Wegovy. We had very reassuring data with liraglutide and type 2 diabetes at high or established cardiovascular risk, the LEADER trial, which reduced cardiovascular outcomes, followed by good cardiovascular data with semaglutide, both in the injectable and the oral forms. We have plenty of other studies showing this class of medications to be very good, very safe.

But, all medications have some risks. While we think there are good cardiovascular benefits, there are risks. Some slight gallbladder risks that we’ve seen recently for sure. There have been thoughts in the past of a risk of pancreatitis, but that really doesn’t pan out in the meta-analyses of these. But, you know, gallstones put people at risk, people with obesity and diabetes have risk of pancreatitis. They do have their side effects, potentially nausea and some other GI side effects that can happen.

I think to your question though, and this is an interesting discussion … would we say, “Hey, maybe everyone could do a little bit better with their diet and stuff with the support?”

I don’t know, but that’s a different discussion because they’re also very expensive and the supply isn’t really what we want it to be. We, the three of us and all of our colleagues, have a lot of patients who have real obesity as a disease that’s not being treated well enough yet. And those who have what I would consider more severe obesity in a complication-centric manner, say obesity complicated by prediabetes, type 2 diabetes, atherosclerotic disease, who are the ones who really get the most benefit from especially this class of medications that is expensive and doesn’t have the great supply.

I suspect most of us are on the same page that we would really discourage the inappropriate off-label use of just doing it to shed a few pounds. If you don’t have real clinical obesity, and probably these should be reserved for those who have more significant complications of obesity or significant amounts of weight to lose and things like that, but certainly there’s a spectrum of nuance within this.

You know, she mentioned tirzepatide, brand name Mounjaro, has some of the best data we’ve seen so far for obesity and type 2 diabetes. It’s approved for type 2 diabetes, so we’re using a ton of it. It is being used off-label for obesity because it has the data behind it, it’s being FDA fast-tracked for obesity, but even then because of the cost and supply and pros and cons, I would suggest it should be encouraged to be used for those who have more severe obesity based upon complications. Not very metabolically healthy, “I need to lose a few pounds and get shredded for the summer” kind of thing.

Faust: Right. Because there’s the Hollywood use, which is sort of that like get-into-shape-for-some-ideal viewpoint of aesthetics, and then there’s the, does that 10 extra pounds that someone’s carrying, it’s not obesity, but just even those 10 extra pounds that someone’s carrying confer some kind of long term hypertension or whatever? It’s a question that we can’t answer, right?

Nadolsky: Yeah. I would say that if somebody has what we would consider adiposity-based complications, like high blood pressure, and we look at them — no matter what their BMI is, we have got to get away from the BMI-centric approach anyways, right? So let’s say they have high blood pressure and maybe some high triglycerides depending on their ethnicity their waist is a little up, but their BMI is 24. That’s obesity by definition of the disease. I see [Stanford] is nodding, and so I think we’re all on the same page with that. It takes a clinical perspective.

Faust: Let me dig back into the research. Dr. Stanford, I do deep dives on clinical research. I love to look for things and see what’s going on, especially industry-funded studies and all of this and looking for “how good is this?” and “how much of this is kind of ‘eh’?” But, I’ve been pretty impressed with this literature. I’m curious what your view is on it.

What’s your overall assessment of the literature on this in terms of how well the studies were conducted and how long these effects last? You mentioned that there can be some sort of rebound. Give me a sense, because I’m still sort of coming at this as a person who hasn’t done the deep dive. I’ve done the sort of superficial dive. Is this as good as it looks like? What’s your assessment of the literature?

Stanford: Yeah, so there are several different trials that have looked at GLP- 1 receptor agonist, the ELIXA, the LEADER, SUSTAIN, EXSCEL, Harmony, REWIND, PIONEER, AMPLITUDE, I mean, we can keep going. What these trials have done is look at both cardiovascular and noncardiovascular outcomes, so what we do have is pretty long-term data. As Dr. Nadolsky said, these medications were initially approved for type 2 diabetes and they have been around for quite some time.

What we see are the following things: we see a significant improvement in major adverse coronary events. For example, Ozempic has gotten approval by the FDA specifically for that indication. It reduces cardiovascular (CV) death, fatal and non-fatal MI, fatal and non-fatal stroke, all-cause mortality, hospital admission for heart failure, and kidney outcomes, including macroalbuminuria. So, these are all very significant.

And this is a meta-analysis that actually looked at the CV and non-CV outcomes that came out in The Lancet Diabetes & Endocrinology from 2021. Sattar and colleagues were the leaders of that particular meta-analysis. So when you look at that and you put together all the studies and you see the significant P values — anything less than 0.05 is significant, we’re looking at less than 0.001 for these outcomes that I just mentioned. When you hear those things, that’s a really great profile for these medications, and their need for sustained long-term use for patients that have obesity or obesity-related diseases.

Faust: You mentioned that there are many modalities that you could choose for a different patient, but my sense as an outsider is that for the most part — you used the classroom analogy before, that “yeah, there’s some people who did well and they got an A-, but most people got a B or C+ and then when they got off of it, they went back to not doing well.” I guess what I’m trying to figure out is, how much better is this than what we’ve had before? I am also curious to follow up on if you stop it, how do things creep back up, what do we see, what happens with that?

Stanford: I’ll answer the second question first, and then I’ll go back to the first question that you asked.

So, with any chronic disease — and people haven’t really gotten into the idea of recognizing obesity for being the chronic disease that it is. So, if we’re using a drug to treat obesity like we were treating diabetes or high blood pressure or anything else, we don’t go on it with the idea that we’ll stop it. You don’t go on high blood pressure medicine and say, “Hey doc, when do I get to go off of that?” If we’re using it to treat high blood pressure, we may be using one or two or three or even four agents, for some people five agents. The goal is to get incremental benefits with the added use of these medications, but you don’t magically think it’ll stop one day.

Just like if we start someone on medications for high cholesterol or medications for diabetes, we don’t say, “Let’s put you on, and then let’s stop and see what your blood sugar does.” This is exactly that thing.

I think we have to get out of the idea of not thinking about obesity in that same way that we think of other chronic diseases. We don’t just say, “Let’s stop it. Let’s see what happens.” We know what’s going to happen. It’s pretty obvious.

So [according to] the data from Wilding and colleagues, when you stop these medications, you do begin to rapidly regain your weight because we’re no longer impacting the areas of the brain or the GI tract that we were impacting. Right? As soon as you pull that away, the four things I just said are no longer going on. So what do we expect? We expect to have regain.

Now when I compare and contrast these medications, yes, on average these medications do have more total body weight loss in, on average, more people, but everyone is not the same person. Even if you look at the three of us on the screen, we’re all physicians, but we are very, very different humans in how our bodies respond to different therapies, and modalities may change or be different. So yes, on average people will do well on these medications, but there may be some that don’t do so well and maybe they only lose 1% or 2% of their body weight. For them, this is not the right medication strategy for them. I might put them on phentermine or a combination of phentermine-topiramate and get significant benefit from that because that worked with their biology, and we know those medications work in different areas.

So for example, phentermine, the first drug approved by the FDA back in 1959, actually inhibits norepinephrine reuptake within the hypothalamus. That’s how that works. Topiramate actually stimulates gamma acid within the brain. Those are different pathways. So often — much like when you’re treating high blood pressure, I think that’s the easiest way to think of it — someone may need a thiazide diuretic, and then they may need an ACE [angiotensin-converting enzyme inhibitor] and maybe they need a calcium channel blocker. You’re using different things to compliment each other to help them get to the happiest, healthiest weight for them.

So I think it’s important for me as I’m working with patients to listen to what their body is telling me. Are they a responder? Are they a non-responder? And we can pick this up relatively quickly. I would say in the first 3 months we know whether or not that person is a responder versus not a responder. And if they’re not, don’t give up. We do have other therapies available. We definitely have things that are more kind of in that traditional realm, and for some of those therapies many of my patients have lost tremendous amounts. We’re looking at about 9% to 10% for phentermine-topiramate, but like I said, I’ve had patients that have lost 50% of their total body weight on those medications. So, it just depends on finding the right therapy for the right person.

Faust: Excellent. Let me kick it over to Dr. Nadolsky. With these medications becoming more popular, and there’s just so much buzz about them, are you seeing a change in your patients — not seeking them because that sounds negative — but they want this. Another way of asking the same question in reverse is: how much are things changing? Are fewer of your patients requiring or wanting to have bariatric surgery and that kind of thing? Are you seeing a real change in landscape in terms of what patients want and what they actually end up doing?

Nadolsky: I would say a little bit of both. Interestingly, to what Dr. Stanford said earlier about treating obesity as a chronic disease and how we need to do a better job of educating, I literally just saw a comment pop up down here.

Because she mentioned when you stop the medications, for example with semaglutide, I think it was [SUSTAIN 4], they had a run-in period, they lost about 7% to 10% of their weight then were randomized to placebo or continued semaglutide, and the placebo group started to go up, right? Because the disease of obesity is not about the person’s willpower or necessarily their diet and exercise. It’s about the biology fighting that person’s abilities to do those things to create a different energy balance.

Someone in the comments just said, “Well, that’s because you guys aren’t treating the root cause of the disease and not their diet and exercise.” Ironically, that’s exactly what she was just talking about. We are treating the root cause of the disease, we’re treating the pathophysiology of obesity. She mentioned the areas in the arcuate nucleus that are part of the literal central problem of what’s driving this; and there’s a lot of genetics.

Everyone has different genetics. I always tell patients that their lives are throwing different monkey wrenches into those genetics driving this. It’s not just easy. We always talk about nutrition and physical activity, but these medications are helping people do that. So, that’s one thing just because I saw that comment pop up and I thought that was perfect timing.

But yes, I think we are getting people to their clinical goals, and so it’s not just about weight loss, you know? When we talk about — I went back to the adiposity-based complications, so someone with high blood pressure, mild triglycerides, they have some significant disease of obesity with complications. Some people don’t have any complications, but we want to prevent those things. And then some people have type 2 diabetes and heart disease — and we need more weight loss — or fatty liver. Let’s say they have NASH, nonalcoholic steatohepatitis, we need a little bit more weight loss to achieve those clinical benefits.

It’s what’s on the inside that counts. That’s what we actually care about, not the weight per se. That’s why we stage the severity based upon that.

Also, we should think about the clinical responses to that. So when she’s talking about a lot of people responding to these and that we have these responses to therapy trials for the phentermine-topiramate, naltrexone/bupropion, the GLPs, if you lose 4% to 5% of your weight in the first 3 months, you suddenly then are into this category where your average weight loss amongst all those people, the responders, is even better, and you start getting the really clinically meaningful 10% to 15% or more weight loss that ultimately translates as a surrogate marker to things like improved glycemia, type 2 diabetes remission — we could debate that since the GLPs do more than just weight for the fatty liver and things like that.

That’s another individual thing — we create individual goals based upon their characteristics, their complications, and where they need to be. It’s not just about the weight, but we think about their clinical responses to therapy.

They also have different characteristics that might make us choose one of these medications over the other, not just because on average these medications help a lot more with weight loss. There are other things. They have certain side effects; people have different characteristics that help us personalize it. I’ll give a little plug for the 2016 AACE [American Association of Clinical Endocrinology] guidelines and algorithm where we tried to be very pragmatically relevant for people to say, “Well, this person has this condition, so maybe this medicine might be more beneficial.”

Faust: This is a perfect segue to the next question. Every patient is different, everyone has different goals. Dr. Stanford, how do you decide when someone doesn’t need to lose any more weight? Because you don’t want to use BMI, but you want to get to some kind of goal. What do you do?

Stanford: I disagree 100% with you. We’re going to have to do a lesson with you afterwards.

I don’t ever give anyone a goal weight. I tell them that we’re trying to get them to the happiest, healthiest weight for them, whether that’s 300 pounds or whether that’s 150 pounds. That varies from person to person. What I’m looking at is their overall health.

I think this is what Dr. Nadolsky was trying to get at: is the weight in relation to not only their actual weight, but what is their fasting blood sugar? Are their insulin levels high? Do they have evidence of fatty liver disease? Do they have evidence of obstructive sleep apnea, type 2 diabetes, arthritis? All of these things are some of the over 200 diseases that are caused by obesity. We want to treat that whole person, not just the size that comes in front of us. I think that’s really important.

So, I think the pendulum swings both ways. We have to make sure, it’s exactly what Dr. Nadolsky said: people that are lean, you look at them and presume they’re healthy, but they may be very unhealthy. We may not be doing a deep enough dive to see what their health status is. This is where we often fail patients, I think, because we make these assumptions.

What we do know in terms of physicians is that 79% to 90% of us have tremendous weight bias towards individuals that carry excess weight. A lot of this has to do with the fact that we have had no competencies and training in obesity at all in our medical education. It’s deplorable, the AAMC [Association of American Medical Colleges] is trying to change it, but this is the largest chronic disease in human history and doctors know nothing about it. But who do they tell you to go see? They go tell you to see your doctor.

I mean, I did 3 years of fellowship training in this space, so I feel very confident in the work that I’m able to do. But if you receive nothing, and then you’re expected to deliver this care, that bias creeps in. So I really want to make sure that we get into these nuances about that piece of the puzzle because that affects the care.

Going back to one of the questions you asked Dr. Nadolsky in terms of who’s getting what and what the percentages are, I still think we have to recognize that only 2% of people that meet criteria for bariatric surgery in this country today are getting it. Only 1% of the people that meet criteria for medications in this country are getting it. That’s based upon my Mayo Clinic Proceedings paper that came out last year.

So we’re talking about 3% of individuals that are getting advanced therapies beyond lifestyle behavior approaches, and we’re wondering why our rates continue to go up, not only here in the U.S., but around the world. This is the largest chronic disease worldwide, not just here in the U.S. Yes, everybody assumes it’s a U.S. issue. We’re actually ranked number 14 out of 200 countries. So we’re not award-winning, we’re not number 1, but we’re behind 13 other countries. So this is a major, global issue.

If you look at it from a global perspective, I published this paper too in the International Journal of Obesity, no one’s teaching medical students, residents, or fellows about the disease. We’re going in and we’re saying the wrong thing. We’re telling the patient to eat less, exercise more, eat less, exercise more, eat less, exercise more. If they all did that and it magically worked, then Karl and myself wouldn’t need to be here. Then it could be: eat less, exercise more.

But the problem is the biology. How is the brain affected by the world that’s around them? Some people can get many perturbations and not be affected. You can give them all the bad things: circadian rhythm, they can be up all night, they can have stress and trauma, they can go on medications that usually cause weight gain, they can do all these things, and they’re still very lean. That’s my husband, but that’s not everyone. Everybody is very different.

So then you have this other person over here that at any perturbation that comes in, they gain weight and they gain weight and that weight compounds, and then you end up with a person that carries 150 pounds in excess of a healthier weight for them. Then we have to figure out why. Then, what do we do for it? That’s my soapbox for the day.

Nadolsky: To jump on that a little bit, we have to find a way to educate better because we’re not treating enough of obesity as the root underlying driving cause of all the complications that are getting treated.

Think about all the medications that people get off when we do the right metabolic bariatric surgery and the right obesity pharmacotherapy in addition to their lifestyle efforts. You were mentioning blood pressure medications and how we do multiple different types of blood pressure medications. They’re some of the fastest meds that we can de-escalate when we’re treating the root issue of the biology that’s driving their obesity.

There’s bias stigma and not enough education. To be fair, I guess it’s a relatively new science and medical understanding of the biology, but we have to do better.

Faust: OK, last question; we’re running out of time. I will need five more of these sessions, but both of you [give] your take on this. We have a pediatric obesity epidemic as well in this country, but it’s not, as I’m learning, it’s not just the number of how much you weigh or what you look like, but it’s about health on the inside. How do you decide when to start children or adolescents in some of these pathways?

Nadolsky: Do you do pediatrics, by the way?

Stanford: I’m a pediatrician, also.

Nadolsky: That’s good. I’m an adult endocrinologist, to be fair.

Stanford: Karl’s like, let’s defer that to you.

I am a pediatrician. My patients range in age from 2 to 90, so a pretty broad spectrum. I think that we have to use the right tool for the size of the problem. So I do send some of my pediatric patients for metabolic bariatric surgery at 13 or 14. I use medications. Medications like liraglutide are approved for ages 12 and up. There are some times we’re using medications off-label, particularly for our younger patients that don’t meet those criteria, because we’re trying to treat the biology.

Then for those people that end up having rare forms of obesity, we actually can test and see that — [it happens] more often in childhood, right? Because we’re able to pick up if they have something called hyperphagia, this insatiable desire to eat. Then you test them and you’re like, “Oh my gosh, they have all of these different mutations that are likely contributors to the obesity.” So we can try and throw all the lifestyle at it, but we can’t overcome what’s going on in their brain.

We can use these therapies across the age spectrum. I do believe in treating more aggressively early on. I did a study that was a head-to-head comparison of adults that go to metabolic bariatric surgery versus my kids, and my kids are all my patients — some of them are now adults. What we find is that while adults do well, the kids do better.

Let’s just think about it. If you’re a kid and you developed diabetes at age 12, you’re now 14, you’ve had it for 2 years. If you’re one of my 55-year-old patients that’s had diabetes for the last 15 years, that’s a much longer time. Whose diabetes is more likely to go on remission and stay in remission? The one that had it for 2 years or a year and a half, maybe you had a high cholesterol for a year, you know who’s going to go in remission and stay in remission.

If we look at that paper that compares those head-to-head outcomes, we saw that on average pediatric patients do well. What’s interesting is that those pediatric patients that become my adult patients, when you’re looking at them in their 30s and 40s, their metabolic profile actually is superior to many of us that have never struggled with our weight.

Let me tell you why I know that — I’m looking at their cholesterol, I’m looking at their blood sugar, I’m looking at all of their things and I’m like, “My gosh, I’ve never seen numbers this amazing.” I think it was that early intervention that made an impact. So I would say for anyone that has a child struggling, make sure they’re getting into care sooner than later. The earlier you can get them in, the better they will do overall.

Nadolsky: I’ll add in as the adult endocrinologist, I would love for everyone to address this even earlier than say the diagnosis of type 2 diabetes. Once kids get type 2 diabetes, even early adults, they do tend to have worse beta-cell failure, pancreatic failure, and ultimately really having overt type 2 diabetes and complications down the road. So, let’s treat it earlier than that.

She mentioned the rare genetic disorders that cause severe early onset obesity. We have some medication now for some of those specific disorders and we probably need to do a better job of screening because it’s probably not as rare as we think.

Dr. Farooqi, the renowned geneticist and endocrinologist who does all these studies over from the U.K., made note that there are kids who have been taken away from their parents because people thought the parents weren’t doing what they needed to do. These little bitty kids have severe obesity. That’s not lifestyle, generally speaking, that’s a genetic disorder driving that.

Faust: OK, I promise this is my final question. I want it to be really short, like almost give me a yes or no for both of you.

On one hand we’ve got, [the fact that] the foods that we eat are increasingly not what we want them to be. They encourage overeating or cravings and all these things that can go against what we want. We are also sedentary. We’re sedentary more and more. But on the other hand, we’ve learned so much about these medications and these other medical interventions.

Ten years from now, do you think that there will be more obesity in this country or less obesity in this country? I’ll start with Dr. Nadolsky.

Nadolsky: Oh my god. Unfortunately, based upon the current data and the trends, I still think we’re going to have more. This is why we gotta do better as a team.

Faust: OK. All right.

Stanford: I agree. I think that we’ll have more because we’re not treating the disease. I think if we start to treat the disease for the disease it is, much like how we’re starting to see cancer rates decline, then we can see a change. But we’re not doing that.

And cancer therapy is covered; obesity therapy is often not covered. There are actually laws in place, particularly Medicare Part D does not include any anti-obesity medications. We know Medicare sets the standard for Medicaid and also for private insurers. I happen to live in Massachusetts where employer-sponsored insurance does cover these medications, so we see a better uptake, but Massachusetts has one of the lowest obesity rates in the country. So here we have the group that has less of a struggle on average getting more treatment and therapy. Maybe we’ll see a turn here first.

But the problem is that no one’s treating this like the disease it is. While I agree that our diet and physical activity can make some change, we aren’t recognizing the over 100 reasons why people have obesity. There’s a pie, and we keep targeting the same part of the pie. What’s the definition of insanity? Doing the same thing and expecting a different outcome.

It was what I saw at the White House conference on health, hunger, nutrition, “Let’s just say this is a diet-related disease.” What I think both Karl and I have said today is that’s not the case. That just isn’t what it is. Let’s treat it for the disease it is, and let’s treat patients fairly and let’s give them the dignity and respect that they deserve.

Faust: You guys are doing great work. I really appreciate it. Where can they find you on social media?

Stanford: For me on LinkedIn, Instagram, and Twitter @askdrfatima.

Nadolsky: And mine is @drkarlnadolsky. We also have a podcast “Docs Who Lift” where we talk about this stuff too. We’ll have to get you guys on there.

Faust: Well, I look forward to continuing this conversation, and thank you for educating me and the audience and for sharing your expertise. Have a great day.

  • Emily Hutto is an Associate Video Producer & Editor for MedPage Today. She is based in Manhattan.



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