Jim Hill:

Welcome to Weight Loss And, where we delve into the world of weight loss. I'm Jim Hill.

Holly Wyatt:

And I'm Holly Wyatt. We're both dedicated to helping you lose weight, keep it off, and live your best life while you're doing it.

Jim Hill:

Indeed, we now realize successful weight loss combines the science and art of medicine, knowing what to do and why you will do it.

Holly Wyatt:

Yes, the “And” allows us to talk about all the other stuff that makes your journey so much bigger, better, and exciting.

Jim Hill:

Ready for the “And” factor?

Holly Wyatt:

Let's dive in.

Jim Hill:

Here we go.

Jim Hill:

Holly, recently a group of experts met to propose a new way to define and diagnose obesity. This new definition was intended to better identify people who most need treatment.

Holly Wyatt:

Yes, Jim, this This is really exciting. You know, we've always defined obesity using body mass index, or BMI, which is our weight in kilograms divided in height in meters squared. And a BMI of 30 or more has been used for decades, really, to define obesity. And now that might be changing. And I'm very anxious to explore this topic today to understand how this new definition might impact those with excess body weight.

Jim Hill:

Yeah, and we have the perfect person to help clear all this up. My colleague and friend, Dr. Eric Ravussin, is joining us. I'm going to give Eric a little bit longer introduction than we usually do. He and I have worked in this field for over 40 years. I think I met Eric first in the early 1980s, and we have both worked in this field in similar ways for all those years. But Eric right now is a professor at the Pennington Biomedical Research Center in Baton Rouge, Louisiana. He also just recently stepped down as the director of their Nutrition and Obesity Research Center. This podcast is a part of the UAB Nutrition and Obesity Research Center, and we like to have other people from these centers to come on the podcast. Eric has spent decades studying the physiological mechanisms behind energy balance, metabolic flexibility, and weight regulation. Terms I love, Holly. Those are key terms. He got his PhD from the University of Lausanne in Switzerland. And he trained with Dr. Eric Jacquet, who's one of the real giants in our field of studying human physiology.

Jim Hill:

He came to the U.S. and he was in Vermont for a while, but he spent a lot of time out in Phoenix studying Pima Indians. And we'll talk a little bit about that because the study of the Pima Indians has taught us so much about body weight regulation. He joined the Pennington Biomedical Research Center in 2001, and he has really been at the forefront of shaping how we view obesity, particularly from a metabolic point of view. So please welcome Dr. Ravussin.

Holly Wyatt:

Welcome.

Eric Ravussin:

Thank you very much. It's a pleasure to join you, Holly and Jim.

Jim Hill:

Okay, Eric, big question. Why the heck do we need a new definition of obesity? I thought we had one. What's the problem?

Eric Ravussin:

I think we had one, but we all know that this is not a perfect one because obesity is really excess body fat. And, you know, the BMI is correlated with body fat, but it's far from being perfect. And as you know, I mean, you have some people who can be very muscular, have a BMI of 32, 35, and have 5 or 10% body fat, which don't characterize them as having excess body fat. And I think that Ansel Keys, who is the one who pushed the idea of using the BMI, was right, because it was a factor which is related to corpulence, but not perfectly body fat. And that's why I think we have to revisit that. And we have also to do more of a differential diagnostic of obesity, not just excess fat, but does it damage organs? Does it damage tissues?

Holly Wyatt:

So, can you explain this new classification system? Kind of tell us where we may be going.

Eric Ravussin:

We may be going. That's a good start because, of course, now we published this paper, 42 pages, which is very, very long. I can spend three hours to talk about that here. But it has to be endorsed. It has to be taken. It has to be implemented. It has to be seen if it's cost-effective of treating these people. Now, your question, Holly, is what are the new things? The new thing is, first of all, you need to confirm that this is excess body fat. And what do you do? I mean, of course, you still use BMI. BMI as 30 or 25 is a good start.

Eric Ravussin:

But then you need to either measure directly body fat by DEXA or bioimpedance, but, you know, it's not going to be available everywhere next year or in two years from now. But you can still use other indices, which is waist on hip circumference or waist circumference. And you need two of those above a given cutoff to declare that this is excess body fat. And then, to be more precise in answering your question, Holly, we characterize two kinds of obesity, confirmed obesity, excess body fat. Either you have dysfunction of tissue or organs related to the excess fat, or you don't. And if you don't, it's called preclinical obesity. we argued about the term preclinical because to me, preclinical is rodents before studying humans and so on. But anyway, it's preclinical obesity. And the other one, as soon as you have dysfunction of organs or tissue, or you cannot manage the daily activities of living, then it is clinical obesity.

Jim Hill:

So, Eric, you've now looked at obesity in sort of in two camps. How is that going to affect clinical care management of obesity?

Eric Ravussin:

I think it's going to be a long process because, as you know, Jim and Holly, Holly, you were one of the first physicians really taking seriously obesity. And the training of the physicians now is kind of poor. In medical school, they have two hours of nutrition, for example. Now, we're going to have to train a physician, specialist in obesity, and we are doing that but the implementation is going to be slow. It is going to change because you are going to have to confirm this obesity or this excess fat and after that you are going to have to check about 18 organs and system for adult and 13 for children to see if you have damage of organs or tissue related to the excess fat. And I think it's going to be a longer process and a longer assessment than just taking your weight on the scale when you walk in the physician office with your jacket and everything, taking the height and then say, "Oh, yeah, you have a disease called obesity." Now, clinical obesity is going to be supported by dysfunction of organs and tissues.

Holly Wyatt:

Yeah, I think we've struggled and we finally, I think, have body mass index as something that most, it's a vital sign, you know, it's routinely collected, but it's taken how long to get that implemented? So now you're saying it's going to even have some more steps involved to it. And just for our listeners, so they're thinking about what this, what do you mean by kind of dysregulation or what are those things that they're going to be checking for?

Eric Ravussin:

Yeah. I mean, you can start from the top of the body to the bottom. I mean, you know, So CNS, are there, you know, sign of cognitive function which are known to be influenced by excess body fat? And we know that obesity in general is related to cognitive impairments. Uh, then you go to the respiratory tract and, you know, do you have respiratory problem, which are linked to excess body fat on the chest? Do you have sleep apnea? Then you go to the cardiovascular system. I mean, do you have, uh, epicardial fat? And, uh, uh, then you go to the kidney. I mean, do you have normal kidney function? Then you continue to go down. I mean, you know, reproductive organs. I mean, do you have, uh, PCOS? I mean, do you have, you know, low sperm count? And then you go down skeletal muscle function and all that. And I think it's very well presented, but the implementation is going to be something else.

Holly Wyatt:

I love that you made that list because I think this is a broader list than most of our listeners would necessarily think about. I think they might think of type 2 diabetes. I think they might think about heart disease. They might think, but this seems like this is really broader and is really going to kind of change how we look at this with this new definition.

Eric Ravussin:

Absolutely. I think it's going to be the major thing is really to check all these organs and tissue in a visit or two. There's lab work. I mean, you know, do you have dyslipidemia and hyperglycemia and this kind of things? There is assessment of the organs and functions, and it's not going to be an easy process really to diagnose that. Some of these organ dysfunction are also present in people without obesity. And we have to make sure, you know, I mean, you can have an accident when you are a kid playing hockey and have a bad knee. And this knee, even if you have excess fat, this knee problem may not come from the excess fat, but from an accident in the past.

Jim Hill:

So, Eric, it makes total sense to me. I mean, I think this is a very, very positive move forward to look at those different systems. But what about our listeners who are overweight, obese, They want to lose weight, but they don't have any of these problems. They're like in the sometimes called the healthy obese. They have excess body fat, but it hasn't yet influenced some of these systems. What do we do with them?

Eric Ravussin:

Yeah, we had a lot of discussion on now what is called preclinical obesity, because, I mean, you know, the metabolically person with obesity is kind of a vague concept, and it's mostly related to lipid profile and insulin resistance. But here, I think that you have two kinds of preclinical obesity. Those who are perfectly healthy, none of these signs of the dysfunction of tissues or organs, and very low genetic susceptibility to disease by knowing their family history. And you have some others who have, you know, I mean, a grandfather or mother having diabetes. And here, you're going to have to be more careful. But the recommendation was really following these people, advising them to engage in lifestyle interventions, and then see them on a regular basis. And now, when it comes to those with very high risk of developing these complications, we can already start using obesity medication.

Jim Hill:

So is this going to affect things like insurance coverage? So I could see insurance saying, "Oh, we'll cover obesity, but not preclinical obesity." Or use of the drugs. So physicians say we only use drugs in those with metabolic problems. Is this a potential negative?

Eric Ravussin:

Yeah, Jim, you know, I'm a physiologist and not a public health person.

Jim Hill:

Yeah, but you know everything, Eric.

Eric Ravussin:

I wish and I think by having now a better definition of clinical obesity or preclinical obesity, this is going to be taken more seriously by the insurances, by the public health system. And you know this is going to be a slow process but yes of course some are going to jump on covering that but they are going to want cost effectiveness of treatment and all these kind of things have to be done and I totally understand your question but I really don't know the answer what is going to be the uptake. Is it going to be you have one on eight people around the world with BMI above a cutoff, 27.5 for Asian people, and are we going to treat the whole population? In the States, it's close to 45 to 50 percent in some states. And this is just a question, are we going to bleed through the nose the cost of this disease called obesity.

Holly Wyatt:

Yeah.

Jim Hill:

We've talked about the medications before, and we've had experts on that said, there is no way we're ever going to have the resources to put everybody on meds who need to lose weight. So I think you're right about beginning a way to prioritize resources.

Holly Wyatt:

So I want to go back to the listener, though, and make sure, because they always want to say, okay, what does this mean for the listener now? Should they be asking their doctor different questions based on this framework? What, how can the listener use this new framework to their advantage or how should they be thinking about it?

Eric Ravussin:

Yeah, I wish we are going to educate the population in general. I think in school, and I'm from Europe where we had more education on health and things like that than in the U.S. And I think that education is very, very important. Now, obesity, as you know, as a genetic background, it's been triggered by the environment. It is higher in lower socioeconomic status or classes. It is influenced by geography and all these kind of things. We're not going to reach everyone, but I hope that the people in general will be better educated on, first of all, the risk of obesity. I mean, to me, this is alarming that kids born now have a lower life expectancy than when I was born. And I think it's a catastrophe. And those are things which are going to influence the people because our life expectancy because of obesity and all the associated condition is decreasing life expectancy. But I think it's going to be education. It's going to be the patients going to their physician, asking the right questions, and educating, of course, the physician, like I said before.

Jim Hill:

Well, I think definitely, Eric, it's good to see some change because what we've been doing hasn't been working. We have not had any success in reversing obesity. So I think changing up things is good. What do you think? What do you hear about how the field is going to embrace this? Have you heard major criticisms or the people you're talking to generally positive? What are your thoughts?

Eric Ravussin:

There was some pushback, of course, like all was. There is also, why didn't you include that or why you do that? And of course, this is all a work in progress. I mean, to me, this 42 pages in Lancet is not the end of the discussion. It's the start of the discussion. And I think that we have to learn from implementing that. And I think some in academic world are going to try to implement this approach to the diagnostic of clinical obesity and all that. And it's going to take time.

Holly Wyatt:

I think it's important to realize you're not throwing away BMI. You're adding to it. And I think that's what some of us were already doing. I always said BMI was the first kind of warning sign, but then it didn't, you know, alone, it didn't mean anything. And then I always went to a waist circumference. And then I always, you know, so I like now, I think you're officially saying this is the steps you can take, but it's not throwing away BMI. It's still using that tool.

Jim Hill:

I think Eric's point about education is really right on. I mean, Holly, look here at UAB. We don't train physicians to understand how to manage obesity. We need to revamp our training programs, both for physicians, for other healthcare professionals, and for the public. So it seems to me this is a good move forward, but we still have some work to do on getting people to understand how to use this.

Holly Wyatt:

Yeah, I agree. This is going to be more complex. Like I said, it took us forever just to get BMI. And now we've got multiple things you've got to check and do, but that doesn't mean we can't do it. Although we've been trying to educate doctors on this my whole career. This is actually, this is how I met Eric was through centers for obesity research and education, where we first started to try to get the word out. So here we are again, how many years later doing the same thing.

Eric Ravussin:

Yeah, and to your question, I think, you know, BMI, we had cutoffs. And these cutoffs, you know, 18.5 to 24.9, 25 to 30, and so on, were totally arbitrary. It's not like type 2 diabetes where you have a bimodal distribution of two-hour glucose during an OGTT or fasting glucose and all that. And I think we are going to have to derive cutoffs. And, the first cutoff which was proposed was 30, and we realized that it didn't apply to the Asian population because they have more intra-abdominal fat, and therefore, they went down to 27.5. And to your point, I think, intra-abdominal fat and its measurement or its assessment is going to be very important. But what are the cutoffs for weight-on-hit ratio? I mean, is that 0.85 for women and 0.9 for men? What is the cutoff for waist circumference? I don't know which one you use, Holly.

Holly Wyatt:

I use 35 for 35 inches and 40 inches. 35 for females.

Eric Ravussin:

Oh, you already beat me here with inches.

Holly Wyatt:

I say inches because most of our listeners will understand inches.

Jim Hill:

So I think, Holly, we can sort of conclude this is a good step forward. But back to what Eric said. it's only the beginning. It's not the end. And hopefully there's going to be more discussion and more refinement. But I like that we're changing things up a little bit. So while we've got Eric, and Eric knows a lot about everything, I told him in coming on, the sky's the limit. We can ask him anything. And I want to sort of switch a little bit and talk about, Eric mentioned before, the whole idea of, you know, there are genetic influences and environmental influences on obesity. And Eric has done a lot of really amazing studies, but one of his studies that I love for the simplicity and the beauty is a study he did several years ago where he looked at Pima Indians in the U.S. and in Mexico. Eric, can you tell us what you learned there?

Eric Ravussin:

Yeah, to me, this is a golden study, and this was my field study, if you want. And I was, like you mentioned in the introduction, I worked 14 years as intramural NIDDK in Phoenix, Arizona, just as a researcher working with the Pima Indian population of South Arizona, the Pima Indians. And we know that they have the highest prevalence of type 2 diabetes in the world, the second highest prevalence of obesity, and these people are not there because they are sloth or glutton or they don't exercise enough and eat too much. They are there because of their evolution, their genetic makeup, and all that. And when I was in Phoenix, I met an anthropologist from Tucson, ASU, no, whatever is, University of Arizona in Tucson. And he told me there is a population calling themselves Pima Indians in Sonora. And I had a friend living in Hermosillo, Maro Valencia, and I contacted him and we decided to write a grant with Leslie Schultz to go and visit these Pima Indians in the mountains, the Sierra Madre, I think it is, the mountains in Sonora. And the first time we went there, I think it was in 1989 or 1990.

It took us about five hours for the last 20 kilometers on a four-wheel drive. Now there is a road which has been built between Sonora and Chihuahua. And we did a first collection with Peter Bennett of blood in these people, and we measured their insulin and glucose and things like that on 35 people only. And then we decided now with this primary data, let's go to NIH to have a grant. And we did a study of the entire population that we published. And what we discovered, the unit of BMI, because that's all what we had, was eight to nine units higher, depending of the sex, in the Pimas in Arizona versus Sonora or Maycoba. And the prevalence of diabetes was about six times higher in Arizona. Now, it means, and you know, when did these two populations separate? If it's on linguistic topics, it's like 450 years ago. If it's on pots and pans, it's like 800 years ago. But they still have the same genetic background, but live in totally different environment. And I think this is one of the best examples of the interaction between the environment and the genetics.

Jim Hill:

I love it. I think that point is so brilliant there. And it's like the Pimas in Mexico are still, they still are heavier than you might expect from a non-genetically prone population living that lifestyle, but they're less than the Pimas in the U.S.

Eric Ravussin:

Yes, and it's not malnutrition or anything like that because they are very, very well in terms of nutrition. And I think what we learn, like you said, they are a little bit heavier and so on than non-PIMAs because we are non-PIMAs in the same group of people. And also we did a follow-up 10 years later and now it's creeping up they didn't have electricity they didn't have running water. They were doing all the work manually and all that they didn't have any cars now there is a road like i said going through the village there is about three or four tiendas where you have mostly ultra processed food that they buy and all this kind of thing, and now their weight and probably their diabetes is creeping up.

Holly Wyatt:

Yeah.

Jim Hill:

We'll get them. We'll send our lifestyle and get them sooner or later, right?

Holly Wyatt:

Yeah, that is a beautiful study. I will say I used, that was one of my very first slides. I actually, when I used slides before PowerPoint was that study and I continue to use it today. So it really hits home the fact that yes, there's a genetic predisposition, there's genes involved, but the expression of those genes, the environment plays a big role. So it really just supports both sides, you know, understanding the genetics and understanding the role of environment. And I don't think there's a better study to date than that one.

Jim Hill:

Agreed. So Eric, you're a physiologist and you've spent a lot of years sort of studying human physiology and lean, obese, people with different diseases. So often in the obesity field, especially in the media, the total focus is on food intake. You've studied metabolic processes, and I think nobody's going to say food intake isn't important. Tell us a little bit about what you've learned on maybe the role of metabolism in body weight regulation, sort of separately related, but separately than food intake.

Eric Ravussin:

There's always some doubts about, you know, I mean, a lot of your patients, I'm sure Holly tells you, I have a slow metabolism. That's why I gain weight.

Holly Wyatt:

Absolutely. Yeah.

Eric Ravussin:

Now, is that true? Yes or no? I mean, in our studies, longitudinal studies in Pima Indians, we clearly showed that those with lower metabolism after adjusting for body composition, sex, and age, were more likely to gain weight. But the magnitude of the weight gain was nothing, you know, we could explain only 20% of the weight gain by this slower metabolism or lower 24-hour energy expenditure. And then we went on to do other studies of energy metabolism, and we looked at fat oxidation. And low-fat oxidation was also related to, you know, larger weight gain when you follow up people over years and years. And now the group in Phoenix, under the leadership of Bogardis and Jonathan Krakow, have done a lot of, is there a way of having a challenge to your metabolism, either fasting or overfeeding? An acute challenge, one day.

And can you basically identify a phenotype which is related to weight change, either weight change in very controlled conditions on a metabolic ward or weight change on free living conditions? And I think all these studies tell us, yes, your energy metabolism plays a role.

How much is that? You know, nicotine increase energy expenditure, decrease intake. And I'm still very intrigued by this opposite way of going. Now all the GLP-1 and trying to preserve against what we call the metabolic adaptation, putting glucagon analog or even tirzepatide now. We didn't show that it was protecting against metabolic adaptation. But all these factors are important.

Jim Hill:

I love it, Eric, because for years we studied people in sort of a steady state and we didn't find any differences. It's when we began to challenge metabolism that I think we began to see some of the differences.

Eric Ravussin:

And you remember, Jim, maybe there was an RFA derived by NIDDK and they convened people in Bethesda. And we kind of said that measuring in steady state is not helpful. Let's have challenges to kind of find not biomarkers, but find phenotypes which would be predictive of weight change. And now, of course, you guys have done the weight registry and with Rena Wing and Holly, and you have identified factors for success of weight loss maintenance. You talk a lot of weight loss maintenance being different of weight loss, and I totally agree with that. And I think that we are still learning.

Holly Wyatt:

Yeah. This has kind of shaped my career. One of my very first studies was just studying RMR under a steady state and didn't find a lot of differences. And really, at that point, we're thinking, well, it's not a big player. And now I've said, you know what? It is a big player. It's how we study it and this kind of concept of metabolic flexibility. And there may be some individuals who, under certain challenges, you know, overeating or exercise or lack of exercise or whatever, that may impact their metabolism. And this slow or sluggish metabolism that people talk about might exist just in a little bit different way than I initially thought about it.

Eric Ravussin:

Yep, I totally agree.

Jim Hill:

So, Eric, I want to push you here a little bit to think outside the box a little bit more. You and I are both working on a large study that's focused on looking at precision approaches, precision nutrition, the idea that different people respond to different diets. In your mind, where is this whole, you know, we're really in this era of nobody's the same. Let's understand why people are different. What's your sense on whether or not that's going to help us in the long run?

Eric Ravussin:

Yeah, I think, every time there's something new coming, there are big hopes. And do they really hold the road on the long term? Not always. And I think it's a good initiative to try to basically tailor the nutrition to the genetic as well as environmental conditions of a person towards precision medicine. But we don't know if it's going to work. We know that one size does not fit all. But on the other hand, I think it's going to be more helpful to target different population or group of people rather than really for you because of your genetic, because of your metabolic pathway, you need to eat this and this and that. To me, it becomes too abstract and I don't think we are going to get there. But we're going to learn a lot.

Holly Wyatt:

I love it. So I have a question. So really hot now, time restricted eating, intermittent fasting. What's your thoughts on that kind of new research area?

Eric Ravussin:

Let me go back to the Pima Indians. The Pima Indians, it's very well documented. They have been through periods of feast and famine. And basically, they have been selected, progressively selective to what James Neel in 1962 described as a thrifty genotype. He was very, I still don't understand his first publication, but he came back two or three years later to explain to people like me what it means. And I think that it makes sense. We were not designed to basically eat calories all the time. And my first shock when I came to this country was to see people eating and drinking in their car.

And now, I mean, snacking is permanent. I still think it's very, very important to have a duration of fast. Now you talk about metabolic flexibility. To me, dropping your, you know, going from a low fat oxidation because you are fed, and you have insulin on board, to a high fat oxidation needs time. It's more rapid for some people than others, but you need to leave the time of this switch from high-carbohydrate substrate oxidation to high-fat oxidation. To your point, Holly, I think that it is really important to have Courtney Peterson, who is at UAB. When she was a postdoc with me, she came with this paper in mice from California and said, we need to do that in humans. And it was the first study in humans of time-restricted eating.

Now, how do you do intermittent fasting? You can extend the fast. You can do alternate day modified fast. There are many strategies to that. And once again, one doesn't fit all. When we did, we thought that alternate day modified fast was going to be easier than constant calorie restriction. And we did that with Christa Varady, we had more dropout in the group of alternate day modified fast than in the caloric restriction.

Jim Hill:

We actually like this idea of you need a period of time without calories coming in that allow you to go and get fat out of your fat stores. And the problem is people are eating all day long, so you never go through this period of being far enough away from food that you allow your metabolism to do what it's supposed to do and liberate fat from fat cells.

Eric Ravussin:

Yep. We are putting ourselves in a condition of permanent fat storage.

Jim Hill:

That's right. You go to the refrigerator rather than your fat cells. I want to ask one more question, Holly, before we go to listener questions.

Jim Hill:

Eric, what's exciting you right now about your studies of metabolism?

Eric Ravussin:

Oh, that's a tough one. I mean, to me, this is to, I'm trying now to find easier biomarkers, which would, Holly, I was telling you that a low metabolic rate is associated with weight gain, a low fat oxidation. What are the biomarkers that you can easily assess? And we are doing studies of proteomics and metabolomics. You're going to tell me it's fishing expedition. It is. But hopefully we can find a marker or a group of biomarkers which would allow us to say this person is more at risk of having a low metabolic rate or low fat oxidation and maybe we can help this person. I mean, this is what is exciting me now. I mean, measuring energy balance we have done that all our life. I mean, that's nice. Exercise from the weight registry, you have shown that these people are religious about their exercise. And I like if you can teach people, Holly, in your practice, engage slowly on exercise. One of our colleagues is and I won't tell his name, but he's telling me, I'd rather sit in a cold bath than exercising. And you know, you have to tailor to the people in front of you.

Holly Wyatt:

Well, I love the idea of finding some markers that can help us identify people. What I get excited about. So you find those markers. What I get excited about is then can we do some intervention that changes them? And that's where I think exercise really has its biggest impact, not on just burning more calories, but on perhaps changing whatever that delay in fat oxidation or poor fat oxidation under certain situations, under certain conditions. What can we do once we identify it? That's the first step. We need to identify those people. I love that. And then what do we do to reverse it, improve it, you know, whatever. So if we can't do anything about it, I'm not as excited about identifying it. But I'm excited about identifying it if then we think we can really tailor a treatment to it.

Eric Ravussin:

You're right. And I spent some time in big pharma. When I was there, he was all, you know, GPCR receptors that you target. But obesity and weight regulation is not one or two or 10 or 50 genes. It's really a complex physiology. And I think the approach of using peptides, natural peptides. We still don't know what they do. We know that they impact the gastric motility. I mean, the GI motility. We know that they impact here. We know that they are independently of weight loss doing a lot of good things, but that's because we don't know exactly what they do, but they are part of the physiology. And I remember I was on a scientific advisory board for amylin, and they had all these peptides lined up. And now, of course, we have, you name it, GIP, glycogon, amylin, back with CagriSema and all these kind of things. I mean, I think you are right, identifying the people, but then the next step is what do you do with that?

Jim Hill:

Holly, let's do a couple of questions from listeners. Do you want to take one?

Holly Wyatt:

Sure. Let me see. we have a couple that will work. You know, everybody's interested in these GLP-1, the new medication. So we get a lot of questions related to that. So if they have someone kind of, if I have this new definition, do you think that the, I can get the medication? Will the insurance pay for it if, with this new definition, do you think we're going to move in that direction? They're already asking that.

Eric Ravussin:

Yeah. And we already talked a little bit about that. I think it's going to take time. The Lancet Commission, it was 56 people, has to continue to work on that. We have to welcome the criticism. We have to adjust the definition as well as the diagnostic of clinical obesity. But at the end, it's really to give a benefit to the patients with obesity because they are going to need treatment. We're going to start with some intensive lifestyle intervention like you have done, and then you introduce drugs. I think it's part of a global approach to the disease of obesity.

Holly Wyatt:

Yeah. So I guess not yet, but I would encourage them to talk to their doctors about it because now I think that the patients can influence and help educate doctors. When we're seeing that. When I started, that wasn't the case. But now patients go to their doctors and say, here's what I'm hearing. And so we may not be there yet, but I think the patients, our listeners can help push this new definition and make everybody more aware.

Jim Hill:

Okay, I'll do one. Here's a question. My BMI is under 30, but I've been told I have obesity-related health risk. Would I qualify as being obese under the new definition?

Eric Ravussin:

Yes, because it's very likely that you have abdominal fat. I'm using now a database from all of us, Jim, that you know, to try to basically pin down the prevalence of preclinical and clinical obesity in about 300,000 people with all the codes, the disease codes, and everything. And yes, I mean, this person would be entitled to treatment and with pharmacology, depending also of the family history and, you know.

Jim Hill:

Good, good. All right, Holly, you know what it's time for?

Holly Wyatt:

Oh, yes. We call them vulnerability questions. This is where we get to ask you something you've got to share that might be a little bit vulnerable, Eric.

Jim Hill:

So I'll start. Eric, if you were king of the world, and I'd vote for you for that, what steps would you take to reduce obesity in the population? Notice I don't say one thing, because I think we all know that one thing won't work. But in thinking about some of the things that we might be able to do as a population, any thoughts?

Eric Ravussin:

Yes, I have a lot of thoughts, but they are not very welcome in general.

Jim Hill:

We love those. I can't wait.

Eric Ravussin:

And, you know, like we said, I mean, the gene pool has not changed. What has changed is the environment. When I saw the curves starting in the 80s going like this, I used to say, well, it's when Reagan came to power. But it was not that. It was really the change in environment. And I think that we have to be more serious in terms of public health to try, first of all, to control better the nutrition companies and ultra processed food. And, you know, they do it in Chile, they do it in the UK and all that. And I think we have to be more serious to do it here. Now, reversing the environment, when I went the first time to Mexico to Maycoba, I took pictures.

I brought back data and I was at the tribal council in Sacaton southeast of Phoenix to present the data. And after a long silence, the chair of the tribal council told me, "You think I'm not going to give a bicycle to my kid because it's bad for him? He'd rather he should walk?" And I said, no, absolutely not. But we have to reverse some of the environment which has been conducive to the increase in the prevalence of obesity.

Jim Hill:

Yeah, I think you're right. We want people to change their behavior, but unless we reduce some of the pressures of the environment, it's extremely difficult for people to do that.

Holly Wyatt:

But I think it's going to be looking for creative ways to do that. It's not about going back, because that's not going to happen. We're not going to get rid of video games. We're not going to get rid of some of the things out there. It's how can we re-engineer it based on where we are to put some more movement and change some of the food environment, etc.

Eric Ravussin:

Yeah, but the parents have a responsibility also. You’re saying we're not going to go away from video game, but we can put limits instead of eight hours a day. I mean, in China now, it seems that they are putting limits on the access to video games and all that in childhood and all that. It's really a tricky situation where you basically interfere with the privacy and the freedom of the people. But changing the environment, you know, each time I go to Europe, I have many more steps than here.

Holly Wyatt:

Yeah. I guess I'm more of a carrot, not a stick person, but maybe a little bit of both would be helpful. So I got another vulnerability question. I've been waiting for this one. Are you ready?

All right. What has been one of the most humbling or surprising lessons in your research career? Something maybe you got wrong or that shocked you or humbling. As scientists, I would think we've all had those.

Eric Ravussin:

We do, but I mean, I don't have one experience, but, you know, whenever you kind of push a hypothesis and you think that you have all the data supporting the hypothesis, you have to be humble and say, let's have other people putting their hands on. And, you know, my publication in New England of low metabolic rate predicting weight gain has been challenged. The metabolic flexibility, you have people at UAB challenging what it is or the metabolic adaptation, I'm sorry.

Jim Hill:

Yeah.

Eric Ravussin:

And you have to be a little bit humble and accept also some of the criticism. Some of the criticism comes because they didn't use the right equipment or they didn't do the right design. I didn't do the right design and all these kinds of things, but I don't have one example where I was totally wrong, I think.

Holly Wyatt:

Okay.

Jim Hill:

Okay. Fair enough. Okay. We need to wind up here. But Eric, give our listeners one takeaway from what we've talked about today with the new definition of obesity. What's one thing that's important for them to take away from this conversation?

Eric Ravussin:

I think we are all concerned as society and individuals by this disease called obesity. And we should really take it seriously. Like I said, it's decreasing life expectancy. It's making the life of people miserable. There is still the stigma of obesity. And I think we have to educate the population, the physicians, the treating groups, about obesity and how to tackle this problem. Part of the responsibility also goes to public health policies and things like that. Transfat, why did it take five more years in the US to ban transfat compared to Europe? There's a lot of things that we can do without totally shaking the boat or whatever. But I think we have to educate people. They have to go to you, Holly, and ask the right question. You are educated for that, but your colleagues may not be. I think this is our responsibility and I hope this commission report is going to start to do that.

Jim Hill:

Well, Eric, thank you so much. This has been a very enlightening conversation. We appreciate your time.

Holly Wyatt:

Yeah, this has been great. I love being able to ask these questions and really get your perspective because this has been eye-opening for me in many ways. So thank you so much.

Eric Ravussin:

You are very welcome. And I'm so glad that I can share that with you because you are part of the game and you do similar studies.

Holly Wyatt:

Absolutely.

Jim Hill:

Okay. So if you enjoyed today's episode, be sure to subscribe, leave us a review or a question. We're here to bring the latest science and real-world strategies for weight loss and beyond. Until next time, keep playing the long game. Thanks, everybody.

Holly Wyatt:

Bye, everybody.

Jim Hill:

And that's a wrap for today's episode of Weight Loss And. We hope you enjoy diving into the world of weight loss with us.

Holly Wyatt:

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Jim Hill:

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Holly Wyatt:

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