Speaker 2
And I have to say, to interject, you've played a huge role in the way that I think. I don't know if you know that, but I'm sure you do, because I do call you freaking out on numerous occasions. And you always say to me, number one, science is a science of uncertainty. Yes,
Speaker 1
absolutely. And
Speaker 2
you always challenge me. Why muscle? Why this? Yeah,
Speaker 1
you're absolutely correct. When we say in science and now research that something is happening, we always say that with a certain level of being uncertain, which means that it might not always happen this way and it might not always happen for everybody in the same way, right? So going back to the workshop, I consider myself relatively, I mean, nobody can really be completely neutral, right, in this debate, but I'm one of the people who kind of understand the arguments from both ends. And then I took on the task of putting all these discussions into a paper that everybody would agree on, and then getting it out there for the public to kind of read.
Speaker 2
And this... Oh, sorry. Go ahead. I'm sure you're going to tell us the arguments and why... Well, I was about to tell you the process. So it took us
Speaker 1
many, many months and drafts and back and forth because everybody needs to agree on the final version of the paper and all the actual words, not just the meaning, but we had back and forth in terms of trying to find the correct words to portray what these people believe and agree on. So that task was not particularly easy so it was one of the more difficult papers for me in terms of getting together all the authors to agree on writing a paragraph and sometimes it took us forever to write the paragraphs. But thankfully it all culminated in a nice paper that was published well, and now it's out there.
Speaker 2
And give us the overarching themes of what people disagree on, what people agree on it. And this really was, what is the cause of obesity? Is this a energy balance issue? Is this a carbohydrate insulin issue? And I have to say, looking at the authors, when I saw this, I couldn't believe it. As you'd mentioned, you have Kevin Hall, you have David Ludwig. There are people that have drastically different views and they're all very well respected.
Speaker 1
Absolutely, yes. Absolutely. There's no question about this. And if you look individually in the literature, there is evidence to support arguments on both ends, right? I mean, that's the reality of human research. But going back to the two different ideas or two different models, let's say, that these two camps represent. One of them is, I would say, the one that we were all pretty much brought up with and the one that we are all more or less familiar with, which is the energy balance model. And what this hypothesis states is that obesity generally develops as a result of people eating more food, more calories than the amount of calories that they burn, right? And the main reason why this happens is that the modern food environment, predominantly the modern food environment, and the characteristics of the modern food supply what they do is that they facilitate overeating below the level of your conscious awareness so you eat more without even realizing it right so that's the general idea so the excess calories regardless of whether you eat more carbs or more fat or more protein when you do not burn them the body typically eventually tends to convert them and store them as fat, right? Yes. So you have an expansion of adipose tissue. So in the energy balance model, overeating or positive energy balance precedes the adipose tissue expansion and the development of obesity. So that's what I would say most textbooks on dietetics and nutrition and obesity kind of portray as well. And
Speaker 2
that's what we've all been taught.
Speaker 1
All right. Correct. Correct. So to try to give you an analogy, right? Imagine that you go, let's say on a Monday morning, you go with your car to the gas station and you put 10 gallons of gas, right? And then you take your car around and as you go around, of course, you burn some of this gas, right? So at the end of the week, by Sunday night, you pretty much are empty. So the next Monday morning, you put again 10 gallons of gas and that goes on and on. But on every Sunday night, you are always at zero. You are always empty, right? So you are in an energy balance in this case but imagine now that you know you decide to change gas station right and this new pump that they are using it kind of works a little bit in your favor meaning that it reads that you are dispensing 10 gallons, but in reality, you are dispensing 11. Okay. So now that you go around your daily life and do whatever you do during the course of the week, but now at the end of the week on Sunday night, you are left with one gallon in the tank, right? Now you think, however, that you are left with nothing. So next morning you put again another 10 gallons of gas, as you think, but in reality, another 11. So if this goes on, you accumulate one
Speaker 2
gallon of gas every week.
Speaker 2
is fat or this gallon, we're talking about fat, are we talking about calories? Correct.
Speaker 1
If you do not, let's say, strive to do something with physical activity, most of the excess calories are being stored as fat. Nonetheless, as the time goes on and your weight increases, imagine this as a form of passive training. So obesity is also associated with an increase in lean mass and muscle mass because you need additional muscle to carry the much more weight of your body, right? So most of the weight gain is fat, but part of it is lean mass and muscle. Lean
Speaker 2
mass and muscle, but that, and I'm just going to mention this and you and I certainly discussed this. It doesn't necessarily
Speaker 1
reflect the health of that tissue. Absolutely. But I will get back to that. We can get back to that. So this is the energy balance model. ultra-processed foods which are calorie-dense, and they have a lot of other ingredients in them that, you know, kind of mask or saturate the ability of our brain to understand how much we eat. That's the general idea. So it all starts with eating more than what you need in the energy balance model. And then the end result is an expansion of adipose tissue and obesity. And muscle. Correct, and muscle to some extent. So also energy expenditure goes up along these lines, right? So the total energy expenditure of the body goes up simply because you have a larger body right now. So for any sort of activity you do, you burn more calories, right? Now, the other model that is, let's say, the contender is the carbohydrate insulin model of obesity, right? And that model suggests that the primary defect is not really the brain that does not understand how much you eat, but it's something that happens in your body, the peripheral organs, say in the liver or in the adipose tissue or the skeletal muscle. So the handling of the incoming nutrients and the incoming food is changed. And it's changed in the way that you cannot utilize all the calories that you ingest for doing all sorts of things that you want to do. Right. To put it back in the analogy of the car. Let's assume now that the pump is functioning correctly. So you put in 10 gallons, but the tubes that transfer the gas or the fuel from your tank to the engine, they have leaks. So you cannot take advantage of all the fuel that you entered in your car, right?
Speaker 2
Does it make sense? So it's almost chicken or the egg. What came first? Is it, are we over-consuming food and then getting an increase in adipose tissue, right? It would be considered hyperplasia. Would that be considered hyperplasia
Speaker 1
or? Well, hyperplasia and hypertrophy refer to two characteristics, ways by which tissues typically increase and grow. Hyperplasia is that I am making more cells. And if you are talking about adipose tissue hyperplasia, then you will make more adipocytes. So the number of cells increases.
Speaker 2
Hypertrophy means that the cells themselves grow bigger. Right? And is that what happens when someone... Typically both
Speaker 1
happen in obesity, although hypertrophy is more pronounced. So typically you develop larger antipocytes rather than more cells when you develop obesity in your adult life. But going back now to the carbohydrate insulin model, so what this suggests is that since your body cannot, let's say, take advantage of all the calories that you just ate, it signals to the brain and it tells your brain that, you know what, I need more food. Right? Even if you have it in your body, but you just can utilize it. the brain then what it does is that it tells you that you either need to burn less so it will make you make your energy expenditure lower to match what you have or what you think you have or most commonly it will make you overeat so in the carbohydrate insulin model the cause that the the causal chain reversed, meaning that you start first from depositing more of the ingested calories into fat, and then this leads you to overeat. I see. So in the carbohydrate insulin model, it's something that happens in your periphery that then signals the brain to eat more whereas in the energy balance model is quite the opposite right the first eat more and then you deposit those calories into fat i see and and as you mentioned the chicken and the egg, that's something that is extremely difficult to dissect in humans, right? Because we would have to take people who have normal body weight and then perhaps overfeed them for a prolonged period of time until they become obese and see what comes first, right? But this is not possible in humans to do. The best model that we have so far for weight gain and obesity is these overfeeding studies where we experimentally feed people more than what they need. But this is typically a very large extent of overfeeding. So let's say we feed them 1,000 or 2,000 calories per day more than what they need for a few weeks, right? That's not typically how obesity develops. Nobody goes to bed being lean and wakes up the next morning being obese. Typically, obesity develops by, at least that's what we think, is by eating a few more calories than what you need on a daily basis for years. we do not have really a very good model for human obesity in research. We
Speaker 2
don't. I want to restate that because many of us who are not academics, and as you know, well, you might not know because you're not on the social media circuit or sphere, but there's a lot of information out there. And the discussion is stated in ways that it seems as if these are absolutes, that this is, we'll review literature, and then you'll have influencers or scientific educators then speak to the public. And a fundamental concept is that I think it's important to highlight is we don't actually have a good model of obesity to study. And the foundation of the work is built on the best that we could do. Is that fair
Speaker 1
to say? Yes. And I would say, you know, all the, so one thing with the, with the social media and the influencers and all these arena is that, you know, you have to always defend or try to convince people why things are not as stated in the social media. You know what I mean? And that's a little bit tiring. Explain
Speaker 2
to me a little bit more. I agree with you. So, you
Speaker 1
know, there is a lot of the new trends and the fads and the diets that come up from time to time stem, for instance, from studies in animals or from a single study in humans. And their results are very good because they are very good to make a headline. But nobody really digs deeply to understand the limitations of the study. What does one study mean? Nothing really. Right. There is no definitive study. Research in humans, at least, or generally speaking, science, you have to consider every study as a little brick, and we are trying to build a building. So if you take a brick and you focus on that brick, and you tell me, look, the story that brick tells you, it's really relevant for the whole building, right? So that's kind of the analogy that I try to give to my students as well when it comes to a single study versus understanding what the whole literature shows. Now, coming back to obesity in herements, for instance, right, to give you an example, in the overfeeding studies, we are very successful. We take people in the lab, we can overfeed them, we can make them gain 5, 10 kilos, right? But remarkably, when we send them home and the study is finished, the majority of them within a few months lose that additional excess weight effortlessly without even doing anything according to their testimonials. So this is completely different to the model, to the real obesity that we have in real life where people struggle to lose weight, right? Yes. So how good of a model that is? Probably not so good. And of course, there is no point in discussing the animal studies because then that's also different species, right?