In this episode, I’m speaking with nutrition expert Alex Leaf, someone you may remember from past episodes.
I’ve been lucky to work closely with Alex for the past few years—he’s a highly informed researcher and science writer, and he’s rare in the world of nutrition. He’s extremely scientifically literate and able to break through popular trends to provide practical and accurate interpretations of sometimes complicated research.
I’m really excited for you to hear our latest conversation…we cover a lot of ground, including what the research says about weight loss and calories in/calories out, low-carb versus low-fat diets, the best diet for fat loss, how a low-protein diet affects life span, and, one topic I know you won’t want to miss; Alex’s opinion on a recent publication showing that time-restricted eating leads to a much higher risk of death from cardiovascular disease…is this true?
To celebrate Alex’s appearance on the podcast, I’m offering The Fat Loss Blueprint for $200 off the regular price of $497. Alex and I collaborated on creating this program, and it’s an evidence-based, no gimmicks approach to very effective fat loss.
Click the button below to enroll in The Fat Loss Blueprint for only $297 with the code “Alex” at checkout.
Links to studies discussed in this episode
- Acylation stimulating protein (ASP): https://pubmed.ncbi.nlm.nih.
gov/10355026 - Japanese become fat after emigration to the US and introduction of Western foods: https://pubmed.ncbi.nlm.nih.
gov/2031486/ - Kevin Hall meta-analysis: https://pubmed.ncbi.nlm.nih.
gov/28193517/ - Fat vs carbohydrate overfeeding: https://pubmed.ncbi.nlm.nih.
gov/7598063/ - Holiday overeating explanation of carbohydrate vs fat: https://pubmed.ncbi.nlm.nih.
gov/29399253/ - DIETFITS study: https://pubmed.ncbi.nlm.nih.
gov/29466592/ - Minnesota Starvation Experiment: https://psycnet.apa.org/
record/1951-02195-000 - Energy flux: https://pubmed.ncbi.nlm.nih.
gov/28531421/ - Energy flux: https://pubmed.ncbi.nlm.nih.
gov/15240648/ - Herman Pontzer: https://pubmed.ncbi.nlm.nih.
gov/26832439/ - Women’s amenorrhea: https://pubmed.ncbi.nlm.nih.
gov/34164675/ - Protein stuff: https://alexleaf.com/why-
protein-restriction-for- longevity-makes-no-sense/ - TRF and CVD study: https://www.abstractsonline.
com/pp8/#!/20343/presentation/ 379
Table of Contents
In this podcast, Alex and I discuss:
- Should you pay more attention to calories or hormones when it comes to weight loss? We deeply discuss the energy balance hypothesis versus the hormone/insulin hypothesis debate currently raging in the nutrition industry.
- The extreme importance of different types of research in backing an idea or concept…not all research is created equally, and can easily be misunderstood and misused to inaccurately prove a point
- The amazing complexity of the human body and nutrition science! For instance, why can some cultures eat nearly 70% of their calories as insulin-stimulating refined carbohydrates yet still experience healthy metabolism?
- The number one reason people rapidly lose weight on a low-carbohydrate diet, and it’s probably not what you think
- If a low-carb or low-fat diet is better for fat loss, based on the results of thorough, well-controlled research…including genetic patterns
- Alex’s top 2 easy-to-implement nutrition recommendations for how to maintain optimal body composition and health over your life
- The real reason why extreme diets often lead to weight loss…it isn’t food sensitivities, reactions to plant “toxins,” or the healthiness of plant-based eating patterns
- Does the body really go into “starvation mode,” leading to plateaus in weight loss after long periods of calorie cutting?
- Our favorite strategy for losing weight and building lean mass that actually involves eating MORE food!
- The idea that you can only burn so many calories per day and how this overlaps with overtraining syndrome…does the research really show that there’s a cap on how many calories you can burn?
- Does a high-protein diet shorten your life?
- Finally, Alex’s interpretation of a recent publication that found a strong connection between a restricted eating window and death from cardiovascular disease
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Transcript
Ari: Alex, welcome back to the Energy Blueprint Podcast. I think this has got to be the 5th, 6th, 7th time that you’ve been on here.
Alex: Yes.
Ari: For those that are just tuning in who haven’t seen previous episodes with Alex, Alex works very closely with me. He is sort of one of my– he’s a co-author on my book, Eat for Energy, and he and I work very, very closely together in designing programs, in the programs we teach, the content we write, especially on nutrition-related topics and metabolic health-related topics. He’s a whiz on these topics. He is one of the most knowledgeable people in the field of nutrition that I’ve ever known and one of the most skilled researchers and most scientifically literate people that I know in that realm. I’m very grateful to call him a close friend and very grateful that I get to work with him so closely and that he’s such a great help in the books that we write and the content we produce together. Given that we’ve worked together for– jeez, how long have we worked together? Five or six years now?
Alex: Yes. Yes, I think so.
What is energy balance?
Ari: We’ve worked really closely together for a long period of time. We know each other’s work and minds very well at this point, and we’ve had a very fruitful collaboration where we’ve had the opportunity to learn from each other, co-develop ideas together, and build literally chapters of books together. Because I respect him so much, I wanted to invite him on the podcast yet again to talk about some of his areas of expertise and to teach all of you guys some really cool novel stuff, I think, and novel perspectives on topics that you certainly have heard before. We’re going to continue that theme. In this podcast, we’re going to be talking about different myths that are out there, nutrition myths, health myths, hormone myths, and things of that nature. Without any further ado, Alex, let’s talk about energy balance first. First of all, can you define what energy balance is for people? Then we’ll go deeper into that from there.
Alex: Energy balance- and that’s funny you start with this one because this is a really big topic. It’s still very controversial, not just in the layman area, but in the scientific fields itself. Energy balance at its simplest form is basically saying that however much energy your body takes in through the food that we consume needs to match however much energy our body expends to get through the day. That includes things that keep us alive, supporting physical activity, everything of that nature. If you’re in balance, then your body weight and your body fat levels should stay relatively stable over time. If you’re in a deficit where you expend more, then over time you can expect to see a loss of your body mass. If you’re in a surplus over time, you’ll gain body mass.
This theory, the energy balance theory, is basically going up against primarily a hormone-centered theory where individuals supporting that will say, “Well, it comes down primarily to insulin, which is the primary fat storage hormone.” How your body responds to insulin signaling will determine what happens to your body fat levels. Individuals supporting this idea, it’s called the carbohydrate-insulin model of obesity, will typically advocate for low-carbohydrate diets because that keeps insulin the lowest. They propose that this is the best way to maintain a healthy body composition and not gain fat mass.
Science 101 when it comes to fat loss studies
Ari: It’s interesting. We’re in 2024. My book, Forever Fat Loss, which spoke in great depth about this subject, came out exactly 10 years ago at this point. It’s funny because I feel like this is old news. I feel like this topic has been clarified and debunked literally more than a decade ago. Yet it’s still so prevalent, and there’s still such widespread misconceptions about it. The basic idea to recap this frame that you’ve presented so far, calories in versus calories out. There are people out there still who continue to present things from this very simple frame. It’s just calories in, calories out. That’s the only thing that matters. All you have to do is count your calories, restrict your calories, count how many calories you burn.
f that math favors calories out, meaning calories out are higher than calories in, you lose weight. It’s that simple. That’s sort of the entirety of that frame. On the other hand, you have people out there still today who basically say, “All those people talking about calories in, calories out, that’s a bunch of nonsense. Really, it’s hormones and it’s insulin, which is a fat-storing hormone. Sort of by its nature, the presence of this hormone creates a biochemical milieu that favors fat storage and or blocks fat burning. Therefore, as long as you are spiking insulin levels or insulin levels are high as a result of eating carbohydrates, therefore, you will be in a hormonal biochemical milieu that makes fat loss impossible or that makes fat gain likely. All those people talking about calories in, calories out, that’s nonsense.
Really, it’s hormones and especially insulin as a result of carbohydrates that are controlling and regulating fat mass.” Okay, so those are the two schools. What are the- it’s interesting how easy this is to test and how many times it has been tested. Take people through like sort of science 101 of how scientists would set up research to test one theory versus another and how we can discern which theory is correct or mostly correct.
Alex: Yes, so there is–
Ari: I should say hypothesis instead of theory here, but yes.
Alex: Yes, so there’s several layers to scientific testing that you can take when you’re approaching a problem. Individuals who are proponents of the carbohydrate-insulin model will typically focus in very heavily on mechanistic data. This is a very important layer of scientific research because this is the layer that explains why something happens. What is going on within the body at a mechanistic level that is explaining the outcomes we observe in the real world? I don’t want to give the impression that mechanistic data shouldn’t be looked at or is crappy data or anything. It’s super important for understanding. When you do focus only on mechanisms like insulin promotes fat storage, you run into two problems. The first is that our bodies are really complex. The way things might play out in a petri dish or just from biochemical reactions or hormone signaling might not create a full picture. Because if one thing happens in the body, there’s probably a bunch of other things that are happening as well.
Ari: Yes, I’m to the point now where when I see a supposed health expert extrapolating complex human health outcomes from mechanistic research, I almost find it laughable just because at this point, I’ve been doing health science since I was a little kid, roughly three decades now. I cannot count how many times I have seen mechanisms, proposed mechanisms of how things work in the body be proven wrong, including how many times I have been wrong based on extrapolating from the mechanism level. I’ve learned the hard way as a result of being wrong and seeing so many people be wrong, extrapolating from the mechanism level that you really have to look at outcomes because very often the complexity of human physiology is way greater than our simplistic conceptualization of these mechanisms would suggest to us.
Alex: Yes, the pharmaceutical industry is a great example of that, actually, because when you think of all of the drugs that they produce and how many of them actually come to market, very, very, very few. It’s because the only approach that they can take where they can make money is let’s create a drug that interacts with a specific biochemical pathway. That’s going to be, that’s going to do great things. Then, 99 percent of those those drugs never make it to market because the animal dies or it’s just not feasible or it didn’t play out the way that they thought it would.
Ari: Even when decades have been invested in it and tens or hundreds of millions or maybe billions of dollars have been invested by pharmaceutical companies to develop drugs and even if it successfully makes it to market, like certain of these Alzheimer’s drugs as a good example of this where they extrapolate from the mechanism level. They say, “Oh, these amyloid plaques, these beta-amyloid plaques in the brain are associated with Alzheimer’s disease. Let’s figure out the biochemistry of how these plaques form and develop a drug that blocks the development of these amyloid plaques.”
They did that successfully and then they discovered when they actually measured hard outcomes of symptom and disease progression and death that although these drugs were effective in blocking the formation of amyloid plaques they actually accelerated the progression of the disease and very often many of these drugs were actually linked to accelerated rate of death or have very serious side effects. Basically, they discovered that it isn’t actually this mechanism it isn’t actually the formation of beta-amyloid plaques that’s driving the progression of the disease.
Alex: Yes, exactly. I mean that’s one issue. The second issue is when you get so focused on a mechanism, you lose sight of other relevant mechanisms and so people who say insulin is the fat-storage hormone, I always love to bring up a thing called acylation stimulating protein or ASP, and this is a protein that your fat cells create in response to, it requires fasting levels of insulin so insulin levels of two to three is what this requires. This protein is perfectly capable of sucking up energy from the bloodstream carbohydrates and fats and then turning them into triglycerides for storage in fat tissue. Even if you never raised insulin on a low carb diet, this protein would be active and it would be facilitating fat storage and the only time this protein cannot work is in type 1 diabetes because there is literally zero insulin. It’s not appropriate to extrapolate from that disease state at all when you’re talking about how insulin works in a non type 1 diabetic body. That’s a mechanism that directly counters this narrative that is pushed when you focus only on insulin.
Ari: Yes, agreed, and another maybe easier to understand example is to distinguish between something that’s necessary for something to happen, for something to function a certain way versus what regulates the function of that thing. A car, I always use the example of a car as a good example, where if I remove the spark plugs from the car or the crankshaft or the pistons or any number of other parts on that engine or even something like the wheels, the car cannot function, cannot drive down the road but none of those things I just mentioned regulate whether or not that car is driving down the road and how fast it’s going and whether the accelerator is being pressed or the brake is being pressed. There’s a different-there’s many parts that are necessary for that car to function but those things do not regulate the function of that car.
Alex: Yes, exactly.
The confusion around low carb diets
Ari: Take us back now to what– Well, let’s go back to science 101, okay, how do we test these two different theories?
Alex: Yes, so okay, so the mechanism explanation is one layer and now we can start testing like yes, insulin promotes fat storage. It’s not the only thing that does, human bodies are complex. There’s technically three but let’s focus on two other ways we can test this. One of them is observational data, let’s look at people who eat the most carbs and let’s see if they’re fatter and this research universally shows that is just not the case. In fact, it’s often dietary fat that’s associated with obesity. Not saying fat makes you fat, I’m just saying that when we look at populations with the highest intake of carbohydrates, they tend to be very thin compared to populations with lower carb, higher fat intake.
Ari: Give an example because certain people who have been maybe influenced by some of the low-carb schools of thought might be skeptical and saying, “Well, don’t Americans eat the most carbs and aren’t they the fattest?”, or something to that effect. What’s an example of a population that eats a lot of carbs that isn’t extremely obese?
Alex: The Japanese and many Asian countries in general traditionally have a carbohydrate intake of 70% of their calories because their diet is based around white rice, which is funny because now it’s not even just carbohydrates, it’s like the most insulin-stimulating refined carbohydrate that you could get and they tend to have BMIs that are in the lower end of normal and it’s-it wasn’t until Western food was brought into their countries when– It wasn’t until that point that obesity rates and diabetes and metabolic problems started to increase. Another example of this are indigenous hunter-gatherer societies across the world but especially in tropical regions, the Amazonians they’re the Hadza, the Tizimay and the Kidavans all have high intakes of carbohydrates that come from tubers and berries and honey and their rates of obesity and metabolic disease are like zero. There’s a lot of reasons why their rates are zero but the point remains that they have a diet based around carbohydrate, often simple sugar carbohydrate or starches and they just, they are not fat. That’s the second layer.
Ari: Okay, so let’s say-to simplify, let’s leave out the complexity of the hunter-gatherer tribes, and let’s talk about the Asians because there is some data, I believe, I haven’t looked into this in a few years but I think that there is some data to support the idea that there is a genetic predisposition for leanness and some protection against obesity among East Asian populations. Maybe we can say, “Oh well, yes, those East Asians don’t count because if Caucasian people or people of African descent or people from other ancestry of different parts of the world were to eat those same East Asian diets that are high in white rice, they would really get fat. It’s just that those East Asians have genetics that keep them lean.” What other body and in general observational data of this kind is generally used to basically form a hypothesis about what’s going on which is then later confirmed in other kinds of research, which you’re going to speak about next.
Alex: Yes, and saving the best one for last is intervention research, preferably randomized control trials. These are basically where you take two groups, two or more groups of people that are equivalent in all of their baseline demographics, their statistics to help eliminate as much confounding as possible. Then you have one group do one intervention and you have another group do something else. It could be just maintaining their usual habits, it could be another intervention entirely. Then you compare the outcomes between them. In the context of low carb versus low fat, if carbohydrates stimulate insulin and cause fat gain then we should expect that groups that are randomized to eat high carbohydrate diets over a period of time will gain more fat mass than groups randomized to eat low carb high-fat diets over that same period of time, because the effects on insulin will be so much different.
Ari: In a way, this is like really, really simple to test this, these two schools of thought. Because at the end of the day, it boils down to a very simple scientific experiment. Give two groups of people, as you said, who are essentially the same, controlled for all the differences and potential differences between individual people. Give these two groups the same exact calories in their diet but radically different amounts of carbohydrates such that they will have very different levels of insulin. You control for calories but you have one group with low insulin levels, the low-carb group after meals, and another group, same exact amount of calories but very high insulin after meals. That simple model basically is a way to very definitively tell you whether it’s calories or the insulin that is regulating whether somebody loses or gains fat.
Alex: Exactly. Overwhelmingly, the data on this topic points in the direction of, in the real world, there’s no meaningful difference. In the real world, where you let people live their normal lives and you tell them to eat low-carb or low-fat diets, at the end of six to 12 months, they’re going to have the same outcomes for body composition.
Ari: Well, okay, Alex, let’s go to the meta, let’s go to the, let’s come back to the real world studies because there’s more complexity there. There’s more nuances to dig into. Let’s go into just like this simple experimental setup, which has been done. These are the metabolic ward studies from Kevin Hall and then there were some previous ones. I think going back, it’s been a few years since I dug into this data, but I think going back maybe even to the 1980s or something were the first metabolic ward studies that tested this. This has been repeated again and again where they do this exact experimental setup. They precisely control for exactly how many calories a person consumes with radically different levels of carbohydrate and therefore insulin. What do those studies show?
Alex: Kevin Hall published a meta-analysis on 31 of these exact types of studies, I think in 2018.
Ari: These are called metabolic ward studies for listeners.
Alex: Yes, where literally everything about the participants is controlled, not just what they eat, but also their physical activity levels. Everything is as equal between the groups as it could possibly get. What this meta-analysis showed is that eating a low-fat diet resulted in about 16 grams of fat loss more than eating a low-carb diet and a daily energy expenditure increase of 16 calories per day. These are very, very tiny numbers that have no real-world relevance, but it shows that in fact opposite of what the carbohydrate-insulin model would suggest, a low-fat diet seems to have an advantage for body composition.
Ari: Just so that little bit doesn’t get blown out of proportion, because as you said, those differences are at the end of the day, so minute that they’re almost immeasurable. That you and I don’t get accused of shilling for the, who knows, the low-fat processed food industry or something, we’re not even necessarily proponents of a low-fat diet. I don’t eat a low-fat diet.
Alex: Yes, me either.
Ari: That particular metabolic ward study did show a slight advantage for that. Then the overall body of evidence, basically, if we leave out any minor differences, basically shows at a given level of calories, they provide the exact same amount of fat loss, whether you have high carbs stimulating lots of insulin after those meals or extreme low carbs. I think some of these metabolic ward studies even were like as extreme, the differences were as extreme of 75% of the calories coming from carbohydrate versus the other group was 5%, like almost zero carbohydrate.
Alex: Yes, exactly.
Ari: Still, at those equivalent levels of calories, it was the exact same amount of fat loss, correct?
Alex: I’ll mention too, those studies equate protein also. It’s not a difference due to protein because when you go low carb, you tend to eat more protein because it’s more readily available. These metabolic ward studies controlled for that and made sure protein was the same between the groups so that it wouldn’t interfere with the results.
Ari: These are metabolic ward studies that were in the context of a calorie deficit that were designed to provide fewer calories than what a person’s burning so that you do get weight loss. You do see weight loss in both groups. That amount of weight loss, again, was equivalent in the different groups regardless of carbohydrate and insulin levels. That basically, this is science 101 for debunking the notion that carbs and insulin are regulating fat storage. Now, let’s go into maybe metabolic ward studies.
There are some, if I remember correctly, that were the opposite, where they were calorie surplus metabolic ward studies. Have you looked at those? Again, it’s been several years since I dug into this research, but–
Alex: Yes, so yes, it’s been a bit since I’ve dug into it, but I do know what you’re referring to. These were overfeeding studies where they had two groups of people and overfed them with either a big surplus of dietary fat or a big surplus of carbohydrate.
Ari: Exactly.
Alex: When we say a big surplus, it’s like, imagine all of the energy you needed in one day and then multiply it by 50% or take half of it and– Oh my gosh, eat one and a half times as much as you would normally to maintain your weight, like a 50% surplus. If I need 2000 calories to maintain my weight, now I’m eating 3000 calories every day. This is a big surplus and it’s coming from either carbs or fats. These studies show that, initially, when it comes from carbs, there’s a body composition advantage. You have less initial fat storage and I’ll explain why. Then after doing it for just several days, everything equalizes. This has relevance. The reason I wanted to mention this is this has relevance for holidays. For any-people tend to overeat on holidays but it’s very short-lived. It’s like you overeat for one day, maybe two days, ideally. A lot of people overeat, day after day after day throughout. For anyone who actually cares about their body composition, they’ll just overeat for a little bit.
If you do that, carbohydrates tend to have an advantage because carbohydrates are more thermogenic. What that means is when you overeat carbs, your body does two things with them before storing them as fat. The first is it tries to burn it off as energy. In overfeeding studies, they’ll report that carbohydrates, even following a single meal of eating 500 grams of carbohydrates, your overall energy expenditure will increase by about 20% because your body will just burn through those carbs and let that energy go as heat in order to try and get rid of it because carbs are difficult to store.
The second thing it does is it pushes as many carbohydrates as it can into your glycogen, your liver, your muscle tissue. It will try and super saturate your glycogen stores to get as much of it into those storage depots as it can. The last thing that it does is it stores it as fat, because that takes energy. When you want to store carbohydrate as body fat, it takes energy for your body to transform the carbohydrate molecule into a fatty acid molecule. Your body doesn’t like wasting energy. It would rather use the carbs for energy and then take all of the dietary fat you’re eating alongside it, if any, and just put that right in your fat tissue because that takes no effort on the body’s part.
Ari: Yes, okay. Here’s one nuance that we can go into quickly. There are some people who, when they adopt a low-carb diet, rapidly lose weight. Oftentimes, people will, and this is an effect that is not seen on, let’s say, a low-fat diet that still is high in carbohydrates. As a result of this rapid weight loss in scale weight, people often conclude that there’s something really magic about a low-carb or keto or carnivore diet in that it just sort of puts you into some magical metabolic state that rapidly sheds the fat. They interpret this weight loss as loss of body fat. What’s going on there?
Alex: It’s just losing body water. The reason being is just because you stop eating carbs initially, doesn’t mean your body stops burning them. What’s happening is your body is going to be working its way through your glycogen stores. Now, this is primarily confined to your liver glycogen unless you’re physically active. If you’re physically active, then you’re also going to lose muscle glycogen that will not be replenished easily.
Ari: On the low-carb diet.
Alex: Correct, yes. You’re going to drop water alongside this because every gram of carbohydrate that you store as glycogen requires three times as much water to store it. If you’re no longer storing as much glycogen, you have a ton of water that your body needs to get rid of. Another reason for this too is that when you stop eating carbs and your insulin drops low, that’s going to significantly reduce antidiuretic hormone levels, which means that your body isn’t going to be as capable of holding on to water and electrolytes as before as it would with high insulin. This is one reason too why some people do feel crappy when they start a low-carb diet. Part of that reason is electrolyte imbalances because now they’re peeing out all of the sodium and potassium that they weren’t, that they aren’t replacing adequately. Some people find that electrolyte drinks or supplements can help avoid- [crosstalk]
Ari: [unintelligible 00:30:26] keto diets in particular.
Alex: Yes, exactly. One other thing too I wanted to bring up with this is a lot of low-carb proponents have shifted and said, well, its primary benefit comes from appetite regulation.
Ari: Yes, this is what I wanted to get in next. Let me just set this up for people. There’s the metabolic ward studies where they’re tightly controlling. Researchers are limiting how many calories these people can consume. There are some proponents of low-carb diets who say, well, those studies don’t really count. They don’t really test the hypothesis thoroughly because yes, calories do matter, but what carbohydrates and insulin are doing is they are stimulating appetite, stimulating you to consume more overall calories, and, or that an equivalent amount of calories from carbohydrates versus fat, the fat is much more satiating relative to the carbohydrates. Therefore it takes many, if you eat a diet that’s higher in carbs and lower in fats, it takes much more calories to get you to a place of satiety.
This is the distinction between a metabolic ward study where researchers are controlling for the calorie intake and not letting people consume how much calories they want. What that means is that those people have to suffer through hunger pangs and fatigue, but in the real world, it’s different. People won’t be forced by other human beings to suffer through that, and they have the ability to eat ad libitum, to eat until they feel satisfied and they feel full. These are different settings, and we also need to know what happens in the real world. Do carbs act to hinder society in some way, or are they less satiating, or do they have other mechanisms? Is insulin inherently appetite-stimulating such that on a higher-carb diet, we end up eating way more and therefore getting fat by virtue of consuming way more calories?
Alex: Yes, and so before I dive into this, I want to emphasize something too. This is a big goalpost shift, and this is important just to point out because this idea actually started with Gary Taubes. Gary Taubes was the first to mainstream the low-carbohydrate idea, and “The insulin is what’s causing our problems” idea. He teamed up with Kevin Hall and created a nonprofit that funded three studies that Gary Taubes all signed off on, saying, “These three studies test my ideas, let’s do them.”
Ari: Just to be clear, he, as a strong proponent, as a thought leader of the low-carb movement and the carbohydrate hypothesis of obesity, he was, from his perspective, funding these studies with the explicit intention to prove the legitimacy of, to prove the truth, essentially, that carbohydrates and insulin are the key thing that regulate fatness.
Alex: Yes, and so the first two of these studies were metabolic ward studies, and those, again, they did not support his beliefs. He did a third study and shifted by saying, “Well, it’s primarily appetite.”, which is a completely different argument than saying it’s insulin, because now you have to admit that it’s not insulin driving fat, but okay, we can say maybe it’s affecting your appetite differently. If that’s the case, they conducted a third study called DIETFITS, where they had two groups of people go either very low-fat or very low-carb for an entire year and just watch what happened to their body composition. What they found is that in both groups, if you plot the data for every participant in each group, and this is hundreds of people, this was a very large study, they were almost identical in terms of like half, or I would say 70% of the participants either had no weight loss or they did lose weight in each group. Another 30% actually gained weight.
What this is showing is that, in the real world, and I’ll come back to a metabolic ward study I think Ari might be thinking of too in a sec, but in the real world, these diets influence appetite pretty much the same. It’s up to you as an individual to recognize which one works better for your own biology and preferences, because two people aren’t going to have the same appetite and satiety responses to one single diet, right? It needs to be tailored to that person.
The DIETFITS study
Ari: Yes. Is the DIETFIT study, the one that came out three, four, five, maybe it’s five years ago at this point, [crosstalk] that it was like this really-
Alex: Yes, by Gardner.
Ari: -yes, by Gardner, the one that was like a year-long, if I remember correctly. This was sort of an, there had been many dozens of low-carb versus low-fat studies prior to this, but they were all four weeks, eight weeks, 12 weeks, 16 weeks. This one was unique in that it was a year long. It was also unique in that they controlled for food quality. They put both people on, it was a healthy low-carb and a healthy low-fat diet instead of, a lot of these previous studies from earlier years were garbage diets, and that didn’t really control for food quality. That didn’t, I think a lot of them didn’t control for protein intake as well, which is a confounding variable that maybe you’ll get to. This study was unique. I think it was uniquely expensive. It was, cost many millions of dollars, maybe tens of millions of dollars to conduct, but it was a really well-designed study at an ad libitum, low-carb versus low-fat, high diet quality, healthy dietary patterns in both groups for a year. They concluded, as you said, no really meaningful difference between the two groups in terms of fat loss.
Alex: Yes, and as an aside to this, just an interesting note. Another aspect of the study is they looked at, they looked at a handful of genetic markers that are related to insulin secretion. They looked at what the insulin response was to carbohydrates in these participants. Then they tested, well, maybe people who have bigger insulin responses to carbs do better on low-fat or on low-carb diets. That didn’t pan out either. It didn’t matter what your insulin secretion level was or what your genetics said. Both diets had similar effects.
How hyper-palatable food affects satiety
Ari: Yes, I almost want to go on a whole tangent around genetics because I find that there’s so much talk of, people are still under the impression that genes control way more about our health than they actually do. I find this amusing how much these ideas still predominate even though we have so much research showing like in the grand scheme of things, these gene variations don’t predict nearly as much as we think they do.
Okay, so maybe talk a bit about protein before we go on. I mean we could probably spend another hour or two talking about nuances of this and practical recommendations that come out of it. I feel like we need to give, maybe we’ve provided some clarity, you’ve provided some clarity for people around the body of evidence, comparing low-carb to low-fat now. Maybe now people might still feel confused. Okay, so what do I actually do? Should I go low-carb? Should I go low-fat? What do I actually do if I want to lose fat? Can you give people like, I know this is a tough ask because it could be a very long discussion, but maybe just a few bits of guidance on that topic?
Alex: Yes, so first and foremost, and Ari and I wrote about this in the Fat Loss Blueprint, but I would say the number one thing that you can do is regardless of macros, you want to just eat a quality diet based around whole foods, that doesn’t come with a lot of the gunk that is designed to increase the palatability of those foods. We have a ton of data showing that, if people just eat these types of diets, regardless of macros, if they just eat whole foods diets that don’t have a lot of palatability to them, which is what gets removed when you eliminate a lot of processed foods, they spontaneously lose weight because they eat less because their appetite-regulating mechanisms work better. Yes, just think about the food industry as a whole, their goal is to make money. The best way they can make money is by having you buy and eat their products. The best way they can do that is by making them hyperpalatable so that when you buy a family-size bag of Doritos, suddenly it’s gone, and you’re like, “What happened? That should have lasted me all week.”
Ari: I think the line from Pringles, I think it’s Pringles, was, “I bet you can’t just eat one.”
Alex: Yes.
Ari: Right?
Alex: Yes.
Ari: People need to understand that these processed food companies literally hire Ph. D. food engineers, food engineers, to use various kinds of chemicals, artificial chemicals, artificial flavoring, and all kinds of, there’s a whole science to the palatability and what’s called the food reward to food, where they know the precise ratios of carbohydrates and fats and sugar and salt and texture, crunchiness, and things like that. They know, there’s a whole body of evidence of how to engineer a food that is as pleasurable, hedonically pleasurable, to the pleasure centers of the brain. We’ll stimulate those pleasure centers in the strongest way possible and make those foods as addictive as possible so that you desire them and you want to eat them very rapidly and go back for more and keep buying them.
Obviously, as you said, that the economic interests of those food manufacturers incentivizes them to create food that is as addictive as possible, which just so happens to be the worst possible thing for trying to lose fat.
Alex: Yes, exactly. I would say, sticking to a whole foods diet, preferably home-cooked meals most of the time is going to be the biggest needle mover. After that, I would probably have you focus in on creating every meal around two items. The first is some type of dense source of protein. This is, a variety of animal products are great sources of protein, or there are, some plant-based sources, like many soy-based products, like tempeh, can also fit this role, depending on your dietary beliefs, and even protein powder, especially for individuals who eat a vegan diet, I always recommend that they just have a protein shake with every meal, because protein’s one of the hardest nutrients to get on a vegan diet in adequate amounts, unless you’re eating a ton of processed soy-based foods, which I don’t think is necessarily healthy.
We can, there’s a whole science around how much protein your body needs to maximize muscle gain and fat loss and all of that, but without getting into all of that and complicating things, it’s just base your meal around protein, and then the second item would be some type of fibrous vegetable. The-
Ari: Yes, sorry, go ahead.
Alex: The fibrous vegetable, it doesn’t matter if you’re low-fat or low-carb, because fibrous vegetables have very few carbohydrates and calories. In fact, for most of them, half of their calories actually come from protein, which I don’t recommend counting, because it’s not very bioavailable, but just as a tidbit, fibrous vegetables are a source of nutrition. They’re like a multivitamin, without supplying a ton of energy or carbohydrates or things of that nature. They fill you up, because one of the primary causes of satiety is the stretching out of the stomach. That physical stretching of your stomach causes you to become full, and that’s where fibrous vegetables can come in helpful.
The potential harms of attributing a specific diet to your weight loss
Ari: There’s one more aspect to this that I think is worth touching on, which is on a lot of these diets, whether it’s keto or carnivore, or there are potentially other diets that could be included in this mix, people might lose a lot of weight on them successfully. As a result of that, like I have a very close friend who has been vegan for most of- maybe the last 10 years. I think he recently reintroduced some whey protein and collagen and maybe some fish occasionally. For most of the last decade, he went vegan, he lost a ton of weight. He really improved his metabolic health profoundly. There are other people who do this on very low-carb or carnivore diets, keto diets, things like that. The tendency when a person does successfully lose weight on any given diet and improve their health dramatically is to attribute that health improvement and that weight loss to the unique dietary composition of that specific diet. It was the metabolic state that this specific diet put me in that led to this weight loss. Can you touch on that and why it’s possible to lose weight and improve health on so many different kinds of diets with radically different composition and macronutrient levels?
Alex: Yes, and to add to this too, you might have great success on a diet, you recommend it to a friend and it’s not doing anything for them. The reason is because for most people, they aren’t meticulously tracking their energy intake or their macro intake. Most people are just eating the appetite. When they adopt a new diet, especially this is a benefit of vegan diets, very high in fibrous plants, it’s low in energy density, they just unconsciously start eating less. They might not be aware of it, they might even feel like they’re eating more because they’re more full, they’re more satiated, but the amount of energy they’re taking into their body is less than what they had been consuming previously. They lose body weight. This isn’t anything magical. It’s just that, hey, you stumbled upon a diet that seems to work for you and make you eat less without you actually having to try. An added benefit too, if you feel like you’re eating more, no, you’re not eating more. I can guarantee that because you’re losing body weight, but it feels that way because whatever you’re eating now is more filling than what you were eating before.
Ari: Yes, it’s interesting. I think this is crystallized in the fact that someone can go on like a very high-fat keto diet or high-fat, high protein, paleo or keto diet or a carnivore diet of all meat and lose lots of weight. You can go, there’s such a thing as the potato diet or even the rice diet, but the potato diet is particularly good example of it where- there are people who have done this, there’s research on it. People eat nothing but potatoes or in the case of carnivore, nothing but meat. In both cases, you can lose lots of weight pretty rapidly and improve your metabolic health as a result of that. Sort of what’s, while these things on the surface might seem radically different, they might seem like radically different diets, what they have in common is that they both dramatically lower the food reward or palatability of that diet.
By virtue of that, they become much more filling per calorie and reduce your appetite. You end up consuming far fewer calories. If you psychologically commit to that, and it’s very hard to do and to have the discipline over prolonged periods of time, to really stick with any of these very regimented, very strict, very extreme diets. Some people might object to some of these diets being labeled extreme, but I think it’s appropriate. Let’s say a diet that makes you, says you can only eat meat or you can only eat potatoes. I would say these are extreme diets. If you have the mental capacity, like the intentionality, the willpower, the discipline to really stick with that and apply that, it will actually, you will eat very few calories before you reach the point of satiety. Again, if you have the mental fortitude to keep doing that, it becomes a very viable strategy to make yourself feel full and to not suffer, be suffering through hunger pangs all the time while you are actually in a calorie deficit and therefore tapping into your body fat stores and losing lots of body fat.
Alex: Yes. Yes, exactly. Yes, man.
Ari: In contrast, a diet that’s much higher in food variety, which is another topic that’s been studied by obesity researchers a lot, you could think of this as a buffet, sort of an all-you-could-eat buffet. The being presented with so many different kinds of foods leads to a phenomenon where you end up consuming way more food before reaching the point of fullness. This is a concept called food-specific satiety. Oftentimes, people experience this very frequently. Anytime they go out to dinner, people will say, “Oh, I’m going to eat this. I’m full, I can’t eat anymore.” Then the waiter or the waitress comes, “Do you guys want dessert?” Oh, all of a sudden, “Yes, I have room for dessert”, right? Food-specific fullness, “I’m full on this, but I’m ready for ice cream or cake, right?”
Alex: Yes, exactly.
Ari: The more that principle is extended in your diet, the more you have many different kinds of foods that you’re allowed to eat, the more calories you will tend to consume before you feel full, and vice versa. The more you are eating some really strict, very limited diet, like a monotonous diet, you’re eating the same few foods again and again and again, the more you will tend to not have a big appetite to consume lots of calories.
Alex: Yes, and that’s a really, really simple path to walk down to. it’s not something you want to do for the rest of your life, but if you’re somebody who really is at a sticking point and you just need some forward movement, especially to motivate you to keep going, that’s a really easy thing you can do. In fact, I remember saying this when I had that debate with Paul Saladino some time ago on your podcast, but I agreed at the outset. I said, look, if most people in the US, 70% of whom are obese or overweight, if all these people adopted a carnivore diet for like six months or whatever, the health of the nation would radically improve, hands down, because they would all just start eating less, and they would not have all the metabolic problems that come from being excessively fat. It’s not something I support for long-term health, but it has utility. It can be therapeutic when used in the right way.
Ari: Just again, based on the principle of limiting food variety and food palatability such that it ends up facilitating weight loss, and the same thing can be achieved on any number of other diets that maybe are healthier in the long-term and more sustainable and provide a broader range, a better sort of range of nutrients to sustain health. There is something to be said about these extreme approaches. Sort of the more extreme approach, if you have, again, the mental fortitude to stick with that very limited range of acceptable foods that you’re “allowed to eat”, the more you tend to go to that extreme, the faster the weight tends to come off. On the other side, the less sustainable or healthy it tends to be in the long-term.
Alex: Yes, exactly.
Is the theory of starvation mode valid?
Ari: Okay, so let’s go to the idea of starvation mode. This is an idea that’s been around for probably, I would guess, maybe more than 50 years or so. The idea that when you go on a diet, your body goes into, it slows the metabolism, and you go into a sort of starvation mode. As a result of this slowing of the metabolism, it predisposes to weight regain. What’s going on with that? What’s the science behind this idea of starvation mode?
Alex: Yes, so there’s two components to starvation mode. One of them was it predisposes to regaining the weight. The other one is that your body holds on to the fat as much as it can. It prevents you from losing weight. These are related but separate topics. I want to address that second one first. A lot of people think if they go on a very low-calorie diet, that at some point their body’s going to be like, “I can’t sustain this anymore, like I’m going to hold on to this fat.”, and you’re not going to lose any more weight until you start eating more calories. On its face, and this gets traction because people will stall out. People will be like, “Well, I’ve been eating barely anything and my weight hasn’t budged at all.”
Ari: It resonates with people’s subjective experience.
Alex: Exactly, yes. Now on its face, this actually just, from a biological standpoint, if this did happen, people would not starve to death. Starvation would just not happen. That just alone shows that this idea doesn’t really make a lot of sense.
Ari: Some people might argue that’s maybe taking the argument too far, taking the logic too far. Maybe it’s not sort of a binary thing where either it happens or it doesn’t happen. Maybe it happens to some extent.
Alex: Okay. If that’s the case, I would argue two things. One is that your body absolutely does downregulate non-essential processes when you diet in order to conserve energy. That’s just a smart thing to do from an evolutionary standpoint because it’ll improve your chances of surviving. It’ll say, “Hey, we don’t need to reproduce right now. We don’t need to have as much energy expenditure, so I’m going to lower thyroid output.” Things of that nature. This does have a meaningful impact on how many calories you’re expending every day. The extent of that impact isn’t to the magnitude that many people think. Ansel Keys in his Minnesota starvation experiment was the one who, to me, really demonstrated this because he took a bunch of already normal-weight men. Over the course of six months, he semi-starved them with 1,000 calories per day to the extent that they lost 25% of their starting body weight and they looked like skeletons that had skin put over them by the end of it.
Because again, they were already at a normal weight when they started. Then he did a ton of measurements throughout this entire process to see what happens. What he found is that by the end of this starvation period, these people had 40% lower energy expenditure than when they started. Of that lower energy expenditure, of the 40, 25% of that came from simply the loss of body weight. They weighed less and they had less muscle tissue and less fat mass. The amount of calories that they needed just to stay alive and move went down. It’s the same exact concept you would see between a 200-pound man and a 120-pound woman. The woman needs less calories because she’s smaller. Everything she does from staying alive to just moving takes less energy so she doesn’t need as much to maintain her weight. That’s what happened, that’s part of it.
Then the other 15% was due to hormonal down-regulation and adaptations that were seen in these participants. That 15% corresponded to about two to 300 calories every day. Now, the number one type of person who complains of starvation mode is small women. This is important because that small woman is active enough to maybe maintain her weight on 16 to 1,800 calories every day. She drops it down to, let’s say, 1,200 calories every day. She has a very mild deficit, no more than four to 500 calories, which is a pound of fat loss per day. Now suddenly her weight is stalling.
Ari: [unintelligible 00:57:58] a pound per week.
Alex: Yes, per week, sorry. Now she’s stalling out. She’s like, “Well, it’s in starvation mode, maybe I need to eat more.” It’s like, well, if you think about it, just the adaptation component alone already cut your deficit in half. Now you’re losing one pound every two weeks. Maybe that’s, and maybe at the same time, your body has also said, “Hey, you’re going to be less physically active. We’re going to reduce your motivation to move around.” Now on top of that, now your energy expenditure, even if your hormones were all normal, is no longer 1,800. Now it’s 1,600, because you’re burning 200 less through physical activity. Suddenly you’re in energy balance again at 1,200 calories because your body’s done all these things in the background to reduce your expenditure. Now it doesn’t mean–
Ari: That also, to add to that, there’s also the whole issue of error in reporting of how many calories one is consuming. Such, and this is sort of notorious in the literature on this, that people are, when they’re tracked properly, they are actually eating more calories than they think they are, or than they report they are eating. There’s, and it’s also the case that when you’re chronically day in, day out, restricting calories in a state of fat loss, it becomes very, very difficult mentally to suffer through hunger pangs and low energy. It’s very natural.
We’re designed by hundreds of thousands of years of survival to do this, to, when you’re in that state and you’re hungry, you don’t just suffer and suffer and suffer, of you’ve got a refrigerator right over there with a bunch of food in it, or a kitchen and a pantry with a bunch of food in it, then you could just, “Oh, just have a little bite of something. Maybe I just have a little, a few bites of this or that. Those little few bites end up adding up in many cases to 2, or 3, or 4, to 500 calories more a day, that many people sort of, “Oh yes, I just had a little snack. It was nothing.” In their minds they don’t think of it as significant, but it may be several hundred calories a day.
Alex: Exactly. This is just a really crappy position to be in, especially for the small women because it’s like, “What do you do? Are you going to try and make it on 500 calories per day to keep things going?” It’s a tough position to be in because really the most feasible way for small women and people who encounter this starvation mode to maintain their fat loss is to be more active. They need to get their energy expenditure back up so that then they can eat more food while maintaining that deficit. Because it’s not entirely the deficit that impacts your hormones, it’s also how much food you’re eating overall. This relates to a concept of energy flux.
Ari: Let’s hold off on that before we get there because that’s an important concept I want to get into. Before we get there, let’s talk about this. I haven’t looked at the research that’s emerged on this in maybe four or five years, but my understanding of this idea of starvation mode, the idea that one’s metabolism slows down, is that that idea has been mostly debunked, correct?
That it’s not really your resting metabolic rate, “your metabolism,” that’s slowing down. There are certain people in the evidence-based fitness circles who say, “Oh, that’s a bunch of nonsense. It’s only quacks who say that your metabolism slows down because look at this study, and this study, and this study that shows the metabolism doesn’t slow down.” Is that accurate to say?
Alex: That is.
Ari: However, from my reading of the literature, what I remember is that there are some adaptations that take place that are not a reduction in resting metabolic rate, but that function to limit one’s energy expenditure and one’s drive to expend energy. You alluded to this in the discussion that you had, but there’s even things like nervous system changes and blood flow changes. The nervous system innervates the muscles differently when you’re in a calorically restricted state where it becomes harder to do high intensity exercise, and you have more limited blood flow to the muscles.
The body is shunting, it’s trying to prevent you from doing high intensity exercise or it’s making it more difficult. Your perceived exertion to do the same workouts that you used to do in a fed state will be more difficult, in a well fed state, I should say. I had an experience when I did a five-day fasting mimicking diet, super low calorie diet. I think I was eating 5 or 700 calories a day. On day three and four, I remember going to the gym and trying to do a weight workout, which they advise you not to do, but I didn’t want to go five days missing workouts. I remember feeling like it was literally 200% harder to do the same exact workout that I would have done normally.
It literally felt twice as hard, or maybe even more than twice as hard to do the same weights as I would have done in a well-fed state. That’s how much the perceived intensity changed by being in that state. Simultaneous to that is the not in the context of a deliberate workout, but non-conscious activity what’s called NEAT. Non-exercise activity thermogenesis, which is like moving in your chair, and tapping your feet, and fiddling around, which is hundreds of calories per day. The drive that one has to do that versus the drive that one has maybe to just rest and lay on the couch becomes very different as well.
Without you even being aware of it, your physical activity levels may be reduced by several hundred calories via that mechanism as well. There is at the end of the day, I think almost a case for this general principle or concept of a kind of starvation mode that exist. It just doesn’t work in the way that the proponents of it originally proposed that it’s through a reduction of metabolic rate. Do you agree with that?
Alex: I think that’s a perfect summary. The takeaway that I would have is that if you want to use the term starvation mode, fine, I’m cool with that, but there’s no metabolic damage. You haven’t done any harm to your body, and your body’s just done what it’s supposed to do and downregulated how much energy you’re burning. That’s important to be aware of because if you’re coming at it from a metabolic damage standpoint or whatever, really it takes power away from you. If you say, “Hey, things have stalled out. I’m being less active. My hormones aren’t increasing energy expenditure as much as they were.”
Now, I can say I have two options. Either I can cut food further and continue fat loss if that’s feasible for you, or I can force myself to be more active, or I could take a break. I could just start eating in maintenance, give my body a rest, let everything upregulate because it does. Once you start eating more, everything starts to return to normal, and then you go on that journey again.
Can you damage your metabolism?
Ari: Well said. For people unfamiliar with the concept of metabolic damage, just define that briefly.
Alex: It’s this idea where if you’ve dieted too hard for too long, that you’ve permanently altered your metabolism to where it’s always going to operate slowly. It’s never going to be where it once was.
Ari: There are certain people who have gone on diets many times during their life over the course of 10, or 20, or 30, 40 years, where they lost 20 or 30 pounds and they were lean for a period of time, and then they regained the weight, then they went on a diet again, and lost a bunch of weight, and regained it. At this point, they’re convinced that they’ve done serious metabolic damage to their system, and that maybe they’re always going to be fat, and they can’t lose the weight and keep it off.
Alex: There’s just no evidence to support that. Our bodies were designed to put on fat and then use that fat when food was scarce. That’s how we stayed alive for millions of years. The idea that cycling between being plump and being skinny is somehow harmful to you, just doesn’t make sense from an evolutionary standpoint.
How FLUX can help you succeed with fat loss
Ari: Now, I think is a good time to go into this idea of flux because I think it’s a critically important concept, and one that it still amazes me because I’ve been talking about it and you’ve been talking about it for many years now. I still find that very few people seem to be aware of it, but it’s such a critically important concept. Explain why, as you were saying earlier, it’s not really the deficit of calories that’s causing these negative metabolic adaptations to take place that try to limit your energy expenditure. It’s not the deficit itself, there’s a broader context to that. Explain that.
Alex: If you want to think about flux, flux basically describes the energy turnover within the body. The energy turnover means how much energy you’re burning through plus how much you’re taking in. It’s both sides of the equation. That’s the simple way of thinking of your flux, energy in plus energy out. The reason that this matters is because from a dieting perspective, using our example of you’re eating 1,200 calories per day, and your body’s going to downregulate physical activity and unnecessary functions that burn energy like thyroid, that’s happening because you are now eating so close to or below the amount of energy needed just to keep you alive.
That’s your resting metabolic rate. Let’s say you’re an athlete and your resting metabolic rate, you’re a muscular athlete, is 2,000 calories. You’re so physically active that you burn 4,000 calories every day. Now you need to diet, you need to lose fat so you’re only eating 3,500 calories. You have so much room with how much you’re eating above what you just need to stay alive that your body does not perceive that deficit as a threat to survival because all of its essential functions can still happen without any issue, plus you have leftover to fuel your physical activity. The signals your body is receiving because you’re still eating so much food, even though you’re losing body fat, the signals your body is receiving are entirely different. We have studies in people with obesity, for example, actual interventions where they say, “These two groups burn the same amount of calories to maintain their weight every day. One group we’re going to have cut their calorie intake by 500 calories. The other group, we’re just going to have them do cardio every day that increases their expenditure by 500 calories. Let’s see what happens.”
Both groups will lose the same amount or very similar amounts of fat mass, but the group that is more physically active and eating more food doesn’t see any of the reductions in parameters of energy expenditure that the other group does, nor do they experience more hunger, plus they tend to have more lean body mass. It literally facilitates the development of the, if we want to call it this, the athletic build. When you see athletes, their bodies just look robust. Part of that is because they’re eating so much food to support that.
Ari: In other words, let’s say someone has a 500 calorie per day deficit where they’re burning let’s say 1,700 calories a day and they’re consuming 1,200, or they can have the same exact calorie deficit that they’re burning 3,500 calories a day and consuming 3,000. The same 500 calorie a day deficit, but at very different levels of total food intake per day. The body behaves very differently in those two different scenarios. In particular, the amount of fatigue and the amount of hunger pangs that somebody will have to suffer through in those two different scenarios is very different. I see those two things as the biggest limiting factors of somebody to adhere to the diet.
At the end of the day, all diets that successfully restrict calorie intake will facilitate weight loss, but the big distinction is behavioral adherence. How well will somebody actually continue to eat that way? For how long will they do it? I see that as, to a large extent, a product of how much suffering will they have to endure on a daily basis? Because we are very bad creatures when it comes to enduring suffering day in day out for extended periods of time. If we have a choice to alleviate that suffering, that’s readily available 20 feet away from us by walking over to our kitchen.
The successful approaches are ones that minimize suffering where the person is losing weight and they feel satiety, they’re not suffering through hunger pangs, and they feel energy. They feel alive instead of fatigued. If you are super low energy and hungry all the time, there’s just no way, maybe with a tiny exception of a very small portion of people on the planet who have that kind of extreme mental fortitude and ability to endure suffering intentionally for long periods of time, but the vast majority of people just cannot sustain that. It has to be an approach that minimizes suffering and doing a high flux calorie deficit is, in my mind, one of the biggest keys to doing that.
Alex: I agree. You’ll notice too, bodybuilders, recreational or professional will do this as well. Instead of cutting their calories even lower, they will be on cardio equipment doing very light intensity cardio for hours every day to increase their energy burns so that they can eat more. This isn’t a fringe concept. I think it’s just something a lot of people aren’t necessarily aware of, but it’s a huge needle mover. If you find yourself stuck, as silly as this sounds, try moving more and eating more.
Should you exercise for weight loss?
Ari: Next one. Next myth that I want to get into or clarifying some of these misconceptions that are out there, there is an idea that there is a cap to energy expenditure, that exercising is futile because there’s only so much calories that your body will actually allow you to burn off. Tell me about this idea and help me understand this because I know you know a lot more about this than I do.
Alex: This idea was put forth by Herman Pontzer, who’s done a ton of amazing research with the Hadza hunter-gatherers. One of the things that he did was he basically made a graph that looked at how many calories is an individual burning and let’s plot it against how physically active they are every day. What he found is there’s a very linear increase where you burn more calories, the more physically active you are initially. Then at some point, and I can’t recall off top my head what this point is, at some point, it tops off where now as physical activity continues to increase, energy expenditure doesn’t, like there’s a ceiling.
This fit not just hunter-gatherer tribes, but when he plots it with people living in America, in the US citizens, it’s the same observation. He proposed that once you start being very, very physically active every day, the body starts to downregulate other processes to keep your energy expenditure down, which is something that we just touched on with the whole dieting and the compensation. There is some truth to this. If you’re super, super physically active, then maybe your body isn’t going to want to produce as much testosterone because reproduction when you’re very physically active doesn’t make sense.
Because it doesn’t know why you’re super physically active, it just knows that that’s what’s happening. My big issue with this study is twofold or with this idea, I should say, is twofold. The first is that there’s a lot of reasons why people burn less energy when they’re very physically active that have nothing to do with compensation mechanisms. People who are very physically active, for example, their muscles actually become more efficient at burning energy, where they lose less of that energy as heat. If you think of your mitochondria creating, it takes in a hundred units of whatever and produces 80 energy.
With more and more physical activity, and with making your mitochondria stronger, more efficient, more robust, now suddenly that same input’s producing 90 energy. You’re not wasting as much. You’re not wasting as much of your energy being lost as heat. That’ll reduce your energy expenditure. It might not seem advantageous from a fat loss perspective, but from a health perspective, it means you’re doing really good. Your body is very efficient.
Ari: It also, I think, dovetails with the idea of flux.
Alex: Exactly. It does. If you’re super physically active, you burn less energy doing those physical activities because you’ve become adapted to them. That’s not a bad thing. It doesn’t mean your body is trying to compensate or downregulate anything, it just means it’s become better. You can’t differentiate those variables in the study that he was looking at or that he had put together. We do know from studies looking at flux, that there isn’t downregulation as long as you’re eating enough calories and not creating huge deficits.
As long as you’re keeping things sensible, the more you’re physically active and the more you eat, the less downregulation the body has because it has so many more resources available. The second issue with this idea is the simple fact that there’s no cap when you just look at athletes. Michael Phelps when he was training for the Olympics, needed to eat 10,000 calories every day to support his training. His body did not cap off. When you’re more physically active, over time, you might become more efficient. If you then decide to exercise more, you’re necessarily going to need to consume more energy to support that because movement takes energy. You can’t just move for free. There’s limits to what your body could compensate for, even if it had to. Your body could compensate as much as it possibly could, and you would still increase your energy expenditure if someone forced you to move.
Ari: How much does this overlap with the idea of overtraining syndrome? Some high-level athletes who are really training intensely many hours a day, I’ve been in this state before for periods of my life as well, where you are doing so much exercise that you end up in what’s called overtraining syndrome. Female collegiate athletes are notorious for losing their menstrual cycle and becoming infertile when they are doing extreme amounts of exercise. How do you see that playing into this or factoring into these ideas of there being a cap to energy expenditure?
Alex: Energy expenditure is one outcome, and it matters for body composition. When we’re looking at health in general, things are more complicated. A woman could lose her menstrual cycle being an athlete, that doesn’t mean she’s going to have problems with fat loss or burning more energy. I would like to look at them as separate issues where these things can happen and they aren’t healthy, but that doesn’t mean when we’re looking at it from a fat loss perspective, that it’s going to make exercise futile or that being more active is going to have these harmful effects.
The other part of it too is that with women specifically, in many of them, the issue is actually that they don’t eat enough to support their activity. There’s been many, many studies looking at this where they actually plot calories for every pound of body weight or lean mass that these women have, and figure out where’s the break off point where the body doesn’t shut off their menstrual cycle. These women typically need to eat more than 32 calories for every kilogram of body weight in order to keep things functioning normal, but they don’t. That’s why they lose their menstrual cycle.
The other part of it too is with physical activity specifically, you have to keep in mind that there are limits to your body’s repair potential. When you do physical activity, depending on the physical activity you’re doing, you’re going to be damaging your body. That’s one of the reasons why it leads to adaptations that make you stronger and more resilient. These are micro fractures and bones, micro tears and muscle tissue, strain on the cardiovascular system.
Eating food supplies the nutrients that your body needs to fix everything and make it even better than it was before, but it can only do that so quickly. If you keep pounding, and pounding, and pounding, and pounding, you’re going to well surpass your body’s ability to repair that damage. That’s what leads to things like overtraining syndrome where your body, it is broken down now.
The role of protein for weight loss
Ari: Let’s go to protein now. There’s a longstanding, very pervasive mythology, ideology around protein, around animal protein. Maybe that’s too broad to go into, too much nuance there. The idea that protein is harmful to health or shortens our lifespan, what can you say about this? I know you’ve spent a lot of time digging into the research on this. What does the research tell us about protein consumption as it relates to longevity?
Alex: This is funny to me because with the energy balance stuff, it’s amazing to me that this is still even a point of controversy. Sticking with longevity specifically, there’s no good evidence that protein is implicated in longevity in terms of a high protein diet shortening it. The best evidence that we could get supporting this idea comes from two animals. One of them is mice and rats, and the other is monkeys. The monkeys are more relatable to us. What the researchers found, there have been just a handful of studies looking at this, is that when the monkeys eat a high-quality energy balanced diet, protein intake has no effect on longevity.
However, when you give one group of monkeys a high protein, high processed food, Western diet that causes them to become overweight or obese, those monkeys have shorter lifespans. It wasn’t an effect of the protein, it was that they had a crappy diet quality that made them fatter. In mice, when you look at protein, it depends on which strain of mice, which species or a breed of mice you’re looking at. Studies that have looked at the longevity effects across 21 different strains of mice, for example, found that more mice, more of those types of mice actually tend to have reduced lifespans with low protein diets compared to those that have increased lifespans.
This just shows that if you publish a study with a specific strain of mouse showing, wow, you’re limiting protein extends lifespans, great. Now, do that with all the other strains of mice because there’s very obviously this genetic confounder. That’s completely ignoring the fact that mice aren’t humans. In that regard, one group of researchers tried to equalize the lifespan effects between mice and humans to estimate dietary protein restriction, what effect would it have theoretically on human longevity.
What they found is that you would need to start the intervention while you were still a child or adolescence for it to have an effect. In adulthood, it wouldn’t do anything. It would increase your maximal lifespan by about three years. That’s not taking into consideration the health detriments from consuming inadequate protein in terms of frailty, sarcopenia, a loss of independence.
Ari: Theoretically, leaving those other confounding variables, or conditions, or potential accidents, you and I have been writing a lot about that lately at the sarcopenia, and frailty, and risk of accidents, falling, and fractures, and things like that that are linked to low protein intake. Leaving that aside, theoretically you could get this three-year extension of lifespan by consuming a low protein diet of how low are we talking here?
Alex: Usually it’s 10% of calories or lower.
Ari: Whoa. What does that equate to in grams of protein a day?
Alex: That would probably be around, I’m guessing, 60 grams of protein per day, maybe a little less.
Ari: Very minimal protein intake. Theoretically, you could get a three-year extension of lifespan, but the complexity of human life, given that we’re not lab rats in a cage, is such that there are also these potential downsides of eating a low protein diet. Talk about that aspect or you talk about the upsides of consuming a higher protein diet.
Alex: The obvious upside to that is within reason when we say high protein, we’re not saying eat a house of protein every day. Specifically, we’re talking usually above 1.6 to 2 grams of protein for every kilogram of body weight that you weigh. As a rule of thumb, let’s just say 1 gram of protein for every pound. That makes it easy. You weigh 200 pounds, 200 grams of protein per day. High protein diets above this, when combined with resistance training, which everyone should be doing without excuse, leads to improved muscle mass, muscle strength, muscle function, and lower fat mass.
That permeates out into not just your ability to function in life as you’re growing older, but into your metabolic health as well, where muscle and fat tissue play central roles. The other point that I want to bring up is eating higher protein diets increases immune function. Your immune cells are very amino acid hungry because they use those amino acids chronically just on a constant basis to defend your body against invaders. Low protein diets will increase the risk of not just catching infections, but also dying from them or having more severe outcomes in general. This is relevant, particularly to mice studies because mice are always studied in sterile environments. They are never at risk of infection. When you look at interventions, for example, something like rapamycin, where they say, “Hey, it extends the lifespan of these rodents,” it’s also a very, very potent immunosuppressant that’s used in organ transplant recipients. If you’re out in the real world on rapamycin, you’re probably going to catch an infection and it could very easily kill you because your immune system is no longer working well. You’re never going to see that in a lab rat study because they don’t want infections to happen. That’s going to confound their results.
Ari: Not only is there just interspecies differences in terms of physiology such that not every intervention that works in rats works in humans. Even going back to some of the research you mentioned before, not even every intervention that works in one strain of rodents, rats and mice, works in a different genetic strain of rats or mice. Even within a given species, different genetic strains respond pretty differently. Now, you could reasonably expect those differences to be much more dramatic when you jump from a rodent to a human.
Now, as you said further than that, there is these differences between being a lab rat in a cage in a laboratory somewhere where you are protected from certain things that a human living in the real world is not protected from. Infectious diseases being one of those and also simply falling down, having an accident such that you trip over something, and fall, and fracture a bone. As you know very extensively because you’ve written a lot about this for our upcoming book, that is one of the leading causes of early disability and death in people over the age of 65. This is a whole major driver of disability and death in humans that doesn’t even exist in rodents in a cage.
They don’t have to worry about it. Further muddying the waters of the complexity of this situation changes dramatically when you look at an intervention that in lab rats theoretically extends lifespan, enhances longevity, but now given these kinds of nuances and complexities of human life, actually that same thing that worked to extend lifespan in rodents might actually be a detriment that shortens lifespan in humans.
Alex: Exactly.
The latest study on fasting and CVD mortality
Ari: Alex, one more. Let’s go to this new research. I actually haven’t looked at it, but I saw this research come out maybe a week or two ago that’s been making the rounds. Lots of people have promoted this, but I haven’t looked in depth at what’s going on here. It’s this new research, this new study that came out that basically said that shorter feeding windows are linked to a dramatically increased risk of, I think it was heart attacks or death by cardiovascular disease. I’m not sure what the heart outcome was that they measured, but I’ve seen lots of people promoting this and it was a huge magnitude of effect size.
It was 70 or 80%, something like that, increased risk of cardiovascular disease linked with a shorter feeding window. I saw all these people going out based on this research saying, “Avoid eating your meals in less than 10 hours a day or 8 hours a day, whatever this research was, and make sure you’re eating 12 or more hours a day.” I had you look into this so that we could talk about it. I don’t know what you’re going to tell me because I haven’t looked into it, but you give me the rundown of what’s going on here.
Alex: First and foremost, I can’t see the full text of the study because it’s a poster presentation. It’s an abstract that was posted online for the American Heart Association. We can’t do any type of deep dive into their methodology, into what the results found when we look at them as opposed to what they report. All we have is just an abstract that they provided. Keeping that in mind, the researchers basically took two 24-hour food recalls and looked at within what time interval did people start and then finish eating. Eating was counted as consuming anything with more than five calories. Then they divided them into the groups.
People eating less frequently than 8 hours per day, 8 to 10, 10 to 12, 12 to 16, and then more than 16. They set 12 to 16 as their reference because that’s the most common eating window for people in America. Then they compared all the other time groups to it. What they found is there were no associations except for those who ate within less than 8 hours per day were at a 96% greater risk of dying from cardiovascular disease than people eating 12 to 16 hours per day. This was strengthened when they looked only at people with preexisting cardiovascular disease, the association was even stronger.
When they looked only at people with cancer, it was even stronger than that, 272% greater risk of dying. They don’t say why. Expectedly, mainstream media jumps on this, tells everyone, “Hey, if you eat in an eight-hour window, you’re going to die.” The entire thing just got completely blown out of proportion given what we were provided with and what’s already known. It’s not even a full-text publication.
Ari: This is one of the problems with media reporting and with the way the general public ends up consuming this information, not through any fault of their own. Part of doing the whole science thing is that each new study, each new piece of data that emerges on a particular topic has to be considered in the context of the body of evidence that exists on that topic. A new study doesn’t come out and then if it has a different finding than 30 other studies that have been done for the last 20 years on that topic, we don’t instantly throw out the 30 other studies that have been done for 20 years and go, “Here’s this new study.
This one trumps all the others, and we must value this one over all the other studies because it’s newer,” irrespective of anything else, irrespective of the quality of study and how it was done. It’s like, “Here’s a new study, this is now the word of God that we must all accept as truth, and we’ll forget about all the other studies anyway.” Things are not positioned in context for the general public to consume this piece of information in the context of the broader body of evidence on that topic.
Alex: Exactly. When you do this, and when you do this with any observational study, you have to ask, “Why did they observe this?” To answer that, we can look at all of the huge mountain of data that we have in animals and in humans looking at time-restricted feeding that overwhelmingly shows it’s beneficial, it’s beneficial for body composition, it’s beneficial for inflammatory biomarkers, it’s beneficial for cognition.
You say, “That’s really strange. Why would this observational study observe this if all of the intervention data and mechanistic data we have shows that it’s beneficial?” Then you start thinking, “Wait a second, what could cause people to eat less frequently that also ends up killing them?” People with Alzheimer’s or dementia forget to eat, they eat less frequently, they waste away. That’s not time-restricted eating killing them, they happen to be eating less because they had a disease that was killing them.
Ari: For people listening, this is a phenomenon called reverse causation.
Alex: Exactly. That’s one reason why they saw the association was even three-fold greater with people who had cancer specifically. One of the biggest concerns with severe cancer is not eating enough and wasting away. Of course, people who eat less than eight hours every day are going to have the highest mortality rates because they have the worst cancer and they aren’t dealing with it, as well as somebody who’s able to eat more food more frequently.
Ari: There’s research showing when you look at the relationship of BMI or body weight to lifespan and mortality, all-cause mortality, they show that obviously people with very high BMIs, people who are obese have a greatly increased risk of dying and from many diseases and all-cause mortality. This is a U-curve where people who have very low BMIs are, maybe in some cases research shows, equally at risk for dying early. This gets at the point you were just making is that there’s a confounding variable at play there, which is that those people with extremely low BMIs are in very many cases already close to death, they’re already in some disease state, in some wasting state where they have a low BMI as a result of that disease state.
Alex: On that point too, funnily enough, some researchers have tried to control for that by looking at the relationship not of BMI, but of muscle mass and body fat. They find that that U-curve disappears when you look at muscle or when you look at body fat levels. The best survival is people with the lowest body fat. The U-curve is even stronger when you look at muscle, where the people with the lowest muscle tissue are the ones dying the most. It shows in that example you gave, it’s not that people are skinny or lean, it’s that they’re wasting away, they don’t have that muscle tissue to support their body. That leads to a host of complications like what we just talked about a little bit ago on protein.
Ari: At the end of the day, this research, I consider it really irresponsible for some of the health influencers that I saw running out and advising people, “Don’t restrict your food intake to less than 10 hours a day. Make sure you’re eating at least 12 hours a day or more because eating less than 10 hours was shown to be whatever it was, a 90-something% increase in risk of cardiovascular disease,” because that’s just not taking into account so much evidence that has been accumulated in recent years from so many other much more well-designed studies that have shown profound health benefits from eating in a shorter time window.
Now, this is another example where you could probably reasonably expect to find a U-curve, where you can take time-restricted feeding to a point where it becomes unhealthy. If someone was to consume only one meal a day, let’s say, and they only ate in a one-hour window or two-hour window a day, I don’t think we have the evidence on this yet, but I think it’s reasonable that we could suspect that might lead to nutrient deficiencies or poor metabolic health in some way and may increase risk of death through various other mechanisms.
There’s so much evidence to show benefits of time-restricted eating that’s in the range of 8 to 10 or 8 to 11, let’s say hours a day, but I think more 8 to 10, in particular, that it seems really irresponsible in my mind for people to be running out and saying, “From this one study taken out of the context of the body of evidence on the topic, time-restricted eating all of a sudden is bad for us. Forget everything that’s come out in the last 10 years on this topic.
There’s one new poorly designed study that we don’t even have the full text of that shows an increased risk of disease. Let’s not even analyze any of these confounding variables you just mentioned, let’s just tell everybody to make sure to do what everybody already does and consume food. The standard American way of eating, Western way of eating is to consume food in over 12 hours a day.” You have all these people warning of the dangers of eating in a window of time less than that now.
Alex: I know. If someone took the study and then recommended against time-restricted eating based on this study, huge red flag because one, everything you just said about how there’s no critical thought they put into it. Two, there’s not even a study for them to evaluate. They’re running with an abstract and with the mainstream medias like presentation of that abstract. I wouldn’t consider them to be a trustworthy source of information if that’s how they are approaching these topics.
The Fat Loss Blueprint
Ari: Alex, thank you so much for coming on. We went much longer than we expected to and we still have more topics that we need to get into. I want to talk to you about diabetes and metabolic health more broadly. There’s so much more stuff that we could get into with nutrition myths, and fat loss myths, and stuff like that. Hopefully, everybody listening found this very enlightening.
As you can see, Alex is really world-class with his knowledge of the details of the science around fat loss, metabolic health, and debunking a lot of these myths, and clarifying a lot of the competing ideologies and competing narratives that exist and that have been promoted by different groups of people over the last few decades. One more thing I want to mention to everybody listening, Alex and I collaborated a few years back on creating a program called The Fat Loss Blueprint. I just decided since we’re recording this episode, that we’re going to run a discount on this for the week after this podcast is released.
The program is normally 497, we’re going to lower the price down to 297. If you want to join The Fat Loss Blueprint, which is really– The other thing that we were going to call it was advanced fat loss strategies because to be honest, it’s really unappealing to me to even offer a program in the realm of fat loss because I just feel that whole space became so saturated with charlatans and people pushing all kinds of pseudoscience, and wacky diets, and wacky claims to try to get attention in this landscape and compete on claims of, “You’ll lose 30 pounds in the next 30 days, or the next 6 weeks, or whatever, ” and these wild claims, and these extreme diets.
It’s all with this incentive to make money, but it’s at the expense of the actual person buying these programs and trying these diets and programs that are just nonsense. I approached Alex a few years back and said, “Let’s put together a program that is just rock solid, evidence-based like here’s the science of fat loss, no BS, no crazy claims of how many pounds per week you’re going to lose, and no extreme diets. None of the garbage and pseudoscience that typically exists in the online fat loss realm, just rock solid science of fat loss.
No BS, no hype, no gimmicks, just science.” That’s what we’ve done. It takes you through the foundational stuff in the first week. Then after that, the whole program is really about advanced fat loss strategies. As you can see from listening to this podcast, there’s a whole lot of important nuances that you need to understand to do fat loss the right way and so that you don’t get duped by a lot of the gimmicks and wacky diets that people are promoting to try to make money. This takes you through, here’s the actual evidence we have on what truly works for lasting sustainable fat loss, not rapid fat loss.
To do that is very easy. Go on any extreme diet, starve yourself for a period of time, you can rapidly lose weight. Problem is it’s not sustainable. What is the science of lasting sustainable weight loss? What’s the collection of advanced evidence-based strategies to facilitate that? That’s what we put together with The Fat Loss Blueprint. I strongly recommend you check that out. You can get it @theenergyblueprint.com. Right now we’re going to put it on sale for $297, again, normally it’s $497. We’ll make the discount code. Alex, how about that?
Alex: That works nice.
Ari: In honor of this podcast we’re doing, you can put in the discount code as Alex and it’ll knock off $200 off the price. To everybody listening, hope you enjoyed this. Alex will record another one soon to get to some of these topics we didn’t get to today. I look forward to the next one. Thanks so much for tuning in, everyone.
Alex: Me too. Thanks for having me, brother.
Show Notes
00:00 – Intro
00:39 – Guest Intro: Alex Leaf
01:52 – What is energy balance?
05:06 – Science 101 when it comes to fat loss studies
14:28 – The confusion around low carb diets
34:24 – The DIETFITS study
38:06 – How hyper-palatable food affects satiety
44:36 – The potential harms of attributing a specific diet to your weight loss
53:30 – Is the theory of starvation mode valid?
1:06:52 – Can you damage your metabolism?
1:08:14 – How FLUX can help you succeed with fat loss
1:15:36 – Should you exercise for weight loss?
1:24:17 – The role of protein for weight loss
1:33:33 – The latest study on fasting and CVD mortality
1:45:20 – The Fat Loss Blueprint