The Melanie Avalon Biohacking Podcast Episode #101 - Gary Taubes

TRANSCRIPT

Melanie Avalon: Hi, friends. Welcome back to the show. I am so incredibly excited about the conversation that I am about to have. I am just glowing. A quick backstory to all of this. You guys know I've been in the whole low carb diet, paleo, health sphere, fasting, all of that for quite a while. Honestly, that started when I first tried a low carb diet over a decade ago. I realized the crazy effects that changing your macronutrients had on, not just weight loss, but your entire metabolism, your experience of life, health benefits, so many things. I became really obsessed with the science of it. One of the first books I read on the topic, once I became obsessed was Good Calories, Bad Calories by an investigative science and health journalist named Gary Taubes. And that book, oh my goodness, I have it out right now, in front of me. It's still all marked up so many notes, it's the deepest dive into the concept of calories and metabolism and the potential myths surrounding everything in the diet sphere.

Since then, Gary wrote some other books, Why We Get Fat, The Case Against Sugar, and most recently The Case for Keto: Rethinking Weight Control and the Science and Practice of Low-Carb/High-Fat Eating. Friends, I have read all of them. They've played a massive, huge role in my understanding of all of this. Gary, thank you so much for being here.

Gary Taubes: Thank you so much for having me and the wonderful introduction. And I'll try not to let you down.

Melanie Avalon: You will not. You are a legend. Everything that I've listened to, interviews with you, and such have just been absolutely incredible. I was so excited to read The Case for Keto, because it dives deep into a huge debate that I'm constantly thinking about, that I'm constantly reading about, interviewing people about, and that is, the whole role of the types of food that we're eating, and how it affects weight gain and weight loss. The role of insulin, the role of carbs, the role of fat, what is going on? Are we getting fat, because we're overeating? Or, are there other factors involved? I'm really excited to dive deep into it today.

A question to start things off, though. You are different from a lot of the authors of books in this sphere, because you are a journalist, and you went to Harvard and Stanford and Columbia and you're the cofounder and president of the Nutrition Science Initiative. Your approach to these topics is, it's like history. It's a very different approach than a lot of the books that I read. That's the question I have for you is, what is the importance of looking at the history of these topics? For example, The Case for Keto, you really dive deep into the history of dieting and the low carb movement. How does understanding the history of a topic practically inform science today and what we do today?

Gary Taubes: Two answers to that. The first is the glib one, and I actually say this in The Case for Keto, if you really want to understand what you're talking about, you have to understand the history of the idea as you're communicating. You have to understand the sort of evidence base for why people came to believe something that you might now believe 100%. This is fundamental core good scientific practices. You can't just trust that everybody who told you, you should think this way really knew what they were doing, you should go back and look at the evidence yourself. As a journalist, when I first got into this about 25 years ago, doing a series of investigative articles for science, I knew I was dealing with controversies. The first one was over whether salt, sodium, causes high blood pressure and hypertension, which we all think is just a given, and we've been told the low salt diet for 20 years, but I realized around 1998, that this was actually a very vitriolic controversy in the medical community.

In order to understand that, I had to go back to literally just go through the history of the field to see how the conventional wisdom that salt causes high blood pressure was formed than what the evidence base for that was. Once I understood what the evidence base for that was, then I could begin to know whether or not I should give credence to the people who are skeptical, like, they are right. If we knew beyond a shadow of a doubt, if you did a randomized control trial and you randomized a few thousand people to low salt diet and a high salt diet and a few thousand on the low salt diet, had their blood pressure drop 20 points, then this is a clear cut when for the salt causes high blood pressure argument, you don't have a controversy. But if there's a controversy, it suggests that the data are surprisingly ambiguous until you have to go back and actually look at the data.

As I did this first for salt and blood pressure, and then for the dietary fat, heart disease story, this idea we were raised that a low fat diet or low saturated fat diet is a healthy diet, I realized not only that I had to go back in time to do these stories, but that when you read reviews of the evidence by leading authorities, you had to check their references, because often, and this was kind of a revelation in the field. Often, there are references were completely wrong or bogus or misinterpreted. Then, you'd go back-- I'm reading an article in 1999, that reviews the evidence, and it's citing articles from say 1978 or 1976, you have to go back and pull those articles to see if they were actually accurately representing what they had done and concluded. And then, those articles will base their opinions on earlier articles. I just kept going further and further back in time. The more I learned, the more I realized how bad the science really was in this kind of nutrition, obesity, chronic disease area.

If you don't understand the history, you can’t really make any claims taking-- If you're claiming then you know what you're talking about, you've got to understand the history of the ideas and the evidence base. So, yeah, my work has become-- is always dominated by a historical perspective. I'm actually working on a new book on the relationship between diabetes and diet, that's sort of a case study of the pathology of medical science. I keep wondering who's going to read it, because it's--

Melanie Avalon: I'll read it.

Gary Taubes: Thank you. That’ll sum up to 11 readers now as far as like-- but it's so deep into the history, which fascinates me because it's about how-- you have basically doctors treating patients. They're not trained to be scientists, they're trained to be doctors, it's a different skill to different mindset. They're treating their patients and they're trying to decide at any point in time how best to treat their patients based on the information they have at the time. What they're not aware of is their decisions on how best to treat their patients based on the existing information. They're going to have long-term effects on, they're going to bias help people see the field ever after. So, they're going to have long-term effects on the science when that science is done. So, you have this fascinating situation we're in. In a field like physics, for instance, nobody’s life depends on World War II-- An extreme example, if you're trying to figure out the theory of everything, or whether or not some obscure supersymmetric particle exists, nobody's life depends on it. You don't have to rush anything, you don't have to jump to any conclusions, you could do the rigorous science necessary to establish.

What the truth is, even if it takes 20 years. But when you're a doctor, you've got patients’ lives on the lines, and you're always pressured to jump to conclusions and assume you know more than you do. Then those assumptions get woven into the conventional wisdom in the field, what is believed to be true. Then, scientists become invested in those beliefs. So, the physician, researchers become invested in those beliefs. And you end up with this, and the kind of arguments have been making in 100 years of thinking by some really smart people who weren't as well trained-- They weren't trained to do what they thought they were doing, could lead to terrible mistakes being made. Then, we see the same debates going on today with things like COVID, shutdowns and the benefits of mask wearing, where everything's now-- you see these arguments happening over the course of weeks, where it used to be years and decades.

Melanie Avalon: Yeah. Well, this is pretty frightening, honestly.

Gary Taubes: Yeah, it's one of the problems I have getting the message across. Magazine article, I wrote a year ago, for the New York Times magazine, that I handed in March 14th 2020, so two days before the world shut down. It was about this enormous mistake that had been made in obesity research when they embraced the idea that it was caused by eating too much, which seems like surely, people get obese because they ate too much, but that's a hypothesis and there are competing hypotheses and they were never tested. I documented how this influenced and by embracing this in 1930 based on one physician’s exceedingly naive studies. It biased everything that came after, and the Times bought it, “We're going to run it.” But then as the COVID crisis deepened, then the arguments about the science got more and more vitriolic, they decided that they really can't publish an article by a freelance journalist claiming a mistake of this magnitude had been made, because if they do that, then it's possible that mistakes of smaller magnitudes are being made all along. It became an argument that couldn't be made, because if I'm right, the implications throughout medical science are too profound.

Melanie Avalon: I don't know if this is a comparison worth making, but recapping the history, is that looking for causational data or is it correlational? Finding that one lie that changed the entire potential trajectory of our concept of dieting and our perspective. Is that a causational thing that happened or is it more correlational, and a lot of different thoughts and opinions and it manifested to where we are today?

Gary Taubes: Well, first of all, a fundamental-- there's a phrase that I use in my books that I picked up when I was writing my second book. My first two books are on physics, and then second book was on this, the big scientific fiasco of the late 20th century, which is something called Cold Fusion. I interviewed 300 people for just one of the stupidest scientific subjects ever, but I was obsessed with how this had happened and how progress. While it was happening, this article circulated through the physics community that was on this subject of pathological science. This was a lecture that had been originally given by a Nobel laureate chemist named Irving Langmuir, IBM, in 1957, and somebody transcribed that, and then it would circulate to the physics community every time somebody was claiming to have discovered-- made some discovery that the physicists were pretty sure was wrong. Pathological science is a science of things that aren't so. It's not fraud, it's not conscious manipulation. It's just people doing science so poorly that they end up seeing what they want to see, even though what they want to see doesn't really exist.

It may be a very common phenomenon in science, although this article was talking about just a few specific examples in physics, and my work suggests it's far more common in other people's work as well. It's far more common than we would like to believe. One of the fundamental mistakes that’s always made in this kind of science, is people have an association between two phenomena, they assume that they're causal. In obesity for instance, the association was, well, we see a lot of-- I'm going to use crude language here, and I apologize to anyone, but it's just going to make it easier and I'm also channeling the way people thought in the era. But what they thought was we see a lot of fat people in these, when we notice these fat people, they're sitting in restaurants eating a lot or drinking a lot. Therefore, people get fat because they ate too much. You have an association that's not even a good association, because when you see somebody not eating a lot, and they're obese, your brain doesn't really pay attention to, and it's like you don't notice. You only notice the people who appear to be gluttons. Then, you assume from that observation, that causality, that gluttony causes obesity.

It's the fundamental mistake in the field. It's a fundamental bad idea. Until 1930, most physicians thought people get fat because they too much, but there may be a dozen researchers in the world or physician researchers who are actually thought of, “We're trying to understand the causality of obesity.” What makes someone become obese when most people-- and back then, obesity was relatively rare. why do some people become obese and why is it so hard for them to fix it once they do?

There was the eat too much hypothesis. The constitutional hypothesis, and the constitutional hypothesis is it's small, it's kind of hormonal. Some people are just driven to accumulate too much fat and they're going to accumulate too much fat almost regardless of how much they eat. If you think in terms of this common phenomenon and comedy teams, Abbott and Costello or Laurel and Hardy. There's a thin one and a fat one. The difference between them isn't how much they eat and exercise. The differences is the fat one was sort of constitutionally predisposed to accumulate fat, and that was going to happen. He might starve himself down to being almost lean, but the lean person can be lean effortlessly. This makes an enormous amount of common sense, and yet, nonetheless, the obesity community embraced this idea that people get fat because they eat too much.

I was just looking at an article before we got on from 1952, written by one of the smartest physicists actually doing some of the best work at the time on cholesterol and lipoproteins and heart disease. Let me see if I could pull up the article quickly. Dietary approaches to atherosclerosis. A, caloric intake and obesity, it's a matter of fairly general agreement that obesity is almost only the result of the ingestion of an excess of calories in the diet. That's the sort of fundamental idea in the obesity field. It's like Newton's laws of obesity. There was always this contrary hypothesis that it was constitutional, hormonal defect. Just as some people are hormonally driven to be 6’8”, and other people only get to 5’2”. Some people are driven to be 280 pounds, and some people's bodies only want to be 150. It's got very little to do with how much they eat.

One hypothesis was embraced and it influenced the field ever after, and the other was kind of ignored. It was seen as an excuse for fat people to not do what lean people did, which was eat in moderation and exercise. If anyone said, “Oh, it's hormones,” that just meant that you were making some kind of excuse for why you didn't want to do the work that lean people do naturally. How can it possibly be true? From the perspective of how could a journalist come along originally in 2007, and then an argue that the entire medical research community is just wrong if any reasonable person would bet on the journalist being a quack before they wouldn't bet on this idea of being wrong, and yet it's awkward position to be in, by the way, when you're the journalist.

Melanie Avalon: I can imagine. I have so many follow-up questions about everything you just said. I don't know the answer to this. This is a very naive question. Is our height potential something that's determined genetically?

Gary Taubes: Oh, yeah.

Melanie Avalon: Does that correlate to a genetic potential for our potential weight?

Gary Taubes: Well, it will, because taller people tend to be heavier than shorter people. So, if you ask the question, why Shaquille O'Neal weighs more than Muggsy Bogues, using basketball, Muggsy was like 5’4”, I think. Shaquille was seven feet tall. A lot of that is not about how much Shaquille ate and how little he exercised. Part of it, is the fact that he's two feet taller, and the other part is his body is programmed to accumulate muscle and fat in a way that Muggsy Bogues was not or Kevin Garnett. I hope you're a basketball fan, otherwise, all this is lost.

Melanie Avalon: I can follow the analogy, but I don't know the names.

Gary Taubes: The height has a huge genetic component and everyone-- taller parents are going to have taller kids on average. That's genetic. Then, the question is what information are the genes conveying? A lot of it is going to be related to growth hormone and various growth hormones and the receptors for those growth hormones. The question becomes, why isn't the same thing true for how thick you are, as opposed to how tall you are and how much fat you accumulate. The reason is because-- probably is, but the field grew up believing that people get fat because they ate too much. They ingest excess calories and the diet, as my buddy, Goffman, said in 1952.

Melanie Avalon: When a person is born, is it predestined the height that they're going to be? Or is it also related on environmental factors?

Gary Taubes: There are environmental influences. For instance, a famine will stunt growth. If famine’s for a short period of time, the child will experience catch up growth afterwards. But if it's long enough, it'll influence-- we see it all the time with immigrant populations, where each successive generation tends to be taller than the population before, and so people emigrate from areas of the world that tend to be impoverished where it’s difficult to get the healthy diet, both enough calories and enough protein. If it's a wealthy, higher socioeconomic status area of the world, people tend not to leave. You stay where you're comfortable, you leave when you're not. So, they come to the US, and each successive generation tends to get taller and taller.

Well, when geneticists talk about this, they talk about-- there's a certain genotype, which is the genes you're born with, and then that interacts with the environment to produce a certain phenotype, which is how the genes in that environment manifest themselves. The environment will have an effect on your genetic predisposition to reach some particular height or your biological predisposition. I have a 12-year-old who's obsessed with basketball. I'm sitting here thinking, his happiness through college is going to be determined basically by--

Melanie Avalon: How tall he ends up being? [laughs]

Gary Taubes: How tall he ends up being? Whose genes did he get? I have a brother who's 6’5”, that's a good thing. If he only gets as tall as I am, it's going to be very hard, 6’2” kid who refuses to practice his shot enough. Anyway, the genes must be communicated primarily through these hormones and enzymes and receptors and like that determine these growth phenomena.

By the way, I’ll just interrupt one more second. As a journalist, I was always proud of my ability to ask naive and stupid questions. Often, I used to tell researcher, especially when I was writing about physics, there were some subjects, like, quantum optics, that even saying the word gives me a headache 20 years later, 30 years later. Where I would say to them, “Explain it to me like you're talking to your dog. Okay?” I was never embarrassed to ask a stupid question. The best scientists were delighted by somebody who is honest enough to ask naive and stupid questions. Some of the questionable scientists would get hoity with you, but the best ones invariably respected someone who wanted to understand the subject at the risk of being embarrassed to do it.

Melanie Avalon: Thank you for saying that. Okay, then here come all my naive and stupid questions. Yeah, the reason I was pondering the height thing was because people reach a certain height, but then they can't eat their way taller, but people seem to reach a certain weight, and yet, seemingly, they could keep eating their way larger. Another question just to clarify to make sure that we're starting on the same page because you've established a dichotomy or two options like thin and obese or thin and fat. What is the importance of-- what could potentially be four options, which would be metabolically healthy thin, metabolically unhealthy thin, metabolically healthy obese, and metabolically unhealthy obese? Is a metabolically healthy obese more similar to metabolically healthy thin person and an unhealthy thin person more similar to an unhealthy metabolically obese person?

Gary Taubes: Yes. It's interesting the way you phrased it, because what we're ultimately concerned with, is this metabolic health issue or unhealth issue. In this sort of alternative hypothesis world in which I live, fat accumulation is a symptom of poor metabolic health but there are a lot of hormones that influence fat accumulation, sex hormones influence fat accumulation. Testosterone and estrogen inhibit fat accumulation. If you remove the testosterone from a young boy and create a eunuch, as people used to do, you have somebody who tends to be fat, not only be fatter than would have been otherwise, but also that fat manifests in a particular sort of female fat distribution. So, more around the hips than around the gut, the waist. And that person could be metabolically healthy because this is a hormonally created obesity, but it's not necessarily related to the diet. Eating a healthy diet, whatever that is, that person is going to become fat anyway, because of the lack of testosterone or in a woman the lack of estrogen, but you could imagine them being metabolically healthy, because the havoc that we're attributing to diet isn't going to influence them. As women get older, and they pass through menopause and they secrete less estrogen, estrogen inhibits fat formation. As you secrete less of it, that releases disinhibition and fat tells want to fill up with fat, so a certain level of excess fat accumulation is still going to be a naturally healthy response to aging. There may not be a way to reverse that with diet.

Then, on top of this, what we're trying to explain is the obesity and the metabolic unhealthiness that comes with modern diet. One of the arguments in my book, and one of the revelations I made by studying the history is that-- and again, this has been understood by the nutrition community, but they didn't go back in time very far, so they didn't try to isolate the factors involved. But any population, the world that transitions from whatever their traditional diet is to a Western diet eventually experiences obesity and diabetes epidemics. You can chart this back as I did to, for instance, the Native American tribe called the Pima in 1902. A Harvard anthropologist goes to study them. This anthropologist has tuberculosis, so he wants to go live in a hot, dry climate, he might extend his life, which he didn't. But before he died, he wrote the seminal study on the Pima that was published, completed, I think, in 1902. When he noticed he observed that they had this high level of obesity in the tribe, despite having, this being at the tail end of a 30-year famine. 30-year famine is like a 30-year calorie-restricted diet, you're not supposed to be obese at the end of it. Yet, the older members of the tribe suffered from obesity, and particularly the women who also did the most work in the tribe. These tribes, women basically did all the work that pack animals did not do. All the men lounged around and occasionally when hunting.

Even the anthropologist suggested that there was something unique about their food that triggered obesity in this community, and they had been put on reservations during these famines and were getting their food from food stations on the reservation. Those included the food they were now eating, included white flour and sugar, which they didn't have previously. You could also find examples which I did in my research of explorers who had passed through the Pima land prior to this famine, and prior to there being kind of reservationized, if that's a word. And these explorers commented on how lean these people tended to be, how healthy and beautiful everyone was. There was only one comment about obesity that was made, and it was describing a group of these Pima women sitting around, eating the food of the-- I'm going to forget what the name of the cactus was, but if you look it up, it's a high fructose fruit, and fructose is half of sugar.

Anyway, that's the kind of observation. So, you know that when people transition to a Western diet and lifestyle, they eventually manifest obesity and diabetes. Then, the question is what is it in their diet and lifestyle that trigger this fat accumulation on top of whatever might happen naturally, due to things like lessening of the secretion of sex hormones?

Melanie Avalon: The Pima, what was the estimated calorie intake in their starvation diet with the flour and sugar?

Gary Taubes: Oh, geez, I have no idea. This was pre-1900s. Well, people had started talking about calories at this point, they were in Washington and Boston and Germany and had devices called calorimeters. But what they knew was that there wasn't enough food to feed people, and that the children, their growth, a sure sign of a population living through famine, which we've now discussed is kids whose growth is stunted. Then, there are signs of malnutrition and diseases related to malnutrition. Wounds that don't heal, blindness, things that might suggest scurvy, beriberi, or one of the vitamin deficiency diseases.

Melanie Avalon: Diving deeper into what's actually happening, because all throughout The Case for Keto, you discuss the massive role of insulin and what's happening with that. I know I've been thinking about this so much. Here's a basic question. The base state of our fat cells or our body, are we naturally in a storing mode or energy-releasing mode? What I mean by that is, are the doors naturally open and insulin shuts the door? Or does insulin stop the cell from releasing its fatty acid contents? I guess, the question I'm asking is what does insulin actually do? Is it as a storage hormone? Is it growth promoting? Or is it just anticatabolic? What does it do?

Gary Taubes: Okay, it's a little of both. There are different ways a hormone can signal a cell to do something. It could signal it by being there or it could signal it by not being there. And then, it's going to have different signals, depending on the cell type and the receptor type that's receiving it. So, that's how that same hormone can have different effects, and will have different effects on different tissues around the body. It's funny, as you explained, these are very good questions, by the way. If you think about when insulin levels are very low, so insulin comes into, you secrete insulin in response to the-- one of the carbohydrates in the diet, and then also, you'll secrete some insulin in response to protein because the protein you consume, I think 50% or 60% of the amino acids will be converted to glucose or carbohydrate and that glucose will stimulate insulin secretion.

I actually think our system, pancreas and insulin and glucagon that secreted was evolved to deal with the protein and the diets. Then, as people shifted to agriculture, and then went from eating unrefined carbohydrates to refined carbohydrates and sugar, that same evolutionary mechanism had to shift it over to dealing with the glucose from the diet. Insulin secreted in response to meals, and it signals the fat to store calories. It also signals the protein, so that's insulin that is anabolic for muscle as well. It tells tissues to burn carbs for fuel, it tells the cells, the mitochondria not to burn fat and not to burn protein. They use those because the idea is you've got the insulin there because of the carbs. So, we're going to keep blood sugar low by burning the carbs. The higher the blood sugar gets, the more insulin, we're going to have to stimulate more carb oxidation. Insulin is going to tell the lean tissue in the liver also to convert some of the carbs to glycogen, to fill up glycogen stores. It’s another way to keep the blood sugar low. It's going to tell the lean tissue to use protein for rebuilding cells and cellular growth. It's going to tell the fat tissue to hold on to the fat that's been consumed so it stimulates lipid uptake in the fat cells. So, it's stimulates the fat cell to take up fat from the bloodstream and store it, and then it inhibits the breakdown of the fat in the fat cells, so that the fat won't leave the fat.

As insulin is coming down, during the day you're in storage mode, you eat more calories, and you can need during the day, so you're technically overeating. And you store a lot of the excess, some of the carbs and most of the fat gets stored at least temporarily until you need it and get stored as either glycogen or fat. Then, after the last meal, insulin level start to come down, you start to shift over and in between meals. If you go long enough in between meals without having a Coca-Cola or a snack, you start to shift over to mobilize in the fat that you've stored and burning that fat for fuel and that's responding to insulin levels going lower. As insulin goes lower, that's what you do. After dinner, when you have a long period of fasting overnight. Now you're technically undereating, you're expending more energy than you're consuming. You store it during the day, and then you burn it at night while you're sleeping. That's one reason why you don't get up every two hours to eat or you shouldn't while you're asleep. As insulin levels come down, you mobilize more and more the fat.

Then, in the morning, there's a point in which insulin will be minimal. Now that fat is freely flowing out of your fat tissue and you're burning it for fuel, but then your insulin levels will go up in the morning. I don't know if this is a conditioned response or a biological clock response. I never really looked into it much. But it'll actually start to go up before you eat, and then that'll tell your fat tissue again to store you’re your convert excess blood sugar into glycogen and lock up the glycogen, that's stored in the liver. And now, your body senses this lack of fuel availability, that's response to insulin secretion. Now you had breakfast, and then you go through the routine again, with breakfast stimulates more insulin secretion, and then stays elevated. Part of the argument is if you're insulin resistant, your insulin stays elevated all day long or for too much of the day. As long as it's elevated, you're going to be burning carbohydrates for fuel, and you're going to be storing fat. If you don't have the carbs available, but the insolence still telling the fat to be stored, you're going to be hungry and you're going to want to snack or have a Coca-Cola or something to get the energy you need to keep going.

Melanie Avalon: First of all, lot of my listeners will be slightly different from that picture, because a lot of them do fasting during the day and then eat late. It sounds like insulin’s purpose is-- because I think when people think insulin, they think the main purpose is to store your food as fat, but it sounds like if we were to give it a purpose, it's more dealing with the potential energy toxicity of meals. It's keeping the energy or fat in storage.

Gary Taubes: That's one of the things it's doing. I think of it as a fuel partitioning hormone. Insulin and glucagon primarily, and leptin also, it's orchestrating fuel partitioning. So, you're eating a mixed meal, and all the different macronutrients have different sort of utility to your body. Protein, ideally, you need that to build muscle and replenish, and rebuild muscle and lean tissue and organ. So, you want to save the protein for that use. The fat is the ideal storage hormone. Fat is also used for insulating neurons and for cushioning. Ideally, just a little bit of storage for periods of famine. Weirdly enough, you can also use the muscle during periods of famine for fuel. That's got kind of dual utility, you can both use the muscles to be strong or to throw spears at wild animals for dinner. But if you need it, you've got calories there that can be used during periods without food.

The carbohydrates are basically only for energy. When you eat a mixed meal, the hormonal response to the meal basically determines how all these macronutrients will be used and maximizes their use in the present and also you want to try and maximize their future utility. Again, storing some fat, and protein for fuel-- The issue is with modern diets, again, by this alternative way of thinking about it, we eat so many carbohydrates, and they're so easily digestible that that does become toxic. The example I use in the book, and I can't believe I didn't use these numbers before, but basically if you're healthy, when you wake up in the morning, before having breakfast, you have about a teaspoon worth of blood sugar circulating in your bloodstream. So, that's about 16 to 20 calories worth of carbs, glucose that your body is using for fuel actually, when you wake up, it should be using fat. But if you're diabetic, you've got about a teaspoon and a half, it's like 10 extra calories worth of carbs, is the difference between being healthy and being diabetic. Yet, you might sit down for breakfast that has 500 calories of carbohydrates in between the cereal and the fruit and toast and the jam and the healthy orange juice or the healthy low fat milk products.

So, your body has to do something with those 500 calories and some of it gets stored as glycogen and some of it is converted in fat. The insulin that might have evolved from much a relatively carb-free world-- it's always debatable how much starchy root vegetables or fruit our paleolithic ancestors might have eaten, but the insulin that was evolved to do that now has to take care of this sort of tsunami of carbohydrates we tend to consume. So, keeping blood sugar low is one of the things that it has to do, and it does it. But I think the original purpose is just to maximize utility of all these different macronutrients. Make sure that they get used in the best possible, most efficient and at least up to a certain age, safest possible way.

Melanie Avalon: Yeah, I've thought about what you just talked about with the tiny difference in blood sugar levels and being the difference between diabetic, prediabetic, especially because it is such a small amount of blood sugar, which would equal in calories term, not that many carbs, but we take in exuberant amount of carbs, but then what confuses me is, we have limited carb stores. Even in overfeeding studies with carbs, there doesn't seem to be that significant conversion of carbs to fat. So, I'm always just haunted about where the carbs going, are we just burning them?

Gary Taubes: In reading the research in the history of the field, people kept asking that question like, “Okay, we can demonstrate that there's a significant amount of what's called de novo lipogenesis in these carb-rich meals, so where do they go?” On some level, there has to be more de novo lipogenesis than we're seeing. And then, a lot of issues you have to look at, they're looking at the liver, they're looking at the fat tissue. The fat tissue doesn't do a lot of de novo lipogenesis in humans, but it does more of it in rats and rodents. But when you're consuming sugar, a lot of fructose stimulates a lot of the de novo lipogenesis in the liver cells. There were studies done, and again, one of my problems in my career is my-- and this is true, I think most people aren't just more willing to acknowledge it. But my understanding of the science tends to peter out circa 2007, when my first book was published.

I've expanded my areas of expertise in writing other books but as of 2007, there was still a controversy over whether how much de novo lipogenesis you're getting, and how much you're getting in the liver versus the fat tissue. This is always dependent on what technology has come along to measure it, because we talk about these things, but we forget that they're excruciatingly difficult to measure. You could do a pretty good job often if you're willing to take the cells out of the body, and then study them in test tubes. But then, you don't know if what you're seeing in the test tube is actually what's happening in the body. Often you get beliefs that last for 10 or 20 years until a new technology comes along, that makes it easier to measure it. In this case, you would do it by tagging the foods you're eating, the glucose and the fat with some radioactive isotope and then following it, but then you have to ask when they follow it, how do they know where it goes? Often, it requires, at least as of 2007, doing it in animals where you can sacrifice the animal at the end and then look in the various tissues to see how much radioactivity is accumulated there. If you try to do in humans, you can't sacrifice your human subjects at the end of the study to remove their liver cells so you can do biopsies. But it's surprisingly confusing.

As you mentioned, the question you ask is a question that's asked repeatedly in the literature. There's no de novo lipogenesis going on. Where are these carbs going? The other issue is, the people studying this field assume that for people to get fat, and I talk about this in The Case for Keto, they're going to convert-- like for pasta, for instance, to be fattening. I'm one of these people who used to be able to eat 2000-3000 calories of pasta at a sitting. For that to be fattening, it's got to be converted into fat. What they didn't think-- so it was interesting, they knew that dietary fat tended to get stored as fat again from doing these kinds of labeling experiments in animals, so the fat you eat mostly gets stored. They assumed that, “Okay, if we eat a low fat diet, we'll store less fat,” that was one of the ideas that pushed the dietary fat, the idea we should all eat low fat diets for weight loss. What they didn't think is that what's determining the storage of the fat is largely insulin, not the initial storage, but the retention of the fat, in the fat tissue is determined not by insulin. So, carbohydrates can be fattening by stimulating the retention of fat in the fat cells without ever being converted to fat themselves.

The fat we eat is the fat we store, but how much of that fat stays stored is then determined by the carbohydrate content, the diet, which is a wonderful system, by the way to make sure that there's this-- when you burn carbs when you have them and then as you begin to deplete the carbohydrates, you now replace the carbs with fat. It's called the glucose fatty acid cycle and was worked out in the 60s by British biochemists. The implication was the amount of fat we stored is going to be determined by the carbohydrates we ate. The more carbs we eat, the more fat we store because if you don't convert the carbs into fat, you don't want to be diabetic, you've got to burn those carbs for fuel. If you're going to burn them for energy, you don't want to be burning fat also, because the fat is relatively benign. You have this system that as long as you've got carbs available, you're telling your system to store the fat, not burn. The problem is, if that regulation gets out of whack as it does when you're insulin resistant, you just keep storing fat from day to day like a ratchet wrench or roach motel that, the fat goes in, it doesn't come out. And then you end up with chronic obesity. Then, all the fat you've stored to excess is the fat you've eaten, but the reason it's stored to excess is because of the carbs.

Melanie Avalon: So, to make sure I'm understanding, so it sounds like some people say that the insulin carb hypothesis is making you store fat because you eat a meal of carbs, and it makes you store more fat. But what you're saying is, it's not so much the storage of that meal right then, like that acute rise in insulin, it's the longer postprandial insulin that the food got stored, but then it's like the lingering insulin that keeps the fat from ever coming out again, like you said.

Gary Taubes: Yeah. Let's put some numbers to this so people can understand what we're talking about. Say a typical breakfast-- I don’t know if it's typical. Let's say have a breakfast that’s 50% carbs, 30% protein, or excuse me, whatever, it doesn't really matter. Mostly carbs, some protein, some fat. You're going to store most of the fat. So, if it's 500 calories, and there's 200 calories of fat. That fat is going to get stored over the course of a day, if you're large human being like I am, I'm 6’2”, 210 or 215 pounds these days, I'm going to eat about 3000 calories a day. If that's half fat, or 40% fat, that's going to be 1200 calories of fat. I'm going to probably store about 900 of that, assuming my body is working correctly. Over the course of the day, after breakfast, after lunch, after dinner, about 900 calories of fat is going to go into my fat tissue from the meal. For me to gain two pounds of fat a year, I have to store in excess 20 calories a day. That's all. Two pounds of fat, say, gain, 20 pounds in my 30s, and went from being nicely proportioned to overweight in my 30s and then the throwing another 20 pounds in my 40s. Now by the time I'm 50, I'm obese. That 20 pounds in a decade is 2 pounds a year, that's about 20 calories being stored as fat a day.

Melanie Avalon: Can I ask you a quick question? Does it have to be an extra 20 calories stored or could it just be an extra 20 calories not released later?

Gary Taubes: Well, that's the point. That's exactly the point because I'm taking in 900 calories. If 880 get released and burnt up for fuel, and 20 calories stay behind, they're trapped, I refer to this as the fat trapping scenario. For some reason, 900 calories go in, 880 calories come out, that's pretty damn good in terms of accuracy, but there's still 20 calories that are left behind that are going to make me obese over the course of 20 years.

Melanie Avalon: It sounds like we gain weight because we can no longer lose it.

Gary Taubes: One of the scientists I talked about, whose work I talked about in my first book, Frenchman named Jacques Le Magnen. He was at Collège de France, fascinating guy. He had encephalitis when he was 12 years old and went blind. And then still went into research, and he was fascinated by this concept because he was blind of how odors that you notice, I always liked to use the smell of cinnamon buns cooking for instance, is going to be very intense at first. Then your body, your nerves, your nose adjust to it after 30 seconds or a minute, you no longer really notice it, even though the molecules are still in the atmosphere, you should still be able to smell it. He started studying then, then he went from there to hunger and similar concepts with hunger and wanted to understand why people actually start a meal, not that hungry usually. And then, they get hungry or as a meal progresses. He did these experiments on rats where he studied the time between meals and the time between feeding and manipulated their insulin levels and their blood sugar levels. He concluded basically that the reason we get fat is because our fat cells store fat and they don't let it all out. So, you don't get fat because you're eating excess food, you get fat because your fat tissue isn't releasing everything that it takes.

What is fascinating is world of research-- not a world, but there are very good research groups around the world that are beginning to study and document this phenomenon. In people with obesity, the fat tissue tends to hang on to the fat they've stored for far longer than it does for lean people. So, in lean people, the fat is going in and the fat is coming out. It's all perfectly in sync. When you burn through all the fat you've stored, your body by then has replenished, and you’re eating and getting a new supply, and your energy expenditure is going to be dependent on the fuel you have available. So, it's basically this finely tuned evolutionary homeostatic system that keeps your fat tissue with a certain level of fat, and always makes enough fuel available, so that the body can run itself. And then you disrupt that with modern foods, and now inswing it, you secrete more insulin than you should, the carbohydrates in the diet, the insulin stays elevated longer, and this is the hypothesis. And then, fat goes into your fat tissue, but not enough of it comes back out again, and day to day, it accumulates.

Melanie Avalon: I have a question about the implications of that as far as the macros go. It sounds like if you are stuck in this state of the fat cells not being able to release their fatty acids, because of the insulin situation, that a low carb diet, reducing the insulin would allow the cells to again release their storage content. Then, once you've reached a point where you're either at homeostasis or even underweight, since fat is so easily stored and carbs, unless we find that magical reason for how they're being stored more than we think they are, hypothetically, if you're at homeostasis or underweight, wouldn't you be less likely to gain weight if you ate just carbs or as low as fat as possible?

Gary Taubes: Well, that depends on this question of where did the carbs go? But it's possible, yeah. We want to fix, when I'm writing my books, I'm thinking about people, the phrase I use in the book that I acknowledge I'm borrowing from 1950s era diet books, because I think it's very appropriate, that some of us fatten easily and some of us don't. Those of us who do, we know who we are, our life is a constant struggle just to maintain a healthy way, just like people who are predisposed to be diabetic, their life is going to be a constant struggle to maintain a healthy blood sugar. There are people whose life is a constant struggle to maintain a healthy blood pressure. These all go together, by the way, which is another part of this argument. For those of us who fatten easily-- I have a brother, when we were young, we both ate as much food as humanly possible and I was thick and he was thin. He became a rower. I became a football player. It's like anatomy is destiny.

We both ate. Not only we ate as much food as humanly possible, we ate as quickly as humanly possible. We'd finish dinner every night, this was back in the era when people talked about portion sizes being smaller, but they forget that we all ate family style. Our mother would cook. There were four of us, she would cook two chickens, and starch and vegetables and we would be done in 18 minutes. If I took more than that, my brother would get too much food and I wouldn't get enough. We ate fast, he was thin, I was fat. Not fat, but thick. He was taller too. Our bodies wanted to do something differently with foods available.

The point is, as I got thicker as I got older, I'm going through this, and again, at the rate of about two pounds a year after I turn 28 or so, that's the issue that I want to take care of, and that's this insulin dysregulation that if I fix, that issue will take care of itself. If I can fix the insulin resistance, the elevated insulin levels, then my fat cells won't accumulate excess fat every day, they'll be tempted to mobilize the fat they have, they’ll engage in unfettered lipolysis, and I'm confident that the other cells in my body will happily burn the excess calories off because that's one of the things they'll do. Once I get lean, then the question becomes-- well, the other way to get around that, you can fix the dysregulation but it's possible that you could also starve the fat tissue or fat, or of calories. We know what happens when you try starve it of calories, you're slightly hungry all the time, and you get these variety of symptoms that are associated with hunger and semistarvation, including being angry and short tempered and depressed and tired and thinking about food constantly. Then, the longer it goes, your hair falls out and your skin gets flaky, and you lose your sex drive and there's that whole documented series of symptoms that go with semistarvation and hunger.

I can imagine you could eat a very low fat, high carbohydrate diet, maybe something like 5% or 7% fat, which is very hard to do-- It's certainly, virtually impossible if you're eating any animal foods, because animal foods tend to come with fat attached. But that if you did that, you could starve your fat tissue of fat, and reduce your fat storage that way. I don't know what the doctors would call long-term sequelae of that would be, are you going to be hungry all the time? Are you going to suffer fat hunger? There going to be side effects to that kind of hack of the system. So, instead of fixing the insulin dysregulation that's causing you to store excess fat, you do an end run around that by starving your body of fat. I could imagine that that's why things like the potato diet works, or at least in one person on the internet, or the Dr. McDougall starch diet or even-- I'm not sure the kind of low fat diets promoted by Ornish or Pritikin are low enough in fat. When I look at people who have been on those diets for a long time, they certainly don't look like they're working, but [laughs] I don’t know. They supposedly have wonderful arteries that I can’t judge, but that was a very unscientific statement I may, just made, but it is what it is.

Yeah, you can imagine ways to sort of hack the system. And bodybuilders would do this, because they want to minimize fat accumulation. On some level, they want insulin because they want to promote-- they want the anabolic effect of insulin, but at some point, they're also going to want to minimize their fat storage to look as ripped as humanly possible. One way to do that might be to in effect live on just protein and no fat, nor as much protein as you can get, you'll still need unhealthy carbs. Again, I'm not that familiar with that world, as those bodybuilders are always willing to tell me on Twitter.

Melanie Avalon: I guess the picture I'm painting in my head right now of the potential options would be-- if you're on a low carb diet, with low insulin that fat could be freely going in and out. So, you could hypothetically, easily lose weight, most likely. You could hypothetically, if you kept putting in more fat gain weight. But then on the flip side, like a high carb, extremely low fat diet, it'd be really hard to lose weight because you would be keeping the fat perpetually locked up. But it might also be hard to gain weight because if indeed, the carbs are not turning into fat.

Gary Taubes: It's just depends how low-- Many of the people in my world, we get here-- I mean, I got here as a journalist, but then I clearly experimented it with what was then called Atkins, and now keto, and it worked so well for me, that I am kept doing it and have experimented over the years with other things like intermittent fasting. What I'm trying to say, I could describe to you, I remember once I lived in LA, from about 1988 to off and on to 2001, at one point, I was writing screenplays with a collaborator who was a little more affluent than I was, and she had a personal trainer, who is the single healthiest person I've ever seen in my life. He had a diet. Again, I played football in college poorly, but I played and I was a lineman, so I wanted to be as heavy as possible back then. Anyway, so I was always trying to keep my weight down and he said if I did his diet, I would lose six pounds in two weeks and more energy than I'd ever had. I did it, and then I did it to the 90s and it worked. I lost six pounds in six weeks and then energy and felt great. Then, over the decade, I gained the weight back and more.

I actually I found this thing, so breakfast is oatmeal, apple juice, cream of wheat with four to five egg whites. I'm only allowed to eat fruit in the morning, and I keep egg whites to snack. I joke that in the 90s, I probably boiled 10,000 eggs and threw out 10,000 yolks. Okay, my lunch was brown rice with chicken, egg whites, pasta, baked potato, yams, chicken, tuna, turkey, so very low fat meat, steamed vegetables, salads, dinner was pretty much the same thing. I wasn't allowed complex carbs at dinner. I was supposed to pull the skin off the chicken, steam chicken in the wok, no dairy, no fried foods. I actually ended up eating oatmeal with apple juice, because apple juice seemed like a fruit. I didn't want the fat from milk and no dairy at all. No sodium. I'm guessing this is maybe a 15% fat diet. Drink is a glass of eight ounces, I'm reading from the-- this has gone from computer to computer with me since 1991. Drink a glass, eight ounces of water, and I used to give this to people because it seemed to work. I went on, I lost six pounds in two weeks. Again, it all came back.

Salad dressing. I was allowed safflower oil and apple cider vinegar, but I don't actually remember ever buying safflower oil. I kept this up for a year. I remember I was doing a science writing fellowship at MIT in Boston. I was making my lunchtime pasta, which I had every day for lunch. I would have pasta with no olive oil in the water, though if the pasta is stuck, there was nothing I was going to do about it. Fresh salsa from the market. I'm thinking, I'm eating 800 calories of pasta to fill myself up. That was half a box. So, half a pound the pasta and I was thinking, “Geez, I get two quarter pounders with cheese, and that would also be 800 calories. [laughs] And I'd be happy.”

The point is, most of the people in my world, we went through periods where we ate low fat, mostly plant dietary. In The Case for Keto, I interviewed 120 odd physicians who had transitioned to this way of thinking out of my rough estimate as a few tens of thousands around the world, and they had all gone through-- Not all, but most of them, had gone through periods where they'd been vegetarians, even vegans, we all did the low fat diet thing in the 90s into the 2000s, and we had gotten fatter anyway, that's how you end up in places like keto, is because everything else has failed for you. Then, you suddenly eat this very low carb, high fat diet and your body seems to fix itself. The argument is, if you look at the physiology of insulin, that would explain pretty much everything people tend to experience when they go on these diets. It doesn't mean it's right, but it's what you would predict would happen when you eat a diet that minimize insulin secretion, which these diets tend to do. But you're right, if you eat too much fat, I think one of the reasons when it fails, is people basically they go from having sugary beverages in between meals, so feeding their bodies on this exogenous source of sugars, to then doing things like having bulletproof coffees and drinking fat all day long, or snacking on fat all day long, instead of allowing their body, forcing their body to burn the fat they've stored.

Melanie Avalon: Yeah. Can I tell you what I think is one of the biggest potential myths or mind-blown moments or misconceptions about fat and insulin?

Gary Taubes: Go right ahead.

Melanie Avalon: People often say when they're doing a low carb diet, that fat doesn't release insulin or doesn't release much insulin, so they can have an unlimited amount of fat. That's the conclusion they draw.

Gary Taubes: Similar, yeah.

Melanie Avalon: Yeah, but when really I feel the reason that fat doesn't release insulin is because it is so easily stored as fat.

Gary Taubes: Well, that's the thing, you don't need insulin to store fat as fat.

Melanie Avalon: It's like the opposite. People think, “Oh, no insulin, it won't be stored,” when really, it's no insulin, because [laughs] it's easily stored.

Gary Taubes: On some level, that's true. So, that's the issue is, how do you balance that out? You know in the book, a lot of this comes down to ultimately self-experimentation, what is working for you. Some of the physicians I interviewed who I think are very smart people think their patients tend to stall on the diets because they try the low fat versions of a low carb diet, that's a natural compromise. You don't have starches, but you have your green vegetables cooked in the wok and your skinless chicken breast, and now you're getting too many calories from protein, which also like said that some of those amino acids will be converted to glucose and stimulate insulin. Your body still needs to store some fat anyway. It's always going to be trying to store some fat because it needs some fat is for reserves, for cushioning, and the insulin. But you're right, without any fat, I mean without any insulin, you're still going to store the fat, some of the fat you've eaten.

For some people, the diets might fail to get them to the weight they would prefer because there's not enough fat. And for others, they might be doing too much fat, and there are all sort of [unintelligible [01:05:48] experiments you could try to go further. I think a lot of people, again, as I said, as we get older, we secrete less estrogen, men secrete less testosterone, our bodies want to be thicker. And that could even be weird evolutionary response. In theory, after your childbearing years, evolution doesn't care about us. But I think that's a little naive. It cares about groups of populations, tribes as well. It's conceivable that people get older, we're lower on the food hierarchy, we're less likely to be fed by others, the hunters and the gatherers, and so they might not need little more fat stores to see them through these periods, and that would explain why as we get older and secrete less hormone. My brother, who's a mathematician calls these Just So Stories, like the Kipling books, how the camel got its hump.

Anyway, the point is, some people will never be as lean as they'd like to be without starving themselves, and then they will be a unhealthy lean. But you could get to the point that's a healthy weight. You began this conversation talking about metabolically unhealthy. The ideas here is the same carbohydrates we're talking about that cause the excess weight, also cause the metabolic complications that go with that excess weight or not, the blood pressure issues, the blood sugar issues, inflammatory issues.

Melanie Avalon: Just really quickly a resource, did you read a study? It came out recently. It was called the 100th anniversary of the discovery of insulin perspective: Insulin and adipose tissue fatty acid metabolism. Did you see that?

Gary Taubes: The one by the fellow in Montreal with the French name. I'm not going to remember at the moment, not necessarily Montreal, but Quebec.

Melanie Avalon: It might have been, I'd have to look it up.

Gary Taubes: I skimmed it. It's a very long article. It was being thrown at me because he talked about this on Twitter. He mentioned that there were other factors that drove fat storage after meals other than insulin and said that they were more important. Although I questioned how he knew that were more important. But then he went on by the end of the article to talk about how insulin determined the retention of the fat after it was stored also, it was sort of completely in line with this thinking.

Melanie Avalon: Yeah, that's definitely the article. I have it all highlighted. Yeah, because he says basically, that insulin doesn't necessarily correlate to fatty acid storage, like the fatty acids more closely resemble the fatty acid circulation after a meal rather than insulin levels, per se. Then, yeah, he does say that insulin leads to extended what you just said.

Gary Taubes: Right, exactly, which is what we're worried about. I actually thought I should email him. I’d be curious if he-- because I've been challenging the thinking in the field, there's a portion of the research community that knows my work and respects it, and this happened to talk to me. There's a portion which may or may not be bigger or smaller that wants nothing to do with me, because the implication is that I think they've failed, and we're not good scientists. I'm always curious if I reach out to someone and say, I would like to talk to them more about this work, whether or not they'll talk to me. In this case, I would just like to ask him-- one of the fascinating aspects of this field-- everything we're talking about, for the most part was worked out by the 1960s. By the 1960s, they needed a couple of technologies to do this. They had to be able to measure fatty acids in the circulation, and that was 1956.

The fascinating thing about the field, when you look at the history, 1956, three different groups sort of pioneered way to measure fatty acids in the blood. We store fat as triglycerides, which are three fatty acids and a glycerol molecule backbone. Then, when I talk about the fat being repolisized, there are enzymes in the fat tissue called hormone sensitive lipases that break down the fat, that triglyceride into fatty acids glycerol separate, and then those can escape into the bloodstream, we then burn the fatty acids for fuel, we oxidize the fat as fatty acids. And the glycerol, which is a carbohydrate can also be used for fuel, preferably by the brain of reading a low carb diet, because that'll provide some of the glucose that the brain will still burn.

You had to measure fatty acids to do this, and then you had to be able to measure insulin levels in the blood. That wasn't doable until couple, Rosalyn Yalow and Solomon Berson, reported on this, created this radio amino acid, that was a way of basically labeling insulin antibodies. You can use it to measure any peptide hormone in the blood, and peptides are tiny proteins, and they're in the blood at about-- very hard to measure. After these two discoveries, there was a revolution and understanding fat metabolism. All this was worked out, and the role of insulin was worked out, and how insulin inhibits lipolysis and stimulate lipid uptake and how inhibits fat oxidation and then lean tissue. It had virtually zero effect on the science of obesity. The obese, by the 1960s, this idea that people get fat because they take an excess of calories from the diet that they eat too much and become conventional wisdom and obesity science was dominated in [dog barking] the 1960s by psychologists and psychiatrists. If you can hear my dog barking in the background, I apologize.

The psychologists, psychiatrists, they didn't care about this endocrinology, this hormonal regulation of fat tissue, they were trying to figure out how to get fat people to eat less. Then they were studying behavioral reasons why fat people might eat too much and consume more calories. This idea that the hormonal enzymatic regulation of fat storage was relevant to a disease of excess fat storage never caught on. It's bizarre. Even when you read the sort of seminal research papers in the field, a guy named George Cahill was the leading metabolism researcher, the 1960s. He was at Harvard. He's studied a lot of what we know about ketones and ketosis came from Cahill's work. 1971, he gives a Banting Memorial address at the-- this is the 50th anniversary of the discovery of insulin, the American Diabetes Association. His talk is on the physiology of insulin in man. He discusses everything we've been talking about and the insulin’s effect on muscle and on fat and how it's regulating this field partitioning and making sure all the different tissues get the fields they need after feeding and during famines. He talks about how insulin stimulates fat storage and inhibits fat release. If your insulin is above a certain null point, every day, you're just going to keep getting fatter. Then, the last paragraph, he says people get fat when they have too much food available.

I interviewed Cahill about five years before he died. He passed away around 2012. I want to go back in time-- and he lived in New Hampshire at this point. Instead of interviewing him on the phone, driving up to New Hampshire and saying, “George, look at what you wrote. Okay, you explained obesity, and then you said fat people eat too much.”

Melanie Avalon: Okay, I have a question about that. Even if it is all hormonal, and it's signaling, and that is what's leading to the accumulation of excess energy, and that's what's letting us not release the fatty acids, didn’t it still require at some point, eating more energy than--

Gary Taubes: Then you expend. Well, if you're getting fat, if you're getting heavy, you're taking more energy than you expend, that's the laws of thermodynamics. You can't make energy from nothing. This is the law of energy conservation. The only way you know there's what's called a positive energy balance is because a person's getting fatter, so you have no idea how much they're eating, you have no idea how much they're expanding. You know they're in positive energy balance because they're getting fatter, getting fatter is positive energy balance. Getting taller is also positive energy balance. If you don't consume enough iodine and you get a goiter, that's a positive energy balance. As long as your body is getting heavier, you're in positive energy balance.

The problem is people take that idea and they say, “Well, then you get fat because you're in positive energy balance.” And that means you're eating too much. That's the phrase we're always throwing around. That's a tautology. Getting fatter is positive energy balance. The question is, how is that happening? Is it happening because you somehow can't regulate how much you eat, or you're not going to the gym enough, or is your fat tissue taking up 20 calories a day and not releasing it? Let's say you're eating 2500 calories every day, and you're storing as fat 900 calories every day, and you're lean, so 900 calories goes into your fat tissue, 900 calories come out of your fat tissue, your body stays the same weight, you're in energy balance. Everybody is so proud of you. They think this is a person who eats in moderation and exercises.

Now, you're eating 2500 calories a day and 900 calories going into your fat tissue and 880 comes out. Now, you're in positive energy balance by 20 calories a day. Actually, if 20 calories get stored as fat and you fixing your intake at 2500 calories, it means you're going to expend 20 calories less than you would have otherwise. You're not going to notice, you have no idea how much you're expanding, but your body will easily burn 20 calories less without you ever noticing. It might do it while you're sleeping, doesn't even matter my do it between now and like 2:07 PM, it's 2:06, you're not going to notice it. You've now been in positive energy balance, you trapped 20 calories in fat tissue, you expended 20 calories less, you haven't changed your intake at all. The positive energy balance is the 20 calories you stored, and that's determined by hormones, that enzymes and maybe even the central nervous system might be involved.

Melanie Avalon: Were the hormones and enzymes determined by the types of foods you ate?

Gary Taubes: Yeah, responding to the types of food you ate, yeah. Not how much you ate, but the type of food you ate. One of the interesting things about when I'm talking about reading these articles, in the 70s and 60s, where they're discussing fat store-- George Cahill does this in his articles. They'll talk about insulin signaling in the fed state. After you eat, insulin levels are increased. They know that insulin is responding to the glucose from carbohydrates and from the amino acids and the protein. But they don't want to say that. They don't want to say insulin signals the carbohydrate-fed state, because they also know that by the 1960s era diet book doctors are arguing for carb-restricted diets and that only quacks don't believe that it's all about the calories. They consciously make something about the calories, which are literally about the macronutrients.

When you're talking about diabetes and insulin secretion, you're talking about response to carbohydrates. When you're talking about anything other than diabetes and insulin, these people are talking about the response to eating because they don't want to give any credence to the idea that obesity might be about something other than fat stored. Again, it's fascinating reading this.

Melanie Avalon: That's really fascinating. All these other dietary or health biomarkers were fine to talk about them as the types of food, but for weight gain, no.

Gary Taubes: As soon as you talk about weight gain, the mantra is a calorie is a calorie. Even the weight gain goes along with diabetes where a calorie is clearly not a calorie. So, you might probably notice that week ago, Science magazine ran an article by two researchers Kevin Hall at NIH and John Speakman who has a position in England and position in China, and travels between the two of them. They claim to basically refute the carbohydrate insulin model. It was a very interesting two-page article in which for the first time almost ever they said insulin is a very important hormone to discuss when talking about obesity, because of its effect on fat stored. So, that was progress from my perspective. They basically took because of my work and a couple of other people's, they were willing to finally acknowledge after 50 years that they can't talk about fat storage without talking about insulin, but then they wanted to put it into an energy balance context, so they wanted to be able to claim that this idea that carbohydrate stimulates insulin, and that's the driver of excess fat was wrong, but that carbohydrates do stimulate insulin, but they make you eat too much. So, it's still energy balance.

Anyway, the point is, they didn't really mention type 2 diabetes, because if you're going to refute the idea that the insulin is being secreted in response to the carbs, you don't want to-- and removing that problem fixes the obesity, you don't want to be in a position where you're acknowledging that removing that same problem also fixes the type 2 diabetes that associates so closely with obesity, many people think of them as kind of two sides of the same coin. Again, there was this sort of conscious deception going on they could-- or unconscious, so they could continue to believe what they wanted to believe, without having to accept something that implies that what they had wanted to believe was not right.

Melanie Avalon: I'm still struggling with, if that's technically true, though, what they said, like, so them saying that the carbs release the insulin, it's still about energy balance, because it makes you eat more or whatever.

Gary Taubes: Yeah, well, to me, again, I'm arguing that this energy balance ideas. I mean, the line I like to use, it was a theoretical physicist named Wolfgang Pauli, who was very famous German for his witty putdowns of work he didn't like. He supposedly read one young kid’s PhD thesis. When the kid asked him what he thought, he said, “It's not even wrong.” This energy balance idea is just not even wrong. It's based on this idea that because getting fatter is positive energy balance, we are going to blame getting fatter on positive energy balance.

Melanie Avalon: Okay, right. It is what's happening, but it's not the cause or the reason?

Gary Taubes: It's like saying people get richer because they make more money than they spend. If they're getting richer, they're making more money than they spend, by definition, the two things are equivalent. One can't cause the other. By the way, I've had these arguments with people where they go, “No, no, of course, you can say people get richer because they make more money than they spend.” It's like, okay, head slap, I give up. You could think of the fat tissue, I've been trying to work on a monetary metaphor for this. You could imagine this hypothesis is basically, insulin stimulates a kind of tax that your fat tissue takes. You think of it, I'm going to a bank or your employer, and your employer pays you $2,000 every month, but takes social security tax outright. The social security tax is like the equivalent of what goes into your fat, stays in your fat tissue, because it's supposed to come back to you when you need it at age 65 or over. But imagine if it never came back, it just continued to accumulate. You put in $2,000, they take a 10% social security-- this metaphor can’t possibly be working by the way.

Melanie Avalon: I'm following.

Gary Taubes: Yeah. Any metaphor that requires being more complicated than the actual thing you're trying to describe is a failed metaphor. So, let's just forget I ever went here. I'll work on this one on my own time.

Melanie Avalon: It's like when you can only take money out of your savings at certain times, like you have a limited number of transfers. Insulin doesn't let you transfer out money, out of savings as much.

Gary Taubes: Yeah, the other way to think about it is, I’ve got to remember, an ATM. You put money in a savings account, so your fat goes into a savings account. Then, you can take it out through the ATM all day long or all week long, you can just take money out as you need it and spend it, but what if your bank just refused to give you all of it back, so kind of forcing you to save it-- we're never going to get anywhere with this, Melanie. I think we should just let your--

Melanie Avalon: Okay. [laughs] We'll circle back. [laughs] If I think of one, I will email you at 3 AM, here's the metaphor. Well, this has been absolutely, absolutely amazing. I'll tell you really quick, my one hack. Because you're talking about people who plateau or they stall on low carb, I found a hack that I think should work for almost anybody and it's because you're talking about people will just reduce the fat, but then they're like miserably hungry. If you do remove all fat, but only make your fat from MCT oil, C8 only, I don't think there's a conversion pathway for-- I keep reading all the studies on it for C8 to fat storage, it's pretty much burned like a carb.

Gary Taubes: By the way, I'm very good at buts. That’s what I do. You're going to get fat, and if you're eating animal products, you're going to get fat in the animal products.

Melanie Avalon: From the intramuscular?

Gary Taubes: Yeah. Well, even if you're eating a lean chicken breast, it's still going to be a significant percentage of the calories from fat.

Melanie Avalon: Like, really, really lean chicken breast though, or 99% or 99% turkey.

Gary Taubes: I don't think any degree of excess weight is worth having eat really, really lean chicken breasts. I mean, to me, it's just one of the tragic consequences of the low fat era, that any of us-- yeah, and you know what you have to do to eat them right, you’ve got to either marinate them something sweet or soy or bread them. Now you can bread them with pork rind, breadcrumbs, but now you're putting fat back again. I know, there's this weird acceptance lately in the low carb world of maybe higher protein diets, but I'm just not-- I have to really work out the implications of them. I mean, it could work.

Melanie Avalon: I've done it personally, I thought it was just me. I basically did higher protein,  , all really, really lean, low fat, but I did thousands of calories with MCT oil with it and I lost weight. I thought it was just me, but I've started seeing it. There's some people on Instagram doing this now too.

Gary Taubes: I mean, so you pour the MCT oil over the--

Melanie Avalon: The C8 version.

Gary Taubes: Over the lean chicken?

Melanie Avalon: Mm-hmm. It tastes really good to me, because it just emphasizes the flavor of whatever you're eating.

Gary Taubes: How much weight did you lose doing?

Melanie Avalon: I don't know. All I know is I started doing it. I did it because I wanted to gain weight because I have a sensitive digestive system. The MCTs aren't treated like normal fat. I was like, I'll just add tons and tons of MCT because I can digest it more than I can add tons and tons of calories. But it had the opposite effect. I just lost weight from there.

Gary Taubes: The only thing that worries me about that-- well, there's two things. What happens when you stop doing, and if you don't stop, I'm pretty confident that would evolve to consume tons and tons of MCT oil. It's one of the things that worries me. I'm doing this book on diabetes now. Again, mostly history, and it's fascinating. So, the idea is until 1921, the discovery of insulin, diabetes is seen as a carbohydrate intolerance disorder. The diet to treat it is basically a ketogenic diet, they don't use the term fatty animal meat and green vegetables had have been boiled three times to get all the carbs out of them. Today, we would call somebody with type 2 diabetes healthy and would prolong the life of somebody who has type 1 diabetes. Then, insulin is discovered, and it goes from being carbohydrate intolerance disorder to insulin deficiency disorder, even though only the acute childhood form is actually an insulin deficiency disorder.

Once you start treating people with insulin, you have to give them carbs to balance the insulin. They start feeding them carbs. Then, it turns out that some doctors say, “Geez, my patients don't want to be in a diet, they want to eat like everyone else. Why don't we just give them a lot of insulin and let them eat as many carbs as they want.” Then, it moves into this sort of free diet era. It runs into the low fat science of the 60s, and they never actually get around to checking whether that animal diet that they fed pre-insulin might be the healthiest way for these people to eat.

The point though is insulin comes along, it's a lifesaver for people with type 1 diabetes. It's miraculous. It seems like a miracle, these people are emaciated skeletal on the brink of death, starving literally, and you give them insulin within like a month, they're back at work, and they looked as healthy as you could imagine-- within two months are fat, but nobody's caring about that. After 10 or 15 years, they start seeing the complications of keeping these diabetic patients alive on insulin, and it's just a tidal wave of neuropathies and retinopathies and renal disease and heart disease. When you read the case studies as I have, some of these patients, they seem like in perfect health, I mean, they've gotten their lives back, they get married, they have children, they have jobs, and then over the course of two to three years, their bodies just crap out. It's tragic to read it, but that thoughts in my mind, because again, even with-- I've got a book called The Case for Keto, there are no long-term trials. You can make a lot of assumptions about why this is a very healthy way for us to eat but I worry about anything that is evolutionarily abnormal. Is it a good idea to consume MCT oil for years to decades? If it's in coconuts, it's cool, because we were eating coconut as well, well, some of us were.

Those are the kinds of things that worry me. You just never know when you're doing in. So, we talked about animal experiments and biohacking. When you're hacking something, it might blow up in your face. There's just never any guarantees.

Melanie Avalon: No, this is so true. Yeah, I don't think it would be a long-term thing, it’d be more for losing the weight and then replacing it with a higher fat from normal-- you call them in the book, vintage fats?

Gary Taubes: Yeah, that's a phrase I borrowed from a book by [unintelligible [01:31:00], collaborator whose name I'm going to embarrassingly forget.

Melanie Avalon: I love that that you discuss in the book, which was the concept of what is safe and are things that are evolutionarily novel, more likely-- Or, the difference between things that are added versus taking away? Is low carb correcting health? Or is it improving health? Listeners, you just have to get the book, because there's just so much in there.

Gary Taubes: Thank you. Just to go a little bit further in this, the idea is we tend to think and people tend to market foods is, when you hear the phrase food is medicine, the idea is there are certain foods we can eat that are going to make us healthier. As opposed to there are foods we eat that make us unhealthy. I buy into the second idea. I think there are foods we then make us unhealthy, and we could remove those and we will become healthier. I don't think there are like-- the advantage of blueberries isn't that they're full of phytonutrients. So, if you eat blueberries every day, you will somehow live three weeks longer than if you don't. I think blueberries are benign, and I love them. And then, they're in season now, so I eat them to excess.

Melanie Avalon: I eat pounds of blueberries every night.

Gary Taubes: Yes, but they're benign, because they don't do harm. Often when you hear these phrases, like I said, my allies in the functional medicine world like to talk about food as medicine, I'm just not sure that's true. I think we can get by in a lot of different foods, but some of them are very bad for us and the healthiest we can be for the most part are by removing the bad foods. Then, if there are good foods, they're probably things that everybody in your neighbor now tells you are bad for the environment.

Melanie Avalon: Speaking to that, the fact that all of the health benefits from fasting, which is the absence of food.

Gary Taubes: Exactly. Yeah, it's a very good argument. I may steal that from you, but I will try to remember to give you credit.

Melanie Avalon: Oh no, please steal. Steal away. That would make my day. Oh, my goodness. I’d be so excited. Well, this has been absolutely incredible. I could talk to you for hours more. I'm just so obsessed with your work, and I can't thank you enough for what you're doing. Do you think there's going to be change? What do you think it will actually take besides having your books and talking about it?

Gary Taubes: Well, I think there are two competing forces at work. One is this way of thinking about diet and health works. It takes people who are unhealthy and makes them healthy. I mentioned that I interviewed 120 plus physicians for this latest book, The Case for Keto. One of the things they said to me over and over again, is they went into medicine to make people healthy. Then, with the obesity and diabetes epidemics, they found themselves just managing chronic disease for a living and it was depressing, and it burnt them out, and it wasn't anything they wanted to do. Basically, they're writing prescriptions, and they're upping doses, and they're switching drugs, and they're managing all those negative complications of obesity and diabetes and hypertension. If you're in family medicine or internal medicine, that's what you do.

When they realize that they can get their patients to change their diets, they could actually do what they wanted their medicine to do, which was to make them healthy. This is such a powerful thing, that it spreads from patient to patient and physician to physician and it's slowly changing the world. The flip side is livestock agriculture is a significant contributor to climate change, and it's cruel to the animals and it's unethical to eat animal products and so we should all eat mostly plants or become vegetarian and vegan, because the health of the world depends on it. That movements also making great progress. I don't actually know how it will balance out in the future. I see more and more physicians buying into them realizing that if they want to make their patients healthiest, best thing they can do is get them off the carbohydrates they're eating. Simultaneously, every one of my next-door neighbors telling me I should go vegan like they do, as I watch them get thicker and thicker as it happens. I don't know how these are going to balance out.

You read about one aspect of this every day in the newspapers, and media leans towards the mostly plant, if you want to be vegan, that's the way to go. It's got the least climate footprint. Behind the scenes, you have all these people converting to low carb, high fat diets, because it makes them healthy. The next 10, 20 years will be interesting. Hopefully, I’ll live long enough to see some kind of significant change, because otherwise people will blame my premature demise on my diet.

Melanie Avalon: That's the thing that we're haunted by.

Gary Taubes: Yeah, exactly. It's like we all have to live full 90, or at least longer than our critics.

Melanie Avalon: The people who are longevity experts, and they put out a number of what they're going to live to, I'm like, “I would never do that,” because [laughs] then you have to live up to that literally in the most literal sense.

Gary Taubes: I admire their optimism, but we could do another two hours on that science.

Melanie Avalon: I will say really quickly. Do you know Robb Wolf? Have you met him?

Gary Taubes: Yes, I know Robb.

Melanie Avalon: Have you read his Sacred Cow?

Gary Taubes: I have owned his Sacred Cow and I've read chapters of it, which I hate to say, because I hate when people say that about my books. I don't think you could discuss the livestock, agriculture issue without reading Sacred Cow.

Melanie Avalon: For listeners, I did an interview with Robb on that, and I'll put a link to it in the show notes. I would encourage you, Gary, to read it, because I think you'll feel a lot better about your concerns and thoughts.

Gary Taubes: The issue I've had-- I've discussed this with Robb and his coauthor--

Melanie Avalon: Diana Rodgers, I think.

Gary Taubes: Diana Rodgers, yeah. It's the same issue people had when they read Good Calories, Bad Calories, or any of my books like, what am I leaving out? Why am I making this look so simple? When I read Sacred Cow, and I have read chapters, I feel like I'm reading-- and people have said this about my books, I feel like I'm reading the prosecution argument or the defense argument in that case. It's always the issue with these very complex social controversies. The only way I would have real faith is if I did the reporting myself. That way, I know I'm going to go out of my way to-- because you can always make one side of an argument look compelling if you don't include the other side. We see this all the time with-- again, in the media with COVID and all the social issues that are-- I have faith. I know, Robb, and I think he does terrific, wonderful work. I don't know Diana as well-- I don't really know Diana, but I mean, I have faith in that level, but the way I'm wired is to be skeptical.

Unfortunately, some arguments. I really have a year or two to do the reporting myself, which I don't. But unless I did that, I don't know, really I'm going to remain a little bit skeptical. When I wrote about these issues in the Wall Street Journal, and that's when we had-- I did an essay for the Wall Street Journal arguing that, in fact, a lot of the arguments for plant-based diets are based on the assumption that they're the healthiest way for us to eat, which is just bad science, and for a significant portion of humanity, and certainly Americans, they may indeed not be the healthiest way to eat or anything close. We have to keep that in mind if when we discuss then the impact of livestock agriculture for instance, are we going to give up. If you have a child who's predisposed to be obese or diabetic, are you going to inflict the vegan diet on them and because you think it's better for the environment, even if it's not better for him or her? These are sort of vitally important questions. My friends in the low carb community got mad at me for even entertaining the possibility that this was bad for the environment.

My counter argument was, “Well, it might not be, but that's the conventional [laughs] wisdom.” Even if it is bad for the environment, if it's bad for our health to eat a plant based-- some of us are going to be less healthy eating a plant-based diet, that's the argument I’ve got to make. And that's when I can make confidently, the other one I would have to report myself.

Melanie Avalon: Just after reading Sacred Cow, I do feel like Rob and Diana did a really good job of not cherry picking, and not being the prosecution-only side. I also recently read and interviewed Dr. Robert Lustig for us Metabolical, and he touched on it too in the book.

Gary Taubes: No, I could be wrong. I've said this. I've learned to be very skeptical. I started my career, my very first book, what we would call embedded today with these physicists at a laboratory in outside of Geneva, Switzerland, watching them discover nonexistent fundamental particles. I ended up writing exposé about this world. The experiment was led by a Nobel laureate, physicist actually won the Nobel Prize when I was there, and I went to Stockholm with him.

Melanie Avalon: With nonexistent particles?

Gary Taubes: Non-exist-- they fucked up, that use the non-technical scatological language. This physicist who won the Nobel Prize was something of a pathological liar. He was one of these very ambitious man-- I used to say, in Hollywood, he would have been a reasonably successful producer, but in science, he could win the Nobel Prize, because the competition of people who are willing to do anything to win wasn't quite as high. Anyway, when you're lied to repeatedly by a Nobel laureate, about the science that you're seeing every day, you tend to end up becoming skeptical of everything. I like to think, I'm as skeptical as my own ideas. When I read Twitter, people insist I'm not, but anyway, it's just how I'm wired.

Melanie Avalon: Wouldn't that make you more skeptical of the plant-based constant?

Gary Taubes: I can imagine a plant based-- There's certain truths I know, because everyone agrees on this, but it doesn't really-- When I wrote that Wall Street Journal essay, if I had said-- while in that particular essay, I could only make one argument. As soon as I started arguing that, okay, the livestock isn't bad for the environment anyway, I'm going to lose people who think it is and it's going to undercut the argument that I want to make. I've always wondered in the US, if you actually look at the numbers for the United States that the Environmental Protection Agency put out pre-Trump, so I think they weren't perverted quite as much as norm by political agendas, but their numbers were that the-- first of all, the contribution of agriculture, in general to climate change is about half what it was, and on the worldwide average, and more was coming from plants than animals.

So, I often wondered, are we being told not to eat meat in the United States, because the Brazilians are cutting down the rainforest to raise cattle that they're going to sell the beef from which they're going to sell in China? Is that why I'm supposed to eat less meat here? But point is, we live in a world that's only going plant based here. That's a reality, the belief system is that-- the defense is, it's a healthier diet for us all anyway. Anything you read from the EAT-Lancet report to books like Jonathan Safran Foer’s Eating Animals, there's always a chapter in there about how this is the healthiest diet for us anyway. So, it's a win-win situation. The argument I wanted to make is, if it's not a win-win situation, we have to keep that in mind. I argue if it's a lose-lose situation-- and I get all the benefits of regenerative agriculture. That's a different-- but I don't know-- always have to be aware that you're getting mostly one side of an argument, even when it's the side you want to believe.

Melanie Avalon: That's why we need people like you, and now I'm like really, really hoping that you randomly get inspired to make your next book about this topic. I would be so excited. Oh, my goodness.

Gary Taubes: Well, the funny thing is because even I think I'm now to-- I started my research on nutrition and obesity. I didn't have a bias. I ate like everyone else. I was eating-- we discussed my diet at length, the only bias I had was that I was getting fatter, but I can look at all the literature without-- and I'm tend to be biased towards people who are skeptical and critical of the research, so that tends to make me more accepting of the renegades in a particular field than of the conventional wisdom. Other than that, I don't have a bias. Now I have a bias, and I'm not sure I could do the reporting anymore, and it would be again the kind of question I would ask Robb and Diana. Once you have a bias, if you're going to do a book to prove that this is true because you think it is, you're going to bias your interpretation of every study in the field. Even if you try to fight, I mean, it's a really tricky business.

Melanie Avalon: I feel like the key would be bringing people who have no connection to the industry, who are able to analyze data, and have them review it for bias.

Gary Taubes: Yeah, exactly. I've always had this fantasy that you can just get the smartest people in science on a sort of supreme court of science-- and this has been voiced and suggested over the years, and there are reasons, I've got papers in my files about why this would never work. The idea would be any time you had a controversial subject that was important, you would basically have the teams of scientists presenting the prosecution case and the defense case to the supreme court of scientists who would be-- they can be retired physicists, for instance, very smart people-- ideally very smart people, very good scientists, but they have no investment in either hypothesis. What you would want them to do is say, is there enough evidence here to accept one hypothesis as true beyond reasonable doubt, and if not, what kinds of experiments have to be done, or clinical trials have to be done to settle this? It's kind of my fantasy.

If you staff that jury, that supreme court with researchers who are already involved in the field, tends to happen when these things are done, then you have a jury that's biased from the get-go. I'm combining, in this court, the jury and the supreme court are the same people.

Melanie Avalon: You probably have to have the court on a quick revolving turnover so that they don't acquire bias.

Gary Taubes: Possibly, but then you’re depending on enough really smart scientists, because one of the things they're going to have to do, and there are people who do this. There's a group that works for the Defense Department called JASON. I don't think JASON stands for anything. It's basically the smartest physicists chemists in the world and they self-appointed, they're organized. They're run by a company called MITRE, and they work for the DOE and DARPA, the Defense Advanced Research Project Agency and the Department of Defense. They meet in La Jolla every year for six weeks over the summer. These agencies give them some problem they want to think about and all the information they need to do it. Then they choose two or three every year that they're going to analyze. I knew a lot of these JASON people in my youth. I would always fantasize-- and there's actually another organization that was founded by some people at Santa Barbara. The unofficial name is JASON for the rest of us, so you can have important scientific subjects that weren't top secret and behind defense walls that could be addressed by these very smart physicists.

A lot of these very smart-- not a lot, but a few of these very smart physicists who I know happen to be people who think climate change science is overblown. They're considered climate change deniers. I never know what to do about that, because these are the kind of people who also taught me how to think or informed my thinking in my youth. It's like any subject, the more you know about it, the more complex it gets, except obesity, which is caused by the carbohydrates in the diet, not how much we eat.

Melanie Avalon: I have actually ultimately found that really freeing about knowledge and information. It's the fact that any thesis-- I probably personally know somebody brilliant, who believes the exact opposite on the same topic. Then, I was like, “Okay, what do we know?” And then, when you think about the left and right brain, and our left brain just comes up with stories to explain everything. I'm like, “Okay, I don't know anything.”

Gary Taubes: Yeah, you can really talk yourself into a condition of-- I remember, there's a wonderful New Yorker writer, Kathryn Schulz, who's written-- time and time again, I'm reading some article, I think, “Boy, this is so good. Who wrote this?” I go back and it's inevitably Kathryn Schulz. She wrote a book I think was called Being Wrong about how our brains fool us and how they fool scientists. I remember one of the studies she was talking about in this book was after the Challenger disaster in 1984, the day after some professor has his students write down exactly where they were and what they were doing when they heard about this. And then, they go back five years later, and he gives the papers to the same students what they wrote five years earlier. They swear that they could not have written that, because that's not what they were doing. That's not how they remembered it. The same kind of things were done for 9/11.

I'm reading this thinking, if this is true, and Schulz is writing it like it's true, so I'm going to assume it's true, then I have no idea even what really happened in my own life. Every time I'm having an argument, I'm discussing with my wife, something that happened 10 years ago, and I'm completely sure that my version is correct. I'm thinking of this Kathryn Schulz-- and the only thing is, if Kathryn Schulz was right, then my wife's version is no more likely to be correct than mine was. I still can't believe that these studies were really done, and then our memories are that faulty.

Melanie Avalon: Thank you so much for your time. This is absolutely incredible. The last question I asked every single guest on this show, it's just because I realized more and more each day how important mindset is. What is something that you're grateful for?

Gary Taubes: My family. It's a cliche, but you know. I also got married late and had children late, and didn't want children. Didn't really want kids for a long time, and my boys can be a pain in the ass, but I am very grateful for all of that.

Melanie Avalon: That's fabulous. Well, thank you so much, Gary, this has been amazing. I am perpetually and forever grateful for your work, I have been for like a decade. So, thank you for this conversation and all that you're doing. I look forward to all of your future work.

Gary Taubes: Well, thank you, Melanie, and thank you for all the intelligent, challenging, occasionally naive, but still very good questions. It doesn't always happen in my world, so this was-- you were terrific. Thank you.

Melanie Avalon: Thank you so much. Bye.

Gary Taubes: Okay. Bye-bye.