0:33 Intro. [Recording date: January 12, 2017.] Russ Roberts: Before introducing today's guest I want to thank everyone who voted in the Survey for Top Episodes of 2016. I'll be announcing the results soon. My guest today is author and journalist Gary Taubes. Our topic is his latest book, The Case Against Sugar. Gary, welcome back to EconTalk. Gary Taubes: Thank you for having me. Russ Roberts: Now, this is an awkward interview for me. I really love Peanut M&Ms, chocolate chip ice cream, cherry pie, bear claws. And Creamsicles are my dreamsicles. What's wrong with sugar? Gary Taubes: Well, possibly everything, except that it tastes great. I just want to say in advance, the title I would have preferred for this book was Stealing Christmas. Okay, [?]. I thought I should get it out there. It's not like I'm not aware that I'm playing this Grinch role. And my editor said, 'Keep it simple.' So, we ended up with just The Case Against Sugar. Okay. Traditionally, historically the argument has always been they are empty calories. So, they add calories to the diet; they don't have any vitamins, minerals, fiber, or anything else attached; so then you've got to get the vitamins, minerals, fiber from your other food. So you consume more of them and you end up over-consuming calories. And that's why you get fat. There's a whole world of problems with that thinking. But nonetheless, that's been ubiquitous for going on 100 years now. The argument that I'm making in this book is that sugar is at least the prime suspect, the cause of a condition called insulin resistance. And insulin resistance is the fundamental defect in Type 2 Diabetes, which is the common form of diabetes that associates with excess weight. And insulin resistance is so closely associated with obesity itself that you could at least hypothesize, as I do, that it's a fundamental cause of that. And obesity and diabetes are associated with an increased risk of every major chronic disease, including cancer and heart disease and dementia. And so, if sugar causes insulin resistance--that is, the dietary trigger of this condition called insulin resistance--then it is why we get fat. It's why we get diabetes. And it's at least an exacerbator or an increaser of the risk of cancer and dementia. And, excuse me, why we get heart--the primary reason, the primary dietary trigger of heart disease as well.

3:25 Russ Roberts: So, there's definitely a correlation, as you mention many times in the book--and you are very honest about it--between the rise of sugar consumption in Western countries and then throughout the world; and the prevalence of many of these diseases. And that's one of the reasons to be open to the possibility that sugar is the underlying cause. But let's talk about some of the magnitudes that we are dealing with here. How much sugar do we consume? How much did we consume? So, what are the kind of changes that we are talking about in sugar consumption? And also, you might want to remind listeners that we take sugar into our bodies in many different ways in the modern world. Gary Taubes: Yeah. And this is--there's so many misconceptions and so many issues that need clarification about sugar. In the very first chapter, as you may have noticed, I grind the narrative to a halt by saying, 'Okay, let's clear up some things first, so we know what we're talking about.' The first thing is: What do we mean by sugar? And it's funny--even very informed commentators, even reviews of my book, still seem to get this wrong. Which clearly, I didn't clarify it enough. But, you know, all carbohydrates, all chemicals that end in--and the molecules that end in -'ose' are technically sugars. And when we talk about blood sugar, we are talking about glucose, which, when I'm talking about sugar is, what the FDA (Food and Drug Administration) calls caloric sweeteners, we're talking about you know, roughly 50-50 combinations of glucose or fructose--and fructose. And it's fructose that makes sugar sweet. Fructose is the sweetest of the carbohydrates. And there are sugars with more or less fructose content. But what dominates American diets are sucrose, which is a white stuff, or brown if you get it from Whole Foods [Whole Foods Markets, a supermarket chain], that we put in our coffee. And high-fructose corn syrup. So, when we call it--and there's a big debate about, 'Do you call these things added sugars? Do you call them refined sugars? Are they better or worse than the same sugars--you know, fructose, glucose, sucrose, when you get them naturally in fruits and potatoes?' and we can talk about that. Or fruits or other vegetables. Russ Roberts: Honey. Gary Taubes: Honey. The point is: Refined sugar was very expensive. And it came out of Indonesia, 6000 years ago. It spread to India and China--the Indian and Chinese started refining it 2000 years ago. Sugar cane, into sugar itself. And it's not basically until the creation of the Caribbean colonies in the 17th century that sugar consumption really starts to become big business. And kind of drives empires. It's the oil of that era. With the Industrial Revolution, sugar refining starts to get cheaper and cheaper; and then with the creation of then with the creation of the sugar beet industry. So, sugar cane can only be grown in tropical climates. Limited the amount, the availability. But once you got sugar beets, you can grow it in temperate climates as well--in Europe, in North America, in Russia. So, second half of the 19th century, sugar consumption and distribution explode. So, these numbers--two are confusing because your question is, 'How much sugar do we consume?' And the only--even vaguely accurate number I can give you is how much sugar does the food industry make available for use by the public?' So, food availability numbers are charted pretty carefully. We don't really know how much of the sugar that ends up, you know, because used in beverages, and cooked--used in baking--actually gets consumed; how much gets transformed in cooking; how much gets thrown out. So the FDA--the USDA (United States Department of Agriculture)--has a formula that it estimates that we can talk about. Russ Roberts: Nah, we can't. Go ahead. It's not that interesting. But it does make the point that there's obviously some--it's a challenge to measure this with any precision. Gary Taubes: It's a challenge even to talk about it. And sometimes I think the sugar industry tries to make it as challenging as possibly. So, they like to say--so, the baseline fact is, 200 years ago we were consuming--maybe the food industry or the sugar industry was making available about 5 pounds of sugar per capita per year. About the amount of sugar-- Russ Roberts: In Western countries. Gary Taubes: In the United States and the United Kingdom. So, you are talking about the sugar equivalent of a 12-ounce can of Coke (Coca Cola) every 6 days. By 1999, when this trend peaked, it was up to 155 pounds of sugar per person, per day. Russ Roberts: A modest increase. Gary Taubes: A 30-fold increase in 200 years. Roughly 20% of our calories were coming from sugar. And I--one of the things that fascinated me in recreating the history of this is that, prior to the 1840s, sugar was still so expensive that it's a luxury. It's primarily a sort of head-of-the-household thing. 1840s, you get the--and in one decade you've got the founding of the candy industry and the chocolate industry and the ice cream industry. So, you begin to mass-produce, again, industrial--the Industrial Revolution, you begin to mass-produce sweets for children and women. Until then it's been exclusively men. And then in the 1870s, 1880s, the soft-drink industry begins to kick into gear with Dr. Pepper and Coca Cola, and then Pepsi. And even with chocolate candies--the candies that I grew up on: Snickers and Milky Ways and Mars Bars were all created from about the 1890s and 1920, 1930. And then there's still a couple of more industries to come. So, the fruit juice industry begins to kick in in the 1930s; and if you think about it, it's not till we've got--you know, in order to have to really saturate your diets with sugary beverages, you need a way to keep them cool, close by. So, it's not about going to the soda fountain at the drug store, which it was in the 1880s. By the 1930s, refrigerators and ice boxes and vending machines start getting to the point that they are cheap enough to be in most American household. And that allows fruit juices, now, to--and Coke and Pepsi and the soda beverage manufacturers start now, you know, putting Cokes in cartons and large bottles so that you could keep it at home in your refrigerator and drink it all day long. And then, finally, post-WWII, the sugary cereals come out[?]--the sugary--the cereal industry was founded by health fanatics. Post [Post Cereals] and Kellogg's both ran sanatoriums for the sort-of well-heeled dyspeptic. And cereal was a way to help their digestion--a high-fiber treat. So, all these industries had nutritionists who said, 'We can't put sugar in the cereal because we know sugar is bad for you.' But by 1848 [1948? --Econlib Ed.], I think it was, Post, introduced Sugar Crisps, the first one. And the rest of the industry--it's like, we see these internal struggles going on between the marketing people and the nutritionists; and the marketing people just completely won out. They were saying, 'We can't survive unless we can compete with Sugar Crisps.' So, one after another, it's the big cereal manufacturers started creating these sugary cereals--sugar-coated cereals. And by the 1960s you've got sugary cereals that are 50% sugar by calories. And the American breakfast has been transformed in this sort of low-fat version of dessert. And Americans are getting sugar--you know, and American kids are getting sugar from pretty much the moment they wake up to the moment they go to sleep, and I bet there was a large part of the population that--you know, didn't go 2 hours without a sugar hit. Russ Roberts: Yeah--I think you said "1848" on Sugar Crisp--although maybe I misheard you. You meant 1948. Gary Taubes: 1948. Yeah. 1948. Might have been 1947.

12:20 Russ Roberts: So, thinking about that story--tragically, or comically, or both, I think about my recent interview with Sam Quinones on Dreamland and the giving of heroin to young teenagers to get them hooked as a marketing technique--you know, here we are--I think about Willy Wonka--the romance that we have about childhood and candy, childhood and cake, childhood and cereal--is really sweet--literally. But it's perhaps tragic. Every family, I think has a story of some member of the family who tries to keep their kids from having sugar. And then a grandparent takes the kid on an outing and stuffs them with something that the kid goes nuts for, and 'love is all around, baby'. But-- Gary Taubes: But this is--yeah, the first--after the Prologue, the first chapter of the book, it's called 'Drug or Food,' but it's addressing this issue. And it starts with a thought experiment, actually, in the early versions: it's about how about a thought experiment. And I'm a big fan of thought experiments, because I have this physics background. When I'm feeling particularly pompous I call them gedankenexperiments. Russ Roberts: Well, that's because you have a very deep weltanschauung; and so as a result of your worldview, you need to have a gedankenexperiment. Go ahead, Gary. Sorry. Gary Taubes: Exactly. So, the thought-experiment: Imagine any drug. We are just going to create a drug that can be taken by mouth--so, it can be consumed orally and it's got no apparent sort of immediate side effects; and it's effective just to make you moderately happy. And when you give it to kids, it makes children moderately happy. So you don't have to inject it; you don't have to snort it; there's not a lot of preparation. You just buy this drug at the store and give it to your children; and if they are feeling pain, it will relieve their pain; and if they are feeling stress, it will distract them. And it will make them happy. And the question is, just with that concept, how long would it take until you get to a point where this drug becomes the way we communicate love? This drug becomes the way we reward success? Every family celebration, every holiday, every kid's soccer game--everything we do has to be, you know, sort of, capped off with this one drug, because it's so effective. And it's so easy. And if it's got side-effects, they don't show up for 30 or 40 years. And then by the time they do, by this time, our experimental population has no way to link the side-effects to the drug because everyone is consuming the drug. And has been for 30-40 years. Russ Roberts: Just think how different human history would be if it had been kale-cycles. As a sign of--you know, you scored a goal; you deserve a kale-cycle. You got an A in math; here's a kale-cycle. Gary Taubes: The media started noticing that a lot of Americans were on a diet in the 1950s. And it's interesting why this happened. And so, artificial sweeteners come along, and post-WWII the FDA is allowing cyclamates to be marketed to people with diabetes or who have some medical need for these drugs--they are kind of like marijuana now. Beginning in early 1950s, several manufacturers started making artificially sweetened sodas, soft-drinks; and they realized that they have a market far beyond people with diabetes. So, the industry starts growing, you know, wildly. And the media catches on that they are selling--soda is, clearly a lot of people are on diets so they start doing articles about how Americans are now on diets. And polls are taken, Gallup polls, about how many people. So, I think it was 1958, maybe, the New York Times Magazine has a cover story called, or had this article called 'The Great American Diet Mania,' or something like that. And the point is, at the end of the article it quotes a professor from Yale saying, 'The next thing you know, all Americans will be eating kale." Like, this is how crazy it's going to get. Russ Roberts: Prescience. [?]

17:05 Russ Roberts: So, let's talk a little bit about the evidence: which is, as you often admit in the book: It's not perfect. It's highly suggestive to you. Less suggestive to others. But let's just start with the basics on obesity, which is something of a review of topics that you've discussed in your previous books and we've discussed in your previous episodes here. But the sugar industry's view has been--strangely enough--that, 'Hey, sure it's just calories. Calories are what make us fat. And people who eat sugar might even eat fewer calories elsewhere, because it fills you up. And so it's really no big deal. It's not a health risk. It's just a pleasant way to take in some calories in moderation, or even some larger amounts: It's not a big deal. What have we learned in the last, say, 100 years, about what might be problematic about that claim? Gary Taubes: Well, so, and this claim is based on the nutritional consensus. This is a point--I have an Op-ed in the New York Times that will probably have run by the time you air this, where I am actually defending the sugar industry, because they--business for the past 50, 60 years has been to pay advertisers and to pay researchers to remind nutritionists and obesity researchers that what they believe applies to sugar, too. So, the conventional thinking since the--1920 has been that we get fat because we consume more calories than we expend. And this is based on the science from 1870-1920, which may be a mistake to base such a fundamental understanding on 100-year-old science. But it is what it is. And so, it's a caloric imbalance problem, as the NIH (National Institutes of Health) website will tell us. And, as such, the only way foods can make you fat--the only effect they can have--is through their caloric content, or their digestible caloric content. And, so sugar is no worse than any other food. There's no such thing as a fattening food or a reducing food: it's all about how much you eat; how many calories you consume and digest. Not about what foods those calories come from or what macro-nutrients those calories comes from. So, the sugar industry's defense through all this period has been 'Look, you know, there's nothing uniquely fattening about sugar. It's just a source of calories as any food is. And in fact if you do an epidemiologic study and you follow people'--this used to be true; I don't know if still it is--'but if you follow a population to see who eats a lot of sugar and how much weight they gain, you'll find that lean people tend to eat more sugar than obese people.' And this feeds into my criticisms of epidemiology over the years, because you would expect people who are lean to drink sugary Coca Cola because they can. Russ Roberts: They can. Gary Taubes: And people, the ones who easily gain weight might drink Diet Coke because they are trying to avoid the calories in the Coke. Because they gain weight so easily. And then you follow them; and lo and behold, they gained weight anyway. But they were the ones drinking the diet soda, so you've got a reverse causality you have to deal with. So, this has been the sugar industry defense. And the arguments I've brought up in my books because I happened to pay attention to the history--I was probably the first--I was the first journalist/historian who bothered to go back prior to WWII and recreate the history of thinking on, clinical history of thinking and research on obesity prior to WWII, back when all major medical science was being done in Europe; and the fields relative to obesity--metabolism, nutrition, genetics, endocrinology--were all sort of born and pioneered in Germany and Austria. And these clinical investigators who actually understood what endocrinology was and even what genetics was, which most physicians didn't, had concluded that clearly obesity must be some kind of hormonal, regulatory defect. And, people don't gain 100 pounds, accumulate 100 pounds of excess fat because they eat too much: they do it because somehow their body is telling them to accumulate fat. And that's going to be a hormonal, enzymatic phenomenon. This theory was lost with the war. And post-war obesity research was sort of recreated by young doctors, lean doctors, and nutritionists at the Harvard School of Public Health, and they thought it was simple and they thought it was a caloric imbalance: basically, [?] loss. And by the 1960s, obesity research was dominated by psychologists and psychiatrists who had concluded that obesity is a behavioral defect, in effect--that it's [?] both eating too much and exercising too little are behaviors. And so they were trying to come up with ways to change the behavior of the fat person so that they would do what lean people seemed to do naturally--which is, not accumulate excess fat: you know, eat less and exercise more. It's almost--it's hard to accept that this fundamental, bedrock concept of obesity research is simply wrong. And I keep thinking of different ways to communicate this to people. So, my latest attempt is to say, like: Imagine if, Russ, you were interviewing me about economics or finance or wealth accumulation instead of health and public health, and we were talking about Bill Gates, and you said, 'Why did Bill Gates get so rich?' And I said, 'Because he made more money than he spent.' You know, you would be wondering why you had ever developed a relationship with me to begin with. Right? Russ Roberts: I always wondered [?], Gary. [*cough*]. Gary Taubes: Yes, true. And if we were talking about climate change and the question was: Why is the atmosphere heating up? And I said, 'Because it's taking in more energy than it expends'--which it clearly is--I'd basically insulted your intelligence. But in obesity, if you want to know why somebody is getting fat, then you tell them they take in more calories than they expend. And it's just almost incomprehensibly naive, to me, at this point. Clearly, if someone's gaining weight, they are taking in more calories than they expend. That's the laws--basically what you are saying is if they are accumulating energy, they are accumulating energy.

24:12 Russ Roberts: Well, the economics analog for me, and the reason I find these topics so interesting, besides the personal and intellectual content, is that, in economics people say things like this all the time. They say things like, 'Well, our national income is C+I+G--it's Consumption plus Investment plus Government Spending--so when government spends a dollar, income goes up by a dollar. And that's obvious. And my thought is: Whoa, whoa, whoa, whoa. Where did the dollar come from? Does it not have any other side effects? Does it matter then--can government just, say, add an extra zero to the money and we're that much richer? What about prices? It generates a lot of questions. But in the case of--and by the way, the thing I learned, the deepest thing I learned from your book, because of its honesty, is the same thing, for better or worse--and this may be my problem--it's the same thing for better or worse that I've learned about the economy: Boy, is the human body complicated. It's so challenging to parse out the independent effect of one, even dramatically increasing variable called sugar, because there's so many other things happening at the same time. Gary Taubes: Right, but this gets--it's funny--two points. One is, I remember, I think my very first interview when we tried to decide which science was worse. I think you said the reason economists like me is I'm suggesting there's a more problematic field of research out there. Second point is: We tend to get confused: Because the human body is so complex and because it's so hard to tease out these different issues, people kind of lose sight of the fundamental question that we want to answer. And so they, one of the things you see written about all the time now is obesity and diabetes are multi-factorial, complex disorders. There's this whole slew of things that are involved--you know, genetics and maybe sleep deprivation, the absence of sidewalks, and maybe-- Russ Roberts: Stress. Gary Taubes: Stress. And antibiotics that are being used in our cattle that make the cattle fat. They get into the rainwater. And to me this is an excuse for why we've completely failed to control these epidemics of obesity and diabetes that are worldwide, and we could and should talk about that failure shortly. But the thing to remember, the question is this: We have these epidemics that are worldwide: Every population that transitions to the Western diet and lifestyle, that goes through what's called a nutrition transition, eventually manifests these explosive increases in obesity and diabetes. In diabetes sometimes they do it quickly, in the course of a couple of generations; sometimes it's a little delayed. But it always manifests itself. And you see when people immigrate, emigrate, to the United States from, like for instance Asian populations and they come to the United States, within two generations they've got levels of obesity, diabetes, breast cancer similar to any other Western population. So that's what we're trying to figure out: What's the cause of those epidemics? They are worldwide; we could begin to understand; we could rule out causes by looking for populations that would manifest the epidemics without our suspected cause. The answer to that is probably simple. So, even though obesity and diabetes are considered multi-factorial, complex diseases. I mean, there's some people who think, 'Well, the answer to that question is Western diets and lifestyles: it's the whole shebang,' and, 'if it's food, it's everything that goes into processed foods.' To me, that violates Occam's Razor. Maybe because I grew up in the physics community I have a devotion to Occam's Razor that's more fierce than it should be. But if you don't start with a simple hypothesis, you'll never make progress. So, 'Never multiply hypotheses beyond necessity' is my favorite variation on Occam's Razor. Einstein's paraphrase, which was that 'The hypothesis should be as simple as possible but no simpler.' So, if you start with the simplest possible hypothesis, and the conventional one is that people just eat too much and exercise too little--so, they think diabetes is caused by obesity; obesity is caused by caloric imbalance-- Russ Roberts: With the sloth part, too--that we just are sedentary. Gary Taubes: Yeah, exactly. You get a more mechanized society; there's less manual labor that's necessary; people don't walk as much because they have cars. This all goes with it. But the end result is caloric imbalance. Yeah. And then my version of it--again, in my earlier books I talk about the effect of refined grains and sugars in general. And now I'm just drilling down on sugar. Funny--I have an email waiting for me from somebody who went into my website and said, 'What about the carbs in beer?' And I want to say, 'Well, clearly beer is fattening, and I could have written a book called The Case Against Beer. And that would be a different story.' Russ Roberts: Somebody already wrote that book. You wrote that book before: it was called The Case Against Carbs. [?] a special chapter. Gary Taubes: Yeah. Anyway, so that's--despite all of the complexity of the human body--when somebody gets cholera, it's a complex physiological response as well. And when somebody gets lung cancer from smoking cigarettes--and only 10% of the people who smoke are going to get lung cancer--that's a complex physiological response. But we can identify the agent. The question, 'What is the agent?' has a simple answer. And what I'm saying the agent is: The agent is sugar. You add sugar to every population, whatever their baseline diet is, you are going to trigger, eventually, obesity and diabetes epidemics through this insulin resistance mechanism, at least. And one of the reasons I'm not saying 'sugar and refined grains' in the answer to this question is that we had populations--Southeast Asia--that ate a lot of refined grains and didn't get obese--that had vanishingly small levels of obesity and diabetes until you added sugar to their populations' diets.

30:56 Russ Roberts: So, it could be that you're right. And I'm curious why--in your book, you say in the very, I think the first page, maybe the first--certainly in the first few pages--that this book is the prosecution: This is a prosecutor's one-sided case against sugar. Shouldn't there be a more nuanced? It's suggestive; and as you point out, we don't have large, randomized clinical trials on people who eat sugar for a long time and people who don't. And, so the evidence is always going to be somewhat imperfect. Why are you so convinced that it's sugar? And why aren't other people rallying to your cause, if it's so clear that it's the one thing? Gary Taubes: Well, again, remember the--well, let me backtrack. I do, indeed--there's an Author's Note in the beginning saying that if this were a legal case, this book would be the prosecution's argument. In defense of my defensiveness, I've had people read the book and say, 'Oh, no, a prosecutor would never be so open about the--' Russ Roberts: True. True, true, true. Gary Taubes: [?] a diet, with the evidence. So, yeah, I do believe that anyone involved in the scientific endeavor has an obligation to be as honest as humanly possible about what can and cannot be interpreted from the evidence. So a thing that has always gotten in the way and still gets in the way, is this energy balance issue and calorie issues. So, clearly, one of the reasons this book is being embraced, if it is, is because as a society we are going after sugar now. The World Health Organization has sat relatively strict limits on the amount of sugar they believe should be in a healthy diet--like, 10% of calories; and then they advise 5% for further benefit. The USDA recently for the first time in the history of their dietary guidelines put a cap on the amount of sugar that they believe is healthy, or the percentage of sugar calories. But it's still always based on this idea that sugar is an empty calorie. And one of the things I point out, that I'm a little embarrassed I didn't notice in my earlier books, is how much this is dependent on the state of nutrition science of 100-150 years ago. So, when you go back to read history of nutrition books, modern nutrition science basically dates to the late 1860s and the invention by German researchers of room-sized calorimeters. So, these are devices that could measure the heat and energy expended by a human subject, or a dog. And up until then they knew how to measure the energy content of a food, by burning it in a small calorimeter and measuring the heat that comes out. But now they could actually measure the heat expended by humans. You could measure the energy in and the energy out. And from 1870-1920, virtually all of nutrition science was calorimetry--measuring this energy content of foods, and how much energy they expended by different types of, you know, kids, and soldiers, and [?] people and healthy people. And then you could also do studies on vito-mineral[?] content; and they were beginning to realize that vitamin- and mineral-deficient diseases, what vitamins were causing them. So all of nutrition science, was not--when we talk about sugar being empty calories, it's empty of vitamins and minerals. Which is the science of the 1870-1920. And it's calories, which is the science. And we couldn't actually understand the way sugar impacts bodies differently than that. And so, not until the first--insulin is discovered in 1921, 1920, I always forget--and growth hormone shortly thereafter, and the science of endocrinology, of hormones and hormone-related diseases, slowly begins to evolve. Like in the 1910-1920s, we still call it 'glands'--'ductless glands' was our word for endocrinological organs. And nobody really understood--doctors didn't understand it at all. I remember reading Graham Greene's brother was a premier British endocrinologist and he wrote an article in the British medical journal, I think it was in the 1950s about how nobody understood--none of his physician colleagues even knew that insulin did or what it meant. And that to disregard it on the basis of ignorance was a bad idea. And then, 1960, they finally have a technology available that cut the radium, you know, assay, by Roslin, Yalow and Solomin, Bersin[?], discovered it. And you can for the first time in history measure hormones in the bloodstream accurately. So, you can now really figure out--you can actually feed people and see the hormonal responses. And, you know, using this assay. If you want to. And you could see--so, 1920, all we know is the calorie content of food. Now, 40 years later we can see how the human body responds hormonally and enzymatically to foods, which is another effect they have, independent of calories. But by this time, again, we've got this theory that it's all about calories.

38:51 Gary Taubes: So, as long as it's all about calories, getting back to the evidence, to demonstrate that there's something unique about sugar, the case against sugar depends on demonstrating that it has effects independent--deleterious effects independent of its calories. That it's not just something we benignly over-consume and we get fat because we over-consume all calories. And that dis-association of the effects of sugar from the caloric content of sugar is excruciatingly difficult to do in a laboratory and an experimental setting. And what I've realized in the last 5 years of my life, tried, and to some extent failed to run a nutrition or, I co-founded a nutrition-science initiative, a non-profit that was going to fund and facilitate studies that could resolve these issues. And I completely under--you know, it was like a heart-beat[?] away--you know, getting involved in a nonprofit. And the revelation was how excruciatingly difficult these experiments are. How easy they are to screw up. And if you don't have people who have been thinking deeply about the hypotheses. So, if you take a whole world of people who for the past 50 years have thought a calorie is a calorie and obesity is a caloric imbalance problem, and you say, 'I want you to do an experiment in which we are going to test your fundamental belief based on this alternative hypothesis--that a calorie is not a calorie and obesity is a hormonal, regulatory disorder--and the way you are going to have to do it is you are going to have to disassociate the effect of the calories from the effect on the human body,' it takes an extraordinary amount of thought and dialogue and argument, and critique and critique and critique, before you are going to get an experiment that even begins to work to do this. And there is an absence of people who are capable of having those debates and the critiques, because nobody has been thinking about it. Russ Roberts: So that leaves you--it seems-- Gary Taubes: Yeah. Which is a, sort of, that, so now, if you had a choice--I remember one of your economics colleagues at Yale called this the $100-bill on the sidewalk problem, right? I mean, what are you going to bet? You've got the entire nutritional obesity research community saying one thing. And you've got this journalist and a few friends, and you know, there is a guy, a professor at Harvard who agrees with us and also worked and independently came to the same conclusions. Who are you going to believe? I mean, if I were a betting man, who would I bet on? And I wake up at 3 or 4 in the morning thinking, 'I must be a quack. This is crazy.' But then I think back to the whole energy balance idea--you know, again, let's say we were--again, we never get to talk about a money-balance theory of wealth: You've got to make more money and spend less, that's how you get wealth--so why--then, I can put a stake on a few things that suggest that I'm at least half not wrong.

40:19 Russ Roberts: So, that leaves you with the possibility of having to admit that you are not sure, or that you don't know. For me, as an economist, the analogy is: 'We're in a Depression. What do we do? If government spending isn't what gets us out, what do we do?' And, you know, and I say, 'I'm not sure, but I don't think it's government spending,'--that nobody wants to listen to you. It's not a good selling point for getting attention. Gary Taubes: Well, even historically, whenever researchers said, 'Look, we're not sure. We need more research,' they were perceived as being self-interested. Right. Because 'need more research' means 'need more funding'-- Russ Roberts: Yeah. For me. Gary Taubes: to do the research. And for me, yeah. So, you know, there's a lot of natural traps that occur when we get into--that's why ideally you never screw up in the first place. Because once you've screwed up--once a discipline or an institution has embraced a dogma--and this is one of the revelations that I'm still trying to wrap my head around--it's almost virtually impossible--we have this concept of a Kuhnian paradigm shift, but once you get to the point where entire institutions are invested in a belief system, it might be beyond the point at which enough data will be allowed to accumulate to overturn that belief system. Certainly that's the case in nutrition, obesity research. If I'm right. And let me say right here, we could just assume that every sentence I say for the next remainder of interview is preceded by the clause, 'If I'm right.' Okay? Russ Roberts: Fair enough. Gary Taubes: But I've been-- Russ Roberts: I've been putting in front of it, the whole time. Gary Taubes: Well, it's got to be in there, right? Because the odds--historically, the odds are, people like me are always wrong. Not always--99.9% of the time. Russ Roberts: You've got ulcers. You've got the tectonic plates. You've got a bunch of places where a lone, crazy quack turned out to be a genius. So, this could be one of those. Gary Taubes: They tend to--even those lone, crazy quacks--tend to be in the field. Although, you could argue, if you look at the times when paradigms shift, they are usually driven by some--they are often driven by people outside the field who have a different perspective or aren't trapped by the belief system of the field. Russ Roberts: No--I go with Nassim Taleb, here: that the field that we're talking about, it's called Nutrition or it's called Epidemiology or it's called Medicine, but it's really Statistics. And most of the people who opine on these issues are not experts. They are faux-experts. It's the--Taleb's example is the: If you want to understand roulette, you don't talk to the carpenter who assembled the roulette wheel. And that person looks like the expert: 'He built the wheel. Come on, how could he not be the person who knows the most about it?' So, the people who--given that we don't really understand enough about how the human body works, a lot of it is--it's not clear who the experts are. So, I think the question of who is inside the field and outside the field, that may be not so pertinent. Gary Taubes: But it's--what even here, it's interesting, because it's one of the things that you notice in the history. So, what I'm basically saying: Because it's a belief in caloric balance, and then gluttony and sloth, a like I said, by the 1960s, 1970s, when endocrinology was maturing as a science, was exploding in its maturation, the obesity research community was dominated by psychologists, who were looking for behavioral explanations. Russ Roberts: Yep. Gary Taubes: So, they make no progress for 20 years. And 1993, I think it was, leptin is discovered. And now you've got an obesity gene. And suddenly, boom: molecular biology, industrial complex kicks in. And the field is swarmed by--it becomes a sub-discipline of molecular biology. And now you've got people looking for the effects of other obesity genes; and then the genomics and proteomics and everything else kicks in. And in the meanwhile, basic endocrinology was left behind. Okay? So, this 20-year period of sort of fundamental medicine--like, when you want to know why somebody is 8 feet tall, you explain it by basic endocrinology from the 1920s to the 1970s, you don't bother getting into whether or not he's got some tall-gene. Right? Or the micro-[?] that's involved in communicating between the insulin-like growth factor and his cells. I mean, it's not that relevant. It's like the guy is over-secreting growth hormone: Do an MRI (Magnetic resonance imaging), find the tumor, and it's: 'Pituitary gland, get it out of there before he becomes 9 feet tall.' And I'm saying that period, and when it came to obesity, was basically ignored. The people played around with the theory, and they didn't like the implications. The implications were that people like Robert Atkins was right. And so, they sort of buried it. And we came out--by 1980, we're discussing a science of excess fat accumulation. A disorder of excess fat accumulation. But the actual hormones and enzymes that regulate fat accumulation in the human body are considered irrelevant. Which, again, one of those things where I say: If nothing else, it should be discussed. Right? You should see it in the papers. When somebody writes a paper on the cause of obesity, it should at least be discussed in why it's not a hormonal or enzymatic issue. And you get to the point, so, last Fall I was doing a BBC (British Broadcasting Corporation) interview by Skype, with, on a program, with a host, with a very charming geneticist, I forget if it was Cambridge or Oxford; and he studied the genetics of obesity. And I said to him, 'Do you know what regulates the flow of fat into and out of fat cells?' And he said, 'Well, we don't know that.' And I responded that, 'No. You don't know that. Because you are a geneticist. And you don't read endocrinology texts. But this was worked out in the 1960s.' So, you've even got people study the experts, who are studying [?]in the long tail[?]-- Russ Roberts: What did he say back to you? Did he say, 'Oh'?' Or did he say [?] Gary Taubes: He said, 'Oh.' That's an interesting--and then I actually sent him an email. I mean, maybe it didn't get through. But we got off the show, I sent him a long email, with references and pages from the--you know, Williams' textbook of Endocrinology and Lehninger's Biochemistry saying, 'Look, just go to a [?] site. Look it up.' And we know what the answer is. It's just not considered relevant to human obesity. Which, like I said, is another one of these areas where I think I'm not entirely crazy. Russ Roberts: It's a comfort.

47:29 Russ Roberts: So, let's get personal here, for a minute. We'll start with me, and then we'll turn to you. I would, in theory, like to weigh 25 pounds less. Ten would be great. Twenty-five would be ridiculous. I weight--oh, I probably weigh 40 pounds, plus, more than I did when I finished a marathon in 1976. That's was when I was the fittest I've ever been. And so I weigh more than I did then. Gary Taubes: You continued running through this period? Russ Roberts: I did not. No, no, no. I ran for another few years. Then I stopped. But I knew that whenever I wanted to lose weight I could cut back on carbohydrates. And it would be like magic. And I got that from a great scientist--my Mom, who read the Atkins book, and it worked for her. So, she told me about it, and I thought, 'I'll try it.' And it works. So, in recent years, the only thing I have good to say about my weight is that it has not gone up. My attempts to keep it down have been successful; but it is not fallen. And what happens to me is the following. During the week, I pretend I don't eat carbs. It's not quite true. I pretend it's a snack on things like an enormous bag of almonds, or peanuts--because I think, 'Well, it's really kind of a low-carb food.' I eat cabbage and protein for lunch almost every day. I tend to skip breakfast. I keep the Jewish Sabbath--so, when Friday night comes around, I eat a couple of challahs, to--to balance my low-carb week. And-- Gary Taubes: That kind of loaves[?] Russ Roberts: And that kind of ruins everything, as you might expect. And what I find is, if I say to myself, 'Well, I'll just taste the bread. I don't need to eat 4 slices or 6'; 'I'll just have one cookie, not 6,' on a Saturday afternoon. I find that very difficult to do. So, coming back to the calorie-in/calorie-out thing, I certainly accept the idea that what I eat matters as much as the calories. But what I find, is that when I eat what I know keeps my weight down, my body wants those other things, and enjoys them so much. So, if I wanted to get the 35-45 pounds less that I'd like to weigh, or certainly the 10 or 15 that would be pleasant, I know what I have to do. But I find it very difficult to do. And I think that's the challenge most of us face. And I'm going to finish--one more thing--this is my wife's question, which I promised her I'd ask, because every time I push your ideas on her, she says, 'Come on: it's just calories in, calories out. That's a fact.' And I say, 'Yeah, because my friend, who is a huge exercise guy, and who liked the China study, and so now he eats, he's a vegetarian; he eats a ton of carbs; and he's thin as a rail.' And she says, 'Yeah, that's because he doesn't eat very much.' It's not because he's not eating. You know, it's not because he eats carbs--he's not gaining weight. It's because he doesn't eat very many carbs. What are your thoughts on that potpourri of personal life experience? Gary Taubes: Okay. So, there's a lot of issues buried in there. Russ Roberts: Help me, Doctor. Help me. Gary Taubes: Yeah. The contents of craving. One is-- Russ Roberts: Gary, I've got to tell you one more thing. I know there are listeners out there who heard your previous episode, and took it to heart. And they write me; and they've lost 40 pounds; and I think they have kept it off. So, those of you out there, you can write in again and comment on this episode and give Gary some comfort on this. Go ahead. Gary Taubes: Okay. So, I have to--okay. Again, multiple issues. Let's start basically with dietary advice. So the argument I've been making is that this is, I had a Nature commentary to this effect--the headline was it's biology, not physics. Okay? So what we're worried about is biology. The question is--and often when I talk to researchers in my vain attempt to get them to either do science right or think like I do even though I'm wrong--I suggest that what they could do to their--it would be an interesting exercise for their students, and themselves, to create a theory of obesity being [?] from the fat cells' perspective. So, the problem in obesity is that fat cells are accumulating too much fat. Much of the excess 40 pounds are in fat cells. You could argue that the part that isn't--that is doing more damage. But what, we'll assume is we're worrying about the fat cell, excess fat storage. So, if I were a fat cell--I'm going to create a theory of obesity from here--the fat cell doesn't know how much we are eating or exercising. Okay? It's got no clue what your body's energy balance is. So, all it sees--it does see hormones. It sees--and it responds to those hormones. And that kind of stuff, we know was worked out in the 1960s, significantly in endocrinology textbooks. And, it sees, or it responds to, you know, blood sugar and fats in the blood and to lipoproteins like LDL (Low-Density Lipoprotein) and HDL (High-Density Lipoprotein). It's got some central nervous system enervation of the fat cell, so it's going to respond to some nerve signal to the brain. From what it sees, what would it take to accumulate excess fat? And the primary thing, what it would take, would be to have insulin over some baseline level. Because insulin is the hormone that is signaling that for it to take a fat that signals these enyzymes that regulate on the membrane and other enzymes to down-regulate inside the cell. So as long as there is, your insulin is elevated, your fat cell is working in a milieu in which it is working to take up fat. Whether or not you need those calories elsewhere in your body. Okay? So, from your position--so here's one of the kickers. When you look at the dietary tradition[?]--two factors. When you look at the dietary triggers of insulin, so we secrete insulin, more or less the carbohydrates in our diet, also some to the protein, because it's broken down into amino acids which are converted into glucose, and we secrete it to that: We don't secrete insulin to the fat content of the diet. Fat is--picked up from your gut by particles called Chylomicrons and taken off to your fat cells. And you don't need insulin to do that. So, insulin is not involved. So, the issue is, now, if you are going to have a dietary way to have insulin get as low as possible, you've got to replace the--get rid of the carbs. The protein should be, you know, enough. But you don't want to go crazy with protein. And then you replace the calories with fat. So, this is the idea that you can eat as much as you want. Although, even Atkins[?] didn't--you know, fully understand the science, but the idea is that you can eat as much as you want. But it should be more fat than protein. So, you are eating very fatty foods. You are living on butter. I mean, as we're talking--the reason I'm awake today--is because I'm very recently become addicted to bullet-proof coffee and I have no idea if it's killing me or not but it's got butter in it. And--you know, coconut butter. So, mentally, you have to accept that you can eat these high-fat foods, and they won't kill you. That's always been the challenge, because we decided in the 1960s, as we discussed, 5 or 7 years ago or whatever, whatever it was-- Russ Roberts: Previous episode-- Gary Taubes: Low fat diet is the way to go.

55:31 Gary Taubes: The second fact, is you actually look at insulin dynamics--and this was studied also in the 1970s, 1980s, and 1990s by a few research groups--there's a threshold. So, insulin levels come down in your bloodstream. And this is your--researchers would refer to the exquisite sensitivity of the fat cells to insulin. So, long after your lean tissue--at levels far below that which your lean tissue is resistant to insulin--your fat cells are still very sensitive to it. So what happens is if you eat a carb-rich meal and you start to eat the challah on Friday night, your blood sugar goes up, and you secrete a lot of insulin, started to tell your lean tissue basically to take up that blood sugar and oxidize it for fuel--it facilitates the, getting the glucose into the cell--eventually the lean tissue becomes resistant because it doesn't want more glucose. But you want the fat tissue to stay sensitive, so it could take care of the excess fuel that's floating around. As the insulin levels come down, the fat tissue continues to be sensitive to insulin. So, it continues to hold onto fat. And then there's a threshold. And below that threshold, basically, your fat tissue starts dumping. The, um, your fat that has accumulated into the bloodstream; and your cells will oxidize it for fuel, and you'll have this rush of energy; you'll convert some of it, maybe even to ketones; and you'll have this rush of energy, something that your body just burning this energy that it then had access to before. So, the problem is, you've got to get below the threshold. And if you are still accumulating fat, you are clearly above the threshold. I mean--the journalist without a Ph.D. or an M.D. giving you a simplistic concept of the science: This is how I understand it from 20 years or 15 years of research. So, in the case--many people can just cut back on carbs and cut back on sugar and they'll lose weight. Younger people can clearly do that. I was one of them, when I was 20. But, by the time I was 40 if I wanted to lose that weight, it required basically shifting over to something that's, you know, very much the Atkins Diet. So, you can't really cheat, because cheating is enough to keep you above the threshold. Russ Roberts: Yeah. That's where I'm at--above the threshold. Which sounds good, by the way, but it's not. Gary Taubes: Yeah. So, in this case you want to be under it, because when you're under it--it's funny: I was looking at the--so, again, what sparked this research is understanding of the hormonal regulation, the fat accumulation--was this discovery, this invention by Yalow and Berson of the radium assay. And by 1965 they had made--you get a brand new technology; you get a rush of discoveries. Including--so, they realized that Type II diabetics didn't suffer from insulin deficiency: this was an insulin resistance problem. They actually had too much insulin floating around. And they realized that obese people also had too much insulin, had excess insulin in their circulation. And by 1965, Yalow and Berson are saying that the release of fatty acids from fat cells--the quote was, 'requires only the negative stimulus of insulin deficiency.' Okay? So, if you want to get fat--so, I had an argument recently, an email discussion where I got nowhere with. One of the major figures in the obesity research community for the past 50 years, [?]. He had written an article, co-authored with a woman whose husband runs my son's baseball/soccer team, in Oakland. Anyway, in his article he had said, 'Negative energy balance is the sine qua non of any successful weight-loss diet.' Negative energy balance being more energy out than in. And, I was thinking, you know, the endocrinological view would have been, 50 years ago, and should have been, that insulin deficiency is the sine qua non of a successful weight-loss diet. That's what Yalow and Bersin would have said: If you want to get fat out of your fat cells--which is what a weight loss diet should do--the way to do it is to get insulin as low as possible. And if you do, then you'll expend more energy than you take in, because you'll lose weight. And--so, you're not doing it. That's the answer. If you were to do it in a concerted manner that gets to the craving issue. Even back in the 1930s, a great, famous biologist at Hopkins named Curt Richter had demonstrated that animals sort of, when they have low fat diets, they crave carbohydrates. And if you jack up the fat, they'll lose the carbohydrate craving. So, I would argue that if you got under the threshold--and now, this is the step that stops the entire medical community dead in its track; and you jack up the fat you are eating and you become somebody like me who thinks or at least dearly hopes that butter and bacon are health foods, you will lose the craving for the carbs. And you won't want to eat--it will be much, much easier to avoid the challah on Friday night. And-- Russ Roberts: So, I just need-- Gary Taubes: the cookie on occasion-- Russ Roberts: So you are saying since the bacon doesn't work for me, I just need to go with more of the fatty pastrami--is what you are saying, with the challah. Gary Taubes: Yeah, yeah. Fatty pastrami. It's funny, because I have this, the Center for Science in the Public Interest, in Washington, has been a sort of prime mover for the past 40 years. Sort of that fat is a killer, salt is a killer. So I've sort of been--much of the past, my professional career, writing about nutrition. Arguing that these people have done more [?] in their advocacy for the American public. They've done far more damage than they've prevented. But they are also anti-sugar. Russ Roberts: hmmm-mmm Gary Taubes: So, I recently had lunch, about a year ago, with the very charming, charismatic, intelligent head of the Center for Science Public Interest, this man, Mike Jacobson. We actually had a very wonderful lunch together in Oakland. And when we left, he was saying, asking me why I wasn't supporting his organization more, because, you know, we are both anti-sugar, and why I wasn't supporting sugar regulation more. And I said, 'Because after you are done taking away sugar, you will then go after my pastrami.' Russ Roberts: Yeah. Gary Taubes: And I happen to believe pastrami is a health food. So, you know.

1:02:38 Russ Roberts: So, that's my next question, actually, because when you said you have a lonely life because there are a few researchers who are sympathetic to you, although you did concede one of them was the head of the Harvard School of Public Health, which is-- Gary Taubes: No, he's not the head. He's-- Russ Roberts: A Harvard researcher. Which is usually--that's a good thing to have. The other people you have on your side--and this makes me a little bit uncomfortable; I'm sure it makes some listeners uncomfortable, so I want to get your response. The other people you have on your side are the Puritans--the people that H. L. Mencken said--he defined Puritanism as "The haunting fear that someone, somewhere, may be happy." And so, when some people hear, 'We need to get rid of sugar,' they hear, 'Oh, this is just the latest nanny state cause. It was tobacco; and then it was fat. And now it's sugar. And they just want to take all the fun out of life. And they are busybodies.' Some of them are well-intentioned; maybe all of them. But they are also tangled up with this desire to run other people's lives. Which is something that scares some of us. And I want you to reflect on that. As you've sort of hinted at, in that anecdote. Gary Taubes: Well, and again--when I first got into this, I was fascinated. I think all my books are about, on some level, good science and bad science. That's my obsession: How hard it is to do science? How easy it is to screw up, to discover non-existent phenomena, to embrace incorrect theories. That's the passion that drives me; it's still the book I would like to write. But should I ever do it, it will not sell nearly as well as books about diets do. Russ Roberts: Yeah. I want to write that book, too, Gary; and my agent says the same thing, 'What else are you thinking about?' Gary Taubes: Well, that's a--yeah. Literally, we're trying to tie it onto book deals. Like, just give me a little money so I can justify the time I'm going to put into that one. Otherwise--anyway--I lost track. So, when I first got into this, it was because friends of mine in the physics community said, 'Look, you should look at the science in Public Health. It's terrible.' And indeed it was. So, everything I had learnt from the physicists in the 1980s when I was writing these books about bad science in high energy physics and the cold-fusion fiasco--so, I learned that you've got to be rigorous and methodical and critical and skeptical; and skeptical and the first principle of science, as Richard Feynman said, is you must not fool yourself, and you are the easiest person to fool; and if you cut a single corner, sweep a single uncomfortable fact under the rug, you are going to end up fooling yourself. And then I get into Public Health, and it's just so hard to do it. It's expensive, and you've got these messy experimental subjects called 'humans' and you've got these diseases that take 20, 30 years to manifest. So, the assumption was, we're just going to--all the things that the physicists had told me were required, we're going to treat as luxuries that we don't have. And we're going to assume that we could establish reliable knowledge without it. Whereas, my physicist friends said, 'You can't.' My physics experience said, 'You can't.' So, this was what I was confronted with, and when I got into nutrition, I thought, 'Okay, my long investigation was on salt and blood pressure; and my second was on this dietary fat dogma that a low-fat diet's a healthy diet. About two years of my life with the Journal of Science on those two articles. And I thought, 'I'm just going to knock down the food police.' And I came out of it thinking, 'I didn't eat an avocado or peanut butter in 15 years because of these people.' And I was mad. And, you know, I wanted to write a book on this; but I knew I couldn't get enough of an advance to prevent me from being in debt when I was done. And there was no self-help [?]--I just wanted to, you know, dig deeper, because it was fascinating. Then I did this infamous New York Times Magazine cover story in 2002: "What If It's All Been a Big Fat Lie?" And in the process of doing that, I began to realize that there was an alternative hypothesis. So remember, we still have to explain these explosions in obesity and diabetes. These are--we are back to this question--I said, 'We've come back to this.' They are pandemic. The numbers are unimaginable. In diabetes, from the mid-1950s there's like a 750% increase in prevalence. Okay? If you go back to, like, the 1890s, as I do in the book, or the 1860s, and you trust the numbers, it's probably been closer to, like, 2000% increase in prevalence. I mean, this is shocking. And these are diseases that are going to overwhelm healthcare systems worldwide, because they increase--you know. So: Why are, why don't we care? And in October, Margaret Chan, Director General of the World Health Organization (WHO), goes to Washington; there's an annual meeting of the National Academies of Science, which is dedicated to, I think what is called 'reversing the dramatic 30-year increases in obesity and diabetes.' And Chan says, she talks about this 400% increase from 1980 in diabetes worldwide. And prevalence. So that's not absolute numbers. Now, in her case that was--I think it was both--absolute numbers and prevalence. And then she calls these epidemics a slow-motion disaster. And she admits that the Public Health community has completely failed to control them. So, they've had 20 years now in which they've known of the existence of the obesity and diabetes epidemic; and they have made no inroads whatsoever in curbing them. And then she states that the chances of preventing bad--quote, "keeping a bad situation from getting much worse," unquote--is virtually zero. So, we have a situation in which the Director-General of the WHO is not only acknowledging that they've completely failed to curb these tragic ends--'slow-motion disasters'--but predicting future failure. And so, yeah, maybe I'm playing the grand troll and this is the food police. But, we have to understand what's causing this. And we are never going to control it without--I mean, again, maybe some day somebody will come up with a drug that works and the pharmaceutical industries can make trillions of dollars and we won't have to. But I'm pessimistic that any such drug is coming shortly. And that when it comes, it won't have unfortunate and unforeseen side effects. So, we have got to understand--that's what I'm trying to do, and I'm fortunate that, you know, the targets happen to be something we all love so much. But if we didn't love so much, we never would have let it saturate our diets and our lives. We never would have consumed it so much. And this wouldn't have happened. So it's a--you know, we're stuck.