| Time | Podcast Episode Highlights |
| 0:36 | Intro. [Recording date: July 11, 2012.] Russ: Guest is Gary Taubes. His latest book is Why We Get Fat. You were a guest on this program back in 2011 in November, and we talked about your earlier book on a similar topic, which was Good Calories, Bad Calories. This latest book covers some of the same ground, but in a more accessible way. And when we talked about that first book we focused on how public opinion and public policy is shaped by research that you argued was mistaken. And I saw a lot of parallels between that research and the evolution of policy in the area of nutrition and health to research in policy in economics--problems of groupthink, confirmation bias. In this conversation, I want to focus, as the second book in the topic does, on what we know about weight loss and what you might know of the micro side of the weight loss equation and diet and nutrition question. The economics analogy here is the challenge of understanding a complex system, where it's difficult if not impossible to hold one factor constant and isolate the impact of other factors, both in practice and in research. So let's start by asking the fundamental question. It would seem that all we need to know about weight loss in the human body is captured by the slogan: Eat less and exercise more. That would seem to be undeniably true. And in the end of the discussion, if we want to lose weight, we could do one or the other; both ideally; and I think that's what most people try to do when they want to lose weight. They try to eat less and exercise more. And yet your book begins with challenging that conventional wisdom. What do you see as wrong with that simple and seemingly compelling phrase? Guest: Virtually everything. The short answer. I believed in this a decade ago, before I started my research. You can think of obesity in one of two different ways. The less I eat, the more I exercise idea comes out of the research called the energy-balance problem: You take in more energy than you expend, that energy has to go somewhere, so our bodies stick it in the fat tissue and that's pretty much all you have to know. And if you want to get the energy out of the fat tissue you just have to increase your expenditure, decrease your intake, and then your body will take the energy from the fat tissue and burn it. And it's this incredibly simplistic idea that basically comes down to we are some dynamic systems and we could be a black box, for all anybody cares. Doesn't matter what's happening inside. It just matters that more energy goes in, you get fat; you get thin the more energy goes out. And as I was doing my research for my books, I realized that actually this was a hypothesis, and it was a controversial hypothesis up until the 1950s, 1960s. And pre-WWII when all meaningful science in virtually all fields was done in Europe, the Europeans had a different conception of what caused obesity. And they thought of it as a sort of hormonal regulatory defect, just like any other growth disorder. And so you have your fat tissue is regulated by a whole complex system of hormones and enzymes and receptors and other central nervous system factors, and if that regulation gets out of whack you will start getting fatter. And if you start getting fatter, if your fat tissue starts growing, you'll take in more energy than you expend. So, dysregulation of the fact tissue is the cause, and this disturbance in energy balance is the effect, in this kind of pre-WWII way of looking at it. And the problem is, WWII comes along; the European and German and Austrians in particular, their school of research on this evaporates. Unlike physics, where we embraced all the European scientists who were chased to the United States, in medication and public health we wanted nothing to do with them. And post WWII this idea vanishes. And it's replaced with an idea of obesity as an eating disorder and basically gluttony and sloth. And what I did in my research was say: If this idea was right, if the Germans and Austrian researchers who were pushing this hormonal defect notion were right, how would the world have played out since then? And you see by the late 1950s, early 1960s, researchers, physiologists, and biochemists figure out what would regulate fat tissue, and it turns out to be fundamentally the hormone insulin that puts fat in our fat tissue. And as soon as you've identified insulin as the culprit, then it's the carbohydrates in our diets that determine insulin levels, independent almost of total calories. And now you've got a hypothesis of obesity that carbohydrates make you fat. And they do it by raising insulin levels. Not total calories. Russ: Which in turn, those higher insulin levels cause fat from our diets to enter into our bodies--is that the right way to think of that puzzle? Guest: Well, that's one way. When you eat a mixed meal, the fat from the meal gets stored in your fat tissue. And this is one of reasons why people always wanted to blame obesity on dietary fat. So, when you eat a mixed meal with fat, protein, carbohydrates, your body wants to burn off the carbohydrates because they get dumped into your bloodstream as glucose. Your glucose is blood sugar; your blood sugar levels start to rise. This has toxic effects to various cells. You secrete insulin in part to control your blood sugar. And one of the ways it does it is that it facilitates the entry of the glucose into your muscle cells so they can burn it. But it also locks the fat away in your fat tissue. Kind of saying: We'll deal with the fat later; let's burn the carbs now. And then when glucose levels start coming down, insulin levels start coming down. The fat is released from the fat tissue and the muscle tissue starts to oxidize it for fuel. And in an ideal world you've got a system where you eat a meal, you store fat, you burn carbs; you burn through the carbs, now you start to burn the fat, now you've gotten your fat back down to where it was originally; you get hungry and eat again. So, it's a beautifully orchestrated system, and it's this hormone insulin that runs it all. But if insulin signaling starts getting out of whack--and the idea is that the kinds of carbohydrates we eat today are new to our species, from brand new to relatively new to brand new--and we haven't evolved to deal with them, and they cause various disorders that are signaling in effect to keep insulin high; and if you are keeping insulin high you are keeping fat locked up in the fat tissue rather than burning it. And you end up in this system where sort of every day you store a little more fat than you should. And even if it's the dietary fat that's being stored, it's the carbohydrate content that the diet that's causing the effect. And this is all just sort of basic 1960s level endocrinology and physiology. And one of my challenges as a journalist and someone writing about this, and now kind of a proponent of this idea, is to get across the idea that we actually solved the obesity epidemic in the 1960s. And all we needed was 1960s-era medicine to do it. And technology to do it. And the problem is we decided that solution wasn't convenient. And we threw it out and decided to ignore it. And that's when we get to the situation we've been in ever since. |
| 9:08 | Russ: So, if I eat lots of calories and watch a lot of television and sit on my couch, but the kind of calories I eat are protein-oriented and vegetables that are not starchy, and therefore I have low carbohydrates, you are suggesting that I will not get fat. Guest: Yeah. Although I would edit that to say that if you are eating--actually, what you want to eat is a moderate protein, high fat diet. Fat is the one nutrient that does not trigger insulin secretion. So if you are already overweight, obese, or Type 2 diabetic, protein levels in the diet should also be kept relatively low. Although you could eat a meat-rich diet and still not get a lot, 15-20%, of your calories from protein. But yeah, the idea is, you could be sedentary, you could eat a lot, and if you don't have these offending carbohydrates in your diet, your body will metabolize the energy that you take in, and it will do it perfectly fine, and it will not just stick it in your fat tissue and make you fat. That's an idea that's exceedingly hard for the establishment researchers to buy or understand. Russ: And similarly, you are going to argue that if I have a low calorie diet of, say, being a male, 57 years old, if I eat 1500 or 1800 calories per day, but they are potatoes, candy bars, and bread, I can be obese despite my low-calorie intake. Guest: Yeah. And again, one of the things I do in Why We Get Fat, the very first chapter includes a list of populations that had high levels of obesity, coincident with extreme poverty. I just did something that I always felt the research community themselves should have done but never bothered. We have this idea that it's the toxic environment we live in today that causes obesity. So that toxic environment is fast food joints on every corner, large portion sizes, energy-dense foods--whatever that means--and there is no reason to be physically active, so we don't let our kids walk to school any more; we are always getting in the car; we don't even roll down our own windows any more. And so we have this combination of too much food, it's too available, it's huge portion sizes, not enough reason to be physically active; and that's why we get fat. And what I did was I just looked for counterexamples. Which to me is basic science. Let's look to see if we can find basic populations that had high levels of obesity and had none of this toxic environment. And I found about a dozen of them. I probably found most of the ones that have been studied but I wouldn't be surprised if there are papers in journals here and there that identified others. These go back to the Pima Indians in 1902, where a Harvard anthropologist who lived with the Pima for 6 months, wrote the seminal text on them. The Pima had gone through 20 years of famine from the 1870s, 1880s, early 1890s. And here they were half a dozen years out of their famine period; they are on a government reservation. And Frank Russell, this anthropologist comments about the high level of obesity in the tribe. And he has a photo of an obese Pima woman in his book, which was published in 1905, 1906, and he calls her 'Fat Louisa.' And he points out, as did another Smithsonian anthropologist who traveled to the area, that most of the obesity is in the women and the women work--they were basically treated like beasts of burden. They did most of the farming; they carried anything that the tribe wasn't loading on mules or horses. So if physical activity is a way to prevent obesity--and this is what this Smithsonian anthropologist, who went on to become Head of Physical Anthropology at the Smithsonian, commented--was that if physical activity made a difference, why is it that the women are fat when the women did far more work than the men did? And you see this same trend in 1928 with reservation Sioux on a South Dakota Crow Creek Reservation--very high levels of obesity in coincidence with extreme poverty. Deficiency diseases. In the early 1960s, studies in Trinidad--MIT nutritionists calculated that the diet was giving no more than 2000 calories per day and it was 21% fat and yet they described the obesity problem among the females as an extreme medical problem. And it goes on. Chile in construction workers in the 1960s. Mexican-American oil field workers in the 1980s. And these are poor, hard-working people, sometimes living on near starvation levels of food and yet still with high levels of obesity. So the question I ask in the book is the question I think everyone should ask: Why were they fat? Because if we could figure out what made those populations fat we'll probably have the answer to what makes us fat. And what we know is that they didn't have computers, they didn't have video games, they didn't have iPads, cars, any kind of labor-saving devices. And in some cases they worked a lot harder than any of us ever do. So, what was going on to disregulate their fat tissue? And the answer is? Guest: One thing that was common to all these populations is they were relatively new to refined grains, like white flour and sugar. Even the Pima--trading post comes into the Pima territory after the 1850s and the trading posts are selling sugar and white flour. And the Pima are living on government rations, and 50% of the government rations actually are mostly white flour and some sugar. So again you can argue that you add these refined grains and sugars to a population, you are going to get obesity, diabetes, diseases that associate with them. And the problem with our toxic environment today is not that we don't get enough physical activity, it's not that there's too much saturated fat or anything else, but that there's too much sugars and refined grains in our diets. And if you get rid of those, which is what you do fundamentally on a low carb diet, you reverse the problem. |
| 16:40 | Russ: When I read your book, I admit I heard that argument, but I heard a subtler version of what's wrong with calories in, calories out that I found extremely interesting and it reminded me a lot of the economic way of thinking. So I want to take a couple of examples from the book and you can talk about how they relate to endocrinology and what's going on in the body. So, you have a fascinating example. You have a picture of your son and, as you point out, most kids eat a lot when they are growing. And we would never say: Oh, my kid's growing because he's eating more than he exercises, so therefore he's able to grow. We say: He's having some kind of hormonal growth spurt and as a result, he's hungry. And so causation isn't just complicated. It's actually the opposite of the way we often think about the relationship between eating and obesity. With eating and obesity we tend to think: Well, I eat too much so I get fat. In fact, there's an argument to be made that because I'm fat, I eat a lot. I'm hungry, I have an urge to eat. And the psychological part of that that I find interesting, and I think this varies a great deal by individual, at least I presume it does--we can talk about that--but I know for myself, the line about you can't just eat one potato chip, which was a marketing slogan, is very true for me. It's not just that it's hard to eat one. There's no number of potato chips that satiate me. There's no number of French fries where if someone said, have another plate, that I would say: No, no, they don't appeal to me; I've had plenty. They are always appealing to me--when I've had some. When I don't eat them they are still appealing but in a different way than if I've had a few. And so that causal relation appears to be the opposite of what actually is the way we tend to think about it. Guest: There are a lot of examples of this that I point out in the book. The growing child--and here again, I'm just channeling the way the pre-WWII Germans and Austrians thought about this problem--and the growing child was one of their metaphors. An argument that I make in the book is that in every growth system that you can imagine, growth is the cause. And an increase in intake of nutrients is the effect. So in the growing child, the child's brain, pituitary gland is secreting growth hormone; the growth hormone is stimulating an insulin-like growth factor, and those are driving the growth of cells and tissues; and compensating for this, the body then needs more energy to both build these tissues and for the energy required for the building. And so the kid is hungry. And often you hear the same thing when your children are growing that they are lying around the house all day long: My son is eating me out of house and home and he's lying around the house all day long, and the reason he is doing that is he is going through a growth spurt and that growth spurt is driven by hormones. Elephants eat more than puppy dogs. And the reason they do--young elephants eat more than young dogs--and the reason they do is they are growing bigger. So, any system you can imagine. When a tumor is growing, that tumor is taking in more energy than it expends, but we don't really care that that's why--it's obvious that it's taking in more energy than it expends because it's growing. What we care about is what genes, oncogenes, tumor suppression genes in that tumor are broken that are driving it toward this unfettered growth. And the fact that if we could cut off the fuel supply to the tumor we could kill it is irrelevant. It doesn't mean that it's the excess fuel that's driving the growth. It means the growth is creating a sort of excess demand for fuel and the tumor--part of what's happening with the mutations that drive the tumor growth are all these mutations that allow it to take in more fuel from its environment to fuel the growth. So the fundamental argument I'm making is obesity is, we should think of it the same way. The reason people are hungry, the reason they tend to eat more when they are getting fatter is because the foods they are eating are stimulating the growth of their fat tissue. Those potato chips, the French fries, they stimulate insulin secretion. The insulin stimulates fat accumulation in the sense that it starts storing all the excess glucose, fatty acids in your bloodstream and locking them away in your fat tissue. So your fat cells are expanding. And the rest of your body perceives that as a kind of absence, relative dearth of metabolic fuels to run the body. And so you respond by wanting to continue eating or to eat more. The French have this wonderful phrase, that the appetite comes with the meal. And you've probably thought about this--I think about this--you might sit down to a meal and not be hungry, and then once you have a few bites of the appetizer, which is often a carb-rich creation, created to stimulate your appetite-- Russ: Yeah, it's called an appetizer-- Guest: For a reason. Yeah. And then suddenly you are hungry. Even though you would think that with each successive bite you would get more satiated and less hungry, that's not actually what happens. For a large portion of the meal you are hungrier than you were before you started eating. So there are all these hormonal factors that regulate this. And what you end up with is just a process of flipping the causality in obesity. I'm always having conversations with people where they are arguing, well certainly there's all kinds of psychological factors that are involved. For instance, I get stressed, I eat more; I get happy, I eat more; I get unhappy, I eat more. But among the things that are happening--for instance, if you got stressed and ate more fat and protein--so you went to the refrigerator and had a piece of rib eye instead of potato chips or pasta, then even though you are stressed you wouldn't get fatter. That's the argument. And then you ask the question: Why is it that when you get stressed, the foods you want, you know, comfort foods, are always rich in carbohydrates--usually sugars? And it turns out that stress hormones also have an effect on fat tissue, on fat cells. And in some ways they are similar to insulin and they work in collaboration with insulin in some ways, and so you could argue that it's the effect of the stress hormones on the fat tissue that in turn makes you crave the carbohydrate-rich comfort foods that calms you down. But the behavior in this sense is always an effect. Our null hypothesis, the assumption going in, is that the behavior is a response to a change in the physiological state of the body. Not a driver of that physiological state. |
| 24:30 | Russ: Let me take a couple of examples here, to bring in a little of the economics. First I'm sure our listeners have noticed that there was a failure to pay attention to Austrian scientist and researchers after WWII. Which is of course true in economics as well. This program has an Austrian flavor because of my deep interest in the work of Friedrich Hayek. Guest: Have you've ever read Siddhartha Mukherjee's brilliant book, The Emperor of All Maladies? Russ: No. Guest: I'm a passive aggressive competitive science journalist. I don't like to call anyone's book 'brilliant' if I can avoid it, but it's really a remarkable book, and it's a history of cancer and cancer research. And this theme just keeps repeating itself, with research done in Europe mutually by Germans and Austrians in the 1920s that just gets ignored and/or forgotten, in part because of the disruption that Europe goes through in the war. And then is finally reconstituted in the United States, you know, in the 1950s, 1960s, even the 1970s in some cases. Russ: It's also a bias against German accents probably. I mean, F. A. Hayek's video presence is not easy to access, because he's not as articulate as John Maynard Keynes. So what can you do? Guest: And it's certainly true--I talk about this in the obesity field. The leading American expert on obesity post WWII was Jean Mayer, who was a French émigré. He had fought in the French resistance, and he simply refused to reference the German research in any of his books. And one of his colleagues told me that: Oh, yeah, Jean Mayer, he hated the Germans; he killed quite a few of them. And my metaphor is, imagine if in physics, instead of embracing these European researchers because we had atomic bombs to build and cold wars to fight, imagine if they had said: We don't care what that Heisenberg fellow had to say or Bohr or Planck or Einstein; what could they tell us? We don't like their accents; we fought a war against them; we don't like their politics; we don't like their attitude. And so we are going to ignore everything they did. And this is what happened in medicine and public health. Russ: So, the other example I wanted to mention is this causation being reversed. One of the strangest things to me is this belief that spending creates prosperity. When in fact I think causation is reversed. It is prosperity that allows spending. But because they happen at the same time, we've come to believe that by spending money with each other we can somehow stimulate economic activity and productivity, when I think what we really want to do is stimulate productivity and that allows us to spend and have a nice standard of living. Now the other examples that you give in the book that are so provocative, besides the growing child--I want to go through a couple more of those before we get to some of the, I want to challenge some of your arguments. But I want to go through some of the metaphors first. You talk about a remarkable experiment. The ovaries are removed on one set of rats and not on the others, and what happens, and how we could have misinterpreted that. Talk about that example. Guest: Well, this is one of the seminal examples that I came upon in my research, where I began to have my paradigm shifted. And this is research done at the U. of Massachusetts in the mid-1970s by someone named George Wade. And George is only interested in reproduction. And so he was studying the effect of female sex hormones on weight gain and reproduction. And he did these experiments where he removed the ovaries from rats, females obviously, and noticed that after the surgery they would get what's called 'hyperphagic'--they would get these voracious appetites and they would quickly grow obese. And effectively what he was doing was removing the estrogen, because if you infused estrogen back into these animals after the surgery, you wouldn't see the hyperphagia and you wouldn't see the obesity. So he said, he's telling me about these experiments: If you do these experiments, if you just do this one experiment, what you think is removing the estrogen, removing the ovaries, works to make the animal hungry, and then that hunger causes the obesity. That eating too much--the hyperphagia. And so you've now confirmed your preconception that eating too much makes people or animals fat. But you could do a second experiment, which he did because he's a good scientist. So now he does the same experiment again--remove the ovaries; but you don't allow the animals to manifest the hyperphagia. You don't allow them to eat any more than they ever did. So you restrict the amount of food they can eat after the surgery to exactly what they were eating before the surgery. And he said to me: What do you think happens? Socratic mode; and I said: I don't know. And it turns out the animals get just as fat, just as quickly. But in the second case they are completely sedentary; actually, their metabolic rate goes down, their body temperature goes down, they expend less energy. And if you only did the second experiment you would imagine that removing the ovaries and the estrogen makes the animal into a couch potato. And they get fat because they expend less energy. But if you do both experiments, what you realize is that removing the estrogen literally makes the animal fatter. It works on the fat tissue and the regulation of fat tissue to increase the accumulation of fat. If the animal can eat more to compensate at will--because now it's losing calories into its fat tissue--so if it can eat more at will. If it can't--if you do the second experiment--it just expends less energy. And what is fascinating about this is you've actually created with this, you've shown in an animal model that the behavior we associate with obesity--gluttony and sloth--can both be effects of the dysregulation of fat tissue. And as Wade explained it to me, what estrogen does is it actually suppresses an enzyme on fat cells called lipoprotein lipase, or LPL. And what LPL does, simplistically putting it, it pulls fat from the bloodstream into whatever cell it happens to be sitting on. So if LPL is on your muscle cell, it pulls fat from the bloodstream in and your muscles burn it for fuel; if it's on your fat cells it pulls fat in and your fat cells store it. And estrogen suppresses LPL on the fat cells. You get rid of the estrogen; LPL blossoms on the fat cells and starts pulling in fat as much as it can. And now the body is sort of suddenly losing all this fuel into the fat tissue. And so it compensates by: you get hungry. And as it turns out, insulin works opposite to estrogen, so insulin actually stimulates LPL all the time. And the argument again is, you change the regulation of the fat tissue. You could do it by removing estrogen; you could do it by increasing insulin--the fat tissue is going to start taking fuel. And the way the pre-WWII Germans referred to it is the fat tissue sort of suddenly has its own agenda. Just like a tumor has its own agenda. It wants to grow and it will take what's necessary from the body to do it. Independent of whatever else the body is doing. Just like a tumor. And then the body has to compensate, because it's suddenly got this drain on its system. So, if it can eat more it does; if it can't it becomes more efficient and gets by with less energy. The cause is the dysregulation of fat tissue; the effect is energy imbalance, taking in more energy than the body expends. |
| 33:00 | Russ: So, that's one way to think about it. And I struggle to reconcile that with what I heard you say in other parts of the book. So let me bring that out, which is: eating less and exercising more, ignoring the kind of calories you are eating, the kind of food--the mainstream view that says the way you get thin is you change, you just have to make sure you are in deficit and then you'll lose weight--a pound of fat is 3500 calories, is that what it is? So every week that you consume more than you take in, that's 3500, if you can have your deficit be 7000 you'll lose 2 pounds, etc. But what you said in the book, and I think most of us in real life understand this quite well, is that that strategy fails not so much because of the science but because of the behavior. And of course the behavior is driven by the science; maybe that's the source of my confusion. But the way you think about it in the book and the way I think about it in real life is if you are exercising like a fiend, and you are dieting on calories like crazy, you are really unhappy. Your body is not happy; you are really hungry; and as a result, it's very hard to maintain the strategy. So, the strategy is a good strategy. If you can eat 1500 calories a day and run 10 miles, you'll start to lose weight. But that's just not a viable lifestyle over the long run. And that's why it fails. But you also are kind of suggesting it's not just that it fails because of that behavioral reason. It fails because it's literally not scientifically going to hold up. Is it more--what am I confused about here? Guest: That's the idea. You can argue that the dieting--eating as little as you can--and the exercise are both ways to sort of minimize the carbohydrates in your diet. So without even thinking about it, you are reducing the carbs you are taking in. And you are burning off some of the carbs through exercise. So you are changing your fat to your--the fundamental argument I make is if you want to lose fat or your body wants to gain it, you have to change the regulation of your fat tissue. There's a whole suite of forces dominated by insulin that work to store fat in fat tissue and that balance of forces has to change to get the fat out. Now you can change that to some extent by eating significantly less and exercising, running your 10 miles a day, in large part because you are going to reduce the carbohydrates and their driving of insulin and the effect of insulin on the fat tissue. But now you are also increasing the need for dietary fat and for protein to rebuild the muscle tissue and restock that and protein stores. And when you are done with exercising, your fat tissue actually tries to restock the fat that it gave up. Because it's still being driven--you have haven't changed significantly this balance of forces, post-exercise. So your body is now trying to grow again. Your fat tissue is trying to grow. Your lean tissue wants to restore and repair protein, cells that have been broken down by the exercise, and now your body wants the fuel to do it. This, again, very simplistically speaking. So, this hunger that you are trying to live with is a result of what you are doing to your, trying to do by forcing your fat tissue and your lean, forcing your fat tissue to give up calories, not providing your lean tissue with enough resources to rebuild. So, you can have an effect. But that effect goes along with the hunger that is in itself a result of these behaviors. And by the way, there are people out there who have spent their whole lives doing extreme physical activities, from people who work jobs, manual labor, to marathon runners, who despite this continue to get fatter year in and year out. And in fact one of my largest supporters now is one of the world's leading experts on endurance running, who is himself a marathon runner who gained 40-50 pounds over the years despite running 5 or 6 marathons a year. Russ: Just to make an observation again about consuming data and studies, etc. My first thought in listening to make that claim is--but I watch the Olympics coming up in a month or so, and I watch the marathon--everybody there isn't just thin. They are frighteningly thin. Art De Vany, a previous guest on this program would say they are dangerously thin or unhealthily thin or emaciated. They don't look healthy. He argues it's not a healthy thing to run long distances at a constant pace. But I presume your argument would be that I have a selectivity bias, that I see the marathoners who happen to be thin; there are others who are not so thin, but they don't make it into the Olympic trials, so my sample of people who exercise like crazy are only the ones who are able to run very quickly. And it's therefore not a representative sample. Would that be correct? Guest: Yeah. That's exactly it. You could argue that if we all play enough basketball, we'd all become 6'8" and built like Michael Jordan. And odds are that won't happen. The ones who are 6'8" and built like Michael Jordan are the ones we end up watching on television. Russ: Of course, Michael Jordan, now that he's retired, or Magic Johnson, or others who are exercising less than they used to weigh more than they once did. Guest: Quite likely. But one could argue that that weight is not due to their decrease in regular exercise but due to the foods they've been eating and the effect of those foods on their fat regulation. |
| 39:37 | Russ: You'd have to look at the data. But let me ask a related question to that. I actually--it's hard to believe for those who know me now--I actually ran a marathon and finished it in 1976. It's a long time ago. I concede that. But when I was a semi-serious runner, what I was told to do was carbohydrate loading. So, before the race, I skipped carbohydrates and went heavy protein for a few days, and I think before the race I ate a pound of pasta. I think many athletes are told this--that carbohydrates are energy producers. And so I assume that many world-class athletes are eating a lot of carbs. Is that not true? Guest: Probably. And this is one of the things that actually drove the acceptance of the high carb diet when we were younger. We're within a year of each other. When I grew up, in the 1960s, pasta was something you had once a week. Thursday night was pasta night. And then by the 1980s we were all making pasta every night, and ordering pasta; every time you had a dinner party, pasta is what you would serve because it was easy to cook. Russ: No, it's because Italians are happy. And so we are getting a little causal problem here. Guest: Yeah, well that could do it also. But part of it was driven by the marathon boom, the exercise boom, this idea about carb loading. Russ: No doubt. The energy. Guest: And one of the fascinating things--carb loading was developed by a Scandinavian exercise physiologist, as I understand it for cross country skiers, Olympic cross-country skiers. And these people would train all year round on very low carbohydrate diets and then they would carb-load before. They were raised to maximize the amount of glycogen they could get into their muscles, which, glycogen is the storage form of carbohydrates and it can be beneficial for a lot of endurance activities and actually shorter form burst activities like sprinting. Interesting enough, and this gets us into a different area of discussion entirely, but if you adapt your body entirely to the state of ketosis, where you are burning only dietary fat and you are getting in effect no carbohydrates in your diet, you can do really rather remarkable feats of physical activity. I have a colleague who is now--he eats once a day. He eats dinner, about 3000 calories, no carbohydrates except within the green vegetables. And he's now capable of doing a 90-minute weight workout followed by, for instance, a 70 mile bicycle race the morning after--without eating. And then he still won't eat until dinner the next day. I think it's a little bit obsessive, but he's in effect adapted to the state of ketosis, and even if you've got, say, 6, 8% body fat, which is very lean, you still have enough fat on your body--I want to say if you are 60 pounds at 6% body fat, that's 9 pounds of fat. Russ: Yeah. Guest: So that's--9 times 3500 is--what, about 32,000, 31,000 calories worth of fat to burn? Russ: Yeah. There's plenty there. Guest: That's a lot of exercise that that will fuel. So, if we make progress with the argument we are making, which is the carbohydrates in the diet that are the problem--we are making progress, but if part of this transformation, and the exercise physiologist I mentioned who runs marathons is a South African researcher named Tim Noakes. He's the author of the book The Lore of Running. And Tim is now doing experiments with ketogenic diets on endurance athletes--triathletes, marathon runners--to see how their performance changes when their bodies are running exclusively on fatty acids and ketones instead of glycogen and glucose. |
| 44:10 | Russ: So I'm going to make a confession now to you and the audience--of which they are actually aware; you are going to be less so--but I'll let you know how this confession informs my questions. Which is that starting back in September of last year, I decided to change my diet and start exercising regularly. The way I changed my diet is during the week I basically have no carbohydrates. I have some on the weekends, but a moderate amount. I've cut out all sugar, all starches, etc. And I lost about 20 pounds. And it's bounced around a little bit around that 20. It's gone down to maybe 15 at one point and now it's about 17 or 18. But I've kept it off for about 10 months, which is a long time for me, and very encouraging. And I want to believe this theory is true. It seems like a good theory. I love the contrarian aspect to it. So, I want to give one more metaphor that you use in the book, to let you explain; and then I'm going to challenge it, even though I do have this deep desire to believe everything you say, Gary. So I have to temper that a little bit. When I tweeted that I was going to be interviewing you people warned me that I need to be careful of my own confirmation bias. Which I'm pretty aware of, but of course, being human, sometimes being aware of it is not sufficient. So, anyway, you give the example in the book, two examples in the book, that are both very provocative, that seem to confirm your antagonism correctly to the calorie-in, calorie-out theory. You show photographs of twins as adults photographed naked so their body types are pretty visible; and one set of twins is really thin, the other set are large and obese. And you make the argument it's hard to believe that these two twins who are both thin just happen to have the same mix of consumption and exercise, and the obese twins, it's hard to believe they just had a different mix but the same for each of them. And similarly you point out that different kinds of cows, there are some cows that are quite fat and some cows that are quite thin. And it's unlikely that the thin cows get a lot of exercise and watch their calories and the fat cows are lazy, watch TV, and gorge themselves at the ice cream bar. But the problem I have with that--and this is where I am trying to challenge my own confirmation bias: Isn't equally hard to believe that those twins had the same patterns of carbohydrate consumption? The same is true for the cows. Isn't a huge portion of what we are talking about genetic? And that I look at families where there is a thin body type member of the parents and a not-so-thin one and they have kids, some of whom are incredibly thin and some of whom spend their whole lives struggling with their weight. And I'm starting to wonder: Maybe this whole carb thing is also wrong. It's just the way I'm born. My body has a certain level of heaviness it wants me to have. I can fight it for a while, but I can't fight it--maybe even for 10 months but I can't fight it forever. I long for those fries. Or, to quote Kingsley Amis: Inside every fat person is a fatter person waiting to get out. That's a great line, isn't it? Guest: Yeah. Russ: So, what's your argument against that genetic argument? Guest: Well, the reason the twins are in there is--obesity has always been known to have a huge genetic component. This was first demonstrated in the 1930s by this Austrian researcher Julius Bauer. The question--you can think of it as a genotype/phenotype issue. We have a certain genetic predisposition that gets triggered by the environment. And some of us have an obese phenotype or diabetic phenotype, and some of us don't. And those of us who do, you ask the question: What is the trigger? We know there's an environmental trigger, because first of all the obesity epidemic and the diabetes epidemic tells us that. The numbers have gone up dramatically in 40 years, 50 years, and that's not enough time for our genetic code to have changed in any significant way. Russ: For sure. Guest: So, something has changed in the environment that's triggered the obese phenotype in more individuals. And then you could just look at other species and say: Why is it that just humans are the only ones who grow chronically obese? So there are hibernators and migrators that put on enormous amounts of fat to migrate or to hibernate or to get through the winters, but they don't become, they don't get the metabolic abnormalities that go with it. They don't become sick. Russ: You have to just make a small correction there, because you haven't seen my cat. You mean, animals in the wild. Guest: Animals in the wild. Very good point. And even elephants, hippopotami, whales that have huge amounts of--actually, elephants, I gather, are not all that fat. A lot of that is just muscle. But the animals that do acquire fat, they are not chronically diseased with it. They don't get heart disease, diabetes. Fat is part of their defense mechanism to survive in their environment. With us we get this obesity as a disease thing. Why? What is triggering it? And so obviously we all have different predispositions to this. One of the arguments I've been making--I didn't make it in the book--you know, I think back to when we were kids. Late 1950s, early 1960s; and there were typically a couple of obese kids, one or two in each year of your school. Russ: Yup. Guest: Your year in school. I was talking to a bariatric surgeon from the U. of Missouri who described himself to me as the fat kid growing up. Back when there was only one. We never saw--when you are kids you don't think of those kids as kids who just eat too much and exercise too little, right? You think of them as people who are different. I'm sure we weren't kind to them. But we didn't think of them as lazy or gluttons. We just thought of them as the fat kids. There was something different about them. So the question just becomes, because we had less obesity 50 years ago, because you could find populations in which obesity didn't exist, because we can't find species in the wild that get obese--only humans and our pets and farm animals--what is it that's triggering that obesity? What is it that triggers the obese phenotype in those of us whose genotype is predisposed to it? And the rational argument, the conventional wisdom is it's too much food available, not enough exercise. And I'm arguing that that's wrong and that the null hypothesis should be the quality and quantity of carbohydrates in the diet. And again, in support of what I'm arguing, until the 1960s the conventional wisdom was that carbohydrates were inherently fattening. Jean Brillat-Savarin, 1825 book The Physiology of Taste, said: I've done conversations with hundreds and hundreds of fat people and they are the ones who want to eat the potatoes, the rice, the bread, the sweets, the beer. As late as 1963 I have a quote that I use in both my books from one of the two leading British dieticians. First sentence of his article in the British journal of nutrition was: Every woman knows that carbohydrates are fattening. And actually, when the 1980s came around and the British government started thinking about pushing low-fat diets for heart disease, one of their reports says we're going to have to figure out a way to get people to eat more carbohydrates when we've been telling them for the last 20, 30 years to eat less because they are fattening. So the argument I am making is it should be the null hypothesis, it should be the hypothesis that requires remarkable evidence to throw out. Particularly because the biochemistry and physiology supports it completely. And then we have this simple fact, as you've experienced, that when you actually do give up the carbs in the diet and replace them with fat, it's, for most of us, almost effortless to lose weight. Except for the French fries craving. |
| 53:29 | Russ: Yeah. I guess the flip side of that, though, is that if you start to indulge a little bit, and then a little bit becomes a little bit more, your body gets very excited about the arrival of those carbs. Guest: Well, I'm considered a hard-liner on this because I suspect for most of us it's easier not to eat any carbohydrates than it is to eat them in moderation. Russ: That's why it's easier to eat zero of something than a little bit. There's something ironic about that, I suppose. But maybe not. I think everybody understands that. Guest: I used to be a smoker. And if I tried to do what you do with carbohydrates with smoking--like I'm only going to smoke on weekends--I might have been able to do it, but the weekdays would be torture. Russ: Yeah. I don't find it hard. But I'm not so sure it's good for me. I think there's some evidence that this kind of on and off is not so good for you. But I want to come back to the twins. So, I've got these really skinny twins; they're grownups now. They grew up perhaps together; I don't know if they grew up in the same house or not; I think they probably did. And there's one set that's really skin; and both twins are really skinny. And there's one set that's really obese, and both are really obese. Are you suggesting that the obese twins had the predilection toward obesity and then just carbed out? Guest: Well, I'm saying they both lived in an environment where carbohydrates were available and a consistent part of the diet, and it triggered obesity in the obese twins. Not in the lean twins. It's not necessarily a one-to-one correspondence. Like if I eat 55% of my diet from carbs and 15% from sugar and my twin eats 57% carbs and 17% total calories from sugar, that twin is going to be 2% heavier. Russ: That's not true. Guest: That's a kind of simplistic way to think about it. Although I've seen those kind of analyses in the literature with populations where because you don't have a 1-to-1 correspondence between carbohydrate availability or sugar consumption, sugar availability in weight in the population, therefore this refutes the hypothesis. What I am saying is if both of them live in a carb-rich environment, they are both eating from it, they will end up at effectively the same obese bodies. And the lean twins who can tolerate the carbs will tolerate it equally well even if they have subtle differences in how much they consume. Russ: So, to take another weakness of mine, a donut--very hard for me to eat, say, half a donut. I'm more likely to have four. And yet it seems to me there are some people who can take it or leave it. Donuts. And there are others more like me, who have struggled to eat a half and are more likely to eat 3 or 4 once they get started. Especially if there's a tray of them and you don't have to go through the trouble of ordering them. My brother has the argument that you should eat one potato chip, put the bag up on the top shelf, very far away. So you can have another one; you just have to impose some cost on yourself. Guest: I used to do this with cigarettes when I smoked. I actually kept my pack four blocks away. Russ: There you go. Guest: Shared it with a fellow at the liquor store where I bought the cigarettes. This is in Santa Monica, California. And every time I wanted a smoke I had to walk four blocks to get a cigarette. It worked fine, within reason. Russ: Of course, sometimes you find yourself sprinting. Not walking. But to go back to the twins: are you suggesting--we can think of different hypotheses. One hypothesis is the thin twins just didn't eat a lot of donuts growing up and still don't. Or, they eat a lot of donuts, as much as anybody, but their bodies process donuts differently. Or, they are a type of person that doesn't have a craving for donuts, doesn't get triggered by the first bite as much. And therefore they can't gain weight if they want to. What do you think? Guest: Well, it's interesting. Again, the second and third possibilities are related. So, if that donut affects fat accumulation through the hormones it regulated, then it also will affect craving. So the person that doesn't have a craving could easily be the person--I would argue is the person whose body doesn't want to store calories as fat even when consuming a donut. Russ: Yep. Guest: Now if that person ate a donut every day for the next ten years anyway, that might--I would argue would have an effect on the regulation of fat tissue, so ten years from now they might find they are addicted to donuts and they weigh 20 pounds more. But it happened more subtly. The argument I'm making is that the physiology will tend to drive behavior, so someone whose body is triggered to store fat by these foods is also going to crave those foods. For the twins, they could both have grown up in the same environment. They could both have eaten the donuts. There are variations in this. Like my wife is capable of ordering a dessert at a restaurant, having one bite, and being perfectly content. And if I have one bite of that food, that dessert then takes over my existence. Russ: Me, too. Guest: You know the thing: you are having a dialog in your head about when can I have the other bite, should I have the other bite, should I just eat the whole damn thing and get it over with? Can I get the waitress over here to clear it before things get out of hand? Russ: I know all about that, yeah. Guest: It's somehow related to my body, to the effect that food has on my body. That's the argument. Or anyone's body. So, if you are predisposed to store fat then it's going to happen because the carbs in your diet and particularly the sweets are going to have an effect on insulin signaling and the hormone leptin and other hormones and that's going to start to get your fat tissue growing, and as it does your body is going to respond by wanting more of these particular foods. Simultaneously, somebody might burn off the carbs easily. So, a Lance Armstrong or a Michael Phelps who can eat 15 donuts and might crave those donuts just as much as you do but in that case their body is going to partition that fuel into being oxidized in the muscle cells, and they are going to work out for 3 hours after they eat their donuts; whereas I'm going to just take a nap for 3 hours after eating donuts. There's a lot of variables involved. It's one of the things that makes this so hard to study. Russ: Yes, just like economics. Guest: Yeah. Because you can imagine doing a study where you said let's feed people 3000 calories--this is one of the studies, recently with a colleague, Dr. Peter Attia, we started a not-for-profit called the Nutrition Science Initiative. We have support from a Houston philanthropist to fund research that we think will help clear up these controversies with the help of the obesity researchers. It's all very exciting. It's happening so fast we don't even have a website up yet. But we started talking about what experiments to do and which experiments have been done in the past and try to assess this. So, often people would say: Let's feed obese individuals 1700 calories of diet; one will be low carbohydrates and one will be low fat. But now what they've done is beside from assuming off the get-go that you have to eat less, you have to eat as little as 1700 calories to lose weight, they've removed hunger from the equation by not letting their subjects eat any more than 1700 calories. So now even if one group is much hungrier than the others--the low carb group loses weight effortlessly as does the low fat group but the low fat group is hungry--it doesn't matter because they can't eat more. They are not given any more. So that's really not a valid experiment. But another way to do it, actually the way we want to do it, is to set calories high. So, we believe if you feed them both, say, 3000 calories a day, you'll be able to see the difference between these two paradigms of the way regulation will manifest itself. That's the regime in which you can demonstrate a difference between total calories consumed and the macronutrient content of the diet. But now one of the problems is you are ignoring satiety. So by fixing calories at all high, now you are saying we don't care if you are satiated at 1700 calories. We want you to eat 3000. So that could be problematic. If we allow them to eat as much as they want. This would work for animals, to some extent, but for humans we'll start getting what we call intervention effects: we're using obese subjects who want to lose weight; that's why they entered the study. So they might decide to eat less and be hungry all the time because they want to lose weight. So now we are not going to see the full physiological effect of the diet. These are the kinds of issues we have to work out. And they have to be thought through very carefully because if they are not you could get the wrong answer, even with a study that's otherwise very meticulously planned and carried out. |
| 1:03:59 | Russ: Yes. It would not be the first time that a meticulously planned and careful study ran afoul of selectivity bias, countervailing things you didn't control for. It's a huge challenge. Of course what you really want to do is put sensors on people from birth, follow them through their life so that you know exactly what they ate rather than relying on a survey after the fact of what they ate 5 years ago, which is unreliable, weigh them every day, and get a massively wonderful data set. As long as you had every human being, you'd be fine. Guest: But even then you'd still only have an observation. Because unless you can not only put sensors on them but put shockers on them so you could stimulate one group every time they go near a donut-- Russ: Correct, you need a control group-- Guest: And the other group gets a very pleasurable sensation every time they go near a rib eye. Russ: Yeah. You hear an aria, when you see the plate of pasta you imagine you are in Italy. It's hard to do. I think one of the themes of both your books which I think is deeply appealing and slightly dangerous but I think for an honest person there is some value there: there is an inevitable tendency to use oneself as a data point. So, if you ask me which is easier--to cut your calorie consumption or cut your carb consumption, I'd say it's carbs. That's much easier to sustain. And so I'm more likely to lose weight and keep it off. That my attempts in the past to reduce intake to moderate my calorie consumption, even if that's a correct theory, have not worked because I can't sustain it. Whereas the carbs has a chance of being sustained. Zero carbs does not--it has a similar problem, I think. Guest: I'm not arguing for zero carbs. Except again, a lot of the arguments kind of get confused along the way. I'm arguing that for some obese individuals, some types of diabetics, 0 carbs may be necessary to restore them to some form of--near 0 carbs, in effect animal products and green leafy vegetables and nothing else--may be necessary to get them to a state of sort of near metabolic health. And that there are gradations of metabolic disturbance, metabolic disease, and the more subtle your disease is, the less carb restriction you need, the more refined grains and sugars you can eat. Although I think everyone would benefit from getting rid of sugars. And then for the 250-, the 300-pounders, the Type 2 diabetics, that's a different problem. Or it's a far greater problem and it requires a far more serious intervention. And this isn't a one-size-fits-all, hey, let's give everybody some whole grains, fruits, and vegetables because we think it's a healthy diet and we don't care if it's only a healthy diet for a subset of the population and for that other subset it may be better than what they've been eating. But it's not good enough, it's not severe enough to redress their health problems. Russ: Yeah. Although I have to say, the economist in me that looks at tradeoffs--I just happened to watch the movie Michael with my children. It's a John Travolta film. There's a really pleasant, delightful scene in there where they order two kinds of pie, of every kind of pie on the menu, and they sit around, and they are really happy. It's a really great scene. Andie MacDowell is not my favorite actress, but she's pretty good in this, sings a song about pie; and there's a great aura of love in the room. And there's a scene later where Michael, who is possibly an angel--we don't know in the movie if he's real or not--but he turns to the dog he's been hanging out with and says: You know, you can never get enough sugar. And it's a metaphor for the sweetness of life. But it is interesting how food is more than just things that make us fat and thin. Guest: No, that's true. But I'm going to give you a counter-metaphor. Russ: Yeah, go ahead. Guest: I used to be a smoker. Smoked first cigarette upon waking up; cigarette after breakfast, cigarette during work, during the morning walk to the gym, after the gym, after meals, between courses, after courses; cigarette after sex, of course. When you are a smoker or this is probably true of any drug, you can't imagine life without it. All pleasures are integrated through this cloud of cigarette smoke and nicotine. I lived in Paris off and on in the mid-1980s, and after I quite smoking I couldn't imagine returning to Paris, my favorite city in the world, because what you do in Paris is smoke and stroll, smoke and shop, smoke and eat, smoke and sit in cafes and smoke. Cigarettes are joy when you are a smoker. Just as food is joy, sugar is joy. And the interesting thing when you try to quit smoking is there's three weeks where you crave it constantly. Then constant cravings fade and then it's kind of longing. You're mildly depressed all the time because cigarettes really did mediate much of the joy you have in life. And then after a year or two that passes and after three or four years you can't imagine ever having smoked. And certainly can't imagine doing it again. And I would argue the same thing happens with the joys of sweets, if you give yourself a chance. The problem is sugar is so much more integrated into our lives and into our foods that it's almost impossible to ever get to that place where it's not consumed. And then fruits have sugars, berries have sugars. So you never get to the state where you are not a sugar eater. Although I know people who have certainly tried, and I would argue maybe a few people succeed. But I am a big believer in the need for joy in life, and what I used to get from the bread pudding at Hal's restaurant on Abbott Kinney in Venice, CA, I can now get from the steak, if I lived in New York, at Peter Lugar's; that I would be able to eat without thinking I was killing myself. Russ: Yeah. There are substitutes. Guest: And there's a lot to be said for eggs and bacon in the morning, if you don't believe you are killing yourself. And if you do, or if you are killing yourself, at least you get a lot of good breakfasts before you go. Russ: Yeah, well, that's the issue. A lot of people, I would just mention, although beer is not on my diet any more, other forms of alcohol are relatively low carb, so there are other kinds of joy, and as you point out a steak, etc. Of course, the complexity here is all these effects are, as you say, mitigated through genetics and life and all kinds of individual differences. Lots of people eat lots of potato chips who live long healthy lives, and lots of people eat lots of steaks and live long, healthy lives. And we just don't know so much about what it will do for us. Guest: Well, that's true. Again, and this is getting back to cigarettes, only 10% of smokers get lung cancer. But we know that cigarettes cause lung cancer--from the people who do get lung cancer, some 80-90% get it because they were smokers. I'm arguing the same thing with obesity. And then the other question to keep in mind, and often you get this thought about these very low carb, high fat diets are too restrictive. Doctors will tell me this: My patients are not going to do this. A counter-argument is: If your patient is a Type 2 diabetic or obese and he or she knew that they could be healthy--not have to take insulin, not have to take their statin, not have to take this drug, the hypertension drug, the blood pressure drugs--and that all it required was making this transition, this dietary transition, akin to a smoker quitting smoking or an alcoholic giving up alcohol, which are not easy things to do. But if their patients knew they could be healthy. And there are clinical trials suggesting that a large proportion of Type 2 diabetics could be drug free if they didn't eat these carbohydrates. How many of them would be willing to make the effort? How many of us would trade off--you and I were talking 20, 30 extra pounds. We're not pre-diabetic; we weren't becoming--I don't think so. There's a lot to be said for being healthy, and I think a lot of us will make the sacrifice if we really had the faith that if by doing so we could and would be healthy. Russ: Well, the other thing I would add, since I've cut out sugar and carbs and starches of that kind, that I have more energy. And it's probably just psychological, but it's working for me, so, hey, that's good enough. Guest: Yeah. |
| 1:13:57 | Russ: I could be fooling myself, but if it is it's working. We're going long here, but I just want to ask you one more question. You are a journalist who works in science. You are very aware of group think; you are very aware of the problems of confirmation bias. And you've accused others, and I think correctly of making terrible errors in scientific judgment because of their failure to avoid these problems. But now you've become a crusader of sorts, and you've got a new religion. You've rejected the old; you've got a new one. And, as I said earlier, I'd love to think it's the true religion. But you do put yourself at risk of being prone to confirmation bias and making the mistakes that you've accused others of. How do you keep that from happening? Surely others have accused you just as you've accused them of ignoring evidence on the other side. Do you think you are guilty of that sometimes? Guest: Yeah, obviously. And at some level it's a very seditious[?] problem. I mean you look at a paper--two papers come out and one of them supports your point of view and the other one doesn't. So you read the other one very closely to find out why you don't believe it. Russ: Yep. Guest: Might spend an hour doing it. And the one that agrees with you, you go: Oh, this is great. You read the beginning and the discussion and that's the end of it. One of the arguments that I've been making--we all come with bias. None of us is bias-free. I have a bias; as I said, this should be the null hypothesis. And once I phrase it like that it gives me the opportunity to say: I need remarkable evidence to refute it. So, this poorly designed free living study isn't good enough; rat studies--you know, we can demonstrate anything with rats, we've just got to find whatever species of rat we decide. So you can come up with a lot of reasons to ignore evidence that seems contradictory. The nature of science isn't every paper that comes out is right, every result is right, every interpretation is right. There's a huge amount of chaff out there, and we all get to choose what we think is the wheat. Ultimately it's a scientific question. I believe that every book I've written is as much about good science and bad science as it is about the subject. My first book I watched physicists at Cern, the huge European physics lab, discover nonexistent elementary particles. My second book, I documented the scientific fiasco called 'fusion.' And then I moved into public health and ended up writing two books about nutrition. They are all basically the same book. The difference in nutrition was that there was this alternative hypothesis that kept getting passed over, swept under the rug, that seemed it obviously should be the null hypothesis. And I just dragged it out and said: Let's just look at this. And now, one of the arguments I'm making is: Let's do the best science we can. Because in all these fields, one thing I can state definitively about nutrition, chronic disease public health research, is: Because of the problem of doing human experiments--the cost, the complexity, the fact that you've got real, free living human beings involved who can think for themselves, it's excruciatingly hard to do the science that is standard rigorously and meticulously enough to get a reliable answer. So one of the things I've said, we've done, actually co-founded a nonprofit that's going to fund research. And we've put together a consortium of people who we think are the best scientists in obesity and chronic disease research to help design and oversee the experiments. And then--it's funny--I'm the one who is always saying: look, we might find that the conventional wisdom was right all along, at which point I better find a shoe store that's willing to hire me as a salesman, because that's what I did in high school and I might still be able to do it. But ultimately it comes down to: you get a hypothesis; people either decide the hypothesis is viable or not. In this case you can test it on yourself, on an n of 1, which gives you an advantage over most other hypotheses. But ultimately I've been arguing: Let's just do good science. Let's just do the kinds of studies--people think these answers were settled in the 1960s. And they weren't. Not even close. So let's do what should have been done in the 1960s. And hopefully--we have some philanthropic benefactors behind us; we hope to get more and it looks like we're going to be able to raise enough money to actually answer these questions definitively. But ultimately that's what we need--just really meticulous, rigorous science. And it can be done. And I think it will be done. |