Thursday, January 31, 2008

Gary Taubes Interview by Seth Roberts

Seth Roberts of Shangri-La diet fame interviewed Gary Taubes who wrote Good Calories, Bad Calories.

Fascinating stuff.


Interviewed November 30, 2007 by Seth Roberts

[part 1]

INTERVIEWER I just spoke to someone who reduced the carbohydrate in his diet, for various reasons, including your book. He found that his performance on mental problems started improving again. It had stopped improving; it had been constant for a long time, and then he started getting better. So it may be that when you reduce the carbohydrate in your diet, your brain starts working better.

TAUBES Well there is evidence that your brain works more efficiently on ketones, as does your heart. So if he reduced his carbohydrate consumption sufficiently, he probably increased the level of ketones in his blood. But I'm just speculating here.

INTERVIEWER: The book seems to have had an unusual beginning. You’d been writing about salt, and you learned that a scientist you didn’t trust about salt was also talking about obesity?

TAUBES Well, I’ve spent over 20 years now writing about controversial science. In the mid-1980s, I lived at CERN for ten months, the big physics lab outside Geneva, watching physicists discover non-existent elementary particles. Then I wrote a somewhat infamous story about prions, the supposed causative agents of Mad Cow Disease. I wrote a book about cold fusion: I got obsessed with this question of how it happened, because it was so obviously wrong. After all that, I developed what I believe is a very good feel for who’s a good scientist, and who’s a bad scientist, just by talking to them. There are certain ways that good scientists describe their data, describe the caveats, and describe the conditions by which they may or may not be right. I had also, obviously, with cold fusion, interviewed some of the worst scientists in the world. I used to joke with my friends in the physics community that if you want to cleanse your discipline of the worst scientists in it, every three or four years, you should have someone publish a bogus paper claiming to make some remarkable new discovery -- infinite free energy or ESP, or something suitably cosmic like that. Then you have it published in a legitimate journal ; it shows up on the front page of the New York Times, and within two months, every bad scientist in the field will be working on it. Then you just take the ones who publish papers claiming to replicate the effect, and you throw them out of the field. A way of cleaning out the bottom of the barrel.

INTERVIEWER I thought your NY Times article,"What if It's All Been a Big Fat Lie," sort of did that. The people who came out against it, they were all the bad journalists. Just throw them out!

TAUBES Well, how I got onto that: I was doing this story for Science on salt and blood pressure, looking into the controversy about whether salt consumption plays any role at all in raising blood pressure and causing hypertension. One of the prime players in this salt/blood pressure controversy was obviously one of the worst scientists I'd ever met -- one of the five worst…you can’t say, in that five, who is the very worst, but they're all pretty bad. This is a group that includes guys like Stan Pons and Martin Fleischman who claimed to have discovered cold fusion. While I'm on the phone with this guy, interviewing him, he takes credit for getting Americans to eat less fat and fewer eggs. I literally finished the interview, called my editor at Science, and I said “You know, one of the worst scientists I’ve ever interviewed just took credit for getting Americans to eat less fat and fewer eggs, and I don’t know what the story is, but when I’m done with this salt story, I’m going to look into fat, cholesterol, and saturated fat.” I had a great relationship with Science. My editors had faith in me. If I said there was a story there, they’d give me the support I needed to pursue it. A year later, I ended up with that first story in Science, saying that there’s no evidence that reducing the total fat in the diet makes a damned bit of difference in our health. The evidence that saturated fat and monounsaturated fats are players is, at best, marginal. And that led to the N.Y. Times article.

INTERVIEWER What did that scientist say that made you rank him so low?

TAUBES There are all kinds of signs. He told me there was no controversy, when there was obviously a controversy. His side might have been right, but to deny there as a controversy was ludicrous. He talked about the legitimacy of throwing out negative data. You measure salt consumption one way; you don’t see any effect on blood pressure, and so you decide that’s obviously the wrong way to measure it. The implication of everything he told me was that he knew what the answer was before he did his experiments, and then he adjusted his experimental techniques and methodology until he got the answer that he wanted. And he believed this was legitimate science. There are other signs. I’m a stickler about the use of words like “evidence” and “proof”. So if someone tells you there’s no evidence for some controversial belief, you can be fairly confident that they’re a bad scientist. There's always evidence, or there wouldn't be a controversy. If somebody says that “we proved that this was true” or “we set out to prove that this was true” that's another bad sign. The point here, as Popper noted, among others, is that you can never prove anything is true; you can only refute it. So researchers who talk about proving a hypothesis is true rather than testing it make me worried.

INTERVIEWER Yeah, I see what you’re saying. They overstate; they twist things around to make it come out the way they want. They are way too sure of what they…

TAUBES Yes, and the really good scientists are the ones, almost by definition, who are most skeptical of evidence that seems to support their beliefs. They're most aware of how they could have been fooled, how they could have screwed up, or how they might have missed artifacts in their experiment that could have explained what they observed. They’re very careful about what they say. If you ask them to do play devil’s advocate, and tell you how they could have screwed up, then at the very least, they’ll say “Well, if I knew how I could have done it, I would have checked it before I made the claim”. So when I'm talking about discerning the difference between a good scientist and a bad scientist, I'm talking about how they speak about their research, the evidence itself, it's presence or absence. My friends in journalism would often ask me this question: by what right do I think make decisions about who's a good scientist and who's not. I’d say “Well, when you're an English major, you can be confident that Norman Mailer was a better writer than John Grisham, even though John Grisham makes 10 to 100 times more money”. It’s just a feel for what you do; I don’t know how else to describe it. I know a good scientist when I talk with one. I might be fooled, on occasion, but....

INTERVIEWER It’s not particularly well-correlated with how famous they are, or how many Nobel Prizes they’ve won.

TAUBES My first book was about a Nobel Prize winner who discovered non-existent elementary particles.

INTERVIEWER Who was that?

TAUBES An Italian physicist named Carlo Rubbia.

[end of part 1/start of part 2]

INTERVIEWER What do you think about prions?

TAUBES Here's the problem with prions: the claim is that here's radical discovery -- an infectious agent that doesn't have nucleic acid -- and it's based fundamentally on a negative result, which is that when researchers have gone looking for the nucleic acids they failed to find them. Therefore, so the logic goes, they must not be there. The original claim, by Stan Pruisner, another Nobel Prize winner, was premature. He made some claims in his early papers that were definitively wrong. Yet everything he’s done since then supports his initial claim, which suggests he's was either remarkably lucky to begin with, or he's only capable of interpreting his results so that they agree with his preconceptions. One of the themes in all of my work is that if you go public on premature data, what happens is that the motivation to do really good science ceases. By “really good science”, what you’re supposed to do, as brutally as you can, is to try to come up with tests that would refute your own hypothesis. The idea is that if your hypothesis survives every rigorous test you can imagine, and all those that everyone else can imagine, then you can start believing itss true. But once you’ve staked a claim based on premature data -- once you've gone out on a limb without doing any of those rigorous tests -- now your motivation becomes to prove that you were right., which you can never do in any case. But the point is that you stop trying to refute your hypothesis, and you start trying to accumulate evidence that supports it and the latter isn't science. It's more like what happens in religions.

INTERVIEW That’s what happened with Peter Duesberg. He was a good scientist until he started making claims about HIV.

TAUBES When I wrote this prion article in 1987, the science was so bad that it was a joke. Still, I never said that the prion concept wasn’t correct; I just said there was excruciatingly little evidence to support it, and there were plenty of reasons to believe it was wrong. How do you get strains of an infectious agent without nucleic acids (RNA or DNA) to encode the information in the strains? If you actually look today, even though Prusiner has won the Nobel Prize, if you go to the WHO website or the NIH website and you read up on prions, you’ll see that it’s still considered a hypothesis. There’s still no way to explain how you can get strains without a virus. Prusiner has these ideas, but they’re along the lines of now “a miracle happens”. It’s another long story, but one of the problems (and this is a theme in my book), when you let an untested hypothesis grow and infect the science to the point where people start to believe it’s true, even though it’s never been rigorously tested, the obstacles against ever overturning it get bigger and bigger. It’s like the dietary fat hypothesis: you let it sit around for 40 years, and it evolves to the point that people consider it dogma; it’s virtually impossible to overturn it. The situation with prions isn't so bad because the public doesn’t care about prions the way that they care about diet, but once the Nobel Prize is awarded, even though it’s still considered a hypothesis, people tend to ignore the studies that suggest it’s wrong. There's one researcher from Yale who is constantly publishing evidence in major journals that she’s found the nucleic acids, and people just ignore her. They believe the question has already been answered.

INTERVIEWER What’s her name?

TAUBES Laura Manuelidis.

[end of part 2/start of part 3]

INTERVIEWER That’s really interesting. I’m really interested in these pathologies of science; I’ve written about them several times. You wrote that New York Times piece, and from my take on it, you had a bunch of evidence, and then you got a book contract. Is it fair to say that you found out that what you wrote in the piece was mostly right?

TAUBES It’s a difficult question. I had actually pitched the New York Times piece on fat as an attempt to determine the cause of the obesity epidemic. The proposal was very open ended. I had several ideas. I actually believed, going in to the story, that the answer was going to be that high-fructose corn syrup was responsible for Americans getting fatter over the last 30 years.

INTERVIEWER I’m glad to hear that.

TAUBES The thing about the obesity epidemic is that we can say when it starts, give or take five years: sometime between the mid-1970s and late 1980s. So we have a starting point, and that happens to coincide with the introduction of a type of high-fructose corn syrup known as HFCS-55, which was developed to taste exactly like sugar when it's put in sodas and juices. In fact, it is effectively identical to sugar, as far as the body is concerned -- sugar (sucrose) is 50-50 glucose and fructose and HFCS-55 is 45 percent glucose and 55 percent fructose -- although I didn’t know that when I pitched the article. But I thought that high-fructose corn syrup is so cheap. Basically this is an idea that Greg Critser in a book called Fatland picked up on, and subsequently Michael Pollan, too, that high fructose corn syrup allows you to saturate the market with sugar, without any fear that price fluctuations will cause you to go out of business, or lose you a lot of money. If the international price of sugar suddenly spikes, as it did in the 70s, and you’re committed to fulfilling this enormous demand for sugar you've created, then you're in trouble. But if you have a cheap reliable source of sugar, at a price that won't change from year to year, then you can create an enormous market without fear. This was, more or less, my naive idea of how the economics of HFCS might have caused an entire nation to get fat. Once they had this dependable low-cost sugar substitute, the sugar industry and the soda industry could then expand their production and sell Big Gulps, etc. Then I did the reporting. I talked with industry analysts, and they said that was nonsense; that the primary cost of selling sodas and fruit juices is the bottling and the shipping, and that the cost of the sweeteners is such a tiny portion of the cost of the end product that it wouldn’t have made any difference whether it was sugar or high-fructose corn syrup. So I moved to my next idea, which was based on the fact that the beginning of the obesity epidemic coincided with the institutionalization of the low-fat dogma. As I’m doing that reporting, I stumbled upon what was, at that time, five trials of the Atkins diet, all of which had been finished, but not yet published. At one point, when I was doing the reporting, I actually got worried that some other journalist would beat me to the punch.

INTERVIEWER What was it about the Atkins diet, that made these trials so important to your article?

TAUBES: Well, remember, my background, as a journalist and in school, was more or less in physics. In the kind of physics I used to write about, you’ve got some complicated detector that’s looking at particles and atoms smashing together inside it and you're looking for some byproduct of a collision that you've never seen before. A new particle. But the first thing you have to do is make sure you understand your detector. Can you believe what it's telling you. So you to have to calibrate it. If you want to know how much you weigh, for instance, one thing you might do before you step on the scale is you calibrate that. You make sure that when you're not on it, the little arrow on the scale is pointing to zero. If it's registering one or two pounds when you're not standing on it, then it might be off by five or ten pounds or more when you are. So you want to calibrate your equipment. You want to know that when you set it to zero, it says zero. That's an idea that's always resonated with me. Measure what happens at an extreme, make sure you understand that, and then see what happens from there. So here's the Atkins diet: in theory, you're removing virtually all of the carbohydrates, but you don't tell people to eat less. You tell them to eat as much as they want. It's like you're setting the diet to zero carbohydrates, and as much fat as possible. According to conventional wisdom, you should certainly not lose weight and you might even gain it. But here were five studies saying that, lo and behold, people really do lose weight when you remove the carbohydrates from the diet, and they lose more weight than they do when you tell them to keep the carbohydrates but eat less calories. What's more, their cholesterol profiles actually improve, so how can fat or saturated fat be bad for your cholesterol, if these high fat, high saturated fat diets make your cholesterol levels better. To me that had to tell you something about the validity of the low-fat dogma and about the underlying physiology. What do carbohydates do, and what does their removal do. So once I learned about those five studies, I was confident that I had a story that was now worth writing. As for your original question, about whether I found out most of what I originally wrote was right, obviously the book supports the message of the article, but I no longer believe a fair number of things I believed when I wrote that story. For instance, when I wrote the Times article I inherently believed that the key was still calories consumed.

INTERVIEWER You mean things that you believed then, that you don’t believe now?

TAUBES Yes, that I don’t believe now. In that original article, I discussed what David Ludwig has argued -- that easily digestible carbohydrates cause these blood sugar and insulin spikes, and that in turn causes blood sugar to plummet, and the result is blood sugar so low a few hours later that this in turn makes you hungry. So you eat more and that's why you get fat with carb-rich diets. Ludwig works with obese children at Harvard and I believed that his hypothesis was probably true. Then I also talked about Michael Schwartz’s research at the University of Washington. Schwartz believes that insulin's primary role is to suppress hunger in the brain, but that somehow we become resistant to that effect and so, once again, we eat too much and that's why we get fat. Both these theories are predicated on the notion that we get fat because we eat too much and that's what I believed. We consume more calories than we expend and we get fat; something about carbohydrates facilitates that excess consumption. Now I believe the causality is reversed, and that's what I discuss in the book and in the lecture. Carbohydrates make us accumulate calories in our fat tissue, and that in turn makes us eat too much. It’s all about the regulation of fat metabolism. All those things that Ludwig and Schwartz were talking about might have been true (I mean, they are true, on some level), but they’re not the driving force of why we get fat, or why removing the carbohydrates makes us lean.

INTERVIEWER I see. So that’s a good summing up of what was in your article that you believe, and what you don’t believe anymore.

TAUBES There are other related facts, as well. I never imagined when I wrote that original article that I would come to believe that exercise won't make you lose weight, even though I’ve been an athlete my entire life and it's never helped me. So it's fair to say that when I wrote that New York Times article five years ago, I had an entirely different conception about the causes and cures of obesity and overweight. Carbohydrates were key, but my understanding of the mechanisms was completely different. That’s the kicker with research and reporting: you don’t know what you'll find until you do it.

[end of part 3/start of part 4]

INTERVIEWER I was impressed with the discussion in your book and in your lecture about obesity coexisting with poverty in all these different cultures and the implications of that. I'd never seen that before.

TAUBES I have this feeling, and I guess that all writers (or all neurotic writers) have to some extent, that my work is being ignored. It’s my Rodney Dangerfield complex. Now that I’ve written the book, I occasionally get emails from friends saying that they had some discussion with some obesity researcher, and they said, “Are you going to read Taubes’s book?” and their response was “Well, we know what Taubes thinks, so why should I bother reading the book?” What's more, the Atkins craze has come and gone, so these people believe it’s old news. Why should they pay attention to the book or what I might have learned in reporting it? In fact, I got more reviews for my cold fusion book than I have for Good Calories, Bad Calories. And The cold fusion book came out three years after the fact. There was also this sense that my article started an Atkins craze, and then Atkins Nutritionals declared bankruptcy, and somehow it all went away, and it’s just the same old diet crap that nobody wants to hear about. Nobody is going to stay on the Atkins diet so who cares? Let's move on. The lecture you heard is an attempt to combat that attitude: I argue that the existence of these obese, impoverished populations living on high carbohydrate diets are counter-examples to the conventional wisdom. As I said in my talk, if you have an obese mother and a malnourished child living in the same family, and this is a common phenomenon, that should be perceived as a refutation of the calories in/calories out hypothesis. In any sort of healthy scientific endeavor, that’s the kind of paradox you look for. Physicists have recently spent a few billion dollars building an accelerator that will, they hope, produce some kind of phenomenon that they can’t explain by their current theory. If they get that, it's front page news and they now have some observation that they can use to improve their theory. These obesity researchers, they have malnutrition and obesity coexisting in the same impoverished population, and they don’t see it as a challenge to their hypothesis. How do I get the word out that there are important issues here that have to be discussed? That's what that lecture is intended to do. When [the New York Times reporter] Gina Kolata reviewed my book in the New York Times Book Review, she swept right over these issues. She went right to the thing that bugged her -- why don't people stay on these low-carb diets? -- and ignored all the evidence that refutes the conventional wisdom about why we get fat. All she cared about in the end was why don't people stay on these diets if they work.

INTERVIEWER As if that’s your fault! I thought that was a very unusual way to review a book.

TAUBES Well, she had written her own obesity book that came out five months earlier, and she blamed obesity, in effect, on genes, without bothering to acknowledge that the genes interact with the environment; we have an obesity epidemic; we have obesity associating with poverty, for instance, so there’s obviously some lifestyle factor.

INTERVIEWER And obesity’s gone way up in the recent past; it can’t be genes.

TAUBES I felt her review was her way of saying “Look, this is why none of the stuff he discusses was in my book.” One point I make over and over again is that obesity is a disorder of excess fat accumulation, so you have to look at the hormonal regulation of fat tissue. If you're discussing growth disorders -- gigantism or dwarfism -- you look at the hormonal regulation of growth. So why not do the same in obesity. Gina didn't, because nobody she interviewed brought it up. Then she turned her review of my book into an excuse for why she didn't mention any of these things. Anyway, that’s life in the publishing industry. If you think about it too much, you just get angry.

[end of part 4/start of part 5]

INTERVIEWER Well, I think your book is a great book, and I don’t think its effect is limited to how many reviews it gets. What books do you think your book resembles? I think of it as a book showing that authorities can be seriously wrong, but what do you think?

TAUBES You know, I don’t know, actually. I can’t answer that question without sounding like a crazed egomaniac, so I won’t. What the book does is try to explain why the paradigm of obesity and chronic disease has to change and then to offer the alternative paradigm. Although I don’t use the word “paradigm” in the second half of the book, that's what it's trying to do. I want people to stop thinking about obesity as a disorder of overeating, calories in over calories out, and think about it as a disorder of excess fat accumulation. That's a classic paradigm shift, or at least so I think. I don’t believe that you can understand obesity and its associated chronic diseases, without thinking of obesity fundamentally as a disorder of excess fat accumulation and asking this question: what regulates fat accumulation? That’s going to be the thing that tells you what the cause of obesity is. If it’s a paradigm shift, then you have to ask yourself how many paradigm shifts are there like this, and what kind of books have been written to directly shift those paradigms, and then I sound like I have some serious ego problems.

INTERVIEWER Then let me put the question differently. I think your book piles up an enormous amount of evidence that is hard to refute. The cumulative effect of all that evidence is not that we’ve been lied to, of course, but that we’ve been misled, badly misled, about something that’s really important, namely our health. So, are there other books like this?

TAUBES I really can’t answer that question either. I'm not erudite enough and then I spent the last five years doing nothing but reading about fats and carbohydrates, so my memory of other subjects fades away. Here's how I think of it, though: when I was talking with my editor about this book when we in the editing process -- and he's a tremendous editor, who has edited maybe eight or nine non-fiction Pulitzers -- I brought up a book called Ashes to Ashes as an example. Ashes to Ashes is by Richard Kluger and it won the Pulitzer and my editor edited it. It's about the cigarette industry and not just the industry itself, but the science and the struggle to understand that cigarettes cause lung cancer. I said to my editor, “Imagine if we lived in a world where the public health authorities were telling us that lung cancer is caused by saturated fat”. Kluger has got to write a different book, and that’s the situation that we are in.

INTERVIEWER Kluger has got to write a longer book? Was that your argument?

TAUBES He’s got to write a different book. His book was actually longer than mine, but it was a narrative, which mine isn't. If you're going to convince the entire public health community that they've made a horrible mistake -- or many of them, in this case, whether about cigarettes or obesity and disease -- then you have to build an argument as carefully and as rigorously as you can. It's like arguing a legal case, more so than telling a story. And that’s one of the reasons why my book can be difficult to read, or challenging.

INTERVIEWER I found it easy to read.

TAUBES Well, good. See, I read the Amazon reviews. I shouldn't but I do. And for every three people who say it’s tremendous, there’s somebody who says “It’s boring” and they couldn't get through 20 pages of it. One problem is that we gave it this diet-like spin, with the title "Good Calories, Bad Calories" and people buy it expecting a diet book. And it's not a diet book. I also have a lot of friends who tell me they bought the book and they’re jumping into it, and I never hear from them about it. It tells me, being a cynic, that they got to the section on VLDL and LDL or some such, and that was the end of that.

INTERVIEWER I think it has a lot of evidence. I think the book is harder to read than it might be, because you feel compelled to have a lot more evidence than usual, because you’re saying something that everyone says is false. If what you’re saying was more conventional or acceptable or went down more easily, you wouldn’t need as much evidence.

TAUBES Well, that’s the thing. This is one of the ironies, again, of reviews like Gina Kolata's or some other that I've got. They’ll say the book’s too long, it goes on and on, and then they’ll say “he doesn’t even mention X," or “he leaves out this evidence”. I’m all too aware of the arguments I left out, the counter-arguments, the counter-counter-arguments, the counter-counter-counter-arguments. At one point I had a draft of the book that was 400,000 words, unfinished. For every section, like the section on salt and blood pressure, I would say “here’s why we believe what we’ve come to believe. Here’s the counter-evidence implicating carbohydrates. Here’s how the authority figures treat that counter-evidence. Here’s why they can look at that evidence and think it’s not a challenge to their beliefs”. And my editor, bless his heart, said “Look, you don’t need this. If you get a chance to lecture on this material, then you can tell the people in the audience why their counter-counter-arguments aren’t actually refutations of the carbohydrate hypothesis. You don’t need fifteen different levels in the book." But, you're right, I’m trying to convince people of something they don’t believe. I was walking this tightrope between making it readable for the lay public, so that they could make their own decisions, and hoping that doctors, researchers, and authorities would read it, and they might say, “Well, you know, Taubes has a point. Maybe we should take this seriously.” What I fear is that on one level, I lose some of the lay public, because it’s too difficult and advanced, and on the other level, the physicians and researchers aren’t going to read it anyway, because they don’t see that a journalist can tell them anything they don’t already know. And then there’s this effect where, after I challenge half a dozen of their most fundamental beliefs, and they’re only 150 pages into it, do they just burn out? The example that I use there is that if somebody came out with a really-well-reviewed book saying that extrasensory perception should be taken seriously as a scientific phenomenon, I wouldn’t be able to read it. No matter how good it was, or other people thought it was, I wouldn’t be able to read it. I might try, because I tell myself I have to be intellectually honest and rigorous, but I could imagine, after 50 pages, I'd just say “I can’t do it. Maybe he’s right, but I can’t process it. My brain won’t allow me to process what he’s saying”. I wonder if that’s going on here, too: “Saturated fat, OK, but salt, fiber? Give us a break.”

[end of part 5/start of part 6]

INTERVIEWER It’s true, when I started your book, I already kind of believed all of your main points. Not all of them, but I was sympathetic. I knew where it was going. I thought “Oh, good. More evidence. This is interesting, and that’s an interesting way to tell that story”.

TAUBES The way I see it is that the establishment has an immune system to protect itself from challenges. Every science needs that kind of immune system to protect itself from quacks and easy-to-swallow but erroneous ideas that might infect the good science in the field. My question is whether I can infect enough people, enough serious scientists, that I can pose a threat to this immune system, that I could compromise the immune system of the establishment and make them take this idea seriously. Because some times these immune systems work against challenges that are legitimate. I honestly don’t know if I can. It’s going to be an interesting year. I hope I don’t become one of those bitter old men who, when I fail to do so, who can’t let it go.

INTERVIEWER How did you end up giving your recent talk at Berkeley? Obviously someone in the establishment was willing to invite you?

TAUBES Yes. It was actually epidemiologists at the School of Public Health who invited me initially to talk about epidemiology after I had a cover story called "Unhealthy Science" in the New York Times. I told them that the subtext of that story was my book. If what I say in the book is correct, then an observational epidemiology has done an enormous amount of damage. One line that was taken out of the New York Times article said that this was a story about the risks and benefits of observational epidemiology. There are certainly some successes in that endeavor, but if we’re living through an obesity and diabetes epidemic because of its failures, then it's conceivable that more people have died because of observational epidemiology than have been saved. You always have to look at the negatives, the false negatives and the false positives. You can’t just look at the true positives and say that this is a valuable field of science. We're digressing again, but the game of poker is relevant here. Are you a poker player?

INTERVIEWER I’ve played a lot of poker, yeah.

TAUBES Bad poker players base their methodology, their strategy, only on what happens when they win. They don’t notice that that strategy is making them lose more money when they’re losing than they win when they’re winning. The best strategy, of course, minimizes the losses and maximizes the gains. But they don’t think like that; the wins are so seductive that that’s all they pay attention to. Anyway, getting back to the question, these Berkeley epidemiologists invited me to lecture on epidemiology; I said “let me talk about the book”; it gives me a chance to sit down and try to convince some unbiased observers, I hope, that their beliefs about calories-in/calories-out has to be questioned.

INTERVIEWER What effect do you think your lecture had?

TAUBES I don’t know actually. I don’t know how many of the people I was preaching to are already converted. I thought it went over well. I mean, I couldn’t believe that I had spoken for almost two hours and had 90% of the audience awake. There were a few people I lost (you know, you focus on the girl in the seventh row on the right, who’s asleep). But most people seemed pretty attentive. But when I say I'm trying to infect others with these beliefs, if I convinced even a few of the faculty Berkeley that these ideas have to be taken seriously I've made progress. OK, now I’ve got a little infection growing at Berkeley. Indeed, I asked one of the epidemiologists who invited me to e-mail, say, ten of his colleagues and say, "You should get Taubes to come lecture, because it’s fascinating, and you might think his book is a little dubious, but when you hear his lecture…”. So we’ll see if it has any effect or if they’ve found it compelling enough that they went through with it. I hope so.

INTERVIEWER I’m just surprised that they found your book dubious. I think they might disagree with your interpretation of the evidence, but I don’t think they would find the reporting dubious.

TAUBES I’ve got to get to the people who take this knee-jerk response that they know what I think, and they don’t have to read the book. For instance, I had lunch with a Berkeley obesity researcher that I’d interviewed five years ago. We spent a couple of hours together five years ago and I sent him a copy of the book when it came out.

INTERVIEWER Who is this?

TAUBES A guy named Marc Hellerstein. He’s a runner and, of course, he believes that sloth is the cause of overweight. He joined us for lunch on Wednesday, but he didn’t eat, and I had about 35 minutes to try and convince him to read the obesity section of the book. The way he sees it, he’s got a lot to do; he’s a busy man, doing all of these experiments, trying to get funding, what could he possibly learn from reading the book and it's a big book? So I was basically sparring with him for 35 minutes trying to inflict enough damage that he might conclude that he might actually learn something about his own subject of expertise if he reads it. And he actually said “OK, OK, OK, I’m going to read it, I’m going to read it”. (If he does, I'd be surprised, because after the lecture I e-mailed him a few follow-up notes, and he never bothered to respond.) I believe his initial response is probably common among obesity researchers, and even if they're tempted, they first have to wade through 200 pages on chronic disease that try to convince them that everything else they believed is wrong. The exceptions are those people like you, who already had reason to agree with me.

[end of part 6/start of part 7]

INTERVIEWER I was a member of the Center for Weight and Health. But the other members didn't know what I was up to, and had no idea it could have anything to do with actual weight loss.

TAUBES That’s one of the things I’ve found most amusing about obesity research, that you have this disconnect from pre-World War Two, when the people doing it were clinicians who were treating obese patients, to post-World War Two, where first, it’s nutritionists, who do rat experiments. Then, by the 1960s, obesity is considered an eating disorder and it’s being treated by psychologists and psychiatrists. So today, if you looking at some of the major obesity centers in the country --- at Yale, at University of Cincinnati, they’re all run by psychologists or psychiatrists. Here's a physiological disorder of the body, and it's being studied by psychologists and psychiatrists. They're not interested in anecdotal evidence, unless it agrees with their preconceptions.

INTERVIEWER In my department, we don’t have any of that. Obesity is not handled much on the Berkeley campus.

TAUBES But think about it: it’s a physiological disorder.

INTERVIEWER Well, hunger is controlled by the brain.

TAUBES I know, I know, but you know, diabetics get hungry. Type I diabetics are starving. Literally starving, without insulin. But it's not psychologists who treat diabetics.

INTERVIEWER I think that with Type I diabetes, you can say, “look at this problem; it’s not in the brain”. But I think with most obesity, it’s no so obvious that the problem isn’t in the brain. Sure, they’re fat, but maybe they’re fat because they’re hungry too much. That could easily be a brain disorder. It could easily have something to do with the brain.

TAUBES It could have something to do with the brain, but the problem is in the body. This is the paradigm problem. If you just think of it as hunger, then…

INTERVIEWER I’m not saying you just think of it as hunger, but you wouldn’t want to rule it out.

TAUBES Yeah, I know. That’s why the book is so long, because I’m trying to do it --- I’m trying to say “Look, your fat tissue is trying to get fat. Hunger and gluttony and sloth are side-effects of what’s happening at a hormonal level in your fat tissue."

INTERVIEWER Right. I love the way you’re answering these questions; it’s so informative. What effect did Weston Price have on you?

TAUBES Price was interesting. It’s funny. He got cut from the book for reasons of length and narrative, but reading Price was a revelation to me, as I say in the acknowledgments. I think that Price should be required reading for every nutritionist in the world. And then, "Nutrition and Physical Degeneration" is a great read, as well.

INTERVIEWER How did you come to read his book?

TAUBES How did I come to Price? I don’t remember, actually. Somebody in the field must have recommended him.

INTERVIEWER It was after your New York Times article?

TAUBES Oh, yes, definitely. I did not read Weston Price prior to that. I have to say, by the way, that I was trying to decide how much to believe of Price's stories. I decided that if his story about migrating, tree-climbing crabs in the South Pacific was true, I would believe everything Price said. This was my calibration. Because some of his stories are wild: about how pygmies, for instance, kill elephants by slowly hamstringing them over the course of a few days. Even with his photos as evidence, they're still hard to believe. So, anyway, this being the 21st century, I googled the tree-climbing crabs , and indeed, there are migrating, tree-climbing crabs in the South Pacific. The article I found didn’t say whether the local natives hunted them by putting nets under the trees and making the sounds of coconuts falling, so that the crabs would climb back down into their nets, which is what Price wrote, but the crabs definitely exist. I decided that’s it. As far as I’m concerned, Weston Price is an unimpeachable source.

INTERVIEWER That’s good to know. I really like his work, too.

TAUBES And those photos of the teeth of populations that do and do not eat sugar and white flour. Compelling stuff. I have a 2 year old and I try to keep him away from sugar and white flour just because of Price's photos. And you know, in this day and age, it's not easy to keep a child away from sugar and white flour. But it’s the photos in Price’s book that keeps me motivated: we’ve got to survive in Manhattan on a science writer’s salary. It would be nice to save the $6,000 for braces, if I could keep him off sugar and white flour. I still don’t understand how the sugar and flour can effect how the teeth actually grow in, but Price makes a compelling argument that they do.

INTERVIEWER There’s disagreement about that. Weston Price thinks it’s one thing. A professor in Illinois thinks it’s that that people who eat the urban diets have soft food, and the people who eat the rural diets have chewy food. The chewy food makes the kids’ jaws grow to be the right size.

TAUBES My problem with that is that he's making the assumption that the addition of sugar and flour removes some significant portion of the baseline diet. It could be true, but again, it’s an extra assumption. Take the Inuits, for example: one of the things I did in the course of my research was try to refute this notion that cancer didn’t exist in the Inuits until the 1930s. So I tracked down whatever memoirs I could find from physicians working with the Inuits to see if any of them mentioned cancer prior to the 1930s. And one of the things I found fascinating was that at the turn of the early years of the 20th century, the Inuit were eating mostly their native diet. By the 1950s, they were eating tons of sugar and flour and drinking beer and other alcohol, and tuberculosis had decimated them, but they were still eating their baseline diet; it’s just that all these other things had been added on top. So they’re still eating seal and whale and caribou, but they’re also eating these Western foods. In general, it's never a good idea to add that extra assumption until you absolutely have to -- that something else critical changes with the addition of sugar and flour. Maybe it's just the addition that's the cause. That's the one thing you know for sure that happened. This is Occam’s Razor. The key thing is that cavities are caused by the sugar and flour. The simplest hypothesis is that the orthodontal problems are too. It is possible that the sugar and flour affect growth hormones -- insulin-like growth hormone, for instance -- which could have local effects on how the teeth grow in. The sugar and flour could affect bacterial growth locally and that could have some effect. Either way, I find the evidence sufficiently compelling to wonder whether my son will grow up with nice teeth if he doesn't eat a lot of sugar and candy and white flour.

INTERVIEWER Changing the subject slightly, you mentioned that the obesity center at Yale is run by psychologists. Did you ever ask Kelly Brownell how he reconciles his toxic environment view with the fact that many people in poor countries are fat?

TAUBES Not yet. I would like to lecture at Yale some day, and I’m hoping that I don’t have to invite myself. You know, I’m fairly confident that if I were to ask many of these people if they'd get me a lecture -- call them and say I'd like to come and talk -- they'd arrange it. They 're intellectually honest enough on that level. But again, it’s people like Kelly Brownell that I was thinking of when I was compiling that list of populations. And what boggles my mind is that people have been peddling this nonsense for 30 years, and they never bothered to look. They never bothered to do their research, to see if there was evidence that refuted their hypotheses. Again, this is what you do in science; you get a hypothesis, and you try to test it. So how would you test the hypothesis that prosperity causes obesity, or that our modern toxic environment, as defined by Brownell, is the cause. Let’s see if we can find examples of non-toxic populations, you know, poor populations without McDonald’s, without televisions, without remote controls, who are obviously physically active, at least by our standards. It’s funny, I was talking with Hellerstein at Berkeley. When I told him about the Pima and the Sioux Indians, and he said “Well, do they live on reservations?” Like, if they live on reservations, then that means they’re sedentary, at least relatively, compared to their previous lives, and so you can evoke sedentary behavior as the cause of their obesity. So now you have this idea that it’s not how sedentary you are, it’s how sedentary you are in comparison to how active you used to be. So like, Sioux Indians, who rode along the Great Plains and chased after Custer --- they were so active that if they only have to move onto reservations and stop riding their horses all the time, they get obese. So it can actually be a detriment to be extremely active, because then being only mildly active causes obesity.

[end of part 7/start of part 8]

INTERVIEWER Marc Hellerstein thought that the obesity epidemic was caused by people being sedentary?

TAUBES He believed that the key is whether you're sedentary compared to how you used to be. When I told him about the Pima and the Sioux Indians and this 1981 study of obesity in oil field workers, he had an excuse for everything. So the Pima and the Sioux Indians, they lived on reservations, so they could be obese because they were relatively sedentary, at least more sedentary than they used to be. And the oil field workers, well, they’re Mexican-American, so they have some kind of “thrifty” gene going. You know…this is what pathological science is: a field in which you can find a reason to explain away all negative evidence. In pathological science, it's no longer possible to refute the hypothesis. Remember, science is about trying to test your hypothesis and refute it, but in a field like this, if you test it and come up with a counter-example, the counter-example is just explained away with whatever comes to mind. Negative evidence never means anything. So you have an obese person who’s sedentary, that’s proof of my hypothesis. If you have an obese person who’s very active -- at least, compared to most people today -- the Sioux indians, for instance, who were so poor they had to walk down to the river to get their drinking water; who had no televisions, no cars; they had to walk outside to evacuate their bowels -- those people are obese because they used to be more active than they are now.

INTERVIEWER Well, that’s a new one on me. I’ve never heard that line before. They used to be more active.


TAUBES But that’s the implication of Hellerstein's knee-jerk reservation hypothesis. They may be poor, and they may be out working in the fields, so compared to us, they’re active, but compared to their former life, they’re sedentary. See what I’m saying?

INTERVIEWER Yeah, I understand the logic. I’ve just never heard it before.

TAUBES Well, the reason you’ve never heard it before is because you’ve never heard anyone have to explain why obesity was common in an impoverished Native American tribe in 1902 or in 1928. When confronted with that observation, they have to come up with an explanation so that they don’t have to question their hypothesis. I happen to challenge someone who believes the conventional wisdom unconditionally, and that’s the response I get: “Well, they’re living on reservations”.

INTERVIEWER Does he actually do research on weight, on obesity?

TAUBES Absolutely, he does.

INTERVIEWER That's unfortunate.

TAUBES This is why the field is in the position it’s in. These people believe so strongly in the calories in/calories out/gluttony/sloth combination that they no longer function as scientists. They can’t imagine the existence of an alternative hypothesis. So everything they see, they have to find a way to interpret it so that it supports what they already believe to be true.

INTERVIEWER They don’t see that they’re operating differently…

TAUBES …than other scientists.

INTERVIEWER Do they see that they’re not making progress?

TAUBES No, because that gets blamed on the obese. If you believe that obesity is caused by sloth, then the reason fat people are fat is because they don't have the moral fortitude to go run ten miles every day the way you do.

INTERVIEWER Well, people have been saying that for 50 or 60 years. So the fact that they’re saying the same thing now as they were saying 60 years is a sign, to me, that they’re not making progress.

TAUBES Yes, that's a very good sign, but these people don't realize they're saying the same things and doing the same experiments and making the same mistakes that their predecessors made a century go because they don't bother reading that literature. For reasons I still don't really understand, these people see no reason to pay attention to the history of their field. Imagine if physicists saw no reason to pay attention to Einstein and Plank and Maxwell and Heisenberg? I mean, these guys all lived a century ago, why would anyone want to know about them or the experiments they did? But in physics, mathematics and even biology, the history is carried along with it. As the science progresses, it takes with it the successful ideas and the students learn about the history along with the science. In obesity research, World War II just cut all of that off. For whatever reason, several generations of researchers grew up with this belief that the history of the field doesn’t matter. And so they don't even know or care that they're saying the same thing and doing the same experiments that their predecessors did 100 years ago. And then this latest generation is full of young molecular biologists, and they start the clock in 1994, when leptin was discovered. They’re not aware that they’re not making progress, because they believe that nothing of value was done until 1994.

INTERVIEWER The birth of a new world. The way I read your book about Atkins was that you seem to place weight on the fact that Atkins was disliked by people he went to school with. Did I read that wrong?

TAUBES I think that was part of it. I think the fundamental problem with Atkins is that his book emerged in 1972 , when the low-fat dogma was really beginning to be taken seriously, not just by the heart disease researchers, but by physicians and public health authorities. It was viewed as a great triumph of modern medicine. We finally understand what causes heart disease Then Atkins goes out of his way to throw the high-fat nature of his diet out there: “You can eat lobster Newberg, double cheeseburgers, and porterhouse steaks" (like my New York Times Magazine cover). The AMA always had this philosophy that even if people wanted to lose weight, they should go to their doctor and discuss it with them. You shouldn’t go on a diet without your physician’s guidance. So here Atkins was end-running all of that. Then he was saying “eat a high-fat diet. It’s harmless”. He actually said “It’s good for you." If you read Atkins, he read a lot of the papers I read. His understanding wasn’t tremendously sophisticated, but he didn’t have the advantage I had, of coming along 40 years later. For the time, he was doing pretty damned good. He believed that triglycerides were the problem, not cholesterol. He believed that insulin was a problem. He was a working physician; he didn’t have the time that I did to read all of the research, and to have the internet available to allow him to track down all of the references. But the establishment thought his diet was dangerous. And then Atkins made these claims that he had patients who consumed 5000 calories a day and still lost weight, so they also believed Atkins was a quack, a shyster trying to sell impossible dreams. And they thought this because they believed that calories in/calories out was all that mattered. They had this inherent belief that in order to lose weight, you have to restrict calories; Atkins said you didn’t. So, to these establishment nutrition types, Atkins was saying that the laws of thermodynamics can be ignored. So they had reason to think that Atkins's diet couldn’t possibly work, on the one hand, and that it would kill you, on the other. So these “responsible physicians,” as they perceived themselves to be, felt an obligation to suppress this threat to the public health. The fact that they knew Atkins personally, that some of them had worked with him and gone to medical school with him and didn't particularly like him, made it all that much more . . .

INTERVIEWER Irresistible.

TAUBES Yes, irresistible. One of the things I mentioned in my lecture was something I didn’t realize this when I wrote the book. Atkins proposed that one reason carbohydrates-restriction worked is that it stimulated the secretion of something that British researchers in the 1950s had called Fat Mobilizing Hormone. The joke is that you didn’t need a Fat Mobilizing Hormone; the thing you have to do to mobilize fat is lower insulin levels and the way to do that is to remove the carbohydrates from the diet. That's what mobilizes fat from the fat tissue. But Atkins was doing what a lot of diet book authors do, which was combing the literature for everything and maybe anything that might support his argument. He talked about insulin, but he also talked a lot about Fat Mobilizing Hormone, which was controversial at the time but not an outrageous idea. At the time Atkins wrote the book, this Fat Mobilizing Hormone had yet to be nailed down, and it never would be. The fundamental requirement to mobilize fat, as I said, is to lower insulin.
So, the American Medical Association publishes this famous article dedicated, effectively, to establishing that Atkins has no credibility and one of the ways they do it is to discuss how Atkins was wrong about this idea of Fat Mobilizing Hormone. Then in the same paragraph they also say “in order to mobilize fat, you have to lower insulin”. Then they go back to talking about how Atkins jumped the gun on Fat Mobilizing Hormone . So they know that insulin controls fat accumulation, and they say actually acknowledge it in the article, but only in the context of it supporting the argument that Atkins has no credibility. They never mention that the way to lower insulin -- and so, apparently, to mobilize fat from the fat tissue -- is to eat less carbohydrates, which is exactly what Atkins was recommending. I was writing my response to Gina Kolata's review when I first really noticed that sentence, and it jumped out at me. “Holy shit!" These people knew what regulates fat tissue, and they know what regulates insulin. They just don’t care. That’s how dedicated they were to trying to squash Atkins.

INTERVIEWER It didn’t matter whether evidence supported them or that there was something there that they couldn’t explain. It just mattered that he was wrong about something.

TAUBES All they wanted to do was establish that Atkins was not a credible source, and people shouldn’t follow these bizarre practices of nutrition, or whatever they called it. One of the things I’m curious about is whether, from here on, the American Heart Association and other health authorities will continue to refer to low-carb diets, the Atkins diet, as these fad diets. Even though, if nothing else, as I point out in the book, these diets constituted the preferred medical treatment of obesity for 150 years, or 100 years, until the low-fat diet came along. It's the low-fat diet that's the fad.

INTERVIEWER That’s an interesting point. What is the fad diet? Is it the absence of the Atkins Diet, or its presence? Which is temporary?

TAUBES The idea that you could somehow lose weight by removing fat and increasing carbohydrates is as ludicrous as the idea that you could do it by eating ice cream for any extended period of time. I’m sure there’s something about the ice cream diet that works in the short term. I’m not sure, but I wouldn’t be surprised.

INTERVIEWER Was your response to Kolata's review published?

TAUBES If you search me in the Times, you can read my response. [end of part 8/start of part 9] Her response to me reminds me a little of Mike Fumento's response to me. Did you read that back-and-forth?

INTERVIEWER Yes. This is an example of the litmus test for who the good journalists are and who the bad journalists are. In your Berkeley talk, you quoted Jane Brody: "eating pasta is a good way to lose weight." There seems to have been some sort of journalistic failure. What was the journalistic failure; what is it?

TAUBES Beginning in the 1960s, when newspapers institutionalized this idea of having diet and health/nutrition writers on newspapers, and its still the case, for the most part, today, the people who got those jobs weren’t the shining intellects on the newspaper, and the shining intellects didn’t want to be diet and health writers. If you’re a whip-smart young guy or girl who wants to go into journalism, you want to be an investigative reporter, a political reporter, or a war correspondent; you don’t want to write about diet and health. Or at least you didn't. So I think that was one of the problems. You got not very smart people; truly mediocre reporters, doing jobs that turned out to have remarkable significance and influence. I do think that Jane Brody is as responsible as anyone alive for the obesity epidemic. She just bought into this idea of the low-fat diet as a healthy diet, and her sources in New York told her that Atkins was a quack, and that fat was bad, and she never questioned any of it. I don’t know if she had the intellectual wherewithal to do it. In any other field of reporting, as far as I know, reporters are supposed to be as skeptical of their sources as scientists are supposed to be skeptical of their data. Certainly, if George Bush tells a political reporter something, that political reporter doesn’t treat it like it’s true. He might faithfully report what George Bush said, but you’re supposed to be skeptical of what government institutions tell you. So now it's 1977, the McGovern Committee and the USDA make these proclamations about what constitutes a healthy diet, and there’s simply no skepticism. (With the possible exception of Bill Broad writing in Science Magazine, which no one outside the field of science was reading.) So the government tells us that we should eat low-fat diets -- and not even learned authorities in the government, but Congressman and USDA bureaucrats channeling 30-year-old congressional staffers -- and lo and behold, all these health reporters decide it must be true. That’s the failure. In my fantasy life, I get a call from the managing editors of the New York Times and the Washington Post and the Wall Street Journal and they say they've read my book and they want to know how they can improve their health and diet reporting. Because they can see, whether or not I'm 100% right, or 80%, or only 50%, surely their reporters did something wrong. Now there's a fantasy for you.

INTERVIEWER Yeah, I agree. That makes sense. So, what would you say?

TAUBES I haven’t figured that one out yet. Get some of your political reporters to do the health writing. Get the smarter people on the paper to do it.

INTERVIEWER Well, I always thought of you as one of the very few science writers who was sufficiently skeptical. Practically none of them are.

TAUBES That’s basically the problem. This lack of skepticism. But I had an advantage. . . You’ll remember, in my first book, I got to live at a physics laboratory and I was lied to regularly by a Nobel Prize-winning physicist. His conception of truth was what he needed to be true at the moment, and what he could get people to believe. So if you called him on the lie, and he was kind of a charming fellow, he would acknowledge that he might have misled you, and then he would step back and try another lie, because it wasn’t in his best interest to tell the truth. Then I did this book on cold fusion where I spent three years, basically, getting lied to constantly by anyone who thought it was in their best interest. There was a period in my life where it was hard for me to trust anyone, because I’d just been around too many people who believed that the truth was what was convenient. I also knew, by the time I got into public health reporting, I knew what it took to do good science. So, if somebody wasn’t doing it, I knew there was no reason to put them on a pedestal. The first article I ever wrote for Science magazine was an investigative piece of an alleged fraud that had happened in the cold fusion episode -- a fundamental result that kept the field alive for another few months couldn’t be explained by nuclear physics. That alone was so remarkable -- as one of the smartest men in the world suggested to me, a physicist named Dick Garwin at IBM -- that it should have made everyone suspect fraud. If something can’t be explained by a very well-tested theory, you would question the ethics of the researcher who did the work before you’d question the theory. This is Hume's idea that eyewitness testimony is never good enough to make you believe in the existence of a miracle, because a miracle is, by definition, something that’s impossible, by all our accepted theories. It’s easier to believe that 10, 100, or 1000 people were deluded or dishonest then it is to believe that the Virgin Mary really did appear in Times Square or whatever your miracle of choice is. Anyway, I’m writing this story for Science about an alleged incidence of fraud that took place at Texas A&M, and the editor had a Master’s degree in mathematics from Texas A&M. He took it upon himself to call some of the professors I interviewed, and he would ask them if they really believed what I said they believed, which was not completely unreasonable, considering I'd never written for the magazine before. But then he would say to me, “Well, I talked to professor so-and-so, and he says he doesn’t believe what you said he believed”. And I would say, “Well, this is six months after the fact. Let’s go look at the lecture he gave six months ago, and here’s the paper he wrote on the lecture, and here’s the sentence where he says what he believed then, which is what we're writing about." And this editor's response was "how could you question him? He’s a PhD, and you’re not."

INTERVIEWER That’s rather unfortunate.

TAUBES This was around 15 years ago; it’s still one of those memorable moments in my life.

INTERVIEWER This guy was an editor at Science magazine?

TAUBES An editor for the journal Science.

INTERVIEWER Oh yeah --- that’s really bad. Really, really bad.

TAUBES It’s a common response you see ---- what right does Taubes have to say this stuff? He’s not a scientist. It’s like "The Wizard of Oz," where in order to be a scientist or be taken seriously in science, somebody has to first give you the piece of paper?

INTERVIEWER On a scale of sharpness of criticism, from one to a hundred, that ranks about a zero.

[end of part 9/start of part 10]

TAUBES I’m definitely more skeptical; even the science journalists I really respect, some of my friends, sometimes I read their stuff and I say, “They just weren’t skeptical enough”.

INTERVIEWER Yeah, that’s my reaction to at least half of the science journalism I read. One of my next questions is, did writing your book radicalize you? But it sounds like you were already radicalized!

TAUBES What do you mean by "radicalize me"?

INTERVIEWER Did it make you even more skeptical of the establishment? Obviously, you were skeptical to begin with.

TAUBES Again, the obesity stuff, in retrospect, is mind-blowing to me. Until I did the research for the book, I never questioned the idea that obesity wasn’t about calories in/calories out. That it wasn't about overeating. Then you realize that there's no arrow of causality in the law of energy conservation. That the correct interpretation is that we overeat because we get fat, we don't get fat because we overeat. Now that's a remarkable shift in causality, and yet nobody picked up on that for fifty years. And nobody seems to care even now. There's one guy I know of -- Robert Lustig at UCSF -- who has written papers discussing this causality issue and getting it right. And nobody else seems to care. It blows my mind that an entire field of research could get it so wrong.

INTERVIEWER But you’d seen Nobel-Prize-winning physicists get it very wrong.

TAUBES But what they were getting wrong were subtle; yes, they’d believe incorrectly that they’d discovered elementary particles, but what they were doing was a real subtle game. What they were misinterpreting were extraordinarily subtle aspects of the data. This obesity screw-up is fundamental; it's like a grade school error in the interpretation of the laws of thermodynamics. And I made it as well, up until five years ago. I never thought differently. But what radicalized me is that they don’t care. If they successfully ward off my threat to their beliefs, then I’m in a very dangerous place. Then it’s, like I said, where I end up a bitter demented old man, one of those guys who’s muttering to himself all the time that they, the establishment, didn’t listen to him...

INTERVIEWER I wondered, too, what other books your book resembles. To me, that’s an interesting question. But there's many possible answers, and one is “Well, there’s been a long list of books that talk about this scam or that scam, and some of them are awful and some of them are pretty good. One of the ones that’s good is that great cholesterol scam, The Great Cholesterol Con. that's a good book. But your book is different, because unlike the author of that book, you really had something to lose. You were a respected science writer who could expect to receive many more assignments in the course of a lifetime and write many, many more times for the New York Times in science, and so forth, and might write other books. For a writer in that position --- this is an incredible book, because…

TAUBES I actually didn’t think --- and this may be my own ignorance --- I didn’t ever think of it as endangering my career.

INTERVIEWER But you clearly have more at stake…

TAUBES I always knew I could write about other subjects. I could go back to writing about high-energy physics; I like it. There’s a new accelerator turning on; there’ll be something to write about. I would have to compete with the whole new younger generation of whiz kids who may be better prose stylists than I am, but I could do it. What stuns me is that people may not take me seriously enough to refute me, to ruin my credibility. That’s what bothers me, not that they could ruin it. Here’s a book that might be similar, OK? Not in terms of prose style, or beauty of presentation, but like The Best and the Brightest. A book that came out during the Vietnam War and exposed the sort of irrationality of it. When I was writing my cold fusion book, I read A Bright and Shining Lie and I read Randy Shilts’s And the Band Played On. I thought we’re all writing about human idiocy. Shilts’s book was particularly important, because it came out at a time when it could still make a difference, when people still had to change their beliefs. So Shilts actually accomplished something. And A Bright and Shining Lie was an extraordinary book. In my fondest dreams, I couldn't imagine writing such a book. But maybe my book may be akin to book And The Band Played On and The Best and the Brightest . Those are books that revealed the establishment’s erroneous beliefs and how they were misleading us, and they did so at a time and in a way that could actually help set us on the right path. You use the term “We were misled”; we were literally misled. Not deceived; we were just led down the wrong path. Often, when I think about this, I imagine this situation in the 50s and 60s, when there were these dual paths that could be followed; two paths through the woods, and the establishment took us on this low-fat path. What I had to do when I did this research is I had to back up, back up, back up until I got back to the woods, to the point where the two paths diverged, and see the existence of the other path, and see where that one led us. Did that get to a place where we could actually understand what was going on, and maybe prevent and cure these diseases.

INTERVIEWER Well, when I think about precedents for your book, sometimes I think of The Jungle. In the sense that there’s this awful thing going on, and it’s in the interests of many people to keep it going on, but it’s really outrageous. It’s very different, in a way, because the meat-packing industry was very obviously horrible, whereas what you’re saying went on isn’t obviously horrible; it’s more complicated than that. But on the other hand, your thing is kind of a bigger issue; it’s everyone’s health. It's not just everyone's health, it’s everyone’s mental health; it’s horrible, being fat; it’s awful every day, not just when you die.

TAUBES I have friends and acquaintances who will often say to me at dinner parties, “Well, who really cares about this stuff, because you want to live well, not just eat the healthiest possible meals." But they’re not overweight, they don’t have cancer running in their family. Their life, rightfully, is a balance between living healthy and living well. But the problem always is that even though those people want to live well, they eventually get to the point where now they’re sick. Inevitably, when you get to that point, you wish maybe you hadn’t lived quite so well. Unless you’re lucky and you have that massive coronary on the golf course, or on your lover, so you don’t have time to think about it. But both my mother and my father died from long, extended, horrible illnesses. There’s a point at which you think, “Maybe if, 30 years ago, I had lived less well and more healthy, I wouldn’t have to go through this," but I guess we all have to die of something.

INTERVIEWER Well, I think understanding what causes obesity is a big, big issue. For the medical establishment to be misled, or deluded, to get the wrong answer and insist on it, is a tragedy. It’s a gigantic tragedy, because of all of the people who are overweight. Not the people who are 5, 10, or even 20 pounds overweight. The people who are 50 or 100 pounds overweight.

TAUBES We’re drowning in diabetics; we’re drowning in obese patients. Obviously, physicians and obesity researchers and public health authorities haven’t got a clue. By what right does anyone flippantly discard an alternative hypothesis that can explain the evidence? You would think they'd be desperate for such a thing. You know, this guy presents a compelling argument that we got it wrong. Well, Jesus, we obviously got it wrong. We haven’t cured a person in 100 years! Let’s take him seriously!

INTERVIEWER Let’s praise him for raising an idea that hasn't yet been proved wrong.

TAUBES We’ll see how it goes. Again, I'm obviously impatient. I expected people to read the book immediately and to send me emails; somebody at NIH saying “Come on down here! Talk to us about what experiments we should do.” If the book has any effect over five years, ten years, that probably would be a great accomplishment. In a sense, I wrote the book for graduate students and post-docs, so that when their professors utter nonsensical statements, like the only that matter is calories in/calories out, these kids will challenge them. It could take awhile; it’s only been a few months.

INTERVIEWER When their ideas failed to produce better ways of losing weight, and fifty years had passed, it was understandable, but not for scientific reasons.

TAUBES As I say in the book, they’re not scientists. The funny thing is, they’re not trained as scientists; a lot of the people involved in this field are nutritionists, medical doctors, public health people, and that’s a different way of thinking. I had an apprenticeship in science; I got to spend my ten months at this physics laboratory; I got to delve into cold fusion for three years. In a way, you have to get an apprenticeship in how to think like a scientist. You have to be mentored. It’s not how we naturally think. These people, it’s not part of their training in any way. Not that there aren’t scientists who started as MDs. There are these yellow berets, the guys who went to NIH instead of Vietnam in the late 60s and early 70s, so suddenly, they're MDs who were working around biologists and PhDs, and they were taught how to do good science. But it’s not how we naturally think; these people just didn’t do it. Then there’s this whole world of nutritionists and epidemiologists who, for whatever reason, far too many of the senior figures in those fields don’t have a clue how to do science. So they passed on this sloppy way of thinking to their students, and the whole field is permeated with less-than-rigorous thinking.

[end of part 10/start of part 11]

INTERVIEWER What happened when you met with the [UC Berkeley School of Public Health] epidemiology students?

TAUBES Again, it was a little discouraging, only because these kids really want to do good, they want to make a difference in the world. That’s why they go into the field. They want to have an effect. But as I say at the end of the book, to do science right, your primary motivation has to be to learn the truth, and if you’re infected with this desire to change the world, to save lives, it takes you away from the fundamental motivation, which is to get it right. If you want to save lives, then you want to get the word out as quickly as possible. You don't want to wait ten or twenty years or more for definitive evidence, for the rigorous tests to be done; you want to give advice and tell people what you've learned, even if you only think that you've learned it. Doing science right takes a long time. So does good journalism. You can say the difference between my book and Gina Kolata's book is -- not counting whatever difference in intellect we begin with-- my book took five years, more than full time, because I wasn’t going to say anything until I was certain that what I was saying was sound. She wrote her book in two years, part-time, while still working full-time as a New York Times reporter.

INTERVIEWER Yeah, they’re very different.

TAUBES Even when I was writing magazine articles, if I was in danger of missing a deadline, which was often the case, I would ask my editors, “Do you want it on time, or do you want it right?”.

INTERVIEWER There was a managing editor at The New Yorker, one of the first, whose motto was “Don’t get it right, get it written."

TAUBES When I was a young journalist working for Discover, which was owned by Time, Inc., the philosophy was that one of the worst things anybody could do was over-report a story. Just get the facts and get it out. Except science doesn’t work like that. Science, you’ve got to get it right, and that takes time, and you can’t do it on deadline. Along those lines, I did read one of your blog entries about settling points versus set points, and I thought it might be… You know, I Google myself, as all writers do fairly regularly, so first you read all news stories that day, hoping that the Google Alert might have missed something, and then you go to the blogs.

INTERVIEWER So you read my article about the most surprising thing in your book?

TAUBES What was the most surprising thing?

INTERVIEWER That you didn’t agree that set points play a role in homeostasis.

TAUBES It’s funny – the more I think about it, the more Claude Bernard was brilliant. (I'd like to do a book on Claude Bernard, but probably can't because my French is terrible.) In particular, this idea of the milieu interieur? The fundamental idea of homeostasis is that the body works to maintain the stability of what he called the milieu interieur, which gets translated to “internal environment”. What he meant by that is the conditions right outside the membrane of the cell, every cell in the body. So the body wants to maintain stable this internal environment -- the pH, the blood pressure, the ionic potential, everything -- of the cell itself. So it wants to make sure that the environment the cell lives in -- every cell -- remains relatively stable. in that sense, we're this huge symbiotic organism made up of billions of individual cells, and homeostasis functions to keep the conditions that these cell live in stable. So each cell lives in this little isolated world, and it’s got to see stable conditions, or it’s going to die. The idea of the set point is that there’s some central controller in the brain that maintains homeostasis, but that's naive. Rather, there's an unbelievably complicated mechanism composed of individual settling points. Like the fatty acid concentration on the interior, and exterior of the fat cell. If there’s more fatty acids on the outside of the cell membrane than the inside, then fatty acids flow into the cell, and you get slightly fatter. There’s no brain in charge. The brain may respond, and the hypothalamus sends signals back and forth, and effects changes in hormones in response to changes in the environment, but there’s so many different interrelated, interconnected feedback loops involved that to refer to a set point is to grossly oversimplify things this beautiful homeostatic system, and it directs attention away from the body, where all these feedback loops interact, to the brain. Did you ever read any books on chaos theory?

INTERVIEWER No, I haven’t.

TAUBES Well, to understand homeostasis you have to understand this concept of dynamic equilibrium, where there can be hundreds of forces acting simultaneously. And the point is, you’ve got these negative feedback loops all over the body, and they involve the brain, but on some level, the dynamic equilibrium you’re looking at is right at the cellular level. That’s where the forces converge to make us leaner or fatter. And the brain is part of these loops, but to concentrate on the brain misses the big picture.

INTERVIEWER The brain is sensitive to the environment --- sure, the set point doesn’t really exist anywhere, and sure it’s a function of about a zillion things, not all of them in the brain, sure. But the reason I like that idea of a setpoint is that it’s easy to imagine something going up and down, rather than a million things going up and down.

TAUBES But the problem is once you oversimplify, there's a tendency to believe the oversimplification. You should go back and read the papers on settling points. There were a couple, if I remember correctly, written by psychologists from the University of Chicago. You should go back and read those original papers. They’re fascinating, and the point they make, is that you don’t need the brain involved. Like we don’t think of the brain regulating blood pressure. You don’t really think of your brain regulating blood glucose. Those cycles I described in my lecture, you know, the triglyceride fatty acid cycle and the Randall cycle, serve to regulate blood sugar. Then hormones are layered on top of those cycles, and the hormones are determined, in part, by the hypothalamus, so you get the brain involved, and the sensing of the environment, but there are other ways to sense the environment, like temperature sensing of the skin, evaporation. There are other ways that we adjust to the environment without the involvement of the brain. One of the things I left out of the book, for instance, is this theory that hunger is perceived by the liver.

INTERVIEWER Perceived, or controlled?

TAUBES Perceived. Or sensed by the liver. You know, your eyes collect photons, and then they send the signal back through the optic nerve. The perception of the universe is done in the inside of the brain, but the eyes are the sense organ that collect the photons. Your ears detect sound waves, but your perception of what you’re hearing is inside of the brain. This theory says that your liver senses fuel availability and then your brain integrates the signals from the liver and registers them as hunger or the absence of hunger.

INTERVIEWER Hunger is internal. It’s like the recognition. Hunger is not something external to the body.

TAUBES Let me re-phrase it. It senses fuel ability. Then your brain perceives it as hunger and initiates --- that would be a better way of putting it. But the sense organ of fuel availability is your liver. I had some discussions with Mark Friedman, a fascinating guy, really smart. He’s at the Monell Institute.

[end of part 11/start of part 12]

INTERVIEWER Did you ever hear of Israel Ramirez? He was one of Mark Friedman’s colleagues.

TAUBES That’s the Ramirez you quoted. I forgot that. I didn’t put it together, because I always knew him as I. Ramirez. I saw that, too --- here’s my other carp, and then I’ll stop. It doesn’t do any good to have somebody discuss my arguments who hasn’t read the book.

INTERVIEWER I asked him to, so it’s my fault.

TAUBES Then other people see someone refuting me, and they don’t care whether they read the book or not. You know what I mean?

INTERVIEWER Well, I appreciate that it would be irritating.

TAUBES The problem is, you can’t ask Mark, because I know what Mark thinks of the book. He’s read it --- he read it in draft and critiqued it for me. He’s in the book, so you can’t ask him, either, even though he would probably say tremendous things about it. You have to find people whose research I don’t discuss. I’ll tell you one guy who would be worth knowing what he thinks: George Wade. He’s at U. Mass Amherst. He did these rat experiments. He’s an expert on animal reproduction and I sent him a draft of the book, and I didn’t ask him to critique it, but I was asking him a fact-checking question and I sent him a copy of the book and he never got back to me. I don’t know if he read it or not. I’d be curious what he thinks, because he was my revelation, Wade. He shifted my paradigm.

INTERVIEWER You said something about that in your Berkeley talk.

TAUBES He was the one who got me to realize that we overeat because we get fat; we don’t get fat because we overeat. That’s the paradigm shift, the literal paradigm shift. He’s describing his ovariectomized rat experiments to me. That’s how he did it.

INTERVIEWER Do you know about someone named Michel Cabanac?

TAUBES Yeah, I read a lot of Cabanac's stuff. I forget what the details were. I only remember that I was disappointed and decided that he was missing the point.

INTERVIEWER Well, he had a big effect on me, at least. His idea is that I’m sure there’s a set point, but that’s an old idea. The new idea is that the set point depends on what you eat. He had some ideas about that.

TAUBES Well, that’s the thing. There is a settling point, whatever you call it. The weird thing is that insulin regulates the settling point. It obviously goes up and down. It obviously goes up, anyway.

INTERVIEWER He might not disagree with your book. I asked him “Can insulin regulate the settling point?” I thought that was unlikely, but he didn’t; he thought, “Why not?”

TAUBES Insulin levels correlate with weight, with fat. The question is whether insulin goes up because we get fat, or we get fat because insulin levels go up. There’s always two ways of interpreting the observations in this business. So the establishment viewpoint is that insulin goes up because we get fat. I tracked that belief down to see if there was evidence for it, and indeed, there’s not; there’s a sort of misinterpretation of these experiments done by Ethan Sims 40-odd years ago. On the other hand, it's easy to show that you can manipulate insulin levels by manipulating the carb content of the diet. If you manipulate the carb content of the diet, then the question becomes, does insulin and the weight still track? So the hypothesis is insulin regulates the settling point and the question is how do we test that rigorously to find out of that's indeed what's happening.

[end of part 12/start of part 13]

INTERVIEWER Well, my book came out of an accidental observation, which is that I lost weight when I drank sugar soft drinks. I lost weight, not gained weight. That happened in Paris, and I came back to Berkeley, and I found out it was the sugar. In other words, if I drink unflavored sugar water, I lost weight. This is what’s not so obvious, right? But Israel Ramirez, who I mentioned a few minutes ago --- his experiments with rats are what led me to this discovery. Because I don’t think most people would have thought it was possible to lose weight by drinking Coke, or whatever. But it has to be unflavored. Anyway, the effect never wore off. I drank sugar water for three years, and my weight went down and stayed down. There was no sign that it was ever going to wear off. So this seems to me to be a big problem with your theory, which is that I did something which obviously raised my insulin level, sugar water. I didn’t measure it. I lost weight and not only did I lose weight, but I kept the weight off, and I lost it without being hungry; I was less hungry than usual. I mean, you’re right, you know, set points, settling points, who cares. . .

TAUBES It’s important to think of it as a settling point. Because it’s important to have this concept of dynamic equilibrium. As long as you’re thinking about what’s happening in the brain, which is what set point implies. My question is, what did the sugar water do to your fat tissue? It should have caused you to accumulate fat, or at least hold on to the fat you had, according to what I know of the underlying regulation of fat tissue. The question is, why did it do what it did?

INTERVIEWER I was less surprised than you are, or than most people are, let's put it that way, because I was led to this observation by a theory. I had a theory which pre-dated all of this. I was kind of surprised my theory was so helpful, because it hadn’t been that helpful before. But, lo and behold, it really turned out to be helpful and it led me to other ways to keep my weight off, and I’m still way down from where I was.

TAUBES What I ask when I talk with these people. What I say is: Look at the regulation of fat tissue. The question is, how can you lose weight, or gain it --- how can you gain weight without either increasing insulin secretion, or increasing the relative insulin sensitivity of the fat tissue to the muscle tissue. Basically, the way we work, at least if you believe the biology that I describe, is that as we secrete insulin in response to the carbohydrates we consume and the insulin works, among other things, to facilitate the movement of glucose into the cells of your muscles and other lean tissues. But blood sugar is kind of toxic, so your muscle tissue doesn’t want the insulin pushing all this blood sugar in, and it becomes insulin resistant. Your fat tissue now remains insulin-resistant, because your body doesn’t like to waste fuel. So if you eat a high-carb diet, your lean tissue takes up some of the glucose for fuel, and the rest gets dumped in your fat tissue, and your fat tissue remains insulin-resistant for a long time --- far longer. Because once your fat tissue becomes insulin resistant, then you just become diabetic; you have no place to put the glucose. You just pee it out. That’s the last resort, because your body doesn’t want to waste fuel.

The thing that Rosalyn Yalow and Solomon Berson reported forty years ago is that organs respond differently to high levels of insulin, and they get insulin resistant at different periods. One of the things I put into a paragraph in the book is that I can imagine a scenario where fat tissue becomes insulin resistant prior to muscle tissue, and the result would be anorexia or bulimia. The person would eat a meal and would have no place to store the calories temporarily. So they would either lose their appetite and not be interested in eating at all (anorexia), or they might just throw it up afterwards. Because they have no place to temporarily store the calories that aren’t being used immediately. Bulimia would be another option. A third option would just be to get on an exercise bicycle and ride for three hours and burn the calories off -- be Lance Armstrong, in effect. So what I’m trying to figure out is what did the sugar water do, unflavored? And it’s interesting --- the idea that it’s unflavored might disconnect some of the sort of Pavlovian responses that you’ve developed.

INTERVIEWER Yeah, I think that’s what was key. The reason I lost my appetite in Paris was that I was drinking unfamiliar sugar water. I think this is the reason that so many diets work in the beginning: because people eat unfamiliar food. Once the food becomes familiar, the diets don’t work so well.

TAUBES This is the problem with anecdotal evidence. The idea that oil could suppress your appetite I could understand, because, as I said in my lecture, you need alpha glycerol phosphate to fix fatty acids as triglycerides. You get the alpha glycerol phosphate from eating carbohydrates, so if you only ate oil it would be shipped off to the fat tissue as triglycerides, then broken down by lipoprotein lipase into fatty acids, but those fatty acids couldn't be stored in the fat. So it would raise the fatty acid level in your blood, and your body would switch over to burning fatty acids, and this would effectively suppress hunger. That makes sense. But I can't see why unflavored sugar water would be any different than say, Coca Cola itself, which is just flavored sugar water, for all intents and purposes.

INTERVIEWER Well, when I talked about it in the beginning, I was using fructose.

TAUBES Well, pure fructose, I can also understand. Friedman and Ramirez did an experiment showing that fructose suppresses hunger apparently because it is metabolized in the liver and they believe that the liver monitors fuel status in the body…

INTERVIEWER This is very interesting: someone who is not dedicated to my being wrong.

TAUBES I’m open-minded.

INTERVIEWER Your book proved that.

TAUBES The experiments that Freedman and I think Ramirez did to demonstrate that the liver must sense hunger, must sense fuel availability, is they did intravenous infusions of fructose, Fructose is metabolized only in the liver. It’s not metabolized in the brain. So they infused fructose into the blood stream of rats and it suppressed eating behavior. That’s one of many experiments they did that suggested that somehow what we sense as hunger is being communicated by the liver. It’s always made sense to me. So if you only use fructose, and you don’t get an insulin response to fructose, it would make sense that it suppresses hunger. In my book, I discuss the hypothesis that whatever prompts an insulin response is what causes us to get hungry. So, the fructose, I can understand. Actually, if you’re now eating real sucrose, that’s where it gets complicated, because with sucrose, you’re going to get an insulin response. Unless the fructose component outweighs the glucose, but then, what is it about the absence of taste? Why would Coke make you fat, and sugar water not?

INTERVIEWER Well, first it was it was that flavorless fructose worked. Then it was flavorless sucrose worked. Then it was flavorless oils work. Then it was flavorless any food worked, in particular flavorless protein.

TAUBES When you talk about flavorless protein, what do you mean? The oils, I understand; the fructose fits with everything I know. The sucrose starts getting tricky. What do you mean by flavorless protein? Give me an example.

INTERVIEWER Oh, for example, eating chicken holding your nose clipped. It’s flavorless in the sense that you don’t smell it.

TAUBES That’s interesting. Remember I told you that Jaques Le Magnen started his career studying olfaction (because he was blind). He was curious why the smell of a particular food can go from being very pleasurable when you're hungry to being nauseating when you're full. The example I used in the book was the smell of a cinnamon bun cooking. You can imagine that being unbelievably enticing when you’re hungry, and then nauseating if you’ve already eaten three cinnamon buns. Le Magnen moved from that to asking similar questions about the taste of a food, which he thought was determined by our level of hunger. It's conceivable that if you don't taste a food it somehow works to suppress hunger, but I have no idea why.

[end of part 13/start of part 14]

TAUBES Now here’s one question for you, you know the Freakonomics guys, right? Did you read their last column on obesity?

INTERVIEWER About bariatric surgery?

TAUBES Yes. In particular, the last two paragraphs, about their recommendation that fat people, in effect, carry around something nauseating. I felt like I was reading something from 150 years ago, where they were using anal suppositories to try to cure obesity. Do you remember those paragraphs?


TAUBES They're saying, “let’s get fat people to have willpower, like we do." Here’s a way they could do it, they could carry some nauseating-smelling thing in a pouch around their neck, and whenever they find themselves going to the refrigerator, they could open it up and smell it.

INTERVIEWER I think they were trying to illustrate the concept of commitment device.

TAUBES I got what they were trying to do, but…

INTERVIEWER You’re saying that trivializes the problem.

TAUBES More than that. I'm saying it misses the point entirely. It's not about how much they eat. Remember, you can starve fat animals, for instance, and they’ll die with their fat tissue intact. It’s not about how much they’re eating; it’s about the regulation of their fat tissue. And if you don't understand that, you're not doing anyone a favor by discussing it publicly. If these guys are going to write about this subject, and they're so now so influential and noticeable, they should have some understanding of what's actually going on physiologically. We talked earlier about how I can become flabbergasted -- your words was "radicalized" -- by the idea that people can write about obesity without stopping to think “what’s the mechanism? Should I know anything about the underlying biology?” And again, I never did until the last five years. It was only when I did the research for the book that I realized that you have to actually pay attention to the underlying biology -- the hormonal and enzymatic regulation of fat tissue -- or you can't understand what's going on. Imagine writing about growth defects, about gigantism or dwarfism, without caring about the hormonal regulation of growth. If the Freakonomics guys are going to write about obesity in the New York Times, then maybe they should read my book (he said, ego-maniacally), so they know what they're talking about. And since I don't know them personally, maybe you could...

INTERVIEWER I’ll recommend your book to them. It’s great that you were invited to Berkeley; that shows people trust you. The fact that they invited you means you’re not a heretic, you’re not off the reservation, you’re a respectable person. The fact that you continue to write for the New York Times, that’s very good. Every article you publish from now on will push your book forward, will push your case forward, will say that you are a serious person who is respected by serious people. Just maybe, just maybe, this is one of the cases where the authorities were wrong. We’re all familiar with this happening in the past, and maybe this is just another case. For everybody but a tiny faction of people at the top of the health establishment, I think they’re perfectly fine with the idea that the authorities are wrong. I think that the lack of progress on the obesity epidemic is making more and more people dissatisfied. That’s just a guess. More and more people, outside of the people who are responsible for the current policies.

TAUBES I think that's true, but there’s this contrary effect that happens. I said this in my lecture. The science I'm trying to get across can be accepted up until the point at which I say the the word carbohydrate, and then people shut down, and they think “Oh, it’s that Atkins stuff again." Their minds close and they turn around and go back to their lives. Anyway, I look forward to seeing the interview and getting your book and reading it. I enjoyed this. Again, I like nothing better than talking about this stuff.

INTERVIEWER I learned a lot from our conversation. I’m sure my blog readers will enjoy this.

[end of part 14]