Transcript: Gary Taubes

An interview with the author and award-winning journalist

What makes us fat? It’s a contentious debate in the world of health science. Is obesity caused by energy imbalance — consuming too many calories — as has long been conventional thought? Or is obesity caused by the effects of carbohydrates on insulin? My guest on this week’s program attended an invite-only global gathering of obesity experts. The resulting paper in Nature Metabolism, co-authored with 15 other researchers and published this fall, compares the two competing hypotheses side-by-side, as equals. Which, my guest writes, “has never before happened in the century-plus history of meaningful research on the cause of obesity.”

Gary Taubes is an award-winning investigative science and health journalist. His latest book is Rethinking Diabetes: What Science Reveals About Diet, Insulin, and Successful Treatments. With the journalist Nina Teicholz, he writes the Substack newsletter Unsettled Science.

This is an edited transcript for paid subscribers. You can listen to the interview for free here.

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TH: I think many people will remember you for your book, The Case Against Sugar. I'm a dessert junkie, so I remember reading that book when it came out and being horrified. It did impact my thinking and my diet going forward. I understand you're currently writing a book about obesity. It's a subject I'm interested in and today we'll discuss some of your work on obesity. In particular a recent article in the journal Nature Metabolism, which you co-authored with 15 obesity researchers. Gary, to set this up for us today, there are two competing hypotheses on the cause of obesity, which of course we've seen a dramatic rise in the past 50 years. Can you outline for us in super layman terms what conventional thought about obesity has been up until now? What's referred to, I guess, as the Energy Balance Model?

GT: Yeah, and you're going to have to stop me because my short discussions very quickly can get into long shaggy dog stories about the history of the field. But basically the obvious conventional thinking, what we all grew up believing, is we get fat because we eat too much. Biblical terminology would be gluttony and sloth. And if you want to turn that into a scientific hypothesis, it becomes the energy balance hypothesis. Basically you consume more energy than you expend. The energy is in calories. So you take in more calories than you expend, and if you do, you get fat. That's the conventional thinking. 

It's been the dominant hypothesis on obesity since the late 19th century. There has always been a challenge, though. The challenge is that, going back again — and here's my shaggy dog story — you go back into the literature and it's there 120 years ago. A clinical investigator studying obesity said, “Look, we know tons of people, friends, colleagues, who become obese and don't eat a lot. They don't eat any more than we do; sometimes they eat less than we do. So, how do you explain them?” The alternative, the way to explain them is that obesity is in effect a hormonal disorder. You're predisposed to get obese. Some hormones are controlling fat storage, whether you burn fat or store fat, and that's the cause of obesity. If that's true for these people who don't eat a lot, maybe it's true for the people who eat a lot also — you don't know. So, maybe this gluttony and sloth energy balance thing is completely wrong and obesity is always a hormonal disorder.

By the 1960s we had pretty much worked out the hormones that dominate the regulation of fat storage, and it's the hormone insulin. We secrete insulin primarily in response to the carbohydrates in our diet. There has always been this sort of alternative conventional thinking that carbohydrates are fattening. That's what my mother grew up believing. It goes back 200 years at least. So, now you have a theory that says: We don't get fat because we eat too much. We get fat because the kind of quality and quantity of carbohydrates we're eating are driving fat storage. If you want to not be fat, don't try to eat less — you just get rid of the carbohydrates. They're literally fattening in this hypothesis. 

As a journalist, I've been fortunate enough — or not, depending on how you like my career path — to have been able to play a major role in bringing this hypothesis to the forefront. There are very influential academic researchers who have come to believe this is probably true. That Nature Metabolism paper from August was a result of an invite-only workshop hosted by the Novo Nordisk Foundation in Copenhagen. The Novo Nordisk Foundation owns the pharmaceutical company, Novo Nordisk, which produces these GLP-1 drugs, Wegovy and Ozempic, that have turned the Novo Nordisk Foundation into a charitable organization that has trouble spending its wealth. But they organized a workshop to discuss the differences. Because it's important whether obesity is caused by eating too much or it's caused by one particular macronutrient in the diet and the form in which we eat that macronutrient. 

TH: We'll get to the Copenhagen workshop in a moment. I found that a fascinating piece. But I first, obesity is famously complex. In the paper that resulted from the Copenhagen workshop, the group of all of you acknowledge the potential role of biological factors like genetic predisposition, and behavioural factors like exercise and sleep, and psychosocial factors like income, and environmental factors like endocrine disrupting chemicals. But you do point out that regardless, some biological mechanism is triggered that leads to weight gain. So if the Carbohydrate-Insulin Model proves correct — and of course it's very difficult to conduct rigorous scientific experiments around nutrition — but if it is right, what are the practical implications to that?

GT: Well, first of all, about the complexity of obesity. There are two ways to look at it. One is it's complex because it is by nature a complex problem. The other is we have these obesity epidemics that are now worldwide. You can actually go to any country in the world, any population in the world, and you'll find at some point in time an explosion of obesity and diabetes that happens after these traditional cultures are impacted by Western diets and lifestyles. So there's something about the Western diet and lifestyle that triggers obesity. This was the argument I was making in The Case Against Sugar — it could be sugar specifically. 

But when you ask the question like that: What is it about Western diets and lifestyles? The answer is likely to be simple, although we disagree on what it is. So, the Energy Balance Model would say it's that people eat too much. You get Westernized, you get too much food available. The food tastes too good, it's energy-dense, it's full of salt, fat, and sugar, and people can't say no to it. Then they no longer have to work in the fields for a living, so they don't get enough physical activity. They suffer from energy imbalance and that's why they get fat. 

Endocrine disrupting chemicals could be the reason. So, we interact with a traditional culture. Somehow they are affected by the endocrine disruptors — pick your chemical. That could be the cause of it. Or, it could be as simple as they start eating sugar, and/or white flour. Which is the argument I've been making. Or it could be seed oils. There is a world of people out there now who will say it's seed oils that are causing obesity and diabetes. But it's probably one or the other that's dominating.

Again, we're arguing that the reason is the carbohydrates. So, the impact is pretty simple. What do you do if you find yourself becoming obese? Or you're the parent of a child who's struggling with weight? Do you get them to exercise, or do you tell them to sleep better, or do you isolate them from the endocrine disruptors in the environment? Ultimately you want to remove the cause, whatever it is that's making them fat or making you fat.

If that's carbohydrates, then you're probably not going to succeed unless you remove the carbohydrates from the diet. That's sort of the ultimate. I also wrote a book called The Case for Keto. The case for Keto is if these carbohydrates are fattening, then the only way we can stop that process and reverse it is by not eating them. Ultimately, I also had a book come out last January called Rethinking Diabetes, which makes a similar argument for diabetes, from a historical perspective. So that's the difference.

If you imagine — and this is true for many of us — you are the parent of a child struggling with their weight, do you tell them to eat less of all calories? Do you try to keep them hungry all the time? So, you never let them eat to satiety? Do you get them out exercising, so they're running three miles a day in an effort to keep their weight under control because you've increased the expenditure? Or do you say, “Look, it's unfortunate, but it's the sugar and the flour that's causing this problem. I know you'd love to have sweets after every meal, and cookies for snacks, and candy like the rest of the kids. But if you want to remain relatively lean, that's not an option. It's unfortunate, but it's not an option.”

Understanding the cause of a disorder is absolutely fundamental to reversing it. Whether we like the implications or not. Which is the problem here — because most people don't like the implications of the Carbohydrate-Insulin Model. I'm always amazed that people would rather run four miles a day, and spend 20 minutes going to the gym, and an hour working out and torturing themselves, and then taking a shower and changing, and 20 minutes coming home. But if you suggest they never eat pasta again, that's too much of a sacrifice. That's kind of the conflict.

TH: It's one I know well. 

GT: We all do. I've been there.

TH: But getting back to this Copenhagen gathering. As you say, it's an invite-only gathering of global experts. It compares both models side by side, which I gather has not been done before. The conference defined terms, delineated models, brainstormed the crucial scientific questions that need to be answered, among other things. What drew me to this is the fact that you managed to bring scientists with opposing views together. It was not an attempt to form consensus, but there were some points of agreement. What were some of the open questions that came out of this collective effort about where the field should go from here?

GT: Again, obesity is a serious problem worldwide. I mean, it's terrific that we now have successful weight loss drugs. I find the prospect scary that people will be on these drugs for decades. I hope that they're benign, but I think that's the best we can say at the moment. In the short term, they can be wonder drugs, certainly. But ultimately obesity is a disorder that increases the risk of virtually every major chronic disease — whether it's technically a disease or a disorder or a condition. I think many people who struggle with it wish that they didn't. So, ultimately we have to identify what the cause is. The benefit of this Copenhagen meeting was, more than anything, it gave our perspective, this Carbohydrate-Insulin Model. It raised that to the level of an equal hypothesis in trying to explain this disorder.

So, you could say that even if, for instance, obesity is caused by endocrine disruptors, you want to know if what those endocrine disruptors do is make people eat too much or spend too little energy. Or do they somehow cause these people to store excess calories as fat? You may not be able to remove the endocrine disruptors from their environment. But then you want to know how to disrupt the endocrine disruptors such that they don't cause obesity. For that, you have to know which pathway it's working through. And these are fundamentally different pathways. It's an overused word, but they're different paradigms. So the conference, what came out of it when we were there was we actually designed experiments that could test these hypotheses.

The good thing is you put people in a room who disagree completely on the fundamental causes of what they've been studying their entire careers. There was a lot of antagonism among the participants prior to the meeting. The Danes, to their credit, had us do an escape room exercise to make us bond on day one. I thought it was a mistake, because I've never done an escape room before. It was like, “Are you sure you're at the right meeting?” By the end of the meeting, for the most part, we had come to realize how much we could like each other when we're not arguing about the fundamental cause of obesity.

What has to happen at this stage is people have to care enough to do the studies. It's not actually that difficult to differentiate between these hypotheses, you just have to design studies that are designed specifically to do that. Then you have to tolerate the fact that it's very hard to do experiments correctly. They're expensive as soon as human beings are involved. They take a long time and you have to care enough to want to do it. 

Much of modern medicine is a very different kind of science now. These are the kind of experiments we would have done in the 1950s or 60s, or actually even pre-World War II. Now we do genomics and genetics and microbiomics and proteomics. People can go their entire careers and never actually see a human subject with the disorder that they are ostensibly studying. So, now we have to convince the medical community at large that this is important enough that they should care enough to get behind us to settle this issue. The book that I'm going to write — that I'm in the process of researching — is a history of obesity research. Because I want to show how this energy balance idea arose. Prior to World War II, it had been rejected by the best medical researchers in the world who said, “This doesn't make any sense. We're surrounded by people who live with obesity and don't eat a lot. How can we blame their obesity on eating too much?” The reason for writing the book is to try and get 50 people in the obesity research community to read it and think to themselves, “Maybe we've made a mistake, and maybe we have to fix this. Maybe we owe it not just to ourselves and our research, but the population to do the studies necessary to figure out what the cause of this disorder is.” Because we're talking about two very different mechanisms here.

TH: I want to switch gears now and talk about science journalism. And about changing your mind, about staying skeptical. In your Substack writeup on this paper, and this conference, you touched on an article in the journal Science, originally published in 1890, by the geologist T.C. Chamberlin. He talks about the dangers of “parental affection for a favourite theory.” I think this affects us as journalists, as well. I know that for your book Nobel Dreams, you learned an early lesson in your career on this. You had the opportunity in the 1980s to go to Geneva to basically embed in a world-class physics lab. Things did not go according to plan for the scientists there. Can you describe for us what happened — and what you learned from that?

GT: This was my learning experience and what set me apart from my colleagues in science. I went off thinking I was going to write about a great discovery of a physicist, who everyone knew was going to win the Nobel Prize for work he had just completed. And was claiming to be on to new work that was going to completely revolutionize physics, the biggest discovery in 40 years. I knew him because I had already written a profile about him for his previous work, and I asked him if I could come live at the lab and document this great discovery they were about to make. I got there and learned that in science, until you have dotted every last “i” and crossed every last “t,” you haven't made any discovery. I spent 10 months living at the lab, living with the physicists, basically watching them learn how they had screwed up. 

The book that I thought was going to be about a great discovery ended up being an expose about the world of high-energy physics, sociology, politics, and personalities. It was a learning experience on how easy it is to screw up in science, how hard it is to get the right answer, and how effortless it is to be fooled. All of the Scientific Method and all the rigours and meticulous checks and balances are about trying to minimize the possibility that you are fooling yourself. After that book came out, I actually thought my career was going to be over. Necause this Nobel laureate, who now didn't like me … He actually won the Nobel Prize when I was in Geneva. I went with him to Stockholm, the Nobel ceremonies, and I'm sure he regrets that to this day. I had a blast, though, I have to say.

Anyway, after the book came out, he was quoted on Page Six of the New York Post calling me an asshole. I'm a 30-year-old journalist. He's a Nobel laureate. I thought, “My career is over.” Instead, what happened was when I would interview researchers, I would tell them about the guy I had written about, this Nobel laureate physicist. They would say, “Oh, if you think he's bad, you should write about so-and-so.” Every field in science seems to have one of these characters who cares more about proving he's right than doing really good science. When you do that, you can go a long way in science, because scientists tend to be gullible when it comes to believing that people are in it for the right reasons. So, basically my career became writing about bad science. My second book was called Bad Science. I became all too aware of how — again, all the thought processes — the way that researchers can make erroneous claims, and then commit to these erroneous claims, and build entire, very successful careers on the basis of erroneous claims.

When I stumbled into nutrition in the late 90s, that seemed to me to be the case. And I've been following it ever since. So, I have a very different perspective than most science journalists, who see their job as translating what the experts think — and we need them to be translated. So here's somebody who might be trained as a reporter and have a science background. Or, they might be trained to be a scientist and have decided to become journalists. What they do when something new is announced, or a paper comes out in the New England Journal or JAMA, is they interview the authorities and they tell them what to say and then they turn it into a newsy story. We're not trained to be critical journalists.

No beat reporter in almost any other beat would ever believe implicitly that what he's being told by the authority he's interviewing — like the politician in Washington, or the bureaucrat in Washington, or the police chief, or the police detective, or the football coach, or the basketball player — you never believe that what they are saying is implicitly true. And you never report it as that. But in science and health journalism, that's how we tend to do it. 

So, on one level, these are very complex subjects. They require a lifetime of study to become experts in. On what basis can we question what they say? But by the time I was done writing my second book, I had been browbeaten into questioning what everyone says — regardless of whether they were a Nobel laureate, a PhD, a quantum physicist. If it didn't make sense to me, I thought they better explain it to me so it does.

And nutrition, obesity, is not rocket science. To use a cliched pun. We can understand it if we make the effort, on a commonsensical level, up to a point. But again, this is what Chamberlain was saying in that 1890s article: How do you embrace a hypothesis? You fall in love with it. It becomes a dominant hypothesis. And often that's the very first hypothesis that the scientists will think of in the field. If it's a field like medicine, where it's hard to really rigorously test your ideas … Again, because you don't want to do too many experiments with living humans. By the time they're dead, you don't know if what you are learning is relevant to what you think was happening when they were alive. It's very complicated, ethically tenuous, and expensive.

And so you end up with people embracing ideas, and eventually asserting them as truths, without ever having really tested them. Anyone who comes along and challenges the idea doesn't get funding. Or, if they do get funding, they can't get their papers published in the major journals. Because their papers are going to contradict what the major journals have been publishing all along. So you have a real problem that we live with. And all of this exploded with Covid.

TH: Yeah, and that's what I want to dig into now, on the science journalism question. I'm a general current affairs journalist. I cover a mixed bag of topics. For 2020 and 2021, I was a full-time current affairs producer on two different radio shows, morning radio shows, and we covered Covid a lot. It was an introduction to science journalism for me. I was really shocked by the state of science journalism, which seemed to me to not be asking basic critical questions. I had Elaine Dewar on this podcast a while back. She's a Canadian investigative journalist, and she wrote one of the first books on the lab leak theory. She made this point about science journalism that you just made as well — that basic journalistic practices, in her case following the money, are often ignored in science journalism. What do you think it would take for science journalism to become more rigorous?