To avoid system errors, if Chrome is your preferred browser, please update to the latest version of Chrome (81 or higher) or use an alternative browser.
Click here to login if you're an NAE Member
Recover Your Account Information
Author: Gary Taubes
RON LATANISION (RML): Hello, Gary, we’re really happy to have this opportunity to talk with you today. I see that you are an aerospace engineer, is that right?
GARY TAUBES: I have a master’s in science and engineering from Stanford.
Photo of Gary Taubes
CAMERON FLETCHER (CHF): Why did you choose a degree in engineering?
MR. TAUBES: I had a physics degree from Harvard with an interest in astrophysics. This was the late ’70s. It sounds naïve 40 years later and I suppose it was, but I wanted to be an astronaut. I thought getting an aerospace degree and then maybe going into the Air Force and becoming a pilot would be a reasonable approach.
CHF: And what happened to that trajectory, those thoughts?
MR. TAUBES: I wasn’t very good at engineering. I was 6'2", 220 pounds, and played football in college. (That’s something I can’t undo; I worry about all the concussions.) Anyway there didn’t seem to be any real demand for a 220-pound astronaut when you could put up a 150-pound astronaut who was just as smart and talented or smarter. And I lived with some Navy pilots while I was at Stanford and realized that I wouldn’t last very long in that kind of authoritative hierarchy. I had trouble with authority figures, a common theme in my journalism career.
When I finished my degree at Stanford, I looked for a few engineering-related jobs in the airline industry, but nothing panned out. Meanwhile, I’d always had this urge to be a journalist, and particularly an investigative journalist. I applied to Columbia Journalism School and they accepted me.
CHF: I’d say that’s worked out pretty well for you.
MR. TAUBES: Yes, it did. Although when you con-sider that my schoolmates at Harvard included Bill Gates and Steve Ballmer, success is relative. Steve Ballmer was the manager on my football team. I occasionally try to track him down to see if I can induce him to fund nutrition clinical trials.
CHF: That brings me to another question. What got you started on diet and nutrition? It looks like that was about 15 years ago?
MR. TAUBES: Twenty now. After journalism school, the best jobs I could get were in science journalism because I had physics and engineering degrees from the best universities in the country. I took a job at Discover magazine in New York. I still wanted to be an investigative journalist, but nobody was hiring me to do that. As it turned out, there’s a demand for critical investigative work in science journalism just as there is in any other endeavor. My first two books covered scientific fiascos, controversies, researchers who did their work poorly and got the wrong answer.
I became fascinated by how hard it is to do good science and how easy it is to screw up, for lack of a more technical term. After I did my second book, on cold fusion, I was still getting guidance from physicists and chemists, superb experimentalists. They suggested that if I was interested in bad science, I should look at some areas of public health because it would live down to my expectations. In particular, they were interested in the question of whether electromagnetic fields from power lines could cause brain cancers and leukemia. The concern was based on the science of epidemiology.
I did a piece for The Atlantic on electromagnetic fields and the science. And much of what I had learned from my first two books, about what it takes to do science right and establish reliable knowledge, was considered a luxury that didn’t have to be done in public health research because it was simply too difficult. The thinking was (is) that they don’t have to do well--controlled experiments or maybe do experiments at all. It’s -hypothesis without the test. They can make observations and then conclude from those, because the experimental tests are too challenging, that the hypotheses are likely to be correct because, well, they seem plausible. Then they can give public health guidance because it’s important that they do so. After all, people are dying out there. That sounds extreme but that’s been the reality. I did my first article on this problem for Science in ’94, “Epidemiology Faces Its Limits,” and this has been a primary focus of my career and interests ever since.
In the late 1990s, I stumbled into the nutrition field purely serendipitously. I was working as a correspondent for Science, a glorified freelancer, and asked my editor for a story so I could pay my rent. A new study was coming out in the New England Journal of Medicine, on dietary approaches to stop hypertension, the DASH diet. It had been leaked to Science before publication by a researcher, and I didn’t know that it had been leaked or why.
Typically, the way a reporter will do these stories, particularly as the article isn’t out yet and there’s an embargo, is you get the article in advance, you call the principal investigator, you interview him or her about what they did, then you ask for the names of two or three people who could comment on the study, even though it hasn’t been published yet. You do three interviews, write up the article, get your paycheck, pay your rent, and move on to the next story.
In this case, the article had been leaked to Science along with a list of people to interview, although I didn’t know that. I interviewed the principal investigator at Johns Hopkins, who told me about the research, which shows that you can reduce blood pressure with this dietary approach as much as or more than some blood pressure medications. Then I contacted one of the people on that list, a former president of the American Heart Association. And she refused to talk to me because she said she’d lose her funding if she did. I said that’s crazy, people don’t lose their funding for talking about a diet study in the New England Journal of Medicine! I said, “Can we go off the record, not for attribution? Tell me what it is that bothers you about this study.” But I couldn’t get her to tell me anything.
My next interview was with a fellow who was one of the grand old men of the field. The PI at Johns Hopkins had given me his name. He started yelling at me that there’s no controversy over salt and blood pressure, when I didn’t think I was calling about salt and blood pressure but about this DASH diet trial in the New England Journal of Medicine.
It turns out that the DASH diet lowered blood pressure without reducing salt consumption, so it spoke to the question of whether salt was the cause of hyper-tension, as we’d all been told. I got off the phone and called my editor at Science and said, “I’m going to write up the story and turn it in because I need my paycheck. But I had a former AHA president refuse to talk to me, and a fellow yelling at me that there’s no controversy over salt and high blood pressure, when I wasn’t calling about that. There must be a controversy over salt and high blood pressure that I know nothing about.”
I spent the next 9 months investigating the salt–blood pressure research, and it turns out to be one of the most vitriolic controversies in medicine. I interviewed 85 people for this one article for Science—researchers, administrators, basically anyone who ever played a role in influencing how people thought about salt in the diet, from the researchers who did the clinical trials to the laboratory researchers to administrators with the FDA or NIH or USDA or around the world. I’m a little relentless as a journalist because I’m obsessed with what I don’t know and if somebody can tell me something I don’t know I want to talk to them.
RML: What is the current thinking about salt and blood pressure? I’ve always thought they were mortal enemies. Is there some disagreement?
MR. TAUBES: There’s actually little evidence to support that hypothesis. Clinical trials, and there have been many, simply failed to confirm it. But the proponents of the hypothesis convinced themselves it’s true anyway; they still select out the results that support their preconceptions and ignore all those that don’t. So this salt–blood pressure connection has become dogma, nonetheless.
In 2013 the Institute of Medicine did a review on sodium and blood pressure in which they managed to balance the review committee so it wasn’t stacked with the usual biased suspects, and the review concluded that there was precious little evidence to tell people or to insist that industry reduce the salt content in their food. And now they’ve just come out with a new review in which they put together a typically biased panel and it returned to the conclusion they’d been espousing all along. And, of course, the reason for the new review is because the folks who had been fighting this battle for the past 40 years, the ones who believe dogmatically that salt leads to high blood pressure, found the -unbiased perspective unacceptable. They believe there’s little more important they could do for the public health than to get people to avoid salt.
CHF: What was the genesis of that contention that salt was associated with hypertension?
MR. TAUBES: If you eat more sodium in the short term your body works to maintain a sodium balance in the circulation. That’s why you get thirsty: your body works to increase the water content to keep the sodium concentration stable; that increases blood pressure in the short term. That much is clear: you can definitely increase your blood pressure in the short term by having a large dose of salt. Then you make observations in populations: those that ate higher-salt diets maybe had higher blood pressure than populations that didn’t. So the hypothesis, based on this observation, is that sodium raises blood pressure in a chronic sense. But in longer-term trials the hypothesis fails the test. You read the papers, it bordered on misconduct how these researchers interpreted their results: negative trials interpreted as positive because they believe what they believe.
I actually printed out a stack of the key studies—about a foot high—and sent them for review to three epidemiologists I’d met over the years who I thought were good scientists and critical thinkers. Importantly, they’d never been involved in the salt debate so they had no bias on this. My interpretation was based on their reviews—very critical—as much as anything.
As I was doing this, one of the people I interviewed at length was that fellow who yelled at me that there was no controversy over salt and blood pressure. This guy was one of the worst scientists I’d ever interviewed—and remember I had done an entire book on cold fusion that was called Bad Science. This guy was clearly in the bottom five. He took credit not just for getting Americans to eat the low-salt diet we’d been eating but the low-fat diet we’d all been following.
After I got off the phone with him I called my editor at Science and said, “One of the worst scientists I’ve ever interviewed just took credit for getting us to eat low-fat diets. Everything I know about science tells me that bad scientists never get the right answer. Nature just isn’t that kind. So if this guy, as he claims, was involved in any substantial way in the low-fat diet movement, there’s probably a good story in that, too.”
When I finished the salt piece, which won a major science journalism award, I turned to dietary fat. I interviewed about 140 people for that article, spent an entire year on it. Won that same major science journalism award. The science behind the dietary fat dogma was as bad as the salt science. Again, it was an interesting hypothesis that was tested at length and simply didn’t survive the test. But the tests are very expensive and if you convince the NIH to let you spend $150 million on a test and you get a negative result, that’s considered a waste of money. So the NIH administrators also didn’t like to admit these trials had failed to confirm their hypotheses and assumed instead that they did the trials incorrectly.
RML: What made it bad science, Gary? Was it because the analysis of the data collected was not straight-forward or not properly handled?
MR. TAUBES: This is the book I want to write. To define bad science, you have to establish what good science is. Richard Feynman put it as well as anyone: “The first principle [of science] is that you must not fool yourself—and you are the easiest person to fool.” Another way it’s described is science as institutionalized skepticism.
Let’s say you do a clinical trial or an observation and you get a result: there’s almost an infinite number of ways you could misinterpret that result or screw up the measurements. So the first thing you do is discuss the results tentatively. Good scientists will always discuss their conclusions tentatively because they know, as Feynman said, that there’s a high likelihood that they’re wrong. Even when they can’t imagine how they could possibly be wrong, there are likely to be people who can and one of them is probably right, because there’s always an infinite number of wrong answers for every right answer.
CHF: Isn’t this part of the argument for replicability?
MR. TAUBES: Absolutely. But when you’ve spent $150 million on an experiment, as I said, it’s hard to convince Congress to give you another $150 million to replicate it. And it needs to be replicated by an independent group of people who are not invested in the hypothesis. And remember, a negative result in this field is considered a waste of money. So if you find that your hypothesis of prevention is wrong—‘Hey, it turns out low-fat diets don’t make us live longer’—that’s considered money poorly spent.
In a drug trial a randomized placebo-controlled trial is necessary to be able to correctly interpret any effect you think you see. But in nutrition studies, you can’t do placebo controls: a low-fat diet doesn’t look or taste like a high-fat diet. The participants know if they’re on the low- or high-fat diet. The nutrition field responds to these challenges not by being even more tentative in their interpretation of the data, but by lowering their standards of what they think is necessary to establish reliable knowledge. They don’t care anymore that they can’t do blinded trials or trials with a placebo control.
One reason for doing the experiments is to get the public to change its behavior, right? If you think salt causes high blood pressure, you want the public to eat less salt, you want the industry to put less salt in food. You can’t be tentative; you can’t say, “We kind of think that salt raises blood pressure. And we kind of think that you should spend the rest of your life eating a bland low-salt diet and if you do you might live a little longer than you would otherwise.”
The numbers, for instance, suggest that if you cut your saturated fat content in half, the probability is that you’ll live a few weeks to a few months longer than otherwise. One of the letters I got in the course of my research was from a researcher who did this assessment at the behest of the Surgeon General’s Office. When he got the results and wrote them up, the Surgeon General’s Office tried to prevent JAMA from publishing his study because his conclusion was that cutting back on saturated fat would only extend your life by this trivial amount. And probabilistically, as he pointed out in this letter to the surgeon general (which he shared with me), it’s not an extra month on your honeymoon, it’s a month at the very end of your life.
RML: In the work that I’ve done and as a practicing engineer, I always take the position that nature is consistent. I’m a materials engineer, and when I put mate-rials into an engineering system and that system is placed in service, sometimes there’s a failure, and it’s usually because the service environment is aggressive to the materials of construction. That’s where nature is consistent. If I expose stainless steel to high--temperature chloride, things that are not good will occur.
That phenomenology is inviolate. Nature will always provide the same result. Understanding it mechanistically or from the point of view of causative factors, that’s where the debate comes in—you may have 100 researchers with 100 different ideas trying to interpret a simple phenomenon.
But in the case of nutritional issues like salt, is nature consistent? And if it is, is it just a matter of interpretation? Why is there a controversy?
MR. TAUBES: Among other things, people are still being told to eat low-fat, low-salt diets and yet we have obesity and diabetes epidemics that actually coincide with that dietary advice.
The dogma has been accepted, but I think it’s based on bad science. The term that physicists use is “pathological science,” coined by the Nobel Laureate chemist Irving Langmuir, who gave a famous lecture at IBM in 1953 on what he called “the science of things that aren’t so.” It’s not fraud or misconduct; it’s where people have a lack of understanding about how easy it is to get the wrong answer, to be misled by threshold interactions or subjective phenomena. That’s how Langmuir phrased it.
The same thing happens in nutrition and public health. On one level, science is a very slow process, and it’s supposed to be a critical exchange of information in which you want your colleagues to explain to you, when you present a new result, all the possible ways you could have misinterpreted it or screwed up (because assuredly you did). You want them to help you realize that before you go public and embarrass yourself. But in nutrition and public health the argument is that people are dying and we have a moral obligation to act as quickly as we can to save lives.
So if you believe your hypothesis is correct, and you get any confirmation from observations and experiments, then you must tell people such that they can act on it. And then if the science should change—and this is what public health administrators told me—“we’ll just change what we tell people.”
But what these public health authorities don’t realize is that this process won’t allow the science to change. When studies then suggest that the public health guidelines are wrong, the proponents of the hypothesis refuse to accept it. They see what they want to see in the data to convince themselves that they were right all along. This is a paraphrase of what Francis Bacon wrote 400 years ago, when he argued for the experimental method in science. It was true then. It’s true now.
RML: But wouldn’t it be a straightforward thing to conduct a clinical trial in which a certain number of people eat a high-salt diet and another group eats a low-salt diet? Then you collect, over a period of years, some indications of whether that’s beneficial or not. What am I missing?
MR. TAUBES: Clinical trials were done. They’re relatively easy with high salt versus low salt. But people still know if they’re eating a high-salt diet or not, and you’re going to get the biases that come with that. And you can’t do these trials for decades, although chronic diseases take years to decades to manifest themselves.
What you want to know is not just whether salt raises blood pressure but whether that salt-stimulated elevation in blood pressure causes chronic disease. The clinical trials that were done ran from months to a year or 2. They showed a slight elevation in blood pressure on the high-salt diet; depending on who is doing the meta-analysis, it might be 3 or 4 millimeters of mercury (with hypertension, blood pressure is significantly -higher than that). But you can’t run the study long enough to see whether the low-salt diet prevents heart attacks or strokes because that takes far more than a couple of years.
The meta-analyses of these studies show that, on average, a high-salt versus a low-salt diet leads to a difference in blood pressure of 3 or 4 mm of mercury. If you believe that salt causes high blood pressure, you say, “Look, it elevated blood pressure. That means we should all eat low-salt diets.” If you don’t believe it or you’re skeptical, you say, “Look, the elevation in blood pressure is trivial for a significant reduction in salt that we’re never going to achieve in public health anyway. So let’s spend our limited public health currency on something more important because this clearly isn’t.” The result is a polarized environment in which the skeptics, who are the minority, are seen as irresponsible.
Moreover, the skeptics tend to leave the field. After I did my article for Science, the NIH had a symposium to discuss the science prompted by my work. The three epidemiologists to whom I had sent that stack of papers for review attended the symposium and gave their critical assessment of the data. But then they left and went back to what they were doing before. They didn’t want to spend their precious time kvetching about bad science on salt. (That was my job.) But the people who, 20 years ago, believed that salt is a killer never stop believing it. They stay in the field and continue proselytizing.
I left the field, too; I didn’t want to write about salt and blood pressure my whole life. Now there’s virtually nobody left to fight the “pro science” argument. And when young reporters come along and write about salt, they don’t see any reason not to trust the “experts,” who are the ones who have been telling us to avoid salt for so long.
RML: Much of your writing today is focused on other aspects of nutrition and dietary issues.
MR. TAUBES: Yes. After I did the dietary fat story for Science I started talking to the New York Times Magazine and we decided I would write an article on the likely causes of the obesity epidemic. This was back in 2000 and awareness of the epidemic was relatively new.
What was clear was that the prevalence of obesity in America jumped in the 1980s. I wanted to know why. The result of my research was a relatively infamous cover story for the New York Times Magazine, headlined “What If It’s All Been a Big Fat Lie?,” the “it” being the idea that eating fat makes us fat. The cover was a Porterhouse steak with a pat of butter. The article led with the idea that if the medical community had some kind of “find yourself standing naked in Times Square” nightmare, it was that the low-fat dogma was wrong and Robert Atkins, of Atkins diet fame, was right.
That article got me a large advance to write the book I wanted to write—although I had no idea what I was getting into. I spent the next 5 years working on it. The internet had come along and made it possible to do what would have been a lifetime’s worth of research in 5 years. You didn’t have to spend 30 years buried in the stacks at some Harvard library. Among other things, I eventually amassed probably one of the largest private libraries in the world on obesity.
The gist of this book was that in the post–World War II era, obesity and nutrition researchers settled on a couple of hypotheses of nutrition and health that seemed obvious—and were wrong. One is that we get fat merely because we eat too much, that it’s a -behavioral problem, not a hormonal regulatory issue. The other is that dietary fat is the evil in our diet.
While they were coming to these conclusions, researchers ignored copious evidence that obesity is the result of a hormonal regulatory defect in fat storage and metabolism, and that the hormone that dominates fat accumulation in the human body is insulin, which we secrete in response to the carbohydrate content of our diet. And there was a conventional wisdom until the 1960s that carbohydrates—bread, pasta, potatoes, sweets, beer—were fattening. One of my favorite quotes is from a 1963 British Journal of Nutrition article by one of the two leading British dietitians; the article begins, “Every woman knows carbohydrates are fattening.”
Between the 1950s and 1980s, though, our public health authorities transformed the “fattening carbohydrate” into the “heart-healthy carbohydrate as diet food.” Hormonal regulatory thinking about fat accumulation was replaced with the idea that people get fat just because they eat too much and it’s a behavioral issue. The research became dominated by psychologists and psychiatrists, trying to figure out how to get fat people to eat less, rather than endocrinologists studying the hormones involved in fattening. We ended up with a full-scale national fiasco, and we’re still mired in it.
The implications are profound. We’re told salt causes high blood pressure, but hypertension is associated with obesity, diabetes, heart disease, and stroke, and not just in individual patients but in populations. When populations go from eating their traditional diets to the Western diet, they get obese and diabetic and they develop heart disease, cancer, hypertension, all simultaneously. It’s a well-documented phenomenon around the world.
So, while American researchers were trying to answer the question “Why do we have so much heart disease in America and how do we stop all these fat people from eating so much?,” British researchers had developed an alternative hypothesis that all these chronic diseases of Western diets and lifestyles—obesity, diabetes, heart disease, stroke, hypertension, and a dozen others—are driven by the carbohydrate content—the quality, not the quantity—and the sugar content particularly.
RML: Well, here’s another question. When I travel in Japan, I’m always amazed at how much thinner they appear. They have a diet that’s quite different from a Western diet. How does that factor into all this? They do consume a lot of fish.
MR. TAUBES: The Japanese actually have an interesting role in this. Death rates from diabetes, from about the Civil War to the 1920s, increased in some American cities 15-fold. Diabetes was virtually nonexistent before the Civil War. But by the 1920s public health authorities were saying, “Look, this explosion of -diabetes -coincides with the creation of the sugar-sweetened food and beverage industry.” The chocolate, candy, and ice cream industry from the 1840s, soft drinks in the 1870s, 1880s—by the early 1900s Coke and Pepsi were everywhere, and Dr. Pepper. By the 1920s diabetes experts and public health experts were saying that the prime suspect for this epidemic is sugar.
But Elliott Joslin, the leading authority on diabetes in the country, didn’t believe sugar was the cause because the Japanese ate a high-carb diet and had very low rates of diabetes. Joslin didn’t understand that sugar is metabolized differently than rice. Rice breaks down into glucose; sugar breaks down into glucose and fructose; fructose is metabolized in the small intestine and liver; glucose in virtually every cell in the body.
RML: The Japanese have a low-fat diet compared to Western diets?
MR. TAUBES: They do.
RML: And do they have the same incidence of coronary and other problems?
MR. TAUBES: In the 1930s the Japanese were used as a reason to say that sugar doesn’t cause diabetes. Then in the 1950s and 1960s, driven by University of -Minnesota nutritionist Ancel Keys, they were cited as a reason to argue that fat was the cause of all these diseases of civilization because they eat a low-fat diet high in carbs and they don’t get fat or diabetic and their heart disease rates were very low. But the obvious suspect, to me anyway, is that the Japanese were also eating a very low-sugar diet.
The Japanese are one of the many populations that, when they transitioned to a Western diet, as in all of Southeast Asia, see a rise in obesity and diabetes. You see the same nutrition transitions in populations like the Maasai, who lived on milk and meat. They didn’t have obesity and diabetes until they transitioned to a Western diet. It’s the same thing with the Inuit, who lived on walrus and caribou and seal and fish and didn’t eat carbs at all. And with Native Americans, whether they’re Plains Indians living on buffalo or Southwestern agriculturalists. Until these populations eat a Western diet you don’t see obesity, diabetes, heart disease, or anything else. (And, yes, you often don’t have Western doctors around to diagnose them, but it was a common observation nonetheless.)
When you look at the regulation of fatty acid metabolism and storage in the human body, it turns out that insulin is the primary driver of fat accumulation. The fructose in sugar and the glucose from these easily digested carbohydrates raise insulin levels, albeit by different mechanisms. This is textbook medicine, but it’s rarely if ever considered relevant to obesity. I discuss why in my books, although I still can’t believe it.
RML: One of the things I imagine our readers will wonder is, What would Gary Taubes say a healthy person should eat?
MR. TAUBES: I’m working on a new book that tries to put all this in context. Part of the problem is the idea that we get fat because we eat too much, which is the way lean people think about obesity. Lean people think, ‘I’m lean. I don’t eat a lot of food.’ And then the natural conclusion is ‘I’m lean because I don’t eat too much, and if fat people just ate in moderation they’d be fine, too.’ But for those of us who are predisposed to put on fat, we get fat even when we eat in moderation. We can’t eat what lean people eat. That’s where the idea that carbo-hydrates and sugars drive fat accumulation comes in. We have to keep our insulin low, and the way to do that is to avoid carbohydrates and replace those foods with fat—i.e., Atkins, or keto, as it’s now called. That’s why this is a controversy, because these low-carb diets tend to be high in fat. You have to replace the carb calories and you do it with fat because that keeps insulin low. So we end up with a diet with which people have ethical issues. It tends to include animal products, which are nutritionally ideal combinations of protein and fat. And for 50 years we’ve been hearing that this way of eating will kill us. But if you want an insulin-lowering diet, you replace the carbohydrates not with lean protein, like skinless chicken breast, but with fatty foods and then you get the calories from fat, which is the one macro nutrient that does not stimulate insulin secretion.
In Michael Pollan’s In Defense of Food, he gives his famous mantra, “Eat food, mostly plants, not too much.” The problem is that for those of us who tend toward obesity and diabetes, “not too much” is meaningless, because we get fatter even when we’re consciously trying to restrict how much we eat, and mostly plants is probably wrong, because plant foods tend to be carbohydrate rich.
There’s one thing I mention in my new book, which I wish I could take credit for but can’t. For the past 50 years physicians have been confronted with this conflict: They’ve been told and dietitians have been told to prescribe diets to their patients by hypothesis: eat a low-fat, low-salt diet, which will keep your LDL cholesterol and blood pressure low, and you should live longer than if you eat otherwise. That’s the hypothesis. But they have no way to know if it’s true, and particularly not for a specific patient, even if they think they have reason to believe it’s probabilistically true. Even if the patient lives to be 100, they don’t know if the diet did that or not. We’re not privy to that information. And the flip side is that patients on the low-carb, high-fat (keto) diet get -healthier: their blood pressure comes down, their blood sugar gets under control, they lose weight relatively effortlessly without hunger. So we’re dealing with diet by hypothesis vs. diet by clinical observation and that observation is a powerful one. Moreover, clinical trials are now demonstrating that patients with type 2 diabetes who eat this way can get off all their diabetes medications.
I took one engineering course as an undergraduate at Harvard, systems operations or some such. I can’t remember who taught it, but he would end every few lectures with the comment, “You pays your money and you takes your chances.” On some level, that’s what I’m arguing with diet: you eat the diet that makes you healthier, and you takes your chances on the long run. People will lose dozens or 100 pounds eating low-carb, high-fat foods and their doctors and friends will try to deter them by saying, “You’re going to kill yourself eating all that fat, all that bacon!” But while they eat that way, it’s clear they’re healthier. Are they going to live longer? Well, you pays your money, you takes your chances. Everything is a risk. If you do the low-fat diet, that’s a risk too. Your doctor just isn’t properly communicating all the possible risks.
RML: This is certainly a familiar concept in an engineering mindset.
MR. TAUBES: Isn’t that one thing engineers effectively do? Manage risk?
In a clinical trial or observational study to assess the benefits of, say, lowering cholesterol through diet, like the famous Framingham Heart Study, they looked at people’s cholesterol at, say, 180 and 150 and then at how long they lived, and then concluded that we should all reduce our cholesterol dramatically. But assuming the numbers are causal—which of course we have no idea—what I want to know is how much longer can I expect to live if I lower my cholesterol by this amount? Isn’t that a reasonable question?
There are two ways to look at it. Maybe everybody shares the benefit and lives 2 weeks to a month -longer, or maybe one person hoards the benefit and doesn’t have a heart attack—that’s a bridge that doesn’t collapse when it could. So then everyone else is going on the diet for nothing.
As I was trying to understand what this meant, I -ended up talking to people like engineers at JPL studying risk assessment. How do we make sense of this because the data don’t contain the information to tell us what we want to know, which is how much longer am I going to live, or if somebody’s not going to have a heart attack, what are the odds that it’s me?
CHF: That actually dovetails with a question I want to ask you, Gary, which is how your engineering background informs your work.
MR. TAUBES: I think it’s a combination of the engineering and science. These are disciplines that provide immediate (and occasionally tragic) feedback if you’re wrong. What engineering on some level tells you is that failure is probabilistic and we need to do everything we can to understand that.
RML: I’m going to have to sign off, I’ve got to get to a meeting. Gary, thank you so much for joining us today.
MR. TAUBES: It’s my pleasure. Thanks, Ron.
Back to your question, Cameron, it’s hard for me to say because so much of what happened in graduate school led me into science journalism. Then I had the opportunity in my first book to talk and work with exquisite experimental scientists. They have a way of thinking about the world and the universe that is very different from most of us, other than maybe very good homicide detectives. They want to establish cause and effect beyond reasonable doubt.
CHF: With the areas that you’re researching now, diet and nutrition and the human body, it’s much “squishier.”
MR. TAUBES: I’ve had nutritionists say to me, this isn’t particle physics, every human is different. So it’s incredibly hard to do this research. But you can’t lower your standards of what it takes to establish reliable knowledge because it’s too hard to rigorously and correctly test your hypothesis.
In my first two books I documented people who got the wrong answer and lived to regret it. In the case of cold fusion, they ruined their careers and their reputations. Studying what happens when researchers get the wrong answer tells you a lot about what it takes to establish the right one, how rigorous you have to be and how easy it is to fool yourself. When I moved into public health I found that nobody seems to care, on a profound level.
CHF: That is certainly vividly illustrated in your book The Case Against Sugar.
MR. TAUBES: Yes, and now you read in the paper about this reproducibility crisis. I would call it a sort of systemic pathology in the science. Some enormous amount of what’s published every day in the medical literature is wrong, misinterpreted, irreproducible. Anyone who bases work on those results is going to build their edifice of science on a foundation of cards. And we have no idea how systemic that problem is. One estimate from my youth is that 90 percent of the results published in the physics journals are wrong or meaningless. The process of science is to sift out the 10 percent of the wheat from the 90 percent of the chaff. (That’s quoting the physicist-turned-philosopher-of-science John Ziman.) But it’s probably worse in other fields, because they’re harder to do.
Researchers are supposed to promote their work, to make it look like it’s worth funding, like it has public health or medical implications, because they’re trying to keep the money flowing and get tenure. All of these are completely contrary to the idea that what you’ve just done is very likely wrong and that you’re fooling yourself. Presenting your data as tentatively as possible is actually the best idea because you don’t want to be locked into believing it’s true. Once you are, all the human biases will kick in to make you confirm over and over again something that isn’t true.
CHF: What polemic is next for you?
MR. TAUBES: Well, all my books so far have been about good science and bad science because that’s what I’m interested in. Eventually I would like to write a book called How (Bad) Scientists Think and what to do about it. But we can’t talk about bad science without talking about what science should be.
CHF: How you would characterize effective public health studies?
MR. TAUBES: An effective public health study is a study that is done rigorously enough that we can trust the result and the interpretation of the result to be reliable.
Public health tends to work when associated with infectious diseases: Ebola, for instance, or cholera. One of the things we want to do is develop effective Ebola vaccines or treatments, and we know what kind of clinical trials you have to do to establish whether a vaccine works or not. And we can test them in the field and see if they work. With chronic diseases, the argument is the trials take too long and cost too much. But that’s an effort problem.
Think about what’s happened in high-energy physics. A few years ago the Higgs boson was discovered. This is the last remaining predicted particle in the standard model, and the Large Hadron Collider that was used to discover it cost almost $5 billion. It was an international collaboration—money came in from all over the world to build it at CERN, straddling the French-Swiss border. The device included four separate experiments, so results could be replicated in real time. The physics community said, “This question is really important to us at the moment and we’re willing to raise the money and make the effort to answer it.”
If the same effort were put into these nutrition questions, if you spent a billion dollars on the right clinical trials, you could do a pretty good job of it. It might not be good enough, but it would be better than what we’re doing. The catch is that you wouldn’t know until after the experiment how you screwed up. This is the unknown unknowns problem. Still, we could do a pretty good job if we’re willing to make that kind of unilateral investment. But that’s not how NIH funds this research. Instead it disseminates a lot of money among thousands of researchers, all working on projects that are completely inadequate to answer any meaningful question.
And, of course, the community shakes off critics, regardless of how credentialed (or not) they might happen to be.
CHF: Being a critic is an important role to play.
MR. TAUBES: Yes. We always need to hear from the people who can point out how we most likely screwed up.
CHF: Presumably, someone plays that role for you.
MR. TAUBES: Yes. A fellow who I thought was the best scientist in the field when I did the research for my book Good Calories, Bad Calories—and I interviewed effectively everyone who was still alive who ever did meaningful research in obesity and chronic disease—does it and he has no compunction about being sensitive to my feelings when he reads my work. Francis Crick once said that you have to be able to tell your colleagues exactly what you think about their ideas without worrying about hurting their feelings. If you can’t do that the collaboration will fail. This fellow has no problem with that.
A few years ago, I attended a seminar on childhood obesity and after every talk somebody in the audience raised their hand and said, “That was a brilliant talk, thank you.” There was no criticism at all. No attempt to challenge the speaker on what they had presented. One of the speakers actually suggested that there’s a gene that makes fat people want to eat at fast food restaurants. And nobody raised their hand to say, “Professor, are you out of your mind?” It was clear to me that whatever this was—and I’m still not sure—it wasn’t science. It wasn’t about forwarding our understanding of childhood obesity.
CHF: That argument about the fast food restaurant gene is in the same category as the meteorological “finding” that—and I’m putting this in quotation marks—tornadoes are more likely to strike trailer parks.
MR. TAUBES: Yes, imagine if the field of climate science became based on the trailer park–tornado assumption and 30 years later there are thousands of papers based on this idea that trailer parks somehow attract tornadoes. Tornado movement would be plotted in computer models based on trailer park locations. It sounds crazy, but that’s effectively what happened in nutrition and obesity research.
CHF: That gives me an idea for another polemic for you: climate change.
MR. TAUBES: I’m staying out of the climate change field.
CHF: That sounds like a fruitful topic for you to help people understand.
MR. TAUBES: Maybe so, but when you’re fighting to remain a credible source in a very contentious field, it helps to remain fixed on the problem at hand. For me that’s obesity and the chronic diseases that associate with it.
CHF: What’s the title of your new book?
MR. TAUBES: It’s The Case for Keto: Rethinking Weight Control, the Science and Practice of Low-Carb, High-Fat Eating. I’m not wild about putting the faddish word “keto” in the title, but I figure I’ve been making the case for this way of eating since 2002, I should live up to it. The book argues that those of us who put on fat easily simply cannot eat like lean people, so we have to eat and think about it differently. And among other things, we have to stop taking lean people’s advice. It’s not true that what works for them works for us.
CHF: When is your book coming out?
MR. TAUBES: In April.
CHF: Thank you so much, Gary, what a blast. I’m so glad you were able to stay on the phone a little longer. I really enjoyed our conversation.
MR. TAUBES: Okay, terrific. Take care.
This conversation took place June 4. It has been edited for length and clarity and references have been inserted for readers’ interest
 Nobel Dreams: Power, Deceit and the Ultimate Experiment (Random House, 1987); and Bad Science: The Short Life and Weird Times of Cold Fusion (Random House, 1993).
 Now the National Academy of Medicine.
 Sodium Intake in Populations: Assessment of Evidence. 2013. Washington: National Academies Press.
 Dietary Reference Intakes for Sodium and Potassium. 2019. Washington: National Academies Press.
] Langmuir I, Hall RN. 1989. Pathological science. Physics Today 42(1):36.
 In the Novum Organum, 1620 (https://oll.libertyfund.org/titles/bacon-novum-organum) .
 Reliable Knowledge: An Exploration of the Grounds for Belief in Science (Cambridge University Press, 1978).