Full Transcript: Is Sugar Slowly Killing Us – The Knowledge Project

Is Sugar Slowly Killing Us – The Knowledge Project

: Welcome to the Knowledge Project. I'm your host, Shane Parrish, the curator behind the Farnam Street blog, which is an online community focused on mastering the best of what other people have already figured out. The Knowledge Project is a podcast where we look at interesting people and uncover the frameworks they use to make better decisions, live life, and make an impact.

: On this episode, I have the fascinating, Gary Taubes. Gary is an award-winning science journalist who has written Good Calories Bad Calories and Why We Get Fat. You're going to learn about the role sugar, carbohydrates, and fiber, how breakfast became the most important meal of the day, what science is, and the state of nutritional science, why he says wine is okay, his next book project, and so much more. I hope you enjoy this conversation as much as I did.

: Before I get started, here's a quick word from our sponsor.

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: Gary, I'm so happy to have you on The Knowledge Project.

: Great. I am happy to be here.

: One of the questions that I have when I think about you is I wonder what your daily diet looks like. Like, how do you think about the food that you consume?

: Yeah, it's funny. When we talked about the things that I didn't want to talk about, one of the things I was thinking, "Can I say I don't want to talk about my daily diet?" Then, I thought I probably can't say that because it'll probably come up at some point in the interview.

: Easiest way to think about it is I don't eat grains, and starches, and sugars anymore because I think they make me fat and unhealthy. And I replaced them, for the most part, with, you know, fat animal products. So, not good for the animals, but I think it's good for me physically. And I'm one of these people who have convinced myself that butter and bacon are health foods. And I hope I'm right.

: Why you do think nutritional science is in such a poor state compared to other areas of medical science? Like, what is it about nutrition that's led to such vast misunderstandings?

: Well, first of all, we don't know that it's actually better than other areas of medical science. One of the questions I'm always … We know what we see, right. So, I study nutrition science. I write about nutrition science. I know nutrition science is, to me, almost not a functional science, but I've never had the opportunity to put that out for investigation into other areas of medicine or other areas of science. You just hope they're better.

: My take on this is sort of historical. The way I see it, science was sort of honed to a very fine edge of, you know, a methodology for establishing reliable knowledge. The universe, in Europe, it's by …. You know, it was at its height in Germany and Austria pre-World War II. And, sort of, these people really understood the rigor necessary to do good science, the skepticism necessary, this idea that Richard Feynman later encapsulated by saying, you know, the first principles of science is you must not fool yourself into the easiest person to fool.

: And this culture of science began to evaporate with World War II. And it crossed the Atlantic in fields like physics because we embraced these European researchers, many of whom were Jews. And the leading scientists in the world, the leading physicists in the world post-World War II in the US tended to be these European emigres who are their students. And many of the key players in the Manhattan Project were European emigres.

: And so, you had this very rigorous approach to science being done in fields like physics. And you could do it in fields like physics because if you think of science as hypotheses and tests, the tests were relatively simple, relatively simple to do. You could come up with an idea. You could build a small, you know, cyclotron like Lawrence did here at Berkeley. You could, then, test the ideas, and you know that other people are going to do the same all around the world. And if you're wrong, it's going to be very embarrassing. So, there was also, sort of, a relatively quick feedback between hypotheses and tests.

: And in fields like nutrition and public health, not only did we not embrace the European emigres, and, in fact, in many cases, we wanted nothing to do with these people. The hypothesis and test, by definition, was much harder to do, or the testing aspect of the hypothesis was much harder to do.

: So, now, instead of dealing with subatomic particles or every particle for all intents and purposes of the like, you know, you can do these experiments. Indeed, you're now dealing with these messy humans who think for themselves in chronic diseases that take decades to manifest themselves. Even if you could do the testing of the hypotheses, it takes a long time to do it. It's very expensive, and it's very difficult, if not impossible to do right.

: And so, what the nutrition and public health research communities did is they just lowered their standards for what they would consider reliable knowledge. And this just became sort of inculcated throughout the entire community such that these people almost … To me, I feel like they almost forget what it takes to do reliable knowledge. And they say, they justify it or they say the issues are so important, people are dying out there; and therefore, we don't have time to dot the Is and cross the Ts, and make sure that we're right about our hypotheses. And, to me, the really scientific response is if we don't have time to dot the Is and cross the Ts, you have no idea whether you're right.

: Right.

: And, you know, we end up in a situation today where we have, you know, these massive unprecedented epidemics of obesity, and diabetes, and related diseases. And medical public health community has no idea, almost literally no idea what to do about it. And everyone insists that the science is good enough to answer these questions; and yet, clearly, if we were good enough to answer these questions, we never would have gotten into this situation, so.

: What role do you think genetics plays in this?

: In the obesity and diabetes epidemics or in obese-

: Yeah.

: I think, clearly, genetics … Well, we know that obesity runs in families. And that's been known for, you know, hundred … Body type runs in families, you know. Identical twins don't just have the same facial features, they have the same body types. Clearly, genetics plays a huge role in whether, you know, someone's going to be tall and thin, or short and squat, or some combination of the two. And if it's playing a role in obesity, it's going to play a role in diabetes as well. And I don't actually know the data for diabetes, but I'm sure there's a strong genetic component there as well.

: But then the question is, and this is the question I addressed in my last book, The Case Against Sugar, we have these diabetes and obesity epidemic that manifest themselves pretty similarly worldwide, independent of the genetic, you know, the genotype, the genetic ancestry of the population.

: So, you know, Inuits near the Arctic Circle, or Native Americans, our First Nations people, or, you know, African populations, or South Pacific Islanders, or Middle Eastern populations, or Southeast Asians, they all experience obesity and diabetes epidemics when their environment changes from their traditional diet and lifestyle to a Western diet and lifestyle. And they manifest these epidemics pretty similarly.

: So, clearly, the underlying genetics are not the key factor there. You know, it doesn't matter what type of human, you know, where your ancestors came from. You get dumped in a modern western lifestyle, you're likely to become obese, and then diabetic. And so, the question I was asking in my book is, what is it about the Western diet and lifestyle that is the agent of these diseases?

: So, what do you think about, like, the Mediterranean diet, the French diet, and all of this stuff? Like are there diets suited to cultures or types of people that grow up in a certain region, or?

: The Mediterranean diet may or may not be healthier than, for instance, an Inuit diet. Like, if you took the Inuits and gave them the Mediterranean diet, they may do just as well as the Greeks do, or they may do more poorly because they haven't had time to adapt to, I don't know, olive oil, or a lot of green vegetables, or, you know, whatever the grains they're consuming in this diet. It's sort of … You know it's one of the ways people tend to confuse the fundamental issue.

: So, to me, the really important issue, the critical issue is these epidemics. And the numbers are just out of … I mean, almost unimaginable. In the US, and according to the Centers for Disease Control, in the US, since the late 1950s, diabetes prevalence has increased 700%, okay. So, 1 in 11 Americans now have diabetes, when the number might have been closer to 1 in 1000 or 1 in 3000 at the beginning of the 20th century. That's almost incomprehensible.

: And nobody really … I mean the fact that there aren't, sort of, teams of investigative scientists, you know, and task force on every street corner walking around with, you know, I don't know, detectors of some sort trying to figure out what the cause of this disorder is, you know, why we have this out-of-control epidemic is another question. But that's the question you have to keep on asking yourself, what's causing these epidemics because we're not going to be able to reverse or prevent them until we identify the fundamental cause.

: And it gets confused with issues of, "Well, should we be eating the Mediterranean diet to prevent heart disease; or should we be eating the DASH diet to lower blood pressure; or should we be eating, you know, Ornish's diet to reduce risk of heart disease?", when the very first thing you want to know is like, "What's causing these epidemics, man, because this is crazy?"

: The Director General of the UN, a woman named Margaret Chan, a year ago referred to them as slow motion disasters. And she predicted. This was fascinating. This was at a keynote address at the National Academy of Medicine in Washington. And she gave a number, a prediction for the likelihood that public health organizations will prevent these slow motion disasters from getting worse. And the likelihood of even preventing them from getting worse, she said, was virtually zero.

: So, you've got the slow motion disasters worldwide. You've got the head of the greatest public health organization in the world predicting that they will fail to control them. And so, the question you want to ask is, "What's the cause?", not whether we should be eating a Mediterranean diet, or a French diet, or you know.

: And then, maybe, you can further ask the question, is there something about the Mediterranean diet, or about the French diet, or about these Blue Zone diets that happens to shed light on this question of what's causing obesity, and diabetes, and the conditions that are associated with it?

: Can you quickly walk listeners through your beliefs on what is causing this?

: Okay. So, again, if you think of it as a criminal case, the first question is, what's the crime being committed? And in this case, like I said, it's obesity and diabetes epidemic showing up everywhere in the world after they transitioned to a western diet. And so, that's the crime. That's what we want. And we want to find out who the perpetrator is. We know what the age and what the vector is. The vector is the Western diet and lifestyle. You know, it's commercialism, and urbanism, and maybe it's processed food. These are all sort of factors of the disease. But what's the age, and then the vector?

: And, you know, the point I make in my book is you can chart this. Go back in time. And, actually, what you would do, again, if we had a criminal case, you would want to know when the crime was committed, the earliest sign of the crime. And so, you could do this using hospital records in the medical literature. And you find out, for instance, in the US that diabetes rates were virtually non-existent. Even though it was a very relatively easy disease to diagnose, you saw very little sign of it pre-1850, and even for the most part, pre-1870s.

: And then, the numbers in hospitals, and you could see this in hospital records in Boston, in Mass, and/or in Philadelphia, at Pennsylvania Hospital. The diabetes diagnoses in hospitals go from like literally zero a year. Remember, 1 in 11 Americans were considered to have diabetes, and the major city hospitals would see, in some years, zero cases. And then, you could see the numbers go to one, to two, to three a year, to five a year, to ten. And then, by the early years of the 20th century are in double digits. And then, they just shoot up from there.

: And you could find experts back then, you know, the head of the New York City Department of Public Health saying it just detracts so closely with sugar consumption from population to population that we seriously have to consider that sugar is a cause. And you look at the industries that evolved in that period. And sugar. over the course of the 19th century, went from being a sort of expensive luxury in the beginning of the 19th century when Americans, for instance, probably consumed less than in the neighborhood of five pounds per person per year. So, that's the equivalent of maybe, you know, I don't know, four ounces of sugary beverage per day, probably less, to by the end of the 19th century, consumed in the neighborhood of maybe 80 or 90 pounds per person per year.

: Wow.

: You know, in the neighborhood of a 20-fold increase. And in all the ways that we consume sugar today were virtually non-existent as industries in the early 19th century. So, in the 1840s, the candy industry is created, the chocolate industry is created, and the ice cream industry are all created. And then, in the 1870s and '80s, you see the soft drink industry with Dr. Pepper first, and then Coca-Cola, and Pepsi. And by the early 20th century, these foods have just exploded. And they're everywhere. And all the major food producers that we deal with today, the sugar purveyors that we deal with today are already sort of in place, and selling nationally, and marketing nationally, and, you know, sort of pioneering their marketing approaches.

: At one point around 1905, a congressman asked the brother, I think, it was one of the founders of one of the main players in Coca-Cola, you know, if he could describe the items on which Coca-Cola was advertised. And he said, "The everyday items," and he said, "would be easier to describe the items on which it's not."

: So, I mean, the goal of Coke, which Coca-Cola always was basically to make sure that everyone in the world, I mean everyone in the world has easy access to Coca-Cola, and is drinking it regularly. And at one point, the CEO of Coca-Cola even complains that the human body needs so many ounces of water, liquid a day, and only like 20% of it is coming from Coca-Cola, and that's just completely unacceptable.

: So, anyway, you see this explode. The one industry that's now a major … But there's a few industries that are major purveyors of sugar that took a while longer to come about. So, the fruit juice industry doesn't really show up until the 1930s, and then explodes post World War II.

: And the cereal industry, cereal was basically, you know, Kellogg, and Post, and those folks were health fanatics. And they were running sanitariums in, you know, Minnesota for dyspeptic wealthy people. And they were, for the most part, anti-sugar. So, cereal was a way to get fiber into the diet, and they didn't really want sugar in their products, and they had nutritionists working for these companies. They didn't want people eating sugar.

: But post World War II, right around 1948, Post with, I think, it was Sugar Crisp finally breaks down the barrier and started selling a sugar coated cereal. And suddenly, every other, you know, cereal producer has to give in or go out of business. And you could see the struggles between their nutritionists and their marketing people. And in every case, the marketing people won.

: And by the 1960s, you know, the American breakfast had been transformed into, basically, a dead desert with fiber or lack of, you know. So, we're drinking fruit juices. We're eating sugar-coated cereals. And then, when the low fat movement comes in in the 1960s, you know, you're adding sort of low fat or no fat yogurt with sugar and skim milk. And it's, you know, sugar from beginning to end.

: So, the people, while this was happening, are arguing, "Look, you know, obesity and diabetes is exploding. Sugar consumption is exploding. Clearly, that's the prime suspect." And then, as we began to understand the physiology of how sugars metabolize, that clearly made sugar a prime suspect as well in actually causing type 2 diabetes and a condition called insulin resistance that we should probably talk about. So, there's-

: Yeah, why don't you walk me through the physiology of sugar?

: Okay.

: And the response it generates in our body?

: Yeah. So, when we're talking about added sugars, particularly sucrose, which the white powdered stuff in high fructose corn syrup, these are simple carbohydrates that are combinations of two simpler carbs. So, glucose, which is the carb when we consume grains and starchy vegetables like potatoes, are broken down in our body into glucose. And the glucose is transported into the bloodstream. And when we talk about blood sugar, we're talking about glucose, blood glucose. So, the glucose gets into the bloodstream. The glucose level rises. So, your blood sugar rises. And that glucose is metabolized by every cell in the body.

: And this is the glycemic index, kind of like the response?

: When we talk about the glycemic index, exactly. That's the response of your blood sugar to the foods you're consuming. So, if you're consuming a food that's almost pure glucose, and it is easy to digest, like white bread, you will have a, sort of, quick rise in blood sugar. And it's one reason why white bread was usually considered sort of a standard by which you would then compare other foods to the glycemic index.

: But there's another half`of the sugar molecule in the case of high fructose corn syrup and other, 55% of it, which is this molecule fructose. So, any molecule that ends in OSE is a carbohydrate. So, fructose is the sweetest of the carbohydrates. So, it's what makes sugar sweet. But the fructose is metabolized not by every cell in our body. It's transported through the portal vein to our liver. And some huge proportion of it is metabolized by liver cells.

: And, you know, this stuff was worked out by biochemists back as early as the early 20th century. But biochemists weren't doctors, and they weren't studying treating diabetes or obese patients. And the doctors, even if they were getting biochemistry, might not have gotten this level of biochemistry. So, the physicians treating diabetes never really understood what sugar was or what made it different than other starches.

: So, when you began to have debates about whether sugar was the cause of diabetes that diabetes specialists tended to say no, because they thought sugar is the same as rice, and they're all carbohydrates. And look, we know that the Japanese eat a lot of rice, and they have low levels of diabetes. Ergo, it's not about sugar or rice.

: They also thought that once you start giving diabetics insulin, which begins in the early 1920s, it's hard to dose the insulin properly. So, the diabetics would often experience episodes of very low blood sugar where they could go into hypoglycemic shock and die, and they had to be rescued from these episodes. And the easiest way to do it was with candy. Ergo, sugar must be good for you. That's how they thought, and you could see this in the literature.

: But physiology. So, when we're talking about diabetes, we're talking about particularly type 2 diabetes, which is the common form that associates with obesity and age. So-

: That's the one you're not born with; that you develop later in life.

: Well, you don't … Yeah, it's not the acute form that hits in childhood, which is type 1, or that typically appears in childhood, which is type 1. It's about 5% of all diabetes. And then, type 2, there are variations now. But for type 2, it's effectively about 95% of diabetes. When we're talking about the diabetes epidemic, it's type 2 diabetes we're talking about.

: And because it associates so closely with excess weight, the assumption of the diabetes experts, going back to the 1920s, is it's caused by being fat. And you get fat because you eat too many calories, you don't exercise enough. And we'll probably talk about that shortly.

: But by the early 1960s, once the scientists had a tool that allowed them to measure hormones in the blood accurately, they realized that type 2 diabetes was a disorder or what's called insulin resistance. So, with type 1 diabetes, you don't have enough insulin or no insulin at all, and you can't properly metabolize the carbohydrates you eat. And in effect, no matter how much you eat, you kind of starve to death because you can't use these fuels for food.

: And the assumption was all diabetes was just sort of an insulin deficit, until the 1960s when they could really measure insulin levels in the bloodstream, and the research community realized that type 2 diabetics actually have both high insulin and high blood sugar. So, the insulin must not be working. So, they're resistant to the insulin they're secreting, or it's not working well enough, so they have to secrete more insulin.

: So, since the early 1960s, we've been aware that type 2 diabetes is the disease of insulin resistance. And then, this went along with the observation that obese people also tended to be insulin-resistant. They had high blood sugar and high insulin levels.

: And that there's a condition that's now known as metabolic syndrome, which is a cluster of abnormalities that's sort of, basically, insulin resistance syndrome. So, this is, you know, elevated blood sugar with glucose intolerance, it's called. And, also, you know, you're getting heavier, or your waist size is increasing, so you're getting fatter. And you've got an elevated level of what are called triglycerides, which are a form that fat appears in the blood. And you've got low HDL cholesterol, which is the good cholesterol. And your blood pressure is elevated. So, it's this whole sort of cluster of metabolic abnormalities that, not only sort of include obesity and diabetes in them, but also associated with heart disease, and stroke, and all these other chronic diseases.

: So, when you start thinking of this whole cluster of insulin-resistant conditions, and you're asking the question, whatever causes insulin resistance causes obesity, diabetes, high blood pressure, heart disease, stroke, cancer, or Alzheimer's, virtually every chronic disease has a link to insulin resistance. And the best research on what caused insulin resistance suggests that it starts in the liver, and it starts with the accumulation of fat in the liver.

: And, in fact, there's another epidemic going on at the moment of now what's called non-alcoholic fatty liver. And it associates with obesity, and diabetes, and metabolic syndrome. So, everything is targeting the liver. And there, you've got the fructose. Now, I'm bringing it back to the case against sugar. Now, you've got the fructose component of sugar being metabolized in the liver.

: And the liver didn't evolve to metabolize at the levels we see today. So, you know, throughout the last two million years, you would only see sugar in small quantities in fruit. It's what makes, you know, fructose in small quantities. It's what makes fruit sweet. And you'd see it in even smaller quantities in green vegetables. But nothing like the amount you would see in like a Coca-Cola, or a glass of apple juice, or a candy bar, or an ice cream cone, or any of those foods where you're really just dumping fructose on the liver. And by the 1960s, the biochemistry had pretty clearly worked out that when you dump fructose on the liver, it converts it to fat.

: And on the other side, you'd have the insulin resistance researchers saying, "Hey, insulin resistance seems to be caused by the accumulation of fat in liver cells." And all I'm saying is, you know, that you've got 150 years a history of people saying when diabetes appears, it does so after sugar consumption goes up. And then, you've got all these biological mechanisms suggesting that sugar is literally at the scene of the crime in the human body when insulin resistance begins, from when insulin resistance begins. You know, you're on the road to this whole slew of chronic disorders that are now becoming epidemic or are already epidemic.

: Why are we so attracted to sugar?

: It's a good question. You know, if you ask that question about any drug of abuse or any addictive substance, nicotine, caffeine, alcohol, heroin, and cocaine, I mean, it's sort of the … On one level, the idea is we've become addicted to foods because there's an area of our brain called the nucleus accumbens or the reward center that rewards. It's there to reward behaviors that are good for the species.

: So, when you have an orgasm during sex, the nucleus accumbens respond by like dosing your body with dopamine, and it feels great, and you want to repeat it. And when you eat foods, you know, which we have to do, to foods that taste good, also, it stimulates a dopamine response in the nucleus accumbens, so you want to continue eating, which means you'll continue to stay alive, and you'll continue to replicate.

: And so drugs of abuse just happen to be things that, for whatever reason, just by chance, you know, over the course of human history, we sampled 10 million leaves, twigs, starches, you know, food animals. And lo and behold, there's a few things that happened to sort of overstimulate the nucleus accumbens and overstimulate dopamine. And those become addictive substances that we, then, want to repeat, and repeat, and repeat. And so, there is evidence that sugar stimulates dopamine secretion in the nucleus accumbens just like these other drugs of abuse.

: And in animals, at least, so rats and mice, we can do these experiments. You could demonstrate that they will be more addicted to sugar than to cocaine or heroin. So, these experiments, some of them were done in France. They are sort of perversely fascinating. You basically addicted your lab rats to a daily bolus of cocaine or heroin. And then, you give it a choice between either sugar or the cocaine. And if it chooses sugar, it can't go back to the cocaine. It can't do both of them. You know, over the course of a couple of days, the rat will switch from cocaine to sugar. It takes a little longer before making the switch from heroin.

: That's fascinating.

: Yeah. I mean, clearly, you can't do these experiments with children, but if you have kids, you probably don't need to. So, there's a lot of … Clearly, sugar is a psychoactive substance. You know, we give it to newborns to when they get circumcisions. You know, a couple of drops of sugar water on the tongue, and you can remove the foreskin, and it doesn't bother them, at least, not in the short run.

: You know, sugar has always been considered a painkiller. And, actually, entered Europe in the 13th to 14th century or 12th Post-Crusade, it's more as a medicinal and perceived as having medicinal uses than as a food or a spice.

: But, you know, my favorite saying this is from Charles Mann, the journalist historian, who's a friend of mine, and somebody who just awes me with how good his work is. And he said in his book, 1493, he was discussing the sugar industry, and he said, "Scientists today debate amongst themselves whether or not sugar is an addictive substance or we just act like it is." And it's like, you know, clearly … Again, I think, I have kids, I don't need scientific research to tell me that this substance has power over my children that no other food does.

: And, you know, even the sort of ardent defenders of sugar, and, you know, historians, and journalists would say, "Well, of course, parents still have the ration to their children's behavior." I mean, they're sugar-eating. You can't allow them to eat all the sugar they want. So, there's clearly … You know, whether it's this effect in the nucleus accumbens, or there's an interesting fact that might drive sugar consumption, also, in the liver, it's a little more technical. But I've always wondered how much role that play. But something about it, clearly, it just becomes something we like because it affects our brain and the body in a way that we want more of it. You know, we want to repeat the experience.

: A lot of people seem to think it's just simply a matter of calories in, calories out. What do you say to that argument?

: Gosh. No. This was … You know, I-

: This is the most common thing I read, right.

: So, when I started my research, okay, journalistic research on this subject, and if you go back the very first infamous New York Times Magazine cover story I had in 2002 that was called What If It's All A Big Fat Lie?, I had a line in there where I said … You know, I was speculating that dietary fat doesn't make people fat, and it's carbohydrates that do. And so I had elaborated. I said, "Clearly, it's excess calories that cause us to eat too much."

: And then, I actually … You know, I get a big book advance. And I could spend five years of my life doing research. And the internet, at this point in time, made it possible for me to learn, you know, to … It's like a new technology had come along. And, suddenly, I can, you know, sit in my office, which was then in New York, and I can get every primary source on obesity, whether it's in the academic literature, or books, or conference proceedings, you know, going back to the 19th century. I mean, back then. Nowadays, you could virtually download them. Back then, 2002 to 2006, I had students all around the country whose job was to go to their local medical libraries and, you know, make copies of the 50 or 100 references I would send to them. And then, I would buy books.

: So, I actually started doing my research, and I realized that this idea that excess calories is what makes us fat is the … And I'm embarrassed that I never thought of this. It's logically equivalent to saying, you know, excess money makes us rich, or I don't know, scoring access points in a football game will make you win. You know, it's almost incomprehensibly naive to me. And I, now, understand where it comes from because I've read all this literature. And to this day, I'm still sort of mystified.

: So, I'm going to pet peeve time. You know, my sugar book came out. I got sort of almost universally wonderful reviews. And then, Jerome Groopman in the New Yorker condescendingly dismissed the book as the work of sort of, you know, wannabe investigative journalist on. And then, his review, he makes this statement that the one undeniable fact about nutrition research is the importance of calories. And, you know, excess calories makes you fat.

: I thought, you know, if this was James Surowiecki writing about economics, and he said the one undeniable factor in the science of wealth is about the importance of dollars, you know, David Remnick or one of his crew would say, "Are you kidding us? Are you out of your mind? Like, of course, dollars, you know." I mean, if we were discussing wealth accumulation, I just kept telling you, you know, he said, Gary Weiss, you know, "Let's talk about why is Bill Gates so rich." And I said, "Well, because he makes more money than he spends." He began, "Why did I book this guy?".

: And if we were talking about climate change, he said, "Why the atmosphere heating up?", assuming it's heating up, which I'm beginning to believe since we just had 100 degree weather here in Oakland a couple of weeks ago, and I said, "Well, clearly, atmosphere is heating up because it's taking in more energy than it's letting out." You know, I've just, in one sentence, sort of nullified billions of dollars worth of research into what it is about the atmosphere and various, you know, and greenhouse gases, and the wavelengths of light they reflect, or, you know, transmitted. I mean, all the intricacies of climate change science would be nullified by this statement that the atmosphere is heating up because it's taking more energy than it's letting out, which it has to be doing.

: So, the point is nutrition science from the 1860s through the 1920s was completely dominated, as all sciences are, by what they could measure, the technologies available to make observations. And all they had were they had devices called calorimeters where they could measure the energy content of a food, and then they could measure the energy expended by humans by putting him in these room-sized calorimeters or dogs. And then, they could do experiments with animals where you, you know, give them vitamin or mineral deficiencies, and see what kind of diseases manifest still from there.

: So, all of nutrition science was calorimetry, energy in and energy out, and vitamins, and minerals. And when people started talking about what the causes of obesity might be, it made absolutely perfect sense to think in terms of calories because that's all they could look at. That's all they had.

: And so, by 1910-1920, they had this very simplistic idea with some, you know, $5 words attached to it to make it seem more complicated that said that people get fatter because they consume too many calories, or they don't expend enough. And it seemed to coincide with what we see in the environment, which is you're unlikely to see obese people running marathons or doing hard physical labor. So, you tend to think of them as sedentary or lazy.

: And you often see obese people, and we have this sort of model of Falstaff and Shakespeare. You know, they're gone, even if they're not. Like you pay attention to them. You'll notice them when they are. And when you see an obese person sitting at a restaurant eating a tiny salad, you don't think it, it doesn't cross your consciousness, it's refuting your belief that they're gluttons. So, it seemed to go along with what seemed to be conventional wisdom. It was easy to believe.

: And then, the weird thing is the research community just bought into it and locked into it in a way that, again, part of it can be explained by … So, not all the research community locked in, the German and Austrian clinicians. And in Germany and Austria, you know, these people were doing far and away the best medical science in the world at the time. And they pioneered all the fields of science relevant to obesity, some metabolism, genetics, endocrinology, the science of hormones, nutrition, all sort of came out of Germany and Austria. These Herr Professor Doktor types who would both see patients and theorize about what the cause of the disorders might be.

: And they had concluded that obesity had to be a hormonal disorder. It had to be because there were all these manifestations. It's sort of hormonal regulatory disorder. You know, they would say things like, you know, look men and women fatten different. Therefore, sex hormones are involved with obesity. You know, we know when people are insulin deficient, they don't have insulin, they can't store body fat. So, insulin must play a role. And I mean these people get emaciated no matter how much you feed them, type 1 diabetics. So, insulin must play a role in storing body fat.

: We know that there are, you know, tumors, fatty tumors called like lipomas that are independent of how much people are eating and exercising. If you have a lipoma, it could starve someone. The lipoma is not going to go away. It's still going to be this cluster of fat.

: And there were even cases in the literature where people had skin grafts. You know, a graft of skin taken from their stomach, and put on, like, the back of their hand to cover a burn. And then, they get older, and they get obese. And one hand got no body fat on it. You know, if you look at the back of your hand, it's a place we just don't store or tend to store body fat. On the other hand, we have this huge tough fat on it. So, they would say there's clearly regulatory enzymes in the skin itself that are determining whether or not this area of the body will accumulate fat. And it's all got to be hormonally and may be regulated to the central nervous system as well.

: And then, the German and Austrian School just evaporates with the Second World War, literally. You know, these people emigrate to the US, end up in … You know, one of the great endocrinologist from the University of Vienna ends up living in Los Angeles writing articles and working for the Hospital of Medical Evangelist, because nobody else wants to hire these European emigres, particularly the Jews.

: And then, after the war, the European researchers have many things to think about more important than obesity. And in America, they just clammed onto this idea that it's all about how much you eat and exercise. You know, a lot of lean research. They didn't want to read the German literature anymore. So, the lingua-franca of medicine pre-World War II was German. The post World War II, you have a lot of young German doctors. I mean, excuse me, young American researchers who had fought in the war who have just naively, you know, justifiably have this natural antipathy to the Germans and Austrians. They're not going to read the literature. They don't cite the pre-World War II studies. And they just recreate the science of obesity as a gluttony and sloth disorder.

: And by the 1960s, the major figures in the field are psychologists who are trying to change the behavior of the fat person and make them eat less. My favorite example was one idea where you would get the obese man's wife to withhold sex if he didn't lose weight that week. And it's just suddenly eating … Obesity becomes an eating disorder.

: And then, later, it becomes sedentary behavior disorder by the 1970s. And none of these people … You know, if you've got psychologists studying it, well, their specialty is psychology. It's not endocrinology. It's not hormones. It's behavior. So, you get this sort of what you see is all there is phenomenon often coming in, and it never went away.

: And even today, the great themes in obesity research are this idea that the obesity is caused by a highly palatable or rewarding foods. And the implication is there something about the brains of obese people. They can't control their appetite in the onslaught of all, you know, the bliss points created by salt and fat, as opposed to the simple idea that there's something about the foods we eat that trigger a hormonal response that tells the body either to store fat, or, you know, mobilize, and use it for fuel, and then bringing this all back to insulin resistance.

: By the early 1960s, it was clear that insulin. the hormone insulin, was the primary regulator of fat accumulation in the human body. So, what it does is you secreted in response to the carbohydrate content. So, your blood sugar starts to go up, and the body puts insulin out to signal your lean tissue to take up the glucose from the blood, and burn it for fuel. The insulin facilitate the technical ways it facilitates the uptake of sugar, of glucose, but it also signals the fat tissue to hold on to any fat and to store whatever fat you've eaten.

: So, it sort of partitioning the fuel use to say, "Look, the immediate problem is we have this rising tide of blood sugar, and high blood sugar is toxic. So, the way we're going to deal with that is we're going to store fat get that out of the way, and then we're going to burn the blood sugar as quickly as we can. And as blood sugar starts coming down, insulin starts coming down. And then, you could mobilize the fat you've stored and use that fat for fuel, which is how your body's supposed to work.

: So, there's a term called metabolic flexibility where when blood sugar starts coming down, fat's coming up. You just switch over from burning glucose to burning fat. Your cells should be perfectly happy to do that. But if your insulin-resistant, your insulin stays high, and you never successfully make that switch. So, blood sugar comes down, but you continue to lock away fat. And sort of like a ratchet wrench. And day-to-day, it only goes in one direction. You just store fat, and that's all you do.

: So, you know, that's the, again, long-winded way to say as long as people believe it's about calories, you're not even paying attention to the hormones and enzymes that regulate fat accumulation. And what stuns me, so that last February, there's an article in The New England Journal on the pathogenesis and mechanisms of obesity, and you can read that article. This is the premier medical journal in the world, and there's actually no discussion of the mechanisms other than an assumption that people eat too much. And so, you know that's the implicit.

: And you can go to the leading textbook in the world, and the medical textbook, the most seminal textbook, and the Harrison's Principles of Medicine, I think, it's called. And the chapter on obesity is written by, you know, a very very smart researcher named Jeff Flier who just, until recently, was Dean of Harvard Medical School. And his wife, who's equally smart and talented, Terry Maratos-FLier. And they do research together.

: And if you actually look for what it is that causes obesity, in that chapter, the assumption is that the overconsumption of calories. It's eating too much. It's a behavioral problem. And there's no discussion of what's been a very well worked-out science on the sort of hormonal regulatory system that controls both the use of fatty acids for fuel and the storage of fat in the fat cells.

: And, to me, I don't see how that can be defended. And, like I said, it's almost mystifying. And I've spent 20 years trying to understand it. And I, kind of, understand every step along the way, how it happened, and when it happened. And I still want to say to people, you're talking about a disorder of excess fat accumulation. Don't you have to discuss the regulatory system that controls fat accumulation, the hormones and enzymes in the fat cells, on the fat cell membranes, elsewhere in the body, and in a very beautiful system worked out by millions of years to regulate this. And it's clearly dysregulated.

: Well, one thing I haven't heard you mention that I'm curious about is what is the role of fiber.

: That's a very good question. Again, it's interesting. I have to talk about these things historically, and I apologize. I think about them-

: No, this is amazing.

: Yeah. To understand the role, you have to know where it came from. So, in 1960s, several British researchers start focusing in on this idea that it's either sugar or sugar and refined grains that cause obesity, and diabetes, and heart disease.

: And so, these two, one of them is John Yudkin, who is the leading British nutritionist, and the one is a fellow named Peter Cleave who was a British naval researcher. And Cleave had the advantage that as a navy man, he had traveled around the world, and he had seen that there are all these disparities in chronic disease rates all around the world wherever you go.

: So, you know, urban, westernized, urban centers had high rates of obesity, and diabetes, and heart disease. But, you know, less westernized areas and non-urban areas had lower rates. So, the question is, what was driving that? He concluded it was the refinement of the grains we were consuming, including sugar. And so, by the 1960s, Yudkin was publishing in the medical journals, and Cleave had written a book called The Saccharine Disease, explaining that it was refined grains and sugars that cause this cluster of diseases.

: And then, into this walks, a guy named Denis Burkitt who, was a missionary physician in Africa in … I forget. Where was ETM? In Uganda. Burkitt was famous for a medical investigation he did that led to the identification of the first virus that causes the cancer that's known as Burkett's Lymphoma, after Burkitt, So, he was a very well-known, very famous physician.

: And ETM comes into power in Uganda. And as he flee back to the UK, and he's looking for things to do, and the leading British epidemiologist in the world named Sir Richard Doll who was famous for identifying cigarettes as a cause and lung cancer, Richard Doll gives him Cleave's book and says, "You should read this. I don't know how much is right, but there's a lot of it that's brilliant." And Burkitt reads it, and he thinks it's brilliant. But then, he kind of thinks we're never going to convince the world to give up sugar, and white bread, and beer. And he's also obsessed, being a Brit, with constipation. Completely obsessed with constipation.

: So, he decides that the problem isn't the presence of the sugar in the white bread and the beer. It's the refinement of the fiber, the absence of the fiber. When you refine these products, so you take a wheat, then you refine it into a white bread, you get rid of all the fiber in the process. And he knows that fiber helps with constipation, and constipation is a disease that's often seen along with this cluster of western diseases.

: So, by the 1970s, Burkitt start publishing articles with another former missionary physician from African named Hugh Trowell saying the problem is the absence of fiber, not the presence of sugar, and highly-refined, high-glycemic index grains. And you can reconcile this fiber hypothesis with the dietary fat idea that's growing along through the '60s as well. So, over the course of 1960s, the bulk of the heart disease nutrition community had decided dietary fat caused heart disease. And if it caused heart disease, it also caused obesity.

: And then, you had Cleave saying, "No, no, no. It's not that." Cleave and Yudkin thing it's not dietary fat, it's sugar and refined grains. And these were seen as competing hypotheses that couldn't be resolved. In parts, if you told people eat less fat, the question is what were they going to eat, if not sugar and grains. So, those two hypotheses couldn't be reconciled.

: But then, Burkitt comes along and said, "No, no, no. It's not a sugar and refined grain. It's the absence of fiber. So, they should eat low fat diets that are high in fiber," and everyone goes. "That's it." You know the bran muffin craze appears. Like bran muffin start appearing on the market, you know, a year after Burkitt's first publication. And that becomes the conventional wisdom ever since.

: And the problem is these are hypotheses, right. And we've talked about how people do a lousy job of testing hypotheses. They're very hard to test. But by the early 2000s, it was pretty clear that both these hypotheses couldn't be confirmed in experiment. In fact, one of the things I talked to, I talked to Richard Doll a few years before he died for my research, and all said to me, "Yeah. it turns out the only thing fiber actually cures is constipation." And I said, "Well, could Cleave have been right all along?" And he said, "Yeah, that's a good point. Cleave really hit on something."

: And all I did in my book is say, "Hey, it looks like Cleave and Yudkin were probably right all along. They're more right. And then, a few other peoples too, like Atkins. So, there, that's the story. You know, fiber, we're still obsessed about fiber. The idea that … So, you know, again, I said science progresses when new technologies come along that allow you to observe new things.

: So, the obesity-diabetes science is completely botched. You know they made no progress. They can't explain it. Even an article that was recently review, an Endocrine Science Society review of obesity written by some of the leading figures in the field that was kind of a response to my work and that of others in which they said, you know, clearly, obesity is caused by eating excess calories, and a calorie is a calorie. And then, they kind of said, but we don't really know what makes people fat or how to make them thin. So, these people are clearly lost.

: And I'm saying one of the reasons why they're lost is because the revolution in endocrinology was obesity, research nullified that, passed it by, never took advantage of it. That was 1960 there of science. So then, obesity becomes a kind of real science to the medical community. In 1993, when the hormone leptin is discovered, then it becomes a subdiscipline of molecular biology, and the genomics, and proteomics. But this 1960, endocrinology which kind of solved it has just left behind.

: So, now, another new technology comes along. Now, you can suddenly sequence the genome of the bacteria in your gut. So, new technology, you get to see new things. And, now, you assume you could learn new things. And we're desperate for a theory of obesity, right, because we don't know what caused it or prevents it. So, the gut biome explodes. And people say, "Wow, clearly, westerners who are obese and diabetic have different gut biomes than, you know, hunter gatherer populations in Africa." What the difference? Well, the hunter gatherers eat more fiber. I don't know. So, then, you get this focus that goes back on fiber. And then there are people like me saying, "Wait a minute. What about this 1960s endocrinology? Remember that?"

: So, you know, to me, I'm afraid of what happened in the 1970s. You add fiber, you can slow down the digestion of the carbohydrates. You could even slow down the digestion of the sugars. So, that would probably help, but you've paid attention to the wrong thing. It's not the absence of the fiber, it's the presence of those other foods. And you could help more by getting the right answer rather than coming up with another wrong answer.

: What have you kind of changed your mind about, or where have your thoughts significantly shifted since you first started to develop your alternative hypotheses, I guess, of obesity, that carbohydrates promote insulin response, which promotes body fat? I mean, what surprised you the most as you dove into this?

: Well, I mean, again, when I started this, I thought that excess calories caused obesity, so, you know. But we're assuming. You're asking basically after I shed myself of that belief. So, the question, is there anything that I used to believe that I'm not convinced it's wrong?

: Yeah. yeah.

: Put simply. Not substantially,no. I mean, we could talk about one of the things I did in all this. In the course of this is I co-founded this not-for-profit called the Nutrition Science Initiative.

: NuSi, yeah.

: Yeah. We call it NuSi. Well, it could be NuSi, I guess. So, NuSI, I co-founded it with Dr. Peter Attia, who's a very, you know, talented physician with also a business background. And our assumption was, particularly with this energy balance issue, with obesity and energy balance issue, is it a hormonal regulatory issue? And the implication is to factor in foods that cause obesity, the caloric content to the effect of those foods, on underlying hormonal state.

: And, again, on some level, I think, you shouldn't have to do the experiments to demonstrate it because, you know, I find the energy balance thing now so naive, but we'll accept that I just talked about it too much, I've convinced myself that it's easy to see the naivety.

: So, we thought if we can get the research community to do the experiments themselves, and to understand the competing hypotheses, and to understand, you know, our arguments, and then we could raise the money for them to do the research, this would have a profound effect on their thinking. And if anything, at this point in time, we have done more harm than good.

: How so?

: So, of the studies we funded, the first one was a pilot study with some very influential obesity researchers. And it was a learning experience for me also. So, in my first book, Good Calories, Bad Calories, I do discuss. The epilogue is, in part, a meditation on how I don't believe nutrition science is a functioning science; that it lacks many of the characteristics that a functioning science has to have, particularly the sort of critical rigorous back and forth between scientists where they're attacking each other's ideas, and being used by each other to understand how they might be fooling themselves.

: You know, Robert Murden, a philosopher of science, said that this kind of critical back and forth in science makes some mother's, you know, parenting of her child look like child's play in comparison. You know, it's supposed to be sort of …

: Francis Crick said a functioning collaboration doesn't work unless you can be rude to each other. You know, you have to critically attack. And what I've seen in these nutrition public health communities are it's too easy to attack each other's work, so they don't do it. And then, they just allow the substandard work to go by.

: So, I discuss that in the epilogue of Good Calories, Bad Calories. It's one place that my editor really let me sort of express my dismay, but it was on a macro level. I had no idea how hard it was to do these experiments on a micro level. In fact, because I am not a scientist or an experimental scientist, and my only experience was with, you know, my first two books being sort of mentored by some of the great physicists in the world and seeing how they did their work. I wasn't aware of how easy it is to screw up an experiment, and how unintended consequences are, unintended phenomenon will appear that will make the interpretation of the experiment almost impossible.

: And, again, if you're working in a world where, like, you know, you could do your cyclotron experiment on Monday, have results on Wednesday, and have your colleagues explain what you screwed up on Friday, and then you could repeat it on Monday, this isn't a huge problem.

: Right.

: And the history of science is full of those kinds of, you know, examples and discussions. But if you're working in a world where the experiment cost you five million bucks, and you're never going to get $5 million to do it again.

: That's so tough, yeah.

: That's difficult. And same kind of problems come on. It's not like the physicists are any better at this than the nutritionists because if you're doing something new that's never been done before, you have no idea how your equipment, or your subjects, or the purveyors of your diets, or whatever are going to screw it up. You can't plan for everything.

: So, part of my revelation was on this micro level, not just how easily the science could be derailed by just bad luck or, you know, the unforeseen, what was it, you know, unknown unknowns. But the tendency among the researchers to pretend it didn't happen or to ignore it because if they actually confront it, they're basically saying, "Here's a paper I've just written that isn't worth reading. So, I'm going to pretend that it is. And the only way I can pretend that it is is by not mentioning all the ways that it isn't."

: And you're supposed to publish negative data, but the truth is it's very hard to get it published. And nobody wants to put in the time to finally get an article published in some forthright journal because it's negative. So, a lot of issues came up actually getting to be involved. And I'm wondering, you know, how naive was I, and will we ever solve these problems?

: What do you think it's going to take for, like, the nutritional research community to get a lot more rigorous? It seems like … I mean, the influence of the epidemiology makes this difficult. Such a large percentage of nutritional studies are based on correlative measures rather than causative ones, leading people to believe that, you know, just about every food either causes or prevents cancer. Like, how does this get fixed?

: Well, that's the question. I'm involved now, I'm supposed to be coauthoring an article for the British Medical Journal on nutrition policy. They were running a series on nutrition policy. So, one of the article is on dietary fat. And I'm honored that they've taken up my work that they've asked me to be a co-author with two epidemiologists.

: One of them is at Harvard, and has not liked my work for 10 years. And so, I wrote a New York Times magazine cover article about the science of epidemiology using the Harvard Cohort Study as a case study of a pseudoscience. So, I can understand why he would might be angry at me and disagree with my way of thinking.

: So, the conflict in this article is that the nutrition community driven by these epidemiologists think in the context of saturated fat that if all of us out there in the lay population were to replace saturated fat with polyunsaturated fats, we'll live longer and be healthier. We'll have less heart disease, less diabetes, maybe less obesity, less insulin resistance.

: So, this means, in effect, replacing … I don't know if they think this far into advance, but it means, in effect, replacing foods we've been consuming for millions of years as a species. You know, mostly animal fats with vegetable oils that a relatively new to the human diet, and particularly like soya oil, and canola oil, and corn oil.

: And with the argument I've been making in e-mails, not successfully, is that if you're going, what you're assuming is that these vegetable oils are inherently healthy, that they're beneficial, they're the equivalent of statins. If we give vegetable oils to everyone,they will be healthier if they consume these things. And this is an idea that if it was a drug, you would never be able to do without long-term clinical trials to establish that you're not going to do more harm than good or, in fact, that you're not going to do any harm at all. It's not good enough to say 80% of the people are going to live longer if we find out that 20% are going to be killed or get diabetes.

: You know, it's one thing for a doctor to say, "I think you should be on a statin. Here's the … You know, the pro side is, I think, we'll get your LDL down, and your inflammation down, and we're going to reduce your risk of heart disease. There is a small chance you'll become diabetic or have muscle aches, in which case, we'll discontinue the statin or switch to a different drug." It's another thing for public health organizations and governments to say the whole nation should be on statins, and not care if 1 out of 30 of the population gets diabetes because the other 29 might live longer.

: So, these are two entirely different scenarios. And if the vegetable oils are supposed to be beneficial, we have to do those kind of tests. We just have to do them. And what I wrote in an email to the lead author is, you know, "You're telling me that if I cook my 11-year-old son's salmon in canola oil instead of butter, they will live longer, my 11-year-old son will live longer, and there will be no negative consequences? I need to know if you better evidence than you do before I accept that because canola oil scares me. Olive oil, maybe I'll give in. Canola oil, corn oil, soya oil, brand new foods to the human population."

: So, their response, the Harvard response is we'll never get these studies done. What you're asking for are virtually impossible. They're very expensive, maybe half a billion dollars or $100 million. You're asking, what you need to test these is maybe 40,000 people that you can randomize to eat either canola oil, or butter, soya oil or coconut fat. Pick your…

: And they're going to have to keep doing it for ten years. And they're going to have to comply pretty well because at the end of 10 years, we're going to want to be able to compare what are called hard endpoints on more heart disease or less. Not just risk factors, like cholesterol levels, but do they actually get more heart disease, you know, more cancers, more diabetes. Are they heavier? Do they have better or worse cognitive function?" I mean there's a whole slew of things that could happen if you feed people a completely new food.

: And they're arguing, because it can't be done, we have to go with the evidence we have. It's just too hard to do this trial. It's too expensive, and the people aren't going to follow our advice, and the people we put on canola oil are going to get bored, and switch to butter. And the people we put on butter are going to get health conscious with the canola, and it's just going to … And we'll find out, as we have in the past, and we've spent half a billion dollars, and we either don't know the answer, or we don't like the answer. And so, we should go with what we have and the broken system.

: So, let me just give you my counter of the counter, which is in physics, the physicists have decided en masse that they wanted to know whether the Higgs Boson existed, and they want to know if there is science behind the standard model. And the best way they know how to do that is to build a huge accelerator, which costs $10 billion. And then it costs a billion dollars a year to run. So, they did that. And then, society funded. We funded that because society thinks that's an important question, and more of a better society if we spend money trying to answer that than if we don't.

: And then, they have collaborations of 1500 scientists on, you know, four detectors on this huge atom smasher, or 1500 scientists on each detector. The papers have lists of names that are longer than the papers itself. But that's what you do because you want to know the answer, you know, in nuclear fusion. So, we think, as a society, we're going to run into some serious energy problems with or without climate change involved, but we're just going to have to fuel the lives of ten billion people by 2050. That's going to take an enormous amount of energy.

: Our, you know, fossil fuel reserves are going to run dry. Can't do it with renewables. It's just not practical. We need nuclear power and, ideally, nuclear fusion; as opposed to nuclear fission. And fusion power is hard to achieve. And so far, we've spent $50 billion on nuclear fusion research worldwide. It'll probably cost another 50 billion before we find out, either get to a, you know, working fusion reactor, and find out it's not possible, but we do it. We spend the money because we think it's important to our species and the survival of our species.

: So, my counterargument is, I mean, these destroyers that ran into ships in the Sea of Japan, two of them in the past six months, those are billion-dollar ships. If we spend a billion dollars. Obesity and diabetes cost, the healthcare system in the US, the estimate is a billion dollars in direct medical costs in a day. If we spend one day's worth of medical cost, I think we could probably answer every one of these studies, but we have to be willing to do it, and we have to decide, as a society, that it's worth it, that epidemiologists and the public health people have to stop arguing that it's just too impractical, and it will never get done, and instead argue to do it.

: And, you know, if people decide, it's all doable. You could even do these studies in a way. If they've actually tried, they could. They know how studies have screwed up in the past. You could figure out ways to do it that will give you the answers. And then, you have to have patience to get the answers.

: You've taken a very public stand in, you know, what seems to be a somewhat heated debate. How do you strive to remain intellectually honest?

: Intellectually honest is easy. I mean, you just do it. Although, my critics would probably argue that I don't.

: Who is your harshest critic of your intellectual honesty?

: I don't know. I mean, there are some bloggers out there who've … I mean, they may be behind. Do you have bloggers who hate you?

: Oh, yeah. I get hate mail all the time.

: Yeah, that's sort of, you know. I mean, the blogosphere just selects for people who … And the more … I mean, there are websites that exist, in part, to argue that I'm an idiot. And the more fiercely they argue that, you know, the more hits they get. In the community, at large, I'm still fighting this tendency to just … You know, it's easier to just ignore me, or where you see shifts, you know, to pay … You don't really have to pay attention to my work because, you know, it's published in books. And it's only a few peer-reviewed articles in the literature. So, it's easier to just ignore me than to confront the arguments.

: And, again, one of the problems I feel with this field, nutrition epidemiology public health for 50 years, is they found it easier to just ignore skeptics, and to confront the issues, and see if the skeptics are right, and the critics are right, and what they have to do if it's possible to fix these problems. So, you know.

: But I do have friends. I have an e-mail. I'm having an e-mail exchange with the head of the Department of Nutrition at Tufts, and he sent me an article that was written by Tom Frieden, the former head of the CDC, that was in the New England Journal of Medicine arguing that observational epidemiologic studies often have to be the base of decisions about public health, and medical public health recommendations, and medical treatment. And we can't hold clinical trials on this pedestal we do because the observational studies are clearly good enough in some cases. And he sent me that just to say that this sort of brilliant article put his position in words better than he could.

: And so, I read the article. And I said, "Well, needless to say, I don't find it brilliant. And here are all the reasons why." And he responded with, "Well, you're cherry picking your data. You know, you're being intellectually dishonest." And it's an easy accusation to make. And if I have time, I will respond saying, "I'm not actually cherry picking my data. Look at the study you sent me. It doesn't actually make the point that you're using it to make. And I'm asking for evidence that does." So, it's sort of that kind of accusation is very easy to make.

: When you do what I do, I mean, it's a problem. You know, you've got a journalist coming along and condemning an entire field, several entire fields of research that are staffed by very smart people who have done very well in their careers, have gotten enormous amount of positive feedback, who believe they're doing good for the world. Any one of them could have gone into, you know, the commercial sector and made more money.

: I mean, these are really well-meaning people. And, you know, some journalists comes along, and says, "You know, missed it. You botched it. You did lousy science." Who's going to accept that? I mean, I couldn't do it. I can't expect them to do it. So, part of my job is to weather the criticism and just keep making the arguments as honestly as I can. And I do have one advantage that they don't have.

: What's that?

: So, you know, the implications are these chronic diseases are caused by the carbohydrates in the diet. And that's the context. And if you remove the carbs and replace it with fat, the chronic diseases won't go away, not for everybody, but for most people. So, this is, in effect, this argument that if, you know, people eat very low carb, high fat diets, the lowest carb, highest fat would be ketogenic, that's the extreme example, they'll get healthier.

: And the world is now full of people who have done that and gotten healthier. And if there's one thing that I and others like me in the tight shelves have been able to accomplish is we've broken down the resistance to these diets as, on some level, fads, but also as deadly. So, the medical community thought they were deadly. So, now, you've got a whole world of people, diabetic, obese individuals, people with neurological disorders, you know, who go on these diets, and they get healthy.

: And sure, you know, maybe they're raising their LDL cholesterol, and they're going to die earlier of heart disease, but this one woman put it in an Instagram post, you know, "I lost 100 pounds, and you're telling me that bacon is going to kill me. Like being 100 pounds lighter and eating bacon is worse than being the way I used to be." So, this sort of growing movement.

: And the physicians do this as well because they have the same health problems and issues as the rest of us. So, if they do and it works, they become passionate about it, and they put their patients on it, and their patients become passionate about it if it works. If it doesn't, you just lose them. And unfortunately, that sort of cognitive bias with what I'm describing. But you've got this movement that people would like to talk about. It's a field, but it's basically fueled as a fad, but it's fueled by this very profound clinical phenomena, the clinical efficacy of these diets to reverse diabetes, or reverse obesity, or you know. And that's hard to stop.

: I'm interviewing these practitioners for my next book, kind of, solipsistic exercise, but it's fascinating. And I was talking to a South African physician who's now working in British Columbia, who's just incredibly passionate about these low carb, high fat diet. And he communicates this to all his patients. And I said, "Why are you so passionate about it?" And he said, "It's because I can't unsee what I've seen. You know, I put that diabetic patient on this diet. I get them to follow. And this is a person, you know, he's on insulin, and overweight, and obese. The rest of his life, he eats the way he does, and the way the Diabetes Associations want them to eat. All we're doing is basically, you know, adding drugs and modulating his insulin injections. And you put him on this diet, and he becomes healthy."

: And that's a low carb, high fat diet?

: A low carb, high fat. And it's an easy diet because you're not hungry. It's not chewies in there. You're not getting deep doughnuts, and french fries, and cereal anymore. But he's replacing it with some pretty … So, that kind of clinical observation.

: You know, there's a startup in San Francisco called Birdhealth that's doing this on a sort of on a larger scale with smartphones, and health coaches, and doctors. And, you know, until recently people believe that even type 2 diabetes was irreversible. Once on insulin always on insulin basically, until you get taken down by the side effects. And, now, people are showing that on these diet, and maybe others as well, but they're showing that this is a reversible disease. It's a disease that can be controlled without drugs. So, that alone is going to change the discussion, and I could see it already happening.

: Do you think that the sugar industry will be eventually treated like akin to the tobacco industry in terms of how it's vilified?

: On some level, that's already happening and much of the sugar industry's dismay. It's funny, I did a NPR thing a few weeks ago with Michael Moss, the author of Sugar, Salt, Fat or Fat, Salt, Sugar, whatever it's called. And the president of the Sugar Association, a young woman, former college basketball player named Courtney Peterson … No, Courtney, I forget her last name.

: And, anyway, afterwards, I got it. Just yesterday, I got a nice card from Courtney thanking me for being on the show with her and discussing it. So, actually, it was really nice to do, but it's sort of like getting a nice card from the president of Tobacco Foundation. They are being vilified. They know it. They see the writing on the wall, you know, the soft drink industry, the purveyors of sugar rich foods.

: On one level, they know they have a product that's going to continue to sell. So, they're not going to get rid of it because people are going to continue to consume it. It's just like some, I don't know, I think, 17% of Americans still smoke. So, the percentage has come way down, but there's some people. Kids are going to start doing it just like kids are going to continue consuming sugary beverages.

: But they see the writing on the wall. They know where it's going, and they're diversifying. Like. man, you could see them diversifying. And, you know, they're in a bad position because, as I've argued in press, unlike the tobacco industry. So, the tobacco industry's job was to somehow try to convince the world that the research community was wrong, and to sow confusion about what the research community was saying.

: What the sugar industry had to do was remind the research community that what they believed in general was true of sugar, in particular. So, the obesity researchers were saying a calorie is a calorie is a calorie when it comes to obesity. And if that's true, then sugar is harmless. You can't vilify a food for being too good to eat.

: Yeah, yeah.

: You know, it's all about calories. And then, the nutritionists and cardiologists were saying dietary fat causes heart disease. So, the sugar industry paid nutritionists and cardiologists to write articles saying, "We believe dietary fat causes heart disease because they did." And then, they had to remind people that the conventional wisdom is a calorie is a calorie.

: So, you almost can't blame them. And I don't really blame them because had the nutritionists and the obesity researchers gotten it right, they would have put the sugar industry in a position where they had to change, rather than more all they had to do was argue that, "Hey, look, guys, we're harmless. The community says we're harmless. Don't blame us."

: But, now, again, you know, once you have epidemics of obesity and diabetes, and it's clearly not being caused by dietary fat consumption, and, you know, sugar is the likely cause whether it's just because people consume too much of it, whatever that means, or because it's toxic, and it's a different world. So, now, when they fight back, people point out how they're fighting back, even if their fighting back is only a delaying tactic to give them time to diversify.

: What practical tips would you offer somebody who wants to know like, "I want to do something about this. What's a step that I can take?"

: You mean about the epidemics in general or about-

: My health, my personal health.

: Okay. And it's interesting, that's what I've spent the last two months talking to researchers about. So, you know, I clearly think that of all the … So, the problem is the carbohydrate content in the diet. And I think the fat content for the most part is benign, if not healthful.

: And this is what I would tell my family, and my kids would tell you that I would tell it to them too much. So, worst of the carbohydrates is the sugars, and the worse of the sugars is the liquid sugars because we consume them and digest them so quickly. So, you get rid of sugary beverages, and ideally switch to non-sweetened beverages, which means, for the most part, water or red wine. And if you're going to drink it all day long, water's probably the better choice, or I'm a caffeine addict, so I'm fine with coffee whether I'm right or wrong.

: I just want to go back there for a second. Wine is okay?

: Wine is the one area or alcohol where I talk about where I think moderation is meaningful.

: Okay.

: So, you know, life … This is one of the lessons I came away from the sugar books. In what I'm doing, and particularly when I go on to sugar, there's clearly a Grinch Who Stole Christmas aspect to it. I'm taking away people's joy, or I'm suggesting that their joy is killing them, and they should get rid of it themselves. You know, it was my wife who like she sees part of her job in life to sort of squelch my Grinch-like tendencies. And she may be right.

: So, in doing the book, you know, one of the revelations was basically, like, the human existence is not all that great. It's getting better because television is getting better. But, you know, for the most part and for most people, it's hard, it's laborious, it's tiresome, and there isn't a lot of pots of gold at the end of the rainbow.

: And so, for the great bulk of humanity, intoxicants, something we can do to intoxicate us makes it worthwhile, gets us through the day. And, you know, that's what addictive substances do. That's why, you know, when I was a smoker, I looked forward to my next cigarette. That literally carried me through the day. With the caffeine addiction, by about 6:00 at night, I'm thinking about the first cup of coffee in the morning, and how good that's going to taste. We need intoxicants.

: The drugs of abuse, their side effects are too severe, and they occur too quickly for most people, and they create behavior that are also dangerous. You gotta have something. And if it's not, sugar. You know, a lot of us self-medicate with sugar. I mean, I'm depressed, I want a doughnut. Let's be serious. What do you do with that?

: And then, the question is, you know, there are people who can tolerate it. There are people who are relatively healthy, who are not, you know, pre-diabetic, or diabetic, or overweight, or obese; and aren't going to get metabolic syndrome; and can eat, you know, cupcakes twice a day their whole life, and be absolutely fine and happy. And I think, they're the luckiest people on earth.

: The problem is they don't know when they're eating the doughnuts. Like smokers don't know whether that cigarette is going to get lung cancer until it's too late. With sweets, you probably have time to reverse it with these strict diets.

: But all that said, I would get rid of sugar. And because I'm an ex-smoker, I could say that when I was a smoker, I couldn't imagine life without cigarettes. And cigarettes, like I said, I lived for my next cigarette on some fundamental level. And you smoked after everything. You know, after a meal, after a workout, after sex. Like most of us don't eat dessert or have a lollipop after sex, but smoking after sex, was like that's what you did. It just made your life worth living.

: And then, you give it up. For three months, you're miserable. For a year, you're unhappy. And you're hoping at the end of the year, you haven't lost all your friends because you overreact to everything because you have no cigarettes to, like, moderate your emotional responses. And then, after a couple three years, you get to the point you can't imagine why you ever smoked.

: So, you can give up sugar, I believe. And I've gotten there where it's like I don't need sugar to make my life worth living. And I think that can be true for most people. But maybe I'm just lucky that I have a particularly challenging, interesting life. So, that's the first thing. Second thing is high glycemic index, grains, starchy vegetables.

: What are the worst in terms of starchy vegetables?

: Well, it's hard to say. And I don't really know. You know, there are people who would say wheat is clearly the worst grain because of the gluten and these other issues. Bill Davis describes in Wheat Belly that starchy vegetables are fine, that sweet potatoes are fine, or if you only eat potatoes and nothing else, you'll be healthy, and lean, and happy. And I don't know if any of that is true.

: What's your take on gluten?

: I don't know. I really don't know. It would be … The way I think is, I mean, I know a lot of people have gone gluten-free. People used to sort of make fun of my low carb lifestyle who are now gluten-free and proud of it, talk about it too much. But when they give up gluten, they end up giving up most carbs.

: Right.

: And then, you find out, they've given … You know, in Wheat Belly, where it recommends Grain Brain. They say give up wheat because of gluten. That's the prime problem, but don't eat sugar either. And other starches can be problematic because they stimulate insulin secretion. So, people who go gluten-free. So there are clearly people who get healthier, and there are clearly people who have gluten-related disorders, who when they don't eat gluten don't have those disorders. It's that simple. And that's supposedly about 5% of the population, if I'm remembering correctly.

: But the these other people, have this sort of general issues. I don't know if they're getting better because they're giving up gluten, or giving up all carbs, or giving up sugar with the gluten or-

: Well, often, when you give up gluten, you give up a whole bunch of packaged foods. I mean, your food selection just totally changes.

: Yeah. Basically, you have to give up many processed foods.

: Yeah.

: So, it wouldn't be an easy experiment to do. That's the fascinating thing. And I know one very high level self-experimenter who did this who said he basically gave up wheat. 400 calories a day of wheat, and replaced it with 400 calories and rice, and got healthier. And I believe in his case, he did. So, the question is, what makes it a relatively easy nutrition experiment to do is you just have to replace gluten-rich foods with gluten-free versions of them.

: So, say, 400k one, you take their thousand subjects, and 500 get, you know, regular wheat bread. And they're supposed to eat four slices a day, and the other get gluten-free bread, and they're supposed to eat four slices a day. And those are the only sources of gluten. And then, you run it out for a few years, and you see-

: The effect on the-

: The effect. So, you're not having to worry about it. One of the big problems with nutrition studies, if I want to study sugar, if I'm going to remove that 18% of our calories that come from sugar, I have to replace it with something. Do I replace it? I can't replace with diet soda because, then, I'm not getting the calories that the sugar has. I could replace with glucose, so I could replace it, you know, with starch. I can replace it with fat, I replace with protein. All of those will have a different effect, and you won't know if any benefit or detriment you see is caused by the absence of the sugar or the presence of whatever you replace it with. But gluten would be easy to do the study if anybody wanted to, just at which point I would have more confidence that I know what to believe.

: Talk to me about fasting.

: Fasting is another way to approach metabolic disorder that's come on the scene in the last three or four years driven by British clinician named Michael Mosley, and Jason Fung, a nephrologist in Toronto, and Valter Longo, I think, at UCLA. So, you know, it's interesting. The idea used to be if you're obese, breakfast was the most important meal of the day. The reason breakfast was the most important meal of the day was one of these typical sort of simplistic nutrition obesity thinking.

: So, obesity researchers noticed that obese individuals tended to skip breakfast, and have most of their calories from early afternoon on into the evening. And they decided that if they skipped breakfast, and they're obese, maybe they're obese because they are skipping breakfast; and therefore, they should eat breakfast. So, we should all eat breakfast, mistaking an association for a causality and never really testing it.

: So, somewhere along the line, and I have to read Jason Fung's work more closely. or Michael Moseley's, people start saying, "What if you actually do skip meals?" So, the idea mind that carbohydrate insulin hypothesis is that as long as you're keeping insulin levels low, you're mobilizing fat, using it for fuel. So, you're actually getting fat out of your fat tissue, which is literally what you want to do when you want to lose weight, and you're burning that fat for fuel.

: So, if you extend the periods, you know, in the morning before breakfast, when you're fasting, that's when your insulin levels are lowest. And the reason you don't get up every three or four hours to eat during the night or every two hours is because your insulin levels have dropped, and you're living off the fat you stored. You're burning fatty acids for fuel at night. So, the idea is as long as you haven't eaten in the morning, your insulin will stay low. You'll continue to burn fat. You can extend the period between meals, and you'll burn more fat, you know, and it's got to be the fat that you've stored because you're not eating anything.

: So, I don't know if that was the original logic. That's why I think it could work. But people found out that if they, you know, extend the period between meals from like 12 hours to, say, 18. So, you have dinner at 7:00 at night, you don't have any snack that night, you skip breakfast the next morning, and your first meal is at lunch at noon or 1:00, you might accelerate fat burning, to use a cliche. And it might not be that hard to do because as long as your insulin is low, you're going to be mobilizing fat and burning it.

: And it does turn out to be relatively easy for people to do. And then, some people, particularly Jason Fung, have realized that, you know, not only can people on low carb diets pretty easily do 18 hour fast, they could actually pretty easily do three-day fast or even three-week fast. And, now, you know, whatever I mean by pretty easily is totally relative.

: And this is a way to get diabetes under control to sort of rest the pancreas, so that when it does start dealing with food again, it's may be restocked. Some of them may have given the beta cells to create insulin time to, you know, get their biological act together. There's a lot of things we don't know, and a lot of things I would like to see clinical trials to document.

: But, again, talking to these practitioners, clearly, a lot of them are embracing intermittent fasting as a way to get people, you know, who go on low carb diets, and they tend to lose a lot of weight to begin with, but then they plateau. You can use intermittent fasting or longer fasting as a way to break through plateaus or to accelerate fat burning. I worry that it's a fad, and that it will turn out that it's harder, you know, that people just get bored of doing it after a while. And if they get bored and go back to the way they used to eat, they're likely to go back to being obese and/or diabetic.

: Right.

: But there's no way to tell. I've actually been experimenting with it myself recently because just I've been talking to people about it so much, and it is remarkably easy. Yeah, I'm surprised at how easy it is to skip breakfast. And I was just going to say it's 12:40 here in California, and I haven't eaten since dinner last night, and I'm clearly energized talking to you.

: That has more to do with me though, right?

: It does, it does. And, also, that I clearly like talking about this stuff some of it is interesting.

: You've written about the history of nutritional sciences, the alternative hypotheses of obesity, and why we get fat, about the harms of sugar, what's the next thing you're writing about?

: Well, I have to write … Again, I'm interviewing practitioners around the world who, you know, have transitioned to using low carb, high fat, or paleo diets to prescribe to their patients for obesity, or diabetes, or other disorders. So, that's going to become a book; although, I have no idea, at the moment, how I'm going to write it. It's been fascinating talking to these people.

: And I would also like to, if there are any listeners, I would like to talk to doctors who are prescribing being in a vegetarian diet now or Mediterranean diet to try and understand what they're seeing with their patients, and the feedback they're getting, and try to take care of the sort of selection bias of, you know, me interviewing people who follow my Twitter feed, that kind of stuff.

: How can they get a hold of you after lunch?

: My website. GATaubes@gmail.com. I don't understand Twitter enough to know when people tweet at me. I don't see how people have time in their lives to pay attention to Twitter feeds or Facebook, even though I do tweet.

: I would like to write a book, and you and I have talked about this, about how science should be done, sort of, functional trench science. So, there's a lot of books and a lot of courses on the philosophy of science over the millennia, literally. And they're fascinating, but all my books have been about this sort of idea that Richard Feynman capsulized what he said, the first principle of science is you must not fool yourself into the easiest person to fool. And I think we've gotten away from that. The incentives of science today are about, "Hey, fool yourself if you can fool other people and get funding," all that's, you know, that-

: Yeah, it's so much about that.

: To live in facetious way to phrase it, but you know. So, a lot of it is about the kinds of learning to recognize or being aware of the kind of cognitive biases that your blog posts are discussing, and how they manifest in science and scientific experiments.

: And when I did my first book. So, I lived at CERN for ten months back in 1984-'85, and I was embedded with these physicists who discovered nonexistent elementary particles, and then had to realize how they had screwed up. And that became my obsession, this question of how easy it is to get the wrong answer in science, and how hard is to do it right. And that's the book I wanna write and interview, you know, experimental scientists who have thought about these issues their whole career. Theorists are a different species entirely, but, you know.

: And from them, and the history, and the literature, I'm reading memoirs of scientists now, and, you know, how you have to think and how you have to approach this because I think a lot of the problems with modern science, when people talk about the reproducibility crisis, I think we're kind of putting band aids on the fundamental problem, which is that the research community really doesn't get the mentoring that they need to truly understand the nature of this scientific endeavor, and what it takes to get the right answer, and how you have to act and communicate steps along the way. So, that's the book I want to write.

: Well, if it's half as good as the books you've already written, it's going to be phenomenal, and I look forward to reading it. Listen, Gary, this has been an excellent conversation. I want to thank you so much for taking the time.

: Well, thank you, Shane. You know, I'm a fan of your website, and one of the few newsletters I still look forward to receiving.

: That's generous of you. Thank you.

: Hey, guys. This is Shane again. Just a few more things before we wrap up. You can find show notes at FarnamStreetBlog.com/podcast. That's F-A-R-N-A-M-S-T-R-E-E-T-B-L-O-G dot com slash podcast. You can also find information there on how to get a transcript. And if you'd like to receive a weekly email from me filled with all sorts of brain food, go to FarnamStreetBlog.com/newsletter. This is all the good stuff I found on the web that week that I've read and shared with close friends, books I'm reading, and so much more. Thank you for listening.

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