Welcome to the Knowledge Project, I'm your host, Shane Parrish, the curator behind the Furnham 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 Tub's 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 of 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 OK. His next book project and so much more. I hope you enjoy this conversation as much as I did.

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Gary, I'm so happy to have you on the knowledge project. I'm 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 I 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 replace them for the most part with 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 have convinced myself that butter and bacon are health foods, and I hope I'm right.

Why do you 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 has said to me almost not a functional science, but I've never had the opportunity to put that effort, investigation into other areas of medicine or other areas of science who just hope they're better. My take on this is sort of historical.

And I'm going to the way I see it, science is sort of home to a very fine edge as a methodology for establishing reliable knowledge of the universe in Europe. It's by, you know, was at its height in Germany and Austria, pre World War two.

And the sort of these people really understood the rigour 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, a fool.

And this culture of science began to evaporate with World War Two, and it crossed the Atlantic in fields like physics, because we embrace these European researchers, many of whom were Jews and the leading scientists in the world, the leading physicists in the world, post-World War Two in the US tended to be these European emigres or 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 hypothesis and test, the tests were relatively simple, relatively simple to do. You could come up with an idea. You could build a small, you know, a 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 hypothesis and test and in fields like nutrition and public health, not only did we not embrace these 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, much harder to do. So now, instead of dealing with subatomic particles or every particle, for all intents and purposes is alike.

And you can do these experiments in days. You're now dealing with these messy humans who think for themselves and chronic diseases that take decades to manifest themselves. And you can no longer, even if you could do the testing of the hypotheses it takes a long time to do. It's very expensive and it's very difficult, if not impossible, to do it right. And so with 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 by they say the issues are so important, people are dying out there. Therefore, we don't have time. To dot the I's and cross the T's and make sure that we're right about our hypotheses. And to me, the really scientific response is what?

We don't have time to dot the I's and cross the T's who have no idea whether you're right. Right. And we end up in a situation today where we have 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 it was 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 obesity and diabetes epidemics?

Yeah, or an obese. I think clearly genetics. Well, we know that obesity runs in families and that's been known for the body type runs in families. Identical twins don't just have the same facial features, they have the same body types. Clearly, genetics plays a huge role and whether 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 on 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 world wide, independent of the genetics of the genotype, the genetic ancestry of the population. So in you, it's near the Arctic Circle where Native Americans are First Nations people or 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. It doesn't matter what type of human, you know, where you or your ancestors came from the get dumped in a modern Western lifestyle, you're likely to become obese and diabetic. And so the question I was asking in my book is, what's the what's 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 our 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, in India with diet.

Like if you took the influence and gave them a 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 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 the really important issue, the critical issue is these epidemics and the numbers are just out of I'm almost unimaginable in the US.

And according to the Centers for Disease Control in the US, since the late 1950s, diabetes prevalence has increased seven hundred percent. So one in 11 Americans now had diabetes when the number might have been closer to one in a thousand and one in three thousand at the beginning of the 20th century. That's almost incomprehensible. And nobody really I mean, the fact that there aren't teams of investigative scientists and task force on every street corner walking around with, you know, I don't know, detectors of some sort are 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 orange just diet to reduce risk of heart disease when the very first thing you want to know is like what's 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 Academies of Medicine in Washington. And she gave a number, a prediction for the likelihood that public health organizations will prevent the slowmotion disasters from getting worse. And the likelihood of even making preventing them from getting worse, she said, was virtually zero.

So you've got these 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 you can further ask the question is there's something about the Mediterranean diet or about the French diet or about the blue zone diet that happens to shed light on this question of what's 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?

OK, 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, it's it's like I said, it's obesity and diabetes epidemics showing up everywhere in the world after they transition to a Western diet. So that's that's that's the crime. That's what we want. We want to find out who the perpetrator is. We know what the aid and what the the vector is. The vector is the Western diet and lifestyle.

You know, it's commercialism and urbanism and and maybe it's processed foods. These are all sort of vectors of the disease. But what the agent in the vector and the point I make in my book is you can chart these go back in time. And actually what you would do if again, if was a criminal case, you would you would want to know when the crime was committed, when at the earliest sign of the crime and until you could do this using hospital records and the medical literature.

And you find out, for instance, in the US that diabetes rates in you are virtually nonexistent, 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 1870. And then the numbers in hospitals and you could see this in hospital records. And in Boston, a mass general in Philadelphia, Pennsylvania hospital, the diabetes diagnoses and hospitals go from like literally zero a year.

Remember to day one in 11, Americans were considered to have diabetes and their major, 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 and double digits. And then they just shoot up from there. And you could find experts. Back then, the head of the New York City Department of Public Health saying it just it tracked 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 the industries that are involved in that period and sugar over the course of the 19th century went from being a sort of expensive luxury and 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, consuming the neighborhood of 80 or 90 pounds per person per year or so.

You the neighborhood of a 20 fold increase. And in all the ways that we consume sugar today, we're virtually non-existent to industries in the early 19th century. So in the eighteen forties you've got the candy industry has created, the chocolate industry is created in the ice cream industry are all created. And then in the eighteen, seventies and eighties 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, that sugar purveyors that we deal with today are already sort of in place and selling nationally. And Mark. Getting national and, you know, sort of pioneering their marketing approaches at one point in Brown ninety five, a congressman asked the brother of I think it was one of the founders of one of the main players in Coca-Cola. And what if he could describe the items on which Coca-Cola was advertised?

And he said the everyday items and he said it would be easier to describe the items on which it's not.

So 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 the easy access to Coca-Cola and is drinking it regularly. And at one point, the CEO of Coca-Cola even complained that the human body needs so many ounces of water liquid a day, and only like 20 percent of it is coming from Coca-Cola. And that's just completely unacceptable.

So anyway, you see, these are 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 to. The fruit juice industry doesn't really show up until the 1930s and then explodes post-World War Two and the cereal industry, Syria was basically Kellogg and Post and those folks were health fanatics and they were running sanitariums in Minnesota for dyspeptic wealthy people. And they 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 who don't want people eating sugar. But post World War Two, right around nineteen forty eight post with anything with sugar. Chris finally breaks down the barrier and start selling us 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 want.

And by the 1960s, the American Breakfast had been transformed into a basically a dessert with fiber. Yeah, for lack of a better word, drink and fruit juices were eating sugar coated cereals. And then when the low fat movement comes in in the 1960s, you're adding sort of low fat or no fat yogurt with sugar and skim milk and sugar from beginning to end so that people, while this was happening, are doing, look, obesity and diabetes is exploding.

Sugar consumption is exploding. Clearly, that's the prime suspect. And then there's as we began to understand the physiology of how sugars metabolize, that clearly made sugar a prime suspect as well. And, you know, in actually causing type two diabetes and a condition called insulin resistance that we should probably talk about.

So why don't you walk me through the physiology of sugar, OK? The response it generates in our body.

So when we're talking about added sugars, particularly sucrose, which the white powdered stuff and high fructose corn syrup, these are simple carbohydrates that are combinations of two simpler carbs. So glucose, which is the car when we consume grains and the starchy vegetables like potatoes are broken down in our body into glucose and the glucose is transported into the bloodstream and blood.

When we talk about blood sugar, we're talking about glucose, blood glucose. So the glucose gets in 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 glycaemic 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's easy to digest like white bread, you will have a quick rise in blood sugar. And it's one reason why white bread was usually considered sort of the standard by which you would then compare other foods to and the glycemic index. But there's another half of the sugar molecule, or in the case of high fructose corn syrup, another fifty five percent of it, which is this molecule fructose.

So any molecule that I say is a carbohydrate. So fructose is the sweetest of the carbohydrate. So it's what makes sugar sweet. But the fructose is metabolized not by every cell in our body. It's transported to the. To our liver and some huge proportion of it is metabolized by liver cells, and this stuff was worked out by biochemist back in the early in 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 a cause of diabetes, the 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 nineteen twenties, it's easy to 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, all sugar must be good for you. That's how they thought you could see this in the literature.

But physiology. So when we're talking about diabetes, we're talking about a particularly Type two diabetes, which is the common form that associates with obesity and age.

So when I'm 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 one, or that typically appears in childhood, which is type one. That's about five percent of all diabetes. And then type two, there are variations now, but for type two is effectively about 95 percent of diabetes. And we're talking about the diabetes epidemic. It's type two diabetes we're talking about. And because it associate so closely with excess weight, the assumption of the diabetes experts going back to the nineteen twenty says it's caused by being fat and you get fat because 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 two diabetes was a disorder or what's called insulin resistance. So with Type one diabetes, you don't have enough insulin or no insulin at all and you can't properly metabolize the carbohydrate to 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 with Type two diabetes.

And the assumption was all diabetes was the sort of insulin deficit until the 1960s when they could really measure insulin levels in the blood stream in the research community, realize that type two diabetics actually have both high insulin and high blood sugar. So the insulin must not be working. So they're are 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 two diabetes is the disease of insulin resistance.

And then this one, along with the observation that obese people also tended to be insulin resistant. They had high blood sugar and high insulin levels. And that was a condition that's now known as metabolic syndrome, which is a cluster of abnormalities that sort of basically insulin resistance syndrome. So this is elevated blood sugar with glucose intolerance. It's called it. It's also 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 in your blood pressure, is elevated. So 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 resistance conditions, then you're asking the question, whatever causes insulin resistance causes obesity, diabetes, high blood pressure, heart disease, stroke, cancer, Alzheimer's.

Virtually every chronic disease has a link to insulin resistance. And the best research on what causes some 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 not what's called non-alcoholic fatty liver and associated with obesity and diabetes and metabolic syndrome. So everything is targeting the liver and then 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 then evolved to metabolize at the levels we see today. So throughout the last two million years, you can only see sugar and small quantities and fruit. That's what makes fructose in small quantities, is what makes fruit sweeter than you'd see it in smaller quantities and green vegetables. But nothing like the amount you would see in a Coca-Cola 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 pretty clearly worked out. And when you dumped fructose on the liver, it converts it to fat. And on the other side, you have these insulin resistance researchers saying, hey, insulin resistance seems to be caused by the accumulation of fat and liver cells. And all I'm saying is know you've got one hundred and fifty years of history of people saying when diabetes appears, it does so after sugar consumption goes up. And then you've got this all these biological mechanisms suggesting that sugar is literally at the scene of the crime in the human body.

When insulin resistance begin, someone insulin resistance begins that, you know, you're on the road to this whole slew of chronic disorders that are now becoming epidemic or already epidemic.

Why are we so attracted to sugar? A good question. 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. So on one level, the idea is we become addicted foods because it's an area of our brain called the nucleus accumbens. The reward center that rewards is there to reward behaviors that are good for the species. So when you have an orgasm during sex, you've the nucleus accumbens responds by like dosing your body with dopamine.

And that feels great and you want to repeat it. And when you eat foods, which we have to do to foods that taste good, also stimulate a dopamine response in the nucleus accumbens. We 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. Over the course of human history, we sample 10 million leaves, twigs, starches, food, animals.

And lo and behold, there's a few things that happen to sort of overstimulate the nucleus accumbens and overstimulate dopamine. And then those become addictive substances that we then want to repeat and repeat and repeat. And so there is evidence that sugar stimulates dopamine, secretion the nucleus accumbens, just like these other drugs of abuse. And in animals, at least some rats and mice, we could do these experiments. You could demonstrate that they are now there will be more addicted to sugar than to cocaine or heroin.

So these experiments, some of them were done in France are sort of perversely fascinating. You basically addict 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 and came out. And, yeah, over the course of a couple of days, the rattle switch from sugar to from cocaine to sugar takes a little longer before making the switch.

That's from heroin. Yeah. I mean, clearly, you can't do these experiments with children, but if you have kids, you probably don't need to be. So there's a lot of you know, clearly sugar is a psychoactive substance. We give it to newborns to when they get circumcisions, a couple of drops of sugar water on the tongue and you can remove the foreskin and it doesn't bother them, or at least not in the short run. You know, sugar has always been considered a pain killer and it actually entered Europe in the 13th, 14th century or 12th post crusades more as a medicinal and perceived as having medicinal uses than as a food or spice.

But in my best my favorite thing on this is from Charles Mann, the journalist historian who's a friend of mine, and somebody who just asked me with how good his work is. And he said in his book, fourteen ninety three, he was discussing the sugar industry. And he said scientists today debate amongst themselves whether or not sugar is an addictive substance, that we just act like it is. And it's 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 in the historians and journalists would say, well, of course, parents don't have duration their children's behavior. I mean, their sugar eating it can't allow them to eat all the sugar they want. So there's clearly, you know, whether it's affecting in the nucleus accumbens or there's an interesting effect that might drive sugar consumption in also in the liver to a little more technical.

But I've always wondered how much role that played. 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. But, 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?

But no, this is this was this is the most common thing I read.

So when I started my research, journalistic research on this subject. And if you go back to 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. I said I was speculating that dietary fat doesn't make people fat and it's carbohydrates that do. But still, I had a line or two clearly at Texas, calories that cause us too much.

And then I actually 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 to like a new technology had come along. And suddenly I can 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 going back to the 19th century.

And I mean, back then, nowadays, you can virtually download a month back then, 2002 to 2006, you could I had students all around the country whose job was to go to their local medical libraries and make copies of the 50 or one hundred references I would send to them and then I would buy books. So I actually started doing my research and I realized that this this idea that excess calories is what makes us fat is and I'm embarrassed that I ever, never thought of this as logically equivalent to saying excess money makes us rich or I don't know, scoring excess points in a football game will make you win.

You know, it's just it's almost unbelievable, incomprehensibly naive to me. And I now understand where it comes from because I've read all this literature and I to this day, I'm still sort of mystified. So I'm going to pet peeve time. My sugar book came out. I got sort of almost universally wonderful reviews. And then Jerome Groopman in The New Yorker sort of condescendingly dismissed the book as the work of a sort of wannabe investigative journalist. And in his review, he makes a statement that the one undeniable fact about nutrition research is the importance of calories and excess calories makes you fat.

And I thought this was a James Surowiecki writing about economics. And he said the one undeniable factor and the science of wealth is about the importance of dollars. You know, the David Remnick or one of his crew would say to you out of here, are you kidding? Are you out of your mind? Like, what if of course, you know, if I mean, if I think we were discussing wealth accumulation. I just kept telling you.

You said, Gary, why is it let's talk about why why is Bill Gates so rich? And I said, well, because he makes more money than he spends. You know, you'd be going on, why did I book this guy? And if we were talking about climate change, said, why is the atmosphere heating up, assuming it's heating up, which I begin to believe since we just had one hundred degree weather here and opened a couple of weeks ago.

And I said, well, clearly the atmosphere was 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, that and greenhouse gases and the wavelengths of light, they reflect or transmit. And I mean, the all the intricacies of climate change science would be nullified by this statement that the atmosphere is heating up because taking more energy than it's letting out, which it has to be doing.

So the point is back. Nutrition science from eighteen sixty to the nineteen twenties was completely dominated by, as all sciences are, by what they could measure the technologies available to make observations and all they had when they had devices called calorimeter, where they could measure the energy content of a food, and then they can measure the energy expended by humans by putting them in these room sized calorimeter or dogs. And then they had they could do experiments with animals where you give them vitamin mineral deficiencies and see what kind of diseases manifest.

So from there, so all of nutrition science was calorimeter energy in and energy out and vitamins and minerals. And when people started talking about what the cause 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 five dollar 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 likely 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 Shakespeares, you know, their guns. Even if they're not, you pay attention to them. You'll notice them when they are and when they see an obese person sitting at a restaurant eating a tiny salad.

You don't think it doesn't cross your consciousness is refuting your belief that they're gluttons. So it seemed to go along with what seemed to be conventional wisdom, and 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 and the German and Austrian clinicians in Germany and Austria was 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.

So metabolism, genetics and technology, the science of hormones, nutrition, all sort of came out of Germany and Austria. This hare professor doctor 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, just had to be because there are all these manifestations of it's sort of a hormonal regulatory disorder. You know, they would say things like, look, men and women fat differently.

Therefore, sex hormones are involved with obesity. 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 one diabetic. So insulin must play a role in storing body fat. We know that there are tumour's fatty tumors called Pomers that are independent of how much the people are eating and exercising. If you have a lipoma, it starves 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 has got no body fat on it. If you look at the back of your hand, it's a place we just don't store tend to store body fat.

And the other hand, I have this huge stuff, the 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 maybe 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 and end up in one of the great endocrinologists from the University of Vienna, ends up living in Los Angeles, writing articles and working for the hospital 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 glom onto this idea that it's all about how much you eat and exercise in a lot of lean research. They don't want to read the German literature anymore. So the lingua franca of medicine, pre World War two was German, but post-World War. We have a lot of young German doctors and I mean, excuse me, young American researchers who had fought in the war who have just after nine, they justifiably have this natural antipathy to the Germans and Austrians are not going to read the literature.

They don't cite the pre World War Two 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 to 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, 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 phenomena from cornerman and it never went away.

And even today and the great themes in obesity researcher, this idea that the obesity is caused by highly palatable or rewarding foods. And the implication is there's something about the brains of obese people that can't control their appetite in the onslaught of all the, you know, the bliss point created by salt, fat, and 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 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 if 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's sort of partitioning the fuel used to say, look, that 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 coming up, you just switch over from burning glucose to burning fat. Your cells should be perfectly happy to do that. But if you're insulin resistance, 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. That's all you do. So that's the, again, long winded way to say it. As long as people believe about it's about calories, you're not even paying attention to the hormones and enzymes. So regulate fat accumulation. And what stuns me so that last February there's an article in the New England Journal on the pathogenesis and mechanism's obesity. And you can read that article. And it's sort of 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 that's 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 Principles of Medicine, I think it's called in the Chapter on Obesity, is written by the very, very smart researcher named Jeff Flyer, who just until recently was dean of Harvard Medical School, and his wife was equally smart and talented emeritus flyer.

And they do research together. And if you actually look for what it is that causes obesity, they just in that chapter on 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'm 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 on the very beautiful system worked out by millions of years to regulate this?

And it's clearly dysregulated.

One thing I haven't heard you mention that I'm curious about is what is the role of fiber?

It's a very good question. And again, it's interesting. I have to talk about these things historically and I apologize. I think about, oh, this is amazing to understand the role, we have to know where it came from. So in the 1960s, several British researchers started 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's the leading British nutritionist, and the one is a fellow named Peter Kleve, who was a British naval researcher.

And Kleve 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, westernised urban centers have high rates of obesity and diabetes and heart disease. But, you know, less westernised areas and non urban areas had low rates. So the question is, what was driving? Then he concluded it was the refinement of the grains we were consuming, including sugar.

And so by the 1960s, Clevedon Yudkin was published in the medical journals and Cleve had written the book called The Saccharine Disease, explaining that it was refined grains and sugars that caused this cluster of diseases. And then into this walk's a guy named Denis Burkitt, who was a missionary physician in Africa in Forget Where was Idi Amin, Uganda. And Birket was famous for medical investigation. He did. That led to the identification of the first virus that causes the cancer that's known as Burkitt's lymphoma after Birket.

So he was a very well known, very famous physician. And Idi Amin comes into power in Uganda and has to flee back to the UK. And he's looking for things to do. And the leading British epidemiologist in the world, a guy named Sir Richard Doll, who is famous for identifying cigarettes as the cause of lung cancer. Richard Dog, some Clèves 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 Birket 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 with being a Brit, with constipation, completely obsessed with constipation. So he decides that the problem isn't the presence of the sugar and the white bread and the beer. It's the refinement of the fibre, the absence of the fibre. When you refine these products. So you take wheat and you refine it into a white bread, you get rid of all the fibre in the process.

And that's how he knows that fibre helps with constipation. And constipation is a disease that's often seen with needs, along with this cluster of Western diseases. So by the 1970s, Birket started saying publishing articles with another former missionary physician from Africa and a new trial, saying the problem is the absence of fibre, not the presence of sugar and highly refined high glycemic index grains. And you can reconcile this fibre hypothesis with the dietary fat idea that's growing along through the 60s as well.

So over the course of the 1960s, the bulk of the heart disease nutrition community had decided dietary fat caused heart disease and it caused heart disease that also caused obesity. And then you had Klebb saying, no, no, no, it's not that Cleavon Yudkin saying it's not dietary fat, it's sugar and refined grains. And these were seen as competing hypotheses that couldn't be resolved. In part, if 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 Burkett comes along and says, no, no, no, it's not the sugar and refined grains, 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 brand muffin craze appears like bran muffins start appearing on the market a year after Burkett'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 and they're very hard to test. But by the early 2000s, it was pretty clear that both these hypotheses couldn't be confirmed. An experiment. In fact, one of the things I talked to I talked to Richard Dolf a few years before he died from my research. And Dahl said to me, yeah, yeah, it turns out the only thing fiber actually cures is constipation.

And I said, what could Cleave have been right all along? And he said, Yeah, that's a good point. Cliff really hit on something. And all I did in my books is say, hey, looks like Cleveland Yadkin. We're probably right all along or more right. Than a few other peoples to like Atkins. But so that's a story I don't fibre. 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 absorb new things.

So the obesity, diabetes science has completely botched. You know, they've made no progress. They can't explain. And even harder. It was recently a review, an Immigrant Science Society review of obesity written by some of the leading figures in the field. It was kind of a response to my work and that of others in which they said, clearly, obesity is caused by eating excess calories in 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 loss is because they just the revolution in endocrinology was obesity research nullified that passed it by, never took advantage of and that was nineteen sixty zero science. So then obesity becomes a kind of real science to the medical community in nineteen ninety three when the hormone left then is discovered and it becomes a subdiscipline of molecular biology and then genomics and proteomics. But this 1960s era endocrinology which kind of solved it, is 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 can't we don't know what caused that or prevents it. So the gut biome explodes and people say, well, clearly Westerners who are obese and diabetic have different gut biomes. Then, you know, Hunter-Gatherer populations in Africa, what's the difference?

Well, the hunter gatherers eat more fiber. I don't know. So then you get this focus goes back on fiber. And then there are people like me saying, wait a minute, what about this 1960s endocrinology? Remember that? So that's I don't to me, I'm afraid of what happened in the 1970s. You add fiber, you can slow down the digestion of the carbohydrates. You can even slow down the digestion of the sugars. So that will 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 your alternative hypothesis, I guess, of obesity, that carbohydrates promote insulin response, which promotes body fat? I mean, what surprised you the most about you?

You do? Well, I mean, again, when I started this, I thought that calorie that excess calories cause 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 it's just that I'm not convinced it's wrong? Yeah. Um, put simply. And, uh.

Not substantially, no. I mean, there is so we could tell one of the things I did know this in the course of this as I co-founded this, some not for profit called the nutrition scientist. Yeah, yeah. We call Nusi. Could be Nusi, I guess so. Nusi. I co-founded it with Dr. Peter Teo, the very talented physician with also a business background. And our assumption was, particularly with this energy balance, that she was obese, had an energy balance issue, or is it a hormonal regulatory issue?

And that the implication is, is the the 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 I shouldn't have to even you shouldn't have to do the experiments to demonstrate it, because the you know, I find the energy balance thing now so naive, but except that I just talked about it too much. I've convinced myself that it's easy to see the naivete.

So we thought if we can get the research community to do the experiments themselves and to understand the competing hypotheses and to understand 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 scientist and particularly the sort of critical, rigorous back and forth between scientists where they're attacking each other's ideas and and being used by each other to understand how they might be fooling themselves.

I'm Robert Merton. The philosopher of science said that this kind of critical back and forth and science is makes some mothers, you know, parenting of her child looked like child's play in comparison. You know, they're supposed to be sort of Francis Crick said a functioning collaboration doesn't work unless you can be rude to each other.

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 in one place from 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 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 your experiment almost impossible. And again, if you're working in a world where, like, you could do your cyclotron experiment on Monday, have results on Wednesday, and have your colleagues explain what you screwed up on on Friday and then you could repeat it on Monday.

This isn't a huge problem and it's the history of science is full of those kinds of examples and discussions. And but if you're working in a world where the experiment cost you five million bucks. Yeah. And you're never going to get five million dollars to do it again. It's so tough. Yeah, that's that's difficult. And so my and same kind of problems come up. It's not like the physicists are any better at this than the nutritionists, because if you're doing something new, it's never been done before.

You have no idea how your equipment or your subjects or they are the purveyors of your diets or whatever are going to screw it up. You can't plan for everything. But the so that the part of my revelation was on this micro level, how. Not just how easily the science could be derailed by just bad luck or unforeseen, what was it? 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 how naive was I and will we ever solve these problems?

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

How does this get fixed? Well, that's that's the question. The I'm involved now. I'm supposed to be coauthoring an article with the for the British Medical Journal on Nutrition Policy. They're running a series on nutrition policy. So one of the articles on dietary fat. And I'm honored that they think it 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 ten years since I wrote the 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 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 the 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 and mostly animal fats with vegetable oils that are relatively new to the human diet and particularly like soy oil and canola oil and corn oil.

And the argument I've been making in the emails, not successfully, is that if you're going what you're assuming is that these vegetable oils are inherently healthy and they're beneficial. They're the equivalent of statins. 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 with that 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 percent of the people are going to live longer if we find out that 20 percent 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 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 or is a small chance you'll become diabetic or you have muscle aches, in which case will 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 one out of 30 of the population gets diabetes because the other twenty nine might live longer. So these are two entirely different scenarios. And if the vegetable oils are supposed to be beneficial, we should 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're and you're telling me that if I cook my son's 11 year old son's salmon in canola oil instead of butter, they will live long, or my 11 year old son will live longer and there will be no negative consequences.

I need to know you have 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, soy 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 one hundred million dollars. You're asking what you need to testees is maybe forty thousand people that you can randomized to either canola oil or butter or soy 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 hardpoint, some more heart disease or less, not just risk factors like cholesterol levels, but they actually get more heart disease, more cancers, more diabetes. They have me. Or 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 the butter. And the people we put on butter are going to get health conscious, which to 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 my let me just give you my counter, the counter, which is in physics, the physicists have decided en masse that they want to know they wanted to know whether the Higgs boson existed and they want to know if there's science behind the standard model. And the only the best way they know how to do that is to build a huge accelerator which cost ten billion dollars, and then it costs a billion dollars a year to run.

So they did that and the society funded we funded that because society thinks that's an important question and more a better society if we spend money trying to answer that than if we don't. And then they have collaboration's of fifteen hundred scientists on four detectors on this huge atom smasher. Fifteen hundred 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 when 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 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. It's hard to achieve.

And so far we've spent fifty billion dollars on nuclear fusion research worldwide. It'll probably cost another 50 billion before we find out either get to a working fusion reaction reactor, 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 counter argument 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 health care system in the US, the estimate is a billion dollars in direct medical costs day. If we spend one day's worth of medical costs, I think we could probably answer every one of these studies. But we have to be willing to do what 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 argued to do it.

And, you know, if people decide it's all doable, you could even do these studies in a way, if they actually tried, they could. They know how studies have screwed up in the past. You could figure out ways to do it that don't give me the answers and then you have to have patience to get the answers.

You've taken a very public stand in what seems to be a somewhat heated debate.

How do you strive to remain intellectually honest, intellectually honest, as you just I mean, you just do what I tell my critics would probably argue that I don't lose your harshest critics city, that your intellectual honesty.

I, I mean, there's some bloggers out there who I mean, there may be bloggers who hate you.

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

I 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 they know the more fiercely they argue that the the more hits they get are the in the community at large. That I'm still fighting this tendency to just it's easier to just ignore me or where you see shifts to, you know, if you don't really have to pay attention to my work because it's it's published in books and it's only a few peer reviewed articles in the literature.

So to just ignore me, then to confront the arguments. And again, one of the problems I feel with these field interest 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 email I'm having an email 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, medical treatment. And we can 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's brilliant. And here are all the reasons why. And and he responded with why you're cherry picking your data. 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 accusations 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, who've got an enormous amount of positive feedback, who believe they're doing good for the world. Any one of them could have gone into the commercial sector and made more money.

I mean, these are really well-meaning people. And some journalist comes along and says you're you know, you just dismissed it. You botched it. You did lousy science. That's 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 whether the criticisms and just keep making the arguments as honestly as I can. And I do have one advantage that they don't have.

What's 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 them with fat, the chronic diseases will go away, not for everybody, but for most people. So this is an effect, this argument that if people eat very low carb, high fat diets, the lowest carb, highest fat would be ketogenic. That's the extreme example. Don't get healthier.

And the world is now full of people who have done then gotten healthier. And if there's one thing that I and others like me that have been able to accomplish is we've broken down the resistance to these diets as on some level fads, but alternate 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 and who go on these diets and they get healthy in the short.

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 one hundred pounds. And you're telling me that bacon is going to kill me, like being one hundred pounds lighter and eating bacon is worse than being the way I used to be. So there's this sort of growing movement and the physicians do this as well because they have the same health problems and issues that the rest of us hope.

They do it in the works. They become passionate about it. Then they put their patients on it and their patients become passionate about it. If it works, if it doesn't, it just lose them. And unfortunately, that's the sort of cognitive bias with what I'm describing. But you've got this movement that people would like to talk about on the 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 was just 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 is now working in British Columbia who is just incredibly passionate about these low carb, high fat diets. 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 the diabetic patient on this diet.

I get them to follow. And this is a person who's, you know, he's on insulin and he's overweight and obese is the rest of his life and feeds the way he does or the way the diabetes associations want them to eat. All we're doing is basically adding drugs and modulating its insulin injections. And you put them on this guy and he becomes healthy.

And that's a low carb, high fat diet, the low carb, high fat. And it's an easy die because he's not hungry. It's not a true he's not getting any doughnuts and French fries and cereal anymore, but he's replacing it with some pretty. So that kind of clinical observation. There's a startup in San Francisco called Virna Health that's doing this on a sort of on a larger scale with some smartphones and health coaches and doctors. And and, you know, until recently, people believe that even Type two diabetes was irreversible.

A one ton insulin, always on insulin, basically, until you get taken down by the the the side effects and now people are showing that on these diets. Maybe others as well. But they're showing that this is a reversible disease, 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 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 much to the sugar industry?

This may be funny. I did a NPR thing a few weeks ago with Michael Moss, the author of, uh, Sugar, Salt, Fat or Fat, Salt, Sugar, whatever it's called. And, um, and the president of the Sugar Association is a young woman, former college basketball player named Courtney Peterson. Now, Courtney, I forget her last name. And anyway, afterwards, I got I just yesterday I got a nice card from Courtney thanking me for being on the show with her and discussing it.

So it was really nice to do. But it's sort of like getting a nice card from the president's tobacco foundation. They they are being vilified. They know what they see the writing on the wall. They're the soft drink industry, the purveyors of sugar rich foods. On one level, they have they know they have a product that's going to continue to sell. So they can they're not going to get rid of it because people are going to continue to to consume it just like some I think 17 percent of Americans still smoke.

So the percentage has come way down. But it's it's some people kids are going to start doing it just like kids are going to continue consuming sugary beverages. And 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 said, the tobacco industry 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 with the sugar industry had to do was remind the research community that what they believed in general was true of sugar in particular, so that 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 vilify a food for being too good to eat.

And, you know, if 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 caused 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 blame them. And I don't really blame them because they had the nutritionists and the obesity researchers got it right, the sugar, 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 more harmless. The community says we're harmless. Don't blame us. So but now, again, there's been once you have epidemics of obesity and diabetes and it's clearly not being caused by dietary fat consumption, then 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 to now when they fight back, people point out how they're fighting back, even if they're fighting back, is only a delaying tactic to give them time to diversify.

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

You mean about the epidemics in general, about my health, my personal health?

OK, so and it's interesting. I've spent the last two months talking to researchers about. So, you know, I clearly think that of all the so that the problem is the carbohydrate content of the diet. And I think the fat content for the most part is benign. It's not healthful. So and this is just 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, the sugars and the worst of the sugars is that 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 is probably the better choice or I'm going to caffeine addicts. I'm fine. Fine with coffee whether I'm right or wrong. I'd tell you to go back there for a second one's OK. One is the one area where or alcohol where I talk about where I think moderation is meaningful.

OK, so I know life. This one of the lessons that came away from the Sugar Book. So in what I'm doing and particularly when I go out 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. Was my wife, who she sees part of her job in life as 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 the human existence is not all that great. It's getting better because television is getting better. But 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 toxicants, something we can do to intoxicate us makes it worthwhile, gets us through the day.

And 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 six o'clock 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. We, you know, the drugs of abuse, their side effects are too severe and they occur too quickly for most people and they create behaviour that's also dangerous.

You've got to have something. And if it's not sugar, you know, a lot of us self medicate with sugar. I mean, I'm depressed. I'm going to go get it. I want a donut. 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 are going to become aren't going to get metabolic syndrome and can eat cupcakes twice a day their whole life and be absolutely fine and happy.

And I I think that the luckiest people on Earth problem is they don't know when they're eating the doughnuts like smokers don't know whether the cigarette is going to be 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 live for my next cigarette on some fundamental level. And you smoked after everything. After a meal, after a workout, after sex. Like most of us don't eat dessert or have a lollipop after sex. But you 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 from cigarettes to moderate your emotional responses.

And then after a couple, three years, you get to the point you can't imagine I 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 and trusting 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 that there are people who would say wheat is clearly the worst grain because of the gluten and these other issues that Bill Bavis describes in wheat belly and then starchy vegetables are fine or 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 them. Talk about it too much. The bread, when they give up and they end up giving up most carbs. Right. And then you find out that even wheat belt.

Where recommends ingrained brain, I say give up weight because of gluten, that's the prime problem, but don't eat sugar either and other starches can be problematic because they stimulate incents creation. So people who go gluten free, they're clearly people get healthier and they're clearly people who are gluten related disorders who when they don't eat gluten, they don't have those disorders. It's that simple. So and that's supposedly about five percent of the population, if I'm remembering correctly.

But the these other people have these 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 often when you give up gluten, you give up a whole bunch of packaged foods. I mean, your food selection just totally changes.

Yeah. You basically you have to give up many processed foods. So it would 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 and wheat replaced it with 400 calories of rice and got healthier. And I believe in his case, he did. So the question is with this, what makes it a relatively easy experience nutrition experiment to do is you just have to replace gluten free gluten rich foods with gluten free versions of them. So, say, 400 can when you take your thousand subjects and five hundred get your regular wheat bread and they're supposed to eat four slices a day and the others 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 effect. So you're not having to worry about that. One of the big problems with nutrition studies, if I want to study sugar, I'm going to remove that 18 percent of our calories that come from sugar. I have to replace it with something. Do I replace I can't replace with diet soda because then I'm not getting the calories that the sugar has.

I could replace with glucose. I can replace it with starch, I can replace it with fat, I could replace it with protein. All of those who have a different effect and you won't know of the 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, that would be easy to do the study if anybody wanted to, just at which point I would know what 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 a British clinician, Michael Mosley and Jason Fong, nephrologist in Toronto, and Valter Longo, I think of the 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. And 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 thus they decided that if they skip breakfast and they're obese, maybe they're obese because they're skipping breakfast and therefore they should eat breakfast.

So we should always breakfast mistaking an association for a causality and never really testing it. So somewhere along the line and I have to read Jason Fong's work more closely with Michael Moseley's people start saying, what if you actually do skip meals? So the idea behind the carbohydrate insulin hypothesis is that as long as you're keeping insulin levels low, you're mobilizing fat and 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 income levels are lowest. And the reason you don't get up to 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 store and 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, I'll 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'll be 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 seven o'clock at night.

You don't have any snack that night. You skip breakfast the next morning and their first meals at lunch at noon or one. You might accelerate fat burning, to use a cliche. And it might not be that hard to do because as long as your insomnia 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 Funt, realize that, you know, not only can people on low carb diets pretty easily do 18 hour fast, they can actually pretty easily do three day fast or even three week fast an hour.

You know, whatever I mean by pretty easily, it's clearly 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 it may be restocked some. Maybe you've given the beta cells that secrete insulin time to 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'll turn out that it's harder than people just getting 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 just surprised at how easy it is to skip breakfast. And I was just going to say it's twelve forty here in California and I haven't eaten since dinner last night and and clearly energized talking to you.

And I have one that has more to do with me that it does too.

And also that I clearly like talking about this stuff to someone interesting.

You've written about the history of nutritional sciences, the alternative hypothesis of obesity and why we get fat, but 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 have transitioned to using low carb, high fat or paleo diets to prescribe to their patients for obesity, 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 vegan and vegetarian diet now or Mediterranean diet to try and understand their what they're seeing with their patients and the feedback they're getting and tried to take care of the sort of selection bias of, you know, me interviewing people who follow my Twitter feed, kind of that kind of stuff.

How can they get a hold of you instead of my website or to Talbert's that Gmail dot com? I don't look at what 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 it's all my books have been about this sort of idea that that Richard Feynman and capsulized when he said the first principle of science, you must not fool yourself or the easiest person to fool. And I think we've gotten away from that. And the incentives of science today are about, hey, fool yourself, you can fool other people and get funding.

All that's you know, that's so much of a little 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. But that's when I did my first book. So I looked at CERN for ten months, back in nineteen eighty four, eighty five. And I was embedded with these physicists who discovered non-existent 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 it is to do it right. And that's the book I want to write an interview. You experimental scientists who have thought about these issues, their whole career theorists are a different species entirely. But 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 bandaids on the fundamental problem, which is that the research community really isn't doesn't get the mentoring that they need to truly understand the nature of this scientific endeavour and what it takes to get the right answer and how you have to act and communicate the steps along the way.

So that's 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, this has been an excellent conversation. I want to thank you so much for taking the time.

Well, thank you so much. 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.

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