Starting with Breakfast, Gary Taubes interview

This is a great interview held with the legendary Gary Taubes that was published on 10th August 2017.

Gary talks about what he ate for breakfast that day and goes on to discuss what we know about how the body lays down fat, and also how mainstream doctors medical researchers have been following the wrong path for at least the past 50 years. As you may already know, Gary believes that it is insulin that directly stimulates fat accumulation within the body.

Here is the YouTube interview to listen to and a list of his published books on the subject, which are a great resource to help understand how we process food and why humans have been getting progressively fatter and suffering more from modern diseases.


As a science writer and journalist who has written consistently on the subject of fat and metabolism for more than 30 years, his bestselling books come highly recommended:

Good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control, and Disease.

Why We Get Fat: And What to Do About It.

The Case Against Sugar.


If you don’t want to sit and listen to the whole interview, here is the interview transcript (courtesy of metabolic notes).

Metabolic: So, let’s start with breakfast, what did you have today?

Gary Taubes: Yeah, so today what did I have for breakfast? It’s not that different. Bacon, smoked salmon on a Swedish low carbohydrate, low glycemic index cracker that I read about in Dr. Bernstein’s Diabetes Solution book. He said it didn’t raise his blood sugar so I figured maybe it wouldn’t raise mine. You’ve got to eat smoked salmon on something so that seemed like a good compromise.

Otherwise, you would have scrambled eggs?

Scrambled egg, yeah, scrambled eggs and bacon. It’s easy to make. It’s nutrient-dense foods and doesn’t raise the blood sugar; won’t stimulate an insulin response. Again, I was somebody who was gaining weight easily. In the ‘90s, in my 30s, I was gaining a few pounds a year, despite living in Los Angeles and working out regularly, every day. That’s all you do in LA. You don’t go to cafes; you go to the gym or go for a run.

I was doing a story for the journal Science, my first investigative piece on dietary fat, and simultaneously I was writing an article for Discover magazine on the mathematics of the stock market. I was up at MIT interviewing a guy up there who runs the laboratory for financial engineering. We started talking about the dietary fat story as well, and he said, “Well if you’re doing a story on dietary fat, you have to try the Atkins diet; it’s fascinating.”

He has a collaborator at Wharton, he told me, and this collaborator’s father lost 200 pounds on the Atkin’s diet. This economist is Asian-American, he said he lost 40 pounds; he basically gave up white rice. I went back to California and I wasn’t married, I didn’t have kids, if I gave myself a heart attack no one would really care, other than my mother. I think my mother had passed away by then.

I tried the diet, and you have eggs and bacon and sausage for breakfast. I’d go to lunch and have half a roast chicken or a piece of meat or fish with green salad and the same thing for dinner, and I lost 25 pounds effortlessly. It was bizarre. I had been working out an hour a day in part to keep my weight under control, thinking I hate to diet but I’m burning 500 calories during this exercise so I could eat freely, even though I keep getting heavier. Suddenly, you’re just eating, seemingly, as much as you want of all these foods that you’ve been programmed to think will give you a heart attack and you lose weight effortlessly.

From a scientific perspective, it was a fascinating observation. Science is about explaining what we observe. That’s how Claude Bernard put it. We observe something in a laboratory or nature or the universe and then the process is scientists try to explain it. Sometimes these observations are personal. Most scientific breakthroughs come with observing something that doesn’t fit what you believe. You have some basic belief system and you observe something that seems contrary to it and then you try to explain that.

So I’ve got this calorie hypothesis programmed in my head, ‘if you want to lose weight you’ve got to starve yourself’ (or semi-starve yourself) and exercise.’ Suddenly, you start eating this diet and it’s like pounds drop off. As a matter of fact, I stopped working out for a while because my reason for working out was to burn calories and I was losing weight anyway. I actually fell off the diet for a while. I went back to eating desserts all the time, which was a mistake in retrospect. It may have been my body’s way of trying to get the carbohydrates it craved, trying a different approach.

When I started this New York Time magazine article, again on the same subject, the ‘Cause of Obesity’ and ‘Carbohydrates and Calories and Fat and Their Roles’, I went back on the diet and lost the weight again and stuck with it ever since. It’s an easy way for me to maintain a healthy weight.

I’d like to think my research was not biased by the fact that eating this way worked for me. Although clearly, if you think this way didn’t work for me, it would bias my research, so I suppose I’m biased either way.

I came to understand the history of it, the history of these competing ways of thinking about obesity and fat accumulation. What happened? Why we embrace this idea that it’s all about energy and calories and why this alternative thinking that, simply put, carbohydrates are fattening. Bread, rice, potatoes, pasta, sweets, beer, sugary beverages, they have some characteristics that makes them uniquely fattening. Calorie per calorie, they’re more fattening than other foods. If you don’t eat them, either you don’t get fat or tend to lose the fat that you’ve stored because you’re eating them. Through the course of my research, I came to understand that.

Take the concrete example of you eating your breakfast this morning, the salmon, and follow the path of that salmon through your body. After it hits your stomach what happens to it?

The salmon is composed of protein and fat. Some of the protein is used to rebuild your muscles; some of it is broken down into amino acids. It’s converted into glucose to fuel your brain. What it doesn’t do, or does very little, is stimulate insulin secretion. We primarily secrete insulin in response to carbohydrates. We think of insulin as a hormone that’s absent or defective in diabetes, but insulin orchestrates a whole variety of responses in the human body that have to do with deciding how you’re going to put to use the fuels you use.

When you secrete insulin in response to carbohydrates, it’s basically telling your body to burn the carbohydrates for fuel and to store whatever fat you’ve consumed. When insulin goes up, you burn carbohydrates and store fat. As insulin starts to come down, your fat tissue can let the fat back out into the bloodstream. Then you start to burn that for fuel when insulin levels are low, say when you’re fasting or after 12 hours without eating or if you’re eating a diet without carbohydrates in it, then you’re going to be burning fat for fuel not carbohydrates

When you’re overweight, when you’re obese, when you’re getting fatter, you’re basically storing calories as fat that you’re not accessing for fuel. For whatever reason, your body will not burn these for fuel.

This alternative hypothesis that should have merged in the ‘60s and never quite made it is that you’re, in effect, over-secreting insulin. You’re insulin levels are staying elevated and they’re constantly telling your fat tissue to store fat, and they’re constantly telling your lean tissue to burn carbohydrates. They’re never lowering enough to reverse the process so that they burn the fat you’re storing. It’s like a ratchet wrench. Every day you store a little more fat than you burn, and that little more fat accumulates and accumulates a couple pounds a year until you go from being lean to obese.

It’s a very simple hypothesis, but it implies that certain foods are uniquely fattening. Those are the foods that work to elevate insulin levels, and that’s contrary to the ‘calorie is a calorie’ belief.

Instead of having the salmon, let’s say instead of having 400 calories of salmon, I had granola, 400 calories of granola and low-fat yogurt. There a significant portion of the calories are carbohydrates, and there’s going to be some sugar in low-fat yogurt or the granola, which was one of the most disappointing moments of my 1990’s when I realized how much sugar, the Swiss Muesli Granola had. The carbs from the grains are going to turn into glucose and go directly into your bloodstream and stimulate insulin secretion. So your blood sugar level is going up. That’s the glucose being converted from the grain, crossing into your bloodstream, elevating blood sugar. Elevated blood sugar is toxic to your body, so you secrete insulin to get it under control and burn the glucose for fuel. While that’s happening, insulin is telling you to store the fat that’s in the low-fat yogurt and the granola, so you’re storing that. Meanwhile, the sugar is half glucose, half a molecule called fructose. The fructose is going directly to your liver and being metabolized there in the context of this high blood sugar and high insulin, so some of that is going to get converted to fat.

So you get this hormonal response that’s entirely different depending on the macronutrient content of the food. One of the ways in which it’s entirely different is in whether it’s signaling the body to store fat and burn carbohydrates, or it may mobilize fat and burn fat, or even use protein for energy rather than for repairing cells. It would be almost a miracle for these different macronutrients to have the exact same effect on any one of these variables, particularly fat accumulation because the body is responding in entirely different ways. Different organs are metabolized in these different fuels, so you would expect them to do something different. If they did the same thing, if the only thing that mattered was how many calories you consumed, that would be remarkable, and you would think that the research community was going this is incredible. It’s like saying, if I give my car gasoline or rubbing alcohol, I get exactly the same mileage. What is my engine doing?

When you first started to understand the more insulin-based or hormonal-based trigger, how did that thesis build up for you? What part of that seemed particularly intriguing or compelling? What was the thread that you followed?

Well, I approach these issues, controversies in science, historically. I was trained as a physicist, so when you’re trained as a physicist, you learn the science with a historical perspective. Great discoveries, laws, they all have names attached to them and experiments that were done. Maxwell’s equations, you learn about James Clerk Maxwell, Einstein’s theory of relativity, Newton’s theory of gravity. Everything has a name attached and a history, too. You learn that so you learn what the evidence was that led people to make these claims, these discoveries. In part, it happens in physics. As physics progressed, the science got more and more complicated, but students could actually do these experiments up until a certain point when you get into quantum physics.

That’s how I think, and as an investigative reporter, a curious human being, when somebody tells you something, the first thought is, ‘gee, why do you think like that? Where did that come from? How did it develop?’ In the course of doing my research as an investigative journalist, I went back historically through the field. I just had an advantage that other journalists didn’t have because I had been exposed to these low-carbohydrate diets. I thought that there was something to this carbohydrate story.

Some of the earliest post-World War II work on that was done by a guy named Pennington who was a physician in the industrial medicine department at DuPont. Because he was doing his writing in 1948, he was referring to pre-World War II German research articles on obesity. I had his articles, and I could get his references.

Suddenly, I’m looking at what people pre-World War II are thinking. The leading medical research of the era who are all Germans and Austrians, how they thought about obesity, and lo and behold, it was entirely different than the Americans did post-World War II.

The lingua franca of medicine shifts from German to English with the war. The German and Austrian medical communities evaporate with the war, and the last thing they’re concerned with is obesity. The whole center of scientific enterprise moves to the U.S., which is the one nation that hasn’t been racked by the war. We have money to spend on funding, and we recreate a lot of these fields of science from scratch by physicians and nutritionist who didn’t have a clue what really good science. And they weren’t all that bright, frankly.

Just by being exposed to the pre-World War II literature through this one window, I suddenly had a whole new world to work from.

Did the pre-WWII German and Austrian scientists understand insulin well, or not?

No. They didn’t. Insulin was only discovered in 1921. They knew that type 1 diabetics lacked insulin and needed insulin to live. They knew that these patients could survive in a diet absent all carbohydrates, although just barely, and they knew that when they got insulin, they tended to fatten up. They’d be emaciated without insulin, starving. No matter how much you fed them, hungry all the time and emaciated, so their emaciation seemed to be independent of how much they were eating if they didn’t have insulin. When you gave them insulin, they put on weight, and they put on fat. It appeared there were many of them who thought insulin was a fattening hormone.

The problem was you have these type 2 diabetes that’s associated with overweight and age. These people, they assumed, also lacked insulin, but they tended to be obese. If insulin is a fattening hormone and they don’t have insulin, why are they obese? Therefore, insulin can’t be the key factor. This was one of the fundamental problems with their ability to figure it out.

Then it’s not until 1959 or 60 that researchers create a test that allows them to measure insulin levels in the bloodstream accurately. This is Rosalyn Yalow and Solomon Berson in New York. Yalow later won the Nobel Prize for this. It’s called the radioimmunoassay. And for the first time in history, 1960, you can measure hormone levels in the bloodstream. One of the first papers that Yalow and Berson published was that people we think of today as type 2 diabetics don’t lack insulin, they have an excess of insulin. They are insulin resistant. So because their cells are resistant to the insulin they secrete, they have to secrete more and more of it, so now you’ve got lots of insulin in association with obesity. Now you can explain the idea that insulin’s a fattening hormone. Yalow and Berson do. But they’re not obesity researchers, they’re diabetes researchers.

Rosalyn Yalow and Solomon Berson
Dr. Rosalyn Yalow and Dr. Solomon Berson
Was it their work that clarified the concept of type 1 and type 2?

That there were two different types of diabetes was well-known. There had been work. Some British researchers, an Austrian researcher who had already claimed that overweight diabetics were insulin resistant, but it hadn’t really caught on. It had a different terminology. It’s insulin dependent diabetes, which is type 1, and noninsulin dependent.

But with Yalow and Berson, now you could definitively measure it, and you knew for sure what was going on. Most type 2 diabetes is a disorder of insulin resistance. You start off with too much insulin, and then, eventually, the ability to secrete insulin wears out. That’s how the theory goes. And then have an absence of insulin, just like type 1. There are a few intermediate forms as well.

Once you had type 2 diabetes, once you knew it was a disorder of insulin resistance, then this idea of insulin as a fattening hormone comes rushing back in. But by this time, obesity research in the United States had been recreated post-World War II by nutritionists at the Harvard School of Public Health. They only studied animal models of obesity and never saw patients. They weren’t doctors, they weren’t dieticians.

They were studying animals in their laboratories, and they had concluded that this is, basically, a glutton and sloth disorder, taking in more energy than you expend. The doctors who took over this field post-World War II who had this naturally understandable anti-German sentiment also embraced this idea that people who got fat had a perverted appetite. Or there was something wrong with their metabolism that they don’t expend enough energy.

The one thing they never paid attention to is this concept that some foods could be uniquely fattening, and that could be mediated through this insulin pathway.

In the 1960s, researchers start understanding how insulin influences fat accumulation and they work out the details. Insulin stimulates the production of an enzyme on the fat tissue called lipoprotein lipase. It works to pull calories of fat, fatty acids into the cell. It inhibits the work of an enzyme inside the fat cell that tends to break down fat into fatty acid so they could get out again. All this science is being worked out, and it’s really beautiful science. But the obesity research community is now dominated by psychologists and psychiatrists who are trying to figure out why fat people eat so much and how to get them to stop. It focuses on all these behavioral techniques to get fat people to eat less.

Instead of saying something simple like, ‘Well, I’ve got an obese person. He’s got, clearly, a disorder of excess fat accumulation.’ You look at the person. You don’t know how much they eat and exercise. All you see is excess fat. You ask the question. What regulates fat accumulation? This was being worked out very carefully in the 1960s, and it was all implicating insulin and carbohydrates.

These people would look at an obese patient and think I have somebody who eats too much sitting in front of me. How can I get him to eat less? Clearly, it’s a behavioral defect. There’s something wrong with fat people that makes them eat too much, and now you’re studying something entirely different.

It’s almost bizarre to think that this mistake was made. I mean, it is bizarre to think that a mistake like this could have been made on this magnitude, and yet, it was clearly made. I document it in my books. I could sit down with anyone and say here are the references. Here are the articles. Here, you could see how the field evolved and what happened, and why the psychologists and psychiatrists got involved, and why they weren’t paying attention to the science on fatty acid storage and metabolism.

When did it start to come back together? When Atkins shows up and starts to talk about this, is he starting to talk about it or thinking about it at all from a hormone insulin point of view?

Very much so. This is where an almost like a perfect storm of circumstance and bad science come together.

These doctors start reading the literature. Atkins had a weight problem. Pennington worked at DuPont where a lot of the executives were overweight and obese, and they were worried about heart disease. They read the literature to see what they can do about it. There wasn’t this firm belief that it was all about calories yet. Nobody was talking about that except one American researcher who had far too much influence.

Who was that?

A fellow named Louis Newburgh at the University of Michigan. It was his theory that this caused by a perverted appetite and a suppressed metabolism. The perverted appetite is, by definition, taking in more calories than they’re expending. Newberg was one of the few researchers in this field whose career spanned the war years, He wrote a few influential articles during the war years. Afterward, when these young doctors and nutritionists were recreating the science of the field, it was easy for them to find Newberg’s articles and say, ‘hey, look. Newberg says it’s all about a perverted appetite, and he’s shown it.’ I mean one of Newberg’s articles is 130 pages long. Nobody can get through that stuff, so you believe you know what they’re talking about. He didn’t.

Pennington at DuPont is trying to lower the weight of the executives. He reads about a guy who’s had great success with low-carb diets, so he tries it. He loses weight. He puts the DuPont executives on the diet. They lose weight. It’s all rather remarkable. He publishes some papers. One of them is in the New England Journal of Medicine.

The 1950s comes along. The Harvard School of Nutrition is building up an influence in powers. It’s the first dedicated nutrition department in the United States. They have a conference on obesity where Pennington speaks, but simultaneously, they’re funded by people like General Foods and the sugar industry. They might’ve been a little biased. Who knows?

They find it an interesting hypothesis. But you have in this mind this idea that all fat people are like Falstaff from Shakespeare. They’re guzzling beer and eating huge amounts of food. It’s just an easy stereotype to think about, particularly if you’re not seeing patients.

Then there’s a gynecologist in Brooklyn named Herman Taller who reads Pennington’s work, starts putting his patients on this low-carb, high-fat diet. Lo and behold, they lose weight. He writes a book that is called Calories Don’t Count. The idea is that it’s not all about this measuring calories and how many I expend and how many I take in. Just don’t eat these fattening foods, and these fattening foods are carbohydrates. Neither Pennington nor Taller really understood that insulin was key because they were before this Yalow and Berson’s radioimmunoassay discovery revolutionized the science of hormones.

Then Atkins came along. He read these guys, read some articles in the journals. He read some of the same stuff I read. He had a weight problem. He tried life without carbohydrates, lost weight effortlessly. He prescribed it to his patients, they lost weight, and he wrote a book about it. It was a huge bestseller, supposedly at the time even outsold the Bible.

What years was this?

This was 1973, Dr. Atkins’ Diet Revolution. Here’s where the perfect storm of circumstance comes in. In the 1960s, the medical community starts focusing on this idea that dietary fat causes heart disease, in particular, saturated fat. So if you want to avoid heart disease, you give up the fat, and you replace it with carbohydrates. Now Atkins comes along and says not only is this wrong but if you want to lose weight and be healthy, you get the carbohydrates replaced with fat, particularly saturated fats. You should eat things like double quarter pounders with cheese without the bun, bacon and eggs for breakfast, Lobster Newberg for dinner. I had a guy write me the other day saying. ‘I just cannot believe that lobster with butter sauce is healthier than an apple, and yet, that’s what you seem to be arguing.’

That’s what Atkins was arguing. He was arguing it at a time when the medical research community, the cardiology community, nutrition community had come together to really believe this ‘dietary fat hypothesis’ of heart disease. When it was tested, it never passed the test.

But they thought Atkins was killing people. These were very well-meaning physicians and researchers who were convinced that anyone who went on this diet would die of a heart attack. Their heart would blow up. In The New York Times in 1965, the most influential nutritionist in America, a guy named Jean Mayer at the Harvard School of Nutrition, is quoted as saying that ‘prescribing a low-carb diet to patients is the equivalent of committing mass murder.’ That’s in The New York Times in 1965 when they’re just beginning to realize that insulin dominates this fat-accumulation process. It’s the only hormone that really tells your body to store calories as fat. Carbohydrates stimulate insulin secretion – they should be fattening!

The medical community goes after Atkins. The American Medical Association runs a critique of his diet that accuses it of being quackery, perverse. I forget the terminologies, ‘perverse principles of medicine’. It’s written by, in effect, one cardiologist, but it’s got the imprimatur of the American Medical Association. The obesity research community, which in the 1970s was dominated by a half a dozen white men from Tufts or Harvard, Columbia, Penn. They all knew Atkins, and they didn’t like him personally. They didn’t like his theory, and they thought he was killing people. In order to get rid of this theory that you should eat a low-carb, high-fat diet if you want to be lean, they had to get rid of the science behind the theory as well.

When I say get rid of it, I mean the same six men would write every textbook chapter on obesity in the medical textbooks and in their own textbooks. They would host the conferences on obesity and write the conference proceedings on obesity. Again, they were well-meaning. They were just misguided.

In order to reject the implication that these low-carb diets are the way to go, they had to render irrelevant the science behind them. By the time you get to 1980, they’ve successfully gotten to the point where they now believe they understand the disorder of excess fat accumulation without ever having to address the issue of what regulates fat accumulation in fat cells.

So in the 1960s, you have this revolution in the science of endocrinology, the study of hormones and hormone-related diseases, that allows you for the first time ever to understand the regulation of fat accumulation in fat cells and in the human body. But by the end of the 1970s, that’s considered irrelevant to a science of excess fat accumulation. Instead, all we’re talking about is how much people eat and exercise and the factors that determine how much people eat and exercise as though the human body is a black box. And the only thing that matters is what comes in the top and what goes out the sides, and nothing that happens in the box can play a role.

This past February, the New England Journal of Medicine, it might’ve been January, published an article on the pathogenesis and mechanisms of obesity written by researchers at the Pennington Biomedical Research Center in Baton Rouge, Louisiana. In this article, they basically have a sentence saying obesity is caused by taking in more calories than you expend, and that’s all they say. Despite the title being about the pathogenesis and mechanisms, the only mechanism is this excess calories thing, and there’s no discussion of this whole science of fat metabolism that’s been very well worked out.

The leading medical textbooks have a chapter on obesity, and they have no discussion of the endocrinological regulation of fat accumulation. It would be like talking about if you had a son who grew to be eight feet tall and never mentioning the word growth hormone or a son who only grew to be five feet tall and never mentioning the word growth hormone or growth hormone receptor. This is what regulates growth. It’s this very sophisticated, wonderful homeostatic endocrine system, and we don’t discuss it.

Other than Atkins, going into the 80s, 90s and more recently, where has this been picked up?

It’s always been, basically, one best-selling diet book after another. The mid-70s was Tarnower, the diet doctor in the Westchester County (The Complete Scarsdale Medical Diet) who got shot by his girlfriend. Protein Power is a variation on Atkins. The South Beach Diet is a variation on Atkins. The Zone is a variation on the science, the higher carb, healthier carbohydrate variation on Atkins. Even some of the very low-fat diet books like Dean Ornish’s very low-fat diet restricts sugar and highly refined grains because of their effect on insulin and insulin’s effect on fat accumulation.

So you got to the situation by 2000 where, basically, the medical community was saying it’s all about how much you eat and exercise. And every diet book had some magic formula that was, for the most part, based on one of two hypothesis. You don’t eat sugar and white flour and other carbs and processed foods, and you replace it with fat. Or you’re eating less fat and you’re also not eating sugar, white flour, processed foods or avoiding all carbs. The diet books were insisting there’s a formula by which you could lose weight. And the medical community was saying it’s all about willpower, how much you eat and exercise.

Did most or any of them talk about insulin or hormones in particular?

The insulin story, like I said, more or less disappeared. I began to revive it when I came on the scene in the late 90s, and with my research and my book. I don’t know if I’m giving myself too much credit.

David Ludwig at Harvard, a pediatric endocrinologist with an obesity clinic, had bought into the idea that carbohydrates are the problem but was focused on blood sugar response. I think I was the one who just brought back the simple idea that you’re talking about a disorder of excess fat accumulation. Insulin directly stimulates fat accumulation. That’s what it does. Why aren’t we starting there?

Yeah. I often sit down – I try to sit down with researchers when they’ll do it and say let’s just do a thought experiment. This is something you could assign your students. If I taught a class on this, I would assign my students this problem. I’d say imagine you’re a fat cell. Okay. They’ll give me a theory of obesity from the fat cell’s perspective.

The fat cell doesn’t know how much the person’s eating or exercising. What does it see in the circulation? What hormonal signals is it responding to? What are those signals saying? What central nervous system signals is it responding to? What are they triggering? You could find all this in the textbooks, and then create a theory of obesity from the fat cell’s perspective. If you do that, it’s going to be insulin-centric because that’s the dominant signal telling the fat cell to store fat. Everything after that is downstream.

I was the first one, just by re-building up from the historical perspective with my shallow journalistic understanding. But I had been trained to think by some very good physicists. Simple as possible hypothesis: why isn’t this about insulin? Especially because obesity and type 2 diabetes are so closely related, it makes perfect sense that they’re both about insulin, both about insulin dysregulation, considering what insulin does. I guess I can give myself credit for that. Like I said, David Ludwig was thinking closely along those lines. He was also thinking that it was about the hunger that comes when your blood sugar drops, that your blood sugar drops because the insulin is keeping your fat cells from being fatty acids from being used for fuel. You over-respond by continuing to burn glucose past the point which it’s comfortable to your body.

Was anybody in the diabetes community thinking about this?

If you read the chapters on diabetes in the textbooks they would talk about the effect of insulin as lipogenic hormones. Lipogenic means fat-forming or fat-creating hormone. Clearly, type 2 diabetics have a problem – when they give themselves insulin, they tend to gain weight. And some people with diabetes don’t want to take their insulin because they don’t want to get fatter. They clearly know that insulin has this role. The endocrinology and biochemistry textbooks, they’ll talk about insulin as a fattening hormone. They talk about how it regulates fat accumulation in fat cells

But then they’ll have a separate section on obesity that says it’s caused by taking in more calories than you expend.

If you go back to the very first cover story I wrote in The New York Times magazine on obesity, I have this line, “of course obesity is caused by consuming excess calories.” Now, I think, boy, what an absurd thing to say. But it just seemed so obvious. How can it be wrong? We’re just not programmed to accept we made those kinds of mistakes.

I mean, I remember. I lived through this period in the 80s when suddenly everybody was eating pasta every night. It’s easy to cook. It’s delicious. You have a dinner party. You’ve got your special pasta you make that all your guests love. I mean, what could go wrong? How could it possibly be unhealthy?

Suddenly, bagels became an everyday food. Something Jews only ate on weekends. People had bagels every day because they didn’t have fat in it. The pasta didn’t have fat in it. It made perfect sense.

I probably went the entire decade of the 1990s without eating one piece of red meat without at least feeling guilty about it. And maybe five or six pieces a year because it killed you, right? It’s a hotbed of dietary fat and cholesterol.

They so successfully got that message across, and we embraced it so well that it’s just hard to shed it.

I’ve been talking to physicians around the world who prescribe low-carb, high-fat diets. Over and over again what I hear is it’s just so hard to convince people they can eat these foods.

Here’s the thing with this field that gives it one advantage. One of the reasons we’ve gotten as far as we have, further than Atkins did, despite his massive bestseller, is, a) we understand the science better than he does now, but b) the internet has removed the gatekeepers. So the American Heart Association will be saying we should eat carb-rich, polyunsaturated fat-rich diets. People don’t care about what the American Heart Association says because their neighbor or somebody on the internet says I went on this low-carb, high-fat diet with a lot of saturated fat. I got healthier. My type 2 diabetes reverted. Then you could find chat rooms to discuss it and eight million articles, and you could identify diet books on Amazon that you could buy. You can get around it, and you could try it for yourself. You also know you can get pretty simple blood tests that will tell you whether you’re getting healthier. And it’s very easy in this day and age to find physicians who understand this diet and prescribe this diet, and then can help you through it.

So when it comes to nutrition, you can experiment. You can see what happens. It’s an advantage.

Nowadays, it’s easy enough, like I said, to get the blood tests. They’re not expensive. You say I’m going to do a blood test now. I’m going to check my lipids, my triglycerides, my HDL, my good cholesterol, my LDL. I’m going to come back in six months or a month, and test it again, and see what happens. Then I can decide.

I can find out if I feel better. It’s not just if I look better, but if I feel better, if I’m healthier, if I’m sleeping better, if I have more energy, if my moods have stabilized when I don’t eat grains and sugars, maybe that’s a good enough reason to keep doing it.

Thanks, for doing this.

My pleasure.


Here is a good clip of Gary Taubes talking about the case against sugar:

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