Gary Taubes is the author of many best selling books, including Why We Get Fat: And What to Do About It. Following lecture is based on the latter. Here is the full transcript of the talk….
I want to thank you for having me and Carol for setting this up. And let me just give you a little bit of background before I start. And you know why a journalist is here, talking about weight and why a journalist has anything to say about this.
And as Michael explained, my obsession over the years has been controversial science, good science and bad science, how easy it is to get the wrong answer in science, and how hard it is to do it right. And after I had finished this book on the scientific fiasco called Fusion, some of my friends in the physics community said to me, if you’re really interested in bad science, you should look at some other stuff and public health, that’s really terrible.
And so in the early ‘90s I moved into public health and I meandered around the field until the late ‘90s, I was writing about nutrition issues. I did a series of exposes for the journal Science in which I spent a year on an entire – twice I spent the year on an entire article first about the idea that salt causes high blood pressure. And then about dietary fat and heart disease and that led me to do a what was a relatively famous cover story for the New York Times Magazine called What If Fat Doesn’t Make You Fat, or What If It’s Been A Big Fat Lie, and I got a large book advance from that.
And one of the things with a large book advance it gives you a lot of time to do the research. I spent four year — five years on the book, the advance lasted four.
When I talked to doctors and researchers about this, I say imagine if you took one of your reasonably smart post dos, who had a reasonably good understanding of science, and said look, we have this obesity epidemic, we have this diabetes epidemic. We think we understand this but the fact that obesity and diabetes have gone wild during our lifetime suggests that maybe we don’t. Could you just go back to the literature and see if we miss something, see if maybe there’s some other explanation that we just blamed on because we thought we understood and one of the common pitfalls in science is as soon as you think you understand something, you ignore all other possible hypotheses.
So that’s in effect what I did, and unfortunately I stumbled upon what I thought were some obvious mistakes it had been made over the past 60 years. And now as a journalist, I am in the position of trying to convince the medical research community and the scientists and the educators that they have to rethink what they’ve been doing. So that’s what I’m going to do tonight with you.
The gist of it is – well, let me – so I wrote this book, Good Calories, Bad Calories. Five years of my life, it’s densely annotated. And after came out I got a lot of emails and letters from people saying that this book changed my life. Now would you please write one that my husband could read, or my father could read, or my children would read? I got letters from patients saying, would you write one that my doctors could read, and I got letters from doctors saying, would you write one that my patients could read. So and see how we’re…
So I wrote Why We Get Fat, which is kind of the airplane weaning version of Good Calories, Bad Calories. Instead of providing the history and the perspective and the background, it’s more of an argument and it’s based on this lecture. And I’m going to argue that what I say is true.
So as we know there’s an obesity epidemic out there. Obesity levels have increased dramatically. This is the epidemic here so and we know that just – as Mike said living in Santa Cruz County, you’ve got obesity and the obesity epidemic. It goes along with the diabetes epidemics. So diagnosis of type 2 diabetes have tripled since 1980 in the United States.
So the conventional wisdom, and I am just going to give you this in background. Obesity is associated with the whole cluster of metabolic diseases. And what we mean by associated means the fatter you’re the, the more obese you are, the greater your risk of getting these diseases. So they include type 2 diabetes, fatty liver disease, heart disease, hypertension, stroke, cancer, asthma, sleep apnea, neuro-degeneration and Alzheimer’s disease is one of them.
And actually just yesterday there was a report that came in the journal Pediatrics said, autism is associated with obesity, in maternal obesity and maternal type 2 diabetes. And the conventional wisdom is that as you get fatter, something about being fat, then increases maybe the inflammatory molecules that are released by your fat tissue, increases the risk of these diseases.
The subtext of what I’m going to argue is that whatever makes us fat also causes all these diseases. So it’s not whatever makes us fat causes heart disease, causes type 2 diabetes, causes cancer, causes Alzheimer’s and it’s kind of a radical position. But I want you to take it seriously. It leads, as I explain to you, why we get fat or hopefully sort of expand your beliefs about why we — open your mind a little bit about why we might get fat.
Why do we get fat
So boom, why do we get fat? Simple question. And the answer is pretty obvious also, as the NIH puts, obesity occurs when a person consumes more calories from food than he or she burns, okay. It’s conventional wisdom – energy in is greater than energy out. Okay, we overeat. Simple enough.
This is the energy balance hypothesis of obesity. That’s how it’s known. We take in, it’s calories in, calories out, whenever you hear somebody say that a calorie is a calories, is a calorie. This is what they’re arguing, and any food will make you fat if you take in more but then you’re expending.
So I just want to ask a question – how many of you believe this is true? Just so I get a feel for – okay, 13 people.
I am going to argue that this is one hypothesis of obesity and there are alternatives. And that obvious as it seems, what we want to do is look at the alternatives and see because this is science. Maybe the alternatives explain the observations better than our energy-in, energy-out hypothesis. So again this is kind of how it’s perceived today in the popular press.
Energy-in greater than energy-out
And one of the things you want to do as a science is we want to explain, not just obesity but the obesity epidemic. So science is about observing things and then figuring out what the causes are, and our explanation for the obesity epidemic is increased prosperity. This is a phrase that the NYU nutritionist Marion Nestle used in a Science article 10 years ago when Marion is still arguing, so the idea is we get richer and as we get richer food is more available. We have to exercise less, basically the food and entertainment industries conspire not consciously but subconsciously to feed us too much and give us too many opportunities to be sedentary watching TV, watching video games, or kids are playing video games or are on the iPads everyday. They’re not outside running.
Kelly Brownell, a Yale psychologist used the phrase the toxic environment to describe this, and toxic environment is an environment that promotes sedentary behavior and overeating. And by doing so makes calories in, more than calories out, as Kelly put it your cheese curls and french fries, drive-in restaurants are more part of environment now than trees, grass and clouds. Your children sit at home and watch television, they play video games as parents are afraid to let them walk or bike to school anymore. So we drive them to school. So there’s all these opportunities to eat too much and expend too little and that’s the toxic environment that we live in today.
And the question we could ask as scientists is pretty simple. We have our hypothesis – increased prosperity leads to overeating. Energy in greater than energy out. And the result is the obesity and the obesity epidemic.
And what we want to do is say, does this hypothesis make sense? Does it explain the observations? Because that’s again what we want our hypothesis – we want it to explain things that we see and it certainly seems to explain what we see today.
But there are some less obvious observations out there, and this is what I did in the course of my research, as I was able to go back in time and looked for examples for populations that had high levels of obesity. But none of the toxic environment that we see today around us.
Pima Indians- History of Obesity
And the first is on the Pima Indians – Native American tribe that live in, on a reservation today in Arizona, south of Phoenix. And the Pima were happened to be among the most affluent Native American tribes through the middle of the 19th century. So they were hunters and gatherers. They hunted in the nearby mountains. They fished in the Gila river. They farmed, they were an agrarian population as well. So they raised wheat and beans. They raised pigs and cattle.
And in late 1840s when army battalion started traveling through the Pima territory, they noted that the Pima were sprightly and in fine health. And they had this great abundance of food, warehouses full of foods so much so that after gold was discovered here in California in 1849, and from the 1850s to 1880s, 20,000 to 60,000 49ers went west on the Santa Fe Trail that lives in the Pima territory. And the US government asked the Pima to feed them which they did.
So in 1846, they were very prosperous tribe and they were described the sprightly and fine health by several observers. This drawing was actually made in 1851.
And then what happens is Anglo Americans and Mexican Americans are moving into the Pima territory in Arizona and they over hunt the local mountains and they divert the Gila river water to irrigate their own streams. And by the 1870s, the Pima are starving. And they go through 20 to 30 years of famine.
And by 1902, a Harvard anthropologist named Frank Russell comes to live with the Pima, and he describes the conditions on the reservation as poor beyond our imagination. They’re trying to make a go at farming and barely doing it. And Russell takes this picture of this Pima Indian that he calls fat Louisa. And he says there is a degree of obesity on the tribe, particularly in the older people completely at odds with the popular image even back then of the Native American lean handsome Native American and popularized thought.
And actually shortly thereafter a physician turned anthropologist named Alex Hrdlicka came to visit the Pima tribe. He was doing a series of explorations in the American Southwest. And he also commented about how obese they were. And what’s interesting is our hypothesis says increased prosperity causes obesity. But here we have an example where they were prosperous and affluent in the mid-century, they go through twenty to thirty years of famine. And then they have an obesity problem in 1902 when they were extremely poor. And 20 to 30 years of famine you could think of as twenty to thirty years on a low calorie diet, right? These people should be lean, if not, emaciated and yet there’s a obesity problem.
So one of the things I did as I said, I went through the research looking for examples like this populations in which obesity levels were measured prior to the 1980s when it became a cottage industry and everyone blamed it on McDonald’s.
So one of the first ones you see it, Sioux Indians on a South Dakota Crow Creek reservation 1928. This was a study done by University of Chicago economists and they went to live on the reservation. And what’s interesting yet, the living conditions were poor beyond our imagination. As matter of fact, in 1927, there was a government report on living conditions in the Indian reservations, and they said they were poor beyond the imagination of the Anglo Americans living in 1927 and here there were 48 people living per room. 15 families with 32 children among them on this population were living on bread and coffee. They had to go to the river to get water. Their toilets were outhouses and yet you have obesity levels that are not that dissimilar to what we have today. 40% of the women, 25% of the men and 10% of the children were distinctly fat. And 20% of the women, 25% of the men and 25% of the children were extremely thin. And in fact, they were on – this combination of obesity and malnutrition or emaciation is a very important observation I am going to come back to it.
But there was plenty of signs that these economists reported the malnutrition deficiency diseases on the population. Certainly these people weren’t getting enough food and they weren’t getting enough protein. They weren’t getting enough minerals and vitamins. And yet they had this high level of obesity – poverty and obesity.
African-American, the Charleston South Carolina 1959. 30% of the women are obese, 18% of the men and the family incomes are $9 to $53 a week. That’s about $360 a week in today’s money.
Zulus in Durban South Africa, 1960. 40% of the women are obese. Women in their forties averaged 175 pounds. Women in America today average around 165 pounds.
So they’ve got again this obesity epidemic in this population and we want to explain that too, not just obesity today.
Trinidad, in the early 1960s, there is a malnutrition crisis going on in Trinidad. Trinidadians are dying of deficiency diseases. The U.S. government sends a team of nutritionists down to help out and these nutritionists come back and they report that a third of women over 25 were obese. And obesity is a potentially serious medical problem in women.
And the next year, an MIT nutritionist goes down to Trinidad to quantify the diet that they were eating, and she reports that the obese women are eating roughly 2,000 calories a day; it’s 21% fat. It’s a low-fat diet, less calories than recommended at the time by the Food and Agriculture Organization for healthy diet. And yet there is explosive obesity in the population.
Bantu pensioners in South Africa mid-1960s, the poorest of a disenfranchise black South African population, and yet 30% of the women are severely overweight.
Rarotonga in South Pacific in 1971. 25% are grossly obese. Factory workers in Chile – okay, these people, they’re working and they’re engaged in heavy labor. You’ve got 30% obesity, nearly 50% of the women over 50 and 10% suffer undernourishment. So there’s a combination again of obesity and not enough food existing in the same population of factory workers in Chile.
And the key observation there – again they’re doing heavy labor like this Mexican American study that was done in 1981. Starr County Texas is about 200 miles south of San Antonio on the Mexican border. A University of Texas Southwestern cardiologist named [William Mueller] was down there studying diabetes in this population and he measured obesity as well. And he reported that 50% of the women in their fifties were obese, 40% of the men in their forties.
And the living conditions, most inhabitants are employed in agricultural labor and/or work in the oil fields in the country. These are hard-working people. Okay, they may not be running marathons or training for triathlons, if you’ll excuse me, they may not be doing CrossFit or belonging to gyms. But they’re working out in the oil fields, they’re working in the fields and they have high levels of obesity and they’re poor. There was actually one restaurant in Starr County Texas in 1981, a Mexican restaurant.
So there’s no aspect of this toxic environment that we think of it today, no fast food joints, no televisions, no video games. They are not keeping their children home from school. They’re not sedentary. They’re not white collar workers, and yet they have high levels of obesity.
Yet why are these populations fat?
So the question you want to ask is: why are these populations fat? Okay, because if we can figure out why they’re fat, we can probably figure out we’re fat, and our explanation for what makes us fat should encompass these populations also. So our toxic environment theory, or increased prosperity theory can’t explain poor hard-working populations with high levels of obesity.
So this is how this was perceived in the 1970s before this idea that obesity was a disorder of over nutrition, of over-consumption of foods set in like ice on a pond. And I am going to have to read it meaning over a little. It’s difficult to explain the high frequency of obesity seen in a relatively impecunious society such as exists in the West Indies. Actually let me interrupt for a second.
This is Rob Richards. Rob Richards was a British-trained diabetes specialist who moved to Jamaica in the early 1960s and started a diabesity clinic at the University of the West Indies in Kingston, Jamaica. And Richards pointed out when he made this statement, he observed the two-thirds of the adult women in Jamaica were obese. So when he says it’s difficult when the high frequency of obesity seen in a relatively impecunious society such as exists in the West Indies when compared to the standard of living enjoyed in the more developed countries, and asking the same question, do we expect the rich countries to have obesity problems, right, not the poor countries.
Malnutrition and sub-nutrition are common disorders in the first two years of life in these areas and account for almost 25% of all missions to pediatric wards in Jamaica. Sub-nutrition continues in early childhood to the early teens – sub-nutrition, the kids aren’t getting enough food.
Obesity begins to manifest itself in the female population from the 25th year of life, and reaches enormous proportions from 30 onward.
Okay, that was how this question was asked circa 1973-74. Now we can look at the same issue, the same observation 2005 after this belief that obesity is just a disease of sort of overconsumption sets in.
This is Benjamin Caballero. He runs the laboratory for human nutrition at Johns Hopkins University, which is a pretty good school. This is from an article in the New England Journal of Medicine called Obesity and malnutrition in nutrition paradox. 2005, this is — a few years ago I was visiting a primary care clinic in the slums of Sao Paulo, Brazil, the waiting room was full of mothers with thin stunted young children exhibiting the typical signs of chronic undernutrition. Their parents sadly would survive few who visit poor urban areas in the developing world.
What might come as a surprise and many the mothers holding those undernourished infants for themselves overweight. Then he says the coexistence of underweight and overweight poses a challenge to public health programs and the aim of programs to reduce undernutrition which is make more food available, is in conflict with those for obesity prevention which is make less food available. And that could pose the challenge to public health programs in perennial in bold print in italics because as coexistence of underweight and overweight in the same populations in the same family doesn’t pose a challenge to public health programs, it poses a challenge to your paradigm.
Okay, if you believe that the mothers got obese because they took in more calories than they expended, they took in superfluous calories that they didn’t need so that they could get fat, in a brutal way of saying that they snuck outside to eat Snickers bars. While their children are starving, then you believe these mothers were eating calories they didn’t need that they could keep from their children to keep their children from starving to death.
Okay. So we have a paradigm of maternal behavior that says mothers will starve themselves to death before they’ll see their children starved. Okay, how many of you are mothers in here? Probably a lot of. How many of you would let your children starve so you could eat a Snickers bar? Okay, that’s what we’re talking about.
So our maternal behavior paradigm says mother starves so children can live. And our obesity paradigm says the mothers are getting fat because you’re eating calories they don’t need. We have to throw out one of the two of them and what makes his observations so interesting is in physics, the field I grew up in, physicists, scientists spend their whole lives waiting for what they call anomalous observations. An anomalous observation is something that your theory can’t explain because if you find something your theory can’t explain, you could then improve your theory or come up with a new theory that, that can explain which then makes progress.
In physics, for instance, they’ve spent billions of dollars building one atom smasher outside of Geneva in this laboratory called CERN so that they could create one reliable observation that their theory can explain.
In obesity and nutrition research, we’ve been sitting on one for arguably 80 to 100 years, and we don’t pay attention. All we care about is that it doesn’t kind of make sense if we want to solve the public health programs, and one of the issues I come back to over and over again in my book is that obesity nutrition researchers and the public health authorities have been so convinced they know the answer. This energy balance thing, this calories in, calories out that they’ve been blinded even to sort of glaringly obvious anomalies that their theories can explain.
So let’s look at some other inconvenient observations here. For starters, if eating more causes us to get fat eating too much, we should be able to eat less and lose the weight. And it’s not that you know – you can argue, okay, once somebody’s 50 or 100 pounds overweight, eating less doesn’t work but you don’t – you’re not born 50 or 100 pounds overweight, or at least most people are, they get overweight in little bits and pieces, one day you notice you’re 10 pounds heavier than you want to be and your pants don’t fit right or you look — you turning to your husband and saying do I look fat in this outfit? Your husband is trying to lie to you desperately.
And at those points when you’re a little bit overweight, you should be able to cut back on calories and lose the weight. And the fact is it doesn’t work and in fact, in the mid-1950s some of the leading experts on obesity said, look, we can define obesity disorder in which eating less doesn’t work because every one who is obese or overweight knows they’re supposed to eat less or exercise more, some combination of both, everyone tries to do with their whole life.
And if they’re still fat, it means it didn’t work. It’s that simple. So it means for third of the American population it didn’t work, for two-thirds of the American population, and you can actually quantify it in clinical trials, you could do experiments where you tell people to eat less and other people not to. And as a cockring collaboration which is a group that was founded to do unbiased reviews of the medical literature put it, “weight loss achieved in trials of calories restricted diet is so small as to be clinically insignificant”.
Eating less doesn’t work?
One of the interesting things is [Hal Brooke] was a leading pediatric obesity researcher in the mid 20th centuries, wrote a great book on obesity in 1957. And she talked about this and she said, it should it come as a surprise that eating less doesn’t work, or that calorie restricted diet doesn’t work, obese people again they spend their whole life trying to eat less. Having a doctor tell you to do with, or a researcher tell you to do it, if that certainly didn’t work, that would be shocking.
Exercising more doesn’t work also?
Now the other problem is that exercising more doesn’t work also. And by exercising more, I mean to quantify this, because I always get in trouble – expending more energy. We have this energy balance thing, so we either eat too much or we expend too little. So you can increase energy expenditure and hope that you will lose weight, and I could quote meta-analyses on this but I find this more compelling.
In 2007 the American Heart Association, the American College of Sports Medicine published Joint Physical Activity Guidelines. These are people who want us to exercise, who like me believe that physical activity is an inherent part of a healthy diet, healthy lifestyle. And you would expect that they would pin the data to make exercise more attractive, and yet this is what they said in their guidelines. It said, “it’s reasonable to assume that persons with relatively high energy expenditures would be less likely to gain weight over time compared with those with low energy expenditures.” That’s like saying it’s reasonable to assume that a marathon runner would be less likely to gain weight over time than a couch potato, or that if you are a couch potato, you would be less likely to gain weight if you become a marathon runner. Then if you remain a couch potato, those are logically equivalent and then they say so far data to support this hypothesis are not particularly compelling.
And the interesting thing about this is this hypothesis is at least a hundred years old. As early as 1907, there was a famous German researcher named Karl von Noorden, diabetes, obesity specialist who said, maybe people get fat because they take in more calories than they expend and if we could just get them to expend more, they won’t get fat.
As early as 1860, there was a famous British Undertaker who went on a diet and wrote a book about it and said, “Look, when I was younger, I told a doctor I just keep getting fatter and fatter, he told me to take up rowing. And I took up rowing, I bought a boat, I took up rowing and I just got hungry and still fatter.”
And the idea – the point I’m making here is that if the best you could say about a hypothesis and notion that increasing energy expenditure should help you lose weight, or prevent you from gaining it, after a century is that the data are not particularly compelling, maybe your notion is incorrect. Maybe your hypothesis incorrect, doesn’t mean it is. Maybe never studied it right, maybe these people didn’t do enough exercise, we know from The Biggest Loser that if we get people to do six hours a day, and starve them, they’ll lose weight but we don’t know what they’ll do as soon as the show ends.
One of the ways to think about this – it was given to me by a British blogger. And he said and I wish I could remember his name, so I could give more credit than that. Imagine that when I came to Santa Cruz tonight, I also came with the top 10 chefs from the Bay Area where I live, and they cooked a feast of monumental proportions, you know 12 courses of the best food that you will ever taste in your entire life. So when you heard about this lecture, you got an invitation saying, “Come here to Gary Taubes lecture, and please come to this feast we’re having with the best food you’ve ever had and there’s going to be a ton of it – bring your appetite. Come hungry. What would you do to make sure that when you got here you could eat as much of that food as humanly possible?
Okay. So you might see skip lunch that day, or eat less over the course of the day. That’s one obvious thing you’d do. And the other thing you might do is exercise more, right? If you run three miles, you run five or if you spend forty minutes at the gym, you spend six, if this was a day off, you go to the gym anyway. You might say look, I only live five miles from the school, I will walk.
So the two things that you would do to assure that you were hungry — eat less and exercise more — the two things we tell obese people to do to lose weight. Does that strike you as odd and perhaps a sign of something that’s wrong here?
What about practicing energy balance?
The CDC says when it comes to maintaining a healthy weight for lifetime, the bottom line is calories count, weight management is all about balance, balancing the number of calories you consume with the number of calories your body uses to burn off.
Okay. How many of you have tried to basically do calorie counting? And thank you — and how many of you have — when you work out at the gym, go to the aerobics machines and look at the calorie counter and say okay I got like 300 calories, I could stop now, or 500? If you ever actually think about this, this is one of the places where when I was doing my research, I actually tend to get angry because you never think about what this entails. And I was reading a 1937 metabolism text book written by the leading expert on metabolism. And he gave me the calculation I’m about to give you with what it entails.
Let’s just ask ourselves, what does this mean to practice energy balance? How do we do it? So a typical American’s food intake average between men and women is 2700 calories a day, it’s about a million calories a year, it’s about 10 million calories in a decade, it’s about 10 to 12 tons of food.
So now you just ask the question – how accurately do I have to balance calories in to calories out? So I don’t gain any more than 20 pounds over the course of a decade, okay because if I gained 20 pounds in a decade that’s 40 pounds in 20 years, I’ll go from being lean in my twenties as many of us were and many of us are, to being obese in my forties as many of us are and many of us will be, and I don’t want that to happen.
So I want to make sure that I don’t gain any more than 20 calories, just ask what do I have to do to do that, how many calories do I over-eat for that to happen? And the answer is 20 calories a day. If I stick 20 calories a day in my fat tissue that I don’t burn, on average I will gain 20 pounds in a decade.
Here’s the calculation. It’s very simple. 20 calories a day times 365 days a year times 10 years, divided by 3500, which is a reasonable number for the calories in a pound of fat, and you come out to 21 pounds in a decade. That’s one bite of food, two sips of soda. If I eat 150 bites of food over the course of a day and I only burn off 149 of them, and the 150 it ends up in my fat tissue, I am going to become obese. And when [Eugene Dubois], the leading expert on metabolism in the U.S. pre-World War II wrote about this, he said, “This tells you that there’s something wrong here. Obviously there’s something going on. Regulating weight that has more to do with it are conscious balance of calories in, calories out because nobody can do this. This is 0.8 percent accuracy.
So even if you were the Guinness World Record holder on calorie counting, you still couldn’t do it because you have no idea how much you are expending over the course of a day and that’s what Dubois said he said there’s nothing strange in the maintenance of a constant body weight under fluctuations of energy intake and energy expenditure. But the question should be not why are some of us fat, if this is what we have to do to remain lean, why aren’t we all fat, or why aren’t half of us fat and the other half end look anorexic because half of us overshoot in one direction, the other half undershoot in the other. And you could argue, you could say there are ways to get around it and the researchers do it and said, well maybe what we do is we oscillate.
So we start to eat too much, we consume a bite of food too much every day, and we start to get fatter and then as we get fatter, we under eat and we under shoot, so we oscillate around perfect energy balance, which is possible.
How do animals do it?
But the question is then, how do animals do it, because they don’t know they’re getting fatter, right? They don’t have mirror, they’re not looking in mirrors and not asking their husbands their clothes aren’t fitting. So if we do it by oscillating, how do they do it? Because the one thing we can bet they’re not doing is counting calories over the course of the day or consciously doing this 20 calories a day thing.
So here’s another way to look at it – some more inconvenient observations and now I am going to show photos of naked human beings — and I apologize – I am going to be channeling the way pre-World War II European researchers thought about this, because they had a different theory of obesity. So I am now going to tell you how they thought about the problem. And I am going to say by the way that pre-World War II all meaningful medical research was done in Europe. The lingua franca of science was German, and if you wanted to be a medical researcher or actually a physicist or a chemist, or any field, you had to at least read Germans, you could read the German literature, and you had to speak German ideally so you could move to Germany and Austria and train with these people that all the leading experts in nutrition and metabolism in the US pre-World War II did.
So this is how those excellent scientists thought about obesity, and today you won’t see photos of naked human beings in obesity textbooks, you might see naked rats. These Europeans thought you could learn a lot from looking at not just whether someone’s fat or not, which is what we get from a BMI or body mass index, but how they get fat, where they get fat, when they get fat. All these things will tell us something about why they get fat.
So for starters we have genetics. Here is a lean pair of identical twins and an obese pair of identical twins. Our calories in, calories out notion might explain why these women are fat, and these women are lean, and these ones took in more calories than they expanded. And these practice perfect energy balance. But that is nothing about why they have the identical bodies and why they have the identical bodies.
We know obesity is a large genetic component. We also know that obese identical twins don’t just look alike, they have the same bodies. Body types run in families.
So what’s controlling that? The amount of calories they took in and expended can’t be doing, it’s something about their genes are giving them the same body even when there is a 50, 70,80 pounds overweight. What’s doing that? Why do they have? Why does the fat go to the same places on these women and on these women too for that fact?
Our calories theory says nothing about this, something else must be regulating where the fat goes and how much. The idea that the genes just regulate how much these women eat and exercise is a little absurd.
Here is another way to look at it. Animal husbandry, for hundreds of years we’ve been breeding farm animals to be more or less something. So here’s a lean breed of cattle, it’s a Jersey cow, it’s a dairy cow. You could see the [swollen other] and here is a meat cow, Aberdeen Angus, it’s a stocky fatty muscular cow, you could see the meat from this cow. Actually this is probably a bone, I should have switched the photos but would have been the same.
You could see the fat accumulation. You could just ask, we know because they are different breeds, what’s regulating this? It’s Genetics, it’s controlling it. What are the genes controlling? Why does this animal so stocky and this animal so lean? And now the gene’s controlling how much they eat and exercise, how much calories per bite per graze of grass this one takes in versus out, maybe this one, the genes tell it to graze only 10 hours a day and this one 12 hours a day, or maybe the genes promote this one – it gets dark it goes for run at night like that far side cartoon. And this one it gets dark and it’s genetics make it go in and watch television.
I mean it’s obviously absurd, right? And what the genes probably — we could think of it this way. This is an animal that — all ethical moral issues aside, we can think of it as a machine that takes in fuel here and converts it to milk. And we want that — that’s a very energy expensive thing to do. We want it to happen as efficiently as possible. We don’t want it bulking up. We don’t want our fuel being lost elsewhere. And this animal, we do want the fuel going to muscle and fat and proteins. It’s not a milk cow, so maybe what the genes do is determine not how many calories animal takes in or expense but how it uses them. The technical term is fuel partitioning.
In this animal, the fuel is partitioned to milk, and in this animal, it’s partitioned to protein and fat. So what our genes determine is this how the animal partitions fuel or how the human partitions fuel.
Here is another problem – sexual variations. Okay, men and women fat in different ways – so it’s been well-known, men get fat above the waist, women get fat below the waist. Both of these people would have taken more calories than they expand to get fat.
But here, this guy it went here — this woman, it went below the waist. This guy doubled his risk of heart disease by getting fat, up here this woman did not. So what do the calories have to do with it? That’s a question. What determined where the fat went and why did the fat in one place double the risk of heart disease where the fat in the other place doesn’t?
You can look at this at puberty. Boys and girls go through puberty. They start out puberty with roughly the same amount of body fat, about 7%. And then as they go through puberty, the boys lose fat and gain muscle and the girls gain fat in very specific places.
So by the time they’re done with puberty, the girls have about 50% more fat than the boys do. Both of them got bigger. Both of them got heavier. They both took in more calories than they expended but the boys lost fat and gained muscle, and the girls gained fat in very specific places.
What do the calories have to do with it? This positive energy balance is – calories-in greater than calories-out have to do with that. And we know why they got – they both grew because they were secreting growth hormone. The boys gained lost fat and gained muscle because of testosterone. The girls gained fat in specific places because of sex hormones. The fact that they were in this positive energy balance taking in more calories than they expended is irrelevant.
Okay. Last slide, by this point in my book, by the way I had more of these in my editors. This looks like a freak show here. We want to sell books, we don’t want a circus sideshow.
Lipodystrophy – that’s a disorder of fat accumulation. Lipo means fat, dystrophy, disorder. This is a rare disorder called progressive lipodystrophy. By the 1950s, there are about 200 of them on record in the United States. This photo again comes from a 1940 textbook.
Progressive Lipodystrophy was called progressive, because in this case, most of the cases were women and they start losing fat in their forehead, all subcutaneous fat and it progresses downward. In one case, the British physician actually measured it at moving downward at the rate of about an inch a year. And then you get to the waist, and often in these cases, it would stop and you would get lower body obesity.
So the way these Europeans thought about it, they used as an example and they said, look, are we going to blame the top half on undereating and the bottom half on overeating? And if this woman had 10 more pounds of fat on her upper body, five more pounds – she actually had a BMI of around 34 anyways. So she was technically obese. But if she had just enough fat so that you couldn’t see the emaciation, you couldn’t see the lipodystrophy, and she’d gone to the doctors and so the doctor would say look, eat less, exercise more.
The point of this is that if overeating can’t explain localized obesity, why can’t use it to explain generalized obesity? Obviously there’s something else going on here. And that’s what we want to find out.
So let me just answer the question – why is it that we believe in this energy balance thing to begin with, and the answer is physics. So the first law of thermodynamics and often when you give — whenever somebody like me argues that it’s not about energy-in, energy-out, somebody accuses you of not believing in the laws of thermodynamics.
I actually was on the Larry King Show, and Jillian Michaels came on the air from Los Angeles and gave me a lecture on the laws of thermodynamics on national television. And I was literally speechless. I mean you could watch this clip on YouTube – I have a physics degree from Harvard. I was a lousy student. I was a B- student but I understand the laws of thermodynamics. It may have been the high or low point in my life depending on how you look at it.
First law of thermodynamics
Why do we believe – the first law of thermodynamics. Energy conservation – change in energy of a system, that’s what we mean by Delta E is equal to the energy-in minus energy-out. Okay, so this is based pretty simple. It means if a system gets more energy and it’s got to take in more energy than expend, and if a system gets less energy, it’s got to let out more energy than it takes in. That’s why it’s called the law of energy conservation. The idea is we can’t create energy from nothing. Energy can only change its form. It can’t be created or destroyed. It’s conserved.
So what we do is we say, look, here is a fat mass, Delta E, and if the energy you eat goes up and you don’t compensate by increasing your expenditure, then Delta E has to go up. So you get fatter, right?
And if you become sedentary, it goes down and you don’t compensate by eating less, Delta E goes up, you get fatter. Therefore eating too much or exercising too little is a cause of obesity. And the point is there is no error of causality here. This is like an eighth grade physics mistake that we all made. Actually I guess in eighth grade you’re not even learning physics, you are just learning science.
So we all make it, it’s been made in the United States since the 1950s. It wasn’t made pre-World War II. By no error of causality, what this law says is that if someone gets bigger, if I get fatter, I have to take in more energy than I expend. But it says nothing about why? There is no causality here. It doesn’t say I got fat because I took in more energy than I expend. It just says that if I get fatter, this has to happen. And if I actually am in negative energy balance, if I am expending more energy than I take in, I have to get thinner. But it doesn’t say that the way to get thinner is to do this. There is no causality in this law. It just says if one thing happens, the other thing has to happen because that’s the way the universe works. Period.
So let me give you an example of how absurd this is that we take this and we put a law of causality on this. Imagine that instead of wanting to know why you get fat, why your fat tissue fills up with such energy, you want to know why is this room full of such energy, instead of energy in the form of triglycerides and fats, so we have energy in the form of people in this room.
And so you asked me, okay, Gary, why is this room so crowded? Why is this so full of energy? I’d say because more people entered than left. Have I told you anything that you didn’t know anything at all meaningful? This is what logicians would call vacuously obvious.
It’s true, of course, more people entered than left. That’s what you say to me, Gary, of course, more people entered than left, but why is the room so crowded? And then I say to you, I have said the equivalent by the way we get fat because you take in more energy than you expend.
So now you say, but why is this so kind of – look, if more people enter than leave, it’s got to get crowded, right? Which is the equivalent of saying, if you take in more energy than you expend, you have to get fatter, but I still haven’t told you anything meaningful. Obviously more people entered the room than left. That’s a given.
The question is why is the room crowded? Well, maybe it was pouring outside, and everybody ran in to get out of the rain. Maybe there was free food, maybe there was free drinks. Maybe there’s a birthday party. Maybe I put large men in motorcycle jackets at the door and they grabbed everyone who walked in and threw them into the room and won’t let them leave. There are lot of explanations for why the room is crowded and it’d have to do with the conditions outside the room, the conditions inside the room, and the conditions at the barrier.
But the fact that more people entered than left is irrelevant, it’s obvious. And what I’m saying is, if you tell someone that they got fat because they took in more energy than they expended, you’re just saying I believe in the laws of thermodynamics, but you’re saying nothing meaningful.
And when a government says that you get fat because you took in more calories than you expended, they’re telling us nothing meaningful. It’s completely irrelevant. If you got fatter, you had to take in more energy than you expended. There’s no causal information in there, and just making that mistake is why obesity researchers went off the rails. And it’s one of the things when I was doing my research and I was reading the literature in the 1950s, and I could see this happening.
After it was explained to me what the mistake was, because I believed just like everyone else that obesity was all about energy balance, I was stunned like how could we do this. How could we actually think this equation says anything about why you get fat. How about thermodynamics says anything about why we get fat. It’s not physics, it’s biology.
So let’s have an alternative hypothesis. I hope I at least made you doubt the idea that this is about energy balance. If there are any doctors in here, I hope that you will never again use the phrase you got fat because you took in more calories than you expended.
Okay. Here’s the alternative hypothesis. Obesity is a disorder of excess fat accumulation. This is the way the Germans and Austrians look at it pre-World War II. So instead of saying obesity is sort of energy balance or overeating or sedentary behavior, they started from first principles, which is what you’re supposed to do in science, you’re supposed to make a statement of the problem that has the least assumptions attached.
So obesity is sort of excess fat accumulation. You could say obesity, having too much fat is a disorder of having too much fat, which sounds so simplistic as to be meaningless. And if you just said that and you’re a doctor you might, first question that might come to mind is, I don’t know what regulates fat tissue. Because if you’re saying it’s about eating too much, exercising too little, you don’t care what’s regulating fat tissue. You only care about what to making somebody eat too much.
Okay. In this hypothesis, overeating and inactivity or compensatory effects are not causes. So by that I mean that whatever makes you fat causes you to eat more or exercise less, causes overeating or sedentary behaviors, it’s not the other way around. And the way this was phrased to me by various researchers, we don’t get fat because we overeat. We overeat because our fat tissue is accumulating excess fat.
So to show that this isn’t the rhetorical argument I am making, an example used by the pre-World War II researchers were growing children. I kind of got into this with the puberty thing but I will do it again.
Here is an extraordinarily cute young child in 2006 who weighed 20 pounds who was one-year-old. Okay, three years later, he weighs 45 pounds. He’s gained 25 pounds in three years, he is overeaten. He has taken in more calories than he expended, right? We know this – as he’s grown. Children grow.
So the question is did he grow because he over ate, or did he overeat because he was growing. And the fact is he was growing because he was the secreting growth hormone and he needed all this energy both for the act of growing and to create new structures and bigger structures. So he grew – he over-ate because he was growing. He didn’t grow because he was overeating.
And what I’m arguing is in any example in biology, here is another one. The tumor cell – cancer. This is a gruesome photograph of cancer cell growing. Here is the tumor. It’s getting bigger and bigger and bigger. It’s taking in more calories than it’s expensed, that’s what the first law of thermodynamics tells us, but we don’t care. Because we know that the reason it’s growing, it’s got various genes that are broken – oncogenes that will stimulate growth and tumor suppressor genes that are supposed to break growth, and because of that is being driven to unfettered growth and not stop, and it’s taking in more calories than it’s expensed because it’s growing.
In every biological system, I can — I’ve yet to find in a counterexample – growth is the cause and eating too much or positive energy balance is the effect, it’s never the other way around, except in human obesity where we put the cause on some positive energy balance.
So this theory was known as a Lipophilia theory. Prior to the First World War, it was a German Austrian hypothesis. The two leading proponents were Gustav von Bergmann who was the leading German authority on internal medicine pre-World War II. And today one of the leading awards in the German Society of Internal Medicine is the Gustav von Bergmann Award; and Julius Bauer who was a University of Vienna endocrinologist and geneticist. He was a very famous man and is still famous today in Austria. So these people weren’t quacks, they were very well respected scientists and was more or less fully accepted in Europe by 1940. And the problem is 1940 was a really bad year.
By that time, Bauer had fled Austria in 1938. The Nazis invaded Austria. The war breaks out. This German school evaporates. This German Austrian school evaporates. And after the war, we don’t pay no attention to this obesity and nutrition research. The beliefs we grew up with were created by young American researchers post-World War II without any concern to what these Germans and Austrians had learned prior to the war because they didn’t like the Germans – for good reason.
So the lingua franca of science went from Germany pre-war to English after the war. In some fields like physics, it didn’t have an effect because the Germans chased all the brilliant scientists out of Europe and we embraced them because he had atomic bombs and hydrogen bonds to build and the Cold War to fight, but in medicine and public-health we wanted nothing to do with these people.
So this pre-World War II theory, this Lipophilia theory was forgotten, and then we created obesity as an eating disorder. But let’s look what this theory was.
Here is Lipophilia in a nutshell by Bauer. This is like a malignant tumor like the fetus, the uterus or the breast of a pregnant woman, the abnormal lipophilic tissue seizes on foods – so lipophilic means love of fat. And the idea is that some tissue will readily absorb fat just like an other tissue won’t – this is what they call Lipophilia. And the metaphor they used was hair growth. We just grow hair in some places but not in others. We grow hair on top of our head but not on our foreheads. We grow fat in some places but not in others and we all know where we grow fat, we all know the places we don’t.
And they said, just like some people are hairier than others, some people are fatter than others. And this is all regulated by hormones and enzymes and central nervous system things and we have to know what those are.
So the abnormal lipophilic tissue seizes on foodstuffs, even in the case of under-nutrition, maintains its stock and may increase it independent of the requirements of the organism. So see, even in the case of under-nutrition, we can begin to explain these obese mothers with their starving children. Doesn’t matter if they’re getting starved, the fat tissue like a tumor is doing what it wants. A sort of anarchy exists. The adipose tissue lives for itself but does not fit into the precisely regulated mechanism of the whole organism.
Okay, think of the fat tissue like a tumor, suddenly something has stimulated it to grow more so in some than others. Some of us are lucky and it never happens. And the question is what is that something?
So you can look at animal models of obesity and just ask the question – there is 100 different ways you can make animals obese nowadays and you can ask the question – when I make them obese, do I make them eat too much and exercise little, or do I change the regulation of their fat tissue?
And [Jean Myard] famous — the most influential nutritionist of the United States 1968, he studied a strain of obese mice and he said, look, these mice will make fat out of their food under the most unlikely circumstances even when they’ve starved. It’s not that they get fat because they eat too much; they get fat if they eat it all.
In fact, there are copious animals model obesity where you could starve the animals and they’ll die with their fat tissue intact. Okay, so you can starve, actually there was type of rate color — and you could put this rate on a diet from birth, and this was actually done by a researcher at UC Santa Cruz in the late 1970s, so you wean them from their mothers and you put them on a diet and then you compare their weights to their littermates that could eat as much as they want and the ones on the diet actually get fatter than the ones who get to eat as much they want. So they don’t weigh as much but they have more fat tissue and this researcher M.R.C. Greenwood said, they cannibalized their brains and their muscle and their organs, so they have smaller brain, smaller muscle, smaller organs in order to feed this drive to get fat.
What you do is you increase the sort of lipophilia, the fat tissue and then they do drive calories into the fat tissue and the animal responds by eating lesser, exercising more. So you just ask some questions – in vertical growth we know that growth is a cause and positive energy balance is the effect. And when we look at animals we know that growth is a cause and positive energy balance in the effects but why not men?
And if obesity is sort of excess fat accumulation, what regulates fat accumulation? So this is a quick course. Now I am going to get a little bit technical. Okay, but in five minutes, you’re going to have to know everything you need to know about your fat tissue. I’d like to say you’ll know more than what your doctors know, but your doctors were actually taught this in medical school, and they were taught it was irrelevant to obesity. And you think about that — we have a disorder of excess fat accumulation and we don’t care what regulates our fat tissue because we know it’s all about eating too much and exercising too little. I am going to tell you what regulates your fat tissue.
So lesson number one is fat circulates in the human body in two forms – three forms but this two we’re interested in – triglycerides and fatty acids. Here’s a fatty acid, it’s a long chain of carbon and oxygen and it bounds together into fatty acids, so you get three fatty acids bound together with the glycerol molecule into a triglyceride.
So fat is stored as triglycerides is big thing, but fatty acids are burned for fuel — this long thin thing – fat enters and exits fat cells as fatty acids, and inside the fat cell, fatty acids continually cycle into triglycerides and back.
Let me show you what this looks like. Here is a fat cell. Here is the fat cell membrane. Your fatty acids outside the membrane, and the reason we store fat as triglycerides because triglycerides are too big to get through the membrane. It’s like if you’ve ever bought a piece of furniture and you brought it home and found out it was too big to fit into the room, through the door into the room that you bought it for, so what you have to do is like take it apart and then rebuild it inside, I had to do this with an IKEA bed once and I wanted to shoot myself. That’s what we do.
In fatty acids, actually they start off in lipoproteins as triglycerides, there is an enzyme here called lipoprotein lipase that breaks them down into fatty acids. The fatty acids are small enough to fit through the fat cell membrane. That’s why they – that’s the way we traffic the fatty acids cross the cell and that’s what we burn fatty acids. Inside the cell they are put together into triglycerides fixed here, because this guy is too big to get out.
And then they are broken down again into fatty acids. There are enzymes in the cell that break them down into fatty acids and as fatty acids they could escape through the cell.
So here’s where our energy balance thing becomes meaningful. If this is like insanely simple – if more fatty acids go into the cell than leave it, you get fatter. At least the fat cell does. And if more fatty acids go out of the cell than go in, you get leaner. So anything that works to move fatty acids this way makes you fatter, anything that works to move fatty acids that way makes you leaner.
What you want to know is what regulates this process, because that’ll tell you whether your fat cells are getting fatter, and if your fat cells are getting fatter, you’re getting fatter and it’s kind of simple actually – remember the German hypothesis vanishes in 1940. At that time they didn’t have the tools necessary to figure out what regulates fat tissue. That was 1956, three groups of researchers discovered a mechanism to measure the fatty acid level in the blood.
In 1959, Rosalyn Yalow and Solomon Berson discovered what’s called the radioimmunoassay (RIA) to measure hormones in the bloodstream. Yalow later got the Nobel Prize for this work. Berson had passed away, and as they pointed out, by 1965, insulin is a principal regulator of fat metabolism. The hormone insulin — this is a diagram from 2010 just to show that this hasn’t gone away. But the hormone insulin is a hormone that puts fat in fat tissue and you could see here’s white fat tissue and here is insulin – insulin – insulin – insulin, putting fat in and here’s insulin suppressing the mobilization of fat. And these other hormones play a little bit of role of getting fat out of fat tissue.
But it’s is the hormone insulin fundamentally that puts fat in, and as Alan Berson said back in ’65, release of fatty acids from fat cells requires only the negative stimulus of insulin deficiency. Okay, again here’s a suppression of fat mobilization from this 2010 book and again it’s insulin – insulin – insulin – if you want to get fat out of your fat tissue and burn it for fuel, you have to lower insulin levels. This was known back in 1965. It’s still true.
Insulin – Fattening hormone
And the funny thing is insulin had always been known to be a fattening hormone. Now there were debates about how it worked and why. But here’s a good example from a textbook you could get online at the Library of Medicine – Endocrinology: An Integrated Approach.
So here’s a young woman’s – it’s the photo of a young woman at age 17 was diagnosed as type I diabetic and for the next 47 years she injected herself with insulin in two spots on her thighs. She ended up with these huge fat masses. And this textbook said the overall action of insulin on the adipocyte – that’s a technical word for fat cell – it’s to stimulate fat storage and inhibit mobilization – the remarkable effects of locally injected insulin and the accumulation of triglyceride fat into fat cells are graphically illustrated here.
This woman also took her 40 years to build those fat masses. She probably didn’t notice at first and you could argue that she was doing to her thighs where we’ve done to our guts and below our waist.
So here is the lesson – the bottom line of adiposity 111 – when insulin is secreted, our chronically elevated fat accumulates in the fat tissue, that is conventional wisdom. That’s in the endocrinology textbook, it’s in the biochemistry textbook.
When insulin levels drop, that escapes in the fat tissue and the fat depots shrink. If you want to get fat out of fat tissue, you got a lower insulin levels, and we secrete insulin primarily in response to the carbohydrate content of our diet.
The way it was described to me by George Cahill, Harvard emeritus professor who did some of this research back in the 1960s as carbohydrate is driving insulin is driving fat. And if you remove these three words, is driving insulin, you have the logical equivalent – carbohydrate is driving fat.
So insulin driving fat is conventional wisdom. Carbohydrate is driving insulin is conventional wisdom. You put all three together, remove these words – carbohydrate is driving fat – and now you’re in quackery.
When I lectured to medical schools, I have given grand rounds at the Mayo Clinic and elsewhere and the doctors are with me – as soon as I mentioned the word carbohydrates, oh, my God it’s that Atkins crap. He’s a quack. You could see it happening on like half of them, their faces – he fooled us, he sounded intelligent, he sounded logical, he is making really fascinating points. And then he said the word “carbohydrates” in cohort with the word “fat” and he became a quack and they leave the room completely unconvinced because they’re unconvinced going in.
By the way – not all carbohydrates drive obesity. We could break it into two – into fat accumulation. They are high glycemic index carbs, that’s like crackers, pasta, bread, potatoes, rice. All the foods of my mother’s generation thought were fattening, they happened to be the base of the food guide pyramid.
And then sugar – sugar, sucrose and high fructose corn syrup, I get that you heard a lecture last year from Robert Lustig but there’s good evidence that these foods – these nutrients which are half fructose and roughly half glucose, roughly half fructose cause a condition called insulin resistance. So the sugars could be the fundamental problem and then make all those other carbohydrates fattening.
The question you can then ask yourself is – should this be surprising? I am now arguing that – if we don’t actually eat too much or exercise too little, we get fat because the quality of the carbohydrates in our diet have changed. We’ve gone from eating carbs that were hard to digest, had a lot of fiber in, to eating refined carbohydrates and sugar in enormous quantities and that causes a condition called insulin resistance – causes to change the way we partition fuels, so that we now partition fuels into our fat tissue because insulin levels stay elevated.
So what’s interesting is from 1825 at least through the mid-1960s, the conventional wisdom was that carbohydrates were fattening. This British Journal of Nutrition article 1963 was written by one of the two leading British dietitians and this was the first sentence – every woman knows that carbohydrates are fattening – this a piece of common knowledge which few nutritionists would dispute.
Dr. Spock’s Baby and Child Care – how many of you have used Dr. Spock to raise your kids? Six editions – from the very first in 1946 to the last before Spock died in 1992 had this sentence in it – the amount of plain starchy foods, cereal breads, potatoes taking is what determines in the case of most people how much weight they gained.
What’s interesting is if you went into a hospital in the late 1940s or 1950s and you were obese, you will be put on a diet for obesity. Harvard Medical School, Stanford Medical School, Cornell Medical School all published their diets in the literature and they were all effectively the same as this one which comes from a British textbook – The Practice Of Endocrinology in 1951, Raymond Greene was the leading British endocrinologist – it’s hormone specialist – he was the brother of Graham Greene, the novelist.
This was their diet for obesity – foods to be avoided: bread and everything else made with flour, cereals, potatoes, foods containing much sugar, all sweets.
You can eat as much as you like at the following: meat, fish, birds, all green vegetables, eggs, cheese, fruit, except bananas, grapes. He didn’t even know about insulin yet.
But when he knew, was these foods you avoid because they’re literally fattening? And these foods, you can eat as much as you want them because they are literally not? Okay. It’s not about the quantity you are taking in, it’s about certain foods are literally fattening and those foods are the foods that have the ability to chronically elevate the hormone that regulates fat accumulation.
So if you just go to conclusions – again it’s biology, it’s not a physics thing. So obesity is sort of fat accumulation, not energy balance, not overeating and sedentary behavior. Fat accumulations regulated fundamentally by insulin and dietary carbohydrates – carbohydrate driving insulin is driving fat and the only non-pharmaceutical remedy of which we have none is to remove the carbohydrates.
So it’s even harder than that. This one makes it so hard to accept – if you remove the carbs, you want to replace those calories because it’s not a caloric issue. It’s not about how much you eat. If you are overweight or obese, you have a lot of body mass to run, you have a large caloric requirement. So you want to replace those calories, so you don’t actually replace them with protein, you replace them with fat. Actually even saturated fat arguably.
So a calorically restricted diet, carbohydrate restricted diet is a high fat diet, and this was a problem. Because if you ask where did the science go – I’m telling you obesity was solved in the 1960s – with 1960s era endocrinology, and we ignore it. We literally threw it out. In my book, Good Calories, Bad Calories, I document – I show this happening in the obesity conference, in the textbook, how the leading authorities in the field were so threatened by this idea that carbohydrates and insulin caused obesity and that diet doctors like Atkins and others jumped on it first, that they threw it out. They said it’s irrelevant. We don’t care. But you could see it happening as early as 1965.
Remember 1965 was when Yalo and Berson were saying the way to get fat out of fat tissues is to lower insulin. The New York Times has an article – New Diet Decried By Nutritionists – dangers are seen in low carbohydrate intake”. So this is the first paragraph – Some of the nation’s top nutrition experts are concerned is a new popularity of the low carbohydrate reducing diet which one of them calls nonsense. Nonsense, because you could tell obese people they could eat as much as they want. And when we know they got fat to begin with by eating too much, right? So it violates the laws of thermodynamics.
In another – this was Jean Meyer, the leading nutritionist of the day compares to mass murder. Mass murder, because you’re putting them on a high fat – high saturated fat diet. When we had come to start believing in the 1960s that fat and saturated fat caused heart disease.
In 1965, there was actually no experimental evidence to support our belief that fat and saturated fat caused heart disease, and I would argue that today there’s still virtually none. At the same year that – physiologists were saying insulin drives fat accumulation, carbohydrates drive insulin. So a reasonable hypothesis – if you want to reduce fat accumulation, reduce insulin, reduce carbs, the nutritionists are saying you’re going to kill people – it’s equivalent to mass murder.
The only thing that happened is the calories in, calories out idea. So if you look at an endocrinology textbook today or biochemistry textbook, this is Lenningers’ Principles of Biochemistry; it’s a leading biochemistry textbook. And you go to adipocyte in the index which is fat cell and then you see what page — you go to the page for fat cell and you look up – what makes fat tissue or fat cell fat? This is what it says.
High blood glucose – that’s high blood sugar which comes from eating a carb-rich meal elicits a release of insulin, which speeds the uptake of glucose by tissues and favors the storage of fuels as glycogen – that’s the storage form of carbohydrates – and triglycerols – fat – while inhibiting fatty acid mobilization adipose tissue.
So what makes a fat cell fat? Dietary carbohydrates driving insulin and blood sugar. What makes people fat to a first approximation of obesity is a result of taking more calories in the diet than are expended by the body’s energy consuming activities.
It’s a different mechanism. I actually had a conversation with the guy who wrote the textbook that I showed you those – 2010 textbook that I showed you those diagrams from. He just retired from Oxford, where he is now an emeritus professor. We were talking on the phone. I was interviewing about this insulin resistance stuff for an article on science. And he spent 20 minutes explaining to me how insulin makes fat cells fat.
And then he started talking about overeating as a cause of obesity. And I said, wait, wait – you just spent 20 minutes explaining that fat cells get fat because of insulin, and then when you got to humans, it was this overeating thing. You switched the mechanism only – why? And he said, “I never thought of that”.
And we are so programmed to believe this is true that it has to be true. That even the people who understand, have spent their whole lives understanding what makes a fat cell fat, and we are the integration of all our fat tissue, can’t understand that the same thing that makes our fat cells fat is what makes us fat.
Okay, by the early 1990s with the food guide pyramid, the same foods at my mother’s generation and every woman knows is fattening were institutionalized as the staple of a healthy diet. Carbohydrates went from being literally fattening to heart healthy diet foods. And I’ve lived through this. Many of you, the older people in this room lived through that transformation.
I lived in Paris in the mid-1980s and no self-respecting Frenchwoman over the age 25 would eat any of these foods, you know the Baguetting. It’s always what about the Baguettes – it’s the 12-year-old you see riding on their bicycles with the baguettes in the back, or the 18-year-olds, not the 30-year-olds or the 40-year-olds because they knew these foods are fattening.
We made this staple of a healthy diet and in doing it we made sugars healthy. Because sugars are low-fat – there is no fat in sugar. So they are all these foods – the iconic example was low-fat yogurt. You take the food that what Michael Pollan would call a food – full fat yogurt. You remove a little bit of the fat, it becomes low-fat yogurt. And you replace it with fruit and high fructose corn syrup.
So you’ve replaced it with that – you’ve taken away about 50 calories of fat and added about 90 calories of high fructose sugar. Now it’s a health food. And we all eat, then we serve it to our kids for breakfast. I’m going to go on for two more minutes with my own stick – what’s the difference between low-fat yogurt and dessert? Maybe the chocolate content, I don’t know the butter content. That’s it.
We started with this question – what made those populations fat? I quoted Richards in 1973 that most Third World countries that have high carbohydrate intake as their economic dependence is predominantly agricultural, the heavy dependence on nondairy produces, it is conceivable that the ready availability of starch in preference to animal protein contributing as it must the main caloric requirements of these populations leads to increased lipogenesis – that’s fat formation and the development of obesity.
And I think the only thing you miss is you probably need sugar in that as well. We solved the obesity problem in the 1960s before the obesity epidemic and we’ve been going backwards ever since. And When I want hoping to get from a room like you folks is to get help bringing us back 50 years in time to when we actually understood this.
Okay, thank you very much.