Dhru Purohit Show - #241: Why We Get Fat and How to Actually Lose Weight with Gary Taubes
Episode Date: October 4, 2021Why We Get Fat and How to Actually Lose Weight with Gary Taubes | This episode is brought to you by Vivobarefoot and InsideTracker. For decades we have been taught that fat is bad for us, and that th...e key to a healthy weight is eating less and exercising more. Yet despite this advice, we have seen unprecedented epidemics of obesity and diabetes. Today on The Dhru Purohit Podcast, Dhru talks to Gary Taubes, an award-winning science and health journalist, and co-founder and director of the Nutrition Science Initiative (NuSI). He is the author of The Case Against Sugar, Why We Get Fat, Good Calories, Bad Calories, and, most recently, The Case for Keto. Gary is a former staff writer for Discover and correspondent for Science. He has written three cover articles on nutrition and health for The New York Times Magazine, and his writing has also appeared in The Atlantic, Esquire, and numerous "best of" anthologies, including The Best of the Best American Science Writing (2010). He has received three Science in Society Journalism Awards from the National Association of Science Writers, and is also the recipient of a Robert Wood Johnson Foundation Investigator Award in Health Policy Research. In this episode, we dive into: -The real cause of weight gain and obesity (7:53) -The missing piece when it comes to obesity research (8:55) -Why people who fatten easily can get fat eating exactly as lean healthy people do (14:39) -Why the obesity and diabetes epidemics continue to get worse (19:33) -The safety of a low-carb, high-fat diet (29:09) -Why obesity is not a calories in, calories out problem (42:44) -The carbohydrate-insulin model and obesity (47:26) -Foods that cause hormonal imbalances and cause our body to store excess fat (53:29) -Why carbohydrate abstinence needs to be approached the same way we approach other addictions (1:02:01) -The connection between insulin resistance and chronic disease (1:07:48) Also mentioned in this episode: -The Carbohydrate-Insulin Model: A Physiological Perspective on the Obesity Pandemic - https://academic.oup.com/ajcn/advance-article/doi/10.1093/ajcn/nqab270/6369073 -How a ‘Fatally, Tragically Flawed’ Paradigm has Derailed the Science of Obesity - https://www.statnews.com/2021/09/13/how-a-fatally-tragically-flawed-paradigm-has-derailed-the-science-of-obesity/ -What If It’s All Been A Big Fat Lie - https://www.nytimes.com/2002/07/07/magazine/what-if-it-s-all-been-a-big-fat-lie.html -The Doctor’s Farmacy Podcast Episode #166 - Who Should Eat Keto and Why - https://drhyman.com/blog/2021/04/14/podcast-ep166/ -Good Calories, Bad Calories: Fats, Carbs, and the Controversial Science of Diet and Health by Gary Taubes - https://amzn.to/3CTeWXr For more on Gary you can follow him on Twitter @garytaubes, and through his website http://garytaubes.com/. Get his book The Case for Keto: Rethinking Weight Control and the Science and Practice of Low-Carb/High-Fat Eating, at https://amzn.to/3m2eAai. Interested in joining The Dhru Purohit Podcast Facebook Community? Submit your request to join here: https://www.facebook.com/groups/2819627591487473/. This episode is brought to you by Vivobarefoot and InsideTracker. Vivobarefoot footwear is designed to be wide, thin, and flexible, so you feel as close to barefoot as possible. They promote your foot's natural strength and movement and studies show that foot strength increases by 60% in a matter of months just by walking around in them. Right now they’re offering my community 20% off their first order at vivobarefoot.com/DHRU. Right now, they’re offering my podcast community 25% off. Just go to insidetracker.com/DHRU. Learn more about your ad choices. Visit megaphone.fm/adchoices
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The fat tissue is exquisitely sensitive to insulin.
It's the most insulin sensitive tissue in the body.
So you have to, for most of us, if you want to get fat out of our fat tissue, we have to
minimize the insulin or our circulation.
Hi, everyone, Drew Brod here.
Today's episode, we're talking about the truth of why we actually get fat.
And it's not because we have more calories coming in than we have calories going out.
there's actually a whole different view on why we get fat.
And today's guest, author and journalist Gary Taubbs, is going to break it down for us.
He's part of a group of scientists and doctors who just published a landmark review paper on this exact topic.
If you're curious and you want to know the truth about why we actually get fat, this episode is for you.
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Welcome to the Drew Perraud podcast.
Each week we explore the inner workings
of the brain and the body
with one of the brightest minds in wellness, medicine, and mindset.
This week's guest is Gary Tobs.
Gary Tobs is an award-winning science and health journalist
and the co-founder and director of the Nutrition Science Initiative.
He's the author of The Case Against Sugar, Why We Get Fat, Good Calories, Bad Calories,
and most recently, the case for keto.
Gary is a former staff writer for Discover and a correspondent for science.
He's written three cover articles on nutrition and health for the New York Times magazine,
and his writing has also appeared in the Atlantic, Esquire, and numerous best-of anthologies,
including the best of the best American science writing.
He's received three Science and Society Journalism Awards from the National Association of Science
Writers and is also the recipient of the Robert Wood Johnson Foundation Investigator Award in Health Policy Research.
On today's podcast, we dive deep into the subject of why we truly get fat as a society.
It's not just calories in and calories out known as the energy balance model.
There's something else that's at play.
And Gary, along with the few of his colleagues, have recently published a major review
paper in the American Journal of Clinical Nutrition called the Carbohydrate Insulin
model of physiological perspective on the obesity pandemic. Gary, thanks for being here on the Drew
Proa podcast. It's a pleasure to finally get the chance to interview you. Drew, it's a pleasure to
be here. Let's jump right in. When it comes to all things obesity, fat, and weight gain,
I'm going to steal a question from Peter Thiel. And I'm going to ask you, what is an important
truth on these subjects that you believe that this?
very few people agree with you on the topics of obesity, fat, and weight loss.
Okay.
That obesity, this is an easy one.
Thank you.
And thank you, Peter Thiel.
That obesity is caused, not caused by overeating, by taking in more energy than we expend,
by gluttony or sloth or, you know, whatever you want to call it.
So I believe it's a hormonal regulatory disorder, a constitutional disorder.
And that one of the reasons we've made so little progress for the past century on treating
and preventing obesity is because of this idea that you get fat because you eat too much.
So the person who's following along with the subject who may not be familiar with all the nuances
can immediately think, but Gary, the World Health Organization, they're out there talking about
calories in and calories out when it comes to this important topic of obesity that they've dressed
over the years. So what is it that we're not getting when it comes to these public institutions
and this legacy debate that's been going on? What is the missing piece of the puzzle that has
them arrived to a different conclusion? Okay. So let's talk about.
first of all, why I'm here. So I'm a journalist, right? I'm not a doctor. I don't have a PhD. I'm not
an academic researcher. I was a very well-respected journalist in some corners. I still am.
I got into this 20 years ago because I wanted to, we have obesity and diabetes epidemics that were
becoming very evident back then, and I wanted to know if maybe our understanding of these disorders were
incorrect. So the one thing I did, which I was the first one to really do it, was to look at the
history of the thinking in these fields. So basically to say, you know, we believe, for instance,
that obesity is caused by eating too much. That's a hypothesis. What's the history of that
hypothesis? Where does it come from? On what basis was it accepted? On what evidence was it accepted?
And maybe because I have a physics background originally, in physics when you learn your science,
You don't learn just what to believe.
You learn the sort of experimental basis on which these ideas were tested.
And so all of learning about physics is this history of, you know, it's a theory and an experiment,
and a theory and an experiment.
You're being inculcated in the scientific method as you're learning it.
In medicine, public health, that doesn't happen.
There are some historical episodes that people are taught,
but for the most part, they're taught what to believe,
not why to believe it.
And so this idea that obesity is caused by eating too much was a sort of general conception
pre-1930.
There were actually two competing ideas.
One was that obesity is a constitutional disorder.
Some people just get fat.
And, you know, they can kind of inhibit that from happening, prevent it from happening,
by starving themselves.
But it's a kind of, you know, inexorable process.
And those of us who fat and easily understand this, we know what it's like to sort of just keep adding weight year in and year out no matter what we do.
And then the other was this idea that it's a behavioral problem caused by how much heat and exercise.
And in 1930, the University of Michigan researcher named Lewis Newburgh claimed to have proven experimentally that obesity was caused by eating too much, always caused by eating too much.
And this idea, and back in the 1930s, there were maybe half a dozen people in the world who were thinking about the cause of obesity.
That's what obesity science was back then.
And the people in the U.S. kind of accepted this as true.
It seemed obvious.
You know, we know it just seemed to coincide with our beliefs about gluttony and sloths.
So it was accepted without ever really being confirmed an experiment.
And after World War II, the major theories of obesity, we're all theories trying to figure out
why people who suffer from obesity eat too much, as opposed to the alternative, which would be
why they accumulate too much fat.
So the assumption was they do eat too much.
If we could figure out why they do, then we would solve obesity by the 1960s.
Obesity research was dominated by psychologists and psychiatrists, trying to figure out what
cognitive mental deficiencies obese people might have that would prompt them to eat too much
when we all know that they should eat in moderation and exercise like the rest of us.
And organizations like the World Health Organization and virtually every health organization
in the world just kind of accepted this belief system.
When they were founded and when they started writing and publishing about obesity, this was
a conventional wisdom.
Nobody ever thought to go back and say, hey, maybe we got something wrong.
maybe this isn't the way to think about obesity.
And then by the early 2000s, when someone like me comes along and says, well, wait a minute,
you go back and look at this energy balance idea.
First of all, it's just an idea.
And second of all, it's kind of ludicrous.
And third of all, you know, it's never really been confirmed in experimental tests.
And in fact, most of the experiments suggest the opposite.
then the natural response is to assume that I'm just wrong, right?
That, you know, maybe I'm a quack, maybe I'm trying to sell books.
Maybe I'm just misguided.
I'm not an expert.
I don't have a PhD.
I'm not even a medical doctor.
So clearly I don't understand this.
And since the early 2000s, this is a battle that we've been fighting.
There's a few, you know, very notable academics who have, you know, been at the forefront of this
sort of struggle to overturn this idea that obesity is caused by eating too much, that it's a
behavioral problem. And we're making progress. Well, we'll get to some of those academics and
you guys recently put together a joint paper on this topic, which is really profound. We'll talk
about that. But let's zoom out even more so. For the person that's out there that's watching
this, maybe it's even somebody under those terms you use who fattenes easily. You know,
they go to their life and they just feel that no matter what they do, they gain weight.
So, you know, that person's watching.
And if that's not you, everybody has somebody like that in their life, a loved one, a friend,
somebody that they care about that's in that camp.
What are the implications, plainly and simply, what are the implications of understanding
the true reason, whether it's calories in and out or the insulin, hormonal,
idea that you're bringing to the table, that it's not just calories in and out, what are the true
profound implications of that when it comes to our battle with obesity and the pandemic, as you guys
have said it, that we're facing. Well, and that's the thing. So we have these epidemics of obesity
that are happening everywhere in the world. And the fact that anywhere in the world where
population shifts from eating their traditional diet, whatever that traditional diet is, it could
be a carb-rich diet like in Southeast Asia. It could be an animal product.
product-rich diet like in the Inuit and North America or the First Nations people or the Native
Americans, it could be a natural, you know, anywhere in the world where people are eating their
traditional diet, then they shift eating a Western diet to a Western diet and lifestyle.
They manifest epidemics of obesity and diabetes.
And this is effectively without exception.
So the question becomes, what is it about the Western diet and lifestyle that triggers
these epidemics?
That's the first thing.
And the conventional wisdom is, well, there's just too much tasty food available.
Maybe these people go from being on the edge of famine to having a surplus of food,
so they eat too much.
And then you have all these labor-saving devices so they don't have to work as hard,
so they eat more and expend less.
And then the flip side is the nature of the foods they eat change.
This is the hormonal constitutional hypothesis that it's not how much they're eating or exercising.
In fact, many of these populations are impoverished populations where both men and women work in manual labor all day long, and yet they still struggle with obesity.
So if you believe that it's a constitutional disorder, and you ask, what is it about the environment that triggers this disorder?
The answer is you change the nature of the carbohydrates you eat, from unrefined grains and then tubers to,
basically white flour and sugar. And the white flour and sugar set up a hormonal milieu in the human
body that channels or sort of partitions or diverts calories into fat so your fat tissue grows.
So on a very basic level, when we're talking about what triggers these epidemics, you've got,
do these people eat too much and exercise too little? It's the food tastes too good.
I was just reading an article today where it's like, you know, stay away from.
many foods that tastes good. Because if you do, you'll overeat and then you'll get fat. And I thought,
boy, I'm going to have to change my entire philosophy of cooking. If I don't want my kids to get,
you know, overweight or obese, I'm going to have to make sure I make food for them that doesn't
taste good. That was kind of the logic. When you get to treatment and prevention on an individual
level, patient to patient level, or, you know, trying to decide what you do yourself.
The conventional wisdom is diets work when they reduce the amount of calories you eat,
or you often see create a negative energy balance.
That means they work if you're taking in less energy than you're expending.
That means you're getting lighter.
And the alternative hypothesis is hormonal regulatory hypothesis is diets.
For a diet to work, it's got to lower insulin levels.
Insulin is a hormone that dominates fat storage and metabolism.
So when your insulin levels are high, you store calories as fat.
When your insulin is low, you mobilize those calories and burn them for fuel.
So, again, one hypothesis says diets work when you create a negative energy balance.
The other hypothesis diets work when you lower or minimize insulin secretion.
The way you do each of those is different.
You minimize insulin secretion by removing the carbohydrates from the diet and replacing them with mostly fat.
Fat's the one macronutrient that doesn't stimulate insulin.
The other, you just eat less and exercise more.
And really what your sort of argument has been since you've been writing about this is that
we've been telling people to do that.
We've been shouting from the rooftops to be able to do that.
Doctors have been telling their patients do that.
We've been trying this for a long time and things continue to get worse.
Yeah.
And that's one of the arguments I made in this article in stat news is we have these epidemics.
The former Director General of the World Health Organization described the obesity and diabetes
epidemics about five years ago as slow motion disasters.
A couple years ago, there was a World Bank report on the obesity and diabetes epidemics
that described them as ticking time bombs.
And this was pre-COVID, and we know that COVID, if anything, obesity and diabetes, people
who suffer from obesity and diabetes are at that risk of much worse outcomes from COVID.
So we've got these, you know, awful epidemics.
There are tremendous burdens to the individuals who suffer from these diseases and
tremendous burdens to the health care systems that have to pay for the complications
of obesity and diabetes.
And yet we've been telling people what to do by this energy balance thinking for 50 years.
anyone who grows up obese, probably anywhere in the world, knows that they are supposed to eat
less and exercise more. And what happens when that fails is it inevitably does, eventually inevitably does.
Then the person who's suffering from this physiological disorder is shamed for failing.
You know, today to walk down the street and, you know, be burdened with obesity is to feel,
and I'm just saying this because many people have said this to me,
every aspect of their life is affected by this disease.
And the assumption of the energy balance model is you just somehow don't have the willpower
to do what's necessary, which is what lean people do naturally.
The situation is tragic, and yet it's conventional.
wisdom. It's establishment science.
You know, on that topic of establishment science, there's been a trajectory that you open up
the stat article that you wrote, which will link to in the show notes for everybody to read.
It's a great summary of this topic and also the paper that you and these colleagues had
written. But I just want to read the opening paragraph here because I thought it was a beautiful
sentence. So I'm going to read your words, if that's okay.
I've been a science reporter for 40 years. I've wanted to assume.
that the experts I interview can be trusted to understand their subjects. Put simply,
to get it right. But watching researchers in the field of obesity, almost blindly following a failed
paradigm has led me to cross a line that few journalists ever do to publicly embrace and promote
a minority opinion that many in the obesity field think it's quackery. When you wrote your first
big article in the New York Times on this subject, what sort of initial response did you have from
people that are out there that, you know, you gave that great example of like in physics or in other
sciences, you know, you're taught to say, why do we believe this and continue to re-question
the premise? What response did you get from people who just thought that this is established?
Like, why are you even writing about this topic? Well, and this is, yeah, it's funny.
because things haven't changed that much. Nobody likes to be told that they've made a mistake.
Okay. So if you're in medicine, you're well respected, you're an obesity research,
or any researcher in a field related to obesity, and this is what you believe, and this is how you've
interpreted your data. And then along comes a journalist of all people, not a Nobel laureate physician
or researcher, not, you know, a professor at Harvard or even Mississippi State University,
just a journalist.
He doesn't even work for the New York Times.
He's a freelancer, and now he's coming along and saying, you've made a mistake.
And it's the biggest mistake you can make in the field.
Actually, one of my favorite stories about this after my first book came out, good calories,
bad calories.
I was giving a lecture at the Pennington Biomedical Research Center in Battenham.
Rouge, Louisiana. This is the sort of largest academic obesity research center in the United
States. And I gave my lecture explaining why this energy balance thinking is fallacious and why it
has to be replaced in the way I see it by a hormonal regulatory hypothesis. And afterwards,
one of the faculty at Pennington, a distinguished-looking gentleman at the time I would think was in his
mid-60s raised his hand and very politely said Mr. Talbs is one subtext of your talk that we are all
idiots.
And he was very kind about it.
And I smiled and thought about it and said, no.
The subtext is that you embraced an idea, a paradigm of how to think about obesity from the generation that came before you.
and you never thought about it critically.
This is the, you know, why does a World Health Organization and every other organization say this idea?
But people don't like to hear that.
They don't like to be told that their fundamental belief is wrong, and they don't like to be told by an outsider.
And so when you tell them that, the assumption is that you're wrong.
And then they look for reasons why, in my case, a well-respected journalist would say such a thing.
And that's when you get to sort of ad hominem explanations.
Clearly, I must have done it for the money.
They're looking for rationale.
So when I first wrote this New York Times Magazine cover story, the story was called,
What If It's All Been a Big Fat Lie?
There were two titles, What If Fat Doesn't Make You Fat?
It was on the cover of the New York Times, July 7, 2002.
And it was the most controversial article they had run in at least a decade.
And the, I knew it was the most controversial article they ever ran.
But I was still stunned at the sort of ferocity of the replies.
Because if I was right, a lot of very, very smart, successful people were wrong.
And that's hard to believe.
And even my friends in journalism, if I was right about this,
my friends who covered this field in journalism were wrong.
They had missed a very important story.
So it's very hard to accept that.
And what we all do, and I do it too, is when people insinuate that you're wrong about things.
You look for reasons why they're wrong about saying you're wrong.
And you reach for anything you can.
And, you know, it's, like I said, it's still going on 20 years later.
This stat article is really my first attempt to directly challenge this energy balance thinking.
It's in every book I've written and mostly every article I've written, but I haven't directly gone after it.
And, you know, the implications are not just profound, but that an entire medical research community could have made such a mistake is almost incomprehensible.
So it creates a cognitive dissonance and the cognitive dissonance manifests itself as anger.
and ridicule and vitriol and, you know, I kind of duck and wait for the stuff to stop coming off the fan long enough to take a breath.
Well, while previously, you know, the public would look on and, I mean, that's even saying it kind of kindly, most people have no idea that this debate is going on the background.
They're just trying to live their lives.
They're trying to eat healthy.
They're trying to think about how do they provide for their kids, maybe lose a little weight, look good for that wedding that's coming up.
And there's a small percentage of people that are paying attention.
But that small percentage of people that are paying attention where previously it was just academics and researchers and occasionally doctors who would actually go and read the science.
Not a lot of doctors would, but some would and try to keep abreast of the latest information.
There's been an explosion.
So that was the way the things were before.
But since then, even the last five, ten years, there's been an explosion of people who their life has just gotten so painful.
Their life has gotten so challenging.
They feel like they could not make any progress when it came to weight gain, that they started
to take matters in their own hand.
And they weren't just waiting for what information was coming out on the news and the media.
They started to go directly to sources like podcast or picking up your book because they saw
you featured on somebody's social media.
And what's that, what that's led to is that now you have a whole group of people that have
been trying something different, trying something and experimenting and seeing the results firsthand.
And I think that this is the right time to reemerge with your article, not that you have been
completely silent, you've been writing books along the way, of really hard hitting the subject
because it feels more than ever people are paying attention. Do you have that sentiment on your
side? Yeah, it just divides up. There's an enormous amount of support out there. As you say,
You know, people have been struggling this with their whole lives.
So it used to be you'd read, you know, what's called a fad diet book.
So Atkins or Sugar Busters or the Ornish book or South Beach or protein power.
And you'd go on that diet.
It might work, might not.
You'd stay on it for a while, lose some weight, and then go to see your doctor and your doctor
say, oh, while you're eating too much fat, you're killing yourself.
got to get you off that diet, or you'd lose 40, 50 pounds, then you'd go back to eating the
way you always did, and then you'd gain the weight back.
And there was no real way to break this thing out of the world of fad diet doctors.
But what the Internet has done is it's allowed people struggling with their weight and their,
you know, their blood sugar status and their blood pressure to go on the Internet and look
for answers, and then you could try the answers.
One thing journalists like myself and Nina Tysholtz in particular have done is when I started writing about this 20 years ago, the idea was these low-carb, high-fat diets would kill you because of the saturated fat content.
So we were all afraid if we did these diets, you would just kill over from a coronary within, you know, weeks of starting.
And everybody would laugh that you were on Atkins.
And that would be the end of it.
Over the course of 20 years, you know, Nina and I, physicians like, well, Mark Hyman and David Ludwig
and have pointed out that the research is consistently shown that this way of eating is very safe.
Probably safer than the way the American Heart Association has been recommending us to eat,
depending on how you define safety.
It certainly makes people healthier.
So we have a whole world of people are now trying this way of eating, restricting carbohydrates
to lower their insulin levels.
And among that whole world of people are a lot of doctors, a lot of physicians.
I estimate at least a few tens of thousands of physicians who were also struggling with their
weight or just got tired of watching their patients struggle with their weight and convincing
themselves that their patients refuse to follow their advice and instead started asking
Maybe my advice is wrong.
So part of what's happening is you get pushback from the establishment,
and that's just part of the job, part of what you have to accept when you imply that people have made mistakes.
But along with this pushback, there's a world of people out there who are clearly benefiting
from basically restricting the carbohydrates in their diets, rather than trying to eat less,
just try and eat less carbs, fewer carbs to be grammatically correct.
Thank you for that.
Let's talk origin story because you've written about it a little bit before.
You've shared it on podcasts.
What even got you interested in the subject to begin with that you wanted to explore this topic?
As you mentioned, your training was originally, you know, going down the pathway of physics.
Pick up a story from there and share with our audience, if you would.
Well, my first two books were about, just by chance, were about scientists, physicists, and
chemists and nuclear chemists who discovered non-existent phenomena.
So I did these sort of intensive investigations of scientists who had screwed up, and I became
obsessed with this issue of how hard it is to do good science, how hard it is to get the right
answer, and how easy it is to screw up, and how rigorous research has to be before it can
be believed before you can believe its results, this sort of endless process of hypothesis and
tests and tests and test and replication. So that was what my journalism focused on. It wasn't all
I wrote about, but whenever I got a chance, I would dive into that subject and do a series of
investigations over the years. And by the late 1990s, I stumbled into the nutrition field by accident.
And I was interviewing a scientist, the research, I'm not going to call him a scientist,
who was clearly one of the five worst scientists I've ever interviewed in my life.
And yet he took credit for putting Americans not just on the low salt diet everyone was eating in the late 1990s.
And many people are still eating, but on a low fat diet.
And I literally got off the phone with them.
I was writing about salt at the time, which is why I was interviewing.
But when he took credit for the sort of low-fat dogma as well, in the late 1990s,
the definition of a healthy diet was a diet that was low in salt and low in fat.
When he took credit for it, I called up my editor, and I said, look, one of the five worst scientists I've ever interviewed.
I thought I had interviewed some of the worst scientists in the world in my earlier books.
This guy was clearly down there, and I said, you know, he just took credit for getting us on the low-fat dogma.
So when I'm done writing about salt, I'm going to write about fat, which I did.
I wrote two investigative pieces for journal science, one.
The first on salt, the second on this idea that high-fat, high-saturated fat diets caused heart disease.
This was 1998 and 2000.
The evidence for both of them was terrible.
You would never believe these hypotheses were true if you didn't believe it before.
before you did the experimental tests.
And while I was doing the dietary fat story, I was interviewing an administrator from the National
Institutes of Health.
I remember we were having a coffee at a Starbucks in Potomac, Maryland.
And he said to me, you know, when we put the whole world on a low-fat diet back in the
1980s, we really didn't know if it would affect cholesterol and heart disease that much, because
that evidence was very wishy-washy, iffy. But we figured if nothing else, people would lose weight
because fat is the densest calories in the diet. And lo and behold, they stopped eating fat.
They shifted to eating carbs, and we triggered an obesity epidemic. And I thought, well, that's
an interesting thought. So after I finished the dietary fat story, I pitched this article to the
journal, well, to the New York Times Magazine on the origins of the obesity epidemic, always with
that NIH administrator's words in my head that what happened was they turned. So in the 1960s,
the idea was that carbohydrates were inherently fattening. And then we decided that dietary
fat causes heart disease. If you want to avoid fat, you have to eat carbohydrates and replace
it with carbohydrates. So carbohydrates went from being.
something that most women thought of as fattening to heart-healthy diet foods.
And the food industry was told to produce as much low-fat food products as they could.
So when you take a fat out of a product, it becomes kind of tasteless.
So often what you had is a kind of yogurts, the iconic example.
You remove the fat from yogurt and you replace that fat with sugar,
or high-fructose corn syrup, which is a form of sugar.
And then you can advertise it as a heart-healthy diet food because it's got, say, 10 fewer calories per serving.
And it's low fat, right?
But now it's high sugar, which it wasn't originally.
So that's the kind of phenomenon that I've been, you know, spent five years writing my first book on and then have been, you know, working on ever since.
So you were mentioning your colleagues a little bit before.
and a few of you all work together, some of the names that you've mentioned and some that you didn't get a chance to mention, on a paper, review paper that was published in the American Journal of Clinical Nutrition just earlier in September, September 13th, actually.
And the title is the carbohydrate insulin model, a physiological perspective on the obesity pandemic.
What was your collective goal as a group with publishing this review paper at this time?
Okay, so one of the problems with challenging the conventional wisdom is it's a little bit of a,
you've got, well, roughly an obesity science, I'd say you've got 150 to 200 papers coming out every week.
That's relevant to the subject of obesity.
And some huge proportion of those are dependent on this sort of conventional thinking about the problem.
that's an energy balance disorder.
And so you get this constant repetition in the literature,
and when the media picks up these articles,
that obesity is a problem of eating too much and expending too little.
And it's the problem you never wanted your science to get to the point
where it accepts a hypothesis that hasn't been well tested
because then it gets harder and harder to dislodge.
Along the way as, you know, various individuals in our world have started arguing that this is just wrong and that there's this carbohydrate insulin model is a much more functional hypothesis to describe what's happening with this in obesity.
you create sort of diehard researchers who consider it their obligation to prove that you're wrong,
or at least to make it look like you're wrong.
And so you start getting articles published that the carbohydrate insulin model is incorrect,
that's been disproven in experiments, or the evidence against it is weak.
So it's actually harder to publish an article establishing or even discussing the theory in a unbiased way than it is to publish an article claiming that the hypothesis is just wrong.
So Professor David Ludwig at Harvard, he's a professor in the School of Medicine as well as the School of Public Health.
He ran the pediatric obesity clinic at Harvard, the Boston Children.
hospital for several decades. David has been, you know, one of the two or three leading
proponents of this idea that obesity is driven by, it's a hormonal regulatory disorder.
And again, I'm speaking for David. I hope I'm getting this right. But David believed that
what we had to get a major paper out there laying out and, you know, what the experiments do
and do not show, laying out what the thinking on this hypothesis really is, sort of fully reviewing
the subject, both the theoretical and experimental sides. So people could see this without the
bias that comes from only reading the articles from its opponents. And in doing this, David also,
so he wrote the first draft of this article, but then he recruited some very influential
co-authors, so 15 other academic researchers among the most influential in the world on the
subjects of nutrition and obesity, who agree that this hypothesis is most likely right, that the
energy balance hypothesis or model is something of a failed paradigm and gave their input into the
paper, helped write it in subsequent drafts and get it out there so we could make a statement
that this is a serious issue.
It's a hypothesis that has to be taken seriously.
If it's right, then there are definite implications for how we treat and prevent obesity
and then this slow motion disaster of these epidemics.
And, you know, sort of whenever we could get this out was the right time to do it
because these epidemics are not going away.
While the medical community has made some recent advances in drug treatment for obesity,
you're not going to put, or I hope they're not going to put the 100 or 150, you know,
probably 100 million obese individuals in America on drug therapy,
if they can solve this issue by changes in diet and lifestyle, the correct changes.
You talked about, you know, reviewing some of the base science and experiments that were conducted on both sides of the equation, right?
The energy balance model and then also looking at things on the carbohydrate insulin model.
Is there one or two anecdotes that stands out from that paper that you all as a team put out together and worked on that you feel really highlights.
this point that the idea of it's all just calories in and calories out is not the complete
story or a picture. Was there one or two anecdotes that were inside of the paper that you can
talk about? Well, we didn't really use anecdotes because, again, it's a nature of scientific
publications to avoid them at all costs. But I think the point, remember when I said earlier,
prior to the 1930s are these two competing hypotheses.
One is people put on fat because they eat too much.
And the other is this idea that you have a sort of constitutional hormonal predisposition
to accumulate excess fat that's triggered by the environment.
And the way you would test this in animal models, we didn't have animal models of obesity
until the late 1930s when obesity can become an experimental science.
But in these animal models, what would happen is often, there are various ways you can make an
animal obese.
You can lesion the ventralmedeal hypothalamus of its brain.
You can do genetic manipulations.
You can do dietary manipulations.
And often when these animals are growing obese, they eat a lot.
The technical term is they become hyperphagic.
And so it was natural for obesity researchers to blame their obesity on this hyperphasia,
this eating too much.
So whatever you do to the animal surgically or genetically or through diet, it makes the animal
eat too much and then the animal gets fat.
And that's to this one, you know, the main obesity research community, that's proof that
the obesity is an eating disorder, that it's a taking in too many calories problem.
What they rarely thought to do was to ask the question, what happens to these animals when you don't let it overeat?
So you measure how much the animal is eating, say, before the surgery, and that's all you let it eat after the surgery, or you take a genetic, an animal that's got a genetic mutation to make it obese, and you feed it, say, half the calories that you would feed a lean animal.
So you literally semi-starve it.
And in all these cases, the animals get, if not obese, they get fatter anyway.
So the eighth grade science one-on-one terminology would be you control for overeating,
and the animals still get obese.
There are experiments out there, famous experiments out there where the animals are literally
semi-starved.
Like I said, you measure exactly how much it leads.
animals eating and you feed your animal that you've manipulated to become obese half of those
calories. So you never let it have a decent meal and it gets obese anyway. And that is pretty much
refutation of the idea that they get fat because they eat too much. I mean, these people, when they
think about it, they go, if we're starving them, then something about the manipulation must make them
expend too little calories.
But the flip side is whatever you've done to these animals is causing what's called a change
in fuel partitioning.
So instead of the problem being how much they eat and exercise, the problem is, you know,
how much food they consume, it's what they do with the food they consume.
And what that food does to the hormonal physiological regulation of fat accumulation.
And so those are the kinds of experiments that are discussed that are, you know, clear evidence,
at least in animals, that obesity in animal models is not an intake problem.
It's a fuel partitioning problem.
They're partitioning calories into fat rather than using them as energy,
which is ideally the reason why they're eating.
And on the contrasting side of the carbohydrate insulin model,
which is everything that you've been sharing over the years.
What is one experiment that is worth noting here to talk about how that idea is so much stronger
of a model to understand why we're all getting obese?
One experiment?
Yeah.
Is there an experiment that comes to mind?
Any of the work of Dr. Ludwig's?
Yeah.
Anything of the years you've written about?
One of the things I've done along the way was after I wrote my second book on this subject,
I co-founded a non-for-profit called the Nutrition Science Initiative.
We had support from Texas philanthropists to fund studies that could ideally resolve this question.
One of the issues with science, when you're looking, when you're trying to establish which of these hypotheses,
they're correct? Is it, you know, the fat accumulation occur because of this, you've created
an imbalance and intake and expenditure, or does the fat accumulation occur because you've created
a hormonal imbalance that's driving fat accumulation? It takes very rigorously well-designed
experiments, and so we funded two that could address this. One that was a pilot study
that was at collaboration between researchers at Columbia University and NIH and Pennington,
which I mentioned, and the Clinical Research Institute in Florida.
And the other was run by David Ludwig at Harvard.
And the idea is, just like in the animal experiments, one thing you can fix in an experiment is how much food.
people eat. So you have this interesting system where they're expending energy in response to how much
food they're eating and how much they weigh. And you can't really fix how much they're expending
and you can't, you can try and fix how much they weigh, but that's surprisingly difficult to do.
But you can fix exactly how much they eat. And so again, this sort of eighth grade,
you know, basic science, fix one variable. And then design.
an experiment in which the two hypotheses would make different predictions.
So in the simplest way to think about it, you say establish how much energy your subjects
are expending on a standard American diet, and then you give them exactly that many calories
of a diet that maximally lowers insulin, so that's a ketogenic diet.
So let's say, for example, you have a, I'm a big guy, so I might expend 3,000 calories
a day if I was eating, you know, sort of the way most Americans eat.
So you measure that, and there are ways to do that.
They're tricky, and it's easy to make mistakes, but there are ways to do it.
And so you measure the energy expended.
And then you feed me exactly 3,000 calories a day of a diet that manipulates insulin levels,
the ketogenic diet.
And now you have two hypotheses that make predictions.
The energy balance prediction says, well, we're feeding you the same amount of calories,
and your weight is determined by the difference between intake and expenditure.
We have no reason to think your expenditure is going to change,
particularly if we feed you the same amount of protein on both diets.
So if you do this experiment, we don't expect to see any difference in weight,
whether on the ketogenic diet or the carb-rich standard American diet.
And this hormonal regulatory disorder says, well, if we maximally lower insulin levels, that means fat is going to be mobilized from the fat tissue and it's going to be oxidized for fuel.
And there's no law of physics that says that the amount of energy you expend can't go up.
So our hypothesis says that if you maximum lower insulin, you're going to see weight loss.
and that weight loss will have to be coincide with an increase in energy expenditure.
So we can measure that as well and see if we see that.
So the nature of science, we funded two experiments to do variations on that experiment.
One saw an effect.
They measured energy expenditure.
They only looked at energy expenditure expecting to ask the question, does it go up or not,
when you switch to a ketogenic diet?
And they measured it by two different mechanisms, and one they saw a small effect that they thought was transient, and the other they saw a large effect.
Nonetheless, they interpreted this as not convincing enough to them to believe the carbohydrate insulin model.
And then the other experiment was done by David Ludwig at Harvard, and David had three levels of carb consumption in his study.
and as carb consumption went down, energy expended went off consistent with this idea that as carbs go down,
you get more and more mobilization of fat from fat cells, more fat being burnt for fuel
and so more energy being produced.
Ideally, we'd have kept funding studies, but by that point, our Texas philanthropists were not wowed by the quality of
of our organizational skills.
And I had books to write.
So the not-for-profit has been someone hibernation since about 2017.
Connected dots fully with where we started off the interview,
that insulin and the hormonal idea, the carbohydrate hormonal idea of weight gain,
connect the dots fully and just help people understand who are still trying to wrap their heads,
Maybe they're watching this on YouTube where they're listening to this because a friend sent it to them.
They're not as well versed in this world as maybe I am or definitely you are who writes about this topic.
What are the things that people are eating on a regular basis that are a huge part of our diet today?
We all know the term carbohydrates, but let's get a little bit more granular.
What is making up our diets that is causing our hormones, in particular our insulin to be out of whack,
creating a whole milieu of problems that lead to the signaling to store excess weight in the body.
It's interesting, just listening to you talk about it.
There's a lot of technical terminology.
I've just talked about a complicated experiment.
We talked about the carbohydrate insulin model and the energy balance model.
The carbohydrate insulin model, when it comes down to it, is it can be captured by the idea that carbohydrates are fattening.
Okay, carbohydrate-rich foods are fattening.
fattening sugar, grains, starches, primarily sugary beverages, beer, major source of calories or carbohydrates.
These foods stimulate the secretion of the hormone insulin.
And insulin, we think of insulin as a hormone that controls blood sugar.
It's the hormone that's either deficient or dysregulated in diabetes.
physicians think of insulin as a hormone that controls blood sugar.
But one way it controls your blood sugar is by telling your fat tissue to store fat.
So basically it's like a conductor in an orchestra.
And after you eat, it's orchestrating what you're going to do with all the different
macronutrients you've consumed.
So the macronutrients are protein, carbohydrates, and fats.
carbohydrates get into your blood sugar, into your circulation as glucose.
They raise blood sugar levels.
Blood sugar is blood glucose.
And high levels of blood sugar can be toxic, are toxic to cells.
So your body works very hard to keep your blood sugar under control.
And one way it does that is insulin tells your tissues, your muscles, and your organs
to burn the glucose, says that the glucose is,
rising, the insulin is like a shoveling it into the cells to make sure to do its best to keep
blood sugar under control. And as it's doing that, it's also signaling the fat cells to take up any
fat from the diet and any fat in the circulation and store that because the primary job is burning
insulin. Protein is being used to rebuild cells and tissue. So that's got a job of its own.
And insulin is orchestrating that as well with other hormones as well. So when
When insulin has secreted, you're storing fat.
That's what you're doing.
You're burning carbohydrates and storing fat.
And we secrete insulin primarily in response to the carbohydrates in our diet,
or the carbohydrates converted, the glucose converted from protein.
But what we're interested here is the carb content.
And like I said, there had always been, for at least 150 years,
the conventional wisdom was that carbohydrates are fattening.
I quote an article in pretty much all my books that was written in 1963 by one of the two leading British dieticians in the British Journal of Nutrition.
In the first sentence is every woman knows that carbohydrates are fattening because that's what every woman thought she knew in the early 1960.
So this is a hypothesis.
There's a very good hormonal explanation for it.
And arguably, you know, it's hard to understand why it's so challenging to the researchers to understand this.
I mean, they'll say, well, because it's wrong, but assuming it's not.
But yeah, so that's it.
Sugar, starches, grains, sugary beverages, carbary beverages like beer.
By this thinking, even something like milk can be fattening because of the lack.
content, to carbohydrate, which makes up more than 50% of the calories.
And those of us who fatten easily, for many of us, it's not enough to just give up the more
obvious sources, the sweets, the sugary beverages, the beer.
For many of us, when you look at insulin dynamics, fat tissue is very sensitive to the hormone
insulin.
The phrase used by metabolism research, when I interviewed them from my books, was that fat
tissue is exquisitely sensitive to insulin. It's the most insulin sensitive tissue in the body.
So you have to, for most of us, if you want to get fat out of our fat tissue, we have to minimize
the insulin on our circulation. And that's when diets like the keto, ketogenic diets,
you know, what was called Atkins and my youth come into play, because those are just diets
that replace virtually all of the carbohydrates with fat. There's been an explosion in
companies and people who are not diabetics using things like continuous glucose monitors to keep
track of their glucose and understand how their different dietary choices are impacting them.
I wear one and it's been really helpful to see that even sometimes a lot of the foods that I thought
were really healthy that I was eating in the world of wellness that are still primarily
carbohydrates that are super refined like tapioca and cassava those have a much higher and lasting
glucose response for me than even just eating you know straight up bread and other things
like that don't tell me this by the way because my kids are they opened a a boba store was
opened down on the the main drag about a third of a mile from here so my kids
religiously now get boba tea and they come back and they say put it die where i get it without
sugar dad and there are these tapioca balls in it have you ever seen this stuff yeah i have i have i
i don't i just don't get it i realize it's a generational thing i don't know it's they're vile to me
but it does it's just you know it's another way to drink carbohydrates and if we're right this is a
problem. That's well said, right? If you're right, this is a problem. And I think that one of the
great thing about continuous glucose monitors is that you could see in real time and you can see the
impact that it has to as things accumulate, especially when you are not in an optimal range. So I was
just going to get your opinion on those, whether you find them helpful, whether you ever used one,
whether you recommend them to people when it comes to getting a better understanding of how food
continuously can either be supporting you or maybe working against you.
Yeah, I have experimented with CGMs and they're fascinating and I recommend anyone do it.
They're not too expensive to get even without a prescription.
Because I already eat a ketogenic diet, I do not eat them any foods that raise my blood sugar.
So for me, it was interesting but not as interesting as it could be because my blood sugar.
because my blood sugar is pretty much flatlined.
For other people eating mixed diets of any kind,
yeah, I think it could be revelator to see what these foods are doing
to your blood sugar and to see how much blood sugar fluctuation there is,
even in, you know, those of us who are healthy
and, you know, showing no signs of diabetes,
and yet our blood sugar can be, you know,
going up and down by the, you know,
50 points, you know, hourly dependent on our snacks.
And it's going to be different for everyone.
So that's why the CGMs is continuous glucose monitors are so useful.
You know, in your last book that you published you on Mark's podcast for it,
you guys had a great interview.
We'll link to it.
The case for keto.
Inside there, you share on this topic of people eating sort of like mixed diets.
You say that for some people, carbohydrate abstinence needs to be approached the same way
that we approach addictions we need to break.
Talk a little bit more about that.
You know, for people that are still in this place where they haven't gone that, you know,
direction of significantly swapping out the calories in their diet that primarily are coming
from these refined carbohydrates, how is it important to think and why is important to think
of it like an addiction?
Well, it's just, and this is my last book I interviewed 120 plus physicians who have sort of
converted to this way of thinking to get their feelings about the risks and benefits to their
patients and the challenges. And many of them said to me that they thought of what they did,
not as sort of treating obesity, but as treating carbohydrate addiction.
We can be pretty confident from the clinical trials, and there are going on 200 of them now,
that people will improve their health by removing these carbohydrates.
hydrate-rich foods from their diets. And this seems to be pretty much universal in the clinical trials.
I'm not saying there might not be other ways to achieve the same benefits, but this is pretty much the
case. So then the question becomes, why is it people find it so difficult to do? You know,
many people, the idea of giving up their bread is like back when I was a smoker, I used to think,
you know, I can't live without cigarettes. And so a lot of people, you know, there are foods that they just,
they will rationalize eating endlessly because they don't want to give them up and it constitutes
their source of joy in their diets. And I understand that completely. But if you think of this
as an addiction, it's a way to get around that problem. Then you say, look, let's just take
two months, do an experiment. Take three months, ideally. You can live without bread for three
months. You could live without your morning orange juice for three months. You could live without, you know, the
cherries you have at lunch or the donut you have at 10 in the morning when your co-workers bring in
donuts and you can't say no to them. Treat it, you see what happens. Or go one month, then go day
by day, but do the diet right, eat correctly, give up, you know, and then see how you feel
because you may find that after a month what you thought you couldn't eat is, you know,
you don't really miss.
And the benefits to your health.
It's funny, I was just, I just did a podcast for stat that will come out in a couple days.
And they asked me if I could do it with somebody I knew who had gone through this sort of
struggled with their weight and then, you know, tried a low-carb or ketogenic diet.
So I asked this young man that I met doing this research.
I met him when he was a student at Yale, a law student at Yale.
He invited me to come speak to the food and nutrition group at Yale Law School.
And when I came, he told me a story, which was that he weighed 400 pounds when he was 18 years old.
And he had been morbidly obese his whole youth.
And his father had actually seen how much he had struggled with his weight and how he didn't eat any.
more than his lean friends did.
He swam, he boxed.
He couldn't stop himself from becoming morbidly obese.
Morbid obesity runs in the mother's side of his family.
And then his father enticed him to try Atkins,
basically gave a copy of my 2002 New York Times Magazine story,
and he lost 170 pounds.
And when the editor, the stat editor who was moderating,
said, but people say this is unsustainable,
And my friend said, well, the people who say that didn't have to wake up every morning and be 400 pounds.
You know, and I did, and now I don't.
And that, to me, is sustainable.
And that to me is a really powerful message.
So people, they think, well, I can't give up my bread.
And if I do, it's not going to make that much of a difference.
But they don't think in terms, if I do this right, maybe I could be the person who no longer has to wake up 300 pounds.
could wake up at 180 or 150.
And when I do, I might have a different attitude towards what foods I'm willing to eat.
I just read an article this morning about a young woman who had endometriosis,
terrible periods, painful periods, and she tried everything.
And she used to think in terms of low-carb, high-fat diets being fads.
Keto was a fad, but she convinced herself to try it for a month.
Just like you might say, I'm going to quit smoking for a month, or I'm going to quit drinking for a month.
I'm not going to eat carbohydrates for a month.
And after about 15 days, she had a period that caught her by surprise because there was no pain that came first, no cramps.
And she was like, this is crazy.
And then the gist of the article was, yeah, maybe keto was a fad diet, but she's never going back because she doesn't have to wake up with endometriosis anymore.
just like my friend doesn't have to wake up and be 400 pounds.
And that's a powerful, you know,
a motivator to break an addiction.
Now you have a reason why.
And I'm glad you brought up the second story
because we've done so many episodes on the topic of insulin
and metabolic health.
And yes, weight, gain, and obesity is a major issue.
And largely the people that are listening to this podcast,
largely, you know, that are in our audio format,
Maybe on YouTube it's a little bit different.
We get people from all walks of life coming in and listening.
Sometimes people listen and they say, well, I'm not struggling with weight loss.
But there's so many other chronic diseases that are deeply tied into having a place of high glucose,
your insulin being out of whack in the way that it's being used and controlled inside of the body.
And so so many chronic diseases, even if somebody is not overweight and they're not worried about obesity,
or even, even weight gain.
It's still something to pay attention to because, as we've talked about before in this podcast,
Alzheimer's, cancer, all these different things, they all connect in.
So it's not just about weight loss.
So I'm so glad you brought up that story about the young woman who was dealing with endometriosis.
You know, PCOS, endometriosis.
We also have infertility in men and erectile dysfunction.
So many of these things are all tied into that same.
idea of how glucose and insulin trigger inside of the body and the cocktail of chronic disease
that can happen because of how deeply linked they are to inflammation.
Well, and that's what, that was the point I made in my first book, Good Calories, Bad Calories.
What's interesting, there's a lot of, a lot of these disorders you can basically do,
and I'm wondering, you can test them yourself. So the idea is you're, you know, I, my wife
joke that if I saw somebody get hit by a car outside the window, I would somehow blame it on
carbohydrates. But the general idea here is we dramatically changed our food system as we
with the Industrial Revolution and moving from, you know, the hunter-gatherers to agriculture
to the Industrial Revolution and the sort of refined processed foods and sugars that we've been
living with. And along with that comes this whole slew of what our sort of diseases
of Western diets and lifestyles.
It weren't really seen previously, or if they were seen, they weren't diagnosed.
And now what we're saying, look, there's a reasonable chance.
There's a chance that these foods are the sugar and carbs and problem.
You can see all of them are related.
There are insulin and blood sugar associations that suggest this hypothesis could be true.
And if you're experiencing symptoms like excess fat accumulation or poor blood sugar control or high blood pressure or endometriosis or polycystic ovary syndrome or memory dysfunction or erectile dysfunction, any symptom gives you the opportunity to do an experiment where you can say, I'm just going to for two months get rid of these carbohydrates and
the diet, eat a low-carb, high-fat, or a ketogenic diet, or a low-glycemic index diet,
and see if they get better. There are people out there, well, you've interviewed Terry Wall,
I think, and, you know, the idea that serious, you know, nervous system disorders will,
at least in some people, symptoms will improve dramatically when they eat low-carb, high-fat
diet. So, you know, the argument is why not experiment? Give it a try and see if it makes a difference.
So it's harder when you're dealing with something like cancer because you can't, you don't
know what would have happened otherwise, right? You can't do a, for something like that,
you need a randomized control trial to really know if what you've done is benefiting you.
But for these other disorders where you experience day-to-day symptoms, then see what happens.
We know when done right, these will make you feel better.
They will lead to weight loss and blood sugar control and lower your blood pressure as well.
Those things are all pretty much well documented.
The question is, will they work on these other disorders?
And you don't need a clinical trial to tell you if they will.
you can try it yourself.
And the addiction thing comes in on one level because of these disorders, for most people,
these are the things that make us unhappy.
You know, these are the biggest burdens in our day.
So why not experiment?
Why not say I'm going to give two months to testing whether or not these people know what
they're talking about or it's relevant to me?
And I think an important note that you really highlight in your book, the case for keto, is that
of the scientists and doctors especially because they're working individually with patients,
the vast majority did not use something to measure ketones for their patients that they were
putting on these diets.
So this doesn't have to be complicated because sometimes people hear ketogenic.
They think like, okay, I got to use a meter to measure my ketones and other stuff.
And you're going to have bulletproof coffee after breakfast.
Right.
Lod up on MCT oil.
And yeah, the phrase I use in my book was, so this is in this very, at one point in time,
might still be true.
The most famous book ever written about food was called the physiology of taste,
written by a French lawyer turned gastronome named Jean-Omthelme, Briat Savoran.
And in his book, written and published in 1825, Briat Savran says,
look, you know, I've had conversations with hundreds and hundreds, 500 people who suffer
from corpulence.
And inevitably, they tell me how much they love bread or how much they love potatoes or how much
they love rice.
And it's clearly caused by the carbohydrates.
He called him farinaceous foods.
And he himself said he struggled with his paunch, his whole life.
And he finally won out over it by eating basically a carb-free diet.
And he said, it's more or less what's necessary.
is more or less rigid abstinence from carbohydrate-rich foods.
Again, he used the 1820s version of that word.
That's it.
It's not complicated.
It's like carbohydrates make you fat.
I mean, those of us who get fat easily,
the link to diet runs through carbohydrates and insulin.
If we don't want to get fatter,
and if we'd prefer not to stay as heavy as we are,
then we can't eat these foods.
Just like cigarettes cause lung cancer,
if we want to minimize our risk of lung cancer, we don't smoke.
So the keto is just the diet where you get rid of,
and affect all the carbohydrates in your diet,
except that in green leafy vegetables and animal products,
all meat and fish also have a little bit of carbs in them.
It's almost complete abstinence.
And for many of us, just a little bit of abstinence, you know, helps.
But that's, it's simple.
These foods are faddening.
Don't eat them.
Yeah.
And then within that, I mean, you had a great discussion with Dr. Hyman that will link to as well.
It's a nice listen for people if they want to go deeper after this.
And he was sharing that, you know, so, yes, it's very clearly that the, you know, limiting the
carbohydrates, reducing the carbohydrates, having abstinence for the carbohydrates, them as one of the
primary methods to fatness up and then cause our insulin to go out of whack. And then there might be
some personalization that happens on the other side. And great, people can do experimentations and
try personalization, but really the fundamental level is limiting or the abstinence around the
carbs. Yeah. And that's it. You might find that's where CGMs can come in handy. You could see,
once you do it, you can see how different foods influence your blood sugar. Because if they
influence your blood sugar, they're influencing your insulin, and if they're influencing your
insulin, they're influencing fat accumulation. So if I'm right, if we are right. Yeah,
we should say one thing. We have to get back to this American Journal of Clinical Nutrition
Paylor. Please, please. There's something I just, I want to say about this. When 20 years ago,
when I started writing about this, and when I did that New York Times Magazine story, there were
maybe half a dozen physicians in the United States who are prescribing low-carb, high-fat diets.
Half of them had written diet books about him.
Atkins was still alive.
It's guys who wrote sugar busters.
Mike and Mary Dan Eads who wrote protein power.
I don't know.
Maybe another half-dozen.
Who knows?
And there were maybe two or three academic researchers who were willing to stand up and say,
I think this is true.
Okay, David Ludwig at Harvard was one of them.
Mark Friedman at the Monell Center in Philadelphia was another.
That was pretty much it.
Everywhere else, it was just, they were just starting to do clinical trials on the Atkins diet at the time
because nobody had ever really thought to test it before.
And we were just in three years into the awareness,
so we had an obesity epidemic on our hands.
Over the years, we've convinced more and more people.
So it's still very much a minority perspective.
But the co-authors on this article include two members of the National Academy of Sciences,
a former chair of the U.S. Department of Agriculture's Dietary Guidelines Advisory Committee,
a former chair of the American Heart Association's and Nutrition Committee,
the most highly cited nutritionists in the world, the three Harvard professors, and probably the most
influential nutritionist and obesity researcher in Europe. So the point of all this is that
very, very serious people are saying, we've made a tremendous mistake, and we have to fix it.
Like I said, they are still a minority, and because the majority still believes obesity is just
caused by this energy imbalance, it's still going to take an enormous amount of work to chip away
at that dogma. But this article was a major step forward, not just in putting the science out there
in a way that was fair and unbalanced, excuse me, fair and balanced, but showing that there is a
ever-growing academic, very influential academic community that thinks this is quite likely, if not most
likely right.
What's one thing that people could do today in addition to checking out your work,
the books that are out there, but specifically for the movement, what's one thing that people
could do today who are listening to this podcast who are like, I've never heard this for my doctor.
Why don't more people know about this?
Like, what's one request you would have at them today this further help spread the message
that you and your colleagues who are involved in this paper are trying to put out there?
Print the paper out.
you're going to have a link to it on your, you know, with the podcast, print the paper out
and give a copy to your doctor.
It's that simple.
Or put it aside so that the next time you go to your doctor, you could give it to them
then.
Yeah.
But yeah, that's, you know, on one level, the research is slowly coming around.
More and more researchers are studying, as we've said this, you know, these low-carb,
high-fat ketogenic diet seem to have remarkable effects.
A lot of disease states, and a lot of people are now studying that.
But we have to get to the physicians.
We have to get them off their knee jerk, just telling people to eat less exercise more
and then shaming them when they don't lose weight.
It's got to stop.
It's got to stop.
And it's really part of the larger of the, it's really part of the larger discussion that's out there
is that really shaming and blaming people when it comes to just health in general is not the
solution. We have to understand the root causes of why things are the way that they are
and understand that if there are contrary ideas, that there may be worth something getting
a chance to pay attention to. I think we, you know, I can imagine the case for an evening
news channel where we have highly spirited debates amongst people that are coming back and
who actually know what they're talking about to really have a chance to have a discussion
around things and that the public would benefit.
It's funny because I get a lot of pushback on Twitter, which is my only real social media
presence.
And from very specific sort of the usual suspects, there's three or four or five academics
who are always looking for an opportunity to tell me I'm an idiot.
And then they explain why I'm an idiot.
And then I say, well, look, your explanation doesn't really make sense.
And I think if you're going to call me an idiot publicly, you should really read my books.
So you understand the arguments that are being made.
And they'll say, well, I don't need to read your books because you're wrong.
And it's sort of the trap you get into when you believe something is true that's never really been tested.
You also can rationalize why you don't have to read anything that implies that it isn't.
Because you know that's a waste of time because you know there.
wrong and you're right. It's sort of the opposite of the way scientists are supposed to think,
but this is a kind of very common phenomenon. But we can get to physicians because physicians
want to make their patients healthier. That's why you go to med school. Of course, and many of them
themselves are struggling and they're looking for hands. Yeah, and many of them themselves. And if
you're in family medicine or internal medicine in 2021, then your waiting room is filled with
people who are suffering from, you know, doctors like to call the negative sequela of obesity
and diabetes and hypertension, and that's what you're treating.
So why not try to treat the root cause and try to understand the possibility that you don't
understand it?
Try to accept the possibility that you just maybe don't understand it.
It's really stepping out of tribalism and stepping into open-minded thinking around it.
It's what we're supposed to all do.
Just being open, just being open and being open enough to even ask the first question.
Gary Tobs, this has been fantastic.
We've covered so much ground here.
I'll have a link to the paper as well as your interview with Mark.
And also your book, it came out at the end of 2020,
The Case for Keto, Rethinking Weight Control and the Science and Practice of Low Carb,
high-fat eating.
That's a great manual for anybody who is here.
It's like, okay, well, how do I get started?
Pick up the book because it's going to show you actually how to get started from there.
Any final words, my friend?
No, that'll do it.
Thank you very much, Drew.
Thank you for coming on.
I really appreciate it.
