The Case Against Sugar: Is Gary Taubes Full Of Sweet Lies & Deception, Or Is Sugar Really Making...

Gary Taubes argues fructose, metabolized mainly in the liver, overwhelms it and drives fatty liver disease, insulin resistance, and obesity. He distinguishes fructose from glucose and points to high-fructose corn syrup in beverages as a culprit, citing the Pima Indians as an example of metabolic damage from sugar exposure.
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Duh, duh, duh, duh. Insert scary music here. Especially if you're holding anything that has sugar in it. I mean, even a freaking jelly bean. You better put that bad boy down. Because I have the ever prolific Gary Taubes on the show today and he of course thinks that all sugar is poison. And you're gonna find out why when I interview him about his book called the Case Against Sugar, which he calls the tobacco of the new millennium. Hmm. We're gonna find out. However, this show is actually brought to you by something that really doesn't have much sugar in it at all. It's called the pili nut. You ever heard of the pili nut? If you haven't, you should have. Because it contains the highest amount of fat and the lowest amount of carbs, AKA sugar of any nut. It's got a ton of magnesium and vitamin B1 and manganese, but probably a lot more importantly than that, it has like an addictively delicious but buttery taste. And the raw pili nut that I get from this company called Wild Mountain Paleo is pre sprouted, so it's optimum for digestibility as well. It's grown without synthetic fertilizers, it's never sprayed with pesticides, and they only work Wild Mountain Paleo does with high integrity suppliers who focus on transparency and sustainability. And extremely extreme, extremely delicious peely nuts. I've got a bunch in my pantry. They're amazing. I sprinkle them on like everything you can. Visit. BenGreenfieldFitness.com WildMountain Just like it sounds. BenGreenfieldFitness.Com WildMountain and here is your peely nut discount code. You ready? It's Ben Pele 10. Ben Pele 10 and Peely is P I L I Ben Pele 10 over at BenGreenfieldFitness.com WildMountain gets you 10% off of your pen tea nuts. This podcast is also brought to you by one of the more potent anti inflammatories that exists and a specific liposomal based anti inflammatory that I did a podcast interview on a few weeks ago. And it's actually, it's amazing when it comes to absorptability. It lowers blood sugar, it has ginger in it, so it has a really good effect on bloating and digestion. And the ginger helps the curcumin to be absorbed a little bit better. And then it has DHA in it in a vegan form of dha. So no fish died to make this particular anti inflammatory supplement. It's like a fantastic Just daily tonic that you can use for inflammation, for joint health, for gut health, for brain health, a whole lot more. It's called Pura Thrive. And you automatically get 15% off of this along with a full 30 days, 100% money back guarantee. And you go to purathrive.com BenGreenfeld I'm gonna warn you, this stuff is addictively delicious. The peeling nut. Honestly, Pura Thrive is P U r a thrive. Purathrive.com BenGreenfield you don't need a coupon code that's automatically going to give you 15% off. Okay? I don't think either of those things I just talked about has sugar in them. So I'm very, very safe. Now I can go talk to Gary Taubes. Let's do this.
In this episode of the Ben Greenfield Fitness Show.
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Hey folks, it's Ben Greenfield. And my guest on today's show just wrote this eye opening expose called the Case Against Sugar. It's kind of a controversial book, but it argues that sugar is basically like smoking the tobacco of the new millennium, I think they call it. And the author of the book says that sugar is backed by powerful lobbies and entrenched in our lives and also making us very sick. He attributes sugar to the fact that nearly 10% of children are thought to have non alcoholic fatty liver disease and of course attributes also the epidemic proportion of obesity to the root cause of sugar. His name is Gary Taubes and Gary is the co founder and the senior scientific advisor of nusci, which is something that stands for the Nutrition Science Initiative. He also wrote a really good book called why We Get Fat. And also good calories. Bad calories, too. Pretty good books that I guarantee you are not going to get through in one night. And he has three science and society journalism awards, which I kind of like because he takes a deep dive into the science in his books, but also pulls in the politics. And frankly, if you know of Gary, you probably know that there's some controversy around him and his ideas and whether or not sugar really is toxic or whether it's too many calories or, you know, whether fat is worse than sugar. There's, there's lots of, lots of little arguments out there for and against these different macronutrients. So we'll delve into that as well on today's show. Everything that you listen into and hear on today's show you can find over in the shownotes. You just go to BenGreenfieldFitness.com Taubes that's T A U B E S. That's Gary's name. And I'll link to his book over there, too. So, BenGreenfieldFitness.com Taubes and the book that we're chatting about today is called the Case Against Sugar. So, Gary, welcome to the show, man.
Thanks for having me, Ben.
Yeah, no problem. I was telling you before we even started recording that I'm kind of surprised by the number of people who are still kind of confused about sugar. Right. And the different biochemical terms we use for sugar like glucose and fructose and sucrose. So before we even dive into some of the really interesting politics of sugar that you get into in the book, can we put on our propeller hats here and talk a little bit about the biochemistry of glucose versus fructose and how that's related to sucrose?
Yeah, happy to do that. As I mentioned in the book, one of the reasons we got to the sort of misconceptions we live with today is because a lot of the leading authorities in the field going back a hundred years just didn't actually know what they were talking about when they were talking about sugar. And so because we talk about blood sugar and then we talk about the sugar that we put on our cereal or, you know, put in our coffee or load up our sodas with. So blood sugar is glucose, probably 98% glucose.
So when I do like a blood sugar analysis, like with one of those accu check sticks from the pharmacy, that's testing the amount of glucose in the blood, not the amount of fructose Exactly.
That's measuring the amount of glucose. And starches and starchy vegetables break down into mostly glucose, almost primarily glucose. And that glucose goes into your bloodstream and raises your blood sugar. And this is a pretty simple explanation. When we talk about glycemic index, you're looking at blood sugar, blood glucose, and so easily digestible starches, grains, breads, pasta, potatoes have a high glycemic index because they are absorbed as glucose. And that glucose is in your blood, and it raises your blood sugar. So sugar, the stuff you sweeten your coffee with, the sweet stuff, is a combination of. It's a 50, 50 combination of glucose and fructose. And they're both simple carbohydrates. Fructose is the sweetest of the carbohydrates, and that's why sugar tastes sweet. And when you consume sucrose or high fructose corn syrup, which is. We typically consume, is 45%.
Yeah.
Glucose, 55% fructose.
They're both mixtures of glucose and fructose. The glucose raises your blood sugar. The fructose is metabolized primarily by your liver, so it's actually metabolized in an entirely different organ. And the interesting thing is the glucose metabolized by virtually every cell in your body. So when you're consuming sugars, sucrose or high fructose corn syrup.
The fructose is what makes them different from the other carbohydrates. So there's a endocrinologist at UC San Francisco, very famous, named Rob Lustic, who.
Talks about fructose being toxic. And the reason he talks about fructose specifically is because it's what differentiates sugar from starches.
Again, do you think fructose is toxic?
I think sugar is toxic because we never consume. I think it's very likely toxic. Let me be precise. We never consume fructose alone, so we never consume fructose, even when we consume. So there's some fructose and some sucrose in fruits. It's what makes fruits sweet. There's some fructose and some sucrose in vegetables, but very small proportions, a few percent, up to maybe 8% in an apple, whereas in sugars, in a sugary beverage, you're getting all your calories from sugar, and 50% of it, or 55% of it is from fructose. And so the argument is that our, specifically, our liver never evolved to deal with the amount of fructose that it has to metabolize and the speed at which it has to metabolize when the sugars are being consumed, particularly as beverages, but in the quantities that we consume them today. And that's where the problem lies. So those of us are concerned about sugar have a very sort of liver centric view of the human body, hepatocentric view, using the medical terminology. And what worries us is the effect of this fructose load on the liver and the fact that the liver can't seem to deal with it properly. And then that results in not only the non alcoholic fatty liver disease you mentioned, but probably insulin resistance itself. And so insulin resistance is a condition where your body can't has trouble.
Responding to the insulin that the pancreas secreting. So I'm going to back up one step further. You secrete insulin in response to the glucose in your diet. So not the fructose, not the fructose. So it gets far more complicated than the sort of authorities wanted to see it 50 and 100 years ago, although it's still pretty simple. So the glucose raises blood sugar, the insulin is secreted to deal with that blood sugar. You actually start secreting it even before digesting and absorbing the glucose, because you want the insulin in your bloodstream as the glucose hits the bloodstream. And then that insulin basically signals the body to hold on to fat, signals the muscle and organ cells to take up that glucose and use it for fuel.
But while you're simultaneously getting fructose as you are in sugar or high fructose corn syrup, now you have a problem because your body's trying to metabolize fructose in this high insulin, high blood sugar environment. And it appears to cause this condition called insulin resistance.
Means your muscles and organs are resistant to the insulin. So you have to secrete more insulin to deal with the blood sugar. Now insulin levels start to go up and blood sugar levels start to go up. You become what's called glucose intolerant. You become pre diabetic, pre diabetes and type 2 diabetes are both affect conditions of insulin resistance. And then this whole slew of chronic diseases follow from there.
Right. Now you had mentioned how in nature, or really you mentioned two things like we don't have this evolutionary adaptation to be able to digest the amount of fructose that we get along with glucose in a lot of packaged products or in table sugar, which is essentially glucose and fructose combined as sucrose. But in.
In nature, you know, if we look at something like an apple, right, or a piece of fruit, how much of that is glucose or is that just pure fructose and water and fiber.
No, no, that's the thing. Most of it, high water content in fruit. And then you get, the primary carbohydrate is still glucose, just like a starch. And then you get some fructose, some. And some sucrose, which also contains fructose. So the sweetness comes from the sucrose and the fructose, but it's primarily glucose, just like a potato is.
And because of that, having like a piece of fruit would be less of an issue for fatty liver and less of an issue for insulin resistance because there is, there's less glucose being consumed along with the fructose and it's balanced out with more water and more fiber.
Yeah. And it takes longer to consume. So if you think about, say an 8 ounce glass of apple juice has the sugar content of about four apples. So you can, it's four medium sized apples. So you could drink that apple juice, you could consume all that sugar and apple juice and what, you know, if you wanted to, five seconds. But let's say you might nurse it for five minutes. It's an eight ounce glass, not even a 12 ounce can.
If you're going to eat four apples in one sitting, which.
You'Re not going to do it in five minutes, you're going to do it over the course.
Of an hour, about half an apple, personally.
Yeah. So the point is, and the apple is full of fiber as well, so that you digest it more slowly. So when you consume the apple juice, especially if you consume it in between meals, you're going to digest that sugar very quickly. The fructose is going to hit your liver relatively quickly. And again, it's four apples worth of fructose hitting your liver in five minutes as opposed to four apples worth of fructose hitting your liver, say over the course of an hour or two, depending how long it takes you to eat the apples and then digest the apples.
So it's not just the quantity, but it's the speed of delivery. And one way I describe it, if I wanted to, and this was pointed out back in the 60s by a British scientist named Peter Cleave, who said what breaks systems is not the sort of absolute quantity of, you know, whatever is delivered to it, but the speed at which it's delivered. So I could, you know, deliver a significant amount of pressure or weight to your shoulder, for instance, by leaning on you for an hour a day. And that's going to be annoying and you're probably going to get pissed off and I'm probably not going to do any functional damage to your shoulder. But then I could deliver the same amount of pressure by punching you, and I could punch you once a day, and I'll probably break your shoulder pretty quickly, you know, cause significant dysfunction. And so what Cleve pointed out is this is what's happening to our body when we consume these easily digestible carbohydrates, and then specifically to our liver when we consume fruit juices. It's the speed of delivery as well as the amount that's being delivered that causes the harm. And the body can't react to that. Didn't evolve, didn't ever see that kind of delivery. And even, you know, pre agriculture, we certainly have fruit in our diet, but it would be seasonal, and then you see it for nine months a year. So you might. Then there are theories about how the metabolism of fruit might actually trigger. And particularly the sugar in the liver and the uric acid produced might sort of flip a switch to tell your body to become a little insulin resistant so that you can store fat. Because you would see the fruit in the summer and particularly the late summer, and you'd want to store fat for the coming year. But now even fruit we see all year round, and we've also bred the fruit to be much easier to digest and sweeter.
Yeah, that's true. I tell people blueberries are pretty good for you, but the big, old, plump, sweet blueberries that you find at the grocery store are actually different than a lot of the blueberries you find out in nature. Like around me out in Washington and state, I'll eat these, really, polyphenol and flavanol, rich little berries called organ grape berries. And they're really good for you. But they're also very tart, they're very sour, they're very small, they're not very sugary. And people read that berries have a low glycemic index, therefore they're a great fruit to be eating, and they'll eat them by the handfuls. But in fact, big, old, plump, juicy berries bred for these huge amounts of sugar are actually different than the kind of berries you find in nature. So there's that.
But even then, I'm down in the Bay Area in California, and my local market gets these delicious, plump, slightly tart blueberries six weeks a year. So they show up mid May and they're gone by July. And, you know, I'll eat them, I love them, and I pay ludicrous amounts for them, but. But again, I know they're gone in July. That's it. That's the end, the blueberries. And you're getting stuff that's either shipped down from Oregon or Washington, shipped up from Argentina. And so that's one of the issues I'm not. There's another issue about fruit specifically that doesn't. I don't even enter.
Into in the case against sugar. Yeah, we tend to give dietary advice to an entire nation as though we are all equally healthy. And so fruits, vegetables, whole grains, the sort of conventional dietary wisdom. And many of us, a huge proportion of Americans are not, are no longer healthy. They're obese or overweight or diabetic. They have metabolic syndrome, which is again, insulin resistance syndrome. And so what a young metabolic, healthy individual might thrive on somebody who's predisposed to become obese or is already overweight or obese or diabetic, might be. Might not be able to tolerate and would be better off not consuming at all.
Gotcha. Now, I want to get into some other aspects of sugar. The first I find kind of interesting because I've called sugar a sometimes drug before, meaning that occasionally I'll encourage its use in like a highly glycolytically demanding event. Right. Like an intense CrossFit workout or a 40k time trial on a bike or something like that. And you actually get into in the book about the history of sugar when it comes to helping men perform extraordinary muscular labor in German research and some of the things that sugar has been used for in terms of climbing and extreme competition. Can you go into in terms of sugar, its history as far as what you found and what you talk about in the book when it comes to how people almost used it like crack cocaine?
Well, this is one of the interesting parts about the history of sugar and of nutrition research. Modern nutrition research dates to the 1860s in Germany when researchers created room size devices called calorimeters that we're going to probably talk about later to measure the energy expended by humans. So they could always measure or since the measure the energy in a food by burning it and measure the heat release. But now, 1860s, you can measure the energy expended by people by putting them in these rooms and measuring carbon oxygen consumption and carbon respiration and then calculating energy. By the 1890s, 1900s, they were beginning to measure how quickly we metabolize different foods. And so by the early 19th century, around 1916, they already knew that we metabolized sugar faster than any other carbohydrate. So it's literally quick energy. And the sugar industry started pitching it as quick energy. And Everyone from health coaches, athletic coaches to as you mentioned, sort of the German government wanted to know if this source of energy would be healthier and better for their troops. So the German government did a study with German army to see if they performed better on sugar, which indeed they did. They, they kept their weights up better during long marches, they had more energy.
Athletic coaches started using it. So rowing coaches started using it with rowers to see if it helped them get through power through exhaustion. Marathoners, marathon coaches started using it with marathon runners to see if they could get through the bonking. And lo and behold, I mean it was terrific. And one of the reasons why the medical community, particularly in diabetes, thought sugar was benign if not healthful substances because they saw how much it helped athletes get through exhaustion and what appeared to be low blood sugar. And once insulin was discovered in the 1921, 22, and they started using it on diabetics and you'd get these, you know, hard to dose insulin, especially when nobody knew what they were doing. It's always hard to dose insulin for diabetics, but back then it was a completely new art. And they'd often overdose and they'd get, you know, these people crashing into hypoglycemic shock from such low blood sugar. And you could give them candy, a piece of hard candy or some orange juice and that would bring them out of it. And they thought, boy, if it'll save diabetics from dying of hypoglycemic shock, it must be good for you.
Well, it's good for performance. I mean it does work for that. And I remember when I do Ironman triathlon before I actually, you and I haven't talked about this much, but I actually did. I switched to more of like a ketogenic approach, approach to training after a while, after I got sick of some of the issues I'll tell you about. But after Ironman, you'd think that after you did an Ironman triathlon you'd just collapse and go to sleep. But I'd be eating about one gel every 20 minutes, about 100 calories of fructose and glucose and maltodextrin. And so over the course of a 10 hour day, right, I'd have about 30 of those energy gels plus a few bars, plus some energy drinks with sugar in them. And I would finish an Ironman triathlon and have to take like two Valium to even be able to fall asleep at night, you know, even though my body was exhausted, I was so high on sugar and my central nervous system was so stimulated, plus all the gut rot and the fermentation, that despite it being a great drug for use during the race, there were some, some pretty significant side effects. And, and granted, I'm, I'm, I, I would say that an Ironman triathlon is not natural and sometimes you need an unnatural means to achieve an unnatural end. But at the same time, despite the performance enhancing effect of sugar, I think that unless you're a pro athlete with a paycheck on the line.
And even then you could argue that you could possibly go just as fast on fats as Jeff Volek showed in his faster study at University of Connecticut, sugar may not be the best thing to be consuming even during some of these especially like longer performance based endurance events. I think for something extremely intense, you definitely don't want empty glycogen levels and you definitely can benefit from slightly higher blood sugar levels. Right. Like a really tough, like 20 to 60 minute, extremely hard workout. But you know, some of the things you talk about in terms of like mountain climbing and marathoning in the book. Yeah, I think that there are, there are even alternatives to sugar for those.
Well, there are, but these are the things. Again, this was, it's hard to, hard for us to imagine sort of how primitive the state of both science and research was 100 years ago.
But yeah, I mean, clearly sugar was a performance enhancing substance and the athletic coaches realized that. He said that the mountain climbers realized that the Parisian cabbies started feeding their horses sugar back in the horse and carriage days. But they realized, I keep, you know, I wrote screenplays back in my screenwriting days, living on sugar. Aunt Annie's pretzels coated with brown sugar and I'd like buzz for an hour. I'm not sure I could have graduated from college without sugar. I would have liked to gone back and see what I could have done in ketosis, but I didn't know about ketosis.
Well, it's a drug. And I mean even related to like what you were doing for wakefulness. When you look at something like caffeine, you could argue that caffeine is sugar. Right? Because, because in many cases you're getting liver glycogenolysis from high amounts of coffee consumption in the morning. And people's blood glucose will spike due to that and the cortisol and they'll scratch their heads about why they had their fatty coffee with the butter in it for breakfast and their glucose is still spiked. And a big reason for that can be because you can overstimulate the body with other things and still get a sugar high, you know, in that case, a release from the liver. But yeah, it's definitely. Ait's a powerful drug. And related to it being a drug, you actually have a fascinating anecdote in the book about the marriage of tobacco and sugar. What's the relationship between tobacco and sugar?
Yeah, so this was interesting. I first read about this about 20 years ago when I was reading a great book on sugar screed against sugar written in the 70s called Sugar Blues. And the author talked about it then and I could never track down the details. And I had tried over the years, but then the Internet eventually makes everything bubble up to light.
So it turns out that the great technological revolution in the tobacco industry in the late 19th century was something called flu curing tobacco, where you cure, you dry the tobacco over hot air that comes up through these flus. And what flu curing tobacco does, aside from dry the tobacco leaves, is it actually increases the sugar content, believe Sucrose, from about 3% to 20%. And so now when you turn those leaves into a cigarette, which was first done, well, famously done by RJR Reynolds in 1913 or so with Camel cigarettes, which became the leading, the first, what was called American blended cigarette. And what Camel was doing was they were blending these flu cured tobacco with this high sugar content, but a relatively low nicotine content with what was called plug tobacco, which was made for chewing tobacco and was literally marinated in what they called a sugar sauce, which was sugar and maple syrup and licorice and that also had a high sugar content and had this aromatic flavoring from the marination, but had a very high nicotine content as well. And because of the sugar content in the leaves, you can actually inhale them deep into your lungs without stimulating a cough reflex. So it was a sugar content to the leaves that made the tobacco capable of being inhaled. And you could then bring the nicotine deep into your lungs as well, which made the nicotine that much more addictive. That sort of revolutionized the cigarette industry. So RJR Reynolds comes out with Camel, and by 1920, it's a leading cigarette in America. By 1930, these American blended cigarettes have spread all around the world. And now you've got this incredibly addictive substance, not only brings the nicotine in the lungs, but can bring the carcinogens deep into the lungs as well. And so you start seeing lung cancer deaths begin. Actually, literally, they show up in the mortality records within two years of Camel appearing, which is.
And then you get this lung cancer epidemic that follows.
So there's actually a high sugar content in tobacco smoke.
There's a high sugar content in tobacco leaves and tobacco smoke. It's what makes the smoke more acidic, which is why you can inhale it.
Right. Because otherwise tobacco is too alkaline to be able to inhale.
Yeah. So in the 1950s, when the sugar industry was beginning to get hammered, people were getting fat, and artificial sweeteners had appeared and.
Sodas, artificially sweetened sodas, had come on the market, and they were like just that business was exploding because Americans were trying to lose weight and have their sugary beverages, too. And the sugar industry was actually worried about how they were going to survive. And so they were looking for different industries where the sugar could be used as a product in a whole host of different possible industries. But one of them was the tobacco industry. And so there was this report written by this functionary at the sugar association, talking about the marriage of sugar and tobacco and how wonderful it was. Tobacco was so dependent on sugar for its explosive growth. And of course, this was 10 years before the Surgeon General's report linked smoking to lung cancer. So at the time, the sugar industry thought, this is great. Even if we can't sell as much sugar for the food and beverage industry, we'll at least be able to use it in tobacco and cigarettes. And then they kind of stopped talking about that. It became clear that that was not a politically acceptable compromise.
Wow, that's amazing. That sugar and tobacco kind of rose up hand in hand. I thought that was a super interesting part of your book, and I actually didn't know that about tobacco. And you know what's scary, I think you mentioned this even, is the fact that sugar caramelizes the tobacco, tobacco and improves the taste. And of course, that's a classic Maillard reaction, right, where you're inhaling, essentially, compounds that have become even more carcinogenic because of the attachment of sugar. So it's scary and very interesting at the same time. I had no clue about the marriage between tobacco and the sugar industry.
The argument I'm making in my book, the case against sugar, is basically about obesity, diabetes, metabolic diseases. So lung cancer doesn't really fit in. But once I came upon the story and I came upon the documentation to support it, and then once I had that documentation, I could find it discussed in other references.
Then I said, how could I leave this out? In fact, that chapter at one point was. I think I labeled it Chapter two and a half, like the John Malkovich floor. And being John Malkovich, if you remember that movie. Cause it's. I had to have it in the book, but it didn't. The theme is about is, are we talking about the trigger of obesity and diabetes and then the chronic diseases that associate.
When it comes to how we respond to sugar individually, you talk about something called metabolic imprinting or perinatal metabolic programming. And the idea that our response to sugar could actually start in the womb, how does that actually work?
Okay, so let me give you a little background on that. Again, what we're trying to explain today are these obesity and diabetes epidemics that have just exploded. And they exploded in populations around the world. Regardless of the ethnic background of the population, whenever that population transitions from eating its traditional diet, whatever that is, to a Western diet. And you can see the most dramatic examples of these populations, these explosions of obesity and diabetes in aboriginal populations. So Native American populations, Inuit, South Pacific Islanders, in part, I think, because they make this transition far more quickly from a native diet to a Western diet. In the US that happened with Native American populations, many of them over the course of like 20 years, basically. World War II was their introduction to the fully loaded modern American diet. The men were drafted and went off to fight in the armed services, where they were just loaded up with sugar. The army's sugar quota for its men was something like 220 pounds per soldier per year, as opposed to about three times when we supposedly consume today. And then the women went to work in munitions plants and in factories. So they went from living in the sort of relatively isolated reservations to.
You know, sort of fully Westernized diets and lifestyles. And when they came back and continued with these Western lifestyles, obesity and diabetes explode. And the. The seminal example is the Pima Indians in Arizona. And in the 1960s, NIH researchers began studying them and realized that 50% of the adults in the population were diabetic. And it's a brand new disease in these populations. So when they start studying them, they're not seeing any of the sequelae of diabetes, none of the blindness or kidney failure or gangrene and amputations. They seem to be healthy, but with diabetic blood sugars. And then within five, 10 years, they're just showing up in hospitals. And the hospitals are overflowing with these diabetic Pima who have all the horrible effects of being fully diabetic. So they start this.
Longitudinal study, it's called, where they're gonna follow the Pima as many of this population as they had, virtually all of them. And they're going to document their health status, and then they're going to follow their kids, and they're going to follow their kids kids. And what they notice in this population is that each generation, the child of a diabetic mother has something like 20 times the likelihood of becoming diabetic themselves when they just reach their 20s than a child of a non diabetic mother. And then their children in turn are far more likely to be a diabetic. So something's happening in the womb of a woman with diabetes or gestational diabetes or as it turns out, obesity that seems to increase the risk of becoming diabetic, the child becoming diabetic. And the theory is, and it's been pretty well worked out, is that a diabetic mother has elevated blood sugar. And if she has elevated blood sugar, the child in the womb sees increased blood sugar as it's in its fuel supply and then as its pancreas is developing, it over develops pancreatic beta cells, which are the cells that secrete insulin to deal with the carbohydrate content of the womb. And then once it's born, it over secretes insulin in response to the carbs. It's getting. And you get fatter, bigger babies, fatter babies, and then babies that become insulin resistant and diabetic as they get older. And this is what's referred to as, again, metabolic imprinting.
That's really interesting.
Hey, I want to interrupt today's show to tell you about oak. Not the tree, the app. The app called Oak. I've got it on my phone and basically what it is, it guides me through meditation, but doesn't have any synthetic or fake sounds because all the background sounds were 100% recorded in nature. It's got guided breathing, like 4, 7, 8 breathing, which I'm not going to demonstrate to you right now because that'd be a really boring podcast anecdote if I did. It's got box breathing, it's got all sorts of different kinds of breathing. You can do advanced meditation, interval chimes, background music. The reason that it works so well is that the fellow who developed this, Kevin Roach, really cool dude, he's been on my podcast before, actually. He used Data from over 10,000 beta testers to improve the cadence or the speed of the meditations, the wording, the tone, made hundreds of edits to these final guided sessions that are now in this completely free app that also is going to have support for things like the Oura ring, the Apple Watch, other forms of self quantification. You can track your HRV and your heart rate while you're meditating. If you're a geek like that. Anyways, though, all of it is free. You go to BenGreenfieldFitness.com oak. Yeah, like the tree. BenGreenfieldFitness.com O A K get you this app absolutely free. This podcast is also brought to you by ZipRecruiter. What is ZipRecruiter? So, look at it this way. We've got this fresh new year that's begun and you might be setting out new goals for your business, like, let's say, new hires. You can scale your business. Well, if you're looking for a new hire and you don't want to tear your hair out, I guess, dealing with whatever, I don't want to name and throw under the bus a bunch of hiring websites. But let's just say that you didn't want to deal with all the frustration that you're going to experience. On most websites, this company, ZipRecruiter, posts your job to over a hundred of the web's leading job boards with one click. They actively look for the most qualified candidate for you. They invite them to reply. They allow you on this simple dashboard to review every application. And you don't have to dig through all the employees aren't a good fit. As a matter of fact, 80% of employers who post on ZipRecruiter get a quality candidate through the site in literally one, count them, one day. ZipRecruiter, the smartest way to hire. So you can find out today why ZipRecruiter has been used by businesses of all sizes and industries to find the most qualified job candidates with immediate results. If you go to ziprecruiter.com green that lets you post jobs for free. Ziprecruiter.com green there you have it. All right, let's get back to Gary.
Have you read Rob Wolf's book Wired to Eat, or heard of it?
I've heard of it. I'm ashamed to say I haven't read it yet.
Well, in that book, he delves into the Israeli research that that highlights how certain people, apparently based on genetics, have differing sugar responses, blood sugar responses to, say, cookies or bananas. Right? Some people's blood sugar will fly up above 140 or 150 or 160 when they have a cookie, and others won't go up at all. Do you think some of that could be due to not just genetics, but perhaps what that individual's mother would have eaten when they were in the womb and their own pancreatic insulin response to sugar.
Yeah, all of that's possible. I mean, clearly there's also what the mother would have gotten. The child's tastes are stimulated and evolve in part related to what the mother's consuming, both when the child's in the womb and then when the child is nursing after it's born. So all these factors can come into it.
You know, it's hard to pinpoint any particular one.
Is key, but clearly we have vast individual differences, not just in terms of our blood sugar responses, but our cravings for these foods. How we. I live in this world where I'm thinking about sugar. Is sugar addictive? Is it.
Just habit forming? Why is it some people can consume it in so effortlessly in moderation, and others, you know, can't stop themselves from binging? All these issues could be as much a product of the, what's called the intrauterine environment and then the nursing environment and the genetic background. And it's hard to tease them out. Yeah, like I said, you know, what I'm trying to explain in this book, are proposing in this book is, you know, what I want to establish.
A potential cause of are these epidemics, since they're worldwide and they're so tragic. And that's an easier, potentially easier thing to explain than why my blood sugar might spike with bananas and oat bran but not spike with corn flakes. And yours might be the exact opposite right now.
Speaking of epidemics, what about hypertension? Because you talk about blood pressure and I've spoken before about how I'm a salt fiend. I travel over the place with Kona black salt and Aztec salt. I love really good salt. I eat the heck out of salt. And I've spoken before on the podcast about how salt really isn't much of an issue when it comes to raising blood pressure, unless it's just like the nasty aluminum caked sodium chloride you find in the salt shaker at a restaurant. But you talk about how sugar might actually be one of the villains when it comes to hypertension. What would be the relationship between sugar and hypertension? How could that actually happen from a physiological standpoint?
Let me give you the salt story first, quickly, because the salt story, that was in my introduction into nutrition research when I realized that there was actually a very vitriolic controversy over the question of whether or not salt sodium caused high blood pressure and hypertension, which was around 1998. And I spent a year one of these science and society journalism awards I won was for an article I wrote called the Political Science of salt. And I spent a year on it. One magazine article, I interviewed about 90 people.
It was one of the longest articles the journal Science had ever run as a piece of journalism. And the conclusion was that the evidence supporting this idea that salt caused high blood pressure was ambiguous at best. Basically, it was a lot of, frankly, not very good scientists who had gotten a hypothesis that they fell in love with that salt caused high blood pressure, and they couldn't get off it. And even though they could never confirm that it was true, they just kept insisting that it had to be true. And we're at the same point today that we were 20 years ago, they're still insisting, and the evidence still religiously comes up situ suggesting that they're wrong. So I had done that story. And the science there is the idea that we try to keep a relatively stable sodium content in our blood. That's kind of a homeostatic system. So if you consume sodium, the sodium gets into your circulation, you want to.
Keep the concentration constant, you have to dilute it out with some water. So then you get thirsty, you drink more water, and then your blood pressure goes up because you have more water and blood together running through your veins and arteries. So that's the sort of general idea, and it's a very simplistic idea. So eat more sodium, more sodium in the circulation, more water to dilute it out, to keep the concentration of sodium constant. Boom. Hypertension. And the world is full of simple ideas that don't pan out. And this just happened to be one of them. So then, as I'm doing the research for my first book, Good calories, Bad Calories, and you start thinking in terms of first you have this disorder of insulin resistance and metabolic syndrome that I talked about. And so turns out that obese individuals, for all intents and most obese individuals, are insulin resistant. And type 2 diabetes is a disorder of insulin insulin resistance. And metabolic syndrome is the primary or leading risk factor for heart disease. So if you have metabolic syndrome and you're insulin resistance, that's a risk factor for heart disease. And.
All these diseases are also what are known as hypertensive conditions. So they associate with high blood pressure and hypertension. One of the diagnostic criteria, metabolic system syndrome, is elevated blood pressure.
So the argument I was making that other researchers, that legitimate researchers had made in the past, academic researchers, is that if obesity, diabetes, insulin resistance, heart disease, gout, are all hypertensive disorders, they're all associated with elevated blood pressure, then maybe whatever causes one causes all of them. And then the question is what's that? And since there are also conditions of insulin resistance, and again, type 2 diabetes is in effect an insulin resistance disorder, the question then becomes, what causes insulin resistance? And what I'm arguing in the book is that sugar is the prime suspect there. I don't know if I'm right, but I'm arguing it's the prime suspect. And if sugar causes insulin resistance, then in effect, it's the diet.
Wait, you said you don't think you're right when you're suggesting that sugar causes insulin resistance?
No, no, I'm saying I'm not necessarily right. I'm proposing it's the prime suspect. That's the best I can do. You know, the argument I make in the book is that when obesity and diabetes epidemics explode in populations, invariably sugar is new to their diets. And almost invariably there's some physician or researcher saying, geez, it's the sugar guys, look how much sugar we're eating. And then in human bodies, physiologically, the heart of insulin resistance appears to be what's happening with the.
Fat accumulation and the genocide.
Even though admittedly, and I know some people will mention this, so I'll mention it. Insulin can be stimulated by other things too. Right? Like when protein is consumed, the beta cells of the pancreas will secrete insulin to shuttle amino acids into cells, you know, so some people would say, oh, you eat too much whey protein in your whey protein powder in your morning protein shake and your afternoon sardines and your evening steak, and you might induce insulin resistance the same way that you would with high sugar intake.
Yeah. So this is the question. So if you think about the questions, we want to know what creates, what's the diet, lifestyle trigger of chronic insulin resistance. So one idea is these high insulin spikes you get from.
Easily digestible high glycemic index carbohydrates might be the cause of chronic insulin resistance. And people who generally believe that think that the problem is refined grains and easily digestible carbs like potatoes. And then sugar is, is bad because it's also a relatively high glycemic index, carbohydrate. So we're digesting the glucose quickly. Since it's only half glucose, the glycemic index isn't as high as it would be, for instance, white bread. And these people would also propose that if we were drinking glucose rich beverages instead of fructose glucose rich beverages, we would probably become insulin resistant too, which is all possible.
These things are possible. So then the question is, what's the most Likely explanation. Where should we be focusing? What I'm arguing is that because of this metabolism of fructose in the liver, that the insulin resistance starts in the liver with the accumulation of fat, or even a form of fat called diacylglycerol, which is two fatty acids instead of three fatty acids. That, that that's the sort of initiating. So first the liver becomes insulin resistant as an organ, and then this sort of fuel flow and orchestration of fuel around the body begins to back up and the whole body becomes systemically insulin resistant. That's kind of the theory. And then saying sugar. So the fact that protein, for instance, stimulates insulin secretion.
Well, first of all, you know, historically, I mean, you had populations that became obese and diabetic that were relatively low protein consumers.
So it's hard to imagine. It's possible, for instance, I guess you could hypothesize that a population like the Pima, which is very poor, I mean almost unimaginably poor, relatively rural Until World War II Native American population, could have been over consuming lean protein.
They simply wouldn't. Whereas again, you look at what they were eating in the history of their, you know, their dietary assessments that were made by various individuals back then, and you can find always, basically they're commenting about the sugar consumption. Suddenly they're drinking sodas and eating candies and eating sweets, which Pre World War II, they simply didn't have access to, or not nearly in the amount. So, you know, we're always making this argument what's more or less likely to be true. And I find that often the people.
Who.
You know, the alternative hypothesis, like a protein hypothesis, you want to answer the question is can that explain not just one population or not just a modern, you know, what's happening wherever I happen to live or at my gym, but can it explain what we're seeing worldwide? And one of the tricks in this business is trying to keep as much of the evidence in your head at one time as humanly possible.
Yeah. And another thing that is important when it comes to insulin resistance is a lot of it's multimodal. Right. You talked about diacylglycerol mediated insulin resistance and that would be as a response to high amounts of fructose intake, for example. But then you would also have, for example, hypercaloric induced insulin resistance from just eating too damn many calories or even inflammation related insulin resistance. There's a whole inflammation hypothesis that high amounts of inflammation or high amounts of cortisol can also induce insulin resistance. And a lot of People are, are inflamed. They're eating excess whey protein and leucine rich protein, which can cause insulin issues. They're eating excess glucose, excess fructose, excess calories. And so it's hard to really put your finger on what exactly the cause for insulin resistance.
Well, that's why when I say it's, it all depends on the question you're asking. So if you're asking, as I am, I want to know what the cause of these epidemics are.
So, and the epidemics, I'm assuming there's one primary cause because they manifest themselves, you know, again, in virtually every population, regardless of the underlying genetics. So even though there's clearly a genetic predisposition or tolerance to whatever this trigger is, you know, if you see the same epidemic in Inuits and South Pacific Islanders and native Africans and African Americans and Caucasians, and, you know, clearly it's not a genetic disorder. So then the question is, what is it about the Western diet and lifestyle that triggers these epidemics? Because to me, the only way you're going to prevent an epidemic and reverse an epidemic is to unambiguously identify the cause. So some people will say it's overeating of all calories and lack of exercise, but I don't really buy that because the world is full of people who, you know, particularly lower socioeconomic groups that work at incredibly demanding manual labor day in and day out. So whatever, even they're probably working harder day in and day out than you are when you were training for your triathlon, although not as condensed. And yet they clearly, and in some cases have higher levels of obesity and diabetes than more sedentary higher groups. So I don't particularly buy that explanation for a lot of different reasons. Some people will say, well, it's processed food, but then the question is, what is it about processed food? Because I bet you we could create processed foods that don't stimulate trigger insulin resistance. So if we do that, what are we not putting in those foods or what are we putting in those foods to prevent the agent? So what's the agent? And then the question is, and that's where I'm arguing the agent, the prime suspect is sugar. It's not enough to say high glycemic index carbs or grains because we had, for instance, all of Southeast Asia, you know, maybe a billion people living on high glycemic index carbs and grains and not becoming obese or diabetic as a population until they started eating a Western diet. So maybe that was more refined Grains, or maybe it was white flour. But again, the prime suspect.
Yeah, or even, I mean, there's so many confounding variables. I mean, we could even say, well, when they adopted a western diet, they also adopted western technology and their circadian rhythms became disrupted and they saw more blue light and got more non native emf. There's so many things that they kind of come into play. But ultimately we, we can say that a modern western diet and modern western lifestyle and modern Western sleep patterns and everything else that's kind of associated with.
Straying from ancestral wisdom and ancestral living appears to cause some form of insulin resistance. Now one more thing I wanted to ask you about before I turn to some of the controversy that's actually surrounding you right now. And Nusai is one other thing you brought up in the book. You talk about the relationship between sugar and a lot of different chronic diseases, including the hypertension that thrust us down that rabbit hole. But you also talk about gout. And a lot of people, they'll go on a low protein or a low uric acid diet to control something like gout. But you argue that sugar could be the primary culprit there. How would that work?
Well, and so this is, I'm going to give you a little history again here. So gout traditionally swept through. There was something called the gout wave that swept through Europe in the 17th century. And it starts with, so first the royalty get gout, then the wealthy get gout, and then slowly it spreads to the population at large. And the assumption was it's just high living, you know, because if rich people are getting gout, they're drinking a lot of alcohol, they're eating a lot of meat, they're eating a lot of everything. So therefore it's sort of of. You'd see it in the literature back then. High living is the cause of gout. And again, it's one of these sort of vague western diet ideas. And the assumption was because then the researchers start realizing 150 odd years ago that the problem is too much uric acid in the bloodstream. And then the uric acid tends to crystallize out and particularly in the joints. And so you get these swollen, arthritic, incredibly painful joints. One famous bon vivant described it as like walking on his eyeballs.
And so the idea of protein is high and it metabolized, you get a lot of uric acid from it. And therefore maybe.
Protein has a lot of uric acid in it. So maybe it's meat consumption which fit the general epidemiologic picture. And so we should eat. If uric acid is the problem, we should eat a low uric acid diet. And again, there's this kind of simplistic idea always that you are what you eat. So if you know, if you want to minimize sodium levels in the bloodstream, the way to do it is to eat less sodium. If you want to minimize uric acid levels in the bloodstream, the way to do it is to eat less uric acid. A more informed way to think about it is you are what your body does with what you eat. Now you want to understand what actually regulates the sodium content of the blood. So when we were talking about hypertension, turns out that when you raise insulin levels, your body doesn't secrete as much sodium, and it tends to hold on to sodium. So you could raise your insulin levels by eating more sodium, but you could raise it much more effectively just by raising your insulin levels. And that's one of the things that links sodium. That's why all those diseases of insulin resistance are hypertensive diseases.
It turns out you sugar, even though there is not uric acid in sugar, when you metabolize sugar in the liver, particularly, part of it is metabolized into uric acid. So that's another way to elevate uric acid levels. So it's interesting. These researchers studied gout. They realized that eating a low meat diet or a low alcohol diet didn't actually help with gout particularly. But they kept. And then in the 1960s, they discovered a drug to treat gout called allopurinol that was relatively cheap and benign. And they just stopped looking. Literally, the research community kind of evaporated because they thought they had a drug that treated gout. And it was, again, cheap and benign. Everyone could take it. So we don't need to do the research anymore. And they went away. And I talked to these guys who did their research, and they told me they just stopped doing it. They stopped getting funded. They did other things. 1970s, people started realizing that the very easy way to raise uric acid levels in the bloodstream is feed, at least in animals. And turns out in humans is feed them sugar. And there was a sugar or fructose. Well, fructose particularly, but the fructose usually comes in sugar. So there's a concept called fructose induced hyperuricemia.
And the interesting thing is, when I started doing my research for good calories, bad calories, early 2000.
Two, thousands. Yeah. I would talk to these researchers who were studying gout, and some of them were studying sugar, and some of them are studying sugar and uric acid. And the ones who were studying the effect of fructose on uric acid didn't realize that sucrose was half fructose. So they thought they were only doing the research in relationship on maybe high fructose corn syrup. They just didn't have a biochemistry background. And the ones who were studying gout and on an epidemiologic level, and these huge epidemiologic populations didn't. Had never even heard of fructose induced hyperuricemia. So once, you know, and I'll take credit for pointing out to these people, because I, as a journalist, I got to talk to everybody. So even though my med school training is somewhat pathetic, you know, my biochemistry is simplistic, I get to learn from all the experts. So I actually could spread the news around that why aren't you guys looking at sugar? And suddenly sugar is an obvious cause of gout because of the fact that even though it does not have uric acid, it increases uric acid levels in the blood. And then there's a researcher at the University of Colorado named Rick Johnson who's considered one of the best kidney specialists in the country, a very smart guy who's been studying uric acid now and fructose and sucrose and glucose for going on 20 years. And he's, he has a very interesting hypothesis. The uric acid is playing the key role in causing insulin resistance.
Interesting.
And again, it's one of these things. He could be right. And at the end of the sugar book, I have in my acknowledgments that I'm always worried that I'm never giving Rick Johnson as the credit he deserves, but because he's virtually the only person doing the research, it's hard to tell whether he's right because you don't see it hasn't caught on widely enough to be widely replicated.
Yeah, it's really interesting that it's that 1, 2 combo of insulin, which you say in the book, decreases uric acid secretion or excretion, and then the combination of sucrose and high fructose corn syrup, because what you say in the book is that that's the worst of all carbs, because the fructose part of high fructose corn syrup and sucrose increases uric acid production and decreases the uric acid excretion. And then the glucose, because it raises insulin, decreases the uric acid excretion. So, yeah, so it's kind of interesting how a lot of people, they'll cut out protein, they'll cut out alcohol, but then they'll go on a vegetarian diet or something like that for gout. And it'll get worse because in many cases an improperly structured plant based diet a lot of times has tortillas and corn chips and high fructose corn syrup and all manner of other issues.
Nature has thrown some sort of jokes into this as well just to make life more complicated. So often when people go on a ketogenic diet, they'll also get gout flare ups, not apparently from the meat, but because uric acid is often stored as well, if I'm remembering correctly, with fat and fat tissue. So as you start mobilizing that fat, you start increasing, the uric acid comes out too and you increase uric acid. And now you've got somebody who goes on a diet that might in the long run be the healthiest diet he could be on, but in the short run makes a gout flare up. And then of course they say, well this is horrible and they get off the diet and that's the end of it.
Yeah, yeah. You know, there's so much more that you get into in the book when it comes to the relationship between a host of chronic diseases and sugar. And one of the things that perhaps because you're such an advocate against particularly high fructose corn syrup and sucrose or table sugar with Nusai, there was some controversy about that. And from what I understand, you guys did a study at Nusai, at Nutrition Science Initiative where you were looking into whether or not eliminating carbohydrates from the diet could somehow eliminate obesity. And I guess, and again, this is all from a little bit of looking into the issue and I haven't talked to you at all about it, but apparently what you found out was that there wasn't a very big link between sugar consumption and obesity and that a ketogenic diet or a low carb diet didn't seem to infer any type of metabolic advantage at all. And that the carb insulin theory of obesity was falsified by your guys own research And I think you've been called out on that. But what is your response to the controversy about there not being a relationship between insulin and obesity?
Okay, so let me give you the full background on that because this gets into the reason I am one of the reasons, I'm sorry, controversial in this field. So one of the things I realized in my research and argued in my books and.
You know, I think as Much as anyone I'm the owner of this idea is that. So we tend to think of obesity as an energy balance disorder. That's the conventional wisdom. And this phrase, energy balance disorder is what you'll see in science papers. And by that we mean the disorder is literally caused by taking in more calories than we expend. And so it's a disorder of consumption versus expenditure. And the research community, when they study it, they ask questions like why do fat people eat so much? Or why do fat people expend so little energy? And you know, I have trouble even talking about that anymore without thinking this is going to sound too simplistic. People are going to bridle when I even say this is what the research community does, but this is what they do. And it comes down to this phrase. Obesity is about calories in, calories out. And if you eat more calories than you expend, you'll get fat. And so therefore that's the cause of obesity. And I've been arguing, and others as well, that this is almost naive beyond belief. It's a 110 year old thinking based on the what could be measured in 1900, 1910? And we never got away from it. So the argument that I came and I realized this doing my research for my first book was that until the Second World War, all the leading research on obesity and metabolism and nutrition and endocrinology, the study of hormone related diseases, genetics, it was all done in Europe, primarily Germany and Austria. America was like this second rate outpost of medical research. And these Germans and Austrians had concluded that obesity in effect had to be a hormonal defect, a hormonal regulatory defect, and that the hormones involved were, you know, sex hormones were obviously involved because men and women fattened differently and stress hormones were involved and insulin was fun, had to be fundamentally involved because insulin works to put fat in fat cells. Although they hadn't really worked that out yet. And then, and so the gist of it was that the American researchers who thought obesity was a sort of gluttony and sloth problem were naive. And these Germans and Austrians would argue that they were naive. But then the war comes along, the German and Austrian literature vanishes. I mean the research community vanishes. The, the lingua franca of the medical literature goes from German Pre World War II to English post World War II. And the only researchers who are left studying obesity post war are Americans. And so the American calorie in calorie out theory carries the day, not because it made any sense, but because The German and Austrian owners of the hormonal regulatory hypothesis vanished. And so what I mean by it not making any sense is like, first of all, it doesn't explain much. If I ask you why men get fat above the waist.
Belly fat, and women get fat below the waist, which is a reasonable thing to ask about a disorder like obesity, how many calories they consume doesn't tell you anything about that. If I ask you why fat accumulates in specific places like double chins or love handles or thick ankles, the amount of calories you consume, consume doesn't tell you anything. Even, you know.
I mean, there's just a whole slew of things that the, you know, saying somebody gets fat because they take in so many calories is like saying somebody gets rich because they take in so much money. You know, it sounds vaguely explanatory, but it doesn't actually tell you anything about why the person gets rich or why.
The person gets fat. And again, this idea that it's fundamentally that the fat cells are very well regulated by hormones and enzymes in the central nervous system. And they're regulated because you want to be able to store calories when necessary and mobilize calories when necessary. So for instance, in a flight and fight response, when you're secreting adrenaline, that adrenaline is telling your fat tissue to dump fatty acids into the bloodstream. Because if we're going to fight a lion or run away from an army, we got to have the fuel available to do it. And that fuel is going to be both glycogen from the liver and fat from the fat tissue. And all of that is very carefully regulated. In order to get obese, you have to dysregulate. It's not enough just to eat more calories.
Or expend less. You literally have to change the rate. So that's what I've been arguing and others. And for one reason or another, a lot of people find this.
Almost impossible to conceive. Like the idea that obesity isn't an energy balance disorder is considered quackery.
So it's not true that you don't see a lot of these issues. If you're eating a high sugar diet in a hypocaloric state.
If you're eating a high sugar diet in a hypocaloric state, it would be an interesting meaning.
Like if I burn like I burn a, a crap ton of calories, I burned like 3200 calories at rest. If I were to shift to like an 800 calorie a day diet comprised of like rice and Coke. You're saying I'd still gain weight.
No, you wouldn't. But again, remember, you're different from. So let me give you an example.
There's a phenomenon now that's known as a dual burden of obesity and malnutrition. So these are usually very poor populations in which the children are malnourished and their growth is stunted. So they're clearly, they have not just macronutrient, micronutrient deficiencies, but they're not getting calories. And you see relatively high levels of obesity in the adults, particularly the women. And you see, for instance, obese mothers with starving children.
So because the children are starving, we're going to assume they're hypocaloric. And because the mothers are going to want to prevent their children from starving, we're going to assume that they can't, so that they are also hypocaloric and yet they're obese.
So now you have to somehow reconcile how a woman.
Could be obese despite getting not enough calories to give excess calories to her starving child. You know what I mean? So if the mother's obese because she's sneaking Snickers bars, which, you know, then why isn't she giving those Snickers bars to her malnourished kid whose growth is stunted because he's not getting enough protein and enough. So this is what I mean by keeping. You have to direct your attention away from your immediate universe and look sort of worldwide, and you can actually find populations that we, for all intents and purposes, we could describe as hypocaloric, and yet they still have high levels of obesity. So now how do you reconcile those facts? And what you find with those populations is that they tend to have the cheapest calories are carbohydrates and sugar. So they still, even though they're poor, they still tend to have high carb, high sugar diets. So this population. So that's the kind of thing that, you know, one of the things I'm often asking the energy balance defenders is how do you explain those populations? And when you do it, and I've actually got a Dropbox now with about 40 papers describing probably 30 populations like that. And I say, look, I'll give you access to, to my Dropbox file.
What you need to do is you need to write a book or write an article entitled something like people who Eat Few Calories But Lots of Sugar Still Gain fat, and then just use all these tribes and all these populations as Examples, I personally suspect that in addition to insulin, there are probably issues with inflammation with leptin dysregulation, with again, the influence of, of sugar potentially on circadian rhythm and on even like mitochondrial function. Right. Which is incredibly important for metabolism. I think there's a host of things, even in addition to insulin, that will be contributing to the inability to be able to burn your own storage fat, even if you're not eating a lot of calories.
And this is the question, it's sort of. I mean, you've got this amazingly intricate, unimaginably intricate homeostatic.
System that's us. And you start screwing with any aspect of it. All those things you mentioned, you know, from leptin and inflammation, everything. The question is then what's cause and what's effect when everything is causing and affecting everything else in the system. And so the easy question to ask is, what's the trigger? So one way I talk about this is, you know, if I hit myself over the head with a hammer, the response is going to be amazingly complex. I mean, the swelling and the inflammation and the pain mediation and the immune response to whatever. You know, there's going to be a whole.
Lifetime worth of research for, you know, laboratories around the country figuring out all the details of the complex response to that hammer hit. But if I ask the simple question, how do I prevent that from happening? The answer is, don't get the damn hammer away from my head. Because the hammer is the fundamental cause of the complex multifactorial phenomena that follows. And so what we're talking about again is like, it's important to keep your sort of eyes on the goal. And the goal is what's the dietary thing that's causing that obesity and diabetes? Because we're going to assume it's not natural. And one reason we know what it's not natural is because we don't see it even in animal populations unless they're eating western diets like our cat, you know, our house pets.
Right, right. Yeah. And you know, I think a big part of it too is once you introduce a lower fiber intake and a lower protein intake, there's also the potential loss of the thermogenic effect of food as well. And so there's again another hit on metabolism. So there's a variety of factors involved here, but ultimately I kind of look at it. But the same way a lot of people look at.
Living a clean and good life, right? They don't know if there's a hell, but just in case there is.
They'Re going to live a sinless life or try to stay away from getting into too much trouble. Kind of the same idea with high fructose corn syrup and sucrose. I mean, for me, I've seen enough anecdotes of evidence to where even if, whether or not there's. There's science that says one way or the other, there's enough anecdotal evidence for me to say that I'm gonna drink a. I'm gonna drink some bone broth instead of some coke and eat a lot of plants and proteins and good fats instead of sucrose.
Well, and that's the argument I make in the book is do I think the evidence is unambiguous enough to regulate sugar? Well, I don't. It worries me. And if they start regulating sugar, they'll go with the same sort of state of ambiguous evidence. They'll regulate things that I think are not only healthy but that I should be consuming. But do I think there's enough evidence for people to decide for themselves? Just as you said, it's like, am I better off not eating it? And is it worth it to me? And particularly if you're a parent, am I better off, like, moderating my child or getting my kid to stop guzzling? And the answer is, I think there's a lot of reasons to worry.
And these obesity and diabetes epidemics are. They were. The director general of the World Health Organization recently referred to them as slow motion disasters. So they're going to overwhelm medical systems worldwide, including our own. And we have to figure out what's causing them. We have to identify what it is and get it out of the. Or, you know, at least convince people that this is the cause and that they should change their behavior accordingly.
Yeah, yeah. Well, if you're listening in, I'm sure that you have your own theories and your own comments on everything that Gary and I just got done talking about. So if you want to leave them, go to BenGreenfieldFitness.com Taubes that's BenGreenfieldFitness.com T A U B E S where I will also put some links to Gary's books, including this one, we just got to talking about the case against sugar. But you should also read Good Calories, Bad Calories, because it's pretty good too. So is the other one better than pretty good?
Although it's a hard one.
Why We Get Fat. If you don't say so yourself.
And leave your comments or questions there and I'll jump in and reply and in the meantime, Gary, thanks for giving your time and coming on the show and sharing all this stuff with us, man.
Well, Ben, thanks for your interest. It's been great.
Awesome. All right, folks. Well, I'm Ben Greenfield along with author and researcher Gary Taubes, signing out from BenGreenfieldFitness.com have a healthy week.
You've been listening to the Ben Greenfield Fitness podcast.
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