January 11, 2018
Podcast from: https://bengreenfieldfitness.com/podcast/nutrition-podcasts/the-case-against-sugar-gary-taubes/
[0:33] Wild Mountain Paleo/Purathrive
[07:35] The Difference Between Glucose and Fructose and How It’s Related to Sucrose
[14:20] The Difference Between the Fructose We Eat Now and The Fructose in Nature
[27:50] Relationship Between Tobacco and Sugar
[33:35] Metabolic Imprinting
[38:08] Oak App/Zip Recruiter
[47:10] The Relationship Between Sugar, Gout, and Uric Acid
[49:20] Why Different People Have Different Blood Sugar Responses to Sugar
[1:05:00] Controversial NuSI Research: No Insulin-Obesity Link
[1:20:56] End of Podcast
Ben: 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 going to 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 going to 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. 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 a.k.a. sugar of any nut. It’s got a ton of magnesium and vitamin b1 and manganese, but probably a lot of important than that, it has an addictively delicious buttery taste. 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, well Mountain Paleo does, with high integrity suppliers who focus on transparency and sustainability and extremely, extremely delicious pili nuts. I’ve got a bunch in my pantry; they’re amazing. I sprinkle them on everything! You can visit BenGreenfieldFitness.com/WildMountain, just like it sounds. BenGreenfieldFitness.com/WildMountain and here is your pili nut discount code. You ready? It’s BENPILI10. BENPILI10. Pili is P-I-L-I. BENPILI10 over at BenGreenfieldFitness.com/WildMountain gets your 10% off of your pili nuts.
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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:
“So the argument that I was making is that other researchers, that legitimate researchers have made in the past is that if obesity, diabetes, insulin resistance, heart disease, gout are all hypertensive disorders, they’re all associated with elevated blood pressure…” “It turns out that when you raise insulin levels, your body doesn’t secrete as much sodium and tends to hold on to sodium. You could raise your insulin levels by eating more sodium but you can raise them much more effectively just by raising your insulin levels.”
Ben: 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. 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 nonalcoholic 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 NuSI which is something that stands for Nutrition Science Initiative. He also wrote a really good book called “Why We Get Fat” and also “Good Calories, Bad Calories.” Two pretty good books I guarantee you’re not going to get through in one night. 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 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 whether fat is worse than sugar. There’s lots of little arguments our there for and against these macronutrients. We will delve into that as well on today’s show.
Everything that you listen into and hear on today’s show, you can find over on the show notes. 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.
Gary: Thanks for having me, Ben.
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 kind of confused about sugar and the different biochemical terms we use for sugar like glucose, fructose, and sucrose. So, before we even dive into some of the really interesting politics of sugar that you get into the book, can we put on our propeller hats here and talk about the biochemistry of glucose versus fructose and how that’s related to sucrose?
Gary: Yeah, I’m happy to do that as I mentioned in the book, one of the reasons we got to this sort of misconceptions we live with today is because a lot of the leading authorities in the field going back 100 years just didn’t actually know what they were talking about when they were talking about sugar. So, because we talked about blood sugar and then we talked about the sugar that we put on our cereal or put in our coffee or load up our sodas with… So, blood sugar is glucose primarily, 98% glucose.
Ben: So, when I do a blood sugar analysis with one of those Accu-Chek sticks from the pharmacy that’s testing the amount of glucose in the blood not the amount of fructose?
Gary: Exactly. That’s measuring the amount of glucose and starches and starchy vegetables break down into mostly glucose, so almost primarily glucose, and that glucose goes into your bloodstream and raises your blood sugar. Then, 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, pastas, 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 is 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 sweets. When you consume sucrose or high fructose corn syrup which we typically consume as 45%…
Gary: 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.
Gary: So, it’s actually metabolized in an entirely different organ and the interesting thing is the glucose is 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 an endocrinologist at UC San Francisco, very famous, named Rob [0:10:23] ______ who talks about fructose being toxic. The reason why he talks about fructose specifically is because it’s what differentiates sugar from starches.
Ben: Do you think fructose is toxic?
Gary: I think sugar is toxic because we never consume… I think it’s very likely toxic, I may be precise, we never consume fructose alone. So, we never consume fructose when we eat… 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 and sugar beverages, you’re getting all your calories from sugar and 50% or 55% of it is from fructose. And so, the argument is that our liver specifically never evolved to deal with the amount of fructose that it has to metabolize and the speed it has to metabolize and when the sugars are being consumed because, particularly as beverages but in the quantities that we consume today and that’s where the problem lies. So, those of us who are concerned about sugar have a very liver-centric view of the human body, a hepato-centric view using medical terminology. 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 that results in, not only the nonalcoholic fatty liver disease you mentioned, but probably insulin resistance itself. Insulin resistance is a condition when your body has trouble responding to the insulin that the pancreas is secreting. So, I’m going to back up one step further…
Gary: To treat insulin in response to the glucose with your diet…
Ben: Not the fructose?
Gary: Not the fructose. So, it gets far more complicated than this sort of authorities wanted to see it 50 to 100 years ago though 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 onto fad 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 is trying to metabolize fructose and this high insulin high blood sugar environment.
Gary: 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 when blood sugar levels start to go up, you become what’s called glucose intolerant, you become pre-diabetic. Prediabetes and type two diabetes are both in effect, conditions of insulin resistance and this whole slew of chronic diseases follow from there.
Ben: Right. Now, you had mentioned how in nature or really you mentioned two things: 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.
Gary: Or all sugary beverages.
Ben: In nature, and if we look at something like the apple or a piece of fruit, how much of that is glucose or is that just pure fructose and water and fiber?
Gary: No, no, that’s the thing, most of it is high water content in fruit and then you get the primary carbohydrate is still glucose, just like a starch, then you get some fructose, 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.
Ben: And because of that, having a piece of fruit would be less of an issue for fatty liver and less of an issue for insulin resistance because there is less glucose being consumed along with the fructose and that’s balanced out with more water and more fiber.
Gary: And it takes longer to consume. So, if you think about an 8-ounce glass of apple juice has the sugar content of about four apples, four medium size apples. So, you could drink that apple juice, you could consume all that sugar and apple juice if you wanted to in 5-seconds, but let’s say you might nurse it for 5-minutes, an 8-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 in five minutes, you’re going to do it over the course of…
Ben: I can handle about half an apple personally.
Gary: 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 when you consume it between meals, you’re going to digest that 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 over the course of an hour or two depending how long it takes you to eat the apples and then digest the apples.
Gary: So, it’s not just the quantity, but it’s the speed of delivery and one way I describe it is if I wanted to, and this is pointed out back in the 60s by British scientist named Peter Cleve, who said what breaks systems is not the absolute quantity of whatever is the liver to it but the speed at which it’s delivered. So, I could 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, but 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 could probably break your shoulder pretty quickly or cause significant dysfunction.
What Cleve pointed out is this 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 the liver as well as the amount that’s being delivered that causes harm and the body can’t react to that, didn’t evolve, didn’t ever see that kind of delivery and even pre-agriculture, we certainly had fruit in our diet, but it would be seasonal.
Gary: And then you won’t see it for nine months a year so you might… Then there are theories about how the metabolism fruit might actually trigger in particularly the sugar in the liver and the uric and they work fast to produce might sort of flip the 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, in particular the late summer, when 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.
Ben: That’s true. I tell people blueberries are pretty good for you but the big old plump sweet blueberries that you find in the grocery store are actually different than a lot of the actual blueberries you find out in nature like around me, in Washington State, I’ll eat these really polyphenol and flavonoid rich berries called Oregon 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 eaten and they’re eaten 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 too.
Gary: Even that, I’m down in the Bay Area in California, and my local market gets these delicious plum, slightly tart blueberries six weeks a year. So, they show up mid-May and they’re gone by July and I’ll eat them; I love them. I pay ludicrous amounts for them, but I know they’re gone in July. That’s it; that’s the end of the blueberries and you’re getting stuff that’s either shipped down from Oregon or Washington or shipped up from Argentina.
Gary: So, that’s one of the issues. There’s another issue about fruit specifically that I don’t even enter into in “The Case against Sugar”…
Gary: We tend to give dietary advice to an entire nation as though we are all equally healthy and so fruits, vegetables, whole grains, those sort of conventional dietary wisdom, and many of us, a huge proportion of Americans, are no longer healthy. They’re obese or overweight, or diabetic; they have metabolic syndrome which again, is an insulin resistance syndrome, and so, what a young metabolic healthy individual might thrive on, somebody who’s predisposed to become obese or already overweight, obese, or diabetic, might not be able to tolerate, would be better off not consuming it at all.
Ben: 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 it’s use and a highly glycolitically demanding event or an event 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’ve found and what you talk about in the book when it comes to how people almost used it like crack cocaine?
Gary: [laughs] Well, this is one of the interesting parts of sugar and of nutrition research, modern nutrition research dates to the 1860s in Germany when research created room-size devices called calorimeters, which we’re probably going to talk about later, to measure the energy expended by humans. So, they could always measure the energy in a food by burning and measuring the heat release, but now in the 1860s, you could measure the energy expended by people by putting them into 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 early 1916, we already knew we metabolize 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, 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 the German army to see if they performed better on sugar, which indeed they did. They kept their weights up better during long marches, they had more energy. Athletic coaches started using it; rowing coaches started using it with rowers to see if it would help or power through exhaustion; marathon coaches started using it with marathon runners to see if they could get through the bonking and low and behold it was terrific.
One of the reasons why the medical community, particularly in diabetes, thought sugar was benign, if not helpful substance, 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 1921-22, they started using it on diabetics and you would get these 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 would often overdose and they’d get these people crashing into hypoglycemic shock from such low blood sugar and you could give them a piece of hard candy and some orange juice and that would bring them out of it and they thought “boy, if it will save diabetics from dying of hypoglycemic shock, it must be good for you.”
Ben: Well, it’s good for performance, it does work for that. I remember when I do Ironman triathlon, I haven’t talked about this much, but I actually switched to a more ketogenic approach to training, after a while I got sick of some of the issues I’ll tell you about, but after Ironman, I would… You think that after you did an Ironman triathlon you’d just collapse and go to sleep, but I’d be eating one gel every 20-minutes, about 100 calories of fructose and glucose and some maltodextrin and so over the course of a 10-hour day. So, I’d have about 30 of those energy gels plus a few bars, plus some energy drinks with some sugar in them and I would finish an Ironman triathlon and have to take two valium to even be able to fall asleep at night even though my body was exhausted, I was so high on sugar, my central nervous system was so stimulated, plus all the gut rot and fermentation that despite it being a great drug to use during the race, there are some pretty significant side effects.
Granted, I would say that an Ironman triathlon is not natural, sometimes you need unnatural means to achieve an unnatural end. At the same time, despite the performance enhancing effect of sugar, I think unless you’re a pro-athlete with a pay check 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 longer performance-based endurance events. I think for something extremely intense you don’t want empty glycogen levels and you definitely can benefit from slightly higher blood sugar levels, like a really tough 20 to 60 minute extremely hard workout, but some of the things you talk about in terms of mountain climbing and marathoning, in the book, I think there are alternatives to sugar for those.
Gary: There are, but these are the things, again this was hard to imagine how primitive this state of both science and research was 100-years ago, but yeah, clearly sugar was a performance enhancing substance and the athletic coaches realized it, the mountain climbers realized it, the Parisian cabbies started feeding their horses sugar back in the horse and carriage days because they realized… I wrote screenplays back in my screenwriting days living on sugar and Auntie Anne’s Pretzels coated with brown sugar and I’d buzz for an hour. I’m not sure I could have graduated college without sugar.
Gary: I would have liked to gone back to see what I could have done about ketosis but I didn’t know about ketosis.
Ben: Well, it is a drug and even related to what you were doing for wakefulness, when you look at something like caffeine, you could argue that caffeine is sugar 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. 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 is because you can overstimulate the body with other things and still get a sugar high, in that case, a release from the liver, but yeah, it’s definitely a powerful drug.
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?
Gary: Yeah, so this was interesting. I first read about this 20 years ago when I was reading a great book on sugar, [28:03] ______ against Sugar written in the 70s called “Sugar Blows.” 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.
It turns out the great technological revolution in the tobacco industry in the late 19th century was called flue curing tobacco where you dry the tobacco over hot air and it comes up to these flue and what flue curing tobacco does aside from dry the tobacco leaves is it actually increases the sugar content; I believe sucrose about 3% to 20%. So now, when you turn those leaves into a cigarette which was first famously done by RJR Reynolds in 1913 or so with Camel cigarettes and leading the first which was called the American Blended Cigarette and what Camel was doing was they were blending these flue 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.
Because of the sugar content in the leaves, you can actually inhale them deep into your lungs without stimulating a cough reflects. It was the sugar content in 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 Camels, by 1920 it’s the leading cigarette in America; by 1930 these American-blended cigarettes had spread all around the world and now you’ve got this incredibly addictive substance that no only brings the nicotine into the lungs but can also bring the carcinogens deep into the lungs as well. So, you start seeing lung cancer deaths. Which then literally show up in the mortality records within two years of Camel appearing which is… And then you get this lung cancer epidemic that follows.
Ben: So, there’s actually a high sugar content in tobacco smoke?
Gary: 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.
Ben: Right, because otherwise tobacco is too alkaline to be able to inhale.
Gary: Yeah. So, in the 1950s, when the sugar industry was beginning to get hammered, people were getting fat and artificial sweeteners had appeared, artificially sweetened sodas had come on the market and that business was exploding because Americans were trying to lose weight and have their sugary beverages too. Sugar industry was actually worried about how they were actually going to survive 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.
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 and 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 will at least be able to use it in tobacco and cigarettes and then they kind of stopped talking about that as it became clear that that was not a politically acceptable compromise.
Ben: Wow, that’s amazing that sugar and tobacco rose up hand and hand. I thought that was a super interesting part of your book and I should know that about tobacco. You know what’s scary? I think you mentioned this even, is the fact that sugar caramelizes the tobacco and improves the taste and of course that a classic mired reaction, right…
Ben: Where you’re inhaling essentially compounds that have become even more carcinogenic because of the attachment of sugar. It’s scary and very interesting at the same time. I had no clue about the marriage between tobacco and the sugar industry.
Gary: The argument that 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 once I had that documentation I could find it discussed in other references, then I said “how could I leave this out.” It’s like that chapter, in one point, I think I labeled it “The Chapter 2 ½,” like the John Malkovich Floor and being John Malkovich if you remember that movie. I had to have it in the book but it didn’t… The theme… We talk about the triggers of obesity, and diabetes, and chronic diseases that associate.
Ben: When it comes to how we respond to sugar individually, you talk about something called metabolic imprinting or prenatal metabolic programming, and the idea of that, our response to sugar could actually start in the womb? How does that actually work?
Gary: Okay, let me give you a little background on that. Again what we’re trying to explain today are these obesity and diabetes epidemics have exploded and they exploded in populations around the world regardless of those ethnic background of the population. Whenever that population transitions from eating its traditional diet, whatever that is, to a Western diet. You can see the most dramatic examples of these populations, these explosions of obesity and diabetes, in aboriginal populations. So, Native American populations, Inuits, South Pacific Islanders and part of it is 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 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 members was something like 220 pounds per soldier per year as opposed to three times what we supposedly consume today. And then the women went to work in ammunition plants and in factories. So, they went from living in relatively isolated reservations to fully Westernized diets and lifestyles. When they came back and continued these Western lifestyles, obesity and diabetes explode and the seminal example is the Pema Indians in Arizona.
In the 1960s INH researchers began studying them and realized 50% of adults in the population were diabetic and it’s a brand new disease. When they start studying and they’re not seeing any of the [35:55] ______ diabetes, none of the blindness or kidney failure or gang green and amputations, they seem to be healthy but with diabetic blood sugars. Then, within 5 to 10 years, they’re just showing up in hospitals and hospitals are over flooding with these diabetic Pema who have all the horrible effects of being fully diabetic.
So, they start this longitudinal study where they’re going to follow the Pema, as many of this population as they can, virtually all of them, and they’re going to document their status, and they’re going to follow their kids, and they’re going to follow their kid’s kids. What they noticed in this population is that in each generation, the child of the diabetic mother has something like 20 times the likelihood of becoming diabetic themselves when they reach their 20s than a child of a non-diabetic mother. Then their children in turn are far more likely to be a diabetic. So, something is 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 in its fuel supply and as its pancreas is developing, it overdevelops pancreatic beta-cells which are the cells that secrete insulin to deal with the carbohydrate content of the womb. Then once it’s born, it over secretes insulin in response to the carbs its getting and you get fatter, bigger babies, fatter babies, and then babies that become insulin resistant and diabetic as they get older. This is what they refer to as, once again, metabolic imprinting.
Ben: That’s really interesting.
Ben: Hey, I want to interrupt today’s show to tell you about Oak, not the tree, the app called Oak. I’ve got it on my phone and basically what it is, it guides me through meditation but that does not mean 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 would be a really boring podcast anecdote if I did, it’s got box breathing, it’s got all sorts of different kinds of breathing that you can do, advanced meditation, interval chimes, background music. The reason that it works so well is that the fellow who developed this, Kevin Rose, 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 going to have support for things like the Oura Ring, the Apple Watch, other forms of self-quantification, and 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 will get you this app absolutely free!
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Alright, let’s get back to Gary.
Ben: Have you read Robb Wolf’s book “Wired to Eat” or heard of it?
Gary: I’ve heard of it, but I’m ashamed to say I haven’t read it.
Ben: Well, in that book he delves into the Israeli research that highlights how certain people, apparently based on genetics, have differing sugar responses, blood sugar responses to cookies or bananas.
Ben: Right, some people’s blood sugar will fly 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 can be due to not just genetics but perhaps what that individual’s mother would have eaten when they were in the womb in their own pancreatic insulin response to sugar?
Gary: Yeah, all of that is possible. Clearly there’s also what the mother would have done via the child’s tastes are stimulated and evolved in part with what the mother is consuming both when the child is in the womb and when the child is nursing when it is born. So, all these factors can come to it. You know, it’s hard to pinpoint any particular one as key, but clearly we have vast individual differences, not just in terms of our blood sugar responses, but our cravings for these foods. I live in this world where I’m thinking about is sugar addictive? Is it just habit forming? Why is it some people can consume it so effortlessly in moderation and others can’t stop themselves from binging? All these issues could be as much a product of the intrauterine environment and then the nursing environment and the genetic background. It’s hard to [42:57] ______ them out.
Gary: Like I said, what I’m trying to explain in this book or proposing in this book, 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.
Ben: Right, now speaking of epidemics, what about hypertension? You talk about blood pressure and I’ve spoken before about how I’m a salt fiend, I travel all 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 the nasty aluminum-caked sodium chloride you find at the salt shaker in a restaurant. 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?
Gary: Let me give you the salt story first.
Gary: 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 whether or not salt, sodium, caused high blood pressure and hypertension, it was around 1998. I spent the year, one of these science and society journalism awards was for an article I wrote called “The Political Science of Salt” and I spent a year on that one magazine article. I interviewed about 90 people, it was one of the longest articles of journal science I had ever run as a piece of journalism. The conclusion was that the evidence supporting 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 cause high blood pressure and they couldn’t get off it. Even though they could never confirm that it was true, they just kept insisting that it had to be true and that we’re at the same point today that we were at 20 years ago, they’re still insisting, and the evidence still religiously comes us suggesting that they’re wrong.
So, I had done that story. Then the science there is 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 and the sodium gets into your circulation you want to keep the concentration constant, you have to dilute it out with water, so 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.
Gary: The world is full of simple ideas that don’t pan out and this just happened to be one of them. Then, as I’m doing 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. So, it turns out that most obese individuals were insulin resistant and type II diabetes as a disorder of insulin resistant and metabolic syndrome is primarily a leading risk factor for heart disease. So, if you have metabolic syndrome and you’re insulin resistant, that’s a risk factor for heart disease and all these diseases are what is known as hypertension conditions. So, they associate with high blood pressure and hypertensions. One of the diagnostic criteria for metabolic system syndrome is elevated blood pressure. So, the argument I was making that the other researchers that legitimate researchers had made in the past, academic researchers is that, if obesity, diabetes, insulin resistant, heart disease, gout, are all hypertensive disorders, they’re all associated with elevated blood pressure, then maybe whatever causes one, causes all of them. Then the question is, what’s the answer since they’re all conditions of insulin resistance and again type 2 diabetes is an effect of insulin resistance disorder, the question then becomes what causes insulin resistance?
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 dietary…
Ben: You said you don’t think you’re right when you’re suggesting sugar causes insulin resistance?
Gary: 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. The argument I make in the book is that when obesity and diabetes epidemics explode in populations, invariably sugar is the new to their diets and almost invariably there’s some physician or research that’s saying “jeez 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 genesis…
Ben: Yeah! Even though admittedly, and I know some people will mention this so I’ll mention this, 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 in the cells and so, let’s say I eat too much whey protein and your when 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.
Gary: Yeah, so this is the question, so if you think about the question, 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 genuinely believe that think that the problem is refined grains and easily digestible carbs like potatoes and then sugar 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 and the glycemic index isn’t as high as it would be for instance, white bread. These people 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, they’re possible.
Then the question is, what’s the most likely explanation where should 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’s the initiating… So, first the liver becomes insulin resistant as an organ and then it 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.
Gary: And then saying sugar. So, the fact that protein, for instance, stimulates insulin secretion… well, first of all, historically, we’ve have populations that became obese and diabetic that were relatively low protein consumers. So, it’s hard to imagine. It’s possible… I guess you could hypothesize that a population like the Pema which were very poor and almost unimaginably poor relatively raw until World War II Native American population could have been overconsuming lean protein because they simply wouldn’t whereas if you look at what they were eating in the history of their dietary assessments that were made by various individuals back then and you could 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 too, or not nearly in that amount. So, we’re always making this argument, what’s more or less likely to be true.
Gary: I find that off in the people who… The alternative hypothesis, the protein hypothesis, you want to answer the question, can that explain not just one population and they’re not just a modern what’s happening wherever I happen to live or at my gym, but can it explain what we’re seeing worldwide? 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.
Ben: Yeah, and another thing that’s important when it comes to insulin resistance is a lot of it is multi-modal, right. We 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, hyper-caloric induced insulin resistance from just eating damn too many calories or even inflammation related insulin resistance, right. 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 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. So, it’s hard to really put your finger on what exactly the cause of insulin resistance.
Gary: That’s why when I say it all depends on the question you’re asking.
Gary: So, if you’re asking, as I am, I want to know what the cause of these epidemics are. In the epidemics, I’m assuming there’s one primary cause because they manifest themselves virtually in every population regardless of the underlying genetics, so even though there’s a genetic predisposition or tolerance for whatever this trigger is, if you see this same epidemic in Inuits and South Pacific Islanders and Native Africans and African Americans and Caucasians, clearly it’s not a genetic disorder.
So, the question is, what is it about the Western diet and lifestyle that triggers these epidemics because, to me, the only way you can 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, particularly lower socioeconomic groups, that work incredibly demanding manual labor day in and day out. They’re probably working even 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.
I don’t particularly buy that explanation for a lot of different reasons. Some people say 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 or trigger insulin resistance. So, if we do that, what are we not putting in those foods? What are we putting in those foods to prevent the agent? So, what’s the agent? That’s why 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, maybe a billion people, living on high index glycemic 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…
Ben: There’s so many confounding variables, 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 come into play, but ultimately we can say that a modern Western diet and modern Western lifestyle and modern Western sleep patterns and everything else is kind of associated with straying from ancestral wisdom and ancestral living appears to cause some form of insulin resistance.
Ben: One other thing I wanted to ask you about before I turn to some of the controversy that’s surrounding you right now and NuSI, is one other thing you brought up in the book, and you talk about the relationships of sugar and a lot of different chronic diseases including the hypertension that thrust us down that rabbit hole, but you also talk about gout. A lot of people will 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?
Gary: Well, so I’m going to give you a little history again here, gout tradition swept through… There was something called the gout wave that swept through Europe in the 17th century and it starts with, first of all, the poor get gout, then the wealthy get gout, then slowly it spreads to the population at large. The assumption was just high living 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, therefore it sort of… You’d see it in literature back then, high living is a cause of gout. Again, it’s one of the sort of vague Western diet ideas and the assumption was because then the researchers start realizing 155 years ago that the problem is too much uric acid in the bloodstream and the uric acid tends to crystalize 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.
So, the idea is [58:30] ______ is high and metabolized you get a lot of uric acid from there and therefore maybe the protein has a lot of uric acid in it. So, maybe it’s meat consumption which fit the general epidemiological picture and so we should eat, if uric acid is the problem, we should eat a low uric acid diet. Again, there’s this kind of simplistic idea that you are what you eat, so 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 sodium content to the blood.
So, we’re talking about hypertension; turns out that when you raise insulin levels, your body doesn’t secrete as much sodium and tends to hold on to sodium. You could raise your insulin levels by eating more sodium but you can raise them much more effectively by just raising your insulin levels and that’s one of the things that links sodium. That’s why all those diseases of insulin resistance or hypertensive diseases, it turns out sugar, even though there’s no uric acid in sugar when you metabolize sugar and the liver particularly part of it metabolized into uric acid, so that’s another way to elevate uric acid levels.
So, it’s interesting as 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 proposing it. 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 again, it was cheap and benign and everyone could take it. So, we don’t need to do the research anymore. So, they went away. 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 a very easy way to raise uric levels in the bloodstream is, at least in animals and it turns out, in humans, is feed them sugar.
Ben: Sugar or fructose?
Gary: Well, fructose particularly, but the fructose usually comes in sugar. So, there’s a concept of fructose induced hyperuricemia. The interesting things is when I started doing my research for “Good Calories, Bad Calories” in the early 2000s, I would talk to these researchers who were studying gout and some of them were studying sugar and some of them were studying sugar and uric acid, and the ones who were studying the effects of fructose in uric acid didn’t realize that sucrose was half fructose. So, they thought they were only doing the research in relationship to high fructose corn syrup, they just didn’t have a biochemistry background.
The ones who were studying gout and on an epidemiological level in these huge epidemiological populations had never even heard of fructose induced hyperuricemia. So once, and I’ll take credit for pointing out to these people, because I as a journalist, I got to talk to everybody so even if my med school training is somewhat pathetic, my biochemistry is simplistic, I get to learn from all the experts. So, actually could spread the news around that “why aren’t you guys looking at sugar” and then 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.
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, very smart guy who has been studying uric acid now and fructose and sucrose and glucose for going on 20 years, and he has a very interesting hypothesis that the uric acid is playing a key role in causing insulin resistance.
Gary: 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 the credit he deserves, but because he’s virtually the only person doing the research, it’s kind of hard to tell if he’s right because you don’t see it hasn’t caught on widely enough to be widely replicated.
Ben: Yeah, what’s really interesting is that one-two 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 you say in the book 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, it’s kind of interesting how a lot of people that cut out protein and 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 the times has tortillas and corn chips and high fructose corn syrup and all manner of other issues.
Gary: Nature has thrown some sort of jokes into this as well just to make life more complicated. Often when people go on a ketogenic diet, they’ll also get gout flare ups.
Gary: Not apparently from the meat but because uric acid is often stored.
Gary: If I’m remembering correctly with fat and fat tissues, when you start mobilizing that fat, you start increasing the uric acid, it comes out too and you increase your 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, might make gout flare up and then, of course, they’ll say this is horrible and they’ll get off the diet and then it’s the end of it.
Ben: Yeah. There’s so much more 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 new NuSI, there was some controversy about that. From what I understand, you guys did a study at NuSI, at Nutrition Science Initiative, where you were looking into whether or not eliminating carbohydrates from a diet could somehow eliminate obesity. 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 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. 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?
Gary: Okay, so let me give you the full background on that because this gets into the reason why I’m one of the reasons I’m so controversial in this field. One of the things I realized in my research and argued in my books and as much as anyone, I’m the owner of this idea, 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 on science papers and by that we mean, the disorder is literally caused by taking in more calories than what we expend. 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? I have trouble even talking about that anymore without thinking this is going to sound too simplistic, people are going to buy that one and I even say this is what the research community does, but this is what they do. It comes down to this phrase obesity is about calories in, calories out, and if you eat more calories in than expend, you’ll get fat and so therefore, that’s the cause of obesity. I’ve been arguing, and others as well, that this is almost naïve beyond belief. It’s a 110-year-old thinking based on 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 this book, until the second World War, all the leading research on obesity and metabolism and nutrition and endocrinology, the study of hormone related diseases, genetics, was all done in Europe primarily, Germany and Austria. America was like a 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… Sex hormones were obviously involved because men and women fatten differently and stress hormones were involved and insulin was fundamentally involved because insulin works to put fat in fat cells that hadn’t really worked that out yet.
Then, so the gist of it was, the American researchers thought obesity was a sort of gluttony and sloth problem were naïve and these Germans and Austrians would argue that they were naïve. But then the war comes along, the German and Austrian literature vanishes, the researcher community vanishes, the lingua franca of medical literature goes from German pre-World War II to English post-World War II. When the only researchers studying obesity post-war are Americans! 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.
So, what I mean by not making any sense, first of all, it doesn’t explain much. If I ask you why men get fat at above the waist, they get belly fat and women get fat below the waist, just 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 doesn’t tell you anything. There’s just a whole slew of things that the… Saying somebody gets fat because they take in so many calories is like saying somebody is getting rich because they take in so much money. It sounds vaguely explanatory, but it doesn’t actually tell you anything about why the person gets rich or why the person gets fat. Again, this idea that it’s fundamentally that the fat cells are very well regulated by hormones and enzymes and 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 fight-or-flight response, when you’re secreting adrenalin, that adrenalin 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. All of that is very carefully regulated and in order to get obese, you have to dysregulate it. It’s not enough to just eat more calories or just expend less. You literally have to change the race.
So, that’s what I’ve been arguing, and others for one reason or another a lot of people find this almost impossible to conceive, like the idea of obesity isn’t an energy balance disorder, it’s considered quackery.
Ben: 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?
Gary: If you’re eating a high sugar diet in a hypocaloric state, it would be an interesting…
Ben: Meaning, if I burn… I burn a crap ton of calories, I burn 3,200 calories at rest, if I shift to an 800 calorie a day diet comprised of rice and coke, you’re saying I’d still gain weight?
Gary: No, you wouldn’t. But again remember, you’re different. So, let me give you an example: there’s a phenomenon now known as a duel burden of obesity in malnutrition. So, there’s are usually very poor populations in which the children are malnourished and their growth is stunted, so they’re clearly not just macronutrient but 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 they camp 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. So, the mother’s obese because she’s sneaking snickers bars, so why isn’t she giving those Snickers bars to her malnourished kid whose growth is stunted because he’s not getting enough protein. 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, 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 in 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, that’s the kind of thing that…
Gary: One of the things I’m often asking the energy balance defenders is how do you explain those populations and when you do it, I actually got a drop box now with about 40 papers describing probably 30 populations like that. So, I’ll say, look, I’ll give you access to my Drop Box file.
Ben: What you need to do is write a book or write an article entitled something like “People Who Eat Few Calories but Lots of Sugar Still Gain Fat” and 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, and with, again, the influence of sugar potentially on circadian rhythm and on even mitochondrial function which is incredibly important for metabolism. I think there’s a host of things, even in addition to insulin, that’d be contributing to the inability to burn your own storage fat even if you’re not eating a lot of calories.
Gary: And this is the question that sort of… You’ve got this amazingly intricate unimaginably intricate homeostatic system that’s us, and you start screwing with any aspect of it, and all those things you mentioned from leptin and inflammation, the question is then what’s causing what’s effect when everything is causing and effecting everything else in the system? So, the easier question to ask is what’s the trigger?
One way I talk about this is, 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, there’s going to be a whole lifetime worth of research for laboratories around the country figuring out all the details of the complex response of 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 multi-factorial phenomena that follows. So, what we’re talking about again is it’s important to keep your eyes on the goal and what’s the dietary thing that’s causing obesity and diabetes because we’re going to assume it’s not natural.
Gary: One reason we know it’s not natural is because we don’t see it even in animal populations unless they’re eating Western diets like our house pets.
Ben: Right, right. Yeah, and 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 a hit on metabolism. There’s a variety of factors involved here, but ultimately, I kind of look at it the same way a lot of people look at living a clean and good life, 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 like the same idea with high fructose corn syrup and sucrose. For me, I’ve seen enough anecdotes of evidence where even if… whether or not there’s science that says one way or another, there’s enough anecdotal evidence for me to say that I’m going to drink some bone broth instead of some Coke and eat a lot of plants and proteins and good fats instead of sucrose.
Gary: Well, that’s the argument I make in the book. Do I think the evidence is unambiguous enough to regulate sugar? I don’t and it worries me. If they start regulating sugar, they’ll go out with the same state of ambiguous evidence that regulate things that are not only healthy but that I should be consuming, but do I think that there’s enough evidence for people to decide for themselves, just as you said. Am I better off not eating it and is it worth it to me?
Ben: Yeah, yeah.
Gary: Particularly if you’re a parent, am I better off moderating my child or getting my kid to stop guzzling and the answer is there’s a lot of reasons to worry.
Gary: And these obesity and diabetes epidemics are, the director general of the World Health Organization recently referred to them as slow-motion disasters…
Gary: So, they’re going to overwhelm medical systems worldwide, including our own. We have to figure out what’s causing them.
Gary: We have to identify what it is and get it out or at least convince people that this is the cause and that they should change their behavior accordingly.
Ben: 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 and so is the other one.
Gary: It’s better than pretty good.
Ben: Right, if you don’t say so yourself. 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.
Gary: Well, Ben, thanks for your interest. It’s been great.
Ben: Awesome. Alright, folks. Well, I’m Ben Greenfield along with author and researcher Gary Taubes signing off from BenGreenfieldFitness.com. Have a healthy week!
My guest on today’s podcast – Gary Taubes – just wrote a groundbreaking, eye-opening exposé entitled “The Case Against Sugar” that makes the convincing case that sugar is the tobacco of the new millennium: backed by powerful lobbies, entrenched in our lives, and making us very sick. Among Americans, diabetes is more prevalent today than ever; obesity is at epidemic proportions; nearly 10% of children are thought to have nonalcoholic fatty liver disease. And Gary believes sugar is at the root of these, and other, critical society-wide, health-related problems. In the book, he delves into Americans’ history with sugar: its uses as a preservative, as an additive in cigarettes, and the contemporary overuse of high-fructose corn syrup. He explains what research has shown about our addiction to sweets. He clarifies the arguments against sugar, corrects misconceptions about the relationship between sugar and weight loss; and provides the perspective necessary to make informed decisions about sugar as individuals and as a society. The ever-prolific Gary Taubes is co-founder and senior scientific advisor of the Nutrition Science Initiative (NuSI). He’s an award-winning science and health journalist, the author of The Case Against Sugar, Why We Get Fat and Good Calories, Bad Calories, and a former staff writer for Discover and correspondent for the journal Science. His writing has also appeared in The New York Times Magazine, The Atlantic, and Esquire, and has been included in 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. He is also the recipient of a Robert Wood Johnson Foundation Investigator Award in Health Policy Research. He lives in Oakland, California. During our discussion, you’ll discover: -The difference between glucose and fructose, and how is that related to sucrose…[7:35] -Why the fructose we eat now is different than the fructose we find in nature…[14:20] Eliminate fatigue and unlock the secrets of low-carb success. Find out how in The Low Carb Athlete – 100% Free. Sign up now for instant access to the book! Email* I'm interested in…* YES, HOOK ME UP! -How German researchers discovered sugar to be just as effective as “crack cocaine”…[21:10] -The fascinating marriage of tobacco and sugar, and why sugar is in cigarettes…[27:50] -How “metabolic imprinting” causes a baby’s pancreatic cells to become dysfunctional…[33:35] -Why salt may not be the cause of hypertension, but sugar may…[44:00] -The relationship between sugar, gout and uric acid, and why gout and uric acid may not just be protein related…[47:10 & 57:00] -Why different people have different blood sugar responses to sugar…[49:20] -What Gary thinks of the fact that he’s been called out on the fact that the NuSci metabolic ward research found no insulin-obesity link, and whether it’s calories, not macronutrients, that are most important…[65:00] -And much more! Resources from this episode: -The Amazon page for all Gary’s books -NuSI Hall Study: No Ketogenic Advantage (ICO 2016) -An effective supplement for regulating blood sugar and insulin response called Kion Lean Show Sponsors: -Wild Mountain Paleo – Visit BenGreenfieldFitness.com/wildmountain and use code BenPili10 for 10% off your Pili Nuts. -Purathrive – Go to Purathrive.com/bengreenfield to automatically get 15% off on Curcumin Gold or Radiant C (a liposomal vitamin C that actually tastes GOOD), or anything else that tickles your fancy. -Oak – Meditation & Breathing – Go to bengreenfieldfitness.com/oak now to download the app, completely FREE. -ZipRecruiter – Post jobs on ZipRecruiter for FREE by visiting ZipRecruiter.com/Green.
Read more at: https://bengreenfieldfitness.com/podcast/nutrition-podcasts/the-case-against-sugar-gary-taubes/
2 thoughts on “[Transcript] – The Case Against Sugar: Is Gary Taubes Full Of Sweet Lies & Deception, Or Is Sugar Really Making Us Fat?”
You mentioned Jeff Bullock out of Univ of Connecticut article on Ketosis but cant seem to locate that reference in the library. Also any link you have to Taubes article from 1990 on salt would be appreciated.
Here's the salt article: http://science.sciencemag.org/content/281/5379/89… For the Ketosis one, try looking through these… https://www.ncbi.nlm.nih.gov/pubmed/?term=Volek+J…