Peter Attia MD#14 – Robert Lustig, M.D., M.S.L.: fructose, processed food, NAFLD, and changing the food system
EVERY SPOKEN WORD
70 min read · 14,220 words- 0:00 – 0:04
Intro
- PAPeter Attia
[instrumental music]
- 0:04 – 7:08
Episode Intro and Guest Background
- PAPeter Attia
Hey everyone, welcome to The Peter Attia Drive. I'm your host, Peter Attia. The Drive is a result of my hunger for optimizing performance, health, longevity, critical thinking, along with a few other obsessions along the way. I've spent the last several years working with some of the most successful top performing individuals in the world, and this podcast is my attempt to synthesize what I've learned along the way to help you live a higher quality, more fulfilling life. If you enjoy this podcast, you can find more information on today's episode and other topics at peterattiamd.com. [upbeat music] In this episode, I'll be speaking with my friend Dr. Rob Lustig, who I suspect a good number of you will have already heard of and certainly have been familiar with through his pretty impressive presence on YouTube and his talk called Sugar: The Bitter Truth that went viral, I believe, in 2011. And that's about the time when I met Rob. Now, this podcast kind of grew out of a really interesting discussion that I think I get into in the podcast a little bit, but I think it was in 2016 when Rob and I were both invited to Hong Kong to speak at the Credit Suisse Asian Investment Conference, and we were on a panel together. And it just so happened that we were on the same flight back to San Francisco, which was not just a long flight, but more importantly a flight where you weren't gonna be sleeping much. And Rob and I ended up huddling together over a laptop going over some really interesting data on NAFLD, which we'll get into in this podcast. And I remember thinking like that just kinda left an impression on my mind, which was, "God, this is the kind of discussion I really enjoy having with people like Rob," 'cause it gets into the nuance and away from the headlines. And obviously many years later, forward, fast-forward to where we are now, I'm starting a podcast. One of the first people I wanted to reach out to was Rob to have this discussion. Rob has very recently stepped down from his clinical responsibilities as a pediatric endocrinologist at UCSF. However, he still has a very active presence in his research department. Rob holds a bachelor's degree from MIT, he got his MD from Cornell, and he also has a Master of Studies in Law from UC Hastings, something that he did probably about four years ago as he began to realize that only one half of the equation in educating people about sugar was going to come from the scientific standpoint. The other half was going to have to be policy related. In this episode, we talk about a lot of things, but among them we talk about why Rob believes the food business has really pushed towards having more and more sugar in it, and why these have led to the epidemics of addiction, depression, et cetera. He talks also about how you can combat that. And I think something that people miss in Rob's headlines is that he is not just talking about avoiding sugar, he's also talking about the importance of fiber. And we actually get into a very nice discussion about the differences between soluble and insoluble fiber and how it's actually not uncommon for people to load up too much through processed foods on the soluble fibers. But they're not getting the full benefit without having the insoluble, which is really stuff that's hard to get without looking towards real foods, particularly vegetables. This was really a fun podcast and I think that comes across in [chuckles] how often we unfortunately probably talk over each other, so I apologize f- for that in advance. This is also one of the first podcasts I record, so I was still sort of, and, and s- am still sort of learning the ropes of how to do this. Unfortunately, Rob had to go to, I believe, to a deposition that morning, and so we had a really hard stop that didn't give us nearly as much time as I think we would have spent on this topic. But I do suspect that Rob and I will talk again. We also get into some of the really, I think, kinda practical stuff around what is it like to be a parent when you're trying to balance the desire to, you know, let your kids be kinda normal and deal with the convenience of not making every meal something that requires a day of planning. But how do you prevent them at the other end of that extreme from, you know, sort of mainlining those nasty Capri Suns and Wheat Thins and things like that. So I think some practical advice there is helpful. We do go really deep on fructose, and there is some biochemistry in there. It does get a little nerdy. Rob can talk kinda fast, and he really knows his stuff on this topic, so he does not pull back from any of that terminology. We're gonna do our best to link in the show notes to some of the definitions and some of the things in there that we get into that will give you a little bit of background. We also get into liver function testing, something that I think many people take for granted when they go to their doctor, but it becomes really important when you're trying to screen out people who might have NAFLD, nonalcoholic fatty liver disease, or NASH, its more progressed sibling. We talk about uric acid, we talk about metabolic syndrome. We just talk about a whole bunch of things, including we talk about heart rate variability near the end. And at the time Rob asked me a question I didn't know the answer to. We have since learned the answer to that question because I was really intrigued by the discussion. And so for anybody who's interested in that little nuance on heart rate variability, we're gonna link to that as well. You'll be able to find a lot more information about this, including information about Rob himself and what he's doing, and also just the stuff that we talk about at peterattiamd.com/podcast. So without further delay, here is my really interesting and intense discussion with Dr. Rob Lustig. [upbeat music] All right, Rob, well, thank you so much for making time today to have this discussion. Oh, Peter, it is my pleasure. My pleasure. We've known each other for I think about six or seven years now. Yeah, about right. And what made me think about talking to you at this point in the podcast, which is to say very early on, is I was thinking back to two years ago when we went to Hong Kong together. Mm-hmm. And by sort of luck, we ended up on the same flight back to San Francisco. Right. And we were probably the two geekiest guys on the airplane 'cause the laptop- We're the only ones not sleeping. [laughs] Right, right. And then the laptop came out, and then it was all data all flight. Right. And it was awesome. And it's- Yeah ... it's experiences like that that have made me think like a podcast can be a fun way to reproduce some of those discussions that I often find myself having and then thinking, "God, I wish-" Everybody could have heard that, 'cause I learned a lot during that time.
- RLDr. Robert Lustig
It's, uh, vice versa, by the way, and people wish they were flies on the wall. So, you know, I'm happy to do this. This is great.
- PAPeter Attia
Awesome. Well, you've spoken so much and so eloquently about sugar and fructose, and certainly we're going to talk about a lot of that stuff today. But I also want to talk about some things that I think are a little less understood, for example, the impact of fructose on inflammation and things like that.
- RLDr. Robert Lustig
Well, what data we have.
- PAPeter Attia
Yeah.
- RLDr. Robert Lustig
By the way, let me qualify. While I do know a whole lot about sugar, fructose, you know, metabolic disease, really my issue is processed food. Processed food has several things wrong with it, sugar being one of them, but lack of fiber being another.
- PAPeter Attia
Mm-hmm.
- RLDr. Robert Lustig
And I think that that is equally important, and I'm very willing to talk about that issue as well.
- PAPeter Attia
Perfect.
- 7:08 – 14:24
Fructose vs. Glucose: Biochemical Differences
- PAPeter Attia
So let's start with a very brief set of the semantics that I think it's important for people to understand when they do confuse fructose and glucose. They're both carbohydrates. What's the difference?
- RLDr. Robert Lustig
Well, they're both monosaccharides. Glucose is the energy of life. Every cell on the planet burns glucose for energy. Glucose is so important to functioning in all eukaryotic organisms. Single cell versus multi-cell, doesn't matter. It's so important that if you don't consume it, your body makes it. It can make it from amino acids. It can make it from fatty acids, called gluconeogenesis. Those amino acids or fatty acids will go to the liver. The liver will metabolize those and produce glucose. And so you can consume zero glucose, but you will still have a blood glucose level. The Inuit, they didn't have any carbohydrate. They didn't have any place to grow a carbohydrate. They had ice. They had whale blubber. They still had a serum glucose level, and we knew that as early as 1928. So glucose is super important, and I don't argue that. It's so important that your body has a fail-safe mechanism. Fructose, however, is completely vestigial to all animal life. It is a storage form of energy in plants. Plants can utilize fructose for energy. We have the capacity to metabolize a limited amount of fructose for energy. Really, when you're consuming fructose, your gut bacteria are more adept, since they are plants, at being able to metabolize that fructose than you are. So when you're consuming fructose, yes, you will absorb some, but for the most part, it's actually more plant food than it is animal food. [chuckles] In addition, there are some very specific biochemical differences between the two molecules. Glucose is a six-membered ring. Fructose is a five-membered ring. Now, that becomes important because both glucose and fructose and every monosaccharide exists in two forms. One's called the ring form, and the other one's called the linear form. The linear form has the capacity to bind to proteins, called the Maillard reaction. It's what makes hemoglobin A1c in diabetics, also known as the Amadori rearrangement. This is a biochemical process that occurs normally. It is the browning reaction. It causes bananas to brown. It causes humans to brown. In fact, we're all browning right now because our mitochondria in our cells are engaged in the Amadori rearrangement. It is what makes people age. It is the aging reaction. And I show a slide which shows newborn rib cartilage nice and white, and 88-year-old rib cartilage nice and brown. Okay? We're all browning. So you can roast your meat in a, an oven for 375 degrees for an hour, or you can roast your meat at 98.6 degrees for 75 years. Ultimately, the answer is the same. You brown. Why do I bring this up? Because glucose causes that browning reaction at a relatively low rate. Fructose makes that reaction occur at seven times faster rate.
- PAPeter Attia
Now, this starts with the Schiff reaction, correct?
- RLDr. Robert Lustig
So it forms a Schiff base.
- PAPeter Attia
Okay.
- RLDr. Robert Lustig
Right. So it starts with... And it's non-enzymatic. It happens just in a test tube with no enzymes needed. You just put it in the sunlight, it will happen. What happens is that the aldehyde moiety of the glucose in the linear form will bind to an epsilon amino group of lysine, which is at position one in hemoglobin, and form a Schiff base, which then spontaneously decomposes to form a covalent linkage, which won't come off, and basically will stay there until that hemoglobin molecule is recycled by the spleen. So this is why you can measure glucose levels through hemoglobin A1C, is because the higher the glucose level in the blood, the more this reaction occurs, and therefore the higher the hemoglobin A1C. Turns out fructose does it seven times faster. And not only that, every time it happens, it's causing those proteins to become less flexible, so less functional, and every time it happens, it throws off a reactive oxygen species, an oxygen radical, a hydrogen peroxide, which then can do damage unless it's quenched by an antioxidant. So in the face of antioxidant deficiency, which is called processed food- It can actually cause inflammation and non-alcoholic steatohepatitis and many other problems related to the inflammatory response. So fructose does that seven times faster than glucose. A third thing that is different is that when you put glucose in the stomach, your hunger hormone called ghrelin goes down. When you put fructose in the stomach, it doesn't change. So when you consume a lot of fructose, your brain doesn't know you've eaten, and so you end up consuming more. And lastly, glucose is metabolized in the brain. The areas that basically metabolize glucose and give you a functional MRI signal are areas that have to do with the sensory motor cortex for the most part and for the basal ganglia. Fructose specifically lights up the reward center and has been now been shown to induce the same physiology in the brain that cocaine, heroin, nicotine, alcohol, any hedonic substance also generates. It is the reward signal, and in fact, we treat it as a reward signal. It's called dessert. [laughs]
- PAPeter Attia
[laughs]
- RLDr. Robert Lustig
So fructose and glucose are not the same. The food industry would have you believe a calorie is a calorie, a sugar is a sugar, you need sugar to live. Those are all food industry mantras. They're all out in the cyber sphere-
- PAPeter Attia
Mm-hmm
- RLDr. Robert Lustig
... and in the blogosphere. It is absolute garbage. They are quite different, and it does matter.
- PAPeter Attia
I want to go back to just something very minor that you mentioned. I get asked this question all the time, and I've never had a compelling answer, but we use hemoglobin A1C as sort of a surrogate proxy for average glucose levels. Now I-
- RLDr. Robert Lustig
Mm-hmm
- PAPeter Attia
... for reasons we won't get into today just for time, I'm not particularly convinced hemoglobin A1C in an absolute sense provides great insight.
- RLDr. Robert Lustig
Oh, I agree.
- PAPeter Attia
On an, on a relative basis, it can be somewhat helpful, but at least directionally it's helpful.
- RLDr. Robert Lustig
Within any given patient, a lowering of a hemoglobin A1C from point A to point B would be a good thing. I won't argue that.
- 14:24 – 23:25
Biomarkers: Uric Acid, ALT, and AST
- PAPeter Attia
So the question becomes, do we have comparable biomarkers that can give us some indication of average exposure to fructose over a given period of time?
- RLDr. Robert Lustig
Right. Awfully good question. So fructose also binds to hemoglobin, but it does not bind at position one, therefore you don't measure it in hemoglobin A1C. So it binds at positions 66 and 110. Now, the hemoglobin A1C assay is not set up to look at 66 and 110. This requires a major research lab. It requires tandem mass spec. It's a huge undertaking. It's only done as a research tool, and the only lab I know that does it is in Japan. So that's not a rational thing to expect right now. People are looking for long-term biomarkers of fructose consumption, and there have been several papers that have come out that are pointing to individual options, but none have been put into clinical practice. None have been shown to really validate consumption in a meaningful way. So at this point in time, we don't have that for consumption. What we do have are some indirect measures of fructose, shall we say, biotoxicity.
- PAPeter Attia
Yeah, like uric acid or ALT would be two examples.
- RLDr. Robert Lustig
Exactly. Those are the ones I was going to bring up. Exactly. Uric acid and ALT. So we know that the more sugar you consume, the higher your serum uric acid goes, and the more risk you have for gout. Benjamin Franklin knew that [chuckles] and wrote about it. The reason that happens is because since fructose can only be metabolized in the liver because the liver has the GLUT5 transporter, every time a fructose molecule enters a liver cell, it has to be phosphorylated. So it goes from fructose to fructose 1-phosphate, and the enzyme that does that is called fructokinase. Well, the phosphate has to be donated, and ATP is the donor. So ATP becomes ADP. Adenosine triphosphate becomes adenosine diphosphate. Now, there is a scavenger enzyme in the liver called adenosine deaminase 1, and what it does is it then takes ADP down to AMP, monophosphate, then to IMP, inositol monophosphate, and finally to uric acid. So the uric acid concentration in the blood is a proxy for total fructose consumption. Now, there are other things that make uric acid go up too, like protein, but all things being equal, they do correlate with each other, and we've shown that serum uric acid in children and adolescents correlate with sugar beverage consumption, for instance. And other people have shown that that uric acid matters because uric acid is the inhibitor of endothelial nitric oxide synthase. That's an enzyme that exists in your vascular tree that vasodilates the blood vessels, and that keeps your blood pressure down. And we have shown that every increase by 10% in fructose consumption increases your blood pressure by two millimeters of mercury consistently, and that increases your risk of stroke by 10%. We have data, and it's also been shown by Dan Feig at UT San Antonio, that if you give an inhibitor of uric acid synthesis, allopurinol, which is what we give to gout patients, you can actually lower adolescents' blood pressures when they have essential hypertension. So this is a mechanistically valid problem, and it is a surrogate proxy biomarker sort of for sugar consumption. ALT Is also a surrogate marker in a similar way. ALT goes up when your liver stores fat.
- PAPeter Attia
What's the difference between-- I mean, patients are sort of familiar with the difference between ALT and AST, but they both show up as liver function tests. But-
- RLDr. Robert Lustig
Right
- PAPeter Attia
... guys like you and I tend to spend a little more time looking at ALT.
- RLDr. Robert Lustig
Right. So AST, which is aspartate aminotransferase, is a biomarker for mitochondrial function, and ALT is alanine aminotransferase, and it is a biomarker for degree of liver fat. So they're both important, but in different ways. AST is much more minute to minute, like what did you eat at your last meal? ALT is a little bit more, shall we say, stable over time, so we tend to use ALT. However, we've shown that when you cut sugar back, AST changes, suggesting mitochondria are actually getting better.
- PAPeter Attia
And the ranges on these things keep drifting upward for what people deem acceptable. I tell my patients I want their ALT below 20.
- RLDr. Robert Lustig
Oh.
- PAPeter Attia
And they say, "But Peter, the range says up to 42."
- RLDr. Robert Lustig
Indeed. This is huge [chuckles] and I'm glad you brought it up. So I entered medical school in 1976, and at that time, the upper limit for normal for ALT was 25. Now, when we talk about upper limits for normal, where do those calculations come from? Basically, you take a bunch of, quote, "normal people," and you figure out the mean, and you look at two standard deviations around the mean, and that's how you decide what is normal. So in 1976, 25 was two standard deviations above the mean. Today, 40 years later, 40 is two standard deviations above the mean. Did something happen to the assay? No. Something happened to us, because now everyone has fatty liver disease. In fact, the Dallas Heart Study showed that 40% of normal people have hepatic steatosis, liver fat. Well, that makes your ALT go up. So what I say is 25 was the upper limit of normal, 25 should still be the upper limit of normal, despite what it says on the lab slip, 'cause that's just looking at two standard deviations above the mean. So we use that very specifically in clinic to show parents and kids what is happening to them and why sugar is the bad guy, 'cause when we get them off sugar, the ALT drops within a month.
- PAPeter Attia
Yeah. And going back to the uric acid thing, I was, um, very influenced by the work of Rick Johnson, and Rick has been always incredibly generous with his time and insights. And-
- RLDr. Robert Lustig
Indeed
- PAPeter Attia
... you know, one of the things-
- RLDr. Robert Lustig
Great guy
- PAPeter Attia
... I started doing probably about three years ago was just basically saying it's non-negotiable. All my patients need a uric acid below five, even though the assay says we will consider normal up to 7.0.
- RLDr. Robert Lustig
Exactly. Same issue. So in clinic, we basically said 5.5 is sort of the break point.
- PAPeter Attia
Mm-hmm.
- RLDr. Robert Lustig
So we're pretty close.
- PAPeter Attia
Yeah.
- RLDr. Robert Lustig
ALT at 25, uric acid of 5.5. You know, we can argue about the-- We're within an order of-
- PAPeter Attia
Right
- RLDr. Robert Lustig
... magnitude of each other. [chuckles]
- PAPeter Attia
And the, and the point is the same, and, and I think it's interesting because when we think about cardiovascular disease, one of the things that the endothelial story gets overlooked a little bit. The inflammation story is now getting its day based on-
- RLDr. Robert Lustig
Yeah
- PAPeter Attia
... these two very recent trials. Well, one recent trial and one that was halted likely because of a significant improvement in the outcome of using methotrexate. But-
- RLDr. Robert Lustig
Yeah. Mm-hmm
- PAPeter Attia
... when you look at the impact of uric acid on nitric oxide synthase, when you look at the impact of homocysteine on asymmetric dimethylarginine, which also then in turn inhibits nitric oxide synthase-
- RLDr. Robert Lustig
Yep. Yep
- 23:25 – 26:28
Does Fructose Have Any Advantage? Sports Drinks and Glycogen
- PAPeter Attia
Now, Rob, is there any situation under which fructose consumed in its natural state, which is to say with water, with fiber, i.e. in fruit-
- RLDr. Robert Lustig
Yep
- PAPeter Attia
... poses an advantage over glucose? 'Cause clearly glucose has many advantages in terms of how metabolically flexible. Like, you know, every organ can basically consume it. You don't have a lot of these other negative-
- RLDr. Robert Lustig
Right
- PAPeter Attia
... reactions. Is there something that fructose does better than glucose?
- RLDr. Robert Lustig
Yes, one thing. So if your liver is glycogen depleted, for instance, if you're a football player, three hours on the gridiron, and you have depleted your glycogen stores from your liver, and you consume a, say, energy drink or sports drink, you will replete your glycogen faster. It will do that. I won't argue that. The reason being-
- PAPeter Attia
But this, to be clear, is only liver glycogen, not muscle glycogen.
- RLDr. Robert Lustig
Absolutely. Only-
- PAPeter Attia
And muscle glycogen is a much bigger store.
- RLDr. Robert Lustig
Absolutely. You will replete your liver glycogen faster. There is a backdoor Where you can turn fructose back into glucose, which can then restore your liver glycogen. Now, the sports drink industry makes a huge deal about this. I think this is truly a tempest in a teapot.
- PAPeter Attia
[laughs]
- RLDr. Robert Lustig
I think this is really irrelevant. And the reason is 'cause after you've spent three hours on the gridiron, you're not gonna spend another three hours on the gridiron. Okay? And you will, by tomorrow, have repleted those glycogen stores anyway just from eating real food. So the idea that somehow you have to replete your glycogen rapidly just to me does not hold water. Yeah, it's fine to expend your glycogen stores in your liver, and real food will get you back to the same place by tomorrow.
- PAPeter Attia
It also doesn't even make sense physiologically because the limit to performance is not liver glycogen.
- RLDr. Robert Lustig
That's right.
- PAPeter Attia
It's muscle glycogen.
- RLDr. Robert Lustig
Well, I'm not even sure that's true because of-
- PAPeter Attia
Well, that's right. When you hit people with glucagon who claim that they've sort of bonked and hit the wall, and there is no more-
- RLDr. Robert Lustig
Right
- PAPeter Attia
... glucose left, you'll still see a transient glucose spike.
- RLDr. Robert Lustig
Absolutely. Plus we have all these people who are now on high fat diets, ketogenic diets, and how about the Ethiopians? They're not eating carbohydrate. [laughs] The fact is, you actually have better sports performance using fatty acids and ketones than you do with carbohydrate, and the reason is insulin. So I don't buy that for a minute as being important. Yes, it is true you will replete your liver glycogen faster, and that's true, true and unrelated. It's like, so what?
- PAPeter Attia
Yeah. You very recently retired. Clinically, yeah, yeah. You're nowhere near retiring.
- RLDr. Robert Lustig
No, no. [laughs] I've got a lot to do.
- PAPeter Attia
But you spent a lot of time... You're a pediatric endocrinologist. You spent a lot of time in clinic with-
- RLDr. Robert Lustig
I did
- PAPeter Attia
... children who had diabetes, have been overweight, have been obese, have had NAFLD, NASH, et cetera.
- RLDr. Robert Lustig
You bet.
- 26:28 – 32:23
Epigenetics and Children's Sweet Taste
- PAPeter Attia
Do you have a concern that children who undergo such metabolic transformation suffer an epigenetic hit that makes it harder for them later in life?
- RLDr. Robert Lustig
What I know about epigenetics suggests that that is possible. I would even go so far as to say likely. I don't-
- PAPeter Attia
And it's frightening if it's t- I mean, it's-
- RLDr. Robert Lustig
Oh, yeah
- PAPeter Attia
... one of these things you hope is so untrue.
- RLDr. Robert Lustig
Right. But I don't know that. Here's what I do know, and it's related but not exactly the same. We know from animal work, from both Children's of Philadelphia and also from the Liggins Institute in New Zealand, that maternal hyperglycemia causes epigenetic changes in-
- PAPeter Attia
This is in utero.
- RLDr. Robert Lustig
In utero. Causes changes in H19, the different epigenetic markers that we have on chromosomes that then portend metabolic dysfunction later on. So if that's true in humans, and no one's proven that that's true in humans, it could explain a lot of the things that we do see. Uh, we know from a biochemical standpoint, animals that are stressed or animals that consume large amounts of sugar during pregnancy end up with offspring that will manifest various aspects of the metabolic syndrome later. Do we know that that's through epigenetics? Not yet. But if the rodent studies are similar to, you know, what happens in primates and humans, it's not too, uh, far field, and it's not too much of a jump. Yes, I'm very concerned about it because as you know, epigenetics is the gift that keeps on giving.
- PAPeter Attia
Yeah.
- RLDr. Robert Lustig
You can change the F1 generation and still find that epigenetic change, and therefore the metabolic alterations in the F4 generation. So it might explain why things keep getting worse year after year is because we're adding on all the time, and more people are entering this epigenetic disaster. But I don't know that. That's a, that's a, that's a guess.
- PAPeter Attia
I mean, it, it's sort of one of those things where we have to sort of take a little bit of the precautionary principle, right?
- RLDr. Robert Lustig
Mm-hmm.
- PAPeter Attia
So you say, well, if there is an epigenetic reprogramming that occurs, then as parents, we need to be thinking a little bit more about the food environment our kids are in, because this is one of those things... You know, we're pretty familiar with the notion that if you don't discipline your kid, you're really not doing them a favor 20 years down the line.
- RLDr. Robert Lustig
[laughs]
- PAPeter Attia
And this would be another variant of that. And of course, you would say, "Well, what if this turns out to be untrue? What if there is no epigenetic signature?" It's like, okay, well, what was the downside of trying to get your kids to eat well?
- RLDr. Robert Lustig
Um, no argument. There's one downside, and it's [laughs] ep-
- PAPeter Attia
It's the effort that's required.
- RLDr. Robert Lustig
Exactly.
- PAPeter Attia
Yeah.
- RLDr. Robert Lustig
That's the downside. So we have these data. How many times do you have to introduce a savory food to an infant before they will accept it?
- PAPeter Attia
Oh, I don't know. Three, four?
- RLDr. Robert Lustig
Median 13.
- PAPeter Attia
Wow. [laughs]
- RLDr. Robert Lustig
How many times do you have to introduce a sweet food to an infant before they'll accept it?
- PAPeter Attia
Let me tell a funny story for that.
- RLDr. Robert Lustig
[laughs]
- PAPeter Attia
When my daughter, who is now 10, turned six months old, and I have this on video, we took her, uh, down to Del Mar for a walk on the beach and got an ice cream cone, and we were like, "All right. She's had nothing but breast milk and some formula for the last six months."
- RLDr. Robert Lustig
Yep.
- PAPeter Attia
What will she do with some soft vanilla ice cream? And our thought was the cold would turn her off. It was a foreign substance, whatever, and it's one of the funniest videos I've ever seen 'cause she puts her face into this vanilla ice cream, and I've never seen her eyes open so much, and w- I joked about it. I was like, "Holy shit. Look at the dope... You can almost see the dopamine firing."
- RLDr. Robert Lustig
You needed to put her in the functional MRI right then and there. [laughs]
- 32:23 – 39:49
Dopamine, Tolerance, Addiction and Drugs
- PAPeter Attia
Because this is the sine qua non of what makes cocaine so dangerous. I mean, I have a number of patients who recreationally use cocaine, and I, I don't wanna be like the alarmist who just says, "Don't do drugs 'cause drugs are bad." I wanna make the point that says, look, not all drugs are necessarily bad, but cocaine has two problems, at least as far as I can see. The first is you have a nonlinear asymmetric risk of something really bad happening as far as cardiac dysrhythmia.
- RLDr. Robert Lustig
Yeah.
- PAPeter Attia
So why would you take that risk? But the second issue is this downregulation of dopamine receptors-
- RLDr. Robert Lustig
Right
- PAPeter Attia
... that develops this tolerance.
- RLDr. Robert Lustig
Right.
- PAPeter Attia
And therefore makes it actually harder for you to experience joy subsequently.
- RLDr. Robert Lustig
Indeed. So here's the deal. Neurotransmitters are either excitatory or inhibitory. Now, neurons like to be excited. That's why they have receptors in the first place. But neurons like to be tickled, not bludgeoned.
- PAPeter Attia
[laughs]
- RLDr. Robert Lustig
They like to receive the neurotransmitter, fire, and then come back to baseline. Chronic overstimulation of any neuron leads to neuronal cell death, period. And we know this because we take care of all these kids with chronic seizure disorders in the ICU, and we're doing our best to try to stop those seizures, not because of the seizure, but because of the brain damage that occurs from continued overstimulation. So any neuron that is an excitatory, that's downstream of an excitatory stimulus, it wants to protect itself. It has a plan B. It has a fail-safe. What it does is it downregulates the receptor. That means that there's less likelihood that any given molecule will find a receptor to bind to, thereby reducing the risk for cell death. So what does this mean in human terms? You get a hit, you get a rush, receptors go down. Next time you need a bigger hit to get the same rush, and the receptors go down, and then a bigger hit, and a bigger hit, and a bigger hit until finally you get a huge hit to get nothing. That's called tolerance. And then when the neurons actually do start to die, 'cause chronic stimulation causes neuronal cell death, that's called addiction. And those neurons don't come back. Once they're dead, they're dead. And that actually limits your ability, even after rehab, of being able to experience that same level of reward because now you don't even have the dopamine to be able to do it because those neurons are dead. So not every drug is stimulatory. There are drugs that are inhibitory. If you're inhibiting the next neuron, do you have to downregulate the receptor? No.
- PAPeter Attia
So like a benzodiazepine, for example.
- RLDr. Robert Lustig
Benzodiazepines are inhibitory. Turns out, haha, psychedelics are inhibitory. So serotonin 2A and 1A are inhibitory. So when the DEA clamped down in 1970 with the Controlled Substances Act that made marijuana and psychedelics and, you know, everything Schedule I and, you know, unavailable, there were a whole bunch of people using psychedelics. They didn't end up in the emergency room.
- PAPeter Attia
Right.
- RLDr. Robert Lustig
They didn't end up with withdrawal. And the reason was because they didn't have downregulation of their receptors because those were inhibitory. So not every drug fries neurons.
- PAPeter Attia
So help me-
- RLDr. Robert Lustig
But cocaine does. [laughs]
- PAPeter Attia
Yeah, help me understand how alcohol fits into this because alcohol is, of course, a gab... Ethanol per se is a GABA agonist, so it should be at least depressing in that sense. But yet ethanol has some of these negative properties in the brain that you've just alluded to.
- RLDr. Robert Lustig
Well, what the problem is ethanol in the brain also, because it's polar and it, it dissolves lipids, it also creates acetaldehyde. So that's the first step-
- PAPeter Attia
Mm-hmm
- RLDr. Robert Lustig
... in terms of metabolism of ethanol, which then can cause that Maillard, uh, reaction because you've made an aldehyde, which then generates reactive oxygen species. So you can kill neurons, not necessarily from excitation, but from the biochemistry of the molecule.
- PAPeter Attia
So we talk a lot, and we might not even get into it today because you've spoken so eloquently about it elsewhere, about the similarities between ethanol and fructose in the liver.
- RLDr. Robert Lustig
In the liver, yes.
- PAPeter Attia
How are they similar in the brain, if at all?
- RLDr. Robert Lustig
So they both stimulate the reward center.
- PAPeter Attia
Though it seems through different mechanisms.
- RLDr. Robert Lustig
Yes, likely through different mechanisms.
- PAPeter Attia
Yeah.
- RLDr. Robert Lustig
There are a lot of different Dopamine stimulators. There are substances, and they're all different, cocaine, alcohol, nicotine, sugar, heroin. They have different mechanisms, but they all ultimately impact on dopamine the same way. We also have behaviors that are addictive. Gambling-
- PAPeter Attia
Mm-hmm
- RLDr. Robert Lustig
... shopping, internet, social media, pornography. Okay? There's an aholic next to every one of those, too, right? Chocoholic, sexaholic, whatever.
- 39:49 – 46:36
Hidden Sugar and Counseling Parents: Eat Real Food
- PAPeter Attia
I want to get into some more geeky biochemistry stuff, but I also know that there's probably at least one person listening to this who's a parent who's thinking, "Oh man, do I have to simmer down how much sugar my kids are eating?" So when you saw kids in the clinic, obviously you're seeing their parents. That's one of the advantages of pediatrics is-
- RLDr. Robert Lustig
It's also one of the disadvantages. [laughs]
- PAPeter Attia
That's right. That's right. You have two patients.
- RLDr. Robert Lustig
Two patients.
- PAPeter Attia
Um-
- RLDr. Robert Lustig
And I don't get paid for both.
- PAPeter Attia
[laughs] But the beauty of it is you have, you have a patient who you need to take care of, which is this child.
- RLDr. Robert Lustig
Yeah.
- PAPeter Attia
But then you also have another caregiver who, for the most part, wants what's best for that child.
- RLDr. Robert Lustig
Mostly.
- PAPeter Attia
And how would you counsel a parent who would say, "Look, Dr. Lustig, there's no way my kid's gonna have no sugar in their life. Can you give me a way to create a sustainable environment and set of rules that's gonna prevent my kid from having the metabolic derangement that hoses them for the rest of their life, but allows them to still be a kid?"
- RLDr. Robert Lustig
Yes. So that's what we did in clinic every single day. Here's the problem. It's not the added sugar you know. It's the added sugar you don't know.
- PAPeter Attia
It's almost, there's like a Rumsfeld tone to that, right? [laughs]
- RLDr. Robert Lustig
Well, yeah. I mean, there's the known knowns-
- PAPeter Attia
Yeah
- RLDr. Robert Lustig
... and then there's the unknown knowns. And the fact is, when you look at the amount of sugar that is in sodas, it's bad. When you look at the amount of sugar that's in candy, cake, ice cream, it's about half as much. That adds up to 50% of the added sugar consumed by children.
- PAPeter Attia
And what is that number, by the way, in grams per day approximately?
- RLDr. Robert Lustig
Oh, it runs the gamut, but the median is 18 teaspoons.
- PAPeter Attia
So that's about 90 grams-
- RLDr. Robert Lustig
About 90 grams
- PAPeter Attia
... of sugar per day.
- RLDr. Robert Lustig
Yeah. And it used to be 120. It's actually come down because of the obesity epidemic. 90 to 94 grams of added sugar per day. Half of the sugar is in foods you didn't know had it.
- PAPeter Attia
Bread, pasta sauce.
- RLDr. Robert Lustig
Pretzels. Why do pretzels have sugar in them?
- PAPeter Attia
[laughs]
- RLDr. Robert Lustig
Okay? Bread, right. Why do they put sugar in bread? Any idea?
- PAPeter Attia
I guess-
- RLDr. Robert Lustig
So if you buy a-
- PAPeter Attia
It probably helps with preserving it, doesn't it?
- RLDr. Robert Lustig
Exactly. So if you buy a loaf of bread at the bakery, how soon before it stales?
- 46:36 – 51:04
Genetic Risk and the Rise of NAFLD
- PAPeter Attia
Is there an economic consideration also?
- RLDr. Robert Lustig
Oh, absolutely.
- PAPeter Attia
What is the-- Do you have a sense of what it costs, all things equal-
- RLDr. Robert Lustig
Yeah, double
- PAPeter Attia
... to go fr- So a parent's gonna basically have to double their food budget if they-
- RLDr. Robert Lustig
Yep
- PAPeter Attia
... want to start eating real food.
- RLDr. Robert Lustig
That's right. They're gonna have to double their food budget, and they're also gonna have to double their food time in terms of preparation.
- PAPeter Attia
That's a big ask-
- RLDr. Robert Lustig
It is
- PAPeter Attia
... for... I mean, when the CDC last looked at this, the estimates of NAFLD, which we'll get into in a moment so we can let you explain that in some detail, but-
- RLDr. Robert Lustig
Mm-hmm
- PAPeter Attia
... when you look in particular along ethnic lines, at the time I last looked at this, 50% of Hispanic boys who were obese had NAFLD.
- RLDr. Robert Lustig
That's right.
- PAPeter Attia
My guess is that's a gross underestimation.
- RLDr. Robert Lustig
Likely. The fact is that Latinos are at more risk of developing-
- PAPeter Attia
Right. There's a-
- RLDr. Robert Lustig
... NAFLD
- PAPeter Attia
... genetic predisposition.
- RLDr. Robert Lustig
They have a specific polymorphism of a specific gene called PNPLA3, uh, patatin-like phospholipase domain, uh, A3, um, and it's been shown that if you have the homozygous form, the GG mutation of polymorphism of this gene, a little sugar in your diet makes a lot of liver fat, and 19% of Latinos have it. So this is particularly worrisome for the Latino population. And yes, they have fatty liver like nobody else. So there are people at more risk, and so it's becomes even more important to get the sugar out of their diet. And we explain all of this to them. We explain why this is, and we show them the lab data. We show them the acanthosis nigricans on the back of the kid's neck to explain how the environment changes the biochemistry. We also then explain how the biochemistry changes the behavior. We know from our study where we actually substituted starch for sugar, the kids actually couldn't even eat as much food as we had to supply. They all of a sudden got satiety back.
- PAPeter Attia
Yeah, this was, uh... Let, let's talk for a moment about that. This is the isocaloric substitution of fructose, uh, for, or glucose for fructose.
- RLDr. Robert Lustig
Glucose for fructose. That's right.
- PAPeter Attia
So let's take a step back and explain what NAFLD is. Let me start with one anecdote before we get, which you'll appreciate. When I was in my residency, so we're talking about, you know, what, 18, 20 years ago, one of the questions you're, if you're a young surgical resident, you're always asking the patient during pre-op is, "How much alcohol do you consume?" And the reason is, going back to the DT thing-
- RLDr. Robert Lustig
Mm-hmm
- PAPeter Attia
... we don't want to ever get into a situation where two days post-op a patient's having DTs.
- RLDr. Robert Lustig
Right.
- PAPeter Attia
So I remember on at least three occasions, but probably more, where a patient claimed they did not consume alcohol or that they, you know, they consume like a beer twice a week. And then we'd get in there to do the case, and they'd have fatty liver. And we would look at each other and go, "Goddammit, this guy lied to me. I can't believe this." You know, I wasn't there to judge him. I just needed to know he clearly is drinking like his life depends on it, and he was in denial. Well, it never registered to me what was going on until 10 years later when I learned about NAFLD, and I said, "Wait a minute, those patients weren't lying to me. They had nonalcoholic fatty liver disease."
- RLDr. Robert Lustig
And you can't tell the difference under the microscope. They look the same. So my first NAFLD patient was in 1996. I had just moved to Memphis, Tennessee, and I had a patient who had ALTs in the 300s, and the liver was enormous.
- PAPeter Attia
Yeah.
- RLDr. Robert Lustig
And they were just sure this... And it was a kid, you know, so it wasn't an alcohol thing, you know, but they were sure this kid had hepatitis or something else. And it turned out, you know, they went and did a liver biopsy, and it was, you know, fatty liver disease. And I said, "What the hell is this?" And soon all my patients had it. Same thing with type 2 diabetes. I saw my first pediatric type 2 diabetic back in 1992, and now one-third of all new diabetes diagnoses in kids is type 2. What's going on? You know, we were at the beginning. We, both of us were seeing this at the beginning of this epidemic, and now everyone's got it. You know, this can't be genetic.
- 51:04 – 55:55
What Drives Fatty Liver: De Novo Lipogenesis
- PAPeter Attia
Let's talk for a moment about that. About four or five years ago, there was certainly a controversy around the etiology of NAFLD. There were camps that said, "Look, it's got to be the fructose," for reasons that you'll articulate. There were other camps that said, "Actually, it's fatty acids. It's kids that are consuming too much fat." Others said, "Actually, it's just a proxy for obesity." In other words, quote unquote, "caloric excess leads to adiposity, which leads to NAFLD." I'd like to hear your thoughts on, in the most unbiased way we could, how do you make the case that it's fructose that is disproportionately driving this versus some of these other factors?
- RLDr. Robert Lustig
It's very easy to imagine how you get liver fat. There's production, and then there's clearance, okay? And the amount of liver fat is the equilibrium between those two phenomena. There are two methods for production. One is through diet, so dietary fat can contribute to hepatic fat. But there's also de novo lipogenesis, which is new fat making. It's the process of turning sugar into fat. Now, that had been discounted for years because of a one study-
- PAPeter Attia
This is Hellerstein's study that basically looked at-
- RLDr. Robert Lustig
Right. The Parks-
- PAPeter Attia
Yeah
- RLDr. Robert Lustig
... Hellerstein study from Journal of Clinical Investigation-
- PAPeter Attia
'96
- RLDr. Robert Lustig
... '98.
- PAPeter Attia
'98, okay.
- RLDr. Robert Lustig
1998, where they said, "Oh, this is a minor pathway. The fractional DNL was only 3%." Well, the reason it was only 3% was because, number one, these were healthy people. Number two, they were fasting, which means they were glycogen depleted.
- PAPeter Attia
Mm-hmm.
- RLDr. Robert Lustig
And so the fructose went into repleting the glycogen like we talked about. And there were also people who hadn't been large fructose consumers in advance. And we now know that fructose absorption at the level of the gut is inducible. We learn this every Halloween because the kid eats a lot of sugar and then ends up having diarrhea like crazy because basically they've got-
- PAPeter Attia
Malabsorption, effectively
- RLDr. Robert Lustig
... they've got malabsorption because their enzyme hadn't been induced yet. But if you continue to supply it, the process increases, and we now know the reason for that is a protein in the intestinal epithelial cell called thioredoxin inhibitory protein, or TXNIP. This is work from Richard Lee at Harvard. There were a whole bunch of reasons why people thought that de novo lipogenesis was a minor pathway. It's not a minor pathway. It is a major pathway. And Donnelly showed in 2005 that de novo lipogenesis was worth about 25% of the fat in the liver.
- PAPeter Attia
Wow. And then, I mean, you're gonna get to this, but how much of that is getting exported in VLDL?
- RLDr. Robert Lustig
That's the clearance side. There are two ways to clear. There's oxidation, fatty acid oxidation. This is why diseases that cause mitochondrial dysfunction like Reye syndrome end up with fatty liver. And then there's export, and the export can be through VLDL or it can be through phosphatidylcholine, but it's basically export out of the liver. So there's oxidation as clearance and export as clearance. So you have two ways coming in.
- PAPeter Attia
Two inputs, two outputs.
- RLDr. Robert Lustig
Two inputs, two outputs. And so the question is, what's changed? And the answer is our dietary fat's gone down. So that ain't it. [chuckles] But our de novo lipogenesis has gone up. And when you look at the exports, we now have fatty liver, which actually makes things worse because it causes inflammation, which ends up making mitochondria less functional, which causes less fatty acid oxidation, and we have data on that. And we have high triglycerides in patients who consume fructose. So if that pathway out is going up, then you know that if you've got fatty liver, it's because more's coming in.
- PAPeter Attia
Bottom line So for the record, you're saying because-
- RLDr. Robert Lustig
The DNL is the driver
- PAPeter Attia
... so we could say because triglycerides typically go up with NAFLD-
- RLDr. Robert Lustig
Yeah
- PAPeter Attia
... that says it's not a problem of exporting. It's not ineffective exporting.
- RLDr. Robert Lustig
Patients who have abetalipoproteinemia, they can't export.
- PAPeter Attia
Right.
- RLDr. Robert Lustig
They can't make the VLDL. You know how many patients that is? Okay, that's like one in 10,000. We have a 40% NAFLD rate in this country. It ain't one in 10,000. It's not 'cause of the fatty acid oxidation defects. It's not because of the export problem. It's not because of the increased saturated fat. It's 'cause of the de novo lipogenesis. By process of exclusion, that's the only pathway that's gone up.
- 55:55 – 1:07:55
Three Paths to Insulin Resistance and Metabolic Syndrome
- PAPeter Attia
Do you believe that insulin resistance is the result of NAFLD or is NAFLD the result of insulin resistance?
- RLDr. Robert Lustig
Yes. [laughs]
- PAPeter Attia
The two feed off each other?
- RLDr. Robert Lustig
Let's talk about metabolic syndrome 'cause the one aspect of metabolic syndrome that everyone agrees on is this phenomenon called insulin resistance. The question is where's the insulin resistance come from? Everyone assumes, well, you get fat, therefore your fat cells make cytokines like TNF alpha and IL-6. Those then go via the portal system to the liver and cause the liver to be dysfunctional, and therefore you increase hepatic glucose output. That then causes your beta cells to have to overproduce insulin, and then that drives the insulin resistance. That's what you learn in medical school. Undoubtedly, there are some patients where that is the pathway. I actually think that's actually a rare way that this happens, maybe 10%. I don't think that's the majority. But that is one way. We'll call it the adipogenic hypothesis of metabolic syndrome.
- PAPeter Attia
Because clearly that patient is not insulin resistant at the adipocyte, as evidenced by the fact that they can increase the size of their adipocyte.
- RLDr. Robert Lustig
Exactly right. So they have liver insulin resistance, but their adipocytes are insulin sensitive because they keep storing.
- PAPeter Attia
And in that model, you haven't necessarily specified what's happening at the level of the muscle, which some would argue is the harbinger of bad things. In other words, once the-
- RLDr. Robert Lustig
Yeah
- PAPeter Attia
... muscle stops disposing of glucose, taking it in.
- RLDr. Robert Lustig
Yeah. In fact, muscles don't need insulin to import glucose. If they did, then every diabetic would be paralyzed. The reason insulin works at the muscle is for import of amino acids, so for muscle growth but not for muscle metabolism.
- PAPeter Attia
So the transporter on muscle is which glute? Glute two?
- RLDr. Robert Lustig
It is glute...
- PAPeter Attia
Or four?
- RLDr. Robert Lustig
It's not four. That's in adipocytes. Glute two is in liver. I'm pretty sure it's three. One is in the brain. I'm pretty sure it's three. I gotta look at that again, but I'm just trying to remember. But it's not glute four.
- PAPeter Attia
Mm-hmm.
- RLDr. Robert Lustig
So that's one pathway of metabolic syndrome, starting at the fat cell.
- PAPeter Attia
Mm-hmm.
- RLDr. Robert Lustig
But I think that's rare. There's a second metabolic syndrome. We see it in clinical depression. Now, clinical depression causes weight loss, so you'd think that that would actually obviate metabolic syndrome, but in fact, clinical depression increases metabolic syndrome. It decreases obesity, but it increases metabolic syndrome. And when you do CT scans or MRIs across the abdomen of people with clinical depression, they have increased visceral fat. Now, why do they have increased visceral fat? Cortisol drives visceral fat accumulation. We know that from the Cushing syndrome patients, okay? Glucocorticoids drive that. So the question is why are stressed people accumulating visceral fat irrespective of their subcu fat? And the answer is because the sympathetic nervous system, normally which is lipolytic, at least acutely, becomes lipogenic chronically. And the reason is because of the cofactor that's released with the norepinephrine called neuropeptide Y. Neuropeptide Y actually changes what would be a lipolytic stimulus to a lipogenic stimulus. So chronic overstimulation of the sympathetic nervous system leads to visceral fat accumulation. And of course, chronic stress increases cortisol. The two together increase visceral fat. Well, that visceral fat will make the cytokines.
- PAPeter Attia
But this is independent. You're saying, 'cause-
- RLDr. Robert Lustig
Independent of subcutaneous fat.
- PAPeter Attia
But also the cortisol and the sympathetic piece, the norepi piece-
- RLDr. Robert Lustig
Yeah
- PAPeter Attia
... you're saying are both basically conspiring to be both pro-lipogenic.
- RLDr. Robert Lustig
Yes. Exactly.
- PAPeter Attia
It's funny, I knew about the, obviously the cortisol connection. Didn't realize the norepi connection.
- RLDr. Robert Lustig
So acutely, norepi will cause lipolysis-
- PAPeter Attia
Right
- RLDr. Robert Lustig
... through the beta three adrenergic receptor at the level of the adipocyte, but it causes lipogenesis when neuropeptide Y is available.
- PAPeter Attia
Can neuropeptide Y be measured or is it too short-lived to wait?
- RLDr. Robert Lustig
Too short-lived.
- 1:07:55 – 1:14:25
Why a Calorie Is Not a Calorie: Fiber and the Gut
- PAPeter Attia
It seems to me that a large part of this now becomes a policy issue, which I know you went back to graduate school-
- RLDr. Robert Lustig
Law school
- PAPeter Attia
... yeah, about what? Six years ago.
- RLDr. Robert Lustig
Five years ago. Yeah.
- PAPeter Attia
Yeah. And I know that even though you've, quote unquote, "retired" from your clinical practice, that's simply given you more time to focus on these other issues.
- RLDr. Robert Lustig
Yeah. No, uh, in, in fact, it's one of the reasons I retired. I realized, oh, about seven, eight years ago, that I could actually take care of a million kids easier than I could take care of one, and so I'm devoting my time now to research. We have a study now that is ultimately, if all goes well, and so far it is, will put the final nail in the coffin on a calorie is not a calorie, and will basically prevent the food industry from ever saying it again. That's my goal.
- PAPeter Attia
And currently, the food industry says... I mean, I haven't really paid much attention to this, to be honest with you, in the last few years. But is the food industry basically still saying that while a can of Coke is not ever deemed, even by Coca-Cola, to be as nutritious as a carrot, in the end, are they basically saying that all calories contribute equally to adiposity-
- RLDr. Robert Lustig
Yes
- PAPeter Attia
... and insulin resistance?
- RLDr. Robert Lustig
Yes. They are all saying it's about obesity, and therefore it's about energy balance, therefore it's about calories, therefore all calories are the same. That's what they say. It is absolutely not true, and we have all the reasons in the world to show why it's not true. We have empiric data, we have mechanistic data, we have plausibility data. We have hard data that show that is just not the case. And if you want, I'll give you examples of it. All right, let's start.
- PAPeter Attia
Yeah.
- RLDr. Robert Lustig
Let's talk about fiber. You eat 160 calories in almonds. How many do you absorb?
- PAPeter Attia
Two-thirds?
- RLDr. Robert Lustig
130. Yeah, I mean, 75%. Okay. Well, what happened to the other 30?
- PAPeter Attia
Presumably, it's going to drag some stuff out in your colon.
- RLDr. Robert Lustig
Well, no. What happens is the soluble and insoluble fiber in the almonds forms a gel on the inside of the intestine. You can actually see it on electron microscopy, a whitish gel. That's gonna act as a secondary barrier, preventing absorption of some of those almond calories early on. Well, if they don't get absorbed in the duodenum, where do they go next? Jejunum.
- PAPeter Attia
Ileum, jejunum.
- RLDr. Robert Lustig
Jejunum.
- PAPeter Attia
Yeah.
- RLDr. Robert Lustig
Well, what's in the jejunum that's not in the duodenum? The microbiome.
- PAPeter Attia
Yeah.
- RLDr. Robert Lustig
The duodenum's essentially sterile. It's got a pH of one. Only H. pylori can live there. You have to get the bicarbonate infusion-
- PAPeter Attia
Wait, you're saying that that lining is formed in the duodenum?
- RLDr. Robert Lustig
Duodenum, yeah. Exactly. To prevent your liver from getting the whole dose, because anything that's absorbed in the duodenum goes straight to the liver.
- PAPeter Attia
So how much fiber is in an apple?
- RLDr. Robert Lustig
A lot. I mean, I can't give you a, a number, but it's a bunch.
- PAPeter Attia
But, but, but I'm just directionally... I, I'm making this number up, but let's say there's how many grams of fructose in an apple? 20?
- RLDr. Robert Lustig
There's 30 calories in a standard apple, half of which would be fructose, so 15.
- PAPeter Attia
That seems low. A, an apple?
- RLDr. Robert Lustig
It's a small apple.
- 1:14:25 – 1:21:30
Changing the Food System: Industry, Subsidies and Policy
- PAPeter Attia
I know that you've got to go soon, otherwise we could do this for another two hours.
- RLDr. Robert Lustig
[laughs]
- PAPeter Attia
But I do want to ask you one sort of final question or final thought on something, which is I looked into this a few years ago, and maybe the numbers have changed, but directionally I think this is still correct.
- RLDr. Robert Lustig
Mm-hmm.
- PAPeter Attia
There were something like nine companies that controlled basically all of CPG-
- RLDr. Robert Lustig
Yep
- PAPeter Attia
... consumer packaged goods.
- RLDr. Robert Lustig
10. There's 10.
- PAPeter Attia
10, okay.
- RLDr. Robert Lustig
10 control 90% of the food in this country.
- PAPeter Attia
Yeah. That's bas- my calculation was 10 of them controlled 85% of the calories that people consumed.
- RLDr. Robert Lustig
Yep.
- PAPeter Attia
You face a very uphill battle-
- RLDr. Robert Lustig
Indeed
- PAPeter Attia
... because you're trying to get them to change the way they do business.
- RLDr. Robert Lustig
Mm-hmm.
- PAPeter Attia
But they answer to shareholders, not to you.
- RLDr. Robert Lustig
No, they're-
- PAPeter Attia
And the way they're doing things right now is working out reasonably for their shareholders. Not great. These aren't the most high performing companies in the world. But how in the world, when such a small group of companies control so much, and going back to what you said earlier-
- RLDr. Robert Lustig
Yeah
- PAPeter Attia
... you're asking parents to double their food budget-
- RLDr. Robert Lustig
Right
- PAPeter Attia
... to feed their kids correctly and spend twice the time doing it.
- RLDr. Robert Lustig
That's right.
- PAPeter Attia
What does this look like in 10 years? How does the story end?
- RLDr. Robert Lustig
Well, I don't know how it ends. This is a battle royal, like tobacco was, and it took a long time to win that, and there are people who say we haven't even won that one yet. You know, e-cigarettes now come, we're having another proposition here in San Francisco tomorrow about, uh, tobacco to kids. Here's the deal. The food system needs to change. They're not gonna change it from the inside because right now sugar is their business model. It's the thing that increases their sales. When high fructose corn syrup and the dietary guidelines of 1977 were, uh, first available, the profit margin of the food industry went from 1% per year to 5% per year. This is their juggernaut. This is their gravy train. They add more sugar, they sell more food, and they know it, and that's why there's sugar in all the food, 'cause when they add it, you buy more for all the reasons we've discussed. They have to change the food, which means they have to change the business model. So how do you change the business model? Well, there are four potential ways to change the business model. One is educate the public so that they don't want that food, in which case then they won't sell it. We're trying to do that. That's one reason I am the chief science officer of a nonprofit trying to do just that, okay, called Eat REAL, and REAL is an acronym, Responsible Epicurean and Agricultural Leadership. We are trying to change the food system by praising the good and hoping that that will induce competition amongst restaurants, cafeterias, hospitals, schools to procure, market, and sell real food. Or you can have executive branch efforts like the FDA or the USDA, but not in this administration. If anything, they've rolled back opportunities for that, like the nutrition facts label. Or you can have Congress legislate specific changes. They're not doing that because they're all paid off from the American Legislative Exchange Council and other concerns like the Koch brothers, what have you. Or you can have judicial impact, and so there are lawsuits against the food industry going on as we speak in an attempt to try to, shall we say, regulate from the bench, which no one thinks is optimal but seems to be the only thing that's available at the moment, aside from education. So those are the four ways to do this. My goal would be to get rid of food subsidies.
- PAPeter Attia
Are the food subsidies what enable the junk food to be basically half the price of real food?
- RLDr. Robert Lustig
That's it.
- PAPeter Attia
Or is it that the real food is twice as much to make? Not independent of the subsidy.
- RLDr. Robert Lustig
It's about the subsidy making junk food cheap. If you got rid of the subsidies, then the market would work. Okay? Right now, any subsidy distorts the market, and there's no reason for food subsidies. In fact, there's no economist worth their salt today that believe in food subsidies because they distort the market. So the question is would food get more expensive if we got rid of all food subsidies? The Jeanine Foundation at UC Berkeley engaged in this exercise several years ago, and they computed what would happen to the price of food, and it turned out that the price of food wouldn't change except for two items. Corn and sugar would go up.
- 1:21:30 – 1:23:20
Closing Remarks
- PAPeter Attia
I hate to end on this note. I know you have to go. I want to respect your time. I hope we can come back and do this again and talk in more detail.
- RLDr. Robert Lustig
Peter, okay, there are a few people that I don't just make myself available for, but that I want to see, and you are on that list.
- PAPeter Attia
All right. That, that means a lot. Thank you, Rob.
- RLDr. Robert Lustig
My pleasure.
- PAPeter Attia
You can find all of this information and more at peterattiamd.com/podcast. There you'll find the show notes, readings, and links related to this episode. You can also find my blog and the Nerd Safari at peterattiamd.com. What's a Nerd Safari you ask? Just click on the link at the top of the site to learn more. Maybe the simplest thing to do is to sign up for my subjectively non-lame once a week email where I'll update you on what I've been up to, the most interesting papers I've read, and all things related to longevity, science, performance, sleep, et cetera. On social you can find me on Twitter, Instagram, and Facebook, all with the ID peterattiamd. But usually Twitter is the best way to reach me to share your questions and comments. Now for the obligatory disclaimer, this podcast is for general informational purposes only and does not constitute the practice of medicine, nursing, or other professional healthcare services, including the giving of medical advice. And note, no doctor-patient relationship is formed. The use of this information and the materials linked to the podcast is at the user's own risk. The content of this podcast is not intended to be a substitute for professional medical advice, diagnoses, or treatment. Users should not disregard or delay in obtaining medical advice for any medical condition they have and should seek the assistance of their healthcare professionals for any such conditions. Lastly, and perhaps most importantly, I take conflicts of interest very seriously. For all of my disclosures, the companies I invest in and/or advise, please visit peterattiamd.com/about.
Episode duration: 1:23:24
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Transcript of episode 6FiYyk0-PWk
