"Doctors Had It All Wrong" - The Shocking Truth About Sugar & Obesity | Dr. Robert Lustig

1. RCDr. Rangan Chatterjee0:00

   What was it in your clinical experience that actually really got you into thinking, "There must be another way here. This can't be right?"

2. RLDr. Robert Lustig0:07

   Right. Well, so I had three aha moments, three, uh, and that sort of got me to where I am today and why I'm saying what I am saying today. The first aha moment came when I worked at St. Jude Children's Research Hospital in Memphis, Tennessee, a pediatric cancer hospital. And I went there in 1995, and I was presented with a cadre of about 40 children who had survived their brain tumors, you know, because of surgery and radiation, sometimes chemotherapy, who had become massively obese. They were perfectly normal weight before the tumor, and now they were on the order of 350 to 400 pounds. Okay? Normal kids before the tumor, and now massively obese. And w- there's a name for this. It's called hypothalamic obesity. It was first, um, you know, written about or first, uh, uh, described in 1901 by Friedreich and Babinski, two of the, you know, greats of, uh, of, uh, of international neurology. And I had all these kids with hypothalamic obesity that I had to take care of. And, like, how do you get them to lose weight? How do you get them to get better? And it had been shown previously that diet and exercise is useless. In fact, George Bray, the father of obesity research in America, in 1975 had taken eight of these kids on his ward and fed them 500 calories a day for a month. What do you think their weight did?

3. RCDr. Rangan Chatterjee2:02

   Well, you would expect it came down, but I suspect in this case it probably didn't.

4. RLDr. Robert Lustig2:07

   It went up.

5. RCDr. Rangan Chatterjee2:09

   Yeah.

6. RLDr. Robert Lustig2:10

   Okay? 500 calories a day, and their weight went up. Like, how does that happen? And the answer is, it happens because they were burning it slower than they were taking it in, because their metabolism of calories had actually c- come to a virtual standstill. So even 500 calories a day was too much. And these kids have, like, no energy. They sit on a couch. They're not interested in anything. The parents would actually complain that that was the worst thing about this. They'd say, "This is double jeopardy. My kid has, you know, survived the tumor only to succumb to the therapy, 'cause my kid is a lump on a log, and he's lost interest in everything. He's lost interest in school. He's lost interest in life. He's lost interest in, in activity. He's lost interest in friends. He's lost interest in everything. All he wants to do is sit and sleep." And so I had to take care of these kids. So I went to the literature, and I said... Oh, um, um, oh, the other thing was that this was exactly when the hormone leptin-

7. RCDr. Rangan Chatterjee3:24

   Yeah

8. RLDr. Robert Lustig3:25

   ... had been discovered. So leptin was discovered in 1994, and I was prepared for that discovery because I worked at Rockefeller University with the guys who discovered it, Jeff Friedman and Rudy Leibel. Okay? We... All the MDs at Rockefeller University all, you know, had to take call in the hospital together, so we were always trading, you know, call d- call dates and everything. So everybody knew what everybody else was doing. So I knew that they were trying to clone this, you know, this hormone, you know, out of these mice. And so when they did in 1994, I was very prepared for it. So I moved to St. Jude, and I had these kids, and it's like, "What am I gonna do for them?" And I postulated right then that these kids must have leptin resistance. These kids can't see their leptin, and the reason is 'cause their hypothalamus is dead, 'cause we killed it because of the tumor or the surgery or the radiation. And so because they can't see their leptin, their brain thinks they're starving. So the question was, okay, their brain thinks they're starving. Is there... What's downstream of leptin? What's actually making them gain the weight? The starvation's why they're hungry, but what's making them gain the weight? Well, we knew that these kids made a lot of insulin, and we knew that there's this, you know, animal model of damaging the hypothalamus, and they put out enormous amounts of insulin, and you could actually stop that by cutting the vagus nerve. The vagus nerve is the nerve that leads from the brain to the pancreas, and then the insulin would go down. So I said, "Well, I can't cut their vagus nerve. I'm not a surgeon, and, you know, that's a little drastic. But what if I gave them a medicine that suppressed their insulin release?" And so we gave them a drug called octreotide, a drug that, you know, is used by endocrinologists to usually suppress growth hormone release, but it also suppresses insulin release. So we repurposed it, and we gave it to these kids, and lo and behold, they started losing weight. And they couldn't lose weight before. You know, George Bray showed they gained weight. They were losing weight, and something even r- more remarkable happened. They started exercising spontaneously. One kid started competitive swimming. Two kids started lifting weights at home. One kid became the manager of his high school basketball team, running around collecting all the basketballs. I mean, these were kids who sat on the couch, ate Doritos, and slept.And now they're active again. And the parents would say, "Oh my God, I've got my kid back." And the kid would say, "This is the first time my head hasn't been in the clouds since the tumor."

9. RCDr. Rangan Chatterjee6:14

   Yeah.

10. RLDr. Robert Lustig6:15

    So something had changed their relationship to the world, not just their relationship to food, but their relationship to the world. So we said, "This is very interesting." So we did a double-blind placebo control trial, and this time built a quality of life measure into the protocol. And sure enough, the lower we got the insulin with the drug, not only the more weight they lost, but the more active they were. So what this did, the reason why this is so important and the reason I'm spending so much time on it, Rangan, is because this turns the first law of thermodynamics on its head. 'Cause the standard interpretation of the first law goes like this. You know, the, the first law is, you know, the total energy inside a closed system remains constant. You know, energy can neither be created nor destroyed, just shifted around. Okay? The standard interpretation that we learn in medical school and the, what, what the general public learns is, if you eat it, you better burn it or you're gonna store it. In which case, the storing part, the fat gain, is secondary to the primary problems, which are the eating and the burning, the gluttony and the sloth. Therefore, the weight gain is secondary to the gluttony and the sloth. Therefore, it's about behavior. Fix the behavior, fix the weight. What we showed in these kids was it's exactly the opposite. Turn it around. What we showed was, if you're gonna store it, that is, a high insulin level leading to obligate weight gain, and you expect to burn it, that is, normal energy expenditure for normal quality of life, because energy expenditure and quality of life are synonyms for each other, then you're gonna have to eat it. And now the storage is primary and the behaviors are secondary. The gluttony and sloth are actually because of leptin resistance.

11. RCDr. Rangan Chatterjee8:39

    So we get sick first, and then the weight comes afterwards.

12. RLDr. Robert Lustig8:45

    That's right. We get sick first, and the weight is secondary. That's exactly right. So this is, you know, monumental. This is huge. Um, but of course, you know, it goes against everything that we are taught, and it's, goes against everything that, you know, doctors routinely believe. But this was my first aha moment. My second aha moment came in 2006. So I realized that insulin was the bad guy, and we started then changing what we did in clinic. Instead of worrying about weight, we worried about insulin. We said, "Get the insulin down any way you can." And that's what my clinic became. It became an insulin reduction clinic. It didn't be- it wasn't a weight loss clinic. It was an insulin reduction clinic. And when we got the insulin down, then they lost weight. So in 2006, I was asked to give a talk at the NIH, okay? Specifically the National Institute of Environmental Health Sciences in Research Triangle Park, North Carolina. They were having their 100 anniversary of public health, and it was a two-day symposium. The first day was on their successes, like lead poisoning and pollution and asthma, things they'd figured out and, you know, been able to do something for the public health. And the second day was on challenges, and the morning was gonna be obesity, metabolic syndrome, and the s- afternoon was gonna be ADD and autism. Okay? So they asked me to give a talk. What do you think is the single most important environmental exposure that leads to obesity and metabolic syndrome? And I figured ... They, they probably figured I was gonna, you know, give a talk about some, you know, like BPA or some other, you know, environmental, you know, toxicant, you know, that's in the water or in the air or, you know, something like that. [sighs] And I thought, [clears throat] thought to myself, "How am I gonna, you know, make this worthwhile?" And I thought to myself, "All right. Wait a second. Let's, let's, let's go backwards here." Children today get two diseases they never got before, type 2 diabetes and fatty liver disease. Those two. Children never got those before. Now, lots of kids get them. All right? So I looked up type 2 diabetes and fatty liver disease, and of course, you know, I know a lot about both of them, but I very specifically looked for origins and causation. And it turns out that in the old days, you know, back in the 1970s, before this pandemic of chronic disease started, those both, both those diseases were the diseases of alcohol. Type 2 diabetes and fatty liver disease were the diseases of alcohol. But kids don't drink alcohol. So I said, "All right. Is there something they're exposed to that's like alcohol?" So I opened up my Lehninger, you know, biochemistry textbook from 1974Sitting at this table that I'm at right now-

13. RCDr. Rangan Chatterjee12:13

    [laughs]

14. RLDr. Robert Lustig12:14

    ... I said, "What the hell is like alcohol?" And there it was. It stared me right in the frigging face, right off the page, from 1974, and the answer was fructose. Fructose and alcohol are, uh, metabolized virtually identically. And it makes sense that that would be the case, 'cause after all, where do you get alcohol from? Fermentation of fructose. It's called wine.

15. RCDr. Rangan Chatterjee12:42

    Yeah.

16. RLDr. Robert Lustig12:43

    We do it in Napa and Sonoma every day. Okay, the big difference between fructose and alcohol is that for alcohol, the yeast does the first step of metabolism, called glycolysis. For fructose, we do our own first step of metabolism, but after that, what the mitochondria see are exactly the same, s- acetyl-CoA. It's just a question of which m- which was the substrate. Was it the ethanol or was it the fructose? But ultimately, they end up with the same fate. So it's very clear, all of a sudden, right, looking at that right there, that this is the substrate that is driving both the type 2 diabetes and the fatty liver disease.

17. RCDr. Rangan Chatterjee13:26

    Mm-hmm.

18. RLDr. Robert Lustig13:27

    So I put together a talk and I went to North Carolina and I said, "This is what I think's going on, and here's why." Half-hour talk. And then there was the bathroom break. And, you know, I got my applause, and then everyone left the room Sorry to interrupt. If you’re enjoying this video and want to dive deeper into the topic of nutrition, I have created a free special guide which contains the five most important changes I think we all need to make when it comes to our diet. If you want to get hold of this free guide, all you have to do is click on the link in the description box below. and they didn't come back. You know, I'm st- standing there at the podium, talking with, you know, this person, that person, and, um, no one's coming back for the next session. And then I had to use the bathroom. So I went out, and I actually got tackled in the frigging bathroom of the NIH by a bunch of crazed toxicologists screaming at me, saying, "Oh my God, oh my God! You're right! This makes perfect sense. This is the toxin. You have to tell everyone about this." And I guess I'm still doing it. [laughs]

19. RCDr. Rangan Chatterjee14:53

    I guess you still are.

20. RLDr. Robert Lustig14:55

    So if the toxicologists went berserk, might be true. And then that was the s- so that was the second aha. And then the third aha was not even my aha. It was my colleague's aha, but I, I, I adopted it. So we got very interested in sugar here at UCSF after that, and we actually have a group of us who we, we call the Sugar Hill Gang.

21. RCDr. Rangan Chatterjee15:23

    [laughs]

22. RLDr. Robert Lustig15:24

    They're actually referenced in, in the book here. Um, but, uh, my colleagues, Kristen Carnes, Laura Schmidt, and Stan Glantz, started looking at the paper trail of the food industry back in the 1960s, and found the actual paper trail that showed that the food industry paid off scientists to exonerate sugar and finger saturated fat as the bad guy. And we actually found their documents that showed the money transfer and the communications, you know, just like what the January 6th committee's doing now. Follow the money. And we, so we actually proved that the sugar industry put their thumb on the scale back in the 1960s to exonerate their product. Because there had been data that had been coming out at that point showing that sugar was not good for you. In fact, that's what John Yudkin found.

23. RCDr. Rangan Chatterjee16:24

    Mm.

24. RLDr. Robert Lustig16:25

    Remember Pure, White and Deadly? And he had found, you know, shown that data. And so people were starting to cast a, a, a, you know, a, a fish eye at, uh, at sugar. And so they had to go into overdrive mode and to, to PR this problem away. And so they approached the chairman of the Department of Nutrition at the Harvard School of Public Health, Fred Stare, and his associate, Marg Hegsted, who ended up becoming the head of the US Department of Agriculture in 1970, to pay them off $6,500 back then, which would be about 50,000 today, to write two review articles to appear in the New England Journal of Medicine that basically said, "Saturated fat's the bad guy, and sugar is no problem whatsoever." So that's the third aha moment. It's all a scam. The whole thing's a put-up job. And that's why I wrote Metabolical.

25. RCDr. Rangan Chatterjee17:26

    If you enjoyed that short clip, I think you are really going to enjoy the full conversation, which you can check out here. [outro music]

Episode duration: 17:47