The Rest Is Science - Why Your Brain Thinks You're Full (Even When You're Not)

Episode Date: August 16, 2026

How did the Gila monster, a desert lizard that eats just five times a year, help unlock the science behind Ozempic, Wegovy and Mounjaro?In this episode of The Rest Is Science, Professor Hannah Fry and Michael Stevens (Vsauce) trace the strange journey from a molecule found in lizard venom to medicines reshaping diabetes and weight-loss treatment, exploring how GLP-1 helps regulate blood sugar, appetite and the hum of ‘food noise’.Early evidence suggests their effects may extend far beyond food, quieting cravings for alcohol and cigarettes, and even the urge to gamble. What might this reveal about the biology of wanting itself, and how much control do any of us really have over what we crave?-------------------For more information about Cancer Research UK, their research, breakthroughs and how you can support them, visit https://www.cancerresearchuk.org/our-research/rest-is-scienceCancer Research UK is a registered charity in England and Wales (1089464), Scotland (SC041666), the Isle of Man (1103) and Jersey (247). A company limited by guarantee. Registered company in England and Wales (4325234) and the Isle of Man (5713F). Registered address: 2 Redman Place, London, E20 1JQ.-------------------Find The Rest Is Science all over the internet by ⁠⁠clicking here.⁠⁠-------------------Video Producer: Adam Thornton + Teo Ayodeji-Ansell + Jack MeekAnimator: Sam BensonVideo & Social: Bex TyrrellAssistant Producer: Lucy LipscombeProducer: Simona RataSenior Producer: Lauren Armstrong-CarterChief Digital Officer: Samuel OakleyExec Producer: Neil Fearn Learn more about your ad choices. Visit podcastchoices.com/adchoices

Hello and welcome to The Rest is Science. I am Michael Stevens. And I'm Hanfri. Michael, you know, if you ask somebody if they want sugar in their tea, and they respond, no thank you, I'm sweet enough. Here's my question for you. How sweet are you? I want to know how much sugar do you think there is in your bloodstream right now? Did you know that I've actually calculated this before? Have you? Yes, I did this entire series of videos for a diabetes medication company for giving to doctors. They were giving to doctors. They were, we're going to doctors. They were, were never public. And the scripts they wrote were so boring. I did a bunch of, like, besawcing them up. And I calculated, like, if a diabetic person with really high blood sugar got bit by a vampire, would they be a dessert? Turns out no. But I don't remember at all what I calculated. But yeah, I did calculate, like, how sweet is my blood, is someone with low blood sugar, high blood sugar? I think that, like, diffused into my whole body, I'm not that sweet. Vampires have

not got sweet tooths, you know, because even a diabetic person with like all this sugar running around in their blood, it's not going to taste that sweet. But you on the other hand, Michael, I mean, I haven't done the exact calculations. I didn't want to sort of email through in advance for your height and weight. But it's about four grams in your blood. That's it. That's it, like a teaspoon, basically. Wow, a little teaspoon. A little teaspoon in your blood at any moment in time. You can eat a massive dessert and your body will be like, nope, too much. Thank you. You need to put, lock some of that away, or you can, like, do a starvation diet and have none there, and your body would be like, what? Not okay. Thank you. You need to put more in. Right. This is like an

incredibly narrow window that your body is continually fighting. High blood sugar doesn't mean 400 grams. It means a little bit more than four. And low blood sugar is a little bit below that, that narrow path, that narrow band where we are fine. Exactly. So what I want to talk about is how your body manages this incredible dance of keeping your blood fine, whatever you throw at it, and then in turn how people are now hacking our own biology via fat drabs in order to disrupt this system to our advantage. This episode is brought to you by.

Cancer Research UK. Our bodies are incredible machines, worrying away making more and more DNA to build the proteins that keep us alive. In fact, in the last minute, your body has made over 200 million new cells and enough DNA to stretch to the moon and back. To the moon and back. That's so much DNA that if you compared it to the size of the cell it fits into, that would be like squeezing the London underground into a suitcase. By the age of 50, you have copied almost 6 trillion miles of DNA. But every time that your body copies DNA, it risks making mistakes. And over time, those mistakes can accumulate. And that collection of errors can lead to cancer. But incredibly, cancer research UK scientists can spot these errors. And by finding them,

they've helped double UK cancer survival over the last 50 years and are driving even more discoveries that could tackle over 200 types of cancer. For more information about Cancer Research UK, their research. and breakthroughs and how you can support them, visit cancer research.uk.org slash rest is science. Okay, there's two main hormones that are in charge of keeping this incredibly fine balance. One of them is insulin, which of course is the one that's the problem when people have diabetes. Do you know how internet actually works, though? It's kind of clever. Okay, I thought you said, do you know how internet works?

And that was like, whoa, it's a bunch of tubes is all. I know. Insulin, I don't remember. At top level, insulin is produced by your pancreas when you have too much blood sugar if you're all fine and good, it will take away excess sugar from your blood and put it into storage. That's sort of like the top line level. When it stores it, it doesn't store it as sugar. Correct. The way that it works is all of your muscle and fat cells, they have, I mean, simplifying slightly here, but they essentially have like little doors in their walls that glucose can pass through. These are like very specific little protein gates. But, But normally those doors are locked close, right?

The glucose can't get in so that any glucose that's within the cell stays within the cell. It's not sort of floating in and out. And then what happens is that insulin is essentially like the lock for this door. So as insulin comes past, it opens up the door, the glucose can wander in. So if you do not have insulin in your body, if you have like a deprivation of insulin in your body, then you can have glucose literally standing right outside of a cell being like, hello, please let me in. and it just can't get in, right? If the insulin doesn't dock into its receptor to open the door,

there's like sort of nothing going on. So this is what's happening when people, especially with type 1 diabetes, this is exactly what happens. Your blood can be completely full of sugar, way, way, way above the four grams that's sort of normal. But because the doors are not unlocking, your cells can't get any.

So your body is like starving to death, despite there being this insane abundance of fuel right next door. Wow. Wow. And by the way, glucose is the type of sugar that our body uses. If I eat a bunch of fructose or lactose or some other kind of sugar, the body goes, okay, cool, but we need to have glucose for the cells to have the energy they need. Exactly. I mean, that's the whole thing about energy is it's glucose plus oxygen equals water plus carbon dioxide plus energy. That's literally the thing that your cells are running on. So I use the energy to move. I breathe out the carbon dioxide. Thank you, glucose. Thank you very much, glucose.

Appreciate it. But without insulin, you're in trouble, right? You're really in trouble. Anyway, at the other end of the spectrum, so that's what happens. If you have too much sugar in your blood, that's what's supposed to happen is that all these doors open, and then it goes in and it gets stored.

At the other end of the spectrum, you have something called glucagon, which is actually also, I think, created very close by in the pancreas. And this gets released when the blood sugar is low instead. So like if you're fasting or overnight or whatever it is. And that goes to the liver. And then the liver is, I mean, it's sort of like the body's pantry. It can break through stored glucose, stored as glycogen.

It can break it back down into glucose. It can pour it into the blood. And it can even manufacture sort of brand new glucose from scratch out of amino acids and other spare parts, right, if you really need to. By the way, gluggan would be a great name for a child. Glucucan. Glucan, put down your sister's toys. Wait, are we saying glucagon is male or female? It could be either. It's just a great name for a child that makes everything sweeter.

Well, that's true. Adds in sugar. Adds in sugar when required. What about insulin as a child's name? Yeah, obviously insulin would be their sibling. Yeah, necessary, but robs the sweetness. That's right. Okay, so here's this puzzle, right? So obviously, people with type 1 diabetes have existed for, I mean, probably as long as people. But he is a real puzzle that bothered doctors and scientists for a really long time.

If you take some glucose and you drink it, right? Let's just say you take some glucose age or something, right? Something really, really sugary and you drink it. Your blood sugar rises, as expected, and your pancreas will dump out loads of insulin to sort of deal with it to kind of clean it up and make sure it doesn't get too much. Fine, expect it. Now, if you take exactly the same amount of glucose, not as lucosate this time, but as the same amount of glucose, and instead you just

inject it directly into a vein. You're bypassing the gut, but it's the same sugar, same blood concentration, you would expect that your pancreas should react in the same way. It should be like, okay, loads of sugar here dumps out loads of insulin. But it doesn't. What actually happens is your pancreas does produce insulin, but way, way less, like half as much as it does if you actually ingest it. People notice this is like that is very strange, right? That like the only difference that's going on here is the root that it gets into your bloodstream, but still it's about being in your bloodstream.

So this was, I think, one of the first clues that people were like, okay, it looks like something is happening in your gut or in your mouth as you're literally ingesting something that is telling your pancreas to produce more insulin. You can't bypass the gut or the pancreas acts. differently. Right. There's something going on here. And so in the 1980s, stomach ulcers used to be a really, really big thing. Do you remember like when I was a kid, you would hear about, it's got a stomach ulcer, like stress, stomach ulcer is really awful. Yeah. And you heard about this in movies and the media all the time. Like every dad had an ulcer that was getting worse because the

kids were loud. I thought that would be a much bigger part of my life today. Yeah, but you don't see them anymore at all. It's like the Bermuda Triangle. Like the 19- full of all these things that I learned to be very, very aware of and fear. And then now I'm just like, A, what happened to the Bruneita Triangle? What happened to ulcers? Not that they've gone away. But yeah, yeah, you're right. Not completely.

But they sort of had because it turns out that they were caused by bacteria. Yeah. There's a great story about how they proved that it was a bacteria because the person who came up with a discovery decided to swallow, to drink the bacteria, deliberately give himself a stomach ulcer in order to then demonstrate that that was the thing that caused it. Anyway, that's not by the bite. Right. So drinking someone's ulcer, bad idea, it's contagious.

Don't lick the inside of someone's stomach if they're infected with ulcers. Let me just write this down because actually, no, I need to cross it off. It's on my list of to-does today. But yeah, ulcers weren't caused by a stressful job. I mean, I think it probably exacerbated it. Your immune system would be more liable to be unable to fight something and so on. Okay. Here's the thing, what they used to do,

which actually seems brutal now, I think, when you think about it, is if people had summer crosses, they would be like, well, I don't know, should just cut out that bit of the stomach? Like, should we just go in there and, like, lop it out, maybe?

I think they would only do it if someone had a particularly nasty ulcer. They'd go in, they would, like, cut out the bottom of your stomach. Okay, and the way your stomach is sort of like this, it's kind of almost like a u-bend shape, right? Sort of like dips below and then comes back up. What then happened was,

Some of these patients started having these really bad low blood sugar attacks. They'd be like really shaky. They'd be really sweaty. They'd be like faint in hypoglycemic. They were like, what on earth is going on with these people? Like, why is this happening? And they worked out that it was because their bodies were pumping out more insulin than it should have been. So it was like depleting all of the sugar that was in their blood really quickly.

the balance was off, essentially. Let me get this straight. So if you eat the glucose, then normally everything's fine. If you inject it and bypass the gut, not enough insulin is made. Correct. If you cut part of the stomach away and you eat the sugar, then too much insulin is made. Exactly. So there's some sort of messaging signal that's going on.

When you ingest food all the way through, some messaging system is going on that is telling the pancreas to release the correct amount of insulin. And they worked out essentially that what was happening that down there in the bottom of the stomach is this little muscular valve. And what it's doing is its whole job is to be really stingy, right? is to like hold back everything in the stomach and then squirt it through really carefully, like drip, drip, drip, drip. Now, if you take that valve out, the food doesn't drip, it like dumps the whole meal kind of comes crashing through into the lower gut all at once, right? And so they were like, okay, well, this signal, maybe this signal is around about there somewhere because as all this food is like getting dumped in, the signal is going,

like what? Like crazy. We need insulin now. We need loads of insulin way, way faster than the body needs it or can handle it. And that's what's making people be high glyclysmite. All of this is going on. These couple of scientists in Boston and Harvard, they were like, okay, this whole thing about glucagon, which isn't their son, unfortunately. Or daughter. Or daughter. Any kind of child should be called glucagon. That's the official policy of me. Okay. Anyway, they were like, right, we want to know what gene is, is. is creating this. And they were particularly interested in the anglerfish, because the anglerfish has this entire organ, which is called the Brockman body, for making glucagon. Okay, so, so like,

normally, you've got like a pancreas and a human or in other animals, and if you want to go in and you want to work out where the glucagon is being made, you've got, like, kind of pick out tiny little bits of glucagon, and it's all mixed in with other bits, really difficult. But in the anglerfish, it's really simple. So what they did is they managed to find the gene for glucagon via this fish. And then they were really surprised to discover that this, this gene also makes two other little peptides. Peptide, by the way, anyone who has like ever experienced a skincare advert will think that it's something that you put on your face. Peptide is just a, it's a cute little chain of amino acids. Okay, that's all it is. It's like a little cute, cute little, cute little

peptide. A cute word for a cute thing. Peptide is another great child's name. Hey, peptide. We got triplets. now. I think peptide should be the pet. Should be like a little mini show hour. It's the little dog. It's the little dog. I love this little family that we're creating, Hannah. We've got to decide what the mom and dad are called at some point.

Yeah, we will. One of them surely is called ulcer. Ulcer. That's the dad. And the mom, TBH, TBD. TBD. What is TBH? To be honest. Oh, gosh. The kids are going to blast me for misusing an acronym. I think you'll feel right.

Okay, so this G that makes glucagon turns out also makes these two little peptides and they're looking at them they're like, well, I don't know what this is, what this one is, oh, it's sort of a bit like a glucagon like a glucagon like peptide, let's call them glucagon like peptide one and glucigan like peptide two.

GLP one and GLP2. There they are. You may have heard of GLP one. Yeah. Because this is the hormone that fat jabs aim to mimic. Things like a Zempeg, Wagovi, Manjaro, all of those. It turns out that you have these little factories. They are essentially this messenger system directly to your pancreas to say,

hello, we're going to get some insulin out there because otherwise our blood sugar is going to end up being a bit too high. Okay, so that's what GLP1 does. It's a messenger to the pancreas to make insulin? Well, yes, but only if the blood sugar is high. The reason why people were so excited about this is because if you have somebody with diabetes, right, and you just whack a load of insulin into their bodies, well, then great, you know, you've dealt with that particular sugar high,

but you need to assess it really carefully because you could accidentally put too much in and then have their sugar levels dropping off the charts instead. It's unbelievably difficult to get that balance, that incredibly fine balance right at all times. Because also, if you have blood sugar that's too low, I mean, your brain literally starves. Yeah.

It cannot function. I mean, it's really, really dangerous. But if you have too high a sugar in your blood, then you're sort of candy all of your internal organs, you know. Your eyes in particular are really, really susceptible to going blind if there's too much sugar in your blood for a long period of time. The thing about this GLP1 that everyone was excited about was like, okay, so intelin is like, it's kind of fixing the problem with a sledgehammer, you know, which is like,

well, better than nothing, but still not great. But GLP 1 will only signal the pancreas to produce more insulin if you have high blood sugar. So if you've got GLP 1 floating around and your blood sugar is low, your pancreas will not go crazy. Right. It's only because the reason why you've got such big spikes in the people who'd had those stomach ulcers removed was because this great big dump of food coming through the stomach coincided with there being a lot of sugar in the blood and therefore the pancreas overreacted. So in 1993, this Danish scientist, he's called Jens Yulholst. He was like, okay, well, let's try this, shall we? Should we just whack a load of this peptides, this cute little peptide,

GLP 1 into people's bodies, see what happens? And he did it with people who had diabetes in particular, right? So this is all about a diabetes medication. So for starters, having GLP in the body did normalize people's blood glucose levels, right? So it worked. But he said, the first problem was that we realized that injecting people with simple subcutaneous injections of this peptide, ultimately. didn't really work. The reason was that the peptide was destroyed in the body within minutes,

so it couldn't be done that way. And you couldn't give them a higher dose because they just start to puke all over the place. So that didn't work either. That's the scientific term, puke all over the place. This is essentially why it's going. Did this scientific study, injected people, they just all started puking all over the place, which is, I mean, tells you that like flooding your body with this stuff is not good. But the other point about how it gets broken down by the body really quickly. Like this made it sort of, okay, maybe there's this miracle drug somewhere, but it's not going to work because essentially your body, in order to keep that incredibly fine balance,

that four grams of sugar, you can't let the GLP1 like float around for too long, you know, because then you'd be, you'd be like carrying on putting out insulin long after it had been the blood sugar had been dealt with. So you also have this little enzyme in your blood, which is called DPP4. I don't know if that's going to be the mother's name. That's the mom. That's the mom. We met her.

She's here. Yeah, maybe we shouldn't call the mom that because it sounds like a very awkward question. What's DPP for? She's here. She's snippy, though, the mom. I mean, that's essentially her job is to go along and cut GLP one and half. And destroy it. I don't think she's, I mean, she's good.

She's keeping everything balancing. But she's sort of, she's doing it by. cutting the play in half, you know? Yeah. Yeah, everyone was like, you know, it feels like we're on to something, but everyone's puking and it doesn't work, so it's not looking so good.

And then enter into the frame, the unusual family pet, the Gila Monster. So this is a lizard, right? Yes. Because the Gila Monster solves everything, my friend. The Gila Monster is the root source of this miracle.

that happened with diabetes. Tell us about the animal. It's a venomous lizard, lives in America. It's quite fat. It's quite, like, chunky. It's got, like, this orange, black skin kind of mottled. They live in the desert. They're, like, they're quite lazy.

They don't move very fast. So they only actually manage to catch and eat a meal about five times a year. No kidding. Yeah. Have you eaten this quarter? Okay, I can see how this is related. But when they do, when they do, they eat like half, their body weight all at once.

Right. Okay. But scientists were like, right, well, this guy over here, this Gila monster is like, he's going very long periods without eating. They've got to have some way to keep this balanced, you know, their metabolism running really smoothly throughout that time. The thing is, one of the reasons why you might know the Gila Monster is that they bite humans.

Oh, they can bite humans. The bite is venomous. It causes this incredible pain. Something else kind of separately that scientists had noticed in the 1990s. 1970s and 80s when people had been bitten was that the victim's pancreas would start secreting all kinds of hormones. Really? I mean, you're absolutely seeing where this is going, right? Yeah. A team of scientists, they decided they would get the venom of this Gila monster and they would test it on pancreas cells to see if any of them did anything, which is really

difficult because it's like this kind of tangled web of molecules, right? But there's one venom in particular that makes a pancreas start secreting and they wrote this paper about it. They just left it. It was untouched for like 10 years. No one touched it. No one went anywhere near it. And then in the early 1990s, this different Dr. John Eng read this paper and was like, oh, I wonder what, I wonder what venom spit from the Gila monster is doing to a pancreas. That's like so weird. He found in this venom, this chain of 30. 29 amino acids, cute little peptide. And he called it Exendin 4.

They really need to get bare names for these things. Exendin 4. Is that the mom? Exendin 4. That's the second wife, maybe. I think there might be the car number plate. Okay, fair enough. Yeah, I like that.

Anyway, the thing is, is it turns out that this little peptide is almost the same. as GLP1. Like, they're really, really similar, but it is different in one important way, which is that venom has to be stable, right? Like, the animal makes the chemicals and the venom and it sort of sits inside the animal's body. So it has to last way longer without breaking down. And the crucial thing is that the peptide in this gila monster spit, instead of, like, disappearing in a few minutes, like gLP1 does, can last for ages and ages and ages. And the reason why is that the enzyme can't cut it. DPP4 can't cut it up. It's blocked. It's blocked. I mean, this is like an unbelievable revelation. I think just really demonstrates the way that science sort of

inches forwards towards progress because over here, someone's looking at venom bites in lizards. Over here, somebody's looking at patients with diabetes. Over here, somebody's looking at stomach ulcers, and then it ends up all coming together, and this lizard that eats four times a year turns out carrying in its spit is an almost perfect human version of the like satiety hormone that sort of makes you feel full, right? It's like, they're absolutely crazy that this is the case. Is that what GLP1 does? It makes you feel full? Yes, well, I'll get to that in a second about because we don't know totally how it completely works. We know a bit of it. We know a bit of about how it works, but one of the things is it makes you feel full. So extend in four,

lasts longer than GLP1. Because it can't be cut. If you inject someone with a bunch of it, does it make them puke all over the place? Well, you still have to be quite careful about that. But, but, okay, for starters, they didn't just, they didn't like harvest the venom of a monster, a spit of a monster to do it. They like manufactured synthetic versions of this same thing. The very first class of these drugs were just, copying the lizard's protein. But the modern ones, what they've done is they've tweaked it a tiny bit. So they've tweaked the spot where the enzyme, where DPP4 can latch onto so that it

can't really get a grip anymore. So there's no risk of it's sort of breaking down. And then they've also added on, I just find this crazy about modern microbiology is obviously astonishing. They've like added on this little tail, this little like fatty tail off it, which can hook onto the albumin, which is. this really big carrier protein that kind of floats around your blood is hitching a ride essentially on like the main train so that it can move around your body. And because it's hitched a ride,

it can't get filtered out by your kidneys. So it's like it stays in your body for longer as well. So you've moved from GLP 1, which is a molecule that you make yourself that lasts about 90 seconds before it gets cut up by the wife. And now you've got semi-glutide, which lasts for a week in your body. That's the whole thing. You haven't. invented anything new, you've just taken like a body's own process and then you've made that process instead of lasting for 90 seconds after you've eaten a biscuit, instead lasts for, you know, a whole seven days. Wow. That really is incredible. Who was the dad again? The dad, dad was ulcer. The dad was ulcer. He's got a bit part in the story, let's be honest. Yeah,

this is the dad who like went out for cigarettes and never came back. GLP one came around, but it still wasn't quite perfect. But then the dad put in the work and he grew as a person and became this manufactured semi-glutide that sticks around, hitches a ride, does the work. That's just incredible. Isn't it? I tell you what, let's go for a break. And then when we come back, I'll answer your question because you have asked about four times, what is it actually doing? And I have got an answer for you, ish. This episode is brought to you by Cancer Research UK. When we talk about beating cancer, we often focus a lot on survival.

And that can mean overlooking impacts that last long after treatment ends. Yeah, for example, take cancers in children and young people. The treatments themselves can be incredibly harsh. They can cause lifelong side effects like infertility or hearing loss. And Cancer Research UK is working to change that because young people, they should be able to grow up hearing the voices of the. people that they love and living their lives at the fullest. That's right.

And one clinical trial led by Cancer Research UK showed that giving another drug alongside chemotherapy nearly halved the number of children losing their hearing. And today, the treatment combination is being used by doctors across the world. For more information about Cancer Research UK, their research and breakthroughs and how you can support them, visit cancerresearchuk.org slash rest is science. Okay, we're back.

You've asked what do they actually do? Yeah. And the answer is there's four things with varying degrees of us understanding them. Hold on. We're talking about GLP1. GLP one, yeah. Okay. Because semaglutin is doing the same thing.

It's like it's the same shape as GOP1 that's doing the same thing. It's just got these additions to stop it being like chopped apart. Yeah. We know GLU2. P1, goes to the pancreas, tells it to make insulin when the blood sugar is also high. Right. That is what makes it an amazing medication for diabetics. It's also why your, you know, your blood sugar doesn't crash to the floor.

It sort of keeps you regulated in a really good way. It also, so as well as increasing your insulin, it also calms down your glucagon. Okay. This is the one, of course, that's telling your liver to sort of pour stored sugar into the blood. Yeah. It's just on both ends of the, on both ends of that spectrum, it's just saying, guys, calm down. All right? Yeah.

No big deal. Just like a good dad, you know? Yeah, it kind of keeps the peace. Let's everyone talk. I love it. Okay. It also, we know that it slows down how fast your stomach empties into your intestines. Mm-hmm.

That means essentially that food is going to sit in your stomach for longer. It's going to, sugar will trickle in much slower instead of. arriving in a flood, which I mean, if you, I don't know, like, you sort of know to do this anyway. I think people broadly know that having something like porridge for breakfast is better, especially with like rolled oats or whatever, is better than having pancakes with maple syrup. And it's because the sugar is being released more slowly. Well, better. Better depends on what your goal is.

If your goal is to get really sugared up, then just drink the syrup. But yeah, if you want that long release of energy, you have the porridge. I mean, this is true. But I think the effect of that is that it also just makes you feel physically fuller for a longer time. Ah, and there's the rub. There is the rub. But here is the ultimate, ultimate rub, because GLP1 manages to talk to your brain. There are receptors for GLP1 in the hypothalamus.

There is a little patch in your brainstem. And when GLP1 lands there, it basically turns down the volume on hunger. It's not like, oh, I'm being disciplined and I'm not going to eat. I'm going to push myself through. It's like you just doesn't even occur to you. The desire is not there. The desire is not there. This is the thing that really makes it this amazing, amazing intervention for obesity.

Because, you know, it's not like, it's not feed. speeding up your metabolism. It's not blocking fat. It's not a stimulant. It's not like, you know, dissecting sections of your stomach like gastric bands used to. It's just changing the demand. Like, that's it. It's just turning down the dial on how you think about it. I'm a little surprised because I thought that the big innovation we would see would be that we would find a way to allow people to continue to desire and consume a lot of food without any problems, health-wise, because that's what made more sense for companies. Like, they need to sell all this food to us.

And the more food we buy, the more their profits go up and the happier their boards are. But a medication that causes a decrease in demand sounded too anti-capitalism to ever take off. And yet, here we are. Except that there's the other capitalism of it on the other side. That's right. That's right. In the sense of like the capitalism of selling the drug. Right.

I think you make a really important point here, which is that when companies have been making foods, whether it's like breakfast cereals or, you know, like crisps that you might snack on over and over again, especially if that food has existed for a really long time. The thing that the company is trying to optimize for is volume, you know? You go in and you have like a sit down, a consumer panel where they all try the stuff. And of course they're asking them, how delicious is it? Did you enjoy it? Was it really tasty? but the thing they care about most was how much did you eat? Right. What volume did you consume?

And I mean, I'm not just saying this is like a hunch, right? Like there is so much evidence that this has been the metric that these companies have optimized for over and over again. And it should have been because if I'm investing in these companies, I need them to have customers that want to consume, consume, consume. Otherwise, they don't grow. Right. Except that. the way to get people to consume more and more food isn't to make it more and more delicious. It is instead to make the food so easy to disintegrate that it never reaches the part of your stomach

which releases these hormones to tell your body that it's full. That whole idea of Pringles being, once you pop, you can't stop. It is literally true. It is literally true. They are so predigested in laboratories, macerated to death that when it enters your mouth, it just evaporates into thin air. And the evolutionary system that your body has spent millions of years perfecting

is no longer capable of telling you you need to stop. That's incredible because I would never eat like three baked potatoes all at once. But if you predigest them for me by mashing them up into a powder, and reconstituting it into a fun shape and adding a lot of fun flavors, I will blow through that and I'll still be hungry. So I will keep buying and buying and buying, and the Pringle's company can make a lot more money

than the potato farmer. But you're not hungry because the calories haven't been consumed. You're not hungry because your body doesn't have the same glucose input. You're hungry because you have overridden the systems that your body has in place to tell you when to stop eating. Right. right, which is wild.

So what GLP1 is doing in a world where all of these products exist, all of these super processed, ultra-processed foods, it's basically like there is this little sort of arms race going on within your own body. So it's like it's extra capitalism rather than less capitalism. It's like you had the capitalism of the food companies, kind of like make people eat more, more, more, more, more. And now you've got the pharmaceutical companies being like, hey, here's the war against it.

So then the solution, if I'm like trying to sell a lot of food, is that in order to keep hitting my benchmarks for profits, I need to make the food probably just more expensive. I need to find a way to say, look, you're going to buy half as much. But now it's like so organic or it's got just the right trendy thing. it that it's worth paying twice as much for, whew, we're not losing money. Or you could do the other thing, which is what apparently some companies are doing, which is to start researching anti-GLP1 foods. Whoa, that's it, isn't it?

The third option is to just buy the GLP company and then you're like, you know, you're- Keep it going around and around around. You sell the food and the toilet paper. You're just there for the whole cycle. So, wow. So anti-GLP food. Additives spark a desire that these GLP-1, I mean, that's not really what they are. They're modified versions of the GLP-1 hormone.

Yeah. You can think of them as GOP-1s. Got it. So, yeah, finding some additive that makes, that sparks a desire for more that GLP-1-like medicines cannot touch would be a goldmine. The thing I think that's really interesting about the GL-1 stuff, like, that is actually sort of aside from the food industry is that the effect that it has on the brain does appear to go beyond just not wanting to eat. That's what I've heard. I've tried them, right? I've,

I've like had them in the past. And you hear people describe food noise. Okay. So like, and I think, actually, I think Oprah Winfrey said something about this when she started on summer glutide. she was saying that it just hadn't occurred to her that people who were thin they didn't think about it. It's not that they were like so capable and strict and like able to resist. It's just that they didn't have to fight the battle in the first place.

That's right. They weren't resisting anything. It wasn't there in the first place. Yeah. Exactly. And so I've definitely had that experience of this food noise being turned down, that dial of food noise being turned down.

Absolutely had that experience. But there is this evidence that actually it turns down. down the dial on all kinds of other overconsumption behaviors. So alcohol, for example, smoking, even gambling, which is incredibly fascinating that actually you could potentially satiate that with a GLP1 mimicer. Yeah. And like we've said, satiate almost isn't the word because you're actually cutting away the desire at the root. It's not there to be sated. There just isn't, you're just, You exist without the desire and the need and the drive to consume, whether it be food or even experiences like gambling.

That is part of human experience, though. So I have heard people complain about how, like, yeah, I'm not like desiring a bunch of sweet pies. But at the same time, my love for my grandmother's pies was a big part of our relationship and now it's gone. Yeah. I mean, I would say when I have been on it, it's not that food tastes less delicious. It's not that you can't plan and enjoy the planning of a really amazing meal. You know, it's not like that. It's just that you, you know, I remember the first week when I had taken it and I was in a hotel in New York, so I was really jet lagged. And like normally in that situation, I will order room service and I will like have a massive burger and I'll sit on the bed and I watch a stupid film and I just eat the entire thing, right?

And I wanted to do exactly the same thing. I was in a bathrobe, you know, whatever, I was there, I was ready and I had this massive burger and I had two or three bites and it was great and then I was done. Right, right. It just stopped. So does it have an effect on our desire to keep scrolling on social media? Like that's another one that goes like, I can't get enough and I just, I need to check my phone. But you, we're not seeing the same.

effect there. I haven't seen any evidence on that. There was one really big hope, actually, about how it might end up having an impact on the development of Alzheimer's in the brain. Really? There was this hope that actually having GLP 1 and these receptors in the brain might end up having this really positive impact on dementia and specifically Alzheimer's, but they did this really big trial with people at early stage dementia, early stage Alzheimer's, I should say. And although some of the things sort of around it were improved, actually really there was no difference to placebo, which is kind of, I think people were kind of were pretty disappointed that this might be this panacea that actually, you know, cures sort of, sort of solves, all kinds of human

ills. That would have been huge. Imagine that if we, if we had medications for dementia, for cognitive decline. And then what comes after that? That's always been my question. Like, it used to be the heart. People can survive heart issues better now, but then you live long enough to hit dementia. After that, you live long enough for what?

What's the next thing? Yeah, I totally agree. I totally agree. And I think that actually, I mean, this thing that I've mentioned a couple of times in this program about how scientists are taking an existing protein or existing peptide, and then they're redesigning it, and they're like adding a bit here and adding a bit there. There's this explosion of research in this type of biology in a really, really,

really, really exciting way. Accelerated bluntly by the amazing use of AI, very domain-specific, very focused, but a sort of AI-assisted way to understand how these molecules and proteins interact with one another. What does the AI do here? There's one in particular, which is called Alpha-Four. fold. All of the stuff that I'm describing, all of the things about proteins, when you get down to that level, it's all about the physical structure of these chains of amino acids. That these long, long, long ribbons of amino acids that fold in this predefined way. But getting from what the ribbon was doing, the kind of chain of molecules, to what the folded pattern was, was incredibly difficult. The first person who managed to work out the folded pattern of a protein won a Nobel Prize, right?

You could, you know, even very recently, an entire PhD would be like, can you work out the folding of this one protein? And then this Demisisaribis, a friend of mine, who's the founder of Deep Mind, him and his colleagues, particularly John Jumper, they won a Nobel Prize for this. They created an AI with the sole focus of working at how to go from the ribbon of amino acids to a folded protein and then essentially folded all the proteins that humans know about and then released it. it for free to the entire world. Which proteins has artificial intelligence discovered for us? Because the Hilo Monster, that discovery

was prior to artificial intelligence. So it's not that artificial intelligence has necessarily discovered proteins, but it has given us this mechanistic understanding and ability to predict what the proteins are going to look like, how they're going to interact with molecules that might be

from drugs or parts of the body, that has just completely shortened in this unbelievable way the work process that you need to go through when it comes to designing medicines, understanding diseases. I mean, this is like, for me, I think this whole thing about Alzheimer's

that we were talking about a moment ago, I don't know, if I was a betting woman, I would put money on the fact that we will come up with some miracle, what feels like a miracle to us now, that I think that there is going to be some miracle intervention for Alzheimer's within the next 10 years or so, purely because of how these AI techniques have just completely accelerated our ability to understand these domains. Right.

Also, my dad had Alzheimer's, right? So I'm on the list, okay? Yeah, my grandfather did too. Yeah. And it's been a big cause for the curiosity box, for the work I do there, is just brain health in general, whether it be cognitive decline or otherwise. Man, but like a lot of other innovations, it's one of those, like there's two doors. And you can use it to find these medicines.

You can also use it to find their antidotes, right? Okay, so we figured out a way to quell the desire, but we could also create desires that slip through. And you've got this arms race, which is the story of human technology. It absolutely is. And there's definitely some quite serious downsides to the potential of biological weapons, biological warfare, all kinds of potential things on the horizon. Well, sure. And these ups and downs were always there in the human story. But now we can get to them faster, which can be even greater or even worse. It's just accelerated. Absolutely. Lots more on the horizon, I think, with all of this stuff.

Yeah, that's my little tour, the history and wonder of GLP-1s and the little family. And the little family we created. Yeah, I love that. But I found this fascinating because I actually had not learned any of this. It was about time that I understood this phenomenon and what's driving it. All right, well, good stuff. As ever, if you would like to send us your questions, your ideas, anything you like, you can email us, the rest of science at goahunger.com.

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