Transcript: Is obesity a choice?

Prof. Giles Yeo

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Hello. My name is Giles. Yo. And I'm a professor of molecular metabolism here at the University of Cambridge. Welcome to my Garden talk is obesity a choice. That is the question. So, so my name is Giles and I'm a geneticist and I think being a geneticist is a perfectly upstanding thing to do. My mother in law still speaks to me. So that that's a good thing. But when people ask me what I study and I say body weight on which one end of the spectrum says obesity. Immediately I become the bad person and I become the bad person because I'm perceived as giving fat people overweight people.

People living with obesity terms I do not use in any pejorative fashion whatsoever. An excuse which philosophically to me has always been an interesting take because if I was studying the genetics of dementia, the genetics of cancer, the genetics of arthritis, would I suddenly be giving those people suffering from those conditions and excuse No right. I hope not. I'd be trying to understand biology, trying to work out mechanism. God forbid I might be trying to help somebody. But yet when we talk about obesity, when we talk about obesity, it suddenly becomes a choice.

It suddenly becomes a bad behavior. Let me open with the story. This is a true story. So, I work at the Cambridge biomedical campus addenbrooke's hospital and we have one of these places where they big famous chains that sell sandwiches and things. And so I was there one day with all the rest of the hospital foraging for my lunch and in front of me there was a shall we say a plus size lady, she was in mufti so she could have been a nurse, she could have been a doctor um looking foraging for her lunch and she had in her hand what would anyone would have thought to be a healthy lunch? She had a yogurt and she had a salad and if the cash tills had been right there she would have paid and she would have walked out and chalk one up for the healthy lunch.

But as you know when you go to these places you have to get in line and this is lunchtime. So the line kind of like an Ikea Disneyland type line, it snakes around the place by the wall of chocolate. These walls exist everywhere. And so this is rush hour shall we say during lunch time. So it probably took us 90 seconds two minutes maybe to clear the line. Now I was standing right behind this lady not minding my own business and so she would come up and she would then right in front of me she picked up a chocolate bar, she looked at it, she put it back down, okay And then she did it again, she now a bag of candy, whatever it was, she did this and every time she put it down internally, I'm not crazy, I went, whoa and she did this 10 times, I'm not exaggerating, she did this 10 times and 10 times she put the food back down she made it to the till and a guard drop.

She got oh I've made it past the wall of chocolate and stood there at the till. The pimply boy. Okay. And suddenly he went two for one cookies. And these are the kind of cookies that first of all the size of my face. You know when you go to at the airport and you like to buy a book and they try and sell you a candy bar the size of an ipad. It's that kind of situation. Four cookies 99 P. She cracked and she bought them. Okay. She probably walked out With an additional 800 calories worth of cookies.

She clearly had not intended to buy. She did not intend to buy. Okay. But she ended up buying it. So here's the question. Who do we blame for this scenario? Okay. I mean do we blame the lady? I hope not. But do we blame the lady right? Is it her choice? Do we blame the supermarket for putting up the wall of chocolate or do we blame the government for not making the supermarket not put up the wall of chocolate. Now I'm not here to give you the answer of what is actually quite a complex question but rather to illustrate the food environment which we are living in.

I think. I think you'll agree this is a situation is not only lunch you can go and get and get diesel, you can go to the pharmacy to get paracetamol and before you pay for your fuel or your chocolate or your pencil. You know you you are accosted you assaulted, almost assaulted by chocolate by candies in front of them. So is this a choice? You know, should people have more willpower? And this is pretty much what I study when faced with food in front of you is their willpower. So we've all seen these scales of justice.

This energy balance type type type of equation, Okay. Where you know, body weight is all about eating an amount of energy expended and it's true. It has to be surely of course our body weight is going to be a function of physics. Which is what it is right? Eat less and move more and you'll lose weight. And that's because it's true. That's because it's physics. But that is the how and this is the interesting point. The how you get to the body weight. You are has to be a function of physics. It has to be but where the biological variation lies, where the complexity lies, where the interest lies, lies in the why why do people behave so very differently around food? So for example, why do some people respond to stress by eating and other people respond to stress by not eating.

It's exactly the same hormone. It's cortisol. How come some people love food. I love food whereas other people appear to use food as fuel, how come some other people appear to take more food to get full up. These are not imagined behaviors. These are behaviors which have huge biological enhance genetic component and that is what I want to study. So where is the evidence from that? There is a genetic basis to body weight. Well, like most human traits, these have come from the study of twins. Okay, so briefly appreciate, so that we're on the same page, you have identical twins and you have non identical twins.

So identical twins are, for all intents and purposes, genetic clones of each other. So they share 100% of their genes, their DNA, whereas non identical twins are going to share as much genetic material as you would with your own siblings or for that matter your parents. 50%. So, if you study enough twins, then you can ask the question about the role that genes play versus the role that the environment plays. Alright, so this is what let me give you an example. So just a couple of examples. So, if I had hair, my hair will be black and I'm going to argue that hair color is very powerfully biologically influenced, with very little environmental impact and no dyeing your hair does not count.

I'm talking about your natural hair color. Let's look at another human trait freckles, particularly in an environment like this. All right. So in terms of freckles. Now, clearly whether or not you have freckles is going to be powerfully genetically influenced as well. But whether or not they appear, how many appear even between identical twins will depend on whether or not you like to stand in the sun. Do I like to wear t shirts? So, that is an example of a powerfully genetically influenced trait with an equally powerful environmental influence.

So, if you do that, maths, okay, and actually look and look at it, then we now understand from these twins that we now understand that the heritability, the percentage of a trait that's down to your genes versus down to the environment. The heritability. Body weight is actually at around 70% amongst identical twins. It's certainly not zero, but it's not 100% either. Okay, so just to give you some perspective, height, which no one here is going to argue that has a genetic influence, has a heritability of around 85%.

So, we know that the heritability of body weight approaches that of height. So, I guess the question is the natural question to ask is, well, what are some of these jeans, what are these jeans doing? So, I mean, we now know of over 1000 genes. 1000 genes. That's right. That that influences our body weight. I'll just give you some examples. Just a couple of examples. I don't want to bore you silly. So, your brain, for example, needs to know two pieces of information in order to influence your food intake, It needs to know number one how much fat you have because how much fat you have is how long you'd last in the wild without any food.

So if your sources of food stopped today, how long would you live for? So it's pretty important piece of information to hold in your head remembering that we never had enough food. We have too much food now as of 30 years ago, but in the past this was not a problem. So how much fat you have? The second piece of information your brain needs to know is what you are currently eating and what you have just eaten. So these are going to be short term signals and they're going to come from your gut, from your stomach and from your gut.

So every mouthful of food you chew as it goes down the esophagus, stomach, small intestines and out the other side your guts release hormones that tend to make you feel full. So these are all hormones, the fat hormones, the gut hormones they circulate in the blood and your brain senses these long term and short term signals and then influences your next interaction with a refrigerator. With the supermarket or with a with a menu. Okay. And some of these genes influence the sensitivity of these, of these sensing pathways, therefore making you eat more.

So for example, imagine if I roughly speaking and probably carrying around 20 kg of fat on me, roughly speaking. Okay, but imagine if because of a slight decrease in sensitivity, my brain only sends us 18 kg. So it's thinking 18, 18, I thought I had 20 it drives you to eat more to get to 20 but I already have 20 kg of fat. And so I end up larger than someone else. So those are these are actually some of the genes that are involved. So I want to give you a few more examples in the fat sensing pathway because just to give you an idea that we walking amongst you.

Okay, everywhere there are people whose body weight are influenced powerfully by their genes. And I want to argue there is actually very little choice involved involved at all. So keeping with the fat sensing pathway. So the fat sensing pathway is called the Leptin milan, a cotton pathway. And I'll give you some examples. So Leptin starting with Leptin is the hormone produced from fat and it circulates in the blood to reflect how much fat you have. And so what happens if you don't have Leptin? Well, if you don't have leptin then your brain cannot sense how much fat you have.

And we know this because we we, my boss and my current head of department Stephen Bradley has identified Children with no leptin genetically have no leptin. And so there, I mean the first child that they identified was this four year old boy who weighs 32 kg. Okay so for some perspective I'm 75 kg. So this is we're looking at a sorry 42 kg. A three year old boy who's 42 kg. So this is a three year old boy who is two thirds who is two thirds of my body weight. So this is not some level of just small chubbiness.

Playstation. A bit too much, a bit too much cola okay, there's something wrong and he in essence has a brain who thinks he's starving because the brain cannot sense how much fat you have. Thinking oh my God I have no fat and no fat. So what do you do when you're starving? You drive yourself to eat, you eat and you eat you'll eat anything that is not poisonous, You eat frozen food, you eat raw food because you're starving to death literally and you eat. And so this is in spite of the fact that this child is so heavy has this really Veronis appetite that that really gets them eating a lot.

So that's one example of the leptin milana courting pathway. But leptin circulates in the blood and signals to the brain and within the brain it hits a set of neurons called the P. O. M. C. Or palm. See neurons now we and others have found Children with mutations in pomc and their severely obese like the Children with no leptin. We have even created mouse models but I thought you'd be interested to know about Labradors. That's right. I said Labradors so Labradors are the most popular pet dog in north America and in the U.

K. Okay. And we use them to sell toilet paper in this country. As you know, the anthrax puppy, other toilet paper is available. And this work was led by a veterinary surgeon colleague of mine, Eleanor raffin. Okay. And the thing about Labradors is not only do they have a wonderful temperament as a lovely family pet, they're also very very food motivated those of, you know who own Labradors? No, you have to keep your compost bin shut. Otherwise the labrador be in with a shot and eat anything that moves.

And Eleanor was always very interested to find out why the Labradors were quite so food motivated to cut a long story short. A percentage of Labradors have a deletion in this gene pomc making them, you know more food motivated and making them more susceptible to obesity. But not all Labradors have it. So about 20 to 25% of Labradors will carry mutations in pomc making them more susceptible to obesity. But the interesting thing is 95% of Labradors are really, really food motivated. And so Eleanor is at the moment throwing the genetic book at that to try and understand why that might be why that might be the case, but that's not the end of the pomc labrador story, because not only are Labradors wonderful family pets, they're also tremendously trainable, Very, very trainable.

In fact, they're so trainable, they're primarily used as guide dogs. Guide dogs for the blind in north America and in the UK. Now guide dogs are like the navy seals of the dog world because they're trained within an inch of their life because they're about to be given a human being to look after for the rest of their life. And they're trained using Pavlovian techniques with food. And the training is really quite, really quite strict that the pyramid is very steep, loads of failure and the failed puppies become pets.

Nothing happens the pets. But then you get the oh, you have the few. Sorry about that. Because then when you actually get to the top, you have the few, the proud, the guide dogs. And what is interesting with guide dogs who have been selected with food is that while 25% of pet Labradors have this deletion in pomc, 80% of Labradors, 80% of successfully trained Labradors for guide dogs have this deletion in pomc. So, here's the concept, imagine if I'm, I'm the guide dog and he is visually impaired Mr smith and I'm taking home? I'm taking him home.

Imagine if a chicken ran across the road. Okay, what are the chances of having chicken for dinner, is it 50 50 is it 80 20 it doesn't matter because the guide dog is trained that if it brings mr smith home safely, it will have a 100% chance of having dinner. So we started by looking at food motivation. Okay. But then because of the selection pressure that these dogs have been put under, Okay, suddenly moved into train ability. So when you go home and look at your Labradors and you see that big googly eyes and said look, Fido, Fido loves me.

Fido doesn't love you. Fido was hungry, almost terrible, terrible thing to say. So what happens with policy policy then signals to a molecule called M. C. Four are the milano coating for receptor. And this, to my mind is the most interesting of this, of this leptin milana court in fat sensing pathway, why do I think it's most interesting because it's the most common cause of severe obesity, not super common. So we've gone and we've looked at a birth cohort. So these are not in a disease cohort, the general population and now know that about 0.

3% 0.3% of the general population carries mutations within the M. C. Four receptor, causing them to be larger. So just for for perspective, if you extrapolate what 40.3% is to the UK population, that's 200,000 people. Okay, if you look at somewhere larger like the United States, then that's more than a million people carrying mutations in the atlantic and four receptor? And what do they look like? So just take it at an age point, say 18 the inflection point between childhood and adulthood. If you carry one copy of a mutated M.

C. Four, you are on average 18 kg heavier. That's £40. Okay, that is nearly five B. M. I points to 20 to 25 25 to 30. And of that 18 kg of weight that you that you know, you would carry 15 kg of which are going to be fat, 200,000 people, Ladies and gentlemen, that is actually around there who have who are so much larger because of a mutation in one gene that that's actually out there. And the moment you begin to think about it and look about because 200,000 people are wandering around, they're not necessarily showing up at hospitals and things, they're just larger.

Okay then you think that's quite that's relatively common. Okay. Is this true in other creatures? Then you begin to look around and you realize that that's true as well. If you look for example, within agriculture, Okay, livestock breeding and in particular, for example for pigs. And so when when you are actually breeding animals for livestock, what are you interested in? You're interested in growth rate, you're interested in fat to lean mass ratio, that kind of thing. And if you look for example at certain pigs which are bred for bacon bread, they're not genetically modified their just bred for their speed of growth.

They also carry mutations in the M. C. Four are in the Milani quoting for receptor. Unless you think that this is some weird mammalian thing. Mm hmm. Let me introduce you to the blind mexican fish. Ladies and gentlemen, that's right. So first of all, why are they blind? And why are they mexican All will be revealed. So that giant asteroid that killed the dinosaurs 65 million years ago hit what is now the Gulf of Mexico. Okay, and when it hit the Gulf of Mexico and and hit the bottom, all these cracks formed in the bottom of the sea bed which got filled in with water and became underwater caves.

And some fish got stuck in these underwater caves. Hence their mexican. Why are they blind? Because underwater caves don't have a lot of light. Don't have any light at all actually. And so over millions of years the eyes of these fish evolved the way and so therefore they become blind. Mexican cave fish. Why am I telling you any of this? I'm telling you this because the other thing which is lacking in an underwater cave is food. So any fish that is remotely blase about a piece of plankton that kind of be floating by? Okay, that didn't snap it up immediately became an ex fish.

All blind. Mexican cave fish that are alive today have mutations in the milan nickel and four receptor in the M. C. Four R. Let me ask you this question folks, where is the choice? I'm talking about a fish that was caught at the wrong place at the wrong time or the right place at the right time. I'm talking about Labradors. I'm talking about 200,000 people living here in the UK and more than a million americans and more throughout the world who really don't have a choice. Their feeding behavior has been hardwired in response to some adaptive pressure.

That has been that has been there. Where is the choice? Okay so this is the fact sensing pathway. Another question however that has emerged because one of the big issues with obesity is because people think it's a choice is there's a lot of weight stigma. There is there is okay, you know kids are cruel. So they call the other kids names, adults are cruel. You know you can't turn on the tv that have someone fat shaming someone else. And this has actually given rise to a movement called the body positivity movement.

Okay. And they say that there is health at every size and I understand the movement. I understand why it's actually come to be but I just want to put it out there that they've probably got it slightly wrong. They've swung too much the other way in terms of trying to look for health at every size because I don't think they can be health at every size. So let's rewind just just for a few minutes. What I mean by this, I guess the question to ask is first of all, what does obesity mean? And don't say B.

M. I above 30 because that's just a number. I think obesity is carrying too much fat so that it begins to influence your health. Okay, let's accept that argument. And this is the interesting thing about obesity. People mistake what happens when you gain weight and lose weight. They think that you gain fat cells and you lose fat cells, which is not true. Your fat cells actually like balloons, they get bigger when you gain weight, they get smaller when you lose weight. Okay, they get balloons. Now the safest place to store fat is in your fat because they are professional fat storing organ where you become ill, where you get issues is when the fat is not in the fact that goes into your muscle goes into your liver, then you end up with diseases like type two diabetes.

The interesting thing is that different people can store different amounts of fat safely okay, before they become ill. So famously, South asian people, indians, Bangladeshis pakistanis, East asian people, people that look like me, we can't get that large before we increase our risk for disease. Okay, compared to white people compared to Polynesians famously who can get far larger before they increase their risk of disease and this is down to safe fat carrying capacity. Not only how big can your fat cells expand, but also where you actually put your fat.

So while they're skinny people with type two diabetes, you can have larger people that are metabolically healthy. But there is no health at every size. They can be health at many sizes in the population because you get skinny people ill and larger people not ill but if you pass your own personal safe factoring capacity, you will become ill. There is no way around around that. And there is just a big difference between blaming the person suffering from the problem and admitting that the problem is a mistake to begin with.

So um 11 thoughts Before I have some closing thoughts. The dessert to me. Have you ever given any thought to the dessert? To me, it does exist really seriously. So let's review imagine if you're out at a restaurant like a proper place, not like some fancy fancy Michelin star place. I guarantee you that by the time you reach the middle to the end of your main meal, you would have achieved your caloric requirements of the day, meaning that if you've burned 2000 calories for example, you would have already recouped to 2000 calories.

But yet when dessert comes, you eat it. Okay, this is the dessert tummy. We understand this phenomenon. We go through it all the time. The interesting question however, to ask is why is it specific for desserts. So for example, if you went to an all you can eat steak and chips place just as an example and you wait till you are, oh my God, I'm feeling ill and the waiter comes along and says more steak, more chips, more steak, more chips. You say no, I feel like I feel like puking, no thanks. But yet when the chocolate cake comes, you eat it, why is it specific for dessert? There is a reason for this and as parole ways evolution plays a role.

So 50,000 years ago, Serengeti, this is an antelope. Now imagine if it's taken me 2000 calories to take down that antelope 50,000 years ago. So what happens when I go back to the village? Well, I better eat at least 2000 calories because otherwise at some point I die. But if I only eat 2000 calories, then I don't buffer against the time that I don't get the antelope because there's no guarantee clearly that you're actually going to get the get the antelope. So a part of your brain called the hedonic region that makes eating feel nice, takes over to make sure you eat more than you need.

But how do you get past the mechanical difficulty of being stuffed with 2000 calories worth of venison? Okay, your brain begins to change the type of calorie that it craves. Okay, so that it begins to increase the caloric density of the foods that it that it begins to crave. So which means that for every given gram of food, there are more calories in it so that you can stuff into all the little nooks and crannies that are there. Okay, so what is high in caloric density, free sugars, which 50,000 years ago would have come from honey ripe fruit um and fat.

What are high in sugar and fat desserts? A dessert tummy is a holdover from the Serengeti to make sure that even when you were stuffed with 2000 calories with the venison, you were still able to continue eating and stuff in all the nooks and crannies that were actually there. And surprisingly, this phenomenon of the dessert tummy is also conserved across the animal kingdom. Now I understand that animals don't eat dessert, but let me give you the example. So the grizzly bear, pacific, northwest hitting the salmon run.

Okay, so now look, the bear is not having a muscat and title citron. I appreciate that. Why is the bear hitting the salmon run? The bears hitting, hitting the salmon run to put on as much weight as possible to survive hibernation, correct. That's that's the reason it's there. So when it first starts, the salmon run, it eats the whole salmon, the whole damn salmon all the way down to the bone. But as it gets fuller and fuller and fatter and fatter. It only eats the skin of the salmon and the fat underneath the skin of the salmon? Because that is the place of the highest caloric density on the salmon? So this phenomenon of increasing the caloric density of foods that your brain craves as you get fuller is a conserved phenomenon.

The dessert tummy is something that is conserved. So I guess let's go back and revisit the question. So is obesity a choice? Well, first of all, am I giving anyone any excuse? Look, you've got to consider your genetic hand of cards. Sorry, you've got to consider your jeans like a hand of cards in poker or any kind of card game. You can have good hands, you can have bad hands. And the only people, you can blame your parents because that that's where you got them from. But you can win with a bad hand of poker, It is just more difficult.

Okay, let me give you another example. I will never, ever run as fast as you say, boat. Ever. Okay. And it's because of my jeans and I'm sticking to it. But it doesn't mean that I won't run faster if I train harder. So people misunderstand what genetics tells us. They think that genetics determines who you are, gives you a point in space and time. Whereas it doesn't clearly genetics offers a bracket of possibilities. It must because they're your jeans, why am I bald? Because of my jeans? Why do I look chinese because of my genes? But within that bracket of possibilities.

You can move up and you can move down. Are you rich? Are you poor commute? You have kids? All of these questions that are there, you can actually move move up and down. That's all we're trying to do. Geneticists are not trying to give anyone any excuse. We're trying to understand the bracket of possibilities and where you can move up and down within that bracket of possibilities. So is it a choice? Okay, so in fact the question is, are we all sinners? Because one of the interesting things about feeding behavior, it's so entrenched in us that it's linked with sin, The seven deadly sins, fourth century religious construct.

Three of them have have to do potentially without feeding behavior. Gluttony sloth, greed. Okay. All of these things are there that you know that apparently have to do with actually with, with, with food. It's been it's been closely linked. So is it a sin? What's a sin? A sin is something you do, even though, you know it's bad. Niven chomping on a piece of pizza. Alright. And you're thinking, well look, you're choosing to chomp on a pizza. Pizza of course is a choice folks, you do not gain or lose weight overnight.

You just, you just don't okay, Whatever, whatever you might think Your body weight is going to be a function of thousands of different feeding events over a number of years previously. Okay, now imagine it because of your genetic hand of cards. You are a little bit less likely to say no, 5% less likely to say no. So one out of every 20 times you may say hang it I'm gonna have to slice of pizza. Okay. 5% over thousands of feeding events is hundreds of thousands of calories different. Which is why some people are small, medium and large in the environment we live in over the period of time that food intake begins to change your body weight.

It isn't a choice to use the casino terms the house will always win. So it doesn't change the physics Mr Smith coming into the to see the doctor with type two diabetes about to go blind about to lose her feet will still need to lose weight. Doctors need to understand that. But until we as society do not until we a society understand that for some people it is more difficult than others that for some people they're fighting their biology. That people with obesity are not bad, not morally bereft. We will never be able to put together a sustainable um strategy in order to solve the obesity crisis.

So listen, my name is Charles. Oh it's been a pleasure to speak to you and I'm hoping that we can do some Q. And A. Thank you so much Giles. It's quite a hot topic right now. I think some of the stuff you've been talking about and that has explained things very clearly. I've definitely learned a lot as have the people in the comments. And I have to say before we get to the questions, there's so much love for you throughout the talk. People definitely want to see you back for another Garden talk.

So hopefully we'll have you back very soon. I want to go straight over to mark our, who says, why can't we artificially create leptin to fool the brain? Oh, that's a good question. Thank you for that. Mark. The problem with leptin as as far as far as the hormones go, is because leptin, is there not to tell your brain you have too much fat, which is what you would do when you actually put leptin in. But when it's there, you have too little fat. So these kids without any leptin at all, if we give them leptin, they do lose weight, but that's because their brain thinks they're starving.

So, so the leptin, is there not to say you have too much fat, but to say that you have enough fat. So as long as you have a little bit of leptin there, it doesn't matter how much more you add, it won't actually change your food intake. So the leptin pathway of the fat sensing is not the pathway to target. Not leptin anyway, but actually you can fool your brain into feeling fuller by using gut hormones and in fact some of the drugs that have just been the new cli drugs that have just been approved by the FDA and here by the the drug committees here in the UK are weaponized gut hormones.

So we know of 20 different gut hormones, 18 of which make you feel fuller. And so one of one called GLP one is the has been weaponized so that when you actually injected, it goes to the brain making you feel fuller, You feel fuller, you eat less, you eat less, you lose weight. And some of the trials of the newest class of these drugs show that you can lose up to 15 to 20% of your body weight over two years with once weekly injections. So leptin is not the panacea, but maybe weaponized gut hormones are Okay, interesting.

Let's get into another question from laura, She says, do you believe that methods of measurement? Like am I inaccurate and perhaps even dangerous because she's read they're far too generic to create a kind of one size fits all health goal. So that's a that's an excellent question, laura, So you'll be unsurprised to know that I'm going to provide a bit of a nuanced answer. So B. M. I just very quickly, B. M. I is your height is your weight in kilograms divided by your height in meters squared away of controlling your height for your weight.

Um the problem with B. M. I is that it just takes those two pieces of information, height and weight, it doesn't tell you how much fat you have, whether you're arnold Schwarzenegger or whether or not you're joe blow joe Schmo on the, on the couch. It doesn't take into account your safe fat carrying capacity. I was telling you about the fact that east asian people myself, my B. M. My risk of getting diab, It's going to be lower than someone white. It doesn't take that into account either. So, for a personal to be used as a the only way to decide whether or not you get treatment and on a personal 1-1 basis, it is terrible.

However, why is it still in use? Because it's very easy to measure its free to measure you need height and you need wait. Um And on average, the higher your B. M. I, the more fat you carry not all of us, a rugby player. So that's the first thing. And on average, the higher the more fat you carry, the more likely you are to be unhealthy on average. So what it is useful for is population level tracking. So the government or or or a town or local council want to understand that if I introduce this particular intervention or this tax, will it influence the health of my population then B.

M. I. Is still the cheapest and easiest way to track whether or not the shifts it's just a terrible thing to use on a 1 to 1 basis. Great. And anne wants to know how does hyper thyroid and low metabolism affect weight loss? Oh my goodness! So, so I think, okay, your thyroid is one of the key controllers of metabolism in your body. So you can have a non functioning thyroid is relatively rare. It's not going to be it's not going to be the reason for the vast majority of body weight changes. But if you are hyper thyroid, meaning that your thyroid gland which sits around here and produces thyroid, if you're producing too much thyroid, what happens is you become hyperactive because it increases your metabolism, you get slightly bulgy eyes, increases your metabolism and you are you tend to be skinny.

Whereas if you actually have hypothyroidism, so your thyroid actually produces less thyroid, then your metabolism slows down and you do end up actually getting quite large and you slow down entirely because of hypothyroidism, but that's relatively rare. But thyroid, your thyroid hormone is a key mediator in normal circumstances for metabolism within the body. Cool, We've had so many good questions, haven't we won from Cindy. She says, what about menopausal weight gain. See all the good questions, all the good questions coming this evening.

Um listen, so let's start with men, I know men don't go into menopause. In fact, in fact, men are very simple creatures were born. We think about food, we think about the other thing and that's it, then we die. Um so women, however, I want to argue are four different, almost entirely different species through their life stages, depending on the stages you choose. Okay, you have a woman pre baby, adult women, a woman pre baby, the pregnant woman who, for all intents and purposes is carrying a parasite.

I'm a father, incidentally, who carries a parasite in them and got to keep it alive. And so the hormonal changes a woman post baby. And we know of women who are like rubber bands, they have babies and snap back into shape. Whereas a lot of women don't lose the baby weight and a woman post menopause. And what marks these four stages of a woman's life marked hormonal changes. And so not when you're younger, you're cycling, some of you may find that. Well, hang on a second, how through my, through my various estrous cycle, I have changes in appetite.

I have changes in a way that I behave. And what happens when you're pregnant? What How come some people can't lose the baby weight now in post menopausal women, what is interesting is that clearly what happens in menopause is that your estrogen levels go away. Okay, this is the so called female hormone and people think that women don't have testosterone, but that's not true women just carry a lot less of it than men, but when a woman is menopausal and estrogen levels go away. It changes the ratio between testosterone and estrogen.

You become a more male, like male, like hormonal profile it's called androgen ization. And what you see in a lot of postmenopausal women is they begin to change shape. They begin to put fat around their waist, which is where men typically put fat as opposed to around their bum. Okay. And so if you see a typical shape, terrible thing to say, but I'm just stating a biological fact, that is what happens. That's why post menopausal women begin to change their body shape because of a shift in their estrogen too.

To testosterone ratio. Really interesting. Okay, thanks Charles. Good one. Next. Actually for Maria, she wants to know can genes influence behavior? So you've been talking quite a lot about physical hunger. What about psychological hunger? Which seems to be the root of compulsive eating? Absolute. So I only gave you the examples from physical hunger because that just happens to be the pathways I specialize in. But I mentioned that there are more than 1000 genes. And some of these genes not only influence the physical hunger that we that we know of hunger or physical fullness, which is different incidentally, but also other genes that influence the reward pathways.

I talk to you about the about the Serengeti grizzly bear scenario, the reward pathways right? Where feeding clearly makes us feel nice. Okay, that's why we keep doing it. It's like sex, why we keep doing it feels nice. Why do we keep eating? It makes it it makes us feel good. But imagine it's because of genes within your feel nice area are slightly less sensitive so that you have to eat more food to give the bang for buck in the brain. And that are going to be what some people carry. Other people are going to be more susceptible to advertisement because they happen to like yellow Ems or something like that.

You know? And I'm being slightly facetious but absolutely you can actually have physical physiological or psychological responses to changes to these changes in your genes. Cool. Giles, I'm learning so much already. We've only been hearing from you from kind of 30 40 minutes and I've got so much more information in my head. We've had loads like I said, loads of love in the comments. And though we've got questions, I have got a comment for you. I just wondered whether you wanted to respond to it from Diane who says I'm not asking a question, but genes do not determine how much you away, it just affects sensitivity to weight gain.

I've got a full set of obesity genes according to 23 me, but I'm not overweight. What would your response be to that? So look, as I said, your genes do not determine. So a couple of things, a couple of things. Let me, let me give you an example. I've taken the 23 test for example to show you that genes are not everything. Even though I study genes okay. And we know that the bottom 20% socioeconomically within the UK Okay are twice as likely to end up with obesity as the top 20% socioeconomically in this country.

Now there is no genetic difference between rich and poor nun accident of birth, yet there's twice 40% versus 20%. And a big part of the reason is going to be access to food. The access to the right foods where they live, Do they have time energy to actually cook fresh food for their kids? All of these, all of these questions that are actually going to be there. It still doesn't change the fact that you're going to have richer people who are going to find it more difficult to say no. And poorer people who are going to find it difficult to say no.

It just so happens that depends on the environment that you actually that you're actually exposed to. You respond slightly differently. So if you are living like me, I live in a comfortable place in the suburbs and I suddenly I'm hungry. I don't have a takeaway close by and I have to go to my fridge. Oh, maybe I have carrots and and I that whereas if you live in a food desert right in the middle of downtown area, you know, and a your cash poor b you don't have time and see you're living, you're living above the kebab shop.

And suddenly you get a hunger pangs, You're gonna end up eating that. And so you're absolutely right. I think your genes do not determine who you are. Your environment. Its interaction with the environment as well. Amazing. We've had so many great comments and questions. So I'm sorry, we're not going to be able to get to them all because there are loads in front of me. Probably two more we can squeeze in. So one from Maria, who says if you come across any genetic evidence that some people's metabolic processes are different or less efficient than others.

So that is an excellent. That is an excellent question. Because everything I've talked about this the last 40 minutes for 30, 40 minutes has been about food intake. What about metabolism? And the genes are there to be found. We know that because just from from studies down done done in twins, that people have different metabolic rates, but yet we haven't found the genes yet. Why? Two reasons. I think the first is what I call measurement error. And the second is effect size. Let me explain each individually.

So measurement error. When you measure food intake, Okay, you are, it's easy. A slice of pizza is a physical entity. You can weigh it and therefore you can measure it when you measure metabolism, you can do it in one of two ways. You can measure it in heat being given off or in changes in ratio to the carbon dioxide oxygen that you breathe out. It's possible within a sealed room, but very difficult at scale. You can't go to sainsbury's and do it to someone there is just too difficult. So there's a measurement error.

It's difficult to get enough clean data. So that's the first thing. The second thing is effect size. Now, what do I mean by this now? If I were motivated, that's like an average size candy bar chocolate bar that you can get from the shops is 240 calories. If I were motivated, I could finish that chocolate bar in less than 90 seconds and I often am. But however quickly or slowly I eat the chocolate bar. I will always need to run on the treadmill for 20-30 minutes. We, as living creatures have been designed to eat our calories far quicker than we can burn them because that's what's kept us alive.

So, while your metabolism will play a role in your weight and your efficiency and some people definitely are more metabolically active than others. The food intake element will over it will will always have a far larger effect, brilliant Giles. I am very sad because we only have time for one more question. So, we're going to take this one from Vlad, which is a really good one. How does the sleep influence the body weight? So, it's over? It does play a role. It's just slightly overstated. So why does it play a role? It plays a role because we are diurnal creatures, which means that we typically are awake when the sun is up and sleep when the sun is down.

Certainly on the Serengeti. And so what happens then is you are therefore more active and more metabolically active. Your metabolism is higher during the daytime so that you can look for food and avoid becoming food and lower at night. So you can save energy and actually and actually go to sleep so clearly if you have disturbed sleep or if you work shifts and so therefore, or jet lag all of the above and you're therefore awake at weird times rather than during the day and asleep at night. Then your body's metabolic um systems go a little bit awry.

And so on. A epidemiological level. At a population level we know, for example, people who work shifts have a slightly higher risk of Type two diabetes and obesity, but it's overstated. It's not the cause of the obesity epidemic, but it definitely does play a role. Thank you for that flat. A great one to end on as that. So, we've got time for today. Thank you to all of you who asked questions including those that we didn't have time to get to. Although we are going to make sure we forward those all on to Giles and Giles.

It's been an absolute pleasure to have you in The Garden. Thanks so much for joining us today. A pleasure and thank you to all of our members for joining this talk. It's been a truly fascinating one that I hope has given you plenty of food for thought, and we hope to see you at your next Garden gathering, but until then stay curious.

Getting Into Your Genes Collection

DNA is the code of life. And it’s the DNA in your genes that determines the traits that make you who and what you are.  Our genes are unique but with so many scientific advancements, what have we learnt about ourselves from our genes?

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