- Welcome to Huberman Lab Essentials, where we revisit past episodes for the most potent and actionable science-based tools for mental health, physical health, and performance. I'm Andrew Huberman, and I'm a professor of neurobiology and ophthalmology at Stanford School of Medicine. This podcast is separate from my teaching and research roles at Stanford.

It is, however, part of my desire and effort to bring zero cost to consumer information about science and science-related tools to the general public. Today, we're going to talk about how hormones impact feeding and hunger, as well as satiety, the feeling that you don't want to eat or that you've eaten enough.

Now, it's important to understand that hormones don't work alone in this context. Today, I'm going to describe some hormones that have powerful effects on whether or not you want to eat more or less or stop eating altogether. But they don't do that on their own. They do that in cooperation with the nervous system.

The first thing that you need to know about the nervous system side, the neural control over feeding and hunger, is that there's an area of your brain called the hypothalamus. Now, the hypothalamus contains lots of different kinds of neurons doing lots of different kinds of things. There's a particular area of the hypothalamus called the ventromedial hypothalamus.

And it's one that researchers have been interested for a long time now in terms of its relationship to hunger and feeding. And the reason is it creates these paradoxical effects. What do I mean by that? What they found was that sometimes lesioning or disrupting the neurons in the ventromedial hypothalamus would make animals or people hyperphagic.

They would want to eat like crazy. And other lesions in other individuals or animals would make them anorexic. It would make them not want to eat at all. It would make food aversive. So that means that the ventromedial hypothalamus is definitely an interesting control station for hunger and feeding and satiety, but it doesn't really tell you what's going on at a deeper level.

In fact, it's a little bit confusing or paradoxical. It turns out that there are multiple populations of neurons in there. Some are promoting feeding and some are promoting not feeding or not eating. Now, the other neural component of all this that you need to know about actually has to do with your mouth.

So there's an area of your cortex. So that's a little bit further up in your brain called the insular cortex. And it processes a lot of different kinds of information, mostly information about what's going on inside you, so-called interoception. The insular cortex has neurons that get input from your mouth, from the touch receptors in your mouth.

An insular cortex has powerful control over whether or not you are enjoying what you're eating, whether or not you want to avoid what you're eating, whether or not you've had enough or whether or not you want to continue eating more. And that has to do, believe it or not, with the touch or sensation of eating.

But the key point right now is to know that you've got these two brain areas, the ventromedial hypothalamus, that's involved in hunger and lack of hunger. And you have this insular cortex that gets input from your mouth and cares about chewing and the consistency of foods and all sorts of interesting things that are just very tactile.

And I think most people think about the touch receptors on, excuse me, the taste receptors on the tongue, but we often don't think about the touch or tactile essence of food. Now, let's get back to the ventromedial hypothalamus. Sometimes it makes animals or people want to eat more, sometimes less.

So what's going on there? There's a classic experiment that was done in which researchers took two rats and so-called parabiose to them to each other. What that meant is that they did a little surgery and they linked their blood supply so that they were forever physically linked to one another and could exchange factors in the blood, but their brains were separate, their mouths were separate, and they essentially did everything separately except that they were linked to one another.

So they had to walk together and go to the same places in order to do it. This parabiosis experiment revealed something really important. When they lesioned the ventromedial hypothalamus in one of the rats that was connected to the other rat, that rat got very, very fat. It's just really obese.

The other one, however, got very thin. It actually lost weight. So what does this tell us? This tells us that there's something in the blood that's being exchanged between the two animals because it was their blood supply that was linked. And that tells us that there's hormone or endocrine signals that are involved in the desire to eat and hunger and appetite.

And so next, we're going to talk about what those endocrine signals are. And then I'm going to immediately point to some entry points that you can use, and you can use these even if you're not parabiosed to anything, and that can allow you to time your meal frequency and predict when you're going to be hungry or not.

So let's talk about the endocrine factors that regulate feeding, hunger, and satiety. One of the really exciting things to emerge in the science of feeding and appetite in the last 20 years is the discovery of another brain area, not just the ventromedial hypothalamus, but it's an area of the brain called the arcuate nucleus.

And the arcuate nucleus has some really fascinating sets of neurons that release even more incredible molecules and chemicals into the blood. And these chemicals act as accelerators on feeding and appetite or breaks. So first of all, there are a set of neurons in this arcuate nucleus. It's the pro-opio-melanocortin system.

Now, the POMC neurons make something called alpha-MSH, melanocyte-stimulating hormone, alpha-melanocyte-stimulating hormone. MSH reduces appetite, and it's a powerful molecule. All right, so just put that on the shelf. MSH reduces appetite. Now, there's another population of neurons in the arcuate nucleus called the AGRP neurons. The AGRP neurons stimulate eating.

The activity in these AGRP neurons goes way up when animals or people haven't eaten for a while. And the activity of MSH, the release of MSH, goes up when we've eaten. Next, let's talk about a hormone peptide that activates hunger. And this is a really interesting one because it relates to when you get hungry in addition to the fact that you get hungry at all.

And it's called ghrelin. It's spelled G-H-R-E-L-I-N. Ghrelin is released actually from the GI tract. And its main role is to increase your desire to eat. And it does that through a variety of mechanisms. Part of that is to stimulate some of the brain areas, the actual neurons that make you want to eat.

In addition, it creates food anticipatory signals within your nervous system. So you start thinking about the things that you happen to like to eat at that particular time of day. This is fascinating. Ghrelin is sort of like a clock, a hormonal clock, that makes you want to eat at particular times.

Now, the signal for ghrelin is reduced glucose levels in the blood. If it drops too low, ghrelin is secreted from your gut. It activates neurons in your brain at various locations. We all know about the famous Pavlovian experiments of Pavlov's dogs. You know, they start salivating to the bell after the bell was presented with food.

You remove the food and then just the bell can stimulate the salivation. We become Pavlovian at times. But rarely is it ever discussed what the neural pathways for that are. And it turns out that these hormones that are secreted from the gut can stimulate the neurons to create a sensation and a desire for certain foods at certain times of day.

You've done this experiment. If you are somebody who eats breakfast at more or less the same time each day, let's say 8 a.m., your ghrelin secretion will start to match when you typically eat. And it's able to override the low levels of glucose in your bloodstream because the ghrelin system also gets input from a clock in your liver that is linked to the clock in your hypothalamus in your brain.

And what this means is if you eat at regular mealtimes, you will start to get hungry a few minutes before those mealtimes. If you've ever wondered why your stomach kind of starts to growl because it's a particular time of day, you're like, "Oh, I must want to eat." Well, that's ghrelin.

So ghrelin is secreted as a kind of food anticipatory signal to get you motivated to go eat at regular times. But what that means is that if you suddenly go from eating on a very regular schedule to skipping a meal or pushing your meal timing out or shifting at all, you're going to have ghrelin in your system.

And that ghrelin is going to stimulate the desire to eat by acting at the level of your brain. So ghrelin stimulates the AGRP neurons, which makes you want to eat. Regularity of eating equals regularity of ghrelin secretion equals regularity of activity of these AGRP neurons, meaning you will be hungry at very regular intervals.

So if MSH inhibits feeding, makes us want to eat less, and ghrelin makes us want to eat more, there's another hormone called CCK, cholecystokinin, that is potent in reducing our levels of hunger. Now, CCK is in the GI tract. It's released from the GI tract. And its release is governed by two things.

One is a subset of very specialized neurons that detect what's in the gut, the specific contents of the gut. And by certain elements of the mucosa, the mucous lining of the gut and the gut microbiome. So what's really interesting is that CCK is stimulated by fatty acids, amino acids, and particular amino acids that we'll talk about, as well as by sugar.

So which fatty acids in the gut stimulate the release of CCK? Omega-3 fatty acids and conjugated linoleic acid, CLA, either from food or from supplements, stimulate the release of CCK, which then reduces or at least blunts appetite. The other thing that stimulates CCK that I mentioned are amino acids.

So when we eat, we have the ability to break down different macronutrients, you know, carbohydrates, fats, or proteins into sugars and glucose that then we can convert to ATP and all that stuff from the Krebs cycle from high school. We're not going to go into that today. That's for a future episode.

Amino acids both can be used as energy through a process called gluconeogenesis of converting proteins into energy, or those amino acids can be broken down and then rebuilt into things like repairing muscle tissue, as well as other forms of cellular repair. They're involved in all sorts of things related to protein synthesis.

What does this mean? If we eat the proper amino acids at the proper levels, if we ingest omega-3s and CLAs, conjugated linoleic acids, at the proper levels, or get them from supplements, there's a blunting of appetite. Appetite is kept clamped and we don't become hyperphagic. We don't overeat. We tend to eat within healthy or normal ranges.

So this is very important because most people don't understand that when we're eating, we are basically fat foraging and amino acid foraging. In other words, even if it's not conscious, we are eating until we trigger the activation of CCK. Now, there are other reasons why we shut down eating too.

The volume of food in our gut can be large and we can feel very distended. That's the physical reason, obviously. But at a subconscious level, the gut is informing the brain via CCK and other mechanisms when we've ingested enough of what we need. So as you can see, feeding is an interplay between brain and body, and it's some of the micronutrients and even the breakdown of particular nutrients that's putting the accelerator or the brake on the feeding process.

You are essentially trying to eat to get these nutrients, and then a signal can be deployed up to your brain that you're not really interested in eating that much more. There's one particular aspect of food that can powerfully impact CCK, and I think most people, I'm guessing 99.9% of people out there are not aware of this.

And it has to do with highly processed foods. There's a lot of reasons why one would want to avoid highly processed foods. In fact, if you're interested in that topic and the history of whole foods transitioning to highly processed foods in this country, I highly recommend you listen to a YouTube video by Dr.

Robert Lustig. He's at University of California, San Francisco. It gives a beautiful description of the history of this and why the food industry started packing in additional sugars and salts and turning foods into commodities. It's really fascinating. It has no conspiracy theory. It's just all scientific facts. It's really a wonderful lecture.

It has millions of views, should be very easy to find. There's another reason to avoid highly processed foods, however. And that has to do with what's called emulsifiers. Now, many of you are familiar with emulsifiers, even though you don't know it. When you put detergent in the laundry, that contains emulsifiers.

The goal of that detergent is to bring together fatty molecules with water molecules and be able to dissociate them and break them up to get the stains out of clothes and things of that sort. There are a lot of emulsifiers put into processed foods. And those emulsifiers allow certain chemical reactions to occur that extends the shelf life of those foods.

Why are emulsifiers bad? Okay, there are a lot of reasons why they're bad, but the reason why they're bad for the mechanisms that we've been talking about today is that when you ingest those foods, you're bringing those emulsifiers into your gut. And those emulsifiers strip away the mucosal lining of the gut.

And they actually cause the neurons that innervate the gut, that extend those little processes we call axons into the gut to retract deeper into the gut. And as a consequence, you're ingesting a bunch of food and the signals like CCK never get deployed. The signals that actually shut down hunger are never actually triggered.

And so as a consequence, you want to eat far more of these highly processed foods. In addition, if you then go from eating a highly processed food to non-highly processed foods, you're not able to measure the amounts of amino acids, sugars, and fatty acids in those foods as accurately.

You've actually done structural damage at a micro level, but structural level damage, excuse me, to the mucosal lining of the gut. Now this can all be repaired if you stay away from highly processed foods for some period of time. But the negative effects of these emulsifiers are quite real.

So to make it really clean and simple, emulsifiers from highly processed foods are limiting your gut's ability to detect what's in the foods you eat, and therefore to deploy the satiety signals, the signals that shut down hunger. In addition to that, there's a parallel mechanism at play that I talked about in a previous episode, but I'll remind you again that you have neurons in your gut that are sensing sugar and are sending a subconscious signal up to the brain via the vagus nerve.

And those neurons trigger the release of dopamine, which makes you crave more of that food. So now you've got parallel signals making you want to eat more sugar, making you unaware of how much sugar you've eaten, and that are disrupting the inputs to the nervous system that signal to the rest of your brain and body that you've obtained enough fatty acids and you've obtained enough amino acids.

So these highly processed foods are really terrible. And I'm not out here to say, never enjoy a processed food of any kind. I'd be a hypocrite 'cause I do eat processed foods from time to time. Although the ones that I tend to eat, I try and make of the healthier variety, but eating whole foods has tremendous value and eating highly processed food has tremendous negative impact on the gut and on the gut brain axis.

The bottom line is that highly processed foods are just bad for you. They increase weight gain. They disrupt the lining of your gut in a way that disrupts things like CCK and proper satiety signals. So there's just so many reasons why these highly processed foods are terrible. And they can explain a lot of the ill health effects that we've seen in the last 50 years, not just in the United States, but all over the world.

The enormous increase in diabetes, juvenile diabetes. It's just remarkable how far down the path of bad we've gone and it's clear, it's almost a smoking gun what the cause of this is. If you'd like to learn more about that, please refer to the Lustig lecture. He also spells out why non-processed foods is far more economical in terms of just at the level of the household or individual, as well as at the societal level.

Really interesting stuff. I highly recommend you check it out. So now let's move on to some other hormones that regulate hunger and satiety. In particular, insulin. Now you've probably heard of insulin before. Insulin is the thing that's lacking in type one diabetics. That's why they have to inject insulin whenever they eat.

The reason they have to do that is because when they eat, their foods are broken down into glucose. And in order to shuttle glucose to the appropriate tissues in the body and also to keep glucose levels in check, you need insulin. So the simplest way to think about insulin and glucose is that when you eat, that food is broken down into sugars.

That's true whether or not it's fats or it's sugars or eventually if it's proteins, they're oxidized into fuels as we say. Your blood sugar needs to be kept in a particular range. Hypoglycemic means too low. Hyperglycemic means too high. And what they called euglycemic, E-U glycemic is the healthy range.

Now, what those healthy ranges are, in general, the healthy range, the euglycemic range is about 70 to 100 nanograms per deciliter. Why is it important that glucose be kept at a particular level? Once you understand that, keeping glucose in check starts to have a rationale behind it and the ways to do that start to make a lot more sense.

So the reason is if glucose levels get too high because of the way that our cells in particular neurons interact with glucose, high levels of glucose can damage neurons. It can actually kill them. You can start getting what are called peripheral, excuse me, neuropathies. One of the symptoms of some forms of diabetes is that people start losing the sensation of touch in their fingers or their hands or their feet, and they can start going blind.

There's diabetic retinopathies. So it's very important that insulin manage your glucose levels. Now, there's also type two diabetes where there's insulin secreted from the pancreas, but people are insulin insensitive. There's a disruption in the receptors and insulin insensitivity isn't quite the same as having no insulin at all, but it parallels some of the same mechanisms.

Now, type one diabetes is often picked up because someone has a sudden weight loss because they're not processing blood sugar the same way they were before. Type two diabetes is often, although not always, associated with being overweight and with obesity. Both of them are challenging conditions. Type two diabetes almost always can be managed by managing one's weight.

And of course, there are prescription drugs and supplements that can help manage those. We're going to talk about all of that. But for most people that don't have diabetes, the important thing is to manage glucose, to keep it in that euglycemic range. And there are a number of different ways to do that.

Some of them are behavioral, some of them are diet-based, and some of them are based on supplements or prescription drugs. So let's talk about those now. So if you eat, and in particular, if you eat carbohydrates, blood glucose goes up. If you eat fats, blood glucose goes up to a far less degree.

And if you eat proteins, depending on the protein, it'll eventually be broken down for fuel or assembled into amino acid chains for protein synthesis and repair of other tissues and bodily functions. But glucose goes up and then is kept in range. When you are hungry, you secrete a different hormone, and that's called glucagon.

And glucagon's main role is to pull stores of energy out of the liver and the muscles. And once those are depleted, you'll eventually tap into body fat. So the two kind of push and pull systems that we're going to think about now to keep this simple is that you have the insulin system managing glucose, and you've got the glucagon system pulling energy out of your liver and muscles for immediate fuel.

And eventually you'll pull fuel out of body fat if you've been active for a very long time and all your glycogen stores are depleted or close to depleted. So what does this all mean? Let's say you had a meal and that meal consisted of rice, a carbohydrate, some meat or fish, let's say a piece of salmon, and some vegetable, some fibrous vegetable like asparagus or cabbage or something like that.

If you were to eat all of that at once, you take a bite of one, a bite of the other, you mix it up, then you will experience an increase in insulin and increase in blood glucose that's moderately fast. It's going to increase pretty quickly. What's remarkable is that the order that you consume each macronutrient has a pretty profound influence on the rate of insulin and glucose secretion into the blood and how quickly those levels rise.

If you were to eat the fibrous thing first, so a lot of chewing, but not a big rise in blood glucose, that will actually blunt the release of glucose until you eat the fish and the rice. But believe it or not, it will actually blunt the glucose increase that the rice would cause.

Now, I'm not talking about neurotically eating each macronutrient separately in sequence. I'm just trying to give you a picture of what's happening ordinarily. So what does this all mean? It means that if you want a steep increase in glucose, you are very, very hungry, then you should eat the carbohydrate-laden food first, or you should eat a bunch of macronutrients combined.

So that would be like the hamburger or the sandwich, the bread, whatever's in that sandwich all together. Usually that's protein and vegetables as well. If you want to have a kind of more modest increase in glucose, or you want to blunt the increase in glucose, then have at least some of the fibrous thing first, and then the protein, and then the carbohydrate.

You will notice that your blood glucose will rise more steadily, and that you'll achieve satiety earlier in the meal. Basically what you're trying to avoid are steep increases in blood sugar. And the order that you eat foods has an enormous impact on that. The other thing that has an enormous impact on how long and shallow or how steep that curve of glucose is, depends on whether or not you recently were moving, are moving, or start moving after you eat.

So it turns out that your blood glucose levels can be modulated very, very powerfully by movement. If you did any kind of intense exercise, or even just walking, or jogging, or cycling, anything before you eat, your blood glucose levels will be dampened somewhat. And even just moving after a meal, even just a calm, easy walk, can really adjust the ways in which blood sugar regulated for the better.

The other thing I'd like to address for a moment is this notion of stable blood sugar versus labile blood sugar, or unstable blood sugar. Some people just have stable blood sugar. They can go long periods of time without eating and feel fine. Other people get really shaky, really jittery, and/or when they do eat, they feel really keyed up.

Sometimes they'll even sweat. But whether or not your blood sugar is all over the place, or whether or not it's stable, can be impacted by a number of things. One of those things is exercise. So these days, there's a lot of interest in what they call zone two cardio, which is that kind of steady state cardio where you can just nasal breathe, even at pretty high output, where you could maybe have a conversation.

Zone two cardio that lasts anywhere from 30 minutes to an hour, or sometimes more for you endurance athletes, can create positive effects on blood sugar regulation such that you, people can sit down and enjoy whatever it is, the hot fudge sundae, or whatever the high sugar content food is.

And blood glucose management is so good, your insulin sensitivity is so high, which is a good thing, that you can manage that blood glucose to the point where it doesn't really make you shaky, it doesn't disrupt you. Basically, doing zone two cardio for 30 to 60 minutes, three to four times a week, makes your blood sugar really stable.

And that's an attractive thing for a variety of reasons. On the flip side, high intensity interval training, or resistance training, aka weight training, are very good at stimulating the various molecules that promote repackaging of glycogen. So sprints, heavy weight lifting, circuit type weight lifting, provided there's some reasonable degree of resistance, those are going to trigger all sorts of mechanisms that are going to encourage the body to shuttle glucose back into glycogen, convert into glycogen into muscle tissue, restock the liver, et cetera.

And I should mention that one of the advantages of high intensity interval training or weightlifting of various kinds is that it also causes long standing increases in basal metabolic rate. Now I'd like to turn to prescription drugs that regulate the hormone systems controlling feeding and satiety. There's a prescription drug, Metformin, which was developed as a treatment for diabetes.

And it works potently to reduce blood glucose. It has dramatic effects in lowering blood glucose. Metformin involves changes to mitochondrial action in the liver. That's its main way of depleting or reducing blood glucose. And it does so through the so-called AMPK pathway, and it increases insulin sensitivity overall. Metformin is a powerful drug.

In fact, I'm surprised that so many people have sought it out given that most of the people that I'm aware of that sought it out are not diabetic. I do want to mention, because I'm sure some of you out there are curious about the ketogenic diet. I'm going to do an entire episode about ketosis and the brain and the body, but the ketogenic diet has been shown in 22 studies to have a notable decrease on blood glucose.

And that is not surprising because the essence of the ketogenic diet is that you're consuming very little or zero of the foods that promote big spikes in insulin and glucose. If you consume enough protein, some of that protein can be converted into glucose, of course, through gluconeogenesis. But the ketogenic diet has very strong support for its role in regulating blood sugar, which is glucose.

But the specific effects of the ketogenic diet, and one particular effect that I'll address later, but I'll mention now, which is the ability of the ketogenic diet to adjust thyroid hormone levels in ways that make it such that if you return to eating carbohydrates after being in ketosis for too long, you don't manage thyroid and carbohydrates as well.

That has been shown as well. So we're going to dive deep into ketosis in a future episode. So for you ketonistas out there, don't worry. I certainly have nothing against ketogenic diet. I actually don't have anything for or against any particular nutrition plan. I know what works for me, at least at this stage of my life, and I'll update it if I need to.

I'm simply trying to get you as much information as I possibly can so that you can navigate through that landscape in a way that's in keeping with your particular goals. So now you understand a lot about blood sugar and how it's managed and the ways that you can manage it better depending on your particular needs.

This is also a good opportunity for us to look back at some of the medical literature, because it really points to just how far we've come in terms of understanding these important mechanisms. And it points us in the direction of some actionable protocols. So diabetes, which is these huge increases in blood glucose, because there's no insulin, was known about as early as 1500 BC, which is just incredible.

And the way physicians then understood that certain people had high blood glucose without actually knowing what blood glucose was, is that they would take the urine of particular patients, and they'd find that ants preferably moved toward and consumed the urine of certain patients and not others. And they understood that there was something in that urine that was correlated with a sudden weight loss and some of the other probably very unfortunate health symptoms that these people were experiencing.

So they knew that there was something in blood and urine. Now, this business of measuring blood sugar from the urine has been something that lasted way beyond these early stages of, you know, 1500 BC. Turns out that as late as 1674, physicians at Oxford University were figuring out who had pathologically high levels of blood glucose by analyzing their urine.

And again, they were measuring the sweetness of their urine, but, and this is medical fact, they would do this by taking urine samples from different patients and tasting them. And they developed an intuitive sense of what excessively sweet urine was relative to the other urines that they had tasted.

So for those of you that are in the medical profession or those of you that are seeking out the medical profession, do understand this is not done anymore. And you can also just reflect on how far we've come in terms of the medical profession itself, in our ability to measure things from the blood and measure things from urine without having to ask ants which urine is sweeter or ask oneself which urine is sweeter.

So indeed we are making progress as a species. Before we close out today, I want to talk about one more tool that many of you will probably find useful. I certainly have. I'm a big consumer of caffeine, although I don't consume a ton of it, I consume it very consistently.

So I'm big on consuming mate, which is a strong caffeinated tea. And I generally do that early in the day. Although I do delay about two hours after I wake up for reasons I've talked about in previous episode to maintain that nice arc of alertness and focus. Mate, also called yerba mate, is an interesting compound because unlike coffee, it has been shown to increase something called glucagon-like peptide, GLP-1, and increase leptin levels.

Now, we didn't talk a lot about glucagon today. Glucagon is really elevated in the fasting state. I mentioned that it's sort of the opposite of insulin in kind of rough terms. That's one way to think about it. But GLP-1 or glucagon-like peptide one is increased by ingesting mate and it acts as a pretty nice appetite suppressant.

Now, I'm not trying to suppress my appetite. I like to eat, as I mentioned before, but it works really well to stimulate the brain and to give you a level of alertness and to do a lot of the things that coffee does. It also contains electrolytes. So we, meaning our neurons and our brain, run on a variety of factors, electrical activity and chemical transmission, et cetera, but they require adequate levels of sodium, potassium, and magnesium.

Actually, if you were to learn the biology or the physiology of the action potential, the firing of a neuron, something we teach every first-year neuroscience student, and I'd be happy to teach you if you're interested, you'll hear about sodium rushing into cells and potassium entering and leaving cells in order to allow neurons to communicate.

Electrolytes are critically important for the function of the nervous system. And many things that act as diuretics that promote excretion of water, like caffeine, can also take electrolytes out along with in particular sodium. And sometimes the lightheadedness or the brain fog that people experience isn't just because electrolytes are low, but because they're kind of out of balance.

So I like mate because it has electrolytes, it has caffeine. It stimulates the release of this glucagon-like peptide, GLP-1, and it's been a big help to me in extending that early morning fasting window out to about noon or so when I eat my first meal. It also just tastes really good.

And the fact that glucagon-like peptide one is enriched or is released more when you drink mate, and the fact that GLP-1 can regulate blood sugar in ways that keep your blood sugar in that we called euglycemic, not too high, not too low mode, is one reason why ingesting mate is attractive to me.

So Yerba Mate, GLP-1 can manage in healthy ways, leptin levels, glucose levels, and glucagon levels in ways that if it serves you, you might want to try. So once again, we covered an enormous amount of material focused on how hormones regulate feeding, hunger, and when one feels they don't need to eat, so-called satiety, that you've had enough.

We've just focused today mainly on things like ghrelin, on things like melanocyte-simulating hormone, incredible, powerful hormone that can suppress appetite, on things like cholecystokinin that comes from the gut and can suppress appetite, on things like food emulsifiers, on the fact that when you're eating, you are amino acid seeking, even though you might not realize it, that you are also seeking out particular fatty acids.

So I've tried to give you a number of actionable tools. Again, always do what's best for your health and do that in company with a healthcare professional. I'm not a physician, I don't prescribe anything. I'm a professor, I profess a lot of things. If you know anyone that's interested in this topic or you think that someone could benefit from it, please suggest the podcast to them as well, and most of all, thank you for your interest in science.

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