Essentials: Healthy Eating & Eating Disorders - Anorexia, Bulimia, Binging

Andrew Huberman: 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. Today, we are going to talk all about healthy and disordered eating. And indeed, we are going to talk about clinical eating disorders, such as anorexia, bulimia, and binge eating disorder, as well as some other related eating disorders. However, before we get into this material, I want to emphasize that today's discussion will include what it is to have a healthy relationship with food. We're going to talk about metabolism. We're going to talk about how eating frequency and what one eats influences things like appetite and satiety, as well as whether or not we have a healthy psychological relationship to food and our body weight and so-called body composition, the ratio of muscle to fat to bone, et cetera. So as we march into this conversation, I'd like to share with you some interesting and what I believe are important findings in the realm of nutrition and human behavior.

Andrew Huberman: I know these days, many people are excited about or curious about so-called intermittent fasting. Intermittent fasting is, as the name implies, simply restricting one's feeding behavior, eating, to a particular phase of the 24-hour or so-called circadian cycle. Other forms of intermittent fasting involve not eating for extended periods of time, for entire days, or some people will extend to two days or three days. Typically, and hopefully, they will drink water during those times, sometimes referred to as water fasting, which means that they are ingesting fluids, and hopefully they are ingesting electrolytes such as salt, potassium, and magnesium as well, because while one can survive for some period of time without ingesting calories, it is extremely important to continue to ingest plenty of fluids and electrolytes. And the reason for that is that the neurons of your brain and body that control your movements, your thoughts, clarity of thinking in general, et cetera, is critically dependent on the presence of adequate levels of sodium, potassium, and magnesium, the electrolytes, and that's because neurons can only be electrically active by way of movement of particular ions, which include things like sodium, potassium, and magnesium. So without those, you can't think, you can't function, and it actually can be quite dangerous.

Andrew Huberman: So why all the excitement about intermittent fasting? Well, a lot of the excitement relates to work that was done by a former colleague of mine down at the Salk Institute for Biological Studies in San Diego named Sachin Panda. Sachin's lab identified some very important and impactful health benefits of restricting one's feeding window to particular times within the 24-hour cycle, or even to having extended fasts that go for a day or two days, or maybe even three days. What they saw was an improvement in liver enzymes, an improvement in insulin sensitivity, which is something that is good. It means that you can utilize the calories and the blood sugar that you happen to have. Being insulin insensitive is not good and is actually a form of diabetes. What Sachin's lab and subsequently other labs showed was that restricting one's feeding window to anywhere from four to eight or even 12 hours during each 24-hour cycle was beneficial in mice. And some studies in humans have also shown that it can be beneficial for various health parameters.

Andrew Huberman: However, the excitement about intermittent fasting seems to be related to the foundational truth about metabolism and weight loss and weight maintenance and weight gain, which is that regardless of whether or not you intermittent fast or whether or not you eat small meals all day long, or you eat one meal in the evening and snack up until then, It really doesn't matter in the sense that the calories that you ingest from whatever source are going to be filtered through the calories that you burn by way of exercise, basal metabolic rate, which is just the calories that you happen to burn, just being alive and thinking and breathing and your heart beating, et cetera. And the reason why many people prefer intermittent fasting to other forms of, let's just call it what it is, diet or nutritional framework is that many people find it easier to not eat than to limit their portion size. And here I'm not talking necessarily about eating disorders, I'm talking about the general population.

Andrew Huberman: So why are we talking about this? And in particular, why are we talking about this during an episode that includes a discussion about eating disorders? The reason is nobody, not the government, no nutritionists, no individual, no matter how knowledgeable they are about food and nutrition and food intake, can define the best plan for eating for any one individual. I'm going to repeat that. Nobody knows what truly healthy eating is. We only know the measurements we can take. Liver enzymes, blood lipid profiles, body weight, athletic performance, mental performance, whether or not you're cranky all day, whether or not you're feeling relaxed. Nobody knows how to define these. These have strong cultural and familial and socio-societal influence. So if you hang out with people that intermittent fast all day, that will seem normal. If you spend time with people that have never heard of intermittent fasting, intermittent fasting is going to seem very abnormal.

Andrew Huberman: Now, we are going to talk about eating disorders that really fall into the category of clinically diagnosable eating disorders for which there's actually serious health hazards and even the serious risk of death. There are clear criteria in the psychiatric and psychological communities to define things like anorexia, bulimia, binge eating disorder, all of which we will talk about. But as we have that discussion, I want to emphasize that self-diagnosis can be both a terrific, but also a very precarious thing. There's always a temptation as one learns about the symptomology of a given disorder, doesn't really matter what the disorder is, to ask the question, well, do I have that? Does so-and-so that I know have that? It's tempting to diagnose them and or ourselves as either having or not having a particular disorder. However, diagnoses really need to be carried out by people who are trained in that particular field and that have deep expertise in recognizing the symptomology, including some of the more subtle symptomology of eating disorders. So if any of the symptoms resonate with you by way of you thinking that you have this particular disorder or someone that you know has a disorder, I would take that seriously, but I would take that information to a qualified healthcare professional that could diagnose or rule out any of these possible disorders.

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Andrew Huberman: So what is an eating disorder? Well, we have to take a step back and confess to the fact that every society, every culture, every family, and every individual has a different relationship to food. Eating disorders, however, have particular criteria that allow us to define them and to think about different modes of treatment as it relates to the particular symptoms, in particular, the psychological and biological symptoms of those disorders. What are the major eating disorders? Anorexia nervosa most commonly referred to as anorexia is perhaps the most prevalent and the most dangerous of all eating disorders in fact anorexia is the most dangerous psychiatric disorder of all even more than depression the probability of death for untreated anorexia is very high and And sadly, the prevalence of anorexia is very high. If you look it up online or you talk to a qualified professional is essentially a failure to eat enough to maintain a healthy weight. You can see all sorts of very troubling symptoms of somebody who's been anorexic for some period of time, a general loss of muscle mass because they're ingesting fewer calories than they burn. They will have a low heart rate. This is the body and brain's attempt to lower energy output. They will have low blood pressure. They will sometimes have symptoms like fainting, loss of bone density, osteoporosis, loss of periods in girls and women, and all sorts of disrupted gut and immune functions. So there are just tons of terrible symptoms of anorexia that really place the anorexic into a very risky state, which is why mortality from anorexia gone untreated is extremely high.

Andrew Huberman: Now, one of the misconceptions about anorexia is that it stems from an overemphasis on perfectionism or that because of all the images in social media and in advertising of extremely thin and fit or muscular people that individuals are looking at themselves and comparing themselves to those images and thinking that they don't match up and developing anorexia. That turns out to not be the case. If you look at the prevalence or the rates of anorexia in the last 10 years or 20 years and when you compare that to when anorexia was first identified, which was in the 1600s and perhaps even earlier, what you find is that rates of anorexia are not going up. Classically defined anorexia has existed at essentially the same prevalence for the last 100, 200, 300, and 400 years, which is incredible and really speaks to the likelihood that there's a strong biological contribution to what we call anorexia nervosa. Anorexia nervosa is extremely common. It's anywhere from one to 2% of women. And the typical onset is in adolescence, close to puberty, but it can show up later in life as well. In fact, the identification and diagnosis of anorexia tends to be in the early twenties. But if you look back at the history of those individuals, there were typically signs of anorexia that stem back into their early teens, or maybe even before that. Now, of course, men can be anorexic as well, but anorexia nervosa does seem to occur at 10 times the rate in women and young girls than it does in men and young boys.

Andrew Huberman: So what is hunger and what is satiety? Satiety, of course, being sated or feeling like we've had enough food. I want to remind people of the basic mechanisms by which the brain and body communicate. The body is communicating two types of information to the brain on a regular basis, but in particular around feeding. And those two types of information are mechanical information and chemical information. When your stomach is full, it sends signals to your brain that are purely based on this mechanical fullness. Has nothing to do with nutrients that says, I'm full. And therefore don't be as hungry. Don't motivate to find or ingest food. Whereas when our gut is empty, Even if we have plenty of nutrients or plenty of body fat stores, we tend to focus on food a bit more. So volume and mechanical influences have a profound effect on how we think and what we consider doing or not doing. Likewise, chemical effects. When we ingest food, our blood glucose goes up. That information is signaled to the brain via neuronal pathways and hormonal pathways. And in particular, there are neurons within our gut that signal to areas of our brainstem that are involved in satiety in our sense of having enough that there's food in our system. So that's chemical information. So how are hunger and feeding and satiety regulated? By way of mechanical and chemical signaling. You have, I have, we all have neurons in our hypothalamus that trigger eating and neurons that trigger cessation or stopping of eating. Your hypothalamus at the base of your forebrain sits more or less above the roof of your mouth. The hypothalamus contains lots of different kinds of neurons, including neurons that stimulate sexual activity and desire, regulate your body temperature and control appetite and ceasing of eating an appetite. There are two types of neurons within a particular area of your hypothalamus that are relevant here. There are the so-called POMC neurons, okay? pro-opioid melanocortin neurons that tend to act as more of a break on appetite by way of another hormone called melanocyte stimulating hormone. And you have a class of neurons called the AGRP neurons. The AGRP neurons are the ones that stimulate feeding and they create a sort of anxiety or excitement about food. If you eliminate or kill these neurons, which has been done in experimental mouse models in the laboratory, but also there are humans that have lesions or neurotoxic effects on these AGRP neurons. And what you find is that they don't want to eat. They have no appetite for food whatsoever. Whereas if you stimulate these AGRP neurons, or in humans that have, say a small tumor near these AGRP neurons, they become hyperphagic. They will eat to the point of bursting.

Andrew Huberman: Now, there are signals coming back from the body to inform the brain about presence of different levels of nutrients. And that generally comes from three sources. First of all is body fat. The more body fat we have, the more we secrete a hormone called leptin, L-E-P-T-I-N, leptin from body fat. Leptin goes to the brain and suppresses appetite. Not incidentally, leptin signaling is disrupted in people that have bulimia and obesity and certain forms of binge eating disorder. The body fat is doing something else really interesting that relates to anorexia. When there's sufficient levels of body fat and leptin circulating in the blood, and that leptin signal gets to the brain, the hypothalamus and the pituitary gland register that signal, and in a completely subconscious way, trigger the deployment of eggs in females and the production of sperm in males. So when body fat stores are very low, the reason why periods shut off or sperm production is reduced or even shut off is because there's not enough leptin getting to the hypothalamus and to the pituitary, and they shut off the signals, the hormones, things like gonadotropin releasing hormone, luteinizing hormone, follicle stimulating hormone that travel to the ovary or to the testes and cause the ovary or testes to ovulate or to produce more sperm. So you've got two categories of neurons, one that acts as an accelerator, the AGRP neuron saying eat, eat, and gets you excited to eat. And then you have a category of neurons, the PMOC neurons that are suppressing hunger. They're acting like a break. And the body is informing the brain all the time about the status of the body and whether or not it needs more food.

Andrew Huberman: So you might ask, why is it that people who are overweight and have a lot of body fat, why they would continue to eat a lot? It seems like that just shouldn't happen. From an evolutionary standpoint, it makes sense that we should eat as often as we can, as much as we can, and as fast as we can. There are circuits in the brain reward eating often, eating fast and cramming as much food into you as possible. Because from a purely evolutionary standpoint, food was scarce and seeking food was dangerous, whether or not it was from animal sources or not. And it's always been competitive. Every animal, including humans, has a hardwired circuit that we were born with that pays attention to how much food is available, how much we are getting now and how much we are likely to get in the future. And without going down the rabbit hole of arcuate nucleus biology, in two sentences, you have a hypothalamic area called the arcuate nucleus. It's actually the area that houses these PMOC neurons and these other types of neurons that regulate hunger and satiety. And these neurons in the arcuate nucleus start getting active when we see food and think about food. And they drive hunger in a way that's responsive to what the food looks like, what it smells like, but also our prior history of interactions with that food. And it takes into account social context.

Andrew Huberman: What's the pathway? How does this work? Well, you can frame all of behavior, good decision-making and bad decision-making in a pretty simple box diagram model. We have knowledge of what we should do in one box. Okay, we should eat that, we shouldn't eat that, we should wait for dinner, we shouldn't wait for dinner. And then we have what we actually do in another box. In between those two boxes are two intervening forces. And those intervening forces are critically important. Those intervening forces are homeostatic processes that regulate the balance of different systems in your body, hot and cold, awake or asleep, dopamine and the desire to pursue things, serotonin and the desire to just relax and chill. So homeostatic processes and reward systems. And as we now move into discussion about anorexia and bulimia specifically, what you'll see is that anorexia and bulimia are not a breaking of the mindset of what one should do or shouldn't do. It's a disruption of these homeostatic and reward processes such that decision-making is completely disrupted and in many cases is not available to the anorexic or bulimic.

Andrew Huberman: I don't want to be abstract here. What I'm saying is that the person who starves themselves to the point where they might die, and in some cases, sadly do die, they can know perfectly well that their behavior is leading to bad outcomes and possibly even death. And yet they are not able to intervene unless they get particular clinical help because the homeostatic processes, the signals from the body and brain that say you need food, those aren't registering in the same way that they are for other individuals. And just as a little teaser of where we're headed, anorexics have a sort of switch that's been flipped such that their decision-making is actually pretty darn good. It might even be better than yours in terms of evaluating food nutritional content, but their habits are disrupted. So they're not even consciously aware of the fact that they're making terrible, and in some cases, very dangerous food choices. It turns out habits and the way that we build and break and rebuild new habits is one of the most effective treatments for anorexia.

Andrew Huberman: I'd like to take a quick break and acknowledge our sponsor, AG1. AG1 is a vitamin mineral probiotic drink that also includes prebiotics and adaptogens. As somebody who's been involved in research science for almost three decades and in health and fitness for equally as long, I'm constantly looking for the best tools to improve my mental health, physical health, and performance. I discovered AG1 back in 2012, long before I ever had a podcast, and I've been taking it every day since. I find it improves all aspects of my health, my energy, my focus, and I simply feel much better when I take it. AG1 uses the highest quality ingredients in the right combinations, and they're constantly improving their formulas without increasing the cost. In fact, AG1 just launched their latest formula upgrade. This next-gen formula is based on exciting new research on the effects of probiotics on the gut microbiome, and it now includes several clinically studied probiotic strains shown to support both digestive health and immune system health as well as to improve bowel regularity and to reduce bloating. Whenever I asked if I could take just one supplement what that supplement would be I always say AG1. If you'd like to try AG1, you can go to drinkag1.com slash Huberman. For a limited time, AG1 is giving away a free one month supply of omega-3 fish oil, along with a bottle of vitamin D3 plus K2. As I've highlighted before on this podcast, omega-3 fish oil and vitamin D3 K2 have been shown to help with everything from mood and brain health to heart health to healthy hormone status and much more. Again, that's drinkag1.com slash Huberman to get a free one month supply of omega-3 fish oil plus a bottle of vitamin D3 plus K2 with your subscription.

Andrew Huberman: So what is an eating disorder? Well, we have to take a step back and confess to the fact that every society, every culture, every family, and every individual has a different relationship to food. Eating disorders, however, have particular criteria that allow us to define them and to think about different modes of treatment as it relates to the particular symptoms, in particular, the psychological and biological symptoms of those disorders. What are the major eating disorders? Anorexia nervosa most commonly referred to as anorexia is perhaps the most prevalent and the most dangerous of all eating disorders in fact anorexia is the most dangerous psychiatric disorder of all even more than depression the probability of death for untreated anorexia is very high and And sadly, the prevalence of anorexia is very high. If you look it up online or you talk to a qualified professional is essentially a failure to eat enough to maintain a healthy weight. You can see all sorts of very troubling symptoms of somebody who's been anorexic for some period of time, a general loss of muscle mass because they're ingesting fewer calories than they burn. They will have a low heart rate. This is the body and brain's attempt to lower energy output. They will have low blood pressure. They will sometimes have symptoms like fainting, loss of bone density, osteoporosis, loss of periods in girls and women, and all sorts of disrupted gut and immune functions. So there are just tons of terrible symptoms of anorexia that really place the anorexic into a very risky state, which is why mortality from anorexia gone untreated is extremely high.

Andrew Huberman: Now, one of the misconceptions about anorexia is that it stems from an overemphasis on perfectionism or that because of all the images in social media and in advertising of extremely thin and fit or muscular people that individuals are looking at themselves and comparing themselves to those images and thinking that they don't match up and developing anorexia. That turns out to not be the case. If you look at the prevalence or the rates of anorexia in the last 10 years or 20 years and when you compare that to when anorexia was first identified, which was in the 1600s and perhaps even earlier, what you find is that rates of anorexia are not going up. Classically defined anorexia has existed at essentially the same prevalence for the last 100, 200, 300, and 400 years, which is incredible and really speaks to the likelihood that there's a strong biological contribution to what we call anorexia nervosa. Anorexia nervosa is extremely common. It's anywhere from one to 2% of women. And the typical onset is in adolescence, close to puberty, but it can show up later in life as well. In fact, the identification and diagnosis of anorexia tends to be in the early twenties. But if you look back at the history of those individuals, there were typically signs of anorexia that stem back into their early teens, or maybe even before that. Now, of course, men can be anorexic as well, but anorexia nervosa does seem to occur at 10 times the rate in women and young girls than it does in men and young boys.

Andrew Huberman: So what is hunger and what is satiety? Satiety, of course, being sated or feeling like we've had enough food. I want to remind people of the basic mechanisms by which the brain and body communicate. The body is communicating two types of information to the brain on a regular basis, but in particular around feeding. And those two types of information are mechanical information and chemical information. When your stomach is full, it sends signals to your brain that are purely based on this mechanical fullness. Has nothing to do with nutrients that says, I'm full. And therefore don't be as hungry. Don't motivate to find or ingest food. Whereas when our gut is empty, Even if we have plenty of nutrients or plenty of body fat stores, we tend to focus on food a bit more. So volume and mechanical influences have a profound effect on how we think and what we consider doing or not doing. Likewise, chemical effects. When we ingest food, our blood glucose goes up. That information is signaled to the brain via neuronal pathways and hormonal pathways. And in particular, there are neurons within our gut that signal to areas of our brainstem that are involved in satiety in our sense of having enough that there's food in our system. So that's chemical information. So how are hunger and feeding and satiety regulated? By way of mechanical and chemical signaling. You have, I have, we all have neurons in our hypothalamus that trigger eating and neurons that trigger cessation or stopping of eating. Your hypothalamus at the base of your forebrain sits more or less above the roof of your mouth. The hypothalamus contains lots of different kinds of neurons, including neurons that stimulate sexual activity and desire, regulate your body temperature and control appetite and ceasing of eating an appetite. There are two types of neurons within a particular area of your hypothalamus that are relevant here. There are the so-called POMC neurons, okay? pro-opioid melanocortin neurons that tend to act as more of a break on appetite by way of another hormone called melanocyte stimulating hormone. And you have a class of neurons called the AGRP neurons. The AGRP neurons are the ones that stimulate feeding and they create a sort of anxiety or excitement about food. If you eliminate or kill these neurons, which has been done in experimental mouse models in the laboratory, but also there are humans that have lesions or neurotoxic effects on these AGRP neurons. And what you find is that they don't want to eat. They have no appetite for food whatsoever. Whereas if you stimulate these AGRP neurons, or in humans that have, say a small tumor near these AGRP neurons, they become hyperphagic. They will eat to the point of bursting.

Andrew Huberman: Now, there are signals coming back from the body to inform the brain about presence of different levels of nutrients. And that generally comes from three sources. First of all is body fat. The more body fat we have, the more we secrete a hormone called leptin, L-E-P-T-I-N, leptin from body fat. Leptin goes to the brain and suppresses appetite. Not incidentally, leptin signaling is disrupted in people that have bulimia and obesity and certain forms of binge eating disorder. The body fat is doing something else really interesting that relates to anorexia. When there's sufficient levels of body fat and leptin circulating in the blood, and that leptin signal gets to the brain, the hypothalamus and the pituitary gland register that signal, and in a completely subconscious way, trigger the deployment of eggs in females and the production of sperm in males. So when body fat stores are very low, the reason why periods shut off or sperm production is reduced or even shut off is because there's not enough leptin getting to the hypothalamus and to the pituitary, and they shut off the signals, the hormones, things like gonadotropin releasing hormone, luteinizing hormone, follicle stimulating hormone that travel to the ovary or to the testes and cause the ovary or testes to ovulate or to produce more sperm. So you've got two categories of neurons, one that acts as an accelerator, the AGRP neuron saying eat, eat, and gets you excited to eat. And then you have a category of neurons, the PMOC neurons that are suppressing hunger. They're acting like a break. And the body is informing the brain all the time about the status of the body and whether or not it needs more food.

Andrew Huberman: So you might ask, why is it that people who are overweight and have a lot of body fat, why they would continue to eat a lot? It seems like that just shouldn't happen. From an evolutionary standpoint, it makes sense that we should eat as often as we can, as much as we can, and as fast as we can. There are circuits in the brain reward eating often, eating fast and cramming as much food into you as possible. Because from a purely evolutionary standpoint, food was scarce and seeking food was dangerous, whether or not it was from animal sources or not. And it's always been competitive. Every animal, including humans, has a hardwired circuit that we were born with that pays attention to how much food is available, how much we are getting now and how much we are likely to get in the future. And without going down the rabbit hole of arcuate nucleus biology, in two sentences, you have a hypothalamic area called the arcuate nucleus. It's actually the area that houses these PMOC neurons and these other types of neurons that regulate hunger and satiety. And these neurons in the arcuate nucleus start getting active when we see food and think about food. And they drive hunger in a way that's responsive to what the food looks like, what it smells like, but also our prior history of interactions with that food. And it takes into account social context.

Andrew Huberman: What's the pathway? How does this work? Well, you can frame all of behavior, good decision-making and bad decision-making in a pretty simple box diagram model. We have knowledge of what we should do in one box. Okay, we should eat that, we shouldn't eat that, we should wait for dinner, we shouldn't wait for dinner. And then we have what we actually do in another box. In between those two boxes are two intervening forces. And those intervening forces are critically important. Those intervening forces are homeostatic processes that regulate the balance of different systems in your body, hot and cold, awake or asleep, dopamine and the desire to pursue things, serotonin and the desire to just relax and chill. So homeostatic processes and reward systems. And as we now move into discussion about anorexia and bulimia specifically, what you'll see is that anorexia and bulimia are not a breaking of the mindset of what one should do or shouldn't do. It's a disruption of these homeostatic and reward processes such that decision-making is completely disrupted and in many cases is not available to the anorexic or bulimic.

Andrew Huberman: I don't want to be abstract here. What I'm saying is that the person who starves themselves to the point where they might die, and in some cases, sadly do die, they can know perfectly well that their behavior is leading to bad outcomes and possibly even death. And yet they are not able to intervene unless they get particular clinical help because the homeostatic processes, the signals from the body and brain that say you need food, those aren't registering in the same way that they are for other individuals. And just as a little teaser of where we're headed, anorexics have a sort of switch that's been flipped such that their decision-making is actually pretty darn good. It might even be better than yours in terms of evaluating food nutritional content, but their habits are disrupted. So they're not even consciously aware of the fact that they're making terrible, and in some cases, very dangerous food choices. It turns out habits and the way that we build and break and rebuild new habits is one of the most effective treatments for anorexia.

Andrew Huberman: I'd like to take a quick break and acknowledge our sponsor, Function. Last year, I became a Function member after searching for the most comprehensive approach to lab testing. Function provides over 100 advanced lab tests that give you a key snapshot of your entire bodily health. This snapshot offers you with insights on your heart health, hormone health, immune functioning, nutrient levels, and much more. Function not only provides testing of over 100 biomarkers key to your physical and mental health, but it also analyzes these results and provides insights from top doctors who are expert in the relevant areas. For example, in one of my first tests with Function, I learned that I had elevated levels of mercury in my blood. Function not only helped me detect that, but offered insights into how best to reduce my mercury levels, which included limiting my tuna consumption. I've been eating a lot of tuna, while also making an effort to eat more leafy greens and supplementing with NAC and acetylcysteine, both of which can support glutathione production and detoxification. And I should say, by taking a second Function test, that approach worked. Comprehensive blood testing is vitally important. There's so many things related to your mental and physical health that can only be detected in a blood test. The problem is blood testing has always been very expensive and complicated. In contrast, I've been super impressed by Function's simplicity and at the level of cost. It is very affordable. As a consequence, I decided to join their scientific advisory board, and I'm thrilled that they're sponsoring the podcast. If you'd like to try Function, you can go to functionhealth.com slash Huberman. Function currently has a wait list of over 250,000 people, but they're offering early access to Huberman podcast listeners. Again, that's functionhealth.com slash Huberman to get early access to function.

Andrew Huberman: Okay, so let's talk about anorexia, this failure to consume enough energy such that the individual is at risk of death. And if not death, then severe metabolic disorders, lack of bone density, et cetera. A careful analysis through medical epidemiology has shown that you find anorexia even in cultures and societies where food is scarce. So that really speaks to biological mechanism. Typically, anorexia starts in adolescence right around puberty. Puberty, at a very broad level, is the most significant and dramatic developmental step anyone goes through in their lifespan. The body changes, the brain changes, perceptions change, one's own self-perception changes, and most of those changes are driven by changes in circuitry within the hypothalamus. So neurons that are controlling the production of the so-called sex steroid hormones, things like testosterone, estrogen, and related hormones, prolactin, et cetera, those are all changing at very rapid rates. Let's look under the hood. Let's look at what's known about the neural circuitry and the sorts of perceptions and behaviors of the neural circuitry is driving in order to understand what they are truly suffering from at the level of cause, not just symptoms. First of all, there's a challenge in studying anorexia because in anorexia, what you're essentially studying is the absence of a behavior. It's very