0:00:00 Welcome to the Huberman Lab Podcast, where we discuss science and science-based tools
0:00:04 for everyday life.
0:00:09 I’m Andrew Huberman, and I’m a professor of neurobiology and ophthalmology at Stanford
0:00:14 School of Medicine.
0:00:15 My guest today is Dr. Zachary Knight.
0:00:18 Dr. Zachary Knight is a professor of physiology at the University of California, San Francisco,
0:00:23 and an investigator with the Howard Hughes Medical Institute.
0:00:26 For those of you that don’t know, Howard Hughes Medical Investigators are selected from an
0:00:31 extremely competitive pool of applicants and have to renew in order to maintain their
0:00:37 investigatorship with the Howard Hughes Medical Institute every five years or so, placing
0:00:42 him in the most elite of categories with respect to research scientists.
0:00:48 His laboratory focuses on homeostasis, in particular, what drives our sense of hunger,
0:00:53 what drives our sense of thirst, and what controls thermoregulation, which is the ability
0:00:58 to maintain body temperature within a specific safe range.
0:01:02 Today, we mainly focus on hunger.
0:01:04 Dr. Zachary Knight explains the biological mechanisms for craving food, for consuming
0:01:09 food, and believe it or not, you have brain circuits that actually determine how much
0:01:13 you’re likely to eat even before you take your very first bite.
0:01:17 He explains the biological mechanisms for satiety, that is, the sense that one has had
0:01:21 enough of a particular food or food group.
0:01:24 Dr. Knight also explains the role of dopamine in food craving and consumption, which I think
0:01:29 everybody will find very surprising because it runs countercurrent to most people’s understanding
0:01:34 of what dopamine does in the context of eating and other cravings.
0:01:38 Today’s discussion also includes a deep dive into GLP-1, glucagon-like peptide, and the
0:01:45 novel class of drugs such as ozempic and mongero and other related compounds that are now widespread
0:01:50 in use for the reduction in body weight.
0:01:53 Dr. Knight explains how GLP-1 was first discovered, and how these drugs were developed, how they
0:01:58 work, and, importantly, why they work, and how that is leading to the next generation
0:02:04 of so-called diet drugs or drugs to treat obesity, diabetes, and related syndromes.
0:02:09 We also discussed thirst and the intimate relationship between water consumption and
0:02:13 food consumption, and we also talk about the relationship between sodium intake, water
0:02:17 intake, and food intake.
0:02:19 By the end of today’s conversation, you have learned a tremendous amount about the
0:02:22 modern understanding of hunger, thirst, and salt intake, as well as this modern class
0:02:27 of drugs such as ozempic and related compounds, all from a truly world-class investigator in
0:02:33 the subjects of researching hunger, thirst, and thermal regulation.
0:02:38 Before you begin, I’d like to emphasize that this podcast is separate from my teaching
0:02:41 and research roles at Stanford.
0:02:43 It is, however, part of my desire and effort to bring zero-cost to consumer information
0:02:47 about science and science-related tools to the general public.
0:02:51 In keeping with that theme, I’d like to thank the sponsors of today’s podcast.
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0:07:04 Now for my discussion with Dr. Zachary Knight.
0:07:07 Dr. Zachary Knight, welcome.
0:07:10 Great to be here.
0:07:11 Today, we’re going to talk about hunger, appetite, thirst, other motivated behaviors, the role
0:07:17 of dopamine, the vagus nerve.
0:07:20 These are terms and topics that a lot of people hear nowadays, and for which there’s a ton
0:07:25 of interest.
0:07:27 Just to march us in sequentially, could you describe some of what’s happening in the brain
0:07:32 and/or body as we get hungry, decide what to eat, and then decide that we’ve had enough
0:07:41 to eat?
0:07:42 I think most people just assume that, “Okay, my stomach’s full,” is what we say.
0:07:47 “I’ve had enough,” or we self-regulate it for some other reason, caloric restriction
0:07:53 or monitoring in some cases.
0:07:57 What’s happening in the brain in terms of the circuitries, and what have you discovered
0:08:01 about what that process looks like in terms of its kind of universality across people,
0:08:09 and then maybe how it sometimes differs between people?
0:08:11 Okay.
0:08:12 There’s a lot in that that I’ll try to unpack.
0:08:14 I can remind of some of the nuances.
0:08:16 In other words, as a biologist, as a neuroscientist, how do you think about this thing that we
0:08:19 call hunger and feeding?
0:08:21 Absolutely.
0:08:22 Absolutely.
0:08:23 At a very high level, a good way to think about the regulation of food intake by the
0:08:26 brain is that there’s two systems, a short-term system and a long-term system, that are primarily
0:08:33 localized to different parts of the brain, operate on different timescales, one on the
0:08:37 timescale of a meal, so 10, 20 minutes, and the other on the timescale of weeks to months
0:08:43 to years and tracks levels of body fat.
0:08:47 These two systems interact so that these short-term behaviors we do eating are mainly
0:08:53 matched to our long-term need for energy.
0:08:58 I think one of the initial experiments that really led to this idea is this great experiment
0:09:02 by Harvey Grill about 50 years ago.
0:09:06 It’s called the de-cerebrate rat, and so essentially what he did was he made a cut in the rat
0:09:11 brain, so he took these rats in the lab, made a cut so that he separated the brain stem,
0:09:15 so the most posterior part of the brain, from the entire forebrain, basically got rid
0:09:20 of 80 percent of the rat’s brain, so basically creating these zombie rats, all they have
0:09:24 is a brain stem, and asked, “What can these rats still do?”
0:09:28 You might imagine they can’t do a lot of things, right, because they basically have
0:09:31 lost most of their brain, but he discovered that one thing they can still do is regulate
0:09:37 the size of a meal, and so, and you have to be careful how we talk about this, because
0:09:45 the way this meal works is you have to actually put food into their mouth, and then they’ll
0:09:48 swallow it as you put food into their mouth, but eventually at some point they’ll start
0:09:53 spitting it out, and that basically is an indication that in some sense they’re becoming
0:09:57 sated, and they’re just using the brain stem that they have left, they’re able to sense
0:10:03 those signals from the gut, and drive the termination of a meal, and he did other experiments
0:10:08 showing that many of these signals that come from the gut, gastric stretch, hormones that
0:10:12 come from your intestine in response to food intake like CCK, these de-cerebrate rats just
0:10:16 have a brain stem.
0:10:18 If you inject those or manipulate the gut in those ways, it can in an appropriate way
0:10:23 change how much the rat eats.
0:10:26 Now what can’t the rat do when it doesn’t have a forebrain?
0:10:28 And the thing it can’t do is it can’t respond to longer term changes in energy need, meaning
0:10:34 if you fast the rat for a couple days, this de-cerebrate rat, then start putting food
0:10:39 in its mouth, the amount that it eats doesn’t change, so basically it doesn’t eat a larger
0:10:43 meal the way you would if you were fasted for several days and then re-fed.
0:10:48 And that experiment along with other events has led to the idea that in the brain stem
0:10:53 and then the most posterior part of your brain, there are neural circuits that control sort
0:10:57 of a meal, and then the time scale of 10 minutes or 20 minutes deciding when a meal should
0:11:01 end, and in the forebrain, primarily in the hypothalamus, there are neural circuits that
0:11:05 then track what is my overall level of energy reserves, what is my level of body fat, things
0:11:10 that would fluctuate on time scale of, say, days when you’re fasting, and those forebrain
0:11:14 centers feed back to talk to the brain stem and modulate those brain stem circuits that
0:11:18 are controlling the size of a meal to sort of match these two time scales.
0:11:22 So that’s at the highest level how I think about the neural circuitry that controls feeding.
0:11:25 There’s obviously a lot more going on underneath that.
0:11:29 Fascinating.
0:11:30 You mentioned body fat and that somehow the brain is tracking the amount of body fat.
0:11:38 That caught my ear because while it makes total sense, I’d like to know how that happens
0:11:44 if we happen to know the mechanism.
0:11:46 And the second question is why body fat and not body fat and muscular mass or body fat
0:11:53 and overall body weight, what is being signaled between body fat and the brain that allows
0:11:59 the brain to track body fat, and why do you think body fat is the critical signal?
0:12:03 I realize it represents an energy reserve, but certainly there are other things about
0:12:08 the bodily state that are important.
0:12:09 Yeah.
0:12:10 Well, there are certainly other things about the bodily state that are important, and there
0:12:13 are other things about physiology definitely that are regulated other than body fat.
0:12:18 But body fat is unique because it represents this energy reserve.
0:12:21 So the neural circuitry that regulates eating behavior is in some ways very unique because
0:12:26 it has this reserve of energy.
0:12:28 So we also study thirst in my lab and drinking, and you don’t have a reserve of water in
0:12:32 your body, right?
0:12:33 And that’s true for basically everything else.
0:12:35 But for fat, we have this reserve of energy, and so it’s very important that the brain
0:12:41 know how much remains and then adjust behavior and coordinates with that so that you know
0:12:50 how urgent it is to get the next meal.
0:12:53 And so the thought is that the major signal of the level of body fat that we have is leptin.
0:12:57 It’s this hormone.
0:12:59 It was discovered.
0:13:00 It was cloned in 1994 actually by my postdoctoral advisor, a scientist named Jeff Friedman at
0:13:04 Rockefeller University, although its history goes back way before 1994.
0:13:08 So the story behind leptin is that there’s a facility called Jackson Labs that I’m sure
0:13:15 familiar with in Maine that since the 1920s has been raising mice and selling them to
0:13:21 academics basically who study physiology and behavior.
0:13:25 And so they breed thousands of mice, the sort of a nonprofit organization that distributes
0:13:29 mice to the scientific community.
0:13:31 And at some point in the 1950s, they spontaneously, just because they were breeding so many mice,
0:13:36 they came across some spontaneous mutations, mutant mice that were extremely fat, like
0:13:41 the fattest mice they had ever seen.
0:13:42 These mice just eat constantly.
0:13:43 They’re just enormous, three times the size of a normal mouse, and it’s all body fats.
0:13:48 They’re just these huge fat mice.
0:13:53 And they came across several different mutant strains that all had the same phenotype in
0:13:59 the sense that they were all extremely fat, all extremely hyperphagic, but they could
0:14:03 tell even in the 1950s that these mutations were on different chromosomes.
0:14:08 They didn’t know anything about how to identify the genes at that point.
0:14:10 That was just science fiction, but they knew that they were chromosomes and they were on
0:14:12 different chromosomes.
0:14:14 And so they labeled one obese, one of these mouse strains obese, and the other one diabetes,
0:14:19 but they’re basically the same.
0:14:20 As people wonder for a long time, well, what’s going on in these mice?
0:14:24 Then there was a scientist at Jackson Labs, Doug Coleman, who had the idea, what if we
0:14:28 do an experiment where we connect the circulations of these two different strains of obese mice
0:14:35 and test the hypothesis that maybe there’s a circulating factor, a hormone that is produced
0:14:39 by one of these strains in the control’s appetite, because at that point insulin was known, glucagon
0:14:44 was known.
0:14:45 There were some hormones that were known that were involved in metabolism, so it was logical
0:14:48 that there could be a hormone that perhaps regulates body fat levels.
0:14:53 And what they found, which was remarkable, when you attach the obese strain to the DB
0:14:57 strains, you basically connect their circulations, so hormones are transmitted between the two.
0:15:03 The OB mouse, that strain dramatically loses weight.
0:15:07 In fact, within a couple of weeks, it looks like a normal mouse.
0:15:10 It just stops eating, it loses almost all of its body fat, and essentially in all respects
0:15:13 becomes a normal mouse.
0:15:15 The DB mouse, nothing really happens.
0:15:17 It still remains obese and still remains hyperphagic.
0:15:20 And based on just that piece of data, Doug Coleman hypothesized that what was going on
0:15:24 is these two mutations were mutations in a hormone and a receptor.
0:15:29 The OB mouse had a mutation in the hormone that comes from fat, so it couldn’t produce
0:15:34 this hormone that comes from fat, and signals to the brain how much fat you have.
0:15:38 And the DB mouse has a mutation in the receptor, so it can’t sense the hormone.
0:15:42 And that was just an idea, it was a hypothesis.
0:15:47 But in the 1980s, as technology advanced, as molecular biology had been invented, it
0:15:53 became possible to clone genes.
0:15:55 A number of people tried to identify what are the genetic mutations that are occurring
0:16:01 in these mice that make them so obese.
0:16:02 And Jeff basically cloned Leptin and showed that, in fact, Doug was exactly right.
0:16:06 The OB mutation is a mutation in this hormone, Leptin.
0:16:11 And later, Millennium Pharmaceuticals showed that the DB mutation is in fact a receptor.
0:16:17 And it was an important discovery for a couple ways, for a couple reasons.
0:16:20 One because this OB gene is just expressed in fat.
0:16:23 It’s exclusively expressed in adipose tissue.
0:16:27 And how much it’s expressed is directly proportional to how much body fat you have.
0:16:32 So as you gain weight, the expression of this hormone increases in a linear manner, and
0:16:37 then it’s secreted into the blood.
0:16:38 So the level of Leptin in your blood is a direct readout of your body fat reserves.
0:16:44 This receptor for Leptin, the Leptin receptor, the functional form of it, is expressed almost
0:16:50 exclusively in the brain.
0:16:52 And it’s expressed in all of the brain regions that we knew from previous work were important
0:16:55 for appetite.
0:16:56 So basically the expression of this receptor gives you a map in the brain of the neurons
0:16:59 that control hunger.
0:17:01 And so what happens is basically when you lose weight, the levels of Leptin in your
0:17:06 blood fall, because basically you’ve lost adipose tissue, the absence of that hormone
0:17:10 sends a signal to all these neurons that have Leptin receptors in the brain.
0:17:12 They’re not getting that signal that I’m starving.
0:17:16 And basically that initiates this entire homeostatic response to starvation.
0:17:20 So a big part of that is obviously increased hunger, but it’s also decreased energy expenditure,
0:17:26 decreased body temperature, even decreased fertility, because you don’t want to reproduce
0:17:31 if you’re starving.
0:17:33 Less spontaneous movement.
0:17:34 Less spontaneous movement, all of this.
0:17:38 And so the thought is, which I think is absolutely correct, is that this hormone Leptin is part
0:17:42 of this negative feedback loop, from the fat to the brain, that basically tells you about
0:17:46 your level of body fat reserves and how urgent it is to find the next meal.
0:17:51 Fascinating.
0:17:52 As I recall, Amgen Pharmaceuticals owned the patent for Leptin in hopes that it would become
0:17:57 the blockbuster diet drug, the logic being that if you were to take this hormone somehow
0:18:03 or activate this pathway, that the brain would be tricked into thinking that there was more
0:18:07 body fat, more energy reserves than there was, and then people would basically be less hungry,
0:18:13 eat less, and lose body fat.
0:18:16 What happened with that?
0:18:18 Do we know why it did not work?
0:18:19 Yeah.
0:18:20 So that’s a great question.
0:18:21 So there was a lot of excitement when Leptin was cloned, because it was thought basically
0:18:25 we’ve cured obesity.
0:18:26 There was an auction for the patent, Amgen one, I think it was something like $20 million
0:18:31 up front payment plus royalties, which at the time, I mean, it still is a lot of money,
0:18:35 but even more money.
0:18:36 It would be a drop in the ocean compared to what companies will invest into potential
0:18:41 diet drugs.
0:18:42 Exactly.
0:18:43 So at the time, and still a lot of money today, and they did a clinical trial, gave obese
0:18:49 people Leptin subcutaneous injections of this hormone, and they didn’t lose a lot of weight.
0:18:55 And the question was why?
0:18:57 And so what was subsequently revealed is that the challenge with Leptin is that individuals
0:19:01 who are obese do not have low levels of Leptin.
0:19:05 For the most part, they actually have high levels of Leptin.
0:19:08 And so what they have is a state of Leptin resistance.
0:19:10 So it’s analogous to someone who has type 2 diabetes.
0:19:13 It’s not because they lack insulin, it’s because they actually have over time a high level
0:19:16 of insulin, and so target tissue stop responding to insulin.
0:19:20 The thought is that it’s the same way in obesity and Leptin.
0:19:23 Now subsequently, they went back and did a reanalysis of that clinical trial.
0:19:29 And asked what if you take all of these people and stratify them according to their starting
0:19:33 Leptin level.
0:19:34 So some people have relatively low levels of Leptin, some have higher, some have really
0:19:37 high levels of Leptin.
0:19:38 And then asked if we reanalyze the data, how effective is Leptin?
0:19:43 And as you might expect, the people with the lowest levels of Leptin, they lost the most
0:19:46 weight when you gave them this drug, and the people with the highest levels of Leptin lost
0:19:50 the least weight.
0:19:51 So there is a rationale there for a scenario in which Leptin could work, either among the
0:19:57 subset of people who just have for some reason lower levels of Leptin, these aren’t people
0:20:02 with mutations like the OB mouse, they have some Leptin, they just don’t have unusually
0:20:05 high levels, or alternatively after weight loss.
0:20:09 So after you’ve lost a lot of weight, your Leptin levels plummet, they become very low,
0:20:13 and that part of the reason, it’s a big part of the reason it’s so difficult to keep weight
0:20:17 off is because those Leptin levels are so low.
0:20:19 And so it’s been thought for a long time that that is a scenario where treating people
0:20:23 with Leptin could be really useful to help them keep the weight off.
0:20:28 Why it never made it as a drug for that application, I really don’t understand, has something to
0:20:32 do, I think, with the pharmaceutical industry, with the economics, with a bunch of other
0:20:36 issues that aren’t necessarily scientific.
0:20:40 But I think there still, in the future, is a possibility that it could come back for
0:20:43 that indication, especially now that we have these GLP-1 drugs, and now there’s just millions
0:20:46 of people losing so much weight, and perhaps they want to transition to a different kind
0:20:50 of drug to keep the weight off.
0:20:52 We are definitely going to talk about GLP-1, Ozympic, and some of the related compounds
0:20:57 in it in a few minutes.
0:20:58 But before we do that, I’d love to get to this issue of what’s happening in the brain
0:21:04 as we get hungry, approach a meal, decide what to eat, and decide when we’ve had enough.
0:21:11 Are there separate circuitries or at least separate neurons for each of those steps?
0:21:15 And if you would, could you walk us through what that process looks like since we do it
0:21:20 every day, most people do it every day unless they’re fasting, multiple times per day, what’s
0:21:24 going on in our brain and body as we think about and approach a meal, consume a meal,
0:21:30 and decide enough?
0:21:33 So there are different neurons that are preferentially involved in different aspects of those processes.
0:21:39 So I think we often divide feeding behavior and many other kinds of motivated behaviors
0:21:44 into a pettitive and consummatory phases.
0:21:47 So a pettitive is the phase of the behavior where you’re, for example, searching for food.
0:21:52 It’s foraging.
0:21:53 It’s all the actions that lead up to the actual behavior itself, which then we call the consummatory
0:21:58 phase.
0:22:00 That’s actually putting the food in your mouth and eating it.
0:22:02 And the general thought is that these four brain circuits in the hypothalamus are more
0:22:07 important, particularly in the hypothalamus, but other parts of the four brain as well,
0:22:11 are more important for the pettitive phase.
0:22:14 And the brain stem circuits are more important for the consummatory phase, the actual putting
0:22:17 it in your mouth and licking chewing, swallowing, and all of that.
0:22:20 Within the hypothalamus, there’s a population of neurons called AGRP neurons.
0:22:24 So it’s just an acronym, AGRP, and it stands for a Goody-related peptide, but it doesn’t
0:22:29 really matter.
0:22:30 They’re absolutely critical for that a pettitive phase, for the searching for food, for the
0:22:34 desire to find food and consume it when you’re hungry.
0:22:37 Sorry, just to touch on the AGRP neurons and this a pettitive phase.
0:22:43 Are they known to connect to areas of the brain and body that stimulate the desire to
0:22:48 move?
0:22:49 Because I think about when I get hungry, if I’m at my desk or something, I need to get
0:22:53 up and find food, need to walk to lunch or go to the refrigerator.
0:22:57 Are they somehow linked to the circuits that promote locomotion?
0:23:01 Well, they have to promote those things, but they’re not directly linked to any of those
0:23:06 circuits.
0:23:07 They’re linked directly to other four brain circuits involved in motivation.
0:23:10 So the way we think about what these kinds of neurons like AGRP neurons are doing, they’re
0:23:15 not directly talking to the motor circuits to tell you to move your legs or arms to pick
0:23:19 up the sandwich or whatever.
0:23:20 They’re rather creating this general problem that the animal has to solve, which is that
0:23:26 I’m hungry, I need to get food, it would be really great if I could have a sandwich.
0:23:30 And then the animal uses all of its mental capacities to solve that problem.
0:23:33 So they’re just there to set the goal, not so much to direct the solution.
0:23:38 So at these AGRP neurons, there are a few thousand neurons at the base of the hypothalamus.
0:23:42 So basically the most ventral, the most bottom part of the forebrain, so a tiny population
0:23:49 of cells, but outsized importance for the control of feeding behavior.
0:23:52 So if you stimulate these cells in a mouse or a rat that’s not hungry, the animal will
0:23:57 voraciously eat like it’s starving.
0:24:00 If you silence these cells, animals will starve to death, so you can basically give
0:24:03 them food, they just won’t eat it voluntarily until basically you have to euthanize them
0:24:07 because they’ve lost so much weight.
0:24:11 And the activity of these AGRP neurons is thought to track the body’s need for energy.
0:24:18 One reason that’s thought is that they express these receptors for leptin, this hormone that
0:24:24 I was just talking about that comes from fat and signals the level of body fat reserves.
0:24:29 And leptin inhibits AGRP neurons.
0:24:31 So as you might expect, if you have lots of body fat, then a neuron that expresses that
0:24:37 controls hunger should be less active than if you have very little body fat.
0:24:40 So that’s one mechanism by which leptin controls hunger.
0:24:45 We at my lab have investigated the role of these AGRP neurons from a slightly different
0:24:50 perspective, which is, and this relates to your question about what happens when we approach
0:24:56 food, when we start a meal, and to ask, what are their activity patterns?
0:25:01 What is the natural sort of firing of this population of neurons when an animal eats
0:25:04 a meal?
0:25:05 It’s a very basic question.
0:25:06 Something I think we’ve wanted to know for a long time was not really addressable until
0:25:11 about 10 years ago because just the technology didn’t exist because these are such a tiny
0:25:14 population of cells so deep in the brain.
0:25:18 So one of the very first experiments we did in my lab was to investigate that, to ask
0:25:21 for the first time what happens to these AGRP neurons when an animal eats.
0:25:24 And so one of my first graduate students, Yu Mingchen, he used a technology called fiber
0:25:30 photometry which allows us to put a fiber optic into the mouse’s brain so then we could record
0:25:35 fluorescence from these AGRP neurons, which we could use as a readout of their activity.
0:25:39 It’s basically using a calcium sensor, so calcium is a surrogate for neural activity.
0:25:45 And one of the very first experiments he did, he said, let’s make the animal hungry.
0:25:49 These AGRP neurons will be very active because the animal is hungry and then let’s give it
0:25:51 some food and see what happens during a meal.
0:25:54 And our expectation was that these AGRP neurons would gradually decline in activity as the
0:25:58 animal eats and levels of hormones in the blood start changing, feeding back to inhibit
0:26:03 these neurons.
0:26:04 What we found was really surprising.
0:26:06 I remember when he made this discovery, basically I’m running into my office and saying, Zach,
0:26:11 I gave the mouse a piece of food but the weirdest thing happened, the neurons shut off almost
0:26:14 immediately.
0:26:15 And I said, Yu Ming, you’ve made a mistake.
0:26:17 It’s okay.
0:26:18 You’re just starting off in graduate school.
0:26:19 This happens.
0:26:20 Go back and repeat the experiment and then we’ll discuss it.
0:26:22 But he did it several times.
0:26:23 He said, you know, Zach, every single time I do this happens.
0:26:25 They give the hungry mouse food and the AGRP neurons within just a few seconds, their activity
0:26:29 has greatly diminished back to the level that would be in a fed mouse, even before they
0:26:34 take the first bite of food.
0:26:36 And so Yu Ming then went to do a series of experiments, tried to understand what was
0:26:39 going on.
0:26:40 And what he basically showed by changing the kind of food he gave them or the accessibility
0:26:44 of the food or how hungry the mouse was in measuring the response of these AGRP neurons
0:26:49 was that what the neurons were doing was predicting.
0:26:53 The mouse looks at the food, it looks at how palatable it is, imagines how hungry the mouse
0:26:57 is, how accessible it is.
0:26:59 And then within a few seconds, these neurons predict how much food the mouse is going to
0:27:02 eat in the forthcoming meal.
0:27:04 And so essentially, these neurons know how much the mouse is going to eat before the
0:27:07 mouse even takes the first bite.
0:27:09 And you can show this by a very simple analysis in which you give the mouse different foods
0:27:14 and you look at how much these AGRP neurons drop when the mouse sees and smells the food.
0:27:18 And then you plot that against–this drop happens in three seconds, four seconds, something
0:27:22 like that.
0:27:23 You look at how much does the mouse go on to eat in the next 30 minutes, you can just
0:27:27 draw a straight line.
0:27:28 This was one of the first results from my lab and it was really surprising to all of us.
0:27:31 I think everyone.
0:27:32 But it illustrated a theme that we’ve now seen again and again, which is that these circuits
0:27:36 that control internal state control things like hunger and thirst, what they’re constantly
0:27:40 doing is predicting the future.
0:27:42 They can sense these signals from the body that tell you about what’s happened but those
0:27:46 signals are slow and you don’t want to wait 20 minutes from the food that you ingested
0:27:51 to reach your stomach and then slowly start entering your intestine to figure out what
0:27:54 was the nutrient content of the meal.
0:27:56 You want to try to figure that out as soon as you can, right?
0:28:00 And so the animals learn presumably through just experience that, okay, something that
0:28:03 smells like this and looks like this, it has about this many calories and I know I’m this
0:28:06 hungry so I’m going to eat about this much and then that information is all transmitted
0:28:10 to these circuits to start the process of satiation before the meal begins.
0:28:15 Is it satiation or it’s ceasing of foraging so that the animal or if I translate to a
0:28:22 person decides, okay, now I’m going to consume this sandwich, this package of food.
0:28:27 That’s a great question.
0:28:28 So we don’t fully know the answer.
0:28:30 So one interpretation of the data I just showed you is exactly what you said, is that what
0:28:34 these neurons do is they control foraging alone, they don’t control eating and so this
0:28:37 is perfect.
0:28:38 You see the food, you know it’s got enough calories, the neurons shut off and then you
0:28:41 stay there and eat it, you transition from this appetitive to this consummatory phase.
0:28:46 But that doesn’t seem to be the whole explanation because if you artificially stimulate these
0:28:51 neurons, so prevent that drop from ever happening, just stimulate them continually, the muscles
0:28:55 just sit there and eat.
0:28:56 So you can’t fully separate, although we like to make this distinction between appetitive
0:29:00 and consummatory and we know that in different parts of the brain there’s more important
0:29:04 for one versus the other, the reality is that the entire behavior is linked and you can’t
0:29:08 fully separate them.
0:29:09 So there’s a number of ideas about what this means.
0:29:12 So one idea that I just mentioned is that starting the process of satiety before the
0:29:16 meal begins.
0:29:18 Another idea which you mentioned which could be part of the answer is that it is reducing
0:29:23 this appetitive drive and allowing the transition to consummatory behavior.
0:29:28 Another idea is that, and I call these ideas because we don’t really fully know the answer
0:29:31 yet for exactly what the purpose is and biology is always hard to answer why something happens.
0:29:35 You can figure out what does happen but then you can, the reason why it evolved that way
0:29:38 is challenging.
0:29:41 Another idea is it’s involved in these, what we call cephalic phase responses that are
0:29:45 necessary to prepare you for a meal, right?
0:29:47 So the famous example, this is Pavlov, basically trains the dog to associate the ring of the
0:29:52 bell with the presentation of food and then eventually the ring of the bell alone causes
0:29:58 the dog to salivate in the absence of any food.
0:30:01 And salivation is one example of a cephalic phase response.
0:30:05 The purpose of that is to have enzymes in your mouth that basically are going to digest the
0:30:08 food and get them there right before you need them.
0:30:10 But there’s also some other things like basically the secretion of insulin occurs in response
0:30:14 to food cues, changes in gastric acid, gut motility, all these things are getting ready
0:30:19 for the meal to happen.
0:30:20 And so another idea is it could be part of that but it probably is doing all of these
0:30:25 things.
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0:32:15 It’s so interesting.
0:32:16 I have a number of questions, but I think the one that I’ll put at the top of the list
0:32:20 is the other night we were out to dinner in New York and I was very hungry.
0:32:25 I hadn’t eaten much that day and I was looking forward to a nice steak.
0:32:30 They brought out bread, French bread, it was French restaurant.
0:32:33 I took one bite.
0:32:34 I realized it was absolutely delicious French bread.
0:32:36 The butter was fantastic and so I had some bread and butter, which I love.
0:32:40 Yes.
0:32:41 Then they brought more and then they started bringing out, I don’t know who ordered them
0:32:44 because I didn’t, appetizers.
0:32:46 And I realized that this was going to be a much more extensive, calorically dense meal
0:32:53 and suddenly my appetite for the appetizers went down because I knew there was more food
0:32:58 coming.
0:32:59 Yes.
0:33:00 Had I not known that there was more food coming, I think I would have consumed more
0:33:03 of the appetizers, which also looked great.
0:33:06 So clearly there’s something going on with these AGRP neurons at the moment.
0:33:09 You’re integrating based on new information.
0:33:13 Exactly.
0:33:15 On the other end of the spectrum, I did a solo episode about eating disorders and anorexia
0:33:19 nervosa in particular and one of the things that I learned from experts in that field,
0:33:24 the psychiatrists who work on this and the scientists who work on this, is that people
0:33:29 with anorexia are unbelievably tuned to the caloric content of food, that their visual
0:33:39 system and presumably other systems have become almost hyperaccurate calculators of the amount
0:33:47 of calories in food.
0:33:49 They’ve devoted a lot of cognition to it.
0:33:51 It sometimes can border on or be placed within the obsessive realm, but that they see food
0:33:56 and they can tell you a tremendous amount about the caloric amounts with these foods.
0:34:02 Even food combinations with a very small margin of error.
0:34:09 That drives in that condition, obviously, food avoidance.
0:34:14 So I have to assume that these AGRP neurons are involved in this kind of thing.
0:34:18 One represents a regulation.
0:34:19 In the case of the example I gave and in the other case, let’s just call it what it is
0:34:23 because anorexia nervosa is the most deadly of the psychiatric conditions, sadly, a pathologic
0:34:29 dysregulation, a maladaptive dysregulation.
0:34:32 So what is known about these AGRP neurons in humans, meaning do they exist in humans?
0:34:40 Presumably they express the leptin receptor.
0:34:44 It’s like they are able to integrate information both cognitive based on immediate experience,
0:34:50 visual, olfactory, but also a lot of prior experience, a hamburger patty.
0:34:55 I can’t tell you how many calories it has.
0:34:57 All I know is that it’s mostly protein and some fat.
0:35:03 What are these neurons doing?
0:35:05 What do they have access to?
0:35:06 They sound like, when any time we hear about hypothalamus, I think very basic drives, but
0:35:10 you’re talking about a pretty sophisticated analysis of a real-time event that is driving
0:35:17 fairly nuanced behavioral decisions and updating that, which is a big deal.
0:35:23 We’re both neuroscientists, but for everyone listening and watching, this is a big deal.
0:35:27 This is as nuanced as deciding whether or not somebody is friend or foe or deciding whether
0:35:31 or not you like a movie or you don’t.
0:35:34 This is some pretty sophisticated processing.
0:35:38 This isn’t eat, don’t eat or eat less or eat more.
0:35:41 These aren’t switches.
0:35:43 These are dials.
0:35:44 Exactly.
0:35:45 Yeah.
0:35:46 There’s a lot there.
0:35:47 I’ll try to unpack that.
0:35:48 The first thing I would say is they are present in humans, and humans have agirapinerons.
0:35:54 Human agirapinerons express the leptin receptor, and we think the functions are very similar.
0:35:59 It’s one of the nice things actually about studying these kinds of things, like basic
0:36:03 mechanisms of hunger, thirst.
0:36:06 Because these things are so important for survival, they’ve been under really strong
0:36:09 selection.
0:36:11 Many of the components of these systems are genetically hardwired, meaning these are cell
0:36:15 types that have a single purpose, in this case, to control hunger.
0:36:18 They’re labeled by specific genes, and those are conserved through revolution.
0:36:23 We also know that this pathway, this agirapineron pathway, is important in humans due to human
0:36:28 genetics.
0:36:31 Just to add a little bit more information here, there’s a companion set of neurons called
0:36:34 POMC neurons that promote satiety, so the yin and yang of hunger, agirapinerons promote
0:36:39 hunger, POMC neurons promote satiety.
0:36:43 They’re intermingled in the same part of the hypothalamus.
0:36:47 They’re axons that project to the exact same downstream brain regions, and then it’s thought
0:36:53 that these two neurons compete with each other to control appetite, and that competition
0:36:58 occurs through neuropeptides that they release, one of which is an agonist for a downstream
0:37:03 receptor, and the other one of which is an antagonist.
0:37:06 We know from human genetics that among severely obese people, mutations in this pathway, agirapinerons
0:37:15 and their direct downstream targets, are quite common.
0:37:18 Really?
0:37:19 So is it fair to say that some amount of obesity is genetic in nature at the level of neuronal
0:37:28 firing or circuitry?
0:37:29 I think a lot of body weight regulation is genetic.
0:37:31 It’s highly heritable.
0:37:34 There’s a question of how much of it is due to single genes, and the number people quote,
0:37:38 and this is among people who are severely obese, so not just people who you’ve seen
0:37:42 someone who’s overweight, but people who have sort of syndromes where they’re very obese
0:37:45 from a very young age.
0:37:47 Among those people, something on the order of 10% have mutations in this pathway, and
0:37:53 it can either be this hormone POMC, or an enzyme within those cells that processes POMC
0:38:00 into the right form, or in the down– and this is the most common mutation, in the downstream
0:38:05 receptor for POMC, it’s called the melanocortin 4 receptor.
0:38:10 And so among the severely obese people who have sort of genetically inherited severe
0:38:15 obesity from childhood, something on the order of 10% have mutations in this pathway.
0:38:19 So it’s very clear that this pathway is involved in body weight regulation in humans.
0:38:25 Genetic obesity, although there’s a very strong genetic component, is not associated with
0:38:30 single gene mutations, like this is associated with effects of many mutations.
0:38:35 But we know that even in that sort of polygenic obesity that has many different genetic causes,
0:38:41 that the brain is important, and one of the reasons we know that, so if you look at the
0:38:45 genes through genetic association studies that have been associated with body weight,
0:38:49 and there’s been lots of genetic association studies try to find mutations that are associated
0:38:52 with whether you’re lean or obese, something on the order of 1,000 genes have been linked
0:38:57 to body weight regulation.
0:39:00 And the vast majority of those are expressed in the brain.
0:39:02 They’re highly enriched for brain processes, which makes sense because body weight is controlled
0:39:06 by food intake, and the brain controls behavior, and also the brain controls energy expenditure.
0:39:11 So maybe it’s not so surprising, but it’s clear that mutations in genes in the brain
0:39:17 are important for body weight, which is consistent with the results of twin studies.
0:39:21 So if you look at monozygotic versus dizygotic twins, the estimates for the heritability of
0:39:25 body weight is something on the order of 80%.
0:39:28 We should explain monozygotic, dizygotic.
0:39:30 I’ve talked about it before in the podcast, just to pressure people up.
0:39:33 Sure, just identical versus fraternal twins, basically.
0:39:35 And so, and by comparing their body weight when they become adults, you can get a sense
0:39:43 for how much of this is genetic versus environmental.
0:39:46 And something on the order of 80% is thought to, the variation between individuals is thought
0:39:51 to be have a genetic component.
0:39:53 Wow.
0:39:54 So I don’t think most people appreciate that.
0:39:57 Yeah.
0:39:58 And a lot of the debate we hear nowadays is, because there are things that people can do
0:40:02 to lose body fat, exercise, eat differently, et cetera, maybe embrace pharmacology, if
0:40:08 that’s appropriate, there seems to be this, to me, silly debate as to whether or not people
0:40:15 should be eating better and exercising or assuming that all of the obesity they might
0:40:21 have arises through genetic causes and therefore take a prescription drug.
0:40:28 I mean, why wouldn’t it be a combination of things?
0:40:31 Yeah.
0:40:32 Like, to me, it just seems like why wouldn’t people embrace some or all of the tools that
0:40:36 they could afford in that are safe for them?
0:40:38 So I just want to get that out there because the moment this comes up, people start thinking,
0:40:41 well, the moment we assign a genetic source to something, we’re removing personal responsibility.
0:40:47 But of course, there are people, I know people who have struggled with their weight, their
0:40:51 entire lives, for whom some of these new pharmaceuticals like Ozempic have provided them the opportunity
0:40:57 to finally be able to lose weight and feel better and exercise safely, for instance.
0:41:04 I completely agree with that.
0:41:06 I think there is a misconception out there about this, about what it means for something
0:41:10 to be genetically heritable.
0:41:11 And I think this gets to the root of why so many people find this sort of hard to believe
0:41:14 that there’s such a strong genetic component to body weight.
0:41:16 And that’s the idea that if you look at people, say, 75 years ago, they were much leaner.
0:41:22 And you look at people today, and starting sometime around the 1970s, there was this explosion
0:41:26 in body weight and increase in obesity.
0:41:29 That’s when it started mid-70s.
0:41:30 And sort of the 1970s is when a lot of that started to happen.
0:41:33 Snacking.
0:41:34 So there’s lots of explanations.
0:41:35 Seed oil, snack.
0:41:36 By the way, I don’t think that’s the reason, folks.
0:41:38 I think there are a lot of reasons.
0:41:39 But the theories that abound right now on social media are, I have a list of the theories
0:41:45 as to why the obesity has increased.
0:41:47 You get everything from seed oils to snacking, to smartphones, to conspiracies, to it’s
0:41:54 wild.
0:41:55 It’s wild.
0:41:56 The range of hypotheses is wild.
0:41:59 Yeah.
0:42:00 I mean, the challenges, I mean, some of them could be true, but it’s just very hard to test
0:42:02 those things experimentally because they’re happening in the whole population, right?
0:42:05 But so I think the thing that people find hard to wrap their heads around, because it is
0:42:08 a little bit of a confusing idea is that how can it be that in, say, 50 or 75 years, there’s
0:42:13 been this explosion in obesity, which is the environment has changed, but human genetics
0:42:18 has not changed in that amount of time.
0:42:19 It’s just not fast enough for people to evolve.
0:42:20 So it can’t be due to mutations in humans, right?
0:42:22 What about devolve?
0:42:24 My understanding is that within a species, evolving nutrients is very slow.
0:42:30 But mutations arise, like the OB mutation, and then you can get very fat versions of
0:42:35 an animal very quickly, right?
0:42:37 Well, you know, if it’s a recessive allele, you need two copies, and the next thing you
0:42:44 know, you’ve got a mouse that’s four times larger than a typical mouse, and it’s all
0:42:47 explained by increased body weight.
0:42:49 So that can happen very quickly within a species.
0:42:52 What’s rare to find is an entire new branch of a species that has a very new adaptive
0:42:59 function.
0:43:00 That seems more rare.
0:43:01 So that’s true.
0:43:02 So definitely, there’s some things that take longer to evolve than others.
0:43:06 But with humans, we’re talking about just two generations.
0:43:08 There just isn’t enough time for any evolution of any significance to happen.
0:43:11 Baby boomers, right?
0:43:13 Generous.
0:43:14 Generous.
0:43:15 That’s me, right?
0:43:16 And then whatever is wise, the millennial guy who’s track after that.
0:43:19 Exactly.
0:43:20 So I think the thing that people find hard to wrap their heads around is how can it be
0:43:22 that this is how, this is, that, that, that increase in body weight is clearly environmental,
0:43:25 right?
0:43:26 Because that’s all that’s changed with the environment.
0:43:27 It’s, then the thing has changed genetically, yet it’s also true what I said that body weight
0:43:31 is extremely heritable.
0:43:32 It’s one of the most heritable features and something on the order of 80%.
0:43:35 The only thing, one of the only things we know about that’s actually more heritable
0:43:38 than body weight is height, right?
0:43:40 Most diseases are not as heritable as body weight.
0:43:42 How can you explain that?
0:43:43 And the idea is this, there’s a distribution of body weights among people.
0:43:47 So in any given society, at any point in time, some people are going to be leaner.
0:43:51 Some people are going to be more obese.
0:43:53 That distribution, where you lie on that distribution is determined primarily by genetics.
0:43:58 So you may be the person who has the thrifty genes that basically cause you to save energy.
0:44:02 And so you would be more on the obese side, or you may be, maybe a person who has different
0:44:06 genes that cause you to be a little bit less hungry, so you would be on the leaner side.
0:44:10 What environment does is then it shifts that whole distribution.
0:44:14 So that basically the mean shifts so that everyone becomes, or most people, become heavier.
0:44:19 And so sort of a phrase that people sometimes use is that, is that genetics loads the gun
0:44:26 and environment pulls the trigger.
0:44:28 So basically genetics sets your propensity, and then environment can basically unmask
0:44:33 that.
0:44:34 And so, as we’ve had this change in environment where there’s all of this, and we don’t know
0:44:38 exactly what the things are that have changed, they’re important, but there’s all this ultra
0:44:41 processed food, highly palatable food, various other things that you mentioned, seed oils,
0:44:46 who knows if that’s important.
0:44:50 Certain people had these latent mutations that made them say very sensitive to palatable
0:44:54 food.
0:44:55 In an earlier time, they may have been lean, but now because they have that latent capacity
0:44:59 to be sensitive to ultra processed food, they now gain tons of weight in the environment
0:45:03 that we’re in.
0:45:04 It’s still because of genetics, but it also requires the environmental component.
0:45:07 I mean, you just take a step back, right?
0:45:09 You can make anyone lean by just putting them, putting them in prison and just only feeding
0:45:14 them 1,500 calories.
0:45:15 I mean, we’ve done those kinds of experiments.
0:45:16 This is a famous experiment, the Minnesota Starvation experiment, right?
0:45:19 They basically, they put people in prison, but this is in World War II, they took a bunch
0:45:24 of healthy volunteers, fed them 1,600 calories a day, just asked what would happen if you
0:45:28 basically semi-starved people and unsurprisingly, they lose an incredible amount of weight.
0:45:31 All they think about is food.
0:45:32 They basically, their body temperature goes down, their heart rate goes down, they just
0:45:35 become obsessed with food.
0:45:36 You could always do that for anyone, right?
0:45:39 But in a given environment where you’re not in that kind of situation, then your propensity
0:45:44 to gain weight will be determined by genetics, so that’s the idea.
0:45:47 I very much appreciate that description, and I know a great number of other people will
0:45:52 as well, because the explanation for the increase in obesity has not been described with that
0:45:59 level of accuracy and detail with respect to the interactions between genetics and the
0:46:04 environment.
0:46:05 Is it fair to say that what’s changed in our environment is the free availability of food?
0:46:11 I was walking through an airport yesterday and every 20 meters or so, there’s a vending
0:46:16 machine or a restaurant.
0:46:18 The cost of calories is fairly low.
0:46:22 Getting high-quality nutritious food that tastes great is expensive, I would argue.
0:46:29 But getting calories is fairly inexpensive.
0:46:33 I think that’s a plausible hypothesis.
0:46:36 It’s one of several plausible hypotheses, and it would be surprising to me if it didn’t
0:46:39 contribute.
0:46:40 But the reality is, these population-level questions, it’s just so hard to actually know,
0:46:44 because you can’t do an experiment.
0:46:45 We can’t create a parallel society where we manipulate one of these variables and see
0:46:49 if the people become obese.
0:46:51 I think probably the availability of food, the free availability, the low cost is one
0:46:55 part of it.
0:46:57 Another part of it is probably, although, again, it’s not proven, is that these ultra-processed
0:47:03 foods have a number of features that make people prone to gain weight.
0:47:08 There’s really beautiful work out of this from Kevin Hall at the NIH who’s investigated
0:47:12 this.
0:47:13 In my opinion, the best person doing this kind of human obesity research today, and he does
0:47:17 these experiments where he takes people into the NIH, into the hospital, hospitalizes them
0:47:21 for several weeks so he can exactly control what they eat.
0:47:23 And he did this beautiful experiment where basically, he had chefs prepare two kinds
0:47:28 of food, one ultra-processed, and the other not ultra-processed sort of more whole foods,
0:47:33 more healthier foods, but had them take a lot of care so that when they gave the foods
0:47:38 to independent raiders, to people to taste, they would say, “This is about equally palatable.”
0:47:41 So I like this ultra-processed dish as much as this non-ultra-processed dish.
0:47:47 What’s an example of an ultra-processed dish?
0:47:48 Like an out-of-package macaroni and cheese with bacon kind of thing versus some pasta
0:47:54 sitting next to a vegetable and some nice piece of salmon or something?
0:47:59 Exactly.
0:48:00 Okay.
0:48:01 Exactly.
0:48:02 And took people into the hospital, basically allowed them to eat just as much as they would
0:48:07 like, first, of the ultra-processed meals.
0:48:10 So they had the selection of ultra-processed meals for a couple weeks and then switched
0:48:14 them to the non-ultra-processed meals and then also did it in the reverse order.
0:48:18 So the other half of the people, they got the regular food first, then they got the
0:48:20 ultra-processed food.
0:48:21 What he found is that even though people rated the foods as equally palatable, they ate much
0:48:26 more of the ultra-processed food and they actually gained weight during that two-week
0:48:30 period when they were being given the ultra-processed foods and then when you switched them, they
0:48:33 lost weight.
0:48:34 So the idea being that you can have two sets of food that you have equal preferences for,
0:48:40 but something about the ultra-processed food is making you eat more of it when you actually
0:48:43 consume it.
0:48:44 And there’s a number of ideas about why that could be.
0:48:46 So one idea is that these ultra-processed foods have been optimized to have the right
0:48:51 percentage of fat and sugar and protein to sort of promote more consumption once you start
0:48:56 eating it.
0:48:57 So that could be part of it.
0:48:58 Another idea is that a big thing about whole foods is that they take more energy to digest
0:49:03 and they have more volume.
0:49:04 So one of the striking things from that study is if you just look at the pictures of the
0:49:08 meals, they’re the same number of calories, but there’s so much more food, seemingly,
0:49:12 on the non-processed food versus the ultra-processed food and that’s just because whole foods are
0:49:16 bigger because they’re not so energy-dense.
0:49:18 So and we know that, for example, volume is a major signal on the short term for regulating
0:49:23 food intake.
0:49:24 So if you just eat more volume, that could be valuable.
0:49:27 And there’s lots of things like that.
0:49:28 So I think that’s another plausible hypothesis, but the truth is we don’t really know.
0:49:32 I have a hypothesis and I don’t want to force you into speculation, but given that you’ve
0:49:37 studied and discovered that the neurons in circuits involved in a pettitive and consummatory
0:49:44 behaviors can learn based on experience and expectation, I think it’s fair game to at
0:49:50 least ask your thoughts on this.
0:49:52 So I’ve been paying a lot of attention to the landscape of what the general public think
0:49:57 about, let’s call them elimination diets, where people will just eat meat or will go
0:50:05 into a vegan diet or do some time-restricted feeding or do any number of different things
0:50:10 that have been shown to promote weight loss, provided people obey the laws of thermodynamics
0:50:16 and consume fewer calories than they burn.
0:50:20 I do believe in calories and calories out.
0:50:23 And there are a number of different routes to get there and some are more painful, some
0:50:27 are less painful and it depends on the individual lifestyle exercise and on and on.
0:50:32 But let’s just suppose for a moment, based on Kevin’s work on highly processed foods
0:50:38 versus whole foods, that there’s a learning that takes place when we eat and that this
0:50:44 learning takes place over time such that our brain and appetite start to link the variables
0:50:50 of taste, macronutrients, proteins, fats and carbohydrates, knowledge about macronutrients.
0:50:57 A piece of fish is mostly protein, has some fat, a bowl of rice is mostly carbohydrate,
0:51:04 has some protein, put a pad of butter on it, has some fat also, it’s sort of obvious.
0:51:10 But taste, macronutrient content, calories, which we already know people with anorexia
0:51:19 are exquisitely good at counting with their eyes.
0:51:24 So it’s possible they represent, again, a pathologic extreme of this.
0:51:28 And micronutrient content, maybe even amino acid content, like how much leucine is there.
0:51:35 Now most people aren’t thinking about how much leucine is in a meal, but we know that
0:51:39 leucine is important for certain aspects of muscle metabolism, it’s present in certain
0:51:44 proteins and not others, you’re gonna find less of it in a vegetable, typically than you
0:51:48 would in a piece of chicken and so on.
0:51:51 And that when people eat mostly non-processed or minimally processed foods and not in combination,
0:51:58 so we’re not talking about stewing all this together or blending all of it together, which
0:52:02 sounds disgusting, right?
0:52:04 Broccoli rice and a chicken breast blended together just sounds horrible, eating them
0:52:07 separately if there’s some olive oil and a little pad of butter involved, like that
0:52:10 sounds pretty good.
0:52:11 But a highly processed food in some ways is a blending together of macronutrients, micronutrients
0:52:18 if there are any, and other features of the food that neurons in the brain seem to pay
0:52:24 attention to, and then giving it a unified taste, a Dorito, right?
0:52:29 Yes.
0:52:30 A candy bar that we attach to the product, we attach to the name of the processed food
0:52:36 to the packaging, but I could imagine, and here’s the hypothesis that that is quote-unquote
0:52:42 confusing to our neural circuits in a way that doesn’t match up well with our thermodynamic
0:52:48 requirements of how much we’re burning versus how much we need to eat.
0:52:52 Whereas when I eat a piece of steak and a vegetable, I actually want less carbohydrate
0:52:58 afterwards.
0:52:59 If I eat the carbohydrate first, for me, it’s difficult because I love the taste of carbohydrates
0:53:03 especially when they’re combined with fat, but there seems to be an easier time regulating
0:53:08 food intake when people step back and say, “I’m going to consume minimally processed
0:53:13 whole foods,” and I’m guessing it’s not just because they’re trying to be healthier.
0:53:18 That might be what stimulates the shift, but that the brain starts to learn the relationship
0:53:23 between food volume, smell, taste, what these things look like, and satiation at the level
0:53:31 of, “Oh, that’s enough amino acids because I had a piece of fish, so maybe I don’t need
0:53:34 to consume as much of some other things,” or, “The vegetables provide volume and fiber,
0:53:38 and often vegetables can taste really delicious too,” so that there’s a linking of nutrients,
0:53:44 calories, and taste in a way that’s more appropriately matched to the energetic demands of the organism,
0:53:50 in this case, us humans, that highly processed foods bypass.
0:53:56 Now, I realize that was long-winded and forgive me, but my audience is used to that.
0:54:02 Whenever I’m trying to table something for no pun intended, for discussion that I would
0:54:06 like to think can at least stimulate some additional thinking about a landscape, in this case, nutrition
0:54:12 and feeding behavior, that for a lot of people is just really confusing, and here’s why,
0:54:17 and this is the last thing I’ll say.
0:54:18 I have several friends who have been very overweight their entire lives, for whom the following
0:54:25 diet has worked exceptionally well.
0:54:28 I’m not a diet coach.
0:54:29 I’m not a nutritionist.
0:54:30 I don’t pretend to be one.
0:54:31 I say eat proteins like meat, fish, eggs, vegetables, and fruit, and do that for a couple
0:54:39 of months, and then add back in starches as you see fit based on your food intake, and
0:54:45 without fail, they all lose a ton of weight.
0:54:48 They’re very happy with that.
0:54:49 They add back in a minimum of starches.
0:54:53 They keep the weight off, and they’re also exercising, but not more than they were before
0:54:57 in most cases.
0:54:59 I don’t think that it’s meat or fish or vegetables per se.
0:55:02 I think it’s that they finally develop an appreciation for what different foods have
0:55:07 in terms of what they actually need, and without fail, they all say, “Oh, I went to this party
0:55:13 and I had a piece of cake, and it didn’t taste good to me after three or four bites.”
0:55:17 That’s interesting too.
0:55:18 I just would like your thoughts on this.
0:55:19 We’re not defining any new diets.
0:55:21 I don’t sell any diets.
0:55:22 I don’t do any of that, but I find it amazing that when people start eating minimally processed
0:55:27 whole foods, I have to assume that their brain changes as it relates to appetite, craving,
0:55:33 and just kind of an unconscious understanding about what food is providing them or not,
0:55:37 and that highly processed foods basically bypass all of this and just get you to consume
0:55:42 more, perhaps in hopes of getting something that you probably aren’t getting at all or
0:55:48 that you need to consume a lot of this food in order to get.
0:55:51 Yeah.
0:55:52 There’s several interesting ideas there.
0:55:54 There’s two that come to mind just thinking about what you just said.
0:55:57 The one is the idea of what’s going on when these people consume simpler diets, more of
0:56:02 whole foods.
0:56:05 One thing I think that’s very likely going on is this phenomenon of sensory-specific
0:56:10 satiety as being engaged.
0:56:14 Sensory-specific satiety is just the idea that as you expose yourself repeatedly to
0:56:17 a certain flavor or taste, you basically lose appetite for that.
0:56:22 You get specific loss of appetite for that flavor or taste.
0:56:26 This is why, as you said, basically if you start off eating the protein, after all, I
0:56:29 don’t want any more salmon, but I would like some carbohydrates now because you have this
0:56:32 sensory-specific satiety.
0:56:36 It’s well-known, actually, that if you simplify your diet, make your diet really simple so
0:56:39 there’s just a few things, then sensory-specific satiety alone can cause you to eat less basically
0:56:45 because there’s just less variety in your diet and you don’t want to eat more of that
0:56:48 same thing.
0:56:49 I think a lot of diets, actually, it’s not about the specific macronutrient or the specific
0:56:53 food, it’s just that they’re reducing the variety in the diet.
0:56:57 Eventually, you just get sick of eating the same thing.
0:57:01 The thought behind that idea is that it’s important evolutionarily so that you eat a
0:57:04 diverse diet.
0:57:05 It’s the reason, probably, that you want sweets after you’ve eaten a savory meal and so on.
0:57:09 A second idea, though, that comes to mind is just, as you mentioned, this idea of learning.
0:57:14 So much about our preferences for food are they’re not innate, they’re driven by learning,
0:57:20 right?
0:57:21 There are some things that are innate.
0:57:22 If you put sugar on a baby’s tongue, it’ll smile, indicating that it likes it, and if
0:57:27 you put something bitter, it’ll frown, and a rat will do the same thing, a neonate rat.
0:57:34 Most of flavor and the perception of food is not just sweet or bitter, it’s this much
0:57:39 more complex sensation that involves smells, it involves taste, and then it involves how
0:57:44 those tastes and smells interact with the post-ingestive effects of the nutrients.
0:57:49 So, the sensing of those nutrients in your stomach and in your intestine, primarily in
0:57:53 your intestine, are thought to then feed back and then change your preference for these
0:57:58 foods.
0:57:59 So, there’s lots of examples of this that you can just imagine from everyday experience.
0:58:02 Most people, the first time they had a beer or the first time they had a glass of coffee,
0:58:05 found it repulsive, right?
0:58:06 Because it’s extremely bitter, but then we come to crave these things because we know
0:58:09 what they do to our body, we like what they do to our body, and that doesn’t just make
0:58:13 us take them like they’re medicine, we actually somehow change our very perception of how
0:58:17 that flavor is.
0:58:18 We actually come to savor that flavor we previously found disgusting, and it’s because our sensation
0:58:22 of whether something is good or bad depends on our internal state.
0:58:27 And so, it’s an interesting idea, perhaps of these ultra-processed foods that have so
0:58:31 many different ingredients and such an unnatural combination, perhaps this process of learning
0:58:36 about the nutrient content of different foods and flavors becomes impaired because it’s
0:58:42 just the brain is not used.
0:58:43 The brain is used to saying, “This is a piece of chicken and this is primarily protein.”
0:58:47 And so, I can gauge from this, I can connect this flavor to an amino acid content, but
0:58:51 something that’s so diverse, it might be harder to do.
0:58:55 And isn’t it the case that the neurons in the gut and the hormones that are produced
0:59:01 by the gut as we digest food, and that the neurons in the brain that control appetite
0:59:06 and feeding have to be tuned to macronutrient content because those are the primary colors
0:59:14 of nutrients, and nutrients are the way in which we can persist on a day-to-day basis,
0:59:22 right?
0:59:23 I mean, I’m not trying to sound more sophisticated where simpler terms would suffice.
0:59:26 What I’m basically saying is that the neurons in our brains that control these behaviors,
0:59:31 both eating and cessation of eating, an ingredient or an entire meal, can’t be tuned to a particular
0:59:37 food product, or to chicken, or to an egg, or to a steak, or to lentils, but rather to
0:59:45 amino acid content, essential amino acid content in particular, essential fatty acids.
0:59:50 And in the case of carbohydrate, whatever is going to replace whatever glycogen we might
0:59:53 have depleted, right?
0:59:54 I mean, we really break it down into biology.
0:59:58 Eating is for a purpose, and my understanding is that the purpose of eating is to replace
1:00:02 those things as needed, rather than to taste savory or taste…
1:00:10 Absolutely.
1:00:11 Absolutely.
1:00:12 Absolutely.
1:00:13 Those sensory cues are just markers that tell the brain what might be in that substance.
1:00:18 I think if you look at broadly at this difference between calories and macronutrients and micronutrients,
1:00:24 I would say what you see is that most of the circuits that are controlling hunger are primarily
1:00:28 calorie specific.
1:00:30 So they can, like for example, an AGR penron, I can put sugar, fat, or protein into the
1:00:36 stomach of a mouse, and to an equal extent inhibit an AGR penron, as long as they have
1:00:40 equal calories.
1:00:41 Really?
1:00:42 Yeah.
1:00:43 So a little drop of olive oil into the belly of an animal that has, let’s say, a little
1:00:49 bit more, let’s say 120 calories of olive oil is equal potent to 120 calories of chicken
1:00:59 breast.
1:01:00 At the level of these AGR penrons, it is.
1:01:02 So they don’t care about the macronutrients?
1:01:03 They don’t care about the macronutrients?
1:01:04 No.
1:01:05 They’re really concerned about…
1:01:06 They’re probably wrong.
1:01:07 They’re really concerned about energy.
1:01:09 There are circuitries that are more concerned with macronutrients individually, although
1:01:13 I don’t think we know nearly as much about how that works.
1:01:15 I think the evidence is clear that the strongest defended macronutrient by far is protein.
1:01:21 So protein, I don’t think really sugar and fat intake are strongly defended in the sense
1:01:27 that you’re fine if you go without eating sugar, right?
1:01:30 Basically, you can synthesize sugar from amino acids, for example, and you don’t develop
1:01:36 a specific sugar appetite in the same way you do.
1:01:39 For example, if you deprive yourself of hunger, you develop a protein hunger, or essential…
1:01:42 I think the difference is that proteins consist of essential amino acids.
1:01:46 There’s this…
1:01:47 I forget if it’s nine amino acids, that your body cannot synthesize.
1:01:51 You absolutely need them, or you will die.
1:01:53 And so whereas sugar and fat can be interchanged with other macronutrients, and there’s other
1:02:00 things also that you absolutely need to ingest, like sodium chloride, right?
1:02:03 So sodium.
1:02:04 So if you deprive an animal of sodium, they will develop this salt appetite.
1:02:10 That’s incredible, basically.
1:02:11 And that’s completely innate.
1:02:13 But that’s, I think, salt appetite and protein appetite are the things that are probably
1:02:19 the most strongly regulated at the level of the macronutrients.
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1:03:59 If we could talk about body weight homeostasis for a moment, I think that would be useful.
1:04:05 Let’s say somebody decides they want to lose some weight.
1:04:09 They caloric restrict slightly, either by exercising more or eating less or both.
1:04:15 Their body weight drops by a bit.
1:04:16 Let’s say they lose 10 pounds, eight of which are body fat.
1:04:20 They lose a little bit of lean mass.
1:04:22 Also, they’re now at a new lower body weight.
1:04:25 Are the AGRP neurons motivated to have them seek out more food?
1:04:29 In other words, are they hungrier and more motivated to find and eat food?
1:04:33 Or do these AGRP neurons learn, “Hey, body weight is lower, and I don’t need to push
1:04:39 to find so much food so often?”
1:04:41 No.
1:04:42 I mean, the idea is that the AGRP neurons are more active when you lose weight.
1:04:46 That chronic activation of those neurons, in part because leptin levels are lower in
1:04:50 the blood because you’ve lost weight, is that drive, that counter-regulatory drive that
1:04:55 drives you to then consume more food.
1:04:57 But then how do people ever keep weight off?
1:04:59 Well, part of the answer is they don’t.
1:05:03 So they’re soaked.
1:05:04 Really?
1:05:05 Because I would argue, I have these friends who were very heavy.
1:05:10 Most of the excess weight was body fat for a long time.
1:05:12 They seemed to be doing great eating the way that I described before.
1:05:15 By the way, I’m not a proponent of any one particular diet.
1:05:19 I have vegan friends, carnivore friends, et cetera, but that pattern of eating I described
1:05:22 before has been enormously successful for them.
1:05:24 I haven’t run a randomized controlled trial.
1:05:27 It’s not my job to do that in the realm of nutrition, but they’re doing great.
1:05:31 They claim to be sated.
1:05:32 They are so happy with the way things are going, and I don’t hear that they’re constantly
1:05:39 hungry.
1:05:40 I hear that they’re constantly sated.
1:05:41 Well, so I would say that there have been efforts for a long time to develop diets that
1:05:48 would help people consistently lose weight, and it has been very unsuccessful.
1:05:53 There are some people who, for various reasons, can successfully lose weight and keep it off,
1:05:57 and I don’t know that I have a good answer for what’s going on in those individual cases,
1:06:01 how they are the exceptions to the rule.
1:06:03 What about them is different that makes no sense?
1:06:04 So I’m also quit drinking alcohol.
1:06:05 Yeah.
1:06:06 So there’s other things.
1:06:07 Right.
1:06:08 So behavioral regulation is better when you’re sober as opposed to being creative.
1:06:11 You can change your environment.
1:06:14 What this is getting at is what is the counter-regulatory response to weight loss?
1:06:19 This has been studied.
1:06:20 It was first studied in the context of energy expenditure, because energy expenditure is
1:06:27 actually surprisingly easier to measure in humans than food intake, because people don’t
1:06:30 tell you accurately what food they eat, if they’re for free-living humans, they have
1:06:33 to fill out a questionnaire.
1:06:36 And the idea is that for every kilogram of weight you lose, so about 2.2 pounds, I think,
1:06:43 your energy expenditure decreases by about 30 kilocalories a day.
1:06:47 Now, so not a ton, but that is significant, right, 30 calories.
1:06:52 And then if you lose, as you said, 10 pounds, then that’s 150 calories, and that adds up
1:06:56 over time.
1:06:59 One interesting thing about that is that if you take people who were obese, and then
1:07:03 they’ve lost a ton of weight, so there’s a study by Rudy Liebel about 25 years ago
1:07:06 that did this, take people who lost like 100 pounds, and then take a control group that
1:07:12 has the same height, weight, basically the same body composition as those people who’ve
1:07:17 now lost 100 pounds, compare their energy expenditure.
1:07:21 The energy expenditure in the people that lost all the weight is about 25 percent lower
1:07:25 than the people who never were obese.
1:07:28 And so those people who lost the weight, we call them the reduced obese, so that’s what
1:07:31 they were called in those studies.
1:07:33 And the idea is that now this chronic deficit, they have to eat 25 percent less than someone
1:07:38 who looks the same as them, is the same height as them, same weight as them, in order to maintain
1:07:42 that body weight.
1:07:43 What’s unclear is whether that’s because those people simply always had a lower metabolism.
1:07:47 They were always destined to be obese, and then you’re just basically comparing two different
1:07:50 groups, or whether something about the process of gaining weight and being in a higher weight
1:07:54 for a longer period of time changes the brain, so that then once you lose the weight, it’s
1:07:57 irreversible.
1:07:59 But there have been studies looking at at least a year, and it doesn’t seem to come
1:08:02 back within a year.
1:08:03 That difference in energy expenditure.
1:08:05 Now a question is, is that really the big effect?
1:08:07 Is that why it’s so hard to lose weight, energy expenditure, or is it because you’re hungrier?
1:08:12 And that’s actually much harder to measure.
1:08:14 But there was another really nice study, again, by Kevin Hall, investigating this, used a really
1:08:19 clever approach, this drug.
1:08:21 So basically what he wanted to do was, is he reasoned that you can measure people’s
1:08:25 body weight, and you can measure people’s energy expenditure.
1:08:30 And because calories in, calories out, if we can measure body weight and energy expenditure
1:08:34 accurately, we can then back calculate how much that person was actually eating.
1:08:40 So let’s see what happens when you have people lose weight.
1:08:43 How does their food intake change?
1:08:45 But the trick to this is, you need to do it in such a way that you don’t just tell them
1:08:49 to go run on a treadmill, because if you tell them to go run on a treadmill and lose weight,
1:08:51 then basically they’re thinking about the fact that they’re doing this.
1:08:54 So you need to do it in some way covertly, so that you increase their energy expenditure,
1:08:57 cause them to lose weight, but without them realizing that’s what’s happening.
1:09:00 So they gave them these drugs, these SGLT2 inhibitors, and it’s a pill you can take.
1:09:06 They’re used for diabetes.
1:09:08 They block this protein, SGLT2, in the kidney that is necessary for glucose to be reabsorbed
1:09:14 into the blood.
1:09:15 So basically what happens is you pee out about like 90 grams of glucose a day, but you don’t
1:09:19 know that you’re doing that.
1:09:20 And that causes you to lose energy, and so these people will lose some weight.
1:09:23 And then measure how their food intake changes.
1:09:26 And what that showed is that for every two pounds or so of weight you lose, your hunger
1:09:30 goes up by 100 calories per day.
1:09:33 So basically you’ve got a 30 kilocalorie decrease in energy expenditure, 100 kilocalorie decrease
1:09:38 in appetite for every two pounds you lose, on average.
1:09:40 Some people will be exceptions, right?
1:09:41 They won’t experience that at all for aspects of their physiology we don’t understand.
1:09:46 And so the increased hunger seems to be the main reason people find it so difficult to
1:09:49 keep weight off.
1:09:50 That seems the perfect segue to talk about GLP1, glucagon-like peptide 1, ozempic manjarro,
1:09:57 and similar drugs.
1:10:00 My understanding of the back history on these is that a biologist obsessed with Gila monsters,
1:10:07 a reptile that doesn’t need to eat very often, discovered a peptide within their bloodstream
1:10:14 called extended, that allowed them to eat very seldom, curbed appetite in the Gila monster
1:10:23 of all things.
1:10:25 And it has an analog homologue, I don’t know the sequence homology exactly, but there’s
1:10:33 a similar peptide made in mice and in humans that suppresses appetite.
1:10:39 If you would, could you tell us what is known about how GLP1 works to suppress appetite,
1:10:44 where in the body and/or brain, and your sort of read of these drugs and what’s happening
1:10:51 there, good, bad, exciting, ugly, anything else.
1:10:58 So the story of GLP1, so the Gila monster is an important term, and I’ll talk about
1:11:02 that.
1:11:03 It actually goes back before that, quite a ways.
1:11:05 So I should take a step back and say these were developed as drugs for diabetes, right?
1:11:10 And diabetes is a condition where basically you have elevated blood glucose, either because
1:11:14 you don’t produce enough insulin, or because your insulin is not effective.
1:11:19 And so back in the 1920s, right around the time insulin was discovered, there was this
1:11:24 phenomenon discovered known as the “Incretan Effect.”
1:11:28 And what it was?
1:11:29 “Incretan?”
1:11:30 “Incretan.”
1:11:31 Yeah.
1:11:32 Not the “Cretan Effect.”
1:11:33 Not the “Cretan Effect.”
1:11:34 You can observe the “Cretan Effect” in numerous places in daily life and online, just kidding.
1:11:37 So it’s called the “Incretan Effect.”
1:11:39 You can think of it as increase insulin, because that’s what the effect is.
1:11:43 And the idea was that if you take glucose by mouth, if you consume glucose orally, versus
1:11:48 if you have the same amount of glucose injected intravenously, more insulin is produced when
1:11:54 you take the glucose orally versus if it’s delivered intravenously.
1:11:58 Suggesting something about the process of ingesting the glucose causes more insulin
1:12:03 to be released and causes you to lower your body sugar more accurately and more strongly.
1:12:08 Interesting.
1:12:09 Which is a little bit counterintuitive, because in the pancreas, right, so insulin is released
1:12:13 from the pancreas, from the beta cell, the pancreas senses the glucose concentration
1:12:17 in the blood directly.
1:12:18 And so it suggests that insulin is being released not just in response to changes in
1:12:21 blood glucose, but in response to a second factor.
1:12:23 And so they call that an “Incretan.”
1:12:26 And through various experiments, it was shown that this “Incretan Effect” comes from the
1:12:31 intestine, that there’s some substance being produced by the intestine that when you eat
1:12:35 a meal, sugar goes through your intestine, that boosts this insulin response to glucose
1:12:41 in the blood.
1:12:42 And people immediately realize this could potentially be very valuable.
1:12:45 And the reason is that, you know, you can treat diabetes with insulin injections, but
1:12:48 insulin is dangerous, right, because if you inject too much insulin, you can kill yourself
1:12:51 by making yourself hypoglycemic, right?
1:12:52 So you have to be very careful.
1:12:54 But the thing about the “Incretan Effect” is it’s not causing insulin release directly,
1:12:59 but it’s rather boosting the natural insulin release that comes when your glucose is higher
1:13:03 in your blood.
1:13:04 So it’s sort of an amplifier on the natural insulin release.
1:13:07 So basically in the years that followed, whenever someone would find a new hormone, they would
1:13:10 test it, “Is it this “Incretan?” and there’s lots of failures, they weren’t the “Incretan.”
1:13:15 But then, so there’s this other hormone that comes from the pancreas called glucagon, right?
1:13:20 And so glucagon, it was also discovered in the 1920s, glucagon is kind of the anti-insulin.
1:13:25 So when blood sugar goes low, glucagon is released in order to cause your liver to release
1:13:30 glucose into the blood.
1:13:32 So glucagon and insulin are these two opposing hormones.
1:13:36 Glucagon was known for a long time, but people discovered in sort of the 1980s that the glucagon
1:13:40 gene is expressed in other tissues other than the pancreas, and it’s differentially processed.
1:13:46 The protein is differentially processed to produce different hormones, hormones other
1:13:49 than glucagon.
1:13:50 And they discovered there was one in the intestine, and so they called it glucagon-like peptide,
1:13:54 because it comes from the same gene, but it’s just slightly different, it’s cut up slightly
1:13:58 differently.
1:14:00 And this hormone wasn’t “Incretan.”
1:14:01 So basically if you put it on beta cells, you get this increased response of insulin
1:14:06 in response to glucose.
1:14:09 And so there was the idea, okay, this could be a great diabetes drug, right?
1:14:12 And I should say there was one other “Incretan” that’s been found, it’s called GIP, G-I-P,
1:14:17 and that will be important to talking about some of these other drugs, also a hormone
1:14:21 that comes from the intestine.
1:14:23 And so the challenge with making GLP-1 into a drug is that it has an extremely short half-life.
1:14:30 So it has a half-life of about two minutes in the blood.
1:14:34 And so even if you inject people with GLP-1, it won’t really be useful for anything.
1:14:38 You don’t decrease appetite, you don’t affect blood sugar, it’s just degraded too fast.
1:14:42 And the reason it’s degraded is because there’s an enzyme, DPP4, is what it’s called, that
1:14:46 degrades GLP-1.
1:14:49 So the first thing people tried was let’s make inhibitors of that enzyme so we can boost
1:14:52 this natural GLP-1 signal.
1:14:53 And those are approved diabetes drugs, they’re called “glyptins,” you’ve probably heard
1:14:58 about them, genuvia is the most common one.
1:15:01 And those boost the level of GLP-1, the natural GLP-1, and produce from the intestine by about
1:15:06 three-fold.
1:15:07 And they’re effective in treating diabetes.
1:15:09 People lose weight.
1:15:10 People do not lose weight.
1:15:12 And that’s one of the key reasons that we know the natural function of GLP-1 is not
1:15:17 really to control body weight because you can boost the level three-fold with these DPP4
1:15:21 drugs, millions of people have taken them, they do not lose weight.
1:15:24 That’s a great question.
1:15:26 So a three-fold is great, but you’d like to increase it even more, right?
1:15:29 And to do that, you can’t block this enzyme, you have to actually produce a GLP-1 that
1:15:35 is more stable in the blood.
1:15:36 And that’s where this lizard that you were mentioning comes into play.
1:15:40 It produces a stabilized form of GLP-1 in its venom.
1:15:44 No one knows why.
1:15:45 One hypothesis is that it’s something to do with the lizard.
1:15:49 As you said, basically having this long time period between meals and it needs to regulate
1:15:52 its blood glucose, who knows if that is true, but it turned out to be fortuitous because
1:15:56 then this GLP-1 from this lizard, it has a half-life of like two hours.
1:16:01 And so the first GLP-1 drug that was approved was just this molecule from this lizard, basically.
1:16:06 And it’s called Exenotide and it was approved in 2005, works well for diabetes, has a half-life
1:16:14 of two hours, you inject it, and doesn’t cause a ton of weight loss.
1:16:20 But two hours is good, but it’s not so great.
1:16:22 So then pharmaceutical industry tried to say, “Can we, you know, basically improve this
1:16:26 even further?”
1:16:27 And so they start engineering this hormone, making mutations, attaching lipid tails to
1:16:31 make it bind to proteins in the blood that would stabilize it.
1:16:35 Chemistry jockey stuff.
1:16:36 Yeah, exactly.
1:16:37 And I think the next big advance was this compound Lira-glutide.
1:16:42 And Lira-glutide was approved for diabetes in 2010 and then for weight loss in 2014.
1:16:47 And so Lira-glutide has a half-life of about 13 hours in the blood.
1:16:51 Now you’re getting up to something serious.
1:16:52 You’ve gone from two minutes, two hours, 13 hours, and you get better effects on aspects
1:16:59 of blood glucose and diabetes control.
1:17:01 And they started to see that some people were losing weight.
1:17:04 Very variable responses.
1:17:05 Not everyone loses weight on Lira-glutide.
1:17:08 And one of the things they noticed that I think is just a fascinating sort of example
1:17:11 of how drug discovery works in the real world, you know, a lot of these people would take
1:17:15 Lira-glutide.
1:17:16 Now it has this longer half-life, they start to get nauseous, and that would limit how much
1:17:19 of the Lira-glutide they could take.
1:17:20 And it’s a known side effect of these GLP-1 drugs that causes nausea and sort of this
1:17:23 gastrointestinal distress.
1:17:26 But they noticed that over time, the nausea would just sort of go away.
1:17:29 And so they would start dose escalating, sort of raising the dose that the person would
1:17:33 take.
1:17:34 So you would go, you know, a month at this dose, and then a month at a slightly higher
1:17:38 dose, and then a month at a slightly higher dose, and you could work your way up.
1:17:41 And these side effects would reappear, but then they go away.
1:17:44 And then once you got up to the highest doses, then people really started losing weight.
1:17:47 And so there’s a couple of things that our pharmaceutical industry realized, wow, these
1:17:50 are potentially really effective weight loss drugs.
1:17:52 And also, this nausea, which we thought was, you know, a killer, people are able to just
1:17:57 get used to it, and then it just goes away.
1:17:59 It undergoes, the word is tachyphylaxis, so the idea is that the receptor that’s affecting
1:18:04 the gut that’s causing these effects undergoes some sort of down-regulation with chronic
1:18:10 exposure.
1:18:12 So Lira-glutide, you know, it’s been around, yeah, it’s been on the market for 14 years
1:18:16 now, was used, but still you’re only getting sort of like seven to 10% weight loss, which
1:18:21 is good, but not like, you know, amazing, impressive.
1:18:26 But then semiglutide came along, and that was approved for diabetes in 2017, and semiglutide
1:18:32 is ozempic, or also marketed as a wig ove for weight loss.
1:18:38 And semiglutide now has a half-life of seven days.
1:18:41 So now we’ve gone from two minutes, two hours, 13 hours, seven days.
1:18:46 And you can really jack up the concentration with a seven-day half-life.
1:18:51 And then they saw people start really losing weight.
1:18:53 And so, in some of those trials, people lost, you know, 16% of their body weight, which
1:18:57 previously had been unattainable.
1:18:59 In what timeframe?
1:19:00 It typically takes about a year.
1:19:02 And most of the loss in body weight is from body fat or from other compartments?
1:19:09 The typical number is that if you lose weight either through dieting or through taking one
1:19:13 of these drugs, and you don’t do anything like eat a high protein diet or do resistance
1:19:17 training, somewhere between 25% and 33% of what you lose is going to be muscle.
1:19:22 The rest is going to be fat.
1:19:23 But as you said, some of that could be offset by resistance training and/or consuming a
1:19:28 higher protein diet?
1:19:30 Yeah.
1:19:31 You can almost completely eliminate that if you eat enough protein and do serious weight
1:19:34 lifting.
1:19:35 Obviously, not the whole population is interested in doing that.
1:19:38 And there’s been a lot of discussion of how serious a side effect this is.
1:19:42 You know, among elderly people, you don’t want to be losing muscle mass because you’re
1:19:46 already losing so much muscle mass.
1:19:48 On the other hand, the counter argument that has been made, which I think is also kind
1:19:51 of convincing, is that true, you’re losing some muscle, but you’re also losing all this
1:19:56 fat.
1:19:57 And you no longer need as much muscle when you’re not carrying around as much body fat.
1:20:01 So people who are heavier naturally have more muscle because they need to to move their
1:20:04 body.
1:20:05 Right?
1:20:06 Yeah.
1:20:07 The calves on very obese people are often enormous and then they lose weight and I mentioned
1:20:14 the calves in particular because they’re carrying a lot of the body load.
1:20:18 Exactly.
1:20:19 Exactly.
1:20:20 So it’s still an open question as to whether as to how serious a problem this lean muscle
1:20:24 mass loss is, although the pharmaceutical industry is all in now on making drugs that
1:20:28 basically are going to prevent that.
1:20:29 So that’s something that will be happening probably in the future.
1:20:32 Is it a, sorry to interrupt, but is the weight loss on these drugs the consequence of reduced
1:20:38 appetite or some other aspect of metabolism, and if it’s the consequence of reduced appetite,
1:20:44 is that occurring at the level of the brain and gut or a combination?
1:20:50 So it’s almost entirely reduced appetite and it’s almost entirely incurring at the level
1:20:54 of the brain.
1:20:55 Which neurons?
1:20:56 It’s thought that the key targets of these drugs are neurons in these two regions.
1:21:01 One’s called the nucleus of the solitary tract and the other one’s called the area posterina.
1:21:05 So we’re back in the brainstem.
1:21:06 Back in the brainstem.
1:21:08 So these are actually the neurons in that de-cerebrate rat story I was telling earlier.
1:21:12 These are the brain regions that are preserved in the de-cerebrate rat.
1:21:14 The de-cerebrate rat still has these very caudal brainstem structures.
1:21:19 They’re two very special brain regions because they get direct input from the vagus nerve.
1:21:23 So the vagus nerve is the nerve that innervates your stomach and intestines and heart and
1:21:27 lungs.
1:21:28 It’s sort of the major pathway from gut to brain.
1:21:30 It provides most of the sensory, the neural input from gut to brain telling you about
1:21:34 things like this, your stomach distention, how many nutrients are in your intestine,
1:21:38 breathing, all that stuff.
1:21:40 And almost all of those vagal nerves terminate on these two structures in the brainstem.
1:21:45 When I hear pustrema, I think about nausea because I was taught that pustrema contains
1:21:50 neurons that can stimulate vomiting.
1:21:53 And this seems to link up well, at least in the logical sense, with the idea that stimulating,
1:21:58 activating receptors in these neurons within pustrema might explain part of the transient
1:22:03 nausea side effect of those M-pick and related drugs.
1:22:08 So the current thought is that a lot of the nausea is coming from activating the neurons
1:22:11 of the area of pustrema, and that a lot of the physiologic satiety is coming from activating
1:22:16 the neurons in the nucleus of the solitary tract.
1:22:18 Now, the whole brain is connected to each other, and so if you really turn on these
1:22:21 neurons in the NTS and the AP, they’re going to talk to the hypothalamus and all these
1:22:24 other brain regions, it’s going to change the whole brain.
1:22:26 So it’s not just those regions, but these drugs don’t have great access to the brain.
1:22:31 They can penetrate a little bit into the brain, but they don’t penetrate into the whole brain,
1:22:34 and it’s thought that if you take fluorescently labeled versions of these drugs and see where
1:22:39 do they, so you can visualize where do they actually go, they’re enriched in these structures
1:22:42 in the brainstem.
1:22:43 So that’s why people think that this is probably where they’re acting.
1:22:46 And is that because there’s an abundance of the receptors for these compounds in pustrema
1:22:53 and NTS, or is it because the blood-brain barrier is somehow weaker at that location?
1:22:59 Just because the blood-brain barrier is weaker.
1:23:01 So basically it’s a region, what’s known as a circumventricular organ, meaning it’s one
1:23:07 of these rare places in the brain where the blood-brain barrier is weakened, and so substances
1:23:10 can come from the outside into the brain.
1:23:13 And that’s important for these big peptides, because these are not small molecules, these
1:23:17 are big peptides with lipid chains on them and other things, and so they can really only
1:23:21 get into areas of the brain where the blood-brain barrier is weakened.
1:23:24 I really appreciate that you mentioned the half-life issue with GLP-1 and the fact that
1:23:30 these DPP-4 antagonists did not lead to weight loss despite increasing circulating GLP by
1:23:38 three-fold.
1:23:40 This is relevant to a number of different claims that people make that a given food or
1:23:45 a given drink increases GLP-1.
1:23:49 I’ve actually said before, I’m a big consumer of Yerba mate, my father’s side is Argentine,
1:23:54 and it’s a known appetite suppressant, but it contains caffeine and other stimulants
1:23:58 that might explain some of that, and it’s not a robust appetite suppressant to the point
1:24:02 where most people would rely on it as a weight loss compound.
1:24:07 But anyway, it’s my preferred source of caffeine, but I’ve said before, there’s some evidence
1:24:12 that it can increase GLP-1, but based on what you’ve said, the increases in GLP-1 that it
1:24:16 creates are very unlikely to produce the kind of appetite-suppressive effect that would
1:24:21 lead to any significant weight loss in somebody that’s obese, presumably, that are separate
1:24:25 from any caffeine stimulatory effects, so you can’t separate because it’s a complex
1:24:30 compound, this Yerba mate thing, it’s got lots of things in it.
1:24:34 But also, I’ve observed you being vocal on social media when people have said, “Hey,
1:24:41 this thing increases GLP-1,” quite appropriately, I think, said, “Wait, ozempic and drugs like
1:24:52 that increase GLP-1 1,000-fold.”
1:24:55 When you talk about a food or drink or maybe a supplement increasing GLP-1, it’s very
1:24:59 unlikely to increase GLP-1 to that level, meaning, unless you’re getting into the 100-fold
1:25:06 or 1,000-fold increases, probably not right to talk about GLP-1 being the source of any
1:25:13 appetite-suppressive effect.
1:25:14 Yeah, that’s all correct.
1:25:16 So I think it’s important sometimes to distinguish between pharmacologic and physiologic effects.
1:25:21 So physiologic is what the hormone naturally does in your body and what can be modulated
1:25:26 by natural things like eating a different food.
1:25:28 And you might get a two-fold change in your GLP-1 by eating a different food, one food
1:25:33 versus the other, but as we know from those DPB4 inhibitors, it’s not going to really
1:25:36 change your appetite because the drugs increase at three-fold.
1:25:40 These GLP-1 agonists are really a pharmacologic effect.
1:25:43 In fact, it only happens with drugs, so you get 1,000 to 10,000-fold higher concentrations
1:25:48 of these drugs in your blood than the natural hormone.
1:25:51 And so there’s no diet that’s ever going to give you that.
1:25:55 And there’s no precedent for it, either.
1:25:57 So should we be at all concerned about that?
1:25:59 I mean, they run clinical trials and address safety, but when you’re talking about a 1,000-fold
1:26:04 increase in essentially a peptide hormone, if we were talking about different peptide
1:26:11 hormone, not pick one, oxytocin or estrogen testosterone, they’re not really broadly speaking.
1:26:20 Most people would be concerned about 1,000-fold dosing of something like that.
1:26:24 And obviously, there are clinical indications where that’s important.
1:26:27 However, my observation of the ever-expanding literature on GLP-1 agonists is that there
1:26:36 seems to be improvements in reduction in alcohol consumption.
1:26:42 And by the way, why would increasing GLP-1 reduce craving for alcohol?
1:26:49 It seems like there’s an ever-expanding list of things that GLP-1 agonism is good for,
1:26:54 but we are talking about, I would say, supra-physiological levels when one takes it.
1:26:59 And again, I’m not against it more for it.
1:27:02 I’m just paying attention to the literature.
1:27:04 So I would say that that’s absolutely right.
1:27:06 When you’re increasing the level of hormone 1,000-fold, you need to be careful and see
1:27:09 what’s happening.
1:27:10 But at the end, it’s an empirical question.
1:27:13 What does it actually do to a person, and they can only be answered through experiments?
1:27:16 And I think the nice thing about these GLP-1 drugs that a lot of people don’t realize is
1:27:20 they’ve been around and proved since 2005, the earliest ones.
1:27:24 And even something like Ozempic, which maybe only entered the public consciousness in the
1:27:27 last year or two, it’s been around for seven-ish years, I think, and big clinical trials with
1:27:33 these drugs.
1:27:35 And the evidence so far is that they seem to be incredibly safe.
1:27:38 And as you said, not just incredibly safe, but they seem to have all these unexpected
1:27:43 health benefits that seem to be, in some cases, even unrelated to weight loss.
1:27:48 And so because of the reasons you mentioned, one of the things the FDA requires from these
1:27:52 pharmaceutical companies for diabetes drugs is these large cardiac outcome trials, so
1:27:58 basically where you measure stroke and where you measure heart attacks and death from any
1:28:03 cardiac cause, big trials, like 20,000 people, four years cost like $1 billion to run.
1:28:09 And the data from the Semiglutai, the Ozempic trial, came out last year.
1:28:14 And as expected, reduced the rate of heart attacks, strokes, all-cause mortality according
1:28:19 to cardiac reasons.
1:28:23 But what was really surprising was a lot of that seemed to happen before the people even
1:28:26 lose weight, lost weight.
1:28:27 So there was already a difference between the placebo group and the Semiglutai group before
1:28:31 the people on the drug had lost a significant amount of weight.
1:28:34 And there was no correlation between the amount of weight they lost and how well they were
1:28:38 protected from heart disease.
1:28:39 And that’s led many people to think that some of these effects actually could be due to
1:28:43 other things that GLP1s are doing that we didn’t expect.
1:28:46 And so one thing is there’s an idea emerging that they are anti-inflammatory.
1:28:52 So these brain regions, the areopostream and the NTS, are also really important for this
1:28:57 reflex known as the inflammatory reflex that basically acts.
1:29:01 It starts with the vagus nerve, goes to these brain regions of the brainstem, and then goes
1:29:04 back down to the body to basically suppress, to prevent out-of-control inflammation.
1:29:10 And so it’s thought that these drugs perhaps have an anti-inflammatory effect that explains
1:29:14 some of that.
1:29:15 It sounds like the patent on these drugs just got extended by another 100 years.
1:29:21 That’s a bio pharma joke.
1:29:24 Just to put context on it, drugs can be patented and sold as a commercial version and not as
1:29:31 generic versions until the patent runs out unless companies are able to find another approved
1:29:36 clinical use in which case it can be remarketed only as a brand name, not generic version.
1:29:42 So a lot of companies once they do the safety testing and all given everything they put
1:29:48 into the R&D, into the research and development, there’s a very big incentive to not necessarily
1:29:53 finding new drugs, but finding new uses for the same drugs and not allowing generic versions
1:29:59 into the picture.
1:30:01 And that’s why it’s likely to be based on these, what sounds like additional uses of
1:30:08 OZMPIC-related compounds a long time before there’s generic OZMPIC available.
1:30:13 Yeah, I think it will be a while.
1:30:15 I don’t know the exact status of the patents, but I’m guessing it’s going to be a while
1:30:18 before there are generic versions, but there’s a lot of competition coming.
1:30:22 So every major pharmaceutical company, or almost every major pharmaceutical company now
1:30:25 has a GLP-1 program.
1:30:28 And some of them are really exciting, actually.
1:30:32 So I mean, the general trend in this area is what people call GLP-1+ which means you
1:30:37 take the GLP-1 agonist, which is already giving you 15% weight loss or so, and then you add
1:30:42 additional things to that to give it additional properties.
1:30:46 So one compound is from Eli Lilly, which makes this other– so there’s this other drug on
1:30:49 the market that we haven’t talked about, but Terzepotide, which is known as Mungaro for
1:30:53 diabetes and Zepbbound for obesity, which is even better, really almost every respected
1:30:57 better drug than OZMPIC, so people lose more weight.
1:31:01 So it’s about 21% weight loss at a year.
1:31:05 Fewer side effects, at least at comparable doses.
1:31:10 That seems to be because this other drug, Terzepotide, it has two targets, not one.
1:31:15 So whereas OZMPIC is just a GLP-1 receptor agonist, Terzepotide is a dual agonist of
1:31:22 GLP-1 and this other incretin that we talked about, GIP, G-I-P, and it seems like having
1:31:29 that GIP agonism actually acts as an anti-nausea effect, the sort of counteract some of the
1:31:34 nausea caused by the GLP-1 in the area post-streamer, there are GIP receptor neurons in the area
1:31:37 post-streamer, this nausea center, it allows you to crank up the dose of the GLP-1 agonism
1:31:42 even further while you’re suppressing the nausea and just get even more weight loss.
1:31:47 So now, talking about the future, things that aren’t available yet, but will be in the next
1:31:51 couple of years.
1:31:52 So Eli Lilly, the company that makes this drug, Terzepotide/Mungaro, they have a triple
1:31:58 agonist that’s in phase three clinical trials now.
1:32:00 So this is now three hormones in one.
1:32:03 That’s the GLP-1, which all these drugs have, the GIP, which is the anti-nausea component,
1:32:09 and then glucagon itself, and so there’s these three hormones all combined in one pill.
1:32:14 And what the glucagon does is it increases energy expenditure, and this is a well-known
1:32:19 effect of glucagon.
1:32:21 And so you’re basically eating less, your nausea isn’t as bad, and now you’re just
1:32:25 burning more calories at baseline, and the results from this drug are incredible.
1:32:28 So basically, there’s been one phase two trial published, and people lost 25% of their body
1:32:33 weight at the end of the, I think it was 48-week period, and they were still losing weight.
1:32:39 So we don’t know where the end point, we don’t know what the maximum is.
1:32:42 So there are bigger, longer trials going on now to figure that out.
1:32:46 But at that point, when you get beyond 25% body weight, you’re talking about basically
1:32:49 bariatric surgery, right, which is currently the best thing we have, like these surgeries
1:32:53 people do to-
1:32:54 What are called stomach staples.
1:32:55 Yeah.
1:32:56 Removing a portion of the stomach.
1:32:57 Removing a portion of the gut.
1:32:58 And really, it’s a pharmacologic version of bariatric surgery.
1:33:02 The other one that I think is really exciting, there’s this compound from Amgen, it’s just
1:33:06 right now it’s just a code, it’s like AMG-133.
1:33:10 But it’s like terzepotide, in the sense that it targets both GLP1 and GIP, so it’s a dual
1:33:16 targeted.
1:33:17 But unlike terzepotide, which activates the GIP receptor, this Amgen compound inhibits
1:33:23 it.
1:33:24 And the reasons that people don’t understand, either activating or inhibiting this receptor
1:33:28 causes you to lose weight.
1:33:30 So it’s still a mystery, there’s a lot of debate about what’s going on there.
1:33:34 But the way this Amgen compound activates the GIP receptor, or inhibits the GIP receptor
1:33:40 rather, is that it’s an antibody.
1:33:43 So all these other things are peptides, but this is a much bigger sexual protein, this
1:33:46 is an antibody.
1:33:47 And because it’s an antibody, it has a much longer lifetime, even than something like
1:33:51 semaglutide, which is seven days, so it lasts like a month in the blood or something.
1:33:55 And so you give people monthly injections of this, and they lose dramatic amounts of
1:33:59 weight.
1:34:00 And then at least in this initial trial, at the end of this, they stopped, and people
1:34:04 maintained the weight loss for six months.
1:34:06 That’s impressive.
1:34:07 Potentially because of the long-lasting effects of this antibody, or potentially because of
1:34:11 other things that we don’t understand.
1:34:12 So, and those are just two, there’s all sorts of other crazy things happening.
1:34:15 So really, I think it’s just created this explosion of interest in pharma once.
1:34:19 Basically, it’s one of these things, you know, it’s, you know, once you see that something
1:34:23 can be done, all of a sudden that changes everyone’s perspective.
1:34:26 And so now, obesity drug discovery has gone from something that 10 years ago everyone
1:34:30 wanted to stay away from, because there were so many nightmare stories about drugs that
1:34:33 turned out to be not safe, till now everybody’s sort of all in on this.
1:34:37 Yeah, I remember in college, the fen-fen debacle where a diet drug was released, and people
1:34:42 had cardiac issues start dying, so it was pulled from market, and then it was essentially
1:34:46 a quiet field for a long time.
1:34:49 In part to bring us back into the brain, and in part because it’s directly relevant to
1:34:54 what we’ve been discussing about ozempic and GLP-1.
1:35:01 There are other neurons in the brain that regulate feeding, and there are other peptides
1:35:06 involved in appetite control, for which I would say niche communities have started to
1:35:11 indulge in, and by the way, people were taking GLP-1 analogs long before they were FDA approved
1:35:17 in kind of niche communities.
1:35:19 These aren’t communities I’m a part of, but every once in a while I’ll stick an ear into
1:35:22 one of these communities and hear what people are taking, and a big thing right now in these
1:35:28 communities is the use of other peptides that are in the melanocyte-simulating hormone pathway.
1:35:36 And you mentioned melanocorticon receptor-containing neurons.
1:35:42 Could you tell us a little bit about what these neurons do in the absence of any pharmacologic
1:35:47 stimulation, and then why it would be that people would perhaps stimulate these pathways
1:35:56 with these drugs?
1:35:57 Not that we’re recommending that, but I do think that given that some of these neurons
1:36:01 are also involved in sexual behavior and FDA approved for the treatment of hyposexual
1:36:06 function in women, things like that, there is FDA approval for some of these compounds
1:36:11 that they’re interesting hypothalamic neurons that are starting to gain more attention and
1:36:15 that I predict based on their potential involvement in feeding appetite and weight control are
1:36:21 likely to enter the picture with more prominence in the not too distant future.
1:36:26 So alpha MSH, as scientists call it, the hormone you’re just referring to, is a product of
1:36:33 the POMC gene.
1:36:34 So in the same way that we just talked about, glucagon can be processed into different things.
1:36:37 In some cells it’s made into the glucagon hormone, in other cells it’s made into GLP-1.
1:36:43 In the POMC, that gene can be processed to produce different hormones, and one is alpha
1:36:46 MSH, which is very important for feeding control.
1:36:49 And so these POMC neurons are in the arcuate nucleus of the hypothalamus, the same region
1:36:54 where these AGRP neurons I talked about earlier are located, and there’s sort of these two
1:37:01 sets of neurons that have opposing effects on body weight regulation.
1:37:04 And so alpha MSH inhibits food intake and AGRP neurons promote food intake.
1:37:10 And where they converge is at this receptor, the melanocortin-4 receptor, which is important
1:37:18 for body weight regulation.
1:37:19 And so alpha MSH is an agonist, it turns on that receptor, and the AGRP peptide is an
1:37:23 antagonist, it turns it off.
1:37:26 And so there’s a lot of human genetics, as I mentioned earlier, implicating this pathway
1:37:32 in body weight regulation.
1:37:34 There’ve been a lot of efforts over many years to turn alpha MSH into a drug.
1:37:39 And it’s been very difficult.
1:37:43 There is one drug that’s now approved, it’s called, I think, I’m going to get the name
1:37:46 wrong, it’s like set malenitide or something like this.
1:37:49 It’s an MC-4 receptor agonist.
1:37:52 It’s mainly used in relatively small populations of people that, for example, have mutations
1:37:56 in this pathway.
1:37:57 It’s not used as a widespread as a drug, and the challenge has been really side effects.
1:38:04 So there’s an increase in blood pressure that happens sometimes with these medicines,
1:38:08 partly because this pathway controls not only appetite, but also autonomic tone, sympathetic
1:38:14 nervous system activation.
1:38:18 So it’s just taking a step back from everything we’ve talked about today.
1:38:23 I talked about this short-term system and the long-term system, the controls on energy
1:38:28 balance and body weight, the long short-term system in the brain stem, the long-term system
1:38:31 in the hypothalamus, the long-term system being leptin and alpha MSH and AGRP.
1:38:36 When I was learning about this stuff 15 years ago or 20 years ago, the dogma was you could
1:38:44 only affect body weight through the long-term system by manipulating the long-term system
1:38:49 because any manipulation you did of the short-term system in the brain stem, the animal would
1:38:53 just compensate.
1:38:54 And there were these famous experiments where they would take CCK, which is a hormone just
1:38:57 like GLP-1, injected into rats, injected several times a day, and CCK is known to decrease
1:39:03 the size of meals, and it would decrease the size of meals, but the rats would never lose
1:39:06 any weight because they would just eat more meals to compensate, and they would just perfectly
1:39:09 compensate by eating more meals.
1:39:10 And so the lore was, it’s just impossible, the animal will always compensate unless you
1:39:14 hit this body weight set point regulating area, which is the hypothalamus, the long-term
1:39:18 system.
1:39:19 But then what the pharmaceutical industry discovered, which I guess maybe shouldn’t
1:39:22 be so surprising, but I guess it was to some people, is that if you just hit that receptor,
1:39:27 that short-term system 24 hours a day, seven days a week, and never let it stop, then you
1:39:31 will lose weight, right?
1:39:32 And so the short-term system alone is enough to cause body weight regulation.
1:39:36 On the other hand, the long-term system with alpha MSH and AGRP neurons and POMC and all
1:39:41 this stuff has been a challenge to pharmaceutical target, because you know, leptin we discussed
1:39:46 didn’t really work.
1:39:48 And so I think there’s going to be, as you mentioned, a reemergence of interest in considering
1:39:53 this other pathway now that we’ve seen the success of the GLP-1s, and I think one area
1:39:59 where it may emerge is in considering their combination, perhaps at different stages of
1:40:04 weight loss.
1:40:05 So perhaps what would make a lot of sense scientifically, I don’t know if it’ll work
1:40:09 in practice, is that you would take a GLP-1 drug to lose the weight.
1:40:13 And then at some point, you might stop that drug and switch to a more hypothalamus-centered
1:40:17 leptin-based drug to keep the weight off.
1:40:20 So basically use the GLP-1 drug to force yourself to lose the weight, and then use the leptin
1:40:25 hypothalamus-based drug to sort of say, “Okay, this is our new body weight set point.
1:40:29 Let’s not resist this weight loss that’s happened.”
1:40:32 Whether that will actually make sense practically is hard to say, because the GLP-1 drugs have
1:40:35 just a lot of benefits even beyond weight loss, so people might not want to stop taking
1:40:38 them.
1:40:40 But that’s one idea.
1:40:41 Very interesting.
1:40:42 I’d love to talk about dopamine.
1:40:45 Sure.
1:40:46 We hear so much about dopamine being involved in pleasure.
1:40:50 I like to think I’ve had at least a small level of impact in convincing people that it’s
1:40:55 also involved in, perhaps, mostly involved in things like motivation, different forms
1:41:00 of learning, and lots of other things, too, folks.
1:41:03 Dopamine does lots of things.
1:41:04 It’s even expressed in the eye and controls adaptation to light, so it does lots of things.
1:41:09 But it certainly is believed that dopamine is involved in our either craving for food
1:41:15 or pleasure from food.
1:41:17 What’s the real story on dopamine as it relates to food and eating behavior?
1:41:22 You had a beautiful paper published in Nature entitled – and we’ll put a link to this
1:41:26 in the show note captions – “Dopamine subsystems that track internal states.”
1:41:32 I love this paper for a variety of reasons.
1:41:34 But if you could give us the high points of your discoveries on dopamine as it relates
1:41:38 to feeding, I know, in fact, that people would find it very illuminating.
1:41:43 Sure.
1:41:44 Fantastic.
1:41:45 The question of what dopamine does with respect to feeding is a great question and a difficult
1:41:50 question, I think, to answer.
1:41:52 There’s a lot of misconceptions.
1:41:54 I think the evidence is dopamine probably isn’t so much involved in the pleasure of
1:41:58 food, that taste, the hedonic experience.
1:42:02 One reason we think this is because you can make mice – the Richard Palmer did this
1:42:07 decades ago – that don’t have any dopamine.
1:42:09 And they still show the same sort of effective responses to foods.
1:42:13 You put something sweet in their mouth, they kind of – they like it, right?
1:42:17 What dopamine seems to be important for with respect to food is two things.
1:42:21 One is the motivation to engage in work to get food, particularly when it’s high levels
1:42:26 of effort.
1:42:27 So if you ask a mouse to press a lever to get a pallet of food, if it doesn’t have
1:42:34 any dopamine, it won’t do it.
1:42:35 And if it has low levels of dopamine, it’ll just work a little bit.
1:42:38 So dopamine is important for sort of energizing action and motivating you to engage in hard
1:42:42 tasks.
1:42:43 The other thing that dopamine is really important for is learning.
1:42:45 And it’s important for learning about which cues predict something useful for the body,
1:42:51 and feeding is a central example of that.
1:42:55 And what that paper of ours is about is the idea that this learning actually happens on
1:42:59 two different timescales for two different kinds of cues.
1:43:03 So what we almost always talk about with dopamine and learning, which is important, is learning
1:43:07 about how external cues in the environment predict something like food availability,
1:43:12 right?
1:43:13 It’s a Donald sign, and you know that that means there’s some tasty food in there.
1:43:18 And so dopamine is involved in that process of sort of learning what that external cue
1:43:23 means.
1:43:24 And that’s a very fast timescale process.
1:43:26 So in the laboratory, for example, we will play a tone and then give an animal a sip
1:43:33 of a solution that has calories in it, for example.
1:43:37 And it can learn the association between that tone and that the food is going to be available
1:43:41 if they’re separated by a few seconds, but that’s all.
1:43:44 And that’s a dopamine-dependent process.
1:43:48 But there’s a second sort of much slower timescale learning about food, which isn’t about where
1:43:52 I go to get a hamburger, but rather about what the experience of eating the food, the
1:43:55 oral sensory experience, its taste, its flavor, its texture, how that relates to the post-ingestive
1:44:00 effects.
1:44:01 And I should say that this seems extremely relevant to the McDonald’s example, because
1:44:06 in your experimental situation, the tone is analogous to the golden arches of the McDonald’s
1:44:11 sign.
1:44:12 Exactly.
1:44:13 But in my experience, and forgive me, but most of the food that I’ve consumed from McDonald’s
1:44:18 does not taste good, relative to other really delicious hamburgers or french fries or something
1:44:24 like that.
1:44:25 I mean, so you’re saying dopamine is required to link the signal, the golden arches or the
1:44:31 tone, to the presence of food at a particular location, but not to the experience of pleasure
1:44:38 from that food.
1:44:39 Exactly.
1:44:40 And I’ve dealt with my experience of McDonald’s, and I probably haven’t had a bite of McDonald’s
1:44:44 in 20 plus years.
1:44:47 I would have to be pretty hungry.
1:44:49 I haven’t either.
1:44:50 And it’s funny, the golden arches thing is just something that people in neuroscience
1:44:53 talks about dopamine use, and so now I’ve started subconsciously just talking about golden
1:44:57 arches, even though I also haven’t eaten at McDonald’s in decades.
1:44:59 In an outburger, the better tasting, from what I understand, probably better sourcing.
1:45:04 We’re not going to get into all of this in detail, but everyone has their preferences.
1:45:08 But I do think it’s interesting because what we’re talking about here is related, I think,
1:45:13 to this notion of highly processed food, packaging, the commodization of food, which is the idea
1:45:18 that we are drawn to food for things other than the taste that we expect for it.
1:45:23 There’s all this context.
1:45:25 So I think an important distinction that people make is the distinction between wanting and
1:45:30 liking.
1:45:31 I don’t know if you’ve talked about this previously on the podcast.
1:45:32 On a Lemke, my colleague at Stanford came on the podcast, talked about dopamine is about
1:45:36 wanting as opposed to enjoying.
1:45:39 In most cases.
1:45:40 Yeah.
1:45:41 So liking is the subjective, hedonic pleasure in the moment of eating it, but wanting is
1:45:44 just what you want.
1:45:46 And these can be uncoupled all the time.
1:45:48 You can want things that at the end of the day, you don’t actually enjoy it when you
1:45:51 get it.
1:45:52 I feel like a lot of life is like that.
1:45:54 Indeed.
1:45:55 And so dopamine is very powerful at making you want something, but not necessarily like
1:46:00 it.
1:46:02 So that’s one element.
1:46:03 There’s this other element that is important, but very much less studied, but I find much
1:46:07 more interesting, which is how you connect the sensory cues associated with food, its
1:46:13 taste, its flavor, its smell with the consequences for the body.
1:46:18 And this is so important because so much of whether we like or dislike a particular food
1:46:23 or drink is related to its post-ingestive effects.
1:46:26 You come to like things, for example, that have calories.
1:46:29 So this is one of the reasons that adults will eat vegetables and other savory foods
1:46:33 that children find disgusting.
1:46:34 Even though they’re a little bit bitter, you learn through experience, this makes me
1:46:36 feel good to eat this.
1:46:37 And even maybe at a completely subconscious level, there’s also a level of learning that
1:46:41 occurs.
1:46:42 And this, of course, happens with other things like coffee and beer and other things like
1:46:46 that.
1:46:47 And so there’s been an idea that this other much slower learning occurs.
1:46:51 And the reason I say it slower is because the time between when you taste the food and
1:46:55 when it actually gets into your intestine and releases the hormones that might drive this
1:46:58 is quite slow, separated by tens of minutes.
1:47:01 But how that works hasn’t been clear.
1:47:02 There’s been an idea that dopamine might be involved, but it hadn’t really received
1:47:07 a lot of attention.
1:47:08 And so we set out to investigate what is the role of dopamine in these post-ingestive responses
1:47:12 and sort of map out for the dopamine system.
1:47:15 How does the dopamine system respond, not when you see the golden arches, which is usually
1:47:19 the kinds of experiments that have been performed, but rather when you deliver nutrients directly
1:47:23 to your stomach or when you deliver water directly to your stomach if you’re thirsty
1:47:26 and so on.
1:47:27 And what we saw was that there are these different populations of dopamine neurons that are
1:47:32 tuned to respond to signals from inside the body.
1:47:35 And so there are some that respond when nutrients are in the stomach and intestine.
1:47:40 There are others that respond in a thirsty mouse when the blood is rehydrated, when you
1:47:45 basically satiate your thirst.
1:47:48 And we showed that the purpose, or at least a purpose of that activation, is to cause
1:47:53 you to learn about the effects of what you just ate, basically to create this connection
1:47:58 between the flavor of something and its post-ingestive effects.
1:48:01 That delayed dopamine signal after ingested food and fluids is reinforcing this connection
1:48:07 between the flavor of what I just ate and that it was something good for me.
1:48:11 One of the interesting things about that paper that was not the direction we initially expected
1:48:15 to go in is that for food, I think it’s kind of intuitive.
1:48:19 There are lots of flavors to food.
1:48:20 You have to learn what all these different flavors mean.
1:48:24 For thirst, people find it a little less obvious because thirst is just water.
1:48:27 Aren’t you just born knowing what water is?
1:48:31 How do you have to learn anything to do with drinking a glass of water?
1:48:34 But it actually is a learning question, in part because for many animals, probably most
1:48:39 animals, thirst is something that’s associated with eating, not drinking.
1:48:44 There’s a study I love of rabbits in New Zealand.
1:48:49 So there’s not a lot of people studying what animals, how they get their fluids in the
1:48:52 wild, because who cares?
1:48:53 But it’s kind of interesting.
1:48:54 And so in New Zealand, there’s this huge rabbit problem because they’re an invasive
1:48:57 pest species that was introduced in the 1800s and they’re just eating all the land.
1:49:02 And so there’s lots of money to study rabbits, to just understand their ecology.
1:49:06 And so a group of researchers did this experiment where they made this big pen outside where
1:49:10 they put a bunch of rabbits in this.
1:49:11 The rabbits couldn’t escape.
1:49:12 But they had all their natural food.
1:49:13 It was like an outdoor area.
1:49:15 And they also put a trough of water.
1:49:17 So the rats always had access to water, which is a clean water, and they could measure how
1:49:20 much water the rabbits drank.
1:49:23 And what they basically found is that nine months out of a year, rabbits drink zero water.
1:49:26 They drink absolutely zero because they get all of their water from food.
1:49:30 The only time they drink is during the winter when all of the greenery has sort of become
1:49:34 shriveled and then they can’t get water from that anymore.
1:49:38 And so it’s just kind of interesting aspect of how many animals are very different from
1:49:42 the way we think about ingestive behavior.
1:49:43 But that fact that animals have to get water from food raises this question, how do they
1:49:48 know which foods are rehydrating?
1:49:50 That’s presumably they have to learn that because you can’t just look at a food and
1:49:53 say if you’ve never had any experience, oh yeah.
1:49:55 This is something that’s very water rich and this will rehydrate me when I’m thirsty and
1:49:59 this one is not.
1:50:00 And so James, the graduate student who led this project, basically investigated this
1:50:05 by giving mice different fluids and then measuring how the dopamine responds.
1:50:11 And he showed there was this delayed dopamine response after the mice had drank the fluids
1:50:17 that correlated with rehydration of the blood.
1:50:19 So a whole bunch of dopamine neurons get strongly activated when the blood is rehydrated.
1:50:23 And he hypothesized this might be a signal, this delayed activation of dopamine neurons
1:50:28 that allows animals in the wild to learn that food I just ate is rehydrating.
1:50:34 And so he did an experiment where he basically gave them two different flavors, mimicking
1:50:38 sort of the flavors of two different foods, one of which was hydrating and one of which
1:50:42 was not.
1:50:43 And the animals couldn’t tell because he infused the water directly into their stomach.
1:50:47 And he showed that basically these dopamine neurons are critical for them learning that
1:50:51 association.
1:50:52 So that’s the story of that.
1:50:54 I love it and I’ll tell you why.
1:50:56 When I was in college for reasons that I don’t recall, I decided to run an experiment on
1:51:00 myself where I would eat one meal that was fairly low water content, like a piece of
1:51:09 meat or something with some cheese, you know what some people call a keto meal, but I wasn’t
1:51:13 ketogenic.
1:51:14 I don’t even think I knew what a ketogenic diet was at that point.
1:51:18 And then the next meal, I would have like a salad and some fruits.
1:51:22 And then I would switch back and forth and I generally would only eat two or three times
1:51:26 a day.
1:51:27 You know, anyway, there’s only so many hours in the day.
1:51:30 And I found it to be incredibly satiating and I found that I felt great and I can imagine
1:51:37 any number of different reasons for that.
1:51:39 And there are these theories that you probably recall that the diet that was being promoted
1:51:44 in the 90s where people would either eat carbohydrates or protein separately, like there was a wackiness
1:51:49 out there.
1:51:50 And as I say that, I’m sure I’ll get assaulted in the comments.
1:51:52 It’s probably not wacky.
1:51:53 I’m sure there’s some enzymatic basis for why that would be useful.
1:51:56 If you enjoy it, go for it.
1:51:58 You know, I don’t have a feeling about it one way or the other.
1:52:02 But one thing I noticed was that low water content containing meals, either by virtue
1:52:11 of the foods that they include or by virtue of the fact that they’re not diluted, so to
1:52:16 speak, it’s a different taste experience to eat those foods than it is to eat like a big
1:52:22 salad or something of that sort.
1:52:25 In any event, I don’t do that any longer.
1:52:27 I just sort of stopped, but it was a fun experiment.
1:52:31 And I think it was efficient because at the time I had very little money as a student.
1:52:34 So, you know, generally fruits and vegetables were less costly than meats and things of that
1:52:37 sort.
1:52:38 So, in all seriousness, to what extent do you think humans overeat or under eat depending
1:52:46 on the water content of the food?
1:52:48 It’s an interesting question.
1:52:49 So you know, there is this advice that you should, if you’re hungry, first drink something,
1:52:54 drink some water and see if you’re still hungry.
1:52:57 And the idea is that perhaps humans can’t always, I mean, our inter-acceptive sense or
1:53:04 our ability to sense what our body needs is not perfect.
1:53:07 And sometimes we could be confused and we could really be thirsty when we’re hungry
1:53:10 and hungry when we’re thirsty.
1:53:12 And there’s some evidence that could help.
1:53:15 I would say it’s probably not a huge effect in most of modern-day life, but it’s an interesting
1:53:21 idea, yeah.
1:53:23 This brings us to the topic of thirst, something that your laboratory has worked on extensively
1:53:27 and the topic of osmolarity, salt consumption and things of that sort.
1:53:36 In broad terms, how do these things link up?
1:53:38 Meaning, are there instances in which what we really need is salt and we end up eating
1:53:44 a bunch of Parmesan cheese?
1:53:46 I got teased yesterday by my team because occasionally when I’m on the road, I don’t
1:53:49 like most of the foods available in most airports and stuff, so I’ll bring a chunk of really
1:53:52 nice Parmesan cheese.
1:53:53 I’ll just break off a piece and eat it.
1:53:55 I’ll have half a cucumber and I’ll have a can of, not a can of tuna, but there are these
1:53:59 wonderful, a jarred filet of tunas that are available that are in olive oil.
1:54:04 They taste really good.
1:54:05 This is not can of tuna.
1:54:06 It’s really good.
1:54:08 I’d rather eat that in most cases until I can get to a decent meal than what’s put
1:54:15 in front of me on an airplane most of the time.
1:54:17 I get teased about this, but I notice that, for instance, sometimes I’ll eat the cheese
1:54:22 and I think, “Oh, actually, what I really just want is the salt.”
1:54:25 I really want the salt.
1:54:26 I’ve been drinking a lot of coffee today.
1:54:28 I’ve had a couple extra glasses of water.
1:54:30 Maybe I’m just craving salt and I’m confused and I’m over-consuming this cheese when in
1:54:36 fact what I’m going for is the salt.
1:54:39 You point out our understanding of exactly what we need is fairly crude and oftentimes
1:54:44 we overshoot the margin, especially when foods are in combination.
1:54:50 Salt, water, and let’s just say calories, how do we accurately or inaccurately pursue
1:54:59 those at the level of biology?
1:55:01 Okay.
1:55:02 I’m drawing tough questions.
1:55:03 I know.
1:55:04 It feels like my qualifying example.
1:55:10 There are separate systems that control salt appetite, thirst for water, and hunger for
1:55:16 calories.
1:55:17 They involve different brain regions for the most part, different neurons, different
1:55:21 signals from the body.
1:55:25 In general, hunger and thirst are pretty separable.
1:55:28 I would say the instance where they interact is in phenomena such as dehydration anorexia.
1:55:34 This is the idea that if I give you some dry food but I don’t give you any water, you’re
1:55:39 going to eat less food because basically you’re going to get dehydrated and you’re going to
1:55:43 decide I need to preserve my fluid balance even if I eat less calories.
1:55:49 We prioritize hydration.
1:55:50 Yes.
1:55:51 You will at some point.
1:55:52 The level of survival.
1:55:53 At some point you will prioritize hydration.
1:55:56 That’s related also to the concept of perennial drinking.
1:55:58 Many animals, including humans, drink most of their water during meals because you basically
1:56:02 want to counteract the osmolites that are in your food.
1:56:07 Salt balance though, and thirst, so the thirst for water and the desire for salt are much
1:56:11 more tightly linked because the purpose of both systems is to maintain the composition
1:56:17 of the blood at its right concentration.
1:56:20 You want to have the right osmolality of the blood, which you can just think of in simple
1:56:24 terms as sort of the total concentration of all the salts.
1:56:29 It’s a little more complicated than that, but it doesn’t really matter.
1:56:33 You also specifically need to maintain the sodium concentration at the right level.
1:56:40 There are really powerful innate mechanisms that drive both.
1:56:42 I think thirst is very intuitive to people.
1:56:45 You get dehydrated.
1:56:46 You lose water.
1:56:47 You become thirsty.
1:56:50 We know now that there are a very small set of neurons in a few brain regions that control
1:56:55 that.
1:56:59 The way their thoughts work is they contain osmosensors.
1:57:05 These neurons are sensors for the osmolality of the blood, and they’re activated when the
1:57:08 blood osmolality gets too high.
1:57:10 It’s an incredibly sensitive system, so you can perceive an increase in your blood osmolality
1:57:15 of 1% as the sensation of thirst, so remarkable.
1:57:20 That’s how critical it is to maintain salt balance.
1:57:22 Exactly.
1:57:23 You get to 10% increase in blood osmolality, and you’re in extreme discomfort and 20% you’re
1:57:28 in the hospital.
1:57:31 Let’s just say a half an ounce sip of seawater inadvertently.
1:57:39 It’s extremely aversive.
1:57:44 You want to drink some non-salty water, some nice clean water immediately.
1:57:51 I should emphasize that there’s two components to the fluid homeostasis system, to the water
1:57:55 homeostasis system.
1:57:56 One is this desire to drink, but the other is, of course, the kidney.
1:58:02 The reason the drinking the salt water won’t put you in a really bad situation is your
1:58:05 kidney would then filter out a lot of that salt and cause you just to pee it out, and
1:58:08 then you’d be fine.
1:58:10 Those two work in balance.
1:58:11 The kidney is controlling how much of the salt gets reabsorbed into the blood, and then
1:58:15 this desire for thirst, this desire to drink, allowing you to replenish the blood with water
1:58:19 at various intervals.
1:58:24 The experiment’s led to the discovery of this thirst circuitry are amazing.
1:58:26 It was this guy, Bank Anderson, working in the 1950s, and he just had this hypothesis
1:58:31 that there was an osmosensor in the brain, which I think there was some evidence to suggest
1:58:36 it, but it was not really strongly supported at the time by the data.
1:58:40 He took these goats, and he just started infusing small amounts of salt into various
1:58:45 places in their brain, reasoning that if there was an osmosensor, I was wild.
1:58:50 I wasn’t chuckling just like I feel for the goats, I feel for everyone involved in that
1:58:56 experiment, but what a wild experiment, just to put salt directly into the brain?
1:59:00 Concentrated saline solution.
1:59:01 Yeah.
1:59:02 And he found this tiny region in and around the hypothalamus that if you infuse salt in
1:59:07 this region, the goats will drink like 8 liters of water in five minutes, just crazy, right?
1:59:13 And then he, and so he reasoned, okay, this must be the osmosensor.
1:59:15 And then he went back and stimulated those neurons, and it’s the same thing, the goat
1:59:19 just drinks like crazy.
1:59:21 And so now we know there’s this couple small regions around the hypothalamus, one’s called
1:59:24 the subphornical organ, and another one’s called, well, it doesn’t really matter what
1:59:27 they’re called, but basically they have these osmosensors.
1:59:32 One of the interesting things about the regulation of fluid balance is you face some of the same
1:59:35 challenges we just talked about with the regulation of food consumption, which is that you have
1:59:39 this behavior, this ingestive behavior that leads to replenishment of the body, but there
1:59:45 are these delays, right?
1:59:46 So if you’re thirsty and you drink a glass of water, it can take on the order of sort
1:59:49 of 20 to 30 minutes for the water to be absorbed into your blood, for the blood to be rehydrated,
1:59:54 and then for these osmosensors that banked Anderson discovered in your brain to be sort
2:00:01 of sense that and return to normal activity.
2:00:02 But of course, if you had the experience of drinking a glass of water, you know that
2:00:05 you can quench your thirst within minutes, right?
2:00:08 And so how does that work within seconds even?
2:00:11 So one of the other experiments we did early in my lab was to ask that question by basically
2:00:17 recording for the first time the activity of these neurons that Banked discovered by
2:00:20 putting the salt in the goat.
2:00:21 So we went back into them now in mice, mice have the same neurons, you have the same neurons,
2:00:24 and recording their activity when a thirsty mice drinks and asks what happens.
2:00:29 And what we saw was that the neurons don’t wait until the blood is rehydrated.
2:00:34 They also don’t do what the AGRP neurons do, meaning they don’t look at the water and
2:00:38 predict how much water they’re going to drink.
2:00:40 But instead, they get a signal from the mouth, which every time the mouth takes a lick of
2:00:43 water, their activity goes down a little bit.
2:00:46 And basically, they track in that way the volume of water that’s passed through the
2:00:49 mouth.
2:00:50 They also get the signal from the blood, relaying the osmolarity of the blood, and they compare
2:00:55 these two.
2:00:56 And basically, when the mouse is drank enough in order for the animal to predict that the
2:01:01 blood osmolarity is going to return to normal, then the animal stops drinking.
2:01:04 Beautiful.
2:01:05 Yeah.
2:01:06 It’s just beautiful.
2:01:07 It’s incredible.
2:01:08 And it’s like the brain is essentially predicting with, it sounds like a high degree of accuracy
2:01:11 how much water one needs to drink, linking it to the pleasure of ingesting good clean
2:01:18 water under conditions where we’re thirsty in anticipation of adjusting blood osmolarity
2:01:23 in 20 minutes.
2:01:25 Exactly.
2:01:26 I mean, it’s, yeah, I mean, this is the kind of thing that just, it delights me because
2:01:31 it just means that the brain as a predictive organ is just so accurate.
2:01:37 It also explains some sort of funny aspects of thirst that you may have noticed from everyday
2:01:42 experience.
2:01:43 So one idea is that just cooling your mouth can sort of quench your thirst, right?
2:01:48 So if you’re in the hospital and you’re not allowed to drink any fluids, they’ll give
2:01:50 you ice chips to suck on to sort of quench your thirst.
2:01:53 So why is that?
2:01:54 And so one idea is that perhaps because water is usually cooler than your body, that sensation
2:01:59 of water passing, it always cools your mouth.
2:02:01 And so you learn, or maybe it’s innate, that just cooling of my mouth means that basically
2:02:05 I’m going to be rehydrated.
2:02:07 So Chris, this was an experiment done by a grad student, Chris Zimmerman.
2:02:10 Chris did the same thing where he was recording these thirst neurons, just put a cold piece
2:02:14 of metal on the mouse’s tongue.
2:02:15 And you can see when you do that, these thirst neurons go down in activity and then you remove
2:02:18 the cold piece of metal and they go back up.
2:02:20 Amazing.
2:02:21 So a lot of these sort of oddities of everyday experience have to do with how the system has
2:02:25 evolved to make the prediction about what’s going to happen to the body.
2:02:29 I mean, few things are as rewarding as the sensation of drinking really nice, clean,
2:02:36 cold water when one is very thirsty.
2:02:38 When my lab was in San Diego, I used to take my dog, High Game Palomar Mountain, and one
2:02:42 day, you know, I really screwed up, he was a bulldog mastiff.
2:02:46 They overheat easily and it was a lot warmer than we thought.
2:02:49 We ran out of water.
2:02:50 It was actually a dangerous situation for him.
2:02:53 We got down to the bottom of the hill, thankfully, with him still alive and there’s this pump
2:02:57 that pumps what was told to a spring water and it came out really cold and you could
2:03:03 just see him fill back up with life.
2:03:07 I filled back up with life knowing he was filling back up with life and it was unlike
2:03:11 the kind of reward that one experiences with food when you’re hungry.
2:03:14 Absolutely.
2:03:15 That basic critical need for water under conditions where you’re clearly dehydrated
2:03:22 is like nothing else.
2:03:24 It’s delicious in a way that no food is delicious.
2:03:27 I would like to actually say something about this.
2:03:28 So that distinction you made is really interesting between hunger and thirst.
2:03:32 So when you stimulate these neurons that make an animal thirsty, the mice hate it.
2:03:36 They will do anything to avoid something that artificially makes them thirsty.
2:03:40 So we can artificially stimulate these neurons, create a state of virtual thirst.
2:03:43 They’ll lever-press hundreds of times to make it stop.
2:03:46 The same neurons that I talked about, the control hunger, the AGRP neurons, they actually
2:03:51 don’t care so much.
2:03:52 They won’t really do much of anything to shut them off.
2:03:55 That raises the question of why do the animals eat then when you stimulate the hunger neurons?
2:03:59 And we think the primary thing that the hunger neuron stimulation does is it makes food itself
2:04:03 more attractive.
2:04:04 It makes the food more delicious, more of an attractive motivational magnet.
2:04:07 It makes the experience of eating more pleasurable.
2:04:10 But it is not itself the most unpleasant state.
2:04:12 At least the mice aren’t willing to do that much.
2:04:15 Whereas for thirst, I think dehydration and thirst is really just unpleasant.
2:04:18 And animals just want to avoid that.
2:04:20 And so I think that distinction is very real.
2:04:22 I think there are two different motivational mechanisms for hunger and thirst.
2:04:25 Hunger is mostly about the reward of food.
2:04:28 Thirst is mostly about this is just really unpleasant.
2:04:31 And removing that unpleasantness.
2:04:32 Exactly.
2:04:33 And you had a paper which I was going to ask you about.
2:04:35 So I will entitle the forebrained thirst circuit drives drinking through negative reinforcement.
2:04:41 And I’m guessing that paper illustrates exactly the point you just made.
2:04:45 So it’s a forebrained circuit.
2:04:47 So does that mean that there’s some elements of learning and cognition around this?
2:04:50 Or are we broadly speaking about the forebrained, for instance, the hypothalamus being in the
2:04:54 forebrained?
2:04:55 Yeah, it’s interesting.
2:04:57 So the thirst circuit for whatever reason is mostly in the forebrained.
2:05:00 So the neurons that, so we talked about the NTS and the area post-stream being important
2:05:05 for hunger and signals from the gut.
2:05:09 Those are, the area post-stream is a circumventricular organ, meaning it’s outside the blood brain
2:05:13 barrier.
2:05:14 There’s only a couple of these in the brain.
2:05:15 The neurons that control thirst are located in the two circumventricular organs in the
2:05:19 forebrained.
2:05:20 One is called the sub-phornical organ.
2:05:22 The other one is called the OVLT, but they’re just acronyms.
2:05:25 But so why it evolved to have the thirst neurons more in the forebrained and the neurons that
2:05:31 sense nutrients more in the hindbrained is a little bit unclear.
2:05:34 And so there is definitely an element of learning.
2:05:37 But a lot of this is those neurons are also just directly sensing the blood and sensing
2:05:40 changes in both the concentration of salt in the blood and then also hormones like angiotensin,
2:05:45 the drive thirst.
2:05:46 I was going to ask you this earlier, but it seems appropriate to ask now a colleague
2:05:50 of mine at Stanford in the psychology department, Dr. Ali Crum, who studies mindsets has done
2:05:56 some interesting experiments where people are told that a given milkshake is calorically
2:06:02 dense, other people are told that a milkshake is calorically sparse, both groups independently
2:06:09 consume the milkshake, and then they measure things like hormone responses in the blood
2:06:15 stream that are associated with satiety.
2:06:17 And what she finds is that even hormone responses to the same shake, meaning the same amount
2:06:25 of calories, fat, sugar, etc., can be significantly modulated based on what we’re told.
2:06:34 And it extends into some other perhaps even more interesting areas in my opinion, whereby
2:06:39 if people are told that let’s say a given meal that has a small piece of fish serving
2:06:45 a vegetables and a carbohydrate is, yes, perhaps a little bit calorically sparse compared
2:06:51 to what would normally eat at a given meal.
2:06:53 But they’re told this is a highly nutritious meal.
2:06:56 This is good for you.
2:06:57 Then just that mere knowledge can drive more satiety, better feelings about the meal, even
2:07:05 I believe I have to double check on this, but as I recall, a heightened sense of it tasting
2:07:11 really good.
2:07:12 So humans are very susceptible to the, in this case, the either inaccurate in the case
2:07:20 of the milkshake experiment or accurate descriptions of food, meaning they shape our perception
2:07:26 of whether or not something is good for us, tastes good or not, and whether or not it
2:07:32 leads to more or less satiety.
2:07:35 And I think this is important given the obesity crisis, to say nothing of these drugs that
2:07:40 are coming out, whereby people often associate dieting with deprivation and pain.
2:07:46 But if they understand that certain foods are nutritious, that can at least partially
2:07:50 offset some of the pain of caloric restriction.
2:07:54 What are your thoughts on that?
2:07:56 Yeah.
2:07:57 Well, one thing I’ve been talking about is how a lot of these circuits are anticipatory.
2:08:02 They’re making predictions.
2:08:03 They’re trying to estimate what’s happening in the future.
2:08:07 And I talked about how these AGRP hunger neurons, how they can sort of see the food or get input
2:08:11 about the site smell of food, and that way predict how many calories the mouse is going
2:08:15 to eat.
2:08:16 But I mean, this is a mouse, right?
2:08:18 This is all based on a mouse.
2:08:19 And a mouse has a thousand times fewer neurons than you do as a person, right?
2:08:23 So the computational capacity that the human brain has to make these predictions is just
2:08:28 vast compared to these mice.
2:08:29 And these mice are already doing amazing things, right?
2:08:31 So when you think about then, what is the human brain able to do in terms of anticipating
2:08:35 changes in traditional state and how information that you’re given can change the expected
2:08:41 physiologic outcomes?
2:08:42 I mean, you’re right.
2:08:43 I mean, there’s just this whole other element that is very hard to study because it’s happening
2:08:48 in the brains of humans and we can’t do these kinds of experiments.
2:08:52 But I’m sure that’s very important.
2:08:53 I mean, so I talked a little bit about these flavor nutrient conditioning experiments.
2:08:58 These are the experiments where essentially an animal learns to consume a certain flavor
2:09:04 because it learns it’s going to be associated with nutrients later, sort of the paradigm
2:09:08 for how you learn to consume bitter vegetables because they’re good for you and you get nutrients.
2:09:13 So people have also done those experiments in humans and that does work.
2:09:17 But what they’ve discovered is it’s very sensitive to what you tell the humans about
2:09:21 the thing that they’re going to consume.
2:09:23 So if you put nutritional labels where you show the different numbers of calories, then
2:09:26 basically they sort of adjust their expectations and nothing happens.
2:09:29 So it really has to be that sort of it’s very sensitive to what information you give them
2:09:33 before the experiment happens.
2:09:35 So I think that’s an example of that kind of thing.
2:09:40 Without any pressure for it to be prescriptive, how do you approach eating given the knowledge
2:09:47 that you have about food?
2:09:48 I like to assume that you can sit down to a meal and not think about your AGRP neurons
2:09:53 too much or any of that.
2:09:55 But given that you have deep knowledge in this, has it shaped kind of how you think about
2:10:00 food cravings, your own, you don’t have to reveal what those are, even if they exist.
2:10:05 How you observe the eating behavior of others and yeah, how has knowledge shaped your feeding
2:10:15 behavior?
2:10:16 Well, I try not to think too much about my AGRP neurons when I’m eating because I think
2:10:24 you know, the circuitry is so complex and we’re just beginning to see what’s happening.
2:10:27 So I wouldn’t use that kind of information at this stage and we’re just beginning to
2:10:32 prescriptively.
2:10:33 But I think there is a set of basic recommendations from physiology and neuroscience.
2:10:40 Very simple things.
2:10:41 You’ve probably talked about with people on your podcast before for sort of shaping your
2:10:46 diet to be healthier, to limit food intake.
2:10:48 So one we’ve already talked about is limiting consumption of ultra-processed food, eating
2:10:53 more whole foods for lots of different reasons because they’re more satiating.
2:10:58 Because they don’t have this sort of engineered palatability that causes you to overeat.
2:11:02 Another big one which I’m sure you’ve talked about with some of your guests is protein consumption,
2:11:06 making sure you get adequate protein consumption both because there’s this concept of protein
2:11:11 leveraging.
2:11:12 So if you don’t eat a minimum amount of protein, that’s going to cause you to eat more calories
2:11:15 just to try to achieve that minimum amount of protein.
2:11:17 Also just because protein is more satiating and also because there’s this idea of thermic
2:11:21 effect of food and so you basically burn more calories metabolizing protein than sugar or
2:11:26 fat.
2:11:27 How about consumption of fluids during meals?
2:11:29 I’ve heard it said before that we’re not supposed to consume too many fluids because
2:11:34 it’s going to dilute the enzymes that allow us to digest our food.
2:11:37 I’ve heard other people say that’s complete myth.
2:11:41 I think that’s a myth, I mean I think drinking water, I mean so humans don’t have a perfect
2:11:48 capacity to determine whether they’re hungry or thirsty and so drinking water will ensure
2:11:51 you’re not eating because you’re thirsty and there’s no idea of diluting it, I don’t
2:11:58 think that meant.
2:11:59 Distention itself, even though water provides a very limited distention signal, the expansion
2:12:03 of your stomach and intestines is one important way that you terminate feeding and so there
2:12:10 is some component of that where you can get distention just from drinking water.
2:12:14 I’m sorry I blurted out, interesting because I didn’t realize that fluid consumption only
2:12:19 provides a limited signal for distention.
2:12:22 Not fluids, it’s water and so the idea is that you can fill your stomach up with fluids
2:12:27 but the rate at which fluids empty out of your stomach depends on their calorie content.
2:12:32 So basically if you drink water it empties very rapidly into your intestine and then
2:12:36 goes through your intestine and is gradually absorbed.
2:12:38 If you drink something like a glass of orange juice it will empty much more slowly and if
2:12:42 you’re drinking something that’s really high in fat, really high in calories it will empty
2:12:44 extremely slowly over hours and that’s because there’s a negative feedback loop from
2:12:49 the intestine that controls gastric emptying.
2:12:51 So as those first nutrients leave your stomach and enter your intestine that produces hormones
2:12:58 that go back and then slow down the rate of gastric emptying.
2:13:01 The purpose for this is that you don’t want nutrients entering the intestine too fast.
2:13:05 That’s really unsafe.
2:13:06 It feels very unpleasant and your intestine can only metabolize nutrients so fast and
2:13:12 so if there’s calories then it slows down gastric emptying a lot but water just kind
2:13:16 of goes through.
2:13:17 What a beautiful system.
2:13:20 There’s regulation at every point, hypothalamus, brainstem, gut, the rate of emptying based
2:13:28 on the difference between water and orange juice, it’s just awesome.
2:13:33 And that’s part of the reason I think it’s so hard to outsmart the system because these
2:13:39 neurons are making predictions based on the site and smell of food but then the gut is
2:13:43 doing its own thing that’s calculating it separately and relaying that information.
2:13:46 So at every step there are these checks basically that are just confirming that what you thought
2:13:50 happened the first time is actually what’s really going on and so which makes sense because
2:13:54 it’s so important for survival of these homeostatic systems so the product of so much natural
2:13:58 selection.
2:13:59 Which I think at least partially explains why thousand fold increases in peptide hormones
2:14:04 like GLP1 are required to see significant long lasting changes in weight because the
2:14:11 system is so strongly regulated.
2:14:13 Exactly.
2:14:14 Exactly.
2:14:15 It’s hard to beat homeostasis and it’s hard to beat it safely but it sounds like you’re
2:14:21 more or less optimistic about where that whole field of what’s called anti-obesity drugs
2:14:27 is headed.
2:14:28 I’m very optimistic.
2:14:29 I mean, I think, look, I mean, I think that you couldn’t have asked for more so far at
2:14:35 this stage with these GLP1 drugs, incredible weight loss, unexpected health benefits, really
2:14:43 safe as far as we can tell.
2:14:44 I mean, it’s always possible that some new side effect will emerge but these drugs are
2:14:50 millions of people and they’ve been in a lot of people for a long time now and nothing
2:14:53 seems to have shown up.
2:14:55 So I’m very optimistic and I think even beyond that just now that the pharmaceutical industry
2:15:00 is reinvigorated to investigate this question.
2:15:02 There’s so many different — in five years people have so many different options.
2:15:05 It won’t just be ozampic or injaro.
2:15:07 There will be five different, ten different drugs that they can choose from that have
2:15:11 slightly different side effect profiles, slightly different efficacy, perhaps used for people
2:15:15 with slightly different metabolic conditions.
2:15:18 And so it’ll really be a whole palette of medicines you can take that will adjust your
2:15:21 physiology and hunger.
2:15:22 And it’s amazing how well it squares with the understanding of the basic biology.
2:15:32 And that’s a perfect opportunity for me to really just say what is in my mind and clearly
2:15:39 in the minds of everyone listening and watching, which is thank you so much for this absolutely
2:15:44 encyclopedic and exceptionally clear explanation of feeding and thirst and salt regulation
2:15:52 and these new drugs that are, you know, in everyone’s minds and everyone’s hearing about.
2:15:58 I’ve learned so much today.
2:15:59 I know everyone else has.
2:16:01 You run a incredible laboratory.
2:16:04 I’ve tracked your career for a very long time.
2:16:06 Every paper is spectacular and you’re in a very competitive field and you’ve contributed
2:16:11 in enormous ways to our understanding of these important processes.
2:16:15 And I don’t just say that as a formality.
2:16:17 I know that to be true given that we, you know, are from the same field and have known
2:16:23 each other for a long time and I’m familiar with your work at a deep level.
2:16:28 Today has just been an absolute privilege and a gift to learn from you and I know everyone
2:16:34 feels the same way.
2:16:35 So thank you for taking time out of your busy research schedule and the other important
2:16:39 areas of your life to come here and educate us all.
2:16:41 I learned so much basic and practical knowledge and I know everyone else did as well.
2:16:47 Thank you so much.
2:16:48 Thank you.
2:16:49 This has been really fun.
2:16:50 I’m really glad we had a chance to do this.
2:16:51 We talked about some of my favorite topics.
2:16:53 So it’s always a pleasure and talk with another neuroscientist about these things is fantastic.
2:16:56 Right.
2:16:57 Well, please come back again.
2:16:59 Meanwhile, thanks for everything you do.
2:17:01 All right.
2:17:02 Thanks.
2:17:03 And for today’s discussion with Dr. Zachary Knight to learn more about his research or
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2:18:47 And last but certainly not least, thank you for your interest in science.
2:18:51 (upbeat music)
2:18:53 you

0:00:00 Welcome to the Huberman Lab Podcast, where we discuss science and science-based tools
0:00:04 for everyday life.
0:00:07 I’m Andrew Huberman and I’m a professor of neurobiology and ophthalmology at Stanford
0:00:13 School of Medicine.
0:00:14 My guest today is Dr. Jonathan Haidt.
0:00:16 Dr. Jonathan Haidt is a social psychologist and professor at New York University.
0:00:21 He is also the author of several important best-selling books, including The Coddling
0:00:25 of the American Mind and, more recently, The Anxious Generation, How the Great Rewiring
0:00:30 of Childhood is Causing an Epidemic of Mental Illness.
0:00:33 And today we talk mainly about the anxious generation, however, it is not a purely pessimistic
0:00:39 conversation.
0:00:40 Indeed, Dr. Haidt offers several clear solutions to the mental health crisis that now exists
0:00:47 and that we have all created through the use of smartphones, in particular in kids entering
0:00:52 and transitioning through puberty.
0:00:55 In today’s episode, we discuss so-called critical or sensitive periods for social development,
0:01:00 for the development of an understanding about competition and violence, about sex, and how
0:01:05 boys and girls are impacted differently by smartphone use and the specific solutions
0:01:09 that do exist and that Dr. Haidt has created that can place boys and girls as well as young
0:01:15 adults back on the trajectory of mental health.
0:01:18 So today’s discussion is really one that brings together an understanding of neurobiology,
0:01:23 psychology, social psychology, and technology in ways that are designed to serve the most
0:01:29 critical members of our species, meaning our youth.
0:01:32 And for those that have already gone through youth, today’s discussion is also relevant
0:01:36 to you because as many of you know and perhaps have experienced, most everybody nowadays is
0:01:41 challenged in some way by smartphones, both for the utility and the ways in which they
0:01:46 can diminish our social and family interactions, academic performance, and more.
0:01:51 So thanks to Dr. Haidt, today’s discussion really is a solution-based one, and it’s
0:01:55 one that is sure to educate, inform, and inspire specific, positive action.
0:02:01 Before we begin, I’d like to emphasize that this podcast is separate from my teaching
0:02:04 and research roles at Stanford.
0:02:06 It is, however, part of my desired effort to bring zero cost to consumer information
0:02:10 about science and science-related tools to the general public.
0:02:13 In keeping with that theme, I’d like to thank the sponsors of today’s podcast.
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0:06:21 And now, for my discussion with Dr. Jonathan Haidt.
0:06:23 Dr. Jonathan Haidt, welcome.
0:06:26 Thank you, Andrew.
0:06:27 I’ve been a longtime listener, I’ve developed many good habits because of you.
0:06:31 Thank you.
0:06:32 Thank you.
0:06:33 Well, you look very healthy, and I’m delighted to have you here.
0:06:36 I’m a longtime fan of your work.
0:06:38 I’ve read The Cuddling of the American Mind.
0:06:40 It’s an incredibly important book, The Anxious Generation, incredibly important book.
0:06:46 I’ll just start off with an easy question, which is, how are we doing as a species?
0:06:52 How are we doing as a species?
0:06:53 Well, as a species, as one of my friends said, “We’re going to be pretty hard to kill off.
0:06:57 We’ll be like cockroaches, and we’re pretty inventive in that way.”
0:07:01 But as a civilization, I think we might well be at a point of, there are peaks and valleys,
0:07:08 and there are some cycles in history.
0:07:11 And we may be at one of those turning points, and it’s going to be pretty unclear what happens
0:07:16 over the next five or 10 years.
0:07:19 It’s a very interesting time to be a social scientist.
0:07:21 I’ll just leave it at that.
0:07:23 I suppose we can’t point to any one factor, but we wouldn’t be sitting here today.
0:07:29 You wouldn’t have written The Anxious Generation, and it wouldn’t be having the incredible impact
0:07:33 that it’s having.
0:07:34 We’re not for the fact that smartphones have dramatically, profoundly changed the way that
0:07:41 we interact as a species.
0:07:43 In fact, a colleague of mine at Harvard, Jeff Lichtman, who’s world famous for neuroplasticity,
0:07:50 said a few years back, “This is probably the first time in human history that humans have
0:07:54 written with their thumbs,” implying that the brain representation of the thumbs is
0:07:58 probably very different in all of us than it was prior to that, because the brain is
0:08:03 an adaptive map of our experience in many ways.
0:08:07 That’s a somewhat innocuous example of the changes that have occurred, the use of the
0:08:12 digits, the thumbs to write.
0:08:16 But there’s so much more going on now as a consequence of smartphones.
0:08:19 So if you were to say the day, the date, the year in which everything changed, would it
0:08:28 be the day that most everyone had and has a smartphone somewhere around 2010, 2011, 2012,
0:08:37 or did all of this start prior?
0:08:38 Right.
0:08:39 Yeah.
0:08:40 Well, actually, if it’s okay with you, I’ll answer that by giving sort of the history, because
0:08:44 the short answer would be 2010 to 2015, but it’ll make more sense if I just sort of go
0:08:47 through how we got there.
0:08:49 So changes in technology, when you connect people more, you get roads, you get telephones,
0:08:54 these things are all great.
0:08:56 They lead to massive gains in knowledge, productivity.
0:08:58 Yes, sometimes there are disruptions, but in the history of humanity, they’ve been great.
0:09:03 The internet was that when you and I are old enough to remember, do you remember the first
0:09:06 time you saw a web browser?
0:09:07 I do.
0:09:08 And it was like, you mean, I just like, I type in a question and I get the answer.
0:09:13 I don’t have to go to the library.
0:09:14 I mean, it was miraculous.
0:09:18 And I can talk to people for free.
0:09:20 We had that by email, which was free.
0:09:22 So in general, connecting people is good, and we were all very optimistic about the internet
0:09:25 in the 1990s.
0:09:26 It was amazing.
0:09:27 And in our conversation today, I want to make it very clear, the internet is absolutely
0:09:30 amazing.
0:09:31 This is not about how the internet is bad.
0:09:34 Smartphones or the iPhone is absolutely amazing, although there are some things about it that
0:09:38 are problematic.
0:09:39 It’s really especially social media, which has changed things.
0:09:42 And so if we look at a kid, let’s take a teenager in 2010, let’s say January 2010.
0:09:51 At that point, there’s no Instagram, there’s no front-facing camera.
0:09:55 They all have mostly, they have flip phones.
0:09:57 The iPhone came out in 2007, but they don’t mostly have them.
0:10:00 So in 2010, most teenagers are using the flip phone as a tool to call each other, text each
0:10:07 other, meet up.
0:10:08 So when technology helps us achieve our goals, that’s good.
0:10:12 By 2015, everything’s different.
0:10:14 By 2015, the great majority of Americans, certainly teens, have a smartphone with a
0:10:19 front-facing camera.
0:10:21 The girls are mostly on Instagram, which was the first social media platform that you had
0:10:25 to be on a smartphone for.
0:10:27 Everything else was web-based.
0:10:28 They have high-speed internet, unlimited texting, and now it’s possible to spend 10, 15 hours
0:10:34 a day on your phone.
0:10:36 Nobody could do that with a flip phone.
0:10:38 So I point to that, it’s that five-year period, 2010 to 2015, which I’ve called the great
0:10:43 rewiring of childhood because it affects everything, everything about what children and teenagers
0:10:48 are doing.
0:10:50 I can recall in 2010, I was actually in New York City visiting friends.
0:10:54 I got my first smartphone and I recall I was up at 1.30 in the morning scrolling on this
0:11:00 thing and thinking, “This is unbelievably addicting.”
0:11:02 Nowadays, I think of it less as addicting, but almost like an OCD of sorts.
0:11:09 Here I’m not talking about clinically diagnosed OCD, but the interesting thing about OCD is
0:11:14 that the compulsions, the behaviors don’t serve to reduce the obsessions, rather they
0:11:20 exacerbate them or reinforce them.
0:11:22 In many ways, I feel like smartphone use and social media use in particular is an OCD
0:11:28 of sorts.
0:11:29 It’s not just a habit.
0:11:30 It’s not just an addiction.
0:11:32 It’s an obsessive-compulsive loop.
0:11:34 It’s already a struggle to pay attention.
0:11:38 Ancient traditions have taught techniques to improve your focus, your attention.
0:11:42 We’re easily distracted.
0:11:46 I don’t work on my phone very much because I hate to type on the phone and I’m always
0:11:51 at a computer, but even for me, sitting at my computer, as soon as the thinking gets
0:11:56 hard, as soon as I’m writing, I’ve been doing something that requires concentration, some
0:11:59 little part of my brain says, “I wonder what the weather’s going to be,” and I go check
0:12:03 the weather.
0:12:04 “Oh, did I get any email?”
0:12:05 I go check my email probably 40, 50 times a day, and I know that’s terrible.
0:12:10 The question is, “Is it a compulsion where I feel pulled, I have to check it, or something
0:12:15 bad will happen?”
0:12:16 No.
0:12:17 It’s more like, imagine trying to do your work.
0:12:21 Imagine trying to be a kid in school and you have on your desk in front of you, you have
0:12:26 your television set, your record player, a walkie talkie to talk to your friends, a
0:12:30 guitar, a painting set, all a raid in front of you, and your teacher is telling you about
0:12:34 geometry.
0:12:35 What are you going to do?
0:12:37 Probably one of these things.
0:12:39 I think the smart phone, whether it’s a flip phone, it’s a tool.
0:12:42 You pull it out if you want to talk to someone, then you put it away, but the smart phone,
0:12:46 there’s no reason to ever put it away.
0:12:48 Talk to us about the scary statistics.
0:12:51 There’s just no way around this.
0:12:53 We will talk about solutions.
0:12:54 You offer some incredible solutions in the book, actually solutions that everyone listening
0:12:59 and watching can participate in, not just by restriction.
0:13:02 We’ll talk about what that means going forward.
0:13:07 Where are we at now, and when did we start to see the trend toward diminished mental
0:13:13 health in particular in girls?
0:13:15 Feel free to hit us with the scary truth.
0:13:18 Sure.
0:13:19 Let’s imagine, in the US, we have really good statistics based on annual or biannual surveys.
0:13:24 There’s three or four big ones that allow us to see what’s happened since the ’70s.
0:13:30 What I’d like listeners to imagine is imagine a bunch of lines, maybe a line for boys, maybe
0:13:35 a line for boys, a line for girls showing the percentage that suffer from anxiety, depression,
0:13:40 or that have self-harm.
0:13:41 Those three really go together.
0:13:43 Imagine these lines.
0:13:44 They move around a little bit, but they’re actually pretty stable from the 1990s all the
0:13:47 way through 2010, even 2011.
0:13:50 There’s no sign of a problem.
0:13:51 On some measures, they’re getting actually a little bit better.
0:13:54 It’s stable and low.
0:13:56 Well, low, if there are around, say, 12%, 15% of girls qualify as having had a major
0:14:01 depression, that’s much higher than we would like.
0:14:05 That’s a problem, but it’s nothing compared to what it is today.
0:14:09 The lines are pretty flat until around 2012, and then all of a sudden, the lines for girls
0:14:15 go up like a hockey stick.
0:14:17 It’s not a subtle thing.
0:14:19 It really is.
0:14:20 There’s an elbow.
0:14:21 It’s not on a light switch in 2012.
0:14:23 That’s for the American data.
0:14:25 Internationally, you see very similar things.
0:14:27 It’s not necessarily 2012 in other countries, but the girls’ graphs are very sharp.
0:14:31 The boys are also up on depression and anxiety.
0:14:34 They’re also way up.
0:14:36 Depending on the measure, everything is in the ballpark of 50% to 150%.
0:14:40 Almost all the numbers are in that range.
0:14:43 We’re not talking 10% or 20% increases here.
0:14:45 For most things, we’re talking close to a doubling, especially for the younger girls.
0:14:50 The boys’ curves, interestingly, are smoother.
0:14:53 That is, the boys are more depressed and anxious, but it’s not 2012.
0:14:58 It actually often begins more like 2009, 2010, and then it just keeps going up gradually.
0:15:04 That’s a real clue, which we’ll come back to when we talk about the boys’ story.
0:15:08 A lot of people say, “Oh, it’s just self-report.
0:15:12 Gen Z, they’re really positive about mental health and they’re willing to talk about it.
0:15:19 It’s a good thing.”
0:15:20 The fact that we see the exact same curves, the very sharp uptick for girls in hospital
0:15:26 admissions for self-harm, psychiatric emergency department visits, and we see this in the
0:15:31 US, Canada, Australia, New Zealand, the UK, the Scandinavian countries.
0:15:37 Something happened across the developed world around 2012.
0:15:45 I mean, Twangie was the first to really raise the alarm.
0:15:47 She and I keep saying, “Well, we can’t find another candidate.
0:15:51 Nothing else fits the pattern.”
0:15:52 Oh, and there’s actually not just correlational data, there’s experimental data, too.
0:15:58 We think, of course, look, everything’s complicated.
0:16:01 Mental health is complicated.
0:16:02 If you want to understand why one person is depressed, there are going to be many stories.
0:16:06 If you want to understand why depression rates rose for girls faster than boys all over the
0:16:11 developed world, unless someone confined like some hormone-disrupting chemical that was
0:16:16 suddenly sprayed over northern Europe and the South Pacific and the US and Canada around
0:16:22 2012, there is no alternative explanation.
0:16:28 We break down smartphone use in these young girls that correlates with and maybe is causal
0:16:35 for this diminishment in mental health.
0:16:38 There are a number of different variables.
0:16:40 There’s the time spent on the phone.
0:16:44 There’s the specific content that they’re viewing, and that’s a vast discussion that
0:16:48 we’ll get into.
0:16:50 There are the social dynamics associated with being on a phone as opposed to in-person interactions,
0:16:57 and then there’s, and I can’t help myself, but as a neuroscientist who trained in the
0:17:00 biology, the visual system, there’s the effect of looking at something at about eight inches
0:17:06 to 12 inches away from you for much of the day as opposed to navigating an environment
0:17:10 the way that we had for hundreds of thousands of years prior.
0:17:14 There are a lot of features within this thing that we call smartphone use.
0:17:18 There’s also the disruption in sleep.
0:17:21 There’s additional blue light exposure.
0:17:23 There’s just so much to it.
0:17:25 If we pull all that together for the time being and put in a basket of smartphone use,
0:17:29 and maybe we’ll pull out each of those variables one by one as we go forward, what are the
0:17:34 numbers in 2012 in terms of how much time girls, maybe you can give us an age range, are spending
0:17:43 with the smartphone?
0:17:44 Was it, they got the smartphone and immediately we’re spending six to eight hours a day on
0:17:47 the thing?
0:17:48 Or has it been gradual?
0:17:49 So let’s start with the time variable.
0:17:52 Sure.
0:17:53 Okay.
0:17:54 So first, the way you put it is actually very helpful.
0:17:55 What I want listeners to imagine, let’s say that I can imagine on the left side of
0:17:59 a slide, I haven’t made this slide, I’m formulating it in my head, imagine on the left side of
0:18:03 the slide, a whole bunch of harmful changes.
0:18:07 If you’re getting less sleep, that’s bad.
0:18:08 If you’re having blue light at night, that’s bad.
0:18:10 If you’re not going out in nature, that’s bad.
0:18:12 If you are sedentary, so imagine about 15 different things, if you’re being contacted
0:18:18 by strange men around the world who want to have sex with you, that’s not good for 11,
0:18:22 12-year-old girls.
0:18:23 So there’s all these different potential harms, and then imagine all these different potential
0:18:28 effects, one of which is depression and another is anxiety and another is self-harm.
0:18:33 If there’s doing worse in school, there’s becoming more shallow, there’s conflicts with
0:18:38 yours.
0:18:39 So there’s a whole bunch, and then we want to look at the causal connections, and what
0:18:43 I’m trying to draw out is, suppose we could quantify the degree to which sheer time, just
0:18:49 spending five hours a day, does that make you more anxious automatically?
0:18:53 Well, maybe a little, but that’s probably not the main effect.
0:18:57 So there’s a gigantic multi-causal network of effects.
0:19:02 Now, I have good numbers for how much teens are using these devices and these platforms
0:19:09 today.
0:19:10 Pew, in particular, has done a great job of tracking changes in this since the 2000s.
0:19:17 What we know today from both Pew and Gallup is that young people in America are now spending
0:19:21 about five hours a day just on social media.
0:19:25 Just social media.
0:19:26 Mostly Instagram?
0:19:28 So the huge time suck is the videos.
0:19:31 So it’s actually TikTok and YouTube are counted in this analysis, they’re counted as social
0:19:35 media.
0:19:36 YouTube is marginally social media, it’s more of an information source.
0:19:40 But the point is, especially the short videos.
0:19:42 The short videos are really, really addictive because the time between action and reinforcement
0:19:47 is so quick that that, as you know, in behaviorism, that’s the key, it’s the quick reinforcement.
0:19:54 So five hours a day, it’s a little bit more than that for girls, a little less for boys.
0:19:58 Just on social media, 35 hours a week of strange stuff coming in from random weirdos on the
0:20:04 Internet.
0:20:05 Imagine letting your kid import 35 hours.
0:20:09 Then you add in everything else, video games, everything else you do on a smartphone.
0:20:14 So now we’re up to seven to 10 hours in that range a day and this is not counting school.
0:20:19 Now, of course, in school, six hours a day for a lot of kids, two or three hours of that
0:20:23 is screen time as well.
0:20:25 So that’s why I say kids used to have a play-based childhood, play is the basic thing mammals
0:20:30 do and since 2010 or 2012, our kids have a phone-based childhood and I don’t think that
0:20:36 is, it’s just incompatible with healthy human development.
0:20:40 Maybe we can back up even before 2010 and talk a bit more about the play-based childhood.
0:20:47 I heard you say last night at a terrific lecture that you gave that when we don’t trust our
0:20:53 neighbors, we are far less likely to let our kids out to play without observation or oversight
0:21:01 and that leads to a whole host of negative consequences.
0:21:04 So if we were to dial back to the history clock even further and talk about, let’s say,
0:21:11 the 1950s, ’60s and ’70s, I was born in ’75, I basically was kicked out of the house every
0:21:16 day to go play.
0:21:17 My mom would say, “Get out of the house.”
0:21:19 I now realize she wanted space, but we would go down the end of the street to the cul-de-sac
0:21:24 and we would just play and do all sorts of things, some of which were destructive, some
0:21:28 of which were good and there were a lot of dynamics that got worked out in the process.
0:21:34 My sister would go hang out with the, basically the older sisters of those boys, that’s kind
0:21:37 of how our neighborhood happened at the Arrangement, that was fortunate and they would do their thing.
0:21:44 So 1950s and ’60s, what did social dynamics look like among kids?
0:21:50 Yeah.
0:21:51 So I think what we need to do is tell this story of what happened as a tragedy in three
0:21:56 acts and the first act is the loss of community, the loss of trust in each other.
0:22:02 So if we go back to the ’50s and ’60s, but we can even go back, my parents grew up in
0:22:08 New York City in the ’30s and ’40s.
0:22:13 Kids all spontaneously organized themselves into villages.
0:22:16 Village life is, it seems to be sort of the default way of living that humans have preferred
0:22:20 for several thousand years.
0:22:25 And it’s where you know your neighbors, the kids run around, all the adults take part
0:22:30 in supervising all the kids, but nobody has to helicopter because the kids are playing,
0:22:34 they’re doing their thing.
0:22:35 If there’s a real threat, if there’s a lion or invaders, then they all come running home
0:22:39 or whatever, but kids need to be out playing with each other, especially outdoors.
0:22:45 We evolved in savannas, we evolved in different parts of the world, we’re attracted to nature.
0:22:51 So that’s the way it always was.
0:22:53 Now especially if we, in the 1950s and ’60s, America had just been through a world war
0:22:59 and the greatest way to make people trust each other, the greatest way to boost social capital
0:23:04 is a foreign attack and of course Pearl Harbor did more for American coherence than anything
0:23:09 else in history, in modern history.
0:23:11 9/11 did that too, but only for a little while and then we lost it.
0:23:16 So for a lot of reasons, people trusted their neighbors, kids were out playing, you know,
0:23:20 my parents grew up in the Depression in New York City, the kids were all out playing stickball
0:23:23 on the street or in a parking lot.
0:23:26 In the 1970s, there is a real crime wave.
0:23:29 Crime goes through the roof actually and it goes through the ’80s, that goes all the way
0:23:33 to the early ’90s.
0:23:34 Even still, you were kicked out of the house to go play.
0:23:37 Even in New York City, all kids went out to play.
0:23:40 That’s just the way it was.
0:23:42 But we’ve been to lose trust in each other for a lot of reasons.
0:23:44 Robert Putnam wrote about this in Bowling Alone, the loss of social capital.
0:23:50 Many reasons for that, the changing media environment, air conditioning and television,
0:23:54 people are not hanging out on their porch in the summertime to get away from the heat.
0:23:59 They close the door and they put on the AC and they watch TV.
0:24:02 Family sizes are shrinking.
0:24:03 There are not that many kids around.
0:24:05 So for a lot of reasons, by the ’90s is the key decade where act two of the tragedy happens
0:24:10 and that’s the loss of the play-based childhood.
0:24:12 So in America and Britain, we freaked out about child abduction and child sexual abuse.
0:24:19 Some of the scandals were real.
0:24:20 The Boy Scouts, the Catholic Church, there were cases where trusted organizations were
0:24:25 covering up abuse.
0:24:26 And I recall the abduction thing, the milk carton thing.
0:24:30 And there was a show, I think my name is Brian, about the kid who was abducted and all he
0:24:36 remembered.
0:24:37 I think it’s a true story.
0:24:38 His name was Brian.
0:24:39 He would just remind himself every night about his real name.
0:24:43 I think they found him eventually in Berkeley.
0:24:46 Not calling out Berkeley.
0:24:47 I lived in Berkeley for a long time.
0:24:48 But seemed to be the discovery of abducted kids, excuse me, in Berkeley.
0:24:55 There are a few other cases there.
0:24:56 I don’t know what that’s about.
0:24:58 In any event, I grew up thinking that you could get kidnapped.
0:25:01 Right.
0:25:02 Yeah.
0:25:03 Which is, so it’s, I mean, it’s the most terrifying possibility for any parent.
0:25:08 But when I was doing the research for the Codling American Mind, I found according to FBI statistics,
0:25:13 there’s only about 100 to 150 true kidnappings a year in our whole country.
0:25:19 Because if a child, like, who would take a child?
0:25:21 Like it’s a really difficult crime and you’re going to, you know, who would steal a child
0:25:25 from a store?
0:25:26 You know, parents are afraid if your kid goes to the next door on the grocery store, they’re
0:25:28 going to be, how are you going to take a kicking and screaming kid out of a store?
0:25:32 And yet, sorry to interrupt, but the show America’s Most Wanted, I believe, was hosted
0:25:36 by a guy whose kid was abducted and eventually found dead.
0:25:39 Exactly.
0:25:40 Adam Walsh.
0:25:41 That’s right.
0:25:42 Right.
0:25:43 So there was this propagation of this fear.
0:25:44 That’s right.
0:25:45 It happens.
0:25:46 I mean, like one of the deepest fears of any parent I can imagine is that.
0:25:48 That’s right.
0:25:49 But the point is that these crimes are extraordinarily rare.
0:25:52 It’s almost always the non-custodial parent who takes a kid.
0:25:55 It’s a family member because there’s a fight within the family.
0:25:59 So we fear the wrong things.
0:26:00 We’re terrified of kidnapping, but locking our kids up, over-protecting them has spiked
0:26:07 the suicide rate so much that the death toll is vastly higher from the extra suicides than
0:26:12 it would be if we could completely wipe out kidnapping, which again, doesn’t, but you
0:26:16 know, you know, the availability heuristic we say in psychology, if it’s visible, if
0:26:20 it comes to mind easily, then people will freak out about that.
0:26:23 And that’s why people sometimes are afraid to fly in a plane.
0:26:26 They think a car is safer.
0:26:28 So for a lot of reasons, we freak out in the ’90s.
0:26:31 We stop letting our kids out.
0:26:32 We think they must always be supervised.
0:26:34 So that’s act two of the tragedy.
0:26:37 And as that act is happening, we’re keeping our kids inside.
0:26:42 And guess what?
0:26:43 These computer things that we started getting in the ’80s, they’re getting interesting because
0:26:47 now we hook them up to the internet.
0:26:49 In the ’80s, what we’re going to do, WordStar and some primitive video games, like, but in
0:26:53 the ’90s, you get the internet.
0:26:55 And now the kids, especially the boys, the early internet, was much more of interest
0:26:58 to boys.
0:26:59 Boys would take computers apart.
0:27:00 They could build computers.
0:27:01 They would learn to program.
0:27:03 So the boys in particular, they’re okay with losing out on the outdoor play because the
0:27:07 internet is so amazing.
0:27:08 And nerddom started to become cool.
0:27:11 Yes.
0:27:12 Revenge of the nerd, Steve Jobs and Steve kind of, and I know because I grew up in Palo Alto,
0:27:16 see Steve downtown.
0:27:17 He had this, it wasn’t really like Rockstar persona, but he kind of, you know, weaved back
0:27:21 and forth.
0:27:22 It was an icon, kind of like a, you know, counterculture guy, but then he was into design
0:27:27 and computers.
0:27:28 Right.
0:27:29 But it was still really geeky.
0:27:30 Like the fonts were lame.
0:27:32 He brought beautiful fonts to it.
0:27:34 He started bringing the aesthetic forward.
0:27:36 And then of course, girls and women got involved in computers more.
0:27:40 Yes.
0:27:41 Although that really, it only really evens out once you get social media.
0:27:45 Boys are more interested in things and mechanics and systems.
0:27:49 Girls have a more evolved and elaborate mental map of social space, they’re more interested
0:27:52 in social relationships.
0:27:54 So once you get social media, that attracts the girls more.
0:27:57 And then it becomes pretty even that all, you know, all boys and girls, they’re just
0:28:00 incredibly attracted to the internet and things on the internet.
0:28:03 But that sets us up for act three, which is the great rewiring.
0:28:07 That’s the arrival of the phone based childhood that we just talked about between 2010 and
0:28:11 2015.
0:28:12 That’s when everything changes.
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0:30:01 Okay, so we’ve got three acts, all of which are tragedies.
0:30:06 Yep, loss of community.
0:30:07 Right.
0:30:08 So community and trust is down.
0:30:09 That’s right.
0:30:10 And then acts two is we take away the play-based childhood because we’re so afraid because
0:30:16 we no longer trust our neighbors.
0:30:18 Then act three is as long as the kids are inside and on computers already, oh, well, now just
0:30:25 a smartphone and a tablet.
0:30:26 These are just cooler computers.
0:30:28 Nothing wrong with that, right?
0:30:30 And that’s what we thought early on.
0:30:31 In the early 2010s, we thought these things were miraculous.
0:30:33 Oh, you know, if my kids use them, maybe they’ll be the next Steve Jobs.
0:30:37 Maybe they’ll be really technically sophisticated, we thought, and it’s not true.
0:30:42 And now we’re in this third act of the tragedy.
0:30:45 You touched on some of the male/female differences.
0:30:49 Maybe you could talk about those a little bit more.
0:30:51 So you said girls tend to focus more on social dynamics, boys more on systems.
0:30:56 I’ve heard you say that the boys in general veer toward more, for lack of a better way
0:31:02 to put it, more on the spectrum type behaviors.
0:31:05 Could you elaborate on that and how it impacts online use and the particular sites that they
0:31:10 tend to gravitate towards and then on the other side for girls?
0:31:14 Yeah, one of the psychological traits that is the biggest differentiator between boys
0:31:20 and girls and between men and women, let me state clearly, that sex differences in ability
0:31:26 are generally pretty small and they’re few and far between.
0:31:30 Sex differences in interest are all over the place and they’re often very large and they’re
0:31:35 true across cultures and some are true across species.
0:31:39 It’s what you enjoy.
0:31:40 And so, and here I’m drawing on the work of Simon Baron Cohen, who’s the cousin of Sasha
0:31:45 Baron Cohen in the UK.
0:31:48 And Baron Cohen’s work on autism shows that because of prenatal testosterone changing
0:31:57 the body, changing the brain, we all start off as girls in utero after conception, but
0:32:02 then the 10th week of gestation, if there’s a Y chromosome, it triggers a little bit of
0:32:06 a testosterone, which then makes the testes develop and then that creates testosterone.
0:32:13 And all of this, the effect on the brain appears to be a shift away, a little bit away from
0:32:18 empathizing in Baron Cohen’s terms.
0:32:20 You can either be a high empathizer or you can be a high systemizer.
0:32:25 Systemizers are people who love subway maps and they pick them up quickly and they like
0:32:29 programming and they like to see how systems are related.
0:32:33 It’s possible to be high on both, but most people are more one way than the other.
0:32:38 So once you see that, now you can understand why this amazing new internet drew everybody,
0:32:46 but it drew the boys and the girls to different parts of it.
0:32:49 And so, you know, metaphor that I’ve started using these days, I actually did get this from
0:32:53 Yasha Monk has a great book called The Identity Trap and Yasha points out that a trap has to
0:32:59 have bait in it that’s attractive.
0:33:01 There has to be something that makes the creature want to go into the trap.
0:33:05 And then once they get the bait, there has to be something that prevents them from leaving.
0:33:09 That’s what a trap is.
0:33:11 And in this case, if you want to catch a girl, don’t show her like the operating system of
0:33:17 a computer, don’t show her war games.
0:33:20 Show her what Maria just said about Julia or what Julia just said about her.
0:33:26 Do you want to know?
0:33:27 Of course you want to know.
0:33:29 And now everybody does, but girls more than boys, they want to understand the social dynamics.
0:33:33 So the girls go rushing into Instagram where everyone’s posting photos of themselves, of
0:33:38 other people, of the party they were at.
0:33:40 The girls go rushing into social media in general, Instagram, Pinterest, and Tumblr
0:33:47 were the three big ones that girls went into in the early 2010s.
0:33:51 And then once they take the bait, they can’t escape because now that everyone is talking
0:33:56 on Instagram, let’s say, if you leave, you’re alone, you’re not going to talk to anyone.
0:34:01 So that’s how you trap girls, and that’s what happened to girls.
0:34:04 How do you trap boys?
0:34:05 What are the things that boys most want to do?
0:34:06 If you let them do whatever they want, what are the two things that really attract them?
0:34:09 One is war and the other is sex.
0:34:11 So if you say, do you want to watch a movie that has violence in it?
0:34:16 Or do you want to watch sports, which is play war?
0:34:19 Boys are more likely to say yes.
0:34:21 Or play a first person shooter game.
0:34:23 Exactly.
0:34:24 That’s right.
0:34:25 It’s hunting and it’s war.
0:34:28 And if you can simulate that, when I was a kid, I remember playing Seawolf.
0:34:33 You shoot torpedoes at a boat in the distance, and it was very primitive technology.
0:34:38 Even the battleship.
0:34:39 Yeah.
0:34:40 Oh, that’s right.
0:34:41 Even battleship.
0:34:42 That’s right.
0:34:43 That was a big deal.
0:34:44 Yeah.
0:34:45 That’s right.
0:34:46 Little plastic boats.
0:34:47 That’s right.
0:34:48 Yes.
0:34:49 Sinking somebody else’s battleship by intuing where the location of their ships were behind
0:34:50 a wall.
0:34:51 It was so satisfying to sing somebody’s battleship.
0:34:53 So boys really want to play at war.
0:34:55 And I really learned this when I was 30.
0:34:58 And I have a group of buddies from college, and we get together once a year.
0:35:02 And one year I hosted in Charlottesville, and we played paintball.
0:35:05 We went to a paintball place, and there were about five or seven other guys, and we divided
0:35:11 up into teams.
0:35:12 And we were divided among ourselves on the teams.
0:35:14 And it was unbelievably thrilling to work with other guys, to hunt and shoot my friends.
0:35:22 And we came out afterwards, all of us.
0:35:23 And it hurts when you get with the paintball.
0:35:26 It hurts.
0:35:27 You’re well.
0:35:28 Yeah.
0:35:29 Which is important.
0:35:30 It’s actually very important.
0:35:31 Because then you really take it seriously.
0:35:32 You really don’t want to get shot.
0:35:34 But it was absolutely thrilling.
0:35:35 It really felt like there was a room in my heart, as a man, there’s a room in my heart
0:35:39 for war that had never been opened.
0:35:42 So boys want to play at that.
0:35:44 And then the multiplayer video games, the first person shooter games, all these things
0:35:47 let them do that.
0:35:48 The other thing, of course, that boys want to do is look at naked women.
0:35:51 And so it used to be Playboy magazine.
0:35:53 Now it’s super hardcore sex with anal sex, and gang bangs, and choking, and all sorts
0:35:58 of things.
0:36:00 So the boys really get– that’s heat trap a boy.
0:36:03 Show them, let them play war games, and give them sex.
0:36:07 And once they do that, they can’t escape.
0:36:08 So interesting.
0:36:09 We did an episode long ago on sexual development, meaning how hormones influence brain development,
0:36:14 which I spent a little bit of time on for my masters.
0:36:16 And by the way, you got the biology exactly right.
0:36:20 And it’s fascinating the way that these hormones organize the brain.
0:36:25 And some people enjoy learning that it’s testosterone from the testes.
0:36:29 It’s the Y chromosome, then the testes, and then testosterone that’s converted to estrogen
0:36:34 that then actually has the organizing effects of–
0:36:36 Oh, yeah.
0:36:37 It’s weird, right?
0:36:38 It’s weird.
0:36:39 –masculinizing the brain.
0:36:40 They’re all these flips in biology, counterintuitive flips.
0:36:41 But I like to mention the flips because they normalize the idea that testosterone creates
0:36:45 maleness and estrogen creates femaleness.
0:36:48 That’s actually not true.
0:36:49 But you got the biology exactly right.
0:36:51 But I was going to add one more thing besides war, violence, and sex.
0:36:58 There seems to be an interest, my boys, in remote control frames.
0:37:05 Oh, absolutely.
0:37:06 I hadn’t had a distance.
0:37:07 Yeah.
0:37:08 Action at a distance.
0:37:09 So remote control cars.
0:37:10 I never had a remote control helicopter.
0:37:11 We would have died to get one.
0:37:12 But remote control car that we built, my dad and I built together, that was thrilling.
0:37:18 And then when we talk about girls and some of the preferences for certain activities,
0:37:23 maybe we’ll get into some others.
0:37:25 But yeah, something about remote control vehicles and vehicles generally.
0:37:30 That’s right.
0:37:31 So there’s an important psychological word called effectiveness made up by White in
0:37:36 the 1950s.
0:37:37 Effectance is the desire to be a cause.
0:37:40 I had this effect on the world.
0:37:43 And a nine-month-old infant in the crib, when he discovers, if I pull this, if I hit
0:37:50 this, a sound happens.
0:37:52 It’s thrilling.
0:37:53 You did that.
0:37:54 And this stays with us for life.
0:37:56 You want to see that the things you do have an effect.
0:37:59 And especially boys are more in the physical world, mechanical world.
0:38:05 And so shooting a gun.
0:38:06 I remember when I was a kid, I had a BB gun that I bought at a church bazaar.
0:38:09 I hid it from my mother, kept it in the closet.
0:38:11 But my best friend and I, we’d set up cans on a row and you shoot them.
0:38:14 And boom, you knock it, it’s amazing, it’s thrilling.
0:38:19 That does seem to be a sex difference.
0:38:21 Now girls, I think, and here I’m speculating, but girls seem to be more interested in having
0:38:26 an effect in the social world.
0:38:28 So everybody wants to have an effect.
0:38:31 But boys are more focused on mechanics.
0:38:32 Girls are a bit more on relationships in the social world.
0:38:35 And I’m sure Freud had a field day with this.
0:38:38 But what is the apparent, I don’t have the numbers on this, obsession of girls and horses
0:38:46 and caretaking of animals.
0:38:48 And yet there are also a lot of wonderful stories about boys taking care of dogs.
0:38:52 Like I read where the red friend grows maybe 50 times and I love dogs and I love taking
0:38:56 care of raising my dog.
0:38:58 But there seems to be something about the stereotype is girls and horses.
0:39:04 Yeah.
0:39:05 That’s right.
0:39:06 Yeah.
0:39:07 The cool part is girls, on average, are a little bit more compassionate.
0:39:11 They feel the pain of creatures more.
0:39:14 Boys are more into animal cruelty as a fun thing to do.
0:39:16 An interesting thing to do, effective.
0:39:19 So girls are more compassionate.
0:39:21 Girls tend more to want to be a veterinarian than boys do because girls love animals.
0:39:26 My daughter was desperate for a pet.
0:39:29 And we got her a leopard gecko when she was about eight or nine.
0:39:34 They’re really cool.
0:39:35 But she was crying one day because she could tell like, it’s never going to love me.
0:39:41 And she desperately wanted to–
0:39:42 You don’t know.
0:39:43 Maybe it’s the link, sir.
0:39:44 No, it’s a reptile.
0:39:45 No, it’s a reptile.
0:39:46 No, they’re not mammals.
0:39:47 They don’t have the bond.
0:39:48 And she was desperate for a dog and she begged for years for a puppy.
0:39:51 We finally got one.
0:39:52 She needed an animal with a four-in-a-brain.
0:39:53 She needed an animal.
0:39:54 Yeah.
0:39:55 She needed a mammal.
0:39:56 She needed a mammal.
0:39:57 Now, the horse thing, that’s different.
0:40:00 I’m not going to speculate on that.
0:40:01 I have heard some speculation that it’s because the musculature, it has a feeling of masculinity.
0:40:09 But I don’t know.
0:40:10 But that’s very Freudian.
0:40:11 I was wondering whether or not it was–
0:40:12 I don’t want to get too–
0:40:13 I don’t even get near that.
0:40:14 Yeah.
0:40:15 I was wondering whether or not it was something about the healthy requirement for caretaking,
0:40:20 the brushing, the cleaning, the caretaking of the animal.
0:40:24 It’s pretty elaborate when it comes to a horse.
0:40:27 My first girlfriend had a horse.
0:40:28 She spent more time with that horse than with me.
0:40:30 And the amount of care, like if the horse was coliquing, she would literally go sleep
0:40:34 with it in the morning.
0:40:36 And it seemed like she loved the amount of love that was available to give to the animal.
0:40:42 Yeah.
0:40:43 Anyway.
0:40:44 Yeah.
0:40:45 I would put that in a giant bucket called biofilia, a term that I love from E.O. Wilson.
0:40:50 Just that our species, we evolved in nature.
0:40:52 We evolved with relationships with animals.
0:40:55 And we crave it.
0:40:57 We seek it out.
0:40:58 We can fall in love with animals.
0:40:59 We have relationships.
0:41:01 So I think that’s the healthy part of life.
0:41:03 And again, it’s another area where a phone-based childhood just takes you away from all of that.
0:41:08 It’s interesting this difference between systems and relationships.
0:41:13 I was obsessed with aquaria.
0:41:15 Still am.
0:41:16 I love aquaria.
0:41:17 I love freshwater tanks, aquascaping is something I plan to get back into at some point soon.
0:41:22 But the most interesting part about it was which fish could go with which?
0:41:27 Who would eat?
0:41:28 Who?
0:41:29 The density of fish needed to be in order to maintain the ecosystem and how to not get
0:41:34 a system crash.
0:41:35 Yeah.
0:41:36 It wasn’t so much about the relationship.
0:41:37 It’s between the fish or to the fish.
0:41:38 That’s right.
0:41:39 So it’d be interesting to see if there’s a sex difference on aquariums, whether it’s
0:41:42 more a boy thing because of the interesting, complex systems.
0:41:47 But you know what I’d really like to do with you now, as long as we’re talking about these
0:41:51 developmental pathways, I’m hoping that we can talk about, let’s stay on sexual development.
0:41:58 Because this is something I just have a little section in the book.
0:42:01 In the chapter on boys, I have a section where I review the research on pornography and huge
0:42:08 amounts of study of pornography over the years.
0:42:11 But the hardcore pornography, high-resolution video, boys watching it for many boys, well,
0:42:20 a large number of boys go every day to pornography sites, often more than once a day.
0:42:28 So I’d love to hear your thoughts on how that would – how is that going to change sexual
0:42:33 development during puberty?
0:42:34 A boy who starts, let’s say, at age 12, 13, and does it for 10 years, could we expect
0:42:40 that that boy will be different when he’s 22?
0:42:43 His dating life will be different.
0:42:46 Tell me what you think is happening there in the brain and socially and hormonally.
0:42:49 Sure.
0:42:50 Absolutely.
0:42:51 And I’m not going to demonize pornography, nor am I going to celebrate it.
0:42:55 All I’ll say is that my understanding of the dopamine reinforcement system, and I like
0:43:01 to call it a reinforcement system as opposed to a reward system because people generally
0:43:04 think that dopamine and dopamine hits relate to pleasure.
0:43:08 But dopamine is more of a motivator.
0:43:10 As a neuromodulator, it creates a kind of an agitation state that puts us in a state
0:43:15 of focus and foraging to resolve some gap between how we feel and how we’d like to
0:43:19 feel by seeking things like sex, like food when we’re hungry, like warmth when we’re
0:43:24 like cool when we’re too warm.
0:43:26 It’s a universal currency of pursuit, of craving and wanting as opposed to having.
0:43:32 Dopamine does a lot more than that.
0:43:34 And other neuromodulators are involved in wanting and craving, but dopamine is central
0:43:38 to that.
0:43:40 So I think it’s not just fair to say, but it’s a ground truth that whether or not it’s
0:43:47 a drug like methamphetamine, cocaine, crack cocaine in particular, or some other drug
0:43:53 that hits the system fast and creates a big, big inflection in dopamine, that the more
0:43:59 rapid the rise in dopamine, the bigger the crash in dopamine afterwards, and the more
0:44:06 miserable you feel afterwards.
0:44:08 And the more repeat of the behavior that initiated the peak will occur, aka addiction, or at
0:44:17 least extreme habit formation, depending on how one defines those.
0:44:21 When it comes to dopamine, the other key thing to know is that dopamine in particular high
0:44:28 inflections in dopamine, big peaks in dopamine that occur without much effort, in particular
0:44:34 the kinds of effort that evolved to bring about the dopamine release, such as courting,
0:44:41 dating, learning your preferences, learning the other person’s preferences, working out
0:44:46 issues of discussion, consent, negotiation, et cetera.
0:44:52 When dopamine arrives quickly without effort, such as with amphetamine, crack cocaine,
0:44:57 or pornography, the whole reinforcement loop becomes wired to these short time scales.
0:45:03 You want something, you want it now, and you get it.
0:45:07 But over time, you get less and less of the dopamine peak, and you get more of the dopamine
0:45:11 trough that occurs.
0:45:12 You drop below baseline afterwards.
0:45:14 So all of that is a bunch of neurobiological-ish nerd speak for absolutely the ready availability
0:45:23 of pornography at a few taps on the phone.
0:45:28 No doubt triggers big dopamine.
0:45:30 The first time requires more and more investment in that behavior to get less and less of the
0:45:35 dopamine.
0:45:36 You never get back to the initial value, and you’re driven further and further down the
0:45:39 pathway of addiction.
0:45:40 There’s the loss of all the learning that the brain has evolved to learn how to evoke
0:45:49 dopamine from, I don’t want to say just mate pursuit, but it’s courtship and eventually
0:45:54 sex.
0:45:55 We know that after ejaculation, after orgasm, there’s a dramatic decrease in dopamine and
0:46:01 a huge increase in prolactin.
0:46:03 What does that do?
0:46:04 Prolactin and dopamine are essentially antagonistic to one another.
0:46:07 It creates states of quiescence, calm.
0:46:10 It’s thought to facilitate pair bonding by keeping mates near one another, smelling one
0:46:15 another, sharing pheromones.
0:46:16 In fact, there’s something called the Coolidge effect.
0:46:19 We could talk about the classic Coolidge effect.
0:46:21 They’re these effects that have to do with the inverse relationship between dopamine and
0:46:27 prolactin.
0:46:28 But with pornography, assuming that boys are masturbating to the pornography, and they
0:46:34 are doing that to the point of ejaculation, then they’re getting this kind of quiescence
0:46:39 of the system.
0:46:40 They’re feeling lethargic, relaxed, maybe depending on their age or their motivation,
0:46:45 they’re doing it again and again.
0:46:46 But neither the dopamine nor the prolactin are being devoted to anything about courtship
0:46:52 and pursuit, nor is it, in the case of prolactin, related to anything related to pair bonding.
0:46:57 They’re just sitting there with their computer in their room.
0:47:01 Of course, this occurred with pornography, as you mentioned before, classic pornography.
0:47:04 When I was growing up, if somebody had a penthouse or a Playboy magazine, they would often stash
0:47:09 it for whatever reason behind a business or something, so no one would get caught with
0:47:12 it.
0:47:13 Then you’d go there like a library.
0:47:15 It was in places where, this is getting a little weird, where people didn’t use the
0:47:19 pornography there.
0:47:20 I think they remembered it, perhaps, but they weren’t spending a ton of time with it.
0:47:25 In fact, there was an unspoken rule.
0:47:27 You didn’t take it with you.
0:47:29 This is most kids’ first exposure to pornography or their dad had a Playboy magazine or something
0:47:34 like that.
0:47:35 I hope I described the landscape of the biology well enough, but the short answer is, absolutely
0:47:41 creates major problems in the dopamine reinforcement system.
0:47:44 It’s training the dopamine reinforcement system for fast reinforcement and diminished reinforcement
0:47:50 over time, and none of it translates to the real world.
0:47:54 It’s not just the content.
0:47:56 I guess what we’re getting at here is it’s not just what they’re seeing as so extreme,
0:47:59 and that’s an issue, clearly.
0:48:02 The whole process takes minutes, and it can be repeated over and over, depending on the
0:48:08 refractory period, as opposed to real-world dating and relationships, which takes effort,
0:48:14 and it takes learning.
0:48:15 There’s hardly any learning in the use of a drug like methamphetamine or cocaine about
0:48:20 how your dopamine system works, unconscious learning.
0:48:23 There’s hardly any, if any, learning about sex and courtship in pornography, and it’s
0:48:28 also training the dopamine system, the whole motivational system around sex, to be observational
0:48:34 as opposed to participatory.
0:48:37 I hear a lot, because I’m in the wellness health space, and I’m a man.
0:48:41 Guys reach out by direct message, “Hey, listen, they’ll reach out that they’re having real
0:48:46 issues with erectile dysfunction, with anxiety,” and these things always existed, but there
0:48:52 was a learning, a communication, hopefully some slow your breathing down and communicate
0:48:57 and get back to a place where you’re more comfortable.
0:49:00 They’re not able to translate anything about their experience of sex and pleasure to the
0:49:04 real world, and as a consequence, they’re retreating into a world where they view, if
0:49:10 they’re heterosexual, the opposite sex, or if they’re homosexual, the same potential
0:49:15 partners as these distant foreign objects that they don’t understand.
0:49:19 Wow.
0:49:20 Andrew, thank you.
0:49:21 That was a really powerful and clear description of what I was trying to say in the book coming
0:49:26 just from the psychological side, which is to turn from a boy into a man, there’s a certain
0:49:34 amount of toughening and skill-building, there’s skills that have to be developed, and I’m
0:49:38 so glad to use the word courtship.
0:49:40 I use that word a lot with my students.
0:49:43 I hear almost nobody else using that word.
0:49:44 It’s such an important word, because we did evolve the ability to pair bond, at least
0:49:48 temporarily, and we do have courtship, and it has to start slowly.
0:49:53 If you jump into bed and have sex right away, there’s no chance of courtship.
0:49:56 That part is over.
0:50:00 As you were talking, I was thinking, and I want the listeners to imagine.
0:50:05 Imagine one 13-year-old boy who really wants sex, would like to have a girlfriend, but
0:50:12 he has a laptop, he has a phone, he has a porn hub.
0:50:17 He masturbates two or three times a day.
0:50:19 He’d still like to have a girlfriend, but he’s sexually satisfied because he has all
0:50:22 this amazing pornography.
0:50:26 He does this every day for 10 years until he’s 23, let’s say.
0:50:30 Then we have another boy who maybe he has a Playboy magazine, or maybe he has nothing.
0:50:36 Maybe he just has his imagination.
0:50:37 He masturbates occasionally, as boys do, but he doesn’t have the hardcore porn.
0:50:41 He doesn’t have the fast dopamine.
0:50:44 In this second boy, he puts more effort into actually having a girlfriend, and he learns
0:50:48 how to talk to girls, and he’s flirting, and one is interested in him, and then they
0:50:54 have their first kiss, because I’m remembering back when I was a teenager in my 20s, the
0:51:01 most beautiful golden days, the most memorable days of my life, it was those days when you
0:51:06 have that first kiss, and you know, oh, this is going to turn into something.
0:51:10 Everything sparkles after that.
0:51:11 Everything sparkles.
0:51:12 The point is, it’s slow, and it’s hard work, and then when you finally do have sex, it’s
0:51:19 not like, oh, dopamine crashed, get out of here.
0:51:22 As you said, it’s like a prolactin rise, you hug, you hold the girl, and at some point
0:51:31 you start thinking about marriage, you start thinking, is this the one?
0:51:35 Crazy thoughts like that, you can’t help but think that when you’re falling in love.
0:51:39 At NYU, I teach an undergrad course, and I also teach an MBA course.
0:51:42 Now, the MBAs are all on the dating apps, they’re in their late 20s, they’re all on
0:51:45 the dating apps.
0:51:46 The undergrads, some of them are on dating apps, but they’re 19, they’re mostly dating
0:51:50 in their circles.
0:51:52 And for the MBAs, I really have to work with them to see that these dating apps are cutting
0:51:58 off courtship in a lot of ways.
0:52:00 I mean, yes, you’re texting, but it’s not the same.
0:52:03 So I’m so glad you explained a lot about that.
0:52:06 One is the fast.
0:52:07 It’s the fast satisfaction that prevents you from learning, where slow hard work towards
0:52:13 a biological goal like sex or dating or marriage or love is what builds you up into a competent
0:52:19 man.
0:52:20 Who would want to hire or who would want to date, let’s put it that way, who would want
0:52:22 to date the kid who’d been masturbating three times a date of porn since he was 13?
0:52:27 So yeah.
0:52:28 Yeah.
0:52:29 And there’s all sorts of things.
0:52:30 My father’s Argentine moved to the States in the late 60s, and so I was raised in a fairly
0:52:36 traditional home from the perspective of masculine, feminine roles, and there were all these things
0:52:42 around chivalry.
0:52:43 I remember going to my first junior high school dance, my dad gave me this whole tutorial
0:52:47 about holding the door and how to, you know, it’s interesting that nowadays guys are often
0:52:53 judged in terms of their latency to respond to text messages, you know, something I’m
0:52:58 terrible at.
0:53:00 And it’s interesting that that sort of replaced chivalry, like how responsive somebody is.
0:53:06 So there’s a kind of a bleeding for it as long as we’re just being very open about the
0:53:09 past, present, and perhaps future of this stuff.
0:53:14 I remember growing up and hearing stories.
0:53:15 This wasn’t how my childhood went, but I remember my dad telling me, you know, in Argentina,
0:53:20 the young boys when they would hit puberty used to be taken to prostitutes, so they would
0:53:24 learn how to have sex.
0:53:26 I mean, that wasn’t that long ago.
0:53:28 That wasn’t my childhood.
0:53:29 And I remember thinking like, you know, is this what’s going to happen next?
0:53:33 But he was explaining that’s kind of how it went.
0:53:35 That doesn’t tend to happen anymore, as I understand.
0:53:37 I haven’t heard of it happening.
0:53:39 Right.
0:53:40 But in terms of learning courtship, learning chivalry, learning, you know, who pays, and
0:53:45 a lot of that’s changed with the, you know, the changing milieu of sex and gender dynamics.
0:53:50 But it’s all iterative.
0:53:53 It’s slow and iterative.
0:53:54 And everything about online use, as you mentioned, is it’s fast.
0:53:57 You can find anything with a keyword search.
0:53:59 Right.
0:54:00 No work.
0:54:01 That’s right.
0:54:02 The technology makes everything easier.
0:54:03 We end up talking about AI at all, which every conversation goes through at some point.
0:54:07 That’s my big fear that AI makes everything easy.
0:54:11 Now, that’s great for us adults when we have 50 things we want to do.
0:54:14 If I can give 30 of them to AI, that would be great.
0:54:17 But you know, how many servants do I want my, you know, my son is now 17.
0:54:21 When he was 10, 11, 12, how many servants would I want him to have to take care of his
0:54:25 knees?
0:54:26 Like probably zero.
0:54:27 Like zero is probably the best number.
0:54:30 But, you know, with porn for the sexual drive, with multiplayer video games for sports or
0:54:35 competition, that’s right.
0:54:38 Our kids are, they’re not, they’re not learning or developing.
0:54:41 And this is why, you know, I work in a business school.
0:54:43 I talked to a lot of people in the corporate world and I always ask them, how, how’s it
0:54:47 going with your Gen Z employees?
0:54:48 I’ve never heard a good word.
0:54:49 I’ve never heard, oh, they’re great.
0:54:51 It’s, they’re often people just surprised at how they don’t take initiative.
0:54:56 If, if, if, you know, if, if something is broken, they don’t fix it.
0:54:59 They want to be told what to do.
0:55:01 They don’t have the confidence.
0:55:02 They’re very anxious.
0:55:04 Um, so, you know, I’m not, I’m not ragging on Gen Z.
0:55:07 I’m saying we blocked their development.
0:55:10 We prevented them from having a thousand, 10, that millions of experiences of social
0:55:15 interaction, of challenge, of failure, of fear, of thrill.
0:55:18 And then when they reach the early 20s and they’re employed, employers find there’s something
0:55:23 lacking.
0:55:24 So it sounds to me like boys on smartphones or this over in this 2010 period forward are
0:55:30 getting this kind of hyper stereotypical male experience, first person shooter games, pornography.
0:55:37 Girls are getting this hyper stereotypical female experience, relational, highly relational.
0:55:43 But there are certain dynamics that are missing or certain components that are missing.
0:55:48 Um, yesterday, I heard you mentioned something very, very interesting to me, which is that
0:55:54 in both groups, it seems conflict and any kind of friction is not being resolved among
0:56:01 the participants, but there’s this sort of looking outward for some rule or policy law
0:56:07 or oversight to come in and intervene.
0:56:09 Yeah.
0:56:10 Um, could you talk a little bit about this?
0:56:11 This relates in an interesting way to cancel culture.
0:56:13 Yeah, that’s right.
0:56:14 That’s right.
0:56:15 Um, it would love to, to learn more about this.
0:56:16 Sure.
0:56:17 So aggression is a part of human nature as is cooperation.
0:56:21 And they kind of, they kind of have to go together.
0:56:23 You know, to make it in this world, you have to be able to play politics.
0:56:25 You have to have friends and allies.
0:56:27 You have to stand up for yourself.
0:56:29 Um, you have to push back sometimes, but you have to learn to bury the hatchet.
0:56:34 And you know, if you grew up with siblings, you know, you’re fighting every day and you’re
0:56:37 cooperating every day, and it’s very important practice.
0:56:40 And if you’re playing, if you’re playing sports outside with a bunch of kids in the neighborhood,
0:56:45 you’re making the rules every day.
0:56:46 And then part of the import, part of what’s important when kids are playing is the infractions.
0:56:51 It’s, it’s everybody, the play stops.
0:56:54 People come together.
0:56:55 You know, that was out of bounds.
0:56:56 No, it wasn’t.
0:56:57 You pushed me.
0:56:58 No, I didn’t.
0:56:59 And then every, you know, everybody gets practice playing judge and jury, uh, because everyone
0:57:03 wants the game to go on.
0:57:04 So they’re very motivated to, to work it out and you have to accept the judgment.
0:57:09 What are you going to do?
0:57:10 Storm off and go home to protest.
0:57:11 Then you look like a loser and you don’t get to play anymore.
0:57:13 So natural play with no adult forces the kids to learn social skills that are essential
0:57:19 for democracy.
0:57:20 How do we make rules together?
0:57:22 Just us.
0:57:23 How do we decide how we’re going to govern ourselves?
0:57:25 What do we do when it looks like someone violated a rule?
0:57:27 Well, we’re not just going to kill them.
0:57:29 We’re not going to spell them.
0:57:30 We have to have a way of going on with the play.
0:57:33 So these are such crucial skills for social development for boys and for girls.
0:57:37 And, um, and kids always learn to work that out.
0:57:41 But what happens when the boys are growing up on video games, there are no disputes.
0:57:45 There can’t be a dispute because the game, the software basically manages everything.
0:57:50 There’s no out of bounds or anything.
0:57:53 So the play is missing a lot of the, of the, of the key skills.
0:57:58 Now, um, how are conflicts resolved?
0:58:01 Well, on social media, instead of like a conflict that two girls might have had just the two
0:58:07 of them or with like a group before, which could get worked out very, very quickly.
0:58:11 It’s somebody posts something indirect, maybe it’s indirect criticism and someone takes
0:58:15 it in a way, maybe it was intended that way, maybe it wasn’t.
0:58:18 But before you know it, it’s accelerated.
0:58:20 People are taking sides.
0:58:21 It could blow up.
0:58:22 You don’t know how big it could get.
0:58:23 It could be the whole school now gets drawn in.
0:58:25 This is terrifying.
0:58:27 So really important idea about play is what’s called low stakes mistakes.
0:58:32 So if you make a mistake while playing soccer with your friends, uh, no big deal.
0:58:37 Like, you know, it’s a foul redo, whatever it is.
0:58:41 Um, but if you make a mistake on social media, it could blow up to the point where you are
0:58:45 now a laughing stock and when a kid, when a, especially in middle school, when a kid is
0:58:50 a laughing stock, when everyone’s laughing at them, that is likely to trigger thoughts
0:58:55 even of suicide.
0:58:57 Shame makes us want to disappear and we’re putting our kids, our kids need to be immersed
0:59:01 in small groups, small groups of other kids that are stable, somewhat stable over years.
0:59:08 That’s the healthiest environment, but instead we’re mixing them in with possibly potentially
0:59:12 gigantic groups, including strangers and people who are not engaging their normal empathy
0:59:18 skills, but are being performative, judgmental, judging in order to be liked by others.
0:59:26 So it’s just an inhumane, it’s a, it’s a, it’s an inhuman world in which to raise kids.
0:59:32 And this is part of my point about the great rewiring in 2010s, American kids still had
0:59:36 a recognizable human childhood with a lot of time together with other friends, but that
0:59:41 plunges in the 2010s to the point where now childhood is largely happening alone on a
0:59:46 screen.
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1:01:23 I’ll never forget in middle school being at some assembly and a kid had got down on
1:01:31 all fours behind me and someone pushed me.
1:01:33 Oh yeah.
1:01:34 I stood up and Kevin Gassman was just sitting there just cackling with his face right in
1:01:39 front of him.
1:01:40 So I hit him.
1:01:41 It turns out it wasn’t Kevin that did it.
1:01:42 And he hit me back and it was a disaster and I don’t remember how it panned out, but
1:01:45 we ended up being friends.
1:01:46 So it was kind of how things got worked out.
1:01:47 Well, that’s right.
1:01:48 Conflict and cooperation.
1:01:49 You need the two together.
1:01:50 Yeah.
1:01:51 Incredibly embarrassing both for getting pushed over and for hitting the wrong kid, but credit
1:01:54 for hitting somebody because that’s how boys work things out.
1:01:57 I’m not suggesting people do this, not suggesting violence.
1:02:00 And then both of us feeling silly and then ultimately, well, I don’t know, I made it
1:02:04 to the eighth grade somehow, right?
1:02:08 And the hierarchy among, I mostly had male friends, but the hierarchy was something that
1:02:13 was very dynamic.
1:02:16 I have a good friend who was a, he was a CEO, a commanding officer in one of the East Coast
1:02:22 SEAL team squadrons, he said the reason they’re so effective in those groups is because they
1:02:29 embrace dynamic subordination where people take over as different skill sets are required
1:02:35 and they are relentlessly hard on each other.
1:02:39 This is something they are like relentlessly hard at the level of humor, but also, I mean,
1:02:43 because it’s so high risk and high consequence, they’re just extremely hard on one another.
1:02:48 But it’s all about this dynamic subordination that sure there are leaders by virtue of who’s
1:02:53 appointed leader in certain amount of authority, but there’s this constant dynamic subordination
1:02:58 and it exists in every group of males I’ve ever been a part of.
1:03:01 And it’s wonderful and very reassuring to me because it means that you both get to potentially
1:03:07 step up, but you also get to rest when you, and trust somebody else’s skills.
1:03:11 I don’t know how it operates with girls.
1:03:13 I’ve only been, you know, born with a Y chromosome, this is all I know, but I imagine it exists
1:03:20 there too in different, but in different ways.
1:03:23 So if online, everything is fear-based where one is fearing a dog pile, like if you say
1:03:30 the wrong thing, you’re going to get dog pile, you kind of wonder why anyone participates
1:03:34 at all.
1:03:35 But it seems like people are in there, are they in there intimidated or is boldness rewarded?
1:03:41 Is it only boldness of, I guess they call, you know, slamming down to what are they called,
1:03:47 dunking on other people?
1:03:48 I mean, and here as I’m describing kids, I want to acknowledge, if you look on Twitter,
1:03:54 X, we now call it, in the academic, tech and finance community in particular, this is how
1:04:02 the men behave.
1:04:03 This is how the women behave, but it’s especially apparent that the adults are kind of acting
1:04:08 like kids and the kids are kind of acting like adults.
1:04:11 So what’s going on?
1:04:13 Are we drawn into this as well as adults and are we modeling this or is this just social
1:04:21 media pulling on these strings of deep, evolutionarily conserved wiring?
1:04:28 Yeah.
1:04:29 Well, so first, let’s not be too sort of monochromatic about social media.
1:04:37 There is a lot of humor.
1:04:39 There’s a lot of jokes.
1:04:40 There are a lot of funny cartoons and videos.
1:04:42 Yeah.
1:04:43 I’m learning.
1:04:44 So there is good stuff mixed in and even the bad stuff is entertaining in the way that
1:04:47 looking at a car crash or a dead body is entertaining, people, it draws the eye.
1:04:53 So young people are very interested and us adults, too, are very interested.
1:05:00 It draws us in, but then, yes, it certainly changes our behavior.
1:05:04 Now, actually, there’s some research on trolls.
1:05:10 Visit that whenever you go on Twitter, you become a jerk and actually know it seems more
1:05:20 that what happens is there’s a small number of men, always men, who have a personality
1:05:24 disorder.
1:05:27 They like to be jerks.
1:05:28 They like to get a reaction from people.
1:05:31 They get blocked a lot.
1:05:32 They get kicked off platforms.
1:05:33 And this small number, in a real community, probably when you were growing up, there were
1:05:38 one or two kids who were like this, and they got in trouble a lot, and they probably ended
1:05:41 up dead or in jail.
1:05:43 But online, I suppose it’s 1% of men, 1% of men are psychopaths.
1:05:47 So I suppose it’s this 2% of men, let’s say, who are jerks like this.
1:05:51 Well, online, that’s who we all see.
1:05:57 So in part, it’s that the online world super empowers extremists and jerks.
1:06:03 It’s also that in the online world, everyone is feeling performative.
1:06:07 Everyone is– even if you’re making a joke, you have to think three steps ahead.
1:06:12 How will it be misinterpreted?
1:06:14 So a metaphor that I have in my head whenever I’m online is it’s really just like being
1:06:18 on thin ice.
1:06:19 You can have fun on thin ice.
1:06:20 It’s not all bad.
1:06:22 But you’re kind of always aware that you’re in danger, whereas when you’re hanging out
1:06:26 with your buddies, you’re good friends, you feel totally safe.
1:06:31 And if you accidentally insult one of them, it’s like, sorry, you’re right, I’m sorry.
1:06:37 Even as followership increases, the ice gets thinner.
1:06:40 Yeah, that’s right.
1:06:41 That’s right.
1:06:42 The higher they go, the harder they fall.
1:06:44 And then a lot of people want to see your fall.
1:06:46 I just want to make one point, that was an interesting concept, that was something in
1:06:50 subordination.
1:06:51 Dynamic subordination.
1:06:52 Dynamic subordination.
1:06:53 Kind of like a flock of birds, is how it was described to me.
1:06:56 But I always thought in the tier one special operations community that people would spend
1:07:03 more years there, further and further.
1:07:06 That’s true too, but this idea that it’s just understood that the hierarchy evolves in real
1:07:11 time and the more people embrace that, the better performing the group is as a pack.
1:07:17 Yeah.
1:07:18 Now, the word hierarchy certainly takes on a bad name, especially in our academic circles.
1:07:23 Hierarchy is bad, and power is bad, and subordination, all these things are bad, power, inequality.
1:07:30 But I think part of what’s going on there, so I teach in a business school, and there’s
1:07:33 a huge amount of writing on leadership.
1:07:36 And I haven’t read much of it, but a key idea that I got, trying to remember the author,
1:07:42 is that the key puzzle is not why people want to be leaders, is why do they want to be followers.
1:07:47 We really need to study followership.
1:07:49 And so people are willing to follow because part of our amazing human ability is to work
1:07:55 together in groups to overcome obstacles.
1:07:57 We don’t have sharp teeth, we’re not very, well, we’re fast in long distance, but not
1:08:00 in sprints.
1:08:01 But we’re able to work together, and when we face a common threat, we very willingly
1:08:07 seed leadership to a leader, but we have to trust him.
1:08:11 And if a leader shows that he’s a narcissist, that he’s putting himself first, that he’s
1:08:14 benefiting at our expense, we don’t trust him.
1:08:17 So what you need to do, and I think this is more clear, males are more hierarchical, this
1:08:21 is true in chimpanzees as well, males are, they take to hierarchy more readily.
1:08:27 Males benefit from having practice, I don’t think it is dominance and submission.
1:08:31 I think what you said is actually more effective, it’s like any practice, like being the leader
1:08:37 of this project, and then being a follower because you grant, like, yeah, you lead us
1:08:41 on this, you take the lead on this, and then something else will reverse.
1:08:45 And if you have a young man who has a lot of that experience, that’s going to be a
1:08:49 young man that you will want to employ when he’s in his mid-20s, whereas one who never
1:08:53 had that, it’s just going to be much more difficult to work with in a business setting.
1:08:57 Yeah, the groups of boys I grew up with and men that I’ve worked with and been friends
1:09:01 with, it’s always been understood, like, this guy’s really terrific for finding stuff, and
1:09:06 this guy’s great with vehicles, and this guy’s great with girls, and this guy’s, that people
1:09:11 have different skill sets, and that the group together can really mesh.
1:09:16 But there isn’t an attempt to be something that you’re not, and you quickly find out
1:09:20 who you are by who you’re not, and you find your unique skill set, and you evolve in that
1:09:30 way by not trying to be everything to everybody, whereas I noticed with my sister and her groups
1:09:34 of friends, it’s changed over time, of course, but that there tended to be one girl that
1:09:38 was really dominant in the play session, like the whole time, the bossy one.
1:09:45 And even though some stories, kids’ books that mainly feature boys have that, I don’t
1:09:52 recall that being such a big part of my reading experience or childhood experience, like in
1:09:57 the Encyclopedia Brown books, like there was like the mean kid, but people would slot in
1:10:03 where they were most adept.
1:10:05 So it was sort of like natural tendencies to excel were complementary, and I don’t know
1:10:09 what it is for girls, but online, it seems, all of that’s erased.
1:10:15 So you’ve got these social dynamics that are very heightened being played out on social
1:10:22 media with girls, but boys and men are on there as well.
1:10:28 And most of what’s on social media is social, it’s relational.
1:10:32 So are boys and men being drawn more toward those sorts of interactions, and how well
1:10:36 are they navigating those interactions?
1:10:38 Is it common for boys to make big mistakes online and then be shunned as a consequence,
1:10:45 or is this more common in females?
1:10:48 Yeah, no, that’s a good question.
1:10:52 Life online is performative for girls, a much bigger element of the performance is perfectionism
1:10:58 about the image.
1:11:00 So girls spend a lot more time choosing a photograph, editing a photograph, making sure
1:11:04 everything’s perfect.
1:11:06 Because guys, I literally don’t notice if my socks don’t match, my wife has to tell
1:11:10 me your socks don’t match.
1:11:13 Guys just don’t notice those things as much.
1:11:15 You’re a professor after all.
1:11:16 Yes, we are.
1:11:17 But my point is that life online, it does affect all kids.
1:11:22 So fear of missing out is something that affects everybody.
1:11:25 On Snapchat you see all your friends over there, and you didn’t even know that there was something
1:11:28 going on.
1:11:29 So again, boys and girls, they’ll have similar insecurities, it’s more a question of degree.
1:11:35 So the perfectionism, the playing out the social dynamics to three steps, like girls
1:11:41 are playing three-dimensional chess about social relationships.
1:11:45 But why did he say that if he also wanted this when he knows that she knows that, and
1:11:51 guys are like, “I don’t even know what you’re saying.”
1:11:54 They’re barely playing checkers.
1:11:56 That’s right, that’s right.
1:11:57 And again, it’s the organizing effects of prenatal hormones.
1:12:02 This is not culturally taught.
1:12:04 This is what kids enjoy doing based on, I believe, and Simon Baron Cohen, I believe, believes,
1:12:10 is the prenatal organizing effects of hormones on the developing brain.
1:12:15 But on YouTube, where it’s my understanding primarily male, there’s a lot of clap-back
1:12:20 type comments.
1:12:22 I know this because I have a YouTube channel.
1:12:25 And in the old days, it seems it wasn’t that long ago, when Rogan had full-length episodes
1:12:31 on YouTube, then he didn’t, now he does again.
1:12:34 The jokes, the comment section on YouTube were like their own show.
1:12:38 It was outrageous.
1:12:40 It was so good.
1:12:41 And some of that’s coming back now that he’s…
1:12:43 Was it men showing off their cleverness?
1:12:45 Right.
1:12:46 I mean, for instance, you might be familiar with Jocko Willink, right?
1:12:50 If you had to draw a Navy SEAL, you draw Jocko, kind of looks like modern day general patent.
1:12:57 And there’s this whole category of jokes based on Jocko, who I think actually has risen to
1:13:01 prominence in the online culture because he’s sort of like the football coach that most
1:13:05 young males never had.
1:13:06 He’s a guy that’s going to tell you what to do, when to do it, do it, even though you
1:13:09 don’t want to.
1:13:11 Just do it.
1:13:12 And you trust him.
1:13:13 He’s a very trustworthy guy, as it were, and he’s a warrior, and he has all the credentials,
1:13:17 et cetera.
1:13:18 But there’s this whole category of jokes, like when Jocko was born, the doctor looked
1:13:24 at his mother and said, “It’s a man.”
1:13:27 Or when Jocko left for college, he looked at his father and said, “You’re the man of
1:13:31 the house now.”
1:13:32 Jokes like that, there are tons and tons of these, right?
1:13:35 So there’s this whole…
1:13:36 So that’s very YouTube-ish, male-type humor.
1:13:38 It’s one hit, it’s done, it gets a ton of likes, and it propagates.
1:13:43 None of this two or three chess moves down the road.
1:13:46 So it’s very clapped back sometimes, or in that case, building up Jocko, who doesn’t
1:13:50 need any more building up, but people do it anyway.
1:13:53 So things of that sort.
1:13:54 So I’m interested in the nuance here because you’re telling me that girls are killing themselves
1:14:02 more.
1:14:03 They’re depressed.
1:14:04 Well, their increase in suicide is larger.
1:14:07 Boys have a much higher suicide rate.
1:14:09 So many more boys die from suicide.
1:14:11 You can say for more violent means?
1:14:13 That’s one of the major reasons, and that’s especially true in America, where we have
1:14:16 so many guns.
1:14:17 Okay.
1:14:18 Boys tend to use a gun or a tall building or a bridge, whereas girls tend to use pills
1:14:22 or cutting their wrists, and the great majority of girls’ suicide attempts don’t lead to
1:14:26 death.
1:14:27 Yeah.
1:14:28 So are most of the issues with girls in online use, social media, it’s sort of, it’s despair.
1:14:37 It’s at home, anxious, sad about self, self-critiquing, this kind of thing.
1:14:42 I mean, you’re telling me there’s a huge, and I believe you, that there’s a tremendous
1:14:46 increase.
1:14:47 I mean, it’s a hockey stick-like function.
1:14:50 And we’re looking at essentially capturing the tip of the pyramid in terms of extreme
1:14:56 social interaction.
1:14:57 So let me, I’m not being very clear here.
1:15:02 We have these neural circuits that evolved for social interactions that are more heightened
1:15:05 in girls.
1:15:06 They’re getting much more of it faster, and the consequences are no less and probably
1:15:13 even more severe than they used to be, but it’s still shunning, shaming, self-attack and
1:15:19 anxiety, depression, et cetera.
1:15:21 In boys, the neural circuits that we’re talking about are related to sex and violence.
1:15:27 Those evolved over hundreds of thousands, not millions of years, and those are heightened.
1:15:33 So we’re sort of capturing the extremes of these neural circuit functions.
1:15:37 I’m looking at this through the lens of the neurobiologist, and this is where it seems
1:15:40 we’re running into trouble because the iceberg below all of that, the portion of the iceberg
1:15:46 below those, those peaks of behavior and interactions, none of that’s happening.
1:15:52 There isn’t the, it’s all happening faster, it’s more potent, and the consequences are
1:15:59 more severe.
1:16:00 That’s right.
1:16:01 That’s right.
1:16:02 I think there’s a good analogy here to junk food, where I’ve heard junk food or a cheeseburger
1:16:05 described as a super stimulus, and ice cream is a super duper stimulus.
1:16:10 It’s got fat.
1:16:11 It’s got sugar.
1:16:12 And a cheeseburger with a milkshake, and the milkshake has candy in it.
1:16:16 Yeah, ice cream.
1:16:17 And then you get a toy.
1:16:18 Yeah.
1:16:19 And they’re playing music.
1:16:20 I mean, that’s a dopamine bath.
1:16:22 That’s right.
1:16:23 Yeah.
1:16:24 So if we think about, if we think about life in the presence of junk food, if you raise
1:16:27 your kids with junk food, you’re going to have all kinds of metabolic problems, developmental
1:16:31 problems, obesity, all sorts of diabetes, all sorts of terrible things.
1:16:35 Now if you have a normal development, and then as an adult, you indulge in more junk food,
1:16:40 you know, it’s not good for you, but it’s very different than being raised on it.
1:16:45 The developing brain, the developing body are much more sensitive.
1:16:49 And so the way you just put it before, it’s like these evolved motives, you super satisfy
1:16:54 them with these overwhelming quick, easy hits.
1:16:58 It may not be so bad for an adult.
1:17:00 We can choose to pay for sex.
1:17:04 We can choose to eat a cheeseburger and a milkshake, but it’s very important for kids.
1:17:12 We have to see, the genes don’t have that much information in them, but they start the
1:17:16 brain developing.
1:17:17 And then the brain has to sort of find its way.
1:17:19 The neurons have to find their way, guide by local signals how to develop.
1:17:23 And then the child has to kind of find its way through its culture, getting a sense of
1:17:27 how do I behave here and who am I and how do I relate to people.
1:17:31 And it’s all a very delicate process that has to be drawn out over many, many years.
1:17:36 Everything about us develops slowly, especially compared to other animals.
1:17:40 And if you intervene in the developmental process and say, “Hey kid, you want the endpoint
1:17:44 without the journey?
1:17:45 Here you go.
1:17:46 Take it.”
1:17:47 You’re cutting off development.
1:17:49 And that’s, I think, what life, that’s what the phone based childhood is doing.
1:17:53 Well, here’s my concern.
1:17:56 There is a reality to these things we call critical or sensitive periods.
1:17:59 Yes, let’s talk about that.
1:18:01 Critical periods implies that it’s open and shut.
1:18:04 And they’re actually sensitive periods for language learning, for brain plasticity.
1:18:07 And the general contour of this is passive experience up until about age 25 dramatically
1:18:13 shapes the maps in the brain that we have of social relationships, of the visual world,
1:18:17 the auditory world.
1:18:18 I mean, there’s just so much data to support this in animals and humans.
1:18:22 Then after about age 25, you can pry open the underlying neurobiological mechanisms for
1:18:30 neuroplasticity and you can rewire your brain, but it takes a hell of a lot of effort and
1:18:34 or pharmacology to assist, which is part of what the excitement about some of the psychedelic
1:18:40 therapies are about because, and I’m not suggesting people just run out and take psychedelics,
1:18:44 but they can foster change.
1:18:45 They can foster change and they’re either neuromodulators or they stimulate the massive
1:18:49 release of neuromodulators like dopamine, serotonin, mostly serotonin and dopamine.
1:18:54 When we talk about psilocybin and MDMA, LSD, et cetera.
1:18:58 But that plasticity needs to be directed, so just taking the drug doesn’t do it on its
1:19:01 own.
1:19:02 Okay.
1:19:03 So, leaving that aside, what do we know for sure?
1:19:05 We know that as the brain progresses from age three, four, five, six, seven, there are
1:19:11 milestones that have to be met.
1:19:13 And in general, if a kid makes it to high school age or college age, regardless of whether
1:19:18 or not they go to, hopefully they do in graduate high school or college, there’s a set of milestones
1:19:26 that they have to reach.
1:19:27 The circuits are going to develop one way or another.
1:19:29 The question is, what are the thresholds under which dopamine is released?
1:19:33 Well, I would argue, and I’ll go on record saying that if a kid watches a lot of intense
1:19:40 high potency, violent porn, and that becomes his dopamine stimulus, well, then other stuff
1:19:47 probably won’t do it for him.
1:19:49 Whereas if there’s a variety of experience or more, let’s just say subtle, dare I even
1:19:54 say healthier, right, stimuli, then the system is, the dopamine system around courting and
1:20:01 sex is more varied.
1:20:03 It’s more of a, at least more of a buffet and hopefully a healthier buffet, right?
1:20:07 Yeah.
1:20:08 Yeah.
1:20:09 Again, no judgment here of different proclivities, but here we’re talking about the wiring of
1:20:12 neural circuits.
1:20:13 Same thing with food.
1:20:14 If one grows up on highly processed, very, very tasty food, for a while, fruits and vegetables
1:20:20 in their pure form, meat and fish in their plane form are boring.
1:20:23 It does not evoke the same reinforcing property.
1:20:27 And earlier, I forgot to mention why I prefer the word reinforcing as opposed to reward because
1:20:31 reward evokes this idea of the thing being the reward, but the reinforcement is a verb.
1:20:39 And so as a verb, it brings the mind to the fact that these circuits are like they’re
1:20:45 churning in the background there.
1:20:46 It’s not just about getting the thing.
1:20:48 It’s the underlying biology that gets you there.
1:20:53 And so I think that where I’m very concerned is that we’ve now got what millions and millions
1:20:58 of kids, boys and girls, whose neural circuits were wired up wrong.
1:21:04 And now there needs to be, it seems, a very active process in unwiring that or at least
1:21:11 shifting those neural circuits towards something that’s more adaptive.
1:21:15 So before we talk about what to do if you’re older, because I have the great good fortune
1:21:20 to be sitting here with you right now, I’d like to ask you to help me expand what I say
1:21:26 in the book.
1:21:27 So you gave a description of critical periods where there’s a hard beginning and end.
1:21:32 And of sensitive periods are periods in which it’s just a lot easier to learn something.
1:21:36 And if you don’t learn, so for example, phenology is one of the clearest cases, you accent.
1:21:41 So when a family moves to America from somewhere else, if you’ve got two kids in the family,
1:21:45 like one of my advisors at Penn and grad school, Henry Gleitme had a very, very heavy German
1:21:51 accent and his younger brother, two years younger, had no accent whatsoever because
1:21:56 Henry was 14 and his brother was 12 when they came to America from fleeing Nazi Germany.
1:22:01 And so there’s a sensitive period that kind of closes at puberty for language.
1:22:05 So I talked about that in the book and then I talked about a more speculative sensitive
1:22:08 period that I’ve read about, you know, a few people think this exists.
1:22:12 And I cited Japanese study of Japanese businessmen who moved to California in the 70s as Japanese
1:22:18 business were thriving.
1:22:19 And they looked at, when did the kids come to feel American?
1:22:23 And the answer was, if they came and left before age nine, nothing.
1:22:28 They went back to Japan.
1:22:29 They were totally Japanese.
1:22:30 If they came when the kid was 15, nothing.
1:22:34 The kid was already Japanese, but wasn’t going to ever feel American.
1:22:37 If they came and spent a few years between about nine and 15, then they go back to Japan.
1:22:41 Now, especially if the kid’s now 15 or 16, the kid now feels American and has trouble
1:22:46 fitting back in.
1:22:47 Puberty.
1:22:48 Well, that’s right.
1:22:49 There’s a period.
1:22:50 It’s early puberty.
1:22:51 It’s, you know, just before puberty to sort of midway through puberty seems to be a sensitive
1:22:56 period for culture learning and for identity.
1:23:00 You’re very deep sense of who you are and how you relate to people.
1:23:03 So this is speculative, but it does seem to fit a lot of interesting data.
1:23:08 And the reason why I focus on this in the book, I decided late in the process, you know,
1:23:12 I knew I had to talk about puberty.
1:23:14 I was going to have like a section on this.
1:23:15 Oh my God.
1:23:16 This is so important.
1:23:17 I need a whole chapter on puberty.
1:23:19 And I talk about initiation rights all over the world.
1:23:24 Adults think kids don’t just turn into men and women.
1:23:28 They need help.
1:23:29 They need to be given the special knowledge.
1:23:31 For boys, there’s usually ordeals more so than for girls.
1:23:35 And so I think what’s going on is we do have this sensitive period for culture learning.
1:23:38 How do you learn to become a person in your culture?
1:23:41 And you know, I was in the Boy Scouts, and Boy Scouts was created around World War One
1:23:45 as like paramilitary training, like learn virtues of, you know, self-denial and, you
1:23:49 know, brave, clean, loyal, trustworthy, revered.
1:23:52 I forgot the order all messed up, but it was a set of virtues.
1:23:55 So would you agree or what would you say about sensitive periods for this really high level
1:24:00 stuff?
1:24:01 We’re not talking vision or phenology, which are fairly low-level cognitive things.
1:24:04 We’re talking like your sense of who you are.
1:24:07 What would you think about a sensitive period for that?
1:24:10 Oh, first of all, puberty is just fascinating and under discussed, in my opinion, as a critical
1:24:16 developmental milestone.
1:24:17 It’s also the fastest rate of aging that we ever undergo.
1:24:21 Aging meaning?
1:24:22 In our life, in terms of change of the brain, in terms of rate of, I mean, there are some
1:24:29 theories that the rate of puberty and the timing of onset of puberty actually might predict
1:24:35 something about longevity.
1:24:37 Which way?
1:24:38 Early puberty is bad.
1:24:39 Early puberty might be bad, but I want to be very careful in saying that some people,
1:24:42 including myself, have a very protracted puberty.
1:24:44 So I hit puberty around 14, but I didn’t get facial hair until I was out of college.
1:24:49 So some people develop the so-called secondary sexual characteristics slowly, but I always
1:24:53 had this voice since I was a little kid, so five years old they call me froggy.
1:24:58 Now, that’s me, and everyone goes through these things differently, but puberty is the
1:25:03 most profound brain change that one can undergo.
1:25:06 Tell me more about it, because I just keep saying, well, it starts in the back of the
1:25:09 brain, but be specific.
1:25:11 What is happening to the brain during puberty that would be relevant here to a sensitive
1:25:15 period?
1:25:16 Okay, so this goes back to the biology that you accurately described earlier, which is
1:25:19 that while we’re in utero, if there’s a Y chromosome, then a bunch of genes are made,
1:25:23 like malaria inhibiting hormone.
1:25:25 The malaria ducts become inhibited.
1:25:28 The testes grow, then testosterone is secreted, and testosterone in some of its derivatives,
1:25:33 like dihydrotestosterone, organize the brain, quote-unquote “male.”
1:25:37 This is dangerous language nowadays.
1:25:39 It’s less dangerous now than it was two years ago.
1:25:41 Okay, well, we’re not talking about gender, we’re talking about biological sex here, and
1:25:44 we’re not talking about the verb sex.
1:25:46 We were talking about that earlier.
1:25:47 We’re talking about biological sex.
1:25:48 So what I’m describing here is not disputed.
1:25:53 So there are these organizing effects of hormones early on, and then there are the activating
1:25:57 effects of hormones that happen during puberty.
1:25:59 So then puberty hits, the testes start secreting testosterone.
1:26:04 If they’re fat stores on the body, they secrete estrogen.
1:26:06 Again, testosterone and estrogen working in parallel, and in males, a number of different
1:26:10 brain areas, in particular the hypothalamus, but also the forebrain and associated areas
1:26:16 undergo massive plasticity in growth, relating the-
1:26:20 Wait, the forebrain, the frontal lobe?
1:26:22 Right, the frontal lobe.
1:26:23 Oh, so one of the most profound changes in puberty that happens, especially in males,
1:26:28 but also in females, is that what we can describe the major function of the prefrontal cortex,
1:26:33 this neural real estate right behind the forebrain, it has many different subdomains involved
1:26:36 in things.
1:26:37 But one of its main functions, this was beautifully described by the guy who’s now the head neurosurgeon
1:26:42 at Neuralink, Matt McDougal, is to say to the impulse-driving actions of the hypothalamus
1:26:48 in particular.
1:26:49 This houses neurons for temperature regulation, sexual drive, hunger, aggression, so much
1:26:57 so that you can go in and stimulate certain neurons, and the ventromedial hypothalamus
1:27:00 with an electrode, and you would go into a rage.
1:27:03 Stimulate neurons also within the ventromedial hypothalamus, just nearby, and you’d want
1:27:09 to go spend some time with your wife alone.
1:27:11 Let’s just put it that way.
1:27:12 A remarkable specificity of the neuronal outputs to behavioral change and state change.
1:27:19 All of that gets set up essentially during puberty, because the neurons of the hypothalamus
1:27:23 are responsive to these hormones that are coming from the gonads.
1:27:26 In females, it’s, yes, mainly secretion of estrogen, but also testosterone.
1:27:32 The brain is changing in dramatic ways, not the least of which is the forebrain is learning
1:27:38 how to suppress impulse, and some of that gets feedback from behaviors, from parenting,
1:27:45 learning how to suppress from social reward or punishment.
1:27:47 If it doesn’t get daily practice in suppressing, if you’re able to give in to all your urges.
1:27:51 Because I’m finding, when I sit on my computer, my rule now, I have to say to myself out loud,
1:27:56 finish what you start.
1:27:58 Finish what you start.
1:27:59 No, don’t go check until you’ve done.
1:28:01 You only have two more pages to read.
1:28:02 Read those two pages, but I can’t do it.
1:28:05 This is the gradual creep of, we don’t want to make it clinical, but an adult ADHD-like
1:28:12 symptoms that we all are suffering from.
1:28:15 We’re at a buffet.
1:28:16 That’s a good example.
1:28:20 That’s one of the main things, this forebrain to hypothalamic wiring.
1:28:24 The other is, and this is not trivial, and you mentioned the context of language learning,
1:28:29 and Dr. Eddie Chang, who’s a neurosurgeon, actually chair of neurosurgery at UCSF knows
1:28:33 a lot about this, and critical periods, is that there are hormone effects on, say, thickening
1:28:37 of the vocal cords, which is why, on average, boys have deeper voices than girls and so
1:28:42 forth.
1:28:43 There’s a lot of feedback from those signals in terms of the social world, because now
1:28:47 a young boy whose voice deepens, who’s also acquiring more knowledge, is talking to other
1:28:53 people about that knowledge, and he’s being treated differently, and there’s feedback
1:28:56 in terms of his self-concept, and that’s where it gets kind of high-level abstract.
1:28:59 In girls, there’s feedback of sometimes his bodily changes, positive or negative feedback
1:29:05 from peers, other girls, and/or boys, but also knowledge.
1:29:10 She’s out there talking about, well, she’s brilliant in math, or brilliant in literature,
1:29:16 and getting the feedback, and then self-knowledge starts to accumulate, and the location of
1:29:21 identity in the brain is unclear, and it’s probably a distributed network.
1:29:25 There’s probably an emergent property of a lot of different things, so we can’t really
1:29:28 point to one area, but it’s learning impulse control, reinforcement contingencies.
1:29:33 On what time scale can I get what I want to meet certain drives, and to what extent should
1:29:38 I suppress those drives?
1:29:40 Traditionally, it was, I think, through religion and parenting and social cues that you learn,
1:29:46 well, if I want something, is it okay to do it, that there are consequences to eating
1:29:50 more or less, consequences to be, okay, so it’s super complex, but that all happens sometimes
1:29:55 in a summer.
1:29:56 This is what’s so amazing about puberty, to me, or the acquisition of facial hair in
1:30:02 a boy, suddenly he’s looked at differently.
1:30:05 People start projecting all sorts of futures on him, but we do this, I notice, I’m not
1:30:10 a child psychologist, obviously, but as soon as my niece started drawing, she’s going
1:30:17 to be an artist.
1:30:18 As soon as a boy starts building, or a girl starts, gets a math problem right, she’s going
1:30:24 to be a mathematician.
1:30:25 We project all this stuff, and there’s no question that that feeds back on identity,
1:30:30 but in terms of online use, I can’t even imagine how much of this is diminished by only showing
1:30:37 a specific part of ourselves, and I can’t even imagine how much of it is exacerbated
1:30:43 in terms of what we are rewarded for during puberty.
1:30:46 Here’s what we know in both animals and humans, which is that neuroplasticity, while it responds
1:30:50 to punishment, is exquisitely sensitive because of a runaway train from more plasticity under
1:30:56 conditions of dopamine reinforcement and reward.
1:30:59 You can imagine that the girl using the filter, the Instagram filter, who gets rewarded for
1:31:05 looking a certain way, maybe excessively thin or something, or what leads to excessively
1:31:09 thin, there’s no question that rewards drive neuroplasticity faster than punishment.
1:31:16 Makes you understand this.
1:31:17 You’re saying, suppose a girl gets on to Instagram, and she’s now consuming stuff about being
1:31:24 thin, and for some reason she finds this rewarding.
1:31:28 Are you saying that the quick dopamine circuits where she posts something and she gets likes
1:31:33 for it, are you saying that that actually will extend neuroplasticity, the fact that
1:31:38 she’s getting more rapid dopamine, that will make her more neuroplastic and her brain will
1:31:42 change more?
1:31:43 Yes, it will accelerate learning for whatever contingency led to that, whatever led to that.
1:31:49 We know this in animals and humans, even though they’re exquisitely sensitive, plasticity
1:31:54 is exquisitely sensitive to punishment, it only takes one shock learning in one corner
1:31:59 of a cage.
1:32:00 We’re getting sick at one particular restaurant that you don’t want to go back again.
1:32:04 When it comes to social dynamics, we know that reward leads to almost what I would call
1:32:11 runaway plasticity in the circuits that generated the behaviors that led to that particular
1:32:17 reward.
1:32:18 There are a number of experiments that explain this, the work of Mike Merzeneck at UCSF who
1:32:24 largely worked on adult plasticity, but showed that when you activate dopamine release in
1:32:29 the brain, fortunately both during development but also in adulthood, you essentially create
1:32:35 a window of superplasticity.
1:32:37 Okay, that’s amazing.
1:32:38 So dopamine reward, that neuromodulator is a window for superplasticity and evolutionarily
1:32:43 it makes sense.
1:32:44 Like, oh my goodness, there’s abundance here of something.
1:32:47 Time to learn something.
1:32:48 That’s right.
1:32:49 We’ve overemphasized the extent to which plasticity is driven by punishment.
1:32:53 But the neuromodulators that allow for plasticity, in particular impuberty and as adults, are
1:33:00 largely dopamine dependent and acetylcholine dependent.
1:33:04 The acetylcholine generally increases focus and broadly speaking.
1:33:08 I mean, it does a bunch of other things, controls, muscular contraction, et cetera.
1:33:12 But so what we’re basically saying here is that if a kid gets a strongly reinforcing
1:33:18 experience, I’d be willing to bet both arms that the neural circuits that help generate
1:33:26 whatever behaviors led to that experience are going to be strengthened in one trial to
1:33:33 the extent that it will be very easy to generate those behaviors again.
1:33:36 Okay.
1:33:37 Thank you.
1:33:38 This is exactly what I wanted to know, to deepen the theorizing that I do in the book.
1:33:44 So now, this is actually the perfect time for us to switch over to the four main recommendations
1:33:50 because they build exactly on what you just said.
1:33:52 They helped me explain why this is so important.
1:33:55 So I think one reason why the book seems to be doing very well and people seem to like
1:34:01 and pass it on is that it’s not just doom and gloom, it’s not just, “Oh, we’ve messed
1:34:04 up our kids.
1:34:05 Oh, these terrible devices.”
1:34:07 Rather, it’s about a vision of childhood, which is actually beautiful.
1:34:11 It’s the one that most of us older people had with the play outdoors and all that.
1:34:18 And so my analysis in the book is that the reason why I got this far is because it’s
1:34:24 a set of collective action traps.
1:34:27 Every 10-year-old needs a smartphone now because every other 10-year-old has one and
1:34:30 you don’t want to make your kid be alone.
1:34:33 So the four recommendations I have are four ways of breaking out on the trap, but the
1:34:36 first two are really about delaying and getting past this period of plasticity and you really
1:34:42 helped me see why it’s so urgent to delay until late puberty at least.
1:34:47 So here are the four norms that I think can break us out of this trap.
1:34:51 Norm number one, no smartphone before high school.
1:34:54 You can give your kid a flip phone.
1:34:56 The millennials had flip phones, they came out fine.
1:34:58 No access or no smartphone of their own.
1:35:01 Your own.
1:35:02 You can’t have your own.
1:35:03 And that would even go for an iPad if you give your kid an iPad and say, “Here, Billy,
1:35:07 this is your iPad.
1:35:08 You can keep it in your room and use it anywhere in the house and you can take it outside even,
1:35:13 although maybe no Wi-Fi, whatever.”
1:35:15 The point is the internet is an amazing thing and you can have a computer in your living
1:35:20 room or kitchen when you have young kids and they can do things on the computer, but you
1:35:24 do not want to give your child the entire internet in his or her pocket.
1:35:30 And you do not want the entire world to be able to reach your child whenever they want
1:35:34 to.
1:35:35 So it’s just insane that we’re giving children, even before puberty, a smartphone.
1:35:42 Let them have a flip phone or a simple phone, watch something like that.
1:35:44 That’s rule number one.
1:35:45 Rule number two is the most relevant to what we’re just talking about and that is no social
1:35:49 media until 16.
1:35:51 There is, I believe, no way to make social media safe for children.
1:35:56 That is, if they’re going to be entering a domain in which prestige is gained by having
1:36:00 posts that get the most likes and followers, you’re making them be brand managers.
1:36:04 You’re making them be performative.
1:36:05 This is not playful.
1:36:06 They’re going to be exposed to horrible, horrible things.
1:36:10 I now ask young people, “Is there something that you saw when you were young that you
1:36:13 really regret seeing?”
1:36:14 And a lot of them have an answer.
1:36:16 My 21-year-old doorman just told me about the gauntlet, running the gauntlet.
1:36:20 It’s a series of 20 videos.
1:36:22 It’s a challenge. Can you watch these 20 videos, which end with a Mexican drug gang dismembering
1:36:28 a person who’s alive?
1:36:30 Things like that.
1:36:31 “Yes, I’m tough enough.
1:36:32 I can do that.”
1:36:33 Really?
1:36:34 At what age do you want your kids watching people being dismembered?
1:36:37 10?
1:36:38 11?
1:36:39 Is that okay?
1:36:40 And those images are forever.
1:36:41 They’re forever.
1:36:42 That’s right.
1:36:43 That’s right.
1:36:44 I didn’t even watch the video.
1:36:45 You know what?
1:36:46 I’m sorry I said that.
1:36:47 No, we won’t provide a link.
1:36:48 No, I’ll say that trauma is defined as an adverse event that forever changes the way the brain
1:36:50 responds in ways that make people less effective in life.
1:36:53 So don’t do it to yourself.
1:36:54 I wouldn’t watch the Dahlmer movie.
1:36:56 Everyone was talking about the Dahlmer movie.
1:36:58 All I had to see was 10 seconds of the trailer to know I’ll pay money not to see that.
1:37:02 That’s right.
1:37:03 Not because I couldn’t get through it.
1:37:05 I’m sure I could force myself to, but I don’t want that in my neural real estate.
1:37:08 That’s right.
1:37:09 That’s right.
1:37:10 That’s right.
1:37:11 For obvious reasons.
1:37:12 So let’s go back to what you said about neuroplasticity.
1:37:15 Because if it’s true that puberty is a sensitive period for many higher level aspects of our
1:37:21 humanities such as identity, relationship skills, all that stuff, then you should be
1:37:26 extra careful.
1:37:27 When your kids are nine to 15 years old, you should be extra careful about what’s going
1:37:32 into their eyes and ears.
1:37:33 And instead that’s when we give up all control.
1:37:35 You know when our kids are little, they pay attention to us.
1:37:37 We read to them.
1:37:38 We have a lot of control about what our kids consume when they’re toddlers and when they’re
1:37:41 very young.
1:37:42 But as they reach middle school and high school, they’re moving away.
1:37:44 They’re seeking out other stuff.
1:37:46 And that’s exactly when you say, here, here’s your own device.
1:37:49 You want to go down a rabbit hole of eating disorder stuff?
1:37:52 You want to go down a rabbit hole of Tourette syndrome?
1:37:58 You’re going to copy people who have these symptoms?
1:38:00 So the last thing we should be doing is exposing our children in this sensitive period to socializing
1:38:06 information from random weirdos on the internet who are selected by an algorithm for the extremity
1:38:11 of their behavior and the degree to which that extremity earned them likes, which makes
1:38:15 them extra prestigious.
1:38:17 So yeah, laws that raise the age to 16 or 18, I think that’s what we need.
1:38:23 This is just not appropriate for minors.
1:38:25 Even if there’s some good stuff on it, I think it’s vastly outweighed by the bad.
1:38:29 So that’s the second norm.
1:38:31 No social media till 16.
1:38:33 The third norm is phone-free schools.
1:38:35 And again, if we expect kids to learn and learning is brain change.
1:38:40 If you’re learning something, you’re developing a skill, something about your brain has changed.
1:38:44 How about instead of learning math or reading or litter or anything else, how about if you
1:38:49 just do more phone stuff?
1:38:51 You just spend more time in school on TikTok.
1:38:53 There was just an article in The Washington and the Wall Street Journal about a teacher
1:38:57 who fought against the phones and finally gave up and quit.
1:39:00 And one of the students in his class has quoted that she used to, she’d come into class and
1:39:06 she would just go on TikTok.
1:39:07 And that’s what she would do all the class long is just watch TikTok in her desk.
1:39:12 And like, no, you should be learning, not doing more TikTok in school.
1:39:16 So it’s just insane that we let kids take the greatest distraction devices ever invented
1:39:20 into the classroom with them.
1:39:21 And I would argue that they are learning, but what they’re learning are these rapidly
1:39:26 reinforced dopamine loops that lead to diminished amounts of dopamine, not just in short periods
1:39:33 of time, but very quickly, and that inhibit other forms of learning.
1:39:37 Yeah, that’s right.
1:39:38 And the ability to pay attention to a teacher, which is not as stimulating as what you’re
1:39:43 seeing on TikTok.
1:39:44 Yeah, there’s tons of learning.
1:39:45 It’s learning of all the wrong things.
1:39:46 That’s right.
1:39:47 That’s right.
1:39:48 So that’s the third norm is phone-free schools.
1:39:51 You have to lock up the phone in the morning, either in a phone lock or a yonder pouch.
1:39:55 If the policy is you keep it in your pocket, that’s not a policy.
1:39:58 That’s just a recipe for constant conflict with the kids because they can’t help it.
1:40:01 They have to text.
1:40:02 If anyone’s texting, they have to be texting.
1:40:04 And the fourth norm is the hardest.
1:40:06 The fourth norm is far more independence, free play, and responsibility in the real
1:40:10 world because what we need to do is not just roll back the phone-based childhood and make
1:40:15 them just sit and do nothing.
1:40:17 We have to do is restore a really fun, adventurous childhood, like what you were saying.
1:40:21 You go out on your bicycle, you’re hanging out with your friends, sometimes something
1:40:24 happens.
1:40:25 And boy, you have memories.
1:40:26 I mean, exciting things happen, scary things happen, but you have memories.
1:40:31 And I worry about what boys today, I have a group of buddy, my group of friends.
1:40:36 That I, you know, we still talk about things that happened, you know, amazing things that
1:40:40 happened when we were in college or after college.
1:40:43 And I wonder what boys, young boys today are going to say, you know, you remember Fortnite
1:40:47 game 27,363 where you were trapped in that elevator shaft and I had to shoot you out?
1:40:51 No, I don’t remember that one.
1:40:53 You know, like the virtual adventures are just not going to cut it.
1:40:57 Our kids need adventure.
1:40:58 They need independence and adventure where they work out the conflicts themselves.
1:41:02 So if we do those four things, I think we can restore childhood in the real world.
1:41:08 No smartphone before high school, no social media till 16, phone free schools, more independence
1:41:13 free play and responsibility in the real world, those four things.
1:41:15 And these are things that we can all do.
1:41:17 If we work together, if we do them at the same time, if you’re the only family that’s
1:41:21 keeping your kid off of smartphone till high school and off of social media till 16, you’re
1:41:26 imposing a cost on your child and she may be lonely and she’ll say, mom, I’m left out.
1:41:30 Yeah, she might still thank you as we saw last night.
1:41:32 So one of the women said, her daughter thanked her for keeping her off, but at the time it
1:41:36 was painful for her.
1:41:37 And so my hope is by spreading these norms, no parent will ever be in that position again
1:41:43 where their kid is the only one in the class who doesn’t have a smartphone at age 10.
1:41:48 To have this fantastic list, I say fantastic because it drives us all of the neurobiology
1:41:55 that I’m aware of and because it offers solutions that it’s really based on knowing what’s
1:42:00 happened and is happening with with smartphone use.
1:42:04 There are a bunch of don’ts, but then there’s some do’s, which I, you know, I’m not again,
1:42:08 I’m not a an expert in behavioral change, but I spent a fair amount of my time talking
1:42:12 to people about what they can do for their health and well-being and not just the don’ts.
1:42:17 And I think it’s important as I understand to have replacement behaviors and also I think
1:42:22 people of all ages want to do something that feels good the first time in every time and
1:42:26 that’s good for them.
1:42:27 And then you create that reinforcement loop in a different direction.
1:42:30 You’re offering all of that in the book in here and it’s fabulous.
1:42:34 What I wonder about and would love to help in any way that I can with is, you know, if
1:42:42 you recall years ago, there was this understanding about the first six years of life being critical.
1:42:46 It was the first six years.
1:42:48 And so parents kind of overstepped it a bit and we’re playing their kids Mozart all the
1:42:51 time and things like that.
1:42:53 But what was interesting is that they were thinking about critical periods and brain
1:42:57 plasticity.
1:42:58 And so as a neurobiologist who say brain development, I was delighted.
1:43:03 It seems to me that if there was an understanding that the biology and psychology and sociology
1:43:10 points to the fact that there is a critical period, maybe not even a sensitive period,
1:43:15 but a critical period in which excessive smartphone use of a particular type is actually leading
1:43:21 to more suicides, depression, anxiety and less learning and adaptive behavior in life.
1:43:29 It seems to me that it should be almost like a law.
1:43:32 It should be implemented at the level, certainly at the national level.
1:43:36 What sorts of barriers do you think exist to that?
1:43:41 You know, obviously, I’m enthusiastic in joining your effort and I know many people
1:43:46 listening will be as well to try and implement these four things.
1:43:49 But what do you think it would really take to get people to take their children’s brains
1:43:56 and lives seriously because children can’t be left to their own self-care to that degree?
1:44:03 This is unfair, right?
1:44:04 I mean, it’s like telling a kid in a candy shop, like, hey, listen, figure it out.
1:44:09 There’s nutritious food down the street, it’s unfair, right?
1:44:12 It’s like a puppy trying to do the Westminster championship.
1:44:16 It’s like, it’s not going to happen.
1:44:20 But this is serious stuff.
1:44:21 I mean, we’re talking about the future, not just of the United States, but of the entire
1:44:24 species.
1:44:26 So what about laws?
1:44:28 What about legislature?
1:44:29 How does that work?
1:44:30 I don’t know anything about that.
1:44:31 Sure.
1:44:32 Sure.
1:44:33 Well, first, so let’s note, I could be wrong about this.
1:44:36 It might be that the phones aren’t doing this.
1:44:38 Now, I think the evidence is pretty good that it is, but let’s suppose there’s a 70% chance
1:44:42 that I’m right.
1:44:43 Let’s suppose there was only a 30% chance I was right.
1:44:46 The consequences are so severe, we should be taking action.
1:44:49 Now, what action to take?
1:44:50 I was over in the UK for the book about three weeks ago, and in the UK and the rest of Europe,
1:44:57 the first thought of everyone is ban it, ban it, ban it, government law ban.
1:45:01 And there are times when we need that, you know, cigarette smoking underage, just ban
1:45:05 it.
1:45:06 Like, you should not have kids smoking.
1:45:07 There was a lot of consideration of, should we ban the sale of smartphones to kids under
1:45:11 14?
1:45:13 And I met with the policy unit at number 10 Downing Street, and I said, now wait a second,
1:45:19 guys.
1:45:20 You know, as an American, it never even occurred to me to suggest that.
1:45:24 You need to get norms first.
1:45:27 If you pass laws that are out of phase with people’s norms, they’re going to really hate
1:45:31 you and they’re going to resent it.
1:45:33 So let’s start with a norm change first.
1:45:36 And so, so I think, I think that’s really happening.
1:45:39 So in Britain, parents are up in arms, they really are changing rapidly over there.
1:45:42 They’re a couple of months ahead of us.
1:45:44 In America, I think it’s happening right now.
1:45:46 And so if we just develop a consensus, we need to see smartphones in the hands of kids
1:45:51 as being like cigarettes in the hands of kids, like, you know, you just don’t do that.
1:45:54 You don’t do that.
1:45:55 Of course, they can be on a laptop, they can be on a computer, they can do some things
1:45:59 on your iPhone sometimes.
1:46:00 It’s not poison, but you don’t want it to be habit-forming.
1:46:04 So, so I think that for keeping smartphones out of the hands of kids, there’s no law.
1:46:10 I don’t want a law banning that, but we just need a norm.
1:46:14 Now for, for raising the age to 16, we can struggle to do that.
1:46:19 I’m doing that with my kids.
1:46:20 I’m saying no for my daughter, no Snapchat until you’re 16.
1:46:24 And she’s the only one who doesn’t have it.
1:46:25 It’s painful for her and she’s 14.
1:46:29 But my hope is that no parent again will be in that situation that in every school a lot
1:46:33 of the parents are going to say no social media till 16.
1:46:36 Now of course, the laws currently state that you have to be 13 in order to sign a contract,
1:46:41 give away your data, and make a deal with a company without your parent’s knowledge
1:46:45 or permission.
1:46:46 But Congress passed this terrible law in 1998, the Copa Child and Online Privacy Protection
1:46:53 Act.
1:46:54 It was supposed to set the age to 16, which is not, which is I think pretty reasonable,
1:46:57 but it got pushed down to 13 with no enforcement.
1:47:00 The law is written such that as long as the company doesn’t absolutely know that you’re
1:47:04 under age, they’re fine.
1:47:06 They’re not responsible.
1:47:07 13.
1:47:08 They’re motivated.
1:47:09 The companies are now, the law motivates the companies to not know how old children are.
1:47:12 There’s barely any forebrain at 13.
1:47:13 That’s right.
1:47:14 That’s right.
1:47:15 And since all you have to do, you just have to be old enough to lie about your age.
1:47:17 If you’re old enough to lie about your age, you can go anywhere on the internet because
1:47:20 there’s no enforcement.
1:47:21 So I’m saying let’s take the age of 13, which is not enforced.
1:47:25 Let’s require age verification, which is complicated, but they’re working on that in Britain.
1:47:29 They’re mandating that.
1:47:30 It’s going to happen in Britain.
1:47:31 We’ll work out the technical details.
1:47:34 So mandate age verification, then raise the age to 16.
1:47:37 That’s the one place where I think we really do need law because social media is a social
1:47:41 trap.
1:47:42 And if half the kids are on it, there’s going to be a lot of pressure on the other half
1:47:45 to join.
1:47:46 So we need to get that down to like only if 5% sneak around, they find a way on.
1:47:51 That’s fine.
1:47:53 So that’s where we definitely need law.
1:47:55 And then the play stuff, there we could use some laws.
1:47:58 So I co-founded an organization called LetGrow.
1:48:00 If you go to letgrow.org with Lenore Scanesi, we advocate for returning play to children.
1:48:06 And one of the things we’ve done is we’ve gotten laws passed in eight states that say
1:48:11 if you let your child out to play, that cannot be taken as evidence of child neglect.
1:48:16 Whereas at present, laws are ambiguous.
1:48:19 So if you send your eight-year-old out to a store, and this has happened to friends
1:48:23 of mine, and some nosy neighbor says, where’s your mother?
1:48:26 Does she know you’re out here?
1:48:27 And then they call 911.
1:48:29 And the police come because no one has seen an eight-year-old on a company since the 90s.
1:48:34 So the police come.
1:48:35 And once the police come, they’re very likely to refer it to child protective services.
1:48:39 And once your family is in the grip of child protective services, you’ve got custody battles,
1:48:43 you’ve got supervision, you’re not allowed along with children.
1:48:45 It’s crazy what happens.
1:48:47 So eight states have now said, no, no more of that.
1:48:49 This is insane.
1:48:51 So law could help to stop incentivizing helicopter parenting, to provide more spaces that are
1:48:58 safe for kids to play in, not car zones.
1:49:01 So the book has– the anxious generation at the whole fourth part of it is suggestions
1:49:05 for governments, for tech companies, for schools, and for parents.
1:49:08 There’s a lot we can do to restore a play-based childhood in the real world.
1:49:14 I realize that some of this is dependent on income for a household, et cetera.
1:49:19 But is there any protective effect of, say, summer camp or protective effect of even just
1:49:27 after-school sport, where both the kids and the parents agree, no phones on the field?
1:49:34 We’re not taping for every goal.
1:49:35 I mean, I love seeing my friends’ kids getting a three-pointer at a game or something like
1:49:41 that.
1:49:42 I delight in that on Instagram.
1:49:43 And it’s wild that my friends, given who I know them to be growing up, have these kids.
1:49:48 And the stories I could tell.
1:49:51 But in all seriousness, it’s wonderful.
1:49:53 And yet, I’m thinking they’re taking a video of their kid playing the game.
1:50:00 Wouldn’t it be wonderful if there were no phones at after-school sports events?
1:50:04 So it’s a couple of hours, three times a week or once a week, even, where at least these
1:50:10 young brains are exposed to a different kind of reinforcement learning.
1:50:14 That’s right.
1:50:15 That’s right.
1:50:16 The British have a saying, “Don’t put your daughter on the stage, Mrs. Worthington,”
1:50:21 which is a line from an old Noel Coward song.
1:50:23 And it acknowledges that especially for girls, for girls to grow up being looked at and admired
1:50:28 and commented on about their looks, it’s just really, really bad for them.
1:50:32 But to grow up always being photographed, everything you do and post it online is really
1:50:36 bad for them.
1:50:38 So yes, in response to your question, first, summer camps are magic.
1:50:41 Never send your child to a summer camp that doesn’t ban phones, because this is the best
1:50:45 chance you have for a detox.
1:50:47 And I hear this story over and over again.
1:50:50 My girl got an iPhone when she was 11.
1:50:53 She suddenly became surly, no longer the sweet, funny child she was.
1:50:56 I sent her to summer camp the next summer.
1:50:59 And lo and behold, the girl that comes back is my wonderful, sweet 11-year-old.
1:51:02 Her personality is back, and then she gets back on her phone and she becomes surly again.
1:51:06 So summer camps are the most powerful technique known for a detox, because the kid isn’t being
1:51:12 deprived.
1:51:13 They are in a bunk with other kids with no phones, and they’re joking and talking and
1:51:18 laughing and fighting and doing all those healthy things.
1:51:21 So summer camp is amazing.
1:51:23 The other thing that the evidence shows is that team sports and religion, those two things
1:51:27 are very, very protective.
1:51:28 So I would strongly urge people to encourage their kids to play team sports.
1:51:32 My kids run track, which is great, but team sports force more cooperation.
1:51:37 So there’s some evidence that team sports are even better for their mental health than
1:51:41 individual sports.
1:51:43 You don’t want super-duper, over-supervised, high pressure sports leagues.
1:51:47 I mean, that’s better than nothing.
1:51:49 But ideally, the more they play games that are more intramural, informal, the kids are
1:51:53 enforcing the rules.
1:51:55 All of that would be better.
1:51:56 Our kids are not rooted in communities anymore, but sports and religion are two things that
1:52:01 do that.
1:52:02 What about music?
1:52:03 I did an episode on music in the brain, and one of the more thrilling and interesting parts
1:52:09 to me was, and I have no musical talent whatsoever, singing or instrumental or otherwise.
1:52:14 I love listening to music, however, was that kids that grew up playing an instrument, especially
1:52:18 cooperatively with other people in a band, a duet or a quartet or band or orchestra or
1:52:25 marching band, there’s some very impressive data in terms of potential for additional
1:52:31 neuroplasticity.
1:52:32 Absolutely.
1:52:33 Brain-wide networks, those are patterns of connectivity are much more broad in kids that
1:52:39 learned an instrument and played it cooperatively than those that try and learn an instrument
1:52:44 later in life, although there’s still advantages to that.
1:52:47 I wonder if that could be added to the list.
1:52:50 Yes.
1:52:51 Playing in a band or singing in a choir, I think definitely should be.
1:52:55 For a while, I was really interested in synchrony, and synchrony has all these really powerful
1:52:59 effects.
1:53:00 There’s a wonderful book called Keeping Together in Time by William McNeill.
1:53:05 He was either he signed up or he was drafted into World War II, training at a camp in Texas.
1:53:11 They’re marching up and down with wooden guns because they don’t have real guns.
1:53:14 At first, it seemed stupid to him, but after a few days, his unit gets it.
1:53:18 When they’re like a unit, they’re like a centipede.
1:53:23 They’re imperfect, and it was like a loss of self.
1:53:26 It was ecstatic.
1:53:28 He goes off to World War II.
1:53:29 He comes back and writes about men in battle.
1:53:32 He writes, that’s a different book title.
1:53:37 Those sorts of being in sync, those experiences, we are an ultra-social species.
1:53:43 We’re much more social than dogs or chimpanzees.
1:53:45 We have this ability to keep together in time and do things synchronously.
1:53:49 All around the world, that’s what rituals used to do.
1:53:52 It’s thrilling.
1:53:56 These self-transcendent experiences that you get from singing in a choir, from playing
1:53:59 in a band.
1:54:00 I don’t have much talent either, but I did play in an informal rock band when I was
1:54:04 at UVA.
1:54:05 We called ourselves Pavlov’s Dogs.
1:54:06 We were all in the psych department.
1:54:09 The first time we got it and we were all really in sync, it was totally thrilling.
1:54:15 The more you give your kids … I have all sections actually in chapter two of the book
1:54:19 on synchrony and attunement.
1:54:23 We need to be in sync, and that’s why face-to-face interaction is so important, whereas when
1:54:28 you’re communicating on Instagram or any social media, it’s asynchronous.
1:54:32 You don’t have the automatic attunement.
1:54:37 Can I get a little new-agey speculative?
1:54:39 All right, let’s go.
1:54:40 I have a question.
1:54:43 I’ve heard you and others say that kids and probably adults nowadays are not familiar
1:54:49 with what it is to be bored.
1:54:51 There’s always an input movie on social media, YouTube.
1:54:57 There’s always word streaming at us in audio or written.
1:55:02 There’s this concept that I love from the world of mindfulness, which used to be considered
1:55:05 new-agey, but now I think every academic campus has at least a few grants focused on meditation
1:55:11 and its benefits and respiration, breathwork, and its benefits.
1:55:14 We’ve come a long way, but there’s this concept of wordlessness, of the importance of being
1:55:20 in states of wordlessness, where we’re not reading, we’re not thinking in complete sentences.
1:55:24 We’re not taking in sensory information, and we, under those conditions, are able to actually
1:55:32 register how we feel about things, that we become better tuned to sense our environment
1:55:38 and input when it comes.
1:55:40 I wonder, because my experience of social media has been whether or not kids are on
1:55:48 Instagram, Snapchat, et cetera, and they’re doing it out of whatever, compulsion, habit,
1:55:52 addiction, whatever you want to call it, but I’m not sure it feels good to them.
1:55:57 I’m not sure it does.
1:55:58 I’m not sure it’s like the ice cream that tastes delicious.
1:56:01 I think it might start that way, and occasionally they’re jackpots, but that in large part adults,
1:56:10 but since we’re talking about kids, let’s talk about kids in this very critical, sensitive
1:56:14 period of life are not feeling good, and they might not even know they’re not feeling good.
1:56:21 They’re just compulsively, and there I’m using the term loosely, not clinically, compulsively
1:56:25 engaging.
1:56:26 I wonder whether or not there’s some benefit to kids not just being bored for experiencing
1:56:32 boredom’s sake, but learning to actually be a better sensor of what they like and don’t
1:56:38 like, because when I talk to my niece or I talk to other young people now, they seem
1:56:44 to be becoming increasingly aware of how much some of the online stuff sucks.
1:56:50 That’s the language.
1:56:51 They’re not like, “Oh, it’s awesome.
1:56:52 Don’t take it away from me.”
1:56:53 They’re like, “I don’t want to miss out,” but it’s also painful to them.
1:56:57 It’s like they’re drinking from a fire hose of nails, and then every once in a while there’s
1:57:01 something that tastes good.
1:57:03 It’s not like they’re like, “This is so cool, and that’s so cool,” but of course, if you
1:57:05 give them a really cool video of an animal thing or a social dynamics thing or a war
1:57:10 game or whatever, they’ll get excited, but I don’t get the impression that they’re like,
1:57:14 “This is awesome.”
1:57:16 It’s more like, “This has me by the short hairs.
1:57:19 It’s got me scruffed, and I’m just doing it, and I don’t know how to stop.”
1:57:23 I think that’s absolutely.
1:57:25 That’s certainly the way that boys reach out, guys, young guys typically reach out about
1:57:31 their porn addictions.
1:57:33 I hear about this thousands of messages, “Help me get over this,” so I refer them to our
1:57:38 episode on addiction by Dr. Anna Lemke from Stanford.
1:57:40 Oh, I love her, yeah.
1:57:41 Yeah, she’s amazing.
1:57:42 Oh, yeah, this is not that episode.
1:57:43 Yeah, she’s spectacular.
1:57:46 It’s just that they’re desperate.
1:57:48 They’re desperate.
1:57:49 I don’t see it as all pleasure.
1:57:50 I see it as mostly pain.
1:57:52 No, that’s right.
1:57:53 That’s right.
1:57:54 So there’s a lot going on here.
1:57:55 For some of them, they are addicted, and they feel bad for the reasons you were talking
1:58:00 about dopamine overshoot, or they feel bad when they’re not doing the addictive activity.
1:58:05 So they are compulsively using it, just like a gambler.
1:58:09 If you’re addicted to slot machines, your life sucks.
1:58:11 You’ve spent all your family’s money.
1:58:13 You’re ashamed of what happened.
1:58:14 You feel terrible.
1:58:15 “Oh, but if I just get back into the zone on the slot machine, I feel good for that two
1:58:19 or three hours.”
1:58:20 Yeah, that’s the most dangerous addiction, because as it’s been described to me, I’m
1:58:23 fortunately not a gambling addict, excuse me.
1:58:27 The gambler really does believe that the next one could change everything.
1:58:32 Right.
1:58:33 It’s going to cause motivated reasoning.
1:58:34 It’s going to cause hopefulness that is dashed.
1:58:37 So for some of them, it is a kind of self-medication.
1:58:41 As soon as the boys move their social lives onto video games and porn, and the girls move
1:58:46 their social lives onto social media, both sexes got really lonely.
1:58:51 They’re getting lots of cheap and easy stimulation, but it’s not satisfying.
1:58:55 So what do they do now that they’re lonely and anxious?
1:58:58 Well, sometimes they do more of it.
1:59:00 So some of it is driven by that feedback cycle, that they’re now uncomfortable, so they need
1:59:05 more of it.
1:59:06 But the other part is the compulsion to consume, because everyone else’s may have to keep up.
1:59:11 And so my students at NYU, I asked them, “Okay, some of you are spending four, five, six hours
1:59:16 a day on social media.
1:59:18 Why don’t you quit?”
1:59:19 “Oh, I can’t, because I have to know what everyone’s talking about.
1:59:23 I have to see the latest video.
1:59:24 I have to keep up with it.”
1:59:26 And since I can’t deal with my email and my text, those two combined, that’s more than
1:59:31 I can handle in a day.
1:59:32 I can’t stand it.
1:59:34 I can’t imagine having five platforms in addition.
1:59:37 I don’t know the exact number, but very few of my students are on a single platform.
1:59:40 Most of them are on two or three regularly, plus email and texting and Snapchat.
1:59:46 So it is kind of like, imagine, food is great, but imagine always having to eat.
1:59:51 You have to always be eating.
1:59:53 Our system can’t handle that.
1:59:55 Imagine a plant always in a shower.
1:59:58 It’s always like, “No, you need times of taking in and times of digesting or processing.”
2:00:05 One of the most valuable, I’ll tell you two of the most valuable exercises that we do
2:00:09 in my flourishing class at NYU, the first is a prerequisite to everything else is they
2:00:14 have to regain control of their attention.
2:00:16 And once they understand that they’ve given away almost all of their attention, any moment
2:00:21 that isn’t taken up by a teacher or something, it’s the phone for a lot of them because there’s
2:00:27 so much to process.
2:00:28 They have so many direct messages, so many group texts.
2:00:31 They have to always be processing or they feel like they’re being left behind.
2:00:35 They’re not participating.
2:00:37 So make them see you’ve got to regain control of your attention.
2:00:39 You’ve got to shut off almost all notifications.
2:00:41 You leave on Uber because you want Uber to interrupt you to say the car is three minutes
2:00:45 away.
2:00:46 That’s good.
2:00:47 But how many of the companies is it that important that they interrupt you?
2:00:52 Very, very few.
2:00:53 So shut off almost all your notifications.
2:00:54 Get social media off your phone.
2:00:55 If you need to use it, you can use it on your computer, but don’t always have it said.
2:00:59 At NYU, in any elevator, as students get on the elevator, the phone comes out because
2:01:04 that’s like 30 seconds and it’s awkward.
2:01:06 Take the phone out.
2:01:07 Scroll.
2:01:08 I would argue the professors too.
2:01:09 Yeah.
2:01:10 That’s true.
2:01:11 We do.
2:01:12 Not you.
2:01:13 I’ve spent time with you in an elevator yet.
2:01:14 No, we do.
2:01:15 We do, but it’s less.
2:01:16 Yeah.
2:01:17 Yeah.
2:01:18 And then the other one that I did that is really memorable, and I talk about this in
2:01:24 the book, is an all walk.
2:01:26 And I got this idea.
2:01:28 My friend, Dacher Keltner, he and I did research on all long ago and he really continued it.
2:01:31 He wrote this amazing book called All.
2:01:34 And there was great episode if you just Google Keltner and Tippet.
2:01:40 So with Krista Tippet, he did this great discussion.
2:01:42 He talks about how he used all walks to help him process his brother’s early death from
2:01:47 cancer and just walking in a beautiful environment, walk a little more slowly than usual.
2:01:53 Don’t have anything in your ears.
2:01:56 Don’t be listening to music.
2:01:57 Don’t even bring your phone and just notice.
2:02:00 And it’s magical.
2:02:01 It’s amazing what happens when you do that.
2:02:04 And for a lot of my students, they’ve never done that because they have to take in so
2:02:08 much stuff.
2:02:09 If I’m going from point A to point B, of course, I’m going to be listening to a podcast or
2:02:13 scrolling on my phone while I’m walking.
2:02:16 And a lot of them, they really had these transformative experiences.
2:02:19 You know, we’re right on Washington Square Park at NYU.
2:02:21 We’re built around Washington Square Park, which is a gorgeous, gorgeous park.
2:02:24 It’s really one of the most beautiful in America, certainly one of the most beautiful
2:02:27 urban parks, I’d say.
2:02:29 And the students who did their all walk through the park, a lot of them had these just amazing
2:02:33 experiences.
2:02:34 It’s almost like their heart is opening.
2:02:37 They feel more love for people.
2:02:39 They, their anxiety goes down.
2:02:41 And so ever since they, and so I did that myself, when I signed it, I did it too.
2:02:45 And I had that sort of experience.
2:02:47 So now, you know, I love my AirPods, they’re amazingly convenient, but I listened to them
2:02:52 a lot less now.
2:02:53 Like when I’m walking in New York City, I often just, just nothing, just nothing.
2:02:56 Just look, process, think.
2:02:58 So yes, I think young people are taking in way too much stuff.
2:03:02 Total quantity of bytes is just, you know, 10 times what it should be.
2:03:05 And they don’t have time to process.
2:03:06 They don’t have time to develop an interior life, to think things through.
2:03:11 So we just got to cut it, cut it way back.
2:03:14 If I step back from everything that you’ve said thus far and is in your book, it seems
2:03:19 as if until 2012 or so, what was rewarded in youth set us up for a more adaptive adulthood.
2:03:30 But now everything that’s being rewarded in youth, except from schools and teachers and
2:03:36 parents, but what’s, you know, being rewarded on a moment-to-moment basis for the majority
2:03:41 of the waking life of these young people is maladaptive.
2:03:46 Yes, that’s right.
2:03:47 I mean, it’s so stark.
2:03:49 That’s right.
2:03:50 Think about it this way.
2:03:52 Imagine that your children are having a life out in the real world, they’re having adventures,
2:03:55 they’re doing things, they’re building forts in the forest, they’re doing all sorts of things.
2:03:59 And then one day, you know, a casino opens up nearby and it welcomes all the kids.
2:04:04 And that’s where they spend all their time is in a casino.
2:04:06 And they’re in the care of a company that is trying to extract as much money as it can
2:04:10 from them.
2:04:11 And that’s what they do eight or 10 hours a day.
2:04:13 It’s an abomination to think that a casino could own our children’s childhood.
2:04:17 What if it wasn’t a casino?
2:04:18 What if it was a brothel for the boys?
2:04:19 Would be more of interest, let’s say.
2:04:21 Like again, inconceivable that we would let that happen.
2:04:24 What we’ve done is we’ve said, well, what if it’s Snapchat?
2:04:27 What if it’s Instagram?
2:04:28 What if it’s Facebook?
2:04:29 Well, not so much Facebook.
2:04:30 What if it’s TikTok?
2:04:32 These companies, these are some of the largest and most powerful companies in the world.
2:04:36 They essentially own our children’s childhood.
2:04:38 This is where childhood is taking place on a few giant, for-profit platforms that use
2:04:42 an advertising-based business model.
2:04:44 So they are motivated, like the casino, to keep them in.
2:04:47 Don’t have a clock.
2:04:48 Don’t let them see what time it is.
2:04:50 Keep them in.
2:04:51 Don’t let them click over to a link to another site.
2:04:53 Keep them in.
2:04:55 We somehow have ceded our children’s childhood to giant companies that have shown that they
2:05:00 don’t really care about our kids’ welfare.
2:05:03 They care much more about profitability and they care about their customers, who are the
2:05:07 advertisers.
2:05:08 And these companies have been granted a special writ from the king.
2:05:13 Congress said in section 230 of the Communications Decency Act in 1996, I think it was, Congress
2:05:20 said, “Oh, and nobody can sue you.
2:05:22 Nobody can sue you for what you showed to their kids.”
2:05:25 There was a reason for that, that you don’t want AOL to be responsible for everything
2:05:28 anyone posts.
2:05:29 But it’s been so broadly interpreted that so far, any attempt to regulate social media
2:05:33 or any attempt to sue them is seen as like, “No, no.”
2:05:36 So it’s just, we somehow slipped into this, and once you see it that way, that it says,
2:05:42 “Though our kids are being raised in Hera’s casino,” like, “No, we’ve got to stop this.”
2:05:49 Last year, I had the opportunity to speak to some of the groups at these companies that
2:05:54 are assigned to controlling the well-being of the young people that use their platforms.
2:06:01 And the major emphasis was on the type of content.
2:06:04 So protecting them against child predators, protecting them against pornography.
2:06:09 But as you recall, at the beginning of the conversation, we broke things down into variables
2:06:12 of time-specific content dynamics and maybe the visual interface itself.
2:06:16 I think for sake of today’s discussion, the visual interface is probably the least interesting.
2:06:20 But I can just tell you, looking at things up close, a lot not good.
2:06:24 The eyeball lengthens, you become nearsighted, which is why spending two hours outside, even
2:06:29 if on a tablet has been shown to offset myopia and thousands of people, children.
2:06:34 Anyway, there’s that piece.
2:06:36 But the time piece is interesting, right?
2:06:39 Maybe limiting the total amount of time on social media.
2:06:43 Obviously the content issue is, it only takes one exposure to a video of the sort that you
2:06:47 described, the gauntlet, “I never want to see it,” whatever has to be done to my phone
2:06:51 so that I never see it.
2:06:53 Please let me know.
2:06:56 But it just seems as if this has been allowed to, it’s almost like an IV drip of glucose
2:07:03 or something happening in the background.
2:07:05 We’re saying, okay, just stay rigged up to the glucose drip.
2:07:09 And then we wonder why we’re up with, let’s just say, cognitively obese children.
2:07:14 Yeah, that’s right.
2:07:16 Whenever there’s new media, the public’s emphasis is always on the content.
2:07:21 And so with television, the emphasis was, violence on TV, is this going to make them
2:07:26 violent?
2:07:27 And it turns out, not really, watching violence on TV doesn’t really make you violent.
2:07:31 And video games, these violent video games, these first person shooter games, are these
2:07:34 going to make our kids into killers?
2:07:36 And there was a lot of research on that.
2:07:37 It looks like, no, it doesn’t really do that.
2:07:40 And so many researchers then say, see, it’s just a moral panic, it’s okay.
2:07:44 But that’s focusing on the content.
2:07:47 And this was the great lesson from Marshall McLuhan and Neil Postman and all these great
2:07:50 media theorists in the 20th century.
2:07:53 McLuhan said the medium is the message.
2:07:55 Don’t focus so much on the content of television.
2:07:58 Focus on the transformation of human life when the television becomes the family hearth
2:08:03 and people sit around watching it.
2:08:05 Now from our vantage point today, that’s pretty darn social.
2:08:08 They’re sitting with their family members together, having an experience.
2:08:12 But McLuhan’s point was, that’s the transformative thing, what the technology does.
2:08:17 It’s not the content.
2:08:18 And so in the same way, a life on social media in some ways is like television, you’re watching
2:08:23 stuff.
2:08:24 But it’s much more behaviorist.
2:08:25 With television, you didn’t have the constant, I do something I’m rewarded, I do something
2:08:29 I’m rewarded.
2:08:30 So social media is much, much more addictive than television ever was.
2:08:34 That’s one aspect of the, television’s not performative.
2:08:37 It doesn’t make you live your life in front of a camera.
2:08:41 You’re not in front of a camera.
2:08:42 You’re a passive recipient.
2:08:43 Whereas social media puts our kids in front of a camera.
2:08:48 So in all these ways, we get distracted and this is the way, in those Senate hearings,
2:08:53 it was all focused on content.
2:08:56 Can’t we reduce the number of beheading videos and the child pornography?
2:09:01 Suppose we, can’t we reduce that by 90% when that’d be great?
2:09:04 Senator, we have the world leading technology in doing this.
2:09:08 Yes, that would be nice for our kids to see less hardcore porn and less violent videos.
2:09:13 That’d be nice.
2:09:14 But if we could make Instagram just be happy girls living beautiful lives and our daughters
2:09:20 were to watch eight hours a day of this, is that good for them?
2:09:23 Hell no.
2:09:25 So you know, it is important to clean up the content, but for kids going through puberty,
2:09:29 I think the only real answer is just delay, just don’t let them do that.
2:09:34 How much of the issue here is modeling of what adults are doing and, you know, and how
2:09:39 terrible our, or good our adults at modulating their behavior.
2:09:45 I say modulating because, you know, I see a lot of parents videotaping everything that
2:09:51 they’re, you know, on the phone all the time in line at the store while their kids are
2:09:56 around, you know, and one of the reasons I think parents like devices so much is that
2:10:00 it’s a terrific low-cost, zero-cost babysitter.
2:10:04 It allows them to then go be on their phones or do other things.
2:10:07 Yeah.
2:10:08 So young children are sometimes copying their parents.
2:10:11 Young children are looking for things to copy and, you know, and so, I mean, I’ve got some
2:10:16 slides in my regular book lecture of toy iPhones that we give to toddlers so that they can
2:10:22 be just like mommy and daddy.
2:10:25 For little kids, I think it might matter.
2:10:27 For teenagers, you know, I’m very often asked that question because, and I think it’s because
2:10:31 parents, they feel a little guilty, like they know that they’re modeling bad behavior and
2:10:34 they’re worried, like, is this setting up my kid for doing that?
2:10:36 And I can’t say for sure, but my intuition as a social psychologist is not really, not
2:10:40 very much.
2:10:41 And the reason is because, you know, while your kids once looked up to you and they once
2:10:45 copied you, like, by the time they’re 12, 13, 14, you know, if I pick up, if I start
2:10:49 reading, you know, the Economist magazine, or if I start knitting or whatever, that’s
2:10:54 not going to make my 14-year-old daughter want to do those things because I’m doing
2:10:58 them.
2:10:59 She is completely focused on what her peer group thinks of her.
2:11:02 Of course she is.
2:11:04 That’s the nature of teenage work.
2:11:05 They’re moving away from the family and they’re trying to make their way on their own in a
2:11:08 peer group.
2:11:09 Lisa DeMora is great on these issues.
2:11:13 So I don’t, you know, it’ll be nice if parents could improve their phone habits and boy, phones
2:11:18 at the table, that’s an important place.
2:11:20 That is a very, very important place.
2:11:22 Get across the idea that when we’re eating, we’re with each other.
2:11:27 We’re looking at each other and we’re tasting our food.
2:11:29 We’re experiencing the food.
2:11:30 It’s going to be there.
2:11:35 Modeling collective behaviors like a meal, I think that is actually very, very valuable.
2:11:37 But if it’s just that, you know, you’re often multitasking.
2:11:39 You’re often on your phone.
2:11:40 Yeah, you know, be nice if you didn’t, but that’s not going to push your kid over into
2:11:44 phone addiction.
2:11:45 So the list of four things that you provided are terrific.
2:11:49 They are somewhat enforcement focused.
2:11:53 As I recall, maybe this is not true, but as I recall, one of the ways that media was effective
2:12:01 in getting kids to stop smoking was to pit them against these wealthy old white men who
2:12:09 were in rooms filled with smoke, writhing their hands together, cackling about the amount
2:12:13 of money they were making, stealing the health of young people, whereas telling teenagers
2:12:19 that smoking was bad for them did very little.
2:12:22 So is there a way to create a rebellion of sorts against the smartphone because kids
2:12:28 love to rebel?
2:12:29 Teens love to rebel.
2:12:30 Not, but first of all, they don’t anymore.
2:12:32 Oh no.
2:12:33 Really?
2:12:34 Well, they’re just much more passive.
2:12:37 I don’t think they’re authority focused.
2:12:40 They’re not as rebellious as they used to be.
2:12:42 That’s disappointing.
2:12:43 Yeah.
2:12:44 Now, of course, now we’d have to pit them against a group of young white men who are
2:12:47 owning the social media companies, I suppose.
2:12:50 But this addiction is very different from tobacco or anything else.
2:12:55 Tobacco is biologically addictive, and you can’t get an entire high school addicted
2:13:00 biologically.
2:13:01 At least, it didn’t happen.
2:13:04 In the peak year of smoking was 1997, 37% of American high school students smoked, two
2:13:09 thirds didn’t.
2:13:11 But with social media, you couldn’t have that.
2:13:13 You couldn’t have just a third.
2:13:15 It’s either none or everybody, and it’s everybody, and it happens in middle school.
2:13:19 So the dynamics of a social media addiction, it’s a social addiction more than a biochemical
2:13:26 like nicotine or cocaine type addiction.
2:13:30 So I think the way to break out isn’t, hey, these people are exploiting you.
2:13:33 That might be helpful.
2:13:34 We should definitely study that.
2:13:36 I think the way to break out is, okay, look, you guys actually, you can see what this is
2:13:40 doing to you.
2:13:41 You mostly agree that this is wasting your time, it’s garbage.
2:13:45 You want to weigh out, but you just feel like you can’t.
2:13:48 There’s such resignation.
2:13:50 But look, the cool kids over there, they have flip phones, and they’re out like every day
2:13:55 after school.
2:13:56 They’re like, they’re doing stuff.
2:13:58 They’re down at, they’re in the mall, they’re getting pizza.
2:14:02 They’re building a fort, whatever, depending on the age.
2:14:06 So I think the way out is to give kids an exciting childhood.
2:14:10 Kids are so lonely now, and they don’t have much in the way of adventure.
2:14:14 They don’t have much in the way of thrills.
2:14:17 I live in New York City.
2:14:19 I would bring my kids out to Coney Island when they were nine, 10 years old, bring
2:14:24 them out.
2:14:25 And then I would just say, I’m just going to sit here.
2:14:26 You guys run around.
2:14:27 You guys go have fun.
2:14:28 I’m not going to be with you.
2:14:29 Yeah, there’s a chance you’ll get kidnapped or struck by lightning, although lightning
2:14:33 is more likely.
2:14:35 And then once they were in more, like 13, now they can actually take the subway out to Coney
2:14:41 Island with a friend.
2:14:42 So that’s cool.
2:14:45 I think that’s the way to do it.
2:14:46 Don’t make it like, we’re going to take away all this stuff from you.
2:14:49 Ha, ha, ha.
2:14:50 Now you have nothing to do.
2:14:52 Make it more like, I’m not trying to hurt you here.
2:14:55 I want you to have fun the way I did and the way your grandparents did.
2:14:59 We all had human childhoods full of adventure.
2:15:01 I want that for you.
2:15:03 And I think most Gen Z will embrace that.
2:15:06 They just don’t want to do it alone.
2:15:07 So the key is, if you’re listening to this podcast, and if you have kids that are in
2:15:12 elementary and middle school, be sure to talk with the parents of your kid’s friends.
2:15:17 So if you want to make some changes in your phone policies, if four families do it together,
2:15:22 now your kid’s not going to feel left out or deprived.
2:15:24 And be sure to give them something.
2:15:26 Give them.
2:15:27 Say, here, you know what, how about every Friday, let’s call it Free Play Friday.
2:15:32 No piano lessons on Friday, no nothing on Friday.
2:15:34 Fridays you all get together.
2:15:35 You can start at anyone’s house, go out, do what you want.
2:15:38 We’ll give you more allowance or we’ll give you money to spend.
2:15:42 You go have experiences.
2:15:44 Then it’s fun.
2:15:45 It’s not deprivation.
2:15:46 I love the trust in kids to sort things out and to be safe enough.
2:15:53 At least the statistics say that they’re more likely to thrive under those conditions than
2:15:57 to be kidnapped or have something terrible happen.
2:16:00 I like it also because it merges your previous book, Coddling of the American Mind with the
2:16:06 current book, The Anxious Generation.
2:16:09 I have a bunch of other questions, but I think the most important one at this stage is, how
2:16:15 optimistic or pessimistic are you about the changes that you’re hoping for?
2:16:21 And then the second question is, how can we all help?
2:16:24 I mean, you mentioned these four action items, no smartphone before high school, no social
2:16:28 media until 16, phone free schools, and to foster this exploration and independence.
2:16:35 And we will propagate those four things as far and wide as we can.
2:16:38 But I think everybody, parents and kids, I’m sure as well, want to know what can we do?
2:16:45 So optimism scale, zero being like you’re doing this as a last-ditch effort, but it’s
2:16:51 hopeless.
2:16:52 Well, you wouldn’t be here if you thought it was hopeless.
2:16:53 So one to 10, one being just a sliver of hope, 10 being, you know, we got this same way we
2:16:58 got other stuff.
2:16:59 Yeah, I’m a 10.
2:17:00 You’re a 10.
2:17:01 10.0.
2:17:02 Yeah.
2:17:03 And the reason is because I’ve never seen a situation like this.
2:17:06 I’ve been involved in a lot of efforts to change attitudes.
2:17:09 I ran a gun control group in college when I was 20, and that was impossible.
2:17:14 And I’ve been involved in political campaigns.
2:17:16 You’re trying to persuade people and you can’t get their attention and how do you message
2:17:21 them?
2:17:22 And it’s really hard.
2:17:23 That’s the way anybody involved in social change has experienced that, that’s most things.
2:17:27 This is like, you drop a spark and everything goes, everything, it just goes everywhere.
2:17:32 So all over the world, all over the developed world, family life has become a fight over
2:17:37 screen time.
2:17:38 Almost every parent of a kid over two recognizes this.
2:17:42 We all hate it.
2:17:43 We’re sick of it.
2:17:44 And we’ve just been confused.
2:17:45 The only real pushback I’ve gotten, I’ve gotten two guys.
2:17:47 One is I am in a normal academic debate with about seven or eight researchers who say there’s
2:17:51 not evidence of causality.
2:17:53 I believe there is, we’re marshalling evidence against each other.
2:17:58 But by and large, almost everyone seems persuaded because they already knew this.
2:18:03 They already thought it.
2:18:04 They already saw it.
2:18:05 And what I’ve done with the book is just given them some psychological concepts and some
2:18:09 clear labels and a way out.
2:18:12 And I’m so confident in part because the revolution started in Britain in February.
2:18:16 Yes, they drew on some of my older articles, but this was before my book came out.
2:18:22 Parents are self organizing.
2:18:23 In Britain, the government is acting.
2:18:24 They actually have a functioning legislature in Britain and the government has led efforts
2:18:29 to pass laws as well.
2:18:31 So I know it’s working in Britain.
2:18:34 And I see it happening here now at a massive scale.
2:18:38 The point of the book is collective action.
2:18:40 And parents all over the country are heeding that.
2:18:43 They’re forming reading groups.
2:18:44 They’re going in in a group to talk with the principal, the principals and teachers.
2:18:48 They all hate the phones.
2:18:49 It makes their lives impossible.
2:18:50 They want a phone free school, but they were afraid of the few parents who freak out if
2:18:55 they can’t text their child during class.
2:18:58 If the schools are overwhelmed by parents saying, please lock up the phones.
2:19:01 Please let my child have six hours a day when she can listen to the teacher instead of do
2:19:05 more TikTok.
2:19:07 So I’m very, very confident that childhood is going to look very different within two
2:19:14 years.
2:19:15 I don’t mean that it won’t be seven year olds on phones, but in the same way that we flipped
2:19:20 on smoking, we used to think it was okay to smoke in an airplane.
2:19:23 We used to think it was okay to smoke in restaurants, it was okay to smoke everywhere
2:19:26 we thought.
2:19:27 And now we don’t.
2:19:28 We don’t think that anymore.
2:19:29 That took a long time to change, but it did change.
2:19:32 I think because of the public disgust with seeing children just spending their childhood
2:19:38 looking at a screen, and because of the public disgust with what we’ve heard about META and
2:19:42 TikTok and a few of the other companies, I think within two years it’s going to be widespread.
2:19:47 There’ll be a norm that you just don’t give kids social media in particular.
2:19:52 I mean, iPads are complicated because you want kids to watch movies is okay, stories
2:19:56 are good.
2:19:57 I’m not saying the iPad is a terrible thing, but our attitudes about this are going to
2:20:01 change radically.
2:20:03 And I think the great majority of schools are going to be phone free within two years.
2:20:08 And we’re going to see, we’re already seeing more kids outside.
2:20:12 Every day I get emails from grateful parents saying, “Because of your book, my six-year-old,
2:20:18 he wanted to ride his bicycle down to the end of our cul-de-sac.
2:20:21 He wanted to ride down, circle, and come back.”
2:20:24 And I never would let him because I was afraid that what would the neighbors say.
2:20:28 But once I read your book, I decided to let him.
2:20:30 And he was so ecstatic, he kept doing it and doing it, and now he’s going further and he
2:20:33 rides to his friend’s houses.
2:20:35 So people in her neighborhood, now they’re seeing a kid on a bicycle.
2:20:39 And if, suppose there were 10 kids doing it, well, now it’s normal.
2:20:43 So we can re-normalize human childhood in the real world, where our kids get the chance
2:20:49 to have independent adventures and learn how to be self-supervising adults ultimately.
2:20:56 We can do this.
2:20:57 Okay.
2:20:58 So you’re a 10 out of 10 on the optimism scale.
2:21:01 What can we do to facilitate and accelerate this whole process?
2:21:08 So once we understand that this is a collective action problem, that we’re all stuck in this
2:21:12 because everyone else is stuck and we can’t leave if we’re the only ones.
2:21:16 Once we understand that, now you see the key is collective action.
2:21:20 So talk to your friends about this.
2:21:24 Talk about the book with them.
2:21:25 You don’t have to buy the book.
2:21:26 Just go to anxiousgeneration.com.
2:21:27 We have all kinds of resources.
2:21:30 I have talks where I’ve summarized the book in videos.
2:21:34 Talk about it with your friends.
2:21:36 Talk about it with your family.
2:21:38 Talk about it with other parents at the school.
2:21:40 If you’re on social media, social media is great for adults who want to pursue projects.
2:21:45 I just don’t think it’s good for kids to be pursued by the social media companies.
2:21:49 But if you’re on Instagram in particular, that’s where a lot of parents are, especially
2:21:53 mothers.
2:21:54 Talk about these issues.
2:21:55 Say you’re going to let your kid have some free-range childhood.
2:21:58 You’re going to try to do these four norms.
2:22:00 And then if you’re able, I hope that you’ll support the projects.
2:22:04 If you go to anxiousgeneration.com, there’s a donate button.
2:22:07 And while you have it set up so that people can donate into a research account for me,
2:22:11 and that’s what I use to pay my small staff.
2:22:14 I have about four or five people working for me, and I hope to grow that to 10.
2:22:16 I hope people donate to me at anxiousgeneration.com.
2:22:21 Or to LetGrow, this wonderful organization that advocates for giving play back and independence
2:22:26 back to kids.
2:22:27 LetGrow.org.
2:22:30 And if you know influential people, if you know state legislators, not a lot of—oh,
2:22:36 in Congress, there is a very important bill, COSA, the Kids’ Online Safety Act.
2:22:40 Contact your legislators about that.
2:22:41 Say you support COSA.
2:22:43 It could be coming up for a vote very, very soon.
2:22:45 This is the one piece that really could get through the U.S. Congress.
2:22:47 Beyond the Congress, a lot of states are acting, which is very, very exciting.
2:22:51 So make your views known to your state legislators if you know them, or the mayor or governor
2:22:54 if you know them.
2:22:56 This is a collective action trap.
2:22:58 The only way out is together.
2:23:00 So if we act together, we can break this.
2:23:02 Terrific.
2:23:03 And we’ll put links to all of those things you just mentioned in the show note captions.
2:23:08 Jonathan, you’re bringing the humanity back.
2:23:13 It’s remarkable.
2:23:14 And as a fellow academic, I have to say your depth of scholarship in terms of developing
2:23:22 and researching these ideas, but also the vigor and the mission that you have around
2:23:29 doing good and making sure that it happens soon as opposed to waiting another 10 years
2:23:33 and seeing just how bad this can get is really inspiring.
2:23:38 I feel it.
2:23:39 I know for sure that people listening and watching feel it.
2:23:43 And so I want to thank you for doing this work.
2:23:46 Again, I loved Coddling in the American Mind because it just woke me up to how much things
2:23:50 had changed and we’re changing and it’s such an important book and the anxious generation
2:23:55 is truly an important book and I don’t say that lightly.
2:23:59 It’s mission driven, goal driven, and it has actionable items that I’m certain many people
2:24:04 listening to this are going to partake in.
2:24:07 So on behalf of the listeners and viewers and also myself, but also the positive change
2:24:13 to calm.
2:24:14 I just want to say thank you for taking the time out of your very busy schedule.
2:24:17 You’re still a professor.
2:24:18 You’re also a public facing health science educator like you.
2:24:22 Yeah.
2:24:23 So I feel like kinship there for coming here and speaking with us today and we’ll provide
2:24:28 links to the books and to these other resources in the show note captions and we’d love to
2:24:33 have you back again, hopefully in the not too distant future so that we can review all the
2:24:37 progress that you’ve stimulated.
2:24:39 So thank you so much.
2:24:40 Thanks so much, Andrew.
2:24:41 And thanks for all the work that you do to bring to make science cool and interesting.
2:24:46 I really appreciate your work and I’m very grateful to you for having me on.
2:24:51 It’s been a pleasure.
2:24:52 Thank you.
2:24:53 Thank you for joining me for today’s discussion with Dr. Jonathan Haidt.
2:24:56 To learn more about Endor to support Dr. Haidt’s work and to find a link to his important
2:25:01 new book The Anxious Generation, How the Great Rewiring of Childhood is Causing an Epidemic
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