Huberman Lab - Essentials: Healthy Eating & Eating Disorders - Anorexia, Bulimia, Binging
Episode Date: July 17, 2025In this Huberman Lab Essentials episode, I discuss both healthy eating and clinically recognized eating disorders, including anorexia, bulimia and binge eating disorder. I explain how brain circuits,... hormones such as leptin and reward systems interact to regulate appetite, satiety and overall eating behaviors. I also discuss the serious health risks associated with anorexia, explain how disrupted eating habits contribute to its development and highlight evidence-based treatments for anorexia. Finally, I explore binge eating and bulimia, discussing the underlying causes and the pharmacological treatments commonly used to support recovery. Read the episode show notes at hubermanlab.com. Thank you to our sponsors AG1: https://drinkag1.com/huberman LMNT: https://drinklmnt.com/huberman Function: https://functionhealth.com/huberman Timestamps 00:00:00 Eating Disorders 00:01:05 Fasting, Intermittent Fasting, Healthy Eating 00:06:10 Self-Diagnosis Caution 00:07:20 Sponsor: LMNT 00:08:52 Eating Disorders, Anorexia Nervosa 00:12:39 Hunger & Satiety; Appetite, Body Fat & Brain 00:17:20 Homeostasis & Reward Systems, Eating Disorders 00:21:12 Sponsor: AG1 00:22:49 Anorexia, Puberty, Hyperacuity & Food 00:25:55 Decision-Making vs Reflexes/Habits, Anorexia 00:29:29 Anorexia & Breaking Habits, Therapies & Family-Based Models 00:32:08 Distorted Self-Image & Anorexia 00:35:03 Sponsor: Function 00:36:43 Bulimia & Binge-Eating Disorder, Impulsivity & Prescription Treatments 00:40:28 Recap & Key Takeaways Disclaimer & Disclosures Learn more about your ad choices. Visit megaphone.fm/adchoices
Transcript
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Welcome to Huberman Lab Essentials,
where we revisit past episodes
for the most potent and actionable science-based tools
for mental health, physical health, and performance.
I'm Andrew Huberman,
and I'm a professor of neurobiology and ophthalmology
at Stanford School of Medicine.
Today, we are going to talk all about healthy
and disordered eating.
And indeed, we are going to talk
about clinical eating disorders,
such as anorexia,
bulimia and binge eating disorder,
as well as some other related eating disorders.
However, before we get into this material,
I want to emphasize that today's discussion will include
what it is to have a healthy relationship with food.
We're going to talk about metabolism.
We are going to talk about how eating frequency
and what one eats influences things like appetite
and satiety, as well as whether or not we have
a healthy psychological relationship to food
and our body weight and so-called body composition,
the ratio of muscle to fat, to bone, et cetera.
So as we march into this conversation,
I'd like to share with you some interesting
and what I believe are important findings
in the realm of nutrition and human behavior.
I know these days, many people are excited about
or curious about so-called intermittent fasting.
Intermittent fasting is, as the name implies,
simply restricting one's feeding behavior, eating,
to a particular phase of the 24-hour
or so-called circadian cycle.
Other forms of intermittent fasting involve
not eating for extended periods of time,
for entire days, or some people will extend
to two days or three days.
Typically, and hopefully hopefully they will drink water
during those times, sometimes referred to as water fasting,
which means that they are ingesting fluids.
And hopefully they are ingesting electrolytes
such as salt, potassium and magnesium as well,
because while one can survive for some period of time
without ingesting calories,
it is extremely important to continue
to ingest plenty of fluids and electrolytes.
And the reason for that is that the neurons
of your brain and body that control your movements,
your thoughts, clarity of thinking in general, et cetera,
is critically dependent on the presence
of adequate levels of sodium, potassium potassium and magnesium, the electrolytes.
And that's because neurons can only be electrically active
by way of movement of particular ions,
which include things like sodium, potassium and magnesium.
So without those, you can't think, you can't function
and it actually can be quite dangerous.
So why all the excitement about intermittent fasting?
Well, a lot of the excitement relates to work
that was done by a former colleague of mine
down at the Salk Institute for Biological Studies
in San Diego named Sachin Panda.
Sachin's lab identified some very important
and impactful health benefits
of restricting one's feeding window
to particular times within the 24 hour cycle,
or even to having extended fasts that go for a day
or two days, or maybe even three days.
What they saw was an improvement in liver enzymes,
an improvement in insulin sensitivity,
which is something that is good.
It means that you can utilize the calories
and the blood sugar that you happen to have.
Being insulin insensitive is not good
and is actually a form of diabetes.
What Sachin's lab and subsequently other labs showed
was that restricting one's feeding window
to anywhere from four to eight or even 12 hours
during each 24 hour cycle was beneficial in mice.
And some studies in humans have also shown
that it can be beneficial for various health parameters.
However, the excitement about intermittent fasting
seems to be related to the foundational truth
about metabolism and weight loss
and weight maintenance and weight gain,
which is that regardless of whether or not
you intermittent fast or whether or not
you eat small meals all day long,
or you eat one meal in the evening
and snack up until then,
it really doesn't matter in the sense that
the calories that you ingest from whatever source
are going to be filtered through the calories that you burn
by way of exercise, basal metabolic rate,
which is just the calories that you happen to burn,
just being alive and thinking and breathing
and your heart beating, et cetera.
And the reason why many people prefer intermittent fasting
to other forms of, let's just call it what it is,
diet or nutritional framework
is that many people find it easier to not eat
than to limit their portion size.
And here I'm not talking necessarily about eating disorders,
I'm talking about the general population.
So why are we talking about this?
And in particular, why are we talking about this
during an episode that includes a discussion
about eating disorders?
The reason is nobody, not the government,
no nutritionists, no individual,
no matter how knowledgeable they are about food
and nutrition and food intake,
can define the best plan for eating for any one individual.
I'm going to repeat that.
Nobody knows what truly healthy eating is.
We only know the measurements we can take.
Liver enzymes, blood lipid profiles, body weight,
athletic performance, mental performance,
whether or not you're cranky all day,
whether or not you're feeling relaxed,
nobody knows how to define these.
And these have strong cultural and familial
and socio-societal influence.
So if you hang out with people that intermittent fast all day
that will seem normal.
If you spend time with people
that have never heard of intermittent fasting,
intermittent fasting is going to seem very abnormal.
Now we are going to talk about eating disorders
that really fall into the category
of clinically diagnosable eating disorders
for which there's actually serious health
hazards and even the serious risk of death.
There are clear criteria in the psychiatric
and psychological communities to define things like
anorexia, bulimia, binge eating disorder,
all of which we will talk about.
But as we have that discussion, I want to emphasize
that self-diagnosis
can be both a terrific, but also a very precarious thing.
There's always a temptation,
as one learns about the symptomology of a given disorder,
doesn't really matter what the disorder is,
to ask the question, well, do I have that?
Does so-and-so that I know have that?
It's tempting to diagnose them and or ourselves
as either having or not having a particular disorder.
However, diagnoses really need to be carried out
by people who are trained in that particular field
and that have deep expertise in recognizing the symptomology
including some of the more subtle symptomology
of eating disorders.
So if any of the symptoms resonate with you
by way of you thinking that you have this particular disorder
or someone that you know has a disorder,
I would take that seriously,
but I would take that information
to a qualified healthcare professional
that could diagnose or rule out
any of these possible disorders.
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So what is an eating disorder?
Well, we have to take a step back
and confess to the fact that every society,
every culture, every family,
and every individual has a different relationship to food.
Eating disorders, however, have particular criteria
that allow us to define them
and to think about different modes of treatment
as it relates to the particular symptoms,
in particular, the psychological
and biological symptoms of those disorders.
What are the major eating disorders?
Anorexia nervosa, most commonly referred to as anorexia,
is perhaps the most prevalent
and the most dangerous of all eating disorders.
In fact, anorexia is the most dangerous
psychiatric disorder of all, even more than depression.
The probability of death for untreated anorexia
is very high.
And sadly, the prevalence of anorexia is very high.
If you look it up online,
or you talk to a qualified professional,
is essentially a failure to eat enough
to maintain a healthy weight.
You can see all sorts of very troubling symptoms
of somebody who's been anorexic for some period of time.
A general loss of muscle mass
because they're ingesting fewer calories than they burn.
They will have a low heart rate.
This is the body and brain's attempt to lower energy output.
They will have low blood pressure.
They will sometimes have symptoms like fainting,
loss of bone density, osteoporosis,
loss of periods in girls and women,
and all sorts of disrupted gut and immune functions.
So there are just tons of terrible symptoms of anorexia
that really place the anorexic into a very risky state, which is why mortality from anorexia that really placed the anorexic into a very risky state,
which is why mortality from anorexia gone untreated
is extremely high.
Now, one of the misconceptions about anorexia
is that it stems from an overemphasis on perfectionism,
or that because of all the images in social media
and in advertising of extremely thin and fit
or muscular people, that individuals are looking
at themselves and comparing themselves to those images
and thinking that they don't match up
and developing anorexia.
That turns out to not be the case.
If you look at the prevalence or the rates of anorexia
in the last 10 years or 20 years,
and you compare that to when anorexia was first identified,
which was in the 1600s and perhaps even earlier,
what you find is that rates of anorexia are not going up.
Classically defined anorexia has existed
at essentially the same prevalence
for the last 100, 200, 300, and 400 years,
which is incredible and really speaks to the likelihood
that there's a strong biological contribution
to what we call anorexia nervosa.
Anorexia nervosa is extremely common.
It's anywhere from one to 2% of women.
And the typical onset is in adolescence, close to puberty,
but it can show up later in life as well.
In fact, the identification and diagnosis of anorexia
tends to be in the early 20s.
But if you look back at the history of those individuals,
there were typically signs of anorexia
that stem back into their early teens
or maybe even before that. Now, of course, men can be anorexia that stem back into their early teens or maybe even before that.
Now, of course, men can be anorexic as well,
but anorexia nervosa does seem to occur
at 10 times the rate in women and young girls
than it does in men and young boys.
So what is hunger and what is satiety?
Satiety, of course, being sated
or feeling like we've had enough food.
I want to remind people of the basic mechanisms
by which the brain and body communicate.
The body is communicating two types of information
to the brain on a regular basis,
but in particular around feeding.
And those two types of information
are mechanical information and chemical information.
When your stomach is full,
it sends signals to your brain that are purely based
on this mechanical fullness.
That's nothing to do with nutrients that says, I'm full.
And therefore don't be as hungry.
Don't motivate to find or ingest food.
Whereas when our gut is empty,
even if we have plenty of nutrients
or plenty of body fat stores,
we tend to focus on food a bit more.
So volume and mechanical influences have a profound effect
on how we think and what we consider doing or not doing.
Likewise, chemical effects.
When we ingest food, our blood glucose goes up,
that information is signaled to the brain
via neuronal pathways and hormonal pathways.
And in particular, there are neurons within our gut
that signal to areas of our brainstem
that are involved in satiety in our sense of having enough
that there's food in our system.
So that's chemical information.
So how are hunger and feeding and satiety regulated
by way of mechanical and chemical signaling?
You have, I have, we all have neurons in our hypothalamus
that trigger eating and neurons that trigger cessation
or stopping of eating.
Your hypothalamus, the base of your forebrain
sits more or less above the roof of your mouth.
The hypothalamus contains lots of different kinds of neurons,
including neurons that stimulate sexual activity
and desire, regulate your body temperature
and control appetite and ceasing of eating and appetite.
There are two types of neurons within a particular area
of your hypothalamus that are relevant here.
There are the so-called POMC neurons, okay?
Pro-opioid melanocortin neurons
that tend to act as more of a break on appetite
by way of another hormone called
melanocyte stimulating hormone.
And you have a class of neurons called the AGRP neurons.
The AGRP neurons are the ones that stimulate feeding
and they create a sort of anxiety or excitement about food.
If you eliminate or kill these neurons,
which has been done in experimental mouse models
in the laboratory, but also there are humans
that have lesions or neurotoxic effects on these AGRP neurons.
And what you find is that they don't want to eat.
They have no appetite for food whatsoever.
Whereas if you stimulate these AGRP neurons
or in humans that have say a small tumor
near these AGRP neurons, they become hyperphagic.
They will eat to the point of bursting.
Now there are signals coming back from the body
to inform the brain about presence
of different levels of nutrients.
And that generally comes from three sources.
First of all, is body fat.
The more body fat we have,
the more we secrete a hormone called leptin, L-E-P-T-I-N,
leptin from body fat.
Leptin goes to the brain and suppresses appetite.
Not incidentally, leptin signaling is disrupted
in people that have bulimia and obesity
and certain forms of binge eating disorder.
The body fat is doing something else really interesting
that relates to anorexia.
When there's sufficient levels of body fat
and leptin circulating in the blood
and that leptin signal gets to the brain,
the hypothalamus and the pituitary gland
register that signal and in a completely subconscious way,
trigger the deployment of eggs in females
and the production of sperm in males.
So when body fat stores are very low,
the reason why periods shut off
or sperm production is reduced or even shut off
is because there's not enough leptin
getting to the hypothalamus and to the pituitary
and they shut off the signals, the hormones,
things like gonadotropin, releasing hormone,
luteinizing hormone, follicle stimulating hormone
that travel to the ovary or to the testes
and cause the ovary and testes to ovulate
or to produce more sperm.
So you've got two categories of neurons,
one that acts as an accelerator,
the AGRP neuron saying eat, eat, and gets you excited to eat. And then you have two categories of neurons, one that acts as an accelerator, the AGRP neuron saying, eat, eat,
and gets you excited to eat.
And then you have a category of neurons,
the PMOC neurons that are suppressing hunger.
They're acting like a break.
And the body is informing the brain all the time
about the status of the body
and whether or not it needs more food.
So you might ask, why is it that people who are overweight
and have a lot of body fat,
why they would continue to eat a lot?
It seems like that just shouldn't happen.
From an evolutionary standpoint,
it makes sense that we should eat as often as we can,
as much as we can, and as fast as we can.
There are circuits in the brain to reward eating often,
eating fast, and cramming as much food into you as possible because from a purely evolutionary standpoint,
food was scarce and seeking food was dangerous,
whether or not it was from animal sources or not.
And it's always been competitive.
Every animal, including humans, has a hardwired circuit
that we were born with that pays attention
to how much food is available,
how much we are getting now
and how much we are likely to get in the future.
And without going down the rabbit hole
of arcuate nucleus biology,
in two sentences, you have a hypothalamic area
called the arcuate nucleus.
It's actually the area that houses these PMOC neurons
and these other types of neurons
that regulate hunger and satiety.
And these neurons in the arcuate nucleus
start getting active when we see food and think about food.
And they drive hunger in a way that's responsive
to what the food looks like, what it smells like,
but also our prior history of interactions with that food.
And it takes into account social context.
What's the pathway?
How does this work?
Well, you can frame all of behavior,
good decision-making and bad decision-making
in a pretty simple box diagram model.
We have knowledge of what we should do in one box.
Okay, we should eat that, we shouldn't eat that.
We should wait for dinner, we shouldn't wait for dinner.
And then we have what we actually do in another box.
In between those two boxes are two intervening forces.
And those intervening forces are critically important.
Those intervening forces are homeostatic processes
that regulate the balance of different systems in your body,
hot and cold, awake or asleep,
dopamine and the desire to pursue things, serotonin
and the desire to just relax and chill.
So homeostatic processes and reward systems.
And as we now move into discussion
about anorexia and bulimia specifically,
what you'll see is that anorexia and bulimia specifically, what you'll see is that anorexia and bulimia
are not a breaking of the mindset
of what one should do or shouldn't do.
It's a disruption of these homeostatic and reward processes
such that decision-making is completely disrupted
and in many cases is not available
to the anorexic or bulimic.
Now, I don't want to be abstract here.
What I'm saying is that the person who starves themselves
to the point where they might die,
and in some cases, sadly do die,
they can know perfectly well that their behavior
is leading to bad outcomes and possibly even death.
And yet they are not able to intervene
unless they get particular clinical help
because the homeostatic processes,
the signals from the body and brain that say,
you need food, those aren't registering in the same way
that they are for other individuals.
And just as a little teaser of where we're headed,
anorexics have a sort of switch that's been flipped
such that their decision-making
is actually pretty darn good.
It might even be better than yours
in terms of evaluating food nutritional content,
but their habits are disrupted.
So they're not even consciously aware of the fact
that they're making terrible,
and in some cases, very dangerous food choices.
It turns out habits and the way that we build
and break and rebuild new habits
is one of the most effective treatments for anorexia.
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So now let's talk about anorexia,
this failure to consume enough energy
such that the individual is at risk of death.
And if not death, then severe metabolic disorders,
lack of bone density, et cetera.
A careful analysis through medical epidemiology
has shown that you find anorexia,
even in cultures and societies where food is scarce.
So that really speaks to biological mechanism.
Typically anorexia starts in adolescence
right around puberty.
Puberty at a very broad level is the most significant
and dramatic developmental step
anyone goes through in their lifespan.
The body changes, the brain changes, perceptions change,
one's own self-perception changes.
And most of those changes are driven by changes
in circuitry within the hypothalamus.
So neurons that are controlling the production
of the so-called sex steroid hormones,
things like testosterone, estrogen,
and related hormones, prolactin, et cetera,
those are all changing at very rapid rates.
Let's look under the hood.
Let's look at what's known about the neural circuitry
and the sorts of perceptions and behaviors
of the neural circuitry is driving
in order to understand what they are truly suffering from
at the level of cause, not just symptoms.
First of all, there's a challenge in studying anorexia
because in anorexia, what you're essentially studying
is the absence of a behavior.
It's very hard to study the absence of a behavior
as opposed to a behavior.
So they did some experiments with anorexics,
giving them a gallery of pictures of different foods
and allowing those anorexic patients
to arrange those foods according to preference
about what they would select, about food nutrient content,
about caloric content.
They essentially ask these anorexics to evaluate food.
And in doing so, they were able to identify
something that's very unique to anorexics
at the level of their perception of food.
Anorexics, rather than being anxious
in the presence of food, have a hyperacuity,
a hyper awareness of the fat content of foods,
almost to the point of being sort of fat content savants.
Now it's a well-known symptom of anorexia,
especially young anorexics
that they have kind of an obsession with food,
caloric contents, macronutrient ratios,
meaning fat, protein, and carbohydrate ratios.
They are actively avoiding high fat content foods,
calorie rich foods,
and defaulting towards very low calorie foods
if they have to eat.
And that's very important because what that means is
that we need to look at the areas of the brain
that drive habit formation and habit execution.
In the case of the NREXIC,
those habits are exactly the place
where things start to go awry
and that drive this very dysfunctional under-eating behavior
that sadly often leads to death
or certainly bad medical outcomes.
And it turns out that the brain areas associated
with habit formation and execution
are the best point of intervention.
So you have reflexes and you have neural processes
that include what are called duration path
and outcome type processes.
A duration path outcome type process,
we can shorten with DPO.
DPO is for all types of goal related behaviors.
So for instance, if you want to go to the grocery store
and pick some stuff up and then head home,
you're going to think duration, how long do I have?
Okay, do I have 45 minutes to get to the store?
How long does it take to get to the store?
Path, which way am I going to drive there?
Which way am I going to navigate through the grocery store?
Outcome, was I able to get in, get the items I need
and get home in time?
Okay, DPO, duration, path, outcome.
It's a very conscious process that requires decision-making
and it's reward-based.
You use these DPO type processes in the short term
to pick up groceries and pick a line at the grocery store
and decide which trajectory to take home.
And you use them for navigating long
extended processes in life, trying to get a degree
or raise children or get through a particularly
challenging year, et cetera.
So duration path outcome, and that entire process relies on your forebrain,
this prefrontal cortex.
The prefrontal cortex is what allows you
to take information from memory,
combine it with information about what's happening
in the present context,
and then to direct your behavior, your speech, et cetera,
toward particular outcomes.
Reflexes on the other hand,
don't involve the prefrontal cortex in the same way.
Habits and reflexes, like once you know how to walk,
that doesn't rely on prefrontal cortex.
It's subconscious as it's sometimes called,
but basically you don't have to use the parts of the brain
that are involved in duration, path,
and outcome type analysis.
But basically you have a brain area, and anorexics have a brain area that's involved in evaluating and path, and outcome type analysis. But basically you have a brain area
and anorexics have a brain area
that's involved in evaluating
and decision-making around food.
And then another brain area that's involved
in the reflexive consumption of particular foods
and the reflexive avoidance of other foods.
There are always homeostatic and reward systems
influencing this kind of thing.
Well, in the brain of the anorexic,
it turns out that the reward systems have been attached
to the execution of habits in a way
that is unhealthy for body weight,
but at least from a purely neural circuit perspective,
the reward is now given,
this chemical reward in the brain is given
for avoiding particular foods and only approaching
these very low calorie, low fat foods.
So there really does seem to be a flip in the switch
in the anorexic brain that rewards them internally.
They feel good when they avoid certain foods
and they approach others.
So it's not a deprivation-based model
where they are flagellating themselves or masochistic
or actively avoiding food in order to punish themselves,
which is interesting
because a lot of psychological theories support that idea.
Rather, once this transitions into a set of habits,
they are actually getting a sense of reward.
They feel good, presumably from the release
of a different neuromodulator called dopamine
by approaching foods that are low fat, low calorie content.
And so their whole brain circuitry is skewed
toward avoiding particular things.
And they actually are rewarded for that.
And they feel good.
They feel better than if they were eating
in a healthy weight supporting way.
So how do you break a habit?
How do you rewire the brain circuitry
that's literally causing a reflex?
And in this case, causing a reflex
that is killing the individual,
or at least leading to very bad health outcomes.
The way that you do that is through a cognitive mechanism
where you teach the individual
what is leading up to the habit.
So let's talk about what those things are
that lead into a habit,
because those turn out to be the exact points of entry
for changing and eliminating and rewiring habits
toward more healthy behaviors.
There are two main features of thinking
that go into the sorts of habits that anorexics execute.
The first is something called weak central coherence.
Weak central coherence is essentially an inability
to see the forest through the trees.
It's a hyper acuity and focus on details
within a given environment.
You miss the big picture.
The other is a challenge in set shifting
that once you identify something
that's of particular interest
and that's driving some sort of reward for the anorexic,
that would be identifying the high fat foods
or identifying the one food on the table
that one could eat without anyone hopefully noticing
that they're eating just the green beans
and not touching any of the other food.
If you ever had a meal with an anorexic,
they become masterful actually
at trying to keep people's awareness
away from what they're doing,
which is to home in on these low fat, low calorie foods.
What's amazing and frankly also important
are these findings that once you teach anorexics
what's happening to them, that they're doing this, they are able to intervene.
Now they need support, right?
And another form of therapy that seems to work well
for anorexics that ideally is combined
with this habit rewiring is a family-based model.
Family-based models are starting to surface a lot now
in various therapy settings. Therapy-based models are starting to surface a lot now in various therapy settings.
Therapy-based models, in short,
are basically where the entire family is made aware
of the individual's challenges
with a particular eating disorder or other disorder.
And in understanding some of the biology
and psychology around it,
they stop condemning the individual,
they start to support that individual
through cueing them towards their own habits
that they observe.
They give them some autonomy.
They realize that none of this changes overnight,
but they're taught about things like neuroplasticity
and the ability to change one's brain
in response to experience.
And so there's a whole internal support network.
All of these things fall under the umbrella
of cognitive behavioral therapy.
And I should mention that cognitive behavioral therapies
are often done in conjunction with pharmacologic therapies.
Before we move on to talking about bulimia
and some related disorders,
I want to talk about an aspect of anorexia
that's very interesting, quite troubling in fact,
but that has received a lot of attention.
And that's the distorted self image.
Now, in the episode on depression,
we talked about a very powerful aspect of major depression,
which is this anti-self confabulation
that people who are depressed seem to genuinely believe
and even confabulate about the fact
that they are performing poorly in life
and that they are no good or worthless, et cetera.
It's literally a lie that they believe
and their statements and their feelings
and their behaviors start to reflect that lie.
They're not conscious of it.
That's why we call it a confabulation.
Anorexics often will see themselves as overweight
or imperfect in ways that are of an obsession for them.
In the case of the anorexic,
the problem seems to be that they have a genuine distortion
of their self-image,
so much so that they don't actually see themselves accurately.
Their visual perceptions are off.
And the reason we know this
is because of some really important and beautiful studies
that were done in my colleague Jeremy Bailenson's lab at Stanford.
What's really interesting about these studies
is they give us a window into the perceptual defect
that anorexics have.
I've actually done one of these experiments.
I'm fortunate to not be anorexic,
but I've done some work with the VR lab over there.
And what you get to do is you get to adjust
this avatar of yourself to the point where you think
it's as accurate
as it could possibly be.
And anorexics really distort this avatar.
In other words, they create this serious mismatch
between their perception of themselves and the reality.
So indeed it does seem to be the case.
Now what's relieving, or I should say what's encouraging
about some of the therapies that we talked about before,
the family-based model, the cognitive behavioral treatments,
yes, and the drug treatments as well,
but this habit intervention model is that
as one starts to shift those things,
it does appear that the perception of self seems to follow,
that the perception of self seems to shift
along with the change in habits.
So it doesn't seem that trying to tell someone,
oh my gosh, you're so thin, you really need to eat,
that doesn't seem to work.
They just don't see themselves the same way
that you see them.
And so I offer that as a point of consideration,
if you know someone that's anorexic,
or if you look at an anorexic and you think,
how is it that they are still critical
of the small, even non-existent amount of body fat
on their triceps or something, how is that?
Well, it's literally that their brain,
as it relates to perceptions,
visual perceptions in particular,
that they're completely off.
And fortunately by changing habits,
you rewire those circuits as well.
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Okay, so let's talk about bulimia,
which is overeating and then purging,
typically by self-induced vomiting
or by ingestion of laxatives.
And then we'll also talk about binge eating disorder,
which has a lot of the same features as bulimia,
but typically no purging.
The criteria that were described to me
is that if somebody is doing this at least once a month
over a period of anywhere from two to three months,
then it likely would qualify.
They're not making the decision to overeat.
They are driven from the inside to ingest far more food
than they need.
And in some cases, then they would want to eat.
So it's a lot like the habit that we described
for anorexia, it's almost like it's turned into a reflex
once they get going.
All the homeostatic signals are being overridden,
all the signals from the body, the leptin,
the insulin, the glucose, all that stuff
is cosmically sky high and yet they're just what we,
you know, the nerds call hyperphagic.
They're just eating like crazy.
There's a lot of shame associated with bulimia,
oftentimes because people are vomiting
and it's hard to hide that vomiting behavior.
People are aware of it.
The hallmark feature of bulimia
that distinguishes it from anorexia,
aside from the fact that it's overeating
as opposed to under-eating,
is a lack of what they call inhibitory control.
And that might come as no surprise,
but first of all, the bulimic, unlike the anorexic,
is hyper impulsive,
and oftentimes has other types of impulse behaviors.
And for that reason,
many of the treatments that you see
for bulimia and binge eating disorder
are the sorts of treatments that don't seem to work so well,
or at least most of the time for anorexia.
So the drugs that increase the neuromodulator serotonin,
for instance, fluoxetine, also called Prozac, Paxil, et cetera,
those things oftentimes can be effective in bulimia.
Some of the drugs that are used to treat attention deficit
hyperactivity disorder and ADD,
some of those same drugs like Adderall, Vivants
and things of that sort can also be used to treat bulimia
and binge eating disorder.
Why would that work?
Well, now you are familiar with the prefrontal cortex.
Prefrontal cortex is involved in this analysis
of duration, path and outcome.
Duration, path and outcome is how we avoid impulsivity.
It's how we think, okay, if this, then that,
if that, then this.
You can imagine how for the obsessive compulsive
or for the anorexic, these are circuits that are overactive.
For the bulimic, this is the circuit
that's going to essentially be underactive.
So really the polar opposite of what you see in anorexia.
So this lack of impulsivity implies a lack
of prefrontal control, what we call top-down control.
They become more impulsive.
So bulimics have an issue with impulsivity
and therefore drugs that can increase serotonin
and sometimes these drugs that increase dopamine
and norepinephrine levels in the brain
allow for more top-down control
and that's also why they're used to treat ADHD
and attention deficit disorder.
These drugs tend to create a hyper focus
and tend to push the brain
and general mode of processing into one
in which you think if this, then that, if this, then that.
So anticipating outcomes.
Do behavioral interventions work for bulimia?
In some cases, yes,
provided that those interventions are done early enough.
Regardless, behavioral interventions
coupled with drug-based interventions
are always more effective than either one alone.
Fortunately, there is a decent size kit of drugs
that can help with bulimia.
We have on the one hand anorexia,
which seems to be a disruption in habit
and a coupling of unhealthy habits,
in this case, food restriction, to the reward pathway.
And on the flip side,
we have binge eating disorder and bulimia,
where a very unhealthy habit of gorging oneself with food,
sometimes followed by purging,
is not necessarily coupled to reward.
They feel terrible when they do that, right?
The anorexic feels great
about restricting their food intake.
They feel like they're winning some sort of game.
The circuitry is flipped somehow that way.
With bulimia, they feel horrible
about the fact that they're binging.
There's immense shame.
They can't control themselves.
The reward is set up before the behavior.
The reward is set up in drawing them to food
and in making food look like something
that's incredibly appetizing and there's no impulse break.
There's no way for them to stop that kind of behavior.
I think for those of us that know anorexics
or have observed anorexia, it's so hard to see somebody
starve themselves to near death or to death.
Equally disturbing is somebody who has an abundance of food
and is gorging themselves and then feels terrible about it.
So these are heavy topics.
These are topics that frankly,
no one really wants to talk about
unless they know someone who's suffering from them
or they themselves suffer from them.
What I've tried to do today is try and give you a window
into what really underlies these things
that we call eating disorders.
I hope I've done that at the level of biology,
neurocircuitry, mechanism, endocrinology,
and some of the psychology.
As with any episode of this podcast,
but especially where we're talking about
mental health issues and mental health disorders,
behavioral disorders,
there's no way that I can exhaustively cover
all the different forms of treatment.
The major takeaways today are,
we should all be asking the question,
what is healthy eating for us?
How do we develop a relationship to food
that we can enjoy food,
hopefully both socially and on our own,
but that we are not neurotic and compulsive about it?
Today, we focus on the extremes of food related behaviors
that really qualify as genuine disorders.
They are in the psychiatric manuals
and they are diagnosable
and they are serious health concerns.
They're not just mentally troubling
and concerning for the people suffering from them
and the people around them,
but they are genuine health concerns.
Just want to reiterate that anorexia nervosa
is the most deadly psychiatric disorder by a huge margin.
And if you look statistically at the number of people
with eating disorders and that die of eating disorders,
it's not far off from the number of people
that die from automobile accidents.
I would love for you to take away this model
that was handed off to me that I think is so powerful
for thinking about all sorts of things, not just eating,
but all kinds of behaviors and perceptions
that you have one box for what you think,
one box for what you do,
and what is intervening between those?
Why is it that you can know better and not do better?
Well, it's because you also have to cope
with the subconscious homeostatic processes
and reward processes.
And those oftentimes can be disrupted
in ways that we find ourselves doing things
that are not good for us,
are not good for other people.
But fortunately, there is this great gift,
which is that knowledge of knowledge
can allow you to do better without question.
And that knowledge of knowledge allowing you
to do better over time leads to this incredible phenomenon
called neuroplasticity, which essentially is translated
into doing better over time,
even if difficult,
eventually makes doing better reflexive.
And last but not least,
I want to thank you for your time and attention
and thank you for your interest in science.
And as mentioned at the beginning of today's episode,
we are now partnered with Momentous supplements
because they make single ingredient formulations
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If you go to livemomentous.com slash Huberman,
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