Healthy Eating & Eating Disorders - Anorexia, Bulimia, Binging | Huberman Lab Essentials
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Andrew Huberman opens his discussion on healthy and disordered eating by addressing the current excitement surrounding intermittent fasting, a practice involving restricting feeding to specific windows within the 24-hour circadian cycle. While research from Satchin Panda's lab at the Salk Institute has shown benefits such as improved liver enzymes and insulin sensitivity in mice and humans, Huberman emphasizes that calorie intake versus expenditure remains the fundamental determinant of weight change regardless of timing or frequency. He clarifies that while intermittent fasting is popular because it simplifies portion control for many, no single nutritional plan can be universally defined as "best" due to strong cultural influences; instead, health should be measured by objective metrics like blood lipid profiles and subjective factors such as mental clarity and mood. Crucially, he warns against self-diagnosis of eating disorders, noting that while social media often links anorexia to perfectionism or body image issues driven by images, the prevalence rates have remained stable for centuries, suggesting a strong biological underpinning rather than purely environmental causes. The core of the episode focuses on clinically diagnosable conditions like anorexia nervosa, bulimia, and binge eating disorder, which are distinct from general dietary habits due to their severe health risks and potential lethality. Huberman explains that anorexia is arguably the most dangerous psychiatric disorder, with untreated cases carrying a high mortality rate comparable to automobile accidents. He details how starvation triggers biological responses like reduced heart rate, loss of bone density, and amenorrhea in women as the body attempts to conserve energy via low leptin levels from depleted fat stores. Contrary to popular belief that anorexics starve out of masochism or punishment, Huberman reveals that their brains have rewired reward pathways so that avoiding high-calorie foods actually releases dopamine, making restriction feel rewarding rather than depriving. This condition is characterized by "weak central coherence," where patients hyper-focus on specific details like fat content while missing the big picture, and a distorted self-image confirmed through virtual reality experiments showing they perceive themselves as heavier than they are. In contrast to anorexia's rigid habit formation driven by reward circuits for restriction, bulimia and binge eating disorder involve a lack of inhibitory control in the prefrontal cortex, leading to hyper-impulsivity where homeostatic signals like leptin and insulin are overridden. These individuals often experience immense shame after episodes of overeating or purging because their behavior is not coupled with an internal reward system but rather driven by intense cravings that feel reflexive once initiated. Huberman notes the neurological differences between these disorders: in bulimia, circuits responsible for "duration-path-outcome" analysis are underactive compared to the overactivity seen in OCD and anorexia. Consequently, treatments often involve a combination of cognitive behavioral therapy (CBT) and pharmacological interventions; drugs that increase serotonin or dopamine/norepinephrine can help restore top-down control from the prefrontal cortex, allowing individuals to anticipate outcomes and break impulsive cycles more effectively than behavior alone might achieve early in the disorder's progression. Huberman concludes by addressing the distorted self-perception common in eating disorders, particularly anorexia, where patients genuinely believe they are overweight despite being underweight due to visual perceptual defects rather than conscious lying or confabulation like those seen in depression. He highlights that family-based models and therapies focusing on habit re-wiring can be effective because changing physical habits eventually shifts these distorted perceptions of self-image as neural circuits adapt through neuroplasticity. The overarching message is that while we all have knowledge of what constitutes healthy behavior, subconscious homeostatic processes and reward systems often dictate our actions, creating a gap between knowing better and doing better. However, he asserts that understanding the biological mechanisms behind these disorders provides the necessary insight to leverage neuroplasticity over time, allowing individuals to rewire their brains for healthier relationships with food without relying on willpower alone against disrupted biology.
Read the full video transcript
Welcome to Huberman Lab Essentials,
where we revisit past episodes for the
most potent and actionable science-based
tools for mental health, physical
health, and performance.
I'm Andrew Huberman, and I'm a professor
of neurobiology and ophthalmology at
Stanford School of Medicine.
Today, we are going to talk all about
healthy and disordered eating.
And indeed, we are going to talk about
clinical eating disorders such as
anorexia,
bulimia, and binge eating disorder, as
well as some other related eating
disorders. However, before we get into
this material, I want to emphasize that
today's discussion will include what it
is to have a healthy relationship with
food. We're going to talk about
metabolism. We're going to talk about
how eating frequency and what one eats
influences things like appetite and
satiety, as well as whether or not we
have a healthy psychological
relationship to food and our body weight
and so-called body composition, the
ratio of muscle to fat to bone, etc.
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 2 days or 3 days.
Typically, and hopefully, they will
drink water during those times,
sometimes referred to as water fasting,
which means that they are ingesting
fluids, and hopefully they are ingesting
electrolytes such as salt, potassium,
and magnesium as well because while one
can survive for some period of time
without ingesting calories,
it is extremely important to continue to
ingest plenty of fluids and
electrolytes. And the reason for that is
that the neurons of your brain and body
that control your movements, your
thoughts, clarity of thinking in
general, et cetera,
is critically dependent on the presence
of adequate levels of sodium, potassium,
and magnesium, the electrolytes. And
that's because neurons can only be
electrically active by way of movement
of particular ions, which include things
like sodium, potassium, and magnesium.
So, without those, you can't think, you
can't function, and it actually can be
quite dangerous. 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
Satchin Panda.
Satchin'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 2 days or maybe even 3
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 Satchin's lab and subsequently
other labs showed was that restricting
one's feeding window to anywhere from 4
to 8 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, etc. 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.
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. 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 than they burn,
they will have a low heart rate. This is
the body and brain's attempt to lower
energy output.
They will have low blood pressure. They
will sometimes have symptoms like
fainting,
loss of bone density,
osteoporosis, loss of periods
in girls and women,
and all sorts of disrupted gut and
immune functions. So, there are just
tons of terrible symptoms of anorexia
that really place the anorexic into a
very risky state, which is why
mortality from anorexia gone untreated
is extremely high.
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 1 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 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. Has
nothing to do with nutrients that says,
"I'm full."
And therefore,
don't be as hungry. Don't motivate to
find or ingest food. Whereas when our
gut is empty, even if we have plenty of
nutrients or plenty of body fat stores,
we tend to focus on food a bit more. So,
volume and mechanical influences have a
profound effect on how we think and what
we consider doing or not doing.
Likewise, chemical effects.
When we ingest food, our blood glucose
goes up. That information is signaled to
the brain
via neuronal pathways and hormonal
pathways.
And in particular, there are neurons
within our gut that signal to areas of
our brain stem that are involved in
satiety and our sense of having enough
that there's food in our system. So,
that's chemical information.
So, how are hunger and eating 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 sensation or
stopping of eating. Your hypothalamus,
at the base of your forebrain, sits more
or less above the roof of your mouth.
The hypothalamus contains lots of
different kinds of neurons, including
neurons that stimulate sexual activity
and desire, regulate your body
temperature, and control appetite and
ceasing of eating 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-opiomelanocortin
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 a category of
neurons, the POMC neurons, that are
suppressing hunger. They're acting like
a brake. 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?" 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 POMC 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 and chill.
So, homeostatic processes and reward
systems.
And as we now move into discussion about
anorexia and bulimia specifically,
what you'll see is that anorexia and
bulimia
are not a breaking of the mindset of
what one should do or shouldn't do.
It's a disruption of these homeostatic
and reward processes
such that decision-making is completely
disrupted and in many cases is not
available to the anorexic or bulimic.
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. 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, etc.
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 controlling the production
of the so-called sex steroid hormones,
things like testosterone, estrogen, and
related hormones, prolactin, etc., 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 asked 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
hyperawareness 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 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 anorexic,
those habits are exactly the place where
things start to go awry
and that drive this very dysfunctional
undereating 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.
It requires decision-making and it's
reward-based. You use these DPO type
processes on 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
uh get through a particularly
challenging year, etc. 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,
etc. 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
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
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 cuz 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 re-wiring 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've ever
had a 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
re-wiring is a family-based model.
Family-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
queuing 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, etc. 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 called it
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 or it's
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 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 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 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. Okay, so
let's talk about bulimia,
which is overeating,
and then purging, uh 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.
Uh the criteria that were described to
me is that if somebody's 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, than 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 the nerds uh call
hyperphagic. They're just eating like
crazy.
There's a lot of shame associated with
bulimia,
uh often times because people are
vomiting and it's hard to hide that
vomiting behavior.
Uh 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, um but first of all,
um the
bulimic, unlike the anorexic, is hyper
impulsive.
And often times 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 often times can
be effective in bulimia. Uh some of the
drugs that are used to treat attention
deficit hyperactivity disorder and ADD,
um some of those same drugs like
Adderall, um Vyvanse 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 um um,
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. Um, they
become more impulsive.
So, bulimics
have an issue with impulsivity. Um, 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 hyperfocus and tend to push the
brain and general motor 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 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, uh these are
heavy topics. Um 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 these
subconscious homeostatic processes and
reward processes, and those often times
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.