Huberman Lab - Healthy Eating & Eating Disorders - Anorexia, Bulimia, Binging

Welcome to the Huberman Lab Podcast,

where we discuss science

and science-based tools for everyday life.

I’m Andrew Huberman,

and I’m a professor of neurobiology and ophthalmology

at Stanford School of Medicine.

Today, we are going to talk all about healthy

and disordered eating.

And indeed, we are going to talk

about clinical eating disorders,

such as anorexia, bulimia, and binge eating disorder,

as well as some other related eating disorders.

However, before we get into this material,

I want to emphasize that today’s discussion

will include what it is to have

a healthy relationship with food.

We’re going to talk about metabolism.

We’re going to talk about how eating frequency

and what one eats influences things like appetite

and satiety, as well as whether or not

we have a healthy psychological relationship to food

and our body weight and so-called body composition,

the ratio of muscle to fat, to bone, et cetera.

So as we march into this conversation,

I’d like to share with you some interesting

and what I believe are important findings

in the realm of nutrition and human behavior.

I know these days, many people are excited about

or curious about so-called intermittent fasting.

Intermittent fasting is, as the name implies,

simply restricting one’s feeding behavior, eating,

to a particular phase of the 24-hour

or so-called circadian cycle.

Other forms of intermittent fasting involve

not eating for extended periods of time,

for entire days, or some people will extend

to two days or three days, typically,

and hopefully they will drink water during those times,

sometimes referred to as water fasting,

which means that they are ingesting fluids,

and hopefully they are ingesting electrolytes

such as salt, potassium, and magnesium as well,

because while one can survive for some period of time

without ingesting calories, it is extremely important

to continue to ingest plenty of fluids and electrolytes,

and the reason for that is that the neurons

of your brain and body that control your movements,

your thoughts, clarity of thinking in general, et cetera,

is critically dependent on the presence

of adequate levels of sodium, potassium, and magnesium,

the electrolytes, and that’s because neurons

can only be electrically active by way of movement

of particular ions, which include things like sodium,

potassium, and magnesium, so without those,

you can’t think, you can’t function,

and it actually can be quite dangerous.

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 I think that’s one reason why there’s so much excitement

about intermittent fasting.

Now, within the context of intermittent fasting

on a circadian timescale, once every 24 hours,

you generally find two categories of people,

people who prefer to not eat in the morning,

either because they are not hungry in the morning

or because they find it relatively straightforward

to just drink things like coffee or water, et cetera,

and push their feeding window out to noon or 2 p.m.

or 3 p.m. and then they’ll eat between say 1 p.m.

and 8 p.m. or 9 p.m., it depends on the individual.

Other groups of people find that they are very hungry

when they wake up in the morning,

they don’t feel well if they don’t eat breakfast.

And so they prefer to eat early in the day,

but then they limit their feeding window

such that they cut off their food intake

or stop ingesting any calories of any kind

somewhere around 5 p.m. or 6 p.m., et cetera.

So the duration of the feeding window

has not been broken down

into the kind of nuanced type of information

that one would really want,

at least not in human studies,

saying, well, a six-hour feeding window

or an eight-hour feeding window is ideal.

It really is going to vary

based on lifestyle and circumstances.

For instance, some families

really want to eat dinner together every night.

So do you want to be the person

that’s sitting there watching everybody eat

because you’re fasting from 5 p.m. onward?

I don’t know, that’s an individual difference.

What you can start to identify, however,

is that people tend to fall

into either one category or the other,

people who prefer to skip eating in the morning

or people that prefer to

or manage to skip eating in the evening.

And there has been no evidence thus far

that one is better or worse,

at least in terms of weight loss

or overall health parameters.

Now, you can imagine that some people

might eat breakfast and dinner.

And indeed, I have several, many colleagues, in fact,

who just choose to skip lunch

because they’re busy during the day.

They eat breakfast and dinner.

That doesn’t afford the long fast associated with sleep.

What do I mean by that?

Well, if you went to sleep at 11 p.m.

and you wake up at 6 a.m.

by extending your fast until 1 p.m. in the afternoon,

you get quite a long period of no ingesting any calories.

Whereas when you don’t eat during the middle of the day,

you are getting a fasting period

that’s probably anywhere from four to seven hours,

but it’s not linked to the longer fasting period

of not eating while you are asleep.

Because most all people, and I want to emphasize most,

do not eat while they are asleep.

But we are going to talk about an eating disorder

that does exist where people actually eat in their sleep.

I know it sounds pretty wild,

but indeed that eating disorder does exist

and has a very interesting underlying mechanism.

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.

We will get to that topic.

But for the time being,

I want to emphasize a new set of findings

that I think many people will find interesting

and at least will want to consider

in light of their current nutritional plan

or pattern of eating,

whether or not you’re intermittent fasting or not.

And I want to cue up an important framework

for the rest of the conversation

on healthy and disordered eating,

which includes an understanding of thinking,

decision-making, and what we call homeostatic processes,

meaning regulation of things

that are going on in our brain and body,

and reward mechanisms.

I’m going to return to that in a moment.

But first I want to share with you these new findings

that were just published in the journal Cell Reports,

a cell press journal, excellent journal.

This was a study that was performed both in mice

and it included a crossover study with a human population.

The human population was women,

but it relates to a previous study

that was also carried out in men.

I’m going to simplify this study.

We will provide a link to the full study

so you can explore it in more detail.

And if you’re really excited about the results,

I would encourage you to explore some of the references

within that paper as well.

What was the study?

The study looked at giving mice or humans two meals

and explored whether or not putting those meals

early in the day or late in the day

had an impact on muscle hypertrophy, muscle growth,

and overall protein synthesis of muscle.

So when we eat, the amino acids from various foods

are broken down and synthesized

into different types of tissues.

They can be utilized for energy,

burned up for moving about and thinking, et cetera,

or it can be synthesized,

those amino acids can be synthesized into skeletal muscle,

the sorts of skeletal muscles

that allow you to move your limbs.

This study explored how protein intake,

which included what are called branch chain amino acids

and amino acids like leucine,

which are important for muscle protein synthesis,

it explored whether or not emphasizing or skewing

the protein intake toward early day or late day

was better in terms of muscle hypertrophy.

And they also looked at some parameters of strength

like grip strength.

Now, mice are nocturnal.

So before you say, wait, mice are nocturnal.

How did they look during the day?

And it’s completely, it doesn’t apply because it’s in mice.

Of course they knew that.

And they looked during the mice’s active phase

of their circadian cycle, which corresponds to our day.

And in humans, they looked at whether or not eating

most of one’s protein early in the day

was better than if the protein intake

and these branch chain amino acids

were placed later in the day.

And yes, they had the mice do resistance training.

They did that by emphasizing overload

to one limb of the mouse.

And that actually generates hypertrophy.

It’s a form of resistance training in mice.

So they don’t have the weight training.

They weren’t doing curls and dips and squats

and things of that sort.

They were moving their own body weight,

but they skewed that distribution of body weight

by restricting a limb and forcing them to use one limb

that did indeed grow in response to that.

And then in humans,

there was an exploration of grip strength.

And then with resistance training,

that was also carried out through a peripheral study.

Basically the takeaway from this study

was that mice and humans can utilize amino acids

that are ingested early in the day

better than they can utilize amino acids

ingested later in the day,

in particular toward muscle hypertrophy and growth

or maintenance of muscle,

which for those of you that aren’t interested

in muscle hypertrophy,

that aren’t trying to grow your muscles,

I’ve talked before in the episode

on building strength and hypertrophy,

that maintaining muscle,

regardless of one’s athletic prowess,

regardless of one’s age is extremely important

because loss of skeletal muscle

is one of the major causes of injury as we age.

It’s one of the major causes, believe it or not,

of cognitive and metabolic deficits as we age.

So maintaining muscle is important.

Building muscle might be important to some of you,

but what they found was ingesting protein early in the day

and these amino acids early in the day

led to more muscle hypertrophy

than if the majority of amino acids and proteins

were ingested late in the day.

So this translates to intermittent fasting

such that if you are interested in muscle hypertrophy,

you might, and I want to emphasize might,

consider making sure that you’re getting

sufficient protein intake early in the day.

What sources of protein you use

is going to be highly individual.

Some of you are meat eaters.

Some of you don’t eat red meat.

Some of you eat chicken and fish and eggs.

Some of you don’t.

Some of you are vegans.

It has been shown that the amino acid leucine

is vital for the cell growth process,

including muscle growth because of its relationship

to the so-called mTOR pathway,

mammalian target of rapamycin.

We can talk about that more if you like in a future episode.

This means that if you’re somebody who wants to maintain

or increase the amount of muscle mass that you have,

ingesting a high protein meal early in the day

ought to be beneficial for that.

Does it mean that you should not eat protein

in the afternoon and evening?


I think a lot of people might’ve misinterpreted this study

and I don’t want that to happen.

This is only pointing out the fact that ingesting

sufficient quality amino acids, including leucine,

early in the day can be beneficial for maintenance

and growth of muscle tissue.

It does not say that you should avoid protein

later in the day.

Now, for you intermittent fasters, this could be relevant.

I, for instance, was somebody who for a very long time

skipped breakfast.

My first meal of the day would be in the early afternoon,

mostly protein and salad.

In my case, animal protein,

because that’s in alignment with my values.

Then in the evening I would eat pasta, vegetables, et cetera.

I might have some protein, some small piece of fish

or chicken or something like that,

but I didn’t really emphasize that.

On the basis of these results, I am experimenting with,

I want to emphasize experimenting with.

I haven’t completely tossed out my old protocol,

but I’m experimenting with eating proteins early in the day

and eating lunch.

And then dinner might be a light supper of some sort,

but not so much protein later in the evening.

Again, if you want to eat six meals a day,

you want to eat around the clock.

I’m not going to stop you.

I’m not telling anybody what to do.

As I mentioned earlier, nobody knows exactly how to eat

for one’s particular goals.

But this study was really interesting

because it really did show that we can utilize the proteins

that are ingested early in the day better

than we can utilize the proteins that are ingested

later in the day.

And of course there will be factors that can shift that.

For instance, if you work out very hard

with resistance training later in the day,

resistance training is known to increase protein synthesis.

So it stands to reason that ingesting amino acids

after that training would be beneficial.

However, in this study, it did not seem to matter

when the resistance training fell

within the 24 hour schedule.

The morning ingestion or early day ingestion

of amino acids seem to be beneficial.

How early?

Between the hours of about 5 a.m. and 10 a.m. for humans.

Now, just a bit of mechanism to explain why this happens.

So why would it be that ingesting protein early in the day

would lead to more synthesis of muscle

than ingesting protein later in the day?

And the reason it turns out is related

to the circadian clock mechanism that is present

in all cells, including muscle cells.

So muscles have fibers.

I think most people are aware of that,

that your muscles are not just one big blob of tissue.

A lot of these little fibers that contract.

Within those fibers, however, there are cells with nuclei.

Those nuclei contain DNA.

DNA is transcribed into RNA.

RNA is translated into proteins.

The DNA of your cells, including these muscle cells,

are under strong circadian regulation.

Each one has a pattern of gene expression

that is different at different times

during the 24 hour cycle.

This is an unescapable reality of all cells in your body,

right from your hair cells, to your brain cells,

to your retinal cells, to your toe on both feet.

These cells make a gene called BMAL, B-M-A-L,

is a clock gene.

And the expression of this clock gene

varies across the 24 hour cycle.

And proteins that are downstream of this BMAL gene

influence protein synthesis.

The circadian regulation of this BMAL gene

turns out to be vitally important

for this protein synthesis mechanism.

How do we know that?

Well, in this particular study,

because they had a mouse that lacked BMAL,

the gene was knocked out.

They had a bunch of these mice.

They were able to explore

whether or not this early day feeding effect

was present or absent in these mice

that lack the gene BMAL.

And indeed it was absent.

In other words, the effect of increased protein synthesis

early in the day was eliminated

in the absence of the BMAL gene.

So what this means is that when you wake up in the morning,

assuming you’re following a standard schedule

of being asleep at night and awake during the day,

your muscle cells are primed to incorporate amino acids

and synthesize muscle,

regardless of whether or not you weight trained

the night before at 8 p.m.

or you don’t weight train at all,

or you weight train afterwards or before.

I said 5 to 10 p.m. is the sort of critical window

for this increased protein synthesis.

All this means is that if you are interested

in maintaining or enhancing muscle tissue volume,

that you might want to consider eating quality protein

and amino acids early in the day.

You could train first, you could train after,

you could not train at all.

That’s an entirely different discussion.

What is quality protein?

Well, quality protein is going to be a protein

that includes most of the essential amino acids

and in particular leucine.

Now, there’s a lot of debate as to whether or not

you can get all the essential amino acids

from a purely plant-based diet

or whether or not you need to ingest

animal-based foods or not.

The term quality protein

has no strict scientific definition.

Some people define quality protein

as a protein that has a high essential amino acid

to caloric ratio.

Now, what that means is a small piece of chicken or steak

or eggs, for instance, will have many essential amino acids

with a low caloric content relative to, say,

beans or plant-based foods

that can also get you essential amino acids,

but it requires more calories

to access those essential amino acids.

Now, that’s a debate that has many exceptions and nuances.

And I, for one, am perfectly respectful of the folks

that just want to ingest plant-based foods

in order to get their high-quality protein.

I think that actually can be done.

One has to be careful and thoughtful in their choices

about how to do that.

So this really isn’t about animal-based

versus non-animal-based foods.

This is about getting quality amino acids early in the day

from whatever foods are in alignment

with your particular values and your particular eating plan.

So that’s a lot of information,

but the key takeaways are every cell in your muscles

has a clock gene.

The clock genes vary such that protein synthesis

is greater early in the day than it is later in the day,

such that in both mice and in humans,

ingestion of quality proteins early in the day

will be more so incorporated into muscle

than the proteins that are ingested late in the day.

And of course, there are the caveats of

if you’re training hard late in the day,

if you’re adjusting your hormone status

through whatever mechanism, et cetera,

protein synthesis can also be high later in the day,

but for most people, it’s going to taper off

due to this circadian B-mal gene related mechanism.

Again, we will provide a link to the study.

And the other key takeaways were that nobody knows,

nobody can tell you what healthy feeding windows are,

what the best feeding windows are.

There’s absolutely no information in that context.

You talk to 10 nutritionists or academics or trainers

or individuals about what healthy eating is,

and you are going to get vastly different answers.

And that’s one of the reasons why I believe that

the internet in particular social media

are so filled with contradictory opinions,

but the calories in versus calories burned formula

is the more or less holy foundation

of all things about nutrition, eating and weight.

And as we transition today into the discussion

about eating disorders, I’d like you to keep this in mind

because for the treatment of eating disorders,

it doesn’t matter what psychological

or early trauma-based effects led to the eating disorder

if the person isn’t adjusting their feeding behavior

in a way that is going to ameliorate

the symptoms of that disorder,

which is ultimately the goal.

Before we begin, I’d like to emphasize that this podcast

is separate from my teaching and research roles at Stanford.

It is however, part of my desire and effort

to bring zero cost to consumer information about science

and science related tools to the general public.

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So let’s talk about eating disorders.

And as we do that, I want to emphasize again

that nobody can really define what healthy eating is

with a single protocol.

However, there is some general agreement

about what unhealthy and disordered eating is.

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.

We talked about this a little bit

in the episode about depression.

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?

Ah, I see this sort of behavior or that pattern of thinking

in that individual.

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.

I say that not to protect us, but to protect you,

because information is valuable.

And I do believe that knowledge of knowledge

can be very valuable in navigating any topic

and improving our thoughts and behaviors around that topic.

But one doesn’t want to, or I should say,

one shouldn’t start to self-diagnose

simply on the basis of information

without running that through the filter

of a qualified professional.

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.

Now that’s a mouthful, no pun intended.

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.

So what is anorexia and how prevalent is it?

Anorexia, 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.

Muscle is very metabolically active.

They tend to lose a lot of muscle mass.

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.

They will have sometimes even hair growth on the face,

something called lanugo,

which is essentially the body’s attempt

to insulate the body because of loss of body heat

when you’re that thin.

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.

So this idea that the images that we’re being bombarded with

are causing anorexia doesn’t seem to be true.

Now, that is not to say that the images

that we in particular young people are being bombarded with

are healthy for their psychological state of mind,

but classically defined anorexia

has existed at essentially the same prevalence

for the last 100, 200, 300, and 400 years,

which is incredible and really speaks to the likelihood

that there’s a strong biological contribution

to what we call anorexia nervosa.

Anorexia nervosa is extremely common.

It’s anywhere from one to 2% of women.

And the typical onset is in adolescence, close to puberty,

but it can show up later in life as well.

In fact, the identification and diagnosis of anorexia

tends to be in the early twenties.

But if you look back at the history of those individuals,

there were typically signs of anorexia

that stem back into their early teens,

or maybe even before that.

Now, of course, men can be anorexic as well,

but anorexia nervosa does seem to occur

at 10 times the rate in women and young girls

than it does in men and young boys.

So while there does seem to be more of a prevalence

of anorexia in boys and young men these days,

that’s probably due to better diagnosis and detection

than it is to some sort of societal shift

related to imagery, et cetera.

Later, we will talk about body dysmorphia

and some of the images that are present in media

and social media and how those are impacting

other forms of eating disorders.

But when you look at anorexia nervosa,

this failure to maintain weight, even to healthy levels,

and often drops in weight that are very dangerous

or even deadly, that has existed for a very long time

and seems to be somewhat hardwired

into the biology of individuals that suffer from it.

Now, when I say hardwired,

that doesn’t mean that it can’t be treated or cured,

and indeed it can.

Bulimia, which is defined as binge eating or overeating.

Let me explain what that is.

Binge eating is consuming vast amounts of calories

in a short period of time.

Overeating can be ingesting more calories than one needs,

but over an extended period of time.

Both can exist, of course, but bulimia is also very common.

It’s more common in young girls and in women

than it is in young boys and in men,

but it is present in both sexes.

Bulimia and rates of bulimia might be increasing.

That’s sort of an interesting finding.

It’s not quite clear whether or not it’s existed

in its same form for a long period of time

or whether or not there are new forms

that are evolving or showing up.

We’re going to drill into bulimia

and what it actually is and what it represents.

But one thing I want to be clear about,

just as the perfectionist mindset

has been associated with anorexia,

and it turns out that’s not the case.

It can be, but it’s not always associated with anorexia.

There was the idea that bulimia is associated

with early trauma in childhood, in particular sexual trauma.

And while that can be the case,

there’s no direct correlation between the two.

Now, obviously, psychological phenomena and trauma

can have a profound impact

on the way that the brain wires up

and the way that people approach food

and other types of behaviors.

But the sort of classic idea

was that all anorexics are perfectionists.

They want to perform well.

It’s all about control and autonomy.

And bulimics are kind of dysregulated

and acting out against some early sexual trauma.

Those stereotypes of the psychological framework

of anorexics and bulimics doesn’t hold up

when you look at the data.

Many meta-analyses have been done.

It just simply is not the case.

And in both instances, both anorexia and bulimia,

there are clear biological underpinnings

to what’s driving the under-eating or the over-eating.

So we’re going to talk about the biology

of under-eating and over-eating

and appropriate levels of eating.

And by doing that, we will start to identify

some of the mechanisms that serve as entry points

for the treatment of both anorexia and bulimia.

And as some of you are probably aware,

anorexia and bulimia can be comorbid.

They can exist with one another.

There are anorexics who will binge and then purge

in order to maintain that unhealthily low weight.

There are bulimics who fit the psychological criteria

of anorexia.

And so there’s a lot of overlap

between those two categories.

Now let’s talk about the categorization for a second

and why the categorization has led to now

a bunch of other eating disorders

as defined by the psychiatric community.

One of the classic symptoms of anorexia

is a loss of menstrual cycles, loss of periods.

And the reason for that is when the body is undernourished,

the body fat stores send signals to the brain

to inform that the body is undernourished

or they turn off the signals that say,

look, there are enough body fat cells out here

to support healthy metabolism.

And therefore let’s shut down ovulation.

Literally signal sent from the fat and muscle to the brain

and the brain, the hypothalamus and pituitary

will send signals down to the ovaries

or they will turn off the signals heading to the ovaries

to deploy eggs, the maturation of eggs in the follicle,

et cetera.

So there are instances in which people have anorexia

or have bulimia, but are still maintaining

healthy menstrual cycles or at least menstrual cycles.

And that has led to a whole set of other categorizations

of eating disorders like binge eating disorder,

where there tends to be a lot of overeating,

but not the purging or categorizations of anorexia

in which people are underfeeding,

but they are not losing their periods.

And so these have a number of different names and acronyms.

Some of them include things like EDNOS.

EDNOS is eating disorder, not otherwise specified.

So that’s a subcategorization or OSFEDS.

So OSFEDS is other specified feeding or eating disorder.

So right now, if you were to look online

or you’re looking to the psychiatric

and psychological textbooks,

what you would find is that there’s a huge constellation

of eating disorders.

Today, we’re mainly going to talk about anorexia, bulimia,

binge eating disorder, and body dysmorphia.

You can even find eating disorders like pica,

where people actually ingest things like dirt

or rocks or metal because they have a genuine appetite

for those things.

I certainly do not recommend sampling

any of those non-food items as foods.

It is incredibly dangerous.

People often poison themselves.

They often can cause structural blockages.

Some people have died from those sorts of things,

but nonetheless, there are aspects of our brain and biology

that when disrupted can lead to very bizarre

types of eating behavior.

Sometimes pica is caused by malnutrition, but not always.

And so today we’re going to focus on the most prevalent

eating disorders, but we are going to build up

toward that understanding by looking at

what healthy metabolism and eating and satiety

and hunger looks like.

Because one, I realized that not everyone out there

has an eating disorder.

And two, I want people to understand this relationship

between how they think, the decisions they take

about what they eat, and how the body and the brain

at subconscious levels are driving some of these behaviors,

healthy or otherwise.

Because I do think that it can lead us

to a better understanding of what healthy eating is

for most of us and to increase compassion

and hopefully even increased improvement in treatment

of eating disorders for those that are suffering from them.

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.

This is vitally important, not just for this discussion,

but for any discussion about how we think,

how we behave, how we feel.

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.

What do I mean by mechanical information?

Well, if you take a deep breath and you hold your breath,

what you’ll find is that you can hold your breath

a lot longer than if you exhale all your air

and you hold your breath with lungs empty.

And the reason is not because when your lungs are full,

you have enough oxygen,

and therefore you can hold your breath.

It’s because when your lungs are full,

a particular class of neurons called baroreceptors

send information to the brain and say,

there’s pressure in the lungs.

And that means that there’s probably oxygen in here.

And so the trigger to breathe is actually suppressed.

When your lungs are empty,

even if you have plenty of oxygen in your system,

those baroreceptors send a different signal to the brain,

which is, there’s no oxygen in here and you should breathe.

And so the impulse to breathe comes earlier.

Likewise, 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 so-called blood sugar or blood glucose levels go 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.

We have an accelerator on eating and we have a break.

And I covered all of this in a lot of detail

in the episode on feeding and metabolism and hunger.

So if you want a lot more detail, see that episode.

But right now, I’m just going to give you the top contour

of how all that works.

Your hypothalamus is an area of your forebrain,

which tells you it’s in the front,

but it’s 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-opioid melanocortin neurons

that tend to act as more of a break on appetite

by way of another hormone

called melanocyte-stimulating hormone.

And not so incidentally,

when you’re getting a lot of sunlight

and you’re viewing a lot of sunlight,

that system is ramped up.

This is why appetite is lower in the summer months

than it is in the winter months.

This is true in animals and this is true in humans.

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.

It can be positive anxiety or it can be negative anxiety.

What do I mean by that?

Well, have you ever seen kids heading in to get ice cream?

They’re absolutely excited.

You see people getting ready to sit down and eat a big meal.

They’re excited to eat.

Sometimes that’s due to social factors,

but they have an increase in overall levels

of autonomic arousal.

And depending on the context,

they can feel excited or anxious,

but it is a ramping up of energy.

These AGRP neurons are what caused that.

In fact, so much so that 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 essentially become anorexic,

meaning they don’t want to ingest food.

They have no appetite for food whatsoever.

Now that’s not exactly what anorexia is,

but these AGRP neurons are like an accelerator

on wanting to eat.

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.

Both animals and humans that have elevated levels

of these AGRP neurons are anxious.

They want to eat and they will ingest food

to the point where they override those mechanical

and chemical signals in the body.

And I know it sounds horrible and it is horrible.

They will eat until the point that they burst.

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.

This is a body to brain signaling mechanism

that says, look, I’ve had enough.

Not incidentally, leptin signaling is disrupted

in people that have bulimia and obesity

and certain forms of binge eating disorder.

So that system is disrupted.

I’ve had enough signal or there’s enough body fat here

such that you don’t need to eat more, right?

Here I’m sort of in the voice of the body fat

trying to talk to the brain.

That signal, that dialogue is mixed up or messed up.

In some cases it’s absent entirely.

So the body fat is signaling to the brain

about how much reserve you have.

It’s sort of like a savings account for energy

because that’s what body fat is.

You got lipids in there and through lipolysis,

they can be metabolized.

If you’re interested in that process,

both how to increase it and just generally how it works,

you can see the episode on the science of fat loss.

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,

all these hormones that you don’t have to remember

the names of if you don’t want to

that travel to the ovary or to the testes

and cause the ovary and testes to ovulate

or to produce more sperm.

So the reason why anorexic stop having periods

when they stop cycling

is because there isn’t sufficient leptin in the bloodstream.

Now, there have been attempts to give leptin to anorexics

because leptin has been sequenced

and the peptide has been synthesized

and so you can inject leptin into people.

There are studies where they’ve done that.

When that happens, it does not tend to alleviate

the anorexia, does not cause people to start eating again

and that actually makes sense because leptin

is also a way of shutting off the hunger signals

it’s the body fat’s way of saying,

hey, there’s a lot of body fat here

or there’s sufficient body fat,

there doesn’t even have to be a lot.

But it has in some cases been shown to rescue

the menstrual cycling in some anorexics.

Okay, so body fat is signaling to the brain,

the gut is signaling to the brain,

there are neurons in your gut that are primarily responding

to meaning they fire electrical signals

when there are sufficient fatty acids

coming from fats you ingest,

amino acids coming from proteins you ingest

and sugars coming from carbohydrates and sugars,

things like fructose, glucose, et cetera.

Those signals are being sent from the fat

and from the gut up to the brain

and therefore your body has multiple signals

of directing you toward eating more or eating less.

So you’ve got two categories of neurons,

one that acts as an accelerator, the AGRP neuron saying,

eat, eat and gets you excited to eat.

And then you have a category of neurons,

the PMOC neurons that are suppressing hunger,

they’re acting like a 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 or not.

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?

Well, past a certain threshold of body fat,

that’s when you start getting into

these so-called metabolic disorders

where blood glucose metabolism is disrupted,

leptin signaling is disrupted

and there are all sorts of changes on both the brain side

and the body end of things such that they’re hungry

despite the fact that the body

has plenty of energy on reserve.

Okay, that I think is sufficient to explain

the basics of hunger and satiety

and a kind of a biological mechanism.

And the important thing again to remember

is that they’re mechanical and chemical signals

that come from fullness or absence of fullness.

They come from the presence of glucose in the blood

or the absence of glucose in the blood.

When you haven’t eaten for a long time,

glucagon levels go up, for instance, GLP-1 levels go up

and those will drive you to seek out food and want food.

And then there are these signals that are coming

from body fat and from neurons in the gut.

So there’s a lot of convergent signal, a lot of pathways.

I don’t offer you all those pathways to confuse you.

I offer you those pathways to clarify the extent

to which something as simple as eating

or the decision to not eat is complicated.

We’ve perhaps heard, or I’ve certainly heard that,

oh, you know, it takes about 20 minutes

for satiety to set in.

You know, so you should eat slowly

that you won’t realize that you’re full

until about 20 minutes.

That’s actually not true.

I don’t know where that got started,

but we should probably all chew our food better

and eat more slowly,

be more mindful of what we’re eating, et cetera.

So in anticipation of this episode,

I consulted extensively with a colleague of mine

at Stanford who sadly for us

is going off to University of Pennsylvania.

So our loss is University of Pennsylvania’s win.

His name is Dr. Casey Halpern.

He’s a MD, medical doctor and neurosurgeon,

and a PhD who studies binge eating disorder

and other types of eating disorders

and how they arise in the brain.

And he’s developed some really pioneering treatments

for them.

We’ll talk more about his work a little bit later

in the episode.

But we got to the discussion of why a body

that has sufficient energy levels

would desire to eat more at all.

And this is not just the case for binge eating disorder

or for bulimia, but why that would be the case.

You know, this is primitive biology

that evolved over many tens,

if not hundreds of thousands of years.

You see it in mice, you see it in humans,

very similar types of pathways and effects.

How is it that human beings who have plenty of fat

on reserve and plenty of glycogen in their liver, et cetera,

in other words, plenty of energy,

why they would be hungry, why they would eat at all?

It seems like that just shouldn’t happen.

And he had a very important and I think clear

and intuitive way of framing up all this stuff

around eating and motivated behaviors

and how they can go awry,

not just in eating disorders, but in all of us.

Basically what he said was 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.

Oh, that sounds crazy.

I was told to eat not too often, not too much,

and to eat slowly and chew my food.

But as Dr. Halpern pointed out,

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.

For those of you that grew up in families

with a lot of siblings, this may resonate with you.

I just one sibling.

We were competitive about certain things,

but typically not competitive about food.

But I had friends that had a lot of siblings.

It was really interesting to see how food was served up

and how it was taken in those households.

It was like food would hit the table

and it was just an absolute war for portions.

And who got what and how much,

and who got a slightly bigger piece of cake, et cetera,

turned out to be a frequent happening in these meals

and at these birthday parties.

Whereas the only children perhaps

were used to having more food presented to them

without having to compete with other members of the species.

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 a fascinating area.

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.

They drive hunger 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,

whether or not we are going to get the whole pizza

to ourselves or whether or not there are going to be others

that we are going to have to compete with.

So there are a lot of signals that this arcuate nucleus

in your brain are paying attention to.

So Dr. Halpern pointed out

that you actually have an accelerator

that increases your level of awareness and anxiety

and sort of constricts your field of view

and all your senses anytime you interact with food

and is driving a primitive reflex

to ingest as much food as you can, as quickly as you can,

and then move on from there

and presumably to do the same elsewhere.

So that changed the way that I think about eating behavior

and eating disorders.

In fact, we could think about eating disorders like bulimia

as an unmasking of that mechanism

without the so-called top-down control,

without the mechanisms that we use to regulate our behavior.

And indeed, bulimia and binge eating disorder

are closely associated with impulsivity

and with impulsive behaviors of other kinds,

something that we also will discuss more.

What’s the pathway?

How does this work?

What is Dr. Halpern and his colleagues doing

in order to try and treat things like binge eating disorder?

Well, you can frame all of behavior,

good decision-making and bad decision-making

in a pretty simple box diagram model.

And I realize that many of you are listening to this,

not watching this, and there is no diagram to look at.

I’ll just explain it

so that you can conceptualize it in your mind.

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.

Okay, now this is true for all behaviors.

We should say something,

or we want to say something, but we don’t.

We shouldn’t say something, but we do anyway.

That’s the knowledge, the kind of looping in your head.

I should do my homework.

I should go for a run.

I shouldn’t do this right now.

I shouldn’t be on social media.

All those kinds of shoulds and shouldn’ts

that are circulating in your head.

That’s one box.

Then there’s what you actually do, the behavior,

whether or not you suppress the behavior,

you turn off your phone and you go read a book

or you go to sleep or whether or not you stay up all night

or you stay up for another hour, even five minutes.

In between those two boxes are two intervening forces.

And those intervening forces are critically important.

Those intervening forces are homeostatic processes,

called by some processes, same thing.

Homeostatic processes that regulate the balance

of different systems in your body,

hot and cold, awake or asleep, dopamine,

and the desire to pursue things,

serotonin and the desire to just relax and chill.

So homeostatic processes and reward systems.

And as we now move into discussion about anorexia

and bulimia specifically,

what you’ll see is that anorexia and bulimia

are not a breaking of the mindset of what one should do

or shouldn’t do.

It’s a disruption of these homeostatic and reward processes

such that decision-making is completely disrupted

and in many cases is not available

to the anorexic or bulimic.

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 for the bulimic or the person that suffers

from binge eating disorder,

they don’t necessarily want to eat that food.

They simply cannot help it.

It’s like a reflex for them

because the homeostatic processes

and the reward processes associated with food

are such that they can’t intervene

between the should do X, Y, or Z,

or shouldn’t do X, Y, or Z,

and what their actual behavior is.

Now, this isn’t just a biological mechanistic explanation

for what could have been summarized in two sentences.

What this is, is a roadmap of where interventions

can really make a difference.

So as we talk about different drug-based interventions

or behavioral interventions or social interventions,

I’d like you to think about whether or not

those interventions are breaking into

or tapping into this box of the thinking,

the sort of pattern of thinking around food,

whether or not it’s the behavior, the actual ingestion,

or the restriction of food,

or whether or not it’s tapping into the homeostatic process,

the balance of energy systems

and kind of getting enough, but not too much,

or it’s tapping into the reward system.

And just as a little teaser of where we’re headed,

what you’ll find based on the data,

clinical data experiments done very carefully

and very well by excellent groups,

what you’ll find is that 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 that 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, et cetera.

As I mentioned earlier, anorexia and things

that almost certainly were and are anorexia

have been described as early as the 1600s

and maybe even earlier.

There are some records from the saints,

from the 1400s of people that refuse to ingest food.

Another common myth is that anorexia

is only the sort of thing that you see in rich societies.

These are spoiled children with so much food

that they decide they’re only going to focus

on how slim they are,

how they look in bathing suits, et cetera.

Not true.

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.

Now it’s hard to unveil in societies where food is scarce

because a lot of people are starving and hungry,

but there are individuals that choose still to avoid food

and seem to have some sort of reward mechanism

that rewards them or makes them feel better

if they don’t eat,

despite the fact that their body

is severely depleted of nutrients.

So that’s very interesting and points again

to some disruption in some biological mechanism.

Now, I want to make sure that I’m emphasizing

that I’m not in favor of people,

in particular young children, adolescents,

and teenagers being bombarded

with unrealistic imagery about bodies.

But the idea that that’s the cause of,

or is amplifying anorexia,

the data just don’t seem to support that.

Anorexia in its classic sense

requires that there be an endocrine,

meaning a hormonal disruption,

menstrual abnormalities, lack of sperm production,

or low testosterone in males,

in order to meet the classification for anorexia.

But as I mentioned earlier,

there are now nuanced and new classifications of anorexia

that even for individuals that still menstruate

or that maintain sperm production,

that anorexia can still be considered

a clinically diagnosable disorder.

Now, typically anorexia starts in adolescence

right around puberty.

Let’s take a look at what puberty is.

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.

Anorexia tends to show up around this time

in a subset of individuals

who on the face of it seem to find food aversive.

Now, the purely psychological theory of this

is that they are fighting for autonomy.

They want control.

Puberty is also a time in which children and parents

are in a tug of war over control.

You were once a small child being told when to go to bed,

sent to your room,

now you’re a child that can talk back and say,

I don’t want to, or I refuse to.

And that happens a lot in various households

as I’m sure you’re familiar with.

Adolescence and puberty is also

when girls start menstruating typically,

or boys develop deeper voice,

they start producing sperm, et cetera.

So there are a lot of bodily changes

that also drive perceptual changes

and perceptual changes that drive bodily changes.

And it is a dramatic shift for a young girl or boy

that doesn’t nourish themselves sufficiently

during that period.

There are a number of downstream negative effects.

I’ll list out some of them.

These are just a subset of the effects.

Hypogonadism, that’s the lack of sperm production

or healthy egg production.

There is amenorrhea, which is the lack of menstrual cycling.

Okay, so a failure to have a menstrual cycle.

Reduced insulin secretion.

Insulin is this hormone that’s released

in order to help shuttle glucose

into various tissues for energy utilization.

That’s down because energy levels are down so much.

One of the symptoms that’s a little more cryptic

and that has actually interesting implications

for sake of the cholesterol hypothesis

is that anorexics who ingest very little food

often have cosmically high levels of cholesterol,

including LDL, low density lipoprotein cholesterol.

You say, well, how could that possibly be?

We were all told and continue to be told from many sources

that ingestion of dietary cholesterol

is what drives high levels of bodily cholesterol.

Cholesterol is manufactured by the liver

and in anorexics who consume very little food,

they often have cosmically high levels of cholesterol,

which is one of the kind of wrinkles

in the so-called dietary cholesterol hypothesis

that all of our cholesterol that we see on a blood panel

is due to what we eat.

But the explanation for it is that under conditions

where there’s not sufficient cholesterol

to synthesize the sex steroid hormones,

things like testosterone and estrogen,

which are required in both males and females,

those are made from cholesterol,

that the body, the liver will start generating

its own cholesterol and will often overshoot the mark

to a dramatic degree.

So the blood lipid profiles in anorexics

are often very unhealthy,

despite the fact that they’re eating very little food.

In addition, they tend to have elevated levels

of things like vasopressin,

which are hormones that regulate body temperature

and blood volume.

They tend to have low blood pressure.

They can pass out.

I mentioned some of the other symptoms earlier.

In other words,

there are a huge number of terrible things happening.

Thyroid levels are down.

Heart rates are down.

If I’m painting a very bleak picture here,

it is indeed a bleak picture.

So we have to ask ourselves,

what can be done for the anorexic, right?

Let’s say it’s a failure of the AGRP neurons

to stimulate appetite and feeding.

Let’s say it’s too much anxiety around food.

Let’s say it’s because of the way that food restriction

was used for reward in the household, right?

I’m making this up,

but you can imagine a hypothetical scenario

where the, let’s just say the mother

of a particular individual

is very vocal about her avoidance of food.

We’ve seen this before, right?

You’ve probably seen somebody who loves to cook

and prepare food, but then sits down

and doesn’t seem to eat.

And they always seem to, in air quotes,

have eaten earlier.

I ate while I cooked.

I ate while I cooked, right?

These people that you never actually see eating.

We all know people like this.

Are they anorexic?

Possibly, we don’t know.

A child observes that kind of behavior.

Maybe that individual is being,

always being told how beautiful they look

or how wonderful or fit they look,

what incredible meals they produce.

And you could imagine a purely psychosocial set of events

that could lead a child to be anorexic.

That doesn’t seem to be the case,

at least not in terms of driving classic anorexia,

of really extreme deprivation of oneself from food.

However, there’s a strong genetic component for anorexia.

So you could imagine a mild form of anorexia in a parent

that is supported or exacerbated by praise

so that the person feels good from the praise

they’re getting, that they want to be a low body weight

for whatever reason, for aesthetic reasons,

or for whatever reasons that happen to appeal to them.

And the child has a genetic predisposition, right?

We never think about genes in terms of controlling behavior.

Genes bias probabilities for behavior, okay?

So you can have a gene for depression or for schizophrenia,

but it’s not deterministic in the same way

that there are genes that determine your eye color

or your skin color or your hair color, okay?

So there’s a genetic predisposition there.

And that genetic predisposition could exist

such that if one is rewarded enough times

for a particular behavior,

that behavior can start to ratchet in

to our neural circuitry,

because behavior drives neural changes,

so-called neuroplasticity.

And you could imagine that that child

could develop a full-blown case of anorexia.

And this is why I raised at the beginning

that no one really knows how to define healthy eating.

And so therefore we have to rely on just identification

of unhealthy behaviors.

But what do we point people to

in terms of what healthy replacement behaviors would be?

So rather than just look at anorexics

and say they’re not eating enough,

and there’s this huge array of terrible things

that they’re doing to their body,

and they need to eat more,

we need to rescue them from themselves.

Let’s look under the hood.

Let’s look at what’s known about the neural circuitry

and the sorts of perceptions and behaviors

that the neural circuitry is driving

in order to understand what they are truly suffering from

at the level of cause, not just symptoms.

It’s clear what they’re suffering from

at the level of symptoms.

Symptoms are how we diagnose.

I listed off a number of those things.

But let’s look under the hood

and try and identify where one could intervene in theory

in order to try and rescue the anorexic

or help the anorexic rescue themselves.

Because it turns out that the answer,

or at least one of the answers of how to do that

is not intuitive at all.

At least to me was very surprising.

I would be remiss if I didn’t start with the obvious,

which is, is there a chemical defect?

Meaning, is there some disruption

in one of the major chemical systems in the brain

that makes anorexics anorexic?

And therefore, can we replace that chemical

or can we reduce some chemical

and essentially eliminate anorexia?

And the answer is not really sort of maybe no.

Here’s why.

There are a lot of different chemicals in the brain and body

but there are a category of chemicals

that are particularly important

that if you’ve listened to this podcast before,

even if you haven’t,

are going to come up again and again and again.

And that is the category of chemicals in the brain and body

called the neuromodulators.

Neuromodulators are different than neurotransmitters

in the sense that neuromodulators modulate

or change the activity of brain areas and neural circuits.

You can think of them as microphones

that are held between particular sets

of connections in the brain

that make those connections in the brain

more likely to be active relative to others, okay?

They make them louder, so to speak.

There are many neuromodulators

but the ones that are important

for sake of today’s discussion are the classic ones.

Dopamine, acetylcholine, norepinephrine, and serotonin.

Let’s focus on serotonin.

Serotonin is a neuromodulator

that tends to increase the activity

of certain neural circuits,

including within the hypothalamus,

but also within the body,

that trigger a sense of satiety of having enough,

enough food, enough warmth, enough social connection,

enough of any motivated goal or drive

or any type of thing or behavior

that one would want more of.

Serotonin tends to make those circuits quiet down.

Now, there are many categories of drugs

that emphasize the serotonergic circuitry,

meaning they cause the release of

or the efficiency of serotonin in the brain and body.

Things like Prozac, Zoloft, Paxil, things of that variety.

Those drugs have been used to some degree of success,

although not much, to treat things like anorexia nervosa.

That should make sense

because if these drugs increase serotonin,

if their general effect is to increase serotonin,

it will be to lower anxiety.

That sounds like a great thing.

A lot of anorexics are really anxious around food.

We’ll talk about why.

Lowering anxiety, you might think,

would lead to ingestion of more food,

but that’s not often what happens.

Increasing serotonin by way of some drug regimen

will tend to make one less hungry.

Because with heightened levels of serotonin

in the blood and brain,

there isn’t the desire to go seek out the things

that will raise serotonin on their own.

Now, some anorexics do well

or benefit from these serotonergic drugs,

these drugs that increase the activity of these circuits

that lead to satiety.

But if you think about the major goal

of treating an anorexic,

it’s to get them to have more hunger, more appetite.

So now I want to focus on some of the work

that’s been done around the habits

and behaviors of anorexics,

because those turned out to be ideal places

for intervention.

The work I’m about to describe

was done by Dr. Joanna Steinglass and colleagues

at Columbia University in New York.

And there are other groups as well.

Of course, they’re doing this type of work,

but they did what I think are really

some beautiful experiments

and some beautiful explorations

of potential treatments for anorexics

that seem to have a quite high degree of effectiveness

when they are applied correctly.

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.

What they found is that anorexics,

rather than being anxious in the presence of food

and that anxiety driving an avoidance of food,

what they found is that anorexics have a hyperacuity,

a hyper awareness of the fat content of foods,

almost to the point of being sort of fat content savants.

Now they don’t necessarily know that they’re doing this.

They’re not looking at an avocado and thinking,

okay, that’s X number of grams of fat rather,

or looking at an apple and saying, okay, that has no fat.

They start to do this more or less reflexively.

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 know caloric numbers,

but then they sort of pass that information

into a memory system in their brain

that allows their interactions with food

to be very reflexive in a way

that they are actively avoiding high fat content foods,

calorie rich foods,

and defaulting towards very low calorie foods

if they have to eat.

Now, this might seem like an almost trivial result

on the face of it.

You think, okay, they don’t like to eat.

When they do eat, they eat low calorie, low fat foods, duh.

But it’s the way in which

they are doing this subconsciously,

that they learn this information

and then they pass it off to a reflexive habit.

And that’s very important

because what that means is that we need to look at

what processes in the brain, what brain areas,

what chemicals drive decision-making and knowledge.

And we also need to look at the areas of the brain

that drive habit formation and habit execution.

Because for any of you that have habits,

and that means all of you,

the hallmark feature of a habit is that it’s reflexive.

You have a mosquito bite on your leg, you scratch it.

You didn’t necessarily even think,

oh, I’m going to scratch that.

In fact, just to take a little bit of a moment of respite

and talk about habits in general,

there’s a beautiful study that was done

out of Caltech University,

looking at the parking lot

of where people park in the morning

without designated parking spots

and the trajectories that they use

to walk to their offices in the morning.

So they put cameras up on the roof of Caltech.

This is the kind of thing that the nerdy kids at Caltech do.

I think at Caltech, if you call someone a nerd,

I think it’s a compliment.

So my apologies to the non-nerds at Caltech.

I think there’s one or two of you.

And for the nerdy ones of you at Caltech, you’re welcome.

They videotaped the behaviors of these faculty

and students and staff.

And what they found is that people follow trajectories

from their car that are remarkably stereotyped.

First of all, they tend to park always in the same spot

if they can.

They tend to get out of their car, of course,

because they’re on the driver’s side

or passenger side in the same place.

They turn and pivot their body

at approximately the same rate every day.

They close the door,

they put their bag on their shoulder or across their chest

or however it is that they carry their briefcase

or whatever it is.

And they follow trajectories onto campus

that are so stereotyped that you’d wonder

if you just trace line after line after line,

what you’d find is that every day

is almost exactly the same.

And you do this too.

You don’t realize it because if you’re being videotaped

doing this kind of behavior,

it’s not being released to you.

But your behaviors are so stereotyped to the point where

if you were to see them laid out in front of you

in kind of diagrammatic format of the lines

and the trajectories that you follow throughout the day,

the lifting of your mug

and how frequently you drink each hour,

you would be amazed and probably a little bit scared

by how much of a robot we all are.

Now that robotic aspect of our neural circuitry is vital

because it’s what allows us to think about other things

and do other things and drive other behaviors.

But the work of Dr. Steinglass and colleagues

showed that in the case of the anorexic,

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 what Dr. Steinglass and colleagues did

is they took anorexics

and they of course had control groups

and they put them in an fMRI scanner,

which are these brain scanners that allow you to evaluate

which brain areas are active during particular tasks.

And because when you’re in one of those scanners,

you’re actually, you know,

I’ve actually been in one of these things,

you’re biting down on a bite bar

and you’re most of the time in most all of these scanners,

you’re immobile.

So you’re looking at things on a TV screen.

Sometimes you can press buttons

to select choices and so forth,

but you can’t really eat within those things.

What they found was that reward-based decision-making,

the drive to pursue a particular food

or the drive to perform a particular task,

which is a lot of what we do throughout our day,

that was controlled by a brain area

called the ventromedial prefrontal cortex.

Let me simplify a little bit of this,

but I’m going to simplify it by giving you a little detail

because it’s the Huberman Lab podcast.

And I believe in mechanism.

Mechanism is the way that you get true understanding

and that you can then be very quick

and give overviews of things, but you need the mechanism.

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 get a particular grade on an exam,

you want to learn something,

you want to complete a workout,

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 and get the items I need

and get home in time?

Okay, DPO, duration path outcome.

It’s a very conscious process.

You tend to take into account different criteria

related to what’s preventing you

from accomplishing what you want to do

and what’s helping you or assisting you.

So of course, as you get to the checkout line

in the grocery store,

you’re going to select the shortest line, for instance.

So that’s all DPO stuff.

It 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.

And if all that sounds like a mouthful, it is,

and it’s very metabolically demanding.

Decision-making is metabolically demanding.

It takes effort, okay?

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,

you get up and you walk.

You don’t have to think about right foot, left foot,

right foot, left foot, you just do it.

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 analyses, okay?

So in this particular study,

they examined brain activity in anorexics

who are selecting different foods.

And as I mentioned earlier,

they have a hyperacuity or awareness

of which foods contain more or less calories

than other foods and what the fat content

of particular foods is in particular, et cetera.

They’re doing all this while in a scanner,

and then they look at what sorts of brain areas are active

after that task is done.

And what they found was really interesting.

What they found was that the dorsolateral prefrontal cortex,

not surprisingly, is involved in the decision-making

and the evaluation of this food,

which foods are going to be best to eat in this context,

which foods are going to be appropriate

for at least that anorexics framework

about what’s okay to eat and what’s not okay to eat

and how much.

However, there are areas of the brain that were active

after that decision-making process.

And those are the brain areas that turn out

to drive the habit of avoiding particular foods

and approaching other foods.

And in that case,

it wasn’t the dorsolateral prefrontal cortex.

It was an area of the brain

called the dorsolateral striatum.

Now, the striatum is a big area in the brain.

It’s involved in a lot of different things.

It includes areas like the caudate and putanum.

And I just want to mention,

as I throw out all these names,

you do not need to remember the names

of these different structures.

They’re just there if you are interested

in that level of detail.

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.

If you remember way back at the beginning of the episode,

I feel like that was a long time ago now,

when we talked about how you have

these sorts of processes in the brain,

but 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.

Now the dorsolateral striatum is a structure

that we should think about in a little bit more depth.

It’s part of a set of circuits that are involved

in what are called go-no-go tasks.

And I don’t want to go into this

in a lot of detail right now

because it would take us too far down the rabbit hole

of neural circuitry.

But basically in terms of behaviors,

we both have DPO type behaviors,

so decision-making reward-based behaviors,

and we have habits that we learn and we acquire

and then we just start to execute reflexively.

Things like walking, things like yawning when we’re tired,

things like taking a particular route

through the parking lot, right?

We learn that the first time we go to a given parking lot

and walk into a building,

but after that we tend to follow the exact same trajectory.

It becomes very automatized.

It’s just like we just do it without thinking.

Well, the go-no-go circuitry

is another aspect of our behavior

where we both have to select behaviors to perform

and we have to select behaviors to suppress.

And the anorexic brain seems to reward suppression

of one set of behaviors, ingestion of high calorie foods,

and to reward focus or even hyper-focus

and consumption of low-fat, low-calorie foods.

So this homeostatic process that we learn about

from like high school onward,

that, oh, everything in your body is designed

to keep everything in balance.

You stay awake for a certain amount of time,

you want to sleep.

You don’t eat for a while,

then you want to eat to maintain weight, right?

You eat too much, then you want to eat less.

Those systems are disrupted.

And so what’s so beautiful about this work

from the Columbia group is that what it says is

the place to intervene has to be the habit.

This stuff has already passed through all the learning.

It’s passed through all the reward systems.

It’s clearly not being overrun

by the homeostatic processes of the body.

There’s very little body fat.

There’s no leptin.

Whatever neurons in the brain respond to leptin

are starved for leptin.

Periods have shut down.

Sperm production and testosterone is lowered.

Bone density is down.

Clearly, this is overriding all those homeostatic processes,

all the signals that would say, eat, eat, eat.

Those don’t matter in the brain of the anorexic.

The brain of the anorexic is just performing habits

and they’re being rewarded for it.

So when you come along and say,

look, you should really eat this whole pie

or this whole pizza, you’ll feel better.

That’s actually aversive to them.

So since it appears to be a habit,

a reflex that’s perpetuating the anorexic phenotype,

as we say in science,

it’s perpetuating anorexia in this individual

and telling them about all this terrible stuff

that’s happening in their body won’t work.

Taking them away from all the images

of thin people online, et cetera, that’s not going to work.

What’s going to work?

What’s going to work is intervening in the neural circuitry

that’s related to the habit itself.

And it turns out that there are ways to do that.

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.

This is a little bit similar to the way

that somebody who suffers from addiction

starts to put in different constraint type behaviors.

Constraint type behaviors are the sorts of things

like where the alcoholic will call a hotel ahead of time

and say, listen, I want the minibar taken out of the room.

I don’t want a television in the room, et cetera.

Constraint type behaviors.

Those are really ways of keeping oneself

from the temptation.

But with these habits,

they work at such a subconscious level

that what seems to work best is a combination

of teaching the individual about their internal state

and how to register their internal state.

What we call interoception,

this ability to perceive your internal state

so that they can start to learn to associate

the interactions with different types of food

with the sorts of cues that are occurring within their body,

quickening of heart rate, hyperacuity of focus

that we talked about earlier.

Once they start to be able to notice

that those things are happening,

then they can start to intervene.

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.

And I should highlight that this isn’t just about

rewiring habits for sake of the anorexic.

These are also the same types of mechanisms

that one would want to incorporate

in order to rewire any habit of any kind.

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 hyperacuity and focus on details

within a given environment.

And there’s actually an interesting probe test for anorexia

that involves something akin to kind of a

where’s Waldo type puzzle,

where an image is put up.

The one that I saw was one in which

there’s a big array of coffee beans.

Actually, they’re all brown coffee beans.

And your job is to identify where in that array

of coffee beans there’s a face.

And indeed there’s a face embedded in there.

It looks a little bit like a coffee bean,

but once you see it, you realize it’s a face,

not a coffee bean.

And it becomes very hard to not notice the face after that.

Anorexics are very good at identifying the face.

They find it much faster than do non-anorexics,

which is really interesting, right?

They somehow are able to home in on details

and find those details and fixate on those details.

Now, eventually most, if not all people find the face,

but once you do what you will find

and what everyone finds is that you can’t unfind the face.

It just jumps out.

So what essentially you’ve lost is the ability

to see the whole picture,

because there’s some detail within that picture

that you’re obsessed by.

So this has kind of elements

of obsessive compulsive disorder,

but it’s not really obsessive compulsive disorder per se.

So we call that weak central coherence.

It’s a hyperacuity on one particular feature.

You miss the big picture.

The other is a challenge in set shifting

that once you identify something

that’s a 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,

you might be familiar with this.

It’s kind of uncomfortable to be around actually.

They go through a lot of elaborate procedures

to kind of hide food,

to they’ll sometimes even chew food,

hold it in their mouth,

and then go to the bathroom and discard it.

Things very elaborate,

very troubling types of things to hear about

and to be around,

but you’ll notice that they push food

around their plate a lot.

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.

And they can’t seem to set shift.

They can’t just relax and enjoy the meal

because the meal for them is essentially

like this where’s Waldo

or find the face in the coffee bean task.

They’re constantly monitoring

how much people are observing them

and trying to navigate this,

what would otherwise be a really pleasant circumstance

for most people.

They’re trying to navigate through this

because remember for them,

the reward is in the avoidance of certain things

and the acquiring of only the foods

that their brain rewards them for

because those are the foods

that have been pre-selected in our now habit.

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 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 cuing 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.

Now for people that live alone,

this isn’t available to them.

This isn’t the kind of thing

that you share with your coworkers.

You might involve a close friend or a spouse

but it’s not the sort of thing

that people that don’t live in a family context

can really benefit from.

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.

I think that there’s this idea out there

that it’s either or when often it’s both.

So cognitive behavioral therapies are often combined

with this habit recognition and rewiring approach

which is starting to become more and more common.

And I think the data on it look really good

that especially when individuals are taught this early

in adolescence that there are positive outcomes over time.

The relapse rate of anorexia is quite high.

It’s about 50% of individuals will relapse at some point

often triggered by a stressful life circumstance.

But the combination of cognitive behavioral therapy

that includes this family model

or at least habit reformation seems to be fairly effective.

And at present might be the most effective treatment.

Now there are additional treatments starting to surface

and that takes us into the realm of chemical treatments

for anorexia.

And I just want to mention that there are clinical trials

meaning legal clinical trials being done

at Johns Hopkins School of Medicine

by Matthew Johnson and others,

exploring how drugs like MDMA,

which increases dopamine and serotonin to very high levels

or psilocybin, so-called magic mushrooms

which increases serotonin and other compounds

to very high levels within the confines

of a professionally supported therapeutic environment

can help people rewire their brain

such that they can get relief from major depression

and various forms of trauma.

And now eating disorders are also being explored

in the context of MDMA and psilocybin clinical trials.

I do want to emphasize that those are clinical trials

that those compounds are not yet legal.

And in many cases, most cases they are still illegal.

I do not think that they should be explored

without a properly trained medical doctor

that the clinical trials are essential to complete

before one explores those compounds in particular

because lately I get a lot of emails about these compounds,

people telling me that they’ve had amazing experiences

and relief from various things, not just eating disorders

but depression, et cetera.

However, I get an equal number of emails

from people saying that they worked

with some self-appointed guide.

This would be outside the clinical trials

I was referring to.

And they are now experiencing chronic visual snow.

They’re getting genuine visual field deficits.

They are having ticks that they never had before.

They have chronic insomnia.

So I’m not passing judgment on any of these compounds

or the people that are doing this sort of thing.

I just want to see the clinical data.

And I do believe that we should wait

until these clinical trials are done

before people start approaching this stuff.

And that’s because they are serious compounds.

They can open plasticity, but whether or not they work

quote unquote for different types of eating disorders

or depression and trauma, the data are looking promising

but that the clinical trials are still not done.

And I know a number of people are going out of the U.S.

and into other countries where this stuff

is being done more regularly.

And there too, I’ve gotten reports back

of people doing so-called ibogaine treatments.

Some of you who are familiar with eating disorders

will immediately be asking, well, what about ibogaine?

Does it work?

Does it work?

Well, the clinical trials in this country are not complete.

I’ve heard evidence direct.

I’ve heard directly from people who have benefited

from the sorts of things for treatment of eating disorders.

But I’ve also heard of people that have developed

chronic seizure disorders from pursuing things

like ibogaine for the treatment of eating disorders.

So again, I’m not passing judgment.

I would just like to see more data.

And it’s very important that the safety,

aspects of safety be in place.

So this is definitely not something to get renegade about.

So it appears that once anorexia is established

that habit breaking through self-awareness

of what the habits are is going to be a primary entry point.

That might seem kind of trivial.

You might say, well, couldn’t you have just told us

that in one sentence?

But I want to return us to this model

about homeostatic processes, reward processes, et cetera.

That leads us to a place where the short answer is no.

You can’t simply say break the habit.

An individual needs to be informed

about where that habit comes from.

And the fact that what currently seems like

a rewarded habit should actually be a punished habit.

Now I don’t mean by actual punishment,

but what I mean is within the brain,

there’s been a switch and the anorexic

needs to learn that there’s been a switch

such that what should be rewarding is now punished.

And what should be punished, starvation is now rewarded.

The beauty of being a human being

is that knowledge of knowledge

can allow you to make better decisions.

I’ll say that again.

The beauty of being a human being

is that knowledge of knowledge

can allow you to make better decisions.

Now, of course, when we are anxious, when we are tired,

when we are intoxicated,

we have less access to that ability

to use knowledge of knowledge to intervene.

The anorexic will often do things

that are in keeping with their habits,

such as over-exercising.

This is a area that anyone who’s treated anorexics

or interacted with anorexics is well aware of

that they are constantly moving.

They’re constantly on the treadmill.

They’re constantly running.

They always want to be moving and burning calories

so that they can feel okay about interacting with food

or because they have the distorted body image.

Well, does breaking a habit mean

that they should stop moving around and exercising?

No, not necessarily.

There’s some really interesting studies

that show that shifting anorexics towards activities

that, for instance, build muscle resistance training

and allow them to eat a bit more food

without necessarily losing weight,

but rather to put more muscle on their body

can actually be beneficial.

Now, I’m not talking about anorexics becoming bodybuilders.

There’s a whole body dysmorphia

associated with bodybuilding,

but certain forms of exercise are just catabolic,

meaning they break down the amount of muscle.

They reduce body weight overall.

Other types of exercises like resistance training

are anabolic.

They allow muscle to be put on.

And there are some interesting studies,

not a lot, but some interesting studies

trying to encourage anorexics not to stop exercising,

but rather to stop exercising in this neurotic,

catabolic way of breaking oneself down,

but rather getting them shifted toward breaking habits

of only approaching low-calorie, low-fat foods,

while also encouraging them to embark on resistance training

and to start to learn and reward the relationship

between exercise for sake of making one’s body strong,

including the bones, not just the muscles,

but the bones, which is important, especially in anorexics,

and then to see food as a way to nourish that process

to building a body that could be of the stable weight.

Hopefully, once the anorexic is of a healthy weight

that they’re maintaining that weight,

but that they don’t have to constantly be on this treadmill,

no pun intended,

of balancing whatever food intake they have with activity.

And along the lines of that,

during the episode on fat loss and metabolism as well,

I talked about this neat

and non-exercise-induced thermogenesis,

where people who tend to be thin,

tend to bounce around a lot, they’re kind of fidgety,

and that burns thousands of calories a day,

anywhere from 800 to 2,000 calories a day.

Now, that can be beneficial for the folks

that are overweight and have a healthy mindset about food,

but are trying to lose weight,

and it turns out that by literally fidgeting

and bouncing around, like, this is why I’m doing this,

it looks ridiculous,

you actually burn a lot of body fat and calories

that way, provided you’re in a caloric deficit,

you’ll burn body fat,

because body fat is not just a passive tissue,

it actually receives input from neurons

that release noradrenaline and adrenaline,

and this neat has been described for several decades now,

and it actually is a pretty terrific way

to burn off more calories.

So with the anorexic, you actually want to encourage them

to not constantly be trying to burn off calories.

That can be very challenging,

so shifting them toward activities,

like weight-bearing activities or resistance training,

that promote this more anabolic type of relationship

to activity, as opposed to catabolic, can be beneficial.

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.

They’ll think, oh, you know,

their arms are a little bit fat, you know,

or, you know, the contour of their face makes,

they don’t like the pictures of themselves,

or they, what I’m describing here

is actually pretty typical behavior of a lot of people.

I mean, how many people do you know

that after you take a picture of them,

they say, can I see the picture?

And then they tell you that you have to throw it away.

That doesn’t necessarily mean they’re anorexic

or they’re suffering from some sort of disorder.

That just means that they’re a human being

that cares about how they appear in the world.

We’re not here to judge that.

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 Balenson’s lab at Stanford.

He’s in the department of communications.

He’s actually collaborated with a Dr. Halpern

that I mentioned earlier.

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.

And that’s a relief, at least I find that reassuring

because changing one’s perception is actually very hard.

As somebody who’s worked almost his entire career

on visual perception and related things,

the perceptual apparati of the brain

are not very amenable to neuroplasticity.

I mean, they don’t change that easily.

Whereas it appears that the circuitry

that’s related to habit formation and decision-making

and the reward circuitry, that stuff can be rewired.

And so anorexics, as they progress out

of their anorexic state into one

which they are intervening in their reflexes,

gaining better habits around food,

eating more, more accurately assessing foods

and environments that they’re in related to food.

As they change their behavior

and they start to put on healthy weight,

maybe they’re also doing the sorts of exercises

that allow them to put on healthy weight

and avoiding kind of extreme exercises of catabolism

and breaking themselves down.

They also managed to somehow,

just as a consequence of all that,

rewire their perception of self.

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,

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,

typically by self-induced vomiting

or by ingestion of laxatives,

sometimes also in concert with people taking stimulants

and fat burners and over-ingestion of stimulants

to try and burn off more energy.

And then we’ll also talk about binge eating disorder,

which has a lot of the same features as bulimia,

but typically no purging.

I’m not going to list off all the clinical criteria

that would allow someone to be diagnosed

as bulimic or binge eating disorder,

but the general features are that they ingest

far more calories than they need,

anywhere from 10 to 30 times their daily caloric intake,

oftentimes within a two-hour period,

which is just a staggering amount of food and nutrients

in a short period of time.

Oftentimes they’re overriding those mechanical signals

from the body that they’re full.

It’s a really troubling thing to think about,

but people are literally gorging themselves with food.

This looks a lot like a laboratory animal

that has these AGRP neurons stimulated,

these neurons that will eat until they almost burst

or burst.

So you wonder, is it these AGRP neurons that are active?

Almost certainly, yes, that they’re involved.

Although I don’t think that that’s going to be

the major point of intervention.

Pat, we’re going to talk about other types of interventions.

There are a number of clinical criteria.

For instance, if somebody has one of these binges

once a year, does that make them bulimic?

Technically, no,

but I certainly don’t recommend people do this.

If you are one of these people

who has so-called cheat days, right?

Some of you may be familiar with cheat days.

I think they’re a little less common now,

but the idea is you eat clean for six days

or five days a week or two weeks,

and then you have a so-called cheat day

where you just kind of go wild

and eat whatever you want in whatever volumes.

Is that bulimia?

Has some of the contour of bulimia,

if you’re vomiting afterwards or binge eating disorder,

if you’re not.

Does it constitute full-blown bulimia

or binge eating disorder?

I mean, it’s pretty hard to say.

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.

And I certainly know people who do these cheat days.

And by those criteria,

they have something like binge eating disorder.

But in general, one of the hallmark features

of bulimia and binge eating disorder

is that people are unable to control their eating.

They’re just simply,

they’re not making the decision to have a cheat day.

They’re not making the decision to overeat.

They are simply driven from the inside

without question by way of neural circuitry.

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 nerds call hyperphagic.

They’re just eating like crazy.

So what’s going on there?

Well, there’ve been a lot of ideas,

you know, about why this arises.

There’s the so-called thyroid hormone hypothesis.

That one’s a tricky one.

It turns out that cortisol

and thyroid hormone concentrations vary

according to when the binge purge happened.

So there were some studies

that looked at thyroid hormone levels

and they found elevated thyroid hormone levels.

Thyroid hormone is involved in metabolism

and not just the burning of energy,

but the use of energy

in converting it to different tissues of the body,

cartilage, bone, fat, and muscle, et cetera.

Did a whole episode on thyroid and growth hormone,

by the way, if you’re interested

in learning more about thyroid hormone.

But thyroid hormone can also be depleted

at other phases of the binge purge cycle.

Now, without listing off all the terrible things

that happen with this binge purge cycle,

there are a number of things

that are really worth pointing out.

One is that the vomiting itself,

the use of laxatives,

that can cause severe disruption to the mucosal lining,

the mucus lining of the digestive tract

can severely disrupt the gut microbiome.

It can cause all sorts of,

even ulceration of the esophagus

and just really terrible stuff.

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.

There’s some social isolation.

So you recall from the beginning,

it does not appear that sexual trauma

is a prerequisite for bulimia,

although sometimes it can occur.

The hallmark feature of bulimia

that distinguishes it from anorexia,

aside from the fact that it’s overeating

as opposed to undereating,

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.

They might have a little bit of alcohol

and then start to eat like crazy,

whereas normally they’re very restrictive.

That’s a common feature of bulimia.

Sometimes they over-ingest alcohol during these binges.

Sometimes they are sexually promiscuous, not always,

but it’s a general issue with satiety

once they start eating and with impulse control generally.

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,

a topic that we’re going to talk about in depth

here on the podcast soon,

some of those same drugs like Adderall,

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.

You probably know more about prefrontal cortex

than you ever wanted to.

Just from this episode,

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 and is under conditions

where they think, oh, you know,

I shouldn’t eat anything, I shouldn’t eat anything.

And then they just tear the refrigerator open

and plow through that.

And then at that point,

they’re plowing through the cupboards

and then they’re ordering food.

And then they’re feeling horrible about themselves.

There do tend to be these cycles of binge and purge

followed by feelings of real shame

because they just can’t control their behavior.

And what is more embarrassing

than not being able to control one’s behavior

as an adult or as a young adult?

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.

Why do we call it top-down?

Because the prefrontal cortex is suppressing the activity

of deeper limbic and hypothalamic circuitry

and things of that sort.

Anytime you feel like you want to say something

really offensive and you don’t, that’s top-down control.

That’s your prefrontal cortex.

Anytime someone says something and you grit your teeth

because you know you shouldn’t say anything,

gritting your teeth is top-down control, okay?

When you explode or burst or say the wrong thing

or say the thing that you shouldn’t say

or do the thing you shouldn’t do,

that’s lack of prefrontal control.

And indeed people who have frontotemporal dementia

due to aging or head injuries see this a lot

and people who play sports,

they get a lot of frontal damage.

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 adrenaline, also called epinephrine,

will increase the tone, as we call it,

the dopaminergic tone or the, it’s called adrenergic,

but 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.

They tend to create a hyper-focus.

They tend to push the brain into,

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.

And for that reason, drugs like Welbutrin, bupreiron,

which is an antidepressant,

which mainly increases the amount of dopamine

and norepinephrine and less so serotonin,

that can also be effective

for certain types of binge eating disorder,

is actually used to treat smoking,

for promoting smoking cessation and for depression,

but also for certain forms of obesity

related to binge eating disorder.

And the data are pretty good.

And there are timed release forms of this

and non-timed release forms.

And I think you have to consult with a psychiatrist

in order to get these prescribed

because they are prescription drugs,

but it’s a very different constellation of neurochemicals

and brain areas and approaches for bulimia.

The treatment of binge eating disorder

has been explored from a new standpoint recently.

And that’s the work of this now, sadly,

former colleague of mine, Dr. Casey Halpern,

who’s at University of Pennsylvania

that I mentioned earlier.

They are using deep brain stimulation

in order to treat binge eating disorder.

Now, why deep brain stimulation?

Well, work from Dr. Halpern and others while at Stanford

showed that there are particular patterns of brain activity

in both the prefrontal cortex,

but also in an area of the brain

called the nucleus accumbens,

very important and very relevant area of the brain

in this context.

And in any discussion about motivated behaviors

of any kind, feeding, sex, drug-related behavior,

people who exercise compulsively,

the nucleus accumbens is in a ongoing dialogue

with the prefrontal cortex.

And the nucleus accumbens has no mind of its own,

but it’s associated with dopamine release.

It’s part of this so-called reward pathway.

And what Dr. Halpern and colleagues discovered

is that there are particular patterns of activity

that ripple through the brain

through these prefrontal networks

and through this nucleus accumbens area.

Those areas are connected.

It’s called delta oscillations,

delta just being a particular frequency

of electrical activity.

For you aficionados is one to four Hertz activity.

But in any case, those delta oscillations

in the nucleus accumbens are associated with food reward

in both mice and humans.

Somehow this reverberatory activity

creates a perception in the individual

that food is hyper rewarding.

Now that’s interesting and has allowed them

to use a targeted deep brain stimulation approach

to treat binge eating disorder.

And this deep brain stimulation

is appearing to be an effective treatment.

There’s still more studies that need to be done.

Actually, if you think you have binge eating disorder,

you can find the criteria for that.

And you could contact Dr. Halpern.

He’s, as I mentioned,

he’s moving to University of Pennsylvania.

They are recruiting patients for these studies all the time.

The studies are fairly invasive.

They involve a FDA approved approach

of literally placing a wire down into an area of the brain

that then allows the individual

to stimulate a particular brain area

to offset some of these activity patterns

that lead to a elevated sense of reward

from food and binge eating.

And the data look really promising.

Now I realize that’s a very invasive approach.

Not everybody is going to be willing

to have this wire inserted into the brain.

But for people that suffer from binge eating disorder,

this is a great and very exciting potential treatment.

Because what I didn’t tell you

is that many people who have binge eating disorder

are obese to the point where their health

is greatly at risk.

Now, obesity causes all sorts of shifts

in the dialogue between the brain and body.

Some of which you’ll recognize

from earlier in the discussion.

For instance, leptin signaling is disrupted.

So the fat, there’s lots of body fat,

but even though that body fat

is secreting this hormone leptin

and that signal should shut down the desire to eat,

the receptors to leptin in the brain are totally screwed up.

And so the signal to eat is there,

but the signal to stop eating is not there.

So again, you have an accelerator and a brake

and it’s like the accelerator is always pushed down.

Some of these brain stimulation approaches

seem to be able to bypass some of that.

And of course there are all the metabolic syndromes

and the problems with having excess levels of body fat,

things like insulin resistance, type two diabetes.

I mean, as disturbing as is to hear,

there are many individuals, actually,

I know some who are so obese

that they start getting bodily sores.

They’re not just bed sores,

but they have skin sores that are very disruptive to them.

They don’t like having these sores.

And in addition to that,

they can get peripheral neuropathies

because of some of these metabolic issues,

they’re not getting enough utilization

of the nutrients in the tissue

because the way that insulin is disrupted,

insulin signaling,

and they actually have to have certain portions

of their limbs amputated,

and yet they continue to overeat.

So this is not an issue of self-control

that can easily be dealt with simply by telling the person,

look, you have to stop eating or you’re going to die,

or you’re going to have your legs amputated.

Like with anorexia,

there’s a distortion in the relationship to food,

but the homeostatic and the reward aspects are disrupted.

So unlike anorexia,

where it seems to be a habit-based mechanism

with bulimia and binge eating disorder,

something deep within the neural circuitry

is causing food to be hyper-attractive and the brake is off.

So if you want to develop some empathy

for what these people are dealing with, consider this.

It’s like driving a car.

You get onto a grade,

maybe a 10 or 15 degree grade,

and you’re heading down and you figure,

well, you’ll just pump the brakes a little bit,

but there is no brake, right?

So you start going faster and faster and faster,

and your only choice is to use the accelerator

or just to coast through it.

That’s essentially what’s happening to these neural circuits.

So the work of Dr. Halpern and others,

I think is really exciting.

And even though it’s highly invasive,

I think it’s going to lead to not just some relief

for the patients that do get that deep brain stimulation,

but also the identification

of what sorts of receptors are present

in those brain areas that could help.

What that means is that once we understand

which brain areas are involved in the disorder

and we understand what receptors those brain areas express,

then there can start to be additional interventions

by way of non-invasive treatments,

things like drug treatments.

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.

I mentioned some of them before,

things like propriron, welbutrin,

some of the serotonergic drugs

and some of the drugs used to treat impulsivity.

So 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.

So really kind of troubling thing to think about.

On either case,

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.

What more could be disturbing?

Well, 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 in this month 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.

You have the Maudley approach.

You’ve got all these different approaches

to depression and to anorexia, et cetera.

What I’ve tried to do is give you a framework.

And in doing that,

I’ve tried to give you a framework of understanding

that also applies to this question

that’s I think equally important

and goes alongside the treatment of eating disorders

is what in the world is healthy eating?

What in the world is a healthy relationship to food?

I like to think that I have a healthy relationship to food.

I know the foods I like, I enjoy them.

There are 10 or 15 foods in particular

that I like very much.

I’ve mentioned a few of them on the podcast before

and was sort of amused, surprised,

and perplexed as to why, for instance,

I do enjoy eating butter, not in huge amounts,

but I do like butter.

So that seemed to be pretty triggering for folks out there.

A small selection of people decided

that the ingestion of butter was a health concern.

Look, to me, ingesting butter in small quantities

is something that I’m comfortable with

and my blood lipid profiles feel good.

They look good to me.

For other people, that might not be the case.

For some people, the idea of eating an animal-based food

is probably so repulsive

that it actually can make them feel physically sick.

And I think that we should be aware

that that kind of mental phenotype exists.

I’m not calling it a pathology.

For other people like myself,

things like butter and meat feel healthy.

Now, what quantities?

Well, I enjoy eating very much.

I’m not shy about this.

I’ve talked about it on the podcast before.

I enjoy eating.

Some people have a very complicated relationship to food.

They don’t think of it as nourishment.

They don’t enjoy it socially.

It’s a stressful thing for them

based on their personal history

or maybe just general anxiety around food.

And I hope that in sharing this information

about the fact that anytime we approach food,

these neurons in the arcuate area of our hypothalamus

actually increase our levels of anxiety.

This is related to that point that Dr. Halpern made,

which was that from an evolutionary standpoint,

it is advantageous to ingest as much food

as often as possible, as quickly as possible.

We now know that to not be healthy

in this age of abundance

where calories are essentially everywhere.

And yet a lot of people feel anxious

in anticipation of a meal.

What could be useful to them?

Well, whether or not they have an eating disorder or not,

it’s very clear that developing methods to calm oneself

in the presence of any anxiety or fear-inducing stimulus

can be beneficial.

I’ve talked about some of these

in episodes related to stress,

things like the physiological side,

two inhales through the nose and a long exhale.

Things like mindfulness meditation certainly can help.

There are data, a lot of studies out there

showing that meditation practice can help people

deal with eating-related anxiety and disorders.

I think as a general rule,

trying to avoid approaching a meal

or sitting down to eat in an anxious state

is probably a good idea, but let’s be realistic.

How often can we do that?

I think most of us are going to have circumstances

where we’re rushing around

trying to just eat before we head out or get to a meal,

and then we sit down and we find ourselves eating.

This is one of the first times in human evolution

where we mostly eat out of a desire to consume food,

not out of a need for food.

Most everybody could go a fairly long period of time

just ingesting water and electrolytes,

and not that I’m suggesting people do that,

but let’s face it.

We largely eat nowadays because of a desire to eat,

not a need to eat,

and yet we need to eat on a fairly regular basis.

And so no topic is more complicated and nuanced

than food and nutrition,

and in particular as it relates to eating disorders.

So 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?

For those of you that intermittent fast,

this also applies, right?

What, you know, God forbid,

if you eat 30 minutes before your eating window starts,

what does that mean?

If it means something catastrophic,

do you have an eating disorder?

I don’t know, maybe you have an anxiety disorder.

That’s for you to explore.

If you don’t manage to eat five meals a day

and that’s your obsession,

well then, you know, the same thing applies.

These are questions that we can all ask ourselves.

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 know that that sounds like a ridiculous number,

but you can look this up.

This is particularly true in certain countries.

Why that is, we don’t know.

But again, this is not a new phenomenon.

This is not just related to body image issues

that are created through social media and media.

And as a final point on that,

many of you are probably asking,

what about plastic surgery?

What about all the steps that people are going through,

excuse me, to preen themselves and change themselves?

Are people addicted to plastic surgery?

Is that a form of body dysmorphia?

And indeed it is.

And so we will do an episode on exercise related

and plastic surgery related body dysmorphia.

I think there is very little question

that those types of disorders are clearly related

to what we’re observing in social media and in media,

that this shift of, for instance, action heroes,

if you look at action heroes in the 80s,

there were very few men that were very large.

You had your Terminator,

you had your Stallones and your Schwarzeneggers

and a few others,

but the men in movies tended to be, if they were muscular,

they were far more svelte than they are now.

There’s this kind of,

there’s literally a hypertrophy of the imagery.

And likewise, there’s been hypertrophy

of the female body shape as it’s portrayed in the media.

There are body dysmorphia that are related

to those types of things

and that relate to things like plastic surgery,

steroid abuse, diet drug abuse, and so on.

Definitely important to think about and consider

and definitely deserving of its own episode.

You’ve learned a lot of neuroscience today.

I hope that was useful in thinking about these disorders

and in thinking about other aspects of feeding

and motivated behaviors.

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 or 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.

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