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.

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

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This month on the Huberman Lab Podcast,

we’re talking all about hormones,

these incredible chemicals that can impact our mood,

our behavior, our feelings of optimism or pessimism.

The amazing thing about hormones

is that hormones impact all those things,

but all those things,

how we feel and what we do and what we think

also can impact our hormones.

And so it’s a really fascinating area of biology

that impacts every single one of us every day,

both in wakefulness and in sleep

and throughout the lifespan.

Today, we’re going to be talking about hormone optimization,

and we’re mainly going to be focusing

on estrogen and testosterone and their derivatives.

Last episode of the Huberman Lab Podcast,

we talked about sexual development.

That is how the chromosomes, the gonads and hormones

impact what we call sexual development,

leading all the way up to puberty.

Today, we’re mainly going to talk about processes

that happen from puberty onward,

although we might talk a little bit

about development as well.

So today we’re going to talk a lot about basic biology,

but we’re going to weave in a lot of practical tools

along the way for how to optimize

these incredibly powerful things that we call hormones.

Before we dive into our discussion

about hormone optimization,

I want to raise what I think is a very important point

that at least I hadn’t heard of until recently,

which is the concept of salutogenesis.

Many of us are familiar with the concept of pathogenesis,

the idea that there are all these scary diseases

like dementia and heart disease and stroke

and all these things that await us

if we don’t take good care of ourselves

and that might await us even if we do.

That’s the pathogenic model.

Salutogenesis is something I learned about

from one of my Stanford Medicine colleagues,

which is a different orientation

toward health and well-being

where you’re taking on particular behaviors,

you’re taking on a particular stance

towards nutrition and exercise, supplementation, et cetera,

in order to promote well-being

above where you would be

if you were not doing those behaviors.

Now, if you think about these two things,

salutogenesis and the pathogenic model

are really two sides of the same coin,

but I’ll just give an example

of how this might affect you in a real way.

If you like exercise because it feels good, great,

but many people exercise or eat well for that matter

in order to avoid heart disease or to avoid dementia,

to avoid negative changes in body composition.

And while that’s powerful and certainly is the case

that exercise will help you move away from all those things,

the salutogenesis model differs in that

it involves a mindset and an orientation

towards doing those things in order to feel good,

in order to enhance your level of energy,

in order to improve endocrine function

and metabolic function.

So it’s really part of the pathogenic model,

and yet salutogenesis is really more of a mindset

toward why you would do these particular behaviors.

And really the most powerful mindset

is going to be one where you are thinking

about the pathogenic model,

doing things so that you don’t end up sick, et cetera,

and to move away from sickness,

as well as the salutogenic model

where you’re doing things

in order to move towards health and well-being.

We think of health and wellness nowadays

or the wellness community or wellness practices.

And in many ways,

that is the essence of the salutogenic model.

But I found it very interesting to know

that within the field of allopathic medicine,

these two models exist,

but we don’t hear about the salutogenic model

quite as often.

So it’s just something to keep in mind,

especially because of some of the mindset effects

that were discussed in previous episodes.

I’m not going to go into these in detail again right now,

but if you might recall from the episode on food and mood,

we talked about some of these incredible studies

that were done by Aaliyah Crum’s group at Stanford

and others,

showing that if you tell people

that the behavior that they’re about to do,

in this case, it was people cleaning up hotel rooms

because that was their job.

If you tell them that it’s good for them,

then you see much greater positive health effects

than if they aren’t aware of that information,

that it’s good for them.

So we should really be thinking about

not just moving away from disease and negative things,

but also why certain things are good for us

because it’s well-established now

from really good scientific studies

that keeping in mind the positive effects of things

can really have an outsized effect on wellbeing

right down to the level of our physiology.

So let’s talk about hormone optimization.

Today, we’re going to talk about hormone optimization

in reference to estrogen and testosterone

and their derivatives.

Now, estrogen and testosterone and their derivatives

are what we call sex steroids.

Now, the sex steroids immediately call to mind sex

for obvious reasons and steroids,

meaning anabolic steroids.

But I just want to emphasize that estrogen and testosterone

are present in everybody.

It’s their ratios that determine their effects.

So today we’re going to talk about

how you can optimize the ratios

depending on your particular life goals

because the ratio of estrogen and testosterone

in every individual has profound influence

on feelings of wellbeing, feelings of optimism,

feelings of anxiety or lack of anxiety,

on reproduction, on sexual behavior,

independent of reproduction.

They are profoundly powerful molecules

and we all make these molecules to some degree or another,

but there are also important behavioral tools,

supplementation tools, as well as prescription drugs

that can impact the ratios of testosterone and estrogen

in really powerful ways.

So we’re going to cover all of that.

I want to emphasize that when you hear sex steroids

or steroid hormones,

most people think about anabolic steroids.

And of course, anabolic steroids

are derivatives of testosterone or testosterone itself.

And they are heavily used and abused in the sports community

as well as outside the sports community.

But there of course are many steroids

that are not anabolic steroids

that are also abused in sports.

Today, we’re not talking about drugs in sports,

but I think that it carries such a heavy weight

when people hear the word steroids,

they think about anabolic steroids.

So while today’s discussion will certainly be relevant

to physical performance,

in fact, we’re going to talk about

how specific types of exercise,

particular patterns of cold exposure,

as well as particular patterns, believe it or not,

of breathing can impact sex steroid hormones,

both estrogen and testosterone.

The discussion isn’t really geared

towards performance enhancement in sport,

although we will do an entire episode,

perhaps even an entire month

related to performance enhancement in physical enterprises.

So one of the first things to understand

if you want to optimize your hormones

is where they come from.

There are a lot of different glands in the body

that produce hormones.

There’s the pineal gland.

Some hormones are made in the hypothalamus.

Hormones are made by the gonads,

the ovaries or the testes.

You’ve got the thyroid gland.

There are a bunch of different glands

that make these different hormones.

But when we’re talking about the sex steroid hormones,

estrogen and testosterone,

the major sources are ovaries for estrogen

and the testes for testosterone,

although the adrenals can also make testosterone.

Now, there are also some enzymes.

Enzymes are things that can change chemical composition.

And the enzymes that we’re going to talk about today

are the aromatases mainly.

The aromatases convert testosterone into estrogen.

So in a male, for instance,

that has very high testosterone,

some of that is going to be converted into estrogen

by aromatase.

And aromatase is made by body fat.

It’s also made in the testes themselves.

A lot of people don’t realize this,

but the testes actually have the capacity

to manufacture estrogen and aromatase,

albeit at low levels.

But this turns out to be important

for optimizing hormone levels in males at later points.

And we’ll discuss that.

It’s important to note that there’s a huge range

in terms of the levels of hormones,

testosterone, and estrogen between individuals.

And it actually occurs within individuals

across the lifespan.

I’m not going to throw out specific numbers

of X picograms per deciliter, et cetera, today,

because that’s going to vary a lot.

It’s going to depend on whether or not you’re measuring

in picograms or nanograms and that sort of thing.

If you want to examine your hormones,

you should do that in conjunction with a medical doctor.

Ideally, an endocrinologist can help you

sort out that information.

But the important thing to know

is that prepubescent females

make very little estrogen.

And when we talk about estrogen,

we mainly talk about estradiol,

which is the most active form of estrogen

in both males and females.

So prepubescent females, very low levels of estrogen.

During puberty, levels of estrogen, aka estradiol,

basically skyrocket.

And then across the lifespan,

estrogen is going to vary

depending on the stage of the menstrual cycle.

But as one heads into menopause,

which typically takes place nowadays

somewhere between age 45 and 60,

levels of estrogen are going to drop

and then post-menopause levels of estrogen are very low.

As well, testosterone will fluctuate across the lifespan.

Testosterone is going to be relatively low

pre-puberty in males.

During puberty, it’s going to skyrocket.

And then the current numbers are that it drops off

at about a rate of 1% per year.

Although we’re going to talk about some data

that show that there’s actually

tremendous variation in testosterone levels.

There’s actually a lot of examples of men in their 90s,

who still have testosterone levels

that mimic pubertal levels, which is remarkable

and speaks to the huge variation

in testosterone levels across individuals.

So let’s talk about other sources of these hormones.

And then it will make clear what avenues

you might want to take in order to optimize these hormones.

The other glands and tissues in the body

that make these hormones, testosterone and estrogen,

as I mentioned briefly, are the adrenals.

So the adrenals ride up top the kidneys.

And the release of these steroid hormones from the adrenals,

in particular testosterone

and some of its related derivatives,

are mainly activated by competition.

So let’s talk about competition,

because it turns out that competition

is a powerful influence on the sex steroid hormones.

And the sex steroid hormones powerfully influence

competition.

So most people don’t realize this,

but most males of a given mammalian species

never get to reproduce.

In fact, they never even get to have sex at all.

And we don’t often think about that,

but testosterone plays a powerful role

in determining which members of a given species

will get to reproduce,

which ones of that species

will actually get access to females.

And so here I’m not talking about humans specifically,

but it’s well-known in species like elephant seals,

in species like antlered animals and rams, for instance,

that the higher levels of testosterone

correlate with access to females.

Now, one interpretation of this

is that the females are detecting

which males have high testosterone and selecting them.

They’re more receptive to them.

We’re going to talk about receptivity for mating

in a moment.

But it’s actually more so

that the males that have higher testosterone

forage further and will fight harder for the females.

And this is really interesting

because there’s very good evidence now

that testosterone can reduce anxiety,

promote novelty seeking,

and promote competitive interactions.

And so before you leap too far with this in your mind

and think about all these human behaviors,

just stay with me

because there’s a little bit of biology here

that makes it all make sense.

And it turns out to be pretty simple.

We have a brain region called the amygdala.

In Latin, that just means almond.

But the amygdala is most famous for its role in fear.

We hear a lot about fear and the amygdala.

But the amygdala is really involved in threat detection.

It sets our thresholds for anxiety

and what we consider scary or too much.

Testosterone secreted from the gonads

and elsewhere in the body

binds to the amygdala

and changes the threshold for stress.

So I’ve said before on previous versions of this podcast

and on other podcasts

that testosterone has this incredible effect

of making effort feel good.

But what I was really referring to

is the fact that testosterone lowers stress and anxiety

in particular in males of a given species.

Now, this is important

because we often think of testosterone

as creating whatever, masculinization

or it’s virilization

or all these terms are thrown around.

But what’s it really doing

when it comes to mate choice and competition?

What it’s doing is it’s reducing the threshold for anxiety.

And in doing so,

it selects individuals of a given species to push further,

being willing to suffer more,

although it also reduces pain.

So maybe they also suffer less

in pursuit of reproduction in females.

Now, it’s well-known in humans

that both males and females

who have elevated levels of testosterone

will engage in more novelty seeking.

And I do want to point out

that even individuals without testes have testosterone

and peaks in testosterone have similar effects

regardless of whether or not

someone has ovaries or testes.

Testosterone increases generally lead to more foraging,

more novelty seeking,

increases in libido and increases in desire to mate.

So it is the case that increases in testosterone

promote competitive and foraging type behaviors

in humans and in non-human mammals.

But it’s also true that competition itself

can increase androgens such as testosterone.

I want to repeat that.

Competitive environments themselves

can increase testosterone.

Now, some people have come to the conclusion

that if you win, your testosterone goes up.

And if you lose, your testosterone goes down.

And to some extent that’s true,

but that’s not a direct effect on the gonads.

That’s actually mediated by the neuromodulator dopamine.

We talked about dopamine

in the episode on motivation and drive.

And dopamine and testosterone

have a remarkable interplay in the body.

Dopamine is actually released in the brain

in ways that has the pituitary,

this gland that sits over the roof of your mouth,

release certain hormones that then go on

to promote the release of more testosterone.

And indeed winning promotes more dopamine

and later more testosterone.

However, in the short term,

just competing increases testosterone

independent of whether or not you win or lose.

So the short version of this

is that competition increases testosterone.

And this may be an ancient mechanism

whereby the androgens such as testosterone

are feeding back to encourage

more competitive type behaviors.

Because every species,

whether or not you’re talking about reproduction

or other resource allocation,

is involved in competition.

Not every individual of a species

gets access to the same number of mates

or the same quality of mates.

And this is true in both directions

for males and females and everything in between.

So I just want to emphasize once more

in case I went through it too quickly,

that increases in testosterone in females

are also going to lead to increase in reproductive behavior

or seeking out reproductive behavior.

They increase libido.

In fact, there’s a particular phase of the menstrual cycle

where testosterone peaks just before ovulation

that on average leads female humans

to seek out sex more than they would otherwise

during their cycle.

And this is all by self-report,

but this is also while measuring things like testosterone,

estrogen ratios, and so forth.

So it’s really interesting that a single molecule,

regardless of chromosomal or gonadal background,

is increasing seeking of mates across individuals,

increasing desire to compete

or willingness to compete

and lowering the threshold for stress and anxiety.

It’s important to point out

that while increases in testosterone

promote seeking of mates and reproduction

in both males and females,

in females, it’s actually increases in estrogen

that promote receptivity to mating.

So testosterone is driving the seeking of sex

and estrogen is promoting the actual act of sex

from females, so-called receptivity,

consensual receptivity.

In males, it’s interesting to point out

that testosterone is promoting seeking of sex,

but it’s also estrogen in males

that’s important for libido.

If estrogen levels are brought too low,

then men will completely lose their libido.

This is often not discussed or overlooked

in the discussion about testosterone therapy

and performance-enhancing drugs.

People think that hyperandrogenized individuals,

meaning people that have very high levels of androgen

will have very high levels of libido,

and they will provided estrogen is available

in sufficient ratios to match that testosterone.

So it’s not simply the case

that high levels of testosterone

produce a lot of sex and mating behavior

and low levels of estrogen are good across the board.

You actually need both in both males and females.

It’s just that in females,

the testosterone levels are always going to be lower

than the estrogen levels,

and in males, the estrogen levels

are always going to be lower than testosterone levels.

So testosterone promotes sex-seeking behavior.

And the real question then is,

does sex itself promote testosterone?

And the answer is somewhat complicated,

but the short version is yes.

And as you recall, sex has multiple stages.

So there’s the physical act of sex,

there’s the seeking of sex,

and then there’s orgasm and ejaculation.

Now, it’s important to distinguish between these

because whether or not sex itself increases testosterone

depends on whether or not the male ejaculates.

And this is very important to understand

because on a previous episode,

I mentioned how dopamine increases with sexual activity.

Remember, dopamine and testosterone

tend to increase linearly with one another.

But then after ejaculation,

there’s a release of prolactin,

and prolactin actually sets the refractory period in males

during which he can’t have sex again.

And the duration of the refractory period

will vary tremendously depending on how much

and how long that prolactin release occurs.

I also described in a previous episode

how some people take vitamin B6,

I’m not suggesting anyone do this,

but take vitamin B6 in order to reduce prolactin levels

and thereby reduce the duration of the refractory period.

But getting at this question

about testosterone and sexual behavior,

it’s important to distinguish

between these different phases of reproduction

or reproductive behaviors.

So there are studies showing

that sexual behavior itself can increase testosterone.

There was a study published in 2011

from Escasa et al, E-S-C-A-S-A.

This is the stuff of textbooks, this is on PubMed.

These are quality studies showing that men who observe sex,

so I guess this would be observing pornography,

will have slight increases in testosterone

during the observation.

These people actually were willing

to have blood draws taken while watching pornography.

They had increases in testosterone

that were very modest of about 10%.

Whereas when people participated in sex,

they actually did this study where people had blood draws

and they had real sex with their partners,

and they had 70% increases in testosterone.

So there are increases in testosterone

that are quite significant during the physical act of sex

and far less so during observing sex.

Now, the question that I often get,

in fact, it’s one of the questions I get most often

in the comments on YouTube, I don’t know why that is,

is whether or not ejaculation adjusts testosterone levels.

And it turns out there are two studies that I could find

that were quality studies on PubMed that address this,

that sex and ejaculation itself

does not reduce testosterone levels,

although it will increase prolactin levels

for the reasons I described a moment ago.

However, abstinence or sex without ejaculation

for a week or more will increase testosterone levels

up to 400%.

So the answer is actually complicated.

It’s not straightforward.

What it means is that sex itself increases testosterone.

However, abstinence also increases testosterone even further.

So it’s a nuanced answer.

And I hope this is satisfactory, no pun intended,

to those of you that have been asking me

what is the relationship between sex and ejaculation

and testosterone and dopamine?

It is nuanced.

And you have to understand that nuance

if you want to understand how certain behaviors

impact hormones and how hormones impact those behaviors.

As I mentioned before, in females,

testosterone also primes the motivation to seek out sex.

And sex itself also increases testosterone,

but it also increases prolactin.

So in both men and women,

sex increases prolactin post-sex.

It’s just the way that the system works.

It’s that testosterone and dopamine increase

in the seeking out and the behavior of sex.

And then after sex, prolactin levels go up.

There’s kind of a quiescence.

The whole nervous system is promoted towards calm.

And this may actually have something to do with pair bonding

and the encouragement of individuals

to spend more time together,

to exchange different smells and hormones

and maybe even pheromones.

And we’re going to talk about pheromones in a moment.

A few years ago, there was a lot of excitement

about the hormone DHEA,

which is mainly made by the adrenals.

DHEA has been promoted as kind of a catch-all

for increasing testosterone and estrogen

in males and females.

And indeed, DHEA will increase

both testosterone and estrogen.

This is something to be mindful of

if you’re thinking about taking DHEA

or you’re taking DHEA already.

DHEA will increase both testosterone and estrogen.

And the extent to which it increases one or the other

will depend on whether or not you’re starting off

with more estrogen than testosterone

or whether or not you’re starting off

with more testosterone than estrogen

and whether or not you have a lot of aromatase.

So for individuals that have a lot of aromatase

being made by the testes or by body fat,

if you take DHEA, there’s a good chance

that a fair portion of that

is going to be shuttled towards estrogen production

and not towards testosterone production.

Whereas in individuals that have low levels of testosterone

to begin with, high levels of estrogen,

there’s a good chance that the DHEA

is going to promote mainly estrogen production.

At least that’s what I could find

from the research studies that I examined.

So the way to think about DHEA,

it’s a kind of global promoter of the sex steroid hormones

and its specific effects are going to depend a little bit

on where you started

and whether or not you have ovaries or testes.

So just as there are behaviors

that can increase testosterone,

there are behaviors that can decrease testosterone.

And one of the most well-characterized ones in humans

is becoming a parent.

So expecting fathers have an almost 50% decrease

in testosterone levels, both free and bound testosterone.

As well, their cortisol levels, a stress hormone,

drop by almost threefold, which is incredible.

And their estradiol levels double.

So their estrogen levels double.

So expecting fathers, many people have known,

put on additional body weight.

Everyone always thought that it’s because they’re eating

in parallel with their pregnant wife.

But it turns out that these effects of reduced testosterone,

increased estradiol and reduced cortisol

can all be explained by an increase in prolactin.

So not just in humans, but in other species as well,

when the male and female of that species are expecting young,

they lay down more body fat.

The assumption is that this is to prepare

for long nights of no sleep,

which occurs in many species, not just in humans.

So it’s really interesting that this hormone prolactin

can start suppressing whole categories of hormones,

sex steroid hormones,

and can start increasing whole categories of other ones.

So we hear about the dad bod.

There are a lot of explanations for the dad bod

that extend well beyond this podcast episode.

But it is a well-known phenomenon

that testosterone is going to drop,

prolactin is going to increase,

estradiol is going to increase in males and females

that are expecting children.

Now, how long that lasts is very interesting.

It actually has to do with how much contact

and how much contact with the smells of the baby,

of the offspring the father happens to have.

So how available or unavailable he is

will actually impact his level of hormones.

Now, I’m definitely not promoting the idea

that fathers or mothers take time away

from their offspring

in order to keep their testosterone levels high

or to restore them.

It’s not what I’m saying at all.

It’s just interesting to point out

that these evolutionary mechanisms push us toward

or bias us toward particular categories of behaviors

by influencing our hormones,

which then feed back and promote more

of that particular behavior.

Because as I mentioned before,

peaks in testosterone in males and females

cause individuals to seek sex, not promote parenting.

Whereas reductions in testosterone,

increases in prolactin and decreases in cortisol

move individuals of both sexes toward parenting behavior

and less toward reproductive behavior.

The other behavior that markedly reduces testosterone

in both males and females

and markedly reduces the desire for seeking sex

and sex itself is illness.

And many of you might say,

well, duh, when people don’t feel sick,

they don’t feel like seeking out mates,

they don’t feel like having sex.

But have you ever wondered why that actually is?

Well, it turns out that it can be explained

by the release of what are called inflammatory cytokines.

So cytokines are related to the immune system,

they travel in the lymph and in the blood

and they attack invader cells like bacteria and viruses.

And under conditions of illness,

we make a lot of different cytokines.

Some of them are anti-inflammatory,

but some of them are pro-inflammatory.

And the best known example of a pro-inflammatory cytokine

is IL-6.

And it’s known that IL-6 when injected into individuals

will decrease the desire for sex

and eventually will reduce levels of testosterone

and estrogen independent of feeling lousy.

So the reason why people don’t want sex when they’re sick

is because levels of IL-6 are increased.

Now, this is important because as we start to think about

the different ways to modulate the sex steroid hormones,

so-called optimize the hormones,

keeping levels of IL-6 low is going to be important

for them to exert their effects.

Now, IL-6 doesn’t just travel to the gonads

and shut down the gonads,

it actually has ways to interact

with some of the receptors that the steroid hormones,

estrogen and testosterone bind to

and impact those receptors

so that the sex steroid hormones can’t have their effect.

In short and put simply,

inflammatory cytokines like IL-6

are bad for sex steroid hormones.

And so we’re going to talk about how to modulate IL-6

in the direction that you would want

and how to increase another cytokine called IL-10,

which is anti-inflammatory in ways that can help promote

or at least support the sex steroid hormones.

So as we move forward,

we’re going to now start to consider

what sorts of behavioral practices,

as well as other things,

can modulate the sex steroid hormones

in the directions that you want them to go.

But before we do that,

and in order to step the stage for that,

you should be asking yourself,

how is it or why is it at a mechanistic level

that behaviors can modulate hormones at all?

If you think about it,

it’s kind of strange that just the mere act

of being a parent or parenting

can change testosterone levels so dramatically

or estradiol levels so dramatically.

What is it?

Is it the sweat of the baby?

Is it their saliva?

Is it the sight of the baby?

Is it holding the baby?

Or is it all those things?

It turns out that many of those effects

are because of smell,

or in some cases, even possibly pheromones.

Now I talked about hormones.

Hormones, again, are a chemical,

travels in the body,

impacts tissues and cells elsewhere in the body.

A pheromone is a chemical

that’s released by one member of a species

that goes and impacts members elsewhere,

but of the same species or even of other species.

Now pheromone effects are absolutely well-established

in lots of animal species,

but they are very controversial in humans.

Today, I’m going to talk

about some of the well-established ones in animals.

I’ve mentioned one or two of these before

on previous podcasts,

but I haven’t mentioned several of them.

And I’m going to talk about the evidence

for pheromones in humans that are well-established.

So the main ones in animals that are discussed

are called the Liebhut effect,

the Witten effect, the Bruce effect,

and the Vandenberg effect,

named after the people that discovered them.

The Liebhut effect is when you house females

of a given species together with no males,

they start displaying longer,

what are called estrous cycles.

In many species, they don’t have menstrual cycles,

which are 28 days.

They have estrous cycles,

which tend to be four days or some variant thereof.

It’s an interesting phenomenon

because what it means is that the presence

of the male itself is changing the ovulation cycle.

Now, many people out there,

imagine mostly the people that are ovulating out there,

will say, of course, I notice I ovulate differently

or my cycle changes when I’m in the presence

of my partner or I’m not.

But the pheromone effect that mirrors

this Liebhut effect in humans

has still not really been identified.

Nobody knows what the exact chemical is,

but nonetheless, this is a strong effect in some animals.

The other one is the Bruce effect.

And this is a very dramatic effect

whereby a pregnant animal will abort or reabsorb her fetus

if the dad of those animals,

the father that sired the litter,

because these are animals, they’re litters,

is removed and a novel male is placed in her vicinity

for about 48 hours.

And what’s interesting is the way that this happens

is a pheromone that comes from male urine

activates the gonadotropin-releasing hormone system

and causes a reintroduction of the estrous cycle

and a spontaneous abortion of the fetus.

Now, a lot of people have taken the Bruce effect

kind of to its extreme and asked whether or not

in humans miscarriages are caused by detecting

the pheromones or odors of novel males,

meaning the non-dad male.

And that’s still an open question.

Nobody knows if that’s true or not.

So I want to emphasize that.

The other one is the Vandenberg effect.

And this is one I alluded to

in a previous episode of the podcast,

which is that puberty in females can be accelerated

by placing a novel sexually competent male

in with a young female who has not undergone puberty.

There’s also a version of this, which I haven’t described,

which is delay of puberty,

where you take juvenile female animals

that have not undergone puberty

and you put them with more mature females

of the same species.

And that introduction of more females will cause a delay,

a significant delay in the onset of puberty.

So these are all pheromone effects.

And we know they’re pheromone effects

because they’re not conscious.

They also don’t require actual contact

with the other members of a given species.

These are all effects that can be mediated

by the urine from a given species

or by the sweat of a given species.

And speaking of sweat,

the one pheromone effect that I’m very aware of

from the published literature

is a paper that was published in 1998

by Stern and McClintock,

which was getting at this question

of synchronization of menstrual cycles.

Now, the whole idea of synchronization of menstrual cycles

is pretty controversial.

For a long time, people said,

oh, this is absolutely a well-characterized phenomenon.

People living in dormitories,

their menstrual cycles would synchronize.

People living in environments together,

their menstrual cycles would synchronize.

And then some studies came out

that kind of undercut those data

and said, no, this actually doesn’t happen.

And it was kind of controversial.

But there is a very clear effect

that was described by Stern and McClintock.

What they did actually was they took females,

they charted their cycles,

and then they had other females wear pads in their armpits

and they collected sweat from those females.

And then they took the sweat from those pads

in those females’ armpits,

and they introduced them to women

who had never had contact with the people who had sweated.

They only had contact with their sweat.

In fact, they swabbed it underneath their nose.

But if that sounds gross, they dilute it in alcohol

so much so that they can’t actually

detect the odor of the sweat.

That’s actually very important

because it’s not the smell,

it’s the pheromone chemical itself.

And it turns out the pheromone chemical itself

can modulate the menstrual cycle,

although it doesn’t necessarily

synchronize it with the sweater.

What it does is it changes the duration

and the pattern of ovulation

relative to so-called follicular phase.

Long and short of this is that

the sweat and pheromones of females

can modulate the menstrual cycle patterns

of other adult females.

It’s just a question of whether or not they synchronize.

And if you’re kind of rolling your eyes now and saying,

well, of course they do, and this is really detailed,

this is how the science is done.

And the reason why people are so skeptical

about the presence of pheromone effects in humans

is that there’s no well-identified pheromone organ.

You know, we have an area of our nose

that’s responsible for smelling, that’s well-established.

It’s been observed in MRIs many, many times,

in cadavers many, many times,

in pretty much all individuals.

But the vomeronasal organ,

which is the pheromone-detecting organ,

hasn’t really been found in humans.

There’s something called Jacobson’s organ,

which is thought to be the organ in the nose.

It’s actually on the top of the roof of the mouth.

And in the kind of back of the nose,

this is for a few wine tasters,

I never can pronounce this,

what are they called, sommelier, sommelier, whatevers,

the people that are excellent at drinking

and detecting the essences of wine

that you have to go through all these tests

in order to get certified as one of them.

Somebody tell me.

They are using probably a similar mechanism

of mixing taste and smell.

And Jacobson’s organ, if it exists,

the vomeronasal equivalent in humans

is thought to be a combination of smell and taste.

Now, it gets even weirder and cooler

when you think about a given study

that was done in humans

where if you take hundreds of t-shirts from boyfriends,

keep them separate, you take those t-shirts,

you wash them many times separately,

and then you offer them to the girlfriends,

the longtime partners of those guys,

and what you’ll find is that the girlfriend

can pick out her boyfriend’s t-shirt

among hundreds of other t-shirts,

not because it smells different,

but because something about it seems different.

It might smell different to her

in some way that’s kind of imperceptible even to her.

And the level of accuracy in detecting that t-shirt,

her partner’s t-shirt,

is way above statistical significant thresholds,

so much so that you almost have to say

there’s something about these effects

that are real pheromone effects.

Although people still argue

that there are no pheromone effects in humans,

that it’s all through olfaction.

I think these are interesting and important to understand

because it means that a lot of things

coming through our nose,

whether or not it’s pheromones or smells,

are impacting hormones and our ability to attach memories

and kind of recognition of mates and other people,

including our children, not just our mates.

And of course, perfume manufacturers

have really picked up on the idea of pheromones

and have entire laboratories set up

to build chemical compounds into perfumes

that are designed to attract other mates.

This is a well-established and well-documented phenomenon.

And the last point I’ll make about pheromones

is that this combination of taste and smell

is such a real thing in the animal world

that there’s something called the Fleming response.

During the mating season for different animals,

you can actually even see this in horses,

but for animals that are seasonal maters,

they’ll do something called the Fleming response

where they actually open their lips and their mouth

and they expose their gums

so that they can capture pheromones

that are floating in the wind and the environment.

They actually are looking for mates using their mouth

and kind of sniffing around.

If you own a dog and you watch the way

that the dog will sniff around,

selecting where they want to urinate, males and females,

there’s often, they’re bringing molecules into their nose.

I know it sounds kind of gross, sniffing urine,

but there are a lot of pheromones in urine of animals.

A lot of pheromones are traveling in the wind.

Again, whether or not this is happening in humans,

I don’t know, but then you think about the perfume thing,

and here people are putting these scents on themselves

that contain putative pheromones, human pheromones,

and walking around hoping that their scents

are going to evoke mate-seeking behavior

from other individuals of the same human species.

So we are among the animals in this behavior,

independent of whether or not

you believe pheromone effects exist.

So let’s get back to behaviors

that can help optimize hormone levels.

One of the main behaviors that’s been shown

to be associated with poor levels of estrogen

relative to age-match controls for people with ovaries,

or lower levels of testosterone

compared to age-match controls for people with testes,

is apnea.

Apnea has everything to do with under-breathing

and the buildup of too much carbon dioxide in the body.

There are other effects of apnea as well.

But if there’s a consistent literature

in this whole story about aging and reductions in hormones

and general health and reductions in hormones, it’s apnea.

I went deep into the literature on advanced menopause,

or when menopausal symptoms are exacerbated.

And I went into the literature on andropause,

or early onset andropause,

so levels of testosterone that are far lower

than they should be for a given age.

And in every case, you could find multiple papers

that showed that apnea, or poor efficiency of breathing

and buildup of too much carbon dioxide in the body,

was a problem.

Mostly sleep apnea, although apnea in general

was shown to be an issue negatively impacting hormones.

Now, the directionality of this effect isn’t entirely clear.

It could be that reductions in estrogen cause apnea.

And actually, there’s some reason to believe

that might be the case.

I found at least one paper

showing that there are estrogen receptors

on some of the neurons that actually innervate the lungs

and allow for the perception

of how full or empty the lungs are.

In other words, reductions in estrogen may adjust breathing

by changing our sensitivity to our own lungs.

Now, that was true for males and females.

Remember, estrogen in both males and females.

But as well, I found papers

in which testosterone reductions were associated with apnea

and testosterone receptors are also found

on a lot of cells in the so-called viscera,

including the lungs.

So again, the directionality of the effect isn’t clear.

But what’s really interesting

is that there are very clear ways

in which patterns of breathing,

especially patterns of breathing in sleep,

can modulate hormones

in ways that are immediately actionable

and can serve to optimize both estrogen and testosterone,

regardless of whether or not you have ovaries or testes.

So what is apnea?

Apnea is under-breathing

or mainly cessation of breathing during sleep.

So people are holding their breath

and then they’ll suddenly wake up.

Actually, I’ve talked about the physiological sigh

on previous episodes of this podcast,

of this pattern of double inhales followed by exhales

that one can do consciously to reduce stress and anxiety

and offload carbon dioxide.

That pattern of breathing

is actually what kicks in spontaneously

anytime we have an apnea episode in sleep.

Although in many people who have apnea,

they don’t engage the physiological sigh.

People who are dramatically overweight

also suffer a lot from apnea during sleep.

There’s actually a lot of buildup

of carbon dioxide in the body.

And that can lead to excessive sleepiness during the day,

inability to access the deeper phases of sleep.

And it’s well-established

that going into deep sleep

and getting the proper patterns

of slow-wave sleep and REM sleep

are important for hormone optimization.

I talked about how to modulate sleep and optimize sleep

in the first month of the Huberman Lab podcast.

So please check out those episodes

if you have sleep issues or you want to work on your sleep.

Also check out Matt Walker’s terrific book,

“‘While We Sleep,’

and that will help you find various protocols

to help you optimize your sleep.

But the issue of breathing itself

can be adjusted in the daytime waking hours

in ways that can powerfully impact both sleep,

reduce incidence of sleep apnea,

and apparently from some emerging literature,

can also help to optimize various hormones

even just by breathing in particular ways while awake.”

So here’s how this works.

There’s now a lot of literature showing

that breathing through the nose, not through the mouth,

is powerful for improving lots of things.

First of all, it improves cosmetic features

of the jaw and face.

This was first well-established by my colleagues

at Stanford in a book called,

“‘Jaws, The Story of a Hidden Epidemic.”

This is by Sandra Kahn and Paul Ehrlich,

who are both faculty at Stanford,

as a forward by Robert Sapolsky,

the great Robert Sapolsky.

And it also has a heavy endorsement up front

by Jared Diamond, the author of,

“‘Guns, Germs, and Steel,’ the Pulitzer winner.”

So a lot of heavy hitters on this book,

“‘Jaws.’

It’s not a book that a lot of people know about,

unfortunately, but it really describes

the benefits of nasal breathing

and the terrible things that happen

when people, in particular children, but adults also,

are heavy mouth breathers.

So mouth breathers have changes in the cosmetics

of their face and jaw that are really bad

in terms of attractiveness.

And this was done in twin studies.

You can look in the book and see some of this.

It’s really dramatic how being a mouth breather

tends to make the chin drop back behind the upper mandible.

There’s a lengthening in the face, a drooping of the eyes.

It can be quite dramatic or modest

depending on how much mouth breathing.

Now, sometimes we have to breathe with our mouths,

but there’s also a lot of data and studies described

in this book, “‘Jaws,’ that describe how nose breathing

in wakefulness and in sleep promotes all sorts

of positive things related to not just cosmetics,

but also the improvement of gas exchange

of carbon dioxide and oxygen in the body.

And as well, it can modify levels

of different neurotransmitters and neuromodulators

in ways that positively can impact hormones.”

So believe it or not, being a nasal breather

and avoiding being a mouth breather

can actually positively impact hormones.

And in particular, the hormones, testosterone and estrogen.

Although the way that it does that

is by making you a better sleeper,

which allows you to produce more testosterone

and the appropriate amounts of testosterone and estrogen.

But it does that in part through indirect mechanisms

because deep sleep supports the gonads,

the ovaries and the testicles,

and their turnover of cells and the production of cells.

Remember in the ovary, particular cells

and the egg follicles themselves make estrogen.

And in the testicle that the Sertoli cells

and the Leydig cells are important for the formation

of sperm and for testosterone respectively.

So what does this all mean?

This means we have to be breathing properly.

It almost sounds kind of, you know, like kind of new agey,

like, oh, you have to breathe properly,

get your hormones right.

But no, you have to breathe properly

to get your breathing and sleep right

so that your sleep can actually be deep enough

and you’re not entering apnea states.

And then that will support gonad function.

And I wouldn’t be putting this out

as one of the main behavioral tools up front

if it weren’t for the fact that the effects of apnea

on these hormones are dramatic and terrible.

And the positive effects of getting breathing right

on these hormones, testosterone and estrogen

are dramatic and wonderful.

So let’s talk about a few of those studies briefly

so I can underscore the value of proper breathing

in order to optimize hormones.

So I was able to find at least four quality studies

showing that when apnea is reduced in sleep or eliminated,

there are significant increases in testosterone in males

and in proper estrogen to testosterone ratios in females.

And the way that it works is very interesting.

Apparently it works by reductions in cortisol.

Now, cortisol is a stress hormone

that is released early in the day as we wake up

and serves healthy roles in protecting us

against infection, reducing inflammation, et cetera.

But you don’t want cortisol to be too high

and you certainly don’t want it elevated too long

throughout the day and night.

And so we all know,

because now we’ve been told a lot in the last decade or so,

that getting proper sleep is important

for all these aspects of health.

Getting proper sleep can really offset

all the reductions in testosterone and estrogen

and reductions in fertility that occur

if we don’t get enough sleep.

But seldom is it discussed how sleep actually adjusts

things like testosterone and estrogen.

And it does it by modifying cortisol.

So the molecule cholesterol can be converted

into testosterone or estrogen,

but there’s a competition

whereby the cholesterol will turn into cortisol

and not testosterone,

or it’ll turn into cortisol and not estrogen

if stress levels are too high.

So the simple version of this

is getting your breathing right during the waking hours,

meaning primarily, unless you’re working out really hard

or there’s some other reason

why you’re maybe eating or speaking

that you need to be breathing through your mouth,

you should be a nose breather.

There’s really good evidence for that now.

And in sleep, you also want to be a nose breather

because that’s going to increase the amount of oxygen

that you’re bringing into your system

and the amount of carbon dioxide that you’re offloading.

There are other positive effects of it as well,

but you’re basically reducing apnea.

Breath holding in sleep

leads to buildup of carbon dioxide

and leads to increases in cortisol,

which then decrease testosterone

and decrease estrogen in negative ways across all sexes.

Okay, so the simple version of this

is get your breathing right.

So how do you do that?

How do you get your breathing right?

Well, for some people that have severe sleep apnea,

they’re going to need the CPAP machine.

This is a machine that you actually put on your face

and it helps you breathe properly in sleep.

Many people, however,

are starting to do this thing of taping their mouth shut.

Now, this sounds a little bit extreme

and you certainly don’t want to do this

in any way that’s dangerous.

James Nestor talked about this in his book,

“‘Breath, The New Science of a Lost Art,”

that simply taping shut the mouth with some tape

that will allow you to open your mouth

if you really need to during sleep

can allow people to shift over

from being mouth breathers and snorers to nose breathers.

In the daytime, the best way to get good at nasal breathing

is to dilate the nasal passages

because a lot of people have a hard time

breathing through their nose.

And one way to do this

is to just breathe through your nose more.

And one way to do that is that when you exercise,

in particular, cardiovascular exercise,

most of the time, provided you’re not in maximum effort,

you should be nasal breathing.

Now, for a lot of people,

nasal breathing during exercise is hard at first,

but as you do it,

because the sinuses have a capacity to dilate over time,

you’ll get better at it.

The sinuses, if you haven’t ever held a skull,

because of my job as a neuroscientist,

I’ve held a lot of skulls,

taken a lot of brains out of a lot of skulls,

teach neuroanatomy and have done that for,

goodness, God knows how many species I’ve done that for,

including human.

But what the sinuses are is they’re actually,

what you’ve got are you’ve got these little portals

in the bone that run up here and down here

behind the nose and into the jaw.

If you ever had a cold and your sinuses are stuffed up,

you feel like you have congestion here and here

and around your ears and in your cheeks and in your face.

And that’s because the sinuses are actually portals

where the bones are fused together,

kind of interdigitated like this.

But they’re lined, of course, with mucus membranes.

And as you start to nasal breathe more,

the nasal passages will start to dilate more.

Don’t worry, you’re not going to get giant nostrils.

But what’s going to end up happening

is you’re going to have an easier time breathing

through your nose just from waking.

So my advice would be breathe through your nose

while exercising, unless you’re in maximum effort.

Pretty soon, what you’ll find is you actually

can create more output than you would

if you were breathing through your mouth.

And of course, there are exceptions to this.

If you’re swimming, follow that breath protocol.

For fighters and martial artists,

there’s reason to do the kind of exhale breathing

through the mouth, the shh kind of thing.

There are reasons to do that sort of thing

for particular sports, but for most people

who are kind of recreational athletes or exercisers,

learn to be a nasal breather.

Has positive cosmetic effects.

It reduces apnea.

It offloads more carbon dioxide.

It increases lung capacity.

It dilates the sinuses.

And it prevents apnea in sleep.

So unless you have severe apnea and you need the CPAP,

becoming a nasal breather can have all sorts

of positive effects by reducing cortisol,

reducing apnea, and indirectly,

raising testosterone and estrogen in the proper ratios.

So this might seem kind of foundational and indirect,

but when you go into the scientific literature,

it comes through as one of the most powerful things

that you can do that is zero cost.

It takes a little effort, but it’s zero cost.

And it has all these positive effects across the board,

both cosmetic and in sleep and hormonal, et cetera.

So that’s the first piece of behavioral advice.

The second piece of behavioral advice relates

to the viewing of light.

And many of you have heard me talk about this before,

and I’m not going to belabor the point

that viewing bright light within the first hour of waking,

whether or not it’s from artificial light

or ideally from sunlight,

has these powerful effects on sleep and wakefulness.

But we have to return to this if you want to understand

how light can impact hormones,

because hormones, light, and dopamine

have a very close-knit relationship,

so much so that your light-viewing behavior

can actually have a direct effect

on hormone levels and fertility.

It can have a direct effect on hormone levels and libido.

It can have a direct effect on hormone levels

and your ability to heal quickly.

And I’m not talking about shining light

on particular injuries.

That may or may not have positive effects.

You know, we can argue about that on a subsequent episode.

It may, but what I’m talking about

is viewing light with your eyes.

So let’s talk about that now,

because the scientific literature on this are robust

and they extend back several decades,

and yet I think most people don’t really understand

how powerful this relationship is

between light, dopamine, hormones,

and all the great things that the sex steroid hormones do

when they’re available in your body in the proper ratios.

In order to understand the powerful effects

that light can have on the sex steroid hormones,

we need to understand seasonal breeding animals.

Now, humans are not seasonal breeders,

but if you understand the biology

of how light impacts various neurotransmitters and hormones,

you’ll set yourself up for a deep understanding

of what you should do with your light-viewing behavior.

So several species of animals,

many species of animals, in fact,

like rabbits and fox and various mustelids

like ferrets and ermines,

change their pellage color across the seasons.

This might be kind of a duh,

but fox in winter are often white or light gray,

and those same animals will be brown or darker colored

in the summertime and spring months.

Now, those same animals breed in the spring

and they shut down breeding.

They actually shut down ovulation.

They often shut down testosterone production

in the winter months.

So right now, I’m just correlating color of fur

with tendency to breed.

Tendency to breed, as we know,

is going to be related to the levels of sex steroid hormones,

estrogen, and testosterone.

Now, why would these two things be linked?

Well, it turns out that dopamine is the link between them.

So dopamine has a precursor.

That precursor is tyrosine,

which is an amino acid, comes from food.

And when dopamine levels are high, as I mentioned before,

there’s a tendency for more

gonadotropin-releasing hormone,

luteinizing hormone, follicle-stimulating hormone,

all the hormones that come

from the hypothalamic-pituitary axis

and stimulate estrogen and testosterone release

from the ovary and testes.

Dopamine basically increases all of that.

The precursor to dopamine is tyrosine,

but the precursor to a lot

of the melanin-producing elements of cells

that give pigmentation, including for the hair,

is tyrosine and tyrosinase, an enzyme.

So yes, the same amino acid-based pathway

and many of the same enzymes

that are devoted to dopamine

and dopamine-increasing the sex steroid hormones

are devoted to giving pigmentation to the hair and skin.

And this is why in the summer months,

when days are longer, animals are breeding more.

And this is also why in the winter months,

when days are shorter, animals are breeding less.

This is also why in humans, many people, not all,

feel an elevation in mood in the spring and summer months

because of the amount of sunlight they’re getting

is increased relative to the winter months.

Now, some of you may be saying,

I love the fall, I love the winter.

Sensitivity to light in these dopamine systems

has a strong genetic component.

So you go to some areas of the world,

I have relatives who are Scandinavian,

and in some areas of Scandinavia,

people know that there’s a kind of seasonal affective

disorder, there’s kind of a seasonal depression,

and people get sadder and more quiet.

And in the winter, there’s actually less going out,

and therefore there’s less sexual behavior,

there’s less partying and things of that sort.

But other people will say, no, during the winter months,

I feel great and I love the holidays around winter, et cetera.

So there’s a lot of variation.

But in general, the pathway is the following.

Increased viewing of sunlight,

and it has to be to the eyes, it’s not to the skin,

increased viewing of sunlight,

increases dopamine levels in the brain,

increased dopamine levels in animals and humans,

increases the amount of these melanocytes

and the activity of these melanin producing cells,

which give pigmentation to the skin and hair,

and indirectly increase the amount of testosterone

and estrogen and thereby reproductive behavior,

feelings of wellbeing, social interactions,

reductions, anxiety, et cetera.

All of which should make sense

based on what we’ve talked about already

in terms of the biology and the impact

of these steroid hormones

on various aspects of the mind and body.

So how does this translate to a protocol?

This translates to the protocol of,

if you want to optimize testosterone and estrogen,

you need to get your light viewing behavior correct.

It’s not just about optimizing your sleep,

which is also important,

it’s about getting sufficient amount of light in your eyes

so you have sufficient levels of dopamine.

So the simple protocols for that I’ve reviewed before,

but it means getting anywhere from two to 10 minutes

of bright light exposure in your eyes early in the day.

It is not sufficient to do this with sunglasses

unless you have to do that for safety reasons.

It’s fine to wear prescription lenses and contacts.

If you can’t get sunlight for whatever reason,

you want to use bright artificial light.

But that is absolutely critical

for timing the cortisol release properly,

limiting cortisol release to the early part of the day,

getting increases in dopamine

that are going to promote the production

of testosterone and estrogen to healthy levels.

The other aspect of light viewing behavior

that’s extremely important

is to avoid bright light exposure to your eyes

in the middle of the night.

If you’re viewing bright light in the middle of the night,

you are suppressing dopamine release.

If you’re suppressing dopamine release,

you are suppressing testosterone levels.

So much so that I would wager that a major effect

of sleep deprivation on reducing testosterone and estrogen

is not necessarily because of the lack of sleep per se,

it’s because usually when people

are not getting enough sleep,

they’re getting too much light in their eyes

in the middle of the night as well.

A study on this has not been completed yet,

but there are two studies published in Cell and Neuron,

both cell press journals, excellent journals,

showing that viewing bright light with the eyes

in the middle of the circadian night

has a detrimental effect on dopamine

and therefore has a detrimental effect

on things like testosterone and estrogen.

So you can’t even begin to talk about supplements

and other ways to optimize testosterone,

diet and its effects on testosterone and estrogen

and fertility and reproductive behavior, et cetera,

until you get your breathing right,

until you get things like

your light viewing behavior right.

So bright light early in the day

and throughout the day is great.

View as much bright light, ideally sunlight, as you can,

as much as you safely can.

You obviously don’t want to burn your retinas

or damage your retinas,

so never look at any light that’s so bright

it’s painful to look at.

But getting a lot of light in your eyes

is not just about adjusting your sleep-wake rhythms,

it’s also about optimizing your sex steroid hormones.

And avoiding bright light in the middle of the night

is not just about not disrupting your sleep,

it’s also about optimizing the sex steroid hormones.

And now that you understand a bit

of how the sex steroid hormones work

and how powerful they are for reducing anxiety

and all these other effects,

this should be straightforward to do

or hopefully it’s inspired you

to get your light viewing behavior

and your breathing behavior correct.

In fact, in thinking about tools,

for many people that are suffering

from low levels of estrogen if they want higher levels

or low levels of testosterone if they want higher levels,

just getting the breathing and light viewing behavior,

which will indirectly support sleep behavior,

can be a huge and positive effect

on levels of sex steroid hormones.

I can already anticipate that in hearing this,

you might wonder whether or not viewing light

is going to, for instance, increase your testosterone a lot

when in fact you want your estrogen increased

or it’s going to increase your estrogen a lot

when you want your testosterone increased.

Everything I’m describing here

is for people regardless of chromosomal

or gonadal background.

So I’m trying to basically offer all this information

in one swoop.

But basically, if you’re somebody who naturally has ovaries

and has higher levels of estrogen than testosterone,

then viewing bright light early in the day

because of dopamine’s effects

is going to promote more estrogen

and subtle increases in testosterone.

Whereas if you’re somebody who starts off

with more testosterone and lower estrogen,

so somebody presumably who has testes

or maybe you’re supplementing with testosterone

through other sources for whatever reason,

bright light viewing is going to increase testosterone

and estrogen in parallel,

but you’re still going to maintain

the ratio of testosterone to estrogen.

In short, you don’t have to worry

that you’re going to increase the wrong hormone.

This is all about optimizing the ratios of hormones

that you already have.

Okay, so we’ve talked about breathing.

We’ve talked about light.

Let’s talk about a third element

that there seems to be some excitement about lately

for other reasons,

but that can actually have some pretty profound influences

on hormone levels, and that’s heat and cold.

So as always, rather than just offer a tool,

I’m going to tell you the underlying science

as it relates to naturally occurring phenomenon,

because in understanding that

and understanding the mechanism,

you’re going to be in a far better position

to understand the tools and mechanisms

and how you might want to adjust them for your own life.

So now you understand the relationship

between light, day length, dopamine, and hormone levels,

and everyone should realize

that temperature and day length are linked,

and I’m sure as I say that,

you’re probably thinking, oh, of course.

In summer, when there’s more sunlight,

days are longer, nights are shorter,

in general, it tends to be warmer out,

and in winter, when nights are longer, days are shorter,

it tends to be colder out.

And in the winter months,

testosterone and estrogen tend to be lower in many animals

and in humans, and in the summer months,

because of the role of dopamine

in promoting the sex steroid hormones,

when days are longer and it’s warmer,

humans tend to make more estrogen and testosterone

relative to the other months of the year.

Now, these effects can be somewhat weak and modulated

as opposed to in seasonally breathing animals

where they’re really dramatic, okay?

But the point is that temperature and day length

and sunlight, those are all intimately related

because of the systems that we evolved in, right?

So before we had artificial light and artificial heating

and artificial cooling,

our biology evolved under systems where temperature,

day length, and the hormones

were correlated with one another.

So nowadays, there’s a lot of interest

in using cold as a way to stimulate testosterone.

This is mainly because in the sports community,

in particular, in the bodybuilding community,

they are always seeking ways to maximize testosterone,

dihydrotestosterone, keep estrogen to its minimum required

to still have libido and still have skin elasticity,

but also walk around with Saran wrap skin.

Then all this kind of extreme stuff that happens there

has led to a recent movement where,

believe it or not, I heard this

and I couldn’t believe I went and checked,

although I didn’t buy them,

that on Amazon, you can actually find people have,

they’re literally underwear that have ice packs,

or I think they’re ice pack underwear,

so that people are making themselves cold

at the level of the gonads

in order to try and increase testosterone and libido.

Sounds pretty crazy, but believe it or not,

that and things like ice baths and cold showers

can have positive effects on the sex steroid hormones,

both testosterone, mainly in males,

and estrogen, mainly in females.

And you might say, wait,

I thought cold makes the reproductive axis

kind of shut down a bit

or reduces testosterone and estrogen,

but it turns out it’s not actually the cold

that’s having these effects in people.

Things like the ice bath, cold showers, cold water swims,

these ice underwear, whatever they are,

can’t believe that these actually exist, but they do exist.

What happens is there’s a rebound

in vasodilation after cooling.

So cooling causes vasoconstriction,

and then after the cooling, there’s a rebound vasodilation,

and there’s more infusion of blood into the gonads.

There’s also an effect that’s neural.

So let me explain how this works,

because there are only a few studies on this,

none of which looking at the frozen underwear,

but that have looked at cold exposure

and levels of androgens and estrogens.

That’s kind of interesting.

So you have to remember that the gonad,

the ovaries and the testes are heavily vascularized.

Remember, even at the level of the brain,

GnRH, gonadotropin-releasing hormone,

comes from neurons that, believe it or not,

start off in your nose early in development,

migrate into the hypothalamus.

I’m not making that up.

They started off in your nose

and migrated into the hypothalamus.

Those neurons extend processes,

we call them axons, into the pituitary

and release GnRH into the pituitary.

There’s a lot of vascularization within the pituitary.

So now those hormones, or GnRH,

can stimulate follicle-stimulating hormone,

luteinizing hormone, which then are released

and travel into the bloodstream.

Then those hormones reach the ovary or testes,

and they have to get into the ovary and testes.

And the way they do that is through the vascular system.

And people forget, but the vascular system

and how constricted or dilated vessels are

is controlled by neurons, right?

This is, we discussed this during the discussion

about stress in the stress episode.

But it’s well-known to neuroscientists

that the best way to shut down neurons is to cool them.

So there are a lot of examples of this

in the scientific literature,

but most people aren’t aware of it

because you’re not digging around

in the methods section of these papers.

But when we want to shut down neurons,

we can do things like inject drugs

that will do that, like lidocaine,

the stuff that makes you numb at the dentist,

or you can use different inhibitors.

But one of the best ways to do it experimentally

is to just cool neurons.

When you make neurons cold,

because there’s a temperature dependence

of when neurons can be active and when they can’t,

the neurons shut down.

So the most plausible explanation for why cold exposure,

either through one to 10-minute ice bath or cold shower,

or the ice underpants thing,

would increase testosterone or increase estrogen

is that you’re cooling the neurons

that control vasoconstriction and vasodilation

and shutting down the entry of blood,

or at least reducing it, and hormones into the gonad.

And then when the gonad

and the surrounding area heats up again,

you’re getting a rebound hypervasodilation

that delivers excessive levels of,

not excessive, but increased levels of GnRH

and other hormones and carriers

and carrier proteins and so forth

that would then stimulate the gonad

to release more testosterone,

or would stimulate the gonad to release more estrogen.

That’s the most plausible explanation I can come up with.

There aren’t a lot of studies

looking at direct effects of temperature on the gonad.

And it’s going to be a difficult study

to carry out in any case,

because unless it were done in vitro in a dish,

it’s very hard to eliminate all the other things

like vasoconstriction, vasodilation.

Put simply, we don’t know whether or not cold and heat

directly affect the production of testosterone and estrogen.

We only know that cold and heat can modulate those

probably through indirect mechanisms

like controlling the amount of blood flow

by way of shutting down or activating the neurons.

Now, there’s a lot of lore

around heating up the gonads too much.

There’s actually a whole set of pseudoscience webpages

out there saying, well, if you want a girl,

you should conceive the child at this room temperature.

And if you want a boy,

you should conceive the child at this room temperature.

I don’t think there’s really any firm scientific evidence

for that, for either one.

But there’s some interesting literature

about temperature dependence of production of hormones.

And I think that it probably relates to these mechanisms

of vasodilation and neural control over vasodilation.

And of course, excessively high heat is not good

for the testes, for sperm production, or for sperm health.

Sperm have all sorts of proteins in the cap,

things like pentraxins and other things

that cause them to swim faster

when they’re expressed properly and in the right locations.

And heat actually alters the location

and the function a lot of those proteins.

They’re very heat sensitive.

And so that’s why excessive heat

is truly not good for fertility,

which may be independent of heat’s roles

in promoting estrogen or testosterone.

Okay, so now we’ve talked about breathing,

we’ve talked about light and temperature,

we talked about parenthood, we talked about competition,

and we talked about some pheromone effects.

Now let’s talk about particular forms of exercise

and how they modulate the steroid hormones.

And then we’re going to talk about various supplements,

both in reference to testosterone

and in reference to estrogen.

So now let’s talk about how exercise in its various forms,

weight training, endurance work, weight training to failure,

or less intense weight training,

can impact testosterone levels.

But I want to remind you that we’re talking about testosterone

both in males and females.

And based on what you know from earlier in the episode,

testosterone can have numerous positive effects

in both males and females,

provided they’re in optimal range.

So if you look on the web, people will say,

oh, you know, testosterone is increased by weight training.

You want to do big, heavy compound movement,

squats and deadlifts and chins and things of that sort.

But what about the scientific studies?

What’s the actual basis for this?

Because if you just take a step back and look at this

from the perspective of a scientist, you’d say, okay,

what is a squat?

A squat is loading up a bunch of weights on a bar

and then sitting down essentially

and standing up over and over again.

What’s a deadlift?

It’s lifting heavy weights from the ground.

Why would that increase testosterone?

This is what’s often not discussed in the weight training

or even the exercise science community.

What would actually stimulate the release of testosterone

from the adrenals and or testes?

And which one is it, adrenals or testes or both?

And that’s often not discussed, but as a neuroscientist,

this is the kinds of things we think about

because we think always that genes don’t create behavior.

Immune systems don’t know when to be activated.

Lungs don’t know when to inhale or exhale.

Hearts don’t know when to beat

except for the information that it gets from neurons.

The nervous system controls all of that.

And so really the answer has to be in the neural system

that’s related to these particular types

of weight-bearing exercises.

So when you go into this literature,

it’s kind of hard to find real mechanism.

You see a lot of effects.

You’ll hear things like androgen receptor content,

meaning testosterone and its derivatives,

receptor content following heavy resistance exercise.

And you’ll find some examples that for instance,

you know, they do muscle biopsies.

They can actually see receptor increases

looking at either high volume or low volume,

really intense exercise.

And you can find a lot of that,

but not a lot of mechanism

about how the nervous system would do this.

And the reason you’d want to know how it can do it

is that you could potentially build better protocols

or figure out exactly what about these movements

is triggering increases in androgen receptors

and testosterone.

So what’s interesting is when you start digging

into the more mechanistic studies,

what you find is that heavy weight training,

so this is weight training where the sets are done

with anywhere from, you know, kind of one to eight rep range.

So this translates differently

depending on ratio of muscle fiber type and so forth,

but where basically people are working at anywhere

from like 70% to 95% of their maximum,

or sometimes even going right down

to their one repetition maximum,

really kind of, you know, max effort.

What you find is that using the nervous system

in a way in which they’re moving heavy loads.

So that I would translate to recruitment

of high threshold motor units for you muscle physiologists.

And there’s a rule in muscle physiology

about the neuron recruitment for moving muscles

where you basically use the minimum number of motor units

of neurons to activate muscle as you possibly can.

As loads increase, you have to recruit more and more neurons.

You always hear about recruiting muscle fibers,

but really it’s recruiting more neurons

to recruit more muscle fibers.

And what you find is that heavy weight training,

but not weight training to failure

where completion of a repetition is impossible

leads to the greatest increases in testosterone.

Now I’m sure there are a bunch of exercise jockeys

out there that are going to, you know,

come at me with a bunch of things where,

oh yeah, but high volume and this

and training to failure and that, sure.

If you’re willing to kind of put things side by side,

adjust for exogenous testosterone treatment

and all the rest, which was done in these studies,

what you find in general is that weight training

with heavy loads, so anywhere from one rep maximum

to somewhere in the, you know,

six to eight repetition range in males or females

increases testosterone significantly.

And it does it for about a day, sometimes up to 48 hours.

And the studies that I found,

which seem to hold the most rigor or weight

based on where they’re published

as opposed to being published in the journal,

never heard of it.

They’re published in good quality

exercise physiology journals.

For instance, the paper by Ratames, R-A-T-A-M-E-S-S et al,

which was published in 2005,

which talks about modulations in androgen receptor content

after heavy resistance exercise,

looks at going to failure, not to failure.

The work of Sciardo et al, published in 2006,

differential effects of strength training

leading to failure versus not failure

on hormonal responses, strength and power gains.

You know, there are a lot of studies here

and I will certainly put the links to these in the caption.

Many of these actually include Duncan French

who runs the UFC training center,

who I’ve had the privilege of meeting

and discussing some of this with before,

as well as other authors, of course.

But they all point to the fact

that there’s something about the engagement of the neurons

that recruit high threshold motor units in muscle

when moving heavy loads, but not to failure,

that has to provide some sort of feedback signal

either to the gonad to produce more testosterone

or is increasing the activity of receptors in the body.

Now, why do I say that?

Well, this is the puzzle, right?

How is it that a particular movement,

just like how is it that interacting with your child

is increasing or decreasing testosterone?

This is the kind of fundamental question

at the mechanistic level.

And we answered the question for child rearing,

has probably something to do with smell and pheromones,

although I’m sure there are other cues as well,

but there’s clearly a influence of hard work

at the neural level and then at the muscular level

for increasing testosterone.

And there’s also clearly an effect of working too hard

and presumably increasing cortisol too much,

although I’m speculating there,

in terms of reducing testosterone.

And so the reason we’re getting nitty gritty about this

is because ultimately we’d really like to understand

what are the optimal protocols?

You know, out there in the literature,

you hear move heavy objects to increase testosterone.

Some of that will be converted

to the more powerful androgen, DHT,

by 5-alpha reductase, et cetera.

But we really don’t understand yet

how these particular behaviors increase testosterone

and whether or not it’s doing that

by modulating the receptors

or it’s modulating testosterone release directly,

presumably testosterone release directly

and sensitivity of the receptors.

That’s what most of the muscle physiology studies

that I was able to find point to.

But this basically boils down

to a particular set of protocols

where if you want to increase testosterone

for whatever reason,

that weight training with heavy loads,

but not to failure seems to be the best supported,

at least scientifically supported solution to that.

Now, it may not raise your testosterone levels

as high as you want,

but it’s definitely taking things in the correct direction.

Now, many of you might be endurance athletes

or also enjoy exercise besides heavy weight-bearing exercise

and there are several studies exploring

whether or not endurance activity

can increase or decrease androgen levels

and whether or not you combine endurance activity

and weight training,

whether or not that has any effect

if you do the endurance activity first or second.

And the takeaway from all of this

was that endurance activity, if performed first,

leads to decreases in testosterone

during the weight training session

as compared to the same weight training session done first

followed by endurance activity.

In other words, if you want to optimize testosterone levels,

it seems to be the case that weight training first

and doing cardio type endurance activity afterward

is the right order of business.

Now, when these are done on separate days,

it doesn’t seem to have an effect.

They showed no statistical interaction,

but it seems that if you’re going to do these

in the same workout episode

that it’s move heavy loads first

then do cardiovascular exercise.

So there’s a little bit of data looking specifically

at how endurance exercise impacts testosterone

and its derivatives.

And it’s very clear that high-intensity interval training,

sprinting, et cetera,

which somewhat mimics the neural activity

that occurs while moving heavy weight loads

is going to increase testosterone.

There’s ample evidence for that in the literature.

And that endurance exercise that extends beyond 75 minutes

is going to start to lead to reductions in testosterone,

presumably by increases in cortisol.

But of course, the intensity of the exercise

is going to be important too.

No one ever, I don’t think anyone really believes

that hiking for the three hours

is going to reduce your testosterone.

Whereas I think if one were to go out

and run hard for three hours,

that you can imagine there’d be reductions in testosterone

by way of increases in cortisol.

And so while this area certainly needs more research,

it’s pretty clear that limiting the endurance exercise

to 75 minutes or less, not making it too intense

is one way to keep cortisol from going through the roof.

But I’ve talked on previous episodes

and there are a lot of others who have talked out there

about how to clamp cortisol,

how to keep cortisol more reduced.

This is also one of the reasons why you can imagine

that various individuals, either for competition

or just for their own purposes,

rely on testosterone therapy, exogenous testosterone,

not just for weight training, but for endurance exercise.

So this is one of the reasons why every once in a while,

professional cyclists will get popped

for performance-enhancing drugs,

meaning they’ll get caught.

And it’s not just that they’re increasing red blood cells

through EPO and things of that sort.

Oftentimes they’re also taking testosterone,

not because they want to be large

or have massively hypertrophied muscles,

but because they’re injecting testosterone,

they don’t have to worry about cortisol-induced reductions

in testosterone.

They can just clamp or keep their testosterone levels high.

Not something I’m recommending,

but I’m just justifying the rationale

for why an endurance athlete would want to do that at all.

So now let’s switch over to talking about estrogen.

So there are many people

who are trying to optimize their estrogen levels.

And one of the places where this shows up a lot,

and I get a lot of questions about, is menopause.

So menopause, as I mentioned earlier,

is this fairly massive reduction in the amount of estrogen

that is circulating in one’s blood,

mainly because the ovary is now depleted

of some estrogen production of its own.

The eggs are not being produced.

They’ve been depleted, et cetera.

So menopause is characterized by a variety of symptoms

and it’s multifaceted,

probably deserves an entire episode on its own,

but things like hot flashes, things like mood swings,

things like headaches, in particular migraine headaches,

there can be a lot of brain fog.

It can be very, very disruptive for people.

Now you sometimes hear about andropause,

which is thought to be the kind of analog to menopause,

but menopause has certain characteristics

that make it a very robust phenomenon for most women.

Whereas for men, andropause is going to sometimes happen,

sometimes won’t.

In fact, without going into the details

of the graphs and the data,

it’s very clear, as I mentioned earlier,

that some men maintain levels of circulating androgens

that are quite high, even as similar as they were

in puberty and their teen years and 20s,

well into their 60s, 70s, and 80s,

if they’re optimizing a lot of other things

and probably genetics plays a role as well.

Whereas some males won’t,

but within the female population

or population of individuals that have ovaries,

there’s a very stereotyped and characteristic reduction

in estrogen levels as the number of eggs becomes depleted.

And that’s what we think of as menopause.

So what are the various things that one can do for menopause?

Well, one of the most common ones

is that physicians will prescribe supplemental estrogen.

So this is hormone therapy

where somebody takes either oral estrogen

or they’ll use a patch or a pellet,

some way to secrete estradiol into the system.

And that has varying success depending on the individual.

Some people respond very well to it.

Other people really have challenges with it.

And there are a lot of side effects associated with it

for some people, not others.

In addition, there’s a concern always

about supplementing estrogen

when there’s a breast cancer background in the family

or there’s concern about breast cancer for any reason,

because a lot of those cancers are estrogen dependent.

And that’s why drugs like tamoxifen and anastrozole

and drugs that block either aromatase

or block, excuse me, estrogen receptors directly

were initially developed.

You see them a lot on the internet,

again, for all the sports folks

who are trying to increase testosterone, reduce estrogen.

But remember, those drugs were initially developed

as ways to prevent estrogen binding

to the estrogen receptor as cancer treatments.

So I want to be very clear, and I’ve said this many times,

we always put in the caption of each episode, of course,

that I’m not a physician, I’m not an MD.

I don’t prescribe anything.

I’m a professor.

I profess things.

I’m here to translate the scientific literature

and point to what might be some useful avenues

for exploration, but this is just for information purposes.

You should definitely talk to your doctor

about anything that I’m talking about now

or in any episode for that matter.

So if you look at the literature on menopause

outside of just standard estrogen therapy,

there are some very interesting compounds out there

that have been used and that are supported

by quality peer-reviewed studies.

And again, I’ll refer you once again

to this amazing website, examine.com,

where you can put in essentially any condition

or any supplement, and it will point you

to the human effect matrix, not animal studies,

but human studies that have explored these things.

Now, there are a huge variety of them here,

so I won’t go into all of them,

but some of the pro-estrogenic compounds

that have been shown to be powerful

in the context of menopause, as well as other conditions

where estrogen is lower than one would like,

include a description and some of the literature,

and I’ll get into this in a moment

of something like black cohosh.

I think that’s the correct pronunciation.

It’s literally the word black and then C-O-H-O-S-H.

And it’s very interesting.

There are 13 peer-reviewed studies

that have reached prominence

in the kind of commercial landscape

where this substance, black cohosh,

has been promoted as a way to increase estrogen.

Turns out that the effects are consistent,

but are fairly minor,

fairly minor increases in estrogen.

So it does seem to be a real effect.

It is significant over the placebo effect,

but there’s also a significant placebo effect

in some of these studies as well.

So what’s interesting when you look at these studies

is that many of them were carried out

over a period of six-plus months.

They’re double-blind studies, et cetera,

and almost all of them led to modest increases in estrogen

and modest decreases in menopause-related symptoms.

Now, a few additional details about these studies.

They were generally carried out on women age 45 to 64.

In some cases, they looked specifically at women

that were clinically obese or overweight,

although not always.

The subject size pools are pretty big,

anywhere from 50 to 87.

These are decent size, 132 subjects, et cetera.

So these look to be like quality studies,

and they basically point to the fact

that black cohosh can have a modest effect

in improving menopause symptoms.

The other one is Panax ginseng.

So P-N-A-A-X ginseng has been shown

to decrease some symptoms associated with menopause,

mostly related to libido,

although the other effects were unreliable.

Other things like maca,

which is known to increase dopamine, actually,

had minor effects.

Things like, the names here are a little hard to pronounce,

so forgive me, things like Valeriana officinalis

has shown that there can be some improvement

in the hot flash symptoms

and some of the insomnia associated with that.

So that might be worth exploring.

Again, discuss with your doctor.

But these were both 100 subject

plus age 45 to 64 individuals,

double-blind, placebo-controlled studies

that showed significant but modest effects.

There was one substance in the gallery

of the compounds that was looked at

that turns out to be particularly interesting,

and this one is also particularly difficult to pronounce,

and it’s pruraria mirifica.

So I’m going to spell this out for you.

It’s P-U-E-R-A-R-I-A,

pruraria mirifica,

M-I-R-I-F-I-C-A.

And there are four studies on this compound

that show, in every case, it to be very potent,

in fact, comparable to estrogen therapy,

estrogen replacement therapy,

in reducing the symptoms of menopause.

So this was pretty striking

because when you go through these studies

and you look, again, they seem to be pretty well-controlled,

as far as I could tell,

and they explored a pretty wide subject pool,

and it seems that every single one of these studies,

when looking side-by-side at pruraria mirifica,

which is also called,

now this is really hard to pronounce, kuau kurukau,

I guess that’s the name that they use in various countries,

that it was comparable to estrogen replacement therapy.

So I mention this because a lot of people contacted me

and said, what about the insomnia in menopause?

What about the headaches in menopause?

Now, I’m not suggesting you run out

and immediately start taking any of these compounds.

Please talk to your doctor.

Any hormone-related compound is a serious consideration

because of the relationship to breast cancers.

But just in general, these compounds are,

estrogen and testosterone are exceedingly powerful

in terms of controlling our mental and physical states.

And so you want to approach them with caution.

But I thought that that one in particular was interesting

and for which there are quite a few PubMed-documented,

peer-reviewed studies in quality journals.

Okay, so now let’s talk about the role of specific compounds,

some of which, many of which

can be taken in supplementation form

or extracted from diet and nutrition

in order to optimize sex steroid hormones.

And again, I just want to emphasize

that I’m not suggesting anyone take anything

or stop taking anything.

This is purely for informational purposes,

but some of the data on these

is quite striking and impressive.

It’s very clear that certain collections of nutrients

are useful for promoting testosterone and estrogen production

in their proper ratios.

And those things are what I would call

the sort of usual suspects.

Vitamin D, which is important

for so many biological functions,

including endocrine functions, zinc, magnesium, et cetera.

And if you want to look into this more deeply

and you want to understand exactly

what the negative effects are

of not having sufficient zinc, magnesium,

and what those levels might actually be,

there’s a paper that’s available.

You can go on PubMed.

I can’t pronounce this last name.

I’m sorry, it looks to me like Wrzosek,

but it’s W-R-Z-O-S-E-K.

I hope I didn’t butcher that too badly.

Wrzosek et al., 2020 in Endocrinology and Metabolism Review.

So there’s a recent paper in a good peer-reviewed journal.

It talks mainly about how

the hypothalamic pituitary adrenal axis

and the sex steroid hormones are negatively impacted

by deficiencies in magnesium,

deficiencies in vitamin D, and deficiencies in zinc.

However, that doesn’t point to the levels

that one should take in order to optimize.

So it doesn’t say take X amount of zinc

or X amount of magnesium or X amount of vitamin D.

For that information, because it’s so context-dependent

and individual-dependent,

I highly recommend you go to examine.com.

You can put in zinc or magnesium or vitamin D,

and they will give you ranges of dosages

that are supported by specific studies.

Again, that information is completely free to you.

And it’s very useful in figuring that out.

I personally have supplemented with zinc, magnesium,

and vitamin D for years,

but many other people do that as well.

And the question is always how much,

and that’s why I’m a proponent of getting blood work done,

because that’s how you know whether or not

your androgen levels,

as well as things like vitamin D levels, et cetera,

are sufficiently high.

So the takeaway from these studies,

looking at what deficiencies cause

in terms of deficits in testosterone and estrogen,

really point in the direction of,

make sure you’re getting adequate zinc, magnesium, and D3,

unless you want these steroid hormone levels

to be reduced for whatever reason.

One of the things that’s been shown time and time again

to have very negative effects on sex steroid hormones,

testosterone mainly in men,

estrogen mainly in women, is opioids.

There’s this whole issue, of course,

of the opioid epidemic.

It’s deserving of an entire episode

where you’re going to talk about that

with experts in addiction

and people that treat pain and so forth.

But the opioids dramatically reduce levels

of testosterone and estrogen.

And they do that mainly by disrupting the receptors

on gonadotropin-releasing hormone neurons.

These neurons within the hypothalamus

that communicate to the pituitary.

And in fact, people that take large amounts of opioids

or even take low levels of opioids

for long periods of time

will develop all sorts of endocrine syndromes.

That’s been shown over and over again.

Gynecomastia or male breast development in males,

disruptions to the ovary in females.

It’s really a quite terrible situation.

So excessive opioids are very problematic

for sex steroid hormones.

I don’t think anyone will have any trouble

finding any literature on that.

You can just go into PubMed.

You can put opioids, testosterone or opioids, estrogen.

But the major effect is actually way up in the hypothalamus

to shut down the production of GnRH,

the very hormone that stimulates

testosterone and estrogen release.

Now there’s an entire industry devoted to supplements

and various things that people can take

to increase testosterone.

Some of which have scientific data to support them.

Some of which do not.

And some of which have anecdotal support

and some of which do not.

And this ranges so broadly.

I mean, things like the material off deer antlers,

which is high in supposedly IGF-1,

which is in the growth hormone pathway,

all the way to actual consumption of bull testes.

You can go on Amazon right now.

I certainly don’t suggest that you do this.

And you can actually buy ground up testes from cows.

And you can consume those.

Now, a lot of that’s going to be broken down in the gut.

I’m certainly not suggesting you do that.

But just to point out, this is a huge and vast literature.

And it actually dates back hundreds of years.

Even though testosterone wasn’t discovered

that long ago as a specific hormone molecule

and characterized and then re-synthesized,

it has a huge industry

because of the powerful effects that it has.

Likewise with estrogen,

the development of the birth control pill

was only made possible

by understanding the structure of estrogen and estradiol.

And we’re going to talk all about birth control

and how it works

and its influence on various other pathways

in a future episode.

But there are these supplement compounds

that are supported by the scientific literature

in terms of their ability to adjust androgens,

things like testosterone and dihydrotestosterone.

One of the ones that has really good evidence for it

is creatine.

It’s very clear that something about creatine,

although the mechanism isn’t exactly clear,

either increases 5-alpha reductase

or makes the testosterone molecule more susceptible

to certain enzymatic reactions

that leads to increases in DHT.

DHT, dihydrotestosterone,

as I mentioned in the previous episode,

has this dramatic role

in creating a kind of masculinization

of the brain prenatally.

It also defines the primary sex characteristic

of the growth of the penis, et cetera.

And beyond infancy and early childhood and later in life,

it has powerful effects in creating balding,

in beard growth, et cetera.

And it has a much higher affinity for the androgen receptor

than does testosterone.

So creatine can increase DHT,

which means that if you take creatine

and you’re very DHT susceptible,

then you might experience some hair loss.

This has been heavily debated.

Does creatine cause baldness?

It’s going to depend.

It’s going to depend on how much 5-alpha reductase you have

and how prone to hair loss you are.

Some people can take creatine without any problem

in terms of hair loss.

Some people cannot.

They start losing their hair to levels

that at least for them aren’t comfortable.

There are a few other things that can increase testosterone

and it has to do with the way that testosterone exists

in its free and its bound form.

So testosterone, the molecule is kind of total testosterone.

That’s usually what’s measured.

This is the kind of levels

that are typically thrown around

of anywhere from 300 to 900 being the kind of natural range

and then super physiological getting up

into 1200, 1600 range.

But testosterone isn’t just roaming around free in the blood.

At least most of it isn’t.

Most of it is bound to either sex hormone binding globulin,

SHBG, or to albumin.

They’re needed as transporters to get testosterone

into cells so that testosterone can have its effects

on gene expression as well as other pathways

within the cells.

So people talk about that the level of free testosterone

is really what’s important

and that you want to optimize free testosterone.

That’s a little bit of a tricky statement.

That’s kind of like it’s true

and yet it’s not really reflective

of a thorough understanding

of how these binding globulins work.

Remember these binding globulins aren’t there

to soak up all your testosterone

just to make it hard for you to free up testosterone

and make gains in the gym or whatever it is

or have increases in libido.

They’re there to actually transport testosterone

to specific tissues, to shuttle them to specific tissues

and to set the rate of bound and unbound testosterone

so that it’s not all unbound at once.

And it’s always interesting to look in the literature

and see how everyone wants to free up their testosterone

so that it can work.

But sex hormone binding globulin

can bind up too much testosterone

to the point where it’s having negative effects on libido

or on muscle growth and fat loss and things of that sort.

This is true in males and females

or it can be doing exactly what it’s supposed to do

which is shuttling testosterone

to the proper tissues and organs

where it has all these effects, including the brain.

So there are supplements in particular Tonga Ali

which has this other name.

It’s something I’ve called Tonga Ali.

Sometimes it’s called and these,

forgive me that it’s hard to pronounce

but uricoma longifolia jack.

They always seem to have these names

that kind of allude to androgenic features.

Like, I don’t know why longifolia jack.

I don’t know.

I think it’s kind of obvious

why that sounds sort of androgenic.

This has been shown in several studies

and you can find these on examine.com

or you can go to PubMed if you like.

I’ve looked at these.

That it does seem to have some pro-fertility,

pro-free testosterone and subtle aphrodisiac effects.

It does also seem to be a slight anti-estrogen.

So the reports of this are people take this

anywhere from 400 to 800 milligrams a day.

Again, I’m not suggesting you do that

but that’s kind of what’s out there.

And there is some decent scientific literature

to support the fact that it liberates

some of the bound testosterone

and allows more free testosterone to be available.

Some of the reported quote unquote side effects

are things like excessive alertness and insomnia

if it’s taken too late in the day and so forth.

But I encourage you to explore that further

if increasing free testosterone

is something that you’re interested in doing.

Examine.com includes a lot of other things

that can increase testosterone.

One of the things that’s been purported

to free up testosterone in the blood

are things like nettles, stinging nettles.

Although I should point out

that the literature points to stinging nettle

also having some fairly potent effects

on the prostate and on the liver.

And so it might be a tricky molecule

and maybe not an attractive one for people to take.

So we talked about creatine.

We talked about Tonga Ali.

It’s clear that boron, which is really interesting.

Believe it or not, I think boron comes from,

I think these were like meteors that landed on earth

that now they extract boron.

It’s one of these crazy stories that when you look at it,

you go, how could that possibly be?

But there’s actually, that’s how it works.

That boron, there’s some scientific support

for it freeing up more testosterone.

And again, freeing up testosterone

may be exactly what you want.

I just don’t think that we should demonize

these carrier proteins like albumin and SHBG.

In fact, albumin is very important for testosterone

to be able to make it into the brain

to have some of the proandrogenic effects

on the cognitive effects of testosterone.

Because in both males and females,

testosterone can shift these behaviors

like mate-seeking, reductions in anxiety and so forth

that we talked about before,

only by making it into the brain.

And there is this thing called the blood-brain barrier,

which is fascinating and deserving of entire episode also.

And getting molecules across the blood-brain barrier,

even if they’re sex steroid hormones,

which are lipophilic and can pass through cell membranes,

requires carriers.

And those carriers often are bound to or include albumin.

And so it’s not the goal to free up all your testosterone,

but getting free testosterone into a range

that works for your particular goals and needs

is an attractive one.

And that’s why we’re discussing these particular tools.

The amounts of boron that people take,

and you can find this again on PubMed or examine,

but people take a couple grams of it a day.

I’m not aware of any specific side effects,

but you always, always, always want to examine

for the particular side effects.

And people with different backgrounds and conditions,

as we talked about for menopause and estrogen,

have to be careful

because when you’re starting to modulate hormones,

you’re starting to modulate not just the tissues

that thrive on binding of those hormones,

but remember, the reason why there’s so much breast cancer,

and there’s a reason why there’s so much testicular cancer

is that any tissue that undergoes rapid reproduction

of particular cells.

So there’s a lot of reproduction of cells

and shedding of uterine lining

and the reproduction of cells and eggs in the ovary.

And in the testes, there’s the production

of Lydig and Sertoli cells.

And there’s this kind of ongoing production of sperm.

That’s why those tissues are particularly vulnerable

to the development of cancers.

And many of those cancers are androgen sensitive.

That’s why one of the major treatments

for prostate overgrowth or prostate cancer

is to give anti-androgenic drugs, okay?

It’s not just a shutdown,

all things related to being androgenized.

It’s really about trying to prevent testosterone

from encouraging growth of tumors.

So I want to really emphasize the caution there

because it’s easy when thinking about optimizing estrogen

and testosterone to just think, oh, more is better.

More is definitely not better.

And it’s not just because they can aromatize

or convert into other things.

It’s because cancers or any tissue

that has a lot of turnover of cells

is going to thrive on androgen,

anything that promotes growth.

It’s going to thrive on estrogen.

Remember, brain tissue doesn’t turn over that much.

There isn’t really much production of new neurons.

Brain cancers happen, but they’re kind of rare.

And when they do happen, they tend to be glial cells,

which have a lot of proliferation.

Glial cells can proliferate.

Adult neurons don’t create more themselves.

They don’t create more neurons in general,

except in a few places in the brain and body.

So any tissue that recycles itself is prone to cancers

and those tissues thrive on androgens and estrogens

to create more tumors.

So you have to be careful

anytime you’re modulating hormones,

especially androgens and estrogens.

And in my scouring of the literature

and looking at kind of what’s out there

and what people are talking about,

and I also mean in the scientific literature,

one of the things that is new to me anyway,

probably not new to a lot of the gym rats out there,

but, or the people that spend a lot of time

on YouTube videos talking about androgens,

are these, forgive me for butchering the name.

Again, are these ectosteroids.

So ectosteroids are molecules

that come from things like spinach, believe it or not,

that have a lot of similarity to the cholesterol molecule.

The one that’s being discussed a lot out there right now

is something called turkosterone.

I wish I knew why it was called turkosterone.

Someone tell me why it’s called turkosterone.

Does it have anything to do with turkeys?

I don’t know why it’s called turkosterone.

Perhaps someone will know.

In any case, these ectosteroids

are similar enough to cholesterol.

Remember, cholesterol is the precursor

to testosterone, cortisol, and estrogen.

And it appears that some of these ectosteroids

do have bioavailability,

or their metabolites are bioavailable.

And this was something that for many years,

people talked about whether or not insect hormones

or hormones from other species

could actually be used by humans,

or whether or not it would have any effect at all.

And it’s pretty clear based on a study

that I was able to find.

There’s a paper that came out in 2019.

It’s a comparative study in the Archives of Toxicology.

This is Eisenmann et al, I-S-E-N-M-A-N-N et al,

that talks about the ectosteroids

and was given in conjunction with strength training

or no strength training.

This is a 10-week intervention.

And their conclusion is that these ectosteroids

had a fairly significant, above placebo controls,

increases in muscle mass, strength, hypertrophy effects,

all the sorts of things that one would expect

with increases in androgen.

Their conclusion of this study is not my conclusion,

although I may or may not agree with them.

This isn’t about my opinions.

It’s just, I want to be clear.

These are their words, not mine.

But they say that, in their words,

our results strongly suggest the inclusion of ectosteroids

in the list of prohibitive substances.

So they’re saying these things are so powerful

that they should be on the list of banned substances,

which might be upsetting to some,

or some of you might be thinking, well, who cares?

The whole issue of augmenting hormones in sport

is a very interesting issue.

In fact, if you just want a little anecdote about that,

I can’t reveal names here, of course,

but what I learned recently was very surprising to me,

which is that many athletes in pro sports

are taking testosterone,

and they are able to do that legally,

not just because it’s available by prescription,

but they are allowed to do that

under the rules of their sport,

in the fine print that no one, including me, had ever seen,

if they’ve had an injury.

So if athletes are injured,

then it opens up the door for certain forms

of testosterone augmentation

and other types of augmentations

that are not available to them if they’re not injured,

which always makes me wonder now

when I see them getting injured,

whether or not that’s an attempt to get some of the support,

because there’s absolutely no question

that estrogens and testosterones

modulate gene expression, modulate strength,

modulate the way the brain works,

modulates our relationship to effort and anxiety, et cetera.

And while we’re talking about supplementation,

the effects of supplementation,

I would say in some individuals can be quite dramatic,

but they’re always, always, always,

except in extreme cases, going to be far subtler,

excuse me, far more subtle, to use the proper English,

far more subtle than would be, for instance,

just in injecting testosterone

or injecting estrogen, et cetera.

So I think we should just be honest and upfront about that.

So thus far, in terms of talking about optimizing hormones

and in the discussion of supplementation,

I haven’t really talked about things

that actually affect the brain directly,

that increase the pituitary output and things of that sort.

We’ve mainly been talking about things

that free up testosterone or that increase estrogen

at the level of the periphery.

But if you remember way back

to the beginning of this episode,

hormones are made in different locations in the body,

and there are hormones that promote the release

and the production of hormones

from other tissues in the body.

And one of the main hormones for that is luteinizing hormone.

Luteinizing hormone, again,

comes from the pituitary, circulates,

and either goes to the ovary

to promote various aspects of egg maturation,

as well as production of estrogen,

and to the testes to promote testosterone

and sperm production.

And the prescription version

of increasing luteinizing hormone

is something called HCG or human chorionic gonadotropin,

which has been synthesized

and is now available as a prescription drug.

It’s taken in various contexts for increasing fertility,

both by males and by females.

It can increase for all the reasons that now make sense.

It can increase sperm production.

It can produce ovulation frequency.

It can produce the number of eggs,

even, that are deployed in a given ovulation,

although that’s not always a good thing.

It basically is pro-fertility, pro-testosterone,

pro-estrogen, depending on your background.

And what’s interesting is HCG was initially synthesized,

collected and synthesized from pregnant women’s urine.

And believe it or not, before it was synthetically made

and sold as a prescription drug,

there was actually a black market

for pregnant women’s urine,

where people would buy the urine.

I don’t know.

I’m guessing that they probably just consumed it,

which is weird.

But in any case, human chorionic gonadotropin

is now available as a prescription drug.

And it’s one of the things that many people use

to increase testosterone or estrogen

for increasing fertility.

In some cases, I think it’s used

to increase sports performance,

or when people have shut down their gonads

for whatever reason, because of excessive hormone therapies,

or they have some sort of,

sometimes they’re actually lesions to the pituitary.

Sometimes people have a tumor in the pituitary.

It’s actually not common,

but among brain tumors and neural tumors,

it’s one of the more common ones.

And then you get deficiencies in LH and FSH.

And so people will take HCG to stimulate the gonads.

So there are a variety of reasons

why these drugs were created.

But there are certain supplements,

not many, that apparently can increase luteinizing hormone

and thereby can increase testosterone and estrogen.

And one of the more well-documented ones

is phadogia agrestis, that’s F-A-D-O-G-I-A,

separate word, A-G-R-E-S-T-I-S,

which, at least according to the literature,

that I was able to find,

can increase levels of luteinizing hormone

and thereby levels of testosterone or levels of estrogen.

And again, if an individual were to take phadogia agrestis,

what they would probably find is that

testosterone and estrogen would increase

in anyone of any chromosomal or gonadal background,

but remember, it’s the ratio of both.

So both, if someone has low estrogen, high testosterone,

let’s say they have testes, just by way of example,

then both of those would be expected to increase.

And if someone has high estrogen and low testosterone,

and let’s just say has ovaries,

then both of those would increase

by taking phadogia agrestis.

The side effect profile of phadogia agrestis

hasn’t really been documented, so it’s a little unclear.

I just want to emphasize that

anytime someone’s going to start taking supplements

or modifying sex steroid hormones,

getting blood work done is extremely important

for safety reasons,

and also just to know whether or not things are working.

And because all of these things

are subject to negative feedback,

talked about this previously, previous episode,

but if testosterone goes high or too high,

it can feed back and shut down luteinizing hormone,

which will then shut down further testosterone production.

Likewise, if estrogens are going too high

or they’re going too high at various phases of the cycle,

that can start to throw off various other hormones,

including FSH, progesterone, LH.

The menstrual cycle itself

is a just absolutely exquisite balance

of feedback of luteinizing hormone kept low and constant,

at least for the first 14 days of the cycle.

Then mid-cycle, there’s a peak,

and that’s typically when ovulation occurs.

That’s why pregnancy is most likely

during the middle of the 28-day cycle.

FSH kind of goes up and then down across the first 14 days.

So taking anything or really modifying one’s estrogens

or testosterone on that background of the menstrual cycle

is really going to disrupt the way those things interact,

and it’s just such an exquisite feedback loop.

So I’m not saying don’t do that,

but you definitely want to be aware of what you’re doing.

And blood draws are one way to do that.

Monitoring cycles for ovulating females

is another way to do that.

And in males, having a good window

into what’s going on with testosterone,

DHT, aromatase, estradiol, LH, et cetera, is just vital.

And it’s really part and parcel

with the practice of thinking about optimizing

these incredible things that we call sextroid hormones,

estrogen, and testosterone, and their derivatives.

The list of supplements and molecules

that can adjust estrogen and testosterone is vast,

and I only touched on a few of these.

I really tried to emphasize the ones

for which there are human studies

or that have mostly human studies,

or maybe even just one human study.

There are other things out there

for which there are scientific data,

things like bulbine natalensis,

which definitely has support for increasing testosterone,

but all the studies were in rats.

I think there is some evidence in humans,

but the evidence mainly comes in the form

of what we call sponsored research,

so companies paying for research,

which is different than independent research

by people who are not biased in terms of the outcome.

And the reason I didn’t throw out things

like bulbine natalensis is they seem

to have liver toxicity,

similar to high levels of anabolic exogenous steroids.

There’s some problems associated with them

that make them important to think about

if you’re curious about this area and the endocrinology,

but also somewhat precarious.

And that’s one category,

so stuff that doesn’t have a lot of evidence in humans

might actually be dangerous.

The other category of things that has been shown

to improve or levels of, or increase, I should say,

I don’t want to say improve,

because it’s up to you whether or not you want to increase

or decrease estrogen and testosterone,

that’s highly individual, how could I know,

are the things that are kind of housekeeping

for production of estrogen and testosterone,

things like magnesium, things like D3, things like zinc.

Those are the things that are going

to create an overall milieu of opportunity

to produce normal endogenous levels

rather than increasing endogenous levels further.

And so I really want to highlight

that there’s a difference between taking something

to create a kind of backdrop of general support

and taking something that’s going to create a big inflection

in the levels of a given hormone.

So once again,

we covered a tremendous amount of information.

We covered some basic science of hormones and pheromones,

estrogen and testosterone and their derivatives.

We talked about supplementation and behaviors,

competition and parenting,

and how all these things interact.

And I hope that you’ll come away from this

with a deeper mechanistic understanding

of how the brain and body are interacting

to control the output and the ways

in which these incredible things

that we call sex steroid hormones work and influence us.

I hope you’ll also come away with some ideas

of things that you can do in particular behavioral practices

that can improve sleep and your relationship

to light, et cetera,

because those things really set the foundation,

not just for healthy steroid hormone output,

but for all sorts of health effects

and for both the psychology

and the biology of your nervous system.

So I’m sure there’ll be many questions.

There are many things that I couldn’t get to today.

I do try and limit these episodes to about 90 minutes,

which is the optimal ultradian cycle for learning.

It’s a lot of information,

but we’ve timestamped everything for you.

So feel free to look over it in parts or circle back

where you might want deeper understanding.

And please put your questions in the comment section below.

Please put suggestions for future episodes

and things that relate to hormones

in the comment section below.

We do look at those and we do use them

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In closing, I hope you’ll leave today’s episode

with a much richer understanding of the mechanisms

that control the endocrine and nervous system

in the context of estrogen and testosterone,

as well as take away various tools

that you might choose to apply.

And next week, we’ll be back with another episode

about the role of hormones

and its important interactions with the nervous system.

And that will, of course,

include both mechanisms and tools as well.

And as always, thank you for your interest in science.

And as always, thank you for your interest in science.