Huberman Lab - How to Optimize Testosterone & Estrogen
Episode Date: April 12, 2021In this episode, I discuss testosterone and estrogen hormones and how they impact the brain, body, and behavior after puberty. I also discuss how various behaviors such as exercise (resistance and end...urance training) and sex or observing sex impact these hormones and their levels. I ask: "what specifically is it about such activities that impact testosterone and estrogen?"; the resounding theme is that when our nervous system is activated in particular ways, it drives our endocrine system and vascular system to activate or repress certain hormone networks in predictable ways. I also discuss peer-reviewed studies and protocols addressing (at a mechanistic level) how light, cold and heat, and respiration (breathing) can positively or negatively impact testosterone and estrogen. We discuss specific supplements and compounds that peer-reviewed studies illustrate can adjust testosterone and estrogen levels by changing their binding to other proteins, raising them directly, or changing other hormones released from the brain and pituitary. I discuss optimization in the normal reference ranges for these hormones, and I discuss pheromones, apnea, menstrual cycles, menopause and andropause. For the full show notes, visit hubermanlab.com. Thank you to our sponsors AG1 (Athletic Greens): https://athleticgreens.com/huberman LMNT: https://drinklmnt.com/huberman Supplements from Momentous https://www.livemomentous.com/huberman Timestamps (00:00:00) Introduction (00:00:26) Sponsors: AG1, LMNT (00:05:50) Hormone Optimization (00:07:00) Salutogenesis: A Powerful Way to Conceptualize Health (00:10:03) Estrogen and Testosterone: Sources, Levels and Ratios (00:15:46) The Power of Competition, Plus: Anxiety, Persistence and Dopamine (00:20:58) Testosterone and Libido Pre-Ovulation (00:21:48) Estrogen and Sexual Receptivity; Libido In Males (00:23:10) How Sex Behavior Impacts Testosterone: Observing vs. Actual vs. Abstinence (00:26:46) Testosterone and Prolactin: Sex Seeking vs Pair Bonding (00:27:30) DHEA (dehydroepiandrosterone): Effects on Levels/Ratios (00:28:45) Behaviors That Decrease Testosterone (and Cortisol): Parenting and Prolactin (00:31:24) How Illness Impacts Testosterone and Estrogen: Cytokines, e.g., IL-6 (00:33:20) How Exactly Do Behaviors Change Hormones? (00:34:18) Pheromones: Miscarriage, Menstrual Cycles, Puberty Onset, and Mate Recognition (00:43:33) Apnea: A Powerful Bi-Directional Influence On Estrogen and Testosterone (00:47:44) Mouth vs. Nose Breathing and Hormone Levels: Effects Via Sleep and Direct Effects (00:51:11) How Sleep Adjusts Cortisol/Testosterone and Cortisol/Estrogen Ratios (00:53:49) 02:CO2 Ratios, Nasal Breathing During Exercise (00:56:30) Light Viewing Patterns and Hormones: Dopamine, GnRH (00:57:44) Spring Fever: Tyrosinase, Hair Color, Mating Frequency (01:04:39) Specificity of Hormone Effects (01:06:03) Temperature: Cold and Hot Gonads (01:14:10) How To Exercise: Types, Effort Level, Sequencing (01:21:42) Cardio/Endurance vs. Resistance Training (First or Last?) Yes, It Matters (01:24:41) Estrogen and Menopause: Compounds That May Ameliorate/Reverse Symptoms (01:33:18) Nutrients That Optimize The Foundation For Hormones (01:36:00) Opioids as Severe Hormone Disruptors (01:37:23) Testes, Antlers and Ovaries (01:38:50) Creatine and Increasing DHT (Dihydrotestosterone) (01:40:14) Free and Bound Testosterone: SHBG (Sex Hormone Binding Globulin), Tongat Ali (01:43:23) Nettles, Prostate, Boron, and Blood Brain Barrier (01:45:27) Hormone Related Cancers: Sometimes Reducing Estrogen and Testosterone Is Optimal (01:47:43) Ecdysteroids: Mimic Mammalian Hormones (01:51:50) Optimizing Brain Hormones: Chorionic Gonadotropin, Fadogia Agrestis (01:57:18) Additional Compounds, Liver Toxicity, Overall Milieu (01:59:17) Summary: And Note About Additional Related Topic Coverage Coming Title Card Photo Credit: Mike Blabac Disclaimer
Transcript
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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.
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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 Hubertman 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.
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 saluda
genesis. 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.
Saluteogenesis 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, etc. in order to promote well-being above
where you would be if you were not doing those behaviors. If you think about
these two things, saluted genesis 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 saluteogenesis 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, saluteogenesis 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, etc. and to move away from
sickness, as well as the saluteogenic 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 saluteogenic model.
But I found it very interesting to know
that within the field of alopathic medicine,
these two models exist,
but we don't hear about the saluteogenic 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 Alia Crums 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 well-being
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'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 well-being,
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 ratios of testosterone in estrogen in really powerful ways.
So we're gonna cover all of that.
I wanna 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 gonna talk about howabolic 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 gonna talk about today
are the aromatases, mainly.
The aromatases convert testosterone indestrogen.
So, in a male, for instance, that has very high testosterone,
some of that is going to be converted indestrogen
by aromatase.
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.
I'll be at it at low levels.
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.
It actually occurs within individuals across the lifespan.
I'm not going to throw out specific numbers of X-peakograms, per desoleter, et cetera,
today, because that's going to vary a lot.
It's going to depend on whether or not you're measuring in peograms 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 pre-pubescent
females make very little estrogen. And when we talk about estrogen, we mainly talk about
estrogen dial, which is the most active form of estrogen in both males and females.
So pre-pubescent females, very low levels of estrogen.
During puberty, levels of estrogen,
aka estradial, basically skyrocket.
And then across the lifespan,
estrogen is gonna 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 postmenopause 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 testosterone levels.
There's actually a lot of examples of men in their 90s, 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 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.
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.
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, you know,
viralization 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, you know, 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 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. 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 Androgen such as testosterone
are feeding back to encourage more competitive type behaviors. Because every species, whether
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 wanna 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 gonadol 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 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 hyper-androgenized individuals, meaning people that have very high levels
of Androgen, will have very high levels of libido.
And they will provide 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 active 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 Eskasa et al.
ESCA, 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, is one of the questions I get most often
in the comments on YouTube, I don't know why that is, Now, the question that I often get, in fact, is 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 addressed 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. We're gonna talk about pheromones in a
moment. A few years ago there was a lot of excitement about the hormone DHA, 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. DHA 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 a body fat, if you take DHA, 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 DHA 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 DHA, it's a kind of global
promoter of the sex-steroid hormones and its specific effects are going to bend 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 apparent.
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 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.
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 gonna drop,
prolactin is gonna increase,
estradiol is gonna 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 am definitely not promoting the idea that fathers or mothers take time away from their offspring
in order to keep their testosterone levels higher 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 biases 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
will 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 into 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 to testosterone levels so dramatically
or estradiolive levels so dramatically.
What is it?
Is it the sweat of the baby? Is it 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, our 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 and humans that are well-established. So the main ones in animals that are discussed
are called the Leiboute effect, the Witten effect,
the Bruce effect, and the Vandenberg effect, named after the people that discovered them.
The Leibhut effect is when you house females of a given species together with no males,
they start displaying longer what are called estrus cycles.
In many species, they don't have menstrual cycles, which are 28 days, they have estrus cycles,
which tend to be four days 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, I 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 fair amount of fact that mirrors this
reboot 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,
or because these are animals, they're litter 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 ester 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're 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
McClendton, which was getting at this question of synchronization of menstrual cycles. Now,
and McClendon, 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 with 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 McClendon.
What they did actually was they took females,
they charted their cycles.
And then they had other females where pads in their armpits and they collected sweat
from those females and then they took the sweat from those pads and 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.
It'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 down 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 condavors, 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 review, wine tasers, I never can pronounce this.
What are they called, sommelier, sommelier, whatever.
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 vomeronazole 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 long-time 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 pheromones or smells, are impacting hormones and our ability to attach memories and recognition of mates
and other people, including our children, not just our mates.
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 Flemmin response.
During the mating season for different animals, you can actually even see this in horses,
but for animals that are seasonal mators,
they'll do something called the Flemmin Response,
where they actually open their lips and their mouth,
and they expose their gums,
so that they can capture fair mones
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 punitive 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 build-up 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 build up 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 innovate 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.
Now, you have 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 side. People who are dramatically overweight also suffer
a lot from apnea during sleep. There's actually a lot of build up 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 Hubert
Moon Lab podcast.
Please check out those episodes if you have sleep issues or you want to work on your sleep.
Also check out Matt Walker's trifit 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 Conn and Paul Erlich, who are both faculty at Stanford, has 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 in 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 test, in the testicle that the Certoli cells and the Lytex 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 and males and in
proper estrogen to testosterone ratios and 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 build up 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
and 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 Nester 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 snores 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 for because of my job as a neuroscientist
of held a lot of skulls, taking a lot of brains out of a lot of skulls, teaching her anatomy
and done that for goodness. I know how many species have done that for including human.
But what the sinuses are is they're actually what you've got are you 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 in your sinuses or stuffed up, you feel like you have congestion
here and here and around your ears and in your cheeks and in your face.
That's because the sinuses are actually portals where the bones are fused together and
are 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 gonna get giant nostrils.
But what's gonna end up happening
is you're gonna 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. 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, that kind of thing.
You know, 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. It 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,
nasal 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, takes a little effort, but it's zero cost and it has all these positive effects across the board
You know both cosmetic and in sleep and hormonal etc
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
Have you 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
story hormones do when they're available in your body and 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 mustolids, like ferrets and hermons, 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 storied hormones
estrogen into 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 come which is a amino acid comes from food and when dopamine levels are high as I mentioned before
There's a tendency for more
Ganatotropin 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 tyrosine
ace and 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.
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 effect of 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, etc.
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 well-being, social interactions, reductions in 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.
The simple protocols for that I've reviewed before, but it means getting anywhere from
two to ten 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 in 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. So you can't even begin to talk about supplements and other ways to optimize testosterone,
diet and it's effects on testosterone and estrogen
and fertility and reproductive behavior, etc.
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, 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
in 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 days are longer nights are shorter, in general 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,
because of the role of dopamine in promoting a 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 breeding 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.
Just still have libido and still have skin elasticity, but also walk around with saran wraps,
and 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 their 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.
You can 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 start off in your nose, migrate into the hypothalamus.
Those neurons extend processes.
We call them axons into the pituitary and release GNons, into the pituitary and release GNRH into the
pituitary. There's a lot of ascolarization 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 what we discussed 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 we, 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 method section of these
papers. But when we want to shut down neurons, we can do things like inject drugs that will
do that like lid 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 you know,
one to ten 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
hypervezodilation 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.
It's actually a whole set of pseudo science, uh,
web pages out there saying, well, if you want a girl, you should, you know,
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 sperm production or for sperm health.
Spirum 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, 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 that episode testosterone can have numerous
positive effects in both males and females provided they're an optimal range.
So if you look on the web, people 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?
Like 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, you know, 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, right? 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 are 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 be 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 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 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 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.
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.
It's, 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 into testosterone.
I'm sure there are a bunch of exercise jockeys out there that are going to 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 Ratamess, R-A-T-A-M-E-S-S, at all, which was published in 2005, which
talks about modulations in Android and Receptor content after a heavy resistance exercise
looks at going to failure, not to failure.
The work of a scaredo at all, 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. 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.
It has probably something to do with smell and pheromones, although I'm sure there are other
cues as well.
But there's clearly an 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, etc. 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 released directly, presumably testosterone
released directly and sensitivity of the receptors. That's what most of the muscle physiology
studies that I was able to find point two.
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
angrogen 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 cardiotype 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, are 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 and hex, it's in 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 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
antigens that are quite high, even as similar as they were in puberty in their teen years
and 20s, well into their 60s, 70s and 80s, if they're optimizing a lot of other things,
and probably genetic 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 tomoxifen
and an astrozole 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'm a professor, 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, but I won't go into all of them, but some of the proestrogenic 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 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 cohoch,
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 is 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, you know, six plus months, their 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 look specifically at women that were clinically obese or overweight,
although not always. The subject size pools are pretty big, you know, anywhere from, you know, 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 cohe can have a modest effect
in improving menopause symptoms.
The other one is Panax Jinseng.
So PNA-AX Jinseng 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
Valoriana, officionalis,
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 Puraria, Mirif Mirifika.
So I'm going to spell this out for you.
It's P-U-E-R-A-R-I-A, Puraria, M-R-E-F-E-K-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,
you look again that 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 piraria,
mereraphica, which is also called,
and now this is really hard to pronounce,
quau kuru kau, I guess that's the name that they use
in various countries, that it was comparable
to estrogen replacement therapy.
So I mentioned this because a lot of people contact 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 storied 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, etc.
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's, it looks to me like, we're ZoSick, but it's WRZOS EK. I hope I
didn't butcher that too badly. We're ZoSick at all, 2020 in Endocrinology and Metabolism Review.
So there's a recent paper and a good peer review journal. It talks mainly about how the hypothalamic pituitary adrenal axis and the sex-storyed 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 in getting blood
work done because that's how you know whether or not your androgen levels as well as things
like vitamin D levels, etc. 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.
Got a comascia, male breast development in males, disruptions to the ovary and females.
It's really a quite terrible situation.
So excessive opioids are very problematic for sex storied 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 to 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.
This range is 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
so you can actually buy ground up testes from cows.
And you can actually buy ground up testes from cows.
And you can consume those. And a lot of that's gonna 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
or that long ago as a specific hormone molecule
and characterized and then re- recynthesized, 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 five alpha reductase or makes the testosterone molecule more susceptible
to certain enzymatic reactions that leads to increases in DHT. DHT, Dihadur testosterone,
as I mentioned 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, etc.
And beyond infancy and early childhood and later in life, it has powerful effects in creating
balding, in beard growth, etc.
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.
It does creatine cause baldness.
It's going to depend.
It's going to depend on how much five 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 a 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 121600 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 wanna 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 globulons work.
Remember these binding globulons aren't there
to soak up all your test
osterone just to make it hard for you to free up test
osterone and, you know, make gains in the gym or whatever it is,
where I have increases in libido.
They're there to actually transport test
osterone 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 shuddling testosterone to the proper tissues
in 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,
it's hard to pronounce but
Erie coma
Longifolia Jack they always seem to have these names that kind of
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 exama.com
or you can go to PubMed if you like.
I've looked at these,
that it does seem to have some profertility,
pro free testosterone and subtle AfroDGiacFX.
It does also seem to be a slight antestrogen.
So the reports of this,
people take this anywhere from 400 day
100 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 test
osterone 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 that's some, if it increasing free testosterone
or something that you're interested in doing.
Examined.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 nettles also having some
fairly potent effects on the prostate and on the liver.
So it might be a tricky molecule, maybe not an attractive one for people to take.
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, how can 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 need 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 into the brain.
And there is this thing called the blood brain barrier, which is fascinating and deserving
of an entire episode also.
And getting molecules across the blood brain barrier, even if they're sex steroid hormones, which are lipophilic and capacitive 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 in 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, you know, 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 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 lidig
and serotonly 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.
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, you know, 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 when any time you're modulating hormones,
especially androgens and Estrogens.
And in my scouring of the literature
and looking at 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 Turkesteroan.
I wish I knew why it was called Turkesteroan.
Someone tell me why it's called Turkesteroan.
Does anything do with turkeys?
I don't know why it's called Turkesteroan.
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 that it's a comparative study in the archives of toxicology.
This is ice and men at all, ISE and M-A, and N at all, 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 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, quote, our results strongly suggest the inclusion of
ectosterone 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 estrogen and testosterone
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 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.
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 gonatotropin, 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
and in a given ovulation,
although that's not always a good thing.
It basically is profertility,
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-chorianic and atrobin 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.
Some cases, I think, it's used to increase sports performance or when people have shut down their
their gonads
for whatever reason because of excessive hormone therapies or they have
Some sort of sometimes there are actually lesions that 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 Fedogia Agrestus.
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 Fedodogia agressis, what they would probably find
is that testosterone and estrogen would increase in any one 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 should, it would be expected to increase.
And if someone has high estrogen and low testosterone, and and let's just say has ovaries, then both of those would increase by taking
phedogioagrestis. The side effect profile of phedogioagrestis 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 that or modifying sex-storyd hormones, getting blood work done is extremely important. It 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,
talk 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 for the 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 feed back of lute-lute-lute-nizing
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 sex-steroid 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 bullbine 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 is 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 bull-buy, 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 you know, 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 in 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, etc., 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 will 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,
I'll trade in 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. Please put suggestions for future episodes and things that relate to
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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.