The Science of Healthy Hair, Hair Loss and How to Regrow Hair | Huberman Lab Podcast

ANDREW HUBERMAN: Welcome to the Huberman Lab podcast,

where we discuss science and science -based tools for everyday life.

[MUSIC PLAYING]

I'm Andrew Huberman, and I'm a professor of neurobiology

and ophthalmology at Stanford School of Medicine.

Today, we are discussing hair.

Hair is a topic that occupies the minds of many people.

There are people that are losing their

hair and want to halt or reverse that loss of hair.

Today, we will talk about all the ways

that science has taught us we can slow or even reverse hair loss.

I confess that researching today's topic

was a particular joy for me not because I'm obsessed with hair,

mine or the hair of others, but because hair turns out to be

fascinating from the perspective of cellular biology and stem cells,

which is a topic that I've long been interested in and that for much

of my career I focused on in the context of development.

When your brain and your nervous system develop, it develops from a small batch

of cells that turns into many trillions of cells.

It does that by cell replication, something that we call the cell cycle.

We'll talk a little bit about this and so-called mitosis today.

I promise not to get into too much detail.

But what makes hair so very interesting from a biological standpoint is that every

hair, every single individual strand of hair has its own little stem cell

niche, meaning its own little pocket down there in the follicle in which specific

stem cells give rise to those hairs for different durations of time,

depending on the hair, where it is on your body, et cetera.

For instance, the hairs on your head will

undergo ongoing growth for 4-6 or even 8 years.

Were you to not cut your hair, it would continue to grow.

One single hair would continue to grow.

I guess we could say all the hairs will continue to grow for up to 8 years.

That is very different from, for instance, your eyebrows, which have a much shorter

period of hair growth lasting on the order of months.

That's why you don't see people with eyebrows that extend down to their waist.

But you can see people with hair on their

head that extends down to their waist if they don't cut it.

Now, that discrepancy illustrates for us

just how incredible hair follicles and the stem cells that reside within

hairs are and their enormous potential to give rise to these things that we call

hairs, which are simply proteins of varying length.

Today, we are going to address what

determines the length of a hair or rather what determines how long a hair continues

to grow before it ceases growing and eventually falls out.

We're going to talk about what regulates those stem cells,

what allows them to continue to produce hair or cease producing hair.

As we do that,

you will learn all the biology in clear, simple terms,

regardless of your background, that will really set the stage

for understanding what we'll also talk about, which is how to slow hair loss or

halt hair loss entirely or even reverse hair loss.

We will talk about hormone -related hair loss in both men and women.

We will talk about some of the mechanical

and stress -related influences on hair loss.

We will talk about the chemical

and mechanical approaches to halting and reversing hair loss,

everything from minoxidil to dutasteride to ketoconazole

to microneedling to thyroid, estrogen, IGF-1 pathways.

Again, all made very clear regardless

of whether or not you have a background in biology or not.

I will also dispel some of the common myths about balding and hair replacement.

If you've heard, for instance, that you inherit your patterns of balding

from your mother's father, that is not true.

Although it is true that you do inherit certain genes that influence whether or

not you have a predisposition to balding in particular parts of your head,

and believe it or not, even in particular parts of your body.

But it is not the case that you can simply

find a photo of your mother's father, say, age 50, or age 60 or 75,

and determine whether or not you'll have the exact same pattern of hair loss.

That's a myth that I'd like to dispel right here and now.

I will dispel some of the other myths

about hair loss, hair replacement, and hair regrowth as well.

Before we begin, I'd like to emphasize

that this podcast is separate from my teaching and research roles at Stanford.

It is, however,

part of my desire and effort to bring zero cost to consumer information about science

and science-related tools to the general public.

In keeping with that theme, I'd like to thank the sponsors of today's podcast.

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Okay, let's talk about hair.

In researching this episode by talking

to experts in the biology of hair, and the stem cells that exist in all of us

that give rise to our hair growth, and the pigmentation in our hair,

and in talking to experts who understand how to halt and even reverse hair loss,

that there is a tremendously interesting biology surrounding hair.

But there's also an incredible psychology around hair.

In fact, most people who experience even

marginal hair loss undergo pretty severe anxiety.

Now, I confess this is not something I can relate to.

I am losing my hair in certain places.

I'm 47 years old.

I've got a couple of patches up front where there's very minimal hair.

I think that, as we'll later learn in this

episode, reflects a higher density of DHT, dihydrotestosterone, receptors

at that particular location as opposed to elsewhere in my scalp.

But keeping my hair is not something that I've fretted about much of my life.

Yet as I was researching this episode, I remembered an anecdote from my childhood

where my father told me, and I think it was because I was stressing

about something, I was trying to get to sleep, and he said,

"Don't stress . Calm down." And here's why.

If you stress too much, it can actually make your hair fall out.

In fact, I have a cousin who lay down one night stressed,

and woke up the next morning , and all of his hair was on his pillow.

I'll never forget that story.

I think he was trying to get me to stress less.

I don't know if that story made me stress less or not.

But in any event, I don't know that that story is true.

I'm not going to challenge the authenticity of that story.

I didn't have a chance to reach out to my father and ask him to verify or not.

But as we will soon learn,

it is true that our psychological well-being can impact both the coloration

,, or lack thereof and the growth rates of our hair.

That's a real thing.

The reverse is also true,

which is that as hair starts to thin, or fall out, or change color,

many people expect intense anxiety or even depression.

This was not something I was really aware of.

Perhaps that's just because I've always kept my hair pretty short anyway.

I always assumed that if my hair started

to really fall out, I would just shaved my head.

But that's me, and that's not most people out there.

I think most people would loathe to lose their hair.

In fact, given the enormous number,

probably up in the high billions of dollars and euros and other currency,

of course, that people invest in trying to halt or reverse their hair loss,

it's clear that hair is very important to people.

What we know is that by age 50, approximately 50% of all men and women

will have experienced significant enough hair loss that they start to notice it.

And a large percentage,

up to 85% of those people will experience some anxiety that leads them to go out

and try and either halt or reverse that hair loss.

Now, why at age 50?

Well, an important point arises from that, which is that the hair loss is not

occurring between the 49th and 50th birthday.

Hair loss is ongoing from about age 30 to age 50.

It's only by age 50, however,

that about 50% of people out there start to notice that hair loss.

This is typically because

they'll be in a bathroom or looking in a mirror and the lighting will be

bright enough that it permeates the outer boundary of their hair.

They'll notice that their hair is thinning in a particular location.

That's usually how this thing happens.

Again, our psychological states can impact our patterns of hair growth or loss

and of course, patterns of hair growth, but more typically,

hair loss and hair graying can really impact psychological states.

This is a subject that people take intense interest in.

Today, we're going to talk about how hair

normally grows, why it grows at the rate , and for the duration that it happens to.

Then as we talk about ways to intervene with that hair loss,

those biological mechanisms will come up because they really provide a nice

framework for explaining why certain treatments work more or less well or why

certain treatments might have certain side effects or total lack of side effects.

It will also highlight a really key theme

that will come up several times in today's podcast, which is that there are both

mechanical and chemical approaches to slowing and reversing hair loss.

Mechanical approaches would be things as

simple as massaging the scalp, but mechanical changes to the scalp can

cause either hair loss or facilitate hair growth.

This is why things like microneedling are

so prominent in the context of trying to reverse hair loss.

But again, there are also chemical

approaches to trying to halt or reverse hair loss.

This relates to the fact that the hair growth itself is strongly regulated

by hormones such as estrogen, thyroid hormone,

insulin-like growth factor, and that other hormones, in particular

the androgens, so things like testosterone,

but mainly it's derivatives like dihydrotestosterone are very much involved

in setting the stage for hair growth by controlling how big or small that pool

of stem cells that gives rise to hair growth is.

If any of the terms I just use are

confusing to you, don't worry, I will make all of those very clear in a moment.

It's actually all pretty straightforward and simple.

I'd like to just start by talking about

what hair is, how it grows, why it stops growing, and why hair normally falls out.

Let's talk about the biology of hair.

In doing so, I also want to talk about stem cells.

Now, keep in mind that when you hear

the word stem cells, you probably, like most people, think about the sorts

of cells that people are getting injected into their face to get rid of wrinkles,

or give them new skin, or to give them more hair if it's

injected in the scalp, or into a joint to repair a joint or a muscle.

Those stem cells are what we call exogenous stem cells.

Exogenous, meaning from outside the body.

The stem cells that we're going to talk about today are so-called endogenous stem

cell, cells that we all make that can give rise to other cells.

That's really the definition of a stem cell.

Stem cells are present in all of us from the very beginning of life.

When sperm meets egg, that cell,

which we think of as the egg, starts to duplicate,

it incorporates the DNA from the sperm and the egg, of course,

starts to duplicate, and then those cells give rise to more

cells and more cells and the ability of all those cells to replicate and create

more cells are because those cells really are stem cells.

Now, at some point we are a completed body plan, as the biologists say.

We end up with a brain, and a spinal cord, and limbs, and fingers, and livers,

and guts, and all the things that we need in order to be a functioning human being.

Even though we're a baby at that time, we haven't grown up,

we have all the bits that we're going to have for our entire life.

At that point, many of the stem cell populations disappear.

For instance, past puberty,

and probably earlier, you don't get many more new brain cells.

You get a few, but you don't get many more new brain cells because the brain doesn't

have many stem cell populations, whereas other organs in your body maintain

little pockets of stem cells, or in some cases, many stem cells that can

give rise to more and more of that tissue across the lifespan.

Hair is one such tissue.

If we take a look at hair, what we find is that, indeed,

there are these things that we call hairs, but there are also stem cells,

and those stem cells are actually what give rise to the hairs that we see

on the head of our scalp or that we see on the surface of our body.

Right off the bat,

you should know that every single hair that you have is there because you have

a stem cell population that is giving rise to that particular hair.

Let's take a step back, or rather,

I should say, let's zoom in on one hair and the stem cell population that gives

rise to that hair, because in doing so, you're going to learn all the different

components that you can tap into if your goal is to halt the loss of hairs or

to replace hairs that have already been lost.

If we were to just zoom in at the level

of one hair, what you would find is that that hair has what typically is

called a hair root, so that's the portion below the skin.

When we say below the skin,

it means that it dives down into a narrow trench, which is in the so-called

epidermis, which is this outer layer of skin.

It also has a shaft.

The shaft is the part that grows out above the skin.

What you see on somebody's head or you see on their arm,

or when you see an eyebrow, you're seeing the shaft of the hair.

The root, of course, goes below the skin.

What most people don't realize, however, is that down at the base of the root,

there's actually a little cave, a little pocket.

If you were to look at this, it would look like a little bulb,

a little round area with a bunch of stuff in it right below the root.

Within that little cave, there are stem cells.

There are populations of cells that have the ability to divide.

We call this mitosis.

It's a process by which cells can actually

divide, and take DNA with them, and then give rise to other cells.

We call those cells that divide and move out, we call those daughter cells.

We call the cells that give rise to them progenitor cells, but they are effectively

stem cells that give rise to these what we call daughter cells.

Those daughter cells then become

the various types of cells that make up the hair.

When you see a hair,

you're not seeing something that grows throughout the lifespan.

You're seeing something that's going to be

born down there in that little cave, then is going to grow.

It's actually going to stack up on top of itself.

That's because hairs are made up of a protein called keratin.

There are a bunch of different kinds

of keratin depending on what kind of hair you're looking at.

But these are little proteins that stack up on top of one another,

and they're structured in a way that makes them pretty darn durable.

I mean, it's possible, of course, to pull a hair out.

But if you've ever tried to tear a hair, in particular,

thick hair like one from the face or even one off the top of your head,

it's actually a pretty tensile strong little thing.

That's because keratins stack up on top

of one another and bind to one another with a really strong bond.

What you end up with is a bunch

of proteins stacked up on top of one another, and that's the actual hair.

We've got the hair shaft, the hair root,

and then we've got the stem cells down there in that pocket that give rise

to the various cells that make up the actual hair.

We also have down there in that little

cave, which, by the way, is actually called the hair bulb,

if you really want to know the technical name because it's shaped like a bulb.

We have not just stem cells, but we have cells that give rise

to the pigment of the hair that create what's called melanin.

Now, some people have very blond hair,

very light hair, some people have darker hair.

But everybody, unless they have what's

called the albino mutation, where the hairs are truly white,

they lack all melanin, and it's a pretty rare condition,

although it does happen, most people have some degree of melanin

in their hairs because there are little pockets of melanin-producing cells.

Melanin is just a protein that essentially

gets injected into the keratin, into the hair, and gives it its darker color.

Now, there are a couple other components

about the hair that you need to know about, especially if you're interested

in reversing hair loss or reversing graying of hair.

One of those components is a little gland.

Next to every hair root within the dermal layer of the skin,

so this is below the epidermis, there is a gland called the sebaceous

gland, and the sebaceous gland makes oily stuff, and the oily stuff is called sebum.

I know the name evokes something gross,

but sebum is actually really cool and really important.

The sebum gets injected, or seeps rather,

into the area right around the hair as the hair starts to approach the surface

where it goes from essentially root to shaft.

The sebum does two things.

First of all, it forms a little bit

of a seal right at the place where the hair exits the skin.

And that seal is very important, actually, for waterproofing of your skin.

So we don't often think of ourselves as waterproof because we are so accustomed

to water just landing on our skin and and rolling off.

But that's because of some of the oily properties of our skin.

Now, it's also true that our skin is pretty densely packed with cells.

But in the absence of sebum, we would not be as waterproof as we are.

Now as I mentioned, sebum has two important properties.

The other important property of sebum is

that it actually is a strong antibacterial and antimicrobial.

Most people don't realize this, the oils of your skin provide a lot

of immune boundary, so that things don't get into the hair

root or the region around it and infect our skin.

So sebum, while the name is sort of unattractive, to be honest,

is actually performing some essential roles both for waterproofing and for our

immune system function, protecting us from various kinds of infection.

We're going to return to sebum later. As it turns out,

sebum is also very important as it relates to psoriasis and as it relates to some

of the fungal components that can cause hair loss.

So I'm just going to file that away.

There's another important component

of the region around hairs, which is the arrector pili muscle.

The arrector pili muscle is a muscle

that lies diagonally between that bulb portion of the hair or a little bit above

it, and goes up to the surface of the skin.

The arrector pili muscle

is a muscle that contracts when we get cold or when we get scared.

So if you've ever had goosebumps, that's because the arrector pili muscle

contracts pulling the skin at the surface down around the little hair follicles,

or at least where the hairs meet the surface of the skin.

And so those little bumps are actually where little micro hairs reside.

And the dimples between them are

the dimples that occur when this arrector pili muscle pulls down.

Now, why would this muscle exist?

It has a couple of important functions.

One of the functions is that when it

pulls down, it causes, as the name suggests, the hairs to stand up.

Maybe not perfectly vertical,

but when you hear, oh, I was so frightened, my hair stood up on end.

And that's because the hair has become erect.

They stand up.

Now, why would this happen when we get cold?

It happens because when the hairs stand

up, air can be trapped between those hairs and can actually warm our body.

This is not so much the case if you have very light hair on your skin.

If you're a very hairy person,

this is going to be a more robust aspect of your physiology.

And yes, this is why dogs like Huskies can go out in the snow and still remain warm.

When they get cold,

their hairs actually stand up a bit on end because of the contraction of these

arrector pili muscle trapping air in there.

And then their body warms the hair trapped beneath the hair.

And it's like they've got a blanket

on made by the interface between the hair, the air, and their skin.

So just to recap all the components

of hair and the different things around it that are going to be relevant

for understanding how to replace hair that's lost.

We have the hair itself, which has the shaft that sticks out over

the skin, goes a little bit into the skin, but basically sticks out over the skin.

We have the root portion which goes down into the skin.

It goes through the epidermis and into the dermis.

Then we have this bulb like region down at the bottom.

Down at the bottom of that bulb, we have stem cells that actually give rise

to the actual hair, and we have pigmented cells that pigment that hair.

In addition, and this is very important, there are capillaries that go

into that bulb region down at the bottom of the hair and that can serve and support

the stem cells, the melanin producing cells, which are called melanocytes.

So the melanin producing cells in the stem

cells get a lot of blood flow that allows them to keep providing new hair or

the proteins that make up hair and the pigment that goes into those hairs

and those little capillaries deliver not just nutrients and things of that sort,

but they also deliver oxygen because it turns out that the whole process

of growing more hair is a very active process.

Now, as soon as you hear oxygen and you

hear that the growth is an active process, that should cue you to why so many

of the stories around how to keep your hair and regrow hair involve statements

like don't wear a hat, it'll make your hair fall out.

Or if you want your hair to grow back,

don't wear hats or massage your scalp or increase blood flow.

Or why some people will suggest

that people take peppermint oil, for instance,

or menthol type oils of different kinds and massage them into the scalp.

Things that make the scalp tingle.

Or there will be light therapies designed to what?

To increase blood flow to the scalp.

The whole rationale there is that you're

trying to increase blood flow to the stem cell and the melanocytes populations

that support the hairs and that actually create the hairs.

Now, whether or not those are approaches work we'll touch on a little bit later.

I'll just give you a little bit of a hint

right now, which is that while no single one of those approaches that I described

is known to regrow hair in a very robust way because of the requirement for oxygen

and nutrients and because it's such an active process for the stem cells

and melanocytes to grow and darken the hairs that grow out of your skin.

It is true that manipulations or treatments that increase blood flow

to those regions can at least slow the loss of hair or can even extend

the duration over which hairs continue to grow.

So if you've heard things like don't wear a hat, if you want to maintain your hair.

Or massage your scalp, if you want your hair to grow faster.

In some sense that's true, but none of those manipulations on their

own is going to robustly enhance the rate of of your hair growth.

Those things are designed to be done

in conjunction with some other treatments that have been shown in many,

many clinical studies to increase the rate and duration of hair growth.

So now you have in mind a picture

of what's happening at the level of individual hairs.

And if you're anything like me, you're probably thinking, Wow,

there's a lot going on down there just below the surface of the skin.

And indeed there is.

But really the things to think about are that stem cell population that actually

give rise to the hair proteins so that actually create the hair.

The melanocytes that darken that hair, that give it pigment.

That sebaceous gland and the oil sebum that provides some important antimicrobial

and other properties to that general region.

And that arrector pili muscle, that arrector pili muscle,

as I mentioned earlier, is important for creating goosebumps

and it's important for keeping Huskies warm in cold environments.

But it's doing some other really important

things as well, and we'll talk about those as time goes on in this episode.

Right now, what I want to do is just talk

for a moment about how hairs actually grow and why they grow the way they do.

This is extremely important toward

understanding hair replacement and slowing hair loss.

There are three basic phases of growth of a hair.

The first phase is the phase

in which the stem cells down in that bulb give rise to the cells that make up

the proteins of the hair, so the actual growth of the hair.

And keep in mind that the hair is actually growing from the bottom up.

Now, you might think, of course, it's growing from the bottom.

Everyone knows that.

But a lot of people think that the hair

starts growing right at the surface of the skin.

That's not the way it works.

The hair is actually growing from deep within the root and stacking up and then

eventually extends out across the top of the skin.

That growth phase is called the anagen phase.

A-N-A-G-E-N.

And this for some people will ring a bell because if you've ever been interested

in weightlifting or even if you're an endurance runner,

you'll hear about things that are anabolic that promote growth, so Anna of Growth.

Or catabolic that promote breakdown.

So the first phase of hair growth is

called the anagen phase, and it's a period of varying duration

depending on which hair in the body we're talking about.

So the anagen or the growth phase

for hairs on the head, as I mentioned earlier, is anywhere from 2 to 8 years.

For most people, it's going to be about six years.

What this means is that if we were to just not cut our hair, just let our hair grow

for 2 to 8 years, that hair would eventually grow

to a length that it was at its maximum and then would stop growing.

So we can say that the anagen phase of hairs on the scalp is 2 to 8 years.

The the duration of the growth phase.

Contrast that, for instance,

with the duration of the anagen phase for hairs of the eyebrows.

The hairs of the eyebrows grow about 4.2mm per month.

Believe it or not, people have measured this thing.

Now that's an average.

So some people are going to have eyebrows that grow much longer per month.

I'm somebody who, for instance, has mostly the same length eyebrow hairs,

but every once in a while I get one of those eyebrow hairs that really seems

to be heading off my head, like really wants out of there.

And so it's much longer than the rest.

What does that mean?

Does it mean that it grew faster?

Maybe.

But chances are the stem cell population in that particular eyebrow follicle

for that one eyebrow hair is longer than it is for the others.

This is really important.

I'm trying to illustrate two principles at once here.

The first principle is that different hairs on your body,

including the hairs on your scalp, have a growth phase of different duration.

This is why the hairs on your head can grow very, very long because they have

a very long anagen or growth phase, and the hairs on your eyebrows will only

grow for a few months before they actually fall out and then have

to undergo replication of the stem cells to give you new eyebrow hair to then grow.

What's important here is not just that there are differences in the duration

of the growth phase, but rather that the rate of hair growth

is not something that tends to differ within a given body region.

You'll hear people say, "Oh,

my hair grows really, really fast." Other people will say, "Oh,

my hair grows really, really slowly.' That is probably not the case.

Well, there could be slight differences in the rate of growth.

That is the addition of more keratin

to the actual hairs, so creation of more hair more quickly.

Almost certainly what's happening is that the duration of the anagen phase

in some people is just much longer than it is in other people.

We don't realize this, and we tend to think more in terms of how

fast hair grows, because if you were to just look

at somebody's hair, you'd say, "Oh, they're all more or less the same length."

I mean, some people's bangs are shorter than the back because they cut them.

But if they were to just grow their hair, you'd say, "Oh, it's all more or less

the same length." But if we were to zoom in with a microscope,

we would see that there are a lot of hairs down there in between the other

hairs that are very, very short or even tiny, tiny, tiny.

Those are coming in as the other ones are finishing their anagen phase.

That's the anagen or growth phase.

After the anagen phase comes the catagen phase.

Again, this resembles the word catabolic or the breakdown phase.

During the catagen phase, the hair is actually receding not

from the top down to the skin surface and then into the root, but the other way.

It's actually receding from that bulb region up toward the surface.

That catagen phase is going to also be

of different duration depending on which area of the body you're in.

It will vary a little bit depending on

who you are, meaning from person to person.

We'll talk about the influences on the anagen and catagen phase in a moment.

Why is it important that it actually recedes from the inside out?

Well, that's important because as it does that, there's actually a change

in that bulb region down below, because normally, there's an interface,

there's a conversation that's occurring between the stem cell population,

the melanocytes, and the hair itself, and they support each other.

Remember, there's blood vessels going

into that area or rather capillaries that are feeding that area as well.

After the catagen phase comes the telogen phase, which means rest.

The telogen phase is a period in which no

new hair proteins are being added by those stem cells.

During that telogen phase,

that bulb down there at the bottom, instead of being nice and oval and really

having a lot of space in it with all these different things like stem cells,

starts to pinch off from the little tube that comes down

from the surface of the skin that normally would have a hair in it.

It starts to pinch off.

At some point, many hair follicles pinch

off that bulb region, and it recedes and dies.

When it recedes and dies,

the stem cell population and the melanocytes go with it.

In other words, there is no longer a population of stem

cells to give rise to more hair after that telogen phase.

There's no longer melanocytes to pigment the hair, and in fact,

the hair isn't there anymore, so there's no hair even to pigment,

after that telogen phase, unless it's a hair of a particular type such as

the hair on your scalp, which can then reenter the cell cycle,

and get back into an anagen phase and regrow more hair from stem cells.

There are three critical stages

of the life cycle of a hair that are relevant to today's conversation.

There's the anagen phase during which the hair grows,

there's the catagen phase during which the hair actually starts to recede and die.

The protein is actually disappearing from the bottom up.

Then we have the telogen phase,

which is the phase in which the stem cell population is what's called a semi

quiescent, semiquiet, or completely quiescent, where it's not active at all.

Those three phases make up the life cycle

of a hair, keeping in mind that for some hairs, they can reenter the life cycle

and go back into the anagen phase, if there's stem cells there,

and if there is oxygen there, and if there is sufficient blood support,

and—and this is a very important and— if there are the appropriate hormonal

signals to support growth, and there is a reduction or an absence

in the hormone signals that actually trigger that telogen phase.

I make this point now because much of the rest of today's discussion is

going to focus on why particular hormones such as dihydrotestosterone cause hair

loss and why inhibiting things like dihydrotestosterone can support

the preservation of hair that you have and the regrowth of hair.

To make a long story very short, and then we'll get into some additional

details that are relevant, and that I hope you'll stick around

to listen to, dihydrotestosterone, which is a derivative of testosterone,

causes changes in that bulb region where the stem cells reside.

It shortens or halt the anagen phase

of hair growth, and it extends and promotes the catagen and telogen phase.

When we hear that, "Oh dihydrotestosterone makes your hair fall

out, or estrogen makes your hair grow," there are real chemical people,

or we should say biochemical legitimate reasons as to why that is.

But it all comes back to this three

phases of hair growth: the anagen growth phase, the catagen,

catabolic or hair loss phase, and the telogen phase,

which is a rest period in which the hairs can either come back,

if it reenters the anagen phase or maybe it's over for good.

Hormones are the accelerator and the brake on each one of those phases.

I'd like to take a quick break

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Now you have in mind the anatomy

of the hair and the area from which it grows, and the stem cells, et cetera.

The fact that there's capillary innervation delivering oxygen and blood

flow to the stem cells that give rise to the hair, and that there are these

three critical phases of hair growth: anagen, catagen, and telogen.

Now, let's talk about the accelerators

on hair growth and the brakes on hair growth.

There are many accelerators on hair

growth, but the first one that I really want to underscore is blood flow itself,

which equates to the delivery of nutrients and oxygen.

This is very important,

and it explains a lot of the treatments for halting and reversing hair loss.

For instance, one of the longest standing

treatments for halting and reversing hair loss is so-called minoxidil.

Minoxidil, sometimes also referred to by the brand name ROGAINE,

was actually a drug that was developed to treat hypertension.

This is a cardiac drug that lowers blood

pressure, and it does that by causing vasodilation.

It allows more blood flow,

not just to the hairs on your scalp, but to hairs everywhere on your body.

Indeed, most people don't realize this,

but minoxidil won't just slow the loss of hair from your scalp,

it is also effective at slowing the loss of hair elsewhere in your body.

How does it do that?

Well, you now know one of the major ways it does that.

It does that by extending the anagen phase, so it basically makes that phase

a bit longer, and does it make it much longer, which is why for most people

who are losing their hair quickly or who have already lost their hair,

minoxidil alone is not going to be a sufficient treatment.

However, minoxidil has been shown to be effective at slowing rates of hair loss

in people that are starting to experience some hair loss.

I'll get into dosages and things

of that sort a little bit later, but right now I just want to really focus

on the logic of why people would take this drug,

which is lowering hypertension at all as it relates to hair loss.

That might seem like crazy until you

understand the anatomy and the growth of hairs, which you now do.

That's what minoxidil is doing.

It's creating more blood flow to the hairs, which because minoxidil

does have this positive effect, at least most people would like to slow

their rates of hair loss on their scalp anyway, it tells you that blood flow

and delivery of oxygen and other nutrients from the blood is pretty

critical, if not very critical, for the support of the hair growth cycle itself.

Now, again, we haven't talked at all about the sorts of chemicals or the signals

within the body, such as hormones that actually direct the growth of hairs.

Here, we're just talking about

a mechanical change, allow more blood flow to the region,

and thereby extend the anagen phase, which is exactly what happens with minoxidil.

Now, minoxidil does have other effects, and this is why dosing of minoxidil

becomes a little bit complicated and can be a little bit tricky to troubleshoot.

It can greatly lower blood pressure or lower blood pressure just a little bit,

depending on how sensitive somebody is to that particular drug.

Oftentimes physicians will start people on Minoxidil dosages that are very low.

Ideally, that would be the case and then ratchet it up in order to figure out

where the minimal effective dose or the critical threshold is beyond which they

start experiencing some pretty uncomfortable side effects,

such as swelling of the ankles or headaches or dizziness.

These things can happen with the use of Rogaine, aka Minoxidil.

Now, Minoxidil has also been associated with increases in the hormone prolactin.

Prolactin is a hormone that's released from the pituitary.

It is a hormone that acts also as a bit of a neurotransmitter, like many hormones,

and it tends to be antagonistic or an opposite to dopamine.

Dopamine is a neurochemical.

It's actually a neuromodulator,

meaning it modulates the activity of a bunch of neural circuits in the brain.

It also controls the release of various hormones in the body.

Dopamine is almost always associated with states of motivation, pursuit, and drive.

It has a little bit of a feel- good

element to it, which is why a lot of people think

dopamine is associated with reward and pleasure.

But it's really about energy, motivation, and drive.

Dopamine and prolactin are,

as I mentioned before, antagonistic to one another.

They're in sort of a push-pull.

People who take Minoxidil, especially if they're very sensitive to it

or they take dosages that are too high, will experience increases in prolactin

that in turn can cause things like reductions in libido,

reductions in overall feelings of well-being, apathy,

and in some cases where the elevations in prolactin are more extreme,

they can experience, for instance, increase in male breast tissue

gynecomastia or even small bits of milk letdown, things of that sort.

In women who take Minoxidil,

the side effects are much like the ones in experienced in men.

So there can be swelling,

edema of the tissues because if you get too much vasodilation

and too, too much lowering of blood pressure, that's not good.

Headaches, dizziness and so on.

Dosing of Minoxidil is really important.

If somebody is going to use Minoxidil

in order to try and slow or reverse hair loss, again, it mainly is going to be used

to slow rates of hair loss, not to actually reverse hair loss.

The really key thing is to get that dosage right.

The ranges of Minoxidil that you'll see

suggested and that people use out there are vast.

I should also mention that there are two

major routes by which people get Minoxidil to the hair follicle.

One is to take it systemically as a pill

where it goes into the general circulation.

The other is to take it topically as a cream.

There are prescription and non-

prescription forms of Minoxidil just to further complicate things.

But the ranges of oral Minoxidil that you'll see out there and that people

take range anywhere from 0.25 milligrams all the way up to five milligrams per day.

That's an enormous range.

It's like a 20-fold range.

The topical Minoxidil is also found in various concentrations.

The typical concentration is going to be

a 5% concentration that people will use once per day.

Topical treatment with Minoxidil at 5%

concentration is thought to just stay at the scalp, but we now know that it

can go systemically, it can get into the general bloodstream.

Why that is should make complete sense

to you because when you put something on your scalp, I've already told you

that these little pits, these little tubes that go down to those

bulb regions below the skin that have direct access to the blood supply.

When you massage something into your

scalp, it not only has the opportunity to get into your general circulation,

it often does, especially if it's something that's very

water-soluble and that way can get into the capillaries and into the general

bloodstream, although topical treatments of which we're going to discuss,

a number of them today don't tend to get into the general circulation as robustly

as taking something by way of pill or capsule.

Minoxidil works by way of increasing blood

flow to the stem cell niche below the hair.

The dosage ranges of the oral Minoxidil

are tremendous, 0.25 milligrams, all the way up to five milligrams once per day.

The dosage range of the topical solutions tends to be a little bit more confined.

Typically, it's a 5% solution and it's

recommended that people use it one time daily, maybe twice daily.

It's also important, by the way, if you're going to take this route,

that you actually leave that solution on the scalp for 3-5 minutes.

This is important and should make complete sense as to why it's important.

You can't just rub the stuff into your

head and then rinse it off and expect it to be absorbed.

It actually needs to seep down into those hair follicles and access the niche.

How do people arrive at the correct dosage for Minoxidil?

Well, for better or for worse, really, in some cases,

it's accomplished by finding out that you have an unwanted side effect, like

dizziness or swelling of your ankles or edema or I would hope this wouldn't be

the case, but something that suggests there's hyperprolactinemia.

You could get a blood test to measure

your prolactin or you perhaps notice a drop in libido or some lethargy.

These sorts of things that are common

to reduce levels of dopamine, increased levels of prolactin.

I would hope that if people are working with a physician or if they're not

in taking Minoxidil, that they would start with the lowest possible dose.

For oral Minoxidil, that would be 0.25 milligrams and then

increase it as needed rather than jumping in right at five milligrams because some

of those side effects, in particular the fluid retention

and the hyper prolactinemia can be pretty uncomfortable and can

disrupt a lot of aspects of life that most all of us consider desirable.

We're really focusing right now on treatments that relate

to the critical requirement for hair stem cells to receive blood flow in order

to receive oxygen and nutrients, to get the hair to grow.

That's really what Minoxidil is about.

It's also what all of those anecdotes you hear are all about, like

massaging the scalp or putting red light on the scalp.

Although red light might do some other

things, in general, heating or lighting of the scalp or

massaging of the scalp is really designed to increase blood flow to the scalp.

Now, the reason Minoxidil works at all is because it is going to increase blood

flow around the clock, and that's because people are taking it

topically and it's seeping into the general circulation,

or at least it stings somewhat restricted to the hair cell niche.

Or they're taking it orally and it makes

it to that hair cell niche below the follicle.

When we massage our scalp, however,

that's a transient thing, like I massage my scalp right now,

I'm no doubt increasing blood flow to certain areas

and probably decreasing blood flow to the areas I'm pushing down on.

But it's all temporary.

I don't know many people that can massage their scalp enough during the day or long

enough during the day rather that it would sufficiently increase blood flow.

With that said,

it is clear that increasing blood flow to the scalp by way of reducing

hypertension, which is effectively accomplished

by broadening by expanding the blood vessels and capillaries,

is an effective way to at least hold on to the hair that you have.

Is it going to completely halt hair loss

if you have a strong genetic bias towards hair loss?

No. Is it going to reverse hair loss?

Very unlikely that it will.

But it can slow hair loss or even maintain the hair that you have.

If we were to take a step back and ask ourselves what other sorts of drug

treatments are out there besides Minoxidil, that increase blood flow

and that might increase the rates of hair growth or more likely increase

maintenance of hair that one already has by increasing blood flow to the niche.

Nowadays, there are more and more doctors

who are familiar with this requirement for blood flow.

Understand the mechanisms by which Minoxidil works and understand

the vast desire out there for people to hold on to the hair they have

and regrow hair and they are prescribing things like low-dose tadalafil,

so 2.5 milligram to five milligram tadalafil.

Tadalafil was initially discovered as a drug to treat prostate health.

It was a drug that we now know can increase blood flow to the prostate

and thereby offset some of the issues associated with an aging prostate.

Higher doses of tadalafil

sometimes also referred to by its brand name, which is Cialis,

are used to treat erectile dysfunction, but at the dosages that are used

to increase blood flow to the prostate and that now a number of doctors are using

to increase blood flow not just to the prostate but to all regions

of the body, including the scalp, such as 2.5-5 milligram tadalafil.

This is something that I think deserves

attention because it falls under the umbrella of increasing blood flow

to the hair stem cell niche in order to maintain hair.

It is not something that most doctors are going to be familiar with as the way

to reverse hair loss because it won't do that.

But the use of low-dose tadalafil

to slow rates of hair loss is very much in a logical mechanistic sense,

exactly the same as the logic of using Minoxidil to slow rates of hair loss.

It's all about increasing blood flow

to support the stem cell niche below the hair follicle.

The critical requirement for blood flow, oxygen and nutrients to the stem cell

niche is also why you hear a lot nowadays about the use of PRP,

platelet-rich plasma for trying to offset hair loss or even reverse hair loss.

We're going to do an entire episode about PRP.

It is pretty controversial in certain

circles and well- accepted in other circles.

A couple of key things to understand about PRP.

First of all,

it is being used in multiple tissues for different purposes in different clinics.

For instance,

board-certified physicians in the United States, Canada,

and Europe are doing PRP injections into ovaries to try and expand the number

of healthy follicles and eggs so that people can conceive later in life or

even earlier in life if they don't have many follicles.

People are getting PRP injections

into their joints in order to try and support joint health.

People are getting PRP injections into just about every tissue you can think of.

However, PRP, despite what you may have heard, is not stem cells.

Somebody tells you they're injecting stem cells, they're either outside the US,

Canada, or Northern Europe, or they're injecting something else.

So you want to really look into that.

The safety issues there are subject totally deserving of an entire episode.

I'm not necessarily opposed to the future of stem cells as a treatment,

but keep in mind that stem cells are cells that can give rise to lots of other

cell types, and they are cells that divide and replicate.

There's a name for that when it happens

in the adult body when you don't want that.

That's called cancer.

Tumors are over-production of cells

from stem cells when those stem cells ordinarily should be quiescent.

Keep in mind the difference between stem cells and PRP.

PRP, platelet-rich plasma,

again, is legal in the US and many other places because it involves drawing

somebody's blood, spinning it down at a particular speed,

which separates out different components within the blood.

Then taking the platelets and re-

injecting those in a solution back into the person's body.

Platelet-rich plasma or PRP is platelet enriched plasma from that person.

But the basis of PRP is really to encourage nutrient delivery

to a particular region in the body using somebody's own platelets,

because those platelets are enriched for various nutrients.

People are getting PRP injections into their scalp.

Those are not stem cell injections.

Those are PRP injections into the scalp with some moderate success.

These are very expensive treatments.

They tend to be transiently successful.

I'm sure there are people out there who are going to say,

"PRP worked fabulously well for me." That might be the case.

I'm not going to dispute that.

And I'm happy for you.

Although there are not sufficient

clinical data to suggest PRP as a treatment right now,

especially given the cost, many thousands of dollars, many, many treatments.

It's also the case that the PRP

injections, when they work, might work for reasons independent of the platelets.

What do I mean by that?

Well, soon, we're going to talk about a different type of treatment,

which is a mechanical manipulation of the hair follicle, typically,

on the scalp, because that's typically where people want to regrow hair.

I don't know many people who are trying

to maintain or accelerate or regrow their back hair, for instance.

They might be out there,

but I don't think there are a lot of them or their leg hair, for that matter.

Almost always, it's going to be scalp hair.

And one way that people are doing that is through mechanical stimulation

of the hair follicle and the stem cell niche using what's called micro-needling.

Micro-needling, as the name suggests,

is taking a bunch of little needles either in a little stamp.

A little square or nowadays, typically, it's a roller.

It looks like a paint roller,

except it's got tons of little needles in rows all over that roller.

Those needles range in length from half a millimeter to 2.5 millimeters.

Millimeters and one rolls that over the scalp.

If you're thinking, ouch, that probably hurts.

Indeed, it can hurt a little bit or a lot,

depending on the thickness and the length of those needles.

Micro-needling has been shown to do two things.

It has been shown to reactivate semi-

quiescent populations of stem cells that are in that telogen phase,

putting them back in antigen phase and thereby stimulate more hair growth.

It has also, and this is I think, the best use of micro-needling.

It has also been shown to be a very

effective augment for some of the hormone- based hair regrowth tools

and pharmacology that we're going to talk about in a few minutes.

Micro-needling and PRP have something very critical in common,

which is the needle, the actual injection into the skin.

For those of you that are hearing this

and thinking, why would disrupting the skin with needles

actually, support hair growth or regrowth, wouldn't that just damage the follicle?

Well, this gets into some of the, I think, interesting, if not fascinating aspects

of our biology, which is that all of the cells in our body

really can respond to both chemical and mechanical cues.

When we hear needle injected into skin, we think, oh, that must just be damaging

everything, causing all sorts of inflammation.

But it turns out that low levels of inflammation caused by things like

micro-needling or PRP injections or even the introduction of any kind of fluid.

For instance, saline fluid injected

into a region can cause changes in the cells in that region, causing,

for instance, stem cell populations that were waning to reactivate again,

causing telogen phase follicles that have melanocytes and stem cells that are dying

off but not completely gone to reenter the cell cycle.

Micro-needling procedures, PRP injections, things like Minoxidil,

they all kind of center around this same general theme of increasing blood flow,

increasing oxygen, delivery of nutrients, or in the case of micro-needling,

increasing inflammation just enough at that local site that certain cascades

of biological function that relate to proliferation of stem cells or

maintenance of stem cell populations are kicked off.

It's sort of like reminding the cells

in that area that they need to stay alive in order to replenish whatever is lost.

Sometimes a wound can actually induce some healing.

Although I do want to point out

that the micro part of micro-needling is absolutely key and this should be

obvious to you when you think about scars.

I don't know about you, but I've never seen a scar with hair

growing out of it, or if there was, it was probably like one hair.

But if you've ever seen a scar,

someone had their appendix out or if someone had a brain surgery,

you see that scar because there is no hair growing out of it.

So the micro portion of micro-needling is extremely important.

We are not talking about causing

significant damage to a tissue in order to activate that stem cell population.

We're talking about causing microdamage

and micro levels of inflammation to stimulate growth.

For those of you that are interested in using micro-needling or micro-needling

in combination with chemical treatments like Minoxidil or some of the other

treatments we'll talk about in a little bit.

Like finasteride and caffeine.

Yes, believe it or not, caffeine is being used to regrow hair.

Very interesting.

Get into that in a moment.

But if you're interested in using m

icro-needling alone or in combination with some of these other treatments,

there's a wonderful review that was just published this last year.

Wonderful, because it's very comprehensive.

Not so wonderful.

Not to the fault of the authors because

most of the studies out there on micro-needling are not superb.

There are ways of gauging the strength of a study mainly relate to their

duration, whether or not they were control groups et cetera.

But the review itself is excellent and the title of the review is M

icro-needling and its Use in Hair Loss Disorders: A Systematic Review.

We will provide a link to this

in the show note captions and this review did a very good job of highlighting both

the strengths and drawbacks of the various studies looking at micro-needling.

It also explored the use of micro-needling

in both men and women and of various ages, and it does appear to be the case

that micro-needling shows some positive benefit in both men and women,

regardless of age, especially when used in combination

with the various other treatments that we're talking about.

I was also able to glean from this review and some of the papers described within it

that needle lengths of about one millimeter to 2.5 millimeters seem to be

more effective than shorter needle lengths.

So if you're scared of the needles and the needle lengths,

keep in mind that done properly, micro-needling shouldn't be too painful.

Some people experience a little bit more

pain than others, but it's not considered a very painful procedure.

It is, however, a procedure that can cause

some bleeding of the scalp, and that bleeding of the scalp can be

very apparent, especially if it's in the front

of the head as opposed to in the top of the head and hidden by some hair or if

you're already quite bald in a given region.

Keep that in mind.

I suppose one could wear a hat or a wig

or something of that sort if they were really self-conscious about it.

But the micro-needling itself is causing

a physical disruption to the scalp, some degree of bleeding, inflammation.

And again, all of that is part

of the process by which micro-needling can actually improve hair growth.

Of course, there's healing that occurs

of the bleeding and the damage to the follicle.

This is a transient thing,

but understanding the cosmetic implications in the short term as well as

in the long-term is certainly worth knowing.

One thing that's very clear is

that the combination of micro-needling and Minoxidil treatment together is far

more effective than either of those treatments alone.

In addition,

the combination of micro-needling and Minoxidil has been shown to be

effective in recovering what are called dead zones.

These are regions of the scalp that are either completely bald or mostly bald,

for which there is essentially no stem cell population there.

The combination of Minoxidil plus

micro-needling is somehow able to recover those stem cell populations and allow

new hair to grow, although the growth of that hair

in those dead zone regions can take a very long time, 30 to even 50 weeks.

Neither Minoxidil treatment alone nor

micro-needling alone has been shown to be effective in recovering these so-called

dead zones when those treatments are done separately.

This, I would say,

is a strong reason to consider combining micro-needling and Minoxidil as opposed

to just doing Minoxidil or just micro-needling.

I should also mention that Minoxidil treatment, if you pursue it,

is likely something that you are going to have to do for the rest of your life.

If you want to hold on to the hair growth that you obtain with Minoxidil or if you

want to maintain the hair that you are already maintaining with Minoxidil.

Some people have been successful in taking Minoxidil, maintaining some hair

growth or even stimulating some hair growth and then coming off Minoxidil.

But most everyone who goes on Minoxidil

has to stay on Minoxidil because when they cease taking Minoxidil,

even if they're doing other treatments, they lose the hair that they gained

with Minoxidil, so that is an important consideration.

The decision to go on Minoxidil is likely

a decision to be on Minoxidil for the rest of your life.

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So, as you're probably starting to realize, there's a relationship between

mechanical stimulation of the follicle and blood flow, both of which turn out

to be critical for maintaining hair and for stimulating hair growth.

Not surprisingly then, an increasingly c ommon treatment for hair loss is Botox.

Botox is the brand name for what is otherwise known as botulinum neurotoxin.

What is botulinum neurotoxin?

Botulinum neurotoxin,

sometimes just called botulinum for short, is a toxin that's a bacterial

toxin that serves to cut the protein that leads to synaptic vesicle release.

What in the world did I just say?

Well, when your nerve cells communicate with one another,

they do that by way of electricity, but the electricity within those nerve

cells, those neurons, triggers the release of chemicals

from neurons into the synapse, the little gap between neurons.

The release of those chemicals allows the next neuron to be chemically active,

or in some cases, it will suppress the electrical activity of that next neuron.

Botulinum neurotoxin serves to cut a protein present in neurons so

that neurons cannot release the chemicals that cause other neurons to be active.

This actually is pretty serious.

If you were to get botulinum neurotoxin

injected into your muscle you would be paralyzed because the nerves that control

contraction of the muscles would not be able to control the release

of that chemical onto the muscle, which makes it contract.

Botulinum neurotoxin is commonly used in what's called Botox.

Botox is something most people are

familiar with because people get it injected in and around their wrinkles

because many wrinkles are triggered by not just loss of tensile strength

in the skin, but rather, the nerves around the skin

and in the skin are hyper contracted, which causes wrinkles.

For instance, I have crow's feet.

I like to think that's because I've laughed a lot and smiled a lot,

and it's probably also because I've squinted a lot in my lifetime.

I have crow's feet because the nerves

there have pinched the skin on either side of my eyes and that's given me

little creases there that are sometimes referred to as crow's feet.

Botox injections can be applied

to the scalp in order to relieve tension of the scalp.

In hearing that, it should be obvious why

Botox is being used to try and offset hair loss.

It's decreasing the squinting,

if you will, or the tensile nature of the scalp skin so that more blood flow

can arrive at that stem cell follicle area.

Botox treatment to the scalp is actually becoming pretty common.

There are a couple requirements with this Botox treatment.

First of all, it has to be done by somebody who's really skilled.

There are numerous images online

and websites online of so-called Botox fails, where people have gotten too much

Botox or the injections have been done too deep or not at the correct locations

on people's face or scalp, and it can give them droopy scalp or droopy eyes.

All sorts of cosmetic nightmares can occur with Botox.

The second thing to understand is that Botox does eventually wear off.

That botulinum neurotoxin doesn't stick around forever.

Provided it's done correctly at the correct dosages,

it doesn't actually kill the neurons that cause that tension of the skin,

so Botox injections have to be done repeatedly.

The efficacy of Botox for offsetting hair loss is not clear.

There aren't a lot of large- scale clinical studies on this just yet,

but it does seem to be at least one reasonably safe alternative to things

like Minoxidil, although I think if one were to just want to increase blood flow

to the scalp, things like low- dose Tadalafil, which doesn't seem to carry any

of the side effects that Minoxidil can carry, we talked about those side effects

earlier, that would probably be the better alternative.

Botox is a fairly invasive procedure, but some people opt for Botox treatment.

In fact, there is a syndrome called cutis verticis gyrata.

Some of you have probably seen this.

It's more typical in men, although it does occur in women.

It literally means a lumping of the skin on the scalp, or gyri of the scalp.

Gyri or gyrus pertains to the Latin word knee, so it means bump or knee.

Any time you hear the word gyrus

in neuroscience or in biology, you're talking about a bump.

You'll sometimes see people will have ridges in the back where it looks as if

the skin was pushed together, kind of like a Shar-Pei dog, but on the scalp.

People with cutis verticis gyrata almost always experience pattern hair loss.

Now, part of the reason for that is

cutis verticis gyrata is also associated with some androgen or

testosterone- related hormone issues that we'll talk about in a little bit.

But in addition to that,

it has been shown that relieving some of those gyrata by injections of Botox

to allow those folds to sit flatter, A, is effective.

It can lead to less of those gyri, those bumps, and can improve hair growth

in those regions, even if those people don't take on any

additional treatments to address the hormone issues.

That's really how people arrived at this understanding that Botox might be a good

treatment in general for reducing the squinting of the scalp that can occur

and the resulting hair loss in those regions.

I'd now like to turn our attention to the chemical variables that control

the duration of the growth phase of hair, the duration of that catagen phase,

which is when that hair essentially recedes from the inside out,

and the quiescent or semi- quiescent telogen phase.

There are a couple of key chemical players here that we should all be aware of.

First of all, the growth factor IGF-1,

insulin growth factor 1, which is produced by the liver,

but that receives stimulation from the brain and pituitary to be

released, is a strong regulator of hair growth.

We can think of it as the accelerator on hair growth.

It does that by extending that anagen, or growth phase, for longer.

It doesn't necessarily speed up growth,

but it extends it for a longer period of time.

In addition, cyclic AMP, which is part of what's called a second

messenger pathway, in fact, cyclic AMP is a second messenger,

is also a key player in stimulating growth of the hair follicle.

Now, cyclic AMP does many different things in many different cell types in the body.

It really acts, as the name suggests,

as a messenger between signals that arrive at the surface of cells

and transmitting or conveying those signals to things that happen deep within

the cells, such as the turning on and off of various genes.

When you hear second messenger, don't let that confuse you or overwhelm you.

Just understand that the whole process of getting signals from the outside

of cells into the center of cells and controlling gene expression,

for instance, causing a stem cell to continue to give

off daughter cells, or causing a hair cell to continue growing for longer,

that whole process is a bit like a bucket brigade of handing off water or

a bucket from one component to the next, or along a chain.

It's like an assembly line.

I think that's probably the simplest way to think about it.

For sake of this discussion, IGF-1 is known to increase the growth

of hair by extending that anagen phase, as is cyclic AMP.

Those are going to be considered

the accelerators, at least in this conversation.

The brakes on hair growth are going to be

the things that either shorten the anagen phase or that extend

the catagen phase or this quiescent phase, which is the telogen phase.

The two major brakes on hair growth

that we want to think about are PDE, which is a phosphodiesterase,

anytime you hear -ase it's likely to be an enzyme, and TGF-beta-2.

This is a particular growth factor that,

somewhat counterintuitively, doesn't stimulate growth,

it actually stimulates lack of growth, or shortens growth.

With all of that in mind, and please do also keep in mind that you

don't need to remember all those specific terms, just understand that there are

some factors, like insulin growth factor 1, that act as accelerators on growth,

and there are factors that act as brakes on growth.

We can start to think about why,

for instance, half of all people by age 50 start to lose their hair.

Well, they start to lose their hair because of something called androgen-

related alopecia, which, translated to English,

means testosterone and testosterone- derivative induced hair loss.

This is true in men and women.

Hearing that, you should probably be wondering the following thing:

Young men have higher levels of testosterone than old men, right?

Well, the answer is yes,

although some older men in their 40s, 50s, even 80s, maintain testosterone

levels similar to many men in their 20s, but most don't.

It's a downward slope starting at about age 40.

How steep that downward slope is depends.

Women, too, have testosterone.

In fact, women have higher levels of testosterone than they do estrogen.

That's right.

A healthy woman has higher levels of testosterone than she does estrogen.

However, women, on average,

have lower testosterone than most men, so they still have far more estrogen

and far less testosterone than most men, but the level of testosterone that they

have within their body is higher than the level of estrogen they have.

Androgens such as testosterone and its

derivatives, such as dihydrotestosterone, which will be much the topic of what we're

getting into next, inhibit IGF-1 and cyclic AMP.

Again, androgens such as dihydrotestosterone inhibit,

prevent the action of IGF-1 and cyclic AMP, which you just learned a few moments

ago, act to extend the anagen or growth phase of hair.

Which then raises the question, well, if young people, both male and female,

have higher levels of testosterone than they do when they're older,

why would people lose their hair when they're older and not younger?

The answer lies in the conversion of testosterone to dihydrotestosterone.

Testosterone most people have heard of.

Dihydrotestosterone, or DHT, is made from testosterone.

There's an enzyme called 5-alpha reductase that converts testosterone

into dihydrotestosterone in both men and women.

Dihydrotestosterone binds to the androgen receptor at five times

the affinity of testosterone, so it is the most powerful androgen

in humans, and it is responsible for a number of things that we all

really want and like, such as mental vigor, physical vigor, strength,

healing capacity, drive, libido, and on and on.

DHT itself is not bad.

If we take a step back and we acknowledge testosterone levels are

higher in males and females at younger ages as opposed to older,

but as they get older, there is more 5-alpha reductase activity,

which is converting more of that testosterone

to dihydrotestosterone and dihydrotestosterone inhibits hair

growth by reducing IGF-1 and cyclic AMP, well, then we should all be aboard why it

is that by age 50, about 50% of people experience pattern hair loss.

That is androgen-dependent alopecia,

but translated to normal English is pattern hair loss.

In a moment you'll understand why some people lose their hair from the crown

region in the back of the head, or back and top of the head,

whereas other people lose their hair in the front of their head,

in the flanks, right on either side of the midline,

or maybe in the midline and front altogether.

That's because different people, depending on their genetic lineage,

have different patterns of androgen receptors on their scalp.

The pattern of androgen receptors

that you inherit indeed does come from your mother's side.

This is what gave rise to the the myth that if you want to know if you're going

to go bald or not, just look at your mother's father.

Doesn't quite work that way.

In fact, if you think about the logic, you should really look at your mother's

mother if you want to know your pattern of androgen receptors on your scalp.

However, most women don't lose as much

hair from their scalp, or they have ways of covering up the hair

loss in their scalp because their hair is just generally longer or they're using

other approaches, so that you never really get a clear picture of what the androgen-

dependent hair loss was in your grandmother.

Now, we don't want to go too far down the genetics rabbit hole because,

as you know, you can't select your parents anyway, but if you want to know

why, for instance, I'm losing a bit of hair on either side

of the midline in the front, it almost certainly has to do

with the fact that I have a higher density of androgen receptors there,

as opposed to, say, on the crown of my head where,

for whatever reason, my hair seems to grow thickest.

Other people lose hair on the crown,

in the back and top, but not in the front, and some people will lose it all over.

Now you understand why hair loss occurs in certain regions of the body.

You should also understand that the androgen receptors on the face

are also what are responsible for beard growth.

This is where it can get a little bit tricky, but a lot of things will start

to make sense if you can understand this and internalize this.

If you have a high density of androgen

receptors on your face, well then as your DHT levels go up

with age, you will be able to grow a thicker and thicker beard.

In fact, it is rare to see someone who can

grow a thick beard in their youth, but not so much as they get older.

In fact, the reverse tends to be true.

The pattern of androgen receptors differs

between the scalp and the face and the back.

On your back you have androgen receptors and their DHT stimulates hair growth.

If you know someone who has a very hairy back, or if you have a very hairy back,

that means you have a high density of androgen receptors on your back.

If you have a beard and that beard is

thick, well then you have a high density of androgen receptors on your face.

However, a high density of androgen receptors anywhere on your scalp is going

to predispose those regions to androgen- dependent alopecia, or hair loss in those

particular regions, which is going to allow us to understand

why all of the rest of the treatments for halting hair loss

and for stimulating hair growth, almost all of those center on inhibiting

either DHT directly, or 5-alpha reductase, the conversion of testosterone to DHT.

Now I'd like to discuss the ways that one can chemically adjust certain things

within the hair growth pathway, things like IGF-1, PDE, TGF beta, etc,

in order to stimulate hair growth or halt hair loss.

The first thing on this list is actually

going to be pretty surprising to a number of you, and that's caffeine.

We all think of caffeine as a stimulant that we drink.

I certainly drink coffee in Yerba Mate,

the occasional energy drink, things of that sort.

Caffeine does many things besides

stimulate our central nervous system and make us feel less sleepy, however.

One of the things that caffeine does is it is a fairly potent PDE inhibitor.

By being a potent PDE inhibitor, it indirectly stimulates IGF-1.

Why?

Well, because PDE can suppress IGF-1, and by ingesting caffeine,

or by applying topical caffeine ointment or cream to the scalp,

you can suppress PDE sufficiently enough to increase IGF-1 and increase some hair

growth, or at least maintain hair growth in that region.

This may come as a shock,

it might seem a little bit esoteric or even outside the margins of typical

treatments, but head to head, topical caffeine application can be as

effective as Minoxidil application without actually lowering things like

blood pressure and potentially increasing prolactin and some of the other negative,

let's call them negative because they are, side effects of Minoxidil.

Caffeine ointments, and caffeine present in various hair treatments

and creams, etc, is starting to become a more prominent theme out there.

I will include a reference to caffeine and its uses for offsetting hair loss.

Keep in mind that topical caffeine ointments shouldn't necessarily be applied

every single day, so this is the sort of thing you might do three times a week.

The concentration of caffeine in different ointments varies tremendously.

Most of the studies of caffeine

on the stem cell niches that control hair growth and extension of the anagen phase

of hair growth have been performed in vitro in a dish.

Although there are some clinical studies exploring this, they are not nearly as

extensive in number or duration as the studies of Minoxidil because this

approach just hasn't been around quite as long.

However, when comparing side effects of Minoxidil, cost of Minoxidil,

comparing the efficacy of caffeine and Minoxidil,

I think caffeine as a topical treatment for offsetting hair loss stands as

a pretty good choice if you're going to start exploring this pathway.

There's no reason to think that if you were to try the caffeine ointment and it

didn't work for you or you didn't like it for some reason or you needed to stop

it for some reason, that you couldn't stop it safely,

because it doesn't carry all the other blood pressure- related effects

and prolactin emia effects that Minoxidil does.

If you look out there into the hair maintenance and hair replacement

literature, and you look at thetreatments that are

being sold, don't be surprised to see caffeine there.

Also, don't be surprised when I tell you

what I'm about to tell you now, which is, no, you can't simply just drink more

caffeine in order to accomplish the goal of offsetting hair loss.

It is true that when you ingest caffeine, it goes systemically.

However, you have so many adenosine receptors throughout your body.

Those adenosine receptors, and the parking of caffeine in those

adenosine receptors, is the main way in which caffeine

exerts its stimulatory effects, making you feel less sleepy.

It does that because then adenosine can't

have its effects, which are to make you sleepy.

Well, those adenosine receptors soak up

so much of the caffeine that you would ingest orally that very,

very little would make it to the scalp and to the hair follicles

at the concentrations that you would want, so that's why you have to rely

on the application of these caffeine ointments about three times a week.

Keep in mind that no one has really

explored the dosages of caffeine in these ointments in a systematic way.

We are still in the early stages of all this, but I do think it's important

to mention caffeine because of the lower incidence of side effects,

at least reported side effects, and the general safety margins,

and the head to head essentially comparable efficacy with Minoxidil

because Minoxidil has a bunch of other issues.

Now keep in mind that both Minoxidil and caffeine are generally used as

a preventative for reducing hair loss over time.

They are not expected, and they do not, as far- as far as we

know, create new hair growth to any sufficient degree.

If any of you have used caffeine, ointments or minoxidil and observed new

hair growth that was robust, please put that in the comment section.

I'd be curious about those experiences, but as far as I know

and from the clinical literature that I read, there's no examples of that.

One other point about caffeine.

It does appear that caffeine can not only indirectly stimulate IGF-1 and the antigen

phase of hair cell growth by way of reducing PD and TGF beta.

But it also seems to reduce apoptosis

which is naturally occurring cell death of that stem cell niche.

We've been talking a lot about the antigen or growth phase of hair.

We also talked about the catagen or

the recession of that hair from the inside out.

But remember that third phase,

the telogen phase, where that whole bulb down at the bottom, the bulge,

as it's called, gets pinched off and the whole thing dies

and takes the stem cells off to the grave with it.

It appears that caffeine can offset the death of that niche and potentially

maintain the stem cell population longer, making caffeine a really good choice

to think about in conjunction with the various chemical treatments

aimed at directly attacking the DHT pathway that we'll talk about next.

So there's one very direct way to increase hair growth and maintain

the hair that you have on your head, and that's to increase IGF-1.

That can be accomplished through prescription drugs such as growth hormone

and things that stimulate the release of growth hormone and IGF-1.

Keep in mind, growth hormone is released

from the anterior pituitary during the first hours of sleep,

especially when you haven't eaten anything for the two hours prior

to sleep, and especially when you get regular bedtimes.

Yes, this is a real thing.

If you are going to sleep at variable bedtimes, especially if you go to sleep

much later than your usual habitual bedtime, you will miss that growth

hormone pulse that normally occurs in the first 2-3 hours of sleep.

This does not mean that you need to be

neurotic about getting to sleep at the exact same time every night.

There's probably a plus or minus 30-

minute window, and it doesn't mean that you can't stay

out late or have a bad night's sleep every once in a while or get woken up.

Your hair isn't going to fall out.

My dad's story notwithstanding,

your hair isn't going to all fallout because of that.

But you do want to try and get

that natural growth hormone release each night.

And as I mentioned,

there are prescription approaches and those are growth hormone itself.

Things like sermorelin, which is a peptide that increases growth hormone.

It's actually a secreted dog.

It causes the secretion of growth hormone and thereby increases in IGF-1.

This is well documented.

Both growth hormone and IGF-1, as I mentioned, are available by prescription.

They are not without their side effects.

They do cause growth of all tissues.

They do increase height in children, They increase bone mass and density.

They can increase mainly fat loss, not so much muscle size,

but they can increase leanness and they increase hair growth,

They can increase turnover of skin, they can make skin look more youthful.

All these things sound wonderful.

And yet they also have problems because

they can increase growth of small tumors that normally might be eliminated.

So there is an increased cancer risk

with growth hormone treatments and IGF-1 or anything that increases IGF-1 such as

sermorelin or ipamorelin, any of the peptides that you hear about nowadays.

That said, a number of people are using sermorelin as an indirect way to increase

IGF-1 and thereby to increase hair growth.

It does seem to be fairly effective in doing that, especially when done

in conjunction with other treatments that we'll talk about.

But keep in mind, these are prescription drugs and they do carry their own risks.

The other thing about stimulating the natural production of IGF-1 is that,

as its name suggests, insulin growth factor one,

it is insulin dependent in many ways, if not for its secretion,

then for its action at the hair follicle and stem cell.

So one of the things you really want to pay attention to is to avoid being

insulin resistant, or rather you want to try to be insulin sensitive.

So if you're carrying a lot of excess

body fat, if you're obese or if you have type two diabetes,

meaning your insulin resistant, you're going to want to deal with that.

There are a number of prescription treatments to deal with that nowadays.

People are very excited about all the GLP one agonists, but in addition to that,

regular cardiovascular exercise and resistance exercise,

making sure that your body fat percentage is not in excess of where it needs to be.

Everyone has a slightly different idea

of where it needs to be, both cosmetically and for health.

So that's a conversation between you and your doctor and you and you frankly.

But you want to avoid being insulin resistant because being insulin resistant

and being obese can indeed lead to hair loss.

There are many people out there who are

not obese who nonetheless are experiencing hair thinning and hair loss because they

are insulin resistant by way of reduced IGF-1 activity.

There are a few supplements. So these are over-the-counter

supplements such as myo-i nositol, taken at dosages of about 900 milligrams

before sleep, which by the way, can also assist in sleep or things like

berberine or metformin, which are known to improve insulin sensitivity.

Each and every one of these has its own profile of positive and negative effects.

The lowest number of side effects is associated with 900 milligram myo-i

nositol taken about 30 minutes before sleep, mostly because it can make people

a little bit drowsy and it does aid sleep in some really

great ways, but really exercise and maintaining

a healthy nutritional program are also going to be key.

You just can't discard those.

Berberine, which is a substance made

from tree bark is sometimes called the poor man's metformin.

Metformin being the equally effective prescription version of berberine.

Or put differently,

berberine is the non-prescription but equally effective version of metformin.

Keep in mind that both berberine

and metformin dramatically reduce blood sugar levels.

And so if you're not going to take them

with carbohydrates, it can lead to some feelings of discomfort.

That's why I'm not a fan of them.

But if your goal is to really improve insulin sensitivity,

they are considered very potent tools on the list of things that can do that.

The other thing that's really important for maintaining proper hair growth,

this antigen phase, is that you need sufficient iron.

This is because iron and ferritin play

a key role in the cell growth pathways that go from the stem cells

to the stimulation of keratin within the hair itself.

I don't have time to go into this

pathway in a lot of detail, but you can have your blood levels of iron measured.

This turns out to be pretty important

because you don't just want to start popping iron supplements because too much

iron can be toxic, too little means you're anemic.

For women, the levels of iron that you want are somewhere between 25 and 100.

And for men, somewhere between 30 and 150.

Fortunately, the tests or the blood tests for iron are usually a very

inexpensive add to your current blood panel.

So if you're going in for a blood panel

for LDL, HDL, typical things, or if you're doing the more elaborate

hormone testing, which I do recommend people do if they

can afford it or if their insurance covers it, do ask for an iron test as well.

And if your iron is low, you may need to supplement your iron.

If your iron is too high, that's not good either.

But iron plays a key role in the antigen

phase of hair growth, so you want to make sure you at least have sufficient iron.

And if you don't, you want to make sure

that you're getting it from nutrition and or supplementation.

Earlier, we were talking about dihydrotestosterone.

Dihydrotestosterone,

just to jog your memory, is a form of testosterone that combine

the androgen receptor at five times the affinity of regular testosterone.

Both men and women have a lot of testosterone relative to estrogen.

It just so happens that men tend to have more testosterone than women do overall.

But both men and women, as they age, convert more of the testosterone they

have to dihydrotestosterone and dihydrotestosterone does two things

that are bad for hair maintenance and hair growth.

First of all, it shortens the antigen phase, that growth phase.

Whatever hair is going to grow is going to occur over a shorter period of time.

Second of all, because of the presence

of androgen receptors on the stem cell niche area and around it,

it actually miniaturize the follicle and the stem cell niche.

In other words, it makes the population of cells that give rise to more hair

protein smaller and can eliminate it altogether.

And that is why anything that reduces 5-

alpha reductase is going to reduce DHT, is going to maintain or extend the growth

phase, the antigen phase of hair growth and is going to offset or prevent some

of the telogen phase, the pinching off and the removal of that stem cell niche.

Now, one substance that we know can

inhibit 5-alpha reductase, although it does it pretty weakly is saw

palmetto, which is an extract of the saw palmetto berry.

To be honest, I don't know how this was initially discovered.

If anyone knows, please put it in the show note captions.

When I looked online I found a bunch of conflicting stories about who was

the first person to start extracting the extract of the saw palmetto berries.

So I have no idea which one of those is true.

Maybe somebody can tell me.

The good thing about saw palmetto

treatment is that it is known to have very few, if any, side effects.

There might be some side effects

in about 1% of people, but it's not associated with a lot of side effects.

It's also known that when taken at about

300 milligrams per day and here it doesn't have to be that strict.

Most of the studies that I explored involved taking anywhere from 200-

500 milligrams of saw palmetto, but most of them focused on about

300 milligrams of saw palmetto per day, divided into two or three doses.

Why? Well, it has a relatively short half-life,

meaning it's going to get cleared from the bloodstream and more importantly,

its biological action is going to be very short-lived.

So if you can get a hold of 50 or 100- milligram capsules or tablets

of saw palmetto and divide those up, take them in the morning,

afternoon and evening, or even just in the morning and evening

to achieve a total of about 300 milligrams per day.

That's going to very likely help you hold on to some of the hair that you would

have otherwise lost, maybe even grow some new hair.

And I say maybe give you some new hair growth because saw palmetto is not

known to be a particularly robust treatment for the reversal of hair loss.

It's known to have some effect,

but it's generally taken in conjunction with a bunch of other things.

And so it's really hard to tease out just what amount of hair growth or

prevention of hair loss is due to saw palmetto specifically.

But I mention it here because

the mechanism of action is logical and fairly well-known,

which is this week effect in reducing 5- alpha reductase and thereby reducing DHT.

So again, because it has relatively low

side effects, even though it's not super effective and because it's fairly low

cost and it's available over the counter, I felt it was important to include.

Now, as soon as people hear things like

saw palmetto berry, they're probably also thinking, "Oh boy,

here comes all the herbals." Now keep in mind that there are some herbal

compounds that have pretty robust biological effects.

And we talked before in our optimizing testosterone episodes about things like

Tongkat Ali and Fadogia agrestis, which taken incorrect dosages

and in the correct way, can be pretty potent for increasing

luteinizing hormone and free testosterone that can have huge effects.

It's not like taking exogenous anabolic steroids, but they can have real effects.

And so herbal compounds can be potent.

However, I do acknowledge that there is a vast market out there of herbal

compounds and plant-based compounds that people are arguing.

Mostly the people who sell them are arguing can increase hair growth.

There are some decent studies of these things.

The hard part about studying these herbal

compounds and these plant-derived compounds for increasing hair growth is

that they are often taken in combination with one another.

In fact, most of the hair growth

supplements that involve these herbal compounds and plant compounds include 5

or 10, sometimes even more things altogether.

So teasing out which ones are effective

and which dosages are effective is nearly impossible.

There are just too many variables.

You will hear, for instance, that green tea extract, Reishi Mushroom,

pumpkin oil, zinc, curcumin, all of these things can increase hair growth.

Perhaps the only thing on that list that makes logical sense with respect

to the biochemistry is that curcumin is known to, in some people,

be a potent inhibitor of 5-alpha reductase and DHD so much so that I can personally

say for me I once took curcumin, turmeric, it's also called in high dosage.

This is about a gram to 2 gram capsules and I felt absolutely terrible.

I mean, just dreadful.

I don't care if it allowed me to keep

my hair forever, I would rather lose all my hair three times over.

I guess that means it would have grown back.

I'd rather lose all my hair.

Let's just put it that way

than ever take curcumin or turmeric in high dosages again.

In saying that, I know that many people take turmeric and curcumin and really like

its anti-inflammatory properties and don't experience any side effects.

I just happen to be particularly sensitive to curcumin by way of this DHT pathway.

I know this by way of blood work, so I'm never going to hear that stuff again.

That said, a lot of these herbal compounds

and cocktails probably will have some minor marginal,

infinitesimally small, somewhere in that range effect

on maintaining hair growth or in stimulating new hair growth.

It's just that there really aren't

clinical studies to support any one of them.

And that's why I singled out saw palmetto as one of the few

for which the biochemical pathway of inhibiting 5-alpha reductase

and the low incidence of side effects and the fact that many people have used it

with some degree of success makes it a standalone.

I wouldn't say recommendation, but a consideration.

Another commonly discussed and use commercial compound for offsetting hair

loss and stimulating hair growth is ketoconazole.

Sometimes this is known as Nizoral where Nizoral is the brand name of a shampoo.

Ketoconazole is an antifungal that was

initially developed to treat dandruff and severe psoriasis.

Ketoconazole has been shown to be effective in increasing hair number.

It's also been shown to be effective

in increasing hair diameter, which is somewhat surprising because one

of the common side effects of ketoconazole is drying, thinning and brittle hair.

So what's going on there is a little unclear.

We'll return to that in a moment.

The mechanism of action for ketoconazole is pretty interesting.

Remember earlier we were talking about

the sebaceous gland and the production of sebum, that oily stuff

whose very name seems to evoke disgust in certain people.

Well, ketoconazole can disrupt some

of the fungal growth that frankly, we all have on our scalp all the time.

I know this is a surprise to many of you, but you are constantly bombarded

with viruses, bacteria and funguses all the time.

But we managed to battle those off

with our immune system, either by physical barriers such as

an oil barrier like the sebum or through antimicrobial action.

Chemical approaches our immune system, the sebum, etc,

ketoconazole acts as an antifungal that in some way seems to reinforce

the properties of sebum at keeping out other fungal infections.

And the net effect, at least as far as we know, is a mild reduction in DHT.

Now exactly how this happens isn't really clear.

What is clear is that the use

of ketoconazole shampoo is 2-4 times per week with a scalp contact

time of about 3-5 minutes has been shown to give about an 80% response rate

of maintaining hair that would otherwise be lost.

So that's pretty dramatic, 80%.

What is less clear is whether or not

ketoconazole shampoo can actually stimulate new hair growth.

But as you're probably starting to realize,

this is always a bit of a tough thing to disentangle maintenance of hair

that you would have lost versus new hair growth.

Certainly, that's an easy thing to disambiguate if

you have a patch of scalp where there is absolutely no hair,

these so-called dead zones that you can resurrect with certain treatments.

But what about areas of your scalp where hair is thinning?

So, for instance, on the top of your head,

this is where many women will first experience pattern, hair loss.

Alopecia is right at their midline,

especially if they have a part right there.

They'll start to notice that under very

bright light, fluorescent lights in particular,

they'll notice a thinning of their hair there or in the forehead region.

They'll start using ketoconazole shampoo.

Again, the typical recommendation is 2-4 times per week with a scalp contact time

of 3-5 minutes and really rubbing it in and then rinsing it out.

You don't need to be super vigorous, but you want to make sure that it gets

down into the follicle and around the follicles, not just sitting on top

of the hair, which is going to be especially

important for people who have long hair to really massage it in.

Well, they will experience a growth of hair in that particular region

that almost certainly were due to miniaturization of the hair follicle

and reduction of the total population of stem cells in that follicle as opposed

to complete loss of the stem cell population.

The reason we say this is that there's no reason to think that ketoconazole can

actually stimulate IGF-1 or activate growth itself.

It's probably offsetting some of the reductions in the antigen phase

and some of the exacerbation of the telogen phase.

Now, if you decide to use ketoconazole as

an approach to offsetting hair loss, it's very important that you get a hold

of a shampoo that's at least 2% concentration of ketoconazole.

This is important because a lot of the ones that are available out there,

especially online, are going to be 1% or lower.

So you want to try and obtain a ketoconazole shampoo of 2% or higher

concentration of ketoconazole because it has other things in it, of course.

I should mention that there are occasional side effects with ketoconazole.

The rates of side effects from the meta analyzes and reviews that I read were

somewhere between 1% and 8% of people will experience some side effects,

but those side effects tend to be pretty mild.

Things like irritation of the scalp,

things like thinning and brittleness of the hair that sometimes can be offset

by using shampoos that contain things like biotin.

I know many people are probably curious

about biotin, which is a protein that can be incorporated into the keratin.

Whether or not different biotin enriched shampoos can really enhance the total

amount of biotin that gets incorporated into the hair isn't clear,

but it is clear that having sufficient biotin around is important.

So if you get a little bit extra from your shampoo,

you can imagine how that would "tap off" the amount of biotin in that hair.

And there are people out there saying

that by biotin-enriched shampoos have done wonders for them.

Who knows? I'm not going to dispute their experience.

So if you're going to use ketoconazole,

keep in mind that the more typical brand names that are out there,

you know which ones they are, oftentimes don't have 2% or if they do

have 2%, they can be very drying and lead to brittle hair.

There are newer and now fortunately,

a greater variety of ketoconazole containing shampoos.

We as a podcast and I don't have any

affiliation to any of these, but I will provide a links to a couple

of the more prominent ones that are known to have 2% concentration of ketoconazole,

as well as some other things in them known to offset some of that dryness

and brittleness that ketoconazole shampoos can trigger.

So by now, I think it will be abundantly

clear why inhibiting 5-alpha reductase and thereby reducing DHT should increase

hair growth because of the negative impact that DHT has on the hair follicle.

The major player in this whole story

around inhibiting 5-alpha reductase and reducing DHT to maintain or increase

hair growth is going to be finasteride and its close cousin, dutasteride.

Finasteride is effective in reducing DHT because of its actions in reducing

the type two isoenzyme or isoform of 5-alpha reductase.

It turns out there's three different

isoforms or what are sometimes called isoenzymes of 5-alpha reductase.

This is getting pretty far down in the weeds.

What I think most of you just need

to know is that finasteride reduces DHT, that's the net product of finasteride

and in doing so, it can increase hair count by as much as 20%.

Pretty remarkable if you think about it.

In addition, finasteride treatment done properly, which we'll define in a moment,

can reduce hair loss in 90% of all people that take it.

That is near staggering.

I mean, there aren't many pharmaceuticals

Out there that have that efficacy, really dramatic.

In addition, it's known to increase hair thickness by about 20- 30% overall,

so not just create new growth of hairs, and thicker hairs, but whatever hair you

do happen to have on your head, it can further thicken those.

The finasteride story is one, I think, of general success.

It really seems to improve hair growth,

and help you hold on to the hair that you have.

The issue with finasteride is twofold.

First of all, it is known to have some pretty significant side effects if it's

not dosed properly, and in particular populations of people.

This is because there is a wide variation

in the amount of the different Isozymes that people make.

This is why I brought up the Isozymes earlier.

Some people make more of Isozyme one and three, some people make more of

Isozyme two and three, and every variation thereof.

When people take finasteride, some people are very strong responders,

and they achieve really effective hair regrowth and maintenance of hair.

Other people less effective, although still pretty impressive.

But the catalog of side effects

that people experience at a given dose, varies widely.

There's a lot of trial and error that has to take place.

Also, I should point out that finasteride comes in two major forms.

There's an oral form and there's a topical form.

This is not unlike our discussion of minoxidil earlier.

Topical finasteride is typically taken

in 1% solution or ointment and rubbed into the head, sometimes it's now also

incorporated into shampoos, but typically it's put into a solution

that people rub into their head, and it is thought that the 1% solutions

are equivalent to one mg of systemic finasteride.

Now we need to take a step back and ask

why was finasteride developed in the first place?

Well, finasteride, as a fairly potent five

alpha reductase inhibitor, it's great at lowering DHT.

It was developed for treatment

of prostate enlargement and various issues of the prostate that are

associated with elevated DHT that occurs with age.

The topical finasteride were designed

with the hope that the finasteride would make it into the hair follicle,

and would inhibit DHT there and allow for more growth of the hair,

which apparently it does, but not make it into the systemic

circulation, or at least not at concentrations

sufficient enough to cause as many side effects as with the oral dosing.

Now, the problem is, it does make it into systemic circulation.

The issue is also,

that topical application of finasteride is harder to dose than oral finasteride.

I'm not saying you should be taking oral rather than topical finasteride,

but keep in mind that the dosages of finasteride that have been shown to be

effective for inducing hair growth, cover an enormous range.

As low as 0.01mg per day and as high as

five mg per day, which is a just staggering range.

Now, when trying to simplify the problem

of how much finasteride to take, either by way of oral tablet,

or by way of topical solution, we can get a bit of leverage on this

by thinking about how much DHT reduction occurs as a function of dose.

There, finasteride shows this really

interesting, what's called logarithmic distribution.

What it means is that,

for a dosage of 0.01mg of finasteride, you're going to achieve approximately

50% reduction in DHT, and that's systemic DHT,

so this is a blood draw measuring your DHT, then taking 0.01mg of finasteride.

Again, 0.01, very low dose of finasteride, repeated a couple of weeks,

measure people's DHT in their blood again, and you see that it's reduced by 50%.

However, at increasing dosages of 0.2mg, one mg, five mg of oral finasteride per

day, over the same period of time, the increase or I should say

the reduction in dihydrotestosterone, doesn't increase linearly.

It's not that you go from 50%-6 0%-75%-

100% with each increasing dose, it tapers off, it flattens out.

It tends to increase a little bit,

but it's a gradual slope increasing as you head from 0.2mg out to five mg.

What this means is that given that reducing DHT can cause various side

effects, sexual side effects, reductions in either sexual function or

sexual drive, as well as overall drive and motivation,

sometimes even some depressive symptoms that everything points to taking

the lowest effective dose of finasteride and starting with a very low dose

of finasteride because low doses of finasteride, even at that 0.01mg taken

orally daily, are already leading to a 50% reduction

in dihydrotestosterone and thereby taken for a long enough period of time,

should offset hair loss and stimulate hair growth.

One of the problems, however,

is that people will start taking finasteride at a low dose 0.1mg or 0.2mg,

maybe even 0.01mg, and there will be a reduction in their

DHT, but because of the long duration of that antigen phase,

they don't see a lot of change in hair growth in the first month or even two

months, and so what they end up doing is increasing their dosage and then they

start to see hair growth, but then they start to experience more side effects.

Now the side effects of oral finasteride

are serious enough and common enough in people that take finasteride

that the topical solutions were developed, but there are two one needs to exercise

caution because if we are going to translate between topical finasteride

and oral finasteride, with the understanding that topical

finasteride can actually make it into the systemic circulation,

we need to look at what's been shown in clinical studies,

which is that for instance, taking one ml of 0.25% finasteride applied

to the scalp, this is a very typical recommendation, translates to the same

thing that would be achieved with 2.5mg of oral finasteride.

When I say translates to the same thing,

what I mean is it leads to the same concentrations in the blood.

Now consider that 0.2mg, 0.2mg

of finasteride in the blood is known to be effective in generating new hair

growth and maintaining hair that one already has when they start the treatment.

If you think that the topical

finasterides are actually creating lower overall systemic concentrations

of finasteride, that is not necessarily the case.

Again, one ml of topical finasteride

at 0.25% leads to a 2.5mg concentration in the blood, when the effective dose

within the bloodstream by taking it orally as a pill is 0.2mg.

That might not seem like a big deal to you, although it is a big deal, right?

We're talking 2.5mg versus 0.2,

but it is a huge deal when you consider that the side effects of finasteride

increase as you increase the concentration of finasteride in the bloodstream.

Where does this leave us?

Should people who are interested in taking finasteride take the oral form

at low dose or take the topical form and simply try and apply it less often or

guess at what their systemic concentration of finasteride is.

Well, it's going to vary from person to person.

Some people are very sensitive to finasteride and not in the good sense.

The side effects just really show up quickly and they tend to be dramatic.

Other people, not so much.

The dosage recommendations that I was able to arrive at based on the clinical

studies and frankly in discussion with some doctors who prescribe

finasteride were the following: 0.5mg to one mg of finasteride as a tablet per

day seems to be an effective and pretty safe starting place for most people.

Now some people will find that even

that 0.5mg dosage is just going to cause side effects that are not going to work

for them, and they're going to either have to reduce their dosage of finasteride or

move to the topical or maybe cease taking finasteride altogether.

But for many people out there, that's going to be pretty well tolerated.

The key thing here is that one is going to have to wait some period of time

to see whether or not any hair growth occurs.

It is a naive and frankly foolish approach based on what we know about

the duration of that antigen phase of the hair to do one of these

treatments, wait a week or two and then decide to up your dose.

Now, it is not foolish to reduce your dose

if you're experiencing bad side effects, but to simply increase your dose because

you're not getting results quickly enough, that's not going to be the best approach.

I really encourage people who are going to explore the finasteride route,

to think of this as a long-term project and to really ratchet up slowly if at all,

starting initially with a low dose taken for a long period of time,

maybe even as long as 25 weeks before considering going up any further.

Certainly, as I mentioned before, if you need to go down further,

that's not going to be a problem, at least not in terms of reducing side

effects, you're not going to get additional hair growth,

but you're certainly not going to increase your side effects if you reduce your dose.

However, I will talk a little bit later about post-finasteride syndrome,

which is something that's getting increasing attention nowadays.

That's something that occurs after

people have taken finasteride for an extended period of time.

Now some of you have perhaps heard and I'll just tell you right here,

that the topical forms of finasteride are associated with far less side effects.

Now that might come as surprising given that topical application of finasteride

can lead to systemic distribution of finasteride.

But the numbers that are out there right

now, it's that topical finasteride is associated with 30-50% fewer side effects

or 30-5 0% less severe side effects than oral finasteride.

There are several things probably responsible for that.

One is that people tend to ratchet up

their dose of oral finasteride pretty quickly.

But keep in mind that the effective dose of finasteride in the blood is 0.2mg.

Earlier I said the typical topical finasteride solutions are 0.25%. People

are taking one ml of it, that equates to 2.5mg,

and so it seems like a massive overdosing but here's the discrepancy and here's

where we can arrive at some reasonable recommendations.

If you decide that finasteride is right for you, you get a prescription.

I would hope that you're monitoring your DHT levels and other hormone levels

that would be ideal, and working with a doctor, please.

0.5mg to one mg per day of oral

finasteride seems to be the best starting place.

For topical finasteride.

It's going to be that one ml of 0.25% that we talked about earlier,

but that's taken only one time per week, and you can fully expect that right after

the application you will have higher levels of finasteride in your bloodstream,

and therefore lower levels of DHT and that will alter across the week.

Most people are not going to be able

to measure their DHT on a day by day or even weekly basis.

It's just too expensive and labor intensive.

But I think those dosing regimens ought

to get people into more or less the same category of optimizing hair maintenance

and hair growth while minimizing finasteride side effects.

One point about finasteride taken either alone or in combination is that in recent

years, really in the last five or so years, there's been increasing discussion

about so-called post- finasteride syndrome.

Now post-finasteride syndrome is indeed a new phenomenon in the sense

that finasteride has been prescribed for a very long period of time

for treatment of the prostate, at dosages of about five mg per day.

That's a very high dose.

Sometimes lower, but as high as five mg per day, and for many years there was no

discussion about this post-finasteride syndrome.

What is post-finasteride syndrome?

Post-finasteride syndrome is when typically it's males.

This is where it's been described.

We'll take finasteride at any range of dosages, from 1mg to 5mg per day.

They're either doing this for prostate or more likely they're doing it to offset

hair loss and increase hair growth, and then they stop taking finasteride

for whatever reason, financial or it wasn't working for them

or the side effects were not to their liking, and they start to experience some

very severe what can only be called syndrome effects,

such as very reduced libido, very reduced erectile function,

very reduced mood to the point of depression, even suicidal depression.

This is pretty scary stuff, especially since it's occurring at an age

when most of these things are not typically occurring in males.

They can occur, but they're not typical

of younger males in their 20s and 30s and early 40s.

We have to ask ourselves what's going on here?

After all, people have taken finasteride for the prostate at fairly high dosages

without this post-finasteride syndrome when they've stopped.

Now these young males are taking

finasteride, they're coming off finasteride

and they're getting this very severe, very debilitating post-finasteride syndrome.

This has become a hot topic,

enough so that medical doctors who have been prescribing finasteride for a very

long time, have been forced to address this.

I think at first they were perplexed

and thought, I don't know, this might be psychosomatic, whatever that means.

As a neuroscientist who works on mind-body

connection, we know that nothing is truly psychosomatic.

Everything is of the mind and body.

But the point is that enough medical attention has been placed on post-

finasteride syndrome and trying to unravel exactly what that is.

Where there are now a few general conclusions about what might be going on.

First of all, it seems that younger males

taking finasteride in particular high dosages to improve hair growth or offset

hair loss seems to be one of the key variables.

We're not seeing this post-finasteride syndrome as much in older males.

In fact, it seems to occur more in males

in their 20s and 30s than males in their 40s and older.

One thing and it may relate to the ways in which Dihydrotestosterone, we know,

has a very key role in early embryonic development.

It's actually what's responsible for the male genitalia.

It's also responsible for certain things

in female development, but mainly in utero,

it's responsible for male development and development of the penis in particular.

Then around the time of puberty,

Dihydrotestosterone acts again, in what's called its activating effects

to further increase growth of the genitalia, increase the musculature

bone growth, et cetera, and increase libido and a number of other things.

It's probably also involved in the activation of puberty.

It's certainly not the only hormone involved in the activation of male

puberty but it's certainly one of the key players.

Dihydrotestosterone has these known early roles in embryonic development

and in puberty, but what post-finasteride syndrome seems to indicate is

that Dihydrotestosterone is likely having further effects on male maturation,

in particular, maturation of the hypothalamus in areas

of the brain that continue well into one's 20s and maybe even one's 30s.

Here I just want everyone to keep in mind

that we tend to think about development as childhood, teenage years, young adulthood,

adulthood, but really development never stops.

Development is something that starts

at conception and birth, of course, and then extends all the way out

until the point when we die, so even if we live to be in our late 90s

or achieve 100 years of age, development is occurring that entire time,

and these different hormones such as Dihydrotestosterone are having different

impact for across the lifespan and in different ways across the lifespan.

There isn't a clear conclusion about what post-finasteride syndrome is really all

about, but it points to the fact that DHT is likely to be involved

in development of the brain and the brain to genital axis,

because I mentioned that because so many of the side effects

that are associated with this post-finasteride syndrome seem to center

on sexual side effects, although there are also the depressive side effects.

Of course, those can be related to one another in either direction.

While I do understand that loss of one's

hair, or potential loss of one's hair can be particularly troubling and anxiety-

provoking, even cause depression in some cases, I am sensitive to that.

You also want to be sensitive to the fact that some of these treatments,

such as finasteride, can carry very serious side effects even

if you come off them AKA post-finasteride syndrome.

As long as we're talking about finasteride and this general pathway of 5α-Reductase

inhibition and thereby DHT inhibition and on and on topics and themes

and nomenclature you are now very familiar with, we have to talk about dutasteride.

Dutasteride is yet another molecule similar to finasteride,

but remember those three isoforms of the 5α-Reductase enzyme?

Well, it inhibits all three,

mainly type one and type two, but also type three, and it does it very potently.

As a consequence, the typical dosage of oral d utasteride,

get this, 0.5mg to 2.5mg taken orally, works 2-5 times faster than typical

finasteride at inducing hair regrowth and reduces DHT by, get this, 95%.

It's just near flatlines DHT, and that can occur at concentrations as

low as 0.5mg, although you will see prescriptions and people taking d

utasteride anywhere from 0.5 mg all the way to 2.5mg orally.

Now, not surprisingly,

dutasteride is associated with a lot of side effects related to the DHT pathway.

Things like reduction in sex drive,

reduction in overall drive, it also tends to impact other hormone

pathways, so it increases in estrogen prolactin.

That's why gynecomastia,

growth of male breast tissue sometimes occurs when people take dutasteride and so

you're probably asking, why would anyone take dutasteride?

Why not just take finasteride and wait for that hair growth?

Well,

the answer is that people are often very impatient, and it turns out that d

utasteride works, about 2-5 times faster than finasteride.

Some people don't want to wait a full 30

weeks or 40 weeks or 50 weeks or more in order to grow their hair back,

and they're very concerned about the hair loss that's occurring.

They will take what I hope would be a very low dose of dutasteride.

I realize that there are ways

to take dutasteride that can be safer, off set some of these side effects.

But by my read of the literature, if one is going to try to mildly inhibit

the DHT pathway, things like saw palmetto, things like topical caffeine,

which has some effect on the androgen pathway, but as we talked about earlier,

tickles other pathways, things like ketoconazole,

mild reduction in androgen receptor pathways in the follicle and very direct

because it's applied directly to the scalp.

Things like that are going to be the best

route for mild reductions in DHT as an attempt to maintain hair or grow hair.

Whereas if one really wants a potent stimulus for increasing hair growth,

that's very likely going to be finasteride, and hopefully low enough

dosages of finasteride and hopefully a patient enough patient person that they

are willing to wait the duration of time required for that hair growth to come back

because they understand that their antigen phase takes some time.

Now the holy grail of all this hair stuff

is in understanding that no one specific treatment is magic, and in fact,

there are now a number of good meta- analysis comparing the various

treatments we've talked about today alone or in combination.

We can summarize that pretty easily by saying that combination treatments

that involve a mechanical stimulus and a chemical stimulus are always going

to be better than either one alone, and within the mechanical category,

the stimulus that seems to work best is microneedling.

The combination of microneedling and finasteride, can lead to some pretty

robust and impressive hair regrowth, so much so that people that were...

I would only describe them as pretty bald

or bald, can regrow significant amounts of hair.

I've never seen examples of people

who were completely bald, meaning lacking all scalp hair to grow

back a full head of hair, but the combination of microneedling

and finasteride is probably the most effective way to go.

If you're going to do that, there's no reason why you couldn't also

use ketoconazole shampoo, could also use saw palmetto.

There's no reason to think that these things collide with one another,

although anytime you're inhibiting a DHT pathway, or whether or not you're

increasing or decreasing any hormone pathway for that matter,

you want to be careful about layering in too many different treatments because

you don't want your DHT level to go too low.

Let's keep in mind that even if you take a very low dose of finasteride and reduce

your DHT and don't have side effects, maybe just the mere addition of

saw palmetto, which leads to a slight reduction in DHT combined with some

caffeine ointment, would be sufficient enough to start

inducing some of the low DHT associated side effects.

You really have to see for you,

and that's one of the major issues in this whole field of hair growth

and regrowth is that people are highly individual in their response,

and in their side effect profile to these various treatments.

There's an enormous range there

and unfortunately, there's no way to know a priori before doing these treatments

what your response is going to be in terms of side effects.

You're simply going to have to explore, and I would hope that you would explore

starting with minimal, possible effective dosages,

and to do that in coordination with a medical professional so you could

really evaluate these things that the level of blood, and cosmetic changes.

In fact, that's a pretty good motivator

for thinking about the different treatments that we talked about today.

Everything from mechanical treatments,

as simple as massage, which we've all heard about,

but for which there really aren't a lot of data for supporting hair growth.

But certainly things like microneedling, which is a mechanical stimulus

for which there are pretty good data that it can improve hair growth.

Also things like saw palmetto, a weak DHT antagonist.

Also things like ketoconazole shampoo, which again is a weak DHT antagonist

and operates through some other pathways as well to stimulate hair growth.

My suggestion is that anyone young, old,

male, female, who's thinking about embarking on various treatments for

offsetting hair loss and stimulating hair growth, consider both mechanical

approaches, and the approaches that attack the chemical pathways,

that can stimulate hair growth, and can inhibit the inhibitors of hair growth.

In fact, that's the reason why we spend so much time on the biology of hair growth

and what shuts down hair growth early on in today's episode,

and then systematically went through each of the various treatments that relies

on and in some cases hinges entirely on either a mechanical stimulus or

a chemical stimulus in order to exert its effects.

My goal today was not to overwhelm you with a ton of biology about hair,

although we did cover a lot of biology of hair and stem cells and hair growth.

My goal in describing all that was really for you to be able to hear about various

treatments, whether or not it's lasers or PRP or finasteride, dutasteride,

or whatever is coming next that we're sure to hear about soon online

and from the medical community, and to be able to place those into bins

related to their known or potential mechanisms and then to be able to step

back and evaluate, which, if any, of those treatments might be right for you.

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All about the biology of hair and hair

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