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. Our first sponsor is Helix Sleep. Helix Sleep makes mattresses and pillows
that are the absolute highest quality. I've talked many times before on this
podcast about the fact that sleep is the foundation of mental health,
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I certainly love mine. Again, if you're interested, go to helixsleep.com /huberman for up
to $350 off and two free pillows. Today's episode is also brought
to us by HVMN ketone-IQ. Ketone-IQ is a ketone supplement
that increases blood ketones. I want to be very clear that I, like most
people have heard of the ketogenic diet, but I, like most people,
do not follow a ketogenic diet. That is, I'm not in ketosis. However, most people don't realize
that you can still benefit from increasing your blood ketones, which is what
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not following a ketogenic diet. I sometimes also use Ketone-IQ prior
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Huberman to get 20% off. Again, that's hvmn.com, and use
the code HUBERMAN to get 20% off. Today's episode is also
brought to us by ROKA. ROKA makes eyeglasses and sunglasses that were designed with the biology
of the visual system in mind. I've spent a lifetime working
on the biology of the visual system, and I can tell you that your visual system
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to save 20% off your first order. Again, that's roka.com,
enter the code Huberman at checkout. 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 and acknowledge one of our
sponsors, Athletic Greens. Athletic Greens, now called AG1,
is a vitamin mineral probiotic drink that covers all of your
foundational nutritional needs. I've been taking Athletic Greens since 2012, so I'm delighted that they're
sponsoring the podcast. The reason I started taking Athletic Greens and the reason I still
take Athletic Greens once or usually twice a day is that it gets me the
probiotics that I need for gut health. Our gut is very important. It's populated by gut microbiota
that communicate with the brain, the immune system,
and basically all the biological systems of our body to strongly impact our
immediate and long-term health. Those probiotics and Athletic Greens are
optimal and vital for macrobiotic health. In addition, Athletic Greens contains a number of adaptogens, vitamins,
and minerals that make sure that all of my foundational nutritional
needs are met, and it tastes great. If you'd like to try Athletic Greens,
you can go to AthleticGreens .com/ huberman, and they'll give you five free
travel packs that make it really easy to mix up Athletic Greens while you're
on the road in the car, on the plane, et cetera, and they'll give you
a year's supply of vitamin D3 K2. Again,
that's athleticgreens.com/huberman to get the five free travel packs
and the year supply of vitamin D3 K2. 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. I'd like to just take a brief break and thank one of our
sponsors, which is LMNT. LMNT is an electrolyte drink that has
everything you need and nothing you don't. That means plenty of salt, sodium, magnesium, and potassium, the so-called
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nerve cells, also called neurons. We now know that even slight reductions in electrolyte concentrations or
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and physical performance. LMNT contains a science-backed electrolyte ratio of 1,000 milligrams,
that's one gram, of sodium, 200 milligrams of potassium,
and 60 milligrams of magnesium. I typically drink LMNT first thing in the morning when I wake up in order
to hydrate my body and make sure I have enough electrolytes,
and while I do any kind of physical training and after physical training as
well, especially if I have been sweating a lot, and certainly I drink LMNT
in my water when I'm in the sauna and after going in the sauna because
that causes quite a lot of sweating. If you'd like to try LMNT, you can go to drinklmnt,
that's drinklmnt.com/huberman. To claim a free element sample
pack with your purchase. Again, that's drinklmnt
, drinklmnt.com/huberman. 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. If you're learning from and or enjoying this podcast, please subscribe
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