Why do we lose hair?
Androgenetic Alopecia
As its name suggests, androgenetic alopecia is a genetic form of hair loss that involves
androgens (male sex hormones). However, it’s also known as androgenic alopecia, AGA, male
pattern baldness (MPB) and female pattern baldness. In this blog, AGA is used. I also use the
term "MPB region" -this refers to both male and female pattern baldness because each
involves the same region of the scalp.
Whatever you call it (I used to call it “the bane of my life”) AGA is a condition, not a disease even
though it might feel like one!
This chapter examines the current theory for AGA and explains why it’s wrong!
1.1 DHT, androgen receptor sites and 5-alpha reductase
1.2 Female pattern baldness
1.3 Problems, problems, problems
1.1 DHT, androgen receptor sites and 5-alpha reductase
There’s been much debate about the true cause of AGA. Several factors have been linked to it
(genetics, hormones, nutrition, etc) and many theories exist that try to explain exactly what
mechanism is taking place.
There’s no doubt that androgens are the main blame -it’s long been known that a derivative of
testosterone called dihydrotestosterone (DHT) is directly related to this condition. But, exactly
how DHT causes AGA is still unclear to the hair loss industry.
Most hair loss professionals believe that DHT chokes the blood supply to the follicles. (A follicle
is basically a pouch through which the hair shaft grows).
Testosterone first gets converted into DHT by 5-alpha reductase (an enzyme produced within
the scalp). DHT then attaches to androgen receptor sites in the follicles (a receptor site is an
arrangement of molecules that binds to other molecules with a complimentary shape).
If DHT is produced in excess, and attaches to a large number of androgen receptor sites, it may
accumulate within a follicle and block its blood supply. This forces it to prematurely enter the
resting stage of the hair growth cycle.*
* The hair growth cycle -Anagen (the growth stage) normally lasts 3 to 5 years. Catagen (a 2
week shedding stage) is followed by telogen (the resting stage) lasting 3 to 4 months. Anagen
then restarts.
If a follicle enters the resting stage earlier than usual, the time spent in its growth stage will
obviously be reduced. This results in hair that becomes both shorter and thinner with each
successive growth cycle, and also causes hair follicle miniaturisation. Eventually the follicle
shuts down - it becomes dormant and hair growth stops.
If you ask almost any hair loss professional (trichologist, dermatologist, etc) for the mechanism
behind AGA, that's what they’ll tell you.
Convinced?
You shouldn't be - this theory has its problems!
I’ll reveal all these problems shortly, but first of all, you might be wondering how hair loss
involving male sex hormones can also affect women.
1.2 Female pattern baldness
Up to 50% of women will experience AGA to some extent during their lives.
The reason for this is simply because women produce a small amount of testosterone (mostly
from their adrenal glands) 1. Both men and women produce a small quantity of each others’
hormones in this way.
For most women, their oestrogen levels are usually high enough to completely overwhelm the
quantity of testosterone they produce. And the opposite is true for men.
It’s when oestrogen levels become low (e.g., due to the menopause) or
there’s an increase in androgen production (e.g., by stress, weight
training, etc) that AGA can start to show itself on the female body.
In women, AGA usually appears as diffuse thinning (this is evenly
distributed hair loss) on the crown of the head (see Figure 1).
Now, let’s get back to the current theory for AGA.
1.3 Problems, problems, problems!
To explain all the problems this current theory has, take a good look at
Figure 2.
This photo shows a typical example of a man with severe AGA, and you
can clearly see that the familiar MPB region of hair loss has almost fully
developed.
This MPB region needs closer examination:
Ok, first of all, notice how his hairline has receded from the left and right
temples, but not entirely from the center front region. In some cases,
this area keep growing reasonably strong, healthy hair throughout life
despite extensive hair loss all around it. I call this, "remnant hair".
You can see more remnant hair trying very hard to grow within the center crown area. And
behind it, another significant area of hair loss has developed into a bald patch at the back of the
head.
His baldness seems to have developed from the front (both left and right temples) and back of
his head independently (i.e., two separate areas of hair loss). And, where these two areas of
loss meet in the middle, some remnant hair continues to grow.
Notice how hair continues to grow normally on the sides and lower back of this head. This, of
course, gives him that familiar “male pattern” profile, or horseshoe shape, synonymous with this
type of hair loss.
Have you ever wondered why this pattern of hair loss always seems to emerge in nearly every
severe case of AGA?
It’s been observed that both the androgen receptor gene 2 and 5-alpha reductase 3 appear to be
more active within the MPB region in those who suffer AGA. According to the current theory,
this observation indicates that hair follicles within just the MPB region must be genetically
programmed 4 for this to occur.
But this still doesn’t explain why only hair follicles in this region should carry the AGA gene(s). In
other words, it still doesn’t give a reason why hair loss should be confined to the MPB region.
It’s been acknowledged by the hair loss profession that the actual mechanism causing hair
follicle miniaturisation within just the MPB region is still unclear. Furthermore, they accept that
several genes may be involved and that some other mechanism must also be taking place 5.
Another problem with this theory is that androgens are hair growth stimulators 6.
That’s right, androgens cause hair to grow!
The most obvious example of this is when pubic, facial and body hair starts growing during
puberty, all of which is caused by androgens (especially DHT).
This fact has been pestering trichologists and dermatologists for years – DHT should help hair
to grow, not hinder it. So there must be something else going on that's causing the follicles to
shrivel.
No explanation has been given by the hair loss industry as to how DHT can cause both hair loss
and hair growth.
Finally, DHT will not cause AGA in someone without the genetic tendency towards it (even in
high concentrations).
All of this now raises several questions concerning AGA. Questions that must be answered
before any theory can be recognized as the true underlying mechanism for this type of hair loss.
The current theory cannot answer these very important questions concerning the hair loss
process:
Q1. Why does remnant hair sometimes continue to grow within the MPB region despite
extensive hair loss all around it?
Q2. What causes the same male pattern profile (horseshoe shape) to develop in almost all
severe cases of AGA?
Q3. How can DHT be linked to both hair loss and hair growth?
Q4. What is the genetic connection to AGA?
Q5. Why does the rate of hair loss vary from person to person? (Up to 20% of men can suffer
rapid hair loss starting as early as puberty. But most don't experience AGA until later on in life,
and for them, this can be a much more gradual process).
Q6. Why does the location of hair loss vary within the MPB region? (Some people only lose hair
from the front (temple recession) or back of the scalp (a bald patch), whilst others lose hair from
both these regions simultaneously).
The next time, I’ll explain how skull expansion causes AGA, and provides answers to all these
questions.
androgens (male sex hormones). However, it’s also known as androgenic alopecia, AGA, male
pattern baldness (MPB) and female pattern baldness. In this blog, AGA is used. I also use the
term "MPB region" -this refers to both male and female pattern baldness because each
involves the same region of the scalp.
Whatever you call it (I used to call it “the bane of my life”) AGA is a condition, not a disease even
though it might feel like one!
This chapter examines the current theory for AGA and explains why it’s wrong!
1.1 DHT, androgen receptor sites and 5-alpha reductase
1.2 Female pattern baldness
1.3 Problems, problems, problems
1.1 DHT, androgen receptor sites and 5-alpha reductase
There’s been much debate about the true cause of AGA. Several factors have been linked to it
(genetics, hormones, nutrition, etc) and many theories exist that try to explain exactly what
mechanism is taking place.
There’s no doubt that androgens are the main blame -it’s long been known that a derivative of
testosterone called dihydrotestosterone (DHT) is directly related to this condition. But, exactly
how DHT causes AGA is still unclear to the hair loss industry.
Most hair loss professionals believe that DHT chokes the blood supply to the follicles. (A follicle
is basically a pouch through which the hair shaft grows).
Testosterone first gets converted into DHT by 5-alpha reductase (an enzyme produced within
the scalp). DHT then attaches to androgen receptor sites in the follicles (a receptor site is an
arrangement of molecules that binds to other molecules with a complimentary shape).
If DHT is produced in excess, and attaches to a large number of androgen receptor sites, it may
accumulate within a follicle and block its blood supply. This forces it to prematurely enter the
resting stage of the hair growth cycle.*
* The hair growth cycle -Anagen (the growth stage) normally lasts 3 to 5 years. Catagen (a 2
week shedding stage) is followed by telogen (the resting stage) lasting 3 to 4 months. Anagen
then restarts.
If a follicle enters the resting stage earlier than usual, the time spent in its growth stage will
obviously be reduced. This results in hair that becomes both shorter and thinner with each
successive growth cycle, and also causes hair follicle miniaturisation. Eventually the follicle
shuts down - it becomes dormant and hair growth stops.
If you ask almost any hair loss professional (trichologist, dermatologist, etc) for the mechanism
behind AGA, that's what they’ll tell you.
Convinced?
You shouldn't be - this theory has its problems!
I’ll reveal all these problems shortly, but first of all, you might be wondering how hair loss
involving male sex hormones can also affect women.
1.2 Female pattern baldness
Up to 50% of women will experience AGA to some extent during their lives.
The reason for this is simply because women produce a small amount of testosterone (mostly
from their adrenal glands) 1. Both men and women produce a small quantity of each others’
hormones in this way.
For most women, their oestrogen levels are usually high enough to completely overwhelm the
quantity of testosterone they produce. And the opposite is true for men. It’s when oestrogen levels become low (e.g., due to the menopause) or
there’s an increase in androgen production (e.g., by stress, weight
training, etc) that AGA can start to show itself on the female body.
In women, AGA usually appears as diffuse thinning (this is evenly
distributed hair loss) on the crown of the head (see Figure 1).
Now, let’s get back to the current theory for AGA.
1.3 Problems, problems, problems!
Figure 2.
This photo shows a typical example of a man with severe AGA, and you
can clearly see that the familiar MPB region of hair loss has almost fully
developed.
This MPB region needs closer examination:
Ok, first of all, notice how his hairline has receded from the left and right
temples, but not entirely from the center front region. In some cases,
this area keep growing reasonably strong, healthy hair throughout life
despite extensive hair loss all around it. I call this, "remnant hair".
You can see more remnant hair trying very hard to grow within the center crown area. And
behind it, another significant area of hair loss has developed into a bald patch at the back of the
head.
His baldness seems to have developed from the front (both left and right temples) and back of
his head independently (i.e., two separate areas of hair loss). And, where these two areas of
loss meet in the middle, some remnant hair continues to grow.
Notice how hair continues to grow normally on the sides and lower back of this head. This, of
course, gives him that familiar “male pattern” profile, or horseshoe shape, synonymous with this
type of hair loss.
Have you ever wondered why this pattern of hair loss always seems to emerge in nearly every
severe case of AGA?
It’s been observed that both the androgen receptor gene 2 and 5-alpha reductase 3 appear to be
more active within the MPB region in those who suffer AGA. According to the current theory,
this observation indicates that hair follicles within just the MPB region must be genetically
programmed 4 for this to occur.
But this still doesn’t explain why only hair follicles in this region should carry the AGA gene(s). In
other words, it still doesn’t give a reason why hair loss should be confined to the MPB region.
It’s been acknowledged by the hair loss profession that the actual mechanism causing hair
follicle miniaturisation within just the MPB region is still unclear. Furthermore, they accept that
several genes may be involved and that some other mechanism must also be taking place 5.
Another problem with this theory is that androgens are hair growth stimulators 6.
That’s right, androgens cause hair to grow!
The most obvious example of this is when pubic, facial and body hair starts growing during
puberty, all of which is caused by androgens (especially DHT).
This fact has been pestering trichologists and dermatologists for years – DHT should help hair
to grow, not hinder it. So there must be something else going on that's causing the follicles to
shrivel.
No explanation has been given by the hair loss industry as to how DHT can cause both hair loss
and hair growth.
Finally, DHT will not cause AGA in someone without the genetic tendency towards it (even in
high concentrations).
All of this now raises several questions concerning AGA. Questions that must be answered
before any theory can be recognized as the true underlying mechanism for this type of hair loss.
The current theory cannot answer these very important questions concerning the hair loss
process:
Q1. Why does remnant hair sometimes continue to grow within the MPB region despite
extensive hair loss all around it?
Q2. What causes the same male pattern profile (horseshoe shape) to develop in almost all
severe cases of AGA?
Q3. How can DHT be linked to both hair loss and hair growth?
Q4. What is the genetic connection to AGA?
Q5. Why does the rate of hair loss vary from person to person? (Up to 20% of men can suffer
rapid hair loss starting as early as puberty. But most don't experience AGA until later on in life,
and for them, this can be a much more gradual process).
Q6. Why does the location of hair loss vary within the MPB region? (Some people only lose hair
from the front (temple recession) or back of the scalp (a bald patch), whilst others lose hair from
both these regions simultaneously).
The next time, I’ll explain how skull expansion causes AGA, and provides answers to all these
questions.
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