2. Skull Expansion Causes AGA
This part explains how skull expansion causes AGA, and by doing so, provides answers to
all questions from part 1
2.1 Bone resorption and remodelling
2.2 Scalp capillary network
2.3 Remnant hair and development of the male pattern profile
2.4 Hormones and hair loss
2.5 Genetic link to AGA
2.6 Rate and location of hair loss
2.7 Re-evaluation of the current theory
2.8 What skull shapes lead to skull expansion?
2.1 Bone resorption and remodelling
When you’re growing up, your skeleton obviously gets bigger and bigger. This, of course,
includes your skull, which not only grows in size, but also changes shape.
Once you reach adulthood, bone resorption and remodelling will continue to maintain skeletal
integrity.
Together, these two essential processes constantly renew the entire skeleton throughout life.
For some, this simply means maintaining the bones – keeping them strong and healthy. But, for
those who suffer AGA, certain bones of the skull will continue to grow.
This is skull expansion, and is the direct cause of AGA within the MPB region of the scalp for
both men and women. It can also be considered as an exaggeration of the bone resorption and
remodelling processes.
2.2 Scalp capillary network
For all those with the genetic predisposition towards skull expansion/AGA, this process will
progressively stretch and pull tight the scalp tissue that overlies the skull. This constricts the
blood vessels which then reduces the blood supply.
Figure 3 shows how the main arterial network of the scalp will provide a strong blood supply to
the back and sides. But, within the MPB region, the follicles are only served by a much weaker
capillary network (not shown in the diagram). This illustrates how the MPB region is the most
likely area of the scalp to suffer a reduction in blood supply.
Skull expansion will, within the MPB region, reduce the flow of blood and so decrease the
supply of nutrients required by follicles to grow hair. In time, hair follicle miniaturisation and hair
loss will result.
2.3 Remnant hair and development of the male pattern profile
If you compare Figure 2 from part 1 with Figure 4 below, you can see that the
bones of the skull that underlie the MPB region are the frontal and parietal bones.
Figure 5 details these two bones. The frontal and parietal eminences represent the areas where
ossification commenced (in other words, where bone initially began growing as a foetus within
the womb).
From these areas, bone grows outwards, pushing against the surrounding bone tissue and so
causing the frontal and parietal bones to grow larger in surface area. It’s through this linear
growth that the full adult skull size is eventually reached.
There are two parietal bones (left and right) so each one obviously has its own parietal
eminence. But, you can also see that there are two frontal eminences as well. That’s because
the frontal bone actually starts out as two bones within the womb.
As these develop, they gradually fuse together and can leave a remnant suture line* (as shown
in Figure 5). This will usually disappear as a baby grows into a child, but the two frontal
eminences remain.
* Suture lines mark the connection between the bones of the skull.
Skull expansion of these two frontal eminences (left and right) will cause hair loss at the front
hairline. This explains why, in most cases, hair recedes at the left and right temples and not
across the entire front hairline.
It also explains why some remnant hair often continues to grow at the front - you can see this in
Figure 2 and Figure 6 below. (Basically, remnant hair will continue to grow wherever there is no,
or little, skull expansion).
This provides the answer to question 1 in part 1.
In Figure 6 you can see how the frontal and parietal bones of the skull relate to the pattern of
hair loss for someone with severe AGA.
Now, can you see how the temporal ridge seems to coincide with hair loss along the sides of
the head?
Well, this is no coincidence!
Within each parietal bone, the parietal eminence (that causes skull expansion) only lies above
the temporal ridge. So, it logically follows that hair loss can also only occur above this line. And,
as a result, the temporal ridge marks an approximate boundary between hair loss and hair
growth on the sides of the head.
Hair will always continue to grow at the lower back of the head because here, the occipital bone
largely remains unaffected by parietal bone expansion. You can clearly see the occipital bone in
Figure 4.
By analysing of the structure of the skull (specifically the frontal eminences, temporal ridge and
occipital bone), the familiar male pattern profile of hair loss can be explained.
This provides the answer to question 2 in part 1.
2.4 Hormones and hair loss
Androgens, like DHT, can be linked to both hair loss and hair growth. DHT causes facial, body
and pubic hair to grow in men during puberty, but it also has a direct connection with AGA.
How can this be?
DHT is a steroid hormone which means that, whilst it stimulates new hair growth, it also has an
anabolic effect on bone formation 7. In other words, it makes bone grow! And it’s through this
continued bone growth (skull expansion) that overwhelms the hair growth promoting effects of
DHT.
This provides the answer to question 3 in part 1.
For men at puberty, steroid hormones are responsible for the rapid increase in bone growth
(and muscle development) they experience. This also explains the connection that exists
between bodybuilding and AGA - bodybuilders often suffer hair loss because intense weight
training will increase testosterone and DHT levels (as do anabolic steroids).
2.4.1 Sebum
Sebum is a waxy, oily substance secreted by the sebaceous glands within hair follicles. Its
production is governed by androgens (including DHT) so it’s easy to see the connection
between DHT and sebum. As well as stimulating the skull expansion process, DHT can also
contribute to hair loss locally (i.e., within hair follicles) through excessive sebum production.
However, this is very much secondary to the skull expansion process.
2.4.2 Female hormones
Women generally experience AGA to a much lesser extent than men due to their much higher
oestrogen and lower testosterone levels.
Whereas steroid hormones like testosterone and its derivatives have an anabolic effect on bone
growth, oestrogen decreases the bone resorption process 8. Since the oestrogen levels in a
healthy pre-menopausal woman's body greatly exceed those of testosterone, there will be a
reduced tendency towards skull expansion.
However, low (post-menopausal) oestrogen levels can often lead to AGA. That’s because
testosterone levels will be higher (relative to the lower oestrogen levels) and so the bone
resorption, remodelling and skull expansion processes will all increase for those women with the
genetic predisposition towards AGA.
So, for all those men and women with this genetic predisposition, DHT will cause the frontal and
parietal eminences to grow during adulthood. This is the true underlying mechanism behind
AGA.
But, why do some have the genetic predisposition towards skull expansion/AGA whilst others
do not?
2.5 Genetic link to AGA
It’s long been known that a genetic link to AGA exists.
Most research currently places focus on the 5-alpha reductase and androgen receptor genes.
However, it’s the genes that determine skull shape and size that are responsible for AGA.
2.5.1 Sexual dimorphism
Sexual dimorphism 9 means that the form (shape, size, etc) can vary between the two sexes.
For example, women usually have wider hips, whilst men are generally taller and heavier (due
to bigger bones and greater muscle development).
Skull expansion is a largely sexually dimorphic characteristic, affecting men much more so than
women. Men will, quite simply, grow a bigger skull than most women. (This reflects the higher
androgen levels men have, as well as differences in genetic inheritance). More specifically to
AGA, this means that, for most women, the frontal and parietal bones will be proportionately
smaller than in the majority of men.
2.5.2 Growth potential
Associated with skull shape and size is its growth potential. This simply means that some skull
shapes are more likely to grow than others.
For example, someone whose skull shape has a high growth potential will be especially prone
to skull expansion, and so invariably develop severe AGA. And it follows that, anyone else with
a very similar skull shape and growth potential will most likely develop AGA to the same
extent.
Of course, very similar skull shapes often run in families, and you may already be aware that, if
your mother or father lost their hair, you too have a very high chance of losing yours as well.
(This explains the strong genetic connection that AGA can have within a family, especially
between fathers and their sons).
You now know that the genetically determined characteristics of skull shape and size form the
genetic link to AGA.
This provides the answer to question 4 in part1.
2.6 Rate and location of hair loss
Skull shape and its growth potential can account for the different rates of hair loss, and the
location (within the MPB region) in which it occurs.
2.6.1 Rate
The rate at which you lose hair is directly related to the extent of your skull expansion. This,
quite obviously means that, the more your skull expands, the more hair you're likely to lose.
For the 20% of men whose skull shape has a high growth potential, this explains why AGA will
rapidly start developing from puberty and can lead to extensive hair loss by the age of thirty.
However, in most cases, AGA won’t start until later on in life and will be a much more gradual
process - these skull shapes have a low growth potential.
Growth potential can, therefore, account for the variations that exist in the rate of hair loss.
This answers question 5 in part 1.
2.6.2 Location
Within the MPB region, the location in which AGA develops can vary.
For some, hair loss develops at the front (temple recession) or back of the scalp (a bald patch).
For others, AGA will affect both these areas simultaneously and will cause either diffuse
thinning throughout the MPB region, or more concentrated hair loss (a bald patch at the back
together with receding temples at the front).
Skull expansion of the frontal bone will form a receding hairline from the temples. Skull
expansion of the parietal bones will cause hair loss at the back of the scalp. And skull
expansion of the frontal and parietal bones simultaneously will create hair loss in the front and
back of the scalp at the same time.
This answers question 6 from part 1.
Convinced?
You should be!
Skull expansion is the true underlying mechanism behind AGA. It has explained how, for those
with the genetically determined characteristics of skull shape and size, DHT will cause the
frontal and parietal eminences to grow during adulthood. It has also explained how DHT can be
associated with both hair loss and hair growth, and provided answers to all six questions from
part 1 (something the current theory cannot do).
And, if you're in any doubt about skull expansion, why not simply contact a hair loss
specialist and ask those six questions – I guarantee they will not know the answers!
2.7 Re-evaluation of the current theory
Although the current theory for AGA could not answer those questions, it did nevertheless, raise
some issues that now need to be addressed.
Referring back to part 1, these involve the following –
1. Androgen receptor sites, 5-alpha reductase and DHT all appear to be more abundant in
the MPB region of the scalp than in non-MPB regions for those with the genetic predisposition
towards AGA.
2. A gene (or possibly several) may make follicles genetically programmed towards hair
loss (but only in the MPB region).
Ok, we’ve already looked at this before, but let’s examine these two fundamental parts to this
theory in more detail –
1. First of all, let me make this perfectly clear: 5-alpha reductase, androgen receptor sites and
DHT all exist in hair follicles for hair growth, not hair loss – your body does not want to lose
something that insulates and protects your scalp from the sun, rain, cold, bugs, etc.
The current theory does not explain how and why any such proliferation of androgen receptor
sites, 5-alpha reductase and DHT should occur within just the MPB region and nowhere else. In
my view, any proliferation of androgen receptor sites is due to upregulation, also known as
reflex hyperandrogenicity 10.
What this basically means is that the body tries (unsuccessfully) to grow more hair (i.e., to offset
skull expansion) by producing more DHT. It creates an increased expression of the androgen
receptor gene within the area of weak hair growth which then causes receptor site proliferation
to occur. (Once again, remember, that's what androgens like DHT do - they stimulate bone,
muscle and hair growth, not hair loss).
Furthermore, 5-alpha reductase, androgen receptor sites and DHT also occur in bone tissue 7.
Coincidence?
No way!
To me, it seems crystal clear that DHT accumulation within the frontal and parietal bones cause
these bones of the skull to continue growing – i.e., skull expansion.
2. The current theory has identified a number of genes that may be involved in AGA. These
include: the androgen receptor or AR gene (STU1), 5a-reductase genes (SRD5A1 and
SRD5A2), CYP17, etc. But, once again, no reason has been given why follicles in just one
(MPB) region of the scalp should suffer hair loss, but not in any other. This theory simply states
that each follicle must be genetically programmed for hair loss and that they appear to have a
greater number of androgen receptor sites 11.
As you now know, it’s the genes responsible for skull growth (i.e., shape and size) that cause
AGA. And, it’s this genetic connection that explains how AGA occurs within just the MPB region.
Through the upregulation of DHT (hyperandrogenicity, as described above) the increased
expression of the androgen receptor gene within the MPB region can be accounted for.
Now you know that skull expansion is the true cause of AGA, there is a new question that needs
to be asked...
Copyright © 2008 by Paul Taylor 16
Skull Expansion – True Cause of Genetic Hair Loss www.top-hair-loss-remedy.com
2.8 What skull shapes lead to skull expansion?
Figure 7 (below) shows two different skull shapes: one with no hair loss at all (i.e., a skull shape
that did not experience any skull expansion), and one with severe hair loss (i.e., the eventual
skull shape reached after, perhaps, many years of skull expansion).
You can see that, for those who suffer no hair loss at all, they’ll generally have a slightly more
square shape to the skull. But, for those who suffer severe AGA, the skull expansion process
will often create a somewhat rounded skull shape. (This rounded shape can also appear in both
front and side profiles).
This is only a very simple explanation, but it does nevertheless reveal the skull shapes that
generally correlate to the two extreme examples shown in Figure 7.
Other skull shape variations exist, and these determine where within the MPB region skull
expansion/AGA develops (front, back or both), and the rate at which this will happen. There are
also several skull shape characteristics that can be recognized and used to accurately predict
whether someone is likely to experience future hair loss and to what extent.
To learn about these skull shape characteristics and find out what skull shapes cause hair loss
at the front, back or both regions of the scalp, you'll need to read the next part.
This part explains how skull expansion causes AGA, and by doing so, provides answers to
all questions from part 1
2.1 Bone resorption and remodelling
2.2 Scalp capillary network
2.3 Remnant hair and development of the male pattern profile
2.4 Hormones and hair loss
2.5 Genetic link to AGA
2.6 Rate and location of hair loss
2.7 Re-evaluation of the current theory
2.8 What skull shapes lead to skull expansion?
2.1 Bone resorption and remodelling
When you’re growing up, your skeleton obviously gets bigger and bigger. This, of course,
includes your skull, which not only grows in size, but also changes shape.
Once you reach adulthood, bone resorption and remodelling will continue to maintain skeletal
integrity.
Together, these two essential processes constantly renew the entire skeleton throughout life.
For some, this simply means maintaining the bones – keeping them strong and healthy. But, for
those who suffer AGA, certain bones of the skull will continue to grow.
This is skull expansion, and is the direct cause of AGA within the MPB region of the scalp for
both men and women. It can also be considered as an exaggeration of the bone resorption and
remodelling processes.
2.2 Scalp capillary network
For all those with the genetic predisposition towards skull expansion/AGA, this process will
progressively stretch and pull tight the scalp tissue that overlies the skull. This constricts the
blood vessels which then reduces the blood supply.
Figure 3 shows how the main arterial network of the scalp will provide a strong blood supply to
the back and sides. But, within the MPB region, the follicles are only served by a much weaker
capillary network (not shown in the diagram). This illustrates how the MPB region is the most
likely area of the scalp to suffer a reduction in blood supply.
Skull expansion will, within the MPB region, reduce the flow of blood and so decrease the
supply of nutrients required by follicles to grow hair. In time, hair follicle miniaturisation and hair
loss will result.
2.3 Remnant hair and development of the male pattern profile
If you compare Figure 2 from part 1 with Figure 4 below, you can see that the
Figure 5 details these two bones. The frontal and parietal eminences represent the areas where
ossification commenced (in other words, where bone initially began growing as a foetus within
the womb).
From these areas, bone grows outwards, pushing against the surrounding bone tissue and so
causing the frontal and parietal bones to grow larger in surface area. It’s through this linear
There are two parietal bones (left and right) so each one obviously has its own parietal
eminence. But, you can also see that there are two frontal eminences as well. That’s because
the frontal bone actually starts out as two bones within the womb.
As these develop, they gradually fuse together and can leave a remnant suture line* (as shown
in Figure 5). This will usually disappear as a baby grows into a child, but the two frontal
eminences remain.
* Suture lines mark the connection between the bones of the skull.
Skull expansion of these two frontal eminences (left and right) will cause hair loss at the front
hairline. This explains why, in most cases, hair recedes at the left and right temples and not
across the entire front hairline.
It also explains why some remnant hair often continues to grow at the front - you can see this in
Figure 2 and Figure 6 below. (Basically, remnant hair will continue to grow wherever there is no,
or little, skull expansion).
In Figure 6 you can see how the frontal and parietal bones of the skull relate to the pattern of
hair loss for someone with severe AGA.
Now, can you see how the temporal ridge seems to coincide with hair loss along the sides of
the head?
Well, this is no coincidence!
Within each parietal bone, the parietal eminence (that causes skull expansion) only lies above
the temporal ridge. So, it logically follows that hair loss can also only occur above this line. And,
as a result, the temporal ridge marks an approximate boundary between hair loss and hair
growth on the sides of the head.
Hair will always continue to grow at the lower back of the head because here, the occipital bone
largely remains unaffected by parietal bone expansion. You can clearly see the occipital bone in
Figure 4.
By analysing of the structure of the skull (specifically the frontal eminences, temporal ridge and
occipital bone), the familiar male pattern profile of hair loss can be explained.
This provides the answer to question 2 in part 1.
2.4 Hormones and hair loss
Androgens, like DHT, can be linked to both hair loss and hair growth. DHT causes facial, body
and pubic hair to grow in men during puberty, but it also has a direct connection with AGA.
How can this be?
DHT is a steroid hormone which means that, whilst it stimulates new hair growth, it also has an
anabolic effect on bone formation 7. In other words, it makes bone grow! And it’s through this
continued bone growth (skull expansion) that overwhelms the hair growth promoting effects of
DHT.
This provides the answer to question 3 in part 1.
For men at puberty, steroid hormones are responsible for the rapid increase in bone growth
(and muscle development) they experience. This also explains the connection that exists
between bodybuilding and AGA - bodybuilders often suffer hair loss because intense weight
training will increase testosterone and DHT levels (as do anabolic steroids).
2.4.1 Sebum
Sebum is a waxy, oily substance secreted by the sebaceous glands within hair follicles. Its
production is governed by androgens (including DHT) so it’s easy to see the connection
between DHT and sebum. As well as stimulating the skull expansion process, DHT can also
contribute to hair loss locally (i.e., within hair follicles) through excessive sebum production.
However, this is very much secondary to the skull expansion process.
2.4.2 Female hormones
Women generally experience AGA to a much lesser extent than men due to their much higher
oestrogen and lower testosterone levels.
Whereas steroid hormones like testosterone and its derivatives have an anabolic effect on bone
growth, oestrogen decreases the bone resorption process 8. Since the oestrogen levels in a
healthy pre-menopausal woman's body greatly exceed those of testosterone, there will be a
reduced tendency towards skull expansion.
However, low (post-menopausal) oestrogen levels can often lead to AGA. That’s because
testosterone levels will be higher (relative to the lower oestrogen levels) and so the bone
resorption, remodelling and skull expansion processes will all increase for those women with the
genetic predisposition towards AGA.
So, for all those men and women with this genetic predisposition, DHT will cause the frontal and
parietal eminences to grow during adulthood. This is the true underlying mechanism behind
AGA.
But, why do some have the genetic predisposition towards skull expansion/AGA whilst others
do not?
2.5 Genetic link to AGA
It’s long been known that a genetic link to AGA exists.
Most research currently places focus on the 5-alpha reductase and androgen receptor genes.
However, it’s the genes that determine skull shape and size that are responsible for AGA.
2.5.1 Sexual dimorphism
Sexual dimorphism 9 means that the form (shape, size, etc) can vary between the two sexes.
For example, women usually have wider hips, whilst men are generally taller and heavier (due
to bigger bones and greater muscle development).
Skull expansion is a largely sexually dimorphic characteristic, affecting men much more so than
women. Men will, quite simply, grow a bigger skull than most women. (This reflects the higher
androgen levels men have, as well as differences in genetic inheritance). More specifically to
AGA, this means that, for most women, the frontal and parietal bones will be proportionately
smaller than in the majority of men.
2.5.2 Growth potential
Associated with skull shape and size is its growth potential. This simply means that some skull
shapes are more likely to grow than others.
For example, someone whose skull shape has a high growth potential will be especially prone
to skull expansion, and so invariably develop severe AGA. And it follows that, anyone else with
a very similar skull shape and growth potential will most likely develop AGA to the same
extent.
Of course, very similar skull shapes often run in families, and you may already be aware that, if
your mother or father lost their hair, you too have a very high chance of losing yours as well.
(This explains the strong genetic connection that AGA can have within a family, especially
between fathers and their sons).
You now know that the genetically determined characteristics of skull shape and size form the
genetic link to AGA.
This provides the answer to question 4 in part1.
2.6 Rate and location of hair loss
Skull shape and its growth potential can account for the different rates of hair loss, and the
location (within the MPB region) in which it occurs.
2.6.1 Rate
The rate at which you lose hair is directly related to the extent of your skull expansion. This,
quite obviously means that, the more your skull expands, the more hair you're likely to lose.
For the 20% of men whose skull shape has a high growth potential, this explains why AGA will
rapidly start developing from puberty and can lead to extensive hair loss by the age of thirty.
However, in most cases, AGA won’t start until later on in life and will be a much more gradual
process - these skull shapes have a low growth potential.
Growth potential can, therefore, account for the variations that exist in the rate of hair loss.
This answers question 5 in part 1.
2.6.2 Location
Within the MPB region, the location in which AGA develops can vary.
For some, hair loss develops at the front (temple recession) or back of the scalp (a bald patch).
For others, AGA will affect both these areas simultaneously and will cause either diffuse
thinning throughout the MPB region, or more concentrated hair loss (a bald patch at the back
together with receding temples at the front).
Skull expansion of the frontal bone will form a receding hairline from the temples. Skull
expansion of the parietal bones will cause hair loss at the back of the scalp. And skull
expansion of the frontal and parietal bones simultaneously will create hair loss in the front and
back of the scalp at the same time.
This answers question 6 from part 1.
Convinced?
You should be!
Skull expansion is the true underlying mechanism behind AGA. It has explained how, for those
with the genetically determined characteristics of skull shape and size, DHT will cause the
frontal and parietal eminences to grow during adulthood. It has also explained how DHT can be
associated with both hair loss and hair growth, and provided answers to all six questions from
part 1 (something the current theory cannot do).
And, if you're in any doubt about skull expansion, why not simply contact a hair loss
specialist and ask those six questions – I guarantee they will not know the answers!
2.7 Re-evaluation of the current theory
Although the current theory for AGA could not answer those questions, it did nevertheless, raise
some issues that now need to be addressed.
Referring back to part 1, these involve the following –
1. Androgen receptor sites, 5-alpha reductase and DHT all appear to be more abundant in
the MPB region of the scalp than in non-MPB regions for those with the genetic predisposition
towards AGA.
2. A gene (or possibly several) may make follicles genetically programmed towards hair
loss (but only in the MPB region).
Ok, we’ve already looked at this before, but let’s examine these two fundamental parts to this
theory in more detail –
1. First of all, let me make this perfectly clear: 5-alpha reductase, androgen receptor sites and
DHT all exist in hair follicles for hair growth, not hair loss – your body does not want to lose
something that insulates and protects your scalp from the sun, rain, cold, bugs, etc.
The current theory does not explain how and why any such proliferation of androgen receptor
sites, 5-alpha reductase and DHT should occur within just the MPB region and nowhere else. In
my view, any proliferation of androgen receptor sites is due to upregulation, also known as
reflex hyperandrogenicity 10.
What this basically means is that the body tries (unsuccessfully) to grow more hair (i.e., to offset
skull expansion) by producing more DHT. It creates an increased expression of the androgen
receptor gene within the area of weak hair growth which then causes receptor site proliferation
to occur. (Once again, remember, that's what androgens like DHT do - they stimulate bone,
muscle and hair growth, not hair loss).
Furthermore, 5-alpha reductase, androgen receptor sites and DHT also occur in bone tissue 7.
Coincidence?
No way!
To me, it seems crystal clear that DHT accumulation within the frontal and parietal bones cause
these bones of the skull to continue growing – i.e., skull expansion.
2. The current theory has identified a number of genes that may be involved in AGA. These
include: the androgen receptor or AR gene (STU1), 5a-reductase genes (SRD5A1 and
SRD5A2), CYP17, etc. But, once again, no reason has been given why follicles in just one
(MPB) region of the scalp should suffer hair loss, but not in any other. This theory simply states
that each follicle must be genetically programmed for hair loss and that they appear to have a
greater number of androgen receptor sites 11.
As you now know, it’s the genes responsible for skull growth (i.e., shape and size) that cause
AGA. And, it’s this genetic connection that explains how AGA occurs within just the MPB region.
Through the upregulation of DHT (hyperandrogenicity, as described above) the increased
expression of the androgen receptor gene within the MPB region can be accounted for.
Now you know that skull expansion is the true cause of AGA, there is a new question that needs
to be asked...
Copyright © 2008 by Paul Taylor 16
Skull Expansion – True Cause of Genetic Hair Loss www.top-hair-loss-remedy.com
2.8 What skull shapes lead to skull expansion?
Figure 7 (below) shows two different skull shapes: one with no hair loss at all (i.e., a skull shape
that did not experience any skull expansion), and one with severe hair loss (i.e., the eventual
skull shape reached after, perhaps, many years of skull expansion).
You can see that, for those who suffer no hair loss at all, they’ll generally have a slightly more
square shape to the skull. But, for those who suffer severe AGA, the skull expansion process
will often create a somewhat rounded skull shape. (This rounded shape can also appear in both
front and side profiles).
This is only a very simple explanation, but it does nevertheless reveal the skull shapes that
Other skull shape variations exist, and these determine where within the MPB region skull
expansion/AGA develops (front, back or both), and the rate at which this will happen. There are
also several skull shape characteristics that can be recognized and used to accurately predict
whether someone is likely to experience future hair loss and to what extent.
To learn about these skull shape characteristics and find out what skull shapes cause hair loss
at the front, back or both regions of the scalp, you'll need to read the next part.
