Wait wait wait slow down.
The entire point of this theory is to explain that androgens exert their negative effect scalp hair exclusively due to mechanical stress from the galea.
Now i've told you that there are mutiple aponeuroses in the body (and sites of varying mechanical stress besides i.e. a knee joint vs the chest) yet over the course of your life androgens exclusively have a negative effect on just the scalp hair. And your response is that scalp hair follicles are of a different type to body hair? Lmao well isnt that obvious? Its androgenetic alopecia, the clue is in the "genetic".
The point is your theory attempts to explain the difference in gene expression on the top of the scalp as being kicked off by mechanical stress from the galea but you cant explain why only the top of the head would lose hair after androgen exposure, even though its pretty obvious that hair across the body is subjected to different levels of mechanical stress. Why not at joints? Why not at the lumbar aponeurosis? Or the abdominal?
All our tissues in our entire body develop from a single cell.
One single cell.
And over the course of our development, multiple genetic, hormonal, and mechanical pressures exert themselves to shape various progeny of that first progenitor cell into the various organs of our body.
Tissues develop in progressively forking pathway where at each fork, something induces change to create a new tissue type.
Some tissues diverge earlier in development, and some diverge very late in development.
The question developmental biologists attempt to answer is: how and why does each fork occur?
This theory explains how the Norwood 1-7 fork of scalp hair development occurs. Nothing more.
Here is a simple diagram of how our tissues fork starting from the bottom as a single celled zygote into the various organs of our body at the top:
Our hearts and our biceps are both made of muscle. But it is very different muscle with very different properties. They both come from our mesoderm, but the fork that generates the difference occurs very early on, and so although they are both muscles, they are not the same. The same can be said for the difference between body hair and head hair.
Pubic hair, chest hair, *** hair, beard hair, etc. have completely different texture, age of growth, rate of growth, density, triggers for growth/maturation compared to head hair. The only thing body hair shares with head hair is they are both hairs (just like heart and biceps are both muscles). Otherwise, they are plainly different in many many capacities. Like our biceps are different from our heart. They are both muscles, but they are developmentally divergent muscles with very different characteristics.
By contrast, the hair on our head all appears essentially identical in terms of texture, growth, length, density, and pattern of growth. If you pluck a hair from a healthy head anywhere on the head and compare it to another hair somewhere else on the head, they will be likely indiscriminable under a microscope. You could not tell the difference. Because they are developmentally almost identical to one another.
This theory posits that: (1) the hair that exists on our head is sensitive to mechanical stress, and (2) mechanical stress induces androgen sensitivity in the Norwood pattern via the galea.
This theory offers no suggestions about the characteristics of body hair, as that would be like trying to draw conclusions about how to treat heart disease by studying a bicep. They are different organs that arise from different developmental pathways, with different growth stimulants and triggers, and displaying different natures altogether.
The notion that hair on your head develops androgen sensitivity in the Norwood pattern due to mechanical stress does not imply that all hairs anywhere in the body must have the same mechanical sensitivity.
This just helps to explain one tiny fork among the thousands that occur in our development to lead to making our adult bodies the way they are.
