It is well known that DHT is linked to androgenetic alopecia. It's also quite well known that the drug finasteride can help reduce the rate at which this type of hair loss develops (and may even encourage new hair growth for some people).
However, it is not so well known that the purpose of DHT in the body is for hair growth, not hair loss. This steroid hormone is used by the body to promote the growth of bone, muscle and hair.
I believe the primary effect of DHT in the hair loss process is that it contributes to skull expansion by stimulating certain skull bones to grow. But DHT also has a secondary effect. This newsletter explains what this secondary effect is, and how finasteride provides some resistance to it.
Hair loss develops because skull expansion causes a reduction in the capillary blood supply to the hair follicles. Eventually, this causes follicle miniaturization which chokes hair growth. The body reacts to this by starting "upregulation" (hyperandrogenicity). This means that the body tries to restore normal healthy hair growth again by increasing DHT production* within the follicles that are affected by skull expansion.
* Remember, that's what DHT does: it stimulates growth, not loss.
Now, higher DHT levels will accelerate mitosis (cell division) and so should help struggling hair to grow.
But, when the rate of mitosis is increased, the blood supply becomes insufficient to grow hair that fast (i.e., because skull expansion has reduced the capillary blood supply). As such, the (papillae) cells in the root of the hair fail to meet the growth demand placed upon them by DHT.
Instead, the result of all this extra DHT is to make the body rush through the growth phase (anagen) and reach catagen (the shedding phase) and telogen (the resting phase) much sooner than it normally would.
This obviously causes the amount of hair loss to increase. It also means that more hair follicles are in the resting phase. And, whilst the hair growth cycle will restart again, strong healthy hair growth is less likely due to the progressive effects of skull expansion and further accumulation of DHT.
Also, since hair growth in the outer (dermal) layer of the scalp has been restricted, DHT will instead promote more rapid cell division at a deeper level of the scalp (called the stratum germinatum layer).
This interference with normal cell division can result in skin cells rising up towards the surface of the skin faster than normal, causing increased shedding of the skin - dandruff. (This was explained in a previous newsletter).
Finasteride treats this secondary effect of DHT by reducing levels of 5 alpha reductase (an enzyme that converts testosterone into DHT). And so, by reducing DHT levels in this way, finasteride extends the shortened anagen phase which, of course, allows more hair to grow.
However, finasteride does not reverse the miniaturization of the hair follicles. I believe this is because it does not effectively treat the skull expansion process (i.e., the underlying cause of hair follicle miniaturization). It only addresses the negative effects caused by the body when it increases DHT production (upregulation).
Another problem with finasteride is that further upregulation can easily occur. Many people experience this when they start using this drug.
Basically, the body can compensate for the reduction in 5 alpha reductase forced upon it by finasteride. Essentially, it tries even harder to increase the quantity of 5 alpha reductase and DHT production in the affected region of the scalp.
This explains why there can be an initial increase in hair loss when people start using finasteride and again when they stop using it.
Although finasteride and other drugs such as dutasteride and minoxidil are used by some people to treat hair loss, there's a risk of developing side effects.
The method I used and recommend is completely drug free.