Virtually everyone on this site knows the cause of MPB is genetically inherited sensitivity to DHT. However, i'm curious to know how this process really works. Does the DHT bind to the follicle, stay there and build up over time or is it a continuous bombardment of DHT to the follicle (coming and going via transportation through the blood) that causes the end result of MPB? I think most agree the first theory is the generally accepted cause. However, how does finasteride help improve existing hair, and in some cases result in hair regrowth in patients experiencing MPB? The drug is designed to inhibit the transformation of testosterone to DHT. Therefore, the only possible benefit would be the preservation of what hair you had left in its current state(thickness). However, a lot of patients, mainly young patients like myself, experience thickening of previously affected hairs and in some cases regrowth. How would this be possible since the DHT already formed and binded to the follicle would not be altered by finasteride since it already has synthesized to DHT? The second theory would make more sense in providing an answer to this question. Hope someone has the answer to this query.

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My Hair Loss Weblog - Hair Transplant with Dr. Tessler

I am not a doctor, but give me about four years...

I have also recently taken a shit ton of undergrad bio courses, biochemistry, and all that crap, so I think I can give you at least as good of an answer as doctors, who probably haven't thought about this crap in years.

DHT is a steroid hormone, meaning that its typical mechanism of action is:

1. Cross cell membrane
2. Bind receptor
3. Receptor/hormone complex binds DNA in the cell, causing "something" to happen.

It can act as a transcription factor, causing certain gene products to be made, or it can do the opposite, inhibiting transcription.

What is most likely, in this case, is the latter. Or the former, in which the gene products being made are then turning around and down-regulating something else, or initiating a cascade of events which ultimately down-regulate whatever process is required for hair growth.

Molecular biology is the biggest pain-in-the-ass, horseshit subject ever. More power to you if you enjoy it.

But anyway, hormone/receptor associations are typically very fast and short-lived. The molecules themselves break down, and each molecule of DHT can only do so much before it does. The idea here is to limit the amount of damage it can do to these cells, by limiting the amount of DHT, in order to sustain the follicle.

Less DHT = less hormone-receptor associations = less expression of those associations.

Does that make sense? Of course not. Its molecular biology. But that's pretty much what's going on. Or at least the general idea.

Found this on another site but it is good information related to your question DHT:
http://www.hairlossinformation.com/h...air-loss.shtml