mattj said:
If that is so then starting to take finasteride when your hairloss is mild, and possibly only progressing very slowly, could mean that you have a DHT overload in later years which moves your hairloss further than it would have done without the medication. Or am I wrong?
No, you are confusing what I am saying. finasteride will reduce scalp and serum levels of DHT. It is very effective at doing this. In fact, its ability to reduce DHT is similar to what one might see in a castrated patient. That is the point behind its efficacy as hairloss treatment. You will not have a "DHT overload."
Rather, what I am talking about is the variability we see in patient response. Some people shed like crazy -- sheds that are essentially TEs, as defined by the "pull method." Other people don't experience these sheds at all.
In light of this, the question then begs asking: Why this variability in response, when the etiology for our pathology is already well-accepted at this point: we all understand the connection among metabolism (testosterone, DHT, DHEA, 5-AR-I/II, &c.), the androgen receptor, and our hairloss.
In simplified terms, I believe that this variability in response is due to the interplay between the pharmacology of the drug and the genomics of the patient. But signal cascades are a complex topic. It would be helpful if we had someone expert in signal transduction.
This is why the literature on Hedgehog and other conserved loci are of interest to me. But the only sh*t I remember about signal transduction was on sevenless -- eye development in fruit fly. This is the classic textbook example -- very good molecular biology -- but not of much use to me at the moment. I have much reading to do... but I am am often so disspirited, I find that I cannot concentrate.
The models we talk about here on this forum are almost exclusively in terms of [DHT] and kinetics. In a sense, taking this perspective makes tings easier for all of us to a degree. But if you were to actually look at the full spectrum of metabolic pathways involved, you would see that the interplay between pharmacology and genes are too poorly understood to make a definitive statement.
This is why, inevitably, the best advice/prognosis you will ever get here -- or anywhere else for that matter -- is: "The only way to know if it will work -- or how long it will work -- is to give it a try." Because as it stands today, it may be a long time before the full picture comes out.
