There are two different mechanisms involved here... a) production of T and its conversion to either ( or both) E and DHT, (b) growth of male pattern hair:
It is largely the DHT that is responsible for male hair.
SP blocks the conversion of T to DHT and leaves the T available to naturally convert to E via the aromatase reaction.
I think the T->DHT conversion is stronger when you are younger, which is why the SP seems to be more necessary when you are younger. ( I'm pretty sure that my DHT level drop off became significant when I was in my late 40's)
From my personal experience, I suspect that long term exposure to PM has the effect of making male body hair finer and more slow growing, although not WHERE it grows. It is next to impossible to separate the effects of PM from those of SP/Finasteride (without doing controlled intakes over long periods of time, of course).
It is largely the DHT that is responsible for male hair.
SP blocks the conversion of T to DHT and leaves the T available to naturally convert to E via the aromatase reaction.
I think the T->DHT conversion is stronger when you are younger, which is why the SP seems to be more necessary when you are younger. ( I'm pretty sure that my DHT level drop off became significant when I was in my late 40's)
From my personal experience, I suspect that long term exposure to PM has the effect of making male body hair finer and more slow growing, although not WHERE it grows. It is next to impossible to separate the effects of PM from those of SP/Finasteride (without doing controlled intakes over long periods of time, of course).