5-alpha reductase

Big Si

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So here's the thing, 5-alpha reductase (5a) as I'm sure you know, is an enzyme that reduces a form of testosterone to DHT as an end product, which is the cause of our common misfortune.
Enzymes however cant reduce their specific substrate if something else attaches to their binding site(the place where substrate goes) first.
This greatly reduces, but does not completely stop, the enzymes efficiency at producing the end product, in our case DHT.

So the question is this: is this how finasteride works?
Enzymes are also subject to a loss of efficiency by a binding to their exterior which completely changes the shape and has a much more marked effect on their ability (or lack of) to produce the end product.
I don't think this is how finasteride works or its results would be markedly better.

What I want to know is this: The limiting factor in enzyme reactions is the substrate concentration, therefore an increase in dosage of finasteride, over time
should have these enzymes choking on finasteride before they get a chance to produce hair f***ing DHT.

I know its a long shot but does anyone know of research or trials where this has been explored? Im interested to know thoughts or experience of gradual increases of finasteride, I want to know why what were all taking does what it does and how we can make it more effective.
 
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