As DHT is a direct metabolite of Testosterone, I should imagine the only effective way to reduce DHT would be to stop it's conversion from Test. I’ve read in a very few places that, in order to keep homeostasis the body can "back track" thought the normal endocrine progress from cholesterol to androgen to create other androgens. However, the function of the 5-ar is to make DHT from test...so I’m not sure how the pathway would operate without the enzyme action present.
This may help a bit:
"Testosterone is easily converted in the body into Dihydrotestosterone (DHT). This reaction is carried out by the enzyme 5-alpha reductase (5-AR). During this reaction, the double bond between C4 and C5 is reduced to a single bond, and two new hydrogen atoms are added, one each to C4 and C5.
DHT:
The hydrogen attached to the C5 is trans to the methyl groups while the H attached to the C4 can be either cis or trans, as there is already one H bonded to that carbon. 5-AR does not convert all steroids to DHT. As with most enzymes, there has to be an exact fit between the enzyme and the substrate, in this case, the steroid. The analogy of a lock and key is sometimes used to describe the specificity of enzymes."
[/url]
http://www.muscletalk.co.uk/article-...aspx]Chemistry and Structure of Anabolic and Androgenic Steroids Part 2[/url]
The "lock and key" analogy leads me to believe that without 5-AR there is no DHT. S0 those compounds that block the 5-AR enzyme would be the most direct way to effect DHT levels in the body.
However, this is an interesting question--the idea of "binding". SHBG will pick up DHT "...binding of the 5α-reduced androgen dihydrotestosterone (DHT) by SHBG acts as an antagonist on SHBG receptors."
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But it will also pick up Test--which I bet is something you don't want:-)
Any other thoughts form the lab-coats among us?
Ronn