Testosterone can compete with DHT for receptor expression and testosterone is way less androgenic. Having lower testosterone will not necessarily lower DHT as this is dependent more on the amount of 5AR enzyme that you have.
To achieve maximal DHT production (the maximum amount you can produce through 5AR) does not require high testosterone. Think why older men have more body facial hair than younger despite lower T.
For example, to max out DHT production for the amount of 5AR you have, say you need 200 ng/dl of testosterone with the normal range for adults being 200-1100 ng/dl. If your T was 800 ng/dl, you would have the same amount of DHT being produced as if you had 200 ng/dl due to the conversion being limited by the amount of available 5AR. However, w/ higher T, the DHT is less active as less of it binds to receptors. It has to compete w/ Testosterone.
So lower testosterone won't lower DHT levels (unless you get really low, like castration levels) but it can make the DHT you normally produce more active. In other words, high T can blunt the effects of DHT (DHT is highly androgenic where as Testosterone is more anabolic) somewhat.
Furthermore, there are actually two types of androgen receptors (A and B, just like estrogen receptors).
"Two
isoforms of the androgen receptor (
A and
B) have been identified." From
https://en.wikipedia.org/wiki/Androgen_receptor.
My hypothesis is that these have different effects, anabolic and androgenic. With estrogen receptors, they up regulate when they are stimulated. SERMs (Selective estrogen receptor modulators) can stimulate only estrogen receptor B and cause an increase in estrogen receptor b expression which is genrally attributed to good effects of estrogen (smooth skin) while estrogen receptor A is associated w/ negative (breast cancer).
Finasteride has been shown to up regulate androgen receptors and yet it still grows hair.
http://ehrs.org/conferenceabstracts/2000marburg/guestlectures/s04-sawaya.htm
When you take finasteride, you remove the primary androgenic stimulus for androgen receptors. This allows testosterone to act more anabolically which would cause an upregulation in the androgen receptor type responsible for anabolic effects and a down regulation in the receptor type responsible for androgenic effects.
So in conclusion, when you have low T, you still have DHT and this DHT is more active due to less Testosterone binding. The more DHT that binds, the more upregulation occurs for androgenic receptor expression. It is a feed forward mechanism.