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Does DHT cross the blood-brain barrier?

I mean, I know that testosterone and estrogen are exchanged freely between brain and bloodstream, but does this apply to DHT as well? Does DHT in the brain derive entirely from testosterone that enters from the bloodstream, or can DHT be produced in peripheral tissues and then proceed to enter the brain? This is what I am wondering.
 
Can I ask why your asking? Is it the mental side of things your concerned about like brain fog etc.....or the libido ect....?
 
I ask because I am very interested in figuring out the mechanism by which finasteride might actually cause HPTA shutdown.

In my own case, all of my other hormones are essentially normal (E2, SHBG, prolactin, etc...), but my testosterone is low (this is 1.5 years after 2.5 years on fin). So, in my case, this is not simply metabolic low T (i.e. high E, high SHBG, high prolactin). I'm trying to elucidate a mechanism by which finasteride could cause shutdown mediated by negative feedback (in essence, similar to anabolic steroid induced hypo).

Finasteride shuts down 5AR type II (expressed preferentially in peripheral tissues), causing serum T to increase. At the same time 5AR type I is immune to finasteride, and continues to convert T to DHT in the hypothalamus and pituitary.

Assuming that DHT does not cross the blood-brain barrier, we might then expect that the elevated serum T would enter the hypothalamus/pituitary, in turn causing an increase in DHT. This increase DHT would have strong negative feedback effects on the HPTA, thus potentially leading to shutown.

This hypothesis is however weakened by two facts: 1) DHT is metabolized in the liver, and thus must permeate the BBB to get there; and 2) the data generally indicate that there is no significant change in LH and FSH during finasteride administration - and thus no real negative feedback (although, interestingly, there was one study that did in fact demonstrate a decrease).

So basically, if DHT does not cross the blood-brain barrier, or does not cross easily for that matter, it might provide support for a possible mechanism of finasteride-mediated HPTA shutdown.
 
galapagos said:
I ask because I am very interested in figuring out the mechanism by which finasteride might actually cause HPTA shutdown.

In my own case, all of my other hormones are essentially normal (E2, SHBG, prolactin, etc...), but my testosterone is low (this is 1.5 years after 2.5 years on fin). So, in my case, this is not simply metabolic low T (i.e. high E, high SHBG, high prolactin). I'm trying to elucidate a mechanism by which finasteride could cause shutdown mediated by negative feedback (in essence, similar to anabolic steroid induced hypo).

Finasteride shuts down 5AR type II (expressed preferentially in peripheral tissues), causing serum T to increase. At the same time 5AR type I is immune to finasteride, and continues to convert T to DHT in the hypothalamus and pituitary.

Assuming that DHT does not cross the blood-brain barrier, we might then expect that the elevated serum T would enter the hypothalamus/pituitary, in turn causing an increase in DHT. This increase DHT would have strong negative feedback effects on the HPTA, thus potentially leading to shutown.

This hypothesis is however weakened by two facts: 1) DHT is metabolized in the liver, and thus must permeate the BBB to get there; and 2) the data generally indicate that there is no significant change in LH and FSH during finasteride administration - and thus no real negative feedback (although, interestingly, there was one study that did in fact demonstrate a decrease).

So basically, if DHT does not cross the blood-brain barrier, or does not cross easily for that matter, it might provide support for a possible mechanism of finasteride-mediated HPTA shutdown.
Click to expand...

interesting
 
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