There has been some comment about the role of finasteride in regulating neurosteroids like allopregnanolone and potentially causing side effects such as something (?) called "brain fog".
Although there are studies on PubMed detailing experiments which reveal that finasteride can block the formation of certain neurosteroids, I assumed that any neurosteroidal changes attributable to 5-alpha-reductase inhibition would be due to an effect on 5ARI rather than 5ARII, since the former is found in the brain. We know that finasteride is selective for 5ARII, whereas dutasteride targets both 'flavours' of the enzyme.
However, I have seen various posts where people have claimed that very large amounts of finasteride can inhibit 5ARI as well as 5ARII. Bryan Shelton, for example, claims that large doses of finasteride taken at regular intervals each day could result in DHT inhibition approaching the levels achieved by dutasteride. Of course, finasteride has a fairly flat inhibition curve, but it's not totally flat - so this seems feasible.
So are the neurosteroidal changes induced by finasteride in various animal studies due largely to the higher levels of inhibition achieved by massive doses of finasteride? I know some research was treating rats with as much as 50mg/kg, which is an enormous amount, equivalent to hundreds of milligrams daily in humans.
A secondary question is, even if finasteride at a low dose could modulate neurosteroids - which dutasteride certainly does - does it matter? After all, apart from physical developmental defects, no other clinical abnormalities have been observed for the intersexuals with a natural deficiency of 5ARII, even though I assume they should have a neurosteroidal profile similar to finasteride or dutasteride users. Equally, women have much lower levels of both 5ARI and 5ARII compared to men (frontal hair follicles in women had 3 and 3.5 times less 5- reductase type I and II, respectively, than frontal hair follicles in men) and there seems to be no medical 'penalty' attached to this.
I'm certainly no physician or biochemist, just an Ordinary Joe trying to interpret the literature. Any comments welcome.
Although there are studies on PubMed detailing experiments which reveal that finasteride can block the formation of certain neurosteroids, I assumed that any neurosteroidal changes attributable to 5-alpha-reductase inhibition would be due to an effect on 5ARI rather than 5ARII, since the former is found in the brain. We know that finasteride is selective for 5ARII, whereas dutasteride targets both 'flavours' of the enzyme.
However, I have seen various posts where people have claimed that very large amounts of finasteride can inhibit 5ARI as well as 5ARII. Bryan Shelton, for example, claims that large doses of finasteride taken at regular intervals each day could result in DHT inhibition approaching the levels achieved by dutasteride. Of course, finasteride has a fairly flat inhibition curve, but it's not totally flat - so this seems feasible.
So are the neurosteroidal changes induced by finasteride in various animal studies due largely to the higher levels of inhibition achieved by massive doses of finasteride? I know some research was treating rats with as much as 50mg/kg, which is an enormous amount, equivalent to hundreds of milligrams daily in humans.
A secondary question is, even if finasteride at a low dose could modulate neurosteroids - which dutasteride certainly does - does it matter? After all, apart from physical developmental defects, no other clinical abnormalities have been observed for the intersexuals with a natural deficiency of 5ARII, even though I assume they should have a neurosteroidal profile similar to finasteride or dutasteride users. Equally, women have much lower levels of both 5ARI and 5ARII compared to men (frontal hair follicles in women had 3 and 3.5 times less 5- reductase type I and II, respectively, than frontal hair follicles in men) and there seems to be no medical 'penalty' attached to this.
I'm certainly no physician or biochemist, just an Ordinary Joe trying to interpret the literature. Any comments welcome.