- Reaction score
- 22
I have been on topical finasteride for the last 5 years or more at various doses ranging from 0.1% to currently 0.5% applying as many ml of the foam as possible per application (around 200ml per month). The foam contains 5% minoxidil as well.
Hairloss was not halted. I don't know if it slowed it down or not.
A recent lab shows the following changes compared to the pre-treatment lab years ago:
DHT: -80%
prolactine: +566%
estrogen: +62%
total T: +34%
free T: -%44
progesterone: -68%
delta 4-androstenedione: +%98
3α-androstendiol glucoronide: +%22.4
LH: +88%
PTH-i: +100%
I have other relevant measurements but I didn't measure them back then. Those are enough to see the systemic side effects of the finasteride applied topically. Luckily I have no noticeable side effects, however I don't like those high levels of prolactine at all. The 80% decrease of DHT hasn't been useful in halting hairloss. It's hard to say if it's doing something at all. What I do notice is that upon sexual stimulation my scalp feels weird, I guess inflammed. The foam helps calming this which is why I still use it. My hair is still in good standing for age 30 but I would like to stop the shedding otherwise I will not reach age 40 with a good hairline.
I know at least one case of success with topical finasteride, halting hairloss without systemic changes. Im trying to understand why some get systemic changes and some don't.
If anyone is familiar with how 5α-reductase interacts with finasteride and with the mentioned hormones I would like to hear your thouhtgs on this. I suspect that either some people have difference in scalp tissue which leads to increased absorption, or it's a matter of genetic differences in the pathways of how you metabolize 5α-reductase. Im not sure which treatment should I try next.
Im familiar with RU and CB but I have heard theories of chronical usage of compounds like those speeding up baldness long term due chronically trying to antagonise the androgen receptors thus ending up with upregulated receptors (higher sensitivity to androgens, thus increased hairloss).
Hairloss was not halted. I don't know if it slowed it down or not.
A recent lab shows the following changes compared to the pre-treatment lab years ago:
DHT: -80%
prolactine: +566%
estrogen: +62%
total T: +34%
free T: -%44
progesterone: -68%
delta 4-androstenedione: +%98
3α-androstendiol glucoronide: +%22.4
LH: +88%
PTH-i: +100%
I have other relevant measurements but I didn't measure them back then. Those are enough to see the systemic side effects of the finasteride applied topically. Luckily I have no noticeable side effects, however I don't like those high levels of prolactine at all. The 80% decrease of DHT hasn't been useful in halting hairloss. It's hard to say if it's doing something at all. What I do notice is that upon sexual stimulation my scalp feels weird, I guess inflammed. The foam helps calming this which is why I still use it. My hair is still in good standing for age 30 but I would like to stop the shedding otherwise I will not reach age 40 with a good hairline.
I know at least one case of success with topical finasteride, halting hairloss without systemic changes. Im trying to understand why some get systemic changes and some don't.
If anyone is familiar with how 5α-reductase interacts with finasteride and with the mentioned hormones I would like to hear your thouhtgs on this. I suspect that either some people have difference in scalp tissue which leads to increased absorption, or it's a matter of genetic differences in the pathways of how you metabolize 5α-reductase. Im not sure which treatment should I try next.
Im familiar with RU and CB but I have heard theories of chronical usage of compounds like those speeding up baldness long term due chronically trying to antagonise the androgen receptors thus ending up with upregulated receptors (higher sensitivity to androgens, thus increased hairloss).
