Just weighing the need for topical AR inhibitors in addition to 5ar inhibitors, wondering if topical spironolactone in addition to oral finasteride is better than oral finasteride in the long term.
Castrated men don't lose any more hair, but do did not seem to regrow a lot either.
The psuedo hermaphradites don't go bald (or is it very rare?) because they don't have 5ar2. Maybe they also have better androgen receptors in their hair follicles.
While dutasteride regrows hair faster at first than finasteride does, one or two small studies reproduced the 6 month hair counts, but showed that at 1 year, the counts were the same as proscar. Why would it be faster at first, but then the same later? Is the native testosterone continuing the damage, or is there some other mechanism going on? We know castrates don't lose more, so I'm blaming the testosterone. We don't know the 5 year results of dutasteride though. Maybe it hits the peak sooner and stays there. Topical spironolactone should give similar effects when combined with finasteride.
Would topical spironolactone compete with estrogen?
Some sources say DHT is 3-4x as strong as testosterone, while others say 30x. I wonder if testosterone and DHT tell the follicle to do something different, and are not just the same signal at different strengths.
What does estrogen tell the follicle to do?
Some guys on oral finasteride continue to lose hair. Is there some other thinning mechanism that all men have?
We know that minoxidil regrows more hair than finasteride. Apple poly, GTE, NANO, and other topicals seem promissing too. Nizoral regrows hair not only through anti-androgenic action, but some other action too.
Old people don't make as much GLA and a few other things in their skin. I wonder if revivogen does more than just inhibit 5ar. Maybe those fatty acids make the scalp more youthful.
Since finasteride might not save everyone, and since castration does not regrow as much as minoxidil, and since there may be mechanisms we don't know about, I think a multi-pronged approach is best. And since EGCG in GTE may have other benifits besides receptor blocking, and is cheap, I want to use it instead of RU.
We also know that estrogen works only systemically, probably because it diffuses into the blood faster than it acts locally. Or it is not taken into the follicle much.
Comments?
Castrated men don't lose any more hair, but do did not seem to regrow a lot either.
The psuedo hermaphradites don't go bald (or is it very rare?) because they don't have 5ar2. Maybe they also have better androgen receptors in their hair follicles.
While dutasteride regrows hair faster at first than finasteride does, one or two small studies reproduced the 6 month hair counts, but showed that at 1 year, the counts were the same as proscar. Why would it be faster at first, but then the same later? Is the native testosterone continuing the damage, or is there some other mechanism going on? We know castrates don't lose more, so I'm blaming the testosterone. We don't know the 5 year results of dutasteride though. Maybe it hits the peak sooner and stays there. Topical spironolactone should give similar effects when combined with finasteride.
Would topical spironolactone compete with estrogen?
Some sources say DHT is 3-4x as strong as testosterone, while others say 30x. I wonder if testosterone and DHT tell the follicle to do something different, and are not just the same signal at different strengths.
What does estrogen tell the follicle to do?
Some guys on oral finasteride continue to lose hair. Is there some other thinning mechanism that all men have?
We know that minoxidil regrows more hair than finasteride. Apple poly, GTE, NANO, and other topicals seem promissing too. Nizoral regrows hair not only through anti-androgenic action, but some other action too.
Old people don't make as much GLA and a few other things in their skin. I wonder if revivogen does more than just inhibit 5ar. Maybe those fatty acids make the scalp more youthful.
Since finasteride might not save everyone, and since castration does not regrow as much as minoxidil, and since there may be mechanisms we don't know about, I think a multi-pronged approach is best. And since EGCG in GTE may have other benifits besides receptor blocking, and is cheap, I want to use it instead of RU.
We also know that estrogen works only systemically, probably because it diffuses into the blood faster than it acts locally. Or it is not taken into the follicle much.
Comments?
