I've personally found that the healthier you are, the higher both 5AR expression and aromatase are.
But, in terms of drugs or chemicals, you can find something to upregulate aromatase expression and maybe try to use it topically. Prostaglandin E2, dexamethasone, and ricinoleic acid all upregulate aromatase expression. Or you could bypass all that and try an ER agonist that is highly selective for ER beta and won't cause HPTA dysregulation. 8b-vinylestradiol and WAY-200070 both fit this specification, in theory due to their exceedingly high selectivity for ERb over ERa.
Chiming in here. Not only ER-beta selectivity is important, but also the Relative Transactivational Capacity or Intrinsic Activity (IA) of your ligand. This seems to be forgotten quite often. I strongly encourage everyone interested in ER-beta ligands to read this paper (hyperlink removed). It contains all information that is currently available for known ER-beta agonists.
In short, the IA determines how many genes will be transcribed upon ligand binding with the receptor. Estradiol (E2) has an IA of 100 for both ER-alpha and ER-beta, which is the reference ligand for all other ligands. An IA higher than 100 means that the transcription will be broader than E2, while an IA lower than 100 means the transcription will be narrower than E2. This means that Estriol (E3), with an IA of 11% at ER-alpha and 17% at ER-beta [R], will not activate a very meaningful degree of transcription upon binding. Hence, there are many users that deem E3 as rather weak.
Back to the selective ER-beta ligands. If you want exclusive ER-beta activation, you need a ligand that is very selective for ER-beta (i.e. a high ERa/ERb RBA ratio), a high IA and a high binding affinity. My attention was initially drawn to 8b-vinylestradiol as well, since it has an exceptionally good selectivity (180-fold, functionally 46-fold [R]). However, when investigating the IA, it was only 45.8 relative to E2 [R]. I have not been able to find anything about WAY-200070, but I would be sceptical. There are not many ligands with a very high IA and simultaneously good selectivity for ER-beta.
The best option would be Erteberel, which has a functional selectivity of 32 for ER-beta, and is a full agonist of both receptors with an IA of 101 at ER-beta and 94 at ER-alpha [R]. Futhermore, Erteberel does not inhibit the HTPA axis as per [R] up until 25mg daily orally, and shows low bioavailability [R]. This makes it theoretically a great choice to effectively use topically in very low dosages. The downside if you want to test this is that it will cost you roughly $1500 per gram (untested from China).
However, personally I am sceptical about selective ER-beta activation. I think there is too little evidence that points exclusively in the direction of ER-beta. Yes, in murine models ER-alpha arrests hair growth [R], but this does not necessarily translate to human hair follicles. In murine models, E2 induces catagen [R], but in human hair follicles, E2 prolongs anagen in
male frontotemporal HF's [R]. Not only does this indicate a completely different mechanism between men and women, it also indicates that there are regional differences in the scalp where E2 can be highly effective or detrimental. Obviously, estrogens are still extremely complex, but I do not think ER-alpha (which is the larger estrogen receptor
by far) can be excluded at all.
Apologies for the lengthy reply. I hope some may find it useful.
Edit: I noticed that links to research that I included (the [R]'s) have been removed because of new member restrictions. If anyone wants to check a source, feel free to ask.