Finasteride blocks a more potent form of Testosterone called DHT Dihydrotestosterone
https://en.wikipedia.org/wiki/DihydrotestosteroneIt is many, MANY, more times more potent than Testosterone at the AR (Androgen Receptor):
QuoteDHT is a potent agonist of the AR, and is in fact the most potent known endogenous ligand of the receptor. It has an affinity (Kd) of 0.25 to 0.5 nM for the human AR, which is about 2- to 3-fold higher than that of testosterone (Kd = 0.4 to 1.0 nM)[44] and 15–30 times higher than that of adrenal androgens.[45] In addition, the dissociation rate of DHT from the AR is 5-fold slower than that of testosterone.[46] The EC50 of DHT for activation of the AR is 0.13 nM, which is about 5-fold stronger than that of testosterone (EC50 = 0.66 nM).[47] In bioassays, DHT has been found to be 2.5- to 10-fold more potent than testosterone.[44]
The terminal half-life of DHT in the body (53 minutes) is longer than that of testosterone (34 minutes), and this may account for some of the difference in their potency.[48] A study of transdermal DHT and testosterone treatment reported terminal half-lives of 2.83 hours and 1.29 hours, respectively.[49]
Unlike other androgens such as testosterone, DHT cannot be converted by the enzyme aromatase into an estrogen like estradiol. Therefore, it is frequently used in research settings to distinguish between the effects of testosterone caused by binding to the AR and those caused by testosterone's conversion to estradiol and subsequent binding to and activation of ERs.[50] Although DHT cannot be aromatized, it is still transformed into metabolites with significant ER affinity and activity.[16] These are 3α-androstanediol and 3β-androstanediol, which are predominant agonists of the ERβ.[16]
A while back I looked into FTM forms and I have read (limitedly) that it is used to gain the more male favorable traits such as thicker beard hair, male pattern baldness/thinning of the hair, and thicker/darker/more body hair. Admittedly I only looked into FTM forums limitedly.
DHT is usually associated with those changes I mentioned. Also, DHT cannot be aromatized into E while T can be changed into E via aromatase. So, if you have T some of that will turned naturally into E while any DHT you have will remain there to act on your cells.
https://en.wikipedia.org/wiki/AromataseIs is true that once you are placed on HRT your T will decline and so will other levels of Androgens, but you will still have some in your lood circulating and interacting with your cells. How much? It depends. You have to do a blood check to find out, plus find out just how much is free to interact with your cells and not binded to SHBG.
Another thing is that exogenous use of Estrogen via injection or other methods will naturally lower your T levels due to it's effect on the hypothalamic–pituitary–gonadal axis. This means that ultimately with the use of Estrogen by itself your T levels will fall. Do you really need to take spironolactone? I don't think so personally if you are taking E as injectable or enough as transdermal. Do you really need to tax your kidneys? Again, by how much it depends on your body and how it reacts. Anyway, in the end some T is ideal. Women have some T naturally in their body something like 100ng/dl max and normally around 80ng/dl. SO in a way you should want some T in your blood.
That is when Fina comes in to block the more potent DHT.
However, Finasteride only blocks 2 forms of DHT and lasts 5-6 hours in your blood.
https://en.wikipedia.org/wiki/FinasterideThis is in contrast with Dutasteride which blocks all three forms of DHT and has a half life of 4-5 weeks.
https://en.wikipedia.org/wiki/DutasterideQuoteIt is a competitive, mechanism-based (irreversible) inhibitor of all three isoforms of 5α-reductase, types I, II, and III (IC50 values are 3.9 µM for type I and 1.8 µM for type II).[1][12][36][37] This is in contrast to finasteride, which is similarly an irreversible inhibitor of 5α-reductase[37][38] but only inhibits the type II and III isoenzymes.[12] As a result of this difference, dutasteride is able to achieve a reduction in circulating DHT levels of up to 98%, whereas finasteride is able to achieve a reduction of only 65 to 70%.[13][2][35][39]
So when it comes down to your money and how much you are getting out of it Dutasteride is likely a better option over Finasteride.
Should you block DHT? I personally think so. Is it worth the money? If you want to stop the masculinazing effects of DHT I would think so.
-edit-
You said your friend mentioned estrogen pills. Are you on E pills or injectable or transdermal E? If you are on pills then spirolactone will likely be needed as pills just tend to be less effective at feminization than transdermal, injectable, or the really nice and new approach of using Estrogen Pellets under the skin ( I tried those and they were amazing, but expensive). Pills do a double pass on your liver if you ingest them.
Your friend might say it is all quack talk, but you really have to do your blood work to check how much T and DHT you have. More than likely you do have some of both, but some T is still beings changed to E while DHT cannot be changed via aromatase. Id prefer to have T over DHT.
