Ranking Strengths Of Anti-androgen Regimens Based On Rates Of Gynecomastia

[IdealForehead]

The different anti-androgen regimens that are broadly available are very different from one another, and there is so little data comparing their effectiveness. I have been trying to conceptualize a good way of comparing them. I think the most reasonable way to do so is to compare them based on side effect profiles.

Any anti-androgen regimen should be capable of inducing anti-androgenic side effects if it is adequate at its job. There is nothing to my knowledge unique about the hair follicle androgen receptors that should allow "selective" blockade of them (without blocking androgen receptors equally elsewhere in the body), unless it is a topical application.

I think the best side effect to rate the strengths of a given anti-androgen is probably gynecomastia. I think that's the best one because it's blatantly obvious when it develops. Unlike sexual side effects which are subjective, gynecomastia is very objective.

Gynecomastia is formed in all cases by a combination of (1) Decreased testosterone and/or DHT levels, or decreased binding of testosterone and/or DHT to breast tissue due to blockade, and (2) Increased estrogen levels from increased aromatization of testosterone into estrogen.

These same causative effects are roughly what we want to happen to the hair follicles to help save them. So I think it makes a good comparison. An anti-androgen that is more likely to cause gynecomastia should also be more likely to be effective in protecting hair.

This is not a perfect analysis, because a medication which increases estrogen predominantly will likely produce gynecomastia but not necessarily protect hair from androgens as well as something that blocks androgens completely and does not increase estrogen. But we can see from even very pure anti-androgens like bicalutamide that relatively pure anti-androgenism can result in high rates of gynecomastia, irrespective.

So I think it may be therefore possible to establish a "ladder" of anti-androgenic power, at least for oral anti-androgens, based on their rates of gynecomastia. This is the ladder I can establish on that principle, with percent risks of gynecomastia listed based on the best references I could find:

1) Finasteride 1 mg - <1% (case reports only) ref, ref
2) Finasteride 5 mg - 0.3-4.5% ref
3) Dutasteride 0.5 mg - 1.8-2.3% ref
4) Spironolactone 25-50 mg - 7% ref, ref
5) Spironolactone 75-100 mg - 17% ref, ref
6) Cyproterone - up to 18% ref, ref
7) Flutamide - up to 19% ref
8) Enzalutamide - 49% ref
9) Spironolactone ≥ 150 mg - 52% ref, ref
10) Bicalutamide - 60% ref

Medication-induced gynecomastia in almost all cases goes away after the offending drug is stopped. Alternatively, it can be treated with anti-estrogen medication. A summary of treatment options I came across when working through all this, for reference, is here.

I think the general principle of ranking medication protocols' strength based on their anti-androgenic side effects makes sense. If anyone has any suggestions for a better side effect to pick for ranking by, I'm open to suggestion.

The most complicating factor which I haven't been able to overcome here is that I haven't delved into durations of studies. Obviously, longer studies will provide a higher percentage for any drug. I tried to pick the longest study data I could where applicable (eg. 2 years for enzalutamide) but it is not exactly possible to compare apples to apples. I have tried to go with the highest rates as those usually reflect the longer studies. In the spironolactone study, they found onset of gynecomastia could vary anywhere between 2 and 100 months, though with a faster onset for higher doses.

The most interesting thing for me was that spironolactone >150 mg starts to equal enzalutamide and bicalutamide in its gynecomastia profile. This is surprising because spironolactone is considered a "weak antagonist" of the androgen receptor. It therefore seems likely it is matching enzalutamide and bicalutamide in this effect moreso by simultaneously reducing testosterone levels and increasing estrogen, probably to a greater extent than those other more "pure" anti-androgens.

Finally, looking at these numbers demonstrates how laughable overblown fears are of medications like finasteride 1 mg, which are so weak as anti-androgenic regimens, they are almost incapable of creating this side effect at all.

For final reference, here is a chart visually demonstrating spironolactone's rates of gynecomastia which increase linearly by dose:

 

[whatevr]

I got puffy nipples from finasteride at 0.5 and 1.25 mg and they haven't gone away fully after quitting, but about 80% less. I have some raloxifene but kinda scared to use it.

RU58841 does not do that thankfully.

I guess it doesn't matter statistically what the rates are, because if it happens to you, you won't find any consolation in that. If you feel that your nipples are itching or burning or anything like that (happened to me within the first week of taking 0.5 mg) - get off that drug immediately.

 

[Ramsey]

Nice job shaking things up and looking at issues in different ways, Ideal.

You've done tons of research and have thought a lot about this, so I'd like to ask your views about a few things. We've all gotten scattered between threads, but this post with your overall comparison of anti-androgens seems as good as any. Questions:

1. The effect of SERMs and estrogen on hair
SERMs, tamoxifen in particular, is often used by men both in the real world and in our hair-world lol to fight against gyno. In the article you linked to, TMX is considered a first-line treatment for gyno.

I asked about the effect of SERMs and estrogen on hair in another thread here (quotes and research links in that thread). What's interesting to me is this fairly detailed 2013 study from Germany which finds that "there is little evidence in the current literature that oestrogens affect human hair growth one way or the other, possibly indicating a role of genetic predisposition in oestrogen-related hair changes... Our results argue against an effect of tamoxifen on hair growth."

That contradicts the standard thinking on hair forums that:

a) anti-androgens protect hair from further A.G.A damage, while estrogen is needed to really get regrowth (Cotsarelis interview 2012: "There seems to be a point of no return with respect to androgen removal; even if you castrate someone who’s bald he won’t regrow all his hair. If you give him estrogen, too, he might.")

and

b) that many (cis-, non-MTF) guys start an anti-androgen, get signs of gyno onset, then either drop the antiandrogen or start a SERM like tamoxifen. If they start with tamoxifen, it stops the gyno but negates the benefits of the anti-androgen and leaves you juggling between the drugs. For example, on that thread, jgray201 reported that he used tamoxifen for gyno when taking 200mg of spironolactone ED, and found that with TMX he "always lost some ground" (he reported that raloxifene much less harmful on his hair).

I'm confused about what's going on. What do you think about SERMs and hair?

More basically, what do you think about estrogen's effect on male hair? I notice you're using spironolactone in your nuke regimen, but haven't added any estrogen, topical or oral.


2. Correlation between AR affinity, hair benefit, gyno
I saw in a couple of threads that you've researched the affinity of different anti-androgens. I'd think that how well an anti-androgen competitively inhibits binding of androgens to the AR - in the hair specifically, if possible - is the most important point in evaluating them... and then side effects, cost, etc.

In this post on gyno, I think you're making the assumption that affinity, hair benefit, and gyno occurrence are all closely correlated, so you can use them as proxies for each other. Of course it's related, but is it true to assume that they're so directly correlated that they're proxies for each other? Maybe I'm being naive, overthinking it, and it's a no-brainer, but does the effect of an antiandrogen on hair necessarily have to correlate to gyno? Is there evidence for that? Again, I might be off here, but I'd thought there's a lot we don't know about the local and systemic differences: for example, synthesis and metabolizing of hormones varies locally by site, even among hair follicles, and afaik we also don't know what percent of androgens (or estrogen etc) come from local synthesis vs. passive diffusion. So I'd think that antiandrogen affinity, hair benefit, and gyno occurrence wouldn't necessarily be directly correlated; high gyno, little hair vertex benefit could be a possibility. Or some hair protection with little gyno (finasteride or low dose spironolactone, maybe).

I'm not criticizing, it's that I really don't know and am genuinely interested in your thinking about this.

3. Topical, systemic, vehicles, and antiandrogen differences
Afaik, there's no research comparing antiandrogens used topically. So based on what you've seen, how would you compare transdermal absorption of the different antiandrogens? To what extent will the metabolism of one drug - daro, let's say - depend on the vehicle vs. a different antiandrogen? Are there differences between the antiandrogens that could make some of them better than others topically at blocking local hair ARs?

 

[IdealForehead]

Nice job shaking things up and looking at issues in different ways, Ideal.

You've done tons of research and have thought a lot about this, so I'd like to ask your views about a few things. We've all gotten scattered between threads, but this post with your overall comparison of anti-androgens seems as good as any. Questions:

1. The effect of SERMs and estrogen on hair
SERMs, tamoxifen in particular, is often used by men both in the real world and in our hair-world lol to fight against gyno. In the article you linked to, TMX is considered a first-line treatment for gyno.

I asked about the effect of SERMs and estrogen on hair in another thread here (quotes and research links in that thread). What's interesting to me is this fairly detailed 2013 study from Germany which finds that "there is little evidence in the current literature that oestrogens affect human hair growth one way or the other, possibly indicating a role of genetic predisposition in oestrogen-related hair changes... Our results argue against an effect of tamoxifen on hair growth."

That contradicts the standard thinking on hair forums that:

a) anti-androgens protect hair from further A.G.A damage, while estrogen is needed to really get regrowth (Cotsarelis interview 2012: "There seems to be a point of no return with respect to androgen removal; even if you castrate someone who’s bald he won’t regrow all his hair. If you give him estrogen, too, he might.")

and

b) that many (cis-, non-MTF) guys start an anti-androgen, get signs of gyno onset, then either drop the antiandrogen or start a SERM like tamoxifen. If they start with tamoxifen, it stops the gyno but negates the benefits of the anti-androgen and leaves you juggling between the drugs. For example, on that thread, jgray201 reported that he used tamoxifen for gyno when taking 200mg of spironolactone ED, and found that with TMX he "always lost some ground" (he reported that raloxifene much less harmful on his hair).

I'm confused about what's going on. What do you think about SERMs and hair?

More basically, what do you think about estrogen's effect on male hair? I notice you're using spironolactone in your nuke regimen, but haven't added any estrogen, topical or oral.


2. Correlation between AR affinity, hair benefit, gyno
I saw in a couple of threads that you've researched the affinity of different anti-androgens. I'd think that how well an anti-androgen competitively inhibits binding of androgens to the AR - in the hair specifically, if possible - is the most important point in evaluating them... and then side effects, cost, etc.

In this post on gyno, I think you're making the assumption that affinity, hair benefit, and gyno occurrence are all closely correlated, so you can use them as proxies for each other. Of course it's related, but is it true to assume that they're so directly correlated that they're proxies for each other? Maybe I'm being naive, overthinking it, and it's a no-brainer, but does the effect of an antiandrogen on hair necessarily have to correlate to gyno? Is there evidence for that? Again, I might be off here, but I'd thought there's a lot we don't know about the local and systemic differences: for example, synthesis and metabolizing of hormones varies locally by site, even among hair follicles, and afaik we also don't know what percent of androgens (or estrogen etc) come from local synthesis vs. passive diffusion. So I'd think that antiandrogen affinity, hair benefit, and gyno occurrence wouldn't necessarily be directly correlated; high gyno, little hair vertex benefit could be a possibility. Or some hair protection with little gyno (finasteride or low dose spironolactone, maybe).

I'm not criticizing, it's that I really don't know and am genuinely interested in your thinking about this.

3. Topical, systemic, vehicles, and antiandrogen differences
Afaik, there's no research comparing antiandrogens used topically. So based on what you've seen, how would you compare transdermal absorption of the different antiandrogens? To what extent will the metabolism of one drug - daro, let's say - depend on the vehicle vs. a different antiandrogen? Are there differences between the antiandrogens that could make some of them better than others topically at blocking local hair ARs?

Hey,

1) Estrogen
I believe that 2013 study you quoted. I don't believe estrogen has a direct positive role in hair growth. For example, if you look at estrogen products for postmenopausal women, you'll note they all list hair loss as a common side effect. Eg. Vagifem: "The most commonly reported side effects of Vagifem® include: headache, breast pain, irregular vaginal bleeding or spotting, stomach/abdominal cramps, bloating, nausea and vomiting, hair loss, fluid retention, and vaginal yeast infection."

I think estrogen has an indirect positive effect on hair retention/growth, because it suppresses testosterone levels. In half of M>F transexuals, estrogen alone can get testosterone adequately suppressed. ref

2) Correlation between gyno and hair results
The reason I chose gynecomastia as a side effect to focus on is because from what we know of gynecomastia, the processes underlying it are the same for at least the listed drugs as what we need to happen to protect hair.

Mechanisms of gynecomastia are discussed here, but the point is, anything that either blocks androgens from binding through the body and/or selectively reduces DHT/testosterone will simultaneously create a risk for gynecomastia and save hair from androgenic damage.

So they seem likely to be correlated well to me.

3) Transdermal antiandrogens
I'm not sure about transdermal antiandrogens. I'm not sure anyone is. DMSO is supposed to carry anything the size of these medications straight through the skin no problem, so probably they will be fine.

 

[folfoxorack]

I take Cyproterone 12.5mg every 2-3 days, its pretty strong. A lot than spironolactone 100-150mg.

 

[IdealForehead]

50mg of Cyproterone Acetate is equivalent in efficacy to 200mg of Spironolactone.

Hey Lacey,

Cyproterone isn't something I know as much about. I haven't seen any guys on these sites taking it. It's also something I've had to look into more deeply, as there seem to be fewer studies on it. I presume this has something to do with the fact that it's not FDA approved in America, so there are no American studies on it.

I've looked into it a bit further. I'll summarize what I learned about the comparison below if anyone is interested in reading it.

Spironolactone
Spironolactone is a diuretic with androgen blocking activities. Because it's a diuretic, it means you might be pissing and drinking water 24/7 while on it.

I've learned in my further reading that spironolactone is also quite unique in the way it performs its androgen blocking activities. It can be termed a "selective androgen receptor modifier". This is because although it is mostly an androgen antagonist, it actually has some activating properties on androgen receptors as well.

This has led to it being prohibited in prostate cancer, as it can actually activates the prostate cancer to a small extent leading to cancer growth. ref This same degree of partial agonism may possibly make it less favorable for hair protection, though it still clearly works well to stop hair loss either way.

The primary long term disadvantage for men of spironolactone is that it has a very high rate of gynecomastia as listed. This rate is not disproportionate to other strong antiandrogens. ie. It is matched by enzalutamide and bicalutamide. But it is much less favorable than cyproterone, which seems to get as good an anti-androgenic effect or better without quite so much gyno.

Cyproterone
Cyproterone is a synthetic progesterone with very powerful anti-testosterone effects. Although it also works to block the androgen receptor (like spironolactone), it seems more so to exert its effects by suppressing testicular production of testosterone.

This mechanism of action is more similar to what happens when guys take estrogen - both estrogen or progesterone (as female hormones) will suppress the testicles' testosterone production. So cyproterone is more "cutting off the problem" (your testicles) at the source. This is advantageous but also more aggressive overall in principle.

In a study comparing flutamide 250 mg three times a day to cyproterone 100 mg three times a day, they both were equally likely to create gynecomastia (22.5% flutamide, 23% cyproterone), but the gynecomastia was much less tender with cyproterone. ref

This is actually a very good gynecomastia statistic for a massive chemical castration dose of cyproterone (300 mg/day). It is actually the highest statistic I can find for gynecomastia on cyproterone. All other references quote 10-18%.

That's less than half the gynecomastia rate on spironolactone's typical max dose. So even with full castration dosing of cyproterone, you're getting less gynecomastia overall.

Cyproterone vs. Spironolactone
It's hard to find direct comparisons between the two drugs. One transsexual doctor suggests spironolacone 100-300 mg should roughly equate to cyproterone 100-150 mg, in terms of typical dose ranges. ref

In a hair study on female pattern loss, spironolactone 200 mg was found equivalent in effectiveness to cyproterone 50-100 mg. ref I think this has to do with the fact that there's only so much benefit you can get from anti-androgenism, and at least in women, that's likely maxed out at cyproterone ~50 mg/day.

Final Quirks/Thoughts
There are a few unique extra quirks to these two drugs to consider, which I will list briefly.

• Spironolactone seems to be better for cholesterol. ref
• Cyproterone may be linked to increased blood clot risk (which can be lethal), though likely not too significant if you're otherwise healthy, cancer-free, and not taking estrogen with it. ref
• Spironolactone can be associated with hyperkalemia (high potassium) which can also be lifethreatening, but it is unlikely if you have normal kidneys. ref
• Cyproterone has a higher depression rate of up to 30%. ref

So these two drugs are really quite different in both their risk and benefit profiles.

 

[SpikeCB]

The <1% for 1 mg finasteride seems hard to believe. I am a lean guy and developed mild gyno after 3 months of starting finasteride. Its been >2 weeks since I'v stopped but the sides haven't decreased.

 

[Ramsey]

@IdealForehead -
Very interesting to read what you're finding as you look at anti-androgens.

Estrogen:
Interesting what you say about estrogen. I've been reading a lot recently about estradiol's effects on hair. It's very complicated. Rat hair is inhibited by it, human hair - maybe - gets benefit, including maybe prolonging anagen, but not always. In humans, men and women respond differently to it. Different areas of the scalp respond differently. Aromatase variations among different sites. Afaik, there are no good studies about its use in men (if there are any, let me know... although I kind of doubt many would be done for obvious reasons lol). From anecdotal reports I've seen, it definitely seems to help and many people on forums - cis-men as well as MTFs - think it's the key that got them regrowth.

In fact, MTF case reports are fascinating. I've read a lot, and I don't see any obvious reasons for the hair-regrowth success stories vs. those who don't have such great results. Age and amount of loss before starting HRT are big factors obviously, but it doesn't exactly correspond with results. At that point, among different treatment protocols, I don't see any clear patterns in what is responsible for re-growth; I've found that it's surprisingly varied and seems very individual. Even good breast growth, which they usually want, doesn't always happen. Please do tell if you've noticed any patterns.

Side effects as ranking method:
I'm not sure if any side effect of an anti-androgen - gyno or anything else - is correlated well enough with hair benefit that it's a good proxy. There's just so much going on, so much variation, between individuals, between properties of each site... But I agree that there will never be any good studies about it, so in the meantime, it's great to have a clear view of what the gyno rates are for each of the antiandrogens; that's very useful , thanks!

Absorption:
Yeah, this is the big questions. How much goes systemic? How does it depend on the vehicle? How does it vary between combinations of different anti-androgens with different vehicles? How much would the percutaneous absorption vary between individuals? I'm a daro fan too, might buy some from the places I mentioned on the daro thread, but before I start topical or oral, I want to try to understand better these issues with antiandrogens and transdermal absorption, topical vs. oral, systemic. How much will stay local for hair benefit? If you know how much is going to go systemic, how would it change your thinking about which drug to take? What about interactions: how would a powerful AR inhibitor like daro interact with other treatments, would it lead to stronger/faster systemic effects? As for benefit-sides-cost analysis, could it actually be better to use weaker-to-mid AR-inhibing anti-androgens orally instead of stronger ones topically? Or a low-dose weak AR-inhibiting anti-androgen orally with topical estradiol, particularly for fronto-temporal area? In what ways should these answers vary by the starting hormone measurements you have?

Sorry that I don't have good answers. Even for those willing to push with anti-androgens, I'm not even sure how much of this we can even have a rough idea about and at what point we accept what we won't know, and then it just becomes a leap of faith.

There's some research on flutamide, have you seen it? Always was considered bad for the liver, so people looked at topical solutions.

- Famous 2000 study from Israel (Simtov, www.ncbi.nlm.nih.gov/pmc/articles/10601691) on topical flutamide. He has an interesting formula for a gel to get it to hopefully stick longer in the skin (glycerol monooleate). Big debate for many years afterwards whether the beneficial hair effect was due to local absorption only, or whether it actually went systemic and got benefit that way.

- 2011 FPHL study from Italy found that low-dose oral flutamide isn't so bad for the liver, after all. Flutamide should "be rightfully considered a first-line therapeutic option at least equal, if not superior, to minoxidil in FPHL treatment". Even bragged that they didn't lose many patients from the study because of liver side effects, instead they lost patients because the low-dose oral worked great and patients didn't need to continue treatment. (Prospective Cohort Study on the Effects and Tolerability of Flutamide in Patients with Female Pattern Hair Loss, Paradisi, 2011, http://www.medscape.com/viewarticle/741433_4)

CPA:
You mentioned that you hadn't seen much reports about it. I understand it's limited in the US, but outside the US, it's used a lot. For example, the pill Diane-35 (it has lots of other brand names in different places) combines 2mg CPA with 35μg ethinylestradiol. Women use it for hormonal contraceptive and acne. It has a good reputation among girls - at least on female-issue forums I've looked at - for its anti-androgentic acne benefits.

For hair loss, some guys on different forums have tried it as a topical; a recent example on gourmetstylewellness.com is @cesarcielo's thread https://www.gourmetstylewellness.com/intera...etate-androcur-diane-35-lotion-urgent.106109/. MTFs use CPA orally, as well as a few cis-men who want to be very aggressive in their hair loss fight. There are quite a few case reports on different forums. For example, on here, check out @chillvisio - note chill's discussion of prolactinoma and dopamine. Another to check out: Antydhtor (cis- non-MTF man) takes CPA 50 mg twice ED orally. He likes it because - according to him - it's powerful blocking AR and stopping production at the goands, it has a long history of use, and it's used for precocious puberty, sex offenders, etc, in addition to cancer use. Anty was banned from this forum and his posts were deleted, but he had a thread here and showed amazing results.

 

[IdealForehead]

@IdealForehead -
Very interesting to read what you're finding as you look at anti-androgens.

Estrogen:
Interesting what you say about estrogen. I've been reading a lot recently about estradiol's effects on hair. It's very complicated. Rat hair is inhibited by it, human hair - maybe - gets benefit, including maybe prolonging anagen, but not always. In humans, men and women respond differently to it. Different areas of the scalp respond differently. Aromatase variations among different sites. Afaik, there are no good studies about its use in men (if there are any, let me know... although I kind of doubt many would be done for obvious reasons lol). From anecdotal reports I've seen, it definitely seems to help and many people on forums - cis-men as well as MTFs - think it's the key that got them regrowth.

In fact, MTF case reports are fascinating. I've read a lot, and I don't see any obvious reasons for the hair-regrowth success stories vs. those who don't have such great results. Age and amount of loss before starting HRT are big factors obviously, but it doesn't exactly correspond with results. At that point, among different treatment protocols, I don't see any clear patterns in what is responsible for re-growth; I've found that it's surprisingly varied and seems very individual. Even good breast growth, which they usually want, doesn't always happen. Please do tell if you've noticed any patterns.

Side effects as ranking method:
I'm not sure if any side effect of an anti-androgen - gyno or anything else - is correlated well enough with hair benefit that it's a good proxy. There's just so much going on, so much variation, between individuals, between properties of each site... But I agree that there will never be any good studies about it, so in the meantime, it's great to have a clear view of what the gyno rates are for each of the antiandrogens; that's very useful , thanks!

Absorption:
Yeah, this is the big questions. How much goes systemic? How does it depend on the vehicle? How does it vary between combinations of different anti-androgens with different vehicles? How much would the percutaneous absorption vary between individuals? I'm a daro fan too, might buy some from the places I mentioned on the daro thread, but before I start topical or oral, I want to try to understand better these issues with antiandrogens and transdermal absorption, topical vs. oral, systemic. How much will stay local for hair benefit? If you know how much is going to go systemic, how would it change your thinking about which drug to take? What about interactions: how would a powerful AR inhibitor like daro interact with other treatments, would it lead to stronger/faster systemic effects? As for benefit-sides-cost analysis, could it actually be better to use weaker-to-mid AR-inhibing anti-androgens orally instead of stronger ones topically? Or a low-dose weak AR-inhibiting anti-androgen orally with topical estradiol, particularly for fronto-temporal area? In what ways should these answers vary by the starting hormone measurements you have?

Sorry that I don't have good answers. Even for those willing to push with anti-androgens, I'm not even sure how much of this we can even have a rough idea about and at what point we accept what we won't know, and then it just becomes a leap of faith.

There's some research on flutamide, have you seen it? Always was considered bad for the liver, so people looked at topical solutions.

- Famous 2000 study from Israel (Simtov, www.ncbi.nlm.nih.gov/pmc/articles/10601691) on topical flutamide. He has an interesting formula for a gel to get it to hopefully stick longer in the skin (glycerol monooleate). Big debate for many years afterwards whether the beneficial hair effect was due to local absorption only, or whether it actually went systemic and got benefit that way.

- 2011 FPHL study from Italy found that low-dose oral flutamide isn't so bad for the liver, after all. Flutamide should "be rightfully considered a first-line therapeutic option at least equal, if not superior, to minoxidil in FPHL treatment". Even bragged that they didn't lose many patients from the study because of liver side effects, instead they lost patients because the low-dose oral worked great and patients didn't need to continue treatment. (Prospective Cohort Study on the Effects and Tolerability of Flutamide in Patients with Female Pattern Hair Loss, Paradisi, 2011, http://www.medscape.com/viewarticle/741433_4)

CPA:
You mentioned that you hadn't seen much reports about it. I understand it's limited in the US, but outside the US, it's used a lot. For example, the pill Diane-35 (it has lots of other brand names in different places) combines 2mg CPA with 35μg ethinylestradiol. Women use it for hormonal contraceptive and acne. It has a good reputation among girls - at least on female-issue forums I've looked at - for its anti-androgentic acne benefits.

For hair loss, some guys on different forums have tried it as a topical; a recent example on gourmetstylewellness.com is @cesarcielo's thread https://www.gourmetstylewellness.com/intera...etate-androcur-diane-35-lotion-urgent.106109/. MTFs use CPA orally, as well as a few cis-men who want to be very aggressive in their hair loss fight. There are quite a few case reports on different forums. For example, on here, check out @chillvisio - note chill's discussion of prolactinoma and dopamine. Another to check out: Antydhtor (cis- non-MTF man) takes CPA 50 mg twice ED orally. He likes it because - according to him - it's powerful blocking AR and stopping production at the goands, it has a long history of use, and it's used for precocious puberty, sex offenders, etc, in addition to cancer use. Anty was banned from this forum and his posts were deleted, but he had a thread here and showed amazing results.

Thanks. I would agree with you it's likely impossible to correlate any side effect exactly with its effectiveness for hair. Cyproterone vs. Spironolactone laid that bare. But as with you, I've found this all educational.

Main problems with topical antiandrogenic treatment is in my opinion the following.

At least in the minoxidil study half of what was applied ended up on the pillow. https://jamanetwork.com/journals/jamadermatology/article-abstract/545803