What is your anti-androgen of choice?

[KayXo]

My DHT is higher than I remembered at 53 ng/l, my T is at 0,2 ng/ml. Progesterone at 3,69 µg/l. not particularly much I think? For comparison, on spiro I had 370 ng/l DHT and 1,06 ng/ml T.

Well it seems I can't, but this is the very first time I hear of CPA supposedly being inferior. 
I'm tempted to go back to spiro for the 3 remaining months but I needed a higher than usual dose and my DHT was still super high, which bothers me.

I think the odds are in my favor considering I'd be the first person to get some growth 8 times faster than the fastest known cases. Most other meds I take have higher risk factors.

You are the one who complained of having androgenic symptoms on CPA vs. Spiro despite lower levels of androgens on CPA. If you want to stay on it, then do but I don't understand why you complain then and why you mentioned this in the first place.  And if you had less of these symptoms on Spiro despite higher blood levels, this goes to show you that blood levels alone don't tell the whole picture, there is more going on.

It could be that Spiro resulted in more E as I read that aromatization of T to E increases on it, and E is apparently released from SHBG due to competitive binding with Spiro. Spiro also does not have the progestogenic (anti-estrogenic) effect CPA has and Spiro can even weakly trigger estrogen receptors, CPA doesn't.

If there is growth, then why change anything? I don't know how you came up with that figure, 8 times faster than the fastest known cases...do you know all transwomen that have ever been on hormones, are you basing yourself on actual studies, have you objectively compared growth?

Like I said, the sooner you see a doctor, the better.

[Vii]

You are the one who complained of having androgenic symptoms on CPA vs. Spiro despite lower levels of androgens on CPA. If you want to stay on it, then do but I don't understand why you complain then and why you mentioned this in the first place.  And if you had less of these symptoms on Spiro despite higher blood levels, this goes to show you that blood levels alone don't tell the whole picture, there is more going on.

It's impossible to find any info on this though and emphasis is always put on blood levels. I'd like to know just what is wrong with CPA, as apart from depressions, so far I've seen myself be the only one who had any issues with it.

It could be that Spiro resulted in more E as I read that aromatization of T to E increases on it, and E is apparently released from SHBG due to competitive binding with Spiro. Spiro also does not have the progestogenic (anti-estrogenic) effect CPA has and Spiro can even weakly trigger estrogen receptors, CPA doesn't.

You replied to me in another thread where I was worried about too high estrogen levels. That shouldn't be the problem. You can only guess how much of it binds to receptors, but my issue was foremost increased body hair, which I don't think is something estrogen plays a big role in, as to my knowledge it's mostly an effect of DHT.

If there is growth, then why change anything? I don't know how you came up with that figure, 8 times faster than the fastest known cases...do you know all transwomen that have ever been on hormones, are you basing yourself on actual studies, have you objectively compared growth?

Like I said, the sooner you see a doctor, the better.

The study I quoted and also pretty much any other you can find on the matter cites patients taking CPA 4 years or longer who have had meningioma growth. By the time I have my SRS and with it, an orchiectomy, I'll have been on CPA for half a year so the fastest known case took 8 times that to become an issue.

[KayXo]

You replied to me in another thread where I was worried about too high estrogen levels. That shouldn't be the problem. You can only guess how much of it binds to receptors, but my issue was foremost increased body hair, which I don't think is something estrogen plays a big role in, as to my knowledge it's mostly an effect of DHT.

E does matter to an extent. So, if E is opposed by CPA (due to progestogenic effect, downregulation of receptors, more estradiol converted to estrone), and was slightly higher on Spiro, it could have made a difference.

J Invest Dermatol. 1997 Sep;109(3):296-300.

"Androgen receptor content in female frontal hair follicles was approximately 40% lower than in male frontal hair follicle. Cytochrome P-450-aromatase content in women's frontal hair follicles was six times greater than in frontal hair follicles in men. Frontal hair follicles in women had 3 and 3.5 times less 5alpha-reductase type I and II, respectively, than frontal hair follicles in men."

Suggesting *perhaps* estrogen reduces androgen receptors, increases aromatase and reduces conversion of T to DHT by resulting in less 5 alpha reductase activity.

Endocrinology. 1987 Jun;120(6):2597-603.

"In summary, estradiol treatment caused a reduction in androgen receptors, and estradiol withdrawal lead to a rise in androgen receptors. We believe that these results provide a mechanism whereby estradiol may directly antagonize androgen action."

Exp Dermatol. 2002 Aug;11(4):376-80.

"For topical treatment of androgenetic alopecia (AGA) in women, solutions containing either estradiol benzoate, estradiol valerate, 17beta- or 17alpha-estradiol are commercially available in Europe and some studies show an increased anagen and decreased telogen rate after treatment as compared with placebo."

"In conclusion, our ex vivo experiments suggest that under the influence of 17alpha-estradiol an increased conversion of testosterone to 17beta-estradiol and androstendione to estrone takes place, which might explain the beneficial effects of estrogen treatment of AGA"

The study I quoted and also pretty much any other you can find on the matter cites patients taking CPA 4 years or longer who have had meningioma growth. By the time I have my SRS and with it, an orchiectomy, I'll have been on CPA for half a year so the fastest known case took 8 times that to become an issue.

Right, I understand now (I misunderstood) BUT I still wouldn't take the risk. To each their own. But why continue on it anyways if you are seeing increased androgenic effects on it?

[Vii]

E does matter to an extent. So, if E is opposed by CPA (due to progestogenic effect, downregulation of receptors, more estradiol converted to estrone), and was slightly higher on Spiro, it could have made a difference.

J Invest Dermatol. 1997 Sep;109(3):296-300.

"Androgen receptor content in female frontal hair follicles was approximately 40% lower than in male frontal hair follicle. Cytochrome P-450-aromatase content in women's frontal hair follicles was six times greater than in frontal hair follicles in men. Frontal hair follicles in women had 3 and 3.5 times less 5alpha-reductase type I and II, respectively, than frontal hair follicles in men."

Suggesting *perhaps* estrogen reduces androgen receptors, increases aromatase and reduces conversion of T to DHT by resulting in less 5 alpha reductase activity.

Endocrinology. 1987 Jun;120(6):2597-603.

"In summary, estradiol treatment caused a reduction in androgen receptors, and estradiol withdrawal lead to a rise in androgen receptors. We believe that these results provide a mechanism whereby estradiol may directly antagonize androgen action."

Exp Dermatol. 2002 Aug;11(4):376-80.

"For topical treatment of androgenetic alopecia (AGA) in women, solutions containing either estradiol benzoate, estradiol valerate, 17beta- or 17alpha-estradiol are commercially available in Europe and some studies show an increased anagen and decreased telogen rate after treatment as compared with placebo."

"In conclusion, our ex vivo experiments suggest that under the influence of 17alpha-estradiol an increased conversion of testosterone to 17beta-estradiol and androstendione to estrone takes place, which might explain the beneficial effects of estrogen treatment of AGA"

Right, I understand now (I misunderstood) BUT I still wouldn't take the risk. To each their own. But why continue on it anyways if you are seeing increased androgenic effects on it?

Thanks for the sources. I'm just not sure whether to use CPA or spiro. As I said before, I'm tempted to switch to spiro again, but it still doesn't quite make sense in my head apart from subjective (and somewhat vague) observation. I'll just give it a try once I'm back home I guess.

[KayXo]

I would personally rely more on how my body responds rather than levels. Many doctors share that view as well. Good luck!

[Vii]

Kind of wish I had access to Bicalutamide...
I read a bit more into CPA and it really does have a devilish list of unwanted effects.

Considering my DHT levels on Spiro and since I'm still shedding despite CPA I'll add Dutasteride too. With that I'm not too bothered by the prospect of going back to Spiro. Probably the next best thing after Bica 

[KayXo]

I'll add Dutasteride too.

Beware of depression/anxiety associated with this drug. It can persist even after discontinuation.
Read entire thread https://www.susans.org/forums/index.php/topic,206700.0.html

[Vii]

Beware of depression/anxiety associated with this drug. It can persist even after discontinuation.
Read entire thread https://www.susans.org/forums/index.php/topic,206700.0.html

Thanks for the warning. But trust me, the depressions on CPA are no joke either.
I'm already pretty used to a variety of depression-inducing meds, but I'll know to be prepared now 

[KayXo]

Thanks for the warning. But trust me, the depressions on CPA are no joke either.
I'm already pretty used to a variety of depression-inducing meds, but I'll know to be prepared now 

Dutasteride and CPA aren't the only way to go about reducing androgens. There are other options where mood wouldn't be adversely affected. Just saying...As always, this needs to be discussed with a professional.