Susan's Place Transgender Resources

When I first started HRT, my Endocrinologist started me on Estradiol, and of Finasteride. I started seeing significant progress. Then I switched to Estradiol, and Spiro. It seemed to stop all of my progress and keep me at the point I was at where I switched. I've since lowered my estrogen , yet still no changes in progression. I made the change from Finasteride to Spiro a handful of months after first starting, so my progress couldn't have been completed coincidentally when I switched. Might Estradiol and Finasteride work better for my body than Estradiol and Spiro? I've heard they work in different ways... Does anyone know the differences in how they effect the body? I started a few months after I turned 21, I'm 23 now - unsure if age is a factor or not to such an abrupt halt in progress when it coincided right when I switched my anti-androgen...





Edited for Dosages

Hi Teeg  :icon_wave:

Welcome to Susan's  :)  Glad to have you here

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V M

Spiro has mild anti-estrogenic and yes, even mild androgenic effect but its anti-androgenic effect should overcome all that. I wouldn't know how to explain this sudden stop.

Finasteride is less potent (strong) than Spiro in terms of anti-androgenic effect. So, again, I'm stumped. Perhaps the increased estradiol has made you more anxious and this increased anxiety has negatively affected your growth? I don't know. Just exploring possibilities. Perhaps some further discussion with your doctor would elucidate the mystery. :)

The hospital endo here says that Spironolactone stunts breasts development so he doesn't prescribe it.  He prescribes Finasteride to combat hair loss - not as an anti-androgen.  We do need to do our own research so we can go back to the doctors with reliable information.

I've never heard of Spiro being detrimental to breast growth...and many women do very well on it. Men who take it often develop gynecomastia.

How would it stunt breast growth? By what mechanism? Despite its mild anti-estrogenic effects, and apparent androgenic effects (in rats), I'd think that its antiandrogenic effects and increased conversion to estrogens from androgens would overcome this or not? I would be very curious as to hear why your doctor thinks so.

He says it's his own observation that women who have been on Spironolactone are more likely to end up with breast implants than the ones who were on Decapeptyl.  I got the idea that he intends to publish something and isn't saying too much before he's ready.

Interesting...

I don't believe in what your endo says. In the studies I've seen there has always been a tendency for gynecomastia/breast growth when you take spiro. And since spironolactone is a stronger anti-androgen than anti-estrogen this will lead to a higher amount of estrogen than testosterone in you, which will stimulate the feminization of your body. Does he have any other evidence than his empirical observations? How many transgender patients has he treated? Because if the number is low this would indicate that it's a standard deviation from the average.

Yes, it would be interesting to find out how many he treated, his sample size...how much Spiro he gave, etc? I think it's probably a matter of equivalence...that a certain dose of Spiro will be as effective as analogues but perhaps that dose results in too many side-effects so cannot be increased so much.

Fwiw my endo is religiously against Spiro unless the person has extremely sensitive t receptors or abnormally high t levels. And even then he prescribes a super low dose of the stuff.

My own take: spiro wasn't necessary for me. I've had excellent feminization from pellets (e+p) alone. I'd say if you want to get off spiro go for it, and maybe a bioidebtical progestin would be a better replacement.

There was also that recent study about spiro and breast augmentation. People who did not take spiro were less likely to have BA than those who didn't. Add me to that statistic ;)

I think just taking bio-identical E (+ P, if necessary) is always best. Can you cite link to study? I'd be interested in reading about it. Thanks. ;)

I would be interested in reading this study too.

Quote from: 930310 on February 04, 2014, 12:37:29 PM
I don't believe in what your endo says. In the studies I've seen there has always been a tendency for gynecomastia/breast growth when you take spiro. And since spironolactone is a stronger anti-androgen than anti-estrogen this will lead to a higher amount of estrogen than testosterone in you, which will stimulate the feminization of your body. Does he have any other evidence than his empirical observations? How many transgender patients has he treated? Because if the number is low this would indicate that it's a standard deviation from the average.

I don't know what evidence he has, but he is the endocrinologist at Charing Cross, which is the only hospital in the UK that does GRS.  Other endos can prescribe but anyone who goes the normal route goes through Charing Cross.

Quote from: MaryXYX on February 04, 2014, 08:25:39 AM
The hospital endo here says that Spironolactone stunts breasts development so he doesn't prescribe it.  He prescribes Finasteride to combat hair loss - not as an anti-androgen.  We do need to do our own research so we can go back to the doctors with reliable information.

My original Endocrinologist prescribed me Finasteride as a mild anti-androgen to, "clean up what Estrogen didn't block naturally". I may be mistaken, but I remember hearing from somewhere that Finasteride (and Dutasteride) directly blocks DHT, and produces an enzyme that converts T to E, or stops the conversion of E to T? I thought this might mean the body would then have, "its own" estrogen that perhaps it might like better. Unfortunately I never had hormone levels checked during this time, but perhaps when I was only on E and Fin my body was exposed to more of my own E, where on Spiro and Cypro they remove the T that converts to my body's E? Also, when I was on E, Finasteride, and Spiro, my E levels were significantly higher than with the same dose of E and Spiro with no Finasteride. Perhaps this is due to that conversion making more E?

Finasteride inhibits Type 2 5 alpha-reductase (while Dutasteride also inhibits Type 1, there are only two types) which converts T to DHT (dihydrotestosterone), about 5x more potent than T and responsible for scalp hair loss and body hair growth (and prostate enlargement and probably many other things as well). If less T converts to DHT, then more T is available and some of that may be converted to E, thereby slightly increasing E levels. E does not convert back to T, it's only one way, always T to E. Finasteride and dutasteride do NOT block T or DHT.

Spiro and Cypro reduce androgen levels (and your own E since A converts to E) and block androgens (T, DHT and other weaker androgens) from binding to receptors. Cypro blocks androgen more strongly. Spiro also increases breakdown of androgens, and conversion of androgen to estrogen. Both Spiro and Cypro, being progestins, are also mildly anti-estrogenic and in rats/mices, somewhat androgenic (I don't know if it's the same for us).

E also reduces androgen and also apparently...

http://en.wikipedia.org/wiki/Polyestradiol_phosphate
"blocks testosterone uptake into prostate cells, where it would be metabolized to DHT by the enzyme 5α-reductase. Estradiol also inhibits 5α-reductase directly, blocks binding of DHT to androgen receptors, and exhibits cytotoxicity on prostate cancer cells.[4][7]"

So there you go. :)

Quote from: KayXo on February 04, 2014, 08:36:45 PM
Finasteride inhibits Type 2 5 alpha-reductase (while Dutasteride also inhibits Type 1, there are only two types) which converts T to DHT (dihydrotestosterone), about 5x more potent than T and responsible for scalp hair loss and body hair growth (and prostate enlargement and probably many other things as well). If less T converts to DHT, then more T is available and some of that may be converted to E, thereby slightly increasing E levels. E does not convert back to T, it's only one way, always T to E. Finasteride and dutasteride do NOT block T or DHT.

Spiro and Cypro reduce androgen levels (and your own E since A converts to E) and block androgens (T, DHT and other weaker androgens) from binding to receptors. Cypro blocks androgen more strongly. Spiro also increases breakdown of androgens, and conversion of androgen to estrogen. Both Spiro and Cypro, being progestins, are also mildly anti-estrogenic and in rats/mices, somewhat androgenic (I don't know if it's the same for us).

E also reduces androgen and also apparently...

http://en.wikipedia.org/wiki/Polyestradiol_phosphate
"blocks testosterone uptake into prostate cells, where it would be metabolized to DHT by the enzyme 5α-reductase. Estradiol also inhibits 5α-reductase directly, blocks binding of DHT to androgen receptors, and exhibits cytotoxicity on prostate cancer cells.[4][7]"

So there you go. :)

Thanks for the info! :)

Do people take actually Polyestradiol phosphate for HRT, and/or might it be possible? Or was that just in terms of comparing its effects to other meds?

It's used in Scandinavian countries mostly, I think, in transsexual women and also for prostate cancer patients. The brand name is Estradurin. It works similarly, I think, to Depo-Estradiol (estradiol cypionate) where not only estradiol acts on receptors but where polyestradiol phosphate also acts on receptors. The most common form used is Estradiol Valerate injections (Delestrogen, Progynon-Depot).

The explanation provided was for estrogen, in general, not specific to only Estradurin which is an estrogen.

Quote from: KayXo on February 05, 2014, 12:01:52 PM
It's used in Scandinavian countries mostly, I think, in transsexual women and also for prostate cancer patients. The brand name is Estradurin. It works similarly, I think, to Depo-Estradiol (estradiol cypionate) where not only estradiol acts on receptors but where polyestradiol phosphate also acts on receptors. The most common form used is Estradiol Valerate injections (Delestrogen, Progynon-Depot).

The explanation provided was for estrogen, in general, not specific to only Estradurin which is an estrogen.

Might you know if there's a difference, good or bad, between those two types of estrogens and say estradiol in tablet form?

How do you mean about polyestradiol phosphate also acting on the receptors?

I tend to prefer bio-identical estrogen over any other estrogen that is not since it tends to have less effect on clotting, liver.

Many doctors wrongly assume that estradiol cypionate or polyestradiol phosphate only become active when they are broken down into estradiol which then acts on the body. What I was saying was that not only does the broken down estradiol act on the body but also, the unbroken molecule of estradiol cypionate or polyestradiol phosphate. Like Ethinyl Estradiol. It affects directly the body and then when it is later converted to estradiol, estradiol also affects the body. So, almost like you get a double whammy. But, where I am a little concerned is that these unnatural estrogens tend to have a stronger than normal effect on the body and estrogen receptors so increase health risks. But, it appears that polyestradiol phosphate (Estradurin) is quite safe in high doses in prostate cancer patients...so I'm not sure about this estrogen in particular.

spiro can cause breast bud fusing and limit breast growth too.

Quote from: Akira21 ♡♡♡ on February 06, 2014, 11:59:31 AM
spiro can cause breast bud fusing and limit breast growth too.

Any studies/evidence?

Quote from: 930310 on February 06, 2014, 12:17:24 PM
Any studies/evidence?

There is some discussion about a study done in the UK here:

https://www.susans.org/forums/index.php?topic=154404.0

The study mostly just points out that women who do not take spiro are less likely to have breast augmentation.

I read the full study which I have access to and the problem with it is that spironolactone doses are not mentioned. Say was used...well, obviously, results weren't good! What if doses of  had been used? Spiro is a weaker anti-androgen and perhaps higher doses are as effective as say,  Androcur or analogues.

I will reread, do more research re: this study because some of the statements intrigue me...namely, this one...

"This is consistent with studies on puberty induction in natal girls in whom rapid estrogen exposure was found to lead to premature breast bud fusion and poor breast development (8). Those transwomen who self-medicate with estrogen may be taking too large a dose at initiation to promote appropriate subsequent breast growth, resulting in a poorer final breast outcome."

And

"The use of spironolactone as an antiandrogen seemed also to be associated with an increased incidence of breast augmentation in transwomen. The other, more specific antiandrogens and GnRH analogs were not. Spironolactone is a mineralocorticoid receptor antagonist that acts as an androgen receptor partial antagonist as well as an estrogen receptor agonist. As such, in addition to blocking the androgen receptor (which is its primary purpose in this situation), it also has a significant estrogenic action at the
doses used in transwomen. One can postulate that this could lead to an excessive estrogenic action and consequent poorer breast outcome by the same mechanism as that seen when patients self-medicate with estrogens."

First I hear of premature fusion due to high dose of estrogen at the onset and of Spiro being estrogenic and exerting estrogenic action at the estrogen receptor. I do know however that Spiro increases conversion of androgen to estrogen.

Regarding Spironolactone having estrogenic activity, this is what another study states, contrary to the above study

CLIMACTERIC 2005;8(Suppl 1):3–63

Pharmacology of estrogens and progestogens: influence of different routes of administration
H. Kuhl
Department of Obstetrics and Gynecology, J. W. Goethe University of Frankfurt, Germany

"The chemical structure of drospirenone, which is a derivative of 17a-spirolactone, is similar to that of the aldosterone antagonist spironolactone"

"The antiandrogenic activity of drospirenone is about 30% of that of CPA. It has no estrogenic and no appreciable glucocorticoid activity"

"Besides the natural progesterone, four types of orally active, synthetic progestins are available: the progesterone derivatives, 19-norprogesterone derivatives (Figure 9), 19-nortestosterone derivatives and the spirolactone derivative drospirenone (Figure 10). They all exert progestogenic and – in some tissues - antiestrogenic activities, but differ largely in their hormonal pattern."

Experimental and Clinical Psychopharmacology Copyright 2007 by the American Psychological Association
2007, Vol. 15, No. 5, 427–444

Progesterone: Review of Safety for Clinical Studies

"Others that are derived from progesterone (17 hydroxyprogesterone derivatives), hydroxyprogesterone (19 norprogesterone derivatives), or spironolactone (drospirenone) have been found to exert estrogenic, glucocorticoid, and mineralocorticoid actions (Pluchino et al., 2006)."

This study, on the other hand agrees with the study from the UK.

I need to read some more...

Quote from: Akira21 ♡♡♡ on February 06, 2014, 11:59:31 AM
spiro can cause breast bud fusing and limit breast growth too.

Quote from: Jennygirl on February 06, 2014, 04:01:32 PM
There is some discussion about a study done in the UK here:

https://www.susans.org/forums/index.php?topic=154404.0

The study mostly just points out that women who do not take spiro are less likely to have breast augmentation.

Are these symptoms reversible? I took Spironolactone for a few months. This may be something related to why I seem to have experienced stunted progress.

Also, might Cyproterone have similar effects to the studies above?

According to the study, there weren't more people in the cyproterone acetate group having BA vs not having it. I personally don't like cyproterone acetate because it has many undesirable side-effects and it also increases cardiovascular risk (thrombosis, see Diane-35).

Here are a few excerpts from the study re:Cypro

"It is interesting that the other antiandrogens, cyproterone acetate and finasteride, do not appear to be used more frequently in those requiring breast augmentation compared with controls"

"Cyproterone acetate use is statistically more likely to cause depression than the other antiandrogen types used in this study. These results are consistent with previous studies using cyproterone acetate to treat hirsutism (11–13). It is, however, the first time this has been reported in transwomen. The incidence of depression was much lower in those using GnRH analogs, which is consistent with the findings of Dittrich et al. in 2005 (14), who found that depression was not a significant problem in transwomen treated with GnRH analogs."

"Because cyproterone acetate was associated with an increased incidence of depression compared with GnRH analogs, it could be argued that GnRH analogs are better for testosterone reduction."

"Of the antiandrogens studied, only cyproterone acetate was significantly associated with depression (8.3%, P
0.05) (see Table 4)."

More on Spiro, and how it increases estrogen...

From Drug-induced gynecomastia: an evidence-based review
September 2012, Vol. 11, No. 5 , Pages 779-795 (doi:10.1517/14740338.2012.712109)

"Spironolactone acts as an anti-androgen by binding to the androgen receptors; lowers circulating testosterone by increasing its metabolic clearance and preventing a compensatory rise in testicular androgen synthesis; displaces estrogen from sex hormone-binding globulin (SHBG) and increases the peripheral conversion of testosterone to estrogen leading to elevated estradiol [12]. Estradiol levels decrease and testosterone increase significantly 3 – 6 months after stopping spironolactone [12]."

From J Urol (Paris). 1981;87(9):635-8.
[The influence of spironolactone on the concentration of gonadotrophins and gonadal hormones in prostatic hypertrophy (author's transl)].

"The authors examined the influence of spironolactone on the concentration of testosterone, 5 alpha - dihydrotestosterone (DHT), progesterone, oestradiol (E2), LH, and FSH in 47 patients with prostatic hypertrophy, aged from 60 to 80 years. The control group consisted of 58 men of the same age. Spironolactone was prescribed at a dose of per day for three months. There was a considerable fall in the concentration of testosterone and of DHT and, at the same time, an increase in the concentration of progesterone, E2 and LH."





DO NOT POST DOSAGES

Quote from: teeg on February 06, 2014, 08:19:31 PM
Are these symptoms reversible? I took Spironolactone for a few months. This may be something related to why I seem to have experienced stunted progress.

Also, might Cyproterone have similar effects to the studies above?

No, the fusing is non-reversible. Depending on the amount of breast tissue that you developed before this would be negligible (which will not be much in a few months but it depends on how much a 'few' is exactly).

All this talk of breast bud fusion and such has made me a bit nervous of Anti-Androgens...

When I first started HRT I was only on E and Finasteride, no AA, and I seemed to do great on that...

Can E block T by itself somewhat?

Quote from: teeg on February 07, 2014, 03:39:21 PM
All this talk of breast bud fusion and such has made me a bit nervous of Anti-Androgens...

When I first started HRT I was only on E and Finasteride, no AA, and I seemed to do great on that...

Can E block T by itself somewhat?

Yes and I volunteer myself as living proof ;)

Yes, E blocks T to some degree (what degree varies by person). In the olden days the standard regimen was in fact estrogen only.

I'm another living proof. :) Never took anything but low dose estrogen, and outgrowing my 42DDD bras at the 4-year mark on HRT.

Quote from: Jennygirl on February 08, 2014, 05:15:57 PM
Yes and I volunteer myself as living proof ;)

Thanks for the confirmation :)

I don't think it's allowed to discuss exact doses and rightly so, but could you shed some light on perhaps some details of your HRT regimen like the medications and such if you'd feel comfortable?

I have an appointment coming up in a couple weeks with my Endo and any information could help given I'm in a small town...

Quote from: Jenna Marie on February 08, 2014, 08:29:29 PM
Yes, E blocks T to some degree (what degree varies by person). In the olden days the standard regimen was in fact estrogen only.

I'm another living proof. :) Never took anything but low dose estrogen, and outgrowing my 42DDD bras at the 4-year mark on HRT.

Wow, grats on the progress!  :D

Might you also be able to give a little information about which type of estrogen? Tablet form, injections, etc.?

Teeg : Patches, and a cis-menopausal-level dose. I'm not sure it'll help you much; even my endocrinologist was startled by the results relative to the dose. (Though she does swear by patches?) I can at least attest that I'm also not the only patient my endo has had who was able to get T levels down to the female range on E only.

Quote from: teeg on February 08, 2014, 08:47:01 PM
Thanks for the confirmation :)

I don't think it's allowed to discuss exact doses and rightly so, but could you shed some light on perhaps some details of your HRT regimen like the medications and such if you'd feel comfortable?

I have an appointment coming up in a couple weeks with my Endo and any information could help given I'm in a small town...

I am on kind of a megadose. A dozen E pellets (one would be equal to cis dose) and a single progesterone pellet every 3 months. There are a few other members here who swear by pellets too.

It's an expensive route if you still have the t makers and want to feminize quickly, but after SRS then it's pretty comparable to the other methods because dosage can be reduced so much. After SRS I will probably drop down to two or three E pellets and one P pellet. My wallet is looking forward to that... big time ;)

Pellets are extremely effective for reducing T regardless of the dose, really. The steady release is what makes that possible with such small amounts of the feminizing hormones (especially cross compared with oral). T doesn't stand a chance with pellets.

Quote from: Jennygirl on February 09, 2014, 05:44:59 AM
I am on kind of a megadose. A dozen E pellets (one would be equal to cis dose) and a single progesterone pellet every 3 months. There are a few other members here who swear by pellets too.

It's an expensive route if you still have the t makers and want to feminize quickly, but after SRS then it's pretty comparable to the other methods because dosage can be reduced so much. After SRS I will probably drop down to two or three E pellets and one P pellet. My wallet is looking forward to that... big time ;)

Pellets are extremely effective for reducing T regardless of the dose, really. The steady release is what makes that possible with such small amounts of the feminizing hormones (especially cross compared with oral). T doesn't stand a chance with pellets.

Yeah i completely agree, switching to pellets from patches was fantastic! I see the same wonderful Endocrinologist as Jenny and highly, highly recommend him, lovely guy and so knowledgeable.

Quote from: Bardoux on February 09, 2014, 07:13:54 AM
I see the same wonderful Endocrinologist as Jenny and highly, highly recommend him, lovely guy and so knowledgeable.

Thanks for the information from both of you. Who might that be? I could try to coordinate some sort of consultation between him and my Endocrinologist...

Dr. John O'Dea, he has offices in northern California and Marina Del Rey. That's a great idea!

Quote from: teeg on February 04, 2014, 08:15:47 PM
My original Endocrinologist prescribed me Finasteride as a mild anti-androgen to, "clean up what Estrogen didn't block naturally". I may be mistaken, but I remember hearing from somewhere that Finasteride (and Dutasteride) directly blocks DHT, and produces an enzyme that converts T to E, or stops the conversion of E to T? I thought this might mean the body would then have, "its own" estrogen that perhaps it might like better. Unfortunately I never had hormone levels checked during this time, but perhaps when I was only on E and Fin my body was exposed to more of my own E, where on Spiro and Cypro they remove the T that converts to my body's E? Also, when I was on E, Finasteride, and Spiro, my E levels were significantly higher than with the same dose of E and Spiro with no Finasteride. Perhaps this is due to that conversion making more E?

There exists no mechanism to convert E to T in the human body.

T will convert to E through aromatization.  This is the process that produces the fully feminine physique in CAIS women.

Quote from: Jennygirl on February 09, 2014, 02:48:26 PM
Dr. John O'Dea, he has offices in northern California and Marina Del Rey. That's a great idea!

Thanks for that! :)

I contacted his office, and although I'm at the opposite end of the country, it seems like we'll be able to set something up. Information on his website really makes sense about HRT.

However, I looked at reviews for his practice online and it seems pretty mixed... mostly either greatly negative or greatly positive... any thoughts?

in Transgender care they poin out that the use of finasteride is essential in feminization.

Finasteride

Finasteride* (Propecia, Proscar). One approach is tablets in the morning and tablets in the evening of finasteride. The finasteride tablets are branded as Propecia, but generics are available. The other method is taking the brand name drug, Proscar which contains finasteride. The tablet is not scored, and it is hard and oddly shaped.

*Without finasteride, results are only minimally improved over an estrogen only program.




Edited for Dosages - Do not post Dosages

Hi friends  :police:

Please keep in mind the Site Terms of Service and rules to live by (https://www.susans.org/forums/index.php/topic,2.msg27408.html#msg27408)

Particularly rule 8

Quote8. The discussion of hormone replacement therapy(HRT) and it's medications are permitted, with the following limitations:
A. You may not advocate for or against a specific medication or combinations of medication for personal gain. This is strictly prohibited.
B. You may not discuss the means to acquire HRT medications without a prescription. The discussion of self medication without a doctors supervision is prohibited.
C. The discussion of recommended or actual dosages is strongly discouraged to prevent information obtained on this site from being used to self medicate.
We can not in good conscience condone the self administering of these medications. Not only may self medication be illegal, but HRT medications can cause serious health problems, and many have the potential for life-threatening side effects that can only be detected and prevented with proper medical supervision.

Thank you

V M

Quote from: teeg on February 12, 2014, 02:28:08 PM
Thanks for that! :)

I contacted his office, and although I'm at the opposite end of the country, it seems like we'll be able to set something up. Information on his website really makes sense about HRT.

However, I looked at reviews for his practice online and it seems pretty mixed... mostly either greatly negative or greatly positive... any thoughts?

Bumping this

Teeg- sorry I've been away for about a week! Yeah I think the mixed reviews make perfect sense. He is incredibly strong willed and very blunt at times. It helps to be prepared for it going in and then I'm sure it will be smooth sailing.

Some things he says could easily trigger a person, but it also just goes to show that he is a no-holds-barred kind of doc and would have no problem showing you the exit over a disagreement :O

With him it's best to be attentive, and ask questions if you do not understand something. As I said he is incredibly strong willed and will give you the best care he can regardless of what ANY other doctor might say about it.

I have my next implantation with him coming up in the next few weeks... Can't wait! :)