[bobie]

So in my search for knowledge i have come across several topics suggesting that spiro causes breast bud fusion

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

http://www.susans.org/forums/index.php/t...852.0.html

Tbh im a little worried right now and seriously considering just using estradiol and finasteride, thoughts on how likely the above is?

[GoneGirl]

Bobie, I'm not worried about it, I'll stay on Spiro. Of course, I'm not trying for DDs...

Clara

[bobie]

Clara since i want to fully transition i am a little worried, not that im greedy (i have actually always preffered small breasts) i would like well formed breasts, its got be worried enough to have just cancelled the order of spiro i had placed that hasnt yet been dispatched, i also think i will start using Oestrogel to limit the number of pills passing through my liver, its probably time i found an endo that knows what they are doing, if the above is true though about spiro it could explain a lot not to mention why those using herbals can get such good results (despite susans saying otherwise lol)

[Lotus]

So in my search for knowledge i have come across several topics suggesting that spiro causes breast bud fusion

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

http://www.susans.org/forums/index.php/t...852.0.html

Tbh im a little worried right now and seriously considering just using estradiol and finasteride, thoughts on how likely the above is?

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.

Bobie, every time I read things like this when someone brings up what a doctor states it has a ripple effect. You can't access the report, I'd suggest possibly doing more research on it, I try to gather all the evidence, make comparisons and then make an informed decision.

Imo regardless of being on NBE or pharma is not to reduce free T, converting to E is a viable option, so again why suppress the one thing to which is the basis of breast growth and feminization.

The science of this is staring us right in the face!

[Lotus]

Just some FYI stuff:

Absorption and metabolism of spironolactone

Spironolactone is rapidly absorbed, with maximum plasma levels being reached in 30 to 60 minutes. Food increases spironolactone absorption. The percentage of drug that is detected in the systemic circulation after its oral administration exceeds 90%, depending on the tablet manufacturer.

Spironolactone is rapidly metabolized by the liver. Canrenone can be inter-converted enzymatically to its hydrolytic product, canrenoate. No un-metabolized drug is passed out via the urine. The major metabolites are canrenone and potassium canrenoate and are excreted through urine and bile.

Mechanism of spironolactone action in treatment of androgenetic alopecia

Spironolactone is a potent antiandrogen. The term antiandrogen, as defined by Dorfman, implies prevention of expression of androgen activity at target sites and does not include other mechanisms of decreasing androgen action, such as a decrease in production of androgens, interference with androgen metabolism, or change in androgen plasma protein binding.

However, the action of Spironolactone is directed at both decreasing production and blocking the effect of androgens at the cellular level. It is evident that Spironolactone decreases testosterone production in the adrenal gland by depleting microsomal cytochrome P450 and by affecting the cytochrome P450-dependent enzymes 17a-hydroxylase and desmolase. The destruction of microsomal cytochrome P450 by spironolactone may be limited to those tissues in which microsomal 17a-hydroxylase activity is high. The binding of spironolactone to 17- hydroxylase-cytochrome P450 may convert spironolactone to a metabolite that destroys the heme portion (molecule containing iron) of cytochrome P450, thereby decreasing steroid 17-hydroxylation.

Spironolactone is also a competitive inhibitor of DHT-receptor binding and interferes with the translocation of this complex into the nucleus. Spironolactone, a strong competitor for the androgen receptor, is a potent agonist, whereas canrenone, a weak competitor, is a potent antagonist. The true antagonists of endogenous or exogenous androgens are the weak agonists, which rely only on a continuous supply of the compound to achieve full inhibition. The antiandrogen effect of spironolactone may be produced by the parent compound on the adrenal gland and the metabolite on the receptor site.

The protestation activity of spironolactone is variable but influences the ratio of luteinizing hormone (LH) to follicle-stimulating hormone (FSH) by decreasing the response of LH to gonadotropin-releasing hormone (GnRH), thereby decreasing androgen production.
http://www.androgeneticalopecia.com/hair...ness.shtml

[bobie]

Thanks lotus some things for me to digest, heres a link to the report they talk about http://press.endocrine.org/doi/full/10.1....2012-2030 which im about to read myself

[bobie]

I will post the bits i find significant from that article:

Self-medication

These data appear to show that those people who self-medicate with estrogen are more likely to be referred for breast augmentation surgery than those who do not. The duration of estrogen exposure and the duration of estrogen use before attending the GIC (and any subsequent mammoplasties) resonate with the initial finding that self-medication is associated with greater need for breast augmentation. 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. As breast hemicircumference was not measured in this study; it was not possible to determine whether individuals who underwent breast augmentation had objectively smaller breasts. It should be noted, however, that unlike the situation in natal women, breast hemicircumference measurements are limited in their ability to quantify the appearance of breast development in transwomen. The median breast development in transwomen is reported to be 19 cm, which is near natal female norms (2). Despite this fact, 60% of transwomen still present for breast augmentation.

[bobie]

Antiandrogen type

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. 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, suggesting that this is not a class effect of antiandrogens.

[bobie]

Clinical usefulness

This report is the first comparison of different estrogen and antiandrogen regimens used in a single assessment center in which funding is not a confounding factor in the recommendation for augmentation mammoplasty. The finding that self-medication with estrogen results in more requests for mammoplasty reinforces the importance of supervised and cautious initiation of estrogen therapy in transwomen with regard to satisfaction with breast development. Clinically, it is important to counsel individuals who are self-medicating that they may compromise their final breast outcome, and there should be strong advice not to self-medicate.

[bobie]

So having read that im left thinking its not the spiro thats the problem, its people self medicating without at least getting blood work done, guess what i will be doing asap, im in two minds whether i should cut back to 2mg a day of estradiol (currently 4mg estradiol, 5mg finasteride and 200mg spiro all oraly) until i can get monitored properly, that said 4mg is still a pretty low dose