I just have some general questions and thought that some of the more knowlegable people in this forum would be able to help.
What is it about estrogen that allows women to take a pill for HRT, yet for test, men have to use a cream, needles, pellets, etc…? Or, why is not estrogen acted upon by the liver in the same way that test is? It seems that the oral steroids that are anabolic and androgenic need to be methylated, but why not estrogen?
Lastly, we know that test acts upon the bodies HPA axis and we’re familiar with all that entails, but it seems as though that’s not a concern at all when it comes to estrogen replacement in women…
Obviously, there’s some inherent difference between test and estrogen that accounts for the differences and I was just wondering what they were.
First, not all BC pills contain the same compounds. They contain more or less estrogen, LH, whatever. I would imagine that the compounds used are methylated or alkylated in the same ways that androgens are.
As far as female HPA, I personally cannot say definitively, as I’m not generally as interested in this topic, but I’ll take a couple guesses:
a) it does effect the female hormonal balances, and this is why it takes a few months off of the pill for a woman’s cycle to become normal again, and perhaps why it takes a while for the pill to be fully effective
b)dosages of hormones in BC tend to be in the range of 1-2 milligrams. This is orders of magnitude lower than the androgen dosages we talk about here. One would think that such a large gap in dosing protocols would result in a large gap in effect.
It is quite hard to find detailed product information relating to oral contraceptives, in my experience. I would guess that if not methylated (or ethylated or alkylated, then there must be some modification to the active hormone(s) to increase oral bio-availability. C|onsidering that some women stay ‘on’ for years at a time, the usual AAS modifications are unlikely, due to liver health.
Also, whilst BC pills increase the risk of stroke, obesity, heart disease and certain cancers, these are generally ‘overlooked’, because lets face it, not having kids is far more important.
Of course the pill affects female mood, appetite, fat storage, lipid profiles, etc, etc. Which is why there must be a period of normalisation post-BC prescription to allow normal menstrual cycle and fetility to return.
Cardiovascular disease is from the progestins. Progesterone is protective. BC is HPOA repressive, so there is less progesterone production. So progestins lower progesterone levels.
Estrogens are transported around the body by SHBG and released. With men, most T is SHBG bound and not bio-available. Bio-T involves FT and albumin bound T. Albumin bound T is released around the body.
Progestins are water soluble. Progesterone has very poor availability. Progestins were created to overcome that.
Oral estrogens have a very high first pass effect on the liver, creating SHBG that can really reduce a women’s T levels, with implications for libido, muscle mass, collagen, skin condition, pelvic floor, urine control, mood, bone loss etc.
That said, let’s just go directly to the OP’s questions.
An estrogen component of a birth control is most commonly supplied as ethinyl estradiol. This does have alkylation toxicity issues but the dosage used – well under 1/10 mg – is much lower than what men require for a useful dose of androgen, and chronic use is tolerable due to very the low dose.
There are various synthetic progestins used: for all or nearly all of them, the same is true as above.
As for effect on women’s hypothalamus and pituitary, suppression is exactly what is being aimed for.
