Hormonal contraception
Almost all methods are composed of steroid hormones, although in India one selective estrogen receptor modulator is marketed as a contraceptive.
Hormonal contraception is primarily used for the prevention of pregnancy, but is also prescribed for the treatment of polycystic ovary syndrome, menstrual disorders such as dysmenorrhea and menorrhagia, and hirsutism.
Birth control pills are often prescribed to reverse the effects of excessive androgen levels, and decrease ovarian hormone production.
The hormonal IUD (Mirena) releases levonorgestrel which thins the uterine lining, preventing excessive bleeding and loss of iron.
[7] Birth control pills are the most commonly prescribed hormonal treatment for hirsutism, as they prevent ovulation and decrease androgen production by the ovaries.
Additionally, estrogen in the pills stimulates the liver to produce more of a protein that binds to androgens and reduces their activity.
[10] The SERM ormeloxifene is less effective than the steroid hormone methods; studies have found a perfect-use failure rate near 2% per year.
[10] While no large studies have been done, it is hoped that newer methods which require less frequent action (such as the patch) will result in higher user compliance and therefore lower typical failure rates.
[15] While unpredictable breakthrough bleeding is a possible side effect for all hormonal contraceptives, it is more common with progestogen-only formulations.
[16] Most regimens of COCPs, NuvaRing, and the contraceptive patch incorporate a placebo or break week that causes regular withdrawal bleeding.
[17] Although high-quality studies are lacking,[18] it is believed that estrogen-containing contraceptives significantly decrease the quantity of milk in breastfeeding women.
Smoking (for women over 35), metabolic conditions like diabetes, obesity and family history of heart disease are all risk factors which may be exacerbated by the use of certain hormonal contraceptives.
[2] Oral contraceptives have also been linked to an inflated risk of myocardial infarction, arterial thrombosis, and ischemic stroke.
Nexplanon has replaced the former Implanon and is also a single rod that releases etonogestrel (similar to the body's natural progesterone).
It is believed that combined hormonal contraceptives work primarily by preventing ovulation and thickening cervical mucus.
[citation needed] Combined hormonal contraceptives were developed to prevent ovulation by suppressing the release of gonadotropins.
[33][34][35] Estrogen was originally included in oral contraceptives for better cycle control (to stabilize the endometrium and thereby reduce the incidence of breakthrough bleeding), but was also found to inhibit follicular development and help prevent ovulation.
Estrogen negative feedback on the anterior pituitary greatly decreases the release of FSH, which inhibits follicular development and helps prevent ovulation.
[33][34][35] Another primary mechanism of action of all progestogen-containing contraceptives is inhibition of sperm penetration through the cervix into the upper genital tract (uterus and fallopian tubes) by decreasing the amount of and increasing the viscosity of the cervical mucus.
The primary mechanisms of action are so effective that the possibility of fertilization during combined hormonal contraceptive use is very small.
These contraceptives inconsistently inhibit ovulation in ~50% of cycles and rely mainly on their progestogenic effect of thickening the cervical mucus and thereby reducing sperm viability and penetration.
High dose progestogen-only contraceptives, such as the injectables Depo-Provera and Noristerat, completely inhibit follicular development and ovulation.
If the endometrium was also thin and atrophic during an ovulatory cycle, this could theoretically interfere with implantation of a blastocyst (embryo).
[38] UPA acts as a partial agonist and antagonist of the progesterone receptor and works by preventing both ovulation and fertilization.
[40] In the United States, UPA is sold under the brand name Ella, which is a 30 mg single pill to be taken up to 120 hours after unprotected sex.
[44] 72% of pharmacies reported the ability to order UPA and the prescription to be filled in a median wait time of 24 hours.
[48][49] In 1921, Ludwig Haberlandt demonstrated a temporary hormonal contraception in a female rabbit by transplanting ovaries from a second, pregnant, animal.
[50] By the 1930s, scientists had isolated and determined the structure of the steroid hormones and found that high doses of androgens, estrogens, or progesterone inhibited ovulation.
[58] A third combined injection, Cyclo-Provera, was reformulated in the 1980s by lowering the dose and renamed Cyclofem (also called Lunelle).
Cycle control is enhanced by the estrogen.Because COCs so effectively suppress ovulation and block ascent of sperm into the upper genital tract, the potential impact on endometrial receptivity to implantation is almost academic.
