What is the mechanism of action of contraceptive pills?
Question posted by Naveen kandpal on 14 Feb 2011
Last updated on 14 February 2011 by suzanne66
There are two different kinds of birth control pills — combination birth control pills, which contain estrogen and progestin and minipills which contain only progestin.
Combination birth control pills suppress ovulation — keeping your ovaries from releasing an egg. Combination birth control pills also thicken cervical mucus and thin the lining of the uterus (endometrium) to keep sperm from reaching the egg.
The minipill thickens cervical mucus and thins the endometrium — preventing sperm from reaching the egg. The minipill also sometimes suppresses ovulation. Unlike combination birth control pills, the minipill doesn't contain estrogen. The progestin dose in a minipill is also lower than the progestin dose in any combination oral contraceptive pill.
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Combined oral contraceptive pills were developed to prevent ovulation by suppressing the release of gonadotropins. Combined hormonal contraceptives, including COCPs, inhibit follicular development and prevent ovulation as their primary mechanism of action.
Progestagen negative feedback decreases the pulse frequency of gonadotropin-releasing hormone (GnRH) release by the hypothalamus, which decreases the release of follicle-stimulating hormone (FSH) and greatly decreases the release of luteinizing hormone (LH) by the anterior pituitary. Decreased levels of FSH inhibit follicular development, preventing an increase in estradiol levels. Progestagen negative feedback and the lack of estrogen positive feedback on LH release prevent a mid-cycle LH surge. Inhibition of follicular development and the absence of a LH surge prevent ovulation.
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.
A secondary mechanism of action of all progestagen-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.
Other possible secondary mechanisms have been hypothesized. One example is endometrial effects that prevent implantation of an embryo in the uterus. Some pro-life groups consider such a mechanism to be abortifacient, and the existence of postfertilization mechanisms is a controversial topic. Some scientists point out that the possibility of fertilization during COCP use is very small. From this, they conclude that endometrial changes are unlikely to play an important role, if any, in the observed effectiveness of COCPs. Others make more complex arguments against the existence of these mechanisms, while yet other scientists argue the existing data supports such mechanisms. The controversy is currently unresolved.
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