**2.3 Mechanism of action**

The main mechanism of action of COCs is the suppression of ovulation through the inhibition of gonadotropin-releasing hormone from the hypothalamus, as well as inhibition of both luteinizing hormone (LH) and follicle-stimulating hormone (FSH), and disruption of the mid-cycle LH surge. These effects are mediated by both the progestogen and estrogen components of the COC working synergistically; however, it is the estrogen's ability to suppress FSH and thus prevent folliculogenesis that is likely the most important mechanism.

The additional estrogen exposure in continuous-use pills, pills with a shorter pill-free interval, and pills with an additional 10 μg of EE in the placebo week results in more complete suppression of FSH and less folliculogenesis. However, a substantial number of women can still develop follicles while taking low-dose COCs [32, 33]. Additionally, the estrogen component stabilizes sufficient endometrium production to maintain a regular withdrawal bleeding pattern, thereby permitting cycle control.

Additional progestogen-related mechanisms that contribute to the contraceptive effect of COCs include:

