Last week we learned the biology behind the menstrual cycle. This week, we’re going to learn how that biological understanding was used to prevent pregnancy ““ using some of the same hormones.
In order to brush up on how the menstrual cycle works, please see The Science of Birth Control Part 1: The Menstrual Cycle.
There are many methods of contraception; my main focus will be on hormonal methods. However, for the sake of completion, I am also including barrier methods as well as a brief discussion of surgical sterility.
These methods include the diaphragm, spermicide, contraceptive sponge, cervical cap, cervical shield, female condom and male condom. As indicated in the heading, these methods work by creating a barrier, blocking the sperm from entering the cervix. Many of these methods, if used properly, can be very effective. However, it should be noted that the male condom has a relatively high failure rate and natural versions (ex. lambskin) do not protect against sexually transmitted infections.
The combined pill ““ This type of oral contraceptive pill contains both estrogen and progestin (progestin is a class of progesterone-like drugs). Different types of combined pills use differing amounts of hormones and alternate members of the progestin family.
The mini pill ““ This pill only contains progestin and is ideal for women over the age of 35, women who cannot take estrogen, women who are nursing and women who are prone to blood clots. These progestin only pills contain different progestins depending upon the type of pill prescribed.
Vaginal Ring ““ A thin, flexible ring inserted into the vagina. It contains the hormones estrogen and the progestin etonogestrel.
The Patch ““ A skin patch worn on the lower abdomen, buttocks or arm. It contains the hormones estrogen and the progestin norelgestromin.
Depo-Provera ““ An intramuscular shot given once every 3 months. This shot only contains the progestin DMPA and can only be given for up to two years as DMPA has been shown to cause reversible bone loss.
The estrogen and the progestin suppress the release of follicle stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary gland. From the previous discussion on the role of FSH and LH in the menstrual cycle, you will remember that FSH and LF play an important role in the development of the follicle and the maturation of the oocyte. Without the release of FSH and LF from the anterior pituitary gland, ovulation will not occur. In addition, the constant level of estrogen and progestin cause a decrease in the amount of endometrial tissue being deposited around the uterus, meaning that a fertilized egg would be unable to implant. Progestins also cause a thickening of the mucus at the cervix, creating a barrier that prevent sperm from entering the uterus.
Interestingly, the effect of progestins seem to be linked to the amount and activity of the specific progestin utilized! While the progestin in the mini pill may not prevent ovulation, in the case of Depo-Provera, the progestin DMPA alone decreases FSH and LH levels, which then prevents ovulation, deposition of endometrial tissue and thickens the mucosal covering of the cervix. Depo-Provera is effective nearly from the moment the shot is applied.
The combined pill, the vaginal ring, the patch and Depo-Provera prevent ovulation, decrease endometrial tissue deposition, prevent implantation and increase the thickness of cervical mucus. The mini pill may prevent ovulation, decreases endometrial tissue deposition, prevents implantation and increases the thickness of cervical mucus.
Hormonal Intrauterine Device- The brand name of this device is Mirena. Mirena releases a low dose of the progestin levonorgestrel directly to the lining of the uterus for up to 5 years. The exact method by which Mirena prevents pregnancy is not entirely understood. However, it is believed that the low level of progestin causes changes in cervical mucus thickness and may alter ovulation as described in the hormonal section above. The presence of the IUD in the uterus may cause chronic inflammation in the fallopian tubes and endometrium and likely fosters an environment that prevents fertilization and implantation.
Copper Intrauterine Device– The brand name of this device is ParaGard. ParaGard is an intrauterine device that releases small amounts of copper for up to 10 years. The copper released by ParaGard causes chronic inflammation in the fallopian tubes and endometrium which creates a hostile environment for implantation of a bastocyst. In addition, copper is directly toxic to the sperm and ova.
Implantable Rod ““ The brand name of this device is Implanon. It is the size of a matchstick and is implanted subdermally in a woman’s upper arm. Implanon releases a steady amount of the progestin etonogestrel for up to three years. Similar to the methods described in the hormonal section above, the progestin inhibits ovulation and thickens cervical mucus.
Surgical Implants – such as Essure or Adiana are permanent methods to ensure lack of fecundity. In the case of Essure, stainless steel coils and PET fibers with an outer nickel covering are placed in the fallopian tubes. These materials were chosen because of a history of scar tissue forming around those materials. The PET fibers cause a benign invasion of monocytes and other immune cells, resulting in complete occlusion or blockage of the fallopian tubes, preventing fertilization. Sterilization is achieved in the case of Adiana by thermally damaging (burning) the lining of the fallopian tubes with radiofrequency waves followed by implantation of a silicone matrix into the damaged area of the fallopian tubes. Occlusion occurs as fibroblasts fill the spaces between the silicone matrix.
Tubal ligation – A tubal ligation is considered major surgery. The fallopian tubes will be altered at their thinnest point (the isthmic portion), closest to the uterus. The fallopian tubes are most commonly cut and sutured in such a way that they cannot reattach. The fallopian tubes can be banded or clipped which causes blood loss and scarring and eventually occlusion. The fallopian tubes can also be cauterized.
Vasectomy – The vasa deferentia of the male is severed, which prevents sperm from entering the ejaculate. Typically, the vasa deferentia are cut, cauterized or clipped. Vasectomy is considered an outpatient procedure.
There are other types of emergency contraception, including implantable contraception, but Plan B, as the most well known, is the method being focused on here.
Even though emergency contraception contains the progestin levonorgestrel, Plan B is believed to work through a mechanism of action a little different from other hormonal birth control methods discussed above. This may have to do with the concentration and activity of levonogestrel itself. It has been shown that Plan B does not effect the implantation of a fertilized oocyte and does not interfere with the endometrial wall in anyway, contrary to popular belief. Therefore, Plan B cannot, in any way, be called an abortifacient. Rather, studies have shown that instead, Plan B impairs the ovulatory process and the function of the corpus luteum, likely though similar methods described above. In addition, Plan B also seems to effect sperm migration and function.
Progesterone released from the corpus luteum is necessary during the maintenance of a pregnancy, especially through the first 9 weeks. One of the major roles of progesterone is to maintain the uterine lining necessary to provide nutrients to a developing embryo. Mifepristone (RU-486) is a competitive progesterone receptor antagonist. What this means is that mifepristone more strongly binds the progesterone receptor than progesterone does and will actually compete and win (in a manner of speaking) for the binding site on the receptor. The term antagonist means that mifepristone will bind to the progesterone receptor but will have no biological effect. Once all the progesterone is competed off the receptors by mifepristone, menstrual bleeding will commence and the uterine lining will slough off, including any implanted material. Additional treatment with prostaglandins aid in contraction and cervical softening.
Of course, there are methods of contraception I have not covered, mainly due to time and space issues. Lack of coverage does not reflect upon the importance of those methods. I hope this series on the biology of the menstrual cycle and contraceptives has been informative. Additionally, I hope you have as much fun reading it as I had putting it together.
Again, a special thank you again goes out to Jen R. L. Disarray for suggesting the topic in the first place!
Did I get something wrong? Have a question? Send me an email at AskDorilysAboutScience@PersephoneMagazine.com