| Hormonal contraception | |
|---|---|
| Background | |
| Birth control type | Hormonal |
| First use | 1960 |
| Pregnancy rates (first year) | |
| Perfect use | Varies by method: 0.05-2% |
| Typical use | Varies by method: 0.05-9% |
| Usage | |
| Duration effect | Various |
| Reversibility | Upon discontinuation |
| User reminders | Must follow usage schedule |
| Clinic review | Every 3-12 months, depending on method |
| Advantages and disadvantages | |
| STD protection | No |
| Periods | Frequently lighter, for some methods periods may stop altogether |
| Weight | No proven effect |
Hormonal contraception refers to birth control methods that act on the endocrine system. Almost all methods are composed of steroid hormones, although in India one selective estrogen receptor modulator is marketed as a contraceptive. The original hormonal method—the combined oral contraceptive pill—was first marketed as a contraceptive in 1960. In the ensuing decades many other delivery methods have been developed, although the oral and injectable methods are by far the most popular. Altogether, 18% of the world's contraceptive users rely on hormonal methods. Hormonal contraception is highly effective: when taken on the prescribed schedule, users of steroid hormone methods experience pregnancy rates of less than 1% per year. Perfect-use pregnancy rates for most hormonal contraceptives are usually around the 0.3% rate or less.[1] Currently available methods can only be used by women; the development of a male hormonal contraceptive is an active research area.
There are two main types of hormonal contraceptive formulations: combined methods which contain both an estrogen and a progestin, and progestogen-only methods which contain only progesterone or one of its synthetic analogues (progestins). Combined methods work by suppressing ovulation; while progestogen-only methods reduce the frequency of ovulation, most of them rely heavily on secondary mechanisms such as changes in cervical mucus. The incidence of certain side effects is different for the different formulations: for example, breakthrough bleeding is much more common with progestogen-only methods. Certain serious complications occasionally caused by estrogen-containing contraceptives are not believed to be caused by progestogen-only formulations: deep vein thrombosis is one example of this.
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In 1921, Ludwig Haberlandt demonstrated a temporary hormonal contraception in a female rabbit by transplanting ovaries from a second, pregnant, animal.[2] By the 1930s, scientists had isolated and determined the structure of the steroid hormones and found that high doses of androgens, oestrogens or progesterone inhibited ovulation.[3][4] A number of economic, technological, and social obstacles had to be overcome before the development of the first hormonal contraceptive, the combined oral contraceptive pill (COCP). In 1957 Enovid, the first COCP, was approved in the United States for the treatment of menstrual disorders. In 1960, the U.S. Food and Drug Administration approved an application that allowed Enovid to be marketed as a contraceptive.[5]
The first progestogen-only contraceptive was introduced in 1969: Depo-Provera, a high-dose progestin injection.[6] Over the next decade and a half, other types of progestogen-only contraceptive were developed: a low-dose progestogen only pill (1973);[7] Progestasert, the first hormonal intrauterine device (1976);[8] and Norplant, the first contraceptive implant (1983).[9]
Combined contraceptives have also been made available in a variety of forms. In the 1960s a few combined injectable contraceptives were introduced, notably Injectable Number 1 in China and Deladroxate in Latin America.[10] A third combined injection, Cyclo-Provera, was reformulated in the 1980s by lowering the dose and renamed Cyclofem (also called Lunelle). Cyclofem and Mesigyna, another formulation developed in the 1980s, were approved by the World Health Organization in 1993.[11] NuvaRing, a contraceptive vaginal ring, was first marketed in 2002.[12] 2002 also saw the launch of Ortho Evra, the first contraceptive patch.[13]
In 1991, ormeloxifene was introduced as a contraceptive in India.[14] While it acts on the hormonal system, this selective estrogen receptor modulator is not a hormone.
There are two main classes of hormonal contraceptives: combined contraceptives contain both an estrogen (usually ethinyl estradiol) and a progestin. Progestogen-only contraceptives contain only progesterone or a synthetic analogue (progestin). Also marketed is ormeloxifene; while not a hormone, ormeloxifene acts on the hormonal system to prevent pregnancy.
The most popular form of hormonal contraception, the combined oral contraceptive pill is known colloquially as the pill. It is taken once a day, most commonly for 21 days followed by a seven-day break, although other regimens are also used. For women not using ongoing hormonal contraception, COCPs may be taken after intercourse as emergency contraception: this is known as the Yuzpe regimen. COCPs are available in a variety of formulations.
The contraceptive patch is applied to the skin and worn continuously. A series of three patches are worn for one week each, and then the user takes a one-week break. NuvaRing is worn inside the vagina. A ring is worn for three weeks. After removal, the user takes a one-week break before inserting a new ring. As with COCPs, other regimens may be used with the contraceptive patch or NuvaRing to provide extended cycle combined hormonal contraception.
A combined injectable contraceptive is a shot given once per month.
The progestogen only pill (POP) is taken once per day within the same three-hour window. Several different formulations of POP are marketed. A low-dose formulation is known as the minipill. Unlike COCPs, progestogen-only pills are taken every day with no breaks or placebos. For women not using ongoing hormonal contraception, progestogen-only pills may be taken after intercourse as emergency contraception. There are a number of dedicated products sold for this purpose.
Hormonal intrauterine contraceptives are known as intrauterine systems (IUS). The only currently available brand is Mirena. An IUS must be inserted by a health professional. Mirena may be used for up to five years. While a copper-containing intrauterine device (IUD) may be used as emergency contraception, the IUS has not been studied for this purpose.
Depo Provera is an injection that provides three months of contraceptive protection. Noristerat is another injection; it is given every two months.[15]
Two types of progestogen-only contraceptive implants are available. Both are inserted under the skin of the upper arm. Jadelle (Norplant 2) consists of two rods that release a low dose of hormones. It is effective for five years. Implanon is a single rod that releases a moderate dose of hormones. It is effective for three years.
Ormeloxifene is a selective estrogen receptor modulator (SERM). Marketed as Centchroman, Centron, or Saheli, it is pill that is taken once per week. Ormeloxifene is legally available only in India.[16]
Modern contraceptives using steroid hormones have perfect-use or method failure rates of less than 1% per year. The lowest failure rates are seen with the implants Jadelle and Implanon, at 0.05% per year.[17][18] According to Contraceptive Technology, none of these methods has a failure rate greater than 0.3% per year.[18] The SERM ormeloxifene is less effective than the steroid hormone methods; studies have found a perfect-use failure rate near 2% per year.[19][20]
Long-acting methods such as the implant and the IUS are user-independent methods.[21] For user-independent methods, the typical or actual-use failure rates are the same as the method failure rates.[18] Methods that require regular action by the user—such as taking a pill every day—have typical failure rates higher than perfect-use failure rates. Contraceptive Technology reports a typical failure rate of 3% per year for the injection Depo-Provera, and 8% per year for most other user-dependent hormonal methods.[18] 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.[22]
The effect of hormonal agents on the reproductive system is complex. Overall, while secondary methods have been theorized, combined hormonal contraceptives work by preventing ovulation. Progestin-only contraceptives can also prevent ovulation, but rely significantly on secondary mechanisms such as the thickening of cervical mucus. Ormeloxifene does not affect ovulation, and its mechanism of action is not well understood.
Combined hormonal contraceptives prevent ovulation by suppressing the release of gonadotropins. They inhibit follicular development and prevent ovulation as their primary mechanism of action.[18][23][24][25][26]
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.[18][23][24]
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.[18][23][24]
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.[26]
Other secondary mechanisms have been hypothesized. One example is endometrial effects that prevent implantation of an embryo in the uterus. Some groups that oppose abortion 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.[26] Others make more complex arguments against the existence of these mechanisms,[27] while yet other scientists argue the existing data supports such mechanisms.[28] The controversy is currently unresolved.
The mechanism of action of progestogen-only contraceptives depends on the progestogen activity and dose.[25]
Low dose progestogen-only contraceptives include traditional progestogen-only pills, the subdermal implant Jadelle and the intrauterine system Mirena. 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.
Intermediate dose progestogen-only contraceptives, such as the progestogen-only pill Cerazette (or the subdermal implant Implanon), allow some follicular development but much more consistently inhibit ovulation in 97–99% of cycles. The same cervical mucus changes occur as with low dose progestogens.
High dose progestogen-only contraceptives, such as the injectables Depo-Provera and Noristerat, completely inhibit follicular development and ovulation. The same cervical mucus changes occur as with very low dose and intermediate dose progestogens.
In anovulatory cycles using progestogen-only contraceptives, the endometrium is thin and atrophic. If the endometrium was also thin and atrophic during an ovulatory cycle, this could theoretically interfere with implantation of a blastocyst (embryo).
Ormeloxifene does not affect ovulation. It has been shown to increase the rate of blastocyst development and to increase the speed at which the blastocyst is moved from the fallopian tubes into the uterus. Ormeloxifene also suppresses proliferation and decidualization of the endometrium.[16] While they are believed to prevent implantation rather than fertilization, exactly how these effects operate to prevent pregnancy is not understood.
Pills—combined and progestogen-only—are the most common form of hormonal contraception. Worldwide, they account for 12% of contraceptive use. 21% of users of reversible contraceptives choose COCPs or POPs. Pills are especially popular in more developed countries, where they account for 25% of contraceptive use.[29]
Injectable hormonal contraceptives are also used by a significant portion—about 6%—of the world's contraceptive users.[29][30] Other hormonal contraceptives are less common, accounting for less than 1% of contraceptive use.[29][30]
While unpredictable breakthrough bleeding is a possible side effect for all hormonal contraceptives, it is significantly more common with progestogen-only formulations.[31] Most regimens of COCPs, NuvaRing, and the contraceptive patch incorporate a placebo or break week that causes regular withdrawal bleeding. While women using combined injectable contraceptives may experience amenorrhea (lack of periods), they typically have predictable bleeding comparable to that of women using COCPs.[32]
Although high-quality studies are lacking,[33] it is believed that estrogen-containing contraceptives significantly decrease the quantity of milk in breastfeeding women.[34] Progestogen-only contraceptives are not believed to have this effect.[34] In addition, while in general the progestogen-only pill is less effective than other hormonal contraceptives, the added contraceptive effect of breastfeeding makes it highly effective in breastfeeding women.[35]
While combined contraceptives increase the risk for deep vein thrombosis (DVT - blood clots), progestogen-only contraceptives are not believed to affect DVT formation.[36]
Combined oral contraceptives can increase the risk of certain types of cardiovascular disease in women with a pre-existing condition or already-heightened risk of cardiovascular disease. 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.[1]
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