Although preliminary experiments on ovulation suppression began in 1921, the oral contraceptive pill (OCP) was not approved for menstrual disorders and contraceptive purposes until 1960. Interestingly, Australia was the second country in the world to have access to the pill!
As is the case with many scientific breakthroughs, the inhibiting action of sex hormones on contraception was found accidentally by a fertility specialist who discovered that high doses of estrogen and progesterone combined can effectively prevent ovulation.
Today, 34% of Australian women choose the OCP as their choice of contraception which comes in various forms. The combination pill contains oestrogen and progesterone and the ingredients tend to include 20 micrograms of ethinyloestradiol and 100 micrograms of levonorgestrel. In saying this, the ratios and doses of these synthetic hormones do vary.
The mini pill is another form of OCP which only contains progesterone— a steroid hormone that activates progesterone receptors in the body. These have the ability to inhibit ovulation and thicken cervical mucus to prevent sperm penetration.
Although some pioneering contraceptive developers derived these steroid hormones from plants, these failed to be effective. As a result, synthetic forms continue to be the norm for most.
The various phases of the female menstruation cycle explained
From the onset of menstruation, a woman’s ovaries will release an egg each month which occurs over four phases and is driven by four main hormones: estrogen, progesterone, luteinising hormone and FSH follicle-stimulating hormone. There are others that come into play, but these four mainly control the show.
The Menstrual phase
During ovulation, follicles are released by the ovaries that develop into a “corpus luteum”. This houses the ovum (egg) and acts as a small temporary hormone producing gland. It’s designed to produce optimal conditions for pregnancy should fertilisation occur. If fertilisation is unsuccessful, the corpus luteum begins to break down, estrogen and progesterone levels drop and the thickened uterine lining is broken down and shed. To assist the removal of the uterine lining, the endometrium produces prostaglandins (hormone like compounds) that cause muscle contractions. This explains the onset of menstrual symptoms and painful cramps for some women.
The reason your pain relievers (Panadol and Nurofen) work well for period-related symptoms is because they stop cyclooxygenases— the enzymes responsible for the creation of inflammatory prostaglandins in their tracks.
Pre-ovulatory/ Follicular phase
This phase begins from day one of menses (shedding of the uterine lining) until ovulation occurs. The drop of steroid hormones that occurs during menstruation signals the hypothalamus and anterior pituitary gland to produce Gonadotropin-releasing hormone (GnRH) and then Follicular Stimulating Hormone (FSH). This causes the ovaries to release an “ovarian follicle” that will mature to become a corpus luteum— an egg containing sac that will be released during ovulation.
The ovulation phase
A consistent level of estrogen and an increase in luteinising hormones (LH) triggers the beginning of ovulation. Ovulation occurs approximately 10-12 hours after a large surge in LH. This is why ovulation kits predominately test for this hormone. During this time, Prostaglandins are also triggered by the increase of LH, which may cause some women to experience ovulation pain. This is technically known as “mittelschmerz”.
Increasing levels of estrogen during this phase causes the endometrium to thicken in preparation for the potential implantation of the ovum.
Our bodies are biologically programmed to procreate at this time and increased levels of the sex hormones estrogen and testosterone are responsible for increased sex drive at this point in the cycle.
The Luteal phase
During the Luteal phase, Follicular Stimulating Hormones and luteinising hormone levels drop and the corpus luteum continues to produce progesterone. During this process, estrogen levels remain high.
If fertilisation doesn’t occur, the corpus luteum begins to break down. This triggering a drop in estrogen and progesterone levels resulting in the shedding of the endometrium and the commencement of the menstrual stage.
How does the pill stop ovulation?
The ovulation process is initiated by the production of gonadotropin-releasing hormone (GnRH) which releases follicles created in the ovaries. The progesterone-only pill stops the production of GnRH and all the other hormones that occur within this hormone cascade. This means that no egg is produced during the monthly cycle.
Breastfeeding mothers produce high levels of prolactin which also inhibits GnRH and prevents pregnancy from occurring. Progesterone also thickens cervix mucus and reduces the sperm’s ability to penetrate.
The combined pill contains estrogen and progesterone, however, the estrogen component of this pill works in 3 ways:
- It works in synergy with progesterone to reduce GnRH and its antifertility functions
- It provides stability to the endometrium
- It reduces the likelihood of breakthrough bleeding.
Side Effects from the OCP
Contraceptives such as the OCP provide childbearing women with the ability to choose safe, affordable and effective methods to better manage their reproductive health and family planning options.
Although the benefits of contraceptive use are numerous and auspiciously liberating, they are unfortunately not without consequence. In fact, side effects are common and many micronutrients are lost when the OCP comes into play.
Obviously, when synthetic hormone production overrides the natural form side effects can occur.
Common side effects include:
- Headaches, migraine, dizziness, nausea
- Breast tenderness
- Breakthrough bleeding
- Decreased libido
- Weight gain
- Fluid retention.
The less common side effects include:
- Venous Thrombosis, (vein blood clots, estrogen can increase blood clotting factors.)
- Breast cancer risk: again, estrogen is linked to this.
- Depression & anxiety: again estrogen, primarily due to its effect on the production of neurotransmitters.