Most people dread taking medications because they don’t understand how the medication works, or because they are expensive and time-consuming. Therefore, many will try to swing their doctor to avoid giving them meds or give them a “generic” to reduce costs. However, when it comes to the fertility meds, many are only available in the Brand name (meaning no generic exist) and are extremely expensive. If until now you have been TTC without fertility meds and have now been introduced to the overwhelming world of fertility drugs, don’t despair! In this article, I will try to demystify the many fertility drugs and will give you hints on how to save money on them.
Oral Fertility Meds (aka the first line of treatment)
The fertility pills such as Clomid (Clomiphene) and Femara (Letrozole) help the pituitary gland improve the stimulation of developing follicles (eggs) in the ovaries. They work by blocking estrogen receptors in the hypothalamus, which in turns releases higher amounts of GnRH into the anterior pituitary, telling it to release higher levels of FSH and LH. Thus the ovaries are “forced” to increase follicle development and estrogen. The increasing levels of circulating estrogen as sensed by the hypothalamus, which then sends an LH surge producing ovulation. The side effects can range from headaches, mood swings, ovarian cysts to weight gain. They also increase your chances of twins. Clomid has been known for causing thinning of the uterine lining, which can potentially impact implantation rates or causes miscarriages.
Injectable medications are the second line of fertility treatment, usually used after several cycles with CC failed. Injectable medications can be subdivided into several categories.
GnRH Agonist (Lupron, Buserelin, Nafarelin, Synarel):
This medication mimics the structure of GnRH molecule in the hypothalamus, thus is able to bind to the GnRH receptor and elicit the response of the anterior pituitary to release FSH and LH during the first 4-6 days. Thus, the blood levels of LH and FSH which are initially raised with the initiation of GnRHa therapy are sustained well above normal for 4-6 days, producing a “flare effect” (a 10x increase in LH). However, it sorts of gets stuck and ultimately blocks the receptor from further activity and inhibits the action of this hormone in the brain. This is referred to as “pituitary down-regulation”. At this point, the pituitary gland becomes depleted of FSH and LH. However, after taking it for 10-20 days, it produces a hypogonadal effect, thus drastically reducing FSH and LH. The administration of subcutaneous GnRHa is rarely associated with significant side effects. Some women experience temporary fluctuations in mood, hot flashes, nausea. It is given subcutaneously.
GnRH Antagonist (Ganirelix, Cetrotide, Cetrorelix, Orgalutron):
Also known as antagon, GnRH antagonists are competitive inhibitors of GnRH. They work by blocking GnRH from binding to its receptor in the hypothalamus and rapidly depleting FSH and LH, preventing premature luteinization (ovulation). Unlike the agonist long course of treatment (10-20 days), the antagonist is effective within 2-3 days of treatment. They are usually recommended in women with PCOS, as they reduced the risk of OHSS. As well, they reduced the possibility of having a cycle cancellation.
Gonadotropins (Menoupur, Follitism, Gonal-F):
There are two gonadotropins, FSH and LH. These gonadotropins are excreted in the urine. Two varieties are commercially available. The 1st is menotropins or urinary-derived Human Menopausal Gonadotropins (hMG). The 2nd is genetically-engineered Recombinant DNA-gonadotropins, (FSHr and LhR). If administered to women at a sufficient dosage beginning early enough in the menstrual cycle, commercially available gonadotropins will prompt the development of multiple follicles each of which houses one egg. LH (and hCG) directly stimulates the tissue surrounding the ovarian follicles ) which in response produces male hormones (predominantly testosterone). The testosterone is then carried to the surrounding follicles where FSH converts it to estrogen. Risks and Side Effects of Gonadotropin Therapy: some women taking gonadotropins report breast tenderness, backaches, headaches, insomnia, bloating, and increased vaginal discharge, which are directly due to increased mucus production by the cervix.
- Human Menopausal Gonadotropins (hMG)– Menopur, Merional 75IU: hMG contains both FSH and LH. Menopur also contains a small amount of added hCG.
- Urinary-Derived FSH (Bravelle) this is essentially hMG that has been processed further to extract most of the LH. It is less expensive than FSHr.
- Recombinant FSH FSHr (Folistim, Gonal-F and Puregon): derived by way of genetic engineering. FSHr appears to be more bioactive than urinary-derived FSH products such as Bravelle and hMG and response to FSHr, more consistent and predictable.
Recombinat LH (Luveris): Since some LH is essential to provoke the ovarian stroma to produce some testosterone for delivery to the follicles for conversion into estrogen, a small amount must be given with FSHr to achieve egg development.
HCG (aka trigger shots Pregnyl, Novarel, Ovidrel):
The effect of the “trigger shot” is to send eggs into a reproductive division known as meiosis where the objective end point is a decrease in the number of chromosomes in the egg from 46 to 23 (half) prior to ovulation or egg retrieval. In the process, approximately half of the chromosomes are expelled from the egg nucleus in a membranous envelopment. This so called first polar body comes to lie immediately under the envelopment of the egg (the zona pellucida) in a region known as the perivitelline space. Ovulation will occur 36 after the HCG trigger is given. This trigger shot comprises one of three medications: a) urinary-derived hCG (hCGu), e.g., Novarel, Pregnyl and Profasi, b) Recombinant hCG (hCGr), e.g., Ovidrel, or c) an agonist such as Lupron, which upon being injected provokes a surge in the release of pituitary gland-derived, LH) is initiated.