There is a lot of misleading information about the “morning after pill” or “emergency contraception”.
Much of this misleading information about the “morning after pill or “emergency contraception” has statements like “Won’t cause an abortion if you are already pregnant” or “It doesn’t harm you or a developing embryo”, or “it just prevents fertilisation of the egg”. These statements misrepresent the science behind ‘emergency contraception’.
In New Zealand, only two forms of “emergency contraception” are available. The “emergency contraceptive” pill, or the copper IUD. There is broad consensus that the copper IUD is capable of preventing an embryo (living human being) from implanting into the uterus. By the traditional definition of pregnancy this in an abortion.
But is the emergency ‘contraceptive’ pill also capable of destroying a human life?
In New Zealand, there is only one form of emergency ‘contraceptive’ pill, and its 1.5mg of levonorgestrel taken once as a single dose, or twice in 750 mcg doses. There are other pills available in other countries, but this is currently the only type of pill in New Zealand.
It’s thought that levonorgestrel works mainly by inhibiting ovulation, but it isn’t reliably able to do this if taken on the day before or the day of ovulation[i]. This coincides with a women’s peak libido and when she is most likely in engage in intercourse[ii]. It’s also the two days when she is most likely to get pregnant. So how does it work when it fails to stop ovulation? The makers of one of these medications is honest enough to admit that the precise mode of action “is not known”.
There are however some clues from the research.
One of the mechanisms that many cite is preventing sperm transport and function. Levonorgestrel doesn’t seem to affect the function of sperm as the concentrations used in emergency ‘contraception’, and sperm can reach the fallopian tube in 5 minutes[iii]. Another possible mode of action is affecting the transport of oocytes (eggs) and embryos in the fallopian tubes. This is plausible as progesterone affects the transport mechanisms in the fallopian tube[iv], and levonorgestrel is a synthetic progestogen. If the transport of the embryo to the uterus was disrupted, or even just slowed, the survival chances of this tiny human being are reduced. If tubal transport was affected then it probable that ectopic pregnancies would be more likely. In New Zealand Medsafe currently have a warning about emergency ‘contraception’ and ectopic pregnancy.
The last suggested mode of action is levonorgestrel inhibiting implantation. This is listed as a mode of action for one brand of levonorgestrel. Changes in the endometrium have been observed after treatment with levonorgestrel[v]. And in a model system only 43% of embryos attached in the presence of levonorgestrel compared with 59% of controls[vi], although this was reported as not statistically significant due to the low number of embryos uses (46 embryos destroyed for this research). No scientist has ever directly observed the implantation of a human embryo into a women’s uterus. So when people make sweeping statements that emergency contraception can’t or never prevents implantation, they don’t have anything conclusive to back up their claims.
The numbers are against them too. There are only 6 days in each month when a women is likely to become pregnant. The greatest probability of conception is on the last 2 of these days. And these are precisely the days when levonorgestrel is ineffective at blocking ovulation. So the question is, how can levonorgestrel be up to 95% effective at preventing pregnancy? Clearly it has modes of action other than blocking ovulation.
There is one way to tell if and when levonorgestrel is causing abortions by killing humans at the embryo stage, before implantation. It’s a very early pregnancy test called the ‘rosette inhibition assay’. It capable of detecting fertilisation within 24-48 hours. That’s days before implantation. This has been used to detect fertilisation in women using interuterine devices[vii]. It could be used to confirm once and for all the mode of action of levonorgestrel. But no one has been interested in publishing the results from this assay for years. I wonder if they are afraid of what they will find?
[i] K. Gemzell-Danielsson and L. Marions, “Mechanisms of Action of Mifepristone and Levonorgestrel When Used for Emergency Contraception,” Human Reproduction Update 10, no. 4 (July 1, 2004): 341–348, doi:10.1093/humupd/dmh027.
[ii] A. J. Wilcox et al., “On the Frequency of Intercourse around Ovulation: Evidence for Biological Influences,” Human Reproduction 19, no. 7 (July 1, 2004): 1539–1543, doi:10.1093/humrep/deh305.
[iii] Kristina Gemzell-Danielsson, Cecilia Berger, and Lalitkumar P G L, “Emergency Contraception — Mechanisms of Action,” Contraception 87, no. 3 (March 2013): 300–308, doi:10.1016/j.contraception.2012.08.021.
[iv] T. Mahmood et al., “The Effect of Ovarian Steroids on Epithelial Ciliary Beat Frequency in the Human Fallopian Tube.,” Human Reproduction 13, no. 11 (November 1, 1998): 2991–2994, doi:10.1093/humrep/13.11.2991.
[v] M F Vargas et al., “Effect of Single Post-Ovulatory Administration of Levonorgestrel on Gene Expression Profile during the Receptive Period of the Human Endometrium,” Journal of Molecular Endocrinology 48, no. 1 (February 2012): 25–36, doi:10.1530/JME-11-0094.
[vi] P. G. L. Lalitkumar et al., “Mifepristone, but Not Levonorgestrel, Inhibits Human Blastocyst Attachment to an in Vitro Endometrial Three-Dimensional Cell Culture Model,” Human Reproduction 22, no. 11 (November 1, 2007): 3031–3037, doi:10.1093/humrep/dem297.
[vii] Y C Smart et al., “Early Pregnancy Factor as a Monitor for Fertilization in Women Wearing Intrauterine Devices,” Fertility and Sterility 37, no. 2 (February 1982): 201–204.