Appendix I: Does the oral contraceptive pill cause abortions?

There has been much discussion in Christian circles about whether the oral contraceptive pill (OCP) causes early abortions. The debate began in 1997 when Randy Alcorn, an American pastor, published a book called Does the Birth Control Pill Cause Abortions? The debate is significant because the OCP is widely used and regarded as an easy and effective method of birth control. There is concern that this controversy will mean many Christian families will be unable to reliably control their fertility. As a result, this has caused much anxiety on the part of believers who wish to protect human life from its earliest stages.

It is worth recognizing at the outset that there are people on both sides of the debate who are sincerely pro-life and have much in common. All are concerned about the protection of unborn human beings from the time of fertilization, given that they are all made in the image of the God who imbues them with dignity and worth. All recognize that since we have been able to work out how fertilization occurs through application of human reason, we now have the responsibility to use that knowledge to ensure that the process of embryonic development is not interrupted.

To understand the debate, you need to know how the OCP works. The OCP is known to work as a true contraceptive, by:

  1. inhibiting ovulation, so there are no eggs available to be fertilized
  2. thickening cervical mucus, making it difficult for the sperm to get through the cervix, so they are not available to do the fertilizing.

People on both sides of the debate agree on these points. But it also has a third effect:

  1. it makes the lining of the womb thinner and hostile to the embryo.

This third effect is where the contention lies.

The argument goes this way: If a woman taking the pill experiences failure of the first mechanism, and she ovulates so that an egg is produced; and if the second mechanism fails and sperm gets through the cervix; and if an embryo is then formed; and if the third mechanism prevails; then it means that the endometrium may be unable to support the embryo that is formed, and an early abortion may occur. The study quoted to support this hypothesis claims to demonstrate that women who had ovulated while taking the pill had atrophic (thinned) endometrium.[1]

The problem lies in the methodology: the investigators’ criterion to ‘establish’ that the women had ovulated was to have a blood progesterone level over 4ng/ml. So far so good. But most medical experts would say that you need a progesterone level over 9ng/ml to be sure that ovulation had occurred,[2] so it is possible that women in the study with progesterone levels over 4ng/ml but under 9ng/ml may not have ovulated. The results therefore do not help prove the theory. If the women did not ovulate then the condition of the endometrium doesn’t matter, because if there is no egg then there is no embryo to implant.

Furthermore, the argument that opposes the abortifacient theory claims that ovulation and endometrial thickening go hand in hand. It rejects the notion that the first two mechanisms could fail and the third mechanism could still prevail. Instead, it suggests that if you had failure of ovulation inhibition, and an egg was produced (this is known as escape ovulation), and if you had failure of cervical mucus thickening and the sperm got through, the hormone surge that normally accompanies ovulation would be released and it would stimulate the endometrium to grow and prepare the uterus for implantation of an embryo, as it is designed to do, over the 7 days it takes for the embryo to reach the womb. In this case, if the egg were fertilized, you would not have an early abortion but an unplanned pregnancy. Supporters of this argument note that the endometrium isn’t ready for an embryo in the two weeks before ovulation in a fertile woman even if she doesn’t take the pill. The endometrium always needs the hormone surge to prepare for an embryo, and it is this thickened endometrial lining that is shed each month in menstruation (the woman’s ‘period’ bleed) when no embryo arrives. It builds up again following ovulation the next month, and so the cycle continues. These doctors see no reason biologically why the pill would stop this automatic response to ovulation.

Nobody disputes that with normal OCP usage, the pill-user has a thin endometrial lining. What is important is to find out what happens when ovulation occurs while taking the pill. Just because the pill can cause endometrial thinning does not mean it relies on that thinning for its effectiveness. Suppression of ovulation is the most important aspect of its function.

Ectopic pregnancy risk

A further line of argument used to support the abortifacient position is related to ectopic (tubal) pregnancy rate for hormonal contraceptives. This argument is a bit more complicated. It is postulated by OCP opponents that if the OCP has no effect after fertilization (i.e. it does not interfere with the embryo once it is formed), then reductions in the rate of intrauterine (normal) pregnancy in pill-users would be the same as reductions in the rate of pregnancy outside the uterus (ectopic pregnancy). They argue that if the action of the OCP is occurring before implantation then it has a general reduction effect on all pregnancies regardless of where they would have ended up if they had been fertilized. Those supporting this position suggest that as there is a lesser reduction in the incidence of ectopic pregnancy (that is, there are more of them) with hormonal contraceptive use compared to non-pill users, the most likely explanation is that the OCP does something to prevent the embryo from implanting in the right place (once again, the hostile endometrium hypothesis) and therefore forces the newly conceived child to implant in the wrong place. They quote papers that they say demonstrate an increased extrauterine/intrauterine pregnancy ratio in women taking the pill.[3]

Those opposing this argument acknowledge that there is an increased tubal pregnancy rate with some contraceptives, but point out that the studies cited put other hormonal contraceptives (which work differently) in the same category as the OCP. They suggest that if you look at the research for the hormonal contraceptives individually, in fact the increase (per pregnancy) in ectopic pregnancy occurs only with the progestin-only pill and Norplant, not with injectables or the OCP.[4] This increased risk of ectopic pregnancy may be the result of progestin acting on the fallopian tube to delay egg transport to the uterus, so the embryo is still in the tube when it is time to implant—but it is not fully understood.[5] There is no evidence to support that it is due to a hostile endometrium. Opponents of the abortifacient theory suggest once again that if escape ovulation occurs, the hormonal surge will prepare the endometrium in time for implantation. They suggest that an incorrect conclusion has been drawn from this research. They postulate that the fact that an embryo can implant in the fallopian tubes or other places in the abdomen suggests that an ideal endometrium is not actually necessary for successful implantation and thus further supports use of the OCP.

This is a simplification of the debate—there have been further lines of argument offered and refuted. Please review the given references if you would like to pursue this question further.[6] And as I said in chapter 6, do not use the pill if your conscience forbids it (Rom 14:23b).


  1. V Chowdhury, UM Joshi, K Gopalkrishna, S Betrabet, S Mehta and BN Saxena, ‘“Escape” ovulation in women due to the missing of low dose combination oral contraceptive pills’, Contraception, vol. 22, no. 3, September 1980, pp. 241-7. 
  2. MG Hull, PE Savage, DR Bromham, AA Ismail and AF Morris, ‘The value of a single serum progesterone measurement in the midluteal phase as a criterion of a potentially fertile cycle (“ovulation”) derived from treated and untreated conception cycles’, Fertility and Sterility, vol. 37, no. 3, March 1982, pp. 355-60. 
  3. J Thorburn, C Berntsson, M Philipson and B Lindblom, ‘Background factors of ectopic pregnancy I: Frequency distribution in a case-control study’, European Journal of Obstetrics and Gynecology and Reproductive Biology, vol. 23, no. 5-6, December 1986, pp. 321-31; J Coste, N Job-Spira, H Fernandez, E Papiermik and A Spira, ‘Risk factors for ectopic pregnancy: A case-control study in France, with special focus on infectious factors’, American Journal of Epidemiology, vol. 133, no. 9, 1 May 1991, pp. 839-49. 
  4. HJ Tatum and FH Schmidt, ‘Contraceptive and sterilization practices and extrauterine pregnancy: A realistic perspective’, Fertility and Sterility, vol. 28, no. 4, April 1977, pp. 407-21. 
  5. MF McCann and LS Potter, ‘Progestin-only oral contraception: A comprehensive review’, Contraception, vol. 50, no. 6, supplement, 1994, pp. S1-195. 
  6. For material that addresses both sides of the debate, see LK Bevington and R DiSilvestro (eds), The Pill, Center for Bioethics and Human Dignity, Deerfield; for material that explains the argument for hormone contraceptives as abortifacient, see R Alcorn, Does the Birth Control Pill Cause Abortions?, 10th edn, Eternal Perspective Ministries, Sandy OR, 2011; for the contrary view, see SA Crockett, JL DeCook, D Harrison and C Hersh, ‘Hormone contraceptives: controversies and clarifications’, ProLife Obstetricians, Fennville MI, 1999, in Bevington and DiSilvestro (eds), op. cit., pp. 71-96. 

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