This term refers to methods used after so-called unprotected intercourse to prevent pregnancy. They are called by various names: emergency contraception, postcoital contraception, the “morning-after pill,” the “72-hour pill,” the “day-after pill,” the “emergency pill,” “Plan B,” “in-case-of-emergency” contraception, or even “rescue” contraception.

These preparations usually contain (the exact dosing regimens are intentionally not listed here):

• Levonorgestrel 0.75 mg or 1.5 mg (POEC),
• Levonorgestrel 0.25 mg and estradiol 50 μg (the Yuzpe method),
• Mifepristone 10 mg (which blocks progesterone receptors and therefore has an abortifacient effect; in higher doses it is used for so-called medical abortion),
• Ulipristal acetate 30 mg (a synthetic progesterone receptor modulator), approved for use up to 5 days after sexual intercourse.

A certain mechanical method is also often proposed to women for postcoital contraception; however, its manufacturers have not labeled it for “emergency” use but only for long-term contraception, so it will not be discussed here.

Preparations used for emergency contraception have several complex and multifaceted mechanisms of action:

• When taken before ovulation, they may inhibit or delay the process leading to ovulation by suppressing the release of FSH and LH from the hypothalamus and pituitary gland [1].
• They affect tubal transport, slowing the movement of sperm, the egg, and even the embryo, which may cause aging and damage to the embryo and, consequently, its inability to implant properly in the uterus [2].
• They influence the function of the corpus luteum, which supports early pregnancy [3].
• They may prevent implantation of the human embryo or inhibit its further development by inducing unfavorable changes in the endometrium [4].
• Some of the substances used in so-called emergency contraception (e.g., mifepristone or ulipristal) block progesterone receptors, which leads to detachment of the embryo from the uterine lining and disruption of the corpus luteum that nourishes the embryo, and thus may directly cause miscarriage.

The mechanism of action of substances used in so-called emergency contraception depends largely on the phase of the menstrual cycle in which “unprotected” intercourse occurred and on the time at which the drug was taken.

“Emergency contraception“ taken after the LH surge can no longer inhibit ovulation. If the egg has been released within the previous 24 hours and sperm can reach the fallopian tube within as little as 30 minutes after intercourse, fertilization may already have begun. The developing human embryo then travels down the fallopian tube toward the uterus; however, a high dose of progestin alters the uterine lining in such a way that it may prevent implantation or disrupt this process [5] (although in rare cases pregnancy may continue despite the use of the so-called “morning-after pill”).

At this point, it is worth recalling what pregnancy actually is. For assisted reproductive technologies and for manufacturers of contraceptive and early-abortifacient agents, the view is often promoted that pregnancy begins only with implantation of the embryo in the uterine cavity. However, every gynecologist, obstetrician, geneticist, and embryologist recognizes pregnancy as beginning at the moment of fertilization – the union of the female and male gametes – and defines its average duration as 266 days from the time of fertilization [6].

“All stages of human development are a changing image of the unchanging human being with his or her characteristic human functions. In other words, throughout the whole of human ontogenesis – from conception to birth – a human being is already a human being; he or she does not become one only after some time.” Prof. Włodzimierz Fijałkowski, MD, PhD

“After fertilization, that is, the fusion of the nucleus of the egg cell with the nucleus of the sperm cell, a completely new genetic entity is formed, distinct from the parental genotypes – a new human person. The set of genes in his or her somatic cells will remain unchanged for the rest of life.” Prof. Bolesław Suszka, PhD

Shortly after fertilization, an immunosuppressive protein called Early Pregnancy Factor (EPF) appears in the blood of a pregnant woman, allowing pregnancy to be detected within the first week [7]. EPF was first described in 1976 by F. Clarke, and its presence can be identified in maternal blood plasma, cervical mucus, and amniotic fluid. It can therefore be regarded as the earliest sign of pregnancy [8]. It is also believed to play a role in protecting the developing human embryo from being rejected as a foreign organism by the mother’s immune system [9]. This test, however, is very expensive and time-consuming, which is why in routine practice pregnancy is detected using tests that identify hCG (human chorionic gonadotropin), a hormone produced by the human embryo only after implantation in the uterine cavity.

It should therefore be obvious that any preparations or devices used after ovulation and fertilization (conception) cannot be called, nor considered, “contraceptive.” Consequently, so-called “emergency contraception” is not solely a contraceptive method (i.e., one that prevents fertilization, the union of the female and male gametes), but may also in part have an anti-implantation or early abortifacient effect, preventing the proper implantation of the embryo in the uterus and its further development.

The mechanism of action of postcoital contraception was originally intended to be limited to preventing fertilization. However, it cannot be denied that it often also blocks implantation [10], that is, it prevents the proper implantation of the blastocyst and leads to the expulsion (abortion) of the human embryo from the woman’s body.

Most of the substances used for emergency contraception are higher doses of those commonly used in hormonal contraception (mainly levonorgestrel). Therefore, they intensify effects that, in some cases, are already associated with the use of hormonal contraceptive pills [11]. This refers in particular to their negative impact on the endometrium, which becomes unsuitable for the reception of the human embryo – thinner and less receptive – resulting in its death and expulsion from the woman’s body.

Moreover, a very important and increasingly discussed issue is the occurrence of ovulation despite regular use of contraceptive pills. With combined oral contraceptives, maturation of ovarian follicles and ovulation may occur in about 2-5% of cases, while with progestin-only pills (so-called low-dose pills), ovulation may occur in as many as 40% of cases [12].

A preparation based on ulipristal acetate may also exhibit an anti-implantation effect, as its chemical structure is similar to that of the abortion pill RU-486 [13]. The following mechanisms of action are described in its documentation [14]: it binds to the human progesterone receptor (but not the estrogen receptor), preventing progesterone from occupying its receptors in such a way that the gene transcription normally triggered by progesterone is blocked. As a result, proteins necessary for the proper completion of embryo implantation in the uterine lining and for the maintenance of pregnancy are not synthesized due to progesterone receptor blockade. Depending on the phase of the menstrual cycle in which the woman takes this preparation, it may disrupt or delay ovulation or, by delaying endometrial development, inhibit implantation of the embryo [15].

Mifepristone, known as the abortion pill, is a typical abortifacient. When used in a low dose for emergency contraception, it may (depending on the phase of the woman’s menstrual cycle) delay or prevent ovulation, and after ovulation has already occurred, it inhibits the development of the secretory endometrium [16], increases uterine contractility during the period of embryo implantation [17], and prevents implantation through its antiprogesterone action [18]. Its detailed mechanism of action is as follows [19]: it damages the decidual layer of the uterine lining by blocking progesterone receptors in the uterus. This leads to separation of the blastocyst, which reduces hCG production and causes a decrease in progesterone secretion by the corpus luteum, further intensifying decidual damage. The drop in endogenous progesterone, together with blockade of progesterone receptors in the uterus, increases uterine prostaglandin levels and sensitizes the uterine muscle to their contractile effects. It also softens the cervix, facilitating the expulsion of the human embryo detached from the endometrium.

According to the information leaflets, an absolute contraindication to the use of preparations for emergency contraception is an already existing pregnancy – understood, in the “modern” (Guillebaud) definition, as the period only after the completion of embryo implantation in the uterus.

Effectiveness of postcoital (emergency) contraception [20]

• When used within 24 hours after “unprotected intercourse”: POEC 99.6%, Yuzpe 98%.
• When used within 25–48 hours after “unprotected intercourse”: POEC 98.8%, Yuzpe 95.9%.
• When taken within 49–72 hours after “unprotected intercourse”: POEC 97.3%, Yuzpe 95.3%.
• With ulipristal acetate, the overall pregnancy rate was 2.1%, but within the first 3 days after “unprotected intercourse” the “effectiveness” reached 97.7%, on day 4 (73–96 hours) 98%, and on day 5 (97–120 hours) 98.7% [21].
• With mifepristone at a dose of 10 mg up to 120 hours after “unprotected intercourse,” effectiveness was 84%; however, up to day 49 of pregnancy (counted from the last menstrual period) it was 92%, between days 50–56 it was 83%, and between days 57–63 it was 77% [22]. When mifepristone is used at a much higher dose, its “effectiveness” reaches nearly 100% (pharmacological abortion).

Can a pregnancy resulting from the failure of “emergency contraception” be harmed?

There is a small risk of a teratogenic effect [23] on the developing child. However, the small number of pregnancies carried to term after the “failure” of postcoital contraception does not allow for representative studies. A large proportion of such pregnancies are “terminated” surgically.

• Very common side effects include: abdominal pain, menstrual disturbances, nausea, vomiting, fatigue, headaches and dizziness, breast tenderness, painful menstruation, heavy bleeding, and mood changes. Less common effects include: depression, anxiety symptoms, insomnia, decreased libido, visual disturbances, hot flashes, diarrhea or constipation, acne, rash, frequent urination, pain in the genital area, abnormal vaginal discharge, and appetite disturbances. Rarely, symptoms such as impaired concentration, drowsiness, vertigo, swelling of the paranasal sinuses, nosebleeds, gastroesophageal reflux, kidney stones, kidney pain, changes in urine color, rupture of an ovarian cyst, inflammatory conditions, fever, chills, toothache, and dehydration may occur.
• A relatively high rate of failure, especially in women who use this method as their main form of contraception, as well as the risk of ectopic (extrauterine) pregnancy.
• Absolute contraindications: an existing pregnancy, porphyria, bronchial asthma, liver disease, and hypersensitivity to any component of the preparation.
• A list of medications that interact with “emergency contraception”.
• The need to use additional “precautionary methods” during intercourse after taking emergency contraception, due to the possibility of delayed ovulation.
• Disturbances of the hormonal cycle – the next menstruation may be delayed by more than 7 days (according to WHO this concerns about 5% of women) if the method is used early enough to delay ovulation, or there may be a tendency toward a shortened menstrual cycle when the tablets are taken after ovulation and the implantation process in the uterus is blocked.

The most important drawback of “emergency contraception,” however, is its possible anti-implantation (anti-nidation) effect, that is, the prevention of proper implantation of the human embryo in the uterus and its subsequent death. Such situations do occur naturally, but there is a fundamental moral difference between a natural loss and one in which human action contributes, especially when that action is taken by the child’s own mother.

Because most women who use “emergency contraception” do not practice fertility‑awareness methods, do not track their menstrual cycles, and do not pay attention to natural signs of fertility, they usually do not know which phase of the cycle they are in. As a result, they cannot be certain which mechanism of action of “emergency contraception” occurred in their case, or which one may have led to them being (or no longer being) pregnant. This uncertainty is one of the reasons why these methods are considered controversial and morally questionable as a means of preventing pregnancy.

Anyone who believes that human life has the highest value and that every person has a right to it, a right that must be defended, should oppose the spread of half-truths about “emergency contraception.” Each of us has the right to reliable information, to a detailed description of the mechanisms of action of preparations approved for use, and to full disclosure of the risks associated with them. Only in this way can the right to free choice and to an informed decision, in accordance with one’s conscience, be truly ensured.

Based on:

[1] A.F. Glasier, “Fertility control”, ”Gynaecology”, pp. 433–450, R.W. Shaw, W.P. Soutter, UK 2003.

[2] D. Loose, G. Stancel, “Estrogens and progestagens”, in Goodman & Gilman’s "The pharmacological basis of therapeutics", Vol. II, pp. 1653–1687, Lublin 2007, also R. Lehmann, Problems of Family Planning. Contraception and Its Effects, pp. 8–32, HLI Europe, Gdańsk 1994.

[3] R.T. Burkman, “Contraception”, in Clinical Gynecology, ed. R. Dębski, Vol. III, pp. 863–874, Kraków 2009. Also D. Loose, G. Stancel, “Estrogens and progestagens”, in Goodman & Gilman’s The Pharmacological Basis of Therapeutics, Vol. II, pp. 1653–1687, Lublin 2007.

[4] W. Lacrimore, J. Stanford, “Postfertilization effects of oral contraceptives and their relationship to informed consent”, Archives of Family Medicine, Vol. 9, pp. 126–133, Feb. 2000. A. Rosenfield, “Emergency contraception: a modality whose time has come”, Journal of the American Medical Women’s Association, No. 53(5), pp. 212–213, 1998.J. Trussell, E.G. Raymond, “Emergency contraception: a last chance to prevent unintended pregnancy”, The Emergency Contraception Website, 2010.

[5] F. Grou, I. Rodriguez, “Morning after pill, how long after?”, American Journal of Obstetrics and Gynecology, Vol. 171, pp. 1529–1534, 1994.

[6] Hieronim Bartel, “Embryology“, Medical Publishing House PZWL, Warsaw 2010.

[7] Ibid., p. 85; also Y. Smart, “Early Pregnancy Factor as a monitor for fertilization in women wearing intrauterine devices”, Fertility and Sterility, 37(2), pp. 201–204, 1982.

[8] W. Straube, “Early embryonal signals”, Zentralblatt für Gynäkologie, 111(10), pp. 629–633, 1989;Y. Smart, T. Roberts, I. Fraser, A. Cripps, R. Clancy, “Validation of the rosette inhibition test for the detection of early pregnancy in women”, Fertility and Sterility, 37(6), pp. 779–785, 1982; X. Fan, Z. Zeng, “A study of early pregnancy factor activity in preimplantation”, American Journal of Reproductive Immunology, 37(5), pp. 359–364, 1997.

[9] H. Morton, “Early Pregnancy Factor”, in Seminars in Reproductive Endocrinology, No. 2, p. 72, 1992.

[10] Prof. J. Guillebaud, “Contraception: questions and answers“, Medycyna Praktyczna, 2nd ed., Kraków 2005.

[11] Randy Alcorn, “Does the birth control pills cause abortion?”, CHMP Assessment Report for EllaOne, Procedure No. EMEA/H/C/001027, European Medicines Agency, UK 2009.

[12] D.A. Grimes, A.J. Godwin, A. Rubin, “Ovulation and follicular development associated with the low-dose oral contraceptives: a randomized controlled trial”, Obstetrics and Gynecology, No. 83, pp. 29–34, 1994.

[13] www.sfkp.pl (Polish Association of Catholic Pharmacists – Gdańsk).

[14] CHMP Assessment Report for EllaOne, Procedure No. EMEA/H/C/001027, European Medicines Agency, UK 2009.

[15] CHMP Assessment Report for EllaOne, Procedure No. EMEA/H/C/001027, European Medicines Agency, UK 2009.

[16] D. Loose, G. Stancel, “Estrogeny i progestageny”, in Goodman & Gilman’s The Pharmacological Basis of Therapeutics, Vol. II, pp. 1653–1687, Lublin 2007.

[17] M. Obara, Z. Słomko, “Metody planowania rodziny”, in Gynecology, ed. Z. Słomko, pp. 589–616, Warsaw 2008.

[18] H. Bartel, “Medical embryology“, pp. 38–42, Warsaw 2009.

[19] D. Loose, G. Stancel, “Estrogens and progestagens”, in Goodman & Gilman’s The Pharmacological Basis of Therapeutics, Vol. II, pp. 1653–1687, Lublin 2007.

[20] Effectiveness of the Yuzpe method (estrogens with progestagens) compared with POEC (progestagen). Results of WHO studies from 1998 and 2002.

[21] CHMP Assessment Report for EllaOne (ulipristal acetate), Procedure No. EMEA/H/C/001027, European Medicines Agency, UK 2009.

[22] I.M. Spitz, C.W. Bardin, L. Benton, A. Robbins, “Early pregnancy termination with mifepristone and misopristol in the United States”, The New England Journal of Medicine, Vol. 338, No. 18, April 1998.

[23] J. Guillebaud, “Contraception: questions and answers“, Medycyna Praktyczna, 2nd ed., Kraków 2005.