The State of the Science: Why Catholic Hospitals Should Not Dispense Plan B: Symposium on Plan B: Part V

Editor’s Note: The editors present this series (read part 1, part 2, part 3part 4part 6) on the recent furor over Plan B as an opportunity for our fellow pro-lifers to slow down, step out of activist mode, and enter into the conversation in a prayerful and thoughtful way.

The Church encourages conversation among faithful scientists and theologians as new science comes to light and as we deepen ethical reflection. Typically such conversations occur in academic settings, but since the recent furor pushed the issue into the open, causing much confusion and scandal, we felt it important to present the latest science and moral reflection in a context of faithful discussion.

We offer this series in a spirit of obedience to the Magisterium, and as an opportunity for faithful Catholics and people of good will to come to a greater understanding of the nuances of the Church’s teaching and the complexities of the science and art of medicine in the difficult situations involving the treatment of women who have been raped. There has been no (and will be no) revision in the Church’s teaching concerning direct abortion or contraceptive sexual acts between spouses. Both are morally illicit without exception.

As with all Truth and Charity Forum articles, opinions belong to the author alone and do not necessarily represent the official position of Human Life International.


The mechanism of action of levonorgestrel emergency contraception (hereafter as LNG EC), sold as Plan B, given to prevent pregnancy after an act of intercourse (or rape) is a politically charged but morally important question. The question of mechanism of action is fundamentally a scientific one.

In the discussion on mechanism of action of LNG EC, there is a lot of confusion concerning terms that are used and how particular studies support or refute a postfertilization effect of LNG EC. This brief article is meant to provide a clear, concise summary of the scientific literature pertaining to the mechanism of action of LNG EC, with special emphasis on the best quality evidence.

Effectiveness of LNG EC to prevent pregnancy depends on when it is given, before or after ovulation.

When given after ovulation, there is good evidence that LNG EC is not effective in preventing pregnancy.1 There is also convincing support that LNG EC given after ovulation (actually after the LH surge which occurs the day before ovulation) neither prevents implantation, nor disrupts an embryo that already implanted.2

Many focus their attention on this scientific literature that indicates LNG EC does not prevent or disrupt implantation when administered after ovulation (or the LH surge) to support the claim that LNG EC is not abortifacient whenever given. The period of time that is concerning, however, is when LNG EC is given before ovulation in the fertile window. Consider the following:

First, when given before ovulation (in the fertile window), there is good evidence that LNG EC is very effective in preventing pregnancy.

A study by Noe et al. in 2010 is the largest (n=337) and most robust to date looking at the effectiveness of LNG EC based on when the drug was administered.3 The day of ovulation was determined by the gold standard of serial ultrasounds to determine follicular rupture (which implies an egg is released). The effectiveness of LNG EC was evaluated based on whether it was given before or after ovulation and whether or not LNG EC was effective was based on the difference between expected and actual pregnancies.

As expected, the effectiveness of LNG EC – given on the day of ovulation or later – was basically non-existent (7 expected and 6 actual pregnancies). In stark contrast, the effectiveness of LNG EC  – given in the fertile window (-5 to -1 days before ovulation) – to prevent of pregnancy was complete (13 expected but 0 actual pregnancies).

Second, when given in the fertile window (before ovulation), the predominant mechanism of action is not to prevent ovulation. 

Again, the study of Noe et al. addresses the question of mechanism of action with this observation: when LNG EC was given in the fertile window, breakthrough ovulations occurred 62 out of 87 times (71%).4 This led the authors to conclude “FR (follicular rupture or ovulation) occurred in some two-thirds of women taking LNG-EC preovulatory; this suggests that other mechanism than suppression of ovulation prevents pregnancy in these women.”  In fact, in a subsequent study (Noe 2011) with a similar robust design, the breakthrough ovulation rate was 80%.5

Note: These studies provides robust evidence that is contrary to the presumption that prevention of ovulation is the predominant mechanism of action for LNG EC given in the fertile window. There is now little scientific support for the presumption that prefertilization effects alone account for the efficacy of LNG EC given in the fertile window. At this point, there should be scientific agreement that the primary mechanism of action of (preovulatory) LNG in the fertile window is POSTOVULATORY, and not primarily to prevent or block ovulation. 
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  • Deacon Tom Davis

    Noe, et al, “Contraceptive efficacy of emergency contraception with levonorgestrel given before or after ovulation,” Contraception 81 (2010):414-20, now leaves no doubt that
    with respect to the narrow window of time causally related to pregnancy, the primary MOA of LNG EC, is post ovulatory. Changes in cervical mucus viscosity or sperm capacitation have also now been excluded as significant. The notion that pre-ovulatory LNG EC results in difficult to fertilize eggs is not supported by the scientific literature. What’s left? The burden of proof rests with those who claim a pre-fertilization MOA. None has been demonstrated (with respect to the critical timing – i.e. fertile window administration with luteal phase effect).

    Alas, some voices simply cannot accept mounting scientific evidence. They appear to accept (how can they not given Noe [2010]?) that the primary MOA is post ovulatory but insist that it is also pre-fertilization, proposing shifting claims with insufficient critical
    examination of their sources. When those sources are distinguished or collapse under critical analysis, they propose yet further tenuous claims lacking intellectual rigor.

    The burden of proof is on the claimants of a post-ovulatory/pre-fertilization MOA. Show us the solid evidence to support it, not conclusory statements form studies or results not associated with critical time periods. All serious voices would welcome it as a potential relief of some of the trauma rape victims endure. But not blindly. To date the evidence of a post fertilization MOA is at least as strong, even stronger, that contrary claims.

    Thank you Dr. Yeung and Dr. Harrison.

    • Patrick Yeung Jr. MD

      I give credit to Deacon Tom Davis for making and emphasizing the point that the terms of the discussion on the mechanism of action of Plan B in the fertile period needs to move AT LEAST from preventing ovulation to POSTOVULATORY.


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  • Dr. Dom Pedulla

    What an excellent essay, especially on the point of where the real burden of proof lies! As the eminent moral theologian Msgr. William Smith on this topic has written: “As I understand Catholic moral thinking, this is one if the three areas to which Probabilism cannot be applied; i.e., the rights of a third party, specifically, the rights of an innocent third party not to be injured.” Or, to refer to Aquinas (S. Th. II-II, Q. 70., article 2), it is precisely because such questions by their very nature admit of scientific uncertainty, and often do not provide demonstrable proof, that we must err on the side of defending the innocent, when such is jeopardized. Citing Aquinas here to allow emergency so-called “contraceptives” is a misuse of his thought. When we can no longer have a reasonable certainty of avoiding embryocidal effects, probabilism, or “imperfect moral certainty” is no longer applicable, precisely because of the grave duty under justice to protect the life of the innocent. How interesting that the scientific rationale of those seeking to exonerate Plan B, having rested until very recently — ENTIRELY — on the allegedly “noncontroversial” mechanism of suppressing egg release, now without even batting an eyelash has abandoned that to pursue extravagant and far-fetched speculative theories such as the “unfertilizable oocyte”, and other such conjecture, since anovulatory effects are no longer tenable. But shouldn’t the finding of an 86% ovulation rate among Plan B users have at least engendered some doubt? Some real re-consideration? The far-flung conjecture of the “unfertilizable oocyte” came from completely unrelated, non-applicable reports among seriously infertile patients (not those fertile and trying to avoid pregnancy) and was first reported in 2000. Why did it take a decade for it to be used as a competing explanatory mechanism used to refute abortifacient effects? Could this “any port in a storm” approach be a case of an a priori conclusion in search of supporting evidence, rather than evidence in search of supportable conclusions?

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