Numerous studies are showing that Plan B often fails to stop ovulation when given in the fertile phase when pregnancy is likely to occur.
Pharmaceutical companies that manufacture contraceptives and finance much of contraceptive research are eager to demonstrate their effectiveness and required to research risks and side effects for FDA approval. But they have little interest in exploring whether or not a certain contraceptive causes early abortion. Knowledge of the potential to cause an abortion would cut into sales, as long as some women who contracept draw the line at abortifacients. The possibility is always stated on the product labeling (as a defense against a lawsuit), but studies usually downplay the likelihood of an abortifacient effect even when one is obvious.
Groups such as ACOG (American Congress of OB-GYNS) are willing to obscure reality by, for example, redefining conception as “the implantation of a fertilized ovum” in its Terminology Bulletin No. 1 (September 1965). Thus, if anything causes the death of the embryo (and a “fertilized ovum” IS in reality an embryo) prior to successful implantation, the drug or device would be classified as contraceptive rather than abortifacient.
The reluctance to publicize discouraging facts about contraceptives has led to a strange phenomenon: The abstract and conclusion of articles discussing contraceptives often don’t reflect the actual findings reported in the guts of the article.
Here’s a simple example. A study earlier this year by Rachel K. Jones and Jenna Jerman of the Guttmacher Institute was designed to determine whether declining abortion rates in the U.S. resulted from either (1) a reduced number of abortion providers or (2) the recent passage of many “restrictive” state laws. The authors found no evidence that either factor was responsible. Then, without even studying the issue of “improved” contraceptive use, the authors confidently concluded that abortion rates declined because more women were using contraception, using it more consistently, and had shifted to more effective contraceptive methods.
But where’s the proof?
Small, Poorly Designed Early Studies into Plan B’s MOAs
The earliest studies into Plan B’s MOAs did nothing to clarify the matter. They suffered from small sample sizes and from imprecise dating of key events in the fertility cycle (relying mainly on women’s recollections of when their last menstrual period began, rather than learning her cycle day via hormone level testing and TVUS).
Non-scientists might assume that a drug will produce an identical effect, i.e., have the same MOA, regardless of when it’s taken in the monthly cycle. Tylenol, for example, will reduce pain in the same way every time it’s taken, no matter what hour of the day or day of the month. But it should be obvious from the opening discussion, that taking a high dose of levonorgestrel (the synthetic progestin in Plan B) will produce different effects at different stages of the fertility cycle.
The Evidence of Plan B’s Abortifacient Effect
One of the largest studies to date, by Noé, Croxatto et al. in 2011, looked at data from 450 women seeking Plan B at Chilean health clinics. The timing of intercourse in relation to the fertile period and the occurrence of ovulation were determined by hormone levels and TVUS. A preovulatory group consisted of 103 women who’d had sexual relations during the period one to five days before ovulation and were given Plan B within 72 hours of relations and before ovulation was expected to occur.
If the primary MOA of Plan B were to delay or prevent ovulation, TVUS of the ovary would show an unruptured follicle and low levels of progesterone, meaning that ovulation had not occurred. Instead, 80% of women in this group ovulated. The closer Plan B was given to the time of ovulation, the less likely it was for Plan B to prevent or delay ovulation: 92% of women who were given Plan B on Day -2 still ovulated and 93% showed higher post-ovulation progesterone levels.
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