Numerous studies are showing that Plan B often fails to stop ovulation when given in the fertile phase when pregnancy is likely to occur.
Before answering that question (and there IS an answer to it) a couple of points need to be addressed that explain why there’s so much confusion about Plan B’s mechanisms of action (MOAs).
What Science Tells Us about the Fertility Cycle: News You Can Use
The fertility cycle is an enormously complex series of interactions among a number of hormones that stimulate and downregulate the production of other hormones at precisely synchronized times. The interplay of hormones is essential (a) to the maturation and release of an ovum, (b) to an environment conducive to allowing sperm to ascend, survive and become capable of fertilizing the ovum, and (c) for the newly conceived embryo to successfully implant in a “hospitable” uterine lining that is capable of supporting embryonic growth and development.
Some facts are well-established, for example, that the likelihood of pregnancy outside the fertile phase is practically nil. The only reason that women are told to take Plan B whenever they’ve had a condom failure or unprotected sex is that most women are ignorant of their fertility cycle and when their fertile phase occurs.
The fertile phase consists of the day of ovulation (when the mature ovum is released) and the five days preceding ovulation. Natural family planning methods allow women to chart their cycle and identify their fertile phase through changes in cervical mucus. A rise in basal body temperature also signals that ovulation has occurred, but unlike changes in mucus, it is not predictive of when ovulation will occur. Devices like the Clearblue Monitor, which track shifting hormone levels, can be used to precisely identify the fertile period.
After ovulation, an ovum is able to be fertilized for only 12 hours before it “dies.” Sperm, however, can remain alive in cervical crypts, and remain capable of fertilizing an ovum, for up to five days preceding ovulation because at this stage the microenvironment of the cervix supports their viability.
We know that after ovulation, the dominant follicle from which the ovum emerged is transformed into a corpus luteum which produces a high level of progesterone to support the endometrium in becoming “hospitable” for implantation in the event an embryo is conceived.
Scientists have been able to identify and measure the rise and fall of various hormones throughout the fertility cycle and to measure the size of ovarian follicles with transvaginal ultrasound (TVUS) to determine precisely how close a woman is to ovulation and to determine whether or not ovulation has occurred by seeing the ruptured follicle.
We know that a large dose of the “wrong” hormone given in the days prior ovulation can delay, blunt or block ovulation. This is one way hormonal contraceptives are designed to work.
Other contraceptives, such as progestin-only mini-pills, are primarily intended to thicken cervical mucus so that sperm have a difficult, if not impossible, time reaching and fertilizing the ovum. If ovulation and fertilization occur, however, the thickened mucus can delay the embryo’s journey down through the fallopian tube to the uterus. This can cause embryonic death due to a tubal (or ectopic) pregnancy (also potentially fatal to the mother) or due to the embryo’s failure to reach the uterus during the optimal “window” for implantation.
Another common MOA of hormonal contraceptives is to create an environment in the uterus or in its lining that is either toxic to sperm and embryos or that can disrupt the implantation process. It is not simply a question of the appearance of the endometrium as “thin” and “atrophic” that impedes implantation. Scientists have discovered numerous essential “implantation factors” which guide and control attachment and implantation through chemical “cell signaling” between the embryo and the cells in the uterine lining. Some of these implantation factors are interleukin-1 ß platelet-activating factor (PAT), insulin growth factor (IGF), leukemia inhibition factor (LIF) and tumor necrosis factor (TNF). Successful implantation also depends on integrins—cell-adhesion molecules present in “mirror” fashion on the embryo and the uterine lining. Much more can be said about glycodelin-A and other critical proteins as well, but I think the point has been made.
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.
The well-respected Wilcox study (1995) established probabilities of pregnancy from sexual relations on each day of the fertility cycle. According to the Wilcox probabilities, 16 women in the preovulatory group who were found to have ovulated should have then become pregnant due to recent sexual relations. But no established (implanted) pregnancies occurred. What happened to those 16 embryos? We don’t know precisely how they died, but we do know that sometime between the hour they were conceived and a week-10 days later when they should have implanted in the uterine lining, they “disappeared.” The researchers concluded that Plan B was 100% successful in preventing an establish pregnancy when given prior to ovulation.
The women who received Plan B on the day of ovulation or later were expected to have 8.7 children and, in fact, had 8 established pregnancies. The authors concluded that Plan B has 0% effectiveness when given at or after ovulation, but the conclusion that Plan B does not interfere with implantation applies only when it is given on the day of ovulation or later. We don’t know if Plan B interferes with implantation when given before ovulation. What we do know is that all of the embryos expected to be conceived and to implant when Plan B failed to stop ovulation did not survive to become an "established pregnancy."
Their findings were corroborated in three other studies that used TVUS and hormone levels to determine the ability of Plan B to delay or block ovulation (Massai, 2007; Croxatto, 2004 and Durand, 2010). Ovulation and higher progesterone levels occurred among 74% of women who received Plan B on Day -4. Taking Plan B on days -3 and -2, produced no delay in ovulation and the great majority of women ovulated.
Noé and Croxatto offered no plausible explanation for why the loss of the expected 16 embryos between fertilization and implantation was not due to an abortifacient effect,
So that is where things stand. Embryos are conceived and die in the first week of their lives and we don’t know exactly by what mechanism these deaths occur. Because Plan B can double the incidence of ectopic pregnancy, due to slowed transport of the embryo through the fallopian tube, one plausible explanation is that embryos may not reach the uterus to begin implantation during the optimal time frame. But whatever the reason, if a hormonal "emergency contraceptive" results in the death of an early embryo, we have to be honest and call it abortifacient.
Susan E. Wills
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