Planned Parenthood Continues its Misinformation Campaign about So-called “Emergency Contraception.”
Planned Parenthood’s misinformation and troubling distribution of so-called “emergency contraception” was highlighted in Americans United for Life’s July 2011 report, The Case for Investigating Planned Parenthood. Although Planned Parenthood subsequently revised some of its literature on “emergency contraception,” its re-write is still rife with misleading and inaccurate information. A grave disservice to women, Planned Parenthood’s materials routinely mischaracterize and misuse studies in an attempt to deny the capacity of these drugs and devices to end the life of a unique, developing human being.
The misinformation campaign is particularly apparent in Planned Parenthood’s materials about the drug ella.
Although the Food and Drug Administration (FDA) approved Ulipristal Acetate (ella) for use as “emergency contraception,” the drug can induce an abortion.[i] This is because, similar to the abortion drug mifepristone, ella “works” by blocking progesterone, a hormone that is necessary for pregnancy. By blocking progesterone, ella can kill a human embryo even after implantation.
Planned Parenthood, the nation’s largest abortion provider, is well-aware that blocking progesterone causes abortions. Planned Parenthood Federation of America’s (PPFA) January 2012 “Fact Sheet” titled “The Difference Between the Morning-After Pill and the Abortion Pill” answers the question “how does the abortion pill work?” with “[m]ifepristone ends pregnancy by blocking the hormones necessary for maintaining a pregnancy.”[ii]
Conversely, the PPFA document states that ella, which similarly blocks progesterone, “works only by preventing ovulation.” But this claim, that ella’s mode of action is limited to preventing ovulation, is dishonest. In fact, the FDA labeling of ella acknowledges that it can “affect” implantation and studies confirm that ella is harmful to a human embryo.[iii]
Moreover, the conclusion that ella “only” prevents ovulation is not even supported by the study PPFA cites in its so-called “Fact Sheet.”
Rather, the cited study explains that progesterone-receptor modulators (drugs that block the hormone progesterone) “including [ella]” can “impair implantation.”[iv] While the study—which was funded by ella’s manufacturer, HRA Pharma—theorizes that the dosage used in its trial “might be too low to inhibit implantation,”[v] it also states affirmatively that “an additional postovulatory mechanism of action,” e.g. impairing implantation, “cannot be excluded.” Thus, the study PPFA uses to claim conclusively that ella “works only by preventing ovulation” in actuality uses clear language that ella’s life-ending mechanisms of action cannot be excluded.
In fact, ella’s deadliness is confirmed by its high “effectiveness.”
Planned Parenthood’s materials highlight that, unlike other so-called “emergency contraceptives,” ella’s effectiveness “does not diminish over the course of five days following unprotected intercourse.” Notably, at the FDA advisory panel meeting for ella, panelist Dr. Scott Emerson, a professor of Biostatistics at the University of Washington, raised the point that the low pregnancy rate for women taking ella four or five days after intercourse suggests that the drug must have an “abortifacient” quality.[vi]
While Planned Parenthood has made some effort to distinguish ella from other so-called “contraceptives,” it still inappropriately conflates the drugs to mask ella’s consequential differences.
Several Planned Parenthood documents state that “emergency contraception,” a definition they insist includes ella, “will not induce an abortion in a woman who is already pregnant” and “nor will it affect the developing pre-embryo or embryo.” However, Planned Parenthood uses a study that looked at a category of drugs that are distinct from ella.[vii] The 1998 study that Planned Parenthood cites as evidence for these statements examined progestin-based drugs to make this point.[viii] ella is not a progestin-based drug. Rather, ella is a progesterone-blocker. In fact, the 1998 study also acknowledges that mifepristone, and similar progesterone-blocking drugs, could be used as “emergency contraception.” There is no debate that mifepristone also causes abortions.
When Planned Parenthood denies or downplays the life-ending effects of “emergency contraception,” it is not advancing women’s right to informed consent.
To many women, it matters how a particular method of “birth control” can work. For women concerned about post-fertilization effects of a birth control method, at least one study has found that whether that was the primary mechanism of action was less important than the fact that it can have such a life-ending effect: “For those women who would not use or would stop using a [birth control] method acting after fertilization, it did not matter whether such effects were common or rare.”[ix]
In his most recent study on “emergency contraception,” Dr. James Trussell, whose associations include serving as a member of the National Medical Committee of PPFA, states, “To make an informed choice, women must know that [emergency contraception pills]… may at times inhibit implantation…”[x] Planned Parenthood’s misuse and mischaracterization of studies to claim the opposite, deprives women of the information necessary to exercise true choice and demonstrates Planned Parenthood does not deserve the “trusted provider” moniker it claims.
[i] “The mechanism of action of ulipristal in human ovarian and endometrial tissue is identical to that of its parent compound mifepristone.” D. Harrison & J.Mitroka, Defining Reality: The Potential Role of Pharmacists in Assessing the Impact of Progesterone Receptor Modulators and Misoprostol in Reproductive Health, 45 Annals Pharmacotherapy 115 (Jan. 2011).
[ii] See http://www.plannedparenthood.org/files/PPFA/Difference_Between_Morning_After_Pill.pdf (last visited Sept. 6, 2012).
[iii] See European Medicines Agency, Evaluation of Medicines for Human Use: CHMP Assessment Report for Ellaone 16 (2009), available at http://www.ema.europa.eu/docs/en_GB/document_library/EPAR_-_Public_assessment_report/human/001027/WC500023673.pdf (last visited Sept. 4, 2012); see also ella Labeling Information (Aug. 13, 2010), available at http://www.accessdata.fda.gov/drugsatfda_docs/label/2010/022474s000lbl.pdf (last visited Sept. 4, 2012).
[iv] Glasier et. al, Ulipristal acetate versus levongestrel for emergency contraception: a randomized non-inferiority trial and meta-analysis, 375 The Lancet 555 (Jan. 2010).
[v]In the Glasier study, “follow-up was done 5-7 days after expected menses. If menses had occurred and a pregnancy test was negative, participation [in the study] ended. If menses had not occurred, participants returned a week later.” Considering that implantation must occur before menses, the study could not, and did not attempt to, measure an impact on an embryo pre-implantation or even shortly after implantation. ella was not given to anyone who was known to already be pregnant (upon enrollment participants were given a pregnancy test, pregnant women were excluded from the study). The only criterion for ella “working” was that a woman was not pregnant in the end. Whether that was achieved through blocking implantation, or even ending implantation, would be indeterminable.
[vi] See Transcript, Food and Drug Administration Center for Drug Evaluation and Research (CDER), Advisory Committee for Reproductive Health Drugs, June 17, 2010, available at http://www.fda.gov/downloads/AdvisoryCommittees/CommitteesMeetingMaterials/Drugs/ReproductiveHealthDrugsAdvisoryCommittee/UCM218560.pdf (last visited Sept. 4, 2012).
Dr. Emerson specifically stated, “What’s very, very bothersome here, again, to me, is that we shouldn’t be seeing this much of an effect according to your presumed mechanisms of action; that if there is no abortifacient aspect of this treatment, no effect on implantation, I just can’t make these numbers jive, unless there is a substantial difference in the demographics according to the women who are presenting with this sort of data. …” He also noted, “So this still comes back to this mechanism of action then. Why would we expect that if — and I’ll even concede that the primary mechanism of action might be delayed ovulation, but not in this group that’s five days out from unprotected intercourse.”
The response to Dr. Emerson’s questions given by Dr. Erin Gainer, representing HRA Pharma, ella’s sponsor, acknowledged that HRA Pharma lacked sufficient data to make an assurance that ella did not have an abortifacient aspect, “Again, given the variability that we know when ovulation actually occurs in a given cycle, it’s very hard to comment on how many of the women treated days 4 and 5 may have been post-ovulation. We don’t have biochemical data on the individual women included. So it is very hard to comment on where those women actually were.”
[vii] Without diminishing the legitimate and serious concerns about the implantation-blocking capacity of progestin-based drugs, it must be acknowledged that ella, by blocking progesterone, is able to end even an “established” pregnancy, and thus “works” in a consequentially different way.
[viii] Van Look & Stewart, Emergency Contraception, Contraceptive Technology 277 (17th ed. 1998).
[ix] See Dye et al., Women and postfertilization effects of birth control: consistency of beliefs, intentions and reported use, 5(11) BMC Women’s Health (2005). See also de Irala J, Lopez del Burgo C, Lopez de Fez CM, Arredondo J, Mikolajczyk RT, Stanford JB, Women’s attitudes towards mechanisms of action of family planning methods: survey in primary health centers in Pamplona, Spain, BMC Women’s Health 7 (2007).
[x] J. Trussell et al., Emergency Contraception: A Last Chance to Prevent Unintended Pregnancy, Office of Population Research at Princeton University (June 2010).