Contraception - Adverse Effects: Cancer / Stroke / Abortion

Does Contraception REALLY Reduce the Need for Abortion?

Many columnists are endorsing legislation which calls for even greater contraceptive access and other measures to reduce the “need” for abortion (“Reducing the Need for Abortion and Supporting Parents Act,” H.R. 6067). The media generally promote artificial birth control with this type of comment: “To lower the abortion rate, we need more contraception”.

One columnist recently illustrated his point with an analogy: “[D]enying that contraceptives reduce your risk of pregnancy is as crazy as denying that an umbrella reduces your risk of getting wet.” Well, if at the end of a school day you tell teenagers that the thunderstorm outside will soon pass, but they can try their luck with this stack of umbrellas, many will do so. But some of them will get soaked when their umbrellas break or slip from their hands in the wind, and all will get a little wet.

The problem is that no one gets only “a little” pregnant.
The real problem is not the use of such rhetorical devices, however; it’s the failure to research the subject.

These media sources continue to fall prey to the Great Contraceptive Fallacy: more contraception reduces unintended pregnancies and abortions. 

Consider these studies:

In a study of abortion patients in 1994-95 [Alan Guttmacher Institute], 58% of patients reported that they ‘currently used’ contraception during the month of their last menstrual period…
[CDC, MMWR, 7June02, "Abortion Surveillance – United States, 1998"]

Two-thirds of unplanned pregnancies occur among women who described themselves as using birth control.
Among the women who became pregnant unintentionally, 65% reported using contraception when they conceived. [May 2003, journal Human Reproduction, Researchers from the Hospital de Bicetre, France;  The Washington Post, 5/5/03]


The facts speak for themselves:
Fact 1.
Contraceptive use is already “virtually universal among women of reproductive age,” according to the Centers for Disease Control and Prevention (CDC). The Alan Guttmacher Institute (AGI) reports that 89% of reproductive-age women already are using contraception and 98% have used it in their lifetime.

There are still unintended pregnancies and abortions because with typical use, the risk of pregnancy over 12 months is 9% with oral contraceptives and 15% with condoms. (

Fact 2. Contraceptive researchers and social scientists measuring effectiveness in large-scale studies have reached (often reluctantly) the same conclusion: increased availability of contraception, and even emergency contraception, fails to reduce rates of unintended pregnancy and abortion. Studies examining the impact of emergency contraception (EC) are reviewed at Research in the U.S., Western Europe and China produced remarkable unanimity:
• “No effect on abortion rates was demonstrated with advance provision of EC… [W]idespread distribution of …EC through health services may not be an effective way to reduce the incidence of unintended pregnancy”
(Glasier et al., Contraception 2004);
• “We did not observe a difference in pregnancy rates…Previous studies also failed to show significant differences in pregnancy or abortion rates among women with advance provision of EC” (Tina Raine et al., JAMA 2005);
• “This study adds to the growing literature casting doubt on the increased use of EC as a quick fix for rising abortion rates” (Hu et al., Contraception 2005);
• “Another commonly held view for which there is no documented evidence is that improving knowledge about and access to Emergency Contraception will reduce the number of teenage pregnancies…Experience of use so far does not give any evidence of effectiveness” (Williams, Scottish Council on Human Bioethics, 2005).
Even AGI’s own 2006 “Contraception Counts” report, which ranks states on policies improving contraceptive access as well as on abortion rates, shows no correlation between better access to contraception and lower abortion rates.
U.S. researcher Douglas Kirby concludes: “Most studies that have been conducted during the past 20 years have indicated that improving access to contraception did not significantly increase contraceptive use or decrease teen pregnancy” (“Reflections on Two Decades of Research on Teen Sexual Behavior and Pregnancy,” 1999 Journal of School Health 3:69).
Fact 3. The effectiveness of EC – in the words of prominent EC researcher Anna Glasier – is “unsubstantiated by randomized trials” and “based on rather unreliable data and a great many assumptions” (2004 Contraception 69:361-366). Among several recent studies questioning the 89% efficacy claimed by Plan B’s manufacturer, one concludes that the “best available estimate” of Plan B effectiveness is only 72% (Stanford and Mikolajczyk, “Methodological review of the effectiveness of emergency contraception,” 2005 Current Women’s Health Reviews 1:119-129).

These authors note that the higher estimate of effectiveness is based on two small samples of women:
British women using natural family planning (NFP) in the 1960s and women in
North Carolina in the 1980s who were trying to conceive. The fertility rate, especially among the British NFP users, was very likely higher than among women in
a key World Health Organization study comparing effectiveness of two methods of emergency contraception. This error led to overestimating EC effectiveness. In addition, Stanford notes, “the methods used for comparison do not take into account the normal variation in the timing of ovulation within the menstrual cycle.”
Fact 4. One columnist dismisses the “argument” made by "opponents” of contraception that “birth control pills, like morning-after pills, can block implantation of an embryo. But there’s no evidence that this has ever happened.” There’s plenty of evidence if one knows where to look.
A leading medical textbook on embryology, Moore and Persaud’s The Developing Human: Clinically Oriented Embryology (6th ed.), explains that “morning after pills” taken “within 72 hours after sexual intercourse usually prevent implantation of the blastocyst…These hormones prevent implantation, not fertilization. Consequently, they should not be called contraceptive pills. … It would be more appropriate to call them ‘contraimplantation pills.’ Because the term abortion refers to a premature stoppage of a pregnancy, the term abortion could be applied to such an early termination of pregnancy” (p. 532).
The leading textbook on obstetrics, Williams Obstetrics, provides a detailed overview of the many female hormones involved in the fertility cycle and their effect on the five major stages of the endometrial cycle. (See 19th ed., pp. 82-93, edited by F. Gary Cunningham, M.D. et al., 1996.)

The editors describe the miraculous process by which the uterus is prepared each month to be a safe haven for a developing embryo as “unique and astonishing” (at 82). They note that “two thirds of the entire endometrium is shed and regenerated more than 450 times, on average, in the life of most women. … [If] the doubling time of endometrial growth experienced from the 5th to the 20th day of the ovarian cycle were maintained for 1 year, the weight of the endometrium would approach 1 ton!” (at 83) This astonishing process can be disrupted, thwarting the implantation of a newly conceived embryo, by counteracting certain hormones.
The most commonly used contraceptive pill is a combination of estrogen and progestin.

Here’s what Williams Obstetrics has to say about its mode of action: “Estrogen alone in sufficient dose will inhibit ovulation. … Implantation also is likely inhibited by altering normal endometrial maturation. Although estrogen accelerates ovum transport, progestins cause slowing; thus their possible role in altered tubal and uterine motility is unclear. “… Similar to estrogens, progestins produce an endometrium that is unfavorable to blastocyst implantation. Finally, progestins also can inhibit ovulation. …“The net or combined effect of estrogen and progestin with respect to contraception is extremely effective ovulation suppression [assuming perfect use!–ed.], sperm penetration blockage by cervical mucus, and unfavorable endometrium for implantation if the first two mechanisms fail” (at 1322-23).

Of progestin-only “mini-pills” using the ingredient in the Plan B emergency “contraceptive”), Williams Obstetrics explains: “They have not achieved wide-spread popularity because of a much-higher incidence of irregular bleeding and a higher pregnancy rate. As with all forms of progestin-only contraception, when failure results in pregnancy, there is also an increased risk that it is ectopic. … These agents, when used alone, impair fertility without always inhibiting ovulation. This likely results from inducing cervical mucus that impedes sperm penetration and from altering endometrial maturation sufficiently to thwart successful blastocyst implantation. … [If] menses are not disturbed, or only minimally disturbed, ovulation is likely not suppressed, and the pregnancy risk is greater. Actual pregnancy rates with progestin-only pills range from 1.1 to 9.6 pregnancies per 100 women in the first year of use” (at 1333-34).

Robert A. Hatcher, MD, principal editor of the definitive guide Contraceptive Technology (18th ed., 2004), has also produced a 171-page Pocket Guide to Managing Contraception, available in print and online at

The mechanisms of action of various forms of contraception are described briefly:
• Combined (Estrogen & Progestin) Oral Contraceptives (COCs): “Suppresses ovulation. … Also causes thickening of cervical mucus, which blocks sperm penetration and entry into the upper reproductive tract. Thin, asynchronous endometrium inhibits implantation. Tubal motility slowed” (at 101).
• The mechanisms of progestin-only contraceptive pills (POPs) are described this way: “Thickens cervical mucus to prevent sperm entry into upper reproductive tract (major mechanism).”

N.B. That action requires 12-24 hours, while sperm in fertile mucus need only 6 hours to be capacitated, that is, capable of fertilizing an ovum. The description continues: “Effect short-lived–requires punctual dosing. Other mechanisms include ovulation suppression (in about 50% of cycles), thin, atrophic endometrium which inhibits implantation; and slowed diminished mobility. Some POPs in Europe suppress ovulation more than the levonorgestrel, norgestrel and norethindrone pills used in the USA” (at 124).

By “punctual dosing,” the authors do mean PUNCTUAL. If a woman is only 3 hours late in taking her daily dose, she is advised to use “backup contraception for 48 hours” and “consider using emergency contraception if [she had] sex in past 3-5 days” (at 127).
Depo-Provera injection. The mechanisms are as follows: “Suppresses ovulation by inhibiting LH and FSH surge, thickens cervical mucus blocking sperm entry into female upper reproductive tract, slows tubal and endometrial mobility, and causes thinning of the endometrium” (at 128).
Implanon (implanted rod with progestin now replacing Norplant, which was withdrawn from the market after a successful class action suit based on risks and unpleasant side effects). Its mechanisms: “…thick cervical mucus prevents normal sperm transport”; “inhibition of ovulation”; and “atrophic endometrium” which will inhibit implantation.

A major study by Marta Durand et al. (2005 Contraception 71:451-457) confirms the frequent failure of levonorgestrel (LNG) to prevent ovulation, when administered as an emergency contraceptive before the LH surge. Instead LNG interferes with the function of the corpus luteum in preparing the endometrium for implantation.

Durand et al. studied levels of glycodelin in the blood and endometrium of women who had been given two doses of LNG 12 hours apart.

One group received LNG 3-4 days before the luteinizing hormone (LH) surge. LH triggers both the release of an ovum from the dominant follicle, and the conversion of the residual follicle into a corpus luteum producing progesterone to prepare the endometrium for a possible implantation. LH is necessary to maintain luteal function for the first two weeks. The second group received LNG at the time of the rise in LH, and the third group 48 hours afterward.

In the first group only, LNG caused a rise in glycodelin 4 days earlier than normal which produces “antifertility activity” during the fertile window, and also causes “deleterious effects on [progesterone] production by the corpus luteum” (at 455). Reduced levels of glycodelin in the endometrium at the time implantation should occur can inhibit implantation and result in an embryo’s death.

Chang-hai He et al. compared the effects of 0.75 mg LNG tablets (Postinor and a Chinese version). The pills were taken by women within 8 hours of every act of unprotected intercourse, and again 24 hours later, during the week before and week after their estimated day of ovulation. (1991 Int J Gynecol Obstet 36:43-48).

Ovulation occurred in all but 14.4% of cycles.

He et al. state: “Earlier we have reported that ovulation was not affected in four out of six women given 0.75 mg levonorgestrel daily for 7 days starting on day 11 of their cycle. Thus, it would appear that the mechanism of action of postcoitally administered levonorgestrel is not inhibition of ovulation in most women but presumably involves an effect on the endometrium, rendering it unsuitable for implantation” (at 47).

If the media does not believe the evidence published in science journals and medical textbooks, perhaps they would believe in the post-fertilization effect of contraceptives if they read about it in The New York Times.

Coincidentally, that newspaper allowed a statement by James Trussell (described therein as “one of the world’s leading experts on contraception”) to appear on its pages earlier this year, maintaining that all hormonal methods of contraception involve postfertilization (i.e., abortifacient) effects.

The Times censor must have been asleep at the switch when he allowed this statement by Trussell to slip past him:
“The evidence is about the same for all hormonal methods of contraception. We can’t rule out a postfertility effect for Plan B, and the same is true for the birth control pill” (quoted in R. Shorto, “Contra-Contraception,” The New York Times, May 7, 2006).

There are other reasons not to support contraceptive-promoting legislation which we’ll save for a later day. But it should be clear that more contraception does not decrease unintended pregnancies and abortions.

And it should be clear what effectiveness contraception does have may depend on post-fertilization, abortifacient effects.
[Life Insight, October-November 2006, Vol. 17, No. 4,]
(“Where the Rubber Meets Roe,” Washington Post, Oct. 1, 2006, at B2)