HOW THE PILL AND OTHER CONTRACEPTIVES WORK
By Chris Kahlenborn, MD / Used with permission. To order copies of this entire publication or to view in PDF, visit www.omsoul.com.

Introduction

The birth control pill is currently being used by more than 10 million women in the US.¹ A number of physicians and researchers have claimed that the birth control pill (BCP) (also called an oral contraceptive) is actually an abortifacient. An abortifacient is a substance that causes an abortion, the death of the zygote, embryo or fetus after conception has occurred. Others do not believe the BCP is an abortifacient as noted in a 1998 publication authored by several physicians: Hormonal Contraceptives: Are they Abortifacients? ²

This booklet uses an easy-reading question and answer format to review the available evidence for determining how the BCP works. All of that evidence, whether microscopic, macroscopic, or immunological, indicates that the BCP sometimes causes an early abortion. When and how often this happens remain unknown.

Questions Regarding the Birth Control Pill

Q1 What is a birth control pill (BCP) and how does it work?

Normally, as shown in Diagram A, the pituitary gland produces two hormones called FSH (Follicle Stimulating Hormone) and LH (Luteinizing Hormone). These hormones serve to stimulate the ovary to produce an egg each month (to ovulate). The ovary is also the production site for the woman's two central female hormones: estradiol (EST), a type of estrogen, and progesterone (PRO), a type of progestin. BCPs are a combination of synthetic estrogen and progestin. BCPs "fool" the pituitary gland so that it produces less FSH and LH. By reducing the FSH and LH required for ovulation, BCPs suppress, but do not eliminate ovulation.

Birth control pills are acknowledged to have two other main effects:

• They thin the inner lining of the uterus (called the endometrium), depleting it of glycogen (a type of sugar) and blood supply, and
• BCPs may thicken the cervical mucus, making it more difficult for the sperm to travel up through the cervix.

Though this latter effect is claimed by BCP manufacturers, the evidence for it is weak^{4, 5} and not strongly supported by the rabbit model.⁶

Of course, BCPs could not cause abortions if they always stopped ovulation so this needs to be the first issue that is raised. A clear indication that ovulation will occur in women taking the BCP is provided by noting what the BCP manufacturers state in the PDR (Physician's Desk Reference, ©1998).⁷ The "efficacy rate" table for each BCP claims a "typical failure rate" of about 3%. The PDR defines "typical failure rate" as the rate of annual pregnancy occurrence in "typical couples who initiate use of a method (not necessarily for the first time) and who use it consistently and correctly during the first year if they do not stop for any other reason." This means that even couples who use the pill consistently over the course of a year will have an average pregnancy rate of 3% according to the BCP manufacturers, who might tend to underestimate this number. A 1996 paper by Potter⁸ gives an excellent overview of the matter. She notes that the most recent data point to a rate of pregnancy for "typical use" as being 7%, which is probably the more accurate statistic, given the immediacy of her research data and the fact that today's BCPs are lower dose and theoretically permit a higher rate of breakthrough ovulation. From these estimates of BCP failure and the common experience of on-pill pregnancies, it is clear that both ovulation and conception occur in couples who use the BCP.

Q2 Could you present the evidence that some physicians and researchers give for their claim that the pill is an abortifacient?

Before presenting that evidence, normal anatomy and histology (the study of the body's tissues on a microscopic level) of the inner lining of the uterus (the endometrium) needs to be explained (see Diagram B).

The endometrium slowly builds up before ovulation (the proliferative phase) and then peaks in the secretory phase (shortly after ovulation and possible conception). The endometrium is thus "ready for the newly conceived child to implant" a few days after ovulation. The blood flow carrying oxygen and nutrients to the glandular cells of the endometrium increases through the cycle as the spiral arteries enlarge during the secretory phase. The size of the endometrial glands also enlarges in the secretory phase. These glands contain important nutritional building blocks for the preborn child about to implant, including glycogen (a type of sugar), mucopolysaccharides (they supply certain building blocks for a cell's growth) and lipids (fats).⁹

Q3 What does the phrase "ready for implantation" mean?

The author of a histology text designed for medical students states: "Thus, the various changes that take place in the endometrium during the second half of the menstrual cycle may be regarded as preparing the uterine lining for the nourishment and reception of the fertilized ovum (blastocyst)."¹⁰ It would appear that a woman's body and the lining of her uterus are "optimal for implantation" a few days after ovulation and conception have occurred.

Q4 Does the BCP cause changes in the lining of the uterus that could be detrimental to the newly conceived child's ability to implant himself or herself?

It would appear so. Since we know that the birth control pill sometimes allows ovulation and conception to occur, unfavorable changes in the endometrium could make it difficult for the preborn child to implant and would support the conclusion that the BCP is an abortifacient.

Q5 What are some of those changes?

The first change that the BCP makes is to markedly decrease the thickness of a woman's endometrial lining. Women who take the pill know this because they can tell you that the volume of menstrual contents (flow) lost in their monthly cycles significantly decreases once they start taking the pill. Obviously, if a woman is losing less menstrual contents each month, the layer of endometrium that is being shed must be thinner and less well developed.

Q6 Is there a technical or quantitative way to measure how much thinner a woman's endometrium becomes when she uses BCPs?

Yes, in 1991 researchers in the US performed MRI scans (Magnetic Resonance Imaging) on the uteri of women, some of whom were taking BCPs and some of whom were not.¹¹ The BCP users had endometrial linings that were almost two millimeters thinner than those of the non-pill users. Although this may sound like a small difference, it represents a 57% reduction in endometrial lining thickness for women using BCPs.

Q7 But is there really any evidence that a thinner endometrium makes it more difficult for implantation to occur?

Yes. Several research papers have studied this issue, and it has been widely described in the medical literature concerning in-vitro fertilization where it has been noted that the newly conceived child is much less likely to implant in a thin uterine lining than a thick one. A small, older study [Fleisher et al¹², 1985] did not find the thickness of the endometrium playing an important role in in-vitro implantation rates. However, later studies found a positive trend [Rabinowitz et al¹³, 1986; Ueno et al¹⁴, 1991] or a statistically significant effect [Glissant et al¹⁵, 1985] of decreasing endometrium thickness, thereby reducing the likelihood of implantation. Additional larger and more recent studies [Abdalla et al¹⁶, 1994; Dickey et al¹⁷, 1993; Gonen et al¹⁸, 1989; Schwartz et al¹⁹, 1997; and Shoham et al²⁰, 1991] have reaffirmed this important conclusion. Most studies have found that a decrease of even one millimeter in thickness substantially decreases the rate of implantation. Two studies showed that when the endometrial lining became critically thin, no implantation occurred [Abdalla,16 Dickey17].

Q8 What does the actual endometrial-lining look like under a microscope for women who take BCPs?

As shown in Diagram B, the uterine lining is at an "optimal state for implantation" when the glands and arteries are at their maximum size. This makes intuitive sense since, at this point, the blood supply and glycogen and lipid levels that the preborn child needs to survive are at their maximal state. Researchers who study the histology of the endometrium find that the BCP causes a number of changes to the endometrium. First, the spiral arteries regress significantly to the point where they are much smaller and may even be difficult to find under a microscope.^21-24 This is important, since an adequate blood supply is critical to the existence of the implanting preborn child. A loss of blood flow means a drastic curtailment in the food and oxygen supply needed for the child's survival. The blood flow to the endometrium is so important that in 1996 Kupesic wrote directly about its relationship to a preborn child's likelihood of implantation.²⁵ She found that the blood flow through the spiral arteries peaks at day 16 to 18 of the menstrual cycle, and then stated: "It seems that endometrial perfusion presents more accurate noninvasive assay of uterine receptivity than uterine artery perfusion alone. Therefore, blood flow velocity waveform changes of spiral arteries may be used to predict implantation success rate to reveal unexplained infertility problems and to select patients for correction of endometrial perfusion abnormalities..."²⁶ (emphasis added). In layman's language, Kupesic is stating that the likelihood of implantation correlates with the blood flow through the spiral arteries.

Q9 In addition to the reduced blood supply from the spiral arteries, what other microscopic level changes to the endometrium are caused by BCPs?

The second prominent effect is that the endometrial glands become much smaller and the "mitotic rate" (rate of cell division) of the cells of the glands decreases.^21-24 Obviously if the glands which supply the glycogen (sugar), mucopolysaccharides, or lipids (fats) are compromised, the preborn child who needs those nutrients will have a more difficult time implanting and/or surviving.

Q10 Many of the studies that examined the endometrial lining are older and were performed when the estrogen content of BCPs was much higher (100 micrograms or more). Would the same effect be occurring with the more recent BCPs?

Yes. First it should be mentioned that if you ask a woman who is taking lower dose BCPs about the amount of monthly menstrual contents that she loses, she will note that she loses significantly less after she started taking the BCP. Obviously if she is losing less menstrual contents, then she is shedding less because the lining of the uterus has become thinner. Even histologic studies for BCPs which contain 50 micrograms of estrogen (a medium dose) and 0.5 mg of a progestin (norgestrel) found that the spiral arteries and the endometrial glands "shrivel up."^22-23

Q11 Is there any new evidence that supports the argument that BCPs act by causing an early abortion?

Yes. In 1996 a researcher named Stephen Somkuti published an article concerning the endometrium and a group of molecules called "integrins." ²⁷ Integrins are a group of adhesion molecules that have been implicated as playing an important role in fertilization and implantation. There are several different types of integrins, and it is believed that the endometrium is most receptive to implantation when it expresses certain types of integrins. Birth control pills change the type of integrins that the endometrial lining produces, theoretically making it more difficult for the preborn child to implant. In the words of Dr. Somkuti: "These alterations in epithelial and stromal integrin expression suggest that impaired uterine receptivity is one mechanism whereby BCPs exert their contraceptive action."²⁸

Q12 Has anyone proven that the BCP causes early abortions?

In order to prove if and how often women are having abortions while taking BCPs, one needs to be able to measure how often women become pregnant while taking them. But early pregnancy tests are currently not accurate enough to confirm pregnancy within the first week, although some researchers have been able to detect the hormonal changes in pregnancy as early as four days after conception.^{29, 30} Until a very early pregnancy test is developed or until researchers physically measure how many abortions are occurring in women who take BCPs, one cannot state with absolute certainty when and how often BCPs cause early abortion. The most accurate description of the current evidence is as follows:

All of the evidence, whether at a microscopic, a macroscopic, or an immunological level, strongly supports the argument that the BCP causes an early abortion at times. Until further studies are done, we should take heed and base our actions and pronouncements on the current evidence.

Larimore and Stanford's comprehensive review article [see Archives in Family Medicine, 2/2000] is an excellent resource for those interested in reading more about the Pill and the evidence for its abortifacient action.

Q13 Recently a group of physicians, many of whom are experienced Ob/Gyns, wrote a booklet entitled "Hormonal Contraceptives: Are they Abortifacients?" In it they write: "The hormonal contraception is abortifacient theory is not established scientific fact. It is speculation..." Could you comment on why a group of physicians would hold this view and on the nature of their arguments?

An overview and rebuttal to the arguments cited in the booklet entitled "Hormonal Contraceptives: Are they Abortifacients?"² are presented here as an Appendix. This author believes that some of their own arguments can be shown to actually support the position that the pill is an abortifacient.

Q14 How frequently do BCPs cause an early abortion?

At this point, no one knows. There are many factors which influence the answer to this question and it is possible that as technology improves, an accurate estimate will be made. One of the determining factors is how often BCPs allow ovulation to occur. If the rate of ovulation is documented to be substantially higher than the pregnancy rate, then one could start to make an estimate of the frequency of abortion in women who take the BCP.

But measuring a woman's ability to ovulate is difficult. Researchers measure ovulation rates in women who are taking the pill by using several parameters including: 1) Ultrasound measurements of the ovary, specifically the size of the largest (dominant) follicle (which contains the egg or oocyte); and 2) hormonal assays of progesterone and estradiol levels. Until now, many researchers have arbitrarily accepted that a pregnancy has occurred when the progesterone levels reaches a certain level. But it is possible that BCPs depress the ovary's ability to produce progesterone despite pregnancy, as noted as early as 1962 by Holmes et al.³¹ It would seem more accurate to measure ovulation rates based on daily pelvic or vaginal ultrasound exams. In 1985, Ritchie³² wrote in his review of the role of ultrasound in the evaluation of normal and induced ovulation: "With daily scanning, ovulation can be demonstrated in >80% of cases." In a 1998 paper Petta et al33 commented on ultrasound in regard to ovulation: "Follicles that disappeared or that were abruptly reduced in size by > 50% after reaching a diameter of 15 mm were considered to have ruptured."

There are a number of other reasons why determining the frequency of ovulation by such a method is important. First, studies of women who take the pill often show a high rate of "ovarian activity" in their dominant follicles which may reach a size that is consistent with those seen in non-BCP users who ovulate. In other words, the ultrasound measurements indicate that these women (the BCP users) are about to ovulate. But these same studies often conclude that ovulation has not occurred because the progesterone level has not reached a critical level.^{34, 35} This is somewhat counter-intuitive in light of a recent study³⁵ that found: "Patients using the lower-dose monophasic and multiphasic pills had follicular activity similar to that of those using nonsteroidal contraception, with the important exception that ovulation rarely occurred." This study, as almost all others, used the criteria that ovulation is confirmed when a progesterone levels reaches a certain level. This may not be accurate.

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