How Do the Pill and Other Contraceptives Work?
Part A: How the pill works
The oral contraceptive pill, also known as the birth control pill, is currently being used by over 10 million women in the U.S. 1. A number of physicians and researchers have noted that the oral contraceptive pill (OCP) is actually an abortifacient (ie, an agent that causes an early abortion; specifically, any agent that causes death of the zygote, embryo, or fetus after conception has occurred). Others have stated that they do not believe the OCP is an abortifacient as noted in the recent publication (1998), written by several physicians entitled: Hormonal Contraceptives: Are they Abortifacients? 2
The ethical question of whether contraception is morally permissible has varied between the Catholic Church and the Protestant churches. Both agreed on the "sin of contraception" before 1930 3, whereas both differ in general on the issue today. This appendix will focus on the medical and technical aspects concerning the cited questions regarding the pill's abortifacient qualities.
In order to answer the question of whether the OCP causes early abortions, a number of basic questions need to be answered such as:
Q-A5A. What is an oral contraceptive pill (OCP) 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 (ie, to ovulate). The ovary is the site of production of the woman's two central female hormones, estradiol (EST), a type of estrogen, and progesterone (PRO), a type of progestin. Oral contraceptive pills (OCPs) are a combination of synthetic estrogen and progestin. Oral contraceptives "fool" the pituitary gland so that it produces less follicle stimulating hormone and luteinizing hormone. These two hormones are needed for ovulation to occur, therefore, OCPs suppress, but do not eliminate ovulation.
Oral contraceptives have two other main effects:
- They thin the inner lining of the uterus (called the endometrium), depleting it of glycogen (ie, a type of sugar), and decreasing its thickness. A thinner endometrium has a decreased blood supply.
- They may thicken the cervical mucus, making it more difficult for the sperm to travel up through the cervix. The evidence for this is weak 4 5 and not strongly supported by the rabbit model 6.
Of course, OCP use could not cause abortions if it always stopped ovulation so this needs to be the first issue that is raised. A clear proof of the occurrence of ovulation is provided by noting what the drug companies which manufacture OCPs state. If one opens up the PDR (Physician's Desk Reference, 1998) one will find a table describing the "efficacy rate" of the OCP. In every table listed under each OCP one notes a "typical failure rate" of 3%. The PDR defines this as the rate of annual pregnancy occurrence noted 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 used the pill consistently over the course of a year had a pregnancy rate of 3%. A 1996 paper by Potter 7 gave an excellent overview of the matter. She noted 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 and the fact that today's OCPs are lower dose ones, theoretically permitting a higher rate of breakthrough ovulation. From these estimates of OCP failure and the common experience of on-pill pregnancies, it is clear that both ovulation and conception occur in couples who use OCPs.
Q-A5B: Could you present the evidence that some physicians and researchers glue to support their claim that the OCP indeed acts as an abortifacient?
Before presenting the evidence, the normal anatomy and histology (ie, the study of the body's tissues on a microscopic level) of the inner lining of the uterus, (ie, the endometrium) need to be explained (see Diagram B). 
The endometrium slowly gets built up before oculation (the proliferative phase) and then reaches its peak in the secretory phase (shortly after ovulation [and conception if it has occurred]). The endometrium is "ready for the newly conceived child to implant" when it reaches its peak in the secretory phase a few days after ovulation. The blood flow, specifically the 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 enlarge in the secretory phase. The glands contain important nutritional building blocks for the unborn child who is about to implant, including glycogen (a type of sugar), mucopolysaccharides (building blocks for a cell's growth), and lipids (fats) 8.
Q-A5C: What does the phrase "ready for implantation" mean?
The author of a histology text designed for medical students noted: "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)" [8]. It would appear that God perfectly designed a woman's body and the lining of her uterus to be "optimal for implantation" a few days after ovulation and conception have occurred.
Q-A5D: Does OCP use 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. Because we know that use of the oral contraceptive pill (OCP) allows ovulation and conception to occur at times, if OCP use causes unfavorable changes in the endometrium it would make it difficult for the unborn child to implant, and would support the conclusion that it acts as an abortifacient.
Q-A5E: What are some of those changes?
The first change that use of the OCP makes is to markedly decrease the thickness of a woman's endometrial lining. Women who take OCPs know this because they can tell you that the volume of menstrual contents lost in their monthly cycles significantly decreases once they start taking OCPs. 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.
Q-A5F: Is there a technical or quantitative way to measure how much thinner a woman's endometrium becomes when she uses OCPs?
Yes, in 1991 researchers in the U.S. performed MRI scans (Magnetic Resonance Imaging) on the uteri of women, some of whom were taking OCPs and some of whom were not 9. The OCP users had endometrial linings that were almost 2 millimeters thinner than that of the nonusers. Although this may sound like a small difference, it represented a 57% reduction in the thickness of the endometrial lining in women who used OCPs in this study.
Q-A5G: But is there really any evidence that a thinner endometrium makes it more difficult for implantation to occur?
Yes. A number of different 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 on a thinner uterine lining than a thicker one. Originally an older smaller study (Fleisher et al 10, 1985) did not find that the thickness of the endometrium played an important role in in vitro implantation rates, however, other studies have found a positive trend (Rabinowitz et al, 1986 11; Ueno et al, 1991 12) or a statistically significant effect (Glissant et al, 1985 13) of the decreasing thickness of the endometrium in relationship to a decreased likelihood of implantation. Larger and more recent studies (Abdalla et al, 1984 14; Dickey et al, 1993 15; Gonen et al, 1989 16; Schwartz et al, 1997 17; Shoham et al, 1991 18) have reaffirmed this important connection. Most studies have found that a decrease of even 1 millimeter in thickness yields a substantial decrease in the rate of implantation. In two studies, when the endometrial lining became too thin, no implantations occurred (Abdalla [14]; Dickey [15]).
Q-A5H: What happens to the actual endometrial lining in women who take OCPs when one looks at it under a microscope?
As we saw in Diagram B, the uterine lining is at an "optimal state for implantation" when the glands and uterine arteries are at their maximal size. This makes intuitive sense because at this point the blood supply and glycogen and lipid levels that the tiny unborn child needs to survive are at their maximal state. It has already been stated that it becomes significantly thinner but what does it look like on the microscopic level?
Researchers who study the histology of the endometrium find that OCP use causes a number of effects. First, the spiral arteries regress significantly, becoming much smaller and even difficult to find when one looks under a microscope 19 20 21 22. This of course is important, because an adequate blood supply is critical to the existence of the implanting unborn child. A loss of blood flow means a drastic curtailment in the food and oxygen supply that the child needs to survive. The blood flow to the endometrium is so important that in 1996 one researcher wrote directly about it as concerns its relationship to an unborn child's likelihood of implantation 23. She first discovered that the blood flow through the spiral arteries peaks at day 16 to 18 of the menstrual cycle and then noted that: "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. . ." [23] (emphasis added). In layman's language, Kupesic is stating that the efficacy of implantation correlates with the blood flow through the spiral arteries.
Q-A5I: Are there any other changes on the microscopic level in addition to the reduced blood supply from the spiral arteries?
Yes. the second Drominent effect is that the endometrial glands become much smaller and the "mitotic rate" (rate of cell division) of the cells of the glands decreases [19-22]. Obviously, if the glands which supply the glycogen (sugar), mucopolysaccharides, or lipids (fats) are compromised, the preborn child who needs those nutrients wild have a more difficult time implanting and/or surviving.
Q-A5J: Many of the studies that examined the endometrial lining are older and were performed when OCPs contained a much higher level of estrogen content (100 micrograms or more). Would the same effect be occurring with more recent OCPs?
Yes. First it should be mentioned that if you ask a woman who is taking lower dose OCPs about the amount of monthly menstrual contents that she loses, she will note that she loses significantly less after she starts taking the OCP. Obviously, if she is losing less menstrual contents then she is shedding less each month because the lining of the uterus has become thinner. But what about at the histologic level? Even studies which looked at OCPs that contained 50 micrograms of estrogen (a medium dose) and 0.5 mg of a progestin (eg, norgestrel) found that the spiral arteries and the endometrial glands "shrivel up." [20,21].
Q-A5K: Some researchers 24 have argued that if breakthrough cycle does occur while a woman is taking OCPs, her endometrial lining would become similar to that of the non-OCP user for that cycle. Is this an accurate statement?
To the best of this author's knowledge, that statement has no support in the literature. If the above statement were true, it would mean that each time a woman had a breakthrough cycle while taking the OCP (if she does not become pregnant), she should experience as heavy a cycle as if she were not taking OCPs. This phenomenon has not been described in the medical literature either.
Q-A5L: Is there any other new evidence that supports the argument that OCPs act by causing an early abortion?
Yes. In 1996 a researcher names Stephen Somkuti published an article concerning the endometrium and a group of molecules called "integrins." 25 Integrins are a group of adhesion molecules that have been implicated as playing an important role in the area of fertilization and implantation. There are different types of integrins and it is believed that the endometrium is most receptive to implantation when it expresses certain types of integrins. Oral contraceptive pills change the type of integrins that the endometrial lining produces theoretically making it more difficult for the unborn 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 OCs exert their contraceptive action." [25]
Q-A5M: Has anyone proven that OCP use causes early abortions?
In order to prove if and how often women are having abortions while taking OCPs 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 4 days after conception 26 27). Until a very early test is developed that can detect pregnancy in women in spite of being on OCPs, or until researchers physically measure how many abortions are occurring in women who take OCPs, one cannot state with absolute certainty how often OCPs cause early abortions. New ultrasound technology, which is capable of detecting ovulation, may give new insights in the future (see answer to question O). As of today, the most accurate description of the current evidence is as follows:
All of the evidence on a microscopic, a macroscopic and an immunological level strongly support the argument that OCP use causes an early abortion at times. Until further studies are done, we should take heed and act upon the current data.
Q-A5N: Recently a group of physicians, many of whom are experienced Ob/Gyns, wrote a booklet entitled: Hormonal Contraceptives: Are They Abortifacients? [2] In it they wrote: "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?" is found in the Addendum to this explanation. This author believes that some of their own arguments can be shown to actually support the argument that OCP use is abortifacient.
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