July/August, 1997 Volume XII Number 7 - FEATURES

How do the Pill and other contraceptives work?
by Chris Kahlenborn, M.D.

There are many types of "contraceptives" and related procedures that are said to work by causing an early abortion either some or all of the time. These include the oral "contraceptive" pill (OCP), the intrauterine device (IUD), Norplant, Depo-Provera, the "morning after pill," as well as the procedure of in-vitro fertilization. Do they really cause early abortions? If so, then how do they do so-and if we come to know that they do and we are Christian and/or otherwise pro-life, does this mean that in order do forego hypocrisy we should no longer use them? Does it mean that Christian doctors should no longer prescribe and /or use these procedures?
Before attempting to explain how the various "contraceptives" work, it is important to understand the normal physiology of a woman's menstrual cycle as well as some of the basic concepts concerning the beginning of human life.
In figure A we see that the "control center" or "hormonal thermometer" exists in the brain in the form of the hypothalamus and pituitary gland. For practical purposes it is easier to focus on the pituitary gland as the "central hormonal thermometer."
The pituitary gland secretes a number of hormones but specifically in regards to a woman's monthly cycle they include follicle stimulating hormone (FSH) and luteinizing hormone (LH). Both follicle stimulating hormone and luteinizing hormone act upon the ovary -- specifically upon the developing follicle called the dominant follicle; the ovary in turn produces two female hormones-an estrogen (EST) and a progesterone (PRO) which will have effects upon the uterine lining. If FSH or LH are depressed, the dominant follicle will not develop.
In figure B we see that the ovary contains thousands of follicles of which one will become "dominant" -- that is, one will develop to become large enough so that conception may successfully occur. The dominant follicle is composed of two integral parts: the oocyte resides within the inner component -- it is literally "the egg," and is surrounded by a layer of cells which I arbitrarily refer to as the "outer layer." This outer layer is composed of two types of cells-theca and granulosa cells. These are important because it is these cells that produce estradiol and progesterone. Estradiol and progesterone are specific types of female steroid sex hormones that each come from two general classes of hormones called estrogens and progestins, respectively.
The dominant follicle in figure B moves along the path of arrow 1; when it grows large enough it will release the oocyte; this is ovulation. The oocyte will travel along the path noted by arrow 2 while the outer layer will curl into a ball of cells called the corpus luteum which remains in the ovary. Note that conception will actually occur high up in the fallopian tube at point "L"; thus the sperm must travel through the cervix, through the uterus and up the fallopian tube in order for conception to take place. After conception, it takes about six days for the newly created unborn child to implant him or herself into the mother's womb depicted at point "I". The timing of this event is critical. For example if the unborn child arrives even two days too early, the inner lining -- called the endometrium -- may not be quite ready to support him or her and she will die since she cannot attach herself to her mother's womb.
In order to understand how the various contraceptives work it is also necessary to be familiar with the basic physiology behind the menstrual cycle. As we travel through a 28 day cycle a number of things occur.
There are three phases in the menstrual cycle. The first is the follicular phase. As figure C shows, the body's level of estradiol is slowly increasing as is the pituitary hormone FSH. The increasing estradiol level serves to start to thicken the inner lining of the uterus-the endometrium. One can start to see more spiral arteries and glycogen particles as we reach the ovulatory phase ("OVU")-when ovulation occurs. The surge in LH serves to trigger ovulation and it is at this point that the oocyte is released down the fallopian tube while the remainder of the follicle becomes the corpus luteum as noted again back in figure B. The corpus luteum produces the estradiol and progesterone that result in the increased level of both of these during the luteal phase. Note that the endometrium continues to thicken during this phase as it awaits implantation of the unborn child.
If conception should occur, the unborn child and early placenta will secrete a hormone called B-hCG (Beta- human Chorionic Gonadotropin). This hormone serves to maintain the corpus luteum which in turn will keep estradiol and progesterone levels up. Estrogens serve many functions, but in regards to conception they play the critical task of building up the endometrium. It is essential that it be thick enough and full of enough sugar (glycogen) so that when the six-day old unborn child-technically referred to at this stage as the "blastocyst"-comes out of the fallopian tube, it can implant itself on an endometrial wall that is full of nourishment. Progesterone is the hormone which serves to "stabilize" the endometrium.
If conception does not occur, B-hCG will not be secreted because the corpus luteum will whither, resulting in plummeting estradiol and progesterone levels (see Figure C) -- the endometrial lining cannot be sustained with low progesterone levels and will start to slough off; this presents itself clinically as the onset of a woman's menstrual flow.
Estrogens and progestins both have effects on several other parts of the body: Progestins serve to thicken cervical mucus while estrogens thin it. Progestins serve to slow down the travel of the newly conceived child through the fallopian tube-estrogens speed it up. Both estrogens and progestins cause the cells of the breast to grow and develop.
Now what are oral contraceptive pills and how do they work?
Oral contraceptive pills (OCP) are a combination of synthetic estrogen and progestin which "fool the pituitary gland" so that the production of FSH and LH is markedly reduced thereby suppressing ovulation. OCPs have three other main effects: 1) they change the consistency of fallopian tube thereby either slowing or speeding up the travel of the unborn child and/or sperm up or down its path; 2) they thin the lining of the uterus-depleting it in glycogen and decreasing its thickness making it extremely difficult for the unborn child to implant if a woman did conceive while taking the pill and; 3) they serve to thicken the cervical mucus, thereby making it more difficult for the sperm to travel up through the cervix.
Now, what about the claim that OCPs work by causing an early abortion? In order for an abortion to occur, fertilization must have occurred and in order for fertilization to have occurred, ovulation and the ability of the sperm to travel up into the fallopian tube (FT) must be present.
Let us go through each in order: first, does ovulation occur?
Over the years OCPs have gradually reduced the content of their artificial estrogen and progestin to the point that "breakthrough ovulation" occurs. That is, because they no longer fully suppress the pituitary gland, it may now stimulate the ovary to ovulate at least a portion of the time. Dr. Vander Vange from the Netherlands noted this in the early 1980's. 1 She was able to determine that ovulation had occurred in women who were taking OCPs by three different measurements. First, by using high-tech ultrasound, the researcher saw that the ovaries of women who were taking OCPs continued to produce a follicle that was consistent with the size of those seen when ovulation occurs-usually about 20 mm in diameter. In her results, she noted that 6.6% of the cycles resulted in follicles that were over 30 mm-certainly consistent with ovulation. She also measured the body's natural estradiol and progesterone levels while the women where taking the OCPs. About 3% of the women's monthly cycles produced progesterone levels consistent with ovulation (implying an intact corpus luteum) and 23% of cycles produced estradiol levels consistent with ovulation.
If we now take the most conservative estimate-that is, taking only those cycles in which all three parameters were consistent with ovulation, namely ultrasound, elevated estradiol and progesterone levels, we calculated a conservative rate of breakthrough ovulation of 3%. Other authors have estimated the rate of ovulation to be between 3 and 10% but these are still likely to be low estimates.
Why? First: as is noted above, 6.6% of the time the ovary produced follicles that were consistent with ovulation-in fact even larger than most follicles are at the time of ovulation. Second: recently a "super low" oral contraceptive has been introduced by the drug companies which contains only 20 micrograms of the synthetic estrogen hormone. This will have the effect of inhibiting ovulation even less and if there is a higher percent of breakthrough ovulation there will be a higher percentage of early abortions. Third: it should be noted in Van der Vange's study and others, that the rate of breakthrough ovulation was measured in women who just started taking the pill when the study began-that is, they were not taking the pill before the study began. This means that we know the rate of breakthrough ovulation in women who have recently been placed on the pill but what about those women who are on it for years? Does the pituitary gland begin to "get fooled" less and less by the OCP as time goes by so that breakthrough ovulation actually increases through the years? To this author's knowledge this has not been studied but before dismissing the notion one should note that this is exactly the phenomenon that occurs with Norplant as will be noted in the discussion of it below. [See table 2]
Now if a woman ovulates at least 3% of the time while taking the pill, does that mean the OCP is causing an abortion at least 3% of the time? No. Ovulation in itself does not prove that conception has occurred. All of the drug companies and endocrinology textbooks note that OCPs thicken the cervical mucus, making it difficult for sperm to get through. Of course, if no sperm get through, conception cannot occur. But animal models give us the first clue that this is not the case.
In Chang's paper in 1970 2, he studied several groups of rabbits: to some he gave artificial estrogen, to some he gave artificial progestin and lastly some-the control group-did not receive any hormone at all. After receiving the hormones for a number of days each rabbit was then artificially inseminated by placing rabbit sperm within their vaginal vaults. Each of the animals was then killed and a comparison was made as to how many sperm had reached the fallopian tubes. Note that if OCPs thickened the mucus to a point that no sperm could get through, one would expect that the rabbits which had taken the progestin-the hormone that is known to thicken the cervical mucus-would not have any sperm in their fallopian tubes. Note that in table 1 this certainly is not the case. In every rabbit which received an artificial progestin (e.g., Norgestrel-which is in Norplant-or Norethynodrel) or an artificial estrogen (e.g., ethinyl estradiol which is found in OCPs) they still had thousands of sperm which reached the fallopian tube-up to at many as 72% of the control group. This is very strong evidence that a large percent of sperm are not inhibited even when large doses of hormones are taken.
What about the OCPs effect on the endometrium? As noted back in figure C, the endometrium gradually gets thicker throughout a woman's menstrual cycle in preparation for the arrival of the unborn child and his or her implantation into it; this reflects two phenomenon.
First, the vascularity of the endometrium increases-that is, there is an increase of blood vessels called spiral arteries. The increased blood supply will serve to bring nutrients and oxygen to the newly attached child. Second, there is an increase in the glycogen stores of the endometrium; glycogen is a type of sugar that serves as a food source for the newly attached child.
What do OCPs do?
Oral contraceptives decrease the body's natural E and Pr levels. This in turn will result in a endometrial lining that is both thin and depleted both in its vascular supply and its glycogen content. This reflects itself clinically when women who take OCPs note that their monthly blood loss decreases. Of course, an endometrium as described above makes it extremely difficult for the unborn child to implant. Both the makers of OCPs as well as the leading gynecology texts make no attempt to hide this effect. Williams Obstetrics-one of the leading textbooks used in the United States says: "Similar to [artificial] estrogens, [artificial] progestins produce an endometrium that is unfavorable to blastocyst implantation."3 Similarly Danforth's Obstetrics and Gynecology notes: "The production of glycogen by the endometrial glands is diminished by the ingestion of oral contraceptives, which impairs the survival of the blastocyst in the uterine cavity."4 Ortho pharmaceutical corporation, in its January, 1996 drug insert describing its "contraceptive" Ortho-Cept writes: "Combination oral contraceptives act by suppression of gonadotropins. Although the primary mechanism of this action is inhibition of ovulation, other alterations include changes in the cervical mucus, which increase the difficulty of sperm entry into the uterus, and changes in the endometrium which reduce the likelihood of implantation."
The evidence thus presented points to the occurrence of breakthrough ovulation as well as penetrance of the sperm into the fallopian tube. In addition to this, an even clearer proof of the occurrence of ovulation is provided for by simply noting what the drug companies which manufacture OCPs have to say. If one opens up the PDR (Physician's Desk Reference)-the annually updated manual that lists virtually every drug and a description of it-and looks up any OCP, one will find a table describing the "efficacy rate" of the OCP. In every table listed under each different OCP one always 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"5 This means that even couples who did not stop using the pill for any known period of time had a "failure rate" of 3%. Of course, by definition, both ovulation and sperm penetration into the FT's had to occur at least 3% of the time in these instances.
Even when the drug companies perform their own trials under "ideal conditions" they still get a "failure rate" of 0.96% or about one in 100. 6 Now the real question becomes: how often does the OCP cause an early abortion? All researchers and obstetricians would agree that the endometrial lining, as noted above, is unsuitable for the unborn child to implant-therefore for every child that does implant, it is likely that many others do not-only to die in an early abortion.
In order to estimate how frequently abortion occurs while women take OCPs let us make the comparison of what occurs during in-vitro fertilization. During in-vitro fertilization several eggs are taken from a woman's ovary and mixed with the sperm of a man in a Petri dish. Several of the now fertilized eggs-tiny unborn children-traditionally three to six at a time are then implanted into a "primed" endometrium; that is, the physicians have primed the uterine lining so that it is thick and full of glycogen and "optimal" for receiving the unborn child. What happens under these circumstances? Speroff reports that even under these optimal conditions only 13.5% "success" occurs in any given attempt. 7 That is, when they implant the three to six unborn children, the success will be only 13.5% per cycle. This in turn implies that the "success rate" for any given child is about 3.0%, or about one in thirty!
Now if even under "ideal conditions" the success rate of implantation is one in thirty, imagine what the rate of implantation would be if the uterine lining were withered and depleted of glycogen as occurs with OCPs! This implies that for each unborn child who is conceived and able to implant himself in the uterine wall, many others are sloughed off and die. If the rate of "failure" (i.e., the rate of pregnancy per year in women who take OCPs) is conservatively estimated at 1% and if even 10% of the unborn children are able to implant-both of these being conservative estimates-at the very least a woman would be undergoing an abortion in 10% of her cycles, or about one abortion every 10 months. Clinically, one obstetrician who does not prescribe the pill has told me that women who take or took the pill have confided in him that every few months they experience an especially heavy "period." This may in actuality be the clinical presentation of the early abortion which we have been speaking about.
What about Norplant manufactured by Wyeth-Ayerst or Depo-Provera made by Upjohn? Both of these "contraceptives" are made of a type of artificial progestin. Norplant is composed of levonorgestrel and Depo-Provera of medroxyprogesterone. Depo-Provera is a long-acting progestin that is injected every three months intramuscularly-it it used worldwide despite the fact that animal and human studies have all shown that it increases the rate of breast cancer in its users-especially women who took it before the age of 25!
Norplant is a particularly obnoxious abortifacient that consists of a series of Silastic (i.e., rubber-like) strips which are filled with levonorgestrel and are implanted under the skin of a woman's upper arm and slowly release the artificial progestin into the woman's body. Because the progestins have a similar mechanism of action as concerns their "contraceptive" action, let's look at how Norplant works realizing that Depo-Provera is quite similar. As a powerful artificial progestin, Norplant has three sites of action like OCPs. They inhibit ovulation, they certainly change the endometrial lining and they thicken the cervical mucus. The main difference is that ovulation can be demonstrated to occur more frequently with Norplant than with the OCPs.
Table 2 shows data taken from Croxatto's paper in 1982;8 since Norplant is placed under the skin for years at a time it is possible to measure the rate of ovulation over many years. Note two important effects: first we see that after the first year, the rate of breakthrough ovulation increases dramatically. If researchers had only looked at the first year of use they may well have concluded that the rate of ovulation was only 11.1%. Second, we see that the overall average rate of breakthrough ovulation over the seven-year period is 44.4%! Since we know that the progestin norgestrel does not adequately inhibit sperm migration in animals (see table 2), and since Norplant is a norgestrel that allows an average breakthrough ovulation of 44.4%, it points to the implication that the progestin "contraceptives" cause a very high rate of abortions-up to as high as 32% of the time. If the rate of breakthrough ovulation were to be measured over a period of years as Croxatto did with Norplant [as noted above], we may well find that OCPs cause an increasing rate of breakthrough ovulation-and therefore more abortions-as years go by. Note also in table 2 that the IUD allowed ovulation 100% of the time. The IUD also works by causing an early abortion by disrupting the endometrial lining of the uterus through its irritative action.
What about "the morning after pill?" When a woman takes a series of high dose OCPs one or two days after she thinks that she may have conceived, the high dose hormones act as an abortifacient by altering the lining of the uterus. The animal model described by Castro-Vazquez in 1971 demonstrates this. Dr. Castro-Vazquez took two groups of rats who had recently conceived. On the 2nd, 3rd, 4th or 5th day after conception, one group of rats received an artificial progestin-lynestrenol while the control rats did not receive anything. Twelve of fourteen of the control rats went on to give offspring. None of the fourteen rats which had received the lynestrenol gave birth. Since conception had taken place in both groups this points to an abortive effect of the group given the progestin. The authors state: "As the time of administration excludes any possible action on the sperm transport, capacitaion, or ovum penetration, a failure of implantation must be assumed." 9 In other words, if rats who conceive and are shortly thereafter given a progestin abort their pregnanies because of a failure to implant, the analogous implication is that women who get high dose hormones after conception will suffer this same phenomenon. No one denies this effect; the "morning after pill" clearly causes an early abortion.
A question that proceeds from this is: "What about the woman who was raped and comes into the ER-should she receive high dose hormonal "therapy?" This is a slightly different situation in the sense that this woman, if she had been raped within a few hours of coming to the ER, may not yet have conceived. Many emergency rooms will give such a woman high dose estrogen and progestin hormones very similar to the "morning after pill." [the exception is often found in Catholic hospitals which may not give the "post-rape pill"]. If ovulation has not yet occurred, then the given hormones may indeed stop ovulation and prevent conception.
But what if ovulation and conception have already occurred? The hormones will then almost certainly work by causing an early abortion in the same way as has just been described for "the morning after pill." Since there is no way to know whether conception has occurred or not, the Christian physician is obligated to refrain from such a "therapy" no matter how awkward the circumstance-to do otherwise may well be to participate in an early abortion and if the physician would not consider performing an abortion on a woman who has been the victim of rape when she is four months pregnant, neither should he consider it in the woman who is two hours pregnant. This is the realm of God-not men.
There are two other situations that need to be addressed. The subject of in-vitro fertilization has already been mentioned. Every method of in-vitro fertilization that this author is aware of, whether it be in-vitro, or GIFT or ZIFT involve the loss of some unborn children during the process. As noted previously, when fewer than one out of thirty unborn children "survive" the process of in-vitro fertilization clearly 29 out of 30 do not. Even GIFT involves the exposure of more than one egg to multiple sperm; a situation in which early abortion is bound to occur.
Lastly, there is one last medical situation in which women may unwittingly conceive and experience an early abortion. Often women are started on estrogen replacement after they experience menopause. This usually has a beneficial effect of reducing the risk of cardiac disease and osteoporosis while increasing the risk of uterine and breast cancer. Unfortunately, many women are now starting to be put on estrogen replacement before they have completely stopped their cycles-that is, they are not always in true menopause, but are still having occasional cycles. If a woman were to start estrogen at a time in which she were to still have an occasional cycle, she could still conceive and have an early abortion. Although this would probably be quite rare, it is still something to be aware of and women who wish to avoid this effect should not start hormonal replacement therapy if they are still having an occasional cycle every few months.
In conclusion OCP, Norplant, Depo-Provera, the IUD, the "morning after pill," the "post-rape pill," and in-vitro fertilization all work by causing an early abortion at least part of the time. The reader may note that the word "contraceptive" was consistently placed in quotations. That is because all of the evidence points to these hormones or procedures as being abortifacients-that is, they cause an early abortion either some or part of the time. Contraception technically means "to prevent conception"-clearly the alluded to hormones cause the death of the unborn child after conception and cannot accurately be solely called "a contraceptive." None of these should simply be referred to as contraceptives.
It is ironic that there are two groups of people, who among others, stand out in their refusal to change their behavior in regards to their use of OCPs and the other abortifacients. Who are they? I have found them to be either those Christians who are taking the OCPs currently or recently, or those Christian doctors-whether they be Ob/Gyns, family practitioners, pediatricians, or internists-who currently prescribe them. It really is no mystery. When one combines the fact that almost no one speaks out against these abortifacients with the fact that few are aware that they are abortifacients, coupled with our human nature-that is, our ability to rationalize, it really is not too surprising. The irony is that while many in our ranks conveniently ignore the hard truth the "other side" has no problem admitting it. As noted before, each and every manufacturer of the pill clearly states in the PDR that one of the effects of OCPs is to cause "changes in the endometrium which reduce the likelihood of implantation." It should also be noted that even the most ardent pro-abortion supporters admit that the OCP and IUD are both abortifacients. In his arguments before the Supreme Court, in a case that received world-wide publicity-the case of Webster v. Reproductive Health Services-Mr. Frank Susman, arguing for the pro-abortion side spoke to Justice Anthony Scalia stating "If I may suggest the reasons in response to your question, Justice Scalia. The most common forms of what we generally in common parlance call contraception today, IUD's, and low-dose birth control pills, which are the safest type of birth control pills available, act as abortifacients. They are correctly labeled as both." 10
I conclude by asking the readers in the audience to comment on what I think may be more than just a curious coincidence. As I was preparing this paper I noted that every OCPs description in the PDR stated that the first birth control pill should always be started on a Sunday-every drug insert to every OCP always asks its users to start them on a Sunday. If you know anyone who is currently taking OCPs ask them what day their doctor told them to start-Sunday-always Sundays! Is this just a coincidence? Some would say that, but think about it. Sunday, the Lord's day, the day when Protestant Christians listen and take in the Word of God-the day when Catholic Christians take in the Body of Christ. Life against death-could Satan possibly be tempting us to choose hypocrisy on this day by pretending to honor the Lord on the same day we start a process that may well result in the destruction of the child He has given to us? He has spoken: "I call heaven and earth to record this day against you, that I have set before you life and death, blessing and cursing; therefore choose life, that both thou and thy seed may live." [Deuteronomy 30:19]. Hopefully after becoming aware of the fact that the discussed items really do act by causing an early abortion, Christians would immediately stop taking these hormones/procedures and certainly stop prescribing them. Let us avoid sin and death-let us choose life, and live.

1 Van der Vange N. Ovarian activity during low dose oral contraceptives. Contemporary Obstetrics and Gynecology. G. Chamberlain (editor). London, Buttersworth, 1988. 315-326.
2 Chang MC, Hunt DM. Effects of various progestins and estrogen on the gamete transport and fertilization in the rabbit. Fertility and Sterility. 1970; 21: 683-686.
3 Cunningham FG et al. Williams Obstetrics. Stamford, CT. Appleton & Lange. 1993. p.1323.
4 Danforth. Obstetrics and Gynecology (Seventh Edition). Philadelphia. JB Lippincott Company. 1994. p. 626.
5 Physician's Desk Reference, 49th Edition. "Description Ortho-Cyclin & Ortho Tri-Cyclen". Montvale, NJ. Medical Economics. 1995. p. 1782.
6 Ibid.
7 Speroff L, et al. Clinical Gynecologic Endocrinology and Infertility (Fifth Edition). Williams and Wilkins. 1994. p 937-9.
8 Croxatto HB, Diaz S, et al. Plasma progesterone levels during long-term treatment with levonorgestrel silastic implants. Acta Endocrinologica; 1982; 101: 307-311.
9 Castro-Vazquez, et al. On the Mechanism of action of oral contraceptives. Fertility and Sterility. 1971; 22: 741-744.
10 Transcripts of oral arguments before court on abortion case. New York Times. April 27, 1989. B 13.

Copyright © 1997 AFLM