Friday, June 27, 2008

How to Decrease the Chances that "The Pill" Kills [Serge]

Although I have explained why I am skeptical regarding the evidence of a post-fertilization mechanism from OCs, if there were a way to decrease even the potential chance, I would be interested. Surprisingly, in my reading of the literature there is a way for women who choose to take OCs to significantly decrease the chance that an embryo will be affected by the so-called "hostile endometrium". I have yet to see this promoted (especially by those who swear that OCS cause "chemical abortions"), yet is almost universally consistent in the literature. It is also a technique which is very doable. The secret is simple:

Take the pill every day at about the same time every day.

Thats it.

In every study that I have seen, the vast majority of "breakthrough ovulations" occur because of non-perfect use of the pill. In other words, a more consistent use of the pill will minimize the risk for ovulation, which will decrease the chance that a conceived embryo will not implant.

So if you choose to take OCs, and wish to minimize the chance that you could cause a "chemical abortion", then take it consistently.

Tuesday, June 24, 2008

What if Breastfeeding Kills? [Serge]

Many state that until we can be absolutely sure that OCs cannot cause any negative post-fertilization effects on an embryo, we should counsel women never to use them. Although this seems like sound reasoning, I wonder if we are willing to consistently apply this across the board.

In a recent webcast (posted on here), James Trussel, one of the leading contraceptive researchers in the country, stated the following after giving evidence that ECPs work predominately if not exclusively on ovulation:

We have about the same level of evidence for each of the following statements:
OCPs may ...
ECPs may ...
the contraceptive effect of breastfeeding may...

inhibit the implantation of an embryo into the uterine lining.
If this is the case, should we begin to counsel women not to engage in sexual activity until after breast-feeding is complete? Or to forgo breastfeeding to decrease the chance of creating a "chemical abortion"? Does this information change things at all? Should we begin to demonstrate in front of docs who advocate breast feeding?

By endorsing a campaign such as "The Pill Kills" and overstating the case for a post-fertilization effect of OCs, we leave ourselves vulnerable to being hypocritical regarding possible dangers to an embryo. There are many reasons to question the use of oral contraceptives, and we should inform women to the best of our ability so they can make an educated choice. However, overstating dangers helps no one.

Sunday, June 22, 2008

Risk Free? [Bob]

The Times of London breathlessly reports on a new test for Down's Syndrome that can detect the genetic anomaly early and thus provide a "risk-free blood test." Sounds good. But for whom is the test really "risk-free"?

What risk does a Down's baby pose to the mother beyond that of a "normal" pregnancy? Absolutely none (correct me if I'm wrong Serge). The risk being referred to here is to the baby who, without such a blood test, has previously been subjected to the dangers inherent in amniocentesis or chorionic villus sampling (CVS), both of which pose a physical risk to the pregnancy. So, given the newly found improvement in technology, the news sounds good. After all say the proponents:
It would have the positive effect of saving normal foetuses from invasive, and potentially dangerous procedures such as amniocentesis. This would also alleviate the stress of pregnant women going through prenatal testing.
But when it comes to the intersection of technology and human life, there is always more to the story. Consider why anyone is doing fetal testing for Down's in the first place. I offer this caution based on experience.

When my wife was pregnant with our first child in 1987, she was given a serum-based alpha-fetoprotein (AFP) test that returned a borderline high result. This prompted what was then called a Level 2 Ultrasound to determine the source of the "abnormally" high reading. Being first-time, naive parents, and because we had not requested any of these tests, we never questioned the process because we assumed that this was standard operating procedure. Along the way we were told that our baby had a decent probability of being born with spinabifida, neurological disorders (to include brain malformation), Down's and several other scary outcomes. I will never forget the feeling of shock and confusion we both felt when the doctor, after going over the combined test results with us, leaned forward and asked, "So do you want to continue with the pregnancy or terminate?"

The second option had never occurred to us. We declined further testing and my wife refused to ever submit to an AFP test for any of our other 4 kids. Sadly some, given the same situation and alternatives, may have chosen to "terminate." In doing so, they would have "terminated" a perfectly normal, happy, healthy child.

I don't share this story to promote my own moral superiority to anyone. At that point in my life I had not even bothered to consider the moral implications of the pro-life position, nor could I have possibly offered an intellectual defense of our decision beyond, "It just doesn't seem right to me." If anything I owe the steadfast wisdom of my wife the credit for that one. My only point is that these newly discovered "risk-free" tests are anything but risk free to the baby. They offer nothing but another means to rationalize the decision to abort.

There is only one reason to undergo a prenatal test for Down's Syndrome and that is to do away with the child who fails the test. If you don't believe me, listen to the thoughts of some Times readers who offered their opinions on the matter:

The earlier this conditions is recognized the better, and if the parents decide the bundle of cells - for that is what it is before 16 weeks - isn't to their liking, it is their decision. End of debate. After sixteen weeks, when the foetus can be supported independently, that's different. ChrisY, Santa Cruz, USA

Children with Down's suffer for their disability as do their parents and thus ideally should not be born ... As the purpose of civilisation is (hopefully) the prevention of suffering, I believe that a viable means to prevent disabled birth of any sort can only be a good thing. Haseeb, London, UK
Yes, there are those who are doing nothing but mentally preparing themselves for the challenges that would come with introducing a Down's Syndrome child into the world. I would not presume to question that motive. Unfortunately, I believe that those folks are in the minority. These tests are not much more than a seek and destroy mission for pro-abortionists. This will do nothing but increase the number of abortions performed by those who don't need any more prompting than they already have, and for those who may never have considered it otherwise.

Tuesday, June 17, 2008

Dominican Republic Mission Trip [SK]

I returned Friday night from leading a two-week mission trip to the Dominican Republic. Five young men, all high school youth, joined me on this exhausting, but unbelievably profitable adventure. While in the DR, we visited a leper colony, helped a widow rebuild her home, conducted church service for poor kids in a village just shy of the Haitian border, and gave pro-life presentations at a local university and a local church. Our host was Kent Norell, Director of YWAM for the Dominican Republic. (Kent and I are long time friends dating back to our college years!)

The young men joining me on this trip were Tyler Klusendorf, Jeff Klusendorf (both are my sons), Justin Jarrell, Nathan Freeze, and Jordan Freeze. Jordan broke two of his toes (when he fell out of a tree) a week into the trip, but still finished strong, continuing to minister to kids for God's glory up until the very end! All of these young men worked very hard and I'm proud of all of them!

Right now, I'm at Cedarville University preparing to speak to students at Summit Ministries, so I'll let the video clip below give you more insights into our trip. Enjoy!

(Song used with permission of the artist.)

Monday, June 16, 2008

Does a Thin Uterine Lining Support the "Pill as Baby Killer" Theory? [Serge]

I believe the most frequently cited evidence for a "baby-killing" mechanism for oral contraceptives (OCs) is the thinning of the uterine lining that occurs when a woman is on OCs. First, I do not dispute this fact: when women are on OCs their uterine lining becomes considerably thinner than when they are not. This is the reason that many women report lighter periods when they are on OCs. I will also concede that this evidence appears compelling at first glance: if a thick, receptive uterine lining is necessary for implantation, and we can show that OCs thin the lining, it almost has to effect implantation. This is the predominant reasoning used by those who support the abortifacient theory.

However, this only covers the issue very shallowly. In order to understand what it really occurring, we have to go deep. This can be complicated and confusing, but I will do my best to simplify it where I can. In order to understand how OCs effect a woman's uterus, we must first examine the regular menstrual cycle in detail.

Normal Physiology

To the right you see a graphical representation of a woman's menstrual cycle. You can see that the cycle can roughly be divided into the follicular phase and the luteal phase. During the follicular phase, the hormones secreted by the pituitary gland, namely LH and FSH stiffly peak at day 13-15 - which results in ovulation. At the time of ovulation, the uterine lining (seen at the bottom) is quite thin and in fact is unreceptive to implantation . This is a surprise to some, but the truth is that if an embryo attempted to implant at the time a woman ovulates, it would most likely not be successful. Thankfully, implantation naturally occurs days later.

The next phase after ovulation is the luteal phase, in which the uterine lining is prepared to accept an embryo. This phase is controlled by the corpus luteum (thus the name), which arises from the follicle from which the ovum is generated. During the luteal phase, the corpus luteum secretes progesterone (and some estrogen) in order to increase the thickness of the uterine lining in preparation for implantation. If implantation occurs, the CL continues to secrete estrogen and progesterone that support the embryo for 2 more months until the embryonic placenta takes over. The pituitary is able to sense these elevated hormones during pregnancy and will not allow the woman to ovulate during this time (in other words, it will not allow the LH and FSH peak to occur). However, if implantation does not occur, then the thickened uterine lining is lost during menstruation.

I hope you're still with me. The point here is during normal cycles, the luteal phase, which is characterized by the hormones secreted by the corpus luteum is in control of preparing the uterine lining for implantation. The progesterone secreted by the CL during the luteal phase is about 20 times its baseline level, and is far greater than hormone concentrations that are found in formulations of OCs.

What happens on the pill?

What about women on the pill? The primary mechanism of action if OCs is to "trick" the pituitary into believing the woman is pregnant. It does so by elevating the amount of estrogen and progesterone to mimic their levels during pregnancy. As in pregnancy, the LH and FSH peak that would normally occur does not, and the woman does not ovulate, at least in theory.

If ovulation does not occur, then there is no corpus luteum formation, so the uterine lining does not thicken as it normally would. Essentially, women on the pill who do not ovulate have no luteal phase of their cycle. Since their uterine lining does not thicken, you would expect, and it is observed, that their uterine linings are thinner than women who are not on the pill. Their linings would be similar to the thickness at time of ovulation for a woman not on the pill, and as I stated before, this lining is most likely unable to accept an embryo.

What if Ovulation Occurs?

So it seems clear that thickening of the uterine lining in preparation for acceptance of the embryo occurs during the luteal phase of the cycle. A woman on OCs that does not ovulate will not have a luteal phase, thus her uterine lining will be thin. It is also reasonable to believe that this thin uterine lining would not accept an embryo - which is not really a problem because ovulation did not occur. However, what if ovulation does occur? What would happen then?

If so-called "breakthrough" ovulation occurs, then the follicle that released the ovum would turn into a corpus luteum, and the woman would once again have a luteal phase to her cycle. Since the luteal phase is responsible for preparing the uterine lining for implantation, and the hormones secreted by the CL are of far greater magnitude then those found in OCs, it seems reasonable to me that the uterine lining would be thickened and prepared to a similar extent than would a woman who was not on OCs. All of the studies that showed a thinned uterine lining did so an a non-ovulatory cycle. It gives us very little information on what would occur if a woman actually ovulates, which of course is a necessary condition for pregnancy.

I have heard some question this thinking, being skeptical that somehow it would be miraculous that a woman's uterine lining could rebound so quickly from a thin state to one that could accept an embryo. However, what is often forgotten is that this happens every single month for women who are not on OCs! Every month the luteal phase, by using hormones secreted by the CL, turns a thin, "hostile" uterine lining into one that is thick and can support pregnancy. If OCs do create a "hostile environment" for an embryo, then you would have to have some evidence that OCs either negatively influence the CL hormones themselves are that they somehow decrease the effectiveness of the hormonal receptors found in the uterine lining. I have not seem even a possible mechanism for any of these events to occur in the literature, so I remain skeptical regarding this theory.

Whew, thats enough for now. I welcome and covet challenges and corrections regarding this information. However, seeing that this topic is a medical issues, and separate from the ethical issues surrounding contraception, I ask for medical citations and documentation regarding claims that are made.

Update: Tired Typos corrected

Tuesday, June 10, 2008

The Dangers of Overstating our Case [Serge]

Jill Stanek, a prominent pro-lifer and nurse, makes this statement in her WND column:

Did you know the birth control pill can cause chemical abortions?

No, probably not, unless you're a radical pro-lifer like me, or a radical pro-abort. We all know.

Sorry, Jill, you are simply wrong here.

I've been interested in this topic for a number of years, and have reviewed much of the medical literature on the topic. I often joke that I am probably the only oral and maxillofacial surgeon who subscribes to the journal Contraception, which I do in order to have electronic access to all of their back issues. In short, I have done my homework here, and can say without a doubt that Jill has seriously overstated the evidence we have for a post-fertilization effect from OCs. I would summarize the evidence we have about the mechanism of OCs in this way:

1. We do not have full knowledge of the actual mechanism of OCs, and there is little prospect that we will gain this knowledge in the near future. There are questions that we simply do not know, and will almost certainly not know anytime soon.

2. There is no direct evidence that OCs cause "chemical abortions". In other words, there is no direct evidence that OCs effect the uterine lining to cause an embryo that would otherwise implant not to.

3. There is indirect evidence that causes some to believe that OCs can cause changes to the uterine lining that would decrease the chance of embryo implantation in the cases in which breakthough ovulation occurs. This indirect evidence includes differing ectopic pregnancy rates with those on OCs and the thinning of the utering lining for women on OCs. I am well aware that some pro-lifers are persuaded by this indirect evidence that OCs cause a hostile endometrium in a minority of cases (like Randy Alcorn and Dr. Walter Larimore). However, there are also a number of pro-lifers that are unconvinced by this indirect evidence - including myself. If prompted by comments, I will go deeply into the literature on this topic to explain my reasoning. In the meanwhile, I would recommend the book "The Pill" by the Center for Bioethics and Human Dignity for good summaries of both sides of this argument.

4. Direct evidence does not exist that would prove that OCs can never act via a post-fertilization mechanism.

5. Both the package insert and the PDR lists the hostile endometrium theory as a possible mechanism of action of the pill. This is not surprising, considering #4 above. For more information on the accuracy of package information and the FDA, see this post here.

There is a real controversy regarding this issue, and science does not have all of the answers. Let me state this plainly: anyone who believes they know absolutely that OCs cause endometrial changes that result in "chemical abortions" is simply wrong. They don't. I don't know for sure either. Cool web sites and T-shirts do nothing to change this fact. Pro-lifers who overstate this case are acting very irresponsibly.