Is Hormonal Birth Control Pro-Life?

| Pro-Life Family Planning guide |

In our Pro-Life Guide for Family Planning, we provide an overview of the various methods a couple can use for family planning. Specifically, we saw that the FDA-approved material for the pill explicitly states that it achieves its effectiveness in part by taking life after conception (i.e. preventing implantation of a baby embryo). Importantly, every form of hormonal birth control utilizes that same mechanism of action, including:

  • Combination Pills (e.g., Yaz),
  • Progesterone-only Pills (the minipill),
  • Emergency Contraception (the morning-after pill),
  • The implant/shot/ring/patch, and
  • IUDs (intrauterine devices)

Because many have used the pill in the past, I realize that this comes as a surprise and can be very controversial. There are plenty of good questions: Is there actually evidence for this or is it just theoretical? How often does this happen? Like I said, these are all good questions. These are all questions that I asked too. On this page we’re going to tackle these. But first, let me lay a quick foundation.

Is an Embryo a Baby?

When conception occurs, a new person’s life begins. I’ve written elsewhere on conception’s significance scientifically and biblically. The scientific evidence is overwhelming that fertilization (conception) marks the point where an individual human [a person] is first alive (see When Does Life Begin Scientifically? and When Is a Person a Person Scientifically?). Perhaps more important for us though, the Scripture is even more clear. The Bible demonstrates that our life, our calling even, begins at conception (see When Does a Person’s Life Begin Biblically?).

So, if hormonal birth control allows conception but then keeps that baby embryo from implanting, it achieves its effectiveness by taking life. Before we explore the evidence for this, let’s double check this foundation. If you aren’t sure if an embryo is a baby from conception, that’s ok. It’s an understandable question, and it’s a question I want to help you resolve once and for all. But rather than recount all of the information here, I’d encourage you to look at our scientific overview and biblical overview of these discussions. From here on, we’ll instead focus on the application of this truth.

How Does Hormonal Birth Control Work?

As I mentioned in the overview, the Physician Desk Reference® is “the most recognized drug information reference available in the U.S.” It tells medical providers how each drug works, known as the drug’s mechanisms of action. Whether taken as a pill, shot, patch, IUD, etc., all hormonal birth control represents either a combination of estrogen and progesterone or just progesterone.

To understand the way the combination dose works (i.e., both estrogen and progesterone), just one example from the PDR will be sufficient. Let’s look at the way Yaz works:

“Both estrogen and progestin ultimately inhibit maturation and release of the dominant ovule. In addition, viscosity of the cervical mucus increases with hormonal contraceptive use, which increases the difficulty of sperm entry into the uterus. Alteration in endometrial tissues also occurs, which reduces the likelihood of implantation of the fertilized ovum.”[1]

The progesterone-only dose works similarly. For example, the PDR’s information on Nor-QD[2] identifies these same three mechanisms of action. Let me outline them here:

  1. Inhibit ovulation which reduces the chances of conception (fertilization),
  2. Thicken cervical mucus which also reduces the chances of conception,
  3. Change the lining of the uterus (endometrium) to reduce the chances that the embryo (fertilized ovum) can implant.

For the sake of clarity: Inhibiting ovulation and thickening cervical mucus operate BEFORE conception (fertilization) so those do not present an issue. However, altering the lining of the uterus (endometrium) operates AFTER conception to prevent implantation of a baby embryo (a.k.a., fertilized ovum).

What’s the Problem?

I realize I started this page with a bold statement, that hormonal birth control relies on taking life for its effectiveness. There is some very legitimate confusion on this point. The biggest part of this confusion undoubtedly centers on when life begins. For example, some studies have demonstrated that the pill does not affect the risk of miscarriage after implantation. Based on this, some people have concluded that the pill does not take life. However, while a clinically recognized pregnancy begins at implantation, a life begins before this, at fertilization/conception (as we’ve discussed elsewhere).

So, while the pill has not consistently been shown to increase the risk of miscarriage (i.e., taking a life after implantation), it has consistently been shown to increase the risk that the embryo does not implant (i.e., taking a life before implantation). In other words, the problem isn’t really about pregnancy loss (i.e., after implantation), but about embryo loss (i.e., after fertilization/conception).

More to the point, as we’ve seen in the third mechanism of action, all hormonal birth control is designed to change the womb to prevent a conceived child from being able to implant. While this may not meet the strictest definition of miscarriage, it nevertheless takes a life. Effectively, it starves the baby embryo of the nutrients they need so that they don’t survive. This is where the issue is.

Furthermore, this third mechanism of action is explicit and is clearly identified in the FDA approved information. Nevertheless, some physicians dismiss it, suggesting that it doesn’t actually do that or that it doesn’t do it very often. Let’s explore the evidence together.

Does it Actually Thin the Uterus?

So, how does hormonal birth control “change” the lining of the uterus (endometrium). We’ll just look at the most obvious effect: the pill thins that lining. A journal article in the Archives of Family Medicine[3] compiled some of the evidence related to this. Allow me to summarize that information here:

The authors identified ten different large studies that all concluded that the thickness of the lining in the uterus is directly related to the ability of the fertilized egg (embryo) to successfully implant in that uterus.  Five of these studies conclusively found that when the lining becomes too thin, implantation cannot occur.  To quantify this, some of the studies measured the thickness required to maintain a viable pregnancy as ranging from 5mm to 13mm as a minimum.

So, the thickness of the endometrium (uterine lining) matters, but does the pill actually thin that lining? More specifically, does the pill thin it below that 5mm minimum? Yes, it does. One study found that the average thickness in a woman taking the pill was 1.1mm[4].  Another article similarly found that women on the pill had an inactive endometrium that consistently measured less than 5mm across multiple studies with a thousand women[5].

In other words, the pill definitively thins the lining of the uterus below the minimum 5mm that is reported to maintain a viable pregnancy. More to the point, “when the endometrial lining becomes too thin, then implantation does not occur”[3], meaning that the actual, measured effects of the pill do prevent implantation.

It’s Real, but is It Rare?

Let me recap quickly:

  • If hormonal birth control prevents implantation of a baby embryo then, in doing so, it takes the life of that conceived child by starving them of the nutrient they need to survive.
  • The FDA approved information for hormonal birth control explicitly states that it does this, that it prevents implantation of an embryo by changing the lining of the uterus (endometrium).
  • Furthermore, this isn’t just theoretical. Studies have consistently demonstrated that hormonal birth control significantly reduces the thickness of the endometrium below what is needed for implantation to be successful.

So, this is real. The pill actually does prevent implantation, taking the life of the conceived child. But, some might still dismiss this on the grounds that it’s rare. How often does this happen? It’s a great question. Let’s see what the evidence says.

How Often Does It Happen?

Specifically, what we want to know is this: How often does the pill prevent implantation of a conceived child? Of course, the simplest way to answer this question would be to look at a study of women who’ve conceived (but not implanted) and see how often women on the pill implant vs. women not on the pill. The reality though is that’s easier said than done because, of course, women don’t know they’ve conceived until after implantation. Nevertheless, we can still answer this question; we just have to work backwards from implantation.

The Evidence

We know of course that implantations (pregnancies) still occur for women on the pill. Specifically, 9 out of 100 women on the pill will become pregnant (implantation will occur) over the course of a year with typical use. By way of background, not all of these implantations occur inside the uterus. In a rare but dangerous condition known as an ectopic pregnancy, sometimes the baby embryo can implant outside the uterus. Now, implantation outside the uterus happens for women on the pill and for women not on the pill. However, this probability is significantly higher for pregnancies among women who are on the pill:

Specifically, several studies[6] [7] [8] [9] [10] found that the ratio of pregnancies that were ectopic among users of oral contraceptives compared to women not on the pill ranged from 1.7 times as likely to 4.5 times. All of these studies included 2.1-2.5 times in their unadjusted 95% confidence intervals; we will use 2.0 for simplicity and in order to be more conservative.

Stated more simply, for every pregnancy observed there were twice as many ectopic pregnancies among pregnant women on the pill when compared to women not on the pill.

The Analysis

There are two possible explanations for this: either (i) the pill increases the chances of implantation outside the womb, or (ii) the pill reduces the chances of implantation inside the womb. Which is it? The pill has not been shown to contribute to the causal factors for ectopic pregnancy (implantation outside the womb) such as inflammation in the reproductive system. By contrast, the pill is explicitly designed to reduce the chances of implantation inside the womb (this is the 3rd mechanism of action). More specifically, we’ve seen that the pill significantly affects the endometrium (lining of the uterus) to reduce the chances of implantation inside the uterus. In short, the second explanation is the one supported by evidence.

In other words, the pill doesn’t cause twice as many implantations outside the womb; instead, this statistic demonstrates that the pill causes half as many baby embryos to implant inside the womb. Importantly, this has nothing to do with the other two mechanisms the pill uses to prevent conception/fertilization. If the pill only prevented conception, then it would affect implantations inside and outside the womb equally. This is due solely to the third mechanism, preventing implantation of a conceived child.

This statistic demonstrates that the pill causes half as many baby embryos to implant inside the womb.

What does this statistic mean? It irrefutably demonstrates that the pill doesn’t just prevent conception but also affects the chances of implantation. More specifically, the pill cuts the chances the baby embryo will implant inside the womb in half.

The Implications

Let me bring this analysis home. Remember that 9 out of 100 women on the pill will become pregnant (implantation will occur) over the course of a year with typical use. Since the pill cuts the chances of embryo implantation in half, there would have been 18 pregnancies (implantations) if the pill hadn’t prevented them. In other words, for every 100 couples on the pill, 9 will lose a child every year to the effects of the pill. This isn’t a rare occurrence we can just ignore; this is an unacceptable risk.

For every 100 couples on the pill, 9 will lose a child to the effects of the pill each year. This isn’t a rare occurrence we can just ignore; this is an unacceptable risk.

For the whole picture: Out of 100 couples, 92 would get pregnant in a year without the use of any contraceptives[11]. The pill reduces this number by 83 couples to just 9. But how did it do that? For 74 of those couples, the pill did so by successfully preventing conception/fertilization. However, for those last 9 couples (83 minus 74), the pill did so by preventing the implantation of a conceived child. In other words, approximately 11% of the pill’s effectiveness (9/83) relies on taking life.

Approximately 11 million women in the US are on the pill (ignoring the other forms of hormonal contraception). Since, for every 100 women on the pill, 9 will lose a child to the effects of the pill each year, the pill alone takes the life of nearly 1 million conceived children in the US every year.

The Weight of This Answer

I realize that this answer might be very offensive, particularly because hormonal birth control is so common. Because my focus has been on working through the evidence for the conclusion, I’ve done a poor job explaining my heart here on this page. As a result, it’s possible that it feels I am trying to condemn people for using the pill. Please know that nothing could be further from the truth. As I explained in telling our story in the overview to this guide, my heart is to do what I wish someone had done for me: tell me the truth about the risks to my kids lives. I know that everyone of us wants to protect the lives of our kids, and I know that very few people really know the truth about hormonal birth control.

Please know that any weight or condemnation you may feel from this answer is not yours to bear. “There is therefore now no condemnation for those who are in Christ Jesus.” (Romans 8:1) I’m sharing the truth with you not to make you feel guilty about the past, but to help guide your decisions in the future.

Also, it’s possible this has left you feeling like you don’t have any options, but you do have options. There are effective, pro-life methods for avoiding conception whether you’re in a season where you are waiting to have kids or you are done having kids. We’ve put together a pro-life guide for family planning to talk through all of these options.

[1] https://www.pdr.net/drug-summary/Yaz-drospirenone-ethinyl-estradiol-98.3934

[2] https://www.pdr.net/drug-summary/Nor-QD-norethindrone-2131

[3] Larimore, W. L., & Stanford, J. B. (2000). Postfertilization Effects of Oral Contraceptives and Their Relationship to Informed Consent. Archives of Family Medicine, 126-133.

[4] McCarthy S, Tauber C, Gore J. Female pelvic anatomy: MR assessment of variations during the menstrual cycle and with use of oral contraceptives. Radiology. 1986;160:119-123.

[5] Hee L, Kettner LO, Vejtorp M. Continuous use of oral contraceptives: An overview of effects and side‐effects. Acta Obstet Gynecol Scand. 2012;91:DOI:10.1111/aogs.12036.

[6] Task Force on Intrauterine Devices for Fertility Regulation, The World Health Organization’s Special Programme of Research Development and Research Training in Human Reproduction. A multinational case-control study of ectopic pregnancy. Clin Reprod Fertil. 1985;3:131-143.

[7] Mol BW, Ankum WM, Bossuyt PM, Van der Veen F. Contraception and the risk of ectopic pregnancy: a meta-analysis. Contraception. 1995;52: 337-341.

[8] Job-Spira N, Fernandez H, Coste J, Papiernik E, Spira A. Risk of chlamydia, PID, and oral contraceptives. JAMA. 1990;264:2072-2074.

[9] Thorburn J, Berntsson C, Philipson M, Lindblom B. Background factors of ectopic pregnancy, I: frequency distribution in a case-control study. Eur J Obstet Gynecol Reprod Biol. 1986;23:321-331.

[10] Li, Cheng; Zhao, Wei-Hong; Meng, Chun-Xia; Ping, Hua; Qin, Guo-Juan; Cao, Shu-Jun; Xi, Xiaowei; Zhu, Qian; Li, Xiao-Cui; Zhang, Jian. (2014, Dec 10). Contraceptive Use and the Risk of Ectopic Pregnancy: A Multi-Center Case-Control Study. PLoS One, 9(12).

[11] C. Gnoth, D. Godehardt, E. Godehardt, P. Frank‐Herrmann, G. Freundl, Time to pregnancy: results of the German prospective study and impact on the management of infertility, Human Reproduction, Volume 18, Issue 9, September 2003, Pages 1959–1966, https://doi.org/10.1093/humrep/deg366