War of the Words

Changing Hearts and Minds One Definition at a Time

You can’t talk about the pill without talking about pregnancy. But when does pregnancy begin?

The definition of pregnancy impacts how people understand conversations about birth control and abortion, and the definition was undisputed until 1965.

Pregnancy

Prior to 1965, everyone understood that pregnancy means a woman has conceived. We have been observing the fusion of sperm and egg since 1870, and our understanding of embryology and DNA have drastically improved since the mid-20th Century.

In 1965, the American College of Obstetricians and Gynecologists (ACOG) began defining pregnancy as beginning with the implantation of the embryo in the uterine wall. This was politically necessary to allow the new wonder drug—the pill—to be described as a product that prevents pregnancy instead of potentially causing an abortion.

At the time no one knew (or would admit) exactly how the pill worked. But they knew that it worked. They just had to change the way the public thought about the word “pregnancy,” and the new definition has been enshrined into US law ever since.

But pro-lifers have always maintained that pregnancy begins at conception.

Pregnancies lost naturally are called a pre-clinical loss or a miscarriage or perinatal-loss. Pregnancies lost unnaturally due to contraception-induced effects are abortions.

My objective is to determine if hormonal contraception is preventing the birth of already-conceived children. Whether you call it abortion or pre-clinical loss, the questions remain:

• Can contraception-induced effects cause abortion?
• Is there any way to know based on past and current research?
• If so, can we determine how likely is it to happen?

We may be closer than ever to answering these questions.

Hormonal Contraception

The term “hormonal contraception” will be used to describe any drug or drug/device combination that uses the administration of exogenous hormones to dysregulate the hypothalamic-pituitary-gonadal axis and is used solely and expressly for the purpose of preventing birth.

That includes the pill, the mini-pill, injectables, patches, rings, hormonal IUDs, and anything else they come up with to put on or in a woman’s body to add hormones in order to prevent birth.

Off-Label = Off-Topic

That also means if we’re talking about the same drugs taken off-label to remedy a legitimate medical condition, that’s a separate discussion. For example, if a woman is taking birth control to manage endometriosis or polycystic ovarian syndrome (PCOS)—even if she knows it may have abortifacient properties—it’s a worthy discussion, but it’s not this one.

Intent matters, and the principle of Double Effect should be considered when facing competing moral interests. However, this discussion will be limited to the context of solely attempting to prevent birth.

When Birth Control Was Birth Control

Remember when birth control was called birth control? In the more honest days, they used the term that described what was happening: births were being controlled. Regardless of how it was happening, it was true that birth control was happening.

Later they began using the term “contraception” that described what they hoped would happen—that conception would be prevented—despite limitations on proving it with direct evidence (emphasis on “direct”). They call it contraception, but is contraception always happening when the births are controlled today?

This is not a discussion on abstinence, barrier only methods, or the fertility awareness method. These are true contraceptive methods and have no potential to cause abortion. This discussion is limited to the methods that are potentially abortifacients.

When a Period Isn’t a Period

“Birth control tricks your body into thinking you’re pregnant all the time.”

This is a common way to describe how the pill works, and nothing could be further from the truth.

What you might not know is that you’re being prescribed the minimum amount of synthetic hormones required to manipulate your body into ceasing production of your natural endogenous hormones.

You’re taking hormones to shut off your hormones until the placebo week (if your pill regimen has one). During the placebo week, the body attempts to recover from the suppression and resume a natural cycle. This leads to a “monthly withdrawal bleed.” This is not the same thing as a normal period.

Failing to make this distinction creates a false sense that your body is acting in a normal yet regulated fashion. But in fact, it’s in a chronic state of dysregulation.

Some suggest a better description is that the pill tricks your body into thinking it’s in menopause. While it’s true that the pill puts you into a similar low-hormone state, that description is not a perfect fit either.

HPG Axis

The most accurate statement you can make is that the pill manipulates the hypothalamic-pituitary-gonadal (HPG) axis to interrupt normal cyclical and synchronous endogenous hormone production that would otherwise occur during the menstrual cycle.

It’s a thing apart from any analogy.

The manipulation of the HPG axis is the intended and primary method of action for all hormonal contraception.

The pill works primarily on the hypothalamus. You can’t get any further upstream. But the downstream effects are many.

You’ve heard the traditional proposed methods of action:

1. Inhibition of ovulation
2. Thickening cervical mucus to block sperm function
3. Impeding tubal motility
4. Altering the endometrium

What may surprise you is that ovulation is not inhibited as often as you might think depending on the type of HC. Progestin-only pills (POPs) can have a 43% ovulation rate.¹ (Milsom, Korver, 2008)

We actually don’t know much about the effect of thick cervical mucus, and what we do know is based on indirect evidence.

“Although cervical mucus changes dramatically in response to both natural and artificial progestogens, little experimental evidence exists to support a contraceptive effect of cervical mucus. The approaches used to evaluate mucus characteristics such as the Insler score, post-coital test, and sperm penetration assay have not been shown useful to predict infertility, and have never been validated as surrogate outcomes for pregnancy in contraceptive studies.”² (Han, Taub, Jensen, 2017)

Tubal motility is a big deal that effects the timing and synchrony required by the embryo and endometrium for successful implantation. For a time, the ART community theorized a “window of implantation” of maximal receptivity that spanned only around 3 days. If the timing between the independent development of the endometrium and the to-be-injected embryo differs developmentally by more than 3 days, failure rates drastically increase.

“The majority of successful [in vitro] pregnancies (84 %) had first detection of urinary hCG from day 8–10 post-ovulation. These data support the concept that under ideal conditions, optimal implantation rates occur with embryo-endometrial developmental asynchrony of ±1.5 days or less. Based on these data, we can infer that successful implantation can still occur with asynchrony of up to 3 days (i.e. optimal synchrony ±1.5 days).”³ (Wan-Tinn Teh, McBain, Rogers, 2016)

Although, a systematic review and meta-analysis of conventional and modern markers of endometrial receptivity in 2019 noted:

“Time has come to reconsider the classical definition for the window of implantation as a time frame of maximal endometrial receptivity surrounded by refractory endometrium. Endometrial receptivity appears to be a continuous variable reflected in the molecular changes triggered by ovulation and progesterone exposure.”⁴ (Craciunas et al., 2019)

Finally a “thin” or “hostile” or “atrophied” endometrium (impaired decidualization)—once hopelessly denied by contraceptionists—is now widely acknowledged.⁵,⁶,⁷,⁸,⁹,¹⁰,¹¹,¹²,¹³,¹⁴,¹⁵,¹⁶,¹⁷

(Yland et al., 2023) (Yaz FDA Label) (Arlier et al., 2023) (Homminga, Meer, Green, Cantineau, Hoek, 2023) (Liao et al., 2022) (Cooper, 2024) (Abuwala, Tal, 2022) (Lv et al., 2022) (Jacobs et al., 2022) (Bitzer, 2021) (Murata, Tanaka, Okada, 2021) (Liao et al., 2021) (Britton, Alspaugh, Greene, McLemore, 2020)

Even the American College of Obstetricians and Gynecologists (ACOG), whose values include that “abortion is an essential component of comprehensive medical care,”¹⁸ acknowledges that “the lining of the uterus also thins”¹⁹ on combined hormonal birth control.

But I want to go beyond the traditional talking points about HC. We will go beyond “life begins at conception” and “hostile endometrium” and “post-fertilization effects.”

We’re going deeper to investigate:

• embryo/endometrial asynchronicity
• maternal/embryo cross-talk, non-communication, and miscommunication
• proliferative (pre-fertilization) effects
• luteal phase dysfunction
• endometrium immunology
• embryo self-selection
• endometrial selection and rejection of embryos

I’ll cite the studies and direct you to all the sources.

Hormonal contraception was developed in parallel with the abortion “rights” movement. Abortionists have long known that the pill can be abused to attempt an at-home abortion.

Why do Protestants—who so vehemently oppose abortion—give the benefit of the doubt to that same community that pushes contraception?

What would it take for them to choose prudence on the pill instead of having faith that it works as anti-family organizations tell them it works?

That’s next on The Christian Gauntlet.

1. Milsom, I., & Korver, T. (2008). Ovulation incidence with oral contraceptives: a literature review. The journal of family planning and reproductive health care, 34(4), 237–246. https://doi.org/10.1783/147118908786000451 ↩︎
2. Han, L., Taub, R., & Jensen, J. T. (2017). Cervical mucus and contraception: what we know and what we don’t. Contraception, 96(5), 310–321. https://doi.org/10.1016/j.contraception.2017.07.168 ↩︎
3. Teh, W. T., McBain, J., & Rogers, P. (2016). What is the contribution of embryo-endometrial asynchrony to implantation failure?. Journal of assisted reproduction and genetics, 33(11), 1419–1430. https://doi.org/10.1007/s10815-016-0773-6 ↩︎
4. Craciunas, L., Gallos, I., Chu, J., Bourne, T., Quenby, S., Brosens, J. J., & Coomarasamy, A. (2019). Conventional and modern markers of endometrial receptivity: a systematic review and meta-analysis. Human reproduction update, 25(2), 202–223. https://doi.org/10.1093/humupd/dmy044 ↩︎
5. Yland, J. J., Wesselink, A. K., Hernandez-Diaz, S., Huybrechts, K., Hatch, E. E., Wang, T. R., Savitz, D., Kuohung, W., Rothman, K. J., & Wise, L. A. (2023). Preconception contraceptive use and miscarriage: prospective cohort study. BMJ medicine, 2(1), e000569. https://doi.org/10.1136/bmjmed-2023-000569 ↩︎
6. https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/021676s012lbl.pdf ↩︎
7. Arlier, S., Kayisli, U. A., Semerci, N., Ozmen, A., Larsen, K., Schatz, F., Lockwood, C. J., & Guzeloglu-Kayisli, O. (2023). Enhanced ZBTB16 Levels by Progestin-Only Contraceptives Induces Decidualization and Inflammation. International journal of molecular sciences, 24(13), 10532. https://doi.org/10.3390/ijms241310532 ↩︎
8. Homminga, I., Ter Meer, A. F., Groen, H., Cantineau, A. E. P., & Hoek, A. (2023). Thin endometrial lining: is it more prevalent in patients utilizing preimplantation genetic testing for monogenic disease (PGT-M) and related to prior hormonal contraceptive use?. Human reproduction (Oxford, England), 38(2), 237–246. https://doi.org/10.1093/humrep/deac258 ↩︎
9. Liao, Z., Liu, C., Cai, L., Shen, L., Sui, C., Zhang, H., & Qian, K. (2022). The Effect of Endometrial Thickness on Pregnancy, Maternal, and Perinatal Outcomes of Women in Fresh Cycles After IVF/ICSI: A Systematic Review and Meta-Analysis. Frontiers in endocrinology, 12, 814648. https://doi.org/10.3389/fendo.2021.814648 ↩︎
10. Cooper DB, Patel P. Oral Contraceptive Pills. [Updated 2024 Feb 29]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430882/# ↩︎
11. Abuwala, N., & Tal, R. (2021). Endometrial stem cells: origin, biological function, and therapeutic applications for reproductive disorders. Current opinion in obstetrics & gynecology, 33(3), 232–240. https://doi.org/10.1097/GCO.0000000000000702 ↩︎
12. Lv, H., Zhao, G., Jiang, P., Wang, H., Wang, Z., Yao, S., Zhou, Z., Wang, L., Liu, D., Deng, W., Dai, J., & Hu, Y. (2022). Deciphering the endometrial niche of human thin endometrium at single-cell resolution. Proceedings of the National Academy of Sciences of the United States of America, 119(8), e2115912119. https://doi.org/10.1073/pnas.2115912119 ↩︎
13. Jacobs, Emily A. et al. Endometrial thickness: How thin is too thin? Fertility and Sterility, Volume 118, Issue 2, 249 – 259. https://www.fertstert.org/article/S0015-0282(22)00342-9/fulltext ↩︎
14. Bitzer, J. (2021). Progestogens in Contraception. In: Carp, H.J. (eds) Progestogens in Obstetrics and Gynecology. Springer, Cham. https://doi.org/10.1007/978-3-030-52508-8_8 ↩︎
15. Murata, H., Tanaka, S., & Okada, H. (2021). Immune Tolerance of the Human Decidua. Journal of clinical medicine, 10(2), 351. https://doi.org/10.3390/jcm10020351 ↩︎
16. Liao, ShuJie; Wang, Renjie; Hu, Cheng; Pan, Wulin; Pan, Wei ; et al.  BMC Medical Informatics and Decision Making; London Vol. 21,  (2021): 1-13. https://www.proquest.com/openview/eb9b7f028ea0c4c0901874391c1e601c/1?pq-origsite=gscholar&cbl=42572 ↩︎
17. Britton, L. E., Alspaugh, A., Greene, M. Z., & McLemore, M. R. (2020). CE: An Evidence-Based Update on Contraception. The American journal of nursing, 120(2), 22–33. https://doi.org/10.1097/01.NAJ.0000654304.29632.a7 ↩︎
18. https://www.acog.org/news/news-releases/2023/09/understanding-acog-policy-on-abortion ↩︎
19. https://www.acog.org/womens-health/faqs/combined-hormonal-birth-control-pill-patch-ring ↩︎