One Pill Daily

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One Pill Daily





One Pill Daily An investigation into Millennial women’s understanding of how birth control pills work By Dana Berger



Start

Introduction

How Does the Pill Work? Survey answers with responses by Kelly Zafman

A Closer Look Imagery and explanations of the female reproductive system from the Department of Cell Biology at Yale

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Con

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Introduction Over 11 million women in the U.S. take birth control pills. The pill was a breakthrough for women’s health. For many, it’s a privilege, a symbol of freedom, and a dependable source of contraception. The 2018 Women’s March launched one of the largest birth control campaigns yet, with access to, and affordability of birth control as major goals of the movement. I started taking birth control pills when I was 17 to regulate my period. Like many of my friends, I didn’t think twice about how it works or many of the side effects. In 2016, my mom was diagnosed with breast cancer. Her diagnosis led me to question the hormones I was ingesting on a daily basis. My inability to explain how the pill works led me to wonder how my peers would respond.

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Introd

tion

While I believe in women’s right to birth control, I also believe in the importance of self-knowledge about the biological mechanisms of birth control and the voicing of their social effects. This book aims to capture narratives that can be overlooked in the midst of political activism.


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The Survey Within three days I received 95 responses to an online survey that I posted in several Facebook groups. The average age of respondents was 22 years old, but the age group ranged from 19-37. The majority of responses came from students that attend or attended Georgetown, Washington University in St. Louis, Cornell, Emory, and the University of Pennsylvania. Part One of the book includes survey responses to the question, “how does the pill work?” Kelly Zafman helps to explain the biological process of birth control pills by “myth-busting” a selection of the survey responses.


Meet Kelly

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Introd

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My name is Kelly Zafman, and I am a candidate for an MD/MSCR (master’s of science in clinical research) at the Icahn School of Medicine at Mount Sinai. I’m currently on a scholarly year between my third and fourth year of medical school, completing a thesis project about the accuracy of ultrasound in predicting large babies. I am planning to apply into OBGYN for residency next year. I have always been interested in women’s health issues and am excited to continue pursuing this as my career! I’m passionate about reproductive issues and think that health education is a critical way to empower women.


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—I started taking the pill in 9th grade because of period pain. It didn’t work but I’m still on it.

—I was excited to take control of sexual decisions without having to worry about biology.

—I began taking it for protection from unwanted pregnancy. I started it about a month prior to having sex for the first time with my boyfriend at the time. I'm not sure what it's like being a young adult not on the pill. I do wish I could stop them and get an IUD instead, but I've heard too many horror stories about IUDs (both insertions and complications post-insertion). I also think it's absurd that women have to ingest so many hormones for their peace of mind and men get away with simply using (or not using) condoms.


— I took them for one year (my freshman year of college). I wish I knew more about how they were directly affecting me.

—I've had a very positive experience with the pill. I feel more confident in my sex life and I have had a extreme reduction in pain due to ovarian cysts.

—Finally I could take control over my body again. I started taking the pill at 17 because I had been getting my period since 13 but it was never regular. The pill was a great way to try to help regulate my periods. I was also sexually active and wanted to be as safe as possible.

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Introd

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—It took a few tries to get one that didn’t mess with my emotions. Honestly, I’m kind of freaked out by the fact that I still don’t get a regular period without it.


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How does the pill work?


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How it

Kelly Zafman (KZ)

They are pretty magical! But then again, there is a science behind the magic. The OCPs have 3 main functions: inhibit ovulation, thin out the endometrial lining (which creates a less cozy environment for a fertilized egg), and thicken the cervical mucus.


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—Depending on the pill, you are either receiving one or two types of hormones. The hormones not only stop you from ovulating, but also thicken the mucus so that sperm have difficulty entering the cervix. I taught sex ed.


KZ

This is spot on! To delve a bit deeper into ovulation inhibition, the hormones present in OCPs negatively inhibit the pituitary gland. In a natural cycle, low levels of estrogen and progesterone induce the pituitary gland to make more FSH and LH. Ovulation depends on an LH surge, the midpoint of the menstrual cycle where estrogen and progesterone are maximized, causing the release of a mature egg. The hormones in OCPs inhibit the pituitary gland, preventing an LH surge. As a result, the egg is not released and any sperm entering the uterine cavity do not meet a match.


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Such a common answer! On a very basic level, OCPs contain hormones, most commonly in different combinations of estrogen and progestin. These are synthetic formulations of the same hormones that are naturally produced by the body to regulate the menstrual cycle. Normally, these hormones are low during a woman’s period (which is why we can feel so crappy). A feedback loop to the pituitary leads to an increase in hormones and causes the cycle to start again. By providing a constant level of estrogen and progesterone, OCPs prevent a natural ovulation/menstrual cycle.

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How it

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—I’m not


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—Honestly, this is sad because I’m tempted to look this up. I should know this and I don’t think I do. But I’ll refrain from researching until I answer the question to the best of my ability! I think there are a few different ways a pill can work... As far as I understand the pill inhibits the release of an egg (like, inhibits ovulation) but you still shed once a month because your body is expecting the egg anyway. But there are other pills that just make the uterus inviable for fertilization because of the hormones it releases. I don’t know which one was the one I took. Or if there are other ways or if either/ both of these are wrong. Oops! Gonna go read up now, thanks for posing a good question and prompting a teachable moment.


—It has to do with estrogen levels (hormones).

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How it

KZ

Birth control pills tend to get a bad rap in terms of their side-effects. The most common worry that women have is that it will cause weight gain. While it’s true that OCPs of our mom’s and grandma’s generation caused weight gain, formulations today are actually much more weight-neutral and can actually lead to a small (2-5 pound) weight loss. The most common side-effect is spotting and irregular bleeding, but some women do experience mood changes. These tend to level off with time. Methods like IUDs, Nexplanon, or rings provide can provide local hormones that do not tend to affect mood.


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—Wow! I guess I'm not really sure. I believe that the pill regulates menstrual cycles through the different levels of chemicals present in each pill.


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How it

KZ

While there are lots of different birth control options available for women, there are essentially two different kinds of OCPs: combination pills or progestin-only “mini pills.” The combination pills are much more common and contain estrogen and progestin, available in lots of different doses and formulations of the two hormones. These pills tend to be a little bit more flexible; you can miss 1-2 pills (depending on the dose) and still be protected. Also, you don’t necessarily need to take them at the exact same time each day. The progestin-only “mini pill” requires more vigilance; you must take it at the same time each day and absolutely can’t skip any pills to be protected.


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—The pill tricks your body into thinking you’re pregnant?

—The pills trick your body into thinking it’s already pregnant so it does not release an egg and also makes the uterine lining unable to hold an egg.


—Gives you more estrogen, makes your body seem like it’s pregnant. Also has progestin.

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How it


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—Umm, I think it thickens the walls of your uterus and tricks your body into thinking you’re pregnant so that you don’t use your eggs?


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How it

KZ

I have used this exact analogy before, so this is a pretty good way to think about it! While it sounds counterintuitive, the body during pregnancy must maintain a supply of progesterone in order to protect the uterine lining; low levels of progesterone cause the uterine lining to be shed. On the “active pills” of the OCP pack, the progesterone component of the pill helps maintain the lining and prevents bleeding. On the “placebo” or “sugar” pills, progesterone is withdrawn and then the lining is shed, which looks like a period. If you have continuous breakthrough bleeding on the pill, you can consider changing to a higher dose which may help better maintain the lining.


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How it

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Dropping an egg makes me think of a chicken or maybe a second grade science experiment, but this is not so far off! Without OCPs, the body’s hormones naturally cause maturation of a few eggs each month. The eggs are normally hanging out in meiosis I (taking you back to high school biology) and as they mature, complete meiosis I and start meiosis II. Only 1-2 eggs actually complete maturation and are released into the fallopian tubes, preparing to be fertilized by oncoming sperm. This process is known as ovulation. Estrogen and progestin in OCPs throw off this natural hormone cycling, preventing ovulation. No ovulation, no eggs “dropped,� no fertilization, no babies.


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How it


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—Yikes I don’t know exactly. I know it thins cervical mucus and prevents an egg from attaching?


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How it

KZ

The pill actually thickens (not thins) cervical mucus, accomplished through the progesterone component of the OCP! This is a particularly important function in progestin-only pills which may not completely inhibit ovulation. The thick cervical mucus acts as an additional barrier for the sperm which must clear the cervix in order to reach the uterus. The thinning you may be thinking of is that OCPs thin out the endometrial lining, the innermost part of the uterus that is shed each month. This is why women with heavy or irregular periods are often prescribed OCPs and why many women experience lighter periods.


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How it

KZ

While not the main mechanism of action of OCPs, these pills do thicken the cervical mucus. This creates an additional barrier for the sperm. Women starting OCPs may notice that they have more clear discharge than usual, which is actually this mucus.


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—Maintains a constant level of estrogen and progesterone to suppress LH and FSH peaks and therefore suppress ovulation.


— ......?

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How it


KZ

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On another foire into high school biology, understanding the fundamentals of the menstrual cycle is the best way to really grasp the mechanism of OCPs. The menstrual cycle can be divided into two phases: follicular and luteal phase. During the follicular phase, follicle stimulating hormone (FSH) and luteinizing hormone (LH) are produced by the pituitary gland and induce production of estrogen and progesterone in the ovaries. This helps to thicken the endometrial lining and mature the growing oocytes (eggs). At the midpoint in the cycle, there is a surge of LH which causes the mature oocyte to be released. At this midpoint, we enter the luteal phase.


The corpus luteum, the lining of the ovary which once housed our developing oocyte, produces progesterone to maintain the uterine lining while the oocyte awaits sperm. Without fertilization, the corpus luteum degenerates, progesterone and estrogen rapidly decline, the uterine lining is shed, and voila-period. OCPs inhibit this cycle by producing negative feedback on LH/FSH, preventing this cycle from occurring. During the placebo pills of the pack, the decline in estrogen and progesterone produces a similar response during the end of the natural cycle-a withdrawal bleed.

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How it


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—I'm realizing right now that I don't know as much as I should, and my doctor did a less-than-ideal job of explaining this as well – but something about taking certain doses of hormones will allow your body to regulate, and the level of hormones in your system can trigger the timing of your period? So something about tripping up that cycle in an artificial way.


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How it

KZ

One way to think about the pills is that it is mimicking pregnancy. In pregnancy, the fetal tissue (i.e. placenta) produces a basal supply of progesterone and some estrogen which is why you maintain the pregnancy and do not have a period. OCPs function in a very similar way. By maintaining a constant supply of estrogen and progesterone, this provides negative feedback to the pituitary gland which decreases the levels of FSH and LH (described above). It is critical that you do not forget to start a new pack of OCPs after 7 days of placebo pills because you will lose that negative feedback and can start the natural cycle of ovulation.


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A Closer Look


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OVARY The human ovary consists of an inner medulla and outer cortex with indistinct boundaries. The medulla contains the blood vessels and nerves, while the cortex is occupied by developing follicles. Visible in this ovary are follicles in various stages of development. Also visible is a corpus luteum, the remnants of a follicle that has burst and sent its ovum into the genital tract.


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LATE PRIMARY FOLLICLES The late primary follicle stage is achieved when the follicular cells proliferate into a stratified epithelium known as the zona granulosa.

EARLY PRIMARY FOLLICLE The primary follicle has a central oocyte and is surrounded by a single layer of cuboidal cells. The zona pellucida is a thin band that separates these two layers.

PRIMORDIAL FOLLICLES An ovarian follicle progresses through several phases before it releases its ovum. During the first five months of development, a finite number of primordial follicles form in the fetal ovary. These follicles consist of oocytes surrounded by a single layer of squamous follicular cells. These primordial follicles remain in the process of the first meiotic division. At puberty, they begin to develop further and become primary follicles.


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SECONDARY FOLLICLE The characteristic feature that distinguishes secondary from primary follicles is the appearance of a follicular antrum within the granulosa layer. This gap contains fluid known as liquor folliculi. Also visible in this image are the oocyte and the zona pellucida. The follicle is surrounded by the theca interna, whose cells produce hormones.


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CORPUS LUTEUM The corpus luteum is the endocrine remains of the collapsed follicle. The center contains the remains of the blood clot that formed after ovulation. Surrounding the clot are glanulosa lutein cells and on the outside theca lutein cells.

GRAAFIAN FOLLICLE The Graafian follicle is the follicular stage after the first meiotic division but before ovulation. It therefore contains a 2N haploid oocyte. It is characterized by a large follicular antrum that makes up most of the follicle. The secondary oocyte, having undergone the first meiotic division, is located eccentrically. It is surrounded by the zona pellucida and a layer of several cells known as the corona radiata. When released from the Graafian follicle and into the oviduct, the ovum will contain three layers: oocyte, zona pellucida and corona radiata.


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LUTEIN CELLS The granulosa lutein cells have an appearance characteristic of steroid-producing cells, with pale cytoplasm indicating the presence of lipid droplets. Theca lutein cells are smaller and more deeply stained. If fertilization and implantation ensue, the corpus luteum will be maintained by hCG and remain active as the corpus luteum of pregnancy.


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ATRETIC FOLLICLE Degeneration of follicle (atresia) can occur at any stage of development. The granulosa cells undergo apoptosis and consequently, the oocyte degenerates. The basement that separated the oocyte from granulosa cells often thickens to become the glassy membrane. Fibrous material replaces the granulosa cells.

CORPUS ALBICANS If fertilization does not occur, the corpus luteum involutes to form the corpus albicans that is filled with fibrous tissue. The secretory cells of the corpus luteum degenerate and are phagocytoses by macrophages.

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OVIDUCT EPITHELIUM The oviduct epithelium consists of two distinct cell types. The ciliated cells dominate and serve to move the ovum away from the ovary and toward the uterus. The non-ciliated secretory cells, also known as peg cells, release a secretion that lubricates the tube and provides nourishment and protection to the traveling ovum. Estrogen is responsible for the initiation of structural changes that prepare the cells of the female reproductive tract for ovulation.

OVIDUCT The oviduct consists of several segments: the infundibulum, which contains fimbriae and is located adjacent to the ovary, the ampulla, the isthmus, and the pars interstitialis. The first two of these regions have a characteristic appearance that is dominated by an elaborate mucosa that is thrown into numerous branched folds, surrounded by a relatively thin layer of smooth muscle. As the tube moves away from the ovary and toward the uterus, these folds become smaller and the smooth muscle dominates.


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UTERUS The uterus is divided into several layers that have distinct structural and functional characteristics. The simplest classification of these layers is their division into a mucosal layer, or endometrium, a muscularis layer, or myometrium, and a serosal layer, or perimetrium. The endometrium itself is divided into two layers, the stratum functionalis and stratum basalis. During the menstrual cycle, the stratum functionalis expands and vascularizes and is subsequently sloughed off during the process of menstruation, whereas the stratum basalis remains relatively constant. The myometrium allows for the expansion and contraction of the uterine cavity and is responsive to the hormone oxytocin.


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CERVIX The cervix lies at the base of the uterus and serves to protect it from bacterial infiltration. It is the site of an important epithelial transition. The upper cervix (endocervix) is lined by a simple columnar epithelium that contains mucous-secreting cells. In contrast, the lower cervix (ectocervix) is lined by a stratified squamous epithelium. The transition point between these two epithelia is known as the external os.

VAGINA The vagina is lined by a stratified squamous epithelium that features a small degree of keratinization. Below the epithelium is a thick layer of dense connective tissue, like that in the dermis of the skin. A layer of loose connective tissue containing many blood vessels and nerves follows this. The cells of the vaginal wall typically contain a relatively large amount of cytoplasm because they produce and store glycogen.


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UTERINE CYCLE The early proliferative phase of the uterine cycle begins at the end of menstrual flow. The uterine glands in this phase are sparse and relatively small, and the epithelial cells develop microvilli and cilia under the influence of estrogen. The late proliferative phase reveals an increased thickness of the stratum functionalis, and the glands are more coiled and densely packed. The secretory phase of the uterine cycle begins at ovulation. In this phase, the glands become even more complexly coiled and the endometrial lining reaches its maximal thickness, whereas the stratum basalis and myometrium remain relatively unchanged. Note the saw-toothed appearance of the glands. Secretions rich in glycogen and glycoprotein can be observed in the lumina of the glands. If fertilization does not occur, the placental tissue does not produce hCG and the corpus luteum degenerates. The uterine lining does not receive the progesterone, causing the spiral arteries constrict and the endometrial tissue to become ischemic. This causes cell death and the sloughing of the stratum functionalis. Estrogen produced by the follicle induces the buildup of uterine lining during this phase.



Responses, continued.


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How does the pill work? The pill has hormones that prevent an egg from being released so that if there is sperm in you, there isn’t an egg for it to attach with.

makes the uterine lining unable to hold an egg. Shed lining and release egg during off week off of pill. It releases estrogen so I don’t ovulate.

I think it provides hormones, which makes your body stop producing hormones/going through the normal cycle. I know it prevents you from ovulating and some pills thicken the cervical mucus. Stops ovulation and affects the uterine lining and mucus so that an egg is less likely to be fertilized and attach to the uterine wall.

It stops you from ovulating through hormonal release. The pill releases estrogen at certain times of the month to give me my period. I cannot tell you how it works. Changes your hormone levels so you can’t plant an egg.

Provides regulated doses of hormones to regulate hormonal levels?

I’m not sure.

N/a

I have no idea.

Lol um I’m pretty sure it sends hormones to the brain that mimics the ones your body would send if you were pregnant? Honestly, idk really.

Estrogen and progesterone are released so you don’t drop an egg therefore you can’t become pregnant.

The active pills have hormones (ex estrogen) that trick your body into thinking it’s already pregnant so it does not release an egg and also

Since there isn’t one in the lining the pills release an additional dosage of estrogen that alters the chemistry of the reproductive system. I used to know more details, but I think I


My understanding is that the pill regulates your cycle, restricting the part where a woman builds a uterine lining to support a pregnancy. That’s why many women skip periods with continued use of the pill. I think it also overloaded my body with high doses of hormones. The mirena IUD option provides a lower dose more concentrated to the baby-making area.

I don’t know. The pill works by releasing hormones into your blood stream that prevent your ovaries from releasing an egg. Even if you are on a birth control pill that allows you to have a “period” each month, it’s not really a period because no egg was ever released. Your body just suddenly stops getting a certain hormone (either estrogen or progesterone) which triggers it to shed the uterine lining.

s, con

It releases hormones (progesterone and estrogen, I think) during points in your cycle to prevent ovulation.

It thickens the cervical mucus to make it harder for the sperm to travel.

se

You take the pill and it puts hormones in your body that trick it into not ovulating? So that you can’t get pregnant? I think lol.

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Small doses of hormones are taken every day to mimic a menstrual cycle that prevents fertilization.

Respon

The pill gives hormones to my body to make it think it is already pregnant.

There are two types of pills: combination (estrogen and progesterone), and progesterone only. Essentially, the pill works by tricking your body into thinking it’s pregnant by increasing the level of progesterone and preventing ovulation. The pills at the ending of the month have no progesterone, and the drop causes a shedding of your endometrial lining (aka period). There are also some pills that are thought to thicken cervical mucus that allegedly contributes to its contraceptive effects.

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remember something about estrogen preventing an egg from being properly released from the fallopian tubes.


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So all your eggs are still there, just shriveling up as time passes. (Kidding about the last part.)

and the progestin makes the environment in the uterus less likely to allow a fertilized egg to implant.

Honestly, this is sad because I’m tempted to look this up. I should know this and I don’t think I do. But I’ll refrain from researching until I answer the question to the best of my ability! I think there are a few different ways a pill can work... As far as I understand the pill inhibits the release of an egg (like, inhibits ovulation) but you still shed once a month because your body is expecting the egg anyway. But there are other pills that just make the uterus inviable for fertilization because of the hormones it releases. I don’t know which one was the one I took. Or if there are other ways or if either/both of these are wrong. Oops! Gonna go read up now, thanks for posing a good question and prompting a teachable moment.

I took a combined oral contraceptive. Progestin and estrogen suppress the release of FSH and LH, which are responsible for the thickening of the endometrium as well as follicular maturation in the ovary. Without these processes occurring, fertilization and implantation are prevented. I don’t know the mechanisms of the biological processes of the pill and its role in treating various syndromes, nor its contributions to increasing or decreasing specific cancer risks that well.

I use a combined oral contraceptive pill that contains synthetic estrogen and progestin. Both of these hormones are given in a specific dosage to prevent variations in estrogen levels that could lead to ovulation,

Makes my body think it doesn’t need to prepare the uterine lining for a baby. It releases the same hormones (estrogen and progesterone) that your body would produce if you were pregnant, thus mimicking pregnancy and tricking your body thus you would be unable to conceive.


Honestly not really sure. At the most basic level, it’s tricking my body to think it is pregnant when it is not right? And so therefore I can’t get pregnant. It also increases the amount of certain hormones in my system (I think?). It is a hormonal drug that mimics the effects of progesterone and estrogen to prevent ovulation.

s, con

The pill works by introducing hormones that both thicken the uterine lining (making it inhospitable for egg implantation) and preventing ovulation.

Um, I think it thickens the walls of your uterus and tricks your body into thinking your pregnant so that you don’t use your eggs?

se

Stops ovulation through regulation of estrogen and progesterone.

The first three weeks of the pill administer estrogen and progestin to your body that tell your body not to release an egg each month, to minimize the chance of fertilization, should you have unprotected sex.

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The pill releases estrogen and progesterone into the body, hormones necessary for regulating pregnancy. These hormones prevent ovulation. The abundance of these hormones leads the body to believe it is already pregnant, and therefore does not need to release another egg. Then, during the sugar pill set, the drop in hormones signals to the body that there is no pregnancy, and the uterine lining is flushed out.

Respon

The pill contains both estrogen and progesterone. The two hormones act together to Increase vagina mucus, delay egg release in the ovary.

Delivers hormones to your body that simulate pregnancy such as thickened cervical mucus and thinned uterine lining, which tricks your body into thinking it is already pregnant and therefore making it harder to become pregnant.

t.

It prevents the release of an egg and affects the cervical mucus.


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The pill controls the level of hormones our body produces so our body never ovulates. I think it also makes the uterus more inhospitable to sperm. It prevents the ovaries from releasing eggs into the uterus, or prevents eggs from implanting, using progestin and/ or estrogen. The hormones stop eggs from being produced/fertilized. That’s about all I know. Makes your uterine lining thicker to help prevent pregnancy. The pill introduces hormones into your bloodstream and in the week you’re not taking the pills your body releases an egg? (tbh idk)

releasing an egg and becoming pregnant. The period on most pills is a fake period. All kinds of the pill work a little bit differently. I know mine has hormones in it that are common for people to need at our age for things like acne. Hormones trick your body into thinking it’s already pregnant so no eggs are released. During the placebo week your bodies realizes it’s NOT pregnant and sheds the uterine lining. And so on. The pill releases hormones that trick the body into thinking it’s already released and egg, and/or causes parts of the menstrual cycle not to occur (not super sure honestly).

Releases a hormone that stops the egg from being released.

The pill contains a certain levels of hormones, which for me, increase my levels of estrogen and decrease levels of testosterone.

Blocks the release of the egg and contains the hormones that the body would produce when pregnant. The hormone makes the body think it is pregnant, which prevents it from

The pill stops the egg from implanting itself to the lining of the uterus by giving paced out doses of estrogen or progesterone within a month or cycle’s time frame.


Estrogen progesterone combination; blocks ovulation, increases thickening of mucus in cervix to block sperm, thins lining of uterus.

Estrogen in the pill suppresses FSH so that follicles do not mature. Progestin in the pill suppresses LH so that ovulation does not occur.

Oh wow... I think it regulates the hormones in your reproductive system; however, the pill goes into your bloodstream in general so sends medication throughout your body.

High levels of estrogen and/or progesterone to prevent ovulation Most BC pills are a combination of two different types of hormones: estrogen and progesterone. These hormones work to prevent pregnancy via two methods; first, they prevent ovulation (so no egg is released), and, second, the hormones thicken the mucous of the cervix, making it “sticky” so that it is harder for sperm to reach an egg to be fertilized.

s, con

Produces hormones which trick my body into thinking I’m pregnant so no eggs available for fertilization.

Thickens the mucus along the uterine walls? Maybe that’s the IUD. Legitimately don’t know.

se

Mimics hormones to block other hormones used for typical menstrual cycle, and then triggers menstruation when hormones aren’t taken.

I should know this better than I do! I believe it stops ovulation and does something to cervical mucus that makes it harder for sperm to reach the egg?

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Honestly not sure.

Respon

The hormones don’t allow the egg to develop in a way that will allow it to be fertilized, thins the uterine lining.

t.

Causes lighter periods and does not allow your egg to be fertile? I really should know better...


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Acknowledgments This book would not have been possible without the 95 women that filled out the survey. I am incredibly thankful for your willingness to share your honest opinions. To Kelly, thank you for tackling the survey responses with humor, empathy, and enthusiasm. Your genuine passion for women’s health and empowerment is inspiring. Thank you to the students and faculty in Communication Design at Washington University in St. Louis and a special thank you to my capstone advisor Penina Acayo, who offered unwavering support and always kept spirits high.


Colophon Typography Calibre by Klim Type Foundry ITC Grouch by Tom Carnase and Ronne Bonder Imagery The images originate from the Female Reproductive System histology database from the Department of Cell Biology at Yale University and the University of Michigan Medical School Histology and Virtual Microscopy Learning Resources website.

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Production This book was printed at Marvel Printing and bound at Hi-Tec, both located in St. Louis, MO.



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