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I've been trying to figure out through online sources (I don't own any medical textbooks) what the exact mechanism behind the birth control pill (henceforth "the pill") is, and I am often finding contradicting information. This surprises me, since so many women take hormonal birth control that what it does should be known and accessible to everyone.

The following is gathered from PBS and Harvard. As I understand it, the female menstrual cycle is controlled by several organs working in feedback loops: after menstruation, there is a low concentration of estrogen and progesterone in the bloodstream, impelling the hypothalamus-hypofysis to secrete FSH and LH. This stimulates the maturation of a single follicle in the ovaries. This follicle secretes estrogen, signalling to the hypothalamus-hypofysis duo to stop producing FSH and LH. With enough estrogen, a sudden burst of FSH and LH is secreted, causing ovulation. The rest of the cycle is high in progesterone, and by lack of implantation, progesterone production slows and we are back at menstruation.

The goal of the pill is to prevent ovulation (rather than prevent implantation) by playing into these feedback loops.


A first confusion is as follows: I know the pill contains estrogen, yet (as both sources attest to) it is supposedly the high levels of estrogen that induce the FSH/LH spike that triggers ovulation. So then, why wouldn't taking exogenous estrogen cause ovulation rather than preventing it? You are essentially replacing the follicle by a blister pack.


A second confusion is that FSH and LH are so often mentioned in the same breath (i.e., you'll see "FSH" and "LH" less than "FSH and LH") that it is unclear to me what their separate role is. On this ScienceDirect page, in the only exercept that mentions "CHC", it is mentioned that we should consider FSH and estrogen as one loop, and LH and progesterone. The former causes maturation of follicles, the latter causes ovulation (maturation of lutheal cells). This is the only place I have found this distinction, and I'm unsure if it is true; in any case, the above point of contention still applies, because as the pill also contains progesterone, taking exogenous progesterone would cause ovulation.

Besides, I am aware that there exist progesterone-only pills. I'm not sure if they use the same mechanism (this thread is too unclear), because if they do, I don't see the point of having the combined pill contain estrogen.


According to Healthy Women, it is actually the change in estrogen rather than a stable level which causes ovulation. (Rephrasing this as an engineer, the hypothalamus-hypofysis duo detects a high derivative rather than a high baseline in order to trigger the FSH/LH spike.) This seems to be confirmed by Cleveland Clinic in saying

"Chronic (long-term) estrogen exposure inhibits FSH release, whereas rising estrogen levels, which normally occur before ovulation, trigger your pituitary gland to increase levels of gonadotropins (FSH and LH)."

On the other hand, the Crash Course Biology video at 6:02 says in a pop-up that FSH and LH are inhibited by low estrogen but boosted by high estrogen. So, we have a third confusion: does the pill mechanism play on the hormone level, or its rate of change?


So far, I've hypothesised two possible pill mechanisms:

  • Pill keeps estrogen constant, which means the derivative is 0, so the FSH/LH spike isn't triggered (and their initial boost after menstruation is triggered due to GnRH from the hypothalamus which is secreted due to the drop in estrogen due to placebo pills, mimicking menstruation).
  • Placebo pills during menstruation cause very low estrogen. This causes GnRH, which causes FSH. Then the pill saturates the body with estrogen to make it seem like a follicle is growing (above a lower threshold), causing FSH to stop, yet a real follicle would keep increasing estrogen (above a higher threshold) to trigger the spike during ovulation.

I don't like either explanation. There should be a clear mechanism that disambiguates all of the above confusions and comports with all sourced cited above (assuming they're all correct), and comports with all the styles of pill (combined vs. progesterone-only).

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    $\begingroup$ +1 for the effort you've put into this post. Please understand there are more than two kinds of HBC; you can't make blanket statements/assumptions unless you specify exactly the pill you are referring to. Please edit your post to include the pill, by name at least, if that's all you have. Two additional nit-picky things: placebo cannot by definition have an active physiological effect - psychological, yes, and mind-body counts - and how the pill works is known and accessible, but requires some preexisting understanding of endocrinology to really understand (as you've discovered.) $\endgroup$ Aug 6, 2023 at 2:00
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    $\begingroup$ @anongoodnurse Glad to hear the mechanism is known. W.r.t. placebo pills, I guess I should have said "placebo pills give way to" rather than "cause", but indeed it is nuance that I'll gloss over. From your question, can I assume that there are multiple pill mechanisms? Note that I am not talking about HBC in general (e.g. progesterone-excreting IUDs), because that obviously involves multiple mechanisms. I am specifically talking about the pill. I have no knowledge of pill brands; AFAIK, there are two types (combined and progesterone-only). That's as far as I can specify. Does that work? $\endgroup$
    – Mew
    Aug 6, 2023 at 11:42
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    $\begingroup$ @Mew There is more variety than that; different doses of the progesterone-only pills work differently, and all of them have multiple mechanisms of action, not just one. It's a complex hormonal dance with multiple phases and interactions and delays and feedback, not something simple like antagonist drugs that primarily block a single receptor protein. $\endgroup$
    – Bryan Krause
    Aug 6, 2023 at 20:42
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    $\begingroup$ @BryanKrause Consider writing an answer sharing your knowledge, in that case. $\endgroup$
    – Mew
    Aug 7, 2023 at 18:18
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    $\begingroup$ The point is that without knowing to which pill you're referring, the "answer" will be w a a a a a a a a a a a a a a a a a a a a y too long, equivalent to a book on Reproductive Endocrinology. Edit to specify a specific pill or you'll not get an answer. Thanks. $\endgroup$ Aug 7, 2023 at 23:06

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The question appears to be over complicating what is a fairly straightforward mechanism of negative feedback characteristic of most endocrine function in the body, in this case, the effect that oestrogen in the usual or predominant form of oestradiol inhibits the release of FSH from the anterior pituitary required for follicle development and consequently ovulation. By far the dominant effect of both exogenous oestrogens and progestogens -- the respective dosages of which are merely variations on the same general mechanism -- is this negative feedback on the release of gonadotropins from the anterior pituitary, thereby circumventing the natural interaction between the pituitary and its target organ.

To quote from 'Wikipedia' which is usually a good place to start such an inquiry;

Estrogen was originally included in oral contraceptives for better cycle control (to stabilize the endometrium and thereby reduce the incidence of breakthrough bleeding), but was also found to inhibit follicular development and help prevent ovulation. Estrogen negative feedback on the anterior pituitary greatly decreases the secretion of FSH, which inhibits follicular development and helps prevent ovulation.

That should resolve the 'first confusion'satisfactorily: that is, the follicular development induced by FSH has been inhibited by exogenous oestrogen, and ovulation cannot therefore occur.

Under normal circumstances, luteinizing hormone (LH) stimulates the theca cells of the ovarian follicle to produce androstenedione. The granulosa cells of the ovarian follicle then convert this androstenedione to estradiol. This conversion process is catalyzed by aromatase, an enzyme produced as a result of follicle-stimulating hormone (FSH) stimulation.

Progestogen negative feedback and the lack of estrogen positive feedback on LH secretion prevent a mid-cycle LH surge. Inhibition of follicular development and the absence of an LH surge prevent ovulation.

That should address the 'second confusion' and its proliferation into the 'third confusion' regarding the peculiarities of feedback, notwithstanding the anomaly that oestrogen positively feeds back on LH secretion.

The rest of that section of the article deals further with the influence of progestogens (progesterone) on cervical mucus and so on.

The relevant references cited are as usual noted at the end of the article.

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  • $\begingroup$ Oh my, I missed the notification for this answer. I do follow the first quotation, which essentially matches my second hypothesised mechanism (it's the level of estrogen, not the rate of change, that inhibits FSH in the hypofysis; correct?). However, it doesn't answer the "first confusion", i.e. why the exogenous estrogen itself doesn't cause the FSH/LH spike. The second quotation essentially says that LH causes (is metabolised into?) estrogen catalysed by FSH, but nothing is said about LH's secretion nor about progesterone, so this doesn't really answer the "second confusion" either. $\endgroup$
    – Mew
    Jan 8 at 14:14
  • $\begingroup$ @mew. You should read your question and my answer very carefully once again, and understand that the primary mechanism of effect is a NEGATIVE FEEDBACK on FSH/LH secretion by oestrogen, endogenous or exogenous, preventing follicle development in the ovary, and therefore making ovulation impossible, regardless of what happens in the mid-cycle: i.e. the effect you mention, that oestrogen also appears briefly to stimulate the release of those gonadotropins (in a mechanism about which I am ill-informed). It's all a lot simpler than you think, and more a medical question than biological. $\endgroup$
    – jeremiah
    Jan 9 at 22:27
  • $\begingroup$ Okay, let me give it a shot: you are saying that taking exogenous estrogen takes over for the follicle's estrogen production, hence shrinking the supply of LSH and LH faster than usual, keeping the follicle underdeveloped and hence even if the "surge" mechanism were to occur at a certain level of estrogen, no mature follicle would exist to be released. Is that what you are conveying? If yes, I still need an explanation on where progesterone comes in and how it is possible that progesterone-only pills exist if estrogen is what we intercept in the feedback loop. $\endgroup$
    – Mew
    Jan 10 at 3:29
  • $\begingroup$ @mew. Correct. 'Negative feedback'. Progesterone only pills function in essentially the same way, through this same typical negative feedback on the HT-Pituitary, to suppress the release of gonadotropins FSH and LH, both of which are necessary for follicular development and thus ovulation. The mid-cycle surge in LH said to trigger ovulation either doesn't occur or is ineffective in most cases. The follicle simply cannot mature. Progesterone also has other contraceptive effects on cervical mucus etc., but is usually prescribed in cases in which oestrogen is problematic. FSH, LH: read wiki. $\endgroup$
    – jeremiah
    Jan 11 at 7:50

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