The question refers to the finding that "(...) breakthrough bleeding is much more common with progestogen-only methods", see Wikipedia, Hormonal Contraception
and inquires about how adding estrogen to progestogen-only pills apparently prevents breakthrough bleeding, as this seems a paradox because estrogen 1. builds up the placenta (the more the build-up, the more the bleeding, presumably) and 2. does not maintain the placenta (as progesterone does, thus preventing bleeding).
The question's argument is confirmed by a comment, see above:
"(...) unopposed estrogen causes out of proportion endometrium but it'll eventually shed."
Some answer is to be found in Wikipedia, Hormonal contraception:
"Estrogen was originally included in oral contraceptives for better cycle control (to stabilize the endometrium and thereby reduce the incidence of breakthrough bleeding)..."
As this answer (as many other sources) lacks explanation the following reasoning tries to explain what is known and what is yet unclear about the mechanism of action of estrogen in "combined" hormonal contraceptive.
First, some basic knowledge (from University of Berkeley):
- occurs during follicular phases when estrogen levels are still low.
- occurs at high concentrations near the end of the follicular phase, estrogen becomes a positive inducer of the anterior pituitary
- positive feedback triggers the anterior pituitary to release more FSH and LH
- more FSH and LH cause the ovary to produce more estrogen
- the ensuing LH surge is responsible for ovulation"
Second, a summary of the following as the question turned out to be a difficult one, with several issues in science yet unresolved:
Estrogen combined to progesterone may compensate for a lack of estrogen caused by supplemented progesterone, the latter reducing the secretion of follicle-stimulating hormone thus preventing ovulation (cp. question's text) and, at the same time, by absence of FSH, not inducing the production of estrogen . Estrogen's regulatory role in the menstrual cycle might include the upholding of the production of progesterone (peaks of estrogen ask for such of progesterone, see quote highlighted above, LH known to induce progesterone production). Supplementation of estrogen might thus prevent any lack of progesterone as supplemented progesterone may downregulate its very production.
Third, explanatory text:
One basic understanding (cp. the comment above) is that it is the lack, the drop, of the progesterone level that causes the bleeding. There is no hormone or signaling molecule that actively initiates bleeding; it is the drop of production of progesterone the function of which is maintenance of (non-bleeding) placenta. As the question and the comment suggest this mechanism applies to estrogene in the same way, which asks for some explanation of the finding that estrogen is able to reduce breakthrough bleeding (as estrogen differs from progesterone in that respect, as it does not maintain the placenta, thereby preventing bleeding).
There is a second basic concept: the regulation of progesterone axis by the estrogen axis, to be distinguished by the feedback regulation of both hormones based on the hormones FSH and LH. Interestingly, feedback works via action of hypothalamic gonadotropin-releasing hormone which is one single hormone acting on both axis, the "pulse" of secretion deciding if the progesterone or estrogen axis is addressed.
Estrogen and progesteron are both dependent on stimulating hormones, i.e. follicle-stimulating hormone, FSH, and luteinizing hormone, LH. Any rise in estrogen or progesterone (by a regulatory feedback loop that uses the inhibin hormones acting on hypothalamus production of gonadotropin releasing hormone) is able to decrease its very production, and, second, there is an order of succession: the production of FSH consecutively leads to the production of LH; there is an "axis" FSH/LH, of estrogen followed by progesterone (in spite of almost simultaneous peaks of FSH and LH at the time of ovulation FSH (ovum) precedes LH (placenta). If there is no new ovulation there will be no new placenta. Estrogen as well as progesteron, in that feedback loop, seem to act on hypothalamic gonado-releasing hormone, thus up- und downregulating each other via FH and FSH homones.
See Wikipedia: "High-dose progestogen-only contraceptives, (...), completely inhibit follicular development and ovulation.": A progesterone-only pill, as it is able to inhibit the production of FSH may by inhibiting pathways decrease its own production (feedback reglation in a strict sense). However, it seem very likely that it downregulates estrogens "peak" function, thus its function to induce (non-supplemented) progesterone rises and possible decrease production. Conversely, the supplementation of estrogen may uphold the production of progesteron thus preventing shedding in case of lack of supplementation.
By suppressing FSH (known action of contraception, "at least when in high dosis", cp. question above) progesterone seems to be able to inhibit estron and and its own upregulation, thus production. Any drop of progesterone that is has been supplemented thus possibly leads to "non-maintainance" of the placenta by diminished substituting production.
As a result, this answer is:
Supplementation of estrogen may uphold the production of progesterone to compensate any drop in levels of supplemented progesterone thus preventing breakthrough bleeding.
Final remark: Any better answer must be simpler...
Search results confirm that there does exist a direct effect of estrogen on production and secretion of progesterone:
"(...) circulating estrogen levels rise (...), they stimulate the hypothalamo-pituitary axis. This estrogen positive feedback is pivotal to stimulate the luteinizing hormone (LH) surge required for ovulation and luteinization of ovarian follicles. ... "Together, these data strongly suggest that estrogen enhances neuroprogesterone synthesis in the hypothalamus that is involved in the positive feedback regulating the LH surge.", see Micevych et al., The luteinizing hormone surge is preceded by an estrogen-induced increase of hypothalamic progesterone in ovariectomized and adrenalectomized rats, Neuroendocrinology 2003 Jul;78(1):29-35
Popular-scientific pages do not explain the mechanisms, e.g.
BBC, Hormones in human reproduction: "The oral contraceptive, which is known as the pill, contains oestrogen or progesterone. These hormones inhibit the production of FSH, and eggs cannot mature."
For some scientific explanation, see e.g.
Reed et al., The Normal Menstrual Cycle and the Control of Ovulation:
"Declining steroid production by the corpus luteum (...) for follicle stimulating hormone (FSH) to rise during the last few days of the menstrual cycle (...). Another influential factor on the FSH level in the late luteal phase is related to an increase in GnRH pulsatile secretion secondary to a decline in both estradiol and progesterone levels (...). This elevation in FSH allows for the recruitment of a cohort of ovarian follicles (...)"
However,Lesoon/Mahesh, Stimulatory and inhibitory effects of progesterone on FSH secretion by the anterior pituitary found: "These results indicate that the anterior pituitary is a major site of action of progesterone in the release of FSH and that 5 alpha-reduction of progesterone plays an important role in FSH release."
Even if the latter finding does not contractict the stated role of estrogen and progesteron, it doesn't surprise that the search result for action of progesteron in hormonal contraception inter alia is:
"Does progesterone affect the mechanism of ovulation?"
"The role of progesterone (P) in the mechanism of ovulation is controversial at best. (...)"
See also, in the context of postmenopausal breakthrough bleeding the conclusion of van de Weijer et al., Relationship of estradiol levels to breakthrough bleeding during continuous combined hormone replacement therapy, 1999:
"The occurrence of breakthrough bleeding during continuous combined hormone replacement therapy with estradiol and dydrogesterone in postmenopausal women was related to serum estradiol levels and not to dydrogesterone levels. Further studies are needed to test the hypothesis that estrogen is a major factor in the incidence of bleeding(...).
There is a related question on Stackexchange Biology: Use of progesterone in preventing ovulation?.
Last not least, some hint at Wikipedia on Human chorionic gonadotropin:
"Human chorionic gonadotropin interacts with the LHCG receptor of the ovary and promotes the maintenance of the corpus luteum for the maternal recognition of pregnancy at the beginning of pregnancy. This allows the corpus luteum to secrete the hormone progesterone during the first trimester."
Progesterone levels that correspond to those during pregnancy thus lack corresponding chorionic gonadotropin. That may also be meant by stating: "Estrogen was originally included in oral contraceptives for better cycle control", see above.