Hormonal Control of the Menstrual Cycle

In a healthy menstrual cycle, the anterior pituitary releases two key gonadotropins—FSH and LH—under the control of hypothalamic GnRH. These two hormones work in tandem to drive follicular development, ovulation, and the formation of a functional corpus luteum. A complete and isolated inability to produce LH, with normal FSH, would disrupt the cycle in a very specific and predictable cascade.

Follicular Phase: Largely Initiated, but Incompletely Matured

The early follicular phase would begin relatively normally because FSH, which is intact, is the principal driver of this stage. Under normal FSH stimulation, several primordial follicles would be recruited and begin to grow, and the granulosa cells of these follicles would proliferate. However, a problem emerges with estrogen production. The ovary produces estradiol through the "two-cell, two-gonadotropin" mechanism: LH stimulates the thecal cells to convert cholesterol into androgens (such as androstenedione and testosterone), and FSH then stimulates the granulosa cells to aromatize those androgens into estradiol. Without LH, the thecal cells fail to produce adequate androgen substrate. This means the granulosa cells have little raw material to aromatize, so estradiol production would be severely deficient. The follicles might develop to an early antral stage under FSH, but they would not mature into a dominant, fully developed Graafian follicle, and the normal rising tide of estradiol that characterizes the mid-to-late follicular phase would be markedly blunted or absent.

Ovulation: Absent (Anovulation)

Ovulation is the stage most catastrophically affected. The trigger for ovulation is the mid-cycle LH surge, a sharp spike in LH that causes the dominant follicle to complete meiosis I, rupture, and release the oocyte. With no LH at all, there can be no LH surge. Consequently, ovulation simply would not occur—the patient would be anovulatory. The compromised estradiol production further compounds this, because even the positive feedback mechanism that would normally trigger a surge depends on high sustained estradiol levels, which are not reached here. The follicle, even if partially developed, would not release its egg.

Luteal Phase: Effectively Nonexistent

The luteal phase depends entirely on ovulation and on LH. After ovulation, the ruptured follicle is transformed into the corpus luteum, and LH is essential both for this transformation and for sustaining the corpus luteum's secretion of progesterone (and some estrogen). Because ovulation never happens in this patient, no corpus luteum forms, and because LH is absent, even a residual structure could not be maintained or stimulated to secrete progesterone. The result is a profound deficiency of progesterone throughout what would have been the second half of the cycle. In essence, the patient has no true luteal phase.

Uterine Lining (Endometrium): Limited Proliferation and No Secretory Transformation

The endometrium responds sequentially to ovarian hormones. During the proliferative phase, estrogen normally drives thickening and regrowth of the lining; during the secretory phase, progesterone from the corpus luteum transforms the lining into a receptive, glandular, secretory tissue prepared for implantation. In this patient, because estradiol is low (due to absent thecal androgen production), endometrial proliferation would be minimal—the lining would remain thin rather than thickening robustly. More decisively, because there is no progesterone, the endometrium would never undergo secretory transformation. The lining would therefore be both underdeveloped and unable to support implantation.

Net Clinical Picture

The overall consequence is an anovulatory cycle with low estrogen, essentially absent progesterone, and a thin, non-secretory endometrium. Without the cyclic rise and fall of progesterone, the patient would likely experience amenorrhea (absence of menstruation) or, at most, irregular and scanty bleeding rather than a normal cyclic period, because there is no organized progesterone withdrawal to trigger a coordinated menstrual shed. Functionally, the patient would be infertile under these conditions, since neither ovulation nor a receptive uterine lining could be achieved. This scenario illustrates that while FSH initiates follicular growth, LH is indispensable for adequate estrogen synthesis, for ovulation itself, and for the entire progesterone-dependent luteal phase.

Overview
Luteinizing hormone (LH) has two critical roles in the normal menstrual cycle: (1) acting on theca cells in ovarian follicles to stimulate production of androgens (substrates for estradiol synthesis), and (2) producing the mid-cycle LH surge that triggers final oocyte maturation, ovulation, and luteinization of the ruptured follicle into a progesterone-secreting corpus luteum. If the pituitary cannot produce LH at all while FSH secretion and regulation are intact, the cycle will be disrupted in predictable ways. Below I describe the cascading physiological effects on the follicular phase, ovulation, the luteal phase, and the endometrium, and note likely laboratory and clinical findings.

Follicular phase

• Early follicular development: Follicle-stimulating hormone (FSH) will still stimulate recruitment and growth of multiple antral follicles. Early follicular growth therefore can proceed to some extent. Granulosa cells will express aromatase under FSH stimulation and attempt to produce estradiol.
• Reduced androgen substrate: Because LH is absent, theca cells cannot make the usual LH-driven androgens (androstenedione/testosterone) that granulosa cells convert to estradiol. As a result, estradiol synthesis from granulosa cells is diminished relative to normal cycles even though FSH is present.
• Dominant follicle selection and maturation: The normal rise in estradiol from the growing dominant follicle is diminished, so the positive-feedback threshold that normally helps generate a robust preovulatory profile is unlikely to be reached. Without adequate estradiol and without LH support to the theca, the dominant follicle may fail to achieve full preovulatory maturity. Follicles may either arrest in growth (anovulatory follicles) or persist as large antral follicles/cysts.

Ovulation

• No LH surge and no ovulation: Because the pituitary cannot release LH, the mid-cycle LH surge that triggers resumption of meiosis in the oocyte, enzymatic follicle wall breakdown, and follicular rupture will not occur. Even if a follicle reaches a large size, it will not ovulate. The patient will have anovulatory cycles and therefore be infertile without intervention.

Luteal phase

• No corpus luteum formation: Without ovulation and luteinization, there is no corpus luteum to produce progesterone (and inhibin A). As a result the quintessential hormonal hallmark of the luteal phase—sustained progesterone secretion—is absent.
• Low luteal progesterone: Serum progesterone measured in the mid-luteal window would be very low, reflecting the absence of luteal function. Because progesterone normally prepares the endometrium for implantation and provides negative feedback on the hypothalamic–pituitary axis, its absence alters downstream regulation.

Uterine lining (endometrium)

• Proliferative but not secretory transformation: During the follicular phase the endometrium will undergo some proliferation in response to whatever estradiol is produced. However, because estradiol levels are likely lower than normal and because there is no luteal progesterone stimulus, the endometrium will not undergo the normal secretory transformation associated with a true luteal phase.
• Irregular/unscheduled bleeding: In anovulatory cycles the endometrium can become unstable and shed irregularly (anovulatory bleeding or oligomenorrhea/menometrorrhagia). Two common scenarios are (a) insufficient estrogen → scant or absent bleeding (amenorrhea or hypomenorrhea), or (b) unopposed or fluctuating estrogen causing proliferative overgrowth and subsequent irregular breakthrough bleeding. Chronic cycles with repeated unopposed estrogen (if estradiol is intermittently sufficient) can also increase the risk of endometrial hyperplasia over time.

Expected laboratory and clinical findings

• Hormones: LH will be absent or undetectable. FSH may be normal or show compensatory changes (slightly elevated if negative feedback is reduced), but the key pattern is very low mid-luteal progesterone and absent mid-cycle LH surge. Estradiol is likely to be lower than a typical preovulatory peak, though some estradiol will be present from granulosa cells and from peripheral (adrenal) androgen conversion.
• Clinical signs: Primary or secondary amenorrhea or irregular menses, anovulatory infertility, possible development of persistent ovarian follicles or functional cysts, and potential symptoms related to hypoestrogenism if estradiol is chronically low (e.g., diminished bone protection). On pelvic ultrasound, multiple small-to-medium follicles that fail to ovulate may be seen.

Summary
Complete absence of pituitary LH with normal FSH production would permit some follicular growth but disrupt androgen substrate production and prevent the LH surge that triggers ovulation. The result is anovulatory cycles: follicles often arrest or form persistent cysts, there is no corpus luteum and therefore little or no luteal progesterone, and the endometrium never progresses to a normal secretory, implantation-ready state. Clinically this produces infertility and menstrual irregularities (oligomenorrhea, amenorrhea, or irregular bleeding), characteristic hormone lab results (undetectable LH, low mid-luteal progesterone, reduced estradiol peaks), and long-term risks related to unopposed or inadequate estrogen exposure to the endometrium and bone if the hormonal imbalance is persistent.