The ovaries are paired almond-shaped organs, about 3 cm long, sitting in the pelvic cavity on either side of the uterus. They make oocytes (eggs) and the dominant female sex hormones — estradiol and progesterone — plus small amounts of testosterone. Unlike the testes, which churn out new gametes indefinitely, the ovaries are born with a finite egg supply and spend the next several decades steadily depleting it.
At a glance
What it does
Runs the menstrual cycle. Each month in reproductive age, a cohort of follicles starts developing in response to FSH from the pituitary. One follicle becomes dominant, the others regress, and the dominant follicle releases its egg at ovulation in response to an LH surge. The ruptured follicle becomes the corpus luteum, which makes progesterone during the luteal phase to support a potential pregnancy. If no pregnancy happens, the corpus luteum regresses, progesterone drops, and the endometrium sheds as menstruation.
Hormonally, the ovaries make estradiol primarily from granulosa cells (from androgen precursors supplied by theca cells — the two-cell model), progesterone from the corpus luteum and in pregnancy from placenta, and small amounts of testosterone from theca and stromal cells. Ovarian androgens contribute to libido, muscle mass, and mood in women.
How it works
Every egg a person will ever have is present at birth, arrested in prophase I of meiosis. This is the foundation of the entire female reproductive timeline. The finite number at birth is roughly 1-2 million. By puberty it is down to a few hundred thousand. By age 37-38 the decline accelerates. By menopause (average age around 51 in industrialized countries, with substantial variation), the follicle pool is essentially exhausted.
Folliculogenesis takes months from the earliest recruited primordial follicle to ovulation, even though the "menstrual cycle" we observe is only the final 2-3 weeks of maturation. Early development is gonadotropin-independent; later stages become FSH-dependent and the dominant follicle surge depends on LH.
Feedback from the ovaries to the hypothalamus and pituitary is mixed. Estradiol at moderate levels suppresses LH and FSH (negative feedback). Estradiol at high levels sustained for ~48 hours flips to positive feedback, triggering the mid-cycle LH surge that causes ovulation. Progesterone in the luteal phase suppresses LH and FSH back down. Inhibin B from granulosa cells specifically suppresses FSH.
Anti-Müllerian hormone (AMH) is produced by granulosa cells of small growing follicles and is a decent marker of ovarian reserve (how many eggs are left). AMH declines through reproductive life and is used in fertility evaluation, IVF response prediction, and rough estimation of menopause timing — though individual variability is significant.
When it goes wrong
Polycystic ovary syndrome is the most common endocrine disorder in reproductive-age women, affecting 8-13% depending on diagnostic criteria. Classic picture: oligo- or anovulation, hyperandrogenism (acne, hirsutism, sometimes alopecia), and polycystic ovarian morphology on ultrasound. Core problem is functional ovarian hyperandrogenism often with insulin resistance. Treatment is multi-pronged: lifestyle for metabolic features, combined oral contraceptives or spironolactone for hyperandrogenism, letrozole or metformin for ovulation induction when fertility is desired, and increasingly GLP-1 agonists for the insulin resistance and weight components.
Primary ovarian insufficiency is the loss of ovarian function before age 40 — affects roughly 1% of women. Causes include genetic (Turner syndrome, Fragile X premutation), autoimmune, post-chemotherapy, post-surgical, and idiopathic. Produces amenorrhea, hot flashes, infertility, and long-term risks from estrogen deficiency. Treatment is hormone replacement until the typical age of menopause.
Ovarian cancer is the deadliest gynecologic cancer, partly because early disease is often asymptomatic and screening tests have not meaningfully reduced mortality. Epithelial ovarian cancer dominates adult disease; germ cell and sex cord-stromal tumors are rarer but occur in younger women. BRCA1/2 mutations dramatically raise risk and are the clearest indication for prophylactic salpingo-oophorectomy after childbearing.
Functional hypothalamic amenorrhea — cycles stopping from undereating, overexercise, or chronic stress — is an under-recognized cause of absent periods and low estrogen in athletes and chronic dieters. The ovaries are fine; the hypothalamic drive is suppressed. Fix is usually eating enough and moderating training load.
Interactions
Aging is the central ovarian story. Fertility declines noticeably starting in the mid-30s and steeply after 37-38; miscarriage rates rise from rising rates of chromosomally abnormal eggs. By 40, monthly natural pregnancy rates are roughly 5% in a healthy couple; by 45 they are essentially zero with own eggs even with IVF. This is biology, not unfairness — and it is what drives the tight timing of egg freezing decisions.
Menopause is defined as 12 months of amenorrhea from ovarian follicle depletion. The perimenopausal transition preceding it can last 4-8 years and produces erratic cycles, hot flashes, sleep disruption, mood changes, and vaginal dryness. Modern menopausal hormone therapy — within 10 years of menopause onset and before age 60 — is reasonable for symptomatic women based on current guidelines, with a better risk-benefit profile than the initial WHI-era fears suggested.
Ovarian hormones interact with bone density (estrogen is net bone-protective), cardiovascular risk (premenopausal cardiovascular protection tracks with endogenous estrogen), mood, and cognition. Oral contraceptives suppress the ovarian cycle by suppressing FSH and LH and are one of the most widely used and well-studied classes of medication, with net benefits that extend beyond contraception in many cases.
Honest take
The biological fertility window is narrower than culture suggests, and AMH is not a reassurance marker for the unworried — it is a flag to plan around. Women who want biological children and are not sure they will try before 35 should at least discuss egg freezing by 30-32; the outcomes are substantially better when eggs are frozen younger, and the decision is often reversed by ignoring it until too late. Meanwhile, the menopause conversation has swung from "all HRT is dangerous" in the 2000s back toward "modern HRT is reasonable for most symptomatic women" in current guidelines, and the pendulum swing is confusing practitioners and patients. Look at the North American Menopause Society's current position — it is a more moderate and evidence-grounded document than the media narrative suggests.
Sources
- Teede et al., Fertility and Sterility (2023) — international guideline on PCOS.
- Webber et al., Human Reproduction — ESHRE guideline on premature ovarian insufficiency.
- The NAMS 2022 Hormone Therapy Position Statement, Menopause.
- Broekmans et al., Endocrine Reviews — ovarian aging and fertility decline.