How Many Hormones Do Females Have and What They Do

There is no single number that captures “how many hormones females have,” because the human body produces well over 50 distinct hormones, and every one of them circulates in both sexes. What differs is the concentrations, the cyclic patterns, and the reproductive roles certain hormones play. A handful of hormones, including estradiol, progesterone, follicle-stimulating hormone (FSH), and luteinizing hormone (LH), orchestrate the menstrual cycle and pregnancy in ways that have no male equivalent. But the full cast extends much further than most people realize, looping in insulin, cortisol, thyroid hormones, melatonin, and even a brain-derived peptide called kisspeptin that acts as a gatekeeper for puberty itself.

The Hormones Most People Think of First

When someone asks about “female hormones,” they usually mean estrogen and progesterone. These two are the dominant sex steroids produced by the ovaries, and they are responsible for most of the physical changes associated with female development and the menstrual cycle. Estrogen, primarily in the form of estradiol, drives breast development, widens the pelvis during puberty, thickens the uterine lining in the first half of each cycle, and helps maintain bone density. Progesterone rises sharply after ovulation, stabilizing the uterine lining for a potential pregnancy and then dropping if no embryo implants, which triggers menstruation.

What surprises many people is the role androgens play. Testosterone, androstenedione, and dehydroepiandrosterone (DHEA) are all produced in the female body, mainly by the ovaries and adrenal glands. Total testosterone production in premenopausal women runs roughly 0.1 to 0.4 milligrams per day, and androgens as a group are actually produced in greater quantities than estrogens.1Sexual Medicine Reviews. Role of Androgens in Female Genitourinary Tissue Structure and Function: Implications in the Genitourinary Syndrome of Menopause These androgens support libido, muscle mass, and bone health. Some are also converted into estradiol in peripheral tissues, which is why the line between “male” and “female” hormones is blurrier than the popular framing suggests.2PubMed. Androgen production in women

The Brain Hormones That Run the Menstrual Cycle

Estrogen and progesterone do not act alone. They take orders from and send feedback to a chain of hormones that starts deep in the brain. The hypothalamus releases gonadotropin-releasing hormone (GnRH) in pulses, which tells the pituitary gland to secrete FSH and LH.3Recent Progress in Hormone Research. The Neuroendocrine Control of the Menstrual Cycle FSH coaxes immature follicles in the ovary to grow and produce estradiol; LH triggers the mature follicle to release an egg at ovulation. After ovulation, the empty follicle becomes the corpus luteum and pumps out progesterone.

The clever part is feedback. During the first half of the cycle, rising estradiol tells the pituitary to hold back on FSH (negative feedback), keeping only one or two follicles growing to dominance. Then, once estradiol reaches a critical threshold, it flips to positive feedback and triggers the massive LH surge that causes ovulation.4Human Reproduction Update. Ovarian feedback, mechanism of action and possible clinical implications After ovulation, progesterone slows GnRH pulses, essentially quieting the system until the next cycle begins.5PubMed. A simple model of estrous cycle negative and positive feedback regulation of GnRH secretion This back-and-forth between the brain and the ovaries repeats roughly every 28 days, though normal cycles can range from about 21 to 35 days.

Kisspeptin and the Start of Puberty

Before any of this cycling can begin, the brain has to “wake up” the reproductive axis. A peptide called kisspeptin, produced by neurons in the hypothalamus, is now recognized as a key trigger. Kisspeptin binds to its receptor and stimulates GnRH release, which in turn drives the pituitary to start producing FSH and LH at adult levels.6PubMed Central. The Role of Kisspeptin in the Control of the Hypothalamic-Pituitary-Gonadal Axis and Reproduction Without a functioning kisspeptin system, puberty does not begin.7PubMed Central. The Role of Kisspeptin in Female Reproduction

Beyond its role in puberty, kisspeptin continues to regulate follicle development, egg maturation, and ovulation throughout a woman’s reproductive years. Researchers are now exploring kisspeptin-based therapies for conditions where ovulation fails to happen normally, making it one of the more exciting areas in reproductive endocrinology.

Anti-Müllerian Hormone and Ovarian Reserve

Anti-Müllerian hormone (AMH) is produced by the granulosa cells of small growing follicles in the ovary. Its job is essentially traffic control: AMH slows the rate at which dormant follicles get recruited into the growth pipeline and reduces how sensitive follicles are to FSH, preventing too many from developing at once.8PubMed. Anti-Müllerian hormone and its role in ovarian function This keeps the ovarian reserve from being depleted too quickly.

AMH has also become a widely used clinical marker. A blood test measuring AMH gives a rough snapshot of how many growing follicles remain, which is useful for fertility counseling and planning assisted reproduction.9PubMed. Anti-Müllerian hormone and folliculogenesis It is worth knowing that AMH tells you about the remaining pool of follicles, not about egg quality. A low AMH does not automatically mean a woman cannot conceive naturally, but it does signal that the window may be narrower.

Pregnancy Hormones Beyond the Usual Suspects

Pregnancy introduces hormones that barely register outside of it. Human chorionic gonadotropin (hCG) is the hormone detected by pregnancy tests. It is produced by the developing placenta and keeps the corpus luteum alive so that progesterone production continues until the placenta can take over. Alongside hCG, placental lactogen and prolactin help prepare the body for milk production and nutrient delivery to the fetus.10PubMed Central. The human placenta: new perspectives on its formation and function during early pregnancy

Relaxin, another pregnancy-associated hormone structurally related to insulin, loosens ligaments and connective tissue to allow the pelvis to widen for delivery. It does this by activating enzymes that break down collagen in cartilage and tendons.11PubMed Central. The effect of relaxin on the musculoskeletal system This is one reason pregnant women sometimes experience joint laxity and back pain. Relaxin also plays roles in bone remodeling and healing of injured muscles and ligaments outside of pregnancy, though at much lower levels.

During lactation, prolactin drives milk synthesis while oxytocin triggers the “let-down” reflex that ejects milk from the breast.12PubMed Central. Prolactin regulation of oxytocin neurone activity in pregnancy and lactation Oxytocin is also released during skin-to-skin contact, labor contractions, and orgasm. It has been called the “bonding hormone,” though that label oversimplifies what is really a versatile signaling molecule involved in social behavior, anxiety regulation, and uterine contractions.

Leptin and the Link Between Energy and Fertility

Your body will not invest in reproduction if it senses an energy crisis. Leptin, a hormone produced by fat tissue, acts as the messenger that conveys energy status to the brain. When body fat drops too low, leptin levels fall, and the hypothalamus responds by dialing down GnRH pulses. The result can be hypothalamic amenorrhea, a condition where periods stop because the brain has essentially decided the body cannot support a pregnancy.

This is not speculation. In a randomized controlled trial, women with hypothalamic amenorrhea who received replacement doses of recombinant leptin over 36 weeks recovered menstruation and saw their reproductive, thyroid, and growth hormone axes normalize.13PubMed Central. Leptin is an effective treatment for hypothalamic amenorrhea Earlier work had already shown that leptin treatment increased LH levels, pulse frequency, and follicular development within just a few weeks.14PubMed. Recombinant human leptin in women with hypothalamic amenorrhea Even women with hypothalamic amenorrhea who maintain a normal body weight tend to have lower leptin levels than matched controls, suggesting it is not just about how much you weigh but about the ratio between energy stores and energy expenditure.15Human Reproduction. Leptin in functional hypothalamic amenorrhoea

Insulin, Androgens, and PCOS

Insulin, best known for regulating blood sugar, has a direct line to the ovaries. When insulin levels stay chronically elevated, as happens with insulin resistance, the ovaries and adrenal glands ramp up androgen production independently of the normal gonadotropin signals.16PubMed Central. Role of insulin and insulin resistance in androgen excess disorders This is a core feature of polycystic ovary syndrome (PCOS), the most common endocrine disorder in women of reproductive age.

The relationship runs in both directions. Excess testosterone from ovarian overproduction worsens insulin resistance, which raises insulin further, which drives even more androgen production. This vicious cycle helps explain why PCOS can be so stubborn to manage and why lifestyle interventions targeting insulin sensitivity, like exercise and dietary changes, often improve hormonal markers alongside metabolic ones.17PubMed Central. Association of Insulin Resistance and Elevated Androgen Levels with Polycystic Ovarian Syndrome (PCOS): A Review of Literature

Cortisol and Reproductive Shutdown Under Stress

Cortisol, the primary stress hormone, is produced by the adrenal glands in both sexes. In women, it interacts with reproductive hormones in ways that can suppress the menstrual cycle. Chronic psychological or physical stress raises cortisol, which in turn can inhibit GnRH pulses and lower gonadotropin levels.18Reproduction. Impact of psychosocial stress on gonadotrophins and sexual behaviour in females: role for cortisol?

Progesterone appears to dampen this stress response. In a study of acute psychosocial stress, higher progesterone levels in women correlated with lower cortisol and adrenocorticotropic hormone (ACTH) responses, suggesting a protective effect.19PubMed Central. Hypothalamic-pituitary-adrenal axis response to acute psychosocial stress: Effects of biological sex and circulating sex hormones This may partly explain why some women feel more resilient to stress during the luteal phase, when progesterone peaks, though individual variation is large and other factors are clearly involved.

Progesterone, Aldosterone, and Fluid Balance

Many women notice bloating or water retention at specific points in their cycle. The hormonal explanation involves an interaction between progesterone and aldosterone, a hormone produced by the adrenal glands that regulates sodium and water balance. During the luteal phase, when progesterone is high, aldosterone levels rise as well. Research shows that progesterone may directly stimulate aldosterone production, independent of the renin-angiotensin system that normally controls it.20The Journal of Clinical Endocrinology & Metabolism. Relationship between Aldosterone and Progesterone in the Human Menstrual Cycle

At the same time, progesterone competes with aldosterone at the kidney. It can block some of aldosterone’s sodium-retaining effects, acting almost like a natural diuretic.21The Journal of Clinical Endocrinology & Metabolism. Inhibition of the Sodium-Retaining Influence of Aldosterone by Progesterone The net effect on fluid retention depends on which side of this tug-of-war wins in a given woman at a given time. Studies confirm that progesterone can increase plasma volume on its own,22PubMed. Progesterone increases plasma volume independent of estradiol which helps explain the cyclical weight fluctuations that are entirely normal and hormonally driven.

Thyroid Hormones and the Menstrual Cycle

Thyroid hormones (T3 and T4) are not sex hormones, but they influence the reproductive system more than most people realize. In a longitudinal study of premenopausal women, those with higher total T4 levels had greater peak progesterone metabolites during the luteal phase and higher estrogen metabolites during the follicular phase compared to women with lower T4.23PubMed Central. Thyroid hormones and menstrual cycle function in a longitudinal cohort of premenopausal women In clinical practice, both underactive and overactive thyroid function are well-known disruptors of menstrual regularity and fertility. Screening thyroid function is a standard step when investigating irregular periods or difficulty conceiving.

Melatonin and the Ovary

Melatonin, the hormone most associated with sleep and circadian rhythm, is produced mainly by the pineal gland in response to darkness. Its relevance to female reproductive health is becoming clearer. Melatonin receptors are present in ovarian tissue, and the hormone acts as a potent antioxidant, protecting developing eggs from oxidative damage. Research indicates that melatonin can delay ovarian aging, help regulate the ovarian biological clock, promote follicle formation, and improve oocyte quality and fertilization rates.24PubMed Central. Research progress of melatonin (MT) in improving ovarian function: a review of the current status This is part of why chronic sleep disruption and shift work have been linked to menstrual irregularity and reduced fertility, though the evidence is still being refined.

Neurosteroids and Mood Across the Cycle

One of the more fascinating recent developments involves allopregnanolone (often shortened to ALLO), a metabolite of progesterone produced in the brain. ALLO enhances the activity of GABA receptors, the brain’s main calming system. In most women, rising ALLO during the luteal phase has a mild sedative and anxiety-reducing effect. But in women with premenstrual dysphoric disorder (PMDD), the brain’s GABA receptors appear to respond abnormally to these fluctuations, triggering severe mood symptoms instead of calm.25PubMed Central. Allopregnanolone in premenstrual dysphoric disorder (PMDD): Evidence for dysregulated sensitivity to GABA-A receptor modulating neuroactive steroids across the menstrual cycle

This reframes PMDD not as “too much” or “too little” of any hormone, but as an atypical brain response to normal hormonal changes. A naturally occurring mirror-image molecule called isoallopregnanolone has been shown to counteract ALLO’s effects at the GABA receptor and alleviate PMDD symptoms in early research.26Translational Psychiatry. Emotion-induced brain activation across the menstrual cycle in individuals with premenstrual dysphoric disorder and associations to serum levels of progesterone-derived neurosteroids Meanwhile, brexanolone, a synthetic form of ALLO given intravenously, is already approved for postpartum depression, making neurosteroids one of the few areas where basic hormone science has rapidly translated into approved treatments.

What Changes at Menopause

As the ovarian follicle supply dwindles in a woman’s 40s, estradiol and progesterone production becomes erratic and eventually drops to very low baseline levels. The pituitary responds by cranking up FSH in an attempt to stimulate follicles that are no longer there. FSH levels begin climbing roughly six years before the final menstrual period and eventually reach a plateau about 14 times higher than typical FSH levels in men.27PubMed Central. Follicle-stimulating hormone: More than a marker for menopause This dramatic shift is not just a marker of menopause. Researchers are now investigating whether chronically elevated FSH itself contributes to conditions associated with the menopausal transition, including bone loss, changes in body fat distribution, and psychiatric symptoms like depression and anxiety.

Androgen levels decline more gradually than estrogen. The ovaries continue producing small amounts of testosterone after menopause, and the adrenal glands keep making DHEA, though at lower levels than in younger years. This is partly why some postmenopausal women maintain reasonable libido and muscle mass while others do not: the degree of residual androgen production varies considerably from person to person.