Female hormones come primarily from the ovaries, but also from the adrenal glands, fat tissue, the brain, and during pregnancy, the placenta. Every one of these hormones starts from the same raw material: cholesterol. Your body converts cholesterol through a chain of enzymatic steps, first into a compound called pregnenolone, then into the specific hormones your tissues need. Where that conversion happens, and which hormone it produces, depends on the organ.
The Ovaries: The Main Source
The ovaries are the central production site for estrogen and progesterone during the reproductive years. Two types of cells within the ovaries handle most of this work: granulosa cells and theca cells, both found inside the follicles that house developing eggs. Theca cells produce androgens (male-type hormones) that serve as raw material. Those androgens are then converted into estradiol, the most potent form of estrogen, by neighboring granulosa cells. This is why ovarian estrogen production is tightly linked to the menstrual cycle: as follicles grow each month, estrogen output rises with them.
After ovulation, the empty follicle transforms into a temporary structure called the corpus luteum. This small gland-like body pumps out large amounts of progesterone, along with smaller amounts of estradiol. Progesterone’s job at this stage is to prepare the uterine lining for a potential pregnancy. If no pregnancy occurs, the corpus luteum breaks down after about 10 to 14 days, progesterone drops sharply, and menstruation begins.
The ovaries also produce about one quarter of a woman’s total testosterone. While testosterone is often thought of as a male hormone, it plays a role in energy, bone density, and sex drive in women too.
The Brain’s Role in Controlling Production
The ovaries don’t act on their own. A signaling chain that starts in the brain determines how much estrogen and progesterone they release at any given time. A small region at the base of the brain called the hypothalamus releases a signaling hormone in pulses. Those pulses tell the pituitary gland, a pea-sized structure just below it, to release two key hormones: follicle-stimulating hormone (FSH) and luteinizing hormone (LH).
FSH drives the growth of ovarian follicles and stimulates estrogen production. LH triggers ovulation and then maintains the corpus luteum so it can keep producing progesterone. The speed and strength of the hypothalamus’s pulses change throughout the menstrual cycle, which is why hormone levels rise and fall in a predictable pattern each month. When estrogen or progesterone levels get high enough, they send a signal back to the brain to slow down, creating a self-regulating feedback loop.
The Adrenal Glands
Sitting on top of each kidney, the adrenal glands are a secondary but important source of hormones in women. They produce large quantities of a weak androgen called DHEA (and its related form, DHEAS), which is actually the most abundantly produced steroid the adrenals make. On its own, DHEA has minimal hormonal activity. It acts as a precursor, a building block that other tissues convert into either stronger androgens or estrogens depending on local needs.
In women of reproductive age, adrenal precursors account for roughly two-thirds of total testosterone production and about half of another potent androgen called DHT. The remaining quarter of testosterone comes directly from the ovaries, and the final quarter from the adrenal glands themselves. The rest is assembled in tissues throughout the body from these adrenal building blocks.
Fat Tissue and Peripheral Conversion
Fat tissue is not just a storage depot. It actively produces estrogen through an enzyme called aromatase, which converts androgens into estrogen. Aromatase is found in immature fat cells (fibroblasts) rather than in fully mature fat cells. The ovaries, skin, and even the hypothalamus also express this enzyme, but fat tissue becomes especially significant in two situations: obesity and menopause.
In obese women, a greater mass of fat tissue means more aromatase-expressing cells, which increases local estrogen production. This is one reason obesity is linked to higher estrogen exposure and a greater risk of estrogen-sensitive breast cancer. Inflammatory signals that increase with excess body fat further ramp up aromatase activity, creating a cycle where more fat leads to more local estrogen production.
After menopause, when the ovaries largely stop producing estrogen, this peripheral conversion becomes the body’s primary estrogen source. The type of estrogen shifts too. Instead of estradiol (the dominant form during reproductive years), postmenopausal women primarily produce estrone, a weaker form. Essentially all postmenopausal estrone comes from the conversion of adrenal androgens in fat and other tissues, not from any meaningful ovarian or adrenal secretion of estrogen itself.
The Placenta During Pregnancy
During pregnancy, the placenta becomes a major hormone factory. For the first 10 weeks or so, the corpus luteum in the ovary continues producing the progesterone needed to sustain the pregnancy. Between weeks 10 and 12, the placenta takes over this role completely. By the time a pregnancy reaches full term, progesterone levels climb to 100 to 200 ng/ml, and the placenta is producing roughly 250 mg of progesterone per day, a dramatic increase over non-pregnant levels.
The placenta also produces large amounts of estrogen and human chorionic gonadotropin (hCG), the hormone detected by pregnancy tests. Rising estrogen during pregnancy triggers a five- to tenfold increase in a transport protein called SHBG, which binds to sex hormones in the blood and keeps them inactive. This surge in SHBG appears to protect the mother from the effects of the dramatically higher androgen levels that pregnancy also brings. In rare cases where women produce very little SHBG due to genetic variation, they can develop signs of excess androgens during pregnancy, like increased body hair and acne.
Oxytocin and Prolactin
Not all female hormones are steroids built from cholesterol. Oxytocin is a protein hormone made in the hypothalamus and released during childbirth, where it stimulates uterine contractions. After birth, when a baby suckles, nerve signals travel to the brain and trigger oxytocin release, causing the “milk letdown reflex” that pushes breast milk toward the nipple.
Prolactin, the hormone that drives milk production itself, comes from a different location: specialized cells in the front portion of the pituitary gland. Prolactin secretion increases in response to suckling, stress, sleep, and rising estrogen levels. Between feedings, the hypothalamus keeps prolactin in check by releasing dopamine, which acts as a brake on its production.
How Hormones Travel Through the Body
Once released, most sex hormones don’t float freely through the bloodstream. They attach to carrier proteins, primarily SHBG and a general-purpose protein called albumin. Only a small “free” fraction remains unbound, and this free fraction is what actually enters cells and produces biological effects. The balance between total hormone levels and the amount of carrier protein determines how much active hormone your tissues see.
This matters in conditions like polycystic ovary syndrome (PCOS), where SHBG levels tend to be lower than normal. With less carrier protein available to bind testosterone, a higher percentage circulates in its free, active form. The result is androgen excess: acne, excess hair growth, and irregular cycles, even when total testosterone may not be dramatically elevated. Obesity worsens this pattern, because excess weight further suppresses SHBG while also raising androgen production from fat tissue and the adrenals.