In females, testosterone is produced by three sources in roughly equal measure: the ovaries, the adrenal glands, and peripheral tissues like fat and skin. Each contributes about 25%, 25%, and 50% respectively, with that last half coming from the conversion of precursor hormones made by the first two. The total amount is small compared to males, with normal levels in adult women falling below 40 ng/dL, but testosterone plays a meaningful role in bone health, sexual function, and energy throughout a woman’s life.
The Ovaries: Theca Cells and LH
The ovaries account for about 25% of circulating testosterone. The production happens in a specific layer of cells surrounding each developing egg follicle called theca cells. These cells respond to luteinizing hormone (LH) from the pituitary gland by ramping up androgen production, including testosterone, androstenedione, and a potent androgen called dihydrotestosterone.
This process is part of a well-established system known as the “two-cell, two-gonadotropin” model. Theca cells make androgens, and then neighboring granulosa cells convert some of those androgens into estrogen using an enzyme called aromatase. So testosterone in the ovary isn’t just an end product. It’s also a raw material for estrogen production, which is why the two hormones are more closely linked than most people realize.
Even after menopause, when estrogen production drops sharply, the ovaries continue making androgens. Women who have had both ovaries surgically removed show measurably lower testosterone levels than women who keep at least one ovary, confirming the ovaries remain an active testosterone source well past reproductive age.
The Adrenal Glands: Precursor Hormones
Sitting on top of each kidney, the adrenal glands contribute another 25% of circulating testosterone directly and produce the bulk of the precursor hormones that peripheral tissues later convert. The specific zone responsible is the innermost layer of the adrenal cortex, called the zona reticularis. This layer specializes in making two precursors: DHEA and its sulfated form, DHEAS.
What makes the zona reticularis unique is an enzymatic quirk. It has very low levels of a particular enzyme that would normally convert these precursors into other steroid hormones. That enzymatic block keeps the steroids on a pathway that favors androgen production. The adrenals also produce about half of the body’s circulating androstenedione, another key building block that gets converted to testosterone elsewhere in the body.
Because the adrenals operate somewhat independently of the ovarian cycle, they provide a steady baseline of androgen precursors regardless of where you are in your menstrual cycle or whether you’ve gone through menopause.
Peripheral Tissues: Fat, Skin, and Local Conversion
The remaining 50% of female testosterone comes not from a gland but from conversion happening in tissues throughout the body, particularly in fat (adipose tissue) and skin. These tissues contain their own set of steroid-processing enzymes that take androstenedione and DHEA delivered through the bloodstream and convert them into active testosterone.
Fat tissue is especially important. It contains both aromatase (which converts androgens to estrogens) and other enzymes that activate androgen precursors into testosterone. This means fat tissue acts as a local hormone factory, adjusting the balance of testosterone and estrogen based on enzyme activity in that specific location. After menopause, peripheral conversion in fat becomes the dominant source of both estrogens and active androgens, making body composition a real factor in hormone levels.
How the Brain Controls Production
Testosterone production doesn’t happen on autopilot. The hypothalamus in the brain releases a signaling hormone (GnRH) that tells the pituitary gland to secrete LH and FSH. LH is the primary driver of testosterone production in the ovaries, directly stimulating theca cells to make androgens. This forms a feedback loop: when androgen levels rise, they signal back to the pituitary to moderate LH release, keeping production in check.
Research on postmenopausal women shows this feedback loop persists even after estrogen levels drop. When researchers blocked androgen activity in postmenopausal women, LH release increased in response to GnRH stimulation, confirming that androgens still actively suppress pituitary signaling. The system stays responsive, even when the ovaries are no longer producing eggs.
How Testosterone Levels Change With Age
A common assumption is that testosterone drops at menopause, similar to estrogen. The reality is different. A landmark study of 1,400 women found that testosterone levels decline gradually starting around age 20 and are not tied to menopause itself. There were no measurable differences between women who were premenopausal, perimenopausal, or postmenopausal once age was accounted for.
The decline is significant but slow. Between ages 18 and 39, average testosterone levels drop by about 25%. Another 25% decline occurs between ages 40 and 58 or 59. By around age 60, levels have fallen roughly 50% from their peak. Then something unexpected happens: testosterone levels begin to subtly rise again, with this upward trend continuing into the eighth and ninth decades of life. Researchers have confirmed this pattern across multiple studies, though the reasons for the late-life increase aren’t fully settled.
What Testosterone Does in the Female Body
Testosterone isn’t just a “male hormone” that happens to be present in women. It serves direct biological functions. Bone mineral density depends on adequate testosterone alongside estrogen, and by menopause many women lack sufficient levels of both for optimal bone health. One in three women experience loss of sexual desire and arousal after menopause, and there is evidence linking this to declining testosterone. Research at Monash University has investigated whether restoring testosterone to premenopausal levels in postmenopausal women can improve both sexual function and bone density.
Beyond bones and libido, testosterone contributes to muscle maintenance, red blood cell production, and overall energy levels. Because so much of it is produced locally in tissues like fat and skin, its effects can vary by body site, not just by blood level.
When Production Goes Wrong: PCOS and Excess Testosterone
The most common condition involving testosterone overproduction in women is polycystic ovary syndrome (PCOS). In PCOS, two things converge to push testosterone levels up. High LH levels overstimulate the ovarian theca cells, causing them to produce excess androgens. At the same time, high insulin levels (common in PCOS) prevent the liver from making enough of a protein called sex hormone-binding globulin (SHBG). SHBG normally binds to testosterone in the blood, keeping it inactive. Without enough SHBG, more testosterone circulates in its free, active form.
This combination of overproduction and reduced binding creates the symptoms associated with hyperandrogenism: acne, excess facial or body hair, thinning scalp hair, and irregular periods. The root issue isn’t a new source of testosterone but a disruption in the regulation of the existing sources, primarily the ovaries responding too aggressively to hormonal signals.