Androgens (in women)

Androgens are a group of steroid hormones that includes testosterone, DHEA, DHEA-S, and androstenedione. They are usually framed as "male hormones," but they are produced and used by women's bodies in important ways. The right level supports libido, mood, muscle, bone, and energy. Excess androgens drive the cluster of symptoms that defines PCOS and related conditions.

The major androgens in women

Four hormones do most of the work:

Testosterone. The most studied. Produced by the ovaries (25%), adrenal glands (25%), and peripheral conversion from precursors (50%).
DHEA and DHEA-S. Mostly from the adrenal glands. Acts as a precursor that converts to testosterone and estrogen in peripheral tissues.
Androstenedione. A precursor that converts to either testosterone or estrogen depending on which enzymes the tissue expresses.

Women produce roughly 10 to 15% as much testosterone as men. The amount is small but the receptors are sensitive: small shifts produce noticeable effects.

What androgens do in women

The functional roles:

Libido. Androgens are the primary driver of sexual desire in both sexes. The mid-cycle libido rise tracks with the small testosterone bump around ovulation.
Muscle and bone. Maintain lean mass and bone density. Postmenopausal androgen decline contributes to sarcopenia and osteoporosis risk alongside estrogen loss.
Mood and motivation. Androgens support dopaminergic signaling. Low androgens can present as low motivation, low mood, and reduced sense of well-being.
Skin and hair. Drive sebum production and the activity of hair follicles, especially in androgen-sensitive areas (face, chest, abdomen, back).
Substrate for estrogen. Aromatase converts androgens to estrogens. This is the main source of estrogen after menopause.

How androgens cycle

Unlike estrogen and progesterone, androgens have only modest cyclic variation:

Testosterone has a small mid-cycle peak around ovulation, driven by ovarian thecal cell activity under LH stimulation.
DHEA-S does not have meaningful cycle variation.
The mid-cycle libido bump that some women notice tracks more with the testosterone peak than with estrogen.

Androgen excess: the clinical picture

Elevated androgens produce a recognizable cluster of symptoms:

Hirsutism. Coarse dark hair growth in androgen-sensitive areas (face, chest, abdomen, lower back). Scored clinically with the Ferriman-Gallwey scale.
Hormonal acne. Especially along the jawline, chin, and lower face. Often persists into adulthood.
Androgenic alopecia. Thinning at the crown and temples (in contrast to female-pattern thinning that affects the whole scalp).
Cycle irregularity. Anovulatory cycles, long cycles (over 35 days), or amenorrhea.
Insulin resistance. Especially in PCOS, where insulin and androgens reinforce each other.
Voice and clitoral changes at very high levels (rare, usually points to a more serious source like an androgen-secreting tumor).

Sources of androgen excess

When androgens are elevated, the source matters:

Ovarian. Most often PCOS. Testosterone is typically the elevated androgen, with normal or only modestly elevated DHEA-S.
Adrenal. Non-classical congenital adrenal hyperplasia (NCAH), Cushing's syndrome, or rare adrenal tumors. DHEA-S is typically elevated.
Mixed. Many women with PCOS have both ovarian and adrenal contributions.
Exogenous. DHEA supplementation, anabolic steroids, certain medications.
Insulin-driven. High insulin (from insulin resistance) directly stimulates ovarian testosterone production and lowers SHBG, increasing free testosterone.

Testing

Useful tests, drawn ideally on days 2 to 5 of the cycle (or any day if cycles are irregular):

Total testosterone. Standard but limited because most is bound to SHBG.
Free testosterone or calculated free testosterone from total testosterone and SHBG. More informative than total alone.
DHEA-S. Identifies adrenal contribution.
Androstenedione. Useful when other markers are equivocal.
17-hydroxyprogesterone. Screens for non-classical congenital adrenal hyperplasia, which mimics PCOS.

A single normal testosterone reading does not rule out androgen excess if symptoms are clear. The pattern of multiple markers and clinical features matters more than any single number.

Free versus total testosterone

SHBG binds testosterone in the blood. Only the unbound (free) fraction is biologically active. This matters because:

A woman with normal total testosterone but low SHBG can have high free testosterone and androgen excess symptoms.
A woman with high total testosterone but high SHBG can have normal free testosterone and few symptoms.
Insulin resistance lowers SHBG, which amplifies the effect of any given testosterone level. This is part of why PCOS symptoms worsen with weight gain.

Androgen excess and cycle syncing

The practical implication: women with elevated androgens often cannot follow the standard cycle syncing template because their cycles are too irregular for phase-based scheduling to work as written. The cycle syncing for PCOS considerations apply: anchor scheduling to symptoms (ovulation confirmation via BBT, cervical mucus, or OPK) rather than calendar dates.

Low androgens in women

The opposite problem (low androgens) is less commonly diagnosed but real:

Low libido that does not respond to relationship or stress interventions.
Persistent low mood and low motivation distinct from depression.
Loss of muscle mass and strength despite normal training and nutrition.
Postmenopausal women, especially those with surgical menopause, often have low androgens contributing to symptoms.
Adrenal insufficiency and certain pituitary conditions.

Androgen replacement in women is controversial. The risks (cardiovascular, acne, voice change) at therapeutic doses are real, and the benefits are smaller than the marketing suggests.

Testosterone in women: the most clinically relevant androgen
DHEA: the adrenal precursor
SHBG: why free versus total matters
PCOS: the most common cause of androgen excess