Lab result explainedHormonesLast updated November 11, 2026

Androstenedione test: normal range in females and males, and what high or low levels mean

Androstenedione · Androgen or hirsutism panel (ordered with total and free testosterone, DHEA-S, SHBG and 17-hydroxyprogesterone); congenital adrenal hyperplasia monitoring · reported in ng/dL (SI units nmol/L; 1 ng/dL = 0.0349 nmol/L)

Androstenedione is a steroid hormone made in roughly equal amounts by the adrenal glands and the ovaries (or testes), and it sits one step before testosterone and estrone in the body's hormone assembly line. It has weak androgen activity of its own, about a tenth that of testosterone, but tissues such as skin, fat and hair follicles convert it locally into testosterone and estrogen, which is why a high level can cause acne, excess facial and body hair and irregular periods even when testosterone itself is only mildly raised. In adult women it typically runs between about 30 and 200 ng/dL before menopause, and in adult men about 40 to 150 ng/dL, with lab-specific ranges.

The test is ordered mostly in women with signs of androgen excess: hirsutism, acne, hair thinning on the scalp, irregular or absent periods, or difficulty conceiving. The common finding is a mildly raised level with polycystic ovary syndrome (PCOS), where androstenedione is elevated in a fifth to a third of women and is sometimes the only androgen above range. It is also the best single blood marker for monitoring treatment of congenital adrenal hyperplasia (CAH), because it reflects how well steroid replacement is suppressing the adrenal overproduction. Very high values, several times the upper limit, raise the question of an adrenal or ovarian tumor and lead quickly to imaging.

Interpreting the number depends on context. Levels peak in the morning and in the days before ovulation, are higher in adolescence than in midlife, fall by about half after menopause, and are pushed up by stress, obesity and insulin resistance. Androstenedione is also sold illicitly as 'andro', a supplement banned in the US since 2004, and DHEA supplements raise it, so medications and supplements are part of the picture. Reference ranges differ between labs, and immunoassays overestimate low values compared with the mass-spectrometry methods most reference labs now use, so a borderline result on one method may be normal on another.

Androstenedione at a glance

  • What it is: an adrenal and ovarian/testicular steroid that is converted to testosterone and estrone; a weak androgen in its own right and a marker of adrenal and ovarian androgen output.
  • Normal (LC-MS/MS, adults): premenopausal women about 30–200 ng/dL, postmenopausal about 20–75 ng/dL, men about 40–150 ng/dL. Prepubertal children are usually under 50 ng/dL. Labs differ; some report nmol/L (multiply ng/dL by 0.0349).
  • Mildly high (up to about 2 times the upper limit) in a woman with irregular periods, acne or hirsutism: most often PCOS; also non-classic congenital adrenal hyperplasia, obesity and insulin resistance, Cushing's syndrome or DHEA/androstenedione supplements.
  • Very high (above about 500 ng/dL, or more than 3–4 times the upper limit), especially with rapid-onset virilization or a testosterone above 150–200 ng/dL: adrenal or ovarian tumor until imaging says otherwise.
  • Low: adrenal insufficiency, pituitary failure, menopause or ovarian failure, glucocorticoid treatment, or over-treatment of CAH; rarely important on its own.
  • Next step: read with testosterone, DHEA-S, SHBG, 17-hydroxyprogesterone, LH/FSH and prolactin; draw in the morning, in the early follicular phase if cycling, and off DHEA or 'andro' supplements.

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What Androstenedione measures

Androstenedione is produced from 17-hydroxyprogesterone (through the enzyme 17,20-lyase) and from DHEA (through 3-beta-hydroxysteroid dehydrogenase) in the adrenal zona reticularis and in the theca cells of the ovary and Leydig cells of the testis. About half of a woman's androstenedione comes from each source, which is why the pattern of the other hormones helps locate a problem: DHEA-S comes almost entirely from the adrenal, testosterone in women largely from the ovary. Androstenedione is then converted to testosterone by 17-beta-hydroxysteroid dehydrogenase or to estrone by aromatase, mostly in fat tissue, which makes it the main source of estrogen after menopause.

Most reference laboratories now measure androstenedione by liquid chromatography tandem mass spectrometry (LC-MS/MS), which is specific and accurate down to a few ng/dL. Older immunoassays cross-react with related steroids and read 20 to 50 percent higher at the low end, so a 'high' result from an immunoassay in a woman or child may normalize on mass spectrometry. Because the hormone follows the cortisol rhythm, levels are highest between 7 and 9 am and can be 30 to 40 percent lower in the afternoon; a morning fasting sample is standard. In cycling women, levels rise around ovulation and in the luteal phase, so testing in the first week of the cycle (days 2 to 5) gives the most reproducible baseline.

Androstenedione is the preferred monitoring hormone in classic congenital adrenal hyperplasia because 17-hydroxyprogesterone swings too widely with stress and timing, while androstenedione more closely reflects the overall adrenal androgen drive: a level in the age- and sex-appropriate range with a 17-hydroxyprogesterone that is somewhat above normal is the target, since fully normalizing 17-hydroxyprogesterone means the glucocorticoid dose is too high. Androstenedione is also measured in children with early puberty or ambiguous genitalia, and occasionally in men with hypogonadism to look at adrenal versus testicular contribution.

Normal range for Androstenedione

Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.

GroupTypical range (ng/dL (SI units nmol/L; 1 ng/dL = 0.0349 nmol/L))Notes
Adult women, premenopausal (LC-MS/MS)About 30–200 ng/dLSome labs quote 25–220 or 50–250 depending on method and age band. Highest in the late teens and twenties and around ovulation.
Adult women, postmenopausalAbout 20–75 ng/dLFalls by roughly half after menopause as ovarian production stops; the adrenal becomes the main source.
Adult menAbout 40–150 ng/dLDeclines slowly with age; a man's testosterone is mostly made directly in the testis, so androstenedione is rarely the key androgen in men.
Children, prepubertal (1–8 years)Usually below 50 ng/dL (often below 25)Rises with adrenarche from about age 6–8 and through puberty; pediatric age- and Tanner-stage ranges are used.
NewbornsUp to about 300 ng/dL in the first weekFrom the fetal adrenal; falls over the first months. Not used alone to diagnose congenital adrenal hyperplasia, which is screened with 17-hydroxyprogesterone.
PCOS, typicalUpper-normal to about 2 times the upper limit (roughly 150–400 ng/dL)Elevated in 20–35 percent of women with PCOS; sometimes the only raised androgen. Correlates with insulin resistance and metabolic risk.
Non-classic congenital adrenal hyperplasiaOften 150–500 ng/dL, with 17-hydroxyprogesterone above 200 ng/dL (morning, follicular)17-hydroxyprogesterone above 1,000 ng/dL basal or after ACTH stimulation confirms the diagnosis.
Suggestive of an androgen-secreting tumorAbove about 500–1,000 ng/dL, or more than 3–4 times the upper limitEspecially with total testosterone above 150–200 ng/dL (ovarian) or DHEA-S above 700 µg/dL (adrenal) and rapid-onset virilization. Imaging follows.
Classic CAH on treatment, targetWithin the age- and sex-specific normal range (morning, before the steroid dose)With 17-hydroxyprogesterone mildly above normal; a suppressed androstenedione suggests over-treatment.

High androstenedione

A high androstenedione means the adrenal glands, the ovaries (or testes) or both are making more androgen precursor than usual, and the degree of elevation and the company it keeps point to the source. In a woman with irregular periods, acne or hirsutism and an androstenedione up to about twice the upper limit, PCOS is by far the most likely explanation: the ovarian theca cells overproduce androgens under the combined push of excess LH and insulin, and androstenedione is raised in roughly a quarter of women with PCOS, often alongside a high-normal or mildly raised testosterone and a low SHBG. Women with PCOS whose androstenedione is high tend to have more insulin resistance and a less favorable metabolic profile than those with a normal level, which makes it a useful marker beyond diagnosis.

If DHEA-S is also high, the adrenal is contributing, and the key next test is a morning follicular-phase 17-hydroxyprogesterone to look for non-classic congenital adrenal hyperplasia, a partial deficiency of the 21-hydroxylase enzyme that affects about 1 in 200 to 1 in 1,000 people in general and up to 1 in 30 in some ancestries. It looks exactly like PCOS clinically, but is treated differently and matters for pregnancy planning. Other adrenal causes include Cushing's syndrome, where cortisol excess comes with androgen excess, and simple obesity, where insulin and inflammation raise adrenal and ovarian androgen output modestly. Androstenedione and DHEA supplements raise the level directly, and some 'prohormone' and bodybuilding products contain them despite the ban.

Very high levels change the urgency. An androstenedione above about 500 to 1,000 ng/dL, or any level with a total testosterone above 150 to 200 ng/dL or a DHEA-S above 700 µg/dL, particularly in a woman whose symptoms started suddenly and progressed quickly (deepening voice, clitoral enlargement, male-pattern balding, muscle bulk), raises the possibility of an androgen-secreting tumor of the adrenal or ovary. These are rare (well under 1 percent of women evaluated for hirsutism) but are found with adrenal CT or pelvic ultrasound, and surgery is usually curative. In postmenopausal women, ovarian hyperthecosis, a non-cancerous overgrowth of androgen-producing ovarian tissue, produces a similar picture with high testosterone and androstenedione. In children, a raised androstenedione with early pubic hair, body odor or growth acceleration is evaluated for premature adrenarche, CAH and tumors; in men it is rarely the primary finding and usually accompanies a high DHEA-S from an adrenal source or anabolic steroid use.

Common causes

  1. Polycystic ovary syndrome (PCOS)

    The commonest cause in women. Excess LH and insulin drive ovarian theca cells to overproduce androstenedione and testosterone; 20–35 percent of women with PCOS have a raised androstenedione, and it may be the only abnormal androgen. Levels are usually under twice the upper limit.

  2. Non-classic congenital adrenal hyperplasia (21-hydroxylase deficiency)

    A partial enzyme block diverts adrenal steroid precursors toward androgens. Presents like PCOS in adolescence or adulthood; diagnosed by a morning follicular 17-hydroxyprogesterone above 200 ng/dL (screen) and above 1,000 ng/dL basal or after ACTH stimulation (confirm).

  3. Classic congenital adrenal hyperplasia (under-treated)

    In children and adults with classic CAH, a high androstenedione means the glucocorticoid dose is not suppressing adrenal androgen output; it is the main hormone used to adjust treatment, together with growth in children and menstrual regularity in women.

  4. Obesity and insulin resistance

    High insulin stimulates ovarian and adrenal androgen production and lowers SHBG; androstenedione rises modestly with BMI and falls with weight loss. Common in prediabetes and type 2 diabetes even without PCOS.

  5. Androgen-secreting adrenal tumor

    Adrenal adenomas and carcinomas can secrete DHEA-S, androstenedione and testosterone in large amounts; adrenal carcinoma often also produces cortisol. Suspected with DHEA-S above 700 µg/dL and rapid virilization; CT or MRI of the adrenals follows.

  6. Androgen-secreting ovarian tumor or hyperthecosis

    Sertoli-Leydig cell tumors, hilus cell tumors and granulosa-theca tumors raise testosterone (usually above 150–200 ng/dL) and androstenedione with normal DHEA-S. Ovarian hyperthecosis in postmenopausal women produces a slower, similar picture.

  7. Cushing's syndrome

    ACTH-dependent Cushing's drives the whole adrenal cortex, so cortisol excess comes with high DHEA-S and androstenedione; adrenal adenomas causing Cushing's usually have low androgens instead.

  8. Supplements and medications

    DHEA and androstenedione ('andro') supplements are converted directly to androstenedione; some bodybuilding prohormones contain them despite being controlled substances since 2004. Valproate raises androgens in women; danazol and some progestins have androgenic effects.

  9. Premature adrenarche in children

    Early activation of adrenal androgen production (pubic hair, body odor, acne before age 8 in girls or 9 in boys) with mildly raised DHEA-S and androstenedione for age; usually benign but is distinguished from CAH and tumors by the degree of elevation and bone age.

  10. Hyperprolactinemia and hypothyroidism

    High prolactin stimulates adrenal androgen output modestly and disturbs ovulation; severe hypothyroidism lowers SHBG and can raise free androgens. Both are checked in any androgen excess work-up.

Symptoms that can go with it

  • Excess coarse hair on the face, chest, abdomen or back (hirsutism) in women
  • Acne that persists past adolescence or is resistant to standard treatment
  • Thinning hair at the crown or temples (androgenic alopecia)
  • Irregular, infrequent or absent periods, and difficulty conceiving
  • Oily skin and, in some women, darkened velvety skin in the neck and armpit folds (acanthosis nigricans) from insulin resistance
  • Rapid-onset deepening of the voice, enlarged clitoris, increased muscle bulk or male-pattern baldness, which suggest a tumor and need prompt evaluation
  • Weight gain around the middle, easy bruising, a rounded face and purple stretch marks when Cushing's syndrome is the cause
  • In children: early pubic hair, body odor, acne or a growth spurt before age 8–9

Low androstenedione

A low androstenedione is seldom a problem in itself, because the hormone is a precursor rather than an end product and its own androgenic effect is weak. It usually reflects reduced output from one or both of its sources: the adrenal glands (Addison's disease, pituitary ACTH deficiency, or suppression by prescribed glucocorticoids such as prednisone), the ovaries (menopause, premature ovarian insufficiency, surgical removal of the ovaries, or suppression by combined oral contraceptives, which lower androstenedione by about 20 to 30 percent) or the testes (hypogonadism). In each case the diagnosis is made from the main hormones of that gland, cortisol and ACTH, estradiol and FSH, or testosterone and LH, with androstenedione as supporting evidence.

The one setting where a low value is specifically acted on is congenital adrenal hyperplasia. In someone with classic CAH on hydrocortisone or prednisolone, a suppressed androstenedione (below the age- and sex-appropriate range), especially with a fully normalized 17-hydroxyprogesterone, means the glucocorticoid dose is higher than it needs to be, which over years costs growth in children and bone density, weight and blood pressure in adults, so the dose is reduced. In women with low libido or fatigue, low adrenal androgens (DHEA-S and androstenedione) are sometimes measured, but trials of DHEA replacement in adrenal insufficiency show at most modest benefits in well-being and the Endocrine Society does not recommend androgen testing or treatment for low libido on the basis of a blood level alone.

Common causes

  1. Primary adrenal insufficiency (Addison's disease)

    Autoimmune or other destruction of the adrenal cortex removes the adrenal half of androstenedione production, alongside low cortisol and DHEA-S and a high ACTH. Women with Addison's often lose pubic and axillary hair for this reason.

  2. Pituitary ACTH deficiency and glucocorticoid treatment

    Without ACTH drive, the zona reticularis shrinks and adrenal androgens fall; prednisone, dexamethasone and even high-dose inhaled or topical steroids suppress them in the same way. Levels recover slowly after steroids are stopped.

  3. Menopause, ovarian insufficiency and oophorectomy

    Loss of ovarian theca cell production roughly halves androstenedione; premature ovarian insufficiency and surgical menopause do the same at a younger age, with high FSH and low estradiol.

  4. Male hypogonadism

    Testicular failure (high LH) or pituitary hypogonadism (low LH) lowers testosterone and, to a lesser extent, androstenedione; the adrenal contribution keeps it from falling to zero.

  5. Combined oral contraceptives and GnRH analogs

    Estrogen-progestin pills suppress LH and ovarian androgen output and raise SHBG, lowering androstenedione by 20–30 percent and free testosterone by more; GnRH agonists and antagonists suppress ovarian and testicular production more completely.

  6. Over-treatment of congenital adrenal hyperplasia

    A glucocorticoid dose high enough to fully suppress 17-hydroxyprogesterone also suppresses androstenedione below normal; this is the signal to reduce the dose.

  7. Severe illness, anorexia nervosa and opioid use

    Critical illness shifts adrenal output toward cortisol and away from androgens; chronic starvation and long-term opioids suppress both gonadal and adrenal androgens.

Symptoms that can go with it

  • Often none; low androstenedione rarely causes symptoms by itself
  • Fatigue, weight loss, dizziness on standing, salt craving and darkening of the skin when the cause is Addison's disease, which needs prompt testing
  • Loss of pubic and underarm hair, low libido and dry skin in women with adrenal insufficiency
  • Hot flashes, missed periods and vaginal dryness when the cause is ovarian failure or menopause
  • Low libido, erectile difficulty, reduced muscle mass and low energy in men with hypogonadism
  • In children with CAH on treatment: slowed growth or weight gain if the steroid dose is too high

Read it alongside

  • Total and free testosterone — the main active androgen; a testosterone above 150–200 ng/dL in a woman points to an ovarian tumor or hyperthecosis, while PCOS usually gives high-normal to mildly raised values.
  • DHEA-S — almost purely adrenal; high DHEA-S with high androstenedione locates the excess in the adrenal (CAH, Cushing's, tumor), normal DHEA-S with high androstenedione favors the ovary.
  • 17-hydroxyprogesterone — the screening test for non-classic congenital adrenal hyperplasia, drawn in the morning in the follicular phase; above 200 ng/dL prompts an ACTH stimulation test.
  • SHBG — low in PCOS, obesity and insulin resistance, raising the free fraction of all androgens; high on the pill, in hyperthyroidism and liver disease.
  • LH and FSH — an LH:FSH ratio above 2 supports PCOS; a high FSH indicates ovarian insufficiency; both low suggest a pituitary cause.
  • Prolactin and TSH — hyperprolactinemia and thyroid disease disturb cycles and androgen levels and are excluded in every work-up for irregular periods or hirsutism.
  • Cortisol (late-night salivary, dexamethasone suppression or 24-hour urine) and ACTH — when Cushing's syndrome or adrenal insufficiency is suspected.
  • Fasting insulin, glucose and A1C (or an oral glucose tolerance test) — insulin resistance drives androgen excess in PCOS and is worth quantifying, since it is the main lever for treatment.

What usually happens next

  1. If the sample was taken in the afternoon, mid-cycle or while taking DHEA or any hormone-containing supplement, a repeat between 7 and 9 am on cycle days 2 to 5, off supplements for 4 weeks, is the first step; many borderline results normalize.
  2. A mildly raised result in a woman with irregular periods or hirsutism is read with testosterone, DHEA-S, SHBG, 17-hydroxyprogesterone, LH, FSH, prolactin and TSH, and usually a pelvic ultrasound; PCOS is diagnosed when two of three features are present (androgen excess, irregular ovulation, polycystic ovarian morphology) and other causes have been excluded.
  3. If 17-hydroxyprogesterone is above 200 ng/dL, an ACTH (cosyntropin) stimulation test confirms or excludes non-classic congenital adrenal hyperplasia; a positive result means genetic counseling before pregnancy, since the partner may carry a 21-hydroxylase mutation.
  4. Very high androstenedione, a testosterone above 150–200 ng/dL, a DHEA-S above 700 µg/dL, or rapid virilization leads to adrenal CT or MRI and transvaginal ultrasound within weeks, not months, and referral to endocrinology.
  5. If you have classic CAH, ask what androstenedione target your team uses and have it drawn at a consistent time relative to your steroid dose; dose changes are based on the trend together with growth, cycles and weight, not one value.
  6. Ask whether insulin resistance has been assessed; in PCOS the lifestyle and medical measures that improve insulin sensitivity are also the ones that lower androstenedione.

Diet, lifestyle and natural levers with evidence

What can move Androstenedione once the cause is known. Nothing here replaces finding the cause.

Weight loss of 5–10 percent in PCOS with excess weight

Strong evidence

Lifestyle programs that produce a 5 to 10 percent weight loss in women with PCOS lower total and free testosterone and androstenedione by about 10 to 25 percent, raise SHBG, restore ovulation in roughly half of women who were not ovulating, and improve hirsutism scores over 6 to 12 months in randomized trials and meta-analyses. Any approach that reduces calories works; adding resistance or aerobic exercise improves insulin sensitivity further even without weight change. This is the first-line treatment in every PCOS guideline.

Myo-inositol

Moderate evidence

Myo-inositol (2 g twice a day, often with 50 mg folic acid, sometimes combined with D-chiro-inositol in a 40:1 ratio) improves insulin sensitivity and, in meta-analyses of randomized trials in PCOS, lowers total testosterone and androstenedione (one meta-analysis found a mean androstenedione reduction of about 0.5 ng/mL, or 50 ng/dL), raises SHBG and improves ovulation rates over 3 to 6 months, with effects comparable to metformin on androgens and better tolerability. The 2023 international PCOS guideline lists it as an option for metabolic features while noting the evidence quality is moderate.

Mild nausea or loose stools at higher doses; high doses of D-chiro-inositol alone may worsen oocyte quality and are not recommended.

Spearmint tea

Preliminary evidence

In a randomized trial of 42 women with PCOS, two cups a day of spearmint tea for 30 days lowered free and total testosterone and raised LH and FSH compared with a placebo herbal tea, with a reduction in self-reported hirsutism; an earlier 5-day study found similar hormonal shifts. Androstenedione was not measured directly, hair growth did not change objectively in a month, and no trial has run longer than 30 days, so this is a plausible adjunct rather than a treatment.

Stop DHEA, 'andro' and prohormone supplements

Strong evidence

DHEA supplements (25 to 50 mg a day) raise androstenedione and testosterone within days in women, with trials reporting testosterone rising two- to threefold and acne and hirsutism as common side effects; androstenedione itself was sold as a muscle-building supplement until it was classified as a controlled anabolic steroid in 2004, and still appears in some prohormone and bodybuilding products. Stopping for 4 weeks before retesting removes this cause entirely. DHEA is also used in some fertility clinics for diminished ovarian reserve, where the androgen rise is intended.

Do not stop DHEA prescribed for adrenal insufficiency or as part of a fertility protocol without discussing it.

Lower glycemic load and regular exercise

Moderate evidence

Insulin is a direct stimulus to ovarian and adrenal androgen production, so measures that lower insulin lower androgens. In randomized trials in PCOS, low-glycemic-index and lower-carbohydrate diets reduced fasting insulin and free androgen index more than conventional healthy-eating diets at equal calories, and structured exercise (150 minutes a week of moderate activity or 75 minutes vigorous, plus resistance training) lowered the free androgen index by around 10 to 20 percent over 12 to 24 weeks, with or without weight loss. The effect on androstenedione specifically is smaller and less consistently reported than on testosterone and SHBG.

When to see a clinician promptly

  • Rapid onset or quick worsening of male-pattern changes in a woman, such as deepening voice, enlargement of the clitoris, new facial hair spreading over weeks to months, or loss of scalp hair in a male pattern: possible androgen-secreting tumor, which needs evaluation within weeks.
  • An androstenedione or testosterone several times the upper limit, or a DHEA-S above 700 µg/dL, even without dramatic symptoms.
  • Pubic hair, body odor, acne or a growth spurt in a child under 8 (girls) or 9 (boys), or genital changes in an infant, which need pediatric endocrine assessment.
  • Severe fatigue, dizziness on standing, vomiting, salt craving or darkening skin with a low androstenedione and low DHEA-S: possible adrenal insufficiency; collapse, confusion or persistent vomiting in someone on or recently off steroids is an adrenal crisis and an emergency.
  • Periods absent for 3 months or more (outside pregnancy and breastfeeding), or fewer than 8 periods a year, which need investigation whatever the androgen level, partly to protect the uterine lining.
  • Signs of Cushing's syndrome alongside high androgens: central weight gain, a rounded face, easy bruising, purple stretch marks, muscle weakness and high blood pressure or blood sugar.

Frequently asked questions

What is a normal androstenedione level in females?

On mass-spectrometry assays, most labs quote roughly 30 to 200 ng/dL for premenopausal adult women and about 20 to 75 ng/dL after menopause, with the exact limits varying by lab and age band. Levels are highest in the late teens and twenties, in the morning and around ovulation. In SI units the premenopausal range is about 1 to 7 nmol/L. A result just above the limit on an afternoon or mid-cycle sample is often normal when repeated correctly.

What does high androstenedione mean in a woman?

Most often PCOS, where the ovaries overproduce androgens under the influence of high LH and insulin; androstenedione is raised in about a quarter of women with PCOS and goes with irregular periods, acne and hirsutism. The other common causes are non-classic congenital adrenal hyperplasia (checked with 17-hydroxyprogesterone), obesity and insulin resistance, DHEA supplements and Cushing's syndrome. Levels several times the upper limit, or with rapid virilization, raise the question of an adrenal or ovarian tumor.

Is androstenedione high in PCOS?

In about 20 to 35 percent of women with PCOS, yes, usually to less than twice the upper limit, and in some women it is the only androgen that is raised, which is why androgen panels include it rather than relying on testosterone alone. Women with PCOS and a high androstenedione tend to have more insulin resistance and a less favorable metabolic profile. Weight loss, exercise, inositol and metformin all lower it; combined oral contraceptives suppress it.

What is the difference between androstenedione, testosterone and DHEA-S?

They are three steps on the same pathway. DHEA-S is made almost only by the adrenal glands and is a marker of adrenal androgen output. Androstenedione is made about equally by the adrenals and the ovaries or testes and is the direct precursor of testosterone and estrone. Testosterone is the main active androgen, made in women partly in the ovary and partly by converting androstenedione in peripheral tissues. Reading all three together tells you whether an excess is adrenal, ovarian or both.

Can androstenedione cause acne and hair loss?

Yes, indirectly. Androstenedione itself is a weak androgen, but skin and hair follicles convert it locally to testosterone and then to dihydrotestosterone, which enlarges oil glands and shrinks scalp follicles in genetically susceptible people. That is why a woman can have persistent acne or thinning hair with a testosterone that is normal and only androstenedione raised. Treatment addresses the source (usually PCOS or insulin resistance) and, where appropriate, blocks the androgen effect in the skin.

Is androstenedione a steroid, and is it legal?

It is a natural steroid hormone, and as a supplement it was sold as 'andro' for muscle building until the Anabolic Steroid Control Act of 2004 classified it as a controlled substance in the US. Trials in men found it did not increase muscle or strength but did raise estrogen and lower HDL cholesterol. It is banned by all major sports bodies. DHEA, which converts to androstenedione, remains legal as a supplement in the US and is a common hidden reason for a high result.

How should I prepare for an androstenedione test?

Have the blood drawn between 7 and 9 am, ideally fasting, and if you have periods, on days 2 to 5 of your cycle. Stop DHEA, 'andro', prohormone or 'hormone support' supplements for at least 4 weeks beforehand, and tell the clinician about oral contraceptives, steroids (including inhaled and skin creams), valproate and any fertility medication. If you are on treatment for congenital adrenal hyperplasia, draw it at the time your team specifies relative to your steroid dose.

What does low androstenedione mean?

Usually reduced output from the adrenals (Addison's disease, pituitary ACTH deficiency, prednisone or other steroid treatment), the ovaries (menopause, ovarian insufficiency, the combined pill) or the testes (hypogonadism). It rarely needs treatment in itself, and the diagnosis rests on cortisol and ACTH, estradiol and FSH or testosterone and LH. In someone treated for congenital adrenal hyperplasia, a low androstenedione means the steroid dose is probably too high and should be reviewed.

References

  1. Teede HJ, Tay CT, Laven JJE, et al.. Recommendations from the 2023 international evidence-based guideline for the assessment and management of polycystic ovary syndrome. Journal of Clinical Endocrinology and Metabolism (2023)View source
  2. Martin KA, Anderson RR, Chang RJ, et al.. Evaluation and treatment of hirsutism in premenopausal women: an Endocrine Society clinical practice guideline. Journal of Clinical Endocrinology and Metabolism (2018)View source
  3. Speiser PW, Arlt W, Auchus RJ, et al.. Congenital adrenal hyperplasia due to steroid 21-hydroxylase deficiency: an Endocrine Society clinical practice guideline. Journal of Clinical Endocrinology and Metabolism (2018)View source
  4. O'Reilly MW, Taylor AE, Crabtree NJ, et al.. Androstenedione as a marker of hyperandrogenism and metabolic risk in women with polycystic ovary syndrome. Journal of Clinical Endocrinology and Metabolism (2014)
  5. Kushnir MM, Blamires T, Rockwood AL, et al.. Measurement of total serum testosterone in adult men and women by LC-MS/MS: comparison with immunoassays and reference intervals. Clinical Chemistry (2010)
  6. Fitz V, Graca S, Mahalingaiah S, et al.. Inositol for polycystic ovary syndrome: a systematic review and meta-analysis to inform the 2023 update of the international evidence-based PCOS guidelines. Journal of Clinical Endocrinology and Metabolism (2024)
  7. Grant P. Spearmint herbal tea has significant anti-androgen effects in polycystic ovarian syndrome: a randomized controlled trial. Phytotherapy Research (2010)
  8. Lim SS, Hutchison SK, Van Ryswyk E, Norman RJ, Teede HJ, Moran LJ. Lifestyle changes in women with polycystic ovary syndrome. Cochrane Database of Systematic Reviews (2019)
  9. Leder BZ, Longcope C, Catlin DH, Ahrens B, Schoenfeld DA, Finkelstein JS. Oral androstenedione administration and serum testosterone concentrations in young men. JAMA (2000)
  10. Androgen excess disorders in women. Merck Manual Professional Version (2024)
  11. Polycystic ovary syndrome (PCOS). Mayo Clinic (2022)View source

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This page is educational and is not medical advice or a diagnosis. Lab results have to be interpreted together with your history, symptoms and other results by a clinician who knows you. Do not start or stop a supplement to change a lab value before the cause is known.