Androstenedione is a hormone produced by both the adrenal glands and the ovaries, and when levels climb above normal in women, the effects tend to show up as excess hair growth, acne, irregular periods, or thinning hair on the scalp. The most common driver is polycystic ovary syndrome (PCOS), but adrenal conditions, rare tumors, and even pregnancy can push androstenedione higher than expected. Understanding the source of the excess matters because treatment depends entirely on which gland is overproducing and why.
Where Androstenedione Comes From
In women, androstenedione is shared between two factories. The adrenal glands, sitting on top of the kidneys, produce it alongside other androgens like DHEA and DHEA-S. The ovaries also make androstenedione, primarily in the theca cells of developing follicles and in stromal tissue, under the influence of luteinizing hormone (LH). Output from the ovaries shifts somewhat across the menstrual cycle.1PubMed. Adrenal and gonadal androgen secretion in normal females Both sources contribute roughly equally under normal circumstances, which is part of what makes diagnosis tricky: a high reading on a lab test doesn’t immediately tell you which gland is responsible.
Androstenedione itself is not the most potent androgen in the body. It acts mainly as a precursor, getting converted into testosterone or estrogen in tissues like fat, skin, and muscle. That conversion is the reason elevated androstenedione can produce effects well beyond the glands that made it. The hormone’s downstream products are what actually bind to receptors in hair follicles, sebaceous glands, and reproductive tissue, setting off the symptoms people notice.
Symptoms That Point to Excess Androgens
High androstenedione rarely announces itself through a single unmistakable sign. Instead, it typically produces a cluster of symptoms that overlap with other forms of androgen excess. The most studied of these are hirsutism (coarse, dark hair in places like the chin, chest, and abdomen), persistent acne that resists typical treatments, thinning hair at the crown or temples, and irregular or absent periods.
A study of 228 women investigated for androgen excess found that those with hirsutism had higher levels of androstenedione, DHEA-S, and salivary testosterone compared to those whose primary complaint was hair loss, while women with acne fell between the two groups. Hirsutism severity correlated positively with androstenedione levels, and women with the most pronounced hirsutism were also more likely to have irregular menstrual cycles.2PubMed. Androgen dependence of hirsutism, acne, and alopecia in women: retrospective analysis of 228 patients investigated for hyperandrogenism The pattern makes intuitive sense: hirsutism is often the most androgen-sensitive visible symptom, so it tends to appear when levels are highest.
Menstrual disruption deserves separate attention. When androgen levels are persistently elevated, they can interfere with ovulation. Chronic anovulation, where the ovary stops releasing eggs regularly, usually shows up as cycles that stretch beyond 35 days (oligomenorrhea) or disappear altogether (amenorrhea). PCOS accounts for about 85% of chronic anovulation cases, and the condition is characterized by raised concentrations of testosterone, androstenedione, or both.3PubMed Central. Anovulation For women trying to conceive, this link between high androgens and absent ovulation is often what brings them to a doctor in the first place.
PCOS and the Androstenedione Connection
Polycystic ovary syndrome is by far the most frequent explanation for elevated androstenedione in premenopausal women. The condition involves a feedback loop between the ovaries, the pituitary gland, and insulin signaling that keeps androgen production higher than it should be. Researchers have found that women with PCOS had roughly three times the risk of elevated androstenedione compared to controls, and the odds of having an elevated level were nearly fivefold higher.4PubMed Central. Elevated and diagnostic androgens of polycystic ovary syndrome Total and free testosterone were also significantly higher in the same group, but androstenedione’s elevation is sometimes the first biochemical clue, especially when testosterone levels fall in the borderline range.
Insulin resistance is a central piece of the puzzle. High insulin stimulates the ovaries to produce more androgens and simultaneously lowers levels of sex hormone-binding globulin (SHBG), the protein that keeps androgens from freely circulating. The combination of overproduction and reduced binding makes more androgen available to tissues. A growing body of research has identified insulin resistance and elevated androgens as the two main drivers that initiate PCOS and influence how severe it becomes.5PubMed Central. Resistance to the Insulin and Elevated Level of Androgen: A Major Cause of Polycystic Ovary Syndrome This means that anything worsening insulin sensitivity, such as weight gain or a diet high in refined carbohydrates, can ratchet androgen levels upward even without any new pathology.
Adrenal Sources of Excess
Not every case of high androstenedione traces back to the ovaries. The adrenal glands have their own set of conditions that overproduce androgens, and differentiating the two sources is one of the trickiest parts of the workup.
Non-classic congenital adrenal hyperplasia (NCAH) is the most common adrenal mimic of PCOS. It results from a partial deficiency of the enzyme 21-hydroxylase: the adrenals can still make enough cortisol to function, but the enzymatic bottleneck diverts precursors into androgen production. The clinical picture, with hirsutism, acne, and menstrual irregularity, closely resembles PCOS, and the two are frequently confused.6PubMed Central. Nonclassic Congenital Adrenal Hyperplasia: What Do Endocrinologists Need to Know? NCAH is relatively common, particularly in certain ethnic populations, and missing it matters because treatment differs. Women with NCAH may benefit from low-dose glucocorticoids that suppress the adrenal’s androgen output, an approach that would not help someone whose androgens come primarily from the ovaries.
Rarer and more alarming is an androgen-secreting adrenal tumor. When hirsutism or other androgenic symptoms appear suddenly and progress rapidly, rather than building gradually over months or years, clinicians are taught to consider the possibility of an adrenocortical carcinoma or adenoma.7PubMed Central. Differentiating Polycystic Ovary Syndrome from Adrenal Disorders Tumors tend to push androgen levels dramatically higher than either PCOS or NCAH, and the speed of symptom onset is a useful red flag. Cushing’s syndrome, where excess cortisol production comes from adrenal or pituitary pathology, can also raise androgens as a secondary effect and usually presents with additional features like central weight gain, thin skin, and easy bruising.
Postmenopausal Androgen Excess
High androstenedione takes on a different set of causes after menopause. With estrogen production declining, androgens become relatively more prominent, and conditions that were previously masked may surface. Ovarian hyperthecosis, a condition in which clusters of hormone-producing theca cells persist in the ovarian tissue, can drive testosterone levels well above normal. Unlike PCOS, hyperthecosis typically pushes testosterone above a threshold where clinicians start considering tumor as a possibility, which can lead to unnecessary alarm if the condition is not recognized.8PubMed Central. Approach to Investigation of Hyperandrogenism in a Postmenopausal Woman Imaging and sometimes surgical biopsy are needed to distinguish hyperthecosis from an ovarian tumor, because blood tests alone can look very similar.
Postmenopausal women who develop new-onset acne, facial hair growth, or a deepening voice warrant a thorough evaluation. Unlike in younger women where PCOS dominates the landscape, the differential diagnosis after menopause leans more heavily toward tumors and hyperthecosis, and the stakes of missing a malignancy are higher.
Pregnancy and Other Physiological Shifts
Androstenedione does not stay constant even under normal physiological circumstances. Pregnancy is one of the most dramatic examples. A study using highly accurate mass spectrometry methods found that androstenedione levels increased by about 80% by the twelfth week of pregnancy and then plateaued for the remainder.9PubMed Central. Steroid hormone levels in pregnancy and 1 year postpartum using isotope dilution tandem mass spectrometry This rise is driven by the placenta and the expanded adrenal activity of pregnancy and is entirely normal. It does mean, however, that lab values during pregnancy need to be interpreted against pregnancy-specific reference ranges rather than standard ones. A result that looks worryingly high in a non-pregnant woman may be perfectly routine at 20 weeks gestation.
Androstenedione is also sold as an oral supplement, marketed to athletes as a “natural alternative” to anabolic steroids under the nickname “andro.”10PubMed Central. Androstenedione (a Natural Steroid and a Drug Supplement): A Comprehensive Review of Its Consumption, Metabolism, Health Effects, and Toxicity with Sex Differences Women taking these supplements can end up with elevated androstenedione on blood work without any underlying glandular problem. If your doctor finds a high level and asks about supplements or performance-enhancing products, that is why. Even products labeled as “natural” or “herbal” can contain precursors that raise androgen levels.
Why the Lab Test Itself Matters
One underappreciated wrinkle in diagnosing high androstenedione is how the hormone is actually measured. Older immunoassay methods, which are still widely used, can give readings that differ substantially from the gold-standard technique, liquid chromatography-tandem mass spectrometry (LC-MS/MS). Research comparing different immunoassay platforms to LC-MS/MS has found that some assays overestimate androstenedione by as much as 66%, while others underestimate it, depending on the specific platform used.11PubMed Central. The Androstenedione Roche Elecsys immunoassay has superior comparability to the LC-MS/MS assay than the Siemens Immulite immunoassay That is an enormous margin of error for a test that guides clinical decisions.
Newer automated immunoassays have improved, with some platforms showing differences from mass spectrometry of less than 2%. But the variation between labs and methods means that a borderline-high result on one platform might read as normal on another.12PubMed. Comparison of Immunoassay and Liquid Chromatography-Tandem Mass Spectrometry Methods in the Measurement of Serum Androstenedione Levels If your results are close to the upper limit and don’t match your symptoms, it may be worth asking which assay method was used or requesting a repeat through an LC-MS/MS lab. This is especially relevant when distinguishing between PCOS and adrenal causes, where the clinical decision hinges on modest differences in hormone levels rather than dramatic ones.
Sorting Out the Source
When androstenedione comes back elevated, the diagnostic process aims to pin down whether the ovaries, the adrenal glands, or both are responsible. A basic workup includes measuring total and free testosterone, DHEA-S (which is almost exclusively adrenal), and 17-hydroxyprogesterone (17-OHP), which screens for congenital adrenal hyperplasia. The timing matters: samples should ideally be drawn in the early follicular phase of the menstrual cycle, when baseline ovarian androgen production is lowest and adrenal contributions are easier to isolate.
If 17-OHP is elevated at baseline, a stimulation test using synthetic ACTH can confirm NCAH. For cases where Cushing’s syndrome is suspected, a dexamethasone suppression test helps determine whether cortisol production is being regulated normally.7PubMed Central. Differentiating Polycystic Ovary Syndrome from Adrenal Disorders Imaging comes into play when androgen levels are very high or symptoms progress quickly, since those patterns raise the possibility of an androgen-secreting tumor in either the adrenals or the ovaries. The goal is never just to confirm that androgens are elevated, but to figure out the specific machinery behind the elevation, because that determines whether the right treatment is a pill, a dietary change, or surgery.
Treatment Depends on the Cause
For androgen-secreting tumors, surgical removal is the definitive treatment and often resolves symptoms completely. For everything else, medical management is the standard approach.13PubMed Central. Practical Approach to Hyperandrogenism in Women The specifics vary widely depending on the underlying condition.
In PCOS, treatment often starts with lifestyle changes. A low-glycemic diet with a mild calorie deficit has been shown to lower total testosterone levels, decrease the free androgen index, and increase SHBG in overweight women within just 60 days.14PubMed Central. Reduction in the Free Androgen Index in Overweight Women After Sixty Days of a Low Glycemic Diet Because insulin resistance is such a strong driver of androgen overproduction in PCOS, improving insulin sensitivity through diet, exercise, or medications like metformin can lower androgens without ever directly targeting the hormones themselves. Combined oral contraceptive pills are another common tool: they suppress LH-driven ovarian androgen production and raise SHBG, effectively reducing the amount of free androgen circulating in the blood. Anti-androgen medications like spironolactone can be added for persistent hirsutism or acne.
For NCAH, low-dose glucocorticoids replace the cortisol the adrenals struggle to make efficiently, reducing the buildup of androgen precursors upstream. This is a fundamentally different approach from treating PCOS, which is why getting the diagnosis right matters so much. Women with NCAH who are treated as if they have PCOS may see partial improvement from oral contraceptives but miss the more targeted benefit of glucocorticoid therapy.
The Emotional and Psychological Side
The physical symptoms of androgen excess carry a psychological burden that clinical discussions often underplay. Hirsutism, acne, hair loss, and weight gain all affect how women feel about their appearance, and research has repeatedly linked these symptoms to worse mental health outcomes. In one controlled study, women with PCOS scored significantly worse on all body image measures compared to women without the condition, even after adjusting for age and body mass index. Depression symptoms were reported by 28% of women with PCOS versus about 19% of controls, and anxiety symptoms were present in roughly 77% versus 57%.15PubMed Central. Body image distress increased in women with PCOS and mediates depression and anxiety The study found that body image distress did not just coexist with depression and anxiety but actually mediated the relationship, meaning that dissatisfaction with physical appearance was a major pathway through which PCOS led to mood disorders.
These patterns are not uniform across all presentations of androgen excess. Research comparing different PCOS phenotypes found that depression, anxiety, and negative body image were most pronounced in phenotypes that combined both hyperandrogenism and disrupted ovulation, compared to milder phenotypes where androgen levels were less dramatically elevated.16PubMed. Depression, anxiety, body image scores, and sexual dysfunction in patients with polycystic ovary syndrome according to phenotypes This suggests that the severity of the hormonal disruption tracks with the emotional impact, and that addressing androgens is not just a cosmetic or reproductive concern but a mental health one.
When Androstenedione Is High but Everything Else Looks Normal
One scenario that confuses both patients and clinicians is a mildly elevated androstenedione level with no clear symptoms and no other abnormal hormones. This can happen for several reasons. Lab variability, as discussed earlier, can produce a false elevation. The blood draw might have been timed at a point in the menstrual cycle when ovarian androgen output peaks. Stress, poor sleep, and intense exercise can temporarily bump adrenal androgen production. And reference ranges themselves are statistical constructs: being slightly above the upper limit does not necessarily mean something is wrong, especially if the range was established using a different assay method from the one that measured your sample.
Clinicians generally look at the full picture rather than acting on a single number. If androstenedione is high but testosterone, DHEA-S, and 17-OHP are all normal, and you have no symptoms of androgen excess, the most common recommendation is to recheck the level after a few weeks, ideally in the early follicular phase, and to make sure the lab uses a reliable assay. A persistently elevated level with no identifiable cause may warrant periodic monitoring but does not always demand treatment. The harm in overreacting to a borderline lab value, launching into medications or invasive workups, can exceed the harm of watchful waiting when symptoms are absent.
Androstenedione Versus Testosterone in Clinical Practice
Testosterone gets most of the attention in discussions of female androgen excess, and for good reason: it is the most potent androgen and the one most directly tied to receptor activation in target tissues. But androstenedione has clinical value precisely because it can be elevated when testosterone is still within the normal range. In PCOS, for instance, androstenedione sometimes rises before testosterone does, making it a useful early marker. Some researchers have argued that panels measuring only testosterone miss a meaningful fraction of women with biochemical hyperandrogenism.
The distinction also matters in adrenal conditions. DHEA-S is a classic adrenal marker, but androstenedione can be elevated from either adrenal or ovarian sources, so tracking it alongside DHEA-S and testosterone helps triangulate the problem. A pattern of high DHEA-S and high androstenedione with normal or mildly elevated testosterone points toward the adrenals. High androstenedione and high testosterone with normal DHEA-S suggests the ovaries are responsible. Neither pattern is perfectly diagnostic on its own, but together they narrow the field and guide further testing like 17-OHP measurement or imaging.