PCOS With Normal Testosterone and DHEAS: What to Test

You went in with irregular cycles, hair thinning at the part line, or acne that never behaved like teenage acne. The panel came back with a total testosterone inside the reference range and a normal DHEAS, and the conversation stopped there. Nothing about the symptoms changed, but the workup did — two normal numbers became the reason not to look further. That is the moment worth slowing down on, because the two labs most commonly used to screen for androgen excess are also the two most capable of reading normal in someone who genuinely has it.

This article is about the lab layer specifically: which androgen measurements get skipped, why the assay your lab used matters as much as the result it printed, and which common medications change what a draw can show. If you are earlier in the process and want the diagnostic framework itself, our post on how PCOS is actually diagnosed against the Rotterdam criteria covers the three-criteria structure this sits inside.

If my testosterone and DHEAS are normal, does that rule out PCOS?

No. Total testosterone and DHEAS are screening labs, not a complete androgen assessment, and both can sit inside the reference range in someone with PCOS-related androgen excess. International guidelines direct clinicians to assess free testosterone alongside total testosterone, to use mass spectrometry rather than direct immunoassay, and to consider androstenedione and DHEAS only as a second look when testosterone is unremarkable. A normal result on two labs narrows the picture; it does not close it, particularly when clinical signs of androgen excess are present.

Why does total testosterone miss androgen excess so often?

Total testosterone counts every molecule of testosterone in the sample, but most of it is bound to sex hormone-binding globulin (SHBG) and to albumin and cannot act on tissue. Only the small unbound fraction is biologically available, which is why two people with identical total testosterone can have very different androgen activity depending on how much SHBG they are carrying.

That distinction is not theoretical. In a study of subfertile women with oligomenorrhea and suspected PCOS, total testosterone measured by mass spectrometry tracked ovarian findings — ovarian volume and antral follicle count — but showed no relationship with metabolic measures, while SHBG and calculated free testosterone tracked both the ovarian and the metabolic side of the picture (Antonio and colleagues, International Journal of Endocrinology, 2018; 66 women). A panel built on total testosterone alone is measuring the half of the problem that is easiest to measure.

Free testosterone is usually not measured directly. It is calculated from total testosterone and SHBG using the Vermeulen equation, or estimated as the free androgen index, and the 2023 international guideline accepts calculation, equilibrium dialysis, or ammonium sulfate precipitation — but specifically not direct free testosterone immunoassays. Asking whether free testosterone was calculated, and whether SHBG was drawn at all, is often the whole difference between a panel that could show the pattern and one that could not.

What does SHBG have to do with a PCOS diagnosis?

SHBG is made in the liver, and insulin suppresses its production. In PCOS, where insulin resistance is common even at a normal body weight, SHBG tends to run low — which mathematically raises the free fraction of whatever testosterone is present. The result is a familiar and easily missed pattern: total testosterone flagged as normal, SHBG low, free testosterone or free androgen index elevated, symptoms entirely consistent with the free number rather than the total.

This is also why we treat SHBG as a metabolic marker, not just a binding protein. When we see it drifting down alongside fasting insulin, it usually says more about the underlying driver than the androgen value does. Our post on normal glucose with a high fasting insulin covers that pattern, and why PCOS behaves like a metabolic condition rather than an ovary problem covers why the metabolic layer keeps determining what the hormone layer looks like.

Could the assay itself be the reason the number looks normal?

Yes, and this gets very little airtime in the exam room. Female testosterone concentrations are low, and the automated direct immunoassays used in most routine panels perform poorly at that range. The 2023 International Evidence-based Guideline is explicit: laboratories should use validated liquid chromatography–tandem mass spectrometry (LC-MS/MS) assays for total testosterone, and should use LC-MS/MS over direct immunoassays, which "have limited accuracy and demonstrate poor sensitivity and precision for diagnosing hyperandrogenism in PCOS."

A direct comparison makes the point. When 117 women referred for suspected PCOS had testosterone and androstenedione measured both ways, mass spectrometry identified slightly more cases than immunoassay did, and the most frequently elevated markers were calculated free testosterone and androstenedione rather than total testosterone (Grassi and colleagues, Journal of Clinical Medicine, 2020). If a result sits just inside the range on an immunoassay, the honest reading is that the method has limited resolution at that level — not that androgen excess has been excluded.

When is androstenedione actually worth adding?

Androstenedione comes from both the ovaries and the adrenal glands and sits upstream of testosterone in the steroid pathway, so it can be the marker carrying the signal when testosterone is not. Guidance places it precisely: if testosterone and free testosterone are not elevated, androstenedione and DHEAS could be considered, with the caveat that both have poorer specificity and that DHEAS falls with age. It is a considered second step, not a routine add-on, and a clinician choosing not to order it is not ignoring the guideline. In a mass-spectrometry series of 122 consecutive women attending a reproductive medicine clinic, the free androgen index outperformed both total testosterone and androstenedione on diagnostic accuracy for PCOS (Barth and colleagues, European Journal of Endocrinology, 2010) — which is the case for putting free testosterone and SHBG first rather than reaching straight past them.

It is also worth knowing what an isolated androstenedione elevation does and does not predict. In a cross-sectional study of 706 women with PCOS, those with elevated free testosterone carried the adverse metabolic profile — higher insulin resistance, worse glucose and lipid measures — while the group with high androstenedione and normal free testosterone showed no significantly increased metabolic risk (Lerchbaum and colleagues, PLOS ONE, 2014). So androstenedione can complete a diagnostic picture without necessarily changing the metabolic one, and the two questions deserve separate answers.

Do normal androgen labs matter less when the symptoms are obvious?

In the diagnostic framework, yes. Clinical hyperandrogenism — hirsutism above all — satisfies the androgen-excess criterion on its own, with no lab required. The guideline's own practice point is that biochemical testing is of greatest value in patients with minimal or no clinical signs, which is the reverse of how a normal panel is usually deployed in conversation.

The caveat runs both ways. Hirsutism is the strongest clinical predictor; isolated acne or female-pattern hair loss are weaker and less specific, and deserve a fuller look rather than a quick yes or no. We see this play out constantly with patients across Long Island who arrive with a folder of normal labs and a symptom history nobody has mapped against the criteria — and it shows up most often in PCOS at a normal BMI, where the metabolic signs that usually prompt a deeper workup are absent.

Can the pill or an anti-androgen hide the picture?

The combined oral contraceptive pill is the largest masking factor and the one most often overlooked. It raises SHBG and suppresses ovarian androgen production, and the guideline states plainly that biochemical hyperandrogenism cannot be reliably assessed on it. A meaningful androgen panel generally needs a stretch of time off hormonal contraception first — our post on what happens to your cycle after coming off the pill covers what that window looks like.

Anti-androgen medications complicate the read differently. Spironolactone works mainly by blocking the androgen receptor, so its clinical effect on hair and skin does not depend on serum androgens falling, and a review of its use in PCOS describes effects well beyond simple receptor blockade (Bashir and colleagues, Current Pharmaceutical Design, 2023). A normal-looking testosterone on spironolactone is not evidence that the untreated level was normal.

The 5-alpha-reductase inhibitors — finasteride and dutasteride — are counterintuitive in the other direction. They block conversion of testosterone to dihydrotestosterone, the androgen most implicated in androgenic hair loss, so DHT falls while serum testosterone does not reliably follow. A meta-analysis of 11 studies covering 1,784 patients found no unequivocal significant increase in serum testosterone on these drugs, with inconsistent results across studies and a proposed explanation involving SHBG binding (Traish and colleagues, Sexual Medicine Reviews, 2019). Two limits matter when reading that: the data is in men treated for prostate or hair-loss indications, and the drugs are used off-label in women. The practical takeaway is narrow but real — neither drug reliably lowers measured testosterone or DHEAS, so labs drawn on treatment are a poor stand-in for an untreated baseline.

If I am trying to conceive, does this change the medication conversation?

It changes the timing of it. Anti-androgens are recommended only alongside effective contraception, because of the risk to a male fetus if pregnancy occurs during treatment; the 2023 guideline attaches that condition to every anti-androgen recommendation it makes. For anyone planning to conceive, the sequencing question — when the medication stops, how long the washout runs, and what gets drawn afterwards — belongs to the prescriber, and dutasteride in particular has a long elimination profile compared with finasteride.

Nothing here is a reason to start, stop, or change a medication on your own. It is a reason to ask one specific question at the next appointment: was an untreated baseline androgen panel ever established, and if not, when would drawing one make sense?

What should be excluded before PCOS is the final answer?

PCOS is a diagnosis of exclusion, and the standard exclusion workup is thyroid function, prolactin, and 17-hydroxyprogesterone to screen for non-classic congenital adrenal hyperplasia (NCCAH), with further testing where the clinical picture warrants it. NCCAH is a genetic adrenal enzyme condition that can present with irregular cycles, acne, hair thinning and mildly raised androgens — close enough to PCOS that it is missed without the specific test, and managed differently once found.

The screening layer is also evolving. A 2023 study of 99 hyperandrogenic women established mass-spectrometry-specific thresholds for basal and stimulated 17-OHP and evaluated serum 21-deoxycortisol, which reached high sensitivity for NCCAH (Ng and colleagues, Journal of Clinical Endocrinology & Metabolism, 2023). Which of these makes sense for you is a question for your endocrinologist or gynecologist, not something to self-order — but knowing that 17-OHP belongs in the workup is enough to ask whether it was done.

What would a fuller androgen workup actually look like?

For someone with symptoms of androgen excess and an unremarkable total testosterone and DHEAS, a more complete picture usually means total testosterone by mass spectrometry, SHBG with a calculated free testosterone or free androgen index, androstenedione as a considered second step, 17-OHP to exclude NCCAH, and thyroid and prolactin as part of the exclusion set — read alongside ovulatory history and, where relevant, ovarian appearance on ultrasound. Timing matters too: androgens are conventionally drawn in the early follicular phase, and a panel run at a random point in an irregular cycle is harder to interpret.

The wider framing is the one we use with every lab set that comes through our Huntington office: a single draw is a photograph, not a direction. Our guide to reading fertility labs when everything comes back normal goes through that logic in detail, and the question of whether you can have PCOS while still ovulating is the other direction the same conversation runs.

What do we do with this at our clinic in Huntington?

We do not order labs, prescribe, or manage medication — diagnosis and prescribing stay with your OB-GYN or reproductive endocrinologist. What we do is work on the drivers that sit underneath the androgen picture: insulin signaling, inflammation, sleep, and the gut side of androgen handling, which is a real and underappreciated route — see what gut bacteria have to do with testosterone in PCOS. For patients coming to us from across Long Island with a normal panel and persistent symptoms, that is usually where the useful work is.

Our approach to PCOS and endometriosis care starts from the metabolic and immune context rather than a single hormone value, and builds a Personalized 90-Day Fertility Roadmap from there.

A normal total testosterone and DHEAS is a partial answer to a partial question. The measurements that most often carry the signal — free testosterone, SHBG, androstenedione — are frequently not on the panel, the assay used may not resolve female androgen levels well, and a medication taken for hair or skin can make any current result a poor proxy for baseline. None of that means every person needs every androgen lab. It means "normal" on those two labs is not the end of the workup when the symptoms are still there.

This article is general education about how androgen testing works. It is not an interpretation of anyone's individual lab results, a diagnosis, or medical advice, and it is not a substitute for a full evaluation with your own clinician.

East to West Fertility is a metabolic and immune-focused fertility clinic in Huntington, Long Island, serving patients across Long Island, NYC, and beyond. Learn more about our Metabolic & Immune Fertility Evaluation or call 631-416-4940.

References:

• 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 & Metabolism, 2023;108(10):2447-2469. (254 recommendations and practice points.)
• Legro RS, Arslanian SA, Ehrmann DA, et al. "Diagnosis and treatment of polycystic ovary syndrome: an Endocrine Society clinical practice guideline." Journal of Clinical Endocrinology & Metabolism, 2013;98(12):4565-4592.
• Vermeulen A, Verdonck L, Kaufman JM. "A critical evaluation of simple methods for the estimation of free testosterone in serum." Journal of Clinical Endocrinology & Metabolism, 1999;84(10):3666-3672.
• Antonio L, Pauwels S, Laurent MR, et al. "Free testosterone reflects metabolic as well as ovarian disturbances in subfertile oligomenorrheic women." International Journal of Endocrinology, 2018;2018:7956951. (66 subfertile women with oligomenorrhea.)
• Lerchbaum E, Schwetz V, Rabe T, Giuliani A, Obermayer-Pietsch B. "Hyperandrogenemia in polycystic ovary syndrome: exploration of the role of free testosterone and androstenedione in metabolic phenotype." PLOS ONE, 2014;9(10):e108263. (706 women with PCOS, 140 BMI-matched controls.)
• Grassi G, Polledri E, Fustinoni S, et al. "Hyperandrogenism by liquid chromatography tandem mass spectrometry in PCOS: focus on testosterone and androstenedione." Journal of Clinical Medicine, 2020;10(1):119. (117 women assessed by both immunoassay and LC-MS/MS.)
• Barth JH, Field HP, Yasmin E, Balen AH. "Defining hyperandrogenism in polycystic ovary syndrome: measurement of testosterone and androstenedione by liquid chromatography-tandem mass spectrometry and analysis by receiver operator characteristic plots." European Journal of Endocrinology, 2010;162(3):611-615. (122 consecutive women in a reproductive medicine clinic.)
• Bashir R, Asrar MM, Shah IA, et al. "Do pleiotropic effects of spironolactone in women with PCOS make it more than an anti-androgen? Evidence from preclinical and clinical studies." Current Pharmaceutical Design, 2023;29(19):1486-1496.
• Traish AM, Krakowsky Y, Doros G, Morgentaler A. "Do 5α-reductase inhibitors raise circulating serum testosterone levels? A comprehensive review and meta-analysis to explaining paradoxical results." Sexual Medicine Reviews, 2019;7(1):95-114. (11 studies, 1,784 patients, all male cohorts.)
• Ng JL, Lim EM, Zhang R, Beilby JP, Watts GF, Brown SJ, Stuckey BGA. "Serum 21-deoxycortisol for diagnosis of nonclassic congenital adrenal hyperplasia in women with androgen excess." Journal of Clinical Endocrinology & Metabolism, 2023;108(12):e1560-e1570. (99 hyperandrogenic women.)