Dihydrotestosterone (DHT)
The DHT test measures serum dihydrotestosterone, the most potent endogenous androgen synthesised from testosterone by 5α-reductase in target tissues. It is ordered to investigate androgen excess when testosterone is normal, to diagnose 5α-reductase deficiency in undervirilised children, and to monitor 5α-reductase inhibitor therapy, interpreted alongside testosterone, SHBG, and androstenedione.
1
Biomarkers
Blood (serum)
Sample
3–5 business days
Turnaround
No
Fasting
What is the DHT test?
The Dihydrotestosterone (DHT) Test quantifies the serum concentration of the most potent endogenous androgen, which is synthesised from testosterone by 5α-reductase in target tissues and circulates at much lower concentration than its precursor. DHT drives virilisation of the external genitalia in male foetal development, supports prostate growth and male-pattern hair distribution in adults, and contributes to sebaceous gland activity in both sexes. Practitioners order DHT when circulating testosterone alone does not explain the clinical picture — for example, signs of androgen excess with normal total testosterone, suspected 5α-reductase deficiency in a child with undervirilisation, or during monitoring of 5α-reductase inhibitor therapy for benign prostatic hyperplasia or androgenic alopecia. Because most DHT is generated peripherally and because tissue expression of 5α-reductase isoenzymes varies, the circulating level is only a partial proxy for local androgen action, yet it remains the only practical systemic marker of this pathway and is essential when distinguishing primary androgen overproduction from exaggerated peripheral conversion.
What does the DHT test measure?
Dihydrotestosterone is synthesised from testosterone by 5α-reductase isoenzymes (predominantly type 2 in androgen-dependent tissues, type 1 in sebaceous glands and hepatic tissue). DHT binds the androgen receptor with two- to threefold greater affinity than testosterone and dissociates more slowly, making it the most potent endogenous androgen. In male foetal development DHT is indispensable for differentiation of the external genitalia and prostate; postnatally it drives development of the prostate, facial and body hair, and sebaceous gland activity. Because 5α-reductase is expressed in skin, prostate, and follicles, local DHT concentration can be high even when circulating testosterone is modest.
DHT measurement is used to investigate androgen excess in both sexes, to confirm 5α-reductase deficiency in cases of ambiguous genitalia or undervirilisation, and to monitor 5α-reductase inhibitor therapy. Elevated DHT underlies many features of hyperandrogenism — notably androgenic alopecia, hirsutism, and acne — when circulating testosterone may be normal or only mildly raised. Because the majority of circulating DHT is produced peripherally rather than secreted by the testes or adrenals, interpretation requires correlation with total and free testosterone, SHBG, and sometimes androstenedione.
Why is the DHT test ordered?
- Investigation of hyperandrogenic signs — hirsutism, androgenic alopecia, acne — in women when testosterone and DHEA-S are normal or borderline, suggesting peripheral conversion
- Paediatric endocrine evaluation of ambiguous genitalia, micropenis, or undervirilisation to assess for 5α-reductase type 2 deficiency
- Monitoring efficacy and compliance with 5α-reductase inhibitors (finasteride, dutasteride) prescribed for benign prostatic hyperplasia or pattern hair loss
- Work-up of male infertility or sexual dysfunction when total and free testosterone are discordant or when a defect in androgen metabolism is suspected
- Assessment of androgen-excess states in women with polycystic ovary syndrome, particularly those with prominent androgenic alopecia or treatment-resistant hirsutism
- Evaluation of precocious puberty or virilisation in children, interpreted alongside testosterone, androstenedione, and 17-hydroxyprogesterone
- Exploration of the androgen milieu in transgender medicine, where both testosterone and downstream metabolites inform hormone therapy adjustments
Sample collection and turnaround
Sample type
Blood (serum)
Fasting required
No
Collection method
Venipuncture at patient service centre
Turnaround
3–5 business days
Collection notes
Phlebotomy via LabCorp; morning collection (before 10:00) is preferred to align with the diurnal rhythm of testosterone, from which DHT is derived. No special preparation is required. Note current use of 5α-reductase inhibitors, androgens, or hormonal contraceptives on the requisition.
Specimen requirements
Minimum 1.0 mL serum; gel separator acceptable. Separate from cells within two hours of collection; serum is stable refrigerated for up to 48 hours or frozen at −20 °C for longer storage. Specify the assay method (LC-MS/MS preferred) if available through the routing laboratory.
What can affect DHT results?
These drugs competitively inhibit 5α-reductase, lowering DHT by 60–90 per cent while raising circulating testosterone through reduced feedback; monitoring DHT confirms therapeutic efficacy and adherence.
DHT tracks testosterone's diurnal rhythm to some extent, though peripheral conversion dampens the amplitude; morning collection is preferred for consistency with testosterone sampling.
Obesity raises peripheral aromatase activity (lowering bioavailable testosterone) while possibly increasing 5α-reductase expression in adipose tissue and skin, leading to variable DHT:testosterone ratios.
Exogenous testosterone raises substrate for peripheral conversion; some synthetic androgens are direct 5α-reduced compounds and cross-react in the immunoassay or elevate measured DHT.
5α-reductase type 1 is abundant in liver; severe hepatic dysfunction can alter DHT synthesis and clearance, though the clinical impact on circulating levels is inconsistent.
Rare loss-of-function variants in the gene encoding 5α-reductase type 2 cause profound reductions in DHT, presenting as 46,XY differences of sex development; milder polymorphisms may modestly lower circulating DHT.
What do DHT results mean?
Elevated
Primary androgen excess from any cause (polycystic ovary syndrome, androgen-secreting tumour, congenital adrenal hyperplasia) can raise DHT. Isolated DHT elevation with normal testosterone suggests increased 5α-reductase activity and is seen in some cases of idiopathic hirsutism, androgenic alopecia, and acne. Exogenous androgen use or androgen precursor supplementation also elevates DHT. Correlate with testosterone, SHBG, androstenedione, and DHEA-S to localise the source.
Normal
A DHT level within the reference interval does not exclude androgen-mediated pathology, because local tissue 5α-reductase activity and androgen receptor sensitivity determine clinical effects. Interpret in conjunction with the full androgen panel, clinical phenotype, and family history rather than in isolation.
Reduced
Low DHT with low testosterone reflects gonadal insufficiency or hypothalamic–pituitary suppression. Disproportionately low DHT relative to testosterone suggests 5α-reductase deficiency, confirmed by an elevated testosterone:DHT ratio; in male infants this presents as undervirilisation and may be associated with SRD5A2 mutations. Suppression by finasteride or dutasteride is expected and dose-dependent.
Note: DHT circulates at 5–10 per cent of testosterone's concentration and requires a sensitive assay; liquid chromatography–tandem mass spectrometry is preferred over immunoassay, particularly in women and children. The testosterone:DHT ratio (normally 10:1 to 20:1) is more informative than either analyte alone when investigating enzymatic defects. Serial comparisons should use the same assay platform because method-specific differences are substantial.
Frequently asked questions
Testosterone is the primary circulating androgen produced by the testes and adrenals, while DHT is synthesised from testosterone by 5α-reductase in peripheral tissues. DHT is two to three times more potent at the androgen receptor and drives virilisation of external genitalia, prostate growth, and male-pattern hair distribution.
How to access the DHT test
The DHT reference page is free and open to all practitioners. Create a free practitioner account to see pricing, save tests to your list, and generate requisition forms. Verification takes 1–2 business days.
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Published: October 7, 2026
Last reviewed: October 7, 2026
- Azzouni F, et al. The 5α-reductase isozyme family: a review of basic biology and their role in human diseases. Adv Urol. (2012)
- Endocrine Society clinical practice guideline on the evaluation and treatment of hirsutism in premenopausal women. J Clin Endocrinol Metab. (2018)
- McConnell JD, et al. The effect of finasteride on the risk of acute urinary retention and the need for surgical treatment among men with benign prostatic hyperplasia (PLESS trial). N Engl J Med. (1998)
- Imperato-McGinley J, et al. Steroid 5α-reductase deficiency in man: an inherited form of male pseudohermaphroditism. Science. (1974)
- Rosner W, et al. Position statement: utility, limitations, and pitfalls in measuring testosterone — an Endocrine Society position statement. J Clin Endocrinol Metab. (2007)
This content is for licensed healthcare practitioners only and does not constitute medical advice. Clinical decisions should be based on the full clinical picture and not on any single test result.