DHT
Dihydrotestosterone
What it is
Dihydrotestosterone (DHT) is the most biologically potent androgen in the human body. It is formed from testosterone by the enzyme 5α-reductase (primarily types 1 and 2), which is expressed at high levels in the prostate, seminal vesicles, skin, hair follicles, and liver. DHT binds to the androgen receptor with approximately three times greater affinity than testosterone and dissociates from it more slowly, producing a more sustained and potent androgenic signal. Unlike testosterone, DHT cannot be aromatised to oestradiol — it is a terminal androgen. Circulating DHT levels are substantially lower than testosterone (approximately 10% of total testosterone), but its local concentrations in androgen-sensitive tissues can be much higher due to intracrine 5α-reductase activity. DHT is responsible for the virilisation of the external genitalia during fetal development, prostate growth, body and facial hair development, and — in genetically predisposed individuals — androgenic alopecia (male pattern hair loss).
Why we measure it
DHT sits at the intersection of two clinically important areas. First, prostate health: the prostate is highly androgen-sensitive, and DHT — not testosterone — is the primary driver of prostate growth, both normal and pathological. Benign prostatic hyperplasia (BPH) and prostate cancer growth are DHT-dependent processes; 5α-reductase inhibitors (finasteride and dutasteride) lower DHT by 60–90%, reducing prostate volume and improving BPH symptoms, and are used as chemoprevention in prostate cancer risk management. Second, androgenic alopecia: hair follicle miniaturisation in pattern baldness is driven by DHT acting on genetically sensitive follicles; the same 5α-reductase inhibitors halt or partially reverse hair loss in predisposed individuals. In the context of the Blueprint androgen panel, DHT measured alongside total testosterone and SHBG provides a more complete picture of androgenic activity — particularly useful for men on testosterone therapy (which can substantially raise DHT via peripheral conversion) and for those managing prostate or hair concerns.
Why every 6 months
DHT does not exhibit as pronounced a diurnal rhythm as testosterone, but its levels are correlated with testosterone and should be measured at the same morning, fasting draw. The six-month interval tracks the impact of interventions — whether dietary, pharmacological (5α-reductase inhibitors, finasteride, dutasteride), or hormonal — on DHT levels, and provides trend data alongside the broader androgen panel.
What movement means
Standard reference ranges for serum DHT in adult males typically fall between 300 and 850 pg/mL (1.0–2.9 nmol/L), with levels declining with age. Ranges vary substantially by assay method; liquid chromatography-mass spectrometry (LC-MS/MS) is the most accurate method. Female reference ranges are substantially lower (approximately 24–368 pg/mL). Interpretation is most meaningful in context — the DHT:testosterone ratio (reflecting 5α-reductase activity), PSA (for prostate health), and clinical signs (hair, prostate symptoms) together give the DHT reading its clinical significance.
Normal (Male)
300 – 850 pg/mL (1.0 – 2.9 nmol/L)
Within the standard reference range for adult males. Levels naturally decline with age. High-normal DHT in men with androgenic alopecia or BPH symptoms warrants consideration of 5α-reductase inhibition.
Standard laboratory reference ranges — vary by assay method; LC-MS/MS preferred
Elevated (Male)
> 850 pg/mL (> 2.9 nmol/L)
Above the upper reference limit. May indicate high 5α-reductase activity or exogenous testosterone use. Associated with accelerated androgenic alopecia progression and BPH in susceptible individuals. Clinical context and PSA monitoring are appropriate.
Standard laboratory reference ranges — vary by assay method
In the protocol
References
- 1.
Imperato-McGinley J, Guerrero L, Gautier T, Peterson RE. “Steroid 5α-Reductase Deficiency in Man: An Inherited Form of Male Pseudohermaphroditism.” Science. 1974.
- 2.
Roehrborn CG, Boyle P, Nickel JC, Hoefner K, Andriole G. “Efficacy and Safety of a Dual Inhibitor of 5-Alpha-Reductase Types 1 and 2 (Dutasteride) in Men with Benign Prostatic Hyperplasia.” Urology. 2002.
- 3.
Andriole GL, Bostwick DG, Brawley OW, et al.. “Effect of Dutasteride on the Risk of Prostate Cancer.” New England Journal of Medicine. 2010.
- 4.
Kaufman KD, Olsen EA, Whiting D, et al.. “Finasteride in the Treatment of Men with Androgenetic Alopecia.” Journal of the American Academy of Dermatology. 1998.