DHT

Dihydrotestosterone (DHT) is the 5α-reduced metabolite of testosterone produced by 5α-reductase action on the testosterone A-ring. The structural change — saturation of the 4,5-double bond — produces a molecule with approximately 3× the androgen receptor binding affinity of the parent and substantially longer receptor dwell time, making DHT the dominant androgen at tissues with high 5α-reductase expression: scalp follicles, prostate, sebaceous glands, and external genitalia.

Reference ranges, adult male:

– Serum DHT: 30–85 ng/dL on LC-MS/MS assay
– DHT:testosterone ratio: ~10% in healthy adult males
– The ratio rises with age as 5α-reductase activity persists despite declining testosterone

Tissue-specific roles:

DHT is essential for embryonic and pubertal development of male external genitalia, prostate, and secondary sexual characteristics. Imperato-McGinley et al. 1974, Science documented the consequences of 5α-reductase Type II deficiency in genetic males — incomplete external virilisation despite normal testosterone, with later masculinisation at puberty as Type I isoform compensates partially.

In adult males, DHT maintains prostate volume, scalp follicle activity (driving androgenic alopecia in genetically susceptible individuals), sebaceous gland function (acne mechanism), and external genitalia trophism. Notably, DHT does not aromatise — it cannot be converted to estradiol via CYP19A1, which is why DHT-derivative AAS (stanozolol, oxandrolone, drostanolone) carry no aromatisation risk.

Clinical implication for AAS users:

Compounds elevating DHT exposure accelerate androgen-driven side effects in genetically susceptible users — male pattern baldness progression, prostate volume increase, acne, sebaceous overproduction. The risk stratifies by mechanism:

– Direct DHT elevation: exogenous testosterone via 5α-reduction, exogenous DHT (rarely used), masteron (DHT derivative), trenbolone (5× AR affinity).
– DHT-derivative bypass: stanozolol, oxandrolone, drostanolone, methenolone — bind scalp AR directly without 5α-reductase involvement.
– 5α-reductase inhibition: finasteride (Type II), dutasteride (both isoforms) — protective for testosterone-dominant cycles, pharmacologically irrelevant for DHT-derivative compounds.

The therapeutic paradox:

DHT is essential for normal male physiology yet drives multiple androgen-related morbidities. Complete suppression (as with dutasteride) produces measurable libido and erectile effects in some users, while incomplete suppression (finasteride monotherapy) leaves residual scalp DHT that may continue driving alopecia in highly susceptible individuals. The clinical balance favours partial suppression in most contexts; complete suppression is reserved for established prostate hyperplasia management.

Bloodwork interpretation:

Isolated serum DHT measurement is rarely informative — scalp tissue DHT is the relevant variable for alopecia risk and is not measurable on standard panels. Suppression-monitoring on finasteride or dutasteride uses serum DHT as a surrogate marker; the threshold for adequate scalp protection is ~70% serum reduction.