DHT
Strongest endogenous androgen, 3–5x more potent than testosterone at the AR. Formed from testosterone by 5α-reductase. Essential for genital development, libido and prostate.
Auch bekannt als: Dihydrotestosteron, Dihydrotestosterone, 5α-Dihydrotestosteron
Overview
Dihydrotestosterone (DHT) is produced by the irreversible reduction of testosterone by the enzyme 5α-reductase (two isoforms: type 1 in skin/liver, type 2 in prostate/genitals). With a ~3–5× higher binding affinity to the androgen receptor than testosterone, it is the most potent endogenous androgen.
Physiological roles
- Embryonic development: Differentiation of male genitalia (5α-reductase deficiency → female phenotype despite XY karyotype)
- Puberty: Deeper voice, pubic hair, beard growth, penis enlargement
- Libido: Strong direct libido mediator in the CNS
- Prostate: Main androgen in the prostate → prostate growth
DHT & hair loss
In genetically predisposed men, DHT binds to AR in hair follicle papilla cells of the scalp → miniaturization of follicles → androgenetic alopecia. 5α-reductase inhibitors (finasteride, dutasteride) block DHT formation and slow/stop hair loss, but also reduce other DHT-mediated functions.
AAS & DHT
Testosterone aromatizes to E2 AND is reduced to DHT. DHT derivatives (Stanozolol, Oxandrolone, Masteron) do not take this route. They have their own androgenic profile directly at the receptor. 19-nor-steroids (nandrolone) are reduced to dihydronandrolone, much less androgenic than DHT → “joint-friendly”.
Sources
- Imperato-McGinley J et al. Steroid 5-alpha-reductase deficiency in man. Science. 1974. PubMed
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