Androgenic Hormones
Androgens (including testosterone, dihydrotestosterone (DHT), dehydroepiandrosterone sulfate (DHEA-S) and androstenedione) are steroid hormones that play a central role in regulating the skin appendages, especially the sebaceous glands and hair follicles. The skin is not just a target organ that receives androgens from the blood; it is also a peripheral endocrine organ with its own complete enzyme machinery to make, convert and amplify androgen signals locally.
How androgens act on skin cells and how they are processed locally:
- Conversion by 5-alpha-reductase and androgen receptor (AR) affinity:
- Free testosterone in the blood passes into sebocytes and dermal papilla cells of the hair follicle. There, 5-alpha-reductase (mainly type 1 in the sebaceous glands and type 2 in the dermal papilla) converts testosterone into dihydrotestosterone (DHT).
- DHT binds the androgen receptor (AR) 5–10 times more strongly than its precursor testosterone and is many times more potent at switching on gene transcription.
- Sebaceous gland stimulation and acne formation (acnegenesis):
- The DHT–AR complex enters the nucleus of the sebocyte and activates the SREBP-1 (sterol regulatory element-binding protein 1) pathway. This drives a surge in lipid production, enlarging the sebaceous glands and causing excess oil production (hyperseborrhea).
- Excess sebum changes its lipid makeup (less linoleic acid, more oxidized squalene), which causes the follicle opening to become blocked with keratin and creates an oxygen-poor environment where Cutibacterium acnes thrives and triggers inflammation.
- Opposite effects on hair follicles (the androgen paradox):
- On the scalp (causing androgenetic alopecia): in the dermal papillae of the crown and frontal scalp, the DHT–AR complex triggers growth inhibitors such as TGF-β1 and DKK-1. The growth phase (anagen) becomes shorter and the resting phase (telogen) longer, so follicles gradually shrink (miniaturization) and thick terminal hairs turn into fine vellus hairs.
- On the body (causing hirsutism): at the same DHT levels, in androgen-dependent areas (chin, chest, abdomen, thighs) DHT instead increases the growth factor IGF-1, converting fine vellus hairs into dark, coarse, long terminal hairs.
Skin Signs of Androgen Excess or Imbalance
| Clinical Sign | How It Looks | Cellular and Molecular Mechanism |
|---|---|---|
| Therapy-resistant acne | Inflamed spots and cysts concentrated on the lower third of the face (jawline, chin, neck), flaring persistently and responding poorly to standard treatment. | Increased 5α-reductase activity in the sebaceous glands, causing excess sebum and blocked follicle openings. |
| Hirsutism | Dark, coarse, thick hairs in a male pattern in women: chin, upper lip, chest, midline of the abdomen, back, thighs. | DHT stimulates peripheral dermal papillae to convert vellus hairs into terminal hairs. |
| Androgenetic alopecia (AGA) | Gradual thinning and widening along the part (Ludwig pattern in women), or a receding frontal hairline and crown balding (Norwood pattern in men). | DHT increases TGF-β1, miniaturizing follicles and shortening the anagen phase. |
| Excess oil and seborrheic dermatitis | Constantly shiny skin, enlarged pores across the face, greasy yellow scale on the eyebrows, sides of the nose and scalp. | DHT activates SREBP-1, increasing triglyceride and squalene synthesis in sebocytes. |
| Acanthosis nigricans | Thickened, darkened, velvety plaques in skin folds (neck, armpits, groin), often seen with PCOS. | Androgen excess combined with high insulin levels (hyperinsulinemia) stimulates IGF-1 receptors on keratinocytes. |
Testosterone vs. Dihydrotestosterone (DHT): Effects on the Skin
| Feature | Testosterone (T) | Dihydrotestosterone (DHT) |
|---|---|---|
| Origin | Secreted directly by the testes, ovaries and adrenal cortex | Converted from testosterone by 5α-reductase in the skin |
| Affinity for the androgen receptor | Moderate (dissociates from the receptor easily) | Very high (5–10 times that of testosterone), with a long-lasting bond |
| Effect on sebaceous glands | Baseline stimulation of the sebaceous glands | Maximal gland enlargement and sebum production |
| Effect on scalp hair follicles | Weak effect on the hair growth cycle | The core cause of follicle miniaturization and balding (AGA) |
| Response to topical/oral drugs | Little affected by local enzyme inhibitors | Strongly suppressed by 5α-reductase inhibitors (finasteride, dutasteride) |
Our Approach
At Haute-Derma, we assess androgen-related skin conditions systematically:
- Clinical Screening and Standardized Scores:
- Hair growth is scored with the modified Ferriman-Gallwey scale (a total score above 8 indicates hirsutism).
- Follicle miniaturization and the degree of hair loss are graded on the Norwood scale (men) or the Ludwig/Sinclair scale (women).
- We take a detailed history of the menstrual cycle, any signs of virilization and current hormonal medications.
- Biochemical Testing and Endocrine Screening:
- A morning androgen panel (on days 2–5 of the menstrual cycle): total testosterone, free testosterone, DHEA-S (to screen for an adrenal source), androstenedione, SHBG (sex hormone-binding globulin) and 17-OH progesterone.
- Insulin resistance (HOMA-IR) and the LH/FSH ratio are added if polycystic ovary syndrome (PCOS) is suspected.
- Polarized-Light Imaging and Trichoscopy:
- Trichoscopy: dermoscopy is used to check variation in hair shaft diameter (balding is indicated when more than 20% of hairs have shrunk to under 0.03 mm), the proportion of single-hair follicular units and the peripilar sign (a brown halo around the hair base).
- Sebaceous gland assessment: fluorescence imaging measures porphyrin density and sebum output across the T-zone and jawline.
Treatment Options at Haute-Derma
Our treatment of androgen-related skin problems combines control of circulating hormones with direct treatment of the skin itself:
- Treating Androgen-Driven Acne and Excess Oil:
- Topical agents targeting the follicle and sebaceous gland: azelaic acid 15–20% or salicylic acid (BHA) 2% to clear blocked follicle openings, combined with oral anti-androgen therapy (spironolactone, or a combined contraceptive containing a newer progestin such as drospirenone) under specialist supervision.
- Light therapy: blue LED (415 nm) to kill C. acnes, combined with red LED (630 nm) to calm dermal inflammation and regulate sebocyte activity.
- Medical Laser Hair Removal for Hirsutism:
- Diode laser (808 nm) selectively destroys the growth centers of the hair follicle through selective photothermolysis, reducing dark, coarse hairs without harming the surrounding tissue.
- A supportive cream containing eflornithine 13.9% (which inhibits the enzyme ODC in the follicle) slows the regrowth of new hair.
- Restoring Hair Follicles in Androgenetic Alopecia (AGA):
- Topical and oral 5α-reductase inhibition: oral finasteride or dutasteride, or delivery by mesotherapy microinjections directly into the scalp's dermal papilla region, to block DHT formation.
- Boosting microcirculation and the anagen phase: minoxidil solution 2–5% combined with microneedle mesotherapy delivering growth peptide complexes (Capixyl, copper tripeptide-1), biotin and B vitamins.
- Low-level laser therapy (LLLT): low-power laser light (650 nm) stimulates the mitochondria of dermal papilla cells to produce more ATP, extending the anagen growth phase of the follicle.
