Androgenetic Alopecia: Understanding Genetic Baldness and Its Treatments
Androgenetic alopecia (AGA) is the cause of over 95% of male baldness and approximately 40% of female alopecia. It is the most common form of hair loss worldwide — and yet one of the least well understood by patients. Understanding this mechanism precisely means being able to choose the right treatment at the right time.
What Is Androgenetic Alopecia?
AGA is a progressive hair loss caused by the genetic sensitivity of hair follicles to dihydrotestosterone (DHT), a testosterone derivative. It is not a disease — it is a hereditary trait. In genetically sensitive scalp areas, follicles undergo progressive miniaturisation under the effect of DHT, producing thinner, shorter hairs until they shut down permanently.
Genetics: Where Does Baldness Come From?
AGA is polygenic. The myth that baldness is inherited solely from the mother is false — it can come from either side. The AR gene (androgen receptor) on the X chromosome strongly influences follicle DHT sensitivity, but other autosomal loci also modify progression and pattern.
Female Androgenetic Alopecia: A Different Profile
In women, AGA presents differently: hair loss is diffuse and centred on the top of the scalp, with progressive widening of the central parting. The frontal hairline is typically preserved. The Ludwig scale classifies this form in 3 stages. It is often aggravated by hormonal factors (menopause, PCOS, post-partum) or deficiencies (iron, vitamin D).
How Is Androgenetic Alopecia Diagnosed?
- Trichoscopy: dermoscopic examination revealing characteristic follicular miniaturisation signs
- Blood tests: ferritin, TSH, androgen hormones — to exclude aggravating secondary causes
- Skin biopsy: rarely needed, useful in atypical cases to distinguish AGA from scarring alopecia
Medical Treatments: Slowing Progression
Minoxidil: First-Line Treatment
The only topical treatment approved for AGA in both men and women. It prolongs the hair growth phase and improves scalp vascularisation. Limitation: it must be applied for life — cessation causes relapse. It does not address DHT sensitivity.
Finasteride: DHT Inhibitor
Inhibits 5-alpha-reductase, the enzyme converting testosterone to DHT. Studies show arrest or marked slowing of hair loss in 80–90% of patients with continuous treatment. Possible side effects in 1–2% (sexual dysfunction). Prescription required.
Dutasteride: A More Potent Alternative
Inhibits both isoforms of 5-alpha-reductase versus finasteride's single-isoform inhibition. Used off-label for AGA-resistant cases in France.
The Definitive Treatment: FUE Hair Transplant
Medical treatments slow AGA — they do not reverse it. For areas already depleted where follicles have permanently shut down, only FUE hair transplantation can restore permanent density. Transplanted grafts from the occipital donor zone are genetically insensitive to DHT — once transplanted, they retain this resistance and grow permanently.
The optimal strategy for moderate AGA combines medical treatment (finasteride ± minoxidil) to stabilise non-transplanted areas, plus FUE transplant for the definitively depleted zones.
When Should You Consider a Transplant for AGA?
Transplanting too early — before age 25–28 on actively progressing baldness — risks an unsatisfactory long-term result. General criteria: baldness stable for 12–24 months, sufficient donor area, realistic expectations, and ideally prior medical treatment to stabilise transitional areas.
Conclusion: Understand Before You Act
AGA is a predictable biological mechanism with documented therapeutic options and a definitive surgical solution for already-affected areas. Phoenix Hair Center offers a comprehensive consultation to assess your degree of AGA, your treatment options, and if indicated, a personalised transplant plan. Free consultation at 52 Avenue de la Bourdonnais, Paris 7th.
