From the Research
Androgenetic alopecia (AGA) is primarily caused by the conversion of testosterone to dihydrotestosterone (DHT) by the enzyme 5α-reductase, leading to miniaturization of hair follicles and shortening of the anagen phase. This process is mediated by the binding of DHT to androgen receptors in hair follicles, resulting in the transformation of thick, pigmented terminal hairs into fine, unpigmented vellus hairs 1. The pathogenesis of AGA involves a complex interplay of hormonal, genetic, and molecular factors, including genetic predisposition, perifollicular inflammation, oxidative stress, and decreased microcirculation around affected follicles 2, 3.
Key factors contributing to the development of AGA include:
- Genetic predisposition, with polymorphisms in the androgen receptor gene on the X chromosome contributing to male pattern baldness
- Hormonal influences, particularly the conversion of testosterone to DHT by 5α-reductase
- Inflammatory and oxidative stress mechanisms, including perifollicular inflammation and decreased microcirculation
- Prostaglandin imbalances, particularly elevated prostaglandin D2 and decreased prostaglandin E2, which further contribute to follicular miniaturization 4, 5
Understanding the pathogenesis of AGA has led to the development of therapeutic approaches targeting DHT production, promoting vasodilation and hair growth, and addressing inflammation. The most effective treatments for AGA include finasteride, dutasteride, minoxidil, and low-level laser therapy, which have been shown to improve hair density, thickness, and growth in both men and women 5. However, the evidence quality for these treatments is generally considered low, and further research is needed to fully validate their efficacy.