Common Causes of Female Androgenetic Alopecia
Female androgenetic alopecia is primarily caused by genetic predisposition combined with androgen activity on genetically susceptible hair follicles, though most women have normal androgen levels. 1, 2
Primary Pathogenic Mechanisms
Genetic Factors
- Polygenic inheritance pattern is the fundamental cause, with multiple genes contributing to susceptibility 3, 2
- The androgen receptor (AR) gene is the only definitively identified genetic contributor to date, though other genes remain to be discovered 3
- Approximately 20% of affected individuals report a positive family history, indicating strong hereditary influence 4
Androgen-Mediated Follicular Miniaturization
- Dihydrotestosterone (DHT) binds to androgen receptors in genetically susceptible follicles, activating genes that transform terminal follicles into miniaturized follicles 2
- Women with androgenetic alopecia demonstrate higher levels of 5-alpha reductase and androgen receptors in frontal hair follicles compared to occipital follicles 2
- Critically, only one-third of women with female androgenetic alopecia show abnormal androgen levels, meaning most have normal hormonal profiles 1
Secondary Endocrinologic Causes
Hyperandrogenic Conditions
When hyperandrogenism is present, specific endocrinologic disorders should be investigated 1:
- Polycystic ovarian syndrome (PCOS) is the most common cause of elevated ovarian androgens 4
- Hyperprolactinemia 1
- Nonclassical (late-onset) congenital adrenal hyperplasia 4
- Androgen-secreting tumors of the ovary or adrenal gland (rare) 4, 1
Clinical Indicators for Endocrine Evaluation
Hormonal testing is only warranted when clinical features of hyperandrogenism are present 4:
- Infrequent menses or oligomenorrhea 4
- Hirsutism 4, 2
- Severe unresponsive cystic acne 2
- Infertility 4
- Clitoromegaly 4
- Virilization 2
- Galactorrhea 2
- Truncal obesity or acanthosis nigricans 4
Important Clinical Caveats
Most women with female androgenetic alopecia have normal menses, normal pregnancies, and normal hormone levels 2. Extensive hormonal testing is unnecessary in the absence of clinical signs of androgen excess 2.
The condition typically begins between ages 12 and 40 years, with incidence equal to that in men 2. The pathogenesis involves a pre-programmed transformation from long growth (anagen) and short rest (telogen) cycles to long rest and short growth cycles, coupled with progressive follicular miniaturization 3.