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Androgenetic alopecia is the most prevalent form of hair loss in both men and women, but its biology is less uniform than its name implies. The male presentation is well characterised: dihydrotestosterone (DHT) acting through dermal papilla androgen receptors drives a progressive molecular suppression of anagen that miniaturises follicles across a predictable frontotemporal-to-vertex pattern. The female presentation is considerably more complex. Many women with female pattern hair loss have entirely normal androgen levels; androgen-independent mechanisms are established; and the oestrogen withdrawal of menopause contributes through pathways that are not simply the mirror image of DHT excess. Understanding where the male and female presentations converge, and where they diverge, changes both treatment selection and client conversation considerably.

Androgenetic alopecia (AGA) is the most common cause of hair loss worldwide, affecting approximately 50% of men by age 50 and up to 40% of women by age 70, with prevalence rising sharply after the menopause. ^[2] It is a non-scarring alopecia – the follicular stem cell populations are not destroyed, and the follicles themselves retain the theoretical capacity to regenerate – but progressive miniaturisation produces a functional hair loss that becomes structural as follicle regression advances. The mechanism is primarily one of anagen duration compression rather than follicle death: each successive cycle produces a shorter anagen phase than the last, the hair shaft produced is progressively finer and shorter, and eventually the inferior segment of the follicle regresses to a depth consistent with vellus rather than terminal hair production.

The Kenogen Phase: An Under-Recognised Contributor

Before examining the DHT mechanism in detail, a lesser-known feature of AGA is worth establishing: the kenogen phase. In normal hair cycling, a new anagen phase begins relatively promptly after the club hair sheds at exogen – the follicle moves from telogen to anagen with a brief latency. In AGA, this latency is progressively prolonged. academic.oup.com The interval between one cycle’s telogen and the next cycle’s anagen – the kenogen phase – lengthens, meaning that even follicles not yet substantially miniaturised are spending an increasing proportion of time in an empty, non-productive state. At the scalp surface, this contributes to visible density reduction independently of shaft diameter changes; the scalp appears thinner in part because more follicles are between cycles at any given moment, not only because individual hairs are finer.

Male AGA: The DHT Mechanism

In male AGA, the mechanism connecting androgen exposure to follicle miniaturisation is well characterised. Testosterone is converted to dihydrotestosterone (DHT) by 5α-reductase enzymes (primarily type II in the scalp dermal papilla), and DHT binds androgen receptors in dermal papilla cells with considerably higher affinity than testosterone. ^[3] The DHT–androgen receptor complex then drives a constellation of changes in DPC signalling output that collectively shorten anagen:

• Wnt/β-catenin suppression: DHT drives withdrawal of Wnt pathway activity in DPCs, reducing the molecular clock signal that maintains anagen duration
• TGF-β2 upregulation: DPCs upregulate TGF-β2 secretion, which promotes premature matrix cell apoptosis and catagen entry
• IGF-1 downregulation: Androgen receptor activation upregulates miR-221 in DPCs, which suppresses IGF-1 expression – directly reducing the survival and proliferation signal that DPCs provide to matrix keratinocytes and to themselves
• FGF-7 reduction: DPC secretion of FGF-7, which normally stimulates matrix keratinocyte proliferation, is reduced
• GAS6 suppression: DPC GAS6 output is impaired, reducing HFSC activation capacity for the subsequent anagen cycle

Together, these changes compress anagen duration progressively across cycles. The follicle is not acutely damaged – it is gradually shifted toward a shorter and shorter productive phase, producing correspondingly finer and shorter hair shafts, until the inferior segment no longer reaches terminal depth. ^[1]

The distribution follows the androgen sensitivity gradient of the scalp: DPCs in the frontal and vertex regions express higher androgen receptor levels and greater 5α-reductase activity than occipital DPCs – which is why occipital hair is retained even in advanced AGA, and why occipital donor hair is preferred in transplantation. ^[3]

Inflammation: A Genuine Mechanistic Component

The perifollicular inflammation visible on AGA biopsy – a lymphohistiocytic infiltrate around the upper follicle – is not merely incidental. Significant CD4+ T cell infiltration into follicles has been demonstrated in both male AGA and FPHL, and current evidence indicates that this inflammatory component actively contributes to follicle cycle disruption and miniaturisation rather than simply accompanying it. ^[4] Perifollicular fibrosis, when present, is a poor prognostic indicator, reflecting structural changes in the follicle environment that limit the capacity for regeneration even if the androgen signal were removed. ijdvl.com The implication for treatment is that anti-inflammatory approaches are not purely supplementary to androgen-targeting treatment, they are addressing a mechanistic component of the condition in their own right.

Female Pattern Hair Loss: Where the Biology Diverges

FPHL shares the final common pathway with male AGA – follicular miniaturisation, anagen shortening, kenogen prolongation – but its aetiology is considerably less homogeneous. ^[2] The critical distinction is that many women with FPHL have entirely normal circulating androgen levels, and FPHL has been documented in women with no androgen receptors. academic.oup.com Androgen-independent mechanisms are established rather than speculative, making FPHL a condition where “androgenetic” is partially a misnomer for a significant proportion of affected women.

In women where androgen excess is present, the mechanism parallels male AGA – elevated DHT or enhanced local 5α-reductase activity in scalp DPCs drives the same Wnt/ TGF-β/IGF-1 suppression cascade. In women where androgens are normal, several other mechanisms are implicated: genetic predisposition producing enhanced follicular sensitivity to normal androgen levels; aromatase gene polymorphisms reducing local oestrogen production in the scalp; and possibly prostaglandin pathway dysregulation. ^[4]

The oestrogen picture adds a further layer. Indirect evidence for a protective oestrogen role is substantial – FPHL prevalence increases sharply post-menopause, pregnancy (high oestrogen) prolongs anagen, aromatase inhibitors and tamoxifen cause hair loss, and GWAS studies associate aromatase gene polymorphisms with FPHL susceptibility. academic.oup.com The mechanism is thought to involve oestrogen’s IGF-1R-mediated signalling in DPCs, which supports anagen maintenance independently of the androgen pathway, meaning that oestrogen withdrawal at menopause removes a DPC protective signal at the same time as any androgen-driven suppression continues or worsens.

FPHL biopsy findings reflect the dual-mechanism picture: terminal:vellus ratio falls from 7:1 (normal) to approximately 1.9:1; telogen proportion rises from 5–10% to 15–20%; perifollicular lymphohistiocytic infiltrate is common; and perifollicular fibrosis – a poor prognostic indicator – may be present. ijdvl.com

Classification and Pattern

Male AGA is classified by the Hamilton-Norwood scale (I–VII), progressing from frontal hairline recession through vertex thinning to confluent crown and frontal baldness. ^[1]

Female pattern hair loss is classified by the Ludwig scale (I–III), characterised by diffuse thinning over the crown and midscalp with preservation of the frontal hairline, the distinguishing clinical feature separating FPHL from male AGA. ^[1] An alternative frontal accentuation pattern (the “Christmas tree” pattern described by Olsen) produces greater density loss toward the frontal midscalp parting, which can be confused with frontal fibrosing alopecia on clinical inspection. ijdvl.com

The most important differential in women presenting with apparent frontotemporal recession is frontal fibrosing alopecia – a scarring alopecia caused by lymphocytic inflammation at the follicle isthmus, producing irreversible follicle destruction. Frontal fibrosing alopecia is distinguished by perifollicular erythema and scale at the receding hairline, eyebrow involvement in most cases, and a band-like recession rather than the diffuse density reduction of FPHL. jcadonline.com Unlike FPHL, frontal fibrosing alopecia produces scarring – follicles in the affected zone are permanently destroyed, not miniaturised – and misclassifying this as FPHL leads to inappropriate treatment and continued irreversible loss.