What is androgenetic alopecia?
Androgenetic alopecia (AGA), commonly called male-pattern hair loss or male-pattern baldness, is a progressive condition driven by the interaction of androgenic hormones — primarily dihydrotestosterone (DHT) — with genetically predisposed hair follicles. DHT is produced from testosterone by the enzyme 5-alpha reductase, which is present in high concentrations in hair follicles on the scalp.
DHT binds to androgen receptors in susceptible follicles, causing them to miniaturise progressively. Each growth cycle produces a shorter, finer hair. Eventually, the follicle no longer produces visible hair.
The Sehgal consensus paper estimates AGA prevalence in Indian males aged 30–50 at approximately 58% — a figure comparable to Western populations, though the pattern and age of onset may differ by population.
The characteristic pattern
AGA follows a predictable distribution described by the Hamilton-Norwood scale: beginning at the frontal hairline and temporal recessions (Norwood types I–III), progressing to vertex (crown) involvement (types IV–V), and eventually connecting the frontal and vertex regions in more advanced cases (types VI–VII).
Not all patients progress through all stages. Genetic background strongly determines the extent of progression; a man whose paternal and maternal grandfathers had minimal hair loss at 70 is unlikely to have severe AGA at 40, though the pattern is not perfectly predictable.
The evaluation before treatment
A common pattern in India: a patient notices hair loss, buys topical minoxidil from a pharmacy, uses it inconsistently for a few months, and either continues indefinitely or abandons it when results are unclear. This approach bypasses the evaluation that determines whether the hair loss is actually AGA, whether other contributing factors are present, and whether the treatment strategy is appropriate for the severity and pattern.
A clinical evaluation of hair loss in an Indian male typically includes:
Dermatoscopy or trichoscopy. Visual examination of the scalp and follicles under magnification. The pattern of miniaturised follicles, perifollicular pigmentation, and follicular unit ratio (single-hair vs multi-hair follicles) confirms AGA and provides a severity assessment that guides treatment planning.
Blood tests. AGA is primarily a genetic and hormonal condition, but several factors can accelerate it:
- Ferritin: iron deficiency accelerates hair loss in genetically predisposed individuals; serum ferritin below 70 ng/mL is associated with accelerated AGA even without anaemia
- Thyroid panel: hypothyroidism produces diffuse hair loss that overlaps with AGA clinically
- Zinc: deficiency is common in Indian diets high in phytate-containing grains and legumes; zinc is required for normal hair follicle cycling
- Vitamin D: low in a significant proportion of urban Indians; associated with hair follicle dysfunction
- DHT and testosterone: elevated androgens may indicate an underlying hormonal condition
Assessment of other conditions. AGA frequently coexists with seborrhoeic dermatitis (which worsens scalp inflammation and may accelerate follicular miniaturisation) and with diffuse telogen effluvium (stress-related or nutritional hair loss that presents simultaneously and complicates the clinical picture).
How doctors think about topical and oral management
Two medications have the strongest evidence for AGA management:
Topical minoxidil (2% or 5% solution, or foam formulations). The mechanism is not completely understood but likely involves vasodilation, prolongation of the anagen phase, and direct cellular effects on follicle keratinocytes. It is applied daily or twice daily to the affected scalp. Results require consistent use over at least four to six months before meaningful assessment. It does not stop the progression of AGA — it slows it and may reverse some miniaturisation — and any benefit is lost on discontinuation.
Oral finasteride (1 mg daily). A 5-alpha reductase inhibitor that reduces DHT levels in the scalp and serum. Randomised trial data show significant reduction in hair loss and some degree of regrowth in the majority of men treated for 12 months or more. It is more effective than topical minoxidil as monotherapy for vertex hair loss. Side effects — reduced libido, ejaculatory dysfunction — occur in a minority of patients and are reversible on discontinuation in most cases.
The decision between topical-only and combined approaches depends on the severity of hair loss, the pattern and rate of progression, the patient's own priorities (including side effect tolerance), and the results of the evaluation described above.
What the evaluation cannot tell you
Androgenetic alopecia is progressive. The rate of progression is variable and only partially predictable from the current pattern. A 28-year-old with Norwood II hair loss may progress slowly over decades, or may progress rapidly to Norwood V by 40. Clinical evaluation can guide treatment; it cannot guarantee trajectory.
Hair follicle transplantation — surgical redistribution of DHT-resistant occipital follicles to affected areas — is a separate consideration for patients with advanced AGA who want a more permanent intervention. It addresses the result of AGA, not its progression; continued medical management post-transplant is typically recommended.