Hair Thinning & Loss

Hair loss causes disproportionate distress and is frequently mismanaged, largely because two very different conditions get treated as one. Telogen effluvium is a diffuse shed. Something — illness, surgery, childbirth, crash dieting, severe stress, iron deficiency, thyroid disease, starting or stopping certain medications — pushes an abnormally large fraction of follicles from the growth phase into the resting phase simultaneously. Two to three months later, those hairs shed together. The delay is the single most useful diagnostic clue and the one patients almost always miss: the cause lies in the past, not the present. Telogen effluvium is self-limiting and reverses fully once the trigger is corrected, though regrowth takes six months or more. Androgenetic alopecia is different in every respect. It is progressive, patterned rather than diffuse, and driven by genetically determined follicular sensitivity to dihydrotestosterone. Affected follicles miniaturise over successive cycles, producing progressively finer, shorter, less pigmented hair until they stop. In men this produces temporal recession and vertex thinning; in women, widening of the central part with preserved frontal hairline. It does not resolve on its own and requires ongoing treatment to maintain any gains. The practical distinction: shedding suggests effluvium, thinning suggests androgenetic loss, and the two frequently coexist — an effluvium episode often reveals underlying pattern loss that was previously unnoticed. Scarring alopecias are a third category and a medical urgency. Loss of follicular openings, scalp redness, scaling or pain requires prompt dermatology referral, because destroyed follicles cannot be recovered.

• •Increased hairs in the shower drain, brush or on the pillow
• •Widening of the central parting (female pattern)
• •Receding temples or thinning at the crown (male pattern)
• •Diffuse thinning across the whole scalp
• •Reduced ponytail thickness
• •Visible scalp under bright light
• •Scalp itching, burning or tenderness — a red flag for scarring alopecia
• •Loss of eyebrow or body hair, suggesting a systemic cause

• •Androgenetic alopecia — DHT sensitivity, genetically determined
• •Telogen effluvium from illness, surgery, fever or COVID-19
• •Postpartum hormonal shift
• •Iron deficiency with low ferritin
• •Thyroid disease, both under- and overactive
• •Rapid weight loss or inadequate protein intake
• •Severe psychological stress
• •Medications: retinoids, anticoagulants, some antidepressants, chemotherapy, hormonal contraceptive changes
• •Alopecia areata, an autoimmune patchy loss
• •Traction from tight hairstyles
• •Scarring alopecias such as lichen planopilaris and frontal fibrosing alopecia

Hair grows in cycles: anagen, an active growth phase lasting two to seven years; catagen, a brief transition; and telogen, a three-month resting phase after which the hair sheds. At any time roughly 85-90% of scalp follicles are in anagen. Anything that disrupts this proportion produces visible loss. Telogen effluvium works by synchronisation. A systemic insult pushes many follicles into telogen at once, and because telogen lasts about three months, the shed appears with that fixed delay. The follicles are undamaged, which is why full recovery is the norm. Androgenetic alopecia works by miniaturisation. In genetically susceptible follicles, type II 5-alpha reductase converts testosterone to dihydrotestosterone, which binds androgen receptors in the dermal papilla and progressively shortens the anagen phase with each cycle. The follicle produces a finer, shorter hair each time until it becomes vellus. Because the process is cumulative and cycle-dependent, early treatment preserves far more than late treatment. Nutritional causes act by substrate limitation. Hair matrix keratinocytes are among the fastest-dividing cells in the body, so iron, protein and calorie deficits hit them early — an evolutionary triage that sacrifices hair to preserve essential functions.