Alopecia: Types, Causes, Symptoms and Diagnosis

A UK clinical guide to every main type of alopecia — how they differ, how they are diagnosed, and which forms of hair loss need urgent specialist assessment.

Part of the Access Doctor Conditions Library.

What alopecia actually means

Alopecia is simply the medical word for hair loss. It says nothing about the cause, the pattern, or whether the hair will return. A woman shedding handfuls three months after giving birth, a child with a scaly patch caused by a fungal infection, a man whose hairline has crept back over fifteen years, and a person who loses every hair on their body in six weeks all have alopecia — and all four need completely different care.

Understanding your own hair loss starts with the hair cycle. Every follicle on the scalp works independently on a repeating three-phase cycle:

Because those cycles are staggered, losing hair every day is entirely normal. The NHS puts normal daily shedding at 50 to 100 hairs from a scalp carrying roughly 100,000 follicles. Hair loss becomes a medical question when shedding rises well above that, when it happens in a defined pattern, when the scalp itself looks or feels abnormal, or when hair simply stops being replaced.

Scarring vs non-scarring: the distinction that matters most

Dermatologists divide every cause of hair loss into two families. It is the first thing a specialist establishes, because it decides both the urgency and the realistic goal of care.

Non-scarring (non-cicatricial) alopecia

The follicle is still there. It may be miniaturised, switched off, or pushed prematurely into resting, but the stem cells that build a hair remain intact. On close inspection the tiny pores — the follicular openings — can still be seen dotting the skin. Regrowth is biologically possible, sometimes spontaneously, sometimes after the trigger is removed or the underlying condition treated. Alopecia areata, telogen effluvium, anagen effluvium, pattern hair loss and early traction alopecia all sit in this family.

Scarring (cicatricial) alopecia

An inflammatory process has destroyed the follicle and its stem cell reservoir, and fibrous scar tissue has taken its place. The skin often looks pale, smooth and slightly shiny, and crucially the follicular openings have disappeared. Hair that has already been lost will not return. The entire purpose of treatment is to switch off the inflammation at the active border and preserve the hair that remains — which is why time matters so much. Frontal fibrosing alopecia, lichen planopilaris, central centrifugal cicatricial alopecia, folliculitis decalvans and discoid lupus of the scalp all sit in this family.

The main types of alopecia at a glance

The table below covers the forms of hair loss seen most often in UK practice. Use it to narrow down what you may be dealing with, then read the relevant section in full — but treat it as orientation rather than a diagnosis, because several of these conditions look almost identical to the untrained eye and two can occur at once.

Alopecia areata, totalis and universalis

Alopecia areata is an autoimmune condition in which the immune system mistakenly targets actively growing hair follicles and forces them to shut down. The crucial point — and the one that gives people the most hope — is that the follicle is switched off, not destroyed. It can restart, sometimes after months, sometimes after years. The lifetime risk is around 2% of the population, and it affects all ages, sexes and ethnicities, with the peak onset in the second and third decades of life.

What it looks like

• One or more smooth, well-defined round or oval patches, most often on the scalp but possible in the beard, eyebrows, eyelashes or anywhere with hair
• Skin within the patch that looks essentially normal — not red, scaly, shiny or scarred, with follicular openings still visible
• Short broken hairs at the edge of a patch that are wider at the tip than the root, described as exclamation mark hairs and characteristic of active disease
• Patches that may appear over days rather than months, sometimes with mild tingling or itching first
• Regrowth that often comes back fine, soft and white or grey before regaining its normal colour

The patterns it can take

Nails and associated conditions

Nail changes occur in roughly 10–40% of people with alopecia areata — most commonly fine pitting, ridging or roughening — and can appear before the hair loss does. Alopecia areata also runs alongside other autoimmune and atopic conditions more often than chance would predict, including thyroid disease, vitiligo, psoriasis, type 1 diabetes, eczema, asthma and hay fever. A family history of alopecia areata or of autoimmune disease is common.

What happens next

The honest answer is that the course is unpredictable. Spontaneous regrowth is common, particularly with a single small patch, but so is relapse — alopecia areata is a condition that tends to come and go over a lifetime rather than one that resolves permanently. Around 5–10% of people progress to alopecia totalis or universalis. Features associated with a less favourable outlook include onset in childhood, very extensive loss, hair loss that has persisted beyond a year, the ophiasis pattern, nail involvement, a strong family history and coexisting atopic or autoimmune disease.

Specialists measure severity using the SALT score (Severity of ALopecia Tool), which expresses the percentage of the scalp affected. It is not just an academic exercise: SALT scores are used in NHS referral pathways to decide who should be assessed in secondary care for specialist options, with extensive disease above 50% scalp involvement a recognised trigger for routine dermatology referral.

Telogen effluvium: shedding after a shock

Telogen effluvium is the most common cause of sudden, alarming, all-over shedding — and one of the most misunderstood. A physical or emotional shock pushes an abnormally large number of follicles out of the growing phase and into resting at the same time. Because resting hairs take around three months to be pushed out, the shedding starts two to four months after the event that caused it. People almost always blame something that happened last week; the real culprit is usually a season ago.

Common triggers

• Childbirth — postpartum shedding typically peaks around three to five months after delivery
• A high fever, severe infection or a significant illness
• Surgery or a general anaesthetic
• Rapid or substantial weight loss, crash dieting, or very low protein intake
• Iron deficiency, with or without anaemia
• An over- or underactive thyroid
• Severe or sustained psychological stress, including bereavement
• Starting, stopping or changing certain medicines, including some used for blood pressure, mood, acne and contraception
• Stopping hormonal contraception or hormonal changes around the menopause

How to recognise it

The shedding is diffuse rather than patchy — the whole scalp thins, the ponytail feels thinner, and hair appears on the pillow, in the shower drain and on clothing. People commonly report losing well over a hundred and sometimes up to around 300 hairs a day. The scalp itself looks normal, and the hairline is preserved. Importantly, telogen effluvium causes thinning, not baldness: it very rarely produces a fully bald area.

Acute and chronic forms

Acute telogen effluvium peaks within a few months of the trigger and then settles, with full recovery of hair density usually within six to nine months once the cause has resolved. Chronic telogen effluvium means shedding that continues or fluctuates for more than six months. It most often affects middle-aged women, frequently has no single identifiable trigger, and can persist for years while the scalp still appears normal — distressing, but not a disease that causes baldness.

Anagen effluvium and cancer-treatment hair loss

Anagen effluvium is hair loss that happens while hair is still in its growing phase, caused by something that abruptly poisons the rapidly dividing cells of the hair matrix. Chemotherapy is by far the commonest cause; radiotherapy to the head and certain toxic exposures can do the same. Unlike telogen effluvium, it is fast — loss begins within days to a few weeks — and because around 85% of follicles are in the growing phase at any time, it can be close to total, affecting eyebrows, eyelashes and body hair as well as the scalp.

Follicles are damaged rather than destroyed, so regrowth normally begins within a few months of finishing treatment and is usually well under way by three to six months. Regrown hair often has a different texture or colour at first — tighter curl, or a change in shade — which usually settles over subsequent growth cycles. A minority of people experience persistent chemotherapy-induced alopecia, where hair has not meaningfully recovered more than six months after treatment ends; this warrants specialist dermatology assessment rather than watchful waiting.

Scalp cooling during chemotherapy infusions is offered by many UK cancer units and can reduce the degree of hair loss for certain regimens. Whether it is suitable depends on the drugs being used and the type of cancer, so it is a conversation to have with the oncology team before treatment starts rather than after.

Pattern hair loss in women and men

Pattern hair loss — androgenetic alopecia — is the single most common form of hair loss in both sexes. Around half of men over 50 and around half of women over 65 are affected to some degree. It is a gradual process of follicular miniaturisation, in which hairs become progressively finer, shorter and lighter over successive cycles until they no longer surface. It is not shedding in the way telogen effluvium is; it is a failure of replacement.

Female pattern hair loss

In women the picture is diffuse rather than focal. Density is lost over the top and crown of the scalp while the frontal hairline is characteristically preserved — a feature that distinguishes it from frontal fibrosing alopecia, where the hairline itself recedes. The earliest sign is usually a widening centre parting, sometimes described as a Christmas-tree pattern when viewed from above, along with a thinner ponytail. Roughly 40% of women show some evidence of hair loss by the age of 50, and it becomes considerably more common after the menopause. Dermatologists grade severity using the Ludwig or Sinclair scales.

Most women with pattern hair loss have entirely normal androgen levels, so it is not usually a sign of a hormonal disorder. Investigation for excess androgens is warranted where hair loss appears alongside acne, irregular or absent periods, or unwanted facial and body hair — a combination that raises the possibility of polycystic ovary syndrome. Thyroid function and iron stores are worth checking in most women with diffuse thinning, because deficiency and pattern loss frequently coexist and correcting one improves the other.

Male pattern hair loss

In men, hair loss follows the familiar sequence of a receding temporal hairline and thinning at the vertex, driven by the effect of dihydrotestosterone on genetically susceptible follicles and graded on the Norwood scale. Because it has its own evidence base, its own staging system and its own established treatments — oral finasteride and topical minoxidil chief among them — we cover it separately and in full.

Traction alopecia

Traction alopecia is caused by sustained mechanical pull on the hair. It is entirely preventable and, caught early, entirely reversible — but left long enough the repeated tension destroys follicles and it converts into a permanent scarring alopecia. That transition is the reason it deserves to be taken seriously rather than dismissed as a styling issue.

What causes it

• Tight braids, cornrows, weaves and hair extensions, particularly when worn continuously
• Dreadlocks, especially heavy or long ones
• Tight ponytails, buns and chignons worn daily
• Long uncut hair twisted or bound tightly, as in some religious practices
• Headwear or pins that place repeated tension on the same point of the hairline
• Chemical relaxing or heat treatment combined with tension, which weakens the shaft and amplifies the damage

How to recognise it

Thinning concentrates where the pull is greatest, most often along the frontal and temporal hairline. A useful clue is the fringe sign: a line of fine hairs is retained right at the very edge of the hairline while the hair immediately behind it thins, because those outermost hairs are not gripped by the style. Early disease may also produce itching, redness, small pustules, tenderness after styling and short broken hairs — all signals that the follicles are being injured and the style needs to change now.

Scarring (cicatricial) alopecias

Scarring alopecias are uncommon, frequently missed, and the group in which delay does the most harm. They share a common mechanism — inflammation destroying the follicle and its stem cells — and a common clinical signature: loss of the follicular openings, so the affected skin looks smooth and featureless rather than pitted with tiny pores. Many are also symptomatic, causing itch, burning or tenderness at the advancing edge, which is a useful distinguishing feature because most non-scarring hair loss is symptom-free.

Frontal fibrosing alopecia (FFA)

FFA produces a uniform band of recession along the front and sides of the scalp hairline. The exposed skin looks pale and shiny compared with the sun-exposed forehead above it, with no visible follicular openings, sometimes with isolated "lonely hairs" left stranded in the bald zone. Classically described in postmenopausal white women over 50, it is now recognised in younger women, in men, in children and across all ethnic groups, and its incidence has been rising internationally.

The single most useful early clue is the eyebrows. Thinning or complete loss of the eyebrows frequently precedes any visible change to the scalp hairline, so unexplained eyebrow loss in a woman over 40 deserves a scalp examination rather than a cosmetic solution. Itching, burning or small rough bumps along the hairline are also common early symptoms. FFA is associated with hypothyroidism and other autoimmune conditions. It is usually slowly progressive, with an average hairline recession of around 1.8 to 2.6 cm, and in most people it eventually becomes self-limiting after several years — but only the hair preserved along the way is kept.

Lichen planopilaris (LPP)

LPP is closely related to FFA and shares its microscopic appearance. It usually appears as irregular patches of loss on the crown and vertex, with redness and fine scale hugging the base of the remaining hairs, and hairs that pull out easily at the active margin. Itching, burning and scalp tenderness are typical. It most often affects middle-aged women but occurs in men and younger adults too, and it can coexist with lichen planus affecting the skin, nails or mouth.

Central centrifugal cicatricial alopecia (CCCA)

CCCA begins at the centre of the crown and spreads outwards in a roughly circular fashion. It is the most common form of scarring alopecia in women of African descent. Some people have marked itching, tingling or tenderness; others notice nothing at all until a partner or hairdresser points out thinning at the crown, which is one reason it often presents late. Because it can look at first glance like female pattern hair loss, and because the two conditions can occur together, a close examination for lost follicular openings is essential.

Folliculitis decalvans and discoid lupus

Folliculitis decalvans presents with recurrent pustules, crusting and painful boggy areas, and a distinctive feature known as tufting, where several hairs emerge from a single enlarged opening. Discoid lupus erythematosus of the scalp produces red, scaly, sharply demarcated plaques with altered pigmentation that heal to leave smooth, permanently bald scarred skin; it may occur alone or as part of wider lupus.

Infections, children and hair pulling

Tinea capitis (scalp ringworm)

Tinea capitis is a fungal infection of the scalp and hair shafts. It predominantly affects pre-adolescent children, with incidence peaking between the ages of three and seven, and is also seen in adults with weakened immunity. It presents as one or more scaly patches with broken-off hairs, sometimes leaving black dots where hairs have snapped at the surface, and it is frequently mistaken for stubborn dandruff or eczema. A severe inflammatory reaction called a kerion produces a painful, boggy, pus-filled swelling that can be misdiagnosed as a bacterial abscess.

Two points matter. First, tinea capitis needs oral antifungal treatment prescribed by a doctor after confirming the diagnosis with scalp scrapings or hair clippings, because creams and shampoos cannot reach the fungus inside the hair follicle. Second, untreated inflammatory disease — particularly kerion — can leave permanent scarring hair loss. It is also contagious, spreading between children and via shared combs, brushes, hats and pillows, and sometimes from pets, so household members may need checking too.

Trichotillomania (hair-pulling disorder)

Trichotillomania is a body-focused repetitive behaviour in which a person feels a recurrent urge to pull out their own hair. Estimates of how many people are affected vary considerably, with figures up to around 4% of the general population reported; onset peaks in the preschool years and again in early adolescence. It is distinguished from alopecia areata by the shape and texture of the loss: patches are irregular rather than perfectly round, the skin contains stubbly hairs of clearly differing lengths rather than being smooth and bare, and the hair pull test is negative. Management depends on age and ranges from simple behavioural strategies in young children to habit reversal therapy and psychological support in older children and adults.

Hair loss in children

Hair loss in a child should always be assessed by a clinician rather than watched. The likeliest causes are tinea capitis, alopecia areata, traction from tight styling, and hair pulling, but rarer structural hair shaft disorders and nutritional causes also exist — and the four common causes are managed completely differently, so guessing is unhelpful.

Systemic and nutritional contributors

Several general medical problems show up in the hair, usually as diffuse thinning rather than a defined pattern: iron deficiency, thyroid disease, coeliac disease, poorly controlled diabetes, systemic lupus, significant protein-calorie undernutrition and, occasionally, untreated syphilis, which can cause a characteristic patchy "moth-eaten" appearance. Severe deficiency of zinc, vitamin D or B vitamins can contribute, though for most people with a normal diet, supplements taken without a demonstrated deficiency do nothing for hair — and excessive vitamin A or selenium can actually cause hair loss.

Symptoms and warning signs

The features that most usefully separate one type of alopecia from another are the pattern of loss, the speed of onset, what the scalp itself looks like, and whether it hurts.

How alopecia is diagnosed

There is no single test for alopecia. Diagnosis is a structured process built mostly on history and close examination, with investigations used to confirm rather than to search blindly.

When to see a GP and when referral is urgent

Not all hair loss needs a doctor. Gradual thinning that follows a familiar family pattern, or shedding that starts a few months after childbirth or an illness and is already settling, can reasonably be watched. Beyond that, an assessment is worthwhile — and in some situations it is important.

Reasons to see your GP

• Hair loss that came on suddenly, in patches, or in clumps
• Any hair loss in a child
• Loss of eyebrows or eyelashes
• A scalp that itches, burns, hurts, scales, or has pustules
• An area of scalp that has become smooth and shiny with no visible pores
• Hair loss that started within weeks of a new medicine
• Hair loss with other symptoms such as fatigue, weight change, heavy periods, joint pain or a rash
• Hair loss that is causing significant distress, whatever the cause

What happens at a referral

NHS guidance is that most alopecia can be assessed and managed in primary care. Referral to dermatology is indicated when the diagnosis is uncertain, when hair loss persists despite appropriate primary care management, and for extensive alopecia areata — typically a SALT score above 50% — where specialist-only options may be considered. Suspected scarring alopecia should be referred promptly, because the hair loss is irreversible and a biopsy may be needed to establish the diagnosis and start treatment before more follicles are lost.

Living with alopecia: hair care, camouflage and wigs

Whatever the underlying diagnosis, there is a great deal that helps day to day — none of it involving medicines.

Looking after the hair you have

• Wash as often as suits your scalp. Washing does not cause hair loss, and avoiding washing simply allows shed hairs to accumulate and come out all at once, which feels far worse
• Handle wet hair gently — it is at its most fragile. Use a wide-tooth comb and detangle from the ends upwards
• Reduce heat styling, and use the lowest effective setting when you do
• Avoid stacking chemical processes. Bleaching, relaxing and permanent colouring in close succession weakens the hair shaft
• Give tight styles a rest, alternate the direction of partings and braids, and never wear tension over an area that is already thinning
• Eat adequately. Crash diets and very low protein intake are a genuine and common cause of shedding

Protecting exposed skin and eyes

A scalp that has not seen daylight for decades has no accumulated tolerance to ultraviolet light and burns easily. Sunscreen of SPF 30 or above on exposed areas, or a hat, is a practical necessity rather than an afterthought — and it reduces long-term skin cancer risk. If eyelashes have been lost, the eyes lose their natural barrier against dust, grit and sweat, so wraparound glasses or sunglasses outdoors are genuinely useful. Loss of nasal hair can similarly mean more sneezing, a runnier nose and more irritation from dust.

Camouflage and hairpieces

Options range from the very simple to the semi-permanent: coloured fibre powders and root-touch sprays that thicken the appearance of existing hair, tinted scalp powders that reduce contrast between skin and hair, scalp micropigmentation, hair toppers and partial pieces, full wigs, and headwear from scarves to caps. Eyebrow pencils, stencils, semi-permanent tinting and microblading can be transformative where brows have been lost. None of these treat the condition, and all of them can meaningfully improve daily life.

Wigs on the NHS

NHS wigs are available to people with significant hair loss, usually accessed through a hospital appliance department following referral. The charges below apply in England; arrangements differ in Scotland, Wales and Northern Ireland, so check locally.

You do not pay these charges if you are under 16, aged 16 to 18 and in full-time education, a hospital inpatient when the wig is supplied, a war pensioner where the hair loss relates to an accepted disablement, in receipt of certain income-related benefits, or you hold a valid HC2 certificate. An HC3 certificate may provide partial help.

The emotional impact and where to get support

Hair loss is routinely treated as a cosmetic problem. For many people it is nothing of the sort. Sudden or extensive alopecia can affect identity, confidence, intimate relationships, work and social life, and is associated with meaningful rates of anxiety and low mood. Children and teenagers may face questions, staring or bullying at exactly the age when fitting in matters most. None of this is vanity, and it is a legitimate reason to see your GP even when the hair loss itself needs no medical treatment.

Practical things that help: telling a few people directly rather than waiting to be asked, agreeing a short form of words for strangers, involving a child's school early so staff can head off comments, and connecting with others who have the same condition. Talking therapies are available on the NHS and can be requested through your GP or, in England, via NHS Talking Therapies self-referral.

Alopecia UK is the national charity for people affected by alopecia, offering local and online support groups, resources for children and parents, dedicated support for men, and funding for research. In 2025/26 it reported 1,805 adults and children attending its support groups and events, 24,625 people receiving peer support through its online communities, and £585,165 awarded in research grants.

Ten myths about alopecia

Where to go next for treatment

This page deliberately stops short of covering medicines, because the right treatment depends entirely on which type of alopecia you have — and choosing one before the diagnosis is settled is how people waste months. Where to go next depends on what the picture above suggests:

• Male pattern hair loss — read our full clinical guide to male hair loss and androgenetic alopecia, which covers the Norwood stages, the evidence for each treatment and how to access them. Where the diagnosis is confirmed, finasteride for male pattern hair loss is available following an online clinical assessment
• Alopecia areata — see your GP. Limited patches are often managed in primary care, and extensive disease can be referred to dermatology for specialist assessment
• Suspected scarring alopecia — see your GP promptly and ask specifically about dermatology referral. This is the one group where waiting has a permanent cost
• Telogen effluvium — the treatment is finding and correcting the trigger, not treating the hair. Ask about iron studies and thyroid function
• Traction alopecia — change the styling now, while the follicles are still there
• Suspected scalp infection — see your GP for confirmation and prescribed treatment, particularly for a child

Getting help from Access Doctor

Access Doctor is a GPhC-registered online pharmacy (#9011198) with pharmacist independent prescribers. Where hair loss is confirmed male pattern baldness, treatment can be arranged online after a clinical assessment. Where the picture points to alopecia areata, a scarring alopecia, a scalp infection or hair loss in a child, the right answer is your GP — and we will tell you so.