What Causes Hair Loss: Types, Hormones, Genetics, and Treatment Options
A comprehensive look at hair loss causes—androgenetic alopecia, telogen effluvium, alopecia areata, and more—plus the science of hair growth and effective treatments.
This article is for informational purposes only. Consult a qualified healthcare professional for medical advice, diagnosis, or treatment.
The Biology of Hair Growth
Each of the roughly 100,000 hair follicles on the human scalp cycles independently through three phases. The anagen (growth) phase lasts 2–6 years for scalp hair, during which the hair shaft actively elongates from the base of the follicle. This is followed by catagen, a brief transitional phase of 2–3 weeks in which growth stops and the follicle shrinks. Finally, telogen (resting) lasts 3–4 months before the old hair sheds and a new anagen phase begins. At any one time, approximately 85–90% of scalp follicles are in anagen and 10–15% are in telogen. Shedding 50–100 hairs per day is entirely normal.
Common Types of Hair Loss
| Type | Pattern | Cause | Prevalence |
|---|---|---|---|
| Androgenetic alopecia (AGA) | Progressive thinning at crown and temples (men); diffuse crown thinning (women) | Genetic sensitivity of follicles to DHT | 50% of men by age 50; 40% of women by age 70 |
| Telogen effluvium | Diffuse shedding across entire scalp | Physiological shock causes premature telogen transition | Very common; typically self-limiting |
| Alopecia areata | Patchy, well-defined bald spots | Autoimmune attack on hair follicles | ~2% lifetime prevalence |
| Traction alopecia | Hairline recession at traction sites | Chronic mechanical tension from tight hairstyles | Common in certain hairstyle cultures |
| Tinea capitis | Patchy loss with scaling and inflammation | Fungal scalp infection (dermatophytes) | Most common in children |
| Scarring alopecia (cicatricial) | Permanent loss with scarring | Inflammatory conditions destroy follicle stem cells (lichen planopilaris, discoid lupus) | Uncommon; urgent specialist referral needed |
Androgenetic Alopecia: The DHT Pathway
Androgenetic alopecia (AGA), commonly called male or female pattern baldness, is the most prevalent form of hair loss. It results from the progressive miniaturization of genetically susceptible hair follicles under the influence of dihydrotestosterone (DHT). DHT is produced from testosterone by the enzyme 5-alpha reductase (5-AR), which is highly expressed in scalp follicles. DHT binds to androgen receptors in follicle dermal papilla cells, signaling them to shorten the anagen phase and progressively reduce the follicle's diameter over successive cycles until it produces only fine vellus hairs or ceases production entirely.
The genetics of AGA are polygenic and complex; over 350 genetic loci have been associated with the condition. The most important is a variant on the X chromosome encoding the androgen receptor (AR)—explaining why maternal grandfather baldness is a stronger predictor than paternal—but variants on dozens of autosomes also contribute. Women with AGA typically have intact hairlines but diffuse crown thinning because their lower androgen levels produce a less aggressive pattern.
Telogen Effluvium
Telogen effluvium (TE) is a reactive, diffuse shedding triggered when a physiological shock causes a large proportion of follicles to prematurely enter the telogen phase. The shedding becomes visible approximately 2–4 months after the trigger event. Common triggers include:
- Childbirth (postpartum effluvium affects up to 50% of new mothers)
- Major surgery or serious illness, including COVID-19 (hair loss is frequently reported 2–3 months after acute infection)
- Rapid weight loss, crash dieting, or caloric restriction
- Iron deficiency or ferritin levels below 30–40 ng/mL
- Hypothyroidism or hyperthyroidism
- Severe psychological stress
- Starting or stopping certain medications (retinoids, beta-blockers, anticoagulants)
Acute TE is self-limiting; hair regrowth typically resumes once the trigger is resolved. Chronic TE (lasting over 6 months) often has an unidentified or persistent underlying cause and requires investigation.
Alopecia Areata
Alopecia areata (AA) is an organ-specific autoimmune disease in which CD8+ T-cells attack the hair follicle immune privilege, disrupting the normal immunological protection that prevents follicle self-antigens from being recognized. It presents as one or more smooth, round bald patches, typically on the scalp but can affect any hair-bearing area. Alopecia totalis (entire scalp) and alopecia universalis (entire body) are severe variants. The condition is associated with other autoimmune disorders—particularly thyroid disease, vitiligo, and type 1 diabetes. JAK inhibitor medications (baricitinib, ritlecitinib) represent a significant treatment advance, with the FDA approving ritlecitinib for AA in 2023.
Evidence-Based Treatment Options
| Treatment | Indication | Mechanism | Efficacy |
|---|---|---|---|
| Minoxidil (topical or oral) | AGA (male and female); TE adjunct | Vasodilator; prolongs anagen; stimulates follicle proliferation | Modest to moderate; must be continued indefinitely |
| Finasteride (oral) | Male AGA | 5-alpha reductase type II inhibitor; reduces DHT by ~70% | Prevents further loss in 83–90%; regrowth in ~66% over 2 years |
| Dutasteride (oral) | Male AGA (off-label in many countries) | 5-alpha reductase type I and II inhibitor; more potent DHT suppression | More effective than finasteride; similar side effect profile |
| Low-level laser therapy (LLLT) | AGA | Photobiomodulation; stimulates follicle activity | Modest evidence; FDA-cleared devices available |
| Platelet-rich plasma (PRP) | AGA, AA | Growth factor-rich plasma injections stimulate follicle activity | Emerging; variable results |
| Hair transplant surgery (FUE/FUT) | Established AGA with stable loss | Follicle unit extraction or strip transplant of DHT-resistant occipital follicles | Permanent; most effective for advanced AGA |
| Corticosteroid injections | Alopecia areata | Local immunosuppression | Effective for limited patchy AA |
| JAK inhibitors (baricitinib, ritlecitinib) | Severe alopecia areata | Inhibit JAK-STAT cytokine signaling in T-cells attacking follicles | Significant regrowth in ~30–40% of patients; must continue therapy |
When to Seek Medical Evaluation
Dermatologist evaluation is recommended when shedding is severe, prolonged beyond 6 months, accompanied by scalp symptoms (redness, scaling, tenderness, pustules), or presents as well-defined bald patches. Sudden widespread shedding warrants blood work including thyroid function, complete blood count, ferritin, vitamin B12, and metabolic panel. Scarring alopecia requires urgent biopsy and treatment to prevent permanent follicle destruction.
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