Hair loss, medically called alopecia, ranges from gradual thinning to complete baldness. Its mechanisms are either disruption of the hair development cycle or damage to hair follicles, arising from genetic, hormonal, infectious, or other systemic or local factors. Because the term covers many disorders, the cause of an individual's hair loss must be identified before treatment can be chosen.
Hair growth cycle
Each hair follicle cycles through a growth phase (anagen), a regression phase (catagen), and a resting phase (telogen), after which the old hair is shed and a new one begins to form. Hair shedding is normally balanced by new growth. Hair loss occurs when this balance is disturbed, so that more hair falls out than grows in. Many forms of hair loss therefore reflect a shift in the proportion of follicles in each phase, or a shortening of the growth phase, rather than the death of the follicle itself.
Classification
Hair loss is commonly divided into two groups. Cicatricial (scarring) alopecia may progress with loss of follicles and cause irreversible hair loss, whereas non-cicatricial forms are usually reversible. In scarring alopecias, inflammation destroys the follicle's stem-cell and growth machinery, which is why regrowth is not expected once the damage is complete. Non-scarring forms are the more common group and include the disorders described below.
Causes
Hair loss can result from many causes, which may include inherited susceptibility, autoimmune disease, inflammation, infection, hormonal or metabolic changes, medications, nutritional deficiencies, physical or chemical injury, abnormalities of the hair shaft. The same visible symptom, such as diffuse shedding or patchy loss, can arise from very different biological processes.
Principal types
The major categories are:
- Androgenetic alopecia, the most common form of progressive hair loss in both sexes.
- Alopecia areata, an autoimmune disorder that causes patchy or widespread loss.
- Telogen effluvium, a temporary increase in shedding caused by a shift of follicles into the resting phase.
- Anagen effluvium, a rapid loss of growing hair caused by agents that interfere with cell division in the follicle.
- Scarring alopecias, a heterogeneous group of inflammatory disorders that permanently destroy follicles.
- Traction alopecia, caused by sustained pulling from tight hairstyles.
Other recognized causes include hair-shaft disorders, infection, and behavioral causes. Trichotillomania is an impulse-control disorder, and its treatment focuses on the underlying psychiatric condition. Tinea capitis, a fungal infection of the scalp, produces patches of alopecia that may be red and scaly and must be treated systemically. Hair breakage from styling is also common: trichorrhexis nodosa occurs when hairs break from trauma, often as a result of styling or overuse of hair products.
Systemic conditions and drugs can also trigger hair loss. Reported examples include weight loss, certain medications including chemotherapy, iron deficiency, skin conditions, fungal infection, lupus erythematosus, hypothyroidism, hyperthyroidism, diabetes, radiation therapy, trauma and sarcoidosis.
Androgenetic alopecia
Androgenetic alopecia (AGA), also called male or female pattern hair loss, is the most common cause of progressive hair loss. It is a common nonscarring condition that affects both men and women, often resulting in psychological distress and reduced quality of life. Its prevalence rises with age; one review estimates that around 50% of men and 25% of women are affected by age 70.
Pathogenesis
AGA is driven by genetic susceptibility and androgen activity. In affected individuals, the enzyme 5-α-reductase converts testosterone into dihydrotestosterone (DHT), which binds androgen receptors in hair follicles, particularly in the frontal and vertex regions. The key structural change is follicular miniaturization. The pathogenesis involves a shortened anagen (growth) phase and an increased telogen (resting) phase, primarily driven by the action of DHT on androgen-sensitive follicles in the scalp. Over successive cycles, terminal hairs are replaced by progressively finer, shorter, vellus-like hairs.
The androgen model has limits. Researchers have noted that androgens are unlikely to be the sole cause of miniaturization, which has led to the search for additional pathways. Studies have implicated the peroxisome proliferator-activated receptor pathway and other signaling networks, although their relative importance is still being evaluated. The cause of female pattern hair loss, in particular, remains unclear, and its pattern differs from the male form.
Clinical patterns
In men, hair thinning in the frontotemporal areas, recession of the frontotemporal hairline, and hair loss in the vertex area are typical. In women, hair thinning occurs over the frontal and parietal areas of the scalp (Ludwig type) or only in the central part of the frontal area (Olsen type). Women rarely develop a complete hairline recession, which is one reason the two sexes are managed differently.
Alopecia areata
Alopecia areata is an autoimmune disorder in which the immune system mistakenly attacks hair follicles, causing hair loss. The current model holds that the follicle loses its normal immune privilege. CD8+ NKG2D+ T cells, driven by inflammatory cytokines such as IFN-γ, attack the follicle. A feedback loop involving interferon signaling and the JAK–STAT pathway amplifies this inflammation. Its lifetime prevalence is 0.7%–3.8%, and 7%–12% of patients progress to total or universal hair loss.
The disease takes several forms. Patchy alopecia areata causes one or more round or oval bald patches, while alopecia areata totalis causes complete hair loss on the scalp and alopecia areata universalis causes total hair loss on the body, including eyebrows, eyelashes, and pubic hair. Patches often regrow spontaneously, but the disorder can recur. Its genetic basis is polygenic, and environmental triggers are also implicated.
Telogen and anagen effluvium
Telogen effluvium is a nonscarring, noninflammatory alopecia of relatively sudden onset, caused by physiologic or emotional stress. It typically appears months after the trigger, and once the precipitating cause is removed, the hair typically regrows. It is common after childbirth. A stressful event can also worsen other forms of hair loss, and the distress that results from hair loss may in turn prolong the shedding.
Anagen effluvium is a rapid loss of growing hair. It occurs when an event impairs the mitotic activity of the hair follicle, most commonly chemotherapy. Other reported triggers include severe chronic illnesses, pregnancy, surgery, high fever, malnutrition, severe infections, and endocrine disorders. Because anagen effluvium interferes with the actively dividing cells of the follicle, hair often regrows once treatment ends.
Diagnosis
Diagnosis usually begins with a history and examination, including the pattern of loss, medications, illnesses, and family history. Some presentations require evaluation by a dermatologist with specific experience in hair and scalp disorders, particularly when inflammation, scarring, rapid progression, or an unusual pattern is present. If a medicine is suspected, a discontinuation trial is reasonable. Blood tests for thyroid function, iron status, and other markers are often used to look for systemic causes.
Treatment
Treatment depends on the cause. Only a few therapies have regulatory approval for specific forms of hair loss, and most options aim to slow loss or stimulate regrowth rather than restore a full head of hair. Most treatments cannot fully restore hair, although wigs, hairpieces, and some medications may help slow or conceal thinning.
Androgenetic alopecia
Topical minoxidil and oral finasteride are the most widely used treatments. Minoxidil promotes vasodilation and prolongs the anagen phase, whereas finasteride reduces DHT levels by inhibiting 5α-reductase, thereby limiting follicular miniaturization. Dutasteride, another 5-α-reductase inhibitor, is also used. Surgical hair transplantation is an option for established patterns of loss. Common limitations include side effects and recurrence after discontinuation. One FDA-related review notes that due to drawbacks such as significant side effects and high relapse rates, neither approved treatment is considered fully satisfactory.
Alopecia areata
Until recently, no systemic agent for alopecia areata had regulatory approval, and treatment was often empirical. The introduction of Janus kinase (JAK) inhibitors changed this. Demonstrated efficacy from large-scale clinical trials of the JAK inhibitor baricitinib led to the first FDA-approved treatment for AA in June 2022. Other JAK inhibitors, including ritlecitinib, are under study. Because the disease tends to recur, treatment often requires long-term medication, and the long-term safety profile of these drugs continues to be assessed.
Psychological and social impact
Hair loss is medically harmless in most cases, but its effects on the person can be substantial. Unwanted changes to appearance can influence self-esteem and social life. In some people, hair loss causes psychological distress, changing self-concept and body image. Alopecia areata in particular is associated with significant psychosocial burden, and patients may benefit from psychological support alongside medical treatment.
Research and open questions
Current research seeks to clarify the signaling pathways that control follicle cycling, the role of inflammation and oxidative stress, and why some patients respond to a given drug. Understanding why androgenetic alopecia progresses in some people but not others remains a central question, and the differences between the sexes in both incidence and treatment response are still being studied.
References
- An overview of the genetic aspects of hair loss and its connection with nutrition - PMCpmc.ncbi.nlm.nih.gov
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- Compounds, compositions and methods for the treatment or prevention of hair lossimage-ppubs.uspto.gov
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- 1 of 3 / Overviewwebmd.com
- Pathophysiological mechanisms of hair follicle regeneration and potential therapeutic strategies - PMCpmc.ncbi.nlm.nih.gov
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- Induction of T cell exhaustion by JAK1/3 inhibition in the treatment of alopecia areatancbi.nlm.nih.gov
- Review: Approving, Using JAK Inhibitors for Better Alopecia Areata Outcomesajmc.com