Alopecia, the medical term for hair loss, has no single cause. It can result from your immune system attacking hair follicles, hormonal changes that shrink them over time, physical stress that pushes hair into a premature shedding phase, or mechanical damage from tight hairstyles. The type of alopecia determines whether the loss is temporary or permanent, and understanding the cause is the first step toward knowing what to expect.
Pattern Hair Loss and Hormones
The most common form of hair loss, androgenetic alopecia, is driven by a hormone called DHT (dihydrotestosterone). DHT binds to receptors in genetically susceptible hair follicles and activates genes that cause those follicles to miniaturize. With each growth cycle, the follicle gets slightly smaller, producing thinner and shorter hair until it eventually stops producing visible hair altogether. This is why pattern hair loss is gradual rather than sudden.
DHT speeds up and shortens the active growth phase of the hair cycle. The follicle can’t grow to its full size before it enters the resting phase, so over many cycles, thick terminal hairs are replaced by fine, nearly invisible vellus hairs. In men, this typically creates a receding hairline and thinning crown. In women, it usually appears as diffuse thinning along the part line.
The susceptibility to DHT’s effects is largely genetic and polygenic, meaning many genes contribute rather than one. Two of the most significant genetic regions are located on the X chromosome (which is why maternal family history matters) and chromosome 20. Researchers have also identified genes involved in the Wnt signaling pathway, which regulates hair growth, as well as genes related to cell death and hormone metabolism. Because so many genes are involved, the severity and pattern of hair loss vary widely from person to person.
Autoimmune Attack in Alopecia Areata
Alopecia areata affects roughly 0.1% to 0.2% of the global population at any given time, with a lifetime risk between 1.7% and 2.1%. It occurs when a specific type of immune cell, known as a cytotoxic T cell, targets hair follicles as though they were foreign invaders.
Hair follicles normally enjoy a form of immune protection, sometimes called “immune privilege,” that shields them from the body’s defense system. In alopecia areata, this protection collapses. The follicles begin producing stress signals on their surface, and T cells recognize these signals, swarm the follicle, and release inflammatory compounds that halt hair growth. This creates a self-reinforcing cycle: the inflammation triggers more stress signals, which attract more T cells, which cause more inflammation. The result is the characteristic smooth, round bald patches that can appear suddenly on the scalp, beard, eyebrows, or anywhere on the body.
The hair follicles themselves are not destroyed in alopecia areata, which is why regrowth is possible. But the immune attack can be unpredictable, with hair regrowing in one area while falling out in another.
Stress, Illness, and Telogen Effluvium
Telogen effluvium is the most common form of temporary, diffuse hair loss. It happens when a significant physical or emotional stressor pushes a large number of hair follicles out of their active growth phase and into the resting (telogen) phase simultaneously. Normally, about 10% of your hair is in the resting phase at any time. Under significant stress, up to 70% of growing hairs can shift into telogen at once.
The shedding doesn’t happen immediately. Because the resting phase lasts two to three months before hair falls out, you typically notice the loss well after the triggering event has passed. Common triggers include high fever, severe infections, major surgery, crash dieting, low protein intake, iron deficiency, hypothyroidism, and stopping estrogen-containing medications. The good news is that once the underlying trigger resolves, hair typically regrows on its own within six to twelve months.
Postpartum Hair Loss
One of the most common forms of telogen effluvium occurs after childbirth. During pregnancy, elevated estrogen levels delay the normal shedding process, so hair feels thicker and fuller. After delivery, estrogen drops sharply and hair cycles synchronize across the scalp. Within about nine weeks postpartum, roughly 30% of scalp hairs enter the resting phase at once. This explains why noticeable shedding typically begins two to four months after giving birth. It usually continues for 6 to 24 weeks, though in rare cases it can persist up to 15 months before resolving.
Nutritional Deficiencies
Low levels of iron and vitamin D are consistently associated with diffuse hair shedding. In one study, people with hair loss had average ferritin levels (a measure of stored iron) of about 15 ng/ml, compared to 25 ng/ml in people without hair loss. Vitamin D levels showed a similar gap: roughly 14 ng/ml in hair loss patients versus 17 ng/ml in healthy controls, with the normal range starting at 20 ng/ml.
Iron plays a role in delivering oxygen to hair follicle cells, and vitamin D is involved in the cycling of hair follicles through their growth phases. If you’re experiencing unexplained diffuse shedding, these are two of the first things worth checking through a simple blood test, particularly if you menstruate heavily, follow a restrictive diet, or get limited sun exposure.
Medications That Trigger Hair Loss
Drug-induced hair loss is typically diffuse and non-scarring. It works through two main pathways. The first, anagen effluvium, involves direct damage to actively dividing hair cells, causing rapid and often dramatic loss. This is the mechanism behind hair loss from chemotherapy drugs. The second, telogen effluvium, involves a delayed, gradual shedding as medications interfere with normal follicle cycling.
Five major drug classes are most commonly associated with hair loss: cancer treatments, immunomodulators (drugs that alter immune function), anti-seizure medications, certain biologic drugs used for autoimmune conditions, and hormonal agents including some forms of hormonal contraception. Cancer drugs account for the largest share, but thyroid medications, certain hormonal therapies, and immune-modulating drugs prescribed for conditions like multiple sclerosis and rheumatoid arthritis are also frequently reported triggers. In most cases, hair regrows after the medication is stopped or changed.
Traction Alopecia From Physical Tension
Traction alopecia develops from prolonged or repeated pulling on hair follicles. Tight ponytails, braids, cornrows, hair extensions, and any style that creates sustained tension along the hairline can cause it. In the early stages, the damage is reversible: follicles shift into their resting phase prematurely, and hair shafts become fragile and swollen. If you stop the offending hairstyle, complete regrowth is possible.
The danger lies in chronic, repeated tension over months or years. Over time, the follicles miniaturize, scar tissue replaces functional follicles, and the stem cells that regenerate hair are permanently damaged. At this stage, the hair loss becomes irreversible. The most common pattern is a receding hairline along the temples and forehead, where tension from pulled-back styles is greatest. Early signs to watch for include small bumps or redness along the hairline, broken hairs of different lengths, and a feeling of tenderness at the roots.
Scarring Alopecia and Permanent Follicle Loss
Scarring (cicatricial) alopecia is the most concerning category because it results in permanent hair loss. Unlike other forms where the follicle remains intact but dormant, scarring alopecia involves the destruction of the stem cells that allow follicles to regenerate. Inflammation, whether driven by the immune system, infection, or injury, targets the upper portion of the follicle where these stem cells reside.
The inflammatory process may directly destroy the stem cell pool or force stem cells to differentiate (become specialized cells) as part of a repair response. Either way, if the inflammatory insult is severe or sustained enough, the follicle’s regenerative capacity becomes exhausted. The follicle is replaced by scar tissue, and no amount of treatment can regrow hair from that site. This is why early diagnosis matters: treatment focuses on stopping the inflammation before more follicles are lost, rather than regrowing what’s already gone. Signs include smooth, shiny patches of scalp without visible pore openings, which distinguishes scarring alopecia from other types where pores remain intact.