Alopecia happens when something disrupts the hair follicle’s natural growth cycle, either by shortening the growth phase, triggering inflammation that attacks the follicle, or permanently destroying the stem cells that regenerate hair. The specific mechanism depends on the type of alopecia, but every form of hair loss traces back to a disruption at the follicle level. Losing 50 to 100 hairs a day is normal. Problems begin when follicles stop replacing what’s lost.
The Hair Growth Cycle
Understanding how hair normally grows makes it easier to see where things go wrong. Each hair follicle cycles through three phases independently of its neighbors: a growth phase, a transition phase, and a resting phase. A follicle goes through this full cycle 10 to 20 times over a lifetime.
The growth phase (anagen) lasts 3 to 10 years, which is why scalp hair can grow so long. During this time, cells at the base of the follicle divide rapidly to build the hair shaft. The transition phase (catagen) lasts just 2 to 3 weeks, during which the follicle shrinks and the hair detaches from its blood supply. Then comes the resting phase (telogen), lasting 3 to 4 months, after which the old hair falls out and a new growth phase begins.
At any given moment, about 84% of your scalp hairs are actively growing, roughly 1% are in transition, and about 15% are resting. This staggered timing is why you don’t lose all your hair at once. Different types of alopecia interfere with different parts of this cycle.
Pattern Hair Loss: Follicle Shrinkage
Androgenetic alopecia, the most common form, affects an estimated 50 million men and 30 million women in the United States. It can start as early as the teenage years, and more than 50% of men over age 50 have some degree of it. In women, it typically becomes noticeable after menopause.
The mechanism here is hormonal. A byproduct of testosterone called DHT binds to receptors on genetically sensitive hair follicles, primarily at the temples, crown, and top of the scalp. Over time, DHT causes these follicles to miniaturize: each successive growth cycle produces a thinner, shorter, lighter hair. The growth phase gets progressively shorter, from years down to weeks, until the follicle produces only a fine, nearly invisible hair or stops producing visible hair altogether. The follicle itself doesn’t die right away, which is why early treatment can sometimes reverse the process.
Genetics determine which follicles are sensitive to DHT and which aren’t. The follicles along the sides and back of the scalp are typically resistant, which is why those areas keep their hair even in advanced baldness.
Alopecia Areata: The Immune System Attacks
Alopecia areata is fundamentally different from pattern hair loss. It’s an autoimmune condition in which the body’s own immune cells target hair follicles as though they were foreign invaders.
Hair follicles normally have a form of immune protection, a biological shield that keeps immune cells from recognizing and attacking them. In alopecia areata, this shield collapses. When it does, immune cells called CD8+ T cells swarm the base of the follicle during its growth phase. These T cells release inflammatory signals that force the follicle out of its growth phase and into the resting phase prematurely. Worse, they can prevent the follicle from re-entering the growth phase afterward, keeping it stuck in a dormant state.
The inflammatory cycle is self-reinforcing. One key signal, interferon-gamma, triggers the follicle to expose surface markers that attract more immune cells. Another signal, IL-15, helps sustain the attacking T cells. Together, these create a feedback loop: the more inflammation there is, the more immune cells arrive, and the more inflammation they produce. This is why alopecia areata can spread rapidly from a single small patch to large areas of the scalp or body.
The good news is that in most cases the follicle stem cells survive. The follicles are suppressed, not destroyed, which means regrowth is possible if the immune attack can be interrupted. Newer treatments work by blocking the JAK signaling pathway, the molecular relay system that these inflammatory signals use to communicate. By blocking that relay, the treatment breaks the cycle and allows follicles to resume growing.
Telogen Effluvium: Stress-Triggered Shedding
Telogen effluvium is a temporary but dramatic form of hair loss triggered by a physical or emotional shock to the body. Normally, about 15% of your hair is in the resting phase at any time. During a telogen effluvium event, up to 70% of actively growing hairs can prematurely shift into the resting phase all at once.
The shedding itself doesn’t happen immediately. Because the resting phase lasts several months, the hair loss typically shows up two to three months after the triggering event. This delay often makes it hard to connect the shedding to its cause. Common triggers include high fever, surgery, major emotional stress, rapid weight loss, childbirth, and stopping certain medications.
Acute telogen effluvium usually resolves within six months as follicles re-enter the growth phase on their own. The follicles aren’t damaged, just temporarily reset. However, if the underlying stressor persists (chronic illness, ongoing nutritional deficiency, prolonged emotional stress), the shedding can become chronic.
Nutritional Deficiencies and Hair Loss
Hair follicles are among the most metabolically active cells in the body, and they need a steady supply of nutrients to sustain the growth phase. Two deficiencies are particularly well documented. In one study of women with pattern hair loss, 54% had vitamin D levels below 20 ng/mL (classified as deficient) and another 38% fell in the insufficient range. For iron stores, 40% had ferritin levels below 30 µg/L (very low) and 34% were in the low range. Overall, 74% of participants had inadequate iron levels.
Low iron limits the oxygen supply to follicle cells, while vitamin D plays a role in cycling follicles from the resting phase back into growth. Neither deficiency typically causes permanent damage. Once levels are restored through diet or supplementation, follicles generally resume normal production, though it can take several months for visible improvement since new hairs need time to grow out.
Scarring Alopecia: Permanent Follicle Loss
Scarring (cicatricial) alopecia is the most serious category because the hair loss is irreversible. In this group of conditions, inflammation targets and destroys the stem cells housed in a region of the follicle called the bulge. These stem cells are responsible for regenerating the follicle at the start of each new growth cycle. Once they’re gone, the follicle can never produce hair again, and scar tissue fills in where the follicle used to be.
The destruction is typically driven by autoimmune inflammation, as seen in conditions like lupus of the skin. Animal studies have confirmed the central role of these stem cells: when researchers selectively destroyed bulge stem cells in mice, the result was rapid and permanent hair loss. Conversely, when immunosuppressive treatment was given early enough to halt the inflammation, the stem cells survived and hair growth was rescued.
This is why early diagnosis matters so much with scarring alopecia. The window for preserving follicles closes once enough stem cells are destroyed. A dermatologist can distinguish scarring from non-scarring types through a scalp biopsy, looking for the telltale loss of follicle openings and the presence of scar tissue.
How Hair Loss Is Evaluated
One simple test dermatologists use is the pull test. They grasp a small section of about 40 hairs and gently tug. If six or more strands come out, it indicates active hair loss. This helps distinguish normal shedding from a process that needs further investigation.
Beyond the physical exam, blood work can reveal hormonal imbalances, thyroid problems, iron deficiency, or vitamin D insufficiency that may be contributing. The pattern and location of hair loss also provide strong diagnostic clues: patchy round spots suggest alopecia areata, diffuse thinning across the entire scalp points to telogen effluvium or nutritional causes, and a receding hairline or thinning crown typically indicates androgenetic alopecia. Smooth, shiny patches where follicle openings have disappeared suggest scarring alopecia, which usually requires a biopsy to confirm.