Alopecia happens when something disrupts the normal hair growth cycle, damages hair follicles, or triggers the immune system to attack them. The specific cause depends on the type of alopecia, but the most common form, androgenetic alopecia (pattern baldness), affects up to 80% of men and 50% of women by age 70. Other types stem from autoimmune reactions, physical stress, nutritional gaps, or mechanical damage to the scalp. Here’s what’s actually going on beneath the surface in each case.
Pattern Baldness and Hormones
Androgenetic alopecia is driven by a hormone called DHT (dihydrotestosterone), which your body produces from testosterone through an enzyme called 5-alpha reductase. DHT binds to receptors inside the dermal papilla cells at the base of each hair follicle. In people who are genetically susceptible, this binding gradually shrinks the follicle, a process called miniaturization. Over time, thick terminal hairs are replaced by finer, shorter, nearly invisible ones until the follicle essentially stops producing visible hair altogether.
Genetics play a major role in determining who is susceptible. The androgen receptor gene, located on the X chromosome, contains a specific repeat sequence (called GGN) that is strongly associated with early-onset baldness. One variant of this sequence appeared at significantly higher rates in men with pattern hair loss, while a different variant was more common in men without it. Because the gene sits on the X chromosome, it’s inherited from your mother’s side, which is why people sometimes look to their maternal grandfather as a predictor.
The timeline differs between men and women. About 30% of men show noticeable thinning in their 30s, and the peak age of reporting for men is in their 20s and 30s. Women tend to experience it later, with the highest rates appearing after menopause, when protective estrogen levels drop. In women, the thinning is usually diffuse across the top of the scalp rather than the receding hairline pattern typical in men.
Autoimmune Attack in Alopecia Areata
Alopecia areata is fundamentally different from pattern baldness. It happens when your immune system mistakenly identifies hair follicle cells as a threat and attacks them. Hair follicles normally have a kind of immune protection, a biological shield that keeps immune cells from recognizing the proteins inside. When that shield breaks down, immune cells called cytotoxic T-cells detect follicle proteins and mount a killing response.
The breakdown involves a cascade of signals. Inflammatory molecules cause the follicle to start displaying identification markers on its surface that it normally keeps hidden. Immune cells then lock onto these markers using a receptor called NKG2D, which interacts with stress signals on the follicle’s surface. The result is round, smooth patches of hair loss that can appear suddenly, sometimes within weeks. In some cases, this progresses to total scalp hair loss or even loss of all body hair.
The triggers for this immune malfunction aren’t fully understood, but alopecia areata is more common in people with other autoimmune conditions like thyroid disease or vitiligo. Emotional or physical stress can also precede episodes, though stress alone doesn’t cause it in someone without the underlying immune predisposition.
Stress-Related Shedding
Your hair naturally cycles through three phases: active growth (which lasts roughly 1,000 days), a brief transition phase (about 10 days), and a resting phase (around 100 days). At any given time, most of your hair is in the growth phase. Telogen effluvium occurs when a physical stressor forces a large percentage of your hair into the resting phase all at once. Under significant stress, up to 70% of actively growing hairs can shift into resting mode and then fall out two to three months later.
Common triggers include high fever, severe infections, major surgery, crash dieting, low protein intake, iron deficiency, and thyroid problems. Certain medications are also known culprits, particularly beta-blockers, blood thinners, and excess vitamin A. The good news is that telogen effluvium is almost always temporary. Once the triggering stressor resolves, follicles re-enter the growth phase and hair regrows over several months.
Postpartum Hair Loss
One of the most common triggers is childbirth. During pregnancy, elevated estrogen and progesterone levels keep hair in the growth phase longer than usual, and some follicles remain actively growing for the entire pregnancy. After delivery, hormone levels plummet and all those extra hairs enter the resting phase simultaneously. The resulting shedding, which usually peaks two to four months postpartum, can be alarming but is a normal physiological process that resolves on its own.
Nutritional Deficiencies That Cause Hair Loss
Hair follicles are metabolically active and depend on a steady supply of specific nutrients. When levels drop below certain thresholds, shedding can increase noticeably.
- Iron: Ferritin (your body’s iron storage marker) below 30 to 40 ng/dL is strongly linked to hair shedding. Some experts recommend maintaining levels above 70 ng/dL to reverse severe hair loss. Most clinicians will recommend supplementation when ferritin drops below 40 ng/dL.
- Vitamin D: Nearly 97% of people with alopecia areata in one study had vitamin D levels below 20 ng/mL, compared to 73% of healthy controls. Average vitamin D levels in people with hair loss were roughly half those of people without it.
- Zinc: Levels below 70 µg/dL show a strong correlation with hair loss. Zinc is essential for cell division in the follicle, and deficiency can push hairs into the resting phase prematurely.
These deficiencies are treatable, and hair typically regrows once levels are restored. They’re worth checking if you’re experiencing diffuse thinning without an obvious hormonal or autoimmune cause.
Traction Alopecia From Styling
Traction alopecia results from repeated mechanical pulling on hair follicles. The constant tension causes inflammation around each follicle, which initially shows up as redness, small bumps, or tenderness along the hairline or wherever the pulling is strongest. If the styling habit continues, the repeated damage eventually destroys the follicle and replaces it with scar tissue, making the hair loss permanent.
The highest-risk styles include tight ponytails, buns, cornrows, dreadlocks, and hair extensions or weaves. Chemical relaxers significantly increase the risk because they weaken the hair shaft by breaking its internal bonds, making it more vulnerable to breakage under tension. African-textured hair is also more susceptible due to its natural curl pattern, which creates geometric weak points along the shaft.
The effects can be striking. One documented case involved a ballerina who wore an uncomfortably tight bun four days a week for 13 years and developed symmetrical patches of hair loss at both temples. South Korean nurses who pinned caps to the same spot on their scalp for eight-hour shifts developed localized bald patches at the pin sites. Sikh men who tightly twist hair under turbans can develop band-like scarring along the frontal hairline. The key with traction alopecia is that early intervention, by changing the hairstyle, can allow full regrowth before scarring sets in.
Scarring Alopecia and Permanent Follicle Loss
Scarring (cicatricial) alopecia is a group of conditions where inflammation targets the middle portion of the hair follicle, right where stem cells and oil glands sit. These stem cells are what allow follicles to regenerate new hairs with each growth cycle. When inflammation destroys this area, scar tissue (fibrosis) replaces the follicle, and hair cannot regrow. This makes scarring alopecia the only category of hair loss that is truly irreversible once established.
Scarring alopecia can result from autoimmune conditions like lichen planopilaris, from infections, burns, or from advanced traction alopecia. Trichoscopy, a magnified examination of the scalp, can reveal telltale signs: areas where follicular openings have completely disappeared, replaced by smooth, pinkish-white patches of scar tissue, sometimes with scale buildup around the remaining hairs. Early treatment focuses on stopping the inflammation before more follicles are destroyed, since lost follicles cannot be restored without surgical transplantation.
How Alopecia Is Diagnosed
Doctors can often distinguish between types of alopecia by examining the scalp with a dermatoscope, a magnifying tool that reveals patterns invisible to the naked eye. In pattern baldness, the key markers are hairs of widely varying thickness, an increased proportion of fine miniaturized hairs, and follicles producing only single hairs instead of their usual clusters of two or three. Alopecia areata looks different: short broken hairs that taper to a point (called exclamation mark hairs), subtle bending of hairs at scalp level, and constricted or irregularly shaped shafts.
A hair pull test, where a doctor gently tugs on a cluster of about 60 hairs, can confirm whether active shedding is occurring. Blood work is typically ordered to check for thyroid dysfunction, iron and ferritin levels, vitamin D, zinc, and hormonal imbalances. In cases of suspected scarring alopecia, a small scalp biopsy may be needed to confirm whether follicle destruction has occurred.