Balding happens primarily because a hormone called DHT shrinks your hair follicles until they can no longer produce visible hair. Nearly 58% of men between ages 30 and 50 have some degree of pattern hair loss, and the process is driven by a combination of genetics, hormones, and the natural aging of your hair growth cycle. But not all hair loss works the same way, and the cause determines whether it’s permanent or temporary.
How DHT Shrinks Your Hair Follicles
Your body converts testosterone into a more potent hormone called dihydrotestosterone, or DHT, using an enzyme called 5-alpha reductase. DHT is responsible for many normal male traits, including body hair and prostate growth. But in the hair follicles on top of your scalp, DHT does the opposite of what it does elsewhere on your body: it gradually destroys hair.
DHT enters the cells of your hair follicles, binds to receptors inside them, and changes how those cells read their own DNA. Over time, this causes the follicle to shrink in a process called miniaturization. Thick, pigmented hairs are slowly replaced by finer, shorter, nearly invisible ones. Eventually, the follicle becomes so small it stops producing hair altogether. This is why balding areas often look thin before they look completely bare.
Your Hair Growth Cycle Breaks Down
Each hair on your head cycles through three phases. The growth phase (anagen) lasts two to eight years and determines how long your hair gets. A brief transition phase (catagen) lasts about two weeks. Then a resting phase (telogen) lasts two to three months before the hair falls out and a new one begins growing.
In a healthy scalp, the ratio of growing hairs to resting hairs is roughly 12:1 or 14:1. In people with pattern baldness, DHT progressively shortens the growth phase and extends the resting phase, dropping that ratio to about 5:1. Each cycle produces a thinner, weaker hair than the one before it. The growth phase also shortens naturally with age, which is why hair becomes finer even in people without genetic hair loss.
Genetics Are the Biggest Factor
Pattern baldness is polygenic, meaning dozens of genes contribute rather than a single one. The most significant is the androgen receptor gene, located on the X chromosome, which you inherit from your mother. Variations in this gene determine how sensitive your follicles are to DHT. People who bald have genetically higher levels of the 5-alpha reductase enzyme and more active androgen receptors in their scalp follicles.
But the X chromosome only tells part of the story. Genome-wide studies have identified risk genes on at least eight different chromosomes, including ones involved in cell signaling pathways that regulate hair follicle development and programmed cell death. Researchers estimate that about 50% of the heritability of baldness comes from autosomal genes (not tied to the X chromosome), meaning your father’s side of the family matters too. For early-onset baldness, the X chromosome contributes about 23% of heritability, while autosomal genes account for roughly 56%.
Hair thinning in genetically susceptible people can begin as early as age 12 to 40. A population study found that 47.5% of men aged 30 to 35 already had visible pattern hair loss, rising to 73% by ages 41 to 45.
Temporary Hair Loss Has Different Triggers
Not all balding is permanent. Telogen effluvium is a common form of temporary, diffuse hair shedding that happens when a large number of follicles are pushed into the resting phase at once. The shedding typically shows up three to four months after a triggering event and is usually self-limiting, lasting about six months.
Common triggers include major surgery, severe illness or high fevers, emotional stress, crash dieting, and significant blood loss. Postpartum hair loss is one of the most recognizable forms: high estrogen levels during pregnancy keep hair in the growth phase longer than usual, and the hormonal drop after delivery causes all that “overdue” hair to shed at once. Once the trigger is removed, new hair growth usually begins within three to six months, though cosmetically noticeable regrowth can take 12 to 18 months.
Autoimmune Hair Loss Works Differently
Alopecia areata causes patchy, often coin-shaped bald spots and has nothing to do with DHT. It’s an autoimmune condition where a specific type of immune cell, cytotoxic T cells, attacks hair follicles directly. These T cells produce inflammatory signals that collapse the protective immune environment around the follicle, creating a self-reinforcing cycle: the inflammation attracts more immune cells, which cause more damage, which triggers more inflammation.
Unlike pattern baldness, the follicles in alopecia areata aren’t permanently destroyed, which is why hair can regrow if the immune attack subsides. The condition can range from a few small patches to complete loss of scalp or body hair.
Smoking and Nutrient Gaps Can Accelerate It
Smoking contributes to hair loss through several pathways. The chemicals in tobacco smoke generate free radicals that damage DNA in follicle cells, both in the nucleus and in mitochondria. Smoking also constricts blood vessels that supply the scalp, reduces antioxidant defenses, and may accelerate cellular aging in the follicle.
Nutritional deficiencies play a role as well, though the evidence is more nuanced than supplement marketing suggests. Zinc stands out as a clear contributor: one study found that women with chronic hair shedding had significantly lower zinc levels (averaging about 50 micrograms per deciliter) compared to healthy controls (about 60 micrograms per deciliter), with the normal reference range being 60 to 120. Iron deficiency, vitamin D deficiency, and low vitamin B12 are often cited, but the same study found no significant difference in the rates of these deficiencies between hair loss patients and controls. Zinc, rather than the more commonly blamed nutrients, appeared to be the critical gap.
How Pattern Baldness Progresses
Pattern hair loss follows a predictable path measured by the Norwood scale, which has seven stages. In stage 1, there’s no noticeable loss. Stage 2 shows slight recession at the temples, often called a mature hairline, and is common enough to be considered normal in adults. Stage 3 is the first clinically significant stage, where the hairline recedes into an M, U, or V shape with bare or nearly bare patches at the temples.
By stage 4, recession is more pronounced and the crown of the head (vertex) is thinning, but a band of hair still connects the two areas. Stages 5 and 6 see those two zones of loss expanding and merging as the connecting band thins and eventually disappears. Stage 7, the most advanced, leaves only a horseshoe-shaped ring of hair around the sides and back of the head. Not everyone progresses through all stages. Some people stabilize at stage 3 or 4 and stay there for decades.
What Treatments Actually Do
The two most established treatments for pattern baldness target different parts of the problem. Minoxidil (a topical solution) increases blood flow to the follicle and extends the growth phase. Finasteride blocks the enzyme that converts testosterone into DHT, reducing the hormone that drives miniaturization. Both can slow hair loss and promote some regrowth, but they work best in combination.
A clinical trial comparing the two treatments alone versus together found that only the combination group achieved statistically significant increases in hair density at both three and six months, with an average gain of 81 hairs per square centimeter by six months. On a photographic assessment scale, 79% of participants using both treatments showed meaningful improvement, compared to 41% using minoxidil alone and just 8% using finasteride alone. Neither treatment reverses advanced baldness or regrows hair on completely bare areas where follicles have been destroyed, but they can meaningfully slow progression and thicken remaining hair when started early.