Your Hair Is Falling Out. Your Genes May Be Driving It.

Your androgen receptor is the lock, and DHT is the key. This gene encodes the protein on your hair follicle cells that responds to DHT, the hormone that shrinks (miniaturizes) hair follicles in people genetically prone to androgenetic alopecia. It’s a normal, essential protein. The problem is how sensitive your follicles are to it.

The AR gene contains a variable repeat section (CAG repeats). The fewer repeats you have, the more sensitive your androgen receptor is to DHT. Studies show that men and women with shorter CAG repeats experience more aggressive hair loss, and they experience it earlier. It’s one of the strongest genetic predictors of androgenetic alopecia in both sexes, though the effect size varies by ancestry.

What you experience: Hair thinning that follows a pattern, receding hairline or widening part, often triggered or worsened by puberty or hormonal events (pregnancy, starting birth control, hormonal shifts at 30-40). Your family history probably includes hair loss too.

This enzyme is the factory that converts testosterone into DHT, the hormone that drives androgenetic alopecia. If you have more of it, you make more DHT. If you make more DHT and your follicles are sensitive to it (AR gene), you lose hair faster.

The SRD5A2 V89L variant (rs523349), carried by roughly 30-40% of people, affects how much of this enzyme your body produces. Carriers make higher DHT levels from the same amount of testosterone. Combined with AR sensitivity, this is a potent combination for hair loss. If you have both the shorter AR repeats and the SRD5A2 variant that boosts DHT production, your follicles are getting hit harder than someone with just one.

What you experience: Androgenetic alopecia that may be more severe or earlier-onset than you’d expect from family history alone. Possibly acne, oily skin, or other signs of higher DHT sensitivity. Women might notice hair loss tied to hormonal cycles or after stopping birth control.

Estrogen is protective for hair. It lengthens the growth phase (anagen) of the hair cycle and delays the shedding phase. The ESR1 gene encodes the receptor that lets hair follicles respond to estrogen. If your estrogen receptor doesn’t work well, your follicles don’t get that protective signal, even if estrogen levels are normal.

The ESR1 PvuII and XbaI variants affect how efficiently the receptor signals. Roughly 40% of people carry variant alleles. In people with these variants, estrogen’s protective effect on hair is blunted. This is why some women experience sudden hair loss after pregnancy (when estrogen drops), after stopping birth control, or during menopause. Men with ESR1 variants lose the protective balancing effect of estrogen, and DHT becomes relatively more dominant on their follicles.

What you experience: Hair thinning or shedding triggered by hormonal changes (postpartum, menopause, stopping hormonal birth control). It might feel like diffuse shedding rather than classic male pattern baldness. Women often notice it more than men notice theirs.

MTHFR is the enzyme that produces methylfolate, the active form of folate your cells use to divide, repair DNA, and regenerate. Hair follicles are among the fastest-dividing cells in your body. They need robust methylation to stay thick and healthy. If your MTHFR enzyme is inefficient, your follicles can’t regenerate fast enough.

The MTHFR C677T variant, carried by roughly 40% of people with European ancestry, reduces enzyme activity by 40-70%. People with this variant make less methylfolate even if their dietary folate intake is adequate. The follicle stem cells that need to divide and regenerate are running on a reduced supply. This typically causes diffuse thinning rather than patterned loss, and it often doesn’t show up on a thyroid panel or iron panel because the deficiency is at the cellular level, not the blood level.

What you experience: Overall hair thinning, reduced hair density, slower hair growth, possibly dull or brittle texture. It often gets worse with stress (which increases methylation demand). You might have normal bloodwork but still feel depleted at the cellular level.

Vitamin D doesn’t just support bone health. The VDR protein is a receptor on hair follicle cells that responds to active vitamin D (calcitriol). This signaling is critical for hair follicles to enter the growth phase and cycle properly. Without adequate VDR function, follicles get stuck in dormancy.

The VDR BsmI and FokI variants, present in roughly 30-50% of people depending on ancestry, reduce receptor sensitivity. This means your follicles don’t respond as well to vitamin D signaling, even if your blood levels of vitamin D are adequate. Vitamin D deficiency is epidemic in northern climates, but even people with normal vitamin D levels can have VDR variants that impair follicle sensitivity. This is especially relevant to alopecia areata and telogen effluvium (shock shedding), where follicles get trapped in the shedding phase.

What you experience: Diffuse shedding, sometimes sudden (telogen effluvium), or patchy loss (alopecia areata if immune factors are also present). Hair that seems to shed more in winter or in low-sun climates. Possibly other signs of vitamin D insufficiency like fatigue, bone aches, or poor immune recovery.

Iron is essential for hair growth. It’s a core component of hemoglobin (which carries oxygen to follicles) and of catalase and other antioxidant enzymes that protect follicle cells from oxidative damage. The HFE gene encodes a protein that regulates how much iron your body absorbs and stores. If HFE variants impair this regulation, you can end up with either too little or too much iron, and both disrupt hair growth.

The HFE C282Y and H63D variants affect iron regulation. C282Y is rare (roughly 0.5-1% homozygous in European ancestry) but causes severe hemochromatosis; H63D is more common and causes milder dysregulation. Both can affect hair loss. High iron (hemochromatosis) causes oxidative stress and inflammation that damages follicles. Low iron (iron deficiency anemia, or iron-induced by malabsorption) starves follicles of the oxygen and enzyme cofactors they need. Hair loss from iron dysregulation often presents as diffuse shedding.

What you experience: Diffuse hair thinning or shedding. Possibly fatigue, joint pain, or other signs of iron dysregulation. Ferritin levels might be high, low, or paradoxically normal despite functional deficiency.