Your Hair Is Thinning, and Your Genes May Be Why.

Your androgen receptor is the lock that DHT fits into. It sits on the surface of your hair follicle cells and determines how responsive those cells are to the hormone signal telling them to shrink. When DHT binds to the androgen receptor, it triggers miniaturization, the process where hair follicles shrink and produce thinner, shorter hairs instead of thick ones. This is the primary driver of androgenetic alopecia.

The AR gene has a variable length section called a CAG repeat. Shorter CAG repeats mean your hair follicles are more sensitive to DHT. If you carry shorter repeats, your follicles need less DHT to trigger miniaturization. This variant is common; it shows up across all ancestral populations and affects both men and women, though the phenotype differs.

What this means for you: even if your DHT levels are in the normal range, your follicles might be responding as if they’re elevated. You might notice thinning on the crown or temples first, then widening of the part line. The shedding might increase during puberty, after pregnancy (when hormones shift), or during periods of high stress (when androgen sensitivity peaks).

DHT doesn’t exist in your bloodstream on its own. Your body makes testosterone, and then the SRD5A2 enzyme converts it into DHT. The more active your SRD5A2 enzyme, the more DHT your follicles are exposed to. SRD5A2 sits right in your hair follicles, your prostate, and your skin, so it has a direct effect on whether hair grows or sheds.

The V89L variant in SRD5A2, carried by roughly 30 to 40 percent of the population, alters how efficiently this enzyme works. Certain SRD5A2 variants increase DHT production, meaning your follicles are bathed in more DHT than someone with the wild-type allele, even if your total testosterone is normal. Your bloodwork might show testosterone in the healthy range, but your scalp is seeing elevated DHT.

What this means for you: you might have shedding that started early, progresses steadily, and doesn’t respond well to standard stress management or general hair supplements. You notice that your hair loss tracks with seasons of high androgens (puberty, certain times of your cycle if female, high-stress periods). The shedding is diffuse or follows a pattern consistent with androgen sensitivity.

Estrogen is protective for hair. During the anagen phase, the growth phase of the hair cycle, estrogen keeps follicles active and delays the transition to telogen, the shedding phase. The ESR1 gene encodes the estrogen receptor that sits on your hair follicle cells and responds to circulating estrogen. If your estrogen receptor doesn’t function well, your follicles can’t sense the protective signal, and they exit the growth phase earlier than they should.

The PvuII and XbaI variants in ESR1, found in roughly 40 percent of people, reduce how effectively your follicles respond to estrogen. You can have normal or even high estrogen levels, but if your follicles have a variant that reduces receptor sensitivity, that protective signal never gets through. This is why some women experience telogen effluvium after pregnancy (estrogen drops), or why others notice increased shedding after hormonal birth control changes, or why shedding accelerates around perimenopause even when hormone levels are still present.

What this means for you: you might notice shedding that fluctuates with your menstrual cycle, or increases dramatically after pregnancy. Your hair might have been thick and healthy until a hormonal event, then never returned to that baseline. You might be female or have sensitive to estrogen-related symptoms. The shedding is often diffuse rather than patterned, and it feels responsive to hormonal timing.

Your hair follicles are among the fastest-dividing cells in your body. They need a constant supply of methyl groups, the building blocks that repair DNA, synthesize new proteins, and regenerate cells. The MTHFR enzyme is the gatekeeper of methylation. It converts folate into the form your cells can use to methylate and regenerate. If this enzyme works poorly, your follicles can’t keep up with their own cellular turnover, and shedding increases.

The C677T variant in MTHFR, carried by roughly 40 percent of people of European ancestry, reduces enzyme efficiency by 40 to 70 percent. You can eat plenty of folate and still have cells that are starving for the methylated form they actually use. Your follicles, being fast-dividing, are hit especially hard. They start to miniaturize or shed because they don’t have the regenerative capacity to maintain the hair cycle.

What this means for you: your hair shedding might be accompanied by other signs of impaired methylation: fatigue, brain fog, mood changes, or a history of miscarriage. You might notice that standard prenatal vitamins or folic acid supplements don’t help (because your cells can’t convert them). Your shedding might be diffuse and subtle at first, then progressive over months or years. The pattern is often telogen effluvium rather than classic androgenic alopecia.

Your hair follicles don’t grow continuously. They cycle through phases: anagen (growth), catagen (transition), and telogen (shedding). The vitamin D receptor, encoded by the VDR gene, sits on hair follicle cells and responds to active vitamin D. When vitamin D binds to VDR, it signals the follicle to stay in the growth phase longer and delays the transition to shedding. VDR is essential for keeping follicles active.

VDR variants, including BsmI and FokI, are carried by roughly 30 to 50 percent of the population and impair how well your follicles respond to vitamin D. Even if your vitamin D blood level is adequate, your follicles might not be able to sense or respond to it. This is especially true if you have the FokI ff (shorter) variant, which has lower transcriptional activity. Your follicles shift prematurely out of anagen and into telogen, and shedding increases.

What this means for you: you might notice seasonal shedding, worse in winter or in climates with less sun exposure. Your vitamin D blood level might be “normal” by standard ranges, but supplementing doesn’t seem to help your hair. You might have diffuse shedding that doesn’t fit a clear hormonal or androgenic pattern. The shedding might be accompanied by other signs of vitamin D insufficiency: bone health concerns, muscle weakness, mood changes.

Hair follicles need iron to produce the proteins and DNA required for growth. Iron is also a critical cofactor for many of the enzymes that support follicle function. The HFE gene controls how your body absorbs and stores iron. If HFE variants cause iron overload, excess iron generates oxidative stress in your follicles and accelerates shedding. If HFE variants cause iron deficiency, your follicles starve for this essential nutrient. Either direction causes hair loss.

HFE mutations, including the C282Y and H63D variants, are carried by roughly 10 to 30 percent of people of European ancestry (higher in some populations). HFE variants can silently shift your iron balance in either direction, and standard iron panels might not catch it because labs check serum iron, not the actual iron status inside your cells. People with HFE variants often develop iron patterns that drive hair loss even when blood tests look normal.

What this means for you: if you have HFE variants, your shedding might be linked to iron imbalance rather than hormones or methylation. You might notice shedding accompanied by fatigue, joint pain, or changes in energy and mood. Iron supplementation might help or hurt depending on which direction your iron is skewed. Standard iron panels might be misleading; you need more detailed iron testing like ferritin, transferrin saturation, and iron content.