Your Skin Type Isn't Random. Your Genes Determine It.

The androgen receptor (AR) is a protein that sits on hair follicles and tells them how to respond to the hormone DHT. Think of it as the ‘sensitivity dial’ on your follicles. When DHT (derived from testosterone) binds to this receptor, it triggers a cascade of changes in the follicle. In some follicles this leads to hair growth; in others it leads to miniaturization (thinning). The strength of that response depends partly on how sensitive your particular AR protein is.

AR sensitivity is determined by the length of a CAG repeat sequence embedded in the AR gene itself. Shorter CAG repeats mean a more sensitive, more active receptor; longer repeats mean a less sensitive one. This variant is X-linked, meaning if you’re female you inherit one copy from each parent, and if you’re male you inherit one from your mother. The length of your CAG repeats directly predicts how sensitive your hair follicles will be to DHT-driven miniaturization. Shorter repeats correlate with earlier, more aggressive hair loss in genetically susceptible individuals.

If you have shorter CAG repeats in your AR gene, your hair follicles are probably more responsive to DHT. This means even normal levels of DHT might trigger thinning, especially if you also carry variants in other hair loss genes. You may notice hair thinning in your 20s or 30s when friends with longer repeats don’t see changes until much later. On the flip side, if your CAG repeats are longer, your follicles are less sensitive to DHT, which is protective even if you have high DHT levels.

The SRD5A2 gene encodes 5-alpha reductase type 2, the enzyme that converts testosterone into DHT. DHT is roughly 10 times more potent than testosterone at triggering follicle miniaturization. This enzyme exists in hair follicles, skin, and prostate tissue, so its activity affects more than just your hair. SRD5A2 controls how much DHT your body produces from circulating testosterone.

The V89L variant (rs523349) is common, affecting roughly 30-40% of people depending on ancestry. Certain variant alleles reduce the enzyme’s efficiency, meaning you convert less testosterone to DHT. Other variants increase activity slightly, meaning more DHT production. If you carry variants associated with higher SRD5A2 activity, you’re converting more testosterone into the hormone that drives hair follicle miniaturization. This is one reason why two people with the same testosterone levels can have completely different hair loss patterns.

If your SRD5A2 variants suggest higher DHT production, you’re probably more responsive to DHT-blocking treatments (finasteride or dutasteride). You might also notice that your scalp is oilier than average, because DHT also stimulates sebum production. If your variants suggest lower SRD5A2 activity, you have a natural advantage in hair retention; hair loss, if it happens, is more likely driven by your AR sensitivity or other mechanisms.

The vitamin D receptor (VDR) is a protein that responds to activated vitamin D and regulates dozens of genes involved in cell cycling, immune function, and barrier integrity. Hair follicles need vitamin D signaling to cycle through their growth phases properly. When VDR function is impaired, hair follicles get stuck in prolonged resting phases, which manifests as thinning or diffuse hair loss. VDR also affects skin barrier function and immune tolerance, so it influences your skin’s ability to defend itself.

Common VDR variants (BsmI, FokI) reduce the receptor’s efficiency, affecting roughly 30-50% of people depending on ancestry. VDR variants that impair function are associated with prolonged telogen (resting) phases in hair follicles and reduced skin barrier resilience. People with these variants often show a pattern of diffuse thinning rather than male-pattern baldness, because the problem is with the hair cycle itself rather than DHT sensitivity. VDR variants also correlate with alopecia areata susceptibility, where the immune system attacks hair follicles.

If you have VDR variants that impair function, your hair and skin need consistent vitamin D signaling to work properly. You might notice that sun exposure (which activates vitamin D in skin) temporarily improves your hair and skin, while winter months or indoor living worsens both. Your follicles probably cycle more slowly, which is why hair shedding might be heavier in certain seasons or why you’re more prone to hair loss after periods of stress or illness.

MTHFR encodes an enzyme critical for converting folate into its active form, which your cells use for DNA synthesis, cell division, and regeneration. Hair follicles and skin cells divide rapidly, which means they have high demands for methylation and nucleotide synthesis. If your MTHFR function is impaired, your cells struggle to regenerate at the rate they normally would. This affects hair growth rate, hair cycle timing, and skin cell turnover.

The C677T variant is carried by roughly 40% of people with European ancestry. This variant reduces enzyme efficiency by 35-40%, meaning your cells convert folate to its active form more slowly. People with the C677T variant often experience slower hair growth, thinner hair overall, and delayed skin cell turnover. It’s not that they can’t grow hair or regenerate skin; it’s that the process is slower than it would be with a fully functional enzyme. This becomes especially noticeable during times of metabolic stress (illness, pregnancy, intense exercise) when cellular demand for methylation is highest.

If you carry MTHFR variants, you probably notice that your hair grows slowly, your nails are a bit thin, and your skin cell turnover is sluggish (which can lead to a dull complexion or slightly congested skin even when you’re being consistent with skincare). You might also struggle with hair loss after pregnancy or stress, because your body’s ability to quickly regenerate cells is already compromised. Conversely, when you optimize your methylation support, you often see noticeable improvements in hair strength and skin clarity within 4-6 weeks.

SOD2 encodes an antioxidant enzyme that works inside the mitochondria, neutralizing free radicals before they can damage your cells. Skin cells have extremely high metabolic demands (they’re constantly dividing, synthesizing collagen, and defending against UV damage). That high metabolism generates a lot of free radical byproducts. If your SOD2 function is compromised, oxidative stress accumulates in your skin cells faster than it can be neutralized. This accelerates visible aging, inflammation, and photodamage.

The Val16Ala variant (rs4880) is common, with roughly 40% of people homozygous for one allele. The Alanine variant reduces SOD2 enzyme activity by about 30-40%, meaning your mitochondrial antioxidant defense is weaker than average. People with the Ala/Ala genotype accumulate oxidative damage in skin cells at an accelerated rate, which translates to earlier visible aging, more pronounced photoaging, and stronger inflammatory responses to irritants. This is one reason why two people with the same sun exposure history can look dramatically different at the same age.

If you carry SOD2 variants that reduce function, you’re probably more photosensitive than average. You might notice that your skin looks duller, more tired, or older than your chronological age. You probably react more visibly to environmental stress (pollution, dry air, sun exposure). You may have more pronounced redness or reactive skin, because oxidative stress in your skin drives inflammation. You probably heal from skin injuries (acne, cuts, irritation) more slowly because your cells are dealing with accumulated oxidative damage.

Filaggrin is a structural protein that forms the foundation of your skin barrier. It aggregates in your outer skin layer (stratum corneum) and holds water, creating a waterproof seal that keeps moisture in and irritants out. FLG loss-of-function variants disrupt this seal, making your barrier genuinely compromised. People with FLG variants often have chronically dry skin, increased permeability to irritants, and high susceptibility to eczema and dermatitis.

Common FLG variants include R501X and 2282del4 (frameshift deletion). These are loss-of-function variants, meaning the protein is truncated or nonfunctional. Roughly 10% of people with European ancestry carry at least one FLG variant; prevalence is higher in East Asian and African populations. FLG variants eliminate your skin’s capacity to form a fully intact barrier, which means your skin is inherently more permeable to water loss and irritant penetration. This is not a moisturizer deficiency; this is a structural defect in your barrier protein. No topical product can replace filaggrin; you can only work around it.

If you carry FLG variants, your skin is dry at baseline, and no amount of moisturizer will make it ‘normal’ in the way that other people experience normal. You probably react to fragrances, certain surfactants, and preservatives that don’t bother most people. Your skin probably gets worse with heat and dry air, and improves noticeably in humid climates. You might have a history of eczema, keratosis pilaris, or atopic dermatitis. You probably can’t skip moisturizing for even one day without your skin becoming uncomfortable. Standard skincare that works for most people doesn’t work for you because the problem is structural, not cosmetic.