Why Hair Falls Out at a Young Age When Hormones Are Normal: The Role of Genetics

Androgenetic alopecia is not always a story about an excess of hormones. What also matters is how the tissue responds to the same signal. This is why a normal level of androgens does not explain how a particular hair follicle will behave.

This difference is easy to miss. A person gets their test results, sees no abnormalities, and starts looking for the cause in shampoo, water, stress or the season. Meanwhile androgenetic alopecia — a type of gradual hair thinning with a pronounced hereditary component, linked to the response of genetically susceptible follicles to androgens — is the most common cause of reduced hair density in adults (Gupta et al., Biology, 2026). The male pattern belongs to highly heritable complex traits: in twin studies, heritability estimates reached about 80% (Nyholt et al., J. Invest. Dermatol., 2003). For the female pattern the evidence base is limited: there are fewer relevant studies, the samples are narrower, and the results agree less well with one another (Ho et al., Genes, 2023). At the same time, the genetics of complex traits describes probabilities, not scenarios. Hereditary variants shift the predisposition relative to a reference population, but do not determine when and how pronouncedly it will appear.

Below — about how this mechanism works, where the possibilities of a genetic assessment end, and when early hair loss is worth considering outside the frame of androgenetic alopecia.

Why Hair Can Thin Even When Hormones Are Within the Normal Range

A blood test shows how much of a hormone circulates in the body. But it does not show how sensitive particular cells and tissues are to its action. In androgenetic alopecia, the local response of the hair follicle is of great importance (Gupta et al., Biology, 2026). Genetic variants can affect the sensitivity of androgen signalling and of other pathways that regulate the hair growth cycle.

In the skin, testosterone is converted by the enzyme 5-alpha-reductase into dihydrotestosterone, a more active form of androgen (Xiao et al., Nat. Commun., 2020). Dihydrotestosterone binds to the androgen receptor, which is encoded by the AR (androgen receptor) gene. Activation of the androgen receptor in genetically susceptible follicles is linked to changes in several signalling pathways. In particular, the WNT/β-catenin pathway, which supports the follicle’s transition to the active growth phase, may be weakened, and TGF-β signalling — transforming growth factor beta, associated with the premature end of this phase — may be strengthened (Gupta et al., Biology, 2026).

These changes do not cause a sudden loss of hair. Instead, the follicle gradually miniaturises: in each successive cycle it forms a thinner and shorter hair, and the growth phase shortens. Over time, this becomes noticeable as a decrease in hair density. This is consistent with the clinical picture: follicle sensitivity cannot be determined from the hormonal background alone. Even in one person, follicles in different areas of the head respond differently: in particular, in the occipital zone they often remain more resistant to the action of androgens (Gupta et al., Biology, 2026).

Why Androgenetic Alopecia Begins Earlier in Some People

The early onset of androgenetic alopecia is linked to the combined contribution of many hereditary variants, not to a single separate genetic factor. The most robust signal is found in a region of the X chromosome, where the AR and EDA2R (ectodysplasin A2 receptor) genes are located (Hillmer et al., Am. J. Hum. Genet., 2005).

Genetic variants in this region are linked to a higher predisposition to male-pattern hair loss, in particular to its early onset. This is one of the best-reproduced genetic loci of male androgenetic alopecia: the association was first described in the early 2000s and later confirmed in independent samples (Hillmer et al., Am. J. Hum. Genet., 2005). In modern genome-wide analyses this locus also gives the strongest association signal (Gupta et al., Biology, 2026).

This is where the widespread notion comes from that the predisposition is passed down the maternal line. It has a real but incomplete basis. Men receive the X chromosome from their mother, so they inherit the variants of the AR/EDA2R locus down the maternal line. However, most of the loci associated with the trait are located in autosomes, which are inherited from both parents. So the family history on the father’s side also remains informative (Pirastu et al., Nat. Commun., 2017; Gupta et al., Biology, 2026).

The practical conclusion here is simple: an early manifestation of androgenetic alopecia does not mean it is a separate disease, and does not indicate a “strong gene”. It may be linked to a higher hereditary predisposition, but it does not show how pronounced that predisposition is or which specific genetic variants are linked to it.

Why There Is No Single “Baldness Gene”

Androgenetic alopecia is a polygenic trait: its hereditary component is linked not to a single gene but to many regions of the genome. A large 2017 genome-wide study identified 71 independent loci, whose associations were confirmed in a separate sample (Pirastu et al., Nat. Commun., 2017).

The identified loci point to several interconnected biological processes. A pathway analysis in the same study grouped the candidate genes into several functionally coherent directions (Pirastu et al., Nat. Commun., 2017):

• androgen metabolism and signalling through the androgen receptor;

• WNT signalling, in particular through WNT10A (Wnt family member 10A), which regulates the follicle’s transition to the growth phase;

• apoptosis (programmed cell death) processes linked to the end of the growth phase;

• follicle morphogenesis and remodelling of the extracellular matrix.

The hypothesis of rare variants of large effect was tested separately. An analysis of the exomes of more than 72,000 UK Biobank participants found associations of rare variants with five genes, two of which, EDA2R and WNT10A, were already known from genome-wide studies. Rare variants can complement the polygenic architecture of the trait, but in the sample studied, adding them improved population prediction only slightly (Henne et al., Nat. Commun., 2023).

This is exactly why a genetic predisposition to this trait is assessed not by a single variant but by a combination of many variants — using a polygenic predisposition score (PRS). A PRS sums up their weighted contribution on the basis of data from genome-wide association studies. Such a score shows how a person’s genetic predisposition relates to a reference population, but it does not predict the individual course and is not a diagnostic tool. An association found in such studies indicates a link between a genetic variant and the trait, but on its own it does not prove causation.

The limit of transferability also matters here. Most large studies of androgenetic alopecia have been carried out in samples of European ancestry, and transferring polygenic models even to individual European populations depends on the composition of the original sample, calibration and external validation. In a study of African men, estimates built mainly on European data had limited discriminative ability, and some of the signals differed from European cohorts (Janivara et al., Hum. Genet. Genom. Adv., 2025).

Why Genetic Data on Male Baldness Do Not Explain Hair Thinning in Women

The female pattern of hair loss is studied far less, and male findings cannot be transferred to it automatically. Individual loci convincingly linked to the male pattern often did not reach statistical significance in female samples or gave contradictory results. This does not prove entirely different genetics, but nor does it allow male models to be transferred to women automatically (Gupta et al., Biology, 2026).

The difference begins with the clinical picture. The male pattern has a characteristic sequence: a recession of the hairline in the temporal areas, then thinning of the hair on the crown. The female pattern more often looks like a diffuse decrease in density in the area of the parting, with the front hairline preserved. These are different phenotypes, and there are no grounds to believe that the same genetic architecture lies behind them.

Interpretation is complicated by the heterogeneity of the samples themselves. Diffuse hair thinning in women is often classified in studies as the female type, although other processes may lie behind it: chronic telogen effluvium, age-related thinning, mixed phenotypes (Ho et al., Genes, 2023). Such phenotypic heterogeneity blurs the genetic signal and reduces the ability to identify reproducible loci (Gupta et al., Biology, 2026). Reviews of the genetics of the female pattern describe exactly this situation: the available data are fragmentary, and the results agree poorly between studies (Ho et al., Genes, 2023).

Individual genetic associations specific to women have only recently begun to appear. In a sex-stratified genome-wide analysis in a Korean population, variants near the FZD1 (frizzled class receptor 1) and GJC1 (gap junction protein gamma 1) genes were statistically significant only in women (Lee et al., Life, 2024). These are preliminary data on possible differences in genetic architecture, but the study covered a single population, and the results require independent confirmation.

The practical implication for women is direct: for early hair thinning in women, the basis of assessment remains a clinical examination, trichoscopy and the relevant tests. Polygenic models of the male pattern cannot be used as a substitute for such an assessment.

When Early Hair Loss Has a Different Mechanism

Not every case of early hair loss is androgenetic alopecia. Some conditions have a different mechanism, different dynamics and, accordingly, require different actions. If the hair is already noticeably thinning or falling out, the clinical type of the process needs to be determined first. Genetic information can complement this assessment, but it will not establish the cause of the symptom.

Telogen effluvium

A synchronous transition of a large proportion of follicles into the resting phase, followed by heavy shedding. It develops as a reaction to a systemic event: an acute illness, a significant restriction of calories, the postpartum period, deficiency states, disorders of the thyroid gland.

Chronic telogen effluvium

Prolonged diffuse shedding without the characteristic picture of thinning. Whether chronic telogen effluvium is a distinct condition is still debated; moreover, it is often confused with the female type of hair thinning (Daunton et al., Am. J. Clin. Dermatol., 2023).

Alopecia areata

Alopecia areata manifests as clearly defined patches of hair loss and has an autoimmune, not an androgen-dependent, mechanism.

Age-related thinning

A gradual decrease in hair density linked to age-related changes in the cycle and structure of the follicle. It may have mechanisms different from classic androgenetic alopecia, but it is able to coexist with it (Gupta et al., Biology, 2026).

To consider all these conditions reversible would be an oversimplification. Their course depends on the mechanism, the duration of the process, the removal of a possible trigger and accompanying factors. In addition, several processes can overlap: diffuse shedding can temporarily worsen hair thinning against the background of already existing androgenetic alopecia.

An examination by a dermatologist or trichologist should not be put off if there is pain, burning or itching of the scalp, redness, flaking or the appearance of crusts, smooth patches without hair, loss of eyebrows or eyelashes, signs of scarring, or a sudden heavy shedding. These conditions can be distinguished during a clinical examination and trichoscopy, with additional tests where needed, and not from a photograph or a genetic assessment.

What Information a Genetic Report Provides and Where the Limits of Its Interpretation Lie

A genetic report describes constant hereditary features. The state of the hair at a particular moment, by contrast, depends on a combination of genetic predisposition with other factors, among them deficiency states, hormonal changes, past or current illnesses, stress, physical and emotional strain. So a genetic assessment complements the clinical picture but does not replace it.

A normal level of androgens in the blood does not rule out a genetic predisposition to androgenetic alopecia. A blood test shows the concentration of hormones, but not the sensitivity of the hair follicles to their action.

The Limits of a Genetic Assessment

A genetic report does not establish the cause of the actual hair loss in a particular person, does not distinguish androgenetic alopecia, telogen effluvium and alopecia areata, and does not give a precise prognosis of whether the trait will appear. A genetic test does not replace an examination by a dermatologist or trichologist, trichoscopy and laboratory tests. The role of a genetic study is different — to show a hereditary predisposition as one of the factors worth taking into account together with the clinical picture and the results of other examinations.

A Prisma genetic test provides an assessment of the hereditary predisposition to the male type of androgenetic alopecia within the Skin, hair and appearance direction.

The Early Onset of Androgenetic Alopecia Does Not Determine Its Further Course

The mechanism of androgenetic alopecia is linked not only to the concentration of androgens but also to the local response of hair follicles to their action. So normal androgen readings on their own do not rule it out, and an early onset on its own does not point to a separate mechanism or a specific genetic cause. A hereditary predisposition affects the probability of the trait appearing, but does not determine the outcome. Data obtained from male samples cannot be transferred directly to the female type of hair thinning. So for early thinning it is worth first working out which process exactly is taking place: this changes not the prognosis but the quality of the decisions.

Answers to Frequently Asked Questions

Does a normal testosterone level mean that hair loss is not linked to androgenetic alopecia?

In androgenetic alopecia, what matters is not only the concentration of androgens in the blood but also the local response of the follicles to their action. So readings within the reference range do not rule out this mechanism.

Is the predisposition passed down the maternal line only?

The best-reproduced locus is located on the X chromosome, which men receive from their mother. However, most of the associated loci are autosomal, so the contribution to genetic risk from the father’s side also matters.

Can a genetic assessment tell me when hair loss will start?

A polygenic score describes a shift in predisposition relative to a reference population. It does not establish the age of onset and is not a prognosis for an individual person.

Is the genetics of hair loss the same in women and men?

The data point to partly shared and partly different mechanisms, but the female genetic architecture is studied far less, so male models are not transferred to women automatically.

When is it worth seeing a doctor rather than looking for a genetic explanation?

In cases of sudden or heavy shedding, the appearance of patches, pain, itching, redness or flaking of the scalp, loss of eyebrows or eyelashes, and also accompanying systemic symptoms. These signs are distinguished during an examination with trichoscopy and tests.

The results of a genetic test are not a diagnosis and not a substitute for a doctor’s consultation. An Apixmed Prism report provides genetic context that complements the findings of examinations and helps you make decisions together with your doctor.

Sources

1. Gupta, A. K., Dennis, D. J., Economopoulos, V., Piguet, V. (2026). The genetic landscape of androgenetic alopecia: current knowledge and future perspectives. Biology, 15(2), 192. https://doi.org/10.3390/biology15020192

2. Pirastu, N., Joshi, P. K., de Vries, P. S., Cornelis, M. C., McKeigue, P. M., Keum, N., Franceschini, N., Colombo, M., Giovannucci, E. L., Spiliopoulou, A., Franke, L., North, K. E., Kraft, P., Morrison, A. C., Esko, T., Wilson, J. F. (2017). GWAS for male-pattern baldness identifies 71 susceptibility loci explaining 38% of the risk. Nature Communications, 8, 1584. https://doi.org/10.1038/s41467-017-01490-8

3. Henne, S. K., Aldisi, R., Sivalingam, S., Hochfeld, L. M., Borisov, O., Krawitz, P. M., Maj, C., Nöthen, M. M., Heilmann-Heimbach, S. (2023). Analysis of 72,469 UK Biobank exomes links rare variants to male-pattern hair loss. Nature Communications, 14, 5492. https://doi.org/10.1038/s41467-023-41186-w

4. Ho, C. Y., Chen, J. Y. F., Hsu, W. L., Yu, S., Chen, W. C., Chiu, S. H., Yang, H. R., Lin, S. Y., Wu, C. Y. (2023). Female pattern hair loss: an overview with focus on genetics. Genes, 14(7), 1326. https://doi.org/10.3390/genes14071326

5. Lee, J., Choi, J. E., Ha, J., Kim, Y., Lee, C., Hong, K. W. (2024). Genetic differences between male and female pattern hair loss in a Korean population. Life, 14(8), 939. https://doi.org/10.3390/life14080939

6. Janivara, R., Hazra, U., Pfennig, A., Harlemon, M., Kim, M. S., Eaaswarkhanth, M., Chen, W. C., Ogunbiyi, A., Kachambwa, P., Petersen, L. N., et al. (2025). Uncovering the genetic architecture and evolutionary roots of androgenetic alopecia in African men. Human Genetics and Genomics Advances, 6, 100428. https://doi.org/10.1016/j.xhgg.2025.100428

7. Daunton, A., Harries, M., Sinclair, R., Paus, R., Tosti, A., Messenger, A. (2023). Chronic telogen effluvium: is it a distinct condition? A systematic review. American Journal of Clinical Dermatology, 24, 513–520. https://doi.org/10.1007/s40257-023-00760-0

8. Hillmer, A. M., Hanneken, S., Ritzmann, S., Becker, T., Freudenberg, J., Brockschmidt, F. F., Flaquer, A., Freudenberg-Hua, Y., Jamra, R. A., Metzen, C., et al. (2005). Genetic variation in the human androgen receptor gene is the major determinant of common early-onset androgenetic alopecia. American Journal of Human Genetics, 77, 140–148. https://doi.org/10.1086/431425

9. Nyholt, D. R., Gillespie, N. A., Heath, A. C., Martin, N. G. (2003). Genetic basis of male pattern baldness. Journal of Investigative Dermatology, 121(6), 1561–1564. https://doi.org/10.1111/j.1523-1747.2003.12615.x

10. Xiao, Q., Wang, L., Supekar, S., Shen, T., Liu, H., Ye, F., Huang, J., Fan, H., Wei, Z., Zhang, C. (2020). Structure of human steroid 5α-reductase 2 with the anti-androgen drug finasteride. Nature Communications, 11, 5430. https://doi.org/10.1038/s41467-020-19249-z