Androgenetic alopecia is caused by the hormone dihydrotestosterone (DHT) miniaturizing genetically susceptible hair follicles over time. It affects approximately 50% of men by age 50 and is the most common form of hair loss worldwide. The condition is driven by two factors: your genetics determine which follicles are susceptible, and DHT triggers the actual miniaturization process.
This guide explains the biological mechanisms, genetic inheritance patterns, and contributing factors behind male pattern baldness.
The DHT Mechanism
DHT is produced when the enzyme 5-alpha reductase converts testosterone into dihydrotestosterone. This conversion happens in several tissues, including the hair follicles of the scalp.
Not all follicles respond to DHT the same way. Follicles on the top and front of the scalp carry androgen receptors that are genetically programmed to respond to DHT. When DHT binds to these receptors, it initiates a cascade that progressively shrinks the follicle.
How Miniaturization Works
| Stage | What Happens | Hair Appearance |
|---|---|---|
| Normal | Full anagen phase (2-6 years), thick terminal hair | Thick, pigmented, full-length |
| Early miniaturization | Anagen phase shortens, hair grows slightly thinner | Slightly thinner, shorter maximum length |
| Moderate miniaturization | Anagen phase under 1 year, telogen lengthens | Noticeably thinner, lighter in color |
| Advanced miniaturization | Anagen phase weeks only | Fine vellus hair (peach fuzz) |
| Terminal | Follicle produces no visible hair | Bare scalp |
This process takes years to decades per follicle. It does not happen overnight, and different follicles progress at different rates. This is why androgenetic alopecia creates a gradual transition from thick to thin hair rather than sudden bald patches.
Why the Back and Sides Are Spared
Follicles in the occipital and temporal regions (back and sides) lack the androgen receptors that respond to DHT. These follicles are genetically different from those on the top of the scalp. This is why hair transplant surgery works: follicles moved from DHT-resistant areas to DHT-sensitive areas retain their genetic resistance and continue growing permanently.
Genetic Factors
Androgenetic alopecia is a polygenic condition, meaning multiple genes influence susceptibility. No single gene determines whether you will lose your hair. The interplay of many genetic variants determines your follicle sensitivity to DHT, your DHT production levels, and the age of onset.
Key Genes Involved
| Gene | Location | Role |
|---|---|---|
| Androgen receptor (AR) gene | X chromosome | Determines follicle sensitivity to DHT |
| SRD5A2 | Chromosome 2 | Encodes 5-alpha reductase type II |
| EDA2R | X chromosome | Associated with hair loss susceptibility |
| PAX1 | Chromosome 20 | Linked to vertex baldness |
| HDAC9 | Chromosome 7 | Associated with hair loss timing |
Inheritance Patterns
The AR gene on the X chromosome is the strongest single genetic predictor. Because men inherit their X chromosome from their mother, there is a correlation between male pattern baldness and the mother's father's hair pattern. However, this is not the complete picture.
| Inheritance Factor | Impact |
|---|---|
| Mother's father bald | Increases risk significantly (AR gene on X chromosome) |
| Father bald | Increases risk (autosomal genes from both parents) |
| Both sides have baldness | Highest risk |
| Neither side has baldness | Lowest risk, but not zero |
| Identical twin concordance | Over 80% (both twins tend to follow the same pattern) |
Family history on both sides matters. A man whose father is bald but whose maternal grandfather had full hair can still develop androgenetic alopecia, and vice versa. The polygenic nature of the condition means that predicting exact patterns from family history alone is imprecise.
Hormonal Factors
Testosterone and DHT Levels
Men with androgenetic alopecia do not have higher testosterone levels than men without it. The difference lies in follicle sensitivity to DHT, not in the amount of DHT circulating. Two men with identical DHT levels can have completely different hair loss outcomes based on their follicular androgen receptor density and sensitivity.
| Hormonal Factor | Relationship to Hair Loss |
|---|---|
| Testosterone level | No direct correlation with pattern baldness |
| DHT level | Slightly higher in balding men, but sensitivity matters more |
| 5-alpha reductase activity | Higher activity in balding scalp tissue |
| Androgen receptor density | Higher in frontal/vertex follicles of balding men |
| Estrogen | Protective effect (why women lose hair differently) |
Age-Related Changes
DHT levels do not increase with age. However, the cumulative effect of DHT on susceptible follicles means that miniaturization progresses over time. This is why hair loss is age-dependent even though the hormonal trigger remains constant.
| Age | Men Affected | Mechanism |
|---|---|---|
| 20-30 | 20-25% | Early miniaturization, temples recede first |
| 30-40 | 30-40% | Progressive thinning, crown involvement begins |
| 40-50 | 40-50% | Established pattern, frontal and crown merge |
| 50-60 | 50-60% | Advanced patterns common, slower progression |
| 60+ | 60-70% | Most susceptible follicles fully miniaturized |
Contributing Factors (Not Primary Causes)
Several factors can accelerate or unmask androgenetic alopecia without being the root cause.
Lifestyle and Environmental Factors
| Factor | Effect on Hair Loss | Evidence Level |
|---|---|---|
| Smoking | May accelerate thinning via reduced blood flow | Moderate |
| Diet (severe deficiency) | Can worsen shedding if iron, zinc, or protein-deficient | Moderate |
| Stress | Triggers telogen effluvium (temporary shedding), does not cause AGA | High |
| Sleep deprivation | Indirect via stress hormones | Low |
| Anabolic steroids | Dramatically accelerates AGA in susceptible men | High |
| Weight lifting | No effect on hair loss | High (no correlation) |
Medical Conditions
Thyroid disorders, iron deficiency anemia, and autoimmune conditions can cause hair loss that mimics or coexists with androgenetic alopecia. If hair loss is sudden, diffuse, or does not follow the typical Norwood pattern, a medical evaluation should rule out other causes.
What You Can Control
You cannot change your genetics, but you can intervene in the DHT pathway. Finasteride and dutasteride reduce DHT levels by 70% and 90% respectively, directly slowing or halting the miniaturization process. The earlier you intervene, the more follicles remain in a state where recovery is possible.
Hair transplant surgery bypasses the genetic issue entirely by relocating DHT-resistant follicles to balding areas, providing permanent coverage regardless of future DHT exposure.
Assess Your Hair Loss Pattern
Upload a photo at myhairline.ai/analyze for a free AI assessment. The analysis identifies your current Norwood stage and the pattern of miniaturization, giving you a clear picture of where your hair loss stands and which interventions are most appropriate.