Androgenetic alopecia, commonly known as pattern baldness, is the most frequent cause of hair loss, affecting many men and women over their lifetimes. This condition is an inherited trait, meaning the predisposition to develop it is passed down through family lines. While it was once thought to be a simple dominant trait, current understanding confirms that the genetics are complex and multifactorial, involving multiple genes inherited from both parents. These genetic factors determine the age of onset, the severity, and the specific pattern of hair thinning an individual experiences.
The Dominant Gene on the X Chromosome
The most significant and well-studied genetic factor contributing to pattern baldness is a specific variation of the Androgen Receptor (AR) gene. This gene is located on the X chromosome. Men inherit their X chromosome exclusively from their mother, while women inherit one X chromosome from each parent.
Because men only receive one copy of the AR gene, the version inherited from their mother has a disproportionately strong influence on their baldness risk. This inheritance pattern is why baldness is frequently traced to the maternal side of the family, particularly the mother’s father. The AR gene is influential, estimated to confer up to 40% of the total genetic risk for pattern baldness.
The AR gene provides instructions for making the androgen receptor protein, which is found inside hair follicle cells and responds to male hormones. Variations in this gene can make the hair follicles highly sensitive to androgens, leading to hair loss. While this strong gene variant is a major predictor, it is not the sole determinant of hair loss.
The Role of Multiple Genes and Autosomal Inheritance
Despite the strong influence of the AR gene on the X chromosome, baldness is not solely determined by maternal lineage; it is a polygenic trait. This means that multiple genes, often dozens, work together to determine an individual’s final hair loss profile. These additional genes are located on the autosomal chromosomes, inherited from both the mother and the father.
Genome-wide association studies have identified hundreds of different genetic loci across the human genome that contribute to the risk of androgenetic alopecia. These autosomal genes act as modifiers, influencing factors like the age at which hair loss begins and the speed and pattern of the thinning. For example, variants near the PAX1/FOX A2 locus on chromosome 20 have been repeatedly linked to hair loss risk.
This complex inheritance pattern explains why tracking baldness risk is difficult. A person might inherit a high-risk AR gene from their mother but also inherit protective or modifying genes from their father. Conversely, a person could inherit a low-risk AR gene but accumulate many high-risk autosomal genes from both parents, still leading to significant hair loss. The cumulative effect of all these variants determines the final outcome.
How Genes Cause Follicle Miniaturization
The primary biological action of the baldness-associated genes is to regulate the hair follicle’s response to Dihydrotestosterone (DHT). DHT is a derivative of testosterone, produced when the enzyme 5-alpha reductase converts testosterone in various tissues, including the scalp. The inherited genetic variants, especially those in the AR gene, dictate the sensitivity of specific hair follicles to DHT.
If a hair follicle has the genetic predisposition, its androgen receptors bind to DHT, triggering follicular miniaturization. This process causes the hair follicle to progressively shrink with each successive growth cycle. The growth phase, known as the anagen phase, is shortened, and the resting phase is prolonged, resulting in the hair shaft becoming visibly thinner and finer over time.
Miniaturization eventually transforms the thick, pigmented terminal hairs into nearly invisible vellus hairs, leading to the clinical appearance of baldness. The inherited trait is not high levels of circulating testosterone or DHT itself. Rather, it is the genetic programming that makes the hair follicles on the top and front of the scalp hyper-responsive to normal levels of the hormone.