Human hair covers nearly all of the body, but its appearance varies dramatically. This variation depends on the two fundamental types of hair that grow from our follicles. Vellus hair is the fine, short, light-colored hair, often called “peach fuzz,” that covers most skin surfaces and helps regulate temperature.
Terminal hair is the longer, coarser, and more pigmented hair found on the scalp, eyebrows, and, after puberty, in the pubic and underarm regions. The density and distribution of terminal hair cause the wide range of visible “hairiness” among individuals. Every hair follicle can produce either vellus or terminal hair, and the conversion between these two types is the core mechanism explaining most variation.
The Genetic Blueprint
An individual’s baseline level of hairiness begins with their inherited genetic blueprint. Hair follicle density, the number of follicles per area of skin, is a polygenic characteristic determined by multiple genes. These genes influence both the total number of follicles an individual is born with and their location on the body.
Genetic studies have identified specific gene variations, or loci, associated with traits like beard thickness, eyebrow thickness, and general body hair density. Variations in genes like TBX15 and BCL2 have been linked to differences in hair follicle activity and overall density. For instance, BCL2 regulates the life and death cycle of the hair follicle, affecting how long the hair grows.
Heredity also accounts for differences in hair distribution and texture across various ethnic backgrounds. Traits such as thickness and curl are strongly genetically driven and vary significantly across populations. For example, a single gene variation in TCHH relates to hair texture differences in people of Northern European ancestry. These inherited factors establish the initial potential for hair growth before hormonal signals cause changes later in life.
Hormonal Drivers of Hair Growth
The most significant factor converting vellus hair to terminal hair is the activity of androgen hormones. Androgens, such as testosterone and dihydrotestosterone (DHT), drive the growth of thick, pigmented hair in specific body regions. This explains the dramatic increase in body and facial hair during puberty when the body produces higher levels of these hormones.
The conversion occurs when circulating androgens bind to receptors within the dermal papilla cells of the hair follicle. This binding triggers cellular events that remodel the follicle. The small vellus follicle grows larger and deeper, producing longer, thicker, and darker terminal hair. Androgens also extend the anagen, or active growth, phase of the hair cycle, allowing hairs to reach greater lengths.
Variation in hairiness among people with similar hormone levels is often due to the differing sensitivity of their hair follicles to androgens. Some individuals have follicles highly responsive to even normal levels of circulating testosterone or DHT. Different body areas also exhibit different sensitivities. For example, follicles in the pubic region and armpits are sensitive to lower androgen levels, while those on the face and chest require higher concentrations to be stimulated.
Medical Conditions and External Factors
Excessive hair growth can stem from factors beyond normal genetic or hormonal fluctuations. Hirsutism, common in women, is characterized by the growth of coarse, dark terminal hair in a male-typical pattern. This growth occurs in androgen-sensitive areas like the upper lip, chin, chest, and back. It usually results from abnormally high androgen levels or increased tissue sensitivity to androgens. Polycystic Ovary Syndrome (PCOS) is the most frequent cause, often involving the overproduction of androgens by the ovaries.
A separate phenomenon is hypertrichosis, defined as increased hair growth anywhere on the body, not limited to androgen-sensitive sites. Unlike hirsutism, hypertrichosis affects both sexes and may involve either vellus or terminal hair. Causes include rare congenital genetic disorders, malnutrition, or certain systemic illnesses.
External factors, particularly certain medications, can also induce hypertrichosis as a side effect. Drugs such as minoxidil, cyclosporine, and some anticonvulsants like phenytoin are known to stimulate hair growth. The mechanism is not always androgen-related; minoxidil, for example, lengthens the hair’s active growth phase, leading to overall longer hair fibers. In these cases, the excess hair growth is often reversible upon discontinuing the medication.