Hirsutism is the medical term for coarse, dark hair growth in women in areas typically associated with male hair growth, such as the upper lip, chin, chest, and back. This condition is common, affecting 5% to 10% of women of reproductive age.
The appearance of excess hair is usually a visible sign of an underlying biological change, often related to the body’s hormonal balance. This article explores the specific biological and medical factors that cause this shift in hair growth patterns, from the hair follicle level to systemic endocrine disorders.
Understanding Hair Follicle Sensitivity
The physical manifestation of hirsutism begins at the hair follicle, which is a complex mini-organ embedded in the skin. Hair follicles exist in two main types: vellus hair, which is fine, short, and lightly colored, and terminal hair, which is coarse, long, and pigmented. On a woman’s face, most hair is normally vellus hair, but a hormonal signal can cause it to transition into terminal hair.
This transformation is directly stimulated by a group of hormones known as androgens, which are present in all women but at lower concentrations than in men. Androgens interact with hair follicles by binding to specialized androgen receptors located primarily in the dermal papilla cells. The strength of this interaction determines whether a vellus hair follicle will be converted into a terminal hair follicle.
The sensitivity of hair follicles to androgens varies significantly based on location and individual genetics. Facial hair follicles, particularly on the chin and upper lip, are highly sensitive to these signals. An enzyme called 5-alpha reductase, found within the hair follicle, converts testosterone into a more potent form, dihydrotestosterone (DHT), magnifying the local hormonal effect. Hirsutism can thus result from elevated circulating androgen levels or from an increased sensitivity of the hair follicles to normal androgen levels.
Primary Endocrine Conditions
The most frequent cause of hirsutism is an underlying medical condition resulting in androgen overproduction. Polycystic Ovary Syndrome (PCOS) accounts for up to 70% of all cases where a hormonal cause is identified. This endocrine disorder is characterized by irregular or absent menstrual periods, high androgen levels, and often the presence of multiple small cysts on the ovaries.
In PCOS, the ovaries are the primary source of the elevated androgens, often triggered by a complex interplay with elevated insulin levels. Insulin resistance, a common feature of PCOS, causes the body to produce excess insulin, which then stimulates the ovarian cells to increase androgen production. This cycle leads to a chronic state of hyperandrogenism, manifesting as hirsutism, acne, and sometimes female-pattern hair loss.
Other, less common, endocrine disorders can also cause androgen excess originating from the adrenal glands or the pituitary gland. Non-classic Congenital Adrenal Hyperplasia (NCAH) is an inherited condition that causes the adrenal glands to produce irregular amounts of steroid hormones, shunting precursors toward the androgen pathway. Although present from birth, the symptoms of NCAH can be mild and only appear later in life, mimicking PCOS.
Androgen-secreting tumors are a rare but serious cause of hirsutism, typically arising in the ovaries or adrenal glands. These tumors usually cause a rapid, severe onset of hair growth over a few months, often accompanied by signs of virilization, such as a deepening voice. Cushing syndrome, resulting from prolonged exposure to high levels of cortisol, is another possibility that can lead to increased adrenal androgen production.
Genetic Predisposition and Medication Side Effects
Not all cases of hirsutism are linked to a diagnosed endocrine disorder involving elevated hormone levels. Sometimes, the cause is related to an individual’s genetic makeup, a condition known as idiopathic hirsutism. In these cases, the woman has normal circulating androgen levels and regular menstrual cycles, but her hair follicles are simply hypersensitive to normal hormonal stimulation.
Family history plays a substantial role, as hair thickness and density are often inherited. Women of certain ancestries, such as Mediterranean or South Asian descent, are genetically predisposed to have more terminal body hair. This is a variation in normal hair growth patterns, not necessarily a sign of hormonal imbalance or disease.
Certain medications can also induce or worsen hair growth as a side effect (iatrogenic causes). These include medications that contain androgens or indirectly promote hair growth. Examples are anabolic steroids, some immunosuppressive drugs like cyclosporine, and Minoxidil, which is used to treat hair loss.
Diagnostic Steps and Medical Consultation
Determining the cause of unwanted facial hair growth requires a systematic diagnostic approach by a healthcare provider. Evaluation begins with a physical examination to quantify the severity and distribution of the hair using a standardized tool, such as the modified Ferriman-Gallwey scale. This scale assigns a numerical score based on hair growth in nine androgen-sensitive body areas.
Blood tests are subsequently used to measure the levels of specific circulating hormones, most importantly total and free testosterone. Elevated levels confirm the presence of hyperandrogenism, directing the diagnostic focus toward the source of the excess hormones. Other hormones, like dehydroepiandrosterone sulfate (DHEA-S), help differentiate between ovarian and adrenal origins of the androgen overproduction.
If symptoms have a rapid or severe onset, or if hormone levels are extremely high, imaging studies are necessary to rule out rare, androgen-secreting tumors. A pelvic ultrasound can examine the ovaries for abnormal growths or the characteristic appearance of polycystic ovaries. A CT scan or MRI may also be used to visualize the adrenal glands.