Androgens are steroid hormones that play a significant role in developing and maintaining male characteristics, but they are naturally present in everyone. Often referred to as “male hormones,” androgens like testosterone are produced in the testes, ovaries, and adrenal glands. Androgen excess, or hyperandrogenism, is a hormonal imbalance where the body produces elevated levels of these hormones. This leads to various physical signs and can affect reproductive and metabolic health, often indicating an underlying medical condition.
Common Physical Manifestations
The effects of elevated androgens are most visible in the skin and hair, which are highly sensitive to these hormones. The most common sign is hirsutism, which is the growth of coarse, dark hair in areas typically associated with male patterns, such as the upper lip, chin, chest, back, and abdomen. This involves thick, terminal hair growth that can be distressing for those affected.
Androgen excess also frequently contributes to persistent or severe acne and oily skin, known as seborrhea. Androgens stimulate the skin’s sebaceous glands, increasing sebum production, which can clog pores and lead to inflammatory acne lesions. Another visible effect is androgenic alopecia, or female pattern hair loss, which involves thinning hair on the scalp, often concentrated at the crown.
In pronounced cases, a process called virilization can occur, involving the development of masculine physical features. Signs include a deepening of the voice, increased muscle mass, and changes in body shape toward central fat distribution. Severe excess can less commonly lead to clitoral enlargement.
Primary Causes of Elevated Androgens
The majority of androgen excess cases in reproductive-aged women are caused by Polycystic Ovary Syndrome (PCOS), a common endocrine disorder affecting up to 10% of women. In PCOS, the ovaries produce excessive androgens due to a complex interplay between hormones and metabolic factors. A significant driver is insulin resistance, where the body’s cells do not respond effectively to insulin, causing the pancreas to produce higher amounts of the hormone.
This elevated insulin level, or hyperinsulinemia, stimulates the ovaries’ theca cells to overproduce androgens. High insulin also reduces the liver’s production of sex hormone-binding globulin (SHBG), a protein that binds to testosterone. This means more “free” and biologically active testosterone circulates in the bloodstream.
While PCOS is the most frequent cause, other less common conditions must be considered. Non-classic congenital adrenal hyperplasia (CAH) is a genetic disorder resulting from a deficiency in an adrenal enzyme, which diverts hormone production toward the androgen pathway. Androgen-secreting tumors of the ovaries or adrenal glands are rare but cause a sudden, rapidly progressing onset of severe androgen excess and virilization, requiring prompt medical evaluation.
Diagnostic Process
Diagnosis begins with a thorough physical examination and a detailed medical history, focusing on the onset and progression of symptoms like hirsutism, acne, and menstrual regularity. Providers often use a standardized scoring system, such as the modified Ferriman-Gallwey score, to objectively assess excess hair growth severity. Reviewing the menstrual cycle history is also important, as irregular or absent periods frequently accompany androgen excess.
Laboratory testing confirms biochemical hyperandrogenism and helps determine the source of the excess hormones. Key blood tests measure total and free testosterone levels. The Free Androgen Index (FAI), which considers the ratio of total testosterone to SHBG, is also a useful measure.
To differentiate between adrenal and ovarian sources, specific hormones are measured. Dehydroepiandrosterone sulfate (DHEAS) is a marker for adrenal androgen production. Testing for 17-hydroxyprogesterone screens for non-classic CAH, and other hormones like prolactin and TSH may be checked to rule out other endocrine disorders. Imaging studies, such as a pelvic ultrasound, are frequently used to check for the characteristic ovarian morphology associated with PCOS.
Treatment Approaches
Treatment focuses on managing symptoms and addressing the underlying cause to reduce circulating androgen levels. For women with PCOS and insulin resistance, lifestyle modifications are foundational. Losing 5 to 10 percent of body weight can significantly improve insulin sensitivity, which helps lower androgen production and improve symptoms like hirsutism and irregular periods.
Pharmacological interventions often begin with combination hormonal contraceptives, such as birth control pills, containing both estrogen and progestin. These medications work in two ways: the estrogen component increases the liver’s production of SHBG, which binds to and inactivates circulating testosterone, and the progestin component helps suppress the ovaries’ own androgen production. This approach effectively lowers overall androgen activity and regulates menstrual cycles.
Anti-androgen medications like spironolactone may be prescribed, often combined with hormonal contraceptives, particularly for managing hirsutism and acne. Spironolactone works by directly blocking androgen receptors in target tissues like the skin and hair follicles, preventing the androgens from exerting their effects. For cases linked to severe insulin resistance, medications like metformin may be used to improve insulin sensitivity, subsequently reducing the ovarian drive for androgen synthesis.
Symptomatic treatments manage the physical manifestations. Common approaches for hirsutism include temporary methods like shaving, waxing, and depilatory creams, as well as long-term solutions like laser hair removal or electrolysis. Topical anti-acne agents, and sometimes oral antibiotics or isotretinoin, are used to manage the acne component.