Dihydrotestosterone (DHT) is a potent androgen, naturally present in females in small amounts. This hormone plays a role in the development of certain physical characteristics, such as body hair and skin oil production. When DHT levels become elevated in women, it leads to hyperandrogenism, which can manifest as hirsutism, acne, and hair thinning on the scalp. The source of this elevated DHT is often traced back to overproduction of precursor hormones or increased efficiency in the conversion process.
The Biochemical Pathway of DHT Production
The primary mechanism for DHT creation involves the conversion of testosterone, a less potent androgen, into its more active form. This transformation is catalyzed by the enzyme 5-alpha reductase, which is found in various tissues including the ovaries, skin, and liver. DHT is significantly more potent than testosterone, binding to the androgen receptor with a much higher affinity.
High DHT levels in a female can result from two general issues: an oversupply of testosterone, or an overactivity of the 5-alpha reductase enzyme itself. The enzyme’s activity can be locally high in target tissues like the hair follicle, which may lead to symptoms even if circulating DHT levels appear mildly elevated. Some tissues also utilize a “backdoor pathway” to synthesize DHT from other precursors, bypassing testosterone as an intermediate.
Primary Cause: Polycystic Ovary Syndrome (PCOS)
Polycystic Ovary Syndrome (PCOS) is the most frequent cause of androgen excess in women, accounting for the majority of high DHT cases. This disorder involves a disruption of the hypothalamus-pituitary-ovarian axis and metabolic issues. The primary mechanism for androgen overproduction begins in the ovaries.
In women with PCOS, there is often an increased frequency of Luteinizing Hormone (LH) pulses from the pituitary gland, which stimulates the ovarian theca cells to produce excess androgens, particularly testosterone. This overproduction provides the necessary precursor for conversion into DHT. High levels of androgens then interfere with the normal development of ovarian follicles, contributing to the cystic appearance of the ovaries.
A significant driver of this androgen excess is insulin resistance, which is common in women with PCOS, even those who are not overweight. The body attempts to compensate by producing extra insulin, resulting in hyperinsulinemia. High insulin levels directly stimulate the ovarian cells to synthesize more androgens and simultaneously reduce the liver’s production of sex hormone-binding globulin (SHBG).
The reduction in SHBG means more testosterone is available in its “free” or biologically active form, leading to a greater pool of substrate for the 5-alpha reductase enzyme to convert into DHT. This cycle of insulin resistance, hyperinsulinemia, and subsequent hyperandrogenemia is central to the development and maintenance of elevated DHT in PCOS. Targeting insulin pathways is a common strategy in managing PCOS-related hyperandrogenism.
Adrenal Gland Conditions
The adrenal glands are the second major source of androgen production in the female body. Conditions affecting them are another cause of high DHT. Congenital Adrenal Hyperplasia (CAH) is an inherited disorder of adrenal steroid synthesis. Non-classic CAH (NCCAH), a milder form, is particularly relevant to hyperandrogenism in adult women.
NCCAH is most often caused by a partial deficiency of the enzyme 21-hydroxylase, which is required to produce cortisol and aldosterone. Because the enzyme is partially blocked, the precursor hormones that would normally be converted into cortisol accumulate. These accumulated precursors are then shunted into the pathway for androgen production.
This diversion leads to an excessive production of adrenal androgens, which are then converted into testosterone and ultimately into DHT in peripheral tissues. The symptoms of NCCAH, such as hirsutism, acne, and menstrual irregularities, frequently overlap with those of PCOS, making a specific diagnosis challenging without appropriate hormonal testing.
Rare and External Causes
While PCOS and adrenal disorders account for the majority of cases, high DHT levels can also result from rare, localized issues or external influences. Androgen-secreting tumors of the ovaries or adrenal glands are uncommon but serious causes of hyperandrogenism. These tumors produce androgens autonomously, leading to very high and rapidly rising hormone levels.
A rapid onset and progression of symptoms, including signs of frank virilization like voice deepening or clitoral enlargement, often signal the presence of a tumor and require immediate medical evaluation. Virilizing ovarian tumors, such as Sertoli-Leydig cell tumors, are more frequent than adrenal androgen-secreting neoplasms.
External factors, or iatrogenic causes, involve the introduction of androgens into the body, which then serve as precursors for DHT. This includes the use of anabolic steroids, derivatives of testosterone, often used for performance enhancement. The use of certain over-the-counter supplements, such as those containing Dehydroepiandrosterone (DHEA), can also significantly elevate precursor levels.
DHEA is a precursor hormone that the body can convert into testosterone and then into DHT. Even topical testosterone products used by a partner can be inadvertently transferred, leading to elevated DHT levels in a woman. A thorough history of medications and supplements is important for identifying the source of hyperandrogenism.