Dihydrotestosterone (DHT) is a derivative of the androgen hormone testosterone, and its activity is directly linked to how hormones regulate oil production in the skin. DHT plays a significant role in stimulating the sebaceous glands. The activity of this hormone is a primary driver in the development of hormonal acne, especially in adult women. Understanding the specific mechanism by which DHT interacts with the skin’s oil-producing structures is key to appreciating why certain treatments are effective.
What is Dihydrotestosterone (DHT)?
DHT is classified as an androgen, a group of hormones present in both men and women. DHT is synthesized from testosterone through the action of an enzyme called 5-alpha reductase (5-AR). This conversion process makes DHT substantially more potent than the testosterone from which it is derived.
The enzyme 5-alpha reductase exists in different forms, but the Type 1 isoenzyme is predominantly found in the sebaceous glands of the skin. Once formed, DHT binds to specialized androgen receptors located within target cells with a much higher affinity than testosterone. This enhanced binding power allows DHT to exert a powerful effect on tissues throughout the body, including the skin.
DHT’s Direct Impact on Sebaceous Glands
The link between DHT and acne is established by the hormone’s direct interaction with the pilosebaceous unit, the structure containing the hair follicle and the sebaceous gland. Sebaceous glands are sensitive to androgens because they possess a high concentration of androgen receptors. When DHT binds to these receptors, it acts as a signal to the glands.
This hormonal signal stimulates the sebaceous glands to grow in size and increase their output of sebum, the skin’s natural oil. Excess sebum is the initial biological step in the formation of acne lesions. This excess oil creates a sticky environment inside the hair follicle, where it combines with dead skin cells that have failed to shed properly.
The resulting mixture forms a plug that clogs the pore, leading to the formation of a microcomedone. This blocked pore creates an ideal environment for the proliferation of Cutibacterium acnes bacteria. The growth of this bacteria triggers an immune response, leading to inflammation, redness, and the visible formation of pimples, cysts, and nodules characteristic of acne.
Hormonal Approaches to Managing Acne
Acne treatments that target the hormonal pathway aim to reduce the influence of androgens like DHT on the sebaceous glands. One common strategy for female patients is the use of combined oral contraceptives (OCs), which contain both estrogen and progestin. These medications work systemically by increasing the production of sex hormone-binding globulin (SHBG) in the bloodstream.
SHBG binds to circulating androgens, including testosterone and DHT, effectively limiting the amount of free hormone available to stimulate the sebaceous glands. Specific progestins, such as drospirenone or cyproterone acetate, also have anti-androgenic properties that further block the effects of DHT at the receptor level.
Another common treatment is the anti-androgen medication spironolactone, often prescribed for women with hormonal acne. Spironolactone acts as an androgen receptor blocker, competitively inhibiting DHT from binding to the receptors on the sebaceous glands. By blocking this signaling pathway, spironolactone reduces the size and activity of the glands, resulting in a decrease in sebum production.
A more direct approach involves medications that inhibit the 5-alpha reductase enzyme itself. This strategy prevents the conversion of less potent testosterone into the more potent DHT within the skin. Blocking this specific enzyme reduces the local hormonal stimulation that drives acne development.