Dihydrotestosterone (DHT) is a potent androgen hormone derived from the more widely known hormone, Testosterone (T). While T handles a wide range of functions, DHT is the primary driver of characteristics like facial and body hair growth, but also conditions such as male pattern hair loss and benign prostatic hyperplasia (BPH). DHT blockers are medications that manage these conditions by interrupting the conversion of T into DHT. Many people worry that blocking this conversion pathway will lead to an overall reduction in their total T levels, but scientific evidence clarifies how this hormonal process is regulated and what happens to the unconverted Testosterone.
The Conversion Pathway: How DHT is Formed
Testosterone functions as the precursor for Dihydrotestosterone. This conversion is catalyzed by an enzyme known as 5-alpha reductase (5-AR), which is distributed throughout androgen-sensitive tissues in the body. The 5-AR enzyme chemically transforms Testosterone into DHT; approximately 5 to 10% of circulating Testosterone is converted daily.
DHT is significantly more potent than Testosterone because it binds to the androgen receptor with a much stronger affinity, estimated to be two to three times greater. This enhanced binding ability allows DHT to exert powerful effects even at lower circulating concentrations, making it the primary androgen in tissues like the prostate and hair follicles. The 5-alpha reductase enzyme exists in two main forms, or isoenzymes, designated as Type 1 and Type 2.
Type 2 5-AR is predominantly found in the prostate, seminal vesicles, and genital skin, making it the most relevant for conditions like BPH. Conversely, Type 1 5-AR is highly expressed in non-genital skin, the scalp, and the liver. Understanding the location of these two isoenzymes is important because different DHT-blocking medications target them with varying selectivity.
The Action of 5-Alpha Reductase Inhibitors
DHT blockers are pharmacological agents called 5-alpha reductase inhibitors (5-ARIs), with common examples being Finasteride and Dutasteride. These drugs function as competitive inhibitors: they physically bind to the active site of the 5-AR enzyme, preventing Testosterone from docking and undergoing conversion. This action effectively shuts down the synthesis of DHT.
Finasteride is known as a selective inhibitor because its primary target is the Type 2 isoenzyme of 5-AR. This selective action results in a significant, though partial, reduction in circulating DHT levels, typically around 70%. Dutasteride, on the other hand, is a dual inhibitor that targets and blocks both the Type 1 and Type 2 isoenzymes.
Because Dutasteride inhibits both major forms, it achieves a more comprehensive and profound suppression of DHT, often reducing serum levels by 90% to 95%. The mechanism of action centers entirely on interrupting the conversion step, which is distinct from reducing the body’s overall production of Testosterone. This difference in isoenzyme targeting explains why Dutasteride is considered the more potent DHT suppressor.
Impact on Serum Testosterone Levels
Clinical data contradicts the concern that DHT blockers lower Testosterone levels, as the opposite effect is typically observed. Since the 5-AR enzyme is inhibited, the Testosterone molecules that would have been converted into DHT remain circulating, increasing the systemic Testosterone pool. This elevation is readily measurable in blood tests.
Studies show that Finasteride treatment results in a slight, compensatory increase in serum Testosterone levels, generally ranging from 10% to 25% above baseline. For Dutasteride, the increase is often slightly higher, with reported median increases of approximately 19% to 26% over years of treatment. This elevation is a direct consequence of the blocked metabolic pathway, not an increase in the production rate of Testosterone.
Despite this measurable increase, the resulting Testosterone concentrations almost always remain within the normal physiological range for men. The body’s endocrine system attempts to compensate for the hormonal shift. The overall change in total Testosterone is not considered clinically significant or harmful compared to the dramatic reduction in the highly potent DHT.
Understanding Other Resulting Hormonal Shifts
The slight increase in circulating Testosterone, a consequence of 5-AR inhibition, leads to secondary hormonal adjustments. Testosterone is a substrate for the aromatase enzyme, which converts androgens into Estrogens. With more unconverted Testosterone available, a greater amount is accessible to the aromatase enzyme.
This increased substrate availability can result in a minor elevation in serum Estrogen (Estradiol) levels. For example, Finasteride has been shown to increase mean circulating Estradiol levels by approximately 15%. Like the Testosterone increase, this minor rise typically stays within the normal reference range and is generally not associated with adverse clinical outcomes.
The body’s central hormonal regulators, the Gonadotropins (Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH)), are also monitored during treatment. Clinical data generally indicate that LH and FSH levels remain stable or are only minimally affected after starting DHT blockers, confirming that the main feedback loop governing Testosterone production is not severely disrupted.