Finasteride is a commonly prescribed medication used to treat benign prostatic hyperplasia (BPH) and male pattern hair loss (androgenetic alopecia). The drug’s mechanism of action involves interfering with hormonal processes, which often leads to questions about its effect on testosterone. It is a frequent misconception that this treatment causes a reduction in total circulating testosterone.
The Role of the 5-Alpha Reductase Enzyme
The primary function of finasteride is to block the conversion of testosterone (T) into a significantly more potent androgen hormone called dihydrotestosterone (DHT). This conversion process is mediated by an enzyme known as 5-alpha reductase (5AR). The 5AR enzyme exists in multiple forms, or isoenzymes, throughout the body, specifically Type I and Type II.
Finasteride acts as a competitive and specific inhibitor of the Type II 5-alpha reductase isoenzyme, which is highly concentrated in tissues like the prostate, hair follicles, and liver. By forming a stable complex with the enzyme, the drug prevents the conversion of testosterone, resulting in the desired therapeutic reduction in DHT levels.
Dihydrotestosterone is substantially more potent than testosterone and is the main androgen responsible for the miniaturization of hair follicles, leading to male pattern baldness. It also drives the growth of prostate tissue, contributing to BPH. Finasteride’s purpose is therefore not to block testosterone itself but to inhibit the enzyme that creates the more powerful androgen metabolite.
Since finasteride targets only the Type II isoenzyme, it does not completely eliminate DHT production, as Type I 5AR continues to function. This specific inhibition mechanism is key to differentiating between the drug’s effects on testosterone and dihydrotestosterone levels.
Measured Effects on Testosterone and Dihydrotestosterone Levels
Clinical studies consistently demonstrate that finasteride causes a profound decrease in dihydrotestosterone (DHT) levels. Patients taking the medication typically see a reduction in serum DHT concentration ranging from 60% to over 70%, with reductions up to 90% reported in prostatic tissue.
In stark contrast to the dramatic decrease in DHT, total circulating testosterone levels do not fall; they actually tend to increase slightly. When the conversion pathway is blocked, the unconverted testosterone remains in the bloodstream, leading to a small but measurable increase in serum testosterone.
Clinical data indicates that total testosterone levels increase by approximately 10% to 20% compared to baseline measurements. This elevation keeps testosterone well within the normal physiological range for men and directly refutes the idea that finasteride causes clinical hypogonadism.
The precise percentage increase in testosterone can vary depending on the dosage, with the 5 mg daily dose used for BPH sometimes causing a rise of 15% to 25%. This slight elevation is an expected consequence of the drug’s action, as the body attempts to maintain hormonal equilibrium.
Hormonal Balance and Potential Clinical Symptoms
While finasteride does not cause a deficiency in total testosterone, the resulting change in the ratio between testosterone and DHT alters the overall hormonal signaling environment. This altered balance can lead to subjective clinical symptoms, which are often mistakenly attributed to “low T” but are instead related to the severe reduction of DHT.
The reduction in DHT can manifest as side effects such as decreased libido or erectile dysfunction in a small percentage of users. These sexual side effects are thought to be mediated by the decrease in DHT and its associated neurosteroids. Other potential consequences include mood changes or breast tenderness (gynecomastia).
Since androgen receptors respond differently to testosterone and DHT, the functional absence of the more potent DHT can disrupt certain androgen-dependent processes, even with slightly elevated testosterone levels. Any patient experiencing concerning symptoms should consult a healthcare professional for a medical evaluation.