Finasteride is the generic name for the brand-name drug better known as Proscar.
Finasteride was originally developed and manufactured by the pharmaceutical company Merck, and was approved by the FDA in 1992 under the brand name Proscar for use in the prescription market.
It was initially approved for the treatment of benign prostatic hyperplasia (BPH), an enlargement of the prostate gland.
However, in 1997, the FDA approved finasteride for the treatment of male pattern baldness (MPB).
For the treatment of MPB, finasteride is sold under a different brand name, Propecia.
The difference between Proscar and Propecia is that Propecia contains only one-fifth the dose of Proscar.
Finasteride is used by bodybuilders and athletes for generally the same reasons it is used in medical settings: to slow or prevent male pattern baldness related to dihydrotestosterone (DHT), and to mitigate or prevent the potential for benign prostatic hyperplasia caused by the same hormone.
When bodybuilders and athletes use testosterone in high doses, they often experience a marked increase in androgenic side effects, such as increased aggression, increased body hair, oily skin, acne, prostate enlargement, and the potential to trigger male pattern baldness.
This is primarily because testosterone is converted into dihydrotestosterone (DHT), a much more potent androgen.
Testosterone itself is moderately androgenic, but DHT is several times more potent as an androgen.
Testosterone is converted (or more formally, reduced) into DHT via an enzyme called 5-alpha reductase (5AR).
This enzyme is found in high concentrations in tissues such as the scalp, prostate, and skin.
As testosterone circulates in the bloodstream and passes through these tissues, the 5AR enzyme binds to a certain percentage of the testosterone present and reduces it into dihydrotestosterone.
As you will soon learn, finasteride is an inhibitor of the 5-alpha reductase enzyme, which is the active mechanism of how finasteride works in the body.
It is important to note that 5AR inhibitors like finasteride only succeed in reducing or blocking the conversion of testosterone to DHT; they are virtually useless if an athlete or bodybuilder uses other anabolic steroids that completely bypass the 5AR enzyme (or are already derivatives of DHT).
Bodybuilders and athletes typically use finasteride on-cycle with moderate to high doses of testosterone.
Therefore, it stands to reason that finasteride will not help at all in mitigating, preventing, or stopping the androgenic effects of the following anabolic steroids:
(Trenbolone, Nandrolone (Deca-Durabolin), Anavar (Oxandrolone), Winstrol (Stanozolol), Masteron (Drostanolone), and several other compounds.)
Finasteride’s Chemical Characteristics
Finasteride is chemically known as a synthetic 4-azasteroid.
As you just learned, the 5-alpha reductase enzyme is responsible for the conversion of testosterone to DHT in the body.
Finasteride works by binding to and inhibiting the 5-alpha reductase enzyme itself, thereby preventing this process.
Through this mechanism of action, finasteride effectively lowers plasma DHT concentrations, thereby mitigating and minimizing the negative androgenic effects caused by high serum DHT levels.
Studies have shown that finasteride has the effect of reducing serum DHT levels by up to 65% 24 hours after administering a 1mg tablet.
Specifically, finasteride inhibits the Type II 5-alpha reductase enzyme.
In reality, there are two variants of the 5AR enzyme present in the body (Type-I and Type-II).
The difference between the two is that one is found in higher concentrations in certain body tissues than the other.
Specifically, Type-I 5AR enzyme is found in higher concentrations in the liver and the skin.
Type II 5AR enzyme is found in higher concentrations in the prostate and the scalp.
In fact, the Type-II variant is responsible for about two-thirds of the body’s total DHT concentration, with Type-I responsible for the remaining one-third.
It stands to reason that since finasteride only inhibits Type-II, it will be far more effective at preventing or treating MPB and hair loss than it will be at addressing other androgenic effects like oily skin/acne.
An important point here is that while finasteride is a very effective DHT inhibitor, research indicates it cannot block DHT conversion by nearly 100%, nor does it work equally in all body tissues where DHT is a concern.
Because finasteride prevents the conversion of testosterone to DHT, research results have shown that finasteride can increase circulating plasma testosterone levels by approximately 15%.
This is, of course, because finasteride leaves less 5AR enzyme available in the body to interact with testosterone.
Individuals considering the use of finasteride for male pattern baldness (hair loss), oily skin, acne, BPH, or other negative androgenic effects must understand that reductase inhibitors like finasteride do not provide 100% protection against these effects.
Drugs like finasteride can only mitigate or reduce/lessen these effects, not eliminate them.
Similarly, finasteride does not stop hair loss once it has begun, nor does it reverse hair loss, as is commonly misunderstood.
Finasteride Side Effects
Although finasteride is a very specific-acting drug with little peripheral or residual effect elsewhere in the body, it does have potential side effects.
Finasteride does not interact with androgen or estrogen receptors, so it has no direct androgenic, estrogenic, anti-androgenic, or anti-estrogenic effects.
It also does not affect other hormones in the body, such as cortisol, thyroid hormones, Luteinizing Hormone (LH), or Follicle-Stimulating Hormone (FSH).
Research results indicate it does not affect cholesterol levels either.
However, studies have shown that 8.1% of subjects and patients reported erectile dysfunction, 6.4% reported a decrease in libido (sex drive), and a small minority of less than 1% reported ejaculation problems, gynecomastia (breast tissue development), and unusual rashes.
Most finasteride side effects are caused by its ability to lower DHT levels in the body.
It must be understood that DHT is a potent androgen, and part of its responsibility is to maintain normal male secondary sexual characteristics, as well as sexual function.
It stands to reason that by lowering circulating plasma DHT levels, both the positive and negative androgenic effects of DHT are reduced.
This is very important, and individuals considering the use of finasteride should keep this in mind.
Furthermore, research and studies have shown that potent androgens actually act as anti-estrogens in the body.
This holds true for DHT as well, and with plasma DHT levels reduced by finasteride, estrogen can become more ‘dominant,’ potentially causing some users to experience estrogenic side effects like gynecomastia or breast tenderness to some degree.
Finasteride Dosage and Administration
For the treatment of androgenetic alopecia (male pattern baldness), the typical dosage is 1mg daily for 6 to 12 months.
For the treatment of benign prostatic hyperplasia (prostate enlargement), a higher dose is prescribed, typically 5mg daily over a long-term period.
The recommended dosage of finasteride for bodybuilders and athletes seeking to reduce the androgenic effects of testosterone converting to DHT is 1mg per day for the duration of testosterone use.
Furthermore, many athletes and bodybuilders adopt an approach of using finasteride only when necessary, and do not automatically take it with every cycle.
