A very common misconception about Finasteride (also known as Propecia and Proscar) is the belief that it lowers testosterone levels.
This is typically derived from the fact that Finasteride can lower libido and cause erectile dysfunction in a minority of users [R, R, R].
Another common misconception is the belief that it increases Estrogen and can cause gynecomastia on its own.
Also, it has become apparent to me that many doctors who are prescribing this drug aren’t properly educated on its mechanism of action and will commonly tell their patients that one of the side effects of Finasteride is lowered Testosterone.
It's actually the complete opposite.
Finasteride’s Mechanism Of Action
After taking Finasteride there are a few hormonal events that unfold in the body.
The first thing that happens is Finasteride inhibits Type II 5-alpha reductase [R].
5-alpha reductase is an intracellular enzyme that regulates the conversion of the androgen testosterone into the more androgenic metabolite dihydrotestosterone (DHT) [R].
If you take Finasteride, or you are planning on taking it, you should be aware that DHT is the byproduct metabolite of testosterone.
It is another hormone entirely and it is significantly more androgenic than any other anabolic hormone in the body, hence why it has the ability to miniaturize hair follicles to a much greater extent [R].
The more androgenic a hormone is the more havoc it can wreak on your hair in a dose dependent manner [R].
DHT is far more androgenic than testosterone, and when there is enough of it circulating in someone prone to male pattern baldness (almost every man on earth) it results in the growth phase of the hair cycle becoming progressively shorter.
The individual hairs in androgen affected areas of the scalp are unable to grow to full size as a result of this shorter window of growth, and the end result is their progressive decrease in size.
This process is referred to as “hair follicle miniaturization” and is the primary mechanism responsible for the progression of hair loss.
The goal of Finasteride is to inhibit the conversion of testosterone to DHT.
By inhibiting 5-alpha reductase, Finasteride effectively prevents a significant amount of testosterone to DHT conversion that would have otherwise occurred.
How Finasteride Increases Testosterone And Estrogen Levels
After Finasteride inhibits 5-alpha reductase, a significant amount of conversion of testosterone to DHT that would have otherwise occurred is no longer going to happen, so that testosterone remains present in the body as unaffected testosterone.
Inhibition of Type II 5-alpha reductase blocks the peripheral conversion of testosterone to DHT, resulting in significant decreases in serum and tissue DHT concentrations.
As there is now a much greater portion of testosterone that the body cannot convert into DHT, serum testosterone levels are raised indirectly simply due to the fact that the testosterone has nowhere to go because 5-alpha reductase is inhibited from completing the job it normally does.
Within 24 hours of oral dosing 1 milligram of Finasteride, serum DHT concentrations in the body are suppressed by 65%, and mean circulating levels of testosterone and estradiol increase by approximately 15% [R].
Estradiol is the primary estrogen hormone in the body, and the reason estrogen increases is because testosterone has also increased.
Testosterone aromatizes into estrogen, and because testosterone increases as a result of 5-alpha reductase inhibition, aromatization into estrogen inevitably increases as well in parallel to it.
What Actually Causes Low Libido And Erectile Dysfunction Side Effects
If someone has a crash in their libido as a result of Finasteride, it is most often the result of their systemic androgen load going down.
Not their testosterone levels going down.
It is typically the DHT suppression that causes libido and erectile dysfunction in a minority of users.
The elevation in Estrogen levels can also play a role, but typically this is only a concern secondarily to DHT suppression.
Finasteride does not inherently decrease sex drive or lower libido; it is the inhibition of DHT and concurrent elevation of aromatization, which largely influences erectile function if there isn't enough free testosterone present in the body to fill the void of those physiological mechanisms.
This is why “Post-Finasteride Syndrome” is more often than not essentially just the result of a low systemic androgen load.
Even if someone has in range Total Testosterone levels, a significant amount of that may be bound up by sex hormone-binding globulin (SHBG).
Reference ranges are also not based on a young and healthy population, so falling within a physiologic reference range may mean nothing at the end of the day if your body needs more of a certain hormone than the next guy.
Another possible scenario is that an individual’s free testosterone levels are simply not high enough to fulfill the androgenic void left by an absence of DHT.
Also, if estrogen levels are pushed too high from increased aromatization and that goes unaddressed, that can cause severe erectile dysfunction as well until those levels are managed correctly via lifestyle changes, diet, losing body fat, supplements, or in worst case scenarios, manual estrogen management via an aromatase inhibitor (not something you want to be using long term).
How To Cure Post-Finasteride Syndrome
As mentioned above, the incidence of sexual dysfunction in men using 5-alpha reductase inhibitors shouldn’t be perceived as a side effect of inhibiting DHT, rather, it should be viewed as a potential consequence of lowering the body’s endogenous androgen load relative to estrogen levels in the body.
There are hundreds, if not thousands of androgens.
These are synthetic, and not endogenously produced in the human body via the endocrine system like testosterone and DHT are, but they can serve similar functions in the body regardless.
In a dose dependent manner, all androgens will induce androgenic effects in the body, and the amount to which they do this is relative to their selectivity for muscle and bone to androgen affected tissues like the prostate, hair follicles, etc.
Hypothetically, if a guy started getting ED while on Finasteride, and he got a blood test, I would with a fairly high level of certainty bet that his free testosterone levels aren’t on the high end of the reference range, his SHBG is too high, or his estrogen levels are too high (or too low).
I used Dutasteride for over a year straight with my Testosterone Replacement Therapy.
I had DHT levels lower than a woman for over a year, confirmed by my blood work, and I had 0 libido issues or erectile dysfunction.
I would actually prefer if my libido was lower, I’d get way more work done.
The reason my libido was unaffected is because I manually keep my Testosterone levels at 1000-1200 ng/dL, and for a fair portion of my hair loss experiments in 2018 I was pushing those levels up to 2000 ng/dL (a supraphysiological level that no human could naturally produce).
Throughout the entirety of that, I had zero issues, because my body simply didn’t need the DHT at all as it had so much present testosterone that is more than androgenic enough to fulfill those physiological functions.
That doesn’t mean that you should start popping Dutasteride and pinning Testosterone though obviously, I’m just trying to provide a real life example of how the androgen-fulfilled functions in the body can be accomplished with hormones other than DHT.
I am confident that a guy with Post-Finasteride Syndrome could in theory use an extremely androgenic DHT derivative like Proviron, Masteron, or even just literal DHT, and successfully restore whatever loss of function they are experiencing in a dose dependent manner, pending they also kept their other values in range (like Estrogen), as those can cause sexual dysfunction irrespective of androgen levels in the body.
It's important to understand how these hormones work before you take Finasteride (or any drug for that matter).
The onus is on us to understand how processes unfold in the body so we can mitigate issues if they are to occur, and ideally prevent them from occurring in the first place.