Is Post Finasteride Syndrome Real? | How To Diagnose And Reverse It

I believe that interpreting blood work correctly and implementing an appropriate lifestyle and/or pharmacological protocol can reverse Post Finasteride Syndrome.

Post Finasteride Syndrome describes negative side effects caused by Finasteride that persist long-term, even after discontinuing its use.

Finasteride-induced side effects can be very real.

Let's talk about why that happens in the first place.

In short, you need a certain amount of androgenic activity in your body to facilitate physiological functions as a male.

For example, maintaining a high libido.

You also need a physiological amount of Estrogen to support many overlapping functions as well.

When you deplete these androgens and/or throw off the balance of androgens to estrogen in the body, you could experience erectile dysfunction, low libido, and a myriad of other issues.

The Importance Of Correctly Interpreting Blood Work

The way Finasteride can cause persistent side effects is typically via a mismanagement of hormone levels.

This is not entirely the fault of the user.

Most doctors are not going to preemptively suggest that you get baseline blood work, which is their own negligence.

Obviously some level of responsibility falls on the patient to research what drugs they are going to be taking prior to taking them, but if a doctor has upwards of a decade of “education”, and they suggest you forgo blood work, or fail to even suggest it to begin with, it just goes to show that they probably shouldn't even be prescribing drugs in the first place.

If you don't have baseline blood work to see what your hormone profile looks like, you will have no idea what to reference afterwards if an issue arises.

Haphazardly giving somebody Finasteride without looking at their baseline hormone levels is a terrible idea.

Which Blood Tests You Should Get Before Taking Finasteride

You should get your baseline total testosterone, free testosterone, DHT, Estradiol and SHBG levels tested.

While getting baseline blood work for as many major endocrine health markers as possible is ideal, the markers above are the bare minimum that you absolutely need.

In addition, the quality of the testing is critical.

If you get your Testosterone and Estradiol levels tested using the more primitive Roche ECLIA methodology (typically the default test most doctors will sign off on), you are going to get a completely inaccurate test result.

I highly recommend you always get your hormone levels tested with high-pressure liquid chromatography tandem mass spectrometry (LC/MS-MS).

It is a more sensitive and specific method when measuring Testosterone and Estradiol concentrations when compared to immunoassay, and the difference in test results between the two methods are night and day.

Prior to starting Finasteride, I advise that you at least get the following high sensitivity hormone profile and add the sensitive assay Estradiol test to your cart on top of that.

High Sensitivity Hormone Profile

Sensitive Assay Estradiol

Direct ECLIA Vs. LC/MS-MS Blood Test Results

Direct ECLIA is stated to be “sufficiently sensitive and accurate” for screening for androgen dysfunctions in men.

I'll tell you right now, it's not.

If you aren't getting highly sensitive and specific testing done via LC/MS-MS, you will not get accurate blood test results.

I have proven this in my own blood work numerous times.

For example, the following test results are wildly different.

These test results came from the exact same tube of blood.

Yes, it makes that much of a difference.

Get high quality blood work when you get it.

99% of individuals don't get blood work at all, and of the 1% that do get it, 99% of those individuals don't get the proper tests.

As a result, they're completely in the dark when it comes to deciphering exactly what deficiencies and/or imbalances they have in their hormone profile.

Male Pseudohermaphroditism Caused By 5-Alpha Reductase Deficiency

The way Finasteride works is by inhibiting 5-alpha reductase.

Finasteride more or less creates a blockade whereby testosterone can't be 5-alpha reduced into DHT as efficiently as it normally would.

Dutasteride inhibits 5-alpha reductase significantly more, and can crush systemic DHT levels as much as 90-99%.

Dutasteride is so powerful that it almost induces a state identical to what pseudohermaphrodites experience as a result of a 5-alpha reductase genetic deficiency.

5-alpha reductase deficiency is a condition where genetic males (1 X and 1 Y chromosome in each cell) with male gonads do not produce enough DHT because they have a mutation in the SRD5A2 gene.

This mutation prevents 5-alpha reductase from converting Testosterone into DHT adequately, which consequently results in a massive DHT deficiency.

Depending on the severity of their deficiency, males with 5-alpha reductase deficiency can be born with genitalia that is not obviously male or female (ambiguous genitalia).

In some cases, their genitalia appears female, or in other cases they definitively have male genitalia, but its unusually small (micropenis) with the urethra opening on the underside of the penis.

During puberty, Testosterone and DHT spike significantly.

DHT is several times more androgenic than Testosterone with a much higher binding affinity for androgen receptors, and is what is majorly responsible for the development of secondary sex characteristics like the deepening of the voice, development of facial hair and body hair, and the growth of the penis and scrotum.

During puberty, men with 5-alpha reductase deficiency do not develop much facial or body hair, they appear to have no androgenic alopecia, and they have a small prostate.

Many males with 5-alpha reductase deficiency are raised as girls until they hit puberty because they didn't have enough DHT to markedly differentiate themselves as males pre-puberty.

Once they hit puberty and Testosterone levels spike, the penis and other androgen supported structures start to enlarge [R].

Expectedly, the penis doesn't grow to a normal size like it would in someone with an adequate amount of DHT, nor does facial hair or prostate growth occur to as significant of an extent.

This genetic mutation is what shed light on the potential therapeutic applications of Finasteride in the first place [R].

It also reinforces the fact that Testosterone also causes hair loss, just to a far lesser extent than DHT.

Supporting Androgen Dependent Tissues Vs. Androgen Levels Necessary During Puberty

Very similar to how HGH and IGF-1 levels determine how tall you get during puberty, Testosterone and DHT levels determine how much sexual development you experience during puberty.

Once you're an adult, these androgens simply support existing androgen dependent functions though.

A teenager in the middle of puberty could severely inhibit his sexual development by taking Finasteride.

An adult could induce androgen deficiency side effects by taking Finasteride, but this could be manually reversed with ease via hormone manipulation.

There's only a certain amount of androgen receptor activation you need in different tissues to support satisfactory function, and the necessity of maxed out DHT levels is lower post-puberty.

This isn't to say that DHT isn't needed, but there's a reason why the majority of Finasteride users are side effect free.

If you could thoroughly evaluate erection quality, libido, etc. before and during Finasteride use, I am sure that these would be hindered to some extent in the majority of users.

You are after all slashing your body's primary androgen by upwards of 70%.

However, that doesn't mean that you can't still support satisfactory function without that 70% DHT, hence why most do not experience any noticeable issues.

It also doesn't mean you can't reach maxed out androgen support if you really wanted to via manual hormone manipulation, which we will delve into later.

Once you create this blockade with Finasteride at 5-alpha reductase, you now have a bunch of testosterone that would have otherwise been 5-alpha-reduced, that now remains as testosterone.

Finasteride will increase testosterone levels by roughly 15%, and Dutasteride will increase testosterone levels by roughly 22%.

This is why males with 5-alpha reductase deficiency also have higher Testosterone levels than normal, and may even be more muscular than those with adequate DHT conversion.

In most cases, Testosterone is more than sufficient to support androgen dependent functions as an adult in the absence of normal DHT levels.

And in cases where it isn't, this is simply due to a lack of sufficient testosterone production, SHBG level being too high, mismanaged estrogen, or a combination of these.

The same androgen dependent functions can be satisfied via any androgen though; Testosterone and DHT aren't special, which we will delve into later.

Unaddressed Estrogen Imbalance

Finasteride raising Testosterone levels might sound like a good thing.

More muscle, less hair loss, how could this be a bad thing?

Another cause of Finasteride side effects is an unaddressed Estrogen imbalance.

When you have this 15% increase in testosterone, you have to take into account that testosterone also aromatizes into estrogen.

If you have a significant increase in testosterone, you also get a parallel significant increase in estrogen in your body.

In addition, DHT acts as an antagonist to estrogen in the body and also frees up bound Testosterone to SHBG.

Testosterone is far less androgenic than DHT too.

So, despite the fact that you're increasing your Testosterone and your estrogen by 15%, the drop in DHT Finasteride causes reduces the overall androgen load in your body.

Estrogen increases by 15%, while you have a simultaneous 70% drop in the most androgenic hormone in your body that acts as an antagonist of estrogen and frees up bound testosterone from SHBG.

Let's just say, hypothetically, you had an estrogen level on the top end of the reference range to begin with, and you take Finasteride and you push it outside of the therapeutic level, that in itself could cause estrogen dominance and result in estrogenic side effects.

Now, what about individuals with side effects who have in-range hormone levels?

This can happen in the following scenarios.

If you had subpar free testosterone and DHT levels (could still be in the reference range, but not high enough), and Finasteride crushed your DHT while you maintained a normal Estrogen level in the reference range.

Or, you have high SHBG levels, and the drop in DHT and/or the spike in Estrogen caused even more Testosterone to get bound up by SHBG, preventing you from getting sufficient free testosterone to facilitate androgen dependent functions that would otherwise be satisfied by endogenous Testosterone.

Keep in mind, estrogen increases SHBG, and DHT lowers SHBG [R, R].

Finasteride or Dutasteride could both cause a hormonal sh*t storm where any of the following occurrences could cause and/or exacerbate a state of estrogen dominance in the body:

• Your androgen load drops significantly via the decrease in DHT
• The decrease in DHT causes SHBG to bind up more testosterone in the body
• The subsequent increase in estrogen via the increase in testosterone causes SHBG to rise even more, consequently binding up even more testosterone

Increased SHBG will bind up even more of your testosterone, preventing it from being bioavailable.

You could have a high total testosterone level, but if your SHBG is so high that you don't have enough free testosterone, you will likely experience androgen deficiency symptoms.

This is also why it is so critical that you get high sensitivity blood tests.

You could get a completely inaccurate blood test result and have no idea why you're still experiencing side effects, but the reality is that you aren't interpreting accurate information.

If too much of your testosterone is bound up by SHBG, you could have low testosterone symptoms (fatigue, low libido, ED, etc.), and the simultaneous spike in estrogen could result in a state of estrogen dominance where you become prone to gynecomastia and a myriad of other estrogenic side effects.

You could be estrogen dominant even with in-range estrogen levels simply due to an insufficient androgen load in the body.

These are all things that are facilitated via an improperly managed hormone profile, and can be manually corrected.

Now, the answer here is not to take an aromatase inhibitor and crush your Estrogen into the ground.

Estrogen is needed to support libido and erections just as much as androgens.

Even if you have sky high Testosterone and DHT levels, if you take a high dose of Letrozole and crush your Estradiol to zero, I promise you that your dick will cease to function.

You need a healthy amount of estrogen, and an optimal balance of androgens to estrogen to maintain peak sexual function.

The Implications Of Forgoing Blood Tests

Users are quick to blame the drug, when the root of the issue is your hormone profile that is not being managed correctly.

In many cases, had accurate blood work been thoroughly evaluated prior to taking Finasteride, it would have become clear that it wasn't a good idea to take Finasteride in the first place.

Had you seen that your baseline bloodwork showed borderline high estrogen levels to begin with, low or low-normal androgens, borderline high SHBG, or a combination of these, it would be a lot easier to make an educated guess about what your risk profile was prior to starting.

Even if you do increase your testosterone and estrogen by 15% with Finasteride and significantly decrease your DHT, the likelihood is that you will be side effect free.

However, the fact remains that there is a possibility of dropping your androgen index to a point where you no longer have sufficient endogenous androgens to support male sexual functions.

For example, if you have a guy who has Testosterone levels on the low end of the reference range, or he has high SHBG, and he's barely hanging on by a thread with satisfactory sexual function, and then he takes Finasteride and consequently crushes the DHT in his body that his penis was just hanging on for dear life to, can you guess what the likely outcome of that would be?

You can predict with a MUCH higher level of accuracy whether you will encounter issues or not when you have a thorough baseline hormone panel to refer to.

And even if you do still encounter issues, you can then pin point exactly what the reasons could be and how to attenuate the issue within short-order.

Muscle Loss Caused By Finasteride?

If you look at the clinical data, inhibiting 5-alpha reductase has no negative effect on the accrual of lean muscle mass.

The following study was evaluated using Dutasteride, which is far more DHT suppressive than Finasteride.

Even by nearly wiping out the participants' DHT levels with Dutasteride, they did not experience hindered muscle growth at all in response to graded testosterone doses.

The DHT-deprived group had no significant disadvantage compared to the group that wasn't using Dutasteride [R].

The reason is that, if anything, the increase in testosterone would help you gain more muscle rather than lose muscle, because testosterone is more anabolic and tissue-selective than DHT.

This comes with the caveat that your SHBG levels don't increase so much that you end up with less free Testosterone, but in most cases, the increase in Testosterone that occurs as a result of inhibiting 5-alpha reductase increases anabolic activity in the body.

DHT is very androgenic, but sucks at building muscle.

Testosterone has a significantly higher anabolic to androgenic ratio than DHT.

In the image above, the man on the left has a 5-alpha reductase deficiency, and his brother on the right doesn't have a deficiency.

The man on the left has a higher testosterone level, is more muscular, and has less androgenic alopecia than his brother on the right who has normal DHT levels.

The True Cause Of “Post Finasteride Syndrome”

Other than supporting male sexual development through puberty, DHT more or less serves to sustain androgenic functions in androgen supported tissues that could otherwise be maintained by high testosterone levels, lowering SHBG and antagonizing estrogen.

Now, these are obviously important, even in adulthood once the reliance on DHT is far lower as sexual development has already completed.

Most individuals will do just fine with 5-alpha reductase inhibitors, however, when you decrease DHT levels in men who are on the threshold of low androgen status to begin with, crushing DHT and spiking Estrogen with Finasteride, regardless of the fact of that their testosterone might be in the therapeutic reference range, can cause their androgen index to drop too low.

This ultimately results in markedly decreased sexual function, and a myriad of other low androgen symptoms.

Keep in mind, the reference range for these hormones are extremely general too.

A doctor will tell you your testosterone levels are fine when you are walking around with a 300 ng/dL total testosterone level.

And that isn't even factoring in that they probably haven't evaluated it with LC/MS-MS.

They also probably haven't looked at your free testosterone at all, or your SHBG, or your sensitive assay Estradiol, or your DHT, or anything that could be useful to you because most physicians don't know a f*cking thing about hormone management.

One time I asked a doctor to get my DHT tested and he told me I should get a blood test for testosterone because Finasteride lowers testosterone.

Most doctors don't even know what hormones the drugs they're prescribing affect, nor do they know how to test them properly.

This onus falls on you to learn how to manage your health.

If you leave your Post Finasteride Syndrome up to a doctor to solve, you will 9/10 times be stuck with a limp dick and assuming that Finasteride ruined your life.

“Post Finasteride Syndrome” is really just a fancy term for mismanaged estrogen levels and/or an androgen-deficiency induced by the Finasteride use.

This is nothing that can't be alleviated simply by increasing your androgen index manually, and/or modulating your Estrogen levels.

Most individuals who experience side effects and stop Finasteride recover with no issues with endogenous DHT levels returning to normal within short order once the Finsasteride has cleared their system and their body starts 5-alpha reducing Testosterone into DHT again [R].

The vertical dotted line represents when treatment was stopped during this study.

The Finasteride treated group was using 5 mg per day for 24 weeks (roughly 6 months), and after stopping treatment, their DHT levels recovered to baseline within a month.

Expectedly, those using 1.0-1.25 mg for hair loss prevention (the standard daily dose of Propecia, or Proscar prescribed off label divided into quarters) would experience a recovery of DHT levels within an even shorter time frame.

Further complicating things is the fact that endogenous androgen secretion decreases with age [R].

After endogenous androgen secretion peaks in a man's youth, those levels plateau and then start to decline fairly quickly year after year.

Total testosterone levels fall by 0.8%-1.6% on average per year, and free testosterone levels fall by 2%-3% on average per year [R].

SHBG levels also increase by 1.6% on average per year, which exacerbates the problem [R].

Total testosterone secretion dropping will decrease the amount of bioavailable free testosterone for the body to use, and the concurrent increase in SHBG binds up even more of the testosterone in the body, further dropping the amount of bioavailable free testosterone in the body.

Most individuals who experience side effects from Finasteride were borderline low androgen status to begin with, and introducing Finasteride pushed them over the border.

You can just imagine what kind of difficulty a borderline androgen deficient male would have trying to recover optimal sexual function when they are losing 2-3% of their bioavailable testosterone per year.

For most who do experience side effects, the restoration of endogenous DHT production is sufficient to reverse the side effects, as they have effectively restored a sufficient enough androgen load to stimulate androgen supported tissues again.

However, for those who experience persisting side effects, this is simply the result of persisting androgen deficiency or estrogen dominance.

How To Reverse Post Finasteride Syndrome

Now, there is debate as to whether or not Finsateride irreversibly inhibits 5-alpha reductase.

The clinical data clearly shows that it doesn't, but even if it did, androgen receptors are still androgen receptors at the end of the day and can be activated by using any androgen, hence why Post Finasteride Syndrome is 100% reversible with hormonal manipulation.

Let's break this down into what you can do naturally, and what you can do should the natural route fail.

Natural Post Finasteride Syndrome Treatment

Post Finasteride Syndrome is more than likely just an underlying androgen deficiency either caused by a lack of sufficient free testosterone and/or DHT.

High estrogen levels, high SHBG levels, suboptimal endogenous testosterone secretion, or a combination of the 3 can exacerbate this.

The goal here is to maximize bioavailable androgens, lower SHBG, and maintain healthy levels of Estrogen (not too low, and not too high).

Should bioavailable androgen levels be at a healthy level, libido and quality erections are typically supported best with an Estradiol level around 30 pg/mL.

These levels should be assessed using sensitive assay testing only, as outlined earlier in the article.

Obviously there are exceptions to this, but in general, most men feel best with high-normal levels of bioavailable androgens, and an Estradiol around 30 pg/mL.

This is the Estrogen sweet spot.

There are some things you can do to try and optimize these levels naturally.

Lifestyle

• Exercise and lift weights often [R].
• Get as close to 10-12% body fat as possible.
  • The leaner you are, the less aromatase activity you will have, thus resulting in lower Estrogen and SHBG levels, consequently increasing free testosterone and DHT levels [R].
  • Obesity is associated with low testosterone concentrations, which are not secondary to an increase in estradiol concentrations [R].
• Gain as much muscle as possible.
  • Muscle mass not only supports improved insulin sensitivity, but it will increase your metabolic rate, consequently keeping you leaner, and thereby supporting a hormone profile with an optimized ratio of bioavailable androgens. These androgens then support increased muscle mass, essentially creating a virtuous circle of hormone optimization.
  • Having enough muscle mass is the only way you will be able to walk around with a lean body composition year round without significantly depriving yourself of calories. Nutrient deprivation is not sustainable and will ultimately result in a slow metabolism and hindered androgen production.
• Get enough sleep.
  • Obvious, but most do not actually get enough sleep. Most have a disrupted circadian rhythm and poor sleep hygiene, leading to suboptimal hormone secretion and inadequate amounts of REM and deep sleep.

Diet

If you have no idea where to start and are feeling overwhelmed, I recommend trying the Vertical Diet.

It is a turnkey easy to follow diet model that will ensure you are hitting your macros and micros, all while maximizing muscle and strength gain potential.

I'm not going to breakdown everything you should be taking into account with diet as that would easily be an essay of content, and the Vertical Diet eBook covers it in elaborate detail, but here are a couple keys that you should adhere to that will help you be successful once you start following the Vertical Diet.

• Eat enough healthy fats. Dietary fat is critical for producing sex hormones. Most don't realize how the body uses fat to produce testosterone in the first place (and consequently DHT), but many shoot themselves in the foot by severely limiting fats when they try and lose fat.
• Ensure you hit your micronutrient needs, not just your macros.
  • Set up a Cronometer account and monitor your micronutrient intake. Most people get so preoccupied with hitting their macronutrient and calorie targets that they completely fail to take into account that the body needs a sufficient amount of micronutrients to produce optimal amounts of androgens and modulate estrogen.

Supplements

• Creatine Monohydrate [R].
  • This is the only supplement that you definitely will not be able to get enough of via a good diet. Use 5 grams per day, every day, for the rest of your life.
• Boron [R, R].
  • The data on Boron is impressive, but I also view with skepticism. With that being said, Boron seems to be safe to supplement with, and may have a significant effect on reducing SHBG and increasing bioavailable androgens in the body. It is also very cheap, so its worth giving a chance.
• Tribulus, Peruvian Maca, Tongkat Ali, Horny Goat Weed [R, R, R, R].
  • The “sexual health” market is full of junk. Of the products that actually contain efficacious ingredients, the standardization (extract) that is used in most commercial products is generally very low too. I developed the sexual health and libido formula “Horny Hippo” for my friend Chris (owner of Happy Hippo Herbals). It contains ingredients that work, at efficacious dosages and standardizations that will actually make a significant difference in your erection quality and libido. I ensured that it had the strongest possible standardization of every extract, with lab work to confirm.
    • Horny Goat Weed 10% Icariins (Industry standard: 1%)
    • Tribulus Terrestis Extract 62.5% Saponins (Industry standard: 45%)
    • TongKat Ali Extract 200:1 (Industry standard: 100:1)
  • With that being said, this product is ultimately just a bandaid. Frankly, I don't care if you buy it or not. This is something that works very well, but I'm telling you right now, you need to be more concerned with your overall androgen index than what random supplements you are taking to bandaid your issues.
• Vitamin D [R].
  • Due to the predominantly indoor lifestyle humans have adapted to over the years, most people are not getting enough Vitamin D from the sun. And many will still not get adequate Vitamin D production even when they are exposed to the sun due to genetic predispositions. Take me for example, my genetics do not allow me to produce or process Vitamin D very well, so I need to supplement with a fairly high dose of it to reach healthy levels.

• • • You can check if you are predisposed to Vitamin D deficiency with 23andMe Genetic Testing.
    • Check your blood work and add it to your hormone profile as well: Vitamin D, 25-Hydroxy Blood Test
    • Vitamin D is critical not only for optimized androgen production, but also for androgen receptors themselves.
      • The vitamin D receptor is expressed in reproductive tissues including prostate, testis and human sperm, and vitamin D receptor-knockout mice have gonadal insufficiency, suggesting a role for vitamin D in reproductive function [R].
      • A research group from Germany and Austria recruited 2,229 men from the prospective Ludwigshafen risk and cardiovascular health study. Levels of 25-hydroxyvitamin D, testosterone, luteinizing hormone and sex-hormone-binding globulin (SHBG) were measured, and the free androgen index calculated. Almost one-fifth of men assessed had hypogonadism. The mean 25-hydroxyvitamin D concentration of these participants was markedly lower than that of men with sufficient testosterone. Regression analyses showed a significant association between 25-hydroxyvitamin D levels and testosterone, free androgen index and SHBG, even after adjusting for age and body mass index. Variations in testosterone and androgen index followed a seasonal pattern similar to that of Vitamin D levels, with androgen levels peaking in the summer, and significantly decreasing in the winter [R].
• I could have also included supplements like fish oil, Magnesium, Zinc, a B vitamin complex, and much more, but those are all things you should be able to get in and meet your micronutrient demands with a healthy diet. Meeting your micronutrient needs via whole foods is ideal and supplementing with nutrients you can easily get via food should be a last resort.

Unnatural Post Finasteride Syndrome Treatment

Testosterone Restores Sexual Function In Male Pseudohermaphrodites

I've seen evidence enough times now to know that testosterone can support all the same functions in the body as DHT, it's just that it requires a lot more of it to facilitate those functions in androgen dependent tissues with a dense amount of 5-alpha reductase production because it's more tissue-selective.

There's a reason why certain tissues have far more 5-alpha reductase production than others.

Now, testosterone is not very tissue selective in regards to myotrophic to androgenic activity, it's just far more so than DHT.

The only reason males with 5-alpha reductase deficiency are able to go through puberty at all is due to the androgenicity of testosterone.

If testosterone was not androgenic, male pseudohermaphrodites would have never developed any male characteristics and would look like genetic females for the entirety of their lives.

This in itself not only exemplifies how testosterone is inherently androgenic, but it also reinforces the fact that testosterone will transcribe androgenic activity in affected tissues following its activation of androgen receptors (such as exacerbate hair loss in those with a predisposition to aggressive AGA).

If you have a hormone that's mildly androgenic, but incredibly anabolic relative to DHT (what testosterone is), you would need more of it than normal in the absence of DHT to prevent androgen-deficiency symptoms.

This is backed up in the clinical data conducted on male pseudohermaphrodites [R].

“Complete spermatogenesis was present on testicular biopsy in one affected subject, suggesting that Testosterone may be more important in regulating spermatogenesis than DHT. The affected males have erections and ejaculations; these also appear to be Testosterone dependent. Furthermore, in two subjects, the administration of pharmacologic amounts of DHT caused loss of libido and impotence. In the adult castrate male rodent, with the exception of one strain of mice, the administration of Testosterone restores sexual function, but DHT is not effective.“

I've proved this myself with my year long Dutasteride experiment.

I took 1.0 mg of Dutasteride for a year straight with exogenous Testosterone.

I kept my Testosterone levels on the brink of high-normal.

Blood work proved that DHT was almost completely wiped out in my body.

It was so low that DHT was not even detectable in my blood.

All I had to support androgen dependent tissues was testosterone, but because I had more than enough of it, I had 0 negative side effects at all.

I had no libido issues at all.

If anything, my libido was too high, and it was annoying.

As you can see in the reference ranges above, a woman would even be considered DHT deficient with a DHT level lower than 5 ng/dL.

By taking 1.0 mg Dutasteride I not only crushed my DHT far lower than what the average woman produces, but I lowered it all the way down to as low, if not lower, than what male pseudohermaphrodites produce.

This experiment to me proved that the functions of DHT can be replaced simply be replacing the disparity in the body's androgen load from baseline after inhibiting 5-alpha reductase.

The reason is because all those same functions are supported just fine by testosterone, with the caveat being that estrogen is in the sweet spot and is modulated correctly.

As long as the androgen load is satisfactory in the body, your androgen index is sufficient with enough bioavailable free testosterone, and your ratio of androgens to estrogen is optimized, sexual function will be sufficiently supported.

And it's not just testosterone that can accomplish this.

Sexual function can be supported by any androgen at the end of the day.

The whole point is, androgen receptors are literally just receptors located in different tissues that can be activated by androgens to regulate gene expression.

It's not like DHT is special, nor is testosterone special.

It's just the fact that your body endogenously produces them to begin with that makes them seem special.

AR activation is AR activation.

Why Can't You Just Inject DHT To Treat Androgen Deficiency?

Why would administering Testosterone fix androgen deficiency symptoms, but DHT administration further exacerbates it?

The reason is that when DHT is administered, or any exogenous anabolic androgenic steroid, you shut down the HPTA.

So, why does shutting down the HPTA matter when you are trying to rely on exogenous androgens anyways?

Well, when you shut down the HPTA with DHT, you are also consequently eliminating the body's source of Estrogen as a result of Testosterone production being suppressed.

DHT on its own doesn't lower libido, but administering exogenous DHT will cause the body to shut down its natural production of Testosterone, and consequently Estrogen and endogenous DHT too.

Hence why administering DHT without a source of Estrogen will crush libido and cause muscle loss too.

And even if it didn't right away, it would eventually once the endocrine system had been suppressed significantly enough and the body enters a state of Estrogen deficiency.

Testosterone administration restores libido because it not only provides a sufficient amount of Estrogen, but it also 5-alpha reduces into DHT.

However, the 5-alpha reduction of DHT isn't what facilitates the restoration of libido, its the sufficient serum concentrations of bioavailable free testosterone in conjunction with a healthy level of Estradiol.

The 5-alpha reduction of DHT certainly helps, but its not necessary for achieving satisfactory levels of androgens.

The only scenario in which injecting straight DHT could restore sexual function and maintain it long-term is if it was used in conjunction with exogenous Estradiol.

However, that would then make you Testosterone deficient and cause muscle wasting because DHT has such poor anabolic activity.

The only way you ensure that all pathways are fulfilled is by injecting Testosterone and monitoring your Estrogen, SHBG, DHT, total T and free T levels closely.

Then you get into the weeds of optimal injection frequency to minimize aromatization, maximize free T, and optimal testosterone replacement therapy (TRT) practices.

I have outlined these practices in other articles, and will not delve into it in detail here.

Why Do Some People With Post Finasteride Syndrome Get Worse After Using Testosterone/TRT?

One thing I can say with a high level of certainty is that the majority of individuals who don't experience relief of Post Finasteride Syndrome with exogenous Testosterone use are not properly incorporating the natural hormone optimization practices outlined above, aren't implementing optimal TRT practices, or have no idea how to properly interpret their blood work (or aren't getting accurate testing to begin with).

If you think that the doctor who prescribed you Finasteride in the first place without evaluating your hormone profile properly is going to be able to prescribe you an intelligently constructed TRT protocol, you're insane.

Exogenous steroid use is on another level from hormone assessment on Finasteride, and has many more moving parts at play.

How many physicians know how to properly monitor hormone levels?

Standard “TRT” is usually an infrequent mega-dose of Testosterone administered with unnecessary harmful aromatase inhibitors (AI's) and a myriad of other horrible practices.

This is not how TRT should be implemented, and can often lead to deleterious outcomes with further diminished quality of life.

The goal here is restoring an adequate androgen index in the body, with a healthy androgen to estrogen ratio.

If that is accomplished, regardless if its done with Testosterone, or by increasing your androgen load with any other androgen under the sun, the end result in a penis function context will be the same.

Obviously, the most predictable and efficacious of those being Testosterone, as it is the literal bioidentical androgen we naturally secrete, and we already know it acts as a precursor to all of the other hormones we need to modulate sexual health sufficiently, with a reasonably predictable risk profile.

But, for the sake of illustrating my point, let's just say you gave me a guy with Post Finasteride Syndrome and then handed me a vial of Drostanolone (Masteron) and a box of micronized Estradiol pills and told me to figure out how to fix him.

Masteron is a very androgenic hormone, but far more tissue selective than DHT still.

After being injected, Masteron would bind to androgen receptors just like Testosterone and DHT would, and then transcribe its effects in androgen-affected tissues in a dose dependent manner.

The result is the exact same as any other androgen, the degree to which these effects occur simply boils down to the drugs inherent androgenicity, and tissue selectivity.

At some dosage, androgen-affected tissues would be adequately stimulated by Masteron, and then micronized Estradiol could be administered to get E2 levels up to 30 pg/mL manually.

Now, obviously you shouldn't do this, but I'm just giving an extreme example of what this “syndrome” essentially boils down to.

If androgens are low, libido and erectile quality will go down.

If estrogen is too low or too high, libido and erectile quality will also go down.

When enough androgens are present as well as enough estrogen, libido and erectile quality will be supported.

That's it.

So, aside from exogenous Testosterone administration, are there any androgens you can administer that will increase the androgen load in the body to satisfactory levels but won't cause endocrine shutdown?

Yes, Proviron is a viable candidate for this.

Proviron Use For Treating Post Finasteride Syndrome

Mesterolone (Proviron) is one of the best compounds that can be used for treating Post Finasteride Syndrome in my opinion.

The reason being that Proviron is minimally suppressive, whereas exogenous Testosterone use will cause HPTA shutdown.

In a clinical setting, Proviron is used to treat androgen deficiency and to support male fertility.

Teenage boys who experienced delayed puberty are also prescribed Proviron to push the process along.

Proviron is not a substrate for 5-alpha reductase or aromatase; therefore it is not potentiated by 5-alpha reduction and does not convert into estrogen.

It also has no progestogenic activity

Proviron is a very poor anabolic agent due to inactivation by 3α-hydroxysteroid dehydrogenase in skeletal muscle tissue, similarly to DHT.

Proviron is not 17α-alkylated, so it has little or no potential for liver toxicity.

Deleterious effects on cardiovascular health are still possible with Proviron, but the overall risk profile in general is lower with Proviron use than with other comparable androgenic agents.

Testosterone Vs. Proviron For Treating Post Finasteride Syndrome

To clarify my stance on Proviron, I do not believe its the ideal candidate for a male who has low testosterone.

For men with low total testosterone levels and low free testosterone levels, TRT is ideal in my opinion.

However, for those who experience persisting androgen deficiency symptoms after Finasteride use, but otherwise have a healthy total testosterone level, then Proviron would be a better choice to start in my opinion.

A “healthy” total testosterone level is not any number in the reference range.

I would assert that as a rough guideline, a healthy total testosterone level is at least 600 ng/dL, with a free testosterone on the upper end of the reference range.

As an experiment, I lowered my TRT down as far as I could to see how low I could go on a 5-alpha reductase inhibitor while still maintaining adequate sexual function.

I got my total Testosterone all the way down to 465.4 ng/dL at my lowest.

And my free Testosterone (direct) was 19.6 pg/mL.

I would prefer to see my total testosterone above 600 ng/dL and closer to 700 ng/dL, but my free testosterone level being high-normal is far more important.

Despite being DHT deficient via 5-alpha reductase inhibitor use, I was still able to maintain a good libido and erection quality with a free testosterone level on the high end of normal and a hardly satisfactory total testosterone level.

Let's just say hypothetically you have a total testosterone level of 350 ng/dL, a free testosterone level on the low end of the reference range and have Post Finasteride Syndrome.

This is a scenario in which I believe an intelligently designed TRT protocol would be worth exploring and would be the best course of action.

I emphasize “intelligently designed TRT protocol” as most physicians will not be knowledgeable enough to provide this, and goes back to my explanation earlier about why TRT can make things worse if it isn't implemented properly.

With that being said, if you have checked off all the boxes in the “natural Post Finasteride Syndrome treatment” subsection I outlined earlier in the article (most important being lifestyle and diet) and you still have low total and low free testosterone, it will likely not resolve itself without exogenous hormones, and would then make you a prime candidate for TRT.

Now, let's just say hypothetically you have a total testosterone level of 750 ng/dL and a free testosterone level on the low end of the reference range and have Post Finasteride Syndrome.

This is a scenario in which I believe Proviron would be worth exploring and would be the best course of action.

The reason being that you clearly have adequate testosterone production if you have a 750 ng/dL total testosterone level.

The issue is not your testosterone production in this scenario, rather, the issue is that you do not have enough bioavailable free testosterone available to actually use.

Even if you have a total testosterone level on the high end of the reference range, if SHBG has too much of it bound up, you won't have enough free testosterone available to support androgen-affected tissues (like your penis).

Most circulating testosterone is bound to SHBG, and a lesser fraction is bound to albumin.

Only a small fraction of your total testosterone is actually available to tissues as free testosterone.

Testosterone weakly bound to albumin can dissociate freely in the capillary bed and become bioavailable for tissue uptake; however, SHBG still binds the majority of your testosterone and renders it inactive.

Proviron not only directly supports tissues via its inherent androgenicity, but it has a very high affinity for SHBG.

Because of this, Proviron is very effective at displacing endogenous testosterone from SHBG, which then significantly improves the ratio of bioavailable androgens relative to estrogen and SHBG in the body [R].

For someone who is on TRT and is encountering issues modulating their hormones, Proviron is extremely effective at facilitating a balancing act in the body and increasing the amount of available free testosterone to tissues.

For someone using Proviron by itself, while Proviron doesn't directly increase free testosterone, it still modulates the androgen index in the body and can correct a hormonal imbalance without causing complete HPTA shutdown.

Proviron is the least suppressive androgen and can be used at high doses without inducing HPTA shutdown.

It is still an anabolic androgenic steroid at the end of the day, but it has some unique characteristics that make it ideal in this context.

As Proviron is still suppressive, its use suppresses total testosterone levels, which consequently reduces estrogen levels in the body.

In addition, via the suppression of testosterone production, Proviron significantly reduces of SHBG [R, R].

Because Proviron has such a high affinity for SHBG, it also displaces a significant amount of bound testosterone that otherwise wouldn't have been available to tissues in the body.

Despite total testosterone production decreasing as a result of endocrine suppression, Proviron effectively frees up so much SHBG bound testosterone that it can maintain free testosterone levels in the body at the exact same serum concentrations as would have been found in baseline blood work.

However, because estrogen and SHBG levels are now significantly lower in the body, via Proviron's inherent androgenicity and the optimization of the body's androgen index, sexual function should significantly improve in individuals who have optimal total testosterone levels on paper and still experience Post Finasteride Syndrome.

Testoserone And Proviron Used At The Same Time For Treating Post Finasteride Syndrome

If someone who had low total testosterone and low free testosterone implemented all of the necessary lifestyle and diet changes, as well as implemented a properly designed TRT protocol and still did not experience relief of Post Finasteride Syndrome, this is where Testosterone and Proviron may be worth exploring.

As mentioned, Proviron is an effective agent for regulating the androgen index in the body in a dose dependent manner.

If you started TRT, and your total testosterone levels are now on the high end of normal, or even above that, and you still can't achieve high free testosterone levels, or you cannot achieve high free testosterone levels without using such a high dose of testosterone that you induce estrogenic side effects from excessive amounts of aromatization, this is where Proviron alongside TRT will become an excellent option.

Proviron more or less helps you maximize the amount of free testosterone in your body.

Meaning, the higher the dose of Proviron, the more you can displace bound testosterone from SHBG and increase your free testosterone.

Therefore, if you can't achieve an adequate free testosterone level because your SHBG is too high, or your Estrogen levels get too high at the TRT dose you need to achieve high free testosterone levels, then Proviron can be implemented to balance everything.

How To Use Proviron With TRT If Your SHBG Is Too High

If your issue is that your SHBG is too high and your total testosterone is at the top of the reference range, or even higher than the reference range, and you still can't achieve high free testosterone levels, then add in 25 mg of Proviron per day and reassess in a couple weeks.

If that doesn't suffice, try 50 mg of Proviron per day and reassess in a couple weeks.

And so on until you have displaced enough bound testosterone from SHBG with the Proviron to achieve high free testosterone levels and have restored sexual function.

There is some dose of Proviron that will displace enough bound testosterone from SHBG that will allow you to reach high free testosterone levels without having to use so much testosterone that your total testosterone is outside the therapeutic reference range.

How To Use Proviron With TRT If Your Estrogen Is Too High

If your issue is that you can only achieve optimal free testosterone levels by using a dose of testosterone that elevates your estrogen too much and causes estrogenic side effects, then lower your testosterone dose to whatever dose you can handle without any estrogenic side effects, and then add in 25 mg of Proviron per day and reassess in a couple weeks.

If that doesn't suffice, try 50 mg of Proviron per day and reassess in a couple weeks.

And so on until your free testosterone levels are high enough that your ratio of bioavailable androgens relative to estrogen does not cause any estrogenic side effects and you have simultaneously restored sexual function.

If you somehow are still having problems even after all that, then you can try to titrate your testosterone dose up a bit more until sexual function is restored, as the increased amount of bioavailable androgens will allow you to get away with a slightly higher estrogen level without any estrogenic side effects than you would have otherwise.

This is why some bodybuilders can use a high dose of testosterone without any estrogenic side effects (not all, but some can), because estrogenic side effects aren't a direct result of the Estradiol blood test result on paper, rather, they're a result of a suboptimal androgen to estrogen ratio.

The higher the bioavailable androgen load in the body is, the more estrogen can be present in the body without inducing estrogenic side effects.

This is also why men can experience gyno with testosterone and estrogen levels in the reference range.

If you are androgen deficient, you can still experience estrogenic effects even with a 35 pg/mL Estradiol level.

Finasteride Is An Anti-Androgen

While it will be difficult, try and find a doctor who knows what they're talking about who will help you work through this and get accurate blood work to monitor your progress.

Doctors shouldn't haphazardly give you something that depletes your DHT levels by as much as 70% without getting your baseline blood work.

While responsibility lies on the doctor, you also need to do you own research.

It’s baffling to me how many people do not understand that Finasteride is an anti-androgen.

While it doesn't fall into the traditional medical definition of an anti-androgen, the fact remains that 5-alpha reductase inhibitors are designed to severely deplete the body's androgen levels.

If you intentionally take a drug that is designed to deplete your androgen levels, you should expect that androgen deficiency symptoms could be a possible outcome.

The main problem lies in the lack of education.

Most doctors have no idea how this drug works, and they also don't know how to educate their patients about how it works, nor do they try.

Harm reduction is also rarely implemented, when it is more than warranted.

Get some f*cking baseline blood work for the guy, you're about to prescribe him a f*cking drug that lowers his DHT levels by 70%!

This isn't a pill that just prevents hair loss and gets rid of an otherwise unnecessary hormone.

DHT supports androgen-affected tissues in the body for a reason.

It's not something that cannot be supported by other androgens, like I've mentioned.

But the fact remains that certain individuals only have so many endogenous androgens to begin with.

Some men are pretty DHT-dependent because they aren't super high T individuals who can support those functions otherwise.

Or they have a poor balance of androgens to estrogen.

Or they have a poor balance of androgens to SHBG.

Inhibiting 5-alpha reductase in these individuals could very likely result in a dysfunctional ratio of hormones in the body.

This is something you need to understand for yourself before you start popping pills, because the likelihood that your doctor will teach you about it is extremely low.

When you walk into a doctor's office and say “I have hair loss,” they're going to say “okay, take Minoxidil or Finasteride.”

They'll gladly prescribe you Finasteride, perhaps briefly outline the potential side effects of it, and then send you on your way without explaining why the side effects occur, or how you could predict if they will occur in the first place.

What they don't communicate to you is that Finasteride is deigned to deplete your androgen levels.

Expecting an outcome where there's zero chance of having androgen deficiency related symptoms is ridiculous.

However, if you fully understand this before going into it, you can assess your baseline hormone profile, and gauge your risk profile with a far greater level of accuracy.

You would also be able to reverse any negative outcomes you may have because you would understand why it occurred and how to fix it.

Summarizing Post Finasteride Syndrome

At the end of the day, what this comes down to is getting accurate blood work, being able to make an educated conclusion based on your blood work if using Finasteride is a viable risk for you to take.

And if you do have Post Finasteride Syndrome, it comes down to getting accurate blood work, knowing how to interpret it, and then implementing an appropriate lifestyle and/or hormonal protocol to address the issue you're having.

There is a ratio of bioavailable androgens relative to estrogen that will restore sexual function in any individual who is an otherwise healthy individual and does not have a mental disorder, or some other outlier medical condition irrelevant to Post Finasteride Syndrome that is causing sexual dysfunction.

If your penis worked fine before using Finasteride, and you are still an otherwise healthy person, there is some optimal ratio that can be manually achieved that will restore satisfactory function.

If somebody has “Post Finasteride Syndrome,” it can easily be resolved by manually increasing your androgen index while modulating your estrogen levels.

In my opinion, anybody who has it is not interpreting their blood work correctly and/or isn't implementing pharmacological intervention to attenuate whatever potential imbalances they have in their hormone profile as a result of inhibiting 5-alpha reductase.

Disclaimer: The information included in this article is intended for entertainment and informational purposes only. It is not intended nor implied to be a substitute for professional medical advice.