How Relevant Is DHT To Hair Loss?
The first thing I want to make clear in regards to my Dutasteride and Testosterone experiment is that DHT is the worst hormone in your body for your hair.
I don’t want anyone to misinterpret my videos and articles exhibiting the androgenicity of Testosterone as disregarding how bad DHT is.
DHT is terrible for hair loss.
It is several-fold more androgenic than Testosterone.
I think I made that pretty clear in my content, but just to clarify before we delve into this.
DHT still needs to be addressed.
The whole point of my article and video addressing Testosterone’s androgenicity was to state that endogenous androgens as a whole need to be addressed, NOT just the DHT.
Using Dutasteride With TRT To Prevent Hair Loss
It came to my attention that there was a thread made referring to my first video addressing Testosterone’s inherent ability to cause hair loss, and how they believe that Dutasteride in conjunction with TRT is the way to maintain “DHT fulfilled” physiological functions, as well as completely prevent hair loss.
I had the same theory a couple years ago.
The person who started that thread was essentially proposing what I believed in 2017.
Back in 2017 I thought to myself okay; if you use Dutasteride you're guaranteed to be protected from hair loss from Testosterone because the 5-alpha reduction to DHT is taken care of.
I realized some very crucial things shortly thereafter.
Finasteride Is A Band-Aid
While using Finasteride, you can reduce systemic DHT by roughly 70%, but you will still have 30% of your systemic DHT left in tact, which is still going to wreak havoc on your hair (common knowledge).
This also is irrelevant to Finasteride’s 41% reduction of scalp DHT in particular, but that’s an entire topic in itself [R].
Finasteride is a bandaid at most, but most guys know that.
All you’re doing with Finasteride is putting your ticking time bomb of hair loss in slow motion.
For many guys this is more than sufficient to stave off horrible hair loss for another several decades, but the fact remains that androgenic alopecia still occurs, albeit much slower while on Finasteride.
The Reason Why Dutasteride Is Also A Band-Aid
My blood work indicated near 100% suppression of my systemic DHT while on 1 mg of Dutasteride per day.
The blood work couldn't even read my DHT because it was below the detection limit.
Even with a supraphysiological amount of Testosterone in my system from administering an exogenous a source of it and pushing my Testosterone up to 2,000 ng/dL (on purpose) I still had nearly zero DHT in my system because Dutasteride is just that effective at inhibiting 5-alpha reductase.
After determining that 5-alpha reductase inhibition is the same regardless of how much Testosterone is present, I hypothesized that if I just crushed my DHT to zero it would be the equivalent of castration, and then I could just fulfill the physiological anabolic properties that I would normally get from androgens via Testosterone administration.
This opened up the possibility to simply increasing exogenous Testosterone usage to whatever dosage would be necessary to fulfill whatever potential androgenic disparity there would be in the body with a complete lack of DHT.
Based on my blood work, Dutasteride still inhibited Testosterone conversion enough to the point where I could hypothetically use unlimited amounts of Testosterone and still inhibit 5-alpha reduction into DHT completely.
I thought okay great, so I can just use more Testosterone and keep all of my hair because DHT is still absent regardless of how much my Testosterone goes up.
But that just wasn't the case.
Even once I accomplished DHT inhibition, I had continuous androgenic side effects just from testosterone.
The entirety of the experiment I had zero DHT, but I still experienced facial hair growth and had to shave my face just as often.
I still experienced body hair growth, and despite it somewhat notably being reduced on my lower back area, I still had to manscape once a week to keep my body hair growth under control in general.
These are things I had to do anyways just as frequently before when I had normal amounts of DHT in my body.
I still had significant androgenic activity in my body, even with 0 DHT present, because Dutasteride does absolutely nothing to protect hair follicles from Testosterone, and actually increases scalp concentrations of Testosterone, which is why a minority of men who are especially sensitive to Testosterone actually experience exacerbated hair loss and what is often perceived to be chronic telogen effluvium while on Dutasteride.
With this being said, Dutasteride will massively slow down hair loss in the majority of individuals, but it still doesn’t address the true root of the issue, and is not a solution for many.
How Prostate Size Correlates With Hair Loss
The first thing that I think needs to be taken into consideration that's largely overlooked is the fact that Finasteride and Dutasteride were created to address prostate size.
The intention of the drug was not to address hair loss, the creators simply realized that a fringe benefit of inhibiting prostate growth by systemically inhibiting DHT conversion is that your hair can grow back because there's less androgen induced miniaturization occurring.
If you reference the clinical data on Testosterone itself, you can clearly see that it stimulates prostate growth itself inherently, just to a lesser extent than DHT [R].
Not relating to DHT conversion whatsoever, but on its own entirely.
Ideally, for hair loss prevention you would want to have an anabolic in your body that fulfills all of the anabolic properties of Testosterone and simultaneously has as minimal of an androgenic effect as possible.
This is typically assessed in preclinical animal models when analyzing the efficacy of possible hormone replacement therapy alternatives by comparing a drugs stimulation of muscle growth relative to the stimulation of prostate and seminal vesicles growth.
The less favorable the myotrophic-to-androgenic ratio is of a drug, the less ideal of a hormone replacement therapy option it is for men seeking to minimize androgenic alopecia.
In general, the more androgenic a hormone is, the more it will increase prostate size and cause hair loss.
On the opposite side of the spectrum, the less androgenic a hormone is, the less it will stimulate prostate growth, and the less it will expedite androgenic alopecia.
The Paradox Of Being A Male When It Comes To Hair Loss Prevention
Lowering androgenic activity in the body is totally counterproductive to being a male, and presents the paradox men face with their endocrine system.
If you're a male, just the fact that you're a male puts you in a position where your hormone profile is counterproductive to keeping hair on your head, and the hormone profile necessary for complete hair loss prevention is counterproductive to being a male.
What I mean by that is you rely on endogenous anabolic androgenic steroids for libido, penile sensitivity, muscle growth, recovery, neuroprotective effects on the brain, maintenance of masculine traits, and many more functions or traits that are fulfilled directly by androgens or androgen receptor activation.
What most guys don’t realize is that Testosterone itself is the sole reason you can even operate and function without any DHT in your system.
The reason is literally because Testosterone is androgenic itself.
At best, it has that two-to-one selectivity for muscle tissue to prostate, and many other studies indicate that a two-to-one ratio is extremely generous.
That's great because it fulfills the androgenic properties that would otherwise be fulfilled by DHT.
Hence why most guys can use Dutasteride with no side effects, and those that experience androgen deficient side effects simply have free-testosterone levels that are too low to fulfill that androgen deficit, or do not understand effective Estrogen/general hormone management.
The side effects would predictably be mitigated with exogenous androgen administration, or Estrogen management in almost all cases, dependent on what the root of the issue was specifically.
But, the problem with that is that by fulfilling those very androgen dependent physiological functions; you will also miniaturize hair follicles.
This is the paradox of being a male.
Maximizing libido, maximizing the sensitivity of the penis and maintaining masculine characteristics all must be achieved via sufficient androgen levels, which will also cause the miniaturization of hair follicles, and is exactly why Finasteride works so well.
Finasteride directly reduces prostate size by inhibiting DHT, which the majority of the population has acknowledged is also what prevents progression of hair loss.
If you look at androgen activity from the opposite side of the spectrum you will note that increased androgen levels in the body result in increased libido, increased penile sensitivity, increased facial hair growth, increased prostate size, and predictably, increased hair loss miniaturization.
It doesn’t matter what androgenic hormone is in the body, whether its pure DHT, Drostanolone, Trenbolone, Anadrol, Dianabol, etc. they all have their own inherent androgenicity and impact on stimulating the prostate and seminal vesicles, as well as all other androgen affected tissues, including hair follicles.
It's all directly correlated to one another.
Transgender Male To Female Transition Hair Loss Reversal
One study I was looking at recently was a study following the progress of a man who had a serum Testosterone level of 455 ng/dL and had already experienced significant male pattern baldness throughout his lifetime [R].
Men who decide to transition from male to female will often be prescribed an oral anti-androgen and oral estrogen.
When he transitioned from male to female, he used oral estradiol and spironolactone.
What did he accomplish with this?
It dropped his serum Testosterone down to 11 ng/dL.
The result of that was significant inhibition of facial hair and body hair growth.
And, he also started re-growing scalp hair and reversing his male pattern baldness.
This is not a coincidence, and is related entirely to their androgen index, and maintaining healthy levels of Estrogen in the absence of Testosterone that would normally aromatize into Estrogen.
This is why some very hair loss prone individuals who truly value their hair more than their masculinity are using oral anti-androgens now in the hair loss community.
This was actually one of the least impressive reversals I could reference, and the only reason I chose this one was because it is in PubMed and clearly states exactly what their hormone levels were before and after.
There are a number of ways to tackle hair loss, with some targeting mechanisms downstream in the cascade of events that eventually lead to the miniaturization of the hair follicle (e.g. Prostaglandin Theory).
While some are effective and are worth exploring for certain individuals (more on that in future articles), the root of the issue still derives from androgens.
My Dutasteride Experiment And Why I Lost Hair On It
Even with DHT crushed to zero, I experienced androgenic alopecia during the entirety of 2018.
I used Dutasteride with Testosterone concurrently with nothing else for a full year.
In my videos filmed in the middle of 2018 you can see that I had fairly substantial thinning in the middle of my Dutasteride experiment compared to my hair pre-Dutasteride usage.
(2018 – Dutasteride Only)
(2017 – No Dutasteride)
I ran it for a year straight on just TRT.
My libido was perfect. I had no erectile dysfunction whatsoever.
Finasteride And Dutasteride Effect On Muscle Growth
I didn't lose any muscle at all while using Dutasteride.
Minimal conversion of Testosterone to DHT occurs in muscle tissue, and the entirety of the human body’s anabolic effects in muscle tissue are mediated by endogenous Testosterone, not DHT.
My priorities have changed over the years as I stopped caring about bodybuilding as much and started caring more about my hair.
I started to give 5-alpha reductase inhibitors more of a chance in my research and experiments.
I used to think they were the devil but I started to research more and realize what the androgenic component of certain anabolics really accomplishes in the body and how it really plays out in the whole cascade of events leading to eventual hair loss progression.
Dutasteride Does Not Protect Hair From Testosterone
I would have kept using Dutasteride if it worked the way I predicted it was going to work in 2017 before the experiment, but it didn't inhibit my systemic Testosterone at all from inducing androgenic activity at the hair follicle.
I self-administered a dosage that pushed my Testosterone levels up to about 2000 ng/dL on purpose.
I already know I’m severely prone to hair loss at that dosage with no protection, and I had to test the true extent of Testosterone’s own androgenic activity with DHT totally taken care of to know for sure what was going on in the body and to confirm my suspicions.
I didn't use a topical anti-androgen for the entire year because I didn't want to skew my experiment results and because I still thought that perhaps I was just experiencing a prolonged shedding phase, and once it concluded then massive regrowth would occur.
It never did, and Testosterone’s lack of anabolic selectivity in the body was revealed and quite obvious once you take into account that my facial hair, body hair and hair loss was nearly unaltered in contrast to what a slightly lower level of Testosterone in my body with DHT present would induce.
While Dutasteride and exogenous Testosterone therapy may be sufficient for many men in the short-term, ultimately hair loss will still be occurring, just at a less expedited rate than if DHT was present, and for those who are very sensitive to Testosterone, it may make things worse (e.g. what happened in my experiment).
Now you might be asking yourself, what if you kept a normal Testosterone level and used Dutasteride, what would happen then?
Well, there would be no point of using exogenous Testosterone in that situation, and the only purpose it truly serves is to offset androgen deficiency side effects that may occur in a minority of individuals who use Dutasteride.
Dutasteride on its own will increase endogenous Testosterone levels by up to 26% [R].
For most men, this is sufficient enough to fulfill all of the androgenic functions typically facilitated by endogenous DHT, but for some, it is not, and that’s where exogenous Testosterone administration would come into play to push systemic Testosterone high enough to fill that void of androgenic activity, with a higher selectivity of anabolic activity relative to androgenic activity than DHT.
Would the dosage needed for that minority of individuals be high enough to cause hair loss like it did in me?
Depends on their sensitivity, as some men can’t even prevent hair loss with 0 DHT and their regular endogenous Testosterone levels.
The reason is because they have no protection from Testosterone.
One thing to note, if it wasn’t obvious, there is no scenario in which someone would need to take enough Testosterone to push their levels up to 2000 ng/dL on Dutasteride (well, at least 99% of the time, the caveat being Free Testosterone and SHBG issues that may occur).
The only reason I did it was to truly establish Testosterone’s myotrophic-to-androgenic selectivity without DHT present for my future reference.
Androgen deficient side effects on Dutasteride like erectile dysfunction should be alleviated in the vast majority of individuals with very basic Estrogen management, and Testosterone optimization still within the therapeutic reference range.
Different Methods Of Preventing Hair Loss
The insight I got out of my Dutasteride and Testosterone experiment was invaluable as I’ve heard far too many self-proclaimed experts for years during my initial research confidently propose misinformation stating that DHT is the only hormone in the body that matters when it comes to hair loss.
It can be difficult to snap your brain out of thinking something that 99% of people believe is true.
The most effective ways to truly prevent hair loss via the androgen pathway in general will involve at least one of the following mediums:
- Topical inhibition of all androgens
- A combination of systemic inhibition of androgens as well as topical
- Complete systemic inhibition of androgens
- Male > Female Transitioning Via Hormone Replacement Therapy
- Hormone replacement therapy with suppressive anabolic agents that exhibit an extremely favorable level of selectivity for myotrophic-to-androgenic activity in conjunction with estrogen administration to make up for the lack of Testosterone aromatization no longer occurring
I don't have a recommendation for which way to go about it, or if you should go about it at all.
However, I can definitively tell you that while it's not as androgenic as DHT, Testosterone still needs to be accounted for if you don’t want a Band-Aid solution and you have very aggressive hair loss.
Genetic Anomalies And Outlier Theories
There are some people that are not sensitive to Testosterone or DHT.
There are some people with 5-alpha reductase defects that are also not sensitive to Testosterone.
There are a variety of genetic anomalies that are extremely rare, but exist nonetheless and can provide near immunity to hair loss progression.
I suspect this is a genetic variant, and while we can get hung up on what this variant is in their DNA, at the end of the day, for 90-99% of us, androgens are what matter and what we should concern ourselves with understanding inside out, because you will very likely not be changing your genetic code in this lifetime.
There are a variety of interesting theories that have branched out attempting to make sense of hair loss in a context that explains why DHT isn’t the only factor at play here.
While some of these hold weight in certain regards, they are totally irrelevant to androgenic alopecia most of the time, and focus entirely on temporary shedding misinterpreted as androgenic alopecia.
This typically applies to alternative theories like chronically elevated estrogen, elevated prolactin, thyroid deficiencies, liver damage, etc.
I have yet to see any of these guys who make these bold claims even get blood work to establish their own theories in practical application.
Instead of actually assessing these theories themselves, they will typically extrapolate data out of a study and then try and design an entire theory around it, and then make a blanket statement stating that the cause of hair loss is definitively (insert random hormone/nutrient/mineral/wild guess here).
If you've seen my other content, you already know that I get my blood work checked a lot.
I get everything checked extensively several times per year because if something is causing my hair loss (or results in a real health concern), I want to know what it is.
Fortunately, my bodybuilding pharmacology background has enabled me to know how to manually address those things prior to even experiencing hair loss.
I already had my blood work checked consistently and I've been monitoring it for years.
Throughout my bodybuilding endeavours in the past I’ve at one time or another experienced severe Prolactin elevation as well as severe Estrogen elevation because I used to use stupid amounts of AAS when I competed in competitions.
I've literally manually adjusted all of these random values so many times and I can definitively tell you that none of them are the root of male pattern baldness.
I've used Caber to drop my Prolactin.
I've had my Prolactin artificially raised from androgens that caused it.
I've kept in the middle just by not using those androgens, and manually managed it at other times when I was using those drugs.
My Estrogen, same thing.
I've been on 500 milligrams of Test with Dianabol in the past (among other heavily aromatizing compounds) and had absurdly out of range Estrogen levels because I was young, stupid and wasn't using an aromatase inhibitor (AI) to manage my hormones correctly.
I had severely elevated estrogen yet still experienced male pattern baldness.
I've crashed my estrogen to zero intentionally to dry out for competitions – still had a hair loss.
Low estrogen can cause telogen effluvium (shedding, not androgenic alopecia) as well, which should be noted.
If you crush your estrogen into the ground with Letrozole or another AI, you're inhibiting a critical hormone that facilitates healthy hair growth, but not causing androgenic alopecia itself.
Shedding is not the same as androgenic alopecia.
I had perfect Estrogen levels throughout the entirety of my Dutasteride experiment (and still do) – still experienced androgenic alopecia.
My liver is perfect.
I don't drink and I don't use methylated oral steroids anymore.
Even when my liver enzymes weren’t in range when I cycled methylated orals like Dianabol and Superdrol several times years ago there was no difference in my androgenic alopecia progression.
Chronic inflammation is another common health marker that's commonly brought up.
I've had a high sensitivity C-reactive protein test many times now to assess my levels of systemic inflammation, and the tests can't even detect inflammation in my body.
Even with undetectable levels of inflammation in my body I still experience male pattern baldness with a high androgen index present.
At one time I abused the hell out of T3 because I wanted to stay leaner with less effort and thought I could just artificially enhance my metabolism (doesn’t work that way by the way, do not try this), so I intentionally kept myself in a state of hyperthyroidism.
I've also been hypothyroid many times as a result of that after coming off of T3.
Both caused shedding, but didn’t progress my androgenic alopecia.
I've been in the sweet spot (where I am in right now) and I've been in that same sweet spot several times in the past.
I get a comprehensive panel done several times per year including my free T3, T4, TSH, reverse T3, Thyroglobulin, Thyroglobulin antibodies and Thyroid peroxidase antibodies.
Androgenic alopecia never let up until I addressed androgens, and to be clear, for 90-99% of men, the same will apply.
The only time it wouldn’t apply is if someone was experiencing temporary shedding from a deficiency, hormone imbalance, autoimmune condition, disease, or an array of other possibilities that cause shedding, which should not to be confused with androgenic alopecia.
From what I’ve seen, every random value that is hypothesized as a potential root of the issue I've at one time or another had it severely elevated, severely crashed, or in the perfect sweet spot like it is right now.
Estrogen elevation is definitely not the cause of androgenic alopecia, and neither are any of the other random values I mentioned.
Estrogen facilitates hair growth and has a protective effect on scalp hair follicles.
This is evidenced time and again in women who have high Estrogen levels, Progesterone levels equivalent to men the majority of the year (1 ng/mL or under), and low androgen levels.
If chronically high Estrogen was the cause of androgenic alopecia, then we’d all have full heads of hair and women would be bald.
I can confidently say you need to address DHT and Testosterone.
I encourage you to get your blood work checked so you can see what's going on at systemic level.
SARMs Potential Role In Hair Loss Prevention
One promising thing I see in the future are selective androgen receptor modulators (SARMs), which for some reason I don't see talked about in the community at all.
If an individual gets to the point where their endogenous androgens are severely expediting their hair loss to the extent where it can’t be managed with topical anti-androgens, growth agonists, 5-alpha reductase inhibitors, and other classic management strategies, the next step above and beyond that would typically either be using stronger topical anti-androgens, or systemically inhibiting the endogenous androgens causing their hair loss.
While this can be accomplished via a variety of mechanisms involving the androgen receptor, one of the most promising ways to potentially facilitate this in my opinion would be by incorporating a less androgenic hormone (like a SARM) in conjunction with Estrogen for hormone replacement therapy.
In theory (and in practical application for many researchers), this would fulfill the anabolic properties that their endogenous production of Testosterone would normally fulfill, with less of an androgenic hit to the body, and simultaneously suppress the androgenic hormones in the body responsible for hair loss.
The Estrogen would be used to bring systemic Estrogen levels up to where they should be in the absence of adequate Testosterone to Estrogen aromatization.
While SARMs have been examined in preclinical rodent models in the context of their efficacy profiles for managing benign prostate hyperplasia, the effect they have on endogenous anabolic and androgenic activity can be reverse engineered to see its blatant potential in hair loss prevention [R].
In preclinical models, even one of the earliest and least effective SARMs showed a greater efficacy profile than Finasteride [R].
LGD-4033, BMS-564,929 and Ostarine are all in human clinical trials right now with impressive efficacy profiles, and I believe it is just a matter of time before SARMs, and other more selective anabolic agents in general start to be looked at very seriously.
When it comes to hair loss prevention, the ratio of selectivity of the anabolic agents in the body is critical.
The tradeoff there is that the lower the androgenic stimulation is in the body, the less sexual sensitivity there will be too, but that's just the paradox of being a male.
The more of an androgen load you have, the more hair follicle miniaturization you have.
Drugs like Proviron and Masteron are androgenic steroids men commonly use for muscle hardening during bodybuilding competitions, but less commonly known is that they are also drugs men use to increase their sex drive and increase their penile sensitivity.
These drugs are extremely androgenic and do an amazing job at boosting libido.
But, predictably, they are two of the absolute worst drugs for prostate growth and hair loss potential.