Boldenone (Equipoise) is believed by many to aromatize into Estradiol at 50% the rate of Testosterone based on a snippet from the book “Anabolics” written by William Llewellyn.
The viability of Boldenone as a useful anabolic is something that has been heavily debated for years in the bodybuilding industry.
How potent is Boldenone at building muscle?
If you are prone to estrogenic side-effects from Testosterone, can it be swapped in as a Testosterone base?
Over the past year I have been compiling more and more evidence that leads me to believe that Boldenone cannot replace Testosterone as a base, and I've seen several blood test results come back showing that it actually crushes Estradiol levels.
For example, if someone wanted to use 500 mg of Testosterone, but they couldn't use that high of a dose and avoid estrogenic side effects without concurrent use of Aromasin or Arimidex, a conclusion many have come to is that you could then just use EQ instead at the same dose to cut the estrogenic activity in half, but still support adequate Estradiol production.
But when you dig into it, is that actually the case?
“Nandrolone aromatizes at 20% the rate of Testosterone” is another assumption similar to this that was passed down the grapevine in our community for years, which we now know is not true.
So, why would the same not apply to Boldenone?
Table of Contents
What Is Boldenone
Boldenone is often lumped together in the narrow category of Testosterone derivatives that can also serve as a Testosterone base because of their interaction with aromatase.
Testosterone bases are anabolic androgenic steroids that are substrates for aromatase and convert to enough Estrogen to support adequate Estrogen receptor activation.
Mistakenly, Boldenone has been placed in this category, even by me.
Adequate Estrogen production facilitates neuroprotection, cardioprotection, the GH/IGF-1 axis, downstream growth factor production, and a myriad of other important functions for both health and performance.
It is commonly stated that Boldenone aromatizes half as much as Testosterone, and William Llewellyn’s book “Anabolics” is commonly referenced to support this claim.
It is assumed by many that Boldenone can be used as a makeshift Testosterone base for those prone to estrogenic side-effects.
In theory, by using Boldenone, one could reduce the risk of encountering Estrogen related side-effects as it should aromatize about half that of Testosterone.
Over the years other theories have developed around Boldenone's mechanism of action.
One of the most recent being that one (or several) of its metabolites act as an aromatase inhibitor (AI).
I have a different theory entirely, which I will delve into after elaborating on the AI hypothesis.
There was an excellent post made on reddit by SwoleTide discussing the metabolites of Boldenone.
I have also compiled my own research, both of which I will discuss further here.
SwoleTide's Reddit Post Compiling The Boldenone Metabolite Research
There’s a theory going around that metabolites of Boldenone are actually what inhibit the enzyme aromatase, consequently preventing Testosterone from aromatizing to Estradiol.
SwoleTide compiled the available research on Boldenone metabolites [R].
SwoleTide starts by going over anecdotes claiming both a need for increased, decreased, or no need at all of an AI.
Logically, one should require more AI on high dose Boldenone if Boldenone aromatizes as much as it is supposed to into Estradiol.
However, a lot of people claim a decreased need of AI when using it, or no need at all.
Boldenone's Aromatization Rate According To Llewellyn’s Book “Anabolics”
William Llewellyn’s book “Anabolics” claims that “aromatization studies suggest that [boldenone's] rate of conversion to estradiol is roughly half that of testosterone”.
Llewellyn references an in vitro study to support this claim, which does not refer to Boldenone anywhere [R].
In a revised edition of “Anabolics” the reference is changed to an obscure study evaluating the role of androgens in growth and development of the fetus, child and adolescent [R].
This study does not refer to Boldenone either.
It could however be a mistake by Llewellyn as a compound with a similar name, Boldione, is mentioned in the first study (the in vitro study) and apparently does interact with aromatase, however, he updated the source in a more recent copy of his book, presumably based on the fact that the new study represented correct information, but there is no mention in the updated study at all.
Other Studies Suggesting Boldenone Aromatizes
One study on rabbits and the effect of Boldenone had on reproductive hormones was investigated [R].
The study had two experimental groups and one control.
The two experimental groups were injected with Boldenone.
The control group did not get any Boldenone.
Both experimental groups had a significant decrease in circulating Testosterone with a simultaneous increase in Estradiol.
In the discussion the researchers speculate that this may be due to Boldenone aromatizing into Estradiol.
Boldenone Metabolite: 1,4 Dienedione or 1,4 Dienedone
SwoleTide goes on to dig into the metabolite that many claim is responsible for the AI-like effects of Boldenone.
Using google also shows no relevant research for 1,4 Dienedione without quotation marks around it in the context of Boldenone.
When searching using quotation marks around it, one compound, Androsta-1,4-didenedione, came up.
When searching for Androsta-1,4-didendione a few studies came up, with one showing that it could cause birth defects, another on “steroids on microplates with fixed silica gel”, and the last being on a ketosteroids.
No results come up when searching for 1,4 Dienedone in quotation marks, it is considered a typo.
One study investigated the metabolites excreted after Boldenone administration in man [R].
5α‐androst‐1‐ene‐3,17‐dione (aka 1-AD)
androsta‐1,4‐diene‐3,17‐dione (aka ADD)
Nine metabolites are produced, with two metabolites (1-AD and ADD) being similar to the ones previously mentioned.
The study does not mention any AI effects.
5α-androst-1-ene-3,17,dione (aka 1-AD)
1-AD is a synthetic androgen and anabolic steroid.
It also acts as a prohormone to 1-Testosterone [R].
In an in vitro study it was shown that 1-AD is a potent inhibitor of aromatase activity and CYP19 mRNA expression [R].
Androsta-1,4-diene-3,17-dione (aka ADD)
ADD is an anabolic androgenic steroid related to Boldenone and Testosterone.
In an in vitro study ADD was shown to inhibit aromatase [R].
WADA Study on Boldenone Metabolizing To ATD
ATD was not listed in the human metabolite study conducted on Boldenone [R].
In an in vitro study ATD was shown to significantly lower Estrogen biosynthesis [R].
1,4 Dienedione: Mistake or Just Plain Wrong?
When comparing the structures of 1-AD, ADD, ATD and the data available behind them, it seems that 1,4 Dienedione is just an incorrect attempt to shorten ADD after all.
PubChem did not show it as a synonym as it was not indexed on PubMed.
SwoleTide speculates why this mistake occurred and explains why it is incorrect.
It is also misleading to call it an AI because it is an AAS as well that just so happens to have AI like effects, but also aromatizes itself.
Major Issue With All The Studies Showing AI effects
All the studies referenced are done in vitro.
In vitro studies and animal studies do not always translate into humans in practical application, so extrapolations should be not taken as fact without digging further.
SwoleTide touches on the importance of acknowledging genetic variability and how it is entirely possible that some individuals may metabolize Boldenone to ADD, 1-AD or ATD at a higher rate than others, or may hyper-respond to these metabolites.
Drug response is different individual to individual, and even the metabolism of naturally produced endogenous steroids vastly differs person to person.
Some individuals simply don't respond to certain drugs at all too, which needs to be considered.
Conclusion by SwoleTide on the Metabolite Research
The research is not clear on if Boldenone acts as an AI, or if it aromatizes into Estradiol.
Major Flaw In The Rabbit Study Explaining the High Estradiol
SwoleTide did an amazing job compiling the research and citing everything.
I want to start with my interpretation of the rabbit study [R].
This study was conducted in a monotherapy context, meaning they only injected the rabbits with Boldenone.
We see a decrease in Testosterone and increase in Estradiol.
Logically, if there is no Testosterone being administered and it is only Boldenone, and Estradiol levels clearly increase from baseline, then Boldenone must aromatize to Estradiol then right?
Wrong, at least in my opinion.
If we look at how they measured these biomarkers we can see that they collected blood and did a subsequent hormonal assay.
Serum Testosterone and Estradiol levels were determined using electrochemiluminescence immunoassay (ECLIA) kits.
Our favourite shitty test, ECLIA.
What is the problem with ECLIA?
ECLIA cross-detects other estrogens in the body.
During my Nandrolone-only experiment I tested my Estradiol with ECLIA and got a 36.8 pg/mL result.
When the same sample of blood was tested using high sensitivity testing, it was revealed that my Estradiol was actually only 9.9 pg/mL.
Why do we see this huge variation?
ECLIA cross-detects other estrogens in the body and detected my Estrone, consequently artificially inflating my ECLIA test results significantly.
This means that we can already conclude that the Estradiol levels in the Boldenone rabbit study are artificially inflated.
In the case of Nandrolone it spikes Estrone significantly, and we can see that ECLIA reflects a false spike in Estradiol levels as a result of this.
Estrone can convert to Estradiol in the body, but it does not occur at a significant rate.
So, we already know that the values via ECLIA are not very accurate when assessing Estradiol.
Is it a coincidence that whenever someone on Boldenone tests their blood via LC/MS/MS their results are vastly different than with ECLIA?
We consistently see crushed Estradiol levels on high doses of Boldenone via high sensitivity testing.
And this brings me to my next piece of evidence to support my theory.
Anecdotes And Blood Work Showing Boldenone Lowering Estradiol Levels
Vigorous Steve’s Experience With High Dose Boldenone + Testosterone
Vigorous Steve has a very good youtube channel and is someone I consider extremely knowledgeable about bodybuilding and pharmacology.
Steve responds very well to high dose Testosterone only cycles and has pushed his dosages pretty high.
Normally when he is on a gram of Testosterone per week, he needs to take 12.5 mg Aromasin every day to ward off estrogenic side effects.
When he blasted a gram of Testosterone and a gram of Boldenone per week however, he noticed he didn't need the same amount of Aromasin per week, as the introduction of EQ had actually reduced his estrogenic burden.
Despite adding 1000 mg of another drug that supposedly aromatizes at half the rate of Testosterone, he needed less AI, on double the amount of drugs.
High Sensitivity Blood Test Results On 300 mg Boldenone And 400 mg Testosterone
A friend of mine gave me high sensitivity blood test results to reference from his last Boldenone cycle.
The results helped shed more light on what is really going on here.
This is the time line of his cycle:
- 2/18/19 – Started blast: 400 mg Testosterone Cypionate / 200 mg NPP weekly (needed 0.25 mg Arimidex twice a week to keep Estrogenic side effects at bay)
- 5/31/19 – Switched to TRT Cruise consisting of: 100 mg Testosterone Cypionate / 900IU HCG (300 IU x 3) per week
- 7/19/19 – Full TRT Labs done. Estradiol blood test result came back at 75 pg/mL.
- 7/19/19 – Started blast phase with Equipoise in it later that day after blood draw of 400 mg Testosterone Cypionate/300 mg Equipoise per week and 20 mg Anavar per day
- 9/2/19 – Drew bloods while still on 400 mg Testosterone Cypionate/300 mg Equipoise per week and 20 mg Anavar per day
- 9/4/19 – Estradiol blood test result came back at 24 pg/mL, despite being on 400 mg of Testosterone Cypionate
He was on 4 times the dose of Testosterone, and 300 mg of Boldenone which supposedly aromatizes at 50% the rate of Testosterone, and yet his Estradiol decreased from 75 pg/mL down to 24 pg/mL.
The first thing I asked was if he was using ECLIA or sensitive assay.
He told me all blood tests were done using ultra-sensitive LC/MS-MS assay.
So this is another individual showing that Boldenone decreased his Estradiol significantly on cycle.
High Sensitivity Blood Test Results On 850 mg Boldenone And 250 mg Testosterone Per Week
Youtuber Symmetry and Fitness took things a step further and not only tested his Estradiol levels on Boldenone via sensitive assay testing, but he also tested his Estrone levels, which came back with some very interesting results.
His cycle was comprised of approximately 850 mg of Boldenone and 250 mg of Testosterone per week.
His results show a massive increase in Estrone, with a result of 662 pg/mL, with the top end of the reference range being 65 pg/mL.
His Estradiol was undetectable with less than 2.5 pg/mL.
Normally on this much Testosterone your Estradiol levels would be above the top end of the reference range.
Even with natural endogenous Testosterone production you would have somewhere around 15-35 pg/mL (depending on how much Testosterone you produce and other factors).
These blood test results show his Estradiol is even lower than a woman in menopause.
If you know anything about Estradiol, you know how important it is to avoid crashing it.
This test result indicates that something in his stack is preventing the Testosterone in his body from aromatizing into Estradiol.
Unpacking this further, we know the Testosterone is legitimately Testosterone, as he tested his blood using LC/MS-MS, which is the gold standard for Total Testosterone to avoid cross-detection of other anabolics.
So, we know he legitimately has a 1431 ng/dL Total Testosterone level.
That amount of Testosterone would normally produce an Estradiol that is high, not one that is crushed into the ground.
So, either the enzyme is being inhibited, or something else is going on.
Fortunately, with his Estrone blood test result, we can finally solve the puzzle here on what is actually happening.
Referring back to the rabbit study, we know that they used ECLIA to test Estradiol [R].
The rabbit study showed an elevation of Estradiol on Boldenone monotherapy, and coincidentally, of all the individuals who have reported proportional Estradiol levels in their blood work to their dose of AAS, none of them were using high sensitivity testing (at least of those that I have seen to date).
Symmetry and Fitness has a verifiably high Testosterone level, no Estradiol, and a cranked through the roof Estrone.
All blood test results showing an elevation in Estradiol are using ECLIA.
So, I hypothesize that Boldenone doesn't actually aromatize into Estradiol, nor does it inhibit the enzyme aromatase, rather, it competes with Testosterone to interact with aromatase to produce its own estrogenic metabolite.
I will delve into this further in the next subsection, but a quick takeaway from this is that you would very likely need to use exogenous Estradiol with Boldenone to actually get a physiological amount of circulating Estradiol into your body.
The reason being that Boldenone clearly does not aromatize into a sufficient amount of Estradiol, and instead produces a far weaker estrogen with completely different pharmacodynamics.
Estrone in particular is not satisfactory to achieve the same health benefits or muscle growth in the body as Estradiol, and there are numerous studies showing how deleterious disproportionately high Estrone levels can be to your health.
Alternatively, a much lower dose of Boldenone would need to be deployed relative to Testosterone if competition is the main thing we're concerned with, but even at a nearly identical dosage scheme, we saw in the second example I gave where only 300 mg Boldenone significantly impaired adequate aromatization of 400 mg Testosterone to Estradiol.
Almost nobody using Boldenone is using less than 300 mg, and if only that much is already that problematic, then it will be difficult to find a place for it in a health conscious protocol, or even just a protocol intended for maximum muscle growth in general.
It is subpar in both categories.
Boldenone's Effects On Estrogen Biosynthesis
As previously mentioned, the use of exogenous Estradiol is most likely necessary to maintain healthy levels on a high dose Boldenone cycle.
The principal pathway Estrone is biosynthesized through involves Androstenedione as an intermediate, with Androstenedione being transformed into Estrone by the enzyme Aromatase.
This is key to remember in the context of this Boldenone deep dive.
Androstenedione transforms into Estrone via the enzyme Aromatase.
This reaction occurs in both the gonads and in certain other tissues, particularly adipose tissue (hence why if you're fatter you aromatize more), and Estrone is subsequently secreted from these tissues.
In addition to aromatization of Androstenedione, Estrone is also formed reversibly from Estradiol by the enzyme 17β-hydroxysteroid dehydrogenase (17β-HSD) in various tissues, including the liver.
Simply put, you would never ever see levels of Estrone in men naturally like Symmetry and Fitness had on his cycle.
Anecdotally, we see that the need for AI usage goes down, and Estradiol levels get crushed, even on a high dose of Testosterone when adding Boldenone to cycles.
We also see blood test results showing sky high Estrone levels.
Some of Boldenone's metabolites are touted to be AI's, but the evidence of this is based on extrapolation from animal studies, in vitro models, and the fact that we see decreased Estradiol levels on high sensitivity blood test results.
This all leads me to believe that Boldenone does not act as an AI, and even if its metabolites do, the degree to which they do is clearly insignificant or else we would't have this massive spike in Estrone in the blood.
What is actually happening in my opinion is that Boldenone is a potent substrate for aromatase too, but does not aromatize directly into bioidentical Estradiol, it aromatizes into Estrone, or another synthetic Estrogen entirely.
Why we all took for granted that it would convert to straight bioidentical Estradiol when it is a synthetic anabolic steroid is beyond me.
If aromatase was inhibited by Boldenone's metabolites, we wouldn't see Estrone levels spike, nor would we see Estradiol levels spike via ECLIA.
That test cross detects other Estrogens, and it is only via high sensitivity testing that we can see what is actually going on.
The fact that Estrogens are being detected at all clearly indicates that the enzyme aromatase is functioning just fine, and something is pushing through it, and clearly it isn't the Testosterone during high dose Boldenone cycles as Estradiol gets crushed into the ground.
My question would be what is the binding affinity of Boldenone relative to Testosterone for aromatase, and what are the Estrogenic metabolites being created during that enzymatic conversion process.
Keep in mind, Symmetry and Fitness had high sensitivity testing for Testosterone and Estradiol, however, his Estrone test was done using ECLIA methodology.
Hence, the Estrone could very well be a cross detection too of another synthetic Estrogenic metabolite.
And that is probably the case after all, as he commented on my video and stated that he had subsequent followup testing done to assess his Estrone levels via LC/MS/MS.
And this time, they came back as normal.
Testosterone To Estradiol Ratios And The Cap On Aromatase Activity
Something that often goes overlooked is that there is a cap on aromatase activity in the body.
Once you start pushing into supraphysiological dosage territory with AAS, your body does not have a proportional amount of aromatase enzymes to process it all and spit out a perfectly proportional amount of Estradiol (or whatever metabolites the AAS you are using may or may not produce).
Studies measuring graded dose response to Testosterone in young and old men have shown that the Estradiol:Testosterone ratio actually decreases the further into supraphysiological dosing territory Testosterone administration goes.
On 25 mg Testosterone per week the total E2-to-T ratio in a young man is about 1.2%.
At 50 mg it goes down to about 0.7%.
At 125 mg it goes down to about 0.4%.
And so on.
You can clearly see that aromatization doesn't occur in a parallel manner to Testosterone dosage, suggesting that there is a limited amount of aromatization that can occur, and that synthetic AAS will likely be competing with Testosterone for that limited aromatase activity.
It is physically impossible for the body to push out a proportional amount of Estrogen when dosages get into supraphysiological territory, so I don't know how anyone could expect that Testosterone will somehow aromatize perfectly fine into Estradiol when it is competing with a huge drug load (Boldenone) that is also a substrate for aromatase.
Analogous to how anti-androgens will compete for the androgen receptor with Testosterone and DHT, Boldenone most likely competes with Testosterone for aromatase.
Another relevant example is what happens after using a 5α-Reductase inhibitor like Finasteride.
When you inhibit 5α-reductase with Finasteride or Dutasteride to lower DHT levels in the body, in the least scientific jargon possible, Testosterone is essentially “out-competed” by Finasteride.
When Testosterone can't convert to DHT because of enzyme inhibition or competition, it is left as circulating Testosterone, which then consequently increases the Total Testosterone level in the body, and as a byproduct increases Estradiol levels because there is now more circulating Testosterone in the body than there would have been if 5α-reductase was available to interact with.
So, if an enzyme has a cap on how much it can interact with hormones to create metabolite hormones, introducing another substrate with comparable binding affinity and/or dosage (there are other factors as well) into the equation just further decreases the amount of available enzymes for the parent hormones to interact with (Testosterone being the parent hormone in this context we are referring to).
I wouldn't be surprised if using Boldenone with Testosterone actually causes a modest spike in Testosterone and DHT levels in the body above and beyond what that same dose of Testosterone would otherwise provide on its own for the exact same reason that Finasteride increases Testosterone and Estradiol in the body.
If aromatase is occupied by a bunch of Boldenone, there will be more circulating Testosterone, and thus more Testosterone to 5α-reduce into DHT.
Now, in theory one could likely still leverage Boldenone if their dose of Testosterone was significantly higher than Boldenone, but blood test results suggest that the Testosterone dose needs to be A LOT higher for there to not be a significant impairment of Testosterone > Estradiol conversion.
Even just 300 mg of Boldenone dropped Estradiol levels far below what they should have been at on 400 mg of Testosterone, consequently impairing health and muscle growth relative to what could have been achieved with another adjunct anabolic that doesn't compete with Testosterone for aromatase.
It should also be considered that Boldenone is considered by most to be a relatively weak anabolic, and to date I have yet to hear of one person who is using high Test with low Boldenone.
There is even a broscience rule that has passed down the grapevine stating that EQ only works well at dosages above 600-700 mg.
I've even seen people say “EQ shines at 1500 mg”.
You know what else shines on 1500 mg EQ?
The big red flashing 0 on your sensitive assay Estradiol blood test results after you get your blood drawn on that dose of EQ.
But I digress.
In my opinion, Boldenone interacts with aromatase itself and produces an estrogenic metabolite that artificially inflates ECLIA blood test results.
It may or may not convert into Estrone, but my guess is that it doesn't convert to anything bioidentical, but does convert to a synthetic estrogen that has its own unique affinity for ERα and ERβ.
Now the question really becomes what is that synthetic Estrogen, and how potent is it at fulfilling the same physiological functions as Estradiol.
At least we know what to expect from the methylestradiol via Dbol and the 7α-methylestradiol via MENT.
With Boldenone we have no idea what's going on, but anecdotally its estrogenic activity seems lacklustre, and the fact that it essentially completely inhibits the aromatization of Testosterone > Estradiol makes it a very difficult compound to leverage effectively and safely.
Research also suggests that Boldenone is one of the most nephrotoxic compounds in existence.
The competition for aromatase, the subsequent inhibition of downstream cascades affecting important physiological functions, the huge spike in blood viscosity, and the potential kidney toxicity all make this a compound that is hard to find a place for in performance enhancing drug stacks.
While there are some unique performance focused scenarios in which I believe it could be leveraged effectively, for most individuals I do not think this is a compound worth messing with.