It’s just bullshit and bro science. I am on nandrolone only and feeling better than with testosterone. Even pros of the past stayed on without test. Testosterone is dirty and carry many colaterals too. I am a prove of it. And that’s why other steroids was created, to substitute testosterone.
Anyways we have to kill this ditactor culture (of everything) and start to experience. I will use the Boldenone and see what happens. Maybe it can work even better, ins’t? My only concern is anxiety for now. That’s why I taped down testosterone for now and I am trying to use other things.
It can be used as evidence, but it isn’t as strong as something with more than N=1.
I don’t doubt some do just fine on it solo. Same with EQ. Same with Test. How would we determine which one of these compounds is the best if we are interested in the lowest probability of negative mental and sexual side effects? Data exists for testosterone and I have seen it. It looks pretty damn favorable on its own. Perhaps you have some data on nandralone solo?
If you search you will see a lot of studyes on nandrolone because it’s the second mostly studied steroid next of testosterone. And mostly of these studyes was it alone because nandrolone, as every other steroid, was created to substitute testosterone to treat certain medicals and clinicals condictions. On note; I am feeling better on nandrolone than testosterome because of estrogen and/or androgenicity. Testosterone gave me anxiety because my body and mind apearantly don’t handle it well, as some people like me, that end up getting off testosterome suplementation. This is not to discuss about and I am not trying to force anyone to do anything. I just want to hear more experiences about Boldenone usage because majority here do use everything and know more than me.
No problem man. FWIW, I have heard of people running EQ solo. I used to think it was a better idea than I currently do. Because it turns out it doesn’t actually convert to E2 at half the rate of test (it basically just converts to E1, and blocks test out from making E2 is a strong hypothesis IMO). I do know a guy who cruises on test / EQ and loves it.
I seem to handle test pretty well, so I’ll hold out until I have solid proof Deca on it’s own is a good idea.
How much testosterone and boldenone does he runs? He are not experiencing anxiety?
/about the nandrolone it is a good ideia if you suffer, as me, from anxiety or other psycological/physiological side effects from testosterone (or seeking other beneficts that testosterone does not gives).
He runs too much to say it simply (500/500). He was running 300/700 Test / EQ for a while, then bumped the test and lowered the EQ. I tell him this is not a good idea long term.
I have had anxiety before and after test. I think it went down a bit with test, but I will admit I handle test well. Just some back acne when running it for a blast.
I never tried EQ monotherapy, but it definitely crossed my mind as something I might try.
Like you mention, I have heard of some guys feeling great on Deca monotherapy.
For most people I think non test monotherapy is not a good idea, sexual dysfunction, libido reduction, low E2. That’s just from word of mouth. It all comes down to your individual reaction to a particular drug, and dosage. If you have tried other stuff, and its not working for you, I can see how you might want to give it a shot.
Yes, a bioidentical hormone that is responsible for you being a man is dirty. If you want to experiment knock yourself out. But saying something is broscience and then following it up with a full on smooth brain comment isn’t exactly how you instill confidence in those you’re trying to convince of your knowledge.
Do you have tryed it or are you just parroting what other people say as truth?
That’s the problem with internet, everyone thinks that knows everything because they are agrouped with other peoples with the same dogmas and ideologies while atacking everyone who thinks different…
Some of us actually do this thing called research. It involves reading and understanding things like studies. You may not be familiar. Discussing other people’s experiences can help establish certain anecdotally based guidelines for people, and voicing a personal opinion is indeed a liberty, and when many people agree on that opinion it is considered a consensus. The consensus may be incorrect, but it is based on collective experience and opinion. The idea that only testosterone can be used to treat a testosterone deficiency, as opposed to other things that are not testosterone and will not in any way elevate testosterone levels, is fairly straightforward as a concept. If that doesn;t work for you, then maybe you are treating the wrong problem.
First of all I am not using anabolics as trt, aside I obviously on permantly now. And I’ve done a lot of search, I don’t come with the nandrolone ideia from nowhere. You guys that aperantly don’t researched this aswell. I’m just teeling you guys to be open minded. For example; I came here thinking about boldenone but you guys tell me this will not work, so I will not do this anymore. I will do something else because of ya’ll.
I will try testosterone + ia or drostanolone (something guys here use in their protocols too) to control my estrogen arise and see if I will feel better and get good results.
Nandrolone solo comes with more downsides than testosterone solo. Period. It certainly can work for some guys and there’s nothing wrong with being one of them. But it’s not a safer alternative.
Boldenone through aromatase gets converted to E2. That is the case. E1 gets converted to E2 in the body. (Seemingly a too small amount)
Look at the upper row of hormones. To get Converted to E1 boldenone would first need to be oxidized by 17b-HSD in the body. It could equally be taken up by aromatase and then get converted so it’s highly unlikely that boldenone always first goes through one enzyme then the other.
I believe because of the evidence I know boldenone gets converted to E2.
TBH with you, that chart does not mean much to me as I don’t have any organic chemistry knowledge. I can make some sense of it, but it appears to apply to testosterone, not Bold. How do we know that these processes apply to Bold?
Are you saying that Bold → E1 → E2, or that Bold -->E2. I would say if case 1, that it doesn’t necessarily get converted to E2. Perhaps you are saying both?
Do you buy that Bold seems to lower E2 when run with Test? How do you explain that if both Test and Bold are converting to E2?
Sorry if I am asking a lot here. I would like to know the answer to this question with some certainty.
Boldenone has the “estradiol body”, the only thing missing is the aromatization which gets provided by aromatase. Since the A ring (left ring of the 4) looks like the one Testosterone has besides on more double bond, it will be converted to the same structure. (Or at least that’s what it does in my estimation, research is rare)
I know the E1 hypothesis comes from moreplatesmoredates, he writes in his conclusion
“Why we all took for granted that it would convert to straight bioidentical Estradiol when it is a synthetic anabolic steroid is beyond me.”
But what he doesn’t explain is in this case chemically why it would not.
I get the case study he provided. I don’t know what to make of it but his hypothesis is in my estimation not plausible AT ALL.
Here’s why:
For boldenone to convert to E1 (Estrone) there need to be 2 different enzymes with two different reactions taking place:
Aromatase to aromatize the A-Ring
17b-HSD to oxidize the D-Ring
For boldenone to convert to E2 (Estradiol) there needs to be one enzyme doing one reaction:
Aromatase aromatizes the A-Ring
So there’s 2 possibilities:
Either the blood work of the guy was screwed up or his body was a complete outlier
There’s an enzyme that nobody ever saw which can convert boldenone directly to E1
Boldenone gets always first converted to Androsta-1,4-diene-3,17-dione and then aromatized.
The second one is extremely unlikely.
The third one is difficult. It could actually be that Boldenone isn’t a substrate for aromatase but it is one for 17b-HSD. And then product of that reaction Androsta-1,4-diene-3,17-dione (ADD) is a substrate for Aromatase. Then point 3 would be correct and the guy would be correct that it only converts to E1.
My problem with that is:
The Aromatase enzyme doesn’t have a problem with aromatizing 17-Keto or 17-hydroxy. It does that quite good. The 17 position is also not at the active site so it’s not that important to the enzyme what’s going on there. (Second argument only makes sense if first is correct, which it is)
But the Aromatase enzyme has a problem with A-Ring variations. But then it couldn’t convert any of the boldenone like A ring derivatives, so it could not convert ADD (similar to exemestane).
The study we need to read is this one (just found it after 2 hours searching, thank god):
Here they state that human placenta (got a lot of Aromatase and 17 Beta-HSD) converts ADD (the metabolite of boldenone) into Estrone (E1) and Estradiol (E2). It also converts it to 17beta-hydroxy-androstendienon which could mean that this builds up faster than it can get converted to E2.
Puh, so if both enzymes are present, both estrogens are synthesized.
In my opinion, boldenone gets converted to E2.
It’s not conclusive, as it could still be that the high amount of HSD in the last study isn’t replicable. But i don’t know that and the researchers state otherwise. I would have to reread it to find the sentence where they explain it, as I didn’t read it well this time.
That’s the picture. I wrote the names next to the 2 compounds.
Sorry of that was a rollercoaster. I had to research while writing and it took me very long so it can seem like it’s not as coherent as usual. I’m tired. Have a good night fellas
Im just speculating now but yes I buy it. If Bold has a lower conversion rate but a higher affinity or is just there in way larger amounts, then T gets thrown out of the enzyme by Bold. Then bold acts as a AI (or rather competitive AI).
There’s just so damn much blood work showing e2 crashed when guys run high doses of bold, even with decent amounts of test. I don’t know what causes it but it’s undeniably happening.
I once read a decent sounding theory about how boldenone has a metabolite that’s similar to arimistane, which is a proven (albeit weaker) suicidal AI. Never dug into it, but if I can find it I’ll post it.
Yes boldenone itself looks a lot like exemestane and the metabolites of boldenone seem to have AI properties. I did not go into the metabolites on purpose as this would have taken me even longer but in my opinion (contrary to the Reddit post moreplatesmoredates takes as pure truth) the evidence suggests that metabolites of boldenone act as AI(s).
Second option could be just this:
In that case Bold itself would cause the low E2. With that hypothesis there would just be the problem that there should be some E2, not E2 below reference range.
It could also be a combination of the two hypothesis.
