How suppressive is primobolan compared to testosterone?

Solution
Substantially less. You could use, e.g., oral primo ace tablets for a mild cosmetic benefit for months continuously and endogenous T secretion would proceed. The same applies to metenolone enanthate i.m.

Since this is a bodybuilding board, this would seem a waste of drugs to most, however. We generally like aromatizable drugs in our stack to augment IGF-I activity and total-body growth & our risk tolerance permits the risk of persistent hypogonadism. Testosterone is a great drug that synergizes well with many others. It also enhances subjective measures like libido, assertiveness, etc.

Nevertheless, strictly to your question, it is a bro-science myth that you must accept total shutdown. This belief arises from the arguably myopic...
I will also think out loud) theoretically, it is possible to increase T not only with anti-estrogens, but also with anti-androgens. If you use only non-flavored aas. For example, bicalutamide blocks ar, the brain receives a signal that there are no androgens in the system, as a result, the release of gonadotropins increases. I haven't tested it with tests, according to indirect sensations (erection, mood, muscle preservation) it works well. After bic, I take dutasteride, T increases even more.
Dutasteride increases testosterone (a bit) because it inhibits 5AR (since less T is converted to DHT, more T).

Taking bicalutamide, an AR antagonist, to increase testosterone's activity is totally self-defeating.

Your indirect sensations test is totally subjective and subject to psychology.
 
Dutasteride increases testosterone (a bit) because it inhibits 5AR (since less T is converted to DHT, more T).

Taking bicalutamide, an AR antagonist, to increase testosterone's activity is totally self-defeating.

Your indirect sensations test is totally subjective and subject to psychology.
So I do it for myself, I don't need to prove anything to anyone)
 
After taking dutasteride, there is more substrate for aromatase, E2 increases and in the absence of dht becomes more active, libido increases and, oddly enough, prostate pain. In this case, taking 50-100 mg of zinc helps me, the pain goes away immediately, but the libido also decreases..
 
Very interesting thread. I like this forum.

I also have one hypothesis. I base it on a very interesting trial that used 25mg chlomiphene per day for threating low testosterone with pretty prominent effect to rase testosterone (to normal range). Similar effects have been reported using tamoxifen 20mg per day.

Estrogen and androgens seem to supress via the negative feedback at the hypothalamic-pituitary axis. So primobolan would suppress the natural production. Let's not forget the body knows if androgenic receptors are being stimulated. So, could it be that the endogenus estrogen effect is also such a factor (that slows down recovery) to the extent that the suppression effect of intra muscle primobolan (half life around ten days) is on the scale that comparisation is similar to testosterone?

@Type-IIx, thank you for the detailed description. Very interesting.
 
Very interesting thread. I like this forum.

I also have one hypothesis. I base it on a very interesting trial that used 25mg chlomiphene per day for threating low testosterone with pretty prominent effect to rase testosterone (to normal range). Similar effects have been reported using tamoxifen 20mg per day.

Estrogen and androgens seem to supress via the negative feedback at the hypothalamic-pituitary axis. So primobolan would suppress the natural production. Let's not forget the body knows if androgenic receptors are being stimulated. So, could it be that the endogenus estrogen effect is also such a factor (that slows down recovery) to the extent that the suppression effect of intra muscle primobolan (half life around ten days) is on the scale that comparisation is similar to testosterone?

@Type-IIx, thank you for the detailed description. Very interesting.
If you're looking for supraphysiological levels, it doesn't matter that they're made endogenously, you're still suffering certain side effects that even bioidentical testosterone produces. That's why nobody is permablasting even if they accept total shutdown.

Also clomid has the zuclomiphene issue and tamoxifen agonized ER highly at the liver and endometrium which is equivalent as prostate in males. It's going to cause liver and prostate cancer at 20mg/day, however, low doses no more than 1mg per day are likely safe long term and are written to antagonize at the liver while high doses agonize.

To avoid androgenic side effects, forget androgenic and anabolic ratios, because no compound is selective enough.

I do wonder if an androgen be developed with EXTRA HIGH breakdown rate and and perhaps hundreds of times the potency in its administered form before it is broken down by a single enzyme that can be administered systemically?

This way I will not mind having to inject every muscle every day. At levels normally considered extremely toxic. Just keep blood levels of breakdown agent high upon this special androgen injection, but let them clear out of the blood and muscle overnight.

First upon injection the androgen enters the muscle. Immediately upon entering bloodstream it reacts with the breakdown enzyme, and by the time it enters (liver, brain...) it is already reduced to inert form.
 
However, it excludes the legitimate use cases that include the use of orals in a pulsed fashion or for peaking strength/performance, prepping for a photo shoot that isn't in FLEX Magazine, etc.
Are you referring to Dr.D method from the 2000's? Specifically his "how to pulse orals"... nostalgic thoughts
 
How suppressive is primobolan compared to testosterone?
It will shut you down. No doubt. At a small oral dose, maybe minimal, probably similar to low dose anadrol. Anadrol at 25mg daily was found to cause minimal supression over 3 weeks. It was a smaller case study though.


My overall advice; If you're going to pin the stuff in any appreciable dose you're probably going to get shut down. From what I know it's easy to recover from. With the amount of PCT knowledge and scientific practice available, unless you're leydig cells are fucked and dead, you can more than likely recover from most compounds. Take care of your nuts, get blood work, study the feedback loops in your body and brain, and make sure you aren't causing irreparable damage. Primobolan is generally considered mild and easy to recover from as far as I know. With that being said... Are you considering being off longer than 3 months? Or are we talking bridging with clomid and SARMs... Lol...
 
Estrogen and androgens seem to supress via the negative feedback at the hypothalamic-pituitary axis. So primobolan would suppress the natural production. Let's not forget the body knows if androgenic receptors are being stimulated. So, could it be that the endogenus estrogen effect is also such a factor (that slows down recovery) to the extent that the suppression effect of intra muscle primobolan (half life around ten days) is on the scale that comparisation is similar to testosterone?
Metenolone (Rimobolan; "Primo Ace") is nonaromatizable so it doesn't increase estrogens.
 
Are you referring to Dr.D method from the 2000's? Specifically his "how to pulse orals"... nostalgic thoughts
No bro. Athletes do this all the time, dopers. They are able to pass testing easier because orals' metabolites generally pass quicker, and they seek acute performance gains rather than increased weight. Besides that, any commonality that might seem shared between my writing here and Dr. D's is purely a coincidence of our probably arriving at similar conclusions based on facts.

Do you have his method to share? I'd be interested in reading it. You can PM it if you prefer.
 
It will shut you down. No doubt.
How can you say this without knowing the dose or duration?

The question does not specify, it simply asks a question that has already been answered.


At a small oral dose, maybe minimal, probably similar to low dose anadrol. Anadrol at 25mg daily was found to cause minimal supression over 3 weeks. It was a smaller case study though.


My overall advice; If you're going to pin the stuff in any appreciable dose you're probably going to get shut down. From what I know it's easy to recover from. With the amount of PCT knowledge and scientific practice available, unless you're leydig cells are fucked and dead, you can more than likely recover from most compounds. Take care of your nuts, get blood work, study the feedback loops in your body and brain, and make sure you aren't causing irreparable damage. Primobolan is generally considered mild and easy to recover from as far as I know. With that being said... Are you considering being off longer than 3 months? Or are we talking bridging with clomid and SARMs... Lol...
 
In brief: a total of 100 subjects (all men) that were intending to start an anabolic steroid cycle within 2 weeks were included in the trial. Various health measurements, including blood tests, were performed on all participants before the cycle (T0), in the last week of the cycle (T1), 3 months after the end of the cycle (T2), and 1 year after the start of the cycle (T3). To be clear: subjects were using their own AAS, the endocrinologists didn’t prescribe it of course.

What’s of particular relevance for this article, is that they also measured testosterone levels and thus could see how it would recover after a cycle. Additionally, 80 of the subjects did PCT (and therefore, 20 didn’t). So this would be the first prospective trial in which the efficacy of PCT might become apparent. (In the end, data was available for 79 subjects doing PCT and 19 subjects not doing PCT).

PCT drugs also weren’t provided by the endocrinologists. People did their own thing. The authors noted that most PCT regimes consisted of tamoxifen (70% of the time) and/or clomiphene (55% of the time) for 4 weeks post-cycle. Which, indeed, would also be my guess as a stereotypical example of PCT.
 
In brief: a total of 100 subjects (all men) that were intending to start an anabolic steroid cycle within 2 weeks were included in the trial. Various health measurements, including blood tests, were performed on all participants before the cycle (T0), in the last week of the cycle (T1), 3 months after the end of the cycle (T2), and 1 year after the start of the cycle (T3). To be clear: subjects were using their own AAS, the endocrinologists didn’t prescribe it of course.

What’s of particular relevance for this article, is that they also measured testosterone levels and thus could see how it would recover after a cycle. Additionally, 80 of the subjects did PCT (and therefore, 20 didn’t). So this would be the first prospective trial in which the efficacy of PCT might become apparent. (In the end, data was available for 79 subjects doing PCT and 19 subjects not doing PCT).

PCT drugs also weren’t provided by the endocrinologists. People did their own thing. The authors noted that most PCT regimes consisted of tamoxifen (70% of the time) and/or clomiphene (55% of the time) for 4 weeks post-cycle. Which, indeed, would also be my guess as a stereotypical example of PCT.
I read it bro, thank you.

Instead of scanning it in order to highlight sections that try to prove PCT works (working backwards from my preconceived notion), I instead chose to read it in its entirety and take it for what it is (work forward from the evidence to move closer towards a conclusion).
 
How can you say this without knowing the dose or duration?

The question does not specify, it simply asks a question that has already been answered.

What?


I'm not going to take this seriously.


To suggest that exogenous anabolic steroids will do anything other than at the very least minimal supression, is dangerous and irresponsible. Downright stupid.


That is a "trial" from 2010 in the Netherlands, it isn't peer reviewed, or considered something valid to me, because it lacks information considered necessary to be anything more than some parrot post. It doesn't even specify sample study size, and there's is extremely limited information. How does some outdated "study" have anything to do with this?

Years of blood work, forum postings, and actual peer reviewed study have proven that PCT is effective, even if it's just time off for natural recovery, with no clomiphene administration. It just takes longer.

This is what I get out of your post right now.



"Hey Kid, primo tabs are fine. When your dick goes in the dirt and doesn't work any more I want you to know that these random endos from the Netherlands said that PCT doesn't work back in 2010"



That's what you sound like.
 
What?


I'm not going to take this seriously.


To suggest that exogenous anabolic steroids will do anything other than at the very least minimal supression, is dangerous and irresponsible. Downright stupid.
But you're arguing against a strawman. Nobody has suggested they don't do just that: minimal suppression.
That is a "trial" from 2010 in the Netherlands, it isn't peer reviewed, or considered something valid to me, because it lacks information considered necessary to be anything more than some parrot post. It doesn't even specify sample study size, and there's is extremely limited information. How does some outdated "study" have anything to do with this?
It's peer-reviewed and a recent study.
Years of blood work, forum postings, and actual peer reviewed study have proven that PCT is effective, even if it's just time off for natural recovery, with no clomiphene administration. It just takes longer.
Nah, the evidence presently suggests that PCT, if anything, slightly delays recovery: it just makes us feel better acutely - which can still be very useful, no doubt.

This is what I get out of your post right now.



"Hey Kid, primo tabs are fine. When your dick goes in the dirt and doesn't work any more I want you to know that these random endos from the Netherlands said that PCT doesn't work back in 2010"
Oh, that's good to know that's what I sound like.

Because clearly, my posts have expressed an opinion that I advocate for a piss weak cycle.
That's what you sound like.
Sub-maximally anabolic doses of weak androgens like metenolone minimally affect the HPG axis. For example, if you ran a (terrible) cycle of 75 mg q.w. metenolone (as enanthate; "Primo") & 20 mg q.d. dehydrochloromethyltestosterone (Oral Turinabol) you would still have > 50% of your endogenous testosterone secretion.

Calm down, your histrionics are not warranted. You just disagree, albeit, while being factually wrong.
 
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But you're arguing against a strawman. Nobody has suggested they don't do just that: minimal suppression.

It's peer-reviewed and a recent study.

Nah, the evidence presently suggests that PCT, if anything, slightly delays recovery: it just makes us feel better acutely - which can still be very useful, no doubt.


Oh, that's good to know that's what I sound like.

Because clearly, my posts have expressed an opinion that I advocate for a piss weak cycle.

Sub-maximally anabolic doses of weak androgens like metenolone minimally affect the HPG axis. For example, if you ran a (terrible) cycle of 75 mg q.w. metenolone (as enanthate; "Primo") & 20 mg q.d. dehydrochloromethyltestosterone (Oral Turinabol) you would still have > 50% of your endogenous testosterone secretion.

Calm down, your histrionics are not warranted. You just disagree, albeit, while being factually wrong.


Disagree with what?


I'll repeat myself again. Trying to promote any type of exogenous anabolic steroid administration without the hazard warning of supression is dangerous, and stupid.



/Discussion
 
But you're arguing against a strawman. Nobody has suggested they don't do just that: minimal suppression.

It's peer-reviewed and a recent study.

Nah, the evidence presently suggests that PCT, if anything, slightly delays recovery: it just makes us feel better acutely - which can still be very useful, no doubt.


Oh, that's good to know that's what I sound like.

Because clearly, my posts have expressed an opinion that I advocate for a piss weak cycle.

Sub-maximally anabolic doses of weak androgens like metenolone minimally affect the HPG axis. For example, if you ran a (terrible) cycle of 75 mg q.w. metenolone (as enanthate; "Primo") & 20 mg q.d. dehydrochloromethyltestosterone (Oral Turinabol) you would still have > 50% of your endogenous testosterone secretion.

Calm down, your histrionics are not warranted. You just disagree, albeit, while being factually wrong.
You're quoting ONE study with a sample size of 100 people.


Vs. decades of peer reviewed research and evidence...



Riiiiiight
 
Disagree with what?


I'll repeat myself again. Trying to promote any type of exogenous anabolic steroid administration without the hazard warning of supression is dangerous, and stupid.



/Discussion
WHO THE FUCK IS PROMOTING AAS ADMINISTRATION?

Are you unable to read words without projecting, inaccurately, what you think someone's opinion & agenda is onto it, FFS?

You think the HAARLEM trial is low quality; go figure. You also think it's from 2010 and isn't peer-reviewed, but that forum anecdotes are.
 
WHO THE FUCK IS PROMOTING AAS ADMINISTRATION?

Are you unable to read words without projecting, inaccurately, what you think someone's opinion & agenda is onto it, FFS?

You think the HAARLEM trial is low quality; go figure. You also think it's from 2010 and isn't peer-reviewed, but that forum anecdotes are.
How about we discuss steroid profiles, and the extraction methods used to make steroids.

Do.you want to have that conversation? How raws are made, and how you're parroting some bullshit from the Netherlands to dismiss these facts?


Do you want me to start posting pictures of tranbolone labs everywhere? Then we can discuss this?
 
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