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Turn me off to tren

KillerStack

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The mental effects of tren probably aren't from its anti-cortisol effects, because all steroids have an affinity for the GR. It's most likely that the mental effects from tren come from its affinity for the ER, this makes since most of the mental effects from all AAS stem from ER effects.

I was hoping someone here who is a member of Victor's "academy" could explain his views on the androgenicity and anti-cortisol effects of tren. I have seen him say tren is the ONLY known steroid that does certain things with the clucorticoid receptors, basically being uniquely anti-catabolic as far as steroids go.
It’s total bullshit saying tren isn’t androgenic. Just pure clickbait bullshit designed to drum him up some $$$
He doesn't say it doesn't have any androgenicity, just that it's a much weaker androgen than people assume. He has posted all sorts of graphs "proving" his point but I don't know what they are based on. I could see him being kind of right. Doesn't change the fact that I think this "Silverback of our tribe" is a complete fuckhead with a horrible attitude.
 

Kaladryn

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I haven't had a PSA test as they start doing them test around 40 years old and up although I'm not surprised if mine has grew and shrunk back down with the anabolics and androgens of use I've haven't used much androgens I've used trest alone and tren , ime they seem the most androgenic and I didn't really use much of them for long periods of time or go high and dosing

Also from experience trest alone seem almost or as potent androgen as tren

I take finasteride which I've heard it's supposed to shrink it as a many guys do take finasteride for prostate although I've also heard that finasteride gives a false positive on it so I got to do more research on that but when I get my test I guess I'll see

My grandfather and Dad have had prostate issues so that's why I'm concerned about prostate it seems to run on his side my dad's side it seems
A PSA test is recommended for anyone on TRT at any age and you should absolutely always track your PSA if you use AAS.
 

Kaladryn

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I was hoping someone here who is a member of Victor's "academy" could explain his views on the androgenicity and anti-cortisol effects of tren. I have seen him say tren is the ONLY known steroid that does certain things with the clucorticoid receptors, basically being uniquely anti-catabolic as far as steroids go.

He doesn't say it doesn't have any androgenicity, just that it's a much weaker androgen than people assume. He has posted all sorts of graphs "proving" his point but I don't know what they are based on. I could see him being kind of right. Doesn't change the fact that I think this "Silverback of our tribe" is a complete fuckhead with a horrible attitude.
I'm pretty unimpressed with most of what I've heard Victor Black say, in fact, it seems like he is pulling most of his facts out of his ass by making loose inferences from studies with a limited overall understanding of molecular biology.

To say tren is the only steroid that interacts with the GR is a total falsehood, along with most of the other stuff I've heard him say.

This is from a 1975 study:
While glucocorticoid hormones act catabolically on skeletal muscle through their binding to glucocorticoid-specific receptors in the cytosol, androgens exert anabolic responses but no androgen-specific binding proteins could be detected in this responsive tissue. However, various nonradioactive androgens were effective in displacing labeled dexamethasone or cortisol from their respective cytoplasmic receptors in muscle, both in vitro and in vivo. The inhibition of glucocorticoid binding by androgens is competitive, and could be observed following a single or repeated administration of the androgens to adrenalectomized-castrated animals. The synthetic androgen fluoxymesterone and the hormone testosterone displayed Ki values of 7.5 X 10(-6) M and 1 X 10(-5) M, respectively, for the inhibition of [3H]dexamethasone binding in muscle cytosol. On the basis of competition experiments it is postulated that interaction of androgens with glucocorticoid receptors prevents the binding of glucocorticoids and might be responsible in part for the anabolic effects of pharmacologic doses of androgens in muscle.
 

Bleed

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I have a similar impression. His career (engineer) leads him to interpolate a lot of data which is where I think he comes up with some of these facts (just a guess on my part). He also seems to take two completely different pieces of information and conflate the meaning to equal some other point he charges people for.

The deal breaker for me was "the tribe" branding. That marketing technique does the opposite effect from what he intends it to at least with me. He may be a good faith actor but he hides behind the paywall and does so because "people want to spoon fed" so it is easy to get the impression he is high on his own supply and just another guy trying to cash in on his internet notoriety.

Although he did have rex losing his shit at 2 AM. That is worth something, just not a monthly subscriber fee.

I'm pretty unimpressed with most of what I've heard Victor Black say, in fact, it seems like he is pulling most of his facts out of his ass by making loose inferences from studies with a limited overall understanding of molecular biology.

To say tren is the only steroid that interacts with the GR is a total falsehood, along with most of the other stuff I've heard him say.

This is from a 1975 study:
 

Type-IIx

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I was hoping someone here who is a member of Victor's "academy" could explain his views on the androgenicity and anti-cortisol effects of tren. I have seen him say tren is the ONLY known steroid that does certain things with the clucorticoid receptors, basically being uniquely anti-catabolic as far as steroids go.

He doesn't say it doesn't have any androgenicity, just that it's a much weaker androgen than people assume. He has posted all sorts of graphs "proving" his point but I don't know what they are based on. I could see him being kind of right. Doesn't change the fact that I think this "Silverback of our tribe" is a complete fuckhead with a horrible attitude.
Sounds like Victor Black actually read the few decent studies on tren that can be extrapolated to humans and made the correct inferences. I'm not a guru person, but this is actually correct. I didn't realize this was controversial whatsoever. I sent @luki7788 some notes on tren that would support this view. A study worth reading would be Ye, et al (2014) doi:10.1016/j.steroids.2014.05.024.
 

Type-IIx

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Tren is a potent androgen in the sense that it binds the AR like a knife and potently activates the receptor. It doesn't cause prostate enlargement/hair loss as it is non-5α-reducible (and non-estrogenic), so it's not "androgenic" in the "sides" sense. The Hershberger Assay is bullshit for many reasons including the rodent levantor ani being a reproductive organ (rather significant). The psychological sides of tren are likely due to its negative action on glucocorticoids. Perhaps similarly, halotestin likely works primarily via this antiglucocorticoid mechanism, as well as weakly exerting an antagonism at the GR to increase aggression).
 

Kaladryn

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Tren is a potent androgen in the sense that it binds the AR like a knife and potently activates the receptor. It doesn't cause prostate enlargement/hair loss as it is non-5α-reducible (and non-estrogenic), so it's not "androgenic" in the "sides" sense. The Hershberger Assay is bullshit for many reasons including the rodent levantor ani being a reproductive organ (rather significant). The psychological sides of tren are likely due to its negative action on glucocorticoids. Perhaps similarly, halotestin likely works primarily via this antiglucocorticoid mechanism, as well as weakly exerting an antagonism at the GR to increase aggression).
This is from Victor Black? Because it's total bs.
 

Love_to_Bodybuild

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Anyone here taking finasteride? Are the sides bad? My urologist didn't want me on it if I can avoid it. He's pretty non-interventionist. I can feel my stream getting weaker every year as my prostate seems to be growing. Certainly didn't shrink down after my heart attack when I got off steroids. Mine seems permanent, but maybe finasteride will shrink it. Just have to deal with the sides of blocking dht.

If an enlarged prostate and cardiac problems doesn't make you chose not to use tren, nothing will.

In the case of the guy I know that pretty much lost his penis, I think he had cancer and there was no other choice other than risk death from cancer. He's a smart guy, retired county coroner.
I'm on finasteride I don't use it when I use deca . On a tr2 dose of 10 or 20 mg for master side can be reduced to 0.25 mg in studies that shown to almost kill is much DHT as a 1 mg does

Some lowered libido it's not that bad though and it depends on the dose of course if I use you know a full 1.5 mg it's more than if I use half a milligram

It does seem to lower my voice a bit which makes me think DHT is the main hormone for a male androgenic voice cuz my voice is on the deeper side since I was 13 years old, finasteride seems to lower it which means it's working

Cialis generally takes care of any sexual sides though

I've been taking it for since 2014 when I got on trt and I'm not having any pee issues
 

Kaladryn

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You want the citations, bro? It's from me having actually read the data. I've seen your broscience and it's hilarious!
Your level of insecurity is ridiculous, I'm wondering where it's from because it's total BS.

1. Tren is EXTREMELY well known to cause BPH, the fact that whoever wrote that thinks that it doesn't just because it doesn't reduce to DHT is laughable.
2. The fact that it's not "androgenic" because it doesn't reduce to DHT is laughable as well.
3. All AAS interact strongly with the GR so that isn't the source of tren's "psychological sides"
4. Halotestin doesn't work "primarily via this antiglucocorticoid mechanism" as you can see from my post above:

"The synthetic androgen fluoxymesterone and the hormone testosterone displayed Ki values of 7.5 X 10(-6) M and 1 X 10(-5) M, respectively, for the inhibition of [3H]dexamethasone binding in muscle cytosol [at the GR]."

I don't know where your insecurity comes from, but no one is attacking you directly, I don't know why you feel the need to insult or what 'broscience' you are talking about. All I'm asking is where that came from because it's not accurate and is easily proven as such.

But here is some armchair psychology for you: I think you have Borderline Personality Disorder, you might want to look into it.
 

Love_to_Bodybuild

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My first 5 years of testosterone replacement I was going every 3 months like clockwork and they never did a PSA test. I'll look back on my blood work to make sure I'm pretty sure though. Next time I go in for labs I'll ask for a PSA test just because I'm on testosterone replacement and I'm concerned about my prostate

As far as tren being not androgenic that's so BS , if Trent is not androgenic how come females grow Jaws get a deep voice and get a big clit on it just like many other steroids that have higher androgenic effects the females that don't they use the lowest androgenic they can get away with. How come one say this is not androgenic when it does this a females and it's like one of the number one steroids for females to stay away from for virization?

I know it's cliche, tren is much more androgenic than testosterone it's like 3 to 5 times more anabolic and androgenic so until I have other information, which I've seen in this thread and does not make sense to me, I'll stick to tren causing androgenic side effects
 

johnjuanb1

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Tren is rough on me at 53. I was doing 50mg tren ace just once a week and I felt like a million backs at first. The pump and strength lasted for 4 days post inject. But after about 6 weeks it caught up with me just not feeling so hot. My urine smelled real bad which made me decide it was time to stop and heal. My body is much more responsive to AAS now than in past years because my doses are much lower. I’m only on 300mg test and 150mg nandrolone per week which is working real well because I’m bulking sloppy. Today for the heck of it I took 20mg Cialis and 50mg dbol about 90 minutes preworkout then did a full upperbody workout in all supersets. It sure felt good to get a pump all over. It helped me forget I’m old AF for a quick minute. 😀
 

Type-IIx

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Your level of insecurity is ridiculous, I'm wondering where it's from because it's total BS.

1. Tren is EXTREMELY well known to cause BPH, the fact that whoever wrote that thinks that it doesn't just because it doesn't reduce to DHT is laughable.
2. The fact that it's not "androgenic" because it doesn't reduce to DHT is laughable as well.
3. All AAS interact strongly with the GR so that isn't the source of tren's "psychological sides"
4. Halotestin doesn't work "primarily via this antiglucocorticoid mechanism" as you can see from my post above:

"The synthetic androgen fluoxymesterone and the hormone testosterone displayed Ki values of 7.5 X 10(-6) M and 1 X 10(-5) M, respectively, for the inhibition of [3H]dexamethasone binding in muscle cytosol [at the GR]."

I don't know where your insecurity comes from, but no one is attacking you directly, I don't know why you feel the need to insult or what 'broscience' you are talking about. All I'm asking is where that came from because it's not accurate and is easily proven as such.

But here is some armchair psychology for you: I think you have Borderline Personality Disorder, you might want to look into it.
I’m assuredly not insecure about this topic, on the contrary, I’m fairly confident about it. I am also free of any personality disorder. Surmising about a poster’s personality disorder because they disagree with your silly beliefs about AAS does say a bit about your character, and certainly about your confidence in making bold statements/disparagement of people who disagree with you.

On 1-2, yes, tren does directly – via its potent AR action – cause these issues. If you refer back to my post, I was saying that the common parlance about “androgenicity” (as relying on the Hershberger Assay [HA]) entails the action of 5α reductase. Since tren is non-5α-reducible, it cannot exhibit “sides” via this commonly understood pathway that the HA is a proxy for. Indeed, its binding the AR “like a knife” means that these are not androgenic “sides” - but rather direct AAS actions as AR ligands. As your earlier cited article by Davey et al. mentions a bit, prostate function for example is AR-mediated.

If you grasp the function of the AR as directly mediating some of the side-effects attributed to the Hershberger Assay’s anabolic:androgenic ratio then we are getting somewhere, and it means you at least agree with some of the original post, contrary to its being "total bs." Following this logic, tren’s (along with all AAS’) androgenicity is impossible to separate from its anabolism. So long as we are on the same page regarding direct harmful action rather than HA concepts of “androgenic sides,” (5α reduction) then great.

On 3, false: A mammalian bioassay reporter method was used to detect activity at the AR, Erα, ERβ, PR, and GR [1]. MENT and fluoxymesterone (Halotestin) are the only two commercially available AAS that have any (very weak, actually) activity at the GR. Rather, tren likely exerts its antiglucocorticoid action via 11β-HSD 2 – the same pathway as Halotestin [2]. Tren’s potent antiglucocorticoid action was measured by Ye et al., demonstrating suppressed expression of GR mRNA (GR expression was 50% lower in tren vs. test) [3]. It is quite reasonable to hypothesize that the cognitive and psychological side-effects shared by tren and halo is downstream of its antiglucocorticoid action (perhaps involving DA signaling and the hypothalolimbic system). It’s not much of a stretch to connect an anti-anxiety effect with some pathological behaviors associated with tren.

On 4, simply confused: since the antiglucocorticoid action is independent of GR activity, that is, it is not mediated by any binding to the glucocorticoid receptor, the study of GR binding is irrelevant. Moreover, since Halotestin is primarily used specifically for boosting aggression (mostly powerlifters and strength athletes use it) its primary purpose is not even skeletal muscle anabolism. Rather, its primary purpose is indeed the putative antiglucocorticoid mechanism cited commonly linked with increased aggression (and myriad other antisocial behaviors).

I have no problems with good broscience, yours is just always wrong. Please don’t go calling me a mean personality disordered person now.

__________________

References:

[1] Houtman, C. J., Sterk, S. S., van de Heijning, M. P. M., Brouwer, A., Stephany, R. W., van der Burg, B., & Sonneveld, E. (2009). Detection of anabolic androgenic steroid abuse in doping control using mammalian reporter gene bioassays. Analytica Chimica Acta, 637(1-2), 247–258. doi:10.1016/j.aca.2008.09.037
[2] Furstenberger, C., Vuorinen, A., Da Cunha, T., Kratschmar, D. V., Saugy, M., Schuster, D., & Odermatt, A. (2012). The Anabolic Androgenic Steroid Fluoxymesterone Inhibits 11 -Hydroxysteroid Dehydrogenase 2-Dependent Glucocorticoid Inactivation. Toxicological Sciences, 126(2), 353–361. doi:10.1093/toxsci/kfs022

[3] Ye, F., McCoy, S. C., Ross, H. H., Bernardo, J. A., Be harry, A. W., Senf, S. M., … Borst, S. E. (2014). Transcriptional regulation of myotrophic actions by testosterone and trenbolone on androgen-responsive muscle. Steroids, 87, 59–66. doi:10.1016/j.steroids.2014.05.024
 

Kaladryn

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I honestly can't even, the way you write is so pseudo-intellectual it's annoying.

On your first point, you are arguing the definition of 'androgenic' at the ANDROGEN RECEPTOR. Anabolic and androgenic aren't separate pathways, so you are just arguing semantics.

On 3, testosterone is a very well-known GR antagonist. The "quite reasonable hypothesis" you are stating isn't reasonable at all if you factor in tren's affinity for the ER and the fact the ER is where most AAS cause psychological issues.

The fact that tren has other pathways for having an effect on the GH is interesting, but that doesn't mean it's well documented GR antagonist effects don't exist.

Halotestin doesn't "boost aggression" that IS broscience, it's used as a hardener for a cosmetic effect on stage, I've used it many times, there are lots of people, myself included, that get no significant "aggression" from AAS.

Honestly, you are extrapolating from studies much like Victor Black does.
 

MightyJohn

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I can't sleep on over 80mg/week(yes per week)
Para 60mg/wk was My sweet spot...100mg/wk couldn't sleep or function
 

Type-IIx

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I honestly can't even, the way you write is so pseudo-intellectual it's annoying.

On your first point, you are arguing the definition of 'androgenic' at the ANDROGEN RECEPTOR. Anabolic and androgenic aren't separate pathways, so you are just arguing semantics.

On 3, testosterone is a very well-known GR antagonist. The "quite reasonable hypothesis" you are stating isn't reasonable at all if you factor in tren's affinity for the ER and the fact the ER is where most AAS cause psychological issues.

The fact that tren has other pathways for having an effect on the GH is interesting, but that doesn't mean it's well documented GR antagonist effects don't exist.

Halotestin doesn't "boost aggression" that IS broscience, it's used as a hardener for a cosmetic effect on stage, I've used it many times, there are lots of people, myself included, that get no significant "aggression" from AAS.

Honestly, you are extrapolating from studies much like Victor Black does.
Kaladryn: tren only causes hair loss and prostate issues because it's as potent at the AR as DHT, not because of 5alpha-reductase (the commonly understood pathway for androgenic sides), so let's say that on this we agree.

On everything else you're saying, you're just confidently pulling shit out of your ass man. This belief "ER is where most AAS cause psych issues" is you being in denial about a) common observation, b) the literature, and c) the paper you already posted as authoritative on the functions of the AR. Psych issues can arise directly from AR action (neurological function of AR and its presence in neural tissue), AAS dysregulation of the hypothalamic-mesolimbic system, as well as there being an observable correlation between the anticatabolic mechanisms of Halo and methyltren (2 compounds that can actually be studied) and aggression... which despite your always-accurate bro science that AAS and Halo don't boost aggression, actually do.

@OuchThatHurts tren is an anabolic/anticatabolic weapon. To deter you, what makes it perhaps uniquely bad versus other AAS would be its particularly deleterious:
- cardiac effects (impaired corticosteroid metabolism and activation of minerolocorticoid receptor (MR) has been associated with cardiovascular disease)
- aggression
- risk of psychosis
- I've never read the amyloid plaque paper, is that specifically on tren? But there's reason to believe anything with a strong AR affinity in high active concentrations (i.e., more than DHT) negatively affects cognitive function, spatial learning and memory
 

MasteroniPepperoni

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Tren is a potent androgen in the sense that it binds the AR like a knife and potently activates the receptor. It doesn't cause prostate enlargement/hair loss as it is non-5α-reducible (and non-estrogenic), so it's not "androgenic" in the "sides" sense. The Hershberger Assay is bullshit for many reasons including the rodent levantor ani being a reproductive organ (rather significant). The psychological sides of tren are likely due to its negative action on glucocorticoids. Perhaps similarly, halotestin likely works primarily via this antiglucocorticoid mechanism, as well as weakly exerting an antagonism at the GR to increase aggression).

Could it be a possibility that tren is competing at the receptor with other compounds since people usually stack with at least test. Knocking off other compounds and being circulated towards other tissues/receptors other than the muscle?
 

Kaladryn

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Kaladryn: tren only causes hair loss and prostate issues because it's as potent at the AR as DHT, not because of 5alpha-reductase (the commonly understood pathway for androgenic sides), so let's say that on this we agree.

On everything else you're saying, you're just confidently pulling shit out of your ass man. This belief "ER is where most AAS cause psych issues" is you being in denial about a) common observation, b) the literature, and c) the paper you already posted as authoritative on the functions of the AR. Psych issues can arise directly from AR action (neurological function of AR and its presence in neural tissue), AAS dysregulation of the hypothalamic-mesolimbic system, as well as there being an observable correlation between the anticatabolic mechanisms of Halo and methyltren (2 compounds that can actually be studied) and aggression... which despite your always-accurate bro science that AAS and Halo don't boost aggression, actually do.

@OuchThatHurts tren is an anabolic/anticatabolic weapon. To deter you, what makes it perhaps uniquely bad versus other AAS would be its particularly deleterious:
- cardiac effects (impaired corticosteroid metabolism and activation of minerolocorticoid receptor (MR) has been associated with cardiovascular disease)
- aggression
- risk of psychosis
- I've never read the amyloid plaque paper, is that specifically on tren? But there's reason to believe anything with a strong AR affinity in high active concentrations (i.e., more than DHT) negatively affects cognitive function, spatial learning and memory
Consider these points: the AR may indeed have psychological effects, I would say it's certain, however, there are situations that prove to me that ER also has them, and in more 'erratic' ways. Look at the psychological issues people have when coming off of AAS when androgens are low and aromatase is probably hyperactive. Consider personal experience with high E2 levels, I assume you have some, I have many. Why androgens may cause some issues (I would characterize as "hyper" levels of "drive" which can be positive or negative depending), estrogens tend to more irrational behavior. Some people may not be able to control their high levels of "drive" and it can get them in trouble, but the irrational behavior that estrogens cause is a far more dangerous psychological issue for many of us. Consider females and issues they have to deal with involving estrogens. Also, consider the PR and anxiety effects there (also amplified by estrogens).

Now look at tren, sure it has a 3x the affinity for the AR as T, but that doesn't explain the fact 300mg of tren will have more of a psychological effect on many people than 1g of test. Now consider that we know that tren has a strong affinity for both the ER and the PR, which is fairly unique compared to the other AAS, much like its psychological effect is on people is somewhat unique.

Call it all broscience if you will, most of it is, but it's pretty sound logic and has some strong anecdotal evidence behind it. I would bet my left nut these effects are accurate.

Also, methy-test is the traditional "aggression" drug used in powerlifting and strongman comps. Methel-tren maybe also. I really don't think halo has been used for that very much.

As for GR interactions, it was Dan Duchaine that first promoted good old test for blocking the GR with this "post AR mediated growth" broscience.

The problem with science, as the guy in my signature pointed out, is that it always operates on an enormous piece of optimism: that there aren't other factors it isn't considering.
 

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Tren makes me a ducking crazy person at 300mg a week.

Like the apathy…..I don’t want to be around anyone I love, I’m like I’d be better off in a camper by the river eating cheese.

And I can’t sleep. Trazadone, ambien, Benadryl….still only 5-6 hours of sleep
You simply run too much tren, a little goes a long ways, try at least halfing that dose.
 

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It’s total bullshit saying tren isn’t androgenic. Just pure clickbait bullshit designed to drum him up some $$$
Put your $$$ where your mouth is and go challenge him on this data. Bring some proof with you and challenge him. If that's what he TRULY said, then challenge him on it, he ask anyone to do this if they think he is wrong on a subject.
 

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