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.
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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