Favorite steroids to use and why

WTF is going on here? Test only cycles yield minimal gains? Huh?

I think most pros off season is mainly test at 2grrams etc. tell me they have no muscle?
 
@Type-IIx i tried pheraplex(madol/dmt) and it makes tren rage look like a little hissyfit, i would smash mirrors on that pheraplex, theres only one place still selling it still some obscure website in russia
 
WTF is going on here? Test only cycles yield minimal gains? Huh?

I think most pros off season is mainly test at 2grrams etc. tell me they have no muscle?
1. Most people here aren’t and never will be pro

2: why the fuck would I run 2 grams of testosterone and feel like shit??? Just run a couple Mg’s of it and add some safer compounds with it like a primo, Anavar etc
 
I have so many reasons to doubt top pros are only running test
They aren’t. Just like bullshitters o YouTube aren’t running “300 test, 300 mast, 300 primo and 20 mg of Anavar” it’s all fucking bullshit. We get it, harm reduction. But nobody is gaining much, if anything from shit like that
 
M1T was too much. Methylsten so good. I am interested in Epistane again, going to do some research on it. I'll steer clear of the madol (I remember a guy that ran it, he had crazy eyes).
that's funny, madol is ridiculous. def try epistane its pretty much everyones favorite prohormone, superdrol coming in a close 2nd
 
I am always skeptical of pro bodybuilders' self-reports of drug regimens/dosages. There's anobsession with obfuscation and insistence on portraying oneself as genetically gifted/running lower dosages than in reality.

Most guys are probably running Test/Deca in the off season, and perhaps Test/Deca/EQ (some rotation thereof). Throwing in orals and plenty of insulin/GH (year round).

Eh, not a fan of the "highest E2 you feel good on." Benefits from aromatization do not come from high E2, but rather in situ aromatization. Higher E2 negatively feeds back on IGF-I/GH response.
@Type-IIx
“Benefits from aromatization do not come from high E2, but rather in situ aromatization.”…

Could you elaborate on that?
 
@Type-IIx
“Benefits from aromatization do not come from high E2, but rather in situ aromatization.”…

Could you elaborate on that?
Without simply dumping a ton of notes with references on this matter on you, I should organize it into a coherent work of some sort.

Put simply, my "thesis" on myotrophic mechanisms of AAS is that these drugs, through:
I. modulating glucocorticoids and muscle IGF-I isoforms (mIGF-I)
II. aromatization
III. ligand dependent- and independent- AR action exert classical genomic effects, mRNA-mediated translation for protein synthesis, as well as rapid nongenomic action

Downstream of aromatization (so with aromatizing androgen only, i.e., Test, Nand, Dbol, a few others) you see a. enhanced growth factor activity (e.g. GH, IGF-1, etc.), b. enhanced activation of myogenic stem cells (i.e. satellite cells) [this occurs via secondary messenger activation]... and perhaps with all androgens, the potential for c. new myofiber formation ["Hyperplasia"] (working on this... I also have a lot to say about rhGH and this).

With aromatization, there are various benefits. That is, benefits from the process itself (in situ aromatization), rather than with its products (chiefly E2, other aromatic products like 17methyl-E2 with MENT)

The chief consideration with aromatizing androgen, is that its estrogen products pose a net negative in the human male. Rather, the aromatization process itself is what we want (and in fact, tamoxifen prevents the T-induced augmentation of serum IGF-I levels).

E2 increases serum IGFBP-1 levels, which reduce free IGF-I availability and (endogenously) unleashes GH secretion by feedback withdrawal. This is why women have 1.5-3x the GH levels of their male counterparts, yet a diminshed IGF-I response (virtually no benefits from rhGH unless they triple the dose... worse with oral estrogens/birth control generally).

The literature points to E2 being of miniscule if any benefit to men.

Benefits from aromatizing androgen (Test!) including augmented glucose metabolism (increased G6PD/Akt activity), potential myostatin attenuation come from in situ aromatization: the process of T/aromatizing androgens being converted to estrogens. Unfortunately, the products themselves through compensatory mechanisms tend to negatively feed back on anabolism.

Sure there are some benefits of estrogens per se (but E2 and the more potent methylestrogens suck!)... there is some interest in an ERx [as yet undetermined] or of course ER-β, which is a very interesting receptor for us: whereas ER-α primarily regulates blood lipids, ER-β primarily regulates muscle tissue remodeling. E2 is just a shit ligand for this (it's why I am intrigued by the potential of phytoecdysteroids).

This falls quite far outside the classical view of primarily AR/ligand-dependent action but is in line with the latest research.

There is certainly an inverse U-shaped curve plotting E2 vs. muscle anabolism. More E2 is definitely not better.
 
Without simply dumping a ton of notes with references on this matter on you, I should organize it into a coherent work of some sort.

Put simply, my "thesis" on myotrophic mechanisms of AAS is that these drugs, through:
I. modulating glucocorticoids and muscle IGF-I isoforms (mIGF-I)
II. aromatization
III. ligand dependent- and independent- AR action exert classical genomic effects, mRNA-mediated translation for protein synthesis, as well as rapid nongenomic action

Downstream of aromatization (so with aromatizing androgen only, i.e., Test, Nand, Dbol, a few others) you see a. enhanced growth factor activity (e.g. GH, IGF-1, etc.), b. enhanced activation of myogenic stem cells (i.e. satellite cells) [this occurs via secondary messenger activation]... and perhaps with all androgens, the potential for c. new myofiber formation ["Hyperplasia"] (working on this... I also have a lot to say about rhGH and this).

With aromatization, there are various benefits. That is, benefits from the process itself (in situ aromatization), rather than with its products (chiefly E2, other aromatic products like 17methyl-E2 with MENT)

The chief consideration with aromatizing androgen, is that its estrogen products pose a net negative in the human male. Rather, the aromatization process itself is what we want (and in fact, tamoxifen prevents the T-induced augmentation of serum IGF-I levels).

E2 increases serum IGFBP-1 levels, which reduce free IGF-I availability and (endogenously) unleashes GH secretion by feedback withdrawal. This is why women have 1.5-3x the GH levels of their male counterparts, yet a diminshed IGF-I response (virtually no benefits from rhGH unless they triple the dose... worse with oral estrogens/birth control generally).

The literature points to E2 being of miniscule if any benefit to men.

Benefits from aromatizing androgen (Test!) including augmented glucose metabolism (increased G6PD/Akt activity), potential myostatin attenuation come from in situ aromatization: the process of T/aromatizing androgens being converted to estrogens. Unfortunately, the products themselves through compensatory mechanisms tend to negatively feed back on anabolism.

Sure there are some benefits of estrogens per se (but E2 and the more potent methylestrogens suck!)... there is some interest in an ERx [as yet undetermined] or of course ER-β, which is a very interesting receptor for us: whereas ER-α primarily regulates blood lipids, ER-β primarily regulates muscle tissue remodeling. E2 is just a shit ligand for this (it's why I am intrigued by the potential of phytoecdysteroids).

This falls quite far outside the classical view of primarily AR/ligand-dependent action but is in line with the latest research.

There is certainly an inverse U-shaped curve plotting E2 vs. muscle anabolism. More E2 is definitely not better.


Care to give your thoughts on aromatase enzyme inhibitors verse selective estrogen receptor modulators for estrogen control on aromatizing steroids?

By which i mean, is it better to inhibit estrogen formation or to inhibit estrogen binding?

I mean with an AI your keeping more of the steroid from converting to estrogen, which would logically mean more bang for your buck from the AAS, but i dislike AIs because my joints always end up hurting when i use them and ive never been able to “dial in” a good dosage, they are just too damn strong. But based on your reply above it sounds like youd lean in favor of AIs over SERMs for estrogen control unless im misinterpreting what you said.
 
and rarely faked
Debatable. There’s a lot of” Dbol”out there that is in fact, not Dbol. It’s definitely my favorite oral behind Superdrol. However, I notice that it wears off on me fast. The first 1-2 weeks are amazing. After that it feels like the effects start to wear off. I think Dbol is a great addition to a testosterone base. Honestly, any oral is. Just don’t run them more than 6 weeks. Take 8-12 weeks off then if everything is g2g- run another oral. Just don’t run testosterone by itself- for the love of all that’s good and holy.
 
Debatable. There’s a lot of” Dbol”out there that is in fact, not Dbol. It’s definitely my favorite oral behind Superdrol. However, I notice that it wears off on me fast. The first 1-2 weeks are amazing. After that it feels like the effects start to wear off. I think Dbol is a great addition to a testosterone base. Honestly, any oral is. Just don’t run them more than 6 weeks. Take 8-12 weeks off then if everything is g2g- run another oral. Just don’t run testosterone by itself- for the love of all that’s good and holy.
Why not by itself?
 
Why not by itself?
Testosterone should be used as a base for estrodial on your cycle so you don’t feel like shit. Can it add a little muscle? Of course. But once you reach a certain threshold, you will only be spinning your wheels. Once you add in another compound *or 2* be prepared to grow. That’s where your gains will come from. The first cycle should always be test only- after that, you’re gonna need another compound. Or you will accomplish nothing
 
Testosterone should be used as a base for estrodial on your cycle so you don’t feel like shit. Can it add a little muscle? Of course. But once you reach a certain threshold, you will only be spinning your wheels. Once you add in another compound *or 2* be prepared to grow. That’s where your gains will come from. The first cycle should always be test only- after that, you’re gonna need another compound. Or you will accomplish nothing
To add to this: the more anabolics used, the more the androgen receptors are targeted. You’re not going to get a full 3D look on just testosterone. Testosterone and Tren? Testosterone and Deca? Testosterone and EQ? Testosterone and *insert whatever compound here*? Yep- that will get you there. If, of course your diet and training are good
 
Also to the OP. Here is a cycle with human grade products that you can easily get from a pharma source that you can try out:
200 mg/weekTest Cyp *for estrodial*
500 DECA or 500 Primo
Last 4 weeks- 25 mg of anadrol daily
you could even replace the test with HCG….even better….you would still get the same amount of gains. Don’t be fooled. Test is not always best. Perhaps maybe if you’re looking to feel good then it is. If you’re looking to get strong, lean, and full then you should probably reconsider!
 
Care to give your thoughts on aromatase enzyme inhibitors verse selective estrogen receptor modulators for estrogen control on aromatizing steroids?

By which i mean, is it better to inhibit estrogen formation or to inhibit estrogen binding?

I mean with an AI your keeping more of the steroid from converting to estrogen, which would logically mean more bang for your buck from the AAS, but i dislike AIs because my joints always end up hurting when i use them and ive never been able to “dial in” a good dosage, they are just too damn strong. But based on your reply above it sounds like youd lean in favor of AIs over SERMs for estrogen control unless im misinterpreting what you said.
What I prefer is designing the cycle to only aromatize sufficiently for optimal anabolism, i.e., keeping E2 under 45, with a complement of compounds that synergize for the current goals (e.g., mass or prep for bodybuilders).

Then, you fall back on:
- exemestane for mitigating absolute estrogens (only necessary with higher test dosages, with athletes with high absolute levels of aromatase)
- ralox for selective ER antagonism (is usually necessary on Test cycles, and should be used with stimulating hCG/hMG [the latter being optimal but not absolutely necessary] for those who aren't committed to BnCing for life)

These compounds have better profiles for performance, in terms of joint arthralgia, have some procollagenous features, are less suppressive of IGF-I, etc.
 
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