Favorite steroids to use and why

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.
What's the reasoning for using ralox with hcg? Not questioning just wanting to learn.
 
What's the reasoning for using ralox with hcg? Not questioning just wanting to learn.
This is a VERY good question, and where I have to basically deviate from the science which tells us that, on one hand, SERMs function as ER antagonists at hypothalamus/pituitary therefore increasing LH & T secretion versus hCG (and hMG) stimulating LH (and FSH)... thus having the same end result via different mechanisms.

I have what I think of as a method for balancing the sides (e.g., acne, estrogens from hCG vs. lipids, joint pain with SERMs) and the different functions of these compounds. For some people, all that is needed is a SERM, then perhaps post-cycle hCG/hMG + exemestane (this makes a great deal of sense). Others, respond poorly to all SERMs in terms of tradeoffs, so may use a low-dose AI + hCG throughout. Some people may actually be served by balancing sides across the different compounds. This effectively boils down to being methodical bro-science. I believe it's a blind spot, though, to ignore these informal experiments.
 
when I added 200 primo to my 750 test I almost changed overnight. Test only is definitely overrated
Thank you, just the kind of feedback I’m looking for. I will never shit on testosterone, it is the bio identical anabolic male hormone and will always be the base of any cycle / blast I run. I’m all for running test at a high dose up to 700-750 (diminishing returns after that) and other compounds get sprinkled on top.

I totally get your point Conner about test alone is limiting but I would not speak of test like it’s just a step above a good supplement like creatine.
 
Thank you, just the kind of feedback I’m looking for. I will never shit on testosterone, it is the bio identical anabolic male hormone and will always be the base of any cycle / blast I run. I’m all for running test at a high dose up to 700-750 (diminishing returns after that) and other compounds get sprinkled on top.

I totally get your point Conner about test alone is limiting but I would not speak of test like it’s just a step above a good supplement like creatine.
I hate to say this because it sounds like such a troll comment; but I honestly had better results with vitamins, protein and creatine as opposed to testosterone. Sadly.
 
I hate to say this because it sounds like such a troll comment; but I honestly had better results with vitamins, protein and creatine as opposed to testosterone. Sadly.
Hhah come on bro! I think you mean the sides you got from high test alone made it less effective as an aesthetic drug, right? RIGHT? I mean, if you use a low test base in your other cycles, that test is doing a lot.
 
@VenomYo

Here's what I wrote up as a quick profile on Epistane:

Epistane [Profile by Type-IIx]

Synonyms:
2α,3α-epithio-17α-methyl-5α-androstan-17β-ol; 2α,3α-epithio-17α-methyl-5α-etioallocholan-17β-ol
17α-methylepithiostanol; methepitiostane; Havoc; Epi-Strong

Potent orally active androgen, with pronounced anabolism relative to low androgenicity; non-aromatizable, non-5α-reducible (as it is already 5α-reduced).

Structurally distinguishable from 5α-DHT by the replacement of the 3-keto with 2,3 alpha-epithio (a sulphur atom spans C2 and C3).

According to the flawed Hershberger Assay, relative to methyltestosterone its anabolic/androgenic ratio is 1,100/91.

[140] demonstrates pyrolysis and metabolic dethionylation to produce Madol (though it is not strictly a prohormone; rather it is active)

Epistane is an orally active, potent androgen. Some of its activity is due to in vivo conversion to Madol as depicted:
Proposed-metabolism-of-Epistane-to-Madol-Figure.MesoRX.png

Its non-methylated counterpart (epitiostanol) is used (or has been used) clinically in Japan. At a 20mg weekly dosage epitiostanol, considered an anti-estrogen agent, was more effective than Drostanolone (Masteron) (at 50mg weekly) in treatment of gynecomastia. Epitiostanol also has demonstrated efficacy in treatment-resistant, relapsing stage IV metastatic breast cancer, as an alternative form of endocrinotherapy faced with relapse.


In "Effects of 2alpha,3alpha-epithio-5alpha-androstan-17beta-ol (epitiostanol) on hypothalamo-pituitary-gonadal axis in humans," the mechanisms proposed for its anti-gynecomastic action is distinguished from SERMs by the remark, "...results seem to suggest that epitiostanol has clinical effects at the target organ level rather than via the suppression of gonadotropin secretion." (similar again to Masteron's proposed mechanisms)

Practical
Frequent complaints of joint pain ("dry joints"), highly hepatotoxic. Cycles are typically 30mg - 40mg daily for 4 - 6 weeks, followed by a SERM PCT to prevent rebound gynecomastia.
 
Yeah, we all know how crappy those golden era guys looked because they didn't use testosterone.
 
Hhah come on bro! I think you mean the sides you got from high test alone made it less effective as an aesthetic drug, right? RIGHT? I mean, if you use a low test base in your other cycles, that test is doing a lot.
I credit my success to Nandrolone, Tren, EQ and Anavar. The testosterone did little for me. Hence why I run it so low. I try not to stay far away from those compounds now *except Anavar * but without them, I wouldn’t have made it where I did. Not that I’m a crazy physique guy but I’m pleased.
 
Yeah, we all know how crappy those golden era guys looked because they didn't use testosterone.
Correct. An off-season in the golden era was
Dbol
Primo
Deca

no test. Test was viewed as a dirty compound because of it being more androgenic than anabolic. How in the world that view changed is beyond me. It still holds true. Testosterone may be bio identical; but I truly can say I got better results from LGD and RAD 140 way back when the Sarms craze was going around
 
I credit my success to Nandrolone, Tren, EQ and Anavar. The testosterone did little for me. Hence why I run it so low. I try not to stay far away from those compounds now *except Anavar * but without them, I wouldn’t have made it where I did. Not that I’m a crazy physique guy but I’m pleased.
What approx. % of your cycles have been test-free?
 
only 1 has been test free. Deca, primo and Dbol. I had pretty good success with it. However, Dbol was not a sustainable replacement long term Other cycles have had very low test.
And I'd say that I think deca provides enough aromatization even at <1g weekly dosages for all the benefits, so that covers everything (Deca, Primo, and Dbol). I think Deca/Primo/Dbol is a great cycle. I wouldn't be so dismissive of test's effects in your other cycles even at low dosages is all. If you look at my post history you'll see me basically arguing what you are, that test is great at lower dosages but its aromatic function can easily be supplanted by deca's (or rhGH, unless JUST running straight tren only, in which case IGF-I might actually drop precipitously). I know your argument is more that "Test is a shitty anabolic," and I'd just modify that a bit, test is a damn GOOD anabolic, but there are great, perhaps even superior, cycles to the test base cycle.
 
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.
Excellent information! Thank you for taking the time, @Type-IIx
 
@VenomYo

Here's what I wrote up as a quick profile on Epistane:

Epistane [Profile by Type-IIx]

Synonyms:
2α,3α-epithio-17α-methyl-5α-androstan-17β-ol; 2α,3α-epithio-17α-methyl-5α-etioallocholan-17β-ol
17α-methylepithiostanol; methepitiostane; Havoc; Epi-Strong

Potent orally active androgen, with pronounced anabolism relative to low androgenicity; non-aromatizable, non-5α-reducible (as it is already 5α-reduced).

Structurally distinguishable from 5α-DHT by the replacement of the 3-keto with 2,3 alpha-epithio (a sulphur atom spans C2 and C3).

According to the flawed Hershberger Assay, relative to methyltestosterone its anabolic/androgenic ratio is 1,100/91.

[140] demonstrates pyrolysis and metabolic dethionylation to produce Madol (though it is not strictly a prohormone; rather it is active)

Epistane is an orally active, potent androgen. Some of its activity is due to in vivo conversion to Madol as depicted:
View attachment 156732

Its non-methylated counterpart (epitiostanol) is used (or has been used) clinically in Japan. At a 20mg weekly dosage epitiostanol, considered an anti-estrogen agent, was more effective than Drostanolone (Masteron) (at 50mg weekly) in treatment of gynecomastia. Epitiostanol also has demonstrated efficacy in treatment-resistant, relapsing stage IV metastatic breast cancer, as an alternative form of endocrinotherapy faced with relapse.


In "Effects of 2alpha,3alpha-epithio-5alpha-androstan-17beta-ol (epitiostanol) on hypothalamo-pituitary-gonadal axis in humans," the mechanisms proposed for its anti-gynecomastic action is distinguished from SERMs by the remark, "...results seem to suggest that epitiostanol has clinical effects at the target organ level rather than via the suppression of gonadotropin secretion." (similar again to Masteron's proposed mechanisms)

Practical
Frequent complaints of joint pain ("dry joints"), highly hepatotoxic. Cycles are typically 30mg - 40mg daily for 4 - 6 weeks, followed by a SERM PCT to prevent rebound gynecomastia.
So, its a androgenic. Mast causes alot of shedding for some. Does this?
 
Favourite steroids now I'm focosing on health - low dose test and primo or deca.

Favourite steroids to build muscle and change my physique quickly - test, tren and hgh. Nothing comes close to that stack imo.
 
Dianabol.

Why?
- intense vasodilation, just taking it on a non workout day i get pumped
- works from day 1, heck, i notice it just 1 hour after taking it
- gets out of the body quick too
- tons of glycogenesis, full as fawk
- boosts my appetite
- feels wonderful
- cheap, readily available, and rarely faked
- massive boost in strength even from day 1
- i retain all the strength gains and a surprising amount of the weight gains post-use

Biggest cons are the estro, but thats pretty easy to mitigate. Gives me an uptick in zits usually on my back, but its nothing extreme. Other than that i tolerate it very well.
Now you have me wanting to try dbol lol. Its just something I never tried. I always like Anavar and that's all I did (besides proviron if that counts). How do you mitigate the estrogen? By watching football, eating wings, and fucking your wife and her best friend? That's where I'm thinking I would start

/s

I just copped some stuff so I'm good for a while.

My favorites have been test, NPP, and MENT+mast p. I haven't ventured it into many orals before nor have I really stayed from what works for me.
 
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Correct. An off-season in the golden era was
Dbol
Primo
Deca

no test. Test was viewed as a dirty compound because of it being more androgenic than anabolic. How in the world that view changed is beyond me. It still holds true. Testosterone may be bio identical; but I truly can say I got better results from LGD and RAD 140 way back when the Sarms craze was going around


My understanding of why guys say you need test as a base for a cycle stems from a belief that only test can fulfill the role of test.
Now you have me wanting to try dbol lol. Its just something I never tried. I always like Anavar and that's all I did (besides proviron if that counts). How do you mitigate the estrogen? By watching football, eating wings, and fucking your wife and her best friend? That's where I'm thinking I would start

/s

I just copped some stuff so I'm good for a while.

My favorites have been test, NPP, and MENT+mast p. I haven't ventured it into many orals before nor have I really stayed from what works for me.

I just take tamoxifen but i hear arm wrestling can work too. In the past i played with exemestane but it seemed to destroy my estro so i stay away from AIs. Basically killed my libido and made my joints feel like they were rusted. It also helps that im rather lean and dont seem prone to gyno. If you got a lot of body fat i think you are much more prone to high estrogen from aromatizing steroids and also gyno formation, so maybe in those guys an AI is a necessity. Experience has led me to prefer a SERM as i get less issues verse AIs.

Dianabol is great, its very popular for a reason. The liver toxicity seems way over exaggerated but i think that has alot to do with a persons genetics too, some ppl just have crappy genes.
 
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