THE MOST POWERFUL NON METHYLS

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    THE MOST POWERFUL NON METHYLS


    Hi Bros
    What do you think are the most powerful non Methyls in order of most powerful on down here is my list from research but I would like some comments from 1st hand experience. Also if you have experience lets us know on stacks or brands that have stacks.

    NON STACKS


    1.TRENBOLONE

    2.MAX LMG 13-ethyl-3-methoxy-gona-2,5(10)-diene-17-one

    3.PROPADROL 12-ethyl-3-methoxy-gona-diene-17 6-17 dihydroxyetiocholove-3-ol proponate

    4. X-TREN estra-4,9-diene-3b,17b-dione ANOTHER WAY TO WRITE THIS COMPOUND 19-norandrosta-4,9-diene-3b,17b-dione

    5. TRENADROL 17b-methoxy-Trienbolone

    6. 3-AD 2-androstenol acetate and androsterone (3-hydroxy-17-oxo-5a-androstane)

    7. BOLD200 1,4-androstadiene-3b,17b-dione

    8.ORASTAN-A, FURAZBOL 5a-androstano[2,3-c]furazan-17b-tetrahydropyranol ether

    9.ORASTAN-E,Stanozol [3,2-c]pyrazole-5alpha-etioallocholane-17b-tetrahydropyranol

    10. 11-OXO 4-androstene-3,11,17-trione

    There are some others but harder to get I put up the most easily available. Please feel free to disagree and change the order of the list or add to the list and add any wisdom you have on the topic. Thanks

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    trenbolone is an injectable steroid, not an oral designer steroid. just because these supplement companies steal the name and reputation of a compound to sell their products....doesnt mean its identical.

    its just bugs the absolute sh!t out of me when ppl call these oral "tren" products trenbolone....BECAUSE THEY ARENT THE SAME.

    #1 non-methyl = "tren"
    #2 non-methyl = Max LMG

    i wouldnt waste my money or time on anything else
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    trenbolone can be taken orally. but it isnt cost effective.
    the tren products sold now are dienolone precursors.

    he forgot 1dhea, 4dhea, and 19nordhea
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    Quote Originally Posted by jbryand101b View Post
    trenbolone can be taken orally. but it isnt cost effective.
    yes it can, but oral trenbolone is methylated and HIGHLY liver toxic
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    Quote Originally Posted by nosnmiveins View Post
    trenbolone is an injectable steroid, not an oral designer steroid. just because these supplement companies steal the name and reputation of a compound to sell their products....doesnt mean its identical.

    its just bugs the absolute sh!t out of me when ppl call these oral "tren" products trenbolone....BECAUSE THEY ARENT THE SAME.

    #1 non-methyl = "tren"
    #2 non-methyl = Max LMG

    i wouldnt waste my money or time on anything else
    I was wondering too if this was referring to orals. Also are you (OP) referring to legal (orals)? What do you mean by powerful? Pounds gained per mg?

    I agree with you Nos, I hate the "Tren" name used to market dienolone precursors. I tried to get people to call it "prodien/prodienolone" and some other names, but I guess it wasn't catchy enough...

    Too bad this thread didn't get stickied: Stop ****ing Saying 'TREN'
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    Quote Originally Posted by nosnmiveins View Post
    yes it can, but oral trenbolone is methylated and HIGHLY liver toxic
    Actually, just plain old trenbolone (17b-hydroxy-androst-4,9,11-triene-3-one) has relatively decent oral bioavailability, but since there are the much more effective injectible esters, why would one bother?
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    Tren and Bold is a good six week run! , bold is mild and both arent harsh on your liver...
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    Quote Originally Posted by Mass_69 View Post
    Actually, just plain old trenbolone (17b-hydroxy-androst-4,9,11-triene-3-one) has relatively decent oral bioavailability, but since there are the much more effective injectible esters, why would one bother?
    yup. and some like to make it into a transdermal. why ppl wont just inject to get the most out of it is beyond me
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    Non-stack, the 19-nors are most powerful hands down.
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    I'm surprised by how strong the Propadrol seems--I'm just over a week into a 61/2 week Epistane/Propadrol cycle and the Propadrol is definitely adding a lot of punch to the Epistane! This is my first time using Propadrol.

    Crowbar
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    Quote Originally Posted by nosnmiveins View Post
    yes it can, but oral trenbolone is methylated and HIGHLY liver toxic
    lol, I aint talkin about oral trenbolone. im talkin about regular trenbolone, most commonly taken orally in the pellet form.

    but trenbolone has moderate oral bioavailability, and quoted from anabolics "though not an ideal mode of delivery, can be used in this manner in adequate dosages"

    even better would be longer ester froms, like trenbolone undeconate.

    but like i said, the cost would for most, out weigh the benifits. esp when you can just inject it.

    methyl trienelone, i would never recomend to anyone. use that sh*t at your own risk.
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    Quote Originally Posted by Mass_69 View Post
    Actually, just plain old trenbolone (17b-hydroxy-androst-4,9,11-triene-3-one) has relatively decent oral bioavailability, but since there are the much more effective injectible esters, why would one bother?
    looks like you beat me to it.

    and you aint alone in the fight to get people to stop callen dienolone precursors tren, i also continue the never ending battle. it probably isn't ever going to stop.

    it's funny, cause people dont call methyl d "methyl tren" and it's just a methylated dienolone.

    edit* fixed.
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    Quote Originally Posted by crowbar46 View Post
    I'm surprised by how strong the Propadrol seems--I'm just over a week into a 61/2 week Epistane/Propadrol cycle and the Propadrol is definitely adding a lot of punch to the Epistane! This is my first time using Propadrol.

    Crowbar
    thats that stuff from est right? i've wondered if it's any good.

    how many cycles have you ran before this one?
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    19-nor for the win easy. and yes im sure almost everyone knows its not really tren. its well known its dienolone which pattrick arnold said its closer to andro.
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    jbryand, I've done ~6 AAS cycles--it's been so long now since my last one that I'd have a hard time giving an exact number. I got out when things just starting getting so fuc*in crazy, legally. This will be my 7th DS cycle.

    Yeah, I was kind of surprised by the Propadrol because I was under the impression that It was kind of a mild DS best for cutting, but the strength and agression have kind of taken me aback. I really only got aggressive on tren but I find this giving me kind of a short fuse; which is not typical for me really.

    Now I know some of you will say bull****, but my squat has increased by 30 lbs. in 1 1/2 weeks! My other lifts have increased but not like my squat. Maybe I just respond really well to this stuff, I don't know. I do know I'm buying a lot more while it's still here. I was thinking, good god, what this could do stacked with Super-Drol, or maybe better yet, because you could run both longer, P-Plex.


    Crowbar
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    Quote Originally Posted by crowbar46 View Post
    jbryand, I've done ~6 AAS cycles--it's been so long now since my last one that I'd have a hard time giving an exact number. I got out when things just starting getting so fuc*in crazy, legally. This will be my 7th DS cycle.

    Yeah, I was kind of surprised by the Propadrol because I was under the impression that It was kind of a mild DS best for cutting, but the strength and agression have kind of taken me aback. I really only got aggressive on tren but I find this giving me kind of a short fuse; which is not typical for me really.

    Now I know some of you will say bull****, but my squat has increased by 30 lbs. in 1 1/2 weeks! My other lifts have increased but not like my squat. Maybe I just respond really well to this stuff, I don't know. I do know I'm buying a lot more while it's still here. I was thinking, good god, what this could do stacked with Super-Drol, or maybe better yet, because you could run both longer, P-Plex.


    Crowbar
    hmm interesting, thanks man, i'll have to pick some up for down the road.
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    Quote Originally Posted by dpfisher View Post
    Non-stack, the 19-nors are most powerful hands down.
    There not progestines?
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    they technically arnt I have heard but DO product prolactin gyno thats why people use p5p,by,l-dopa,vitex with good results and prefer clomid and some have caber on hand when dosing 120-150mg
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    Quote Originally Posted by bigwhiteguy29 View Post
    19-nor for the win easy. and yes im sure almost everyone knows its not really tren. its well known its dienolone which pattrick arnold said its closer to andro.
    19-nor could be used to describe a plethora of compounds (but you did say "tren"). 19-nor is what most of the older members of this board used to call 19-norandrostenediol (a nandrolone precursor). These "tren" compounds are dienolone precursors, not dienolone itself. PA must have been referring to the chemical structure being similar to androstenedione, as they are the same with the addition of a double-bond at the 9(10) position. The results of the two are much different. The chemical similarities are what marketers use to refer to prodienolone as "tren" since they are the same chemically with tren(bolone) having another double-bond at the 11th position. Again, chemically similar, physically different results.

    Quote Originally Posted by bigwhiteguy29 View Post
    they technically arnt I have heard but DO product prolactin gyno thats why people use p5p,by,l-dopa,vitex with good results and prefer clomid and some have caber on hand when dosing 120-150mg
    The 19-nor structure allows them to bond easier to progesterone receptors typically giving them progesterone-like activity, which is why they are usually referred to as progestins. Progesterone and prolactin aren't even in the same class of hormone and receptors (PRG is a steroidal hormone, PRL is a peptide hormone). I haven't seen any scientific evidence that progestins cause additional prolactin production or activity.

    Quote Originally Posted by jbryand101b View Post
    looks like you beat me to it.

    and you aint alone in the fight to get people to stop callen dienolone precursors tren, i also continue the never ending battle. it probably isn't ever going to stop.

    it's funny, cause people dont call methyl d "methyl tren" and it's just a methylated dienolone precursor.
    Good analogy
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    Dienolone is actully almost identical to nandrolone in its AR (134; both are greater than test here; trenbolone is in the 170's) and PR (in the 60-70 range I think) binding affinities, and it causes the shutdown typical of nandrolone and other 19-nor steroids that interact with the progesterone receptor. It's A:A rating is 100:10 (so a Q factor of 10) and given its effectiveness, it is almost silly to compare it to andro. It's molecular structure looks almost identical to trenbolone (extra double bond I think for dienolone and that's it) which is probably why the supp companies all jumped on the "tren" bandwangon. Also, the parent compound that converts to dienolone is an active anabolic itself, just not as strong as dienolone. Reference Anabolic Pharmacology by Seth Roberts-the only book I know of that describes scientifically dienolone and its parent compound ("tren").

    Also, methyldienolone isn't a pro-anything. It is an active steroid, banned in 2004.

    Lastly, the majority of cases of gyno have nothing whatever to do with prolactin, including steroids that interact with the progesterone receptor (according to the aforementioned book which is the most technical steroid book I own), contrary to the opinions of countless bros. I am sure that many will disagree with that statement, but bro-lore has its limitations. BTW, letrozole is pretty effective at treating the nipple lump gyno and the bitch tit and enlarged nipples ("Prolactin gyno" though a misnomer) type of gyno. And letro doesn't really have anything to do with prolactin either.
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    Quote Originally Posted by dumbhick3 View Post
    It's molecular structure looks almost identical to trenbolone (extra double bond I think for dienolone and that's it) which is probably why the supp companies all jumped on the "tren" bandwangon.
    I outlined this in my last post. Trenbolone has the additional double-bond at the 11 position. For a comparision, see below:

    Nandrolone - 19-norandrost-4-ene-3-one-17b-ol
    Dienolone - 19-norandrost-4,9-diene-3-one-17b-ol
    Trenbolone - 19-norandrost-4,9,11-triene-3-one-17b-ol

    Androstenedione - androst-4-ene-3,17-dione
    Prodienolone - 19-norandrost-4,9-diene-3,17-dione

    Quote Originally Posted by dumbhick3 View Post
    Also, methyldienolone isn't a pro-anything. It is an active steroid, banned in 2004.
    This is correct.

    Quote Originally Posted by dumbhick3 View Post
    Lastly, the majority of cases of gyno have nothing whatever to do with prolactin, including steroids that interact with the progesterone receptor (according to the aforementioned book which is the most technical steroid book I own), contrary to the opinions of countless bros. I am sure that many will disagree with that statement, but bro-lore has its limitations. BTW, letrozole is pretty effective at treating the nipple lump gyno and the bitch tit and enlarged nipples ("Prolactin gyno" though a misnomer) type of gyno. And letro doesn't really have anything to do with prolactin either.
    THANK YOU!!
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    Wow looks like I am going to have to buy Seth Roberts book
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    Quote Originally Posted by dumbhick3 View Post

    Also, methyldienolone isn't a pro-anything. It is an active steroid, banned in 2004.
    yea, I have just quickly glanced at the nomenclature, so figured it was similar to m14add in that it was active by itself, but could convert.

    but at another glance, I see it is the parent compound with the 3 one 17b hydroxy group there already.

    i've thought about getting seths book, I have Llewellyn's anabolics 09, and i love it.

    im not so sure about the prolactin thing though....

    ESTROGEN, GH AND IGF-1, PROGESTERONE, & PROLACTIN

    "Estrogen and progesterone act in an integrative fashion to stimulate normal adult female breast development. Estrogen, acting through its ER a receptor, promotes duct growth, while progesterone, also acting through its receptor (PR), supports alveolar development (15). This is demonstrated by experiments in ER a knockout mice which display grossly impaired ductal development, whereas the PR knockout mice possess significant ductal development, but lack alveolar differentiation (28,6).
    Although estrogens and progestogens are vital to mammary growth, they are ineffective in the absence of anterior pituitary hormones (13). Thus, neither estrogen alone nor estrogen plus progesterone can sustain breast development without other mediators, such as GH and IGF-1, as confirmed by studies involving the administration of estrogen and GH to hypophysectomized and oophorectomized female rats, which resulted in breast ductal development. The GH effects on ductal growth are mediated through stimulation of IGF-1. This is demonstrated by studies of estrogen and GH administration to IGF-1 knockout rats that showed significantly decreased mammary development when compared to age-matched IGF-1- intact controls. Combined estrogen and IGF-1 treatment in these IGF-1 knockout rats restored mammary growth. (23, 40). In addition, Walden et al. demonstrated that GH-stimulated production of IGF-1 mRNA in the mammary gland itself, suggesting that IGF-1 production in the stromal compartment of the mammary gland acts locally to promote breast development (49). Furthermore, other data indicates that estrogen promotes GH secretion and increased GH levels, stimulating the production of IGF-1, which synergizes with estrogen to induce ductal development.

    Like estrogen, progesterone has minimal effects in breast development without concomitant anterior pituitary hormones; again indicating that progesterone interacts closely with pituitary hormones. For example, prolonged treatment of dogs with progestogens such as depot medroxyprogesterone acetate or with proligestone caused increased GH and IGF-1 levels, suggesting that progesterone may also have an effect on GH secretion (33). In addition, clinical studies have correlated maximal cell proliferation to specific phases in the female menstrual cycle. For example, maximal proliferation occurs not during the follicular phase when estrogens reach peak levels and progesterone is low (less than 1 ng/mL [3.1nmol}), but rather, it occurs during the luteal phase when progesterone reaches levels of 10-20 ng/mL (31- 62nmol) and estrogen levels are two to three times lower than in the follicular phase (42). Furthermore, immunohistochemical studies of ER and PR showed that the highest percentage of proliferating cells, found almost exclusively in the type 1 lobules, contained the highest percentage of ER and PR positive cells (42). Similarly, there is immunocytological presence of ER, PR, and androgen receptors (AR) in gynecomastia and male breast carcinoma. ER, PR and AR expression was observed in 100% (30/30) of gynecomastia cases (41). Given these data and the fact that PR knockout mice lack alveolar development in breast tissue, it appears as if progesterone, analogous to estrogen, may increase GH secretion and act through its receptor on mammary tissue to enhance breast development, specifically alveolar differentiation (28, 18).

    Prolactin is another anterior pituitary hormone integral to breast development. Prolactin is not only secreted by the pituitary gland but may be produced in normal mammary tissue epithelial cells and breast tumors. (44, 25). Prolactin stimulates epithelial cell proliferation only in the presence of estrogen and enhances lobulo-alveolar differentiation only with concomitant progesterone. "

    it looks like it isn't any one thing, but a combination of things that enable the growth of breast tissue. I found this in a recent thread a board admin posted in responce to all the got gyno for w/e reason threads, in hopes of clearing up peoples understanding of why gyno happens. i think it's too complicated for most, and long.
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    Quote Originally Posted by Mass_69 View Post
    19-nor could be used to describe a plethora of compounds (but you did say "tren"). 19-nor is what most of the older members of this board used to call 19-norandrostenediol (a nandrolone precursor). These "tren" compounds are dienolone precursors, not dienolone itself. PA must have been referring to the chemical structure being similar to androstenedione, as they are the same with the addition of a double-bond at the 9(10) position. The results of the two are much different. The chemical similarities are what marketers use to refer to prodienolone as "tren" since they are the same chemically with tren(bolone) having another double-bond at the 11th position. Again, chemically similar, physically different results.

    The 19-nor structure allows them to bond easier to progesterone receptors typically giving them progesterone-like activity, which is why they are usually referred to as progestins. Progesterone and prolactin aren't even in the same class of hormone and receptors (PRG is a steroidal hormone, PRL is a peptide hormone). I haven't seen any scientific evidence that progestins cause additional prolactin production or activity.

    Good analogy
    Thank you for this post. I was screaming at the pc and banging my had on my keyboard while reading through this thread...a lot of wreckless posting going on
    RcB Since 09-06-2011 20:55 EST, Post 49
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    Quote Originally Posted by stxnas View Post
    Thank you for this post. I was screaming at the pc and banging my had on my keyboard while reading through this thread...a lot of wreckless posting going on
    i like to post how I drive, wreckless and fast..... expect mistakes to be made.
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    Quote Originally Posted by jbryand101b View Post
    i've thought about getting seths book, I have Llewellyn's anabolics 09, and i love it.

    im not so sure about the prolactin thing though....

    ESTROGEN, GH AND IGF-1, PROGESTERONE, & PROLACTIN

    "Estrogen and progesterone act in an integrative fashion to stimulate normal adult female breast development. Estrogen, acting through its ER a receptor, promotes duct growth, while progesterone, also acting through its receptor (PR), supports alveolar development (15). This is demonstrated by experiments in ER a knockout mice which display grossly impaired ductal development, whereas the PR knockout mice possess significant ductal development, but lack alveolar differentiation (28,6).
    Although estrogens and progestogens are vital to mammary growth, they are ineffective in the absence of anterior pituitary hormones (13). Thus, neither estrogen alone nor estrogen plus progesterone can sustain breast development without other mediators, such as GH and IGF-1, as confirmed by studies involving the administration of estrogen and GH to hypophysectomized and oophorectomized female rats, which resulted in breast ductal development. The GH effects on ductal growth are mediated through stimulation of IGF-1. This is demonstrated by studies of estrogen and GH administration to IGF-1 knockout rats that showed significantly decreased mammary development when compared to age-matched IGF-1- intact controls. Combined estrogen and IGF-1 treatment in these IGF-1 knockout rats restored mammary growth. (23, 40). In addition, Walden et al. demonstrated that GH-stimulated production of IGF-1 mRNA in the mammary gland itself, suggesting that IGF-1 production in the stromal compartment of the mammary gland acts locally to promote breast development (49). Furthermore, other data indicates that estrogen promotes GH secretion and increased GH levels, stimulating the production of IGF-1, which synergizes with estrogen to induce ductal development.

    Like estrogen, progesterone has minimal effects in breast development without concomitant anterior pituitary hormones; again indicating that progesterone interacts closely with pituitary hormones. For example, prolonged treatment of dogs with progestogens such as depot medroxyprogesterone acetate or with proligestone caused increased GH and IGF-1 levels, suggesting that progesterone may also have an effect on GH secretion (33). In addition, clinical studies have correlated maximal cell proliferation to specific phases in the female menstrual cycle. For example, maximal proliferation occurs not during the follicular phase when estrogens reach peak levels and progesterone is low (less than 1 ng/mL [3.1nmol}), but rather, it occurs during the luteal phase when progesterone reaches levels of 10-20 ng/mL (31- 62nmol) and estrogen levels are two to three times lower than in the follicular phase (42). Furthermore, immunohistochemical studies of ER and PR showed that the highest percentage of proliferating cells, found almost exclusively in the type 1 lobules, contained the highest percentage of ER and PR positive cells (42). Similarly, there is immunocytological presence of ER, PR, and androgen receptors (AR) in gynecomastia and male breast carcinoma. ER, PR and AR expression was observed in 100% (30/30) of gynecomastia cases (41). Given these data and the fact that PR knockout mice lack alveolar development in breast tissue, it appears as if progesterone, analogous to estrogen, may increase GH secretion and act through its receptor on mammary tissue to enhance breast development, specifically alveolar differentiation (28, 18).

    Prolactin is another anterior pituitary hormone integral to breast development. Prolactin is not only secreted by the pituitary gland but may be produced in normal mammary tissue epithelial cells and breast tumors. (44, 25). Prolactin stimulates epithelial cell proliferation only in the presence of estrogen and enhances lobulo-alveolar differentiation only with concomitant progesterone. "

    it looks like it isn't any one thing, but a combination of things that enable the growth of breast tissue. I found this in a recent thread a board admin posted in responce to all the got gyno for w/e reason threads, in hopes of clearing up peoples understanding of why gyno happens. i think it's too complicated for most, and long.
    jbry, is that quoted from W. Llewelyn's book? Here's the full article: http://www.endotext.org/male/male14/male14.html

    You're right though, gyno does seem to be "the perfect storm" of hormonal changes.
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    Quote Originally Posted by Mass_69 View Post
    jbry, is that quoted from W. Llewelyn's book? Here's the full article: http://www.endotext.org/male/male14/male14.html

    You're right though, gyno does seem to be "the perfect storm" of hormonal changes.

    na, I got that from the thread a board admin posted. i bumped it. i'll post the link.
    GYNECOMASTIA: ETIOLOGY, DIAGNOSIS, AND TREATMENT

    your link must be where he got it. lol.
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    what about propadrol. ive never used it but it looks like a good non methyl.
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    Quote Originally Posted by bigwhiteguy29 View Post
    19-nor for the win easy. and yes im sure almost everyone knows its not really tren. its well known its dienolone which pattrick arnold said its closer to andro.
    Would 1-T TREN by PP fall under to this 19-nor category?

    Edit: and yes i realize it contains "19-Norandrosta-4,9-diene-3,17-dione", a precursor to Dienelone which has the words 19-Nor, but I wasn't sure if this specific chemical was included under the category of 19-nor you were talking about.
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    tren.. get it while ya can
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    Gyno is probably caused in most cases by an ideal environment for breast growth/cell proliferation, and the factors are numerous. I think that people just go overboard on the whole prolactin thing sometimes. Like it is the devil-so go buy some cabergoline and risk heart fibrosis on top of the strain steroids already put on your heart, just to be safe. I think it can contribute, but a lot of cofactors need to be present too.

    I have Seth's and Lewellyn's book-they complement each other nicely. Seth's is much more technical while Lewellyn's is more practical (though both include sample stacks, but again, Seth explains why these two are a good match or a bad match in pharmacological detail).

    Seth does make the very astute observation that the ancillary drugs used by bodybuilders are often more deleterious to one's health than any of the AASs. Likewise for IGF-1 peptides-they seem to activate oncogenes faster than AAS and definitely cause more organ growth than AAS also (and by organ, I don't mean your penis-I mean your internal organs). But hey, they aren't illegal, so go get some! Don't forget the "cab" while you are there, LOL!
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