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Tren alone?


Jul 15, 2010
A friend of mine says that when hes PCT he uses tren still, sometimes just uses tren when he doesnt wanna be on test and orals.

I dont know much about this so can someone chim in on what hes doing. He's pretty damn massive....
I have never heard of anyone doing this that knows what they are doing. His libido has to be nowhere near. I don't see any reason why someone would do this exspecially on PCT cause what would be the use of PCT? I'm no genius but i'd say don't follow your friends lead IMO.
PCT and tren make no sense.... but I have heard of people cruising on low doses of tren for HRT and I have a huge medical study saved somewhere on my computer regarding the use of trenbolone as an alternative to testosterone for HRT.
I'd be really interested in reading that Tren/HRT study if you could post a link here, Bro.
Some people can run Tren alone. Emeric has talked about it.

To Nemesis. For PCT? Laugh at that guy. If he's using Tren, he's not in PCT! LOL!

I can just hear that conversation:
Hey you look great!
What are you doing for PCT?
Tren,Dbol,Aromasin, 'Lil 500mg Test... And it feels like I didn't even come off!!

Last edited:
I would never recommend this. If you are ever considering running one substance solo make it test hands down.
PCT and tren make no sense.... but I have heard of people cruising on low doses of tren for HRT and I have a huge medical study saved somewhere on my computer regarding the use of trenbolone as an alternative to testosterone for HRT.

I would like to see this study too if you can find it.
Tren with PCT doesn't make a whole lot of sense to me. Would love to see that article tho.
What he is doing is not PCT. He is just running tren in between cycles. If he is going to blast and cruse he should be using test to cruse with .
Sorry I didn't realize this thread got moved...

This study basically states the differences in androgen receptor binding of testosterone/DHT/estrogen from trenbolone and its metabolites. It proposes the possibility of it being used as an alternative to to testosterone because of its lack of DHT or Estrogen metabolism. Trenbolone being extremely androgenic does have a very positive effect on libido which is cancelled out by its progesterone and prolactin production (especially prolactin), this study makes me wonder if at a significantly low dose (35-75mgs/wk) trenbolone could be equally as androgenic and more anabolic than testosterone, yet have little to no progesteronic or prolactin effects, all without DHT or estrogen, thus prostate safe! Its all speculation, but it would be the holy grail of HRT!
Steroids. 2010 Jun;75(6):377-89. Epub 2010 Feb 4.

Tissue selectivity and potential clinical applications of trenbolone (17beta-hydroxyestra-4,9,11-trien-3-one): A potent anabolic steroid with reduced androgenic and estrogenic activity.
Yarrow JF, McCoy SC, Borst SE.

Geriatric Research, Education & Clinical Center, VA Medical Center, Gainesville, FL 32608, United States.

1. Introduction
Testosterone, and its more potent metabolites, dihydrotestosterone (DHT) and estradiol (17â-E2), are known to influence the development and maintenance of numerous tissues, including skeletal muscle [1], bone [2], adipose tissue [3], and sex-organs [4]. In males, reduced testosterone (i.e., hypogonadism) induces losses in skeletal muscle mass and bone mineral density (BMD) and increases adiposity [5]. However, administration of testosterone at replacement doses results in only minor improvements in skeletal muscle mass and strength in hypogonadal older men [6]. In contrast, administration of supraphysiological doses of testosterone results in robust increases in skeletal muscle mass and BMD and reductions in adiposity in both humans [7], [8], [9], [10], [11], [12], [13], [14], [15], [16], [17] and [18] and animals [19], [20] and [21], but also results in a variety of adverse events, of which prostate enlargement and polycythemia appear to be most prevalent [22]. Alternative pharmacological treatments such as selective androgen receptor modulators (SARMs) [23] or combined treatment with high-dose testosterone plus 5á reductase inhibitors (e.g., finasteride or dutasteride) [7], [19], [20] and [24] have been proposed as a means of producing the desired anabolic effects with a lower incidence of adverse effects. Our main objective is to review current research related to the potent anabolic steroid 17â-hydroxyestra-4,9,11-trien-3-one (trenbolone; 17â-TBOH), especially its SARM-like properties that may make it beneficial for the treatment of several clinical conditions [25] and [26]. Additionally, we will offer brief overviews on androgen signaling and on the recent developments with SARMs.

2. Androgen receptor signaling
Classical, or genomic, androgen signaling begins with binding of testosterone or DHT to cytosolic androgen receptors (ARs) and ultimately results in altered gene expression. Most of the familiar effects of androgens on muscle, bone, and male sexual development are genomic effects which require the synthesis of new protein; thus, they may take days to months to manifest. More recently, rapid non-genomic testosterone signaling has been discovered [27] which is mediated by cell-surface, G-protein (GP) coupled receptors [28]. An example of non-genomic signaling is the rapid, testosterone-induced release of calcium (Ca2+) from intracellular stores occurring in mouse IC-21 macrophages [28]. The non-genomic, actions of testosterone are not inhibited by classical androgen blockers such as cyproterone and flutamide, suggesting that the genomic and non-genomic effects of androgens may be quite different. For example, we [29] and others [30] have shown that long-term administration of testosterone to male rats confers cardioprotection against ischemia/reperfusion (IR) injury. However, when testosterone is added in vitro to the working heart preparation, it worsens IR injury [31].

The genomic effects of androgens occur through two distinct pathways. In the first pathway, binding of androgens to cytosolic ARs cause ARs to translocate to the nucleus and bind to chromosomal DNA as homodimers [32] (Fig. 1). The specific regions of DNA that bind ARs are called hormone response elements (HREs) and they regulate the transcription of specific genes, producing androgenic effects. In the second pathway, the actions of androgens are mediated by interaction of ARs with the Wnt/â-catenin pathway. Wnts are a family of secreted glycoproteins that regulate differentiation in a wide variety of tissues. Canonical Wnt/â-catenin signaling involves binding of Wnt to the cell-surface frizzled receptor (FZ), which through its interactions with Axin, Frat-1 and Dsh, results in the inhibition of glycogen synthase kinase-3 (GSK3). GSK3 phosphorylates â-catenin, marking it for proteasomal degradation. As a result, inhibition of GSK3 results in the accumulation of â-catenin in the cytosol and increased translocation of â-catenin into the nucleus, where it interacts with transcriptional regulators to alter gene expression [33]. It is hypothesized that androgen signaling bypasses the canonical Wnt pathway by interacting with downstream Wnt effectors [34] to stimulate the commitment of mesenchymal pluripotent cells to the myogenic line and to inhibit their commitment to the adipogenic line [3]. By this mechanism, androgens increase the number of muscle satellite cells [35]. In culture, androgens have been shown to induce translocation of â-catenin to the nucleus in mouse 3T3 preadipocytes and inhibit their differentiation into mature adipocytes [34]. Wnt/â-catenin signaling has also been implicated in androgen-induced masculinization of external genitalia [4].

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Fig. 1. Androgen receptor signaling pathways. A = androgen, AR = androgen receptor, Ca2+ = calcium, FZ = frizzled receptor, GP = G protein, GSK-3 = glycogen synthase kinase 3, HRE = hormone response element, PLC = phospholipase C, SR = sarcoplasmic reticulum, TCF = T cell factor, LEF = lymphoid enhancer factor 1, Wnt = Wingless-Int.

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The metabolism of testosterone also plays an important role in its actions. Testosterone may be converted to DHT by either 5á reductase isoenzyme [36] and to 17â-E2 by aromatase [37]. Tissues expressing 5á reductase include the prostate, testes, accessory sex organs, beard and scalp, sebaceous glands, liver, brain, and skin [38] and in these tissues the effects of circulating testosterone are amplified by two known mechanisms. First, DHT has an approximate 3-fold greater affinity for the AR than does testosterone [39]. Second conversion of testosterone to DHT prolongs the androgen action because testosterone can be converted to the weaker androgen androstenedione, while DHT maintains a longer presence [36]. Aromatization of testosterone occurs within specific tissues (e.g., bone and brain) and systemically in some species [40] and [41]. In men, significant systemic aromatization also occurs in adipose tissue [42] and because of the resulting elevation of serum 17â-E2, may cause adverse effects (e.g., fluid retention, gynecomastia, and worsening of sleep apnea) in obese men receiving testosterone [43]. Thus, the biological effects associated with testosterone may result from classic AR mediated pathways, interactions with the Wnt/â-catenin pathway, or from AR or ER activation following conversion of testosterone to DHT or 17â-E2, respectively.

3. Recent advances in SARMs
Selective androgen receptors modulators (SARMs) are a class of drugs that have action in some tissues expressing ARs and reduced action in others [44]. One of the key goals in the development of SARMs has been to find orally available agents that have anabolic effects on muscle, bone, and erythropoiesis, but that do not cause prostate enlargement or other common adverse events associated with supraphysiological testosterone administration [23]. The name SARMs is analogous to the older drug class of selective estrogen receptor modulators (SERMs), which act as agonists in some tissues and antagonists in others [45]. SARMs are under development in many major pharmaceutical firms as a potential means of treating the symptoms associated with hypogonadism and various muscle and bone wasting conditions [23] but much of the work defining their mechanism of action and structure-activity relationships has not been published. Much of the pioneering work in developing non-steroidal SARMs was done at Ligand Pharmaceuticals and at the University of Tennessee [46] and [47] where the first generation of SARMs including S1 and S4 were developed [48]; both of which prevent atrophy of the levator ani muscle without significant prostate enlargement in a castrated rat model [49]. The following SARMs are leading candidates in each of the major chemical classes. LGD2226 is quinolinone analog, developed by Ligand Pharmaceuticals [50]. S4 is an aryl proprionamide analog developed by Gao and coworkers [49]. BMS564929 is a hydantoin analog developed by Bristol-Myers Squibb [51]. S40503 is a tetrahydro-quiniline analog developed by Kaken Pharmaceuticals [52]. Each has been shown to have strong anabolic actions in skeletal muscle and bone with partial agonist activity in the prostate [44]. Although, the non-steroidal SARMs are a chemically diverse group of compounds, in many cases, their tissue selectivity may derive from the drug not being a substrate for the 5á reductase and/or aromatase enzymes [53].

Testosterone is not effective when administered orally due to a high liver first-pass effect [54] and is readily 5á reduced or aromatized in a variety of tissues. In contrast, some orally available synthetic testosterone analogs may have SARM-like activity. For example, oxandrolone (17-á methyl-DHT) is not a substrate for aromatase [53]. Similarly, nandrolone (19-nortestosterone) is 5á reduced, but to a relatively weak androgen, dihydronandrolone, and is a poor substrate for aromatase [55]. However, both nandrolone and oxandrolone cause liver toxicity at high doses. Conversely, 17â-TBOH (trenbolone) has a low oral bioavailability (because it is not methylated at the 17á position), but may have SARM-like properties considering that it is not a substrate for 5á reductase and may not be a substrate for aromatase. The toxicity of 17â-TBOH has not been scientifically studied in humans, but anecdotally has been reported to have a low potential for liver toxicity because this drug is generally administered intramuscularly.
4. 17â-TBOH metabolism
17â-acetoxyestra-4,9,11-trien-3-one (17â-TBOH-acetate) is a highly potent anabolic androgenic steroid which is primarily used legally as a growth promoting agent in ******** livestock production within the US [56] either alone, as Finaplix (Intervet, Inc., Millsboro, DE), or in combination with 17â-E2, as Revalor (Intervet, Inc., Millsboro, DE), or 17â-E2-benzoate, as Synovex (Wyeth, Madison, NJ) [57]. Following administration, 17â-TBOH-acetate is rapidly converted to the biologically active steroid 17â-TBOH [58] which, along with its metabolites, are included on the World Anti-Doping Association (WADA) prohibited substance list [59] due to their potential ability to augment skeletal muscle mass and improve athletic performance. As such, a variety of testing methods have been proposed to detect the presence of 17â-TBOH or its metabolites in human urine or blood [60], [61], [62], [63], [64], [65], [66], [67], [68] and [69]; although, evaluation of these methods is beyond the scope of this review.

Most evidence regarding the in vivo mammalian metabolism of 17â-TBOH is derived from studies on livestock and rodents [58], [70] and [71]; however, several studies have evaluated 17â-TBOH metabolism in humans [68] and [72]. Some variation in the in vivo metabolism of 17â-TBOH exists among mammalian species [58] and [68], but the primary metabolites are 17â-hydroxy- and 17-oxo-metabolites of trenbolone in rodents or 17á-hydroxy-metabolites of trenbolone in ruminants [58]. Similarly, in humans, ingested 6,7-3H labeled 17â-TBOH is primarily excreted intact, as 17â-TBOH, as the 17á epimer (epitrenbolone; 17á-TBOH) or as trendione (TBO) (Fig. 2) [68]. In addition, several yet to be identified polar metabolites of 17â-TBOH have also been detected in human urine, albeit in much lower concentrations than the primary metabolites previously listed [68]. 17â-TBOH has a greater affinity for the AR than any of its primary metabolites [39] and [73], suggesting that biotransformation of 17â-TBOH reduces the biological activity of this steroid [26] and [68]. This is in contrast to testosterone, which undergoes irreversible 5á reduction [36] or aromatization [37] and [74] to the more potent DHT and 17â-E2.

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Fig. 2. Structures of trenbolone and it primary metabolites in humans, epitrenbolone and trendione, along with testosterone and its metabolites dihydrotestosterone and estradiol. 17â-TBOH = trenbolone, 17á-TBOH = epitrenbolone, TBO = trendione, DHT = dihydrotestosterone, 17â-E2 = estradiol.

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4.1. 17â-TBOH and 5á reductase
Despite its structural similarities to testosterone, 17â-TBOH does not undergo 5á reduction due to the presence of a 3-oxotriene structure, which prevents A ring reduction (Fig. 2) [58]. In fact, 17â-TBOH undergoes biotransformation to less biologically active androgens [26] and [68], similar to other anabolic androgenic steroids, such as 19-nortestosterone [55]. Indirect evidence indicates this is true, as 17â-TBOH administration has been shown to reduce prostate mass in growing male rodents when compared with control animals [75]. Similarly, 17â-TBOH exerts less pronounced effects than testosterone in androgen-sensitive tissues which express the 5á reductase enzyme including the prostate and accessory sex-organs [25], [26], [36], [76], [77], [78], [79] and [80], despite the fact that 17â-TBOH binds to the human AR [26] and [39], along with ARs of various model species [26], [81] and [82], with approximately three times the affinity of testosterone. Despite its inability to undergo 5á reduction, 17â-TBOH remains highly anabolic, evidenced by equal or greater growth in the levator ani skeletal muscle (an androgen responsive tissue which lacks the 5á reductase enzymes), compared to testosterone [25], [26], [76], [77], [78], [79], [80] and [83]. Thus while testosterone exerts enhanced effects in tissues expressing 5á reductase, 17â-TBOH exerts equal effects in those tissues expressing 5á reductase (e.g., prostate and accessory sex-organs) vs. those not (e.g., skeletal muscle) [36]. Taken together, these reports indicate that 17â-TBOH produces a ratio of anabolic:androgenic effects that may be favorable compared to the effects of testosterone. However, we are unaware of any paper that has reported the effects of 17â-TBOH administration on the growth of androgen-sensitive tissues in humans.
4.2. 17â-TBOH and aromatase
17â-TBOH and other C19 norandrogens [84] are reported to not be substrates for the aromatase enzyme [85] and [86] and to be relatively non-estrogenic [87] and [88]; although some debate exists regarding 19-nortestosterone (a C19 norandrogen) to undergo aromatization and induce estrogenic effects [84] and [89]. In vitro bioassays and cell culture experiments demonstrate that 17â-TBOH and its metabolites have a very low binding affinity for ERs and have low estrogenic activity with approximately 20% of the efficacy of 17â-E2 [87]. Reports also suggest that 17â-TBOH reduces serum 17â-E2 concentrations in vivo [81], [90] and [91], inhibits estrus in ovariectomized estrogen-treated female rats [92], and exerts a variety of anti-estrogenic effects [92], perhaps through hypothalamic feedback inhibition of the production of testosterone (a substrate necessary for endogenous 17â-E2 biosynthesis) [93] and [94]. Additionally, in various fish models, environmental exposure to 17â-TBOH downregulates brain CYP19B (aromatase B) and upregulates gonadal CYP19A (aromatase A) expression in females, but not males [95] and [96], while reducing tissue concentrations and tissue-specific gene expression of vitellogenin (VTG), a protein found in oviparous animals which is positively associated with exposure to estrogenic compounds, in both sexes [81], [88], [93], [94], [95], [96], [97], [98], [99], [100] and [101]; together these may represent compensatory responses resulting from reduced endogenous estrogen concentrations [101]. Conversely, others report that 17â-TBOH either increases [81] and [102] or has no effect [81], [90] and [103] 17â-E2 concentrations in ruminants and oviparous animals.

The mechanism(s) through which 17â-TBOH alters estrogenic activity remain to be elucidated, but may be related to the (1) inhibition of endogenous androgen synthesis [104] and [105] (presumably through pituitary or hypothalamic feedback inhibition [93] and [106]), (2) altered expression or activity of the aromatase enzyme [96] and [107], and/or (3) down-regulation of ERá or ERâ expression [95] X. Zhang, M. Hecker, J.W. Park, A.R. Tompsett, J. Newsted and K. Nakayama et al., Real-time PCR array to study effects of chemicals on the hypothalamic-pituitary-gonadal axis of the Japanese medaka, Aquat Toxicol 88 (2008), pp. 173–182. Abstract | Article | PDF (797 K) | View Record in Scopus | Cited By in Scopus (12)[95] and [108]; however, they do not appear to be mediated by direct androgen receptor activation as co-treatment with 17â-TBOH and flutamide (an AR antagonist) also results in anti-estrogenic activity in female fathead minnows [81]. To summarize, 17â-TBOH is not a substrate for the aromatase enzyme, but may exert both anti- and pro-estrogenic effects, with the bulk being anti-estrogenic.

5. Mechanisms of body growth
The growth promoting effects of 17â-TBOH administration are well known [56], [109] and [110], as numerous studies have reported that administration of 17â-TBOH or its acetate ester enhance total body growth and skeletal muscle mass in various rodent and livestock models when administered alone [25], [26], [75], [76], [77], [78], [79], [80], [83], [86], [90], [102], [103], [111], [112], [113], [114], [115], [116], [117], [118], [119], [120], [121], [122], [123], [124], [125], [126], [127], [128], [129], [130], [131], [132], [133], [134], [135] and [136] or when administered in combination with 17â-E2 [86], [90], [103], [104], [111], [112], [123], [127], [128], [129], [137], [138], [139], [140], [141], [142], [143], [144], [145], [146], [147], [148], [149], [150], [151], [152], [153], [154], [155], [156], [157], [158], [159], [160], [161], [162], [163], [164], [165], [166], [167], [168], [169], [170], [171], [172], [173], [174], [175], [176] and [177]. Interestingly, several studies have reported that administration of 17â-TBOH in combination with 17â-E2 results in greater body growth and skeletal muscle mass than either steroid alone [103], [112], [127], [128], [171], [172] and [173]; indicating that 17â-E2 enhances the anabolic effects of 17â-TBOH, as others have suggested [109] and [110]. Ultimately, enhanced body mass results from increases in lean mass (predominantly comprised of muscle and bone) and/or fat mass; thus, the known effects of 17â-TBOH on each of these tissues will be discussed. In addition, the effects of 17â-TBOH on erythropoiesis will be briefly discussed because androgens are known to exert potent effects on red blood cell production.

5.1. Effects of 17â-TBOH on skeletal muscle
Skeletal muscle expresses ARs to varying degrees among species [178], [179], [180], [181] and [182]. As such, androgens induce skeletal muscle protein accretion following dimerization of ARs (Fig. 1). Skeletal muscle expresses 5á reductase and dose-dependently converts testosterone to DHT [183], however, our laboratory [19] and [20] and others [24] have recently demonstrated the 5á reduction of testosterone is not required for skeletal muscle maintenance in hypogonadal animals or humans. In addition, skeletal muscle expresses ERs within both sexes of various species [184], [185] and [186] and 17â-E2 administration has been shown to protect against loss of muscle strength in ovariectomized female rodents [187] and [188]; suggesting that aromatization might contribute to the effects of testosterone on skeletal muscle in males.

In ruminants, 17â-TBOH, alone or in combination with 17â-E2, has been shown to increase the cross-sectional area (CSA) of type I, but not type II, skeletal muscle fibers and induce a fiber switch from more glycolytic to more oxidative fibers, indicating an increase in the oxidative capacity of skeletal muscle [152] and [189]. However, the presence of 17â-E2 is not required for 17â-TBOH to augment skeletal muscle mass as demonstrated in rodent models which experience significant growth of the levator ani muscle [25], [26], [76], [77], [78], [79], [80] and [83] and other skeletal muscles [25], [26], [76], [77], [78], [79], [83], [117], [126] and [133] following 17â-TBOH administration, despite lacking the primary source of endogenous 17â-E2. However, not all rodent models experience peripheral (i.e., hindlimb) muscle growth following 17â-TBOH administration [115], [118] and [126]; although, elevated skeletal muscle DNA concentrations are present in muscles that do not increase in mass in response to 17â-TBOH treatment [117]. The inconsistent skeletal muscle response to 17â-TBOH in rodents may occur because certain peripheral rodent skeletal muscles possess a low percentage of AR positive myonuclei (i.e., extensor digitorum longus with 7% AR positive myonuclei) [181]. Conversely, human myonuclei are approximately 50% AR positive [182] and ruminants are highly sensitive to androgen-induced myotropic stimuli due to a high concentrations of ARs in bovine skeletal muscle [178] and [179] and skeletal muscle satellite cells [180]. Similarly, the androgen-sensitive levator ani muscle in rodents contains approximately 74% AR positive myonuclei [181] and thus experiences robust atrophic responses to castration [190] and hypertrophic responses to androgen administration [25], [26], [76], [77], [78], [79], [80] and [83].

The underlying mechanism(s) through which 17â-TBOH enhances skeletal muscle growth have not been completely characterized; although, it is suspected that 17â-TBOH exerts direct anabolic effects on skeletal muscle primarily via AR activation and associated nuclear translocation and transcription or via modulation of the Wnt/â-catenin pathway, similar to other androgens [26] (Fig. 1). In vitro evidence indicates that 17â-TBOH induces translocation of human ARs to the nucleus in a dose-dependent manner and induces gene transcription to at least the same extent as DHT, the most potent endogenous androgen [26]. Further, 17â-TBOH treatment of cultured bovine satellite cells upregulates AR mRNA expression [191], perhaps explaining the observations that administration of 17â-TBOH increases satellite cell activation and proliferation in various species [117], [191] and [192].

Additionally, 17â-TBOH may induce anabolic effects via mechanisms associated with alterations in endogenous growth factor concentrations [193] or the responsiveness of skeletal muscle to such growth factors [117] (Fig. 3). For example, 17â-TBOH alone or in combination with 17â-E2 upregulates insulin-like growth factor (IGF-1) mRNA in a variety of tissues, including the liver and skeletal muscle in vivo [140], [141], [160], [170], [191], [194] and [195] and satellite cells in vitro [140], via distinct androgen- and estrogen receptor mediated mechanisms [180] and [196]; although 17â-TBOH alone (without the addition of 17â-E2) does not appear to alter skeletal muscle IGF-1 mRNA [184]. Ultimately, the upregulation of IGF-1 mRNA translates into increased serum IGF-1 in 17â-TBOH treated animals [138], [140], [148], [150], [160], [165], [170], [192], [194], [197] and [198], which may stimulate satellite cells proliferation and fusion as has been shown in vitro [117]. Interestingly, 17â-TBOH administration also appears to increase the responsiveness of satellite cells to the proliferating and differentiating effects of IGF-1 and fibroblast growth factor [117]. These results are intriguing considering that the inhibition of several of the downstream targets of IGF-1 (e.g., Raf-1/MAPK kinase (MEK)1/2/ERK1/2, or phosphatidylinositol 3-kinase (PI3K)/Akt) suppresses 17â-TBOH induced satellite cell proliferation in culture [180]. Thus, it seems likely that increased growth factor expression resulting from 17â-TBOH administration is one mechanism underlying the anabolic responses to this steroid in skeletal muscle, especially considering that binding of IGF-1 to the type 1 IGF receptor is required for proliferation of satellite cells [180].

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Fig. 3. Potential mechanisms underlying the anabolic effects of trenbolone on skeletal muscle. 17â-TBOH = trenbolone, GR = gluccocorticoid receptor, AR = androgen receptor, IGF-1 = insulin-like growth factor 1, IGF-1R = insulin-like growth factor 1 receptor.

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17â-TBOH may also preserve or increase lean mass via anti-catabolic effects associated with reductions in endogenous glucocorticoid activity [126] and [135] or with the suppression of amino acid degradation within the liver [118], [122], [134], [199] and [200] (Fig. 3). For example, 17â-TBOH administration has been shown to reduce circulating corticosterone concentrations in rodents [115], [118] and [122] and resting cortisol in cattle [150]. In vivo [122] and in vitro [201] evidence indicates that 17â-TBOH works in the adrenals to suppress adrenocorticotropic hormone (ACTH)-stimulated cortisol synthesis and to suppress cortisol release. Further, 17â-TBOH has been shown to reduce the ability of cortisol to bind to skeletal muscle glucocorticoid receptors (GRs) [121] and to down regulate skeletal muscle GR expression [108] and [121]. Thus the multiple anti-glucocorticoid actions induced by 17â-TBOH explain, in part, the 17â-TBOH-mediated increase in total body nitrogen retention [133], [151], [155], [156] and [202] and the reductions in total [80], [129] and [156] and myofibrillar protein degradation in several species [126], [135], [156], [202] and [203]; especially considering that 17â-TBOH reportedly reduces skeletal muscle protein synthesis in male rodents [80] and [133]. As a result of its anti-glucocorticoid actions, 17â-TBOH produces a more robust inhibition of protein degradation than does testosterone, which only slightly reduces protein degradation while increasing protein synthesis [204]. Thus, future research comparing the effectiveness of 17â-TBOH and the endogenous androgens in altering skeletal muscle degradation via the ubiquitin proteasome system or other pathways associated with muscle atrophy [205] is warranted and may further elucidate the anti-catabolic mechanism(s) underlying the potent augmentation of skeletal muscle mass associated with 17â-TBOH.
5.2. Effects of 17â-TBOH on bone
Testosterone promotes bone development and maintenance directly, via interactions with skeletal ARs, and indirectly following 5á reduction to DHT and subsequent AR activation and following aromatization to 17â-E2 and subsequent ER activation [2]. Interestingly, we [19] and [20] and others [7] have recently demonstrated that the 5á reduction of testosterone to DHT is not required for skeletal maintenance; although, exogenous DHT administration, which suppresses testosterone and 17â-E2 via feedback inhibition [206], is capable of preventing bone loss in gonadectomized animals [2]. However, the large part of the action of testosterone on bone development is thought to be mediated by conversion to 17â-E2 within bone [2] and [40]. As evidence, several boys have been identified as having an inborn aromatase deficiency, a condition that results in osteopenia which can be treated with 17â-E2, but not testosterone [207]. Similarly, male aromatase knockout (ArKO) mice experience adverse skeletal development in the absence of 17â-E2 [208] and [209]. The role of aromatase action on bone maintenance in skeletally mature men is less clear, as several recent human studies indicate that anastrazole administration (a potent aromatase inhibitor) reduces serum 17â-E2 concentrations, but does not alter BMD or markers of bone resorption or bone formation in older men [210] and [211]; although it is currently unknown whether anastrazol suppresses aromatase action within bone. Recent reviews have suggested that at least small concentrations of 17â-E2 are required for bone maintenance in men [212] and that administration of non-aromatizable androgens may be detrimental to bone maintenance due to their ability to reduce endogenous androgen and estrogen biosynthesis, via hypothalamic-pituitary feedback mechanisms [213].

Preliminary evidence from our laboratory indicates that the enanthate ester of 17â-TBOH protects against hypogonadism induced cancellous bone loss to the same extent as supraphysiological testosterone (unpublished laboratory results), perhaps indicating that the 5á reduction and aromatization of testosterone are not required for skeletal maintenance in rodents. The mechanisms through which 17â-TBOH protects against bone loss require further elucidation; although they may be related to reductions in bone remodeling or increases in cortical bone area which have been shown to occur in stag turkeys following 17â-TBOH-acetate administration [125]. Further, implantation of 17â-TBOH plus 17â-E2 has been shown to increase bone maturity in ruminants [139], [142], [143] and [161]; although, it is not possible to differentiate between the effects of 17â-TBOH and 17â-E2 on bone maturity in these studies. However, chondrodystrophic skeletal abnormalities (i.e., reduced longitudinal bone growth with normal appositional growth) appear in immature and stag turkeys administered 17â-TBOH and to a lesser degree following testosterone or 17â-E2 administration [124] and [125]; perhaps demonstrating the influence of androgen- and/or estrogen-induced suppression of longitudinal bone development [2] or the deleterious effect of exogenous androgen administration on bone development of poultry [214]. Thus, 17â-TBOH, a non-5á reducible and an apparently non-aromatizable steroid, appears to be capable of inducing cancellous and cortical bone maintenance in various skeletally mature hypogonadal animal models, but may be detrimental to developing bone.

5.3. Effects of 17â-TBOH on adipose tissue
Androgens induce potent lipolytic effects directly through ARs expressed in adipose tissue [215]. Additionally, testosterone may reduce intramuscular fat by stimulating commitment of mesenchymal pluripotent stem cells to the myogenic lineage and inhibiting their commitment to the adipogenic lineage [3]. 17â-TBOH administration alone or in combination with 17â-E2 also reduces subcutaneous fat, intramuscular fat [139], and muscle marbling (a gross measurement of intramuscular fat content) [112], [143], [159], [162], [171] and [173], along with other stores of body fat in various livestock species [90], [120], [125], [131], [143], [146], [147], [150], [151], [155], [162], [163], [197] and [216]. We have also observed that 17â-TBOH-enanthate administration reduces retroperitoneal fat mass, perirenal fat mass, and perhaps other fat depots, in male rodents in a dose-dependent manner (unpublished laboratory results), similar to what has been reported in at least one other study [117]. In our hands, the lipolytic effects of 17â-TBOH-enanthate are even more potent than that of supraphysiological testosterone-enanthate (unpublished laboratory results). The mechanism(s) through which 17â-TBOH reduces body fat remain to be determined, but may involve a direct stimulation of lipolysis, as demonstrated by an increased expression of enzymes involved in lipolysis in the liver, including enoyl-coA-hydratase (EnoylCoA) and acyl-coA-dehydrogenase very long chain (ACACvl) expression in heifers administered 17â-TBOH [108]. In fact, the reported inability of male rodents to gain body weight following 17â-TBOH administration [115], [118] and [126], may result from a reduction in total body fat mass or perhaps intramuscular fat content, similar to what has been observed in other species [117], [125], [139], [143], [217] and [218]; although, this was not observed in all studies [142], [145], [161], [219], [220] and [221]. Regardless of the mechanism(s), it is apparent that 17â-TBOH induces potent fat reducing effects in several rodent and livestock model species.

5.4. Erythropoiesis
Androgen deprivation reduces hematocrit and hemoglobin, while testosterone administration results in dose-dependent increases in both hematocrit and hemoglobin [222]. In fact, erythrocytosis is one of the more prominent adverse event associated with high-dose testosterone administration [22]. The mechanism(s) through which androgens augment red blood cell production may be related to direct stimulation of kidney erythropoietin secretion or bone marrow, among others [223]. Interestingly, the aromatization of testosterone does not appear to be required for erythropoiesis as administration of DHT (a non-aromatizable endogenous androgen) augments erythropoiesis in men [224], while exogenous testosterone, but not 17â-E2 administration, increases hematocrit in aromatase deficient men [225]. Together, these reports suggest that androgens directly elevate erythropoiesis via AR mediated mechanisms. Additionally, the 5á reduction of testosterone may not be required for erythropoiesis as high-dose testosterone administration in combination with finasteride (a type II 5á reductase inhibitor) increases hematocrit and hemoglobin concentrations in hypogonadal men to the same extent as testosterone alone, despite a nearly 65% lower serum DHT concentrations in the finasteride group [7]. Preliminary evidence from our laboratory indicates that 17â-TBOH increases hemoglobin concentrations in orchiectomized male rodents in a dose-dependent manner and to a greater extent than supraphysiological testosterone, even though circulating DHT is suppressed by over 50% following 17â-TBOH administration (unpublished laboratory data). Together, the studies provide evidence that the 5á reduction of androgens is not required for erythropoiesis and provide a basis for studies examining the mechanisms through which 17â-TBOH alters erythropoiesis.

5.5. Potential adverse events associated with 17â-TBOH
In order to understand the potential adverse effects associated with 17â-TBOH one must consider typical androgen-mediated side effects (i.e., those associated with testosterone or DHT administration), along with other potentially unique adverse events resulting directly from 17â-TBOH. We are unaware of any controlled studies which have been published regarding the effects of 17â-TBOH administration in humans; thus, the evidence we will discuss regarding potential adverse events associated with 17â-TBOH primarily results from studies on animals or from clinical research on other androgens (e.g., testosterone or DHT). However, at least one case-report has linked the use of 17â-TBOH in combination with a variety of other anabolic agents with severe rhabdomyolysis [226]; although, the exact role of 17â-TBOH in this condition is difficult to determine due to the polypharmacy in this case.

5.6. Potential androgen-mediated clinical side effects
The potential side effects associated with supraphysiological testosterone administration are well documented, of which prostate enlargement, accelerated growth of clinically manifested or early-stage undetected prostate cancers, polycythemia, gynecomastia, fluid retention, worsening of sleep apnea, and disruption of the HPG axis occur most frequently [22] and [43]. However, the most prevalent and the most serious adverse events associated with high-dose testosterone administration appear to be mediated by either the 5á reduction [227] or the aromatization [228] and [229] of testosterone to DHT and 17â-E2, respectively; but not directly by testosterone [6]. In fact, a recent review [230] and a separate meta-analysis [22] suggest that little direct evidence exists to support the idea that testosterone administration increases prostate cancer risk (the most potentially serious adverse risk associated with androgen administration in men) even when administration results in supraphysiological androgen concentrations. However, the risk of prostate enlargement (the most prevalent side effect associated with androgen administration in men) and worsening of undiagnosed prostate cancer remains a concern. As such, human clinical trials are currently underway in our laboratory and by others evaluating the effects of supraphysiological testosterone administration plus finasteride (a type II 5á reductase inhibitor) or dutasteride (a dual type I and II 5á reductase inhibitor) on prostate symptoms. Our laboratory was the first to demonstrate that supraphysiological testosterone does not induce prostate enlargement in rodents when administered in combination with a 5á reductase inhibitor (MK-434) [19] and [20]; results which have been verified by others in a human clinical trial examining the effects of high-dose testosterone administration in combination with finasteride [7] and [24]. These results are expected, considering that finasteride alone is an effective therapy to prevent prostate enlargement [231] and that it reduces the incidence of low-grade prostate cancer and the most commonly detected intermediate- and high-grade prostate cancers by approximately 20–50% [232] and [233]; despite the fact that finasteride treatment increases endogenous testosterone concentrations [234]. Further, several other prominent side effects associated with high-dose androgen administration are influenced by the tissue-specific or systemic aromatization of testosterone (e.g., gynecomastia [228] and prostate cancer [235]) or by a reduced ratio of circulating testosterone/17â-E2 (e.g., side effects associated with fluid retention, including sleep apnea) [229], but not directly by testosterone [6] and [236]. Altogether, these studies suggest that the 5á reduction and/or aromatization of androgens may be primarily responsible for the most prevalent and the most serious adverse events associated with testosterone administration; thus, limiting the 5á reduction and/or aromatization of androgens may prove to be clinically beneficial.

To this effect, 17â-TBOH is a promising candidate to reduce the incidence of androgenic and/or estrogenic side effects associated with androgen administration because 17â-TBOH (1) reduces serum testosterone [104], [105] and [237] and DHT (unpublished laboratory results) presumably through pituitary or hypothalamic feedback inhibition [93] and [106], (2) does not appear to undergo 5á reduction or aromatization [58] and [68], and (3) is metabolized to less potent androgens in vivo [39], [58] and [68]. Ultimately, research examining the prevalence of androgen- and/or estrogen-mediated side effects associated with 17â-TBOH administration and the mechanisms through which 17â-TBOH reduces prostate growth is warranted.
5.7. Disruption of hypothalamic-pituitary-gonadal axis
A primary concern with administration of any exogenous androgen, including 17â-TBOH, is disruption of the hypothalamic-pituitary-gonadal (HPG) axis. In this pathway, gonadotropin-releasing hormone (GnRH) released from the hypothalamus stimulates pituitary release of luteinizing hormone (LH) and follicle stimulating hormone (FSH), which in turn stimulate release of sex-hormones from the gonads. Upon entering the circulation, both androgenic and estrogenic hormones are capable of crossing the blood brain barrier and exerting direct feedback inhibition on the pituitary and hypothalamus, ultimately downregulating GnRH release [238]. Disruptions of the HPG axis, including reductions in serum luteinizing hormone (LH) [90], [104], [105], [106], [150] and [237], follicle stimulating hormone (FSH) (unpublished laboratory results), testosterone [81], [90], [105], [106], [150] and [237], DHT (unpublished laboratory results), and 17â-E2 [81] have been observed in a variety of species following 17â-TBOH exposure. Additionally, indirect evidence indicates disruptions of the HPG axis are present in livestock which experience reduced testicular circumference and weight [153], [237] and [239] and delayed puberty [240] following administration of 17â-TBOH. The mechanisms through which 17â-TBOH affects the HPG axis require further clarification; although they may be related to direct hypothalamic feedback inhibition, as evidenced by reduced GnRH transcription in the brains of fish models [94] or perhaps through direct effects on testicular steroid biosynthesis, as demonstrated by downregulated expressions of testicular CYP17 (the enzyme required for synthesizing androstenedione, the precursor of testosterone) and the testicular LH receptor in male and female fish models [94].

5.8. Androgenization and teratogen activity
The majority of unpublished industry studies indicate that 17â-TBOH is non-teratogenic [241]. However, exposure to 17â-TBOH or its 17á-epimer have been shown to induce androgenization/masculinization [81], [97], [98], [101], [242] and [243] and reduce fecundity [94], [95], [101], [240] and [244] in females of various species. Specifically, 17â-TBOH has been shown to induce androgenic alterations of accessory sex-organs in female ruminants [128] and [240], to inhibit ovulation in menstruating rats [92], and to induce developmental alterations in external genitalia and in the age of puberty onset when administered in utero [242] in some, but not all studies [130]. In addition, in ovo exposure to 17â-TBOH causes teratogenic effects in male avian species, including delayed puberty, reduced proctodeal gland area (an indicator of reproductive development which is dependent upon circulating testosterone), and reduced copulatory behavior and copulation success in Japanese quail [85] and [245]. Together these studies indicate that exposure to 17â-TBOH or to its less potent 17á epimer appear to induce significant masculinization in females of different species and perhaps demasculinizing effects in developing males, which may ultimately alter reproductive ability. Thus, administration of 17â-TBOH would appear to be inappropriate in children, adolescents, and pregnant/lactating females; similar to other drugs which alter endogenous sex-steroid metabolism (e.g., finasteride and dutasteride).

5.9. Genotoxicity and cytotoxicity
The genotoxicity and cytotoxicity of 17â-TBOH, and its primary metabolite 17á-TBOH have been previously investigated because residues of these growth promoters remain in the meat, fat, and organs of treated animals which is intended for human consumption [246], [247], [248] and [249]; although, 17â-TBOH is not significantly bioavailable. An in-depth review of the genotoxic and cytotoxic potential of 17â-TBOH, or its metabolites, is beyond the scope of this paper; however, interested readers are directed to the several previous reviews on this topic, which generally conclude that 17â-TBOH and 17á-TBOH are neither genotoxic nor cytotoxic when studied in various in vivo and in vitro assays [57], [250] and [251]. In addition, the Joint FAO/WHO Expert Committee on Food Additives has stated that 17â-TBOH-acetate is an acceptable anabolic agent to use in the production of meat for human consumption [241] based on the results of numerous studies indicating few biological effects exist following consumption of 17â-TBOH residues (or metabolites thereof) in meat. Regardless, additional evidence relating to the incidence and severity of potential adverse events associated with 17â-TBOH administration in humans is required prior to declaring the safety of this anabolic agent.

6. Conclusion – future research focus and potential therapeutic use of 17â-TBOH
Androgens exert both genomic and rapid non-genomic actions. The genomic actions occur following classic androgen/AR mediated signaling pathways or by interactions with the Wnt/â-catenin pathway, while the non-genomic actions are mediated by androgen interaction with cell-surface G-protein coupled receptors. Testosterone, the most prevalent endogenous androgen, dose-dependently augments skeletal muscle mass and BMD, reduces adiposity, and elevates erythropoiesis in men [7], [8], [9], [10], [11], [12], [13], [14], [15], [16], [17], [24] and [222] either directly, via AR activation, or indirectly, via AR and ER activation, following its conversion to DHT and 17â-E2, respectively [2]; while many of the side effects associated with supraphysiological testosterone administration appear to be primarily mediated by the more potent testosterone metabolites, DHT and 17â-E2. As such, the metabolism and the biological effects of testosterone are influenced by the tissue-specific localization and expression of the 5á reductase isoenzymes and the aromatase enzyme. These considerations have led to the development of steroidal and non-steroidal SARMs which are intended to induce anabolic effects in skeletal muscle and bone without inducing prostate growth or other adverse events commonly associated with androgen administration.

17â-TBOH, a potent synthetic testosterone analogue, promotes gains in skeletal muscle mass and BMD and reduces adiposity in various model species. Additionally, the use of 17â-TBOH in athletics [252] and [253] suggests that this steroid is capable of producing potent anabolic effects in muscle and perhaps other tissues in humans; although, we are unaware of any published reports which have evaluated these effects in humans. The metabolism of 17â-TBOH differs from that of testosterone because 17â-TBOH is neither 5á reducible nor aromatizable; as such the primary metabolites of 17â-TBOH are the less potent androgens 17á-TBOH and TBO in humans. Due to the reduced potency of its metabolites, 17â-TBOH appears to induce fewer systemic and tissue-specific androgenic and estrogenic side effects than testosterone. The mechanisms through which 17â-TBOH produces anabolic responses appear to be related to the direct activation of tissue-specific AR mediated signaling pathways, alterations in endogenous growth factors, and reductions in glucocorticoid activity; although, future research is warranted in order to fully elucidate these and other mechanisms.

17â-TBOH is a highly anabolic steroid which exhibits reduced androgenic side effects in various model species. As such 17â-TBOH may produce SARM-like effects and this provides a foundation for future clinical studies examining the safety and efficacy of 17â-TBOH (or its metabolites) in enhancing skeletal muscle mass and BMD in individuals with muscle or bone wasting conditions or with androgen deficiency syndromes. Further, the potent lipolytic effects of 17â-TBOH are intriguing as 17â-TBOH may have clinical potential as a pharmacological agent to reduce central adiposity and its associated health decrements [254]. Future studies examining the mechanisms through which 17â-TBOH increases erythropoiesis are also warranted and may ultimately result in improved treatment options for individuals with various anemias, as has been suggested for other androgens [223]. In addition, research reporting on the incidence and severity of side effects associated with 17â-TBOH administration may provide useful clinical information regarding the potential health risks associated with an anabolic steroid that is used rampantly, yet illegally, in athletic competition. Lastly, it is possible that future studies evaluating the anabolic effects of 17â-TBOH may assist in determining the direct actions of androgens in various target tissues, independent of 5á reductase and aromatase, because 17â-TBOH is not a substrate for either enzyme and has not been acted upon by these enzymes, in contrast to the endogenous androgens testosterone and DHT.
PCT and tren make no sense.... but I have heard of people cruising on low doses of tren for HRT and I have a huge medical study saved somewhere on my computer regarding the use of trenbolone as an alternative to testosterone for HRT.

I think that the original drug Finaject was used for that purpose. Trenbalone I believe though is even more suppressive than taking test itself. This guy is foolin himself if he calls it PCT. What he is doing is basically staying on year around, or cruising if hes using really low dose tren.

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