The Science of Trenbolone

The Science of Trenbolone by Chest Rockwell

I. Preface

Many of you may have already come across my original Science of Trenbolone “article” that has been circulating bodybuilding boards for many years. I use the term “article” quite loosely though, as I never realized at the time that it would become so widely shared. The original intent of that “article” was simply to make a post on a private bodybuilding board that I spent about ten minutes putting together. It was designed to be a quick and dirty reference guide to help answer many questions that were being asked about regularly. So, it goes without saying that whenever I see it being shared, I get a pang of embarrassment as it has my name attached to it and has grown to become a bit of an authority piece on trenbolone.

II. Introduction

Trenbolone is a hormone that has an almost mythical reputation within bodybuilding circles. Because there is very limited data on humans, we often must rely upon anecdotes when trying to form hypotheses. As can be seen on just about any bodybuilding board, experiences with trenbolone vary widely – with some absolutely worshipping the compound and others either advising extreme caution or telling folks to avoid it at all costs. Despite this large divide in opinion, there is no disputing its popularity as numerous surveys over the years have demonstrated it to be one of the most frequently used anabolic compounds, with anywhere between 20-25% of enhanced bodybuilders reporting they’ve used it within the last twelve months [1, 2, 3].

My goal with this article will be to use what information is available to try and form some more solid conclusions with regard to how the compound works. At the same time I hope to help dispel some myths that are still being propagated far too often.

As I mentioned, there are only one or two controlled human trials that I’m aware of so the vast majority of cited material is going to come from either animal studies or in vitro analysis. The question that must be asked is can we take this data and apply it to bodybuilders with any semblance of accuracy? Personally, I feel there are going to be some very concrete bits that are universally applicable to humans and then there are some that may require disclaimers. I will try and do my best to point these out as the article goes on.
III. Basics of Trenbolone

Trenbolone is a selective androgen receptor modulator (SARM) not designed for human use [4]. Despite this designation, it continues to be heavily used by bodybuilders for muscle growth, fat reduction, and body composition purposes [5–6]. SARMs are modified analogues of male sex hormones normally exhibiting favorable anabolic activity while simultaneously having moderate-to-minimal androgenic activity in vivo as compared to native androgens [7, 8, 9]. They are under development by many pharmaceutical firms in an attempt to create alternative means to treat conditions such as hypogonadism, as well as other muscle and bone wasting states. In essence, the goal is to recreate the positive aspects of supraphysiological doses of testosterone while simultaneously removing the risk for adverse events that tend to occur when using these high doses [10].

Most all SARMs start off life as a testosterone molecule. The chemical structure of the testosterone molecule is then traditionally modified in one of three ways [11–12]:

Esterification at the 17β-hydroxyl group which increases hydrophobicity or the likelihood of a molecule to be repelled from a mass of water
Alkylation at the 7α-position which reduces 5α-reductase binding affinity
Strategic modification of the C1, C2, C9, C11, or C19 carbons to achieve a wide range of therapeutic effects

Trenbolone is a C19 norandrogen (19-nor), derived from nandrolone (nortestosterone). Removal of the methyl group at position 19 of the steroid backbone significantly reduces the susceptibility of 19-nor androgens to aromatize as well as undergo 5α-reduction [4]. We’ll be getting deeper into the underlying mechanisms later but, for now, just understand that subtle modifications to the cholesterol backbone of the testosterone molecule can directly translate into significant changes to the behavior of the new SARM molecule. Some of these changes can include the SARM’s binding affinity for the androgen receptor as well as its binding affinity with numerous enzymes capable of converting SARMs to other steroids [13]. Trenbolone has SARM-like properties in that it has significant less affinity for testosterone’s downstream pathways. We’ll talk much more about this later.
IV. History of Trenbolone

The enormous anabolic potential of trenbolone, as well as its analogs, was reported as far back as the 1960s. There was also an oral version created (methyl-trenbolone), however it has never been marketed as an anabolic agent due to its extreme liver toxicity – causing intrahepatic cholestasis at orally administered amounts as small as 1mg/day [14].

It has never been approved for human use and trenbolone is now primarily used as a growth promoting agent in livestock [15–16]. It is used natively as well as in combination with estradiol (E2) [17]. The use of implants containing the combination of androgenic and estrogenic steroids was approved by the FDA in 1992 [18] and now approximately 90% of beef cattle in the United States are being treated with a growth-promoting mix of estrogens, androgens, and/or progestins [19]. Implants are big business with up to 20 million cattle per year implanted with trenbolone and annual revenues likely exceeding a billion dollars [20].

Despite the FDA’s approval, there are still safety concerns as trenbolone acetate (TBA) and its metabolites have been identified as potential endocrine disrupting chemicals (EDCs). EDCs are exogenous molecules that can mimic or inhibit the action of sexual hormone receptors such as estrogen, androgen and thyroid hormone receptors. These EDCs can also disrupt the synthesis, movement, metabolism, and secretion of naturally occurring hormones which may lead to serious issues down the line including obesity, diabetes and even cancer [21–22].

Because of the potential severity of EDCs, the last two decades has seen higher international attention on environmental exposure, and the effects of EDCs in humans and wildlife [23–24]. As mentioned just a moment ago, TBA and its metabolites have been identified as EDCs through many studies, can be widespread in agricultural environments, and are associated with reproductive toxicity [25, 26, 27]. And it only takes exposure in very low concentrations to cause potential problems, as has been demonstrated in animals like fish with skewed sex ratios and decreased fertility [28].

It will also be important to be able to distinguish the various types of TBA implants, as many of the studies we’ll be reviewing later use different types on their subject animals. What follows is a list of common implant types used in the United States, along with their hormonal concentrations:

Revalor-XS (200mg TBA / 40mg E2)
Revalor-200 (200mg TBA / 20mg E2)
Revalor-H (140mg TBA / 14mg E2)
Revalor-S (120mg TBA / 24mg E2)
Revalor-IS (80mg TBA / 16mg E2)
Revalor-IH (80mg TBA / 8mg E2)
Revalor-G (40mg TBA / 8mg E2)
Synovex PLUS (200mg TBA / 28mg E2)
Synovex-C (100mg Progesterone / 10mg E2)
Synovex-ONE Grass (150mg TBA / 15mg E2)
Synovex-S (200mg Progesterone / 20mg E2)
Synovex-H (200mg Testosterone / 20mg E2)

V. Metabolism and Physiology

We made passing mentions to TBA’s metabolites, so let’s spend some time getting into the particulars. It is worth restating now that the vast majority of our knowledge on trenbolone’s in vivo metabolism comes from livestock and rodents [29, 30, 31]. It is also paramount to understand that there are marked differences in the amounts of various metabolites observed in rat and cow models, the two most heavily studied mammals [32]. We will circle back around to this in a moment after first going over some more of the basics.

The chemical alias of TBA is 17ß-hydroxy-estra-4,9,11-trien-3-one-17-acetate, sometimes shortened to 17β-TBOH-acetate. Following an intramuscular injection, it is rapidly hydrolyzed to the biologically active metabolite known as 17β-hydroxy-estra-4,9,11-trien-3-one, or 17β-TBOH [33]. From there it is further broken down into metabolites including glucuronides (e.g. trendione/TBO) and five other polar hydroxylated metabolites [34]. A general flow of the process can be summarized as follows:

17ß-hydroxy-estra-4,9,11-trien-3-one-17-acetate / 17β-TBOH-acetate (trenbolone acetate)
17ß-hydroxy-estra-4,9,11-trien-3-one / 17β-TBOH
Estra-4,9,11-triene-3,17-dione / TBO (trendione)
17a-hydroxy-estra-4,9,11-trien-3-one / 17α-TBOH (epitrenbolone)

17β-TBOH has a greater affinity for the AR than any of its primary metabolites suggesting that the biotransformation of trenbolone reduces the biological activity of the steroid [25–26,34]. To put this into perspective, in one study the high affinity of 17β-TBOH to the human androgen receptor and the bovine progesterone receptor was reduced after being metabolized into 17α-TBOH and TBO to less than 1/24th of the original compound [35]. This behavior is in stark contrast to testosterone whose conversion to DHT and estrogen leads to more potent compounds as it relates to receptor binding affinity [36–37]. However, TBA’s behavior is similar in nature to other 19-nor behavior (such as nandrolone), whose AR affinity decreases when it is 5-alpha reduced [38].

As mentioned earlier, there is some variation in the metabolism of 17β-TBOH among mammals as the primary metabolites are 17ß-hydroxy-estra-4,9,11-trien-3-one and Estra-4,9,11-triene-3,17-dione together with their 16α and 16ß-hydroxylated in the rat. In the cow, these metabolites were negligible and 17α-TBOH was the major product together with small amounts of 16α and 16ß-hydroxy-17α-TBOH [29–30]. A detailed chart comparing the differences between animals follows:
Comparison of the biliary metabolites of 17beta-trenbolone acetate in rat and cow
Comparison of the biliary metabolites of 17beta-trenbolone acetate in rat and cow.

Fortunately for us, there has been a human trial, which I affectionately refer to as the “human hamburger trial”, that helps elucidate how humans metabolize trenbolone – at least after being orally ingested [34]. The trial was designed to investigate the impacts of ingesting tainted food and therefore the research team injected 17β-TBOH into a 5g piece of fried hamburger, at a dose of 0.04 mg/kg of body weight. After a single oral consumption, 63% of the administered dose was excreted via urine by the 72 hour mark; at 24 hours 50% of the administered dose was seen in urine samples.

The results also revealed that, in humans, ingested 17β-TBOH is primarily excreted intact as 17β-TBOH, as epitrenbolone (17α-TBOH), or as trendione (TBO) – with the vast majority being in 17α-TBOH form. In this respect, the biotransformation of 17ß-TBOH in humans more closely resembles that of cows than rodents. In addition, several yet to be identified polar metabolites of 17β-TBOH have been detected in human urine, albeit in a much lower concentration than those metabolites previously mentioned above [39].

17β-TBOH has a low oral bioavailability because it is not methylated at the 17α position. Results from two Hershberger assays demonstrate that trenbolone was about 80–100 fold less effective via the oral route than via injection [25]. Despite this, TBA and 17β-TBOH have still been shown to disrupt the reproductive system of humans, pigs, mice, rats, and other mammalian species at relatively low dosage levels when administered orally.

VI. Effects on HPG Axis

In vertebrates, the hypothalamic-pituitary-gonadal (HPG) axis controls reproductive processes through a variety of hormones which act on target tissues either directly or indirectly. At a high level, in males, gonadotropin-releasing hormone (GnRH) released from the hypothalamus stimulates the pituitary to release luteinizing hormone (LH) and follicle stimulating hormone (FSH). These, in turn, stimulate the release of sex-hormones from the testes [1–2]. The strongly interwoven nature of the HPG axis means that no single component of the system operates in isolation. Upon entering circulation, both androgenic and estrogenic hormones are capable of crossing the blood-brain barrier and exerting negative feedback inhibition on the pituitary and hypothalamus, thereby downregulating GnRH release and suppressing the entire axis [3].

The administration of trenbolone is associated with numerous types of HPG axis disruptions, which is in line with what has been witnessed with various other androgen treatments over the years [4]. Some of the trenbolone-induced disruptions seen over the years include reduced levels of serum LH [5, 6, 7, 8, 9, 10], reduced serum FSH levels [11], reduced testosterone levels [5, 6, 7, 8, 9, 10, 12, 13, 14, 15, 16], reduced DHT levels [11], reduced estradiol levels [13,15], testicular atrophy [7,17–18], and a delayed onset of puberty [19]. These effects occur quite rapidly as, was demonstrated in one trial, within ten days of trenbolone enanthate administration, castrated rats had 80% suppression rates of serum testosterone and 70% suppression rates of DHT as compared to control animals [20]. It is worth noting, enanthate is a long ester variant of trenbolone (TBE) so the use of acetate (TBA) would have produced these effects even more rapidly.

It is not precisely understood what mechanisms are behind trenbolone’s suppressive effects on the HPG axis, however there have certainly been some trials over the years which provide clues. One popular hypothesis involves direct hypothalamic feedback inhibition, as evidenced by reduced GnRH transcription seen in the brains of fish models. This may be additive to its direct effects on testicular steroid biosynthesis, as supported by downregulated expression of testicular CYP17 [21]. CYP17 is a very important enzyme in steroid biosynthesis, and sequentially catalyzes two key reactions in the production of sex steroids in males.

It is also interesting to note that whatever the mechanism is, it does not appear to be androgen receptor (AR) dependent [22–23]. Further supporting this line of thought, in ovary tissue cultures from fish, non-aromatizable androgens such as trenbolone had direct and non-genomic, anti-androgen-insensitive inhibitory, effects on estrogen production [24]. It is highly likely that the underlying feedback mechanisms at work are similar to other androgens, resulting in inhibited GnRH levels and ultimately inhibited FSH and LH production [25].

One other potential gene candidate involved in decreased sex steroid concentrations, noted in fish trials in which they had been exposed to the strong exogenous androgen 17-trenbolone, is hydroxysteroid (17β) dehydrogenase 12a (hsd17b12a). Hsd17b12a catalyzes the conversion of androstenedione to testosterone which, in turn, is converted to 17β-estradiol by the aromatase enzymes. Thus, down-regulation of hsd17b12a, as seen in these trenbolone-exposed fish, is predictably expected to lead to declines in both testosterone and estradiol [14].
VII. Effects on Anabolic Pathways

As we’ve covered previously, trenbolone expresses SARM-like behaviors and I’d like to use this section to discuss them in more depth.

Despite a structural similarity to testosterone, trenbolone does not undergo 5α reduction due to the presence of a 3-oxotriene structure which prevents A ring reduction [26]. This is the pathway used for converting testosterone into its more potent form dihydrotestosterone (DHT). As trenbolone is not a substrate for 5α reductase, it has been shown to stimulate less pronounced androgenic effects than testosterone in androgen-sensitive tissues which express the 5α reductase enzyme, including the prostate and accessory sex organs [27, 28, 29. 30. 31, 32]. To put this statement into perspective, testosterone has an approximately three-fold higher potency in androgenic tissues that express 5α reductase despite having a significantly lower binding affinity to the AR than trenbolone [33]. We’ll discuss how this impacts hypertrophy potential in these tissues a bit later.

As you can already start to imagine, one particular reason trenbolone is beginning to pick up steam in scientific communities is due to its potential to lower the risks associated with prostate cancer in those patients being treated for hypogonadism. The current de facto treatment strategy for these individuals includes providing them with testosterone, in a manner designed to restore hormone levels to natural reference ranges. However, in adult males, benign and malignant growth of the glandular prostate tissue is largely regulated by sex hormones. And furthermore even moderate increases in circulating testosterone have been shown to directly translate into pronounced hyperplastic effects in prostate tissues, mediated via its 5α reduction into DHT [34–35]. Later in the article, we’ll dig deeper into the available literature to see if trenbolone’s potential to lower prostate cancer risk actually pans out.

Seemingly one of the more asked about questions is whether or not trenbolone has impacts on serum estrogen levels, as well as whether or not it can aromatize like testosterone. Popular opinion in the scientific community is that trenbolone and other 19-nor compounds are not substrates for the aromatase enzyme [36–37]. With that said, please understand this is not the same thing as saying they cannot convert to estrogen as C19 norandrogens can induce estrogenic effects [38–39].

Following this line of thought, trenbolone-itself is largely thought to be non-estrogenic [40–41] and there have been numerous animal trials that have demonstrated it reduces serum estradiol concentrations [13, 14, 15, 42, 43, 44]. Keep in mind that there have been a few trials that did not show this suppressive effect on estrogen levels [10,45–46] but, by and large, the body of literature as a whole does support the hypothesis that trenbolone possesses anti-estrogenic effects.

Based upon what we now know about the HPG axis, this would tend to make a lot of sense as the anti-estrogenic effects caused by trenbolone administration likely have to do with its negative feedback on the axis. This negative feedback would cause the inhibition of endogenous testosterone production, thereby leading to suppressed levels of aromatization via the aromatase enzyme, which is necessary for endogenous estrogen biosynthesis in males. This impact on the HPG axis would cause a more severe rate of estrogen inhibition as compared to any potential direct effects trenbolone would have on estrogen receptors and/or the aromatase enzyme [5–6, 8, 21, 47]. There may even be a secondary mechanism at work here which is related to trenbolone’s ability to downregulate expression in both the estrogen alpha and beta receptors [48].

There have been some other interesting discoveries with regard to the mechanisms behind trenbolone’s relationship with estrogen, as well as the compensatory responses associated with suppressed hormone levels. Trenbolone has been shown to reduce tissue concentrations, and gene expression, of VTG (vitellogenin) which is a protein positively associated with exposure to estrogenic compounds [13–14,21,41,47,49,50,51,52,53,54]. It has also been shown to downregulate brain CYP19B (aromatase B) and upregulate gonadal CYP19A (aromatase A) in female fish, but interestingly not in males [14,54].

Similar to what we’ve seen already in the HPG axis, the impacts of trenbolone on estrogen do not appear to be AR-dependent as trials have shown co-treatment with an AR antagonist (flutamide) resulted in the same anti-estrogenic activity in fish [13]. Interestingly, there has been another fish trial that reported trenbolone to have low-affinity with the estrogen receptor and can potentially even activate it [44]. Whether or not this is species-specific is a matter of debate, as I have not seen this occur in any other trials I’ve reviewed. However, cell culture experiments and bioassays do show that trenbolone and its metabolites have a very low binding affinity with estrogen receptors, roughly 20% of the efficacy of estradiol [40].

So can it aromatize? Although I have found nothing which definitively suggests it can, there has been a hypothesis thrown out there by Holland et al [55] which I find intriguing enough to include in its entirety:

“We previously reported that trenbolone enanthate potently reduced visceral fat mass in young and older ORX animals, indicating that fat loss occurs in response to androgen administration, even in the absence of an androgenic substrate for aromatase. However, our previous work did not account for the possibility that androstenedione (derived from dehydroepiandrosterone) can be aromatized to estrone and, subsequently, converted to E2 by actions of 17β-hydroxysteroid dehydrogenase in tissues, such as fat, expressing the required enzymes”

Trenbolone has been shown to have a high affinity for the bovine progestin receptor, and it is assumed that it has a similar affinity to the progesterone receptor as progesterone itself [56]. In vitro analysis has revealed that the relative binding affinity to the bovine progesterone receptor, as compared to progesterone, was 137.4% for 17β-TbOH and 2.1% for 17α-TbOH [57]. And finally, the relative binding affinity of trenbolone to human SHBG, as compared to DHT, is 29.4% for 17β-TbOH and 94.8% for 17α-TbOH.
VIII. Effects on Metabolic Health Markers

One of the primary reasons the anti-trenbolone crowd admonish against its use is related to how harsh the compound seemingly is on one’s health markers. I had hoped to have some actual reference blood work to add to this article, however unfortunately my crowdsourcing efforts were not successful as not many individuals run trenbolone by itself. So what I will do in this section is go over the available animal literature covering various health markers and trenbolone’s impacts upon them.

Arguably the most intriguing relationship to me is trenbolone and the thyroidal axis. Although the effects have been a bit inconsistent, there does seem to be a pattern which suggests trenbolone has an overall suppressive effect on the thyroidal axis. In one trial, trenbolone-alone decreased T4 in heifers while trenbolone plus estradiol decreased T4 in steers, while no impact was seen on T3 uptake [58]. In another trial, trenbolone plus estradiol actually increased T3 whereas trenbolone by itself decreased both T3 and T4 [59]. We must remember that estradiol stimulates the GH/IGF axis, which acutely increases the conversion of T4 to T3. This may help to explain why co-treatment with estradiol can result in higher T3 levels whereas trenbolone-only has the opposite effect, as estradiol levels are highly suppressed. Even in trials where thyroid levels are not significantly different, trenbolone decreased fasting metabolic rates, leading to less intake requirements for creating intake surplus [60].

Therefore, it may be reasonable to speculate the increased feed efficiency seen in numerous studies over the years could be related to trenbolone-mediated suppression of metabolic rate. Of course, it should be noted that leaner cattle just tend to grow faster, and use feed more efficiently, so it also may just be a byproduct of this [61]. Before I wrap this article series up, I’ll talk a bit more about the practical applications here and why these impacts may want to be considered when deciding how to use trenbolone for bodybuilding purposes.

Generally speaking, there is a strong correlation between fat loss and favorable changes in serum lipid levels, particularly in men [62–63]. Therefore, because trenbolone has been consistently shown to improve body composition, it is reasonable to speculate that it may have favorable impacts on lipid markers. So, let’s see what animal trials have shown us.

Studies on rats have shown that both testosterone and trenbolone elicit similar protections against elevated cholesterol despite trenbolone’s ability to elicit more visceral fat loss. This suggests that serum cholesterol levels may be governed primarily by overall body composition, independently of changes in visceral stores. In one trial, serum total cholesterol, HDL, and LDL were all significantly lower in trenbolone-treated intact rats than in control rats (- 62%, – 57%, and – 78% respectively). The byproduct of this was that treated rats had a greater HDL:LDL ratio. Serum triglycerides were also significantly decreased by 51% as compared to control rats [15]. In another trial, both testosterone and trenbolone reduced circulating cholesterol in rats fed a high fat and high sugar diet, but only trenbolone reduced circulating triglyceride levels [64].

It is strongly suggested to keep an eye on cholesterol levels when using supraphysiological doses of androgens, as they tend to have the ability to increase catecholamine-stimulated hormone-sensitive lipase (HSL) activity in both the liver and cardiac tissues [65–66]. This increased HSL activity tends to result in an increased rate of triglyceride breakdown and suppressed rates of HDL hydrolyzation. Having chronically suppressed levels of HDL seems to be an independent cardiovascular risk factor so prolonged use of androgens resulting in suppressed HDL levels should be done with extreme caution [67]

There are quite a few hepatic markers commonly used to assess overall liver functionality and health, as well as hepatic damage. Albumin is a marker indicative of overall liver function while AST, ALT, ALP are all general markers of hepatic damage.

Recent rodent trials have shown that trenbolone does not appear to induce significant damage to hepatic tissues. In one trial, hepatic tissue samples of trenbolone-treated rats showed a similar morphology to those of control rats. AST, ALT, ALP, and albumin were all at similar level in trenbolone-treated rats as compared to control [15]. In a follow-up trial, similar liver enzyme values were seen with rats fed high fat and high sugar diet in all treatment groups, including testosterone and trenbolone treatments [64].

This is another hormone that tends to have a direct correlation with body fat, and specifically visceral fat levels. Visceral fat accumulation and elevated circulating triglyceride levels are both associated with insulin resistance [68]. Conversely, calorie restriction and weight loss in viscerally obese non-diabetics induced significant improvements in insulin sensitivity [69]. In addition to obesity, there is also compelling evidence which shows that low androgen levels also promote insulin resistance [70]. It has been hypothesized that trenbolone treatment in animal models may promote insulin sensitizing effects through similar mechanisms to those achieved by calorie restriction in human males so let’s see what the trials have actually demonstrated.

One trial showed serum insulin to be significantly lower in trenbolone-treated rats (38% reduction) as compared to control rats which translated into a significantly lower HOMA-IR value, a metric used to measure insulin resistance [15]. Fascinatingly, rats being fed high fat and high sugar diets had significantly elevated serum insulin levels that were only partly restored with testosterone, yet trenbolone significantly reduced insulin levels [64]. In fact, trenbolone was also the only treatment group to reduce HOMA-IR values indicating increased beta-cell function and lowered insulin resistance. So albeit limited, the evidence does suggest that trenbolone has superior insulin sensitizing effects as compared to testosterone.

Adiponectin is a 30 kDa insulin sensitizing adipokine that is primarily secreted by visceral adipose tissues [71–72]. Generally speaking, serum adiponectin levels are inversely proportional to fat mass [73]. Testosterone and trenbolone tend to reduce total adiponectin levels to a similar degree in rats [74].

Erythropoiesis is just a fancy term for the body’s production of red blood cells (RBCs). One of the most commonly reported side effects of TRT treatments tends to be elevated levels of hematocrit and hemoglobin. Specifically, androgen deprivation reduces both hematocrit and hemoglobin whereas testosterone administration results in a dose-dependent increase in both [75–76].

The mechanisms by which androgens augment RBC production may be directly related to stimulation of kidney erythropoietin secretion or even bone marrow [77]. And based upon existing evidence, it would appear as if androgens directly elevate erythropoiesis via AR-mediated mechanisms [11]. It does not appear as if the aromatization of testosterone is required for erythropoiesis as DHT administration also increases the process in male subjects [78]. Furthermore, it has also been demonstrated to occur in male subjects with aromatase-deficiencies [79]. Similarly, 5α reduction of testosterone does not appear to be required for erythropoiesis as the co-administration of testosterone and finasteride (5α reductase inhibitor) increased both hematocrit and hemoglobin to the same extent as testosterone alone despite 65% lower DHT concentrations in the finasteride group [80].

If trenbolone can reduce the elevations of hematocrit and hemoglobin seen with traditional TRT treatments, then this would be another potential reason it could be an interesting candidate for HRT. Let’s see what the trials indicate.

Preliminary evidence indicates that trenbolone increases hemoglobin in male rodents in a dose-dependent manner, and to a slightly greater extent than supraphysiological testosterone (8-10%), despite DHT being suppressed by over 70% following administration [20]. In another trial, at administered doses which were seven times higher than testosterone, trenbolone treated rats had nearly identical levels of hemoglobin, although both were significantly elevated as compared to controls [81].

IX. Anabolism

Before we get into the studies, it is important to point out that there are differences between humans and the animals most commonly used in trenbolone studies (e.g. sheep, mice, cows, etc). As we dive deeper into the studies, I’d like for us to all keep these differences in mind, as they can certainly impact the relevancy to humans.

Most rodent skeletal muscle possesses a very low percentage of AR positive nuclei. An example is the extensor digitorum longus, located near the front of the leg, with only 7% AR positive myonuclei [1]. This is not universally true, as the levator ani/bulbocavernosus (LABC) muscle complex (located near the pelvis) contains 70-75% AR-positive myonuclei and experiences robust myotropic response to androgen administration [2,3,4]. So, if you are comparing multiple rodent studies, and they used combinations of these muscles in the trial, then you can likely expect a wide disparity in results.

Conversely, cattle are generally highly sensitive to androgen-induced stimuli due to high concentrations of ARs in bovine skeletal muscle and satellite cells [5,6,7]. We’ll need to further understand that bulls are mature, and intact, males whereas steers are males that have been castrated before reaching sexual maturity. The vast majority of trials are going to be performed on steers as implantation of trenbolone does relatively nothing to intact bulls. They are likely already at their maximum growth potential with their elevated endogenous hormone levels, however combined TBA/E2 implants are necessary to produce maximum growth and feed efficiency in castrated steers [8]. Heifers are young females that have never calved; they are also used on occasion for implantation trials.

Intact bulls produce very high levels of testosterone. In addition to having a very poor response to implantation, they also generally have larger muscle fibers than steers [9]. Bulls also tend to have a higher percentage of fast-twitch oxidative-glycolytic fibers combined with a lower percentage of fast-twitch glycolytic fibers in the longissimus dorsi (LD) muscles than steers have [10]. It is for these reasons that bulls produce higher total carcass yields but they are generally lower quality grade. Castrated steers tend to have more external fat and marbling however they are offset by a decreased rate of weight gain and lower feed efficiency. So in the quest for higher yields with higher quality meat, researchers began to investigate anabolic implants to see if they can produce the best of both worlds.

Lastly, a quick little side-note – humans are quite similar to cows in that we also respond robustly to androgenic stimuli due to the high percentages of AR-positive myonuclei [11].
Androgen Receptor Affinity

Trenbolone has been shown to bind with both the human AR, as well as ARs of various other species, with approximately three times the affinity than testosterone, or approximately equal to that of DHT [12,13,14,15,16]. In human ARs, the active metabolite 17β-TbOH showed a 109% binding affinity as compared to DHT, with the inactive metabolite 17α-TbOH coming in at 4.5% [13]. With this said, receptor binding studies should be seen as a cheap and rapid tool for an initial evaluation of a ligand, not factoring in things such as subsequent initiation of gene transcription, etc. In other words, because trenbolone binds with a three times higher affinity than testosterone to the AR, this does not literally mean it will produce three times the hypertrophy.

Furthering this point, in comparison trials, trenbolone was shown to produce either equal or slightly greater growth in the LABC muscle complex as compared to testosterone [14,17,18,19,20,21,22]. The LABC is an androgen responsive tissue which lacks the 5α reductase enzymes. Whereas testosterone exerts enhanced effects in tissues expressing 5α reductase, trenbolone exerts equal effects in those tissues versus those that do not which produces a favorable anabolic:androgenic ratio compared to testosterone [23]. We’ll go more into this when we discuss prostate cancer risks later in the article series.
X. Hypertrophy

I had originally planned to do a very deep-dive into the mechanisms behind hypertrophy however I think that may be better done in its own article as it is a very complex topic. I will still need to cover the foundational elements of hypertrophy though, or else a lot of this topic may be more confusing than it needs to be. So therefore, I will not be diving too deeply in intracellular signaling pathways, as this would take this article and make it unnecessarily inflated. If there is enough interest, perhaps an article on that topic can be a future project.
Hypertrophy Fundamentals

Before we get into the studies, let’s talk a little about what hypertrophy is and how it occurs in mammals. Again, this is going to be more of a high-level pass at the topic but hopefully deep enough that the terms used later will be better understood.

The number of muscle fibers in mammals is essentially fixed at birth, so postnatal muscle growth must result from the hypertrophy of existing muscle fibers. This fiber hypertrophy requires an increase in the number of myonuclei present within these fibers; however the nuclei present in muscle fibers are unable to divide, so the nuclei must come from outside the fiber [24]. The source of the nuclei needed to support fiber hypertrophy happen to be a group of mononucleated myogenic cells (satellite cells) located between the basal lamina and the plasma membrane (sarcolemma) of muscle fibers [25]. There is a strong correlation between rates of postnatal growth and the rates at which satellite cells accumulate within muscle tissues. This would seemingly make sense as there will be more overall machinery available to fuel the hypertrophy process [26].

These muscle satellite cells play a crucial role in postnatal muscle growth by fusing with existing muscle fibers, providing the nuclei required for postnatal fiber growth. In newborn animals, a much higher percentage of muscle nuclei are satellite cells, but this percentage significantly decreases with age [27]. Not only is there a reduction in satellite cell numbers, but those cells still present withdraw from the proliferative state of the cell cycle and enter a state of quiescence, which consequently leads to a growth plateau. So finding ways to overcome these physiological limitations can hypothetically lead to superior postnatal growth rates.

To ensure there are adequate numbers of usable satellite cells, they first must be activated which will allow them to progress through the cell cycle and ultimately contribute DNA to the existing muscle fiber. After these dormant satellite cells have been activated, there is subsequently a need for growth factors capable of stimulating satellite cell proliferation and differentiation. Both IGF-1 and fibroblast growth factor-2 (FGF-2) are examples of potent stimulators of satellite cell proliferation [28–29]. IGF-I is unique in that it promotes muscle cell differentiation in skeletal muscle, whereas FGF-2 inhibits differentiation [30]. I’ll talk more about the relationship between trenbolone and IGF-1 a bit later in the article.

So taking a slight step backward, when a hypertrophy activation event occurs (e.g. exercise or muscle damage) it leads to satellite cell proliferation. This satellite cell proliferation causes them to fuse with existing muscle fibers, providing new nuclei for hypertrophy and repair, and to support ramped-up protein synthesis. An overly-simplified way to think about this – satellite cells can be activated to proliferate (divide) and donate their DNA (nuclei) to the existing muscle fiber (differentiation).

This donated DNA leads muscle fibers to form the fusion of myoblasts (proliferating cells) into multinucleated muscle fibers called myotubes. These myotubes may fuse to existing myofibers, or even each other, directly generating new muscle fibers. This is about as deeply as I want to take this topic for now.
Growth Promoting Effects

The growth promoting effects of trenbolone are well-known and have been studied by researchers for decades. The goal has always been to find ways to promote greater meat yields along with a higher quality finished product. We’ll focus primarily on the meat yields for now, as the quality of meat often tends to coincide with the amount of intramuscular fat content. This falls more into the realm of lipolysis, which we’ll be covering later in this article series.

Trenbolone has been shown to increase total body growth and skeletal muscle mass in various animal trials when administered alone [3, 14, 17, 19, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44], in combination with estradiol [45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66], in combination with testosterone and estradiol [67], as well as in combination with estradiol plus growth hormone [68]. This hypertrophy potential is pretty much universally observed, and crosses many different administration methods as well as species of animals.

Interestingly, numerous studies have shown that a combined TBA/E2 implant is more effective than either TBA or E2 alone in stimulating the growth of feedlot steers [8, 45, 52, 54–55, 69, 70, 71, 72, 73, 74]. The hypothesis that estradiol enhances the anabolic effects of trenbolone has been floating around as far back as the 1970s [75–76]. Potentially even more interesting is that the combined treatment increases hypertrophy potential despite the fact that it results in serum trenbolone levels which are actually lower, by roughly half [8].

One of the reasons I suspect this to be the case, particularly in steers, is that implantation with trenbolone suppresses endogenous estradiol levels due to its impacts on the HPG axis. Estrogen and, more specifically, aromatase activity is a potent stimulator of the GH/IGF axis. Supporting this hypothesis, implantation with trenbolone-only has been shown to lower, serum GH levels [8,68,69,70,71]. Conversely, steers implanted with E2 alone have been shown to have increased circulating concentrations of both GH and IGF-1 [77–78]. These combined TBA/E2 implants likely result in increased GH levels, and may even alter the number and/or affinity of GHRs in tissues such as the liver [79]. As we learned earlier, having adequate growth factors to stimulate satellite cell proliferation and differentiation is a crucial step in the hypertrophy process.
Optimal TBA / E2 Ratios

Since combined treatments seem to have enhanced anabolic characteristics, many trials over the years have attempted to answer the question what is the optimal TBA/E2 ratio for eliciting maximal growth ratio? There have been some that proclaim the answer lies somewhere between 5:1 and 8:1 [52,54] however results have varied quite a bit over the years. In fact, in one trial, average daily growth rates (ADG) were quite similar in steers implanted with either 25mg E2, 120mg TBA, or a combined 120mg TBA + 24mg E2 implant [80].

Another trial demonstrated that 120mg TBA + 24mg E2 increased average rates of gain by 20-25% and feed efficiency by 15-20% [55]. In fact, it has been shown that combined treatments lead to 50% more actively proliferating satellite cells from the semimembranosus muscle (hamstring) of control steers [81]. As you recall from earlier, the proliferation of satellite cells is a crucial step in the hypertrophy process. Other trials have similarly shown a trenbolone-induced increase in both satellite cell activation and proliferation [82–83]. It appears that trenbolone and testosterone increase satellite cell numbers per muscle fiber to a similar degree [22] so this is not a unique effect of trenbolone. Its effects on satellite cells may be, at least partially, mediated via the IGF-1 receptor as inhibition of several downstream targets of IGF-1 (e.g. MAPK, MEK/ERK, PI3K/Akt) suppressed trenbolone-induced satellite cell proliferation in cell cultures [7].

In 2007 the FDA approved Revalor-XS which is 200mg of TBA + 40mg of E2, designed to have a delayed release of hormones due to a specialized polymer coating on six of the ten pellets in the pack. This is beneficial as traditional implant methods require multiple implants having the potential to add stress which could negatively affect cattle performance. Much of the variation in trial results over the years could very well be related to this. Trials investigating Revalor-XS have found that the higher dose of TBA/E2 improved steer performance when steers are on feed for longer periods [65,140]. Despite the speculation that multiple implants can cause added stress to steers, the delayed release pattern of Revalor-XS did not actually provide any unique effects on steer performance, or quality grade, when compared with a reimplantation strategy of an equal TBA + E2 dose.
Effects of IGF-1

TBA/E2 implants have been shown to significantly increase IGF-1 levels. These combined treatments have resulted in increased serum IGF-1 levels [59,84,85,86], increased hepatic IGF-1 mRNA expression [56], and increased IGF-1 mRNA expression in skeletal muscle tissues [59,61,81].

TBA-only implants have also been shown to increase IGF-1 levels in various species, however not nearly to the degree of combined implants [87,88,89]. In fact, trenbolone does not significantly increase either autocrine or endocrine IGF-1 in a manner greater than testosterone. One trial even demonstrated that testosterone increases autocrine IGF-1 levels slightly higher than TBA [4]. Evidence seems to suggest that any effects on IGF-1 may be mediated via estradiol, and may even be stimulated via distinct androgen and estrogen receptor mechanisms, which include involvement of the G-protein-coupled receptor (GPR30) [90]. One trial in particular found that increased autocrine expression of IGF-1 in skeletal muscle requires estrogen, and TBA-only implants resulted in no increases in muscle IGF-1 mRNA levels [91]. It is certainly reasonable to speculate that there may be a threshold that must be met, which may not be realistic to see in animal trials. Let’s move along to cell studies to see if this hypothesis pans out.

In vitro studies using bovine satellite cells (BSCs) showed a dose-dependent relationship between trenbolone and IGF-1 mRNA levels. In the cells treated with 1nM or 10nM of trenbolone for 48 hours, IGF-1 mRNA levels were 1.7 times higher, however mRNA levels were not affected by treatments of 0.001, 0.01, or 0.1nM [92]. It also appeared that the effects were at least partially mediated via the AR as co-treatment with flutamide (AR inhibitor) completely negated the increased IGF-1 expression seen in these cultures [90].

It does not take much time at all to see increased levels of IGF-1 after an implantation. In one trial, lambs implanted with Revalor-S (120mg TBA / 24mg E2) showed increased serum IGF-1 levels by day 3 and day 10 of 43% and 62% respectively [56]. This increased IGF-1 was maintained for the entire 24 days of the study and steady state hepatic IGF-1 mRNA levels were 150% higher in implanted lambs than in controls, suggesting the liver is likely a primary source of the increased circulating IGF-1. Autocrine IGF-1 mRNA levels were also 68% higher in the longissimus muscles of implanted lambs than were seen in controls. The dosage of TBA and E2, per kilogram of body weight, was approximately three times higher than that approved for use in steers though. Because of the species and dosage differences, caution should be used when trying to take these results and apply them to steers.

Using this same dose in steers has been shown to produce higher serum IGF-1 levels as compared to non-implanted cattle, within 6-42 days of implantation [93]. Within only 48 hours, implanted steers had a 13.4% increase in serum IGF-1 concentrations [84]. On days 21 and 40, implanted steers had 16% and 22% higher IGF-1 levels as compared to controls. Now where it gets interesting is that IGF-1 levels peaked during this timeframe and subsequently began falling through day 115 of the study where they ended up similar to day 1 values. With that said, control steers still had lower IGF-1 levels than day one. So although the increases in IGF-1 levels appear transient, implants still seem to provide an overall additive effect, even with long-term use.

Other trials on cattle have shown muscle samples with higher IGF-1 mRNA within 30-40 days of implantation [56,61]. These implanted animals also showed more proliferating satellite cells than non-implanted steers suggesting TBA/E2-induced increases in muscle IGF-I may be at least partially responsible for the muscle growth observed in implanted steers. As we discussed earlier, it is well established that postnatal muscle growth depends on fusion of satellite cells with existing fibers to provide myonuclei necessary to support growth [24]. This increase is also important because only a small number of satellite cells are present at this time in yearling cattle, and many of the existing cells have become quiescent or left the cell cycle. It is also worth mentioning that IGF-1 overexpression extends the replicative lifespan of satellite cells, at least in cell cultures [94]. Therefore, it seems reasonable to hypothesize that increased muscle IGF-I expression plays a role in the AAS-induced increase in muscle satellite cell numbers.

In another trial, hepatic steady state IGF-1 mRNA levels were shown to be 69% higher in implanted steers, again suggesting that the liver may be a large contributing factor to increased circulating IGF-1 in implanted animals [61]. Please note that there has been at least one study, which I’m aware of, to show no differences in IGF-1 concentrations between implanted steers and control cattle [95]. This would tend to be the exception and not the rule, however.

An androgen response element (ARE) has been identified in the promoter region of the IGF-I gene, suggesting that the androgen receptor-ligand complex may interact with this ARE to stimulate transcription of the IGF-I gene. Androgens tend to act via multiple mechanisms on muscle though, and estrogen tends to act on the hypothalamus/anterior pituitary to stimulate GH/IGF axis [96]. The relationship between estrogen and the GH/IGF axis has been shown to be additive [97–98].
Estrogen Primer

Since we are kind of heading this direction anyway, let’s take a brief moment to focus our attention more on estrogen before moving forward.

In vitro studies have shown that treatment of bovine satellite cell cultures for 48 hours with E2 significantly increases IGF-1 mRNA expression [92]. This is in line with what we already know about E2, as it has been shown to stimulate expression of IGF-1 mRNA in a number of tissues [99–100]. Interestingly enough, co-treatment with ICI (estrogen receptor antagonist) did not suppress this E2-stimulated IGF-1 expression. This seems to suggest that the mechanism by which E2 stimulates IGF-I mRNA expression in BSCs may be different than the mechanism acting in other tissues which have been examined to date.

Even though the IGF-I gene does not contain a traditional estrogen response element (ERE) in its regulatory region, E2-stimulation of IGF-I mRNA expression can occur via a pathway involving the AP-1 enhancer [101]. As mentioned previously, in addition to the classical estrogen receptors, G-protein-coupled receptor 30 (GRP30) may play a role in mediating the actions of estrogen [102,103,104]. This is relevant to our interests as muscle tissue contains GPR30 mRNA and immunohistochemical studies have localized GPR30 receptor protein within skeletal muscle cells [105]. Furthermore, the effects of GPR agonist/antagonist strongly indicate the GPR30 receptor is involved in the E2-stimulated increase in IGF-1 mRNA observed in bovine satellite cell cultures [90].
Effects on Muscle Fibers

Implantation with TBA/E2 increases the cross-sectional area (CSA) of muscle fibers due to an initial increase in DNA transcription followed by an increase in nuclei within the muscle fiber which support hypertrophy [106]. TBA (either alone or in combination with E2) has traditionally been shown to increase the CSA of type I but not type II muscle fibers [9,107]. Combined implantation of feedlot steers has also been shown to increase type I and IIA CSA in LM muscles [110]. There have been exceptions, as one trial has been shown to increase type IIB fibers without any impact on the size or number of type I fibers [57]. These trials, when taken as a whole, seem to suggest that trenbolone induces a fiber switch from more glycolytic to more oxidative fibers, which indicates an increase in the oxidative capacity of the skeletal muscle fibers.

Getting back to the potential differences seen in species, despite the increase in muscle weight and muscle fiber size, the number of myonuclei per fiber was not enhanced with rats being administered either trenbolone or testosterone [22]. This contradicts the results from an earlier trial, however testosterone was administered beginning at the onset of puberty which is a rapid growth phase for the LABC muscle versus the more mature muscles in the previous study [108]. It is highly likely that androgen-induced hypertrophy in adult rats without exercise stimulus may not require myonuclear addition [109], which kind of goes against the grain of what we’ve been talking about the entire article. But these are also exactly the types of things to keep an eye out for when looking over animal trials and trying to establish patterns which may be potentially translated to humans.
Effects of Androgen Receptors

There have been multiple in vitro experiments that indicate trenbolone upregulates AR mRNA expression [111–112]. There does appear to be a ceiling effect though, where higher doses fail to alter mRNA levels to a degree relative to those present in untreated control cultures [92].

This has not universally been demonstrated in trials however, as some have shown no trenbolone-mediated effects upon AR mRNA expression [4,91]. This discrepancy may be because the elevated AR expression occurs at an earlier time point than data collection was taken in these trials, but that is speculative. In vitro evidence also indicates trenbolone induces translocation of human ARs to the cell nucleus in a dose-dependent manner, and it also stimulates gene transcription to at least the same degree as DHT [14].
XI. Atrophy / Anti-Catabolism

Trenbolone’s reputation as a muscle-preserving hormone is actually well deserved. I would like to briefly go over the basics of skeletal muscle atrophy before diving into the literature associated with trenbolone-specifically.

During various catabolic states, the ubiquitin-proteasome pathway increases protein breakdown leading to skeletal muscle atrophy. Specifically two ubiquitin ligases, MuRF1 and MAFbx (also called Atrogin-1) serve as markers of skeletal muscle atrophy under these various catabolic states such as fasting, cancer, renal failure, and diabetes [113,114,115]. Trenbolone has been shown to significantly decrease MuRF1 and atrogin-1 mRNA expression in the skeletal muscle tissues by a factor of 3 in castrated rats. Atrogin-1 rates were suppressed in these animals to an even greater degree than testosterone administration [4].

Glucocorticoids are steroid hormones which help regulate whole-body metabolic homeostasis. They also exert their influence on skeletal muscle with elevated exposure to them potentially leading to atrophy of tissues. The major members of the glucocorticoid family are cortisol, corticosterone, and cortisone. They bind with the intracellular glucocorticoid receptor (GR) where they activate and exert their effects. It is worth mentioning that cortisol can bind to both the GR and mineralocorticoid receptor (MR), however a deep dive on this is beyond the scope of this article series.

Trenbolone has been shown to lower glucocorticoid binding capacity by causing a decreased number of GRs in skeletal muscle tissues [36,116]. In vitro studies have demonstrated trenbolone to act as a glucocorticoid receptor antagonist [14] despite 17β-TbOH possessing only a 9.4% relative binding affinity to the bovine glucocorticoid receptor as compared to cortisol [13]. Other studies have shown that trenbolone reduces the ability of cortisol to bind to skeletal muscle GRs as well as downregulating overall GR expression [117–118]. In fact, trenbolone suppresses GR expression 50% more than testosterone [4]. And its anti-glucocorticoid actions likely help it produce a significantly more robust inhibition of muscle protein breakdown (MPB) than testosterone, which only slightly reduces MPB while simultaneously increasing MPS [119].

Trenbolone has been shown to reduce circulating corticosterone concentrations in rodents [37,39,116,120] as well as cortisol in implanted cattle [50]. Evidence suggests that trenbolone works in the adrenals to suppress ACTH-stimulated cortisol synthesis as well as suppressing cortisol release [121].

We may now try and extrapolate a bit further on what these lowered glucocorticoid levels may do. For example, glucocorticoids inhibit glucose uptake and help stimulate glycogen breakdown in skeletal muscle by attenuating insulin-induced GLUT4 translocation to the cell membranes [122]. Insulin signaling in muscle tissues is essentially suppressed by glucocorticoids [123]. With this said, is it possible that trenbolone administration could create an environment of enhanced glucose utilization? We’ve already seen its ability to increase insulin sensitivity in rat models, what if one were to run it alongside exogenous insulin?

Glucocorticoids also tend to increase intramuscular triglyceride levels [124]. Is it thereby reasonable to speculate that the cosmetic effects traditionally attributed to trenbolone may have something to do with this? If trenbolone is reducing intramuscular triglyceride levels, then could this be a primary factor behind why many tend to have drier looking muscles? I’ll circle back to some of these questions in my closing remarks of the article series.
Effects on Protein Synthesis and Breakdown

One of the more amusing bits of information on trenbolone is that the rate of muscle protein synthesis (MPS) actually decreases with administration. This has been demonstrated in trials with either TBA implants or TBA+E2 implants [17,32,48]. Many folks hear this and wonder how trenbolone can be such a potent anabolic when it reduces MPS rates? The key here goes back to trenbolone’s impacts on MPB, as it is very adept at lowering rates of MPB to a greater degree than MPS, which results in a net-anabolic state.

In fact, despite lowering rates of MPS, trenbolone has been shown to increase whole body nitrogen retention in various species [32,125,126,127]. Again, this has a lot to do with trenbolone’s impacts on MPB rates. It has been shown to cause significantly decreased rates of total and myofibrillar MPB in various species [32,34,36,120,128].

It is worth noting that in vitro studies have actually shown trenbolone-induced concentration-dependent increases in MPS rates. They can be significant, with up to a 1.7-fold increase using the highest 10 nM dose in the study [129]. So, similar to what we saw earlier with IGF-1 expression, there may be a point where trenbolone stops suppressing MPS and begins increasing it. It is likely this point extends beyond realistic real-world use cases though, as in vivo studies in various animals do not show this same effect. In these cells, rates of protein degradation were also lowered, with the highest dose of TBA causing rate of degradation to be 70% of that shown in cultures with no TBA. This was, at least, a partially AR-mediated effect as flutamide suppresses trenbolone’s ability to stimulate protein synthesis as well as suppress protein degradation rates. Treatment of the cell cultures with JB1 (IGF-1 inhibitor) also impacts trenbolone’s effects on protein synthesis/degradation so it is highly likely these effects require both the AR and IGF-1 receptor to some degree.

Trenbolone has also been shown to suppress amino acid degradation within the liver [37,130]. This can also be a key factor to the overall effects on MPB, as the first step in amino acid degradation takes place there – the removal of nitrogen. In fact, the major site of amino acid degradation in mammals is the liver.
Effects on Bone

Age-related hypogonadism is a major factor contributing to the loss of bone in older men [131]. As we’ve discussed previously, the de facto treatment for hypogonadism is testosterone (TRT). The problem is that TRT only produces modest improvements on bone mineral density in treated subjects [132–133]. Conversely, supraphysiological doses of testosterone fully protects against bone loss, however it comes with a lot of unwanted side-effects [134,135,136]. So, we are back at the place we were at earlier, where we are looking for the protective effects of supraphysiological doses but without the unwanted sides.

Early indications are promising as rodent trials demonstrate trenbolone prevents hypogonadism-induced bone loss in castrated rats to a degree equal to that of supraphysiological testosterone, but without inducing prostate growth or elevations in hemoglobin which are frequently seen with testosterone treatments [3,20].

Trenbolone potentially exerts part of its influence on bone through reductions in circulating corticosterone, via its anti-glucocorticoid activity [14,39]. And, despite trenbolone suppressing estrogen, it still possesses bone-preserving characteristics similar to testosterone. This is similar to what was seen with DHT so it appears as if non-aromatizing androgens are capable of bone protection directly through AR mediated pathways [137–138]. There are still lines of thought out there that believe a small degree of skeletal-specific aromatization of testosterone to E2 is essential for bone protection in males [139]. So, before any conclusions can be drawn, long-term trials with TBA will have to be conducted.


It is well-known that carrying excess body fat can lead to long-term health complications. What I hope to achieve in this section will be to outline some of the specific problems associated with obesity and then illustrate what effects androgens, and specifically trenbolone, have on stored fat.
Metabolic Syndrome

Obesity is a significant concern in western cultures, as it is one of the primary factors leading to metabolic syndrome. Metabolic syndrome is the name given to a group of risk factors that raise one’s risk for heart disease and other health problems [1]. It can also be traditionally characterized by increased visceral adiposity, dyslipidemia (elevation of cholesterol), and insulin resistance [2].

Including the aforementioned characteristics, there are other primary conditions described as being independent risk factors including:

High Triglyceride Count
Low HDL Cholesterol
High Blood Pressure
High Fasting Blood Glucose

Simply stated, with each independent risk factor that one possesses the odds of developing heart disease, diabetes, and stroke increase significantly.
Androgen Deficiency

Another correlation has been found in males between obesity-associated metabolic syndrome and androgen deficiency [3]. Androgen deficiency occurs in approximately 1 in 200 men [4] however this number is significantly increased in males with obesity-related metabolic syndrome [5–6]. It is quite clear that there is a causal effect of obesity on androgen levels in males [7].

In those males who have androgen deficiency plus metabolic syndrome there is a significantly higher risk of cardiovascular disease as well as increased mortality rates, particularly in older males [8–9]. Although not traditionally identified as a unique risk factor, androgen deficiency certainly does appear as if it could be classified as such. Fortunately for us, there have been many animal experiments performed in an attempt to document how androgens, and trenbolone in particular, impact various aspects of metabolic syndrome.

In normogonadic rats trenbolone was shown to improve multiple components of metabolic syndrome, as well as improve myocardial tolerance to ischemia reperfusion, to a degree greater than testosterone [10–11]. This was somewhat surprising considering that trenbolone is not a substrate for the aromatase pathway, and estrogen has traditionally been seen as cardioprotective.

Ischemia reperfusion is a fancy phrase for describing the tissue damage caused when blood supply returns to tissue after a sustained period of low oxygen supply [12,13,14]. It is speculated that these cardioprotective effects of trenbolone are mediated both through direct androgenic activity in the myocardium as well as indirectly through improvements in body composition, lipid profile, and insulin sensitivity. In fact, one of the primary characteristics of androgen-deficiency-induced impairment of ischemia reperfusion is that it causes myocardial desensitization to insulin [15]. There is further speculation that this cardioprotection may be modulated directly via the AR and independent of estrogenic activity, or possibly even via crosstalk between trenbolone and estradiol receptors in the myocardium.
Trenbolone’s Effects on Body Fat

As should be pretty clear by now, if we can find ways to decrease adiposity then this should only serve to lower the risk of numerous, negative metabolic consequences. To cut right to the chase, trenbolone administration has been shown to reduce body fat stores in multiple species. In fact, the lipolytic effects of trenbolone are even more potent than testosterone, especially in visceral fat depots [16]. In castrated rats, the lipolytic effects of trenbolone have been demonstrated to be dose-dependent [17].

In various cattle trials, trenbolone has been shown to reduce intramuscular fat and marbling content [18, 19, 20, 21, 22, 23] however this was not universally observed [24]. It is possible that the discrepancies in these trials could be due to the use of a particular cattle genotype, which may have a greater than average potential to marble. In support of this line of thought, one trial showed that TBA implants did not alter intramuscular lipid deposition (measured by marbling score), total lipid content, fatty acid content, adipocyte cellularity, or lipogenic enzymes expression. This supports the hypothesis that anabolic implants may not have a direct effect on intramuscular lipid deposition, particularly in cattle with a high genetic propensity to deposit intramuscular fat [25].

Getting back to the body of literature as a whole, trenbolone administration has been shown to reduce visceral fat [26], whole-body adipose tissue levels [10, 24, 27, 28, 29, 30], backfat thickness [31, 32, 33], rib-section thickness [34–35], and retroperitoneal and perirenal fat mass [36]. So despite a few trials showing anabolic implants having no impact on body fat levels [24–25,37], the body of evidence as a whole suggests that trenbolone is actually a potent stimulator of lipolysis.
Mechanism of Action

Androgens induce potent lipolytic effects directly via ARs expressed in adipose tissues [38–39]. They elicit these effects by inhibiting lipid uptake in addition to increasing beta-adrenergic receptor expression within these tissues [40–41]. Androgens may also decrease the rate of adipocyte proliferation [42]. It is worth noting that ARs are more densely expressed in visceral than subcutaneous adipocytes and many androgens display an affinity for visceral fat depots [43–44].

Animal models have helped to further demonstrate a clear relationship between the AR and adiposity. Male mice who have been genetically altered to not signal via the androgen receptor (ARKO) develop significant late-onset visceral adiposity [45–46]. Furthermore, ARKO specifically within adipose tissues show that AR signaling in these tissues plays a critical role in both insulin and glucose homeostasis [47].

In addition to the previously described mechanisms, trenbolone may stimulate lipolysis directly by increasing enzymes involved in the lipolytic process within the liver, such as Enoyl CoA and ACACvl [48]. The process of adipogenesis (where preadipocytes become adipocytes) is partly mediated by the estrogen receptor alpha (ERα) expressed in these preadipocytes [49]. Therefore, it may be reasonable to speculate that trenbolone’s ability to suppress aromatization, and consequently reduce estrogen activity, may be a contributing factor with regard to reductions in adipose tissues seen across numerous trials.

In vitro studies have helped us understand that androgens may simply suppress adipogenesis. More specifically, when androgens cause progenitor cells to go down the myogenic pathway, they also simultaneously block their entry to the adipogenic pathway [50]. This was specifically seen in cell lines where activation of the Wnt/β-catenin pathway enhanced myogenesis and inhibited adipogenesis [51]. The number of myogenic cells and myosin protein levels increased in a dose-dependent fashion in response to testosterone and dihydrotestosterone treatments. In parallel, these two steroids decreased the number of adipocytes formed while simultaneously down-regulating C/EBP-α and PPAR-γ protein expression. All of this is just continuing to show that androgens have the ability to simultaneously activate myogenic pathways while suppressing adipogenic pathways.
β-Adrenergic Agonists

I don’t want to spend too much time on this topic, however there have been quite a few trials that combined TBA with β-adrenergic agonists so I’ll include a just a bit on these compounds for completeness. Although clenbuterol and albuterol are likely the most popular family members, most of the trials referenced here used ractopamine.

Ractopamine is predominantly a β1-adrenergic agonist that has binding affinity for both β1- and β2-adrenergic receptors [52]. Binding of ractopamine to the β-adrenergic receptor elicits a response that results in increased lean muscle mass with a minor effect on adipose tissue deposition [53]. Most β-agonists used in livestock stimulate increased lipolysis, decreased lipogenesis, or stimulate protein disposition by binding to the β1- or β2-adrenergic receptors [54].

Steroidal implants and β-adrenergic agonists work through separate mechanisms however both ultimately act to increase protein deposition [55]. β-adrenergic agonists are repartitioning agents that redirect absorbed nutrients away from adipose tissue, favoring protein accretion [56].

As you recall from earlier, satellite cell proliferation is a crucial step in hypertrophy which results in increased nuclei, available for fueling the process. Unlike what is seen with steroidal implants, evidence suggests that during the initial 3 to 5 weeks of β-adrenergic agonist treatments, hypertrophy occurs yet no change in the number of nuclei is observed. It appears as if β-adrenergic agonists cause existing nuclei within the muscle fiber to become much more efficient at increasing muscle protein accumulation without the support of additional DNA from satellite cells. However, over time, it becomes difficult for skeletal muscle to sustain this level of fiber hypertrophy without any additional DNA and thus responsiveness to the β-adrenergic agonists is ultimately suppressed [57]. Therefore, it should come as no surprise that the use of β-agonists alongside trenbolone has been shown to have an additive effect as it relates to hypertrophy [35,58].
XIII. Side Effects

To begin to understand the potential side effects associated with trenbolone administration, we’ll first want to review those which have been observed with other androgen treatments, as there are no controlled trials published discussing the effects of trenbolone administration on humans. We can then branch out a bit more and begin to investigate those undesirable effects seen in various animals exposed to trenbolone.

Quite frankly, most of the major side effects associated with high-dosed testosterone treatments are associated with either the 5α reduction to DHT or the aromatization to estradiol and not directly caused by testosterone itself [59, 60, 61, 62, 63]. As I’ve touched on earlier in the article series, trenbolone and other SARMS have been created largely out of the demand to find compounds which possess the positive attributes of supratherapeutic testosterone without the negatives.

Prostate cancer is the second most commonly diagnosed cancer as well as the fifth leading cause of cancer-related deaths in American men [64]. Despite very little evidence to suggest testosterone administration increases prostate cancer risk, even when administered in supraphysiological doses, prostate enlargement remains a serious concern [65–66].

One of the more accepted theories on the mechanisms behind prostate cancer would be Pitts’ unified theory [67]. He believes that androgen-induced prostate hyperplasia occurs in the absence of malignancy and the subsequent development of prostate cancer is primarily induced by, and reliant upon, circulating estradiol derived via testosterone aromatization. In fact, supporting this line of thought, when testosterone is co-administered with finasteride (5α-reductase inhibitor), it does not induce prostate enlargement in human subjects [68–69].

So, if we follow this line of thought just a bit further, although trenbolone has been shown to increase prostate mass the subsequent lack of circulating estradiol may ultimately lower the risk of malignancy down the line. Of course, what would be the consequences related to long-term aromatase suppression? It will be valuable at some point for us to evaluate the effects of long-term estrogen suppression, as estrogen plays critical roles in many metabolic processes in males such as GH secretion, bone remodelling, and adipose tissue regulation [70]. Scenarios like this are exactly why we are going to need actual human trials at some point should trenbolone ever truly be a serious candidate for HRT strategies in the future.

There have been a few animal trials that provide us with actual in vivo data on how trenbolone impacts the prostate. In one trial, the prostates of trenbolone-treated rats showed a 49% greater mass than those in control rats over 8 week treatment period [10]. In a follow-up, the prostates of trenbolone-treated rats increased in size, but only by approximately 75% of that seen in testosterone-treated rats [11]. Another trial showed that the prostates of trenbolone-treated rats were not significantly different than control rats, yet significantly smaller than testosterone treated rats [71].

In a slightly older, but arguably more thorough examination on castrated rats, trenbolone administration resulted in a dose-dependent effect upon prostate mass. The highest dose resulted in a 68% higher prostate mass than control rats, however neither the low or moderate dosing groups resulted in increased prostate mass. Rats administered testosterone, for comparison, increased mass by 84% which was greater than even the high-dosed trenbolone rats [17]. Intact male rats showed a very similar pattern.

For decades, male androgen deficiency has been known to alter cardiac structure and function, which is subsequently restored with TRT treatments [72, 73, 74]. Specifically, testosterone therapy has been shown to decrease ejection fraction as well as increase left ventricular dimension during diastole, or the dilation of the left ventricle [75].

Alternatively, AAS abuse is associated with a wide range of cardiovascular pathologies [76, 77, 78, 79, 80]. Various problems have been observed over the years including increased risk of atrial fibrillation [81–82] and even sudden cardiac-related death [83-84]. Although the mechanisms remain unclear, the fibrotic response to androgen treatments may be driven by localized disruption to redox homeostasis in the cardiac myocyte [85]. As is often the case with hormones, the ideal spot to reside for health may reside somewhere in the middle.

Interestingly, the role of testosterone’s key androgenic metabolite DHT has not been considered in most of the literature on this topic despite the role it may have with regard to cardiovascular remodeling. In fact, cardiovascular remodeling is highly dependent upon 5α reduction which would naturally be increased with testosterone therapy [86]. It is possible the decreased DHT activity associated with trenbolone therapy may partially explain why no adverse changes were observed in cardiovascular structure or cardiac response in rats [10]. More specifically, there were no differences observed in trenbolone-treated rats with regard to anterior diastolic/systolic, left ventricular wall thickness, posterior diastolic/systolic wall thickness, ejection fraction, or fractional shortening as compared to control rats over eight week treatment period. Stroke volume and raw cardiac output were also similar between groups.

In a follow-up trial, both testosterone and trenbolone treated rats protected against left-ventricular size reduction following their castration to a similar degree [11]. The amount of replacement fibrosis observed with trenbolone treatment was relatively modest when compared to that of testosterone-treated rats though. It was only revealed in a single section of sampled myocardium, whereas the fibrosis observed in the hearts of testosterone-treated rats was widespread. It is worth mentioning that the H&E staining used in this study is not the gold standard for fibrosis assessment however this is still fascinating, nonetheless.

Trenbolone has been shown to have the ability to cross the blood-brain barrier as well as the placental barrier in rodents. The concentration of trenbolone was highest in the hippocampus with concentrations higher in male rats than females. The hippocampus is well-known to be a target for the modulatory actions of both androgens and estrogens so this did not come as a total shock [87]. A few years ago, when the infamous Ma et al study [88] came out, it caused a bit of a stir in bodybuilding circles as it was concluded by many that trenbolone led to brain damage or neurological disorders. Okay, I may be embellishing a bit, however there were a significant amount of folks that were legitimately concerned. So let’s take a moment to go over the study a bit deeper to see what we can really glean from it.

The research team was largely looking into the amyloid hypothesis which states that imbalances between production of β-amyloid peptides and Aβ clearance rates may play a major role in the neurodegeneration associated with disorders like Alzheimer’s Disease [89–90]. The main hallmarks of Alzheimer’s Disease in the brain are extracellular β-amyloid peptide (Aβ) plaques (senile plaques) and intracellular neurofibrillary tangles (NFTs). The senile plaques consist mainly of Aβ40 and Aβ42.

Male rats showed elevated Aβ42 levels in the brain within 48 hours of trenbolone injection, in a dose-dependent manner, and this elevation was mediated via both the AR and ER in vivo and in vitro. Increasing concentrations of Aβ42 in the brain (hippocampus) will increase the Aβ42 burden, leading to aggregation and deposition, and ultimately neuron damage. Decreased Aβ42 levels in cerebrospinal fluid are regarded as another predictor of Alzheimer’s Disease [91]. Although cerebrospinal fluid Aβ42 concentrations did not significantly change in the treated rats, the fact that neurons increased Aβ42 production is still worth noting.

Trenbolone also caused a down-regulation of PS-1 protein levels in neurons to the same degree in both low and high dose treatments. Loss of PS-1 in neurons leads to weakening its normal functions and increases the vulnerability of neurons to apoptosis. It actually did induce apoptosis of the primary hippocampal neurons which is a primary feature of both acute/chronic neurodegenerative diseases [92]. Fascinatingly, adding testosterone “protected” the neurons by resisting the activities of PS-1. Even more fascinating, this did not occur when trenbolone was added first. Why testosterone and trenbolone behaved differently is certainly a question worth asking.

Now, this has the tendency to sound pretty severe, and it could be. However further trials are going to need to be conducted before drawing any definitive conclusions on how this may relate to humans.

As is always the case, especially with powerful androgens, females should use extreme caution and avoid exposure whenever possible. Exposure to trenbolone, or even its metabolites, has been shown to induce androgenization and masculinization of females in various species [93, 94, 95, 96, 97].

There have also been trials which demonstrated its ability to induce androgenic alterations of accessory sex organs in female cows [98–99] as well as produce increased incidences of external female genital malformations in female rats [100]. Exposure has also been shown to decrease fertility of females in various species [97, 99, 101, 102, 103] as well as inhibits ovulation in menstruating rats [104].

To be blunt, trenbolone is not a female friendly androgen and I would not recommend it being used by women ever.
Case Studies

Case studies can be helpful, although often conclusions cannot be drawn from them due to the wide amount of potential confounding variables in play. I’m aware of three case studies which focused on trenbolone in the literature, so I present them to you now.

In the first, a 23 year old bodybuilder suffered from a myocardial infarction following chronic trenbolone acetate consumption [105]. Of course, there is no way to ascertain that is the only hormone he was using, so trying to conclude trenbolone caused his heart attack is pretty thin.

In another, trenbolone along with a combination of other anabolic compounds led to rhabdomyolysis, or severe breakdown of skeletal muscle tissue, in a 34 year old Dutch bodybuilder [106]. Again, because we know trenbolone has the opposite effect on skeletal tissues, I have to speculate something else is at play here. Could it have been the purity of hormones he was using? Because trenbolone is not approved for human use, bodybuilders are often at high risk for sourcing poor quality (or even contaminated) hormones. Could it have been the injection technique in use? Perhaps this individual was not sanitizing the injection area beforehand? Way too many questions to be able to draw any conclusions, or place blame on any single factor.

The third case study described a 21 year old bodybuilder who experienced yellow skin and pruritus, which is a severe itching of the skin, following a trenbolone cycle [107]. I found this particularly interesting as I’ve long suspected that trenbolone may have an impact on increasing histamine levels, which is the most well-known agent to evoke pruritus. If this is true, it could very likely explain a number of sides reported by bodybuilders such as acid reflux, impaired sleep, fatigue, etc. Unfortunately, there is very limited literature specifically examining trenbolone’s impacts on histamines [108–109] and thus I’ll just have to remain speculative for now, based upon anecdotes.

Before moving onto my closing thoughts, there are some other unwanted effects that should be briefly mentioned. Similar to high-dose testosterone treatments, trenbolone has been shown to induce testicular atrophy in intact male pigs [110]. High doses of trenbolone have been demonstrated to negatively impact male immune function in castrated mice [111]. Anecdotally, trenbolone has been associated with acid reflux, changes in emotional state, and insomnia. Insomnia is such a prevalent occurrence that the bodybuilding community has actually bestowed the name trensomnia on the condition. I’ve tried to determine the underlying cause for years but have never been able to pinpoint it, however it does seem significantly more prevalent during periods of food restriction.

And finally, understand that many of the early safety tests performed on the compound are not publicly available, and only available within the WHO Database [112] as abstracts. There is still some interesting information to glean for those that want to deeper-dive, so I will leave the link for you.
XIV. Closing Thoughts / Practical Applications

We’ve covered a lot of ground in this article series, and believe me when I say there was even more content which I had to leave out of the series purely in respect to length. I’m going to use this final section to kind of bring things together and offer some more of my personal thoughts on the topic, which have been formed from years of first and second-hand experience. I am not giving out sample stack designs, nor will I be providing dosing recommendations. I find this to be difficult to do for many reasons and I also personally feel that it may just be ethically wrong. Furthermore, we all know that individual responses to hormones varies so wildly that what works for one may be a trainwreck for others.

As I mentioned at the beginning of this series, trenbolone has an almost mythical reputation and a lot of it is fairly well-deserved. It is a very powerful, yet diverse, compound and it is largely for these reasons that I’ve changed many of my philosophies over the years. In fact, if you have read the original Science of Trenbolone article, you probably remember me being very much against using trenbolone in a growth phase. Conversely, I felt that trenbolone truly shined during dietary phases and contest preps.

This would seemingly make a lot of sense after dissecting trenbolone’s affinity for preserving lean mass, right? Well, there is a lot more to it that this, and these days I honestly don’t feel it takes much to prevent skeletal muscle atrophy in an enhanced bodybuilder-diet phase. In addition, over the years I saw trenbolone wreak havoc on dieters, time and time again. It would lead to misery as sleep was severely impacted, because of this significant fatigue would set in, and ultimately mood shifts would occur. It is likely that systemic stress levels would also increase leading folks to become very irritable, even with their loved ones. And it didn’t take long for these symptoms to manifest, particularly if one was in a state of very low body fat.

Interestingly enough, very few of these symptoms would pop-up when equivalent doses of trenbolone were used during periods of growth. I cannot explain why this happens, but I’ve seen it way too many times to chalk it up to coincidence. I still don’t necessarily advocate it being used frequently in growth phases however, in the right scenario, it can be a very nice accessory compound. I still feel as if solid growth stack design methodology calls for a stack anchored by compounds such as testosterone, nandrolone, dianabol, or anadrol.

Because of trenbolone’s unique impacts on glucocorticoids, and consequently insulin sensitivity, I currently feel a strong case could be made that it can be a useful hormone to run alongside GH+insulin. My personal favorite use of trenbolone tends to be in this very fashion, using a very modest amount during a growth phase alongside either nandrolone or testosterone. Many years ago, I jokingly coined the phrase “golden growth stack” when attempting to describe how well I looked and felt on a TRT + modest trenbolone + higher nandrolone based stack design. Even though I was largely being flippant at the time, it still tends to be the basic methodology I use in a lot of growth stack designs.

Another reason why trenbolone may not be suited to run during times of caloric restriction is its potential impacts on the thyroidal axis. Although the evidence is not overwhelming, there is enough out there to suggest that trenbolone directly impacts thyroidal output, and may even lead to a suppressed metabolic rate. Obviously, neither of these are going to be effects that are necessarily advantageous on a diet when intake levels are already going to be low. Perhaps this could be overcome if one were to use exogenous thyroid alongside their trenbolone, but now you have two compounds with reputations of being very harsh on quality of life potentially making the dietary experience even more rough than it otherwise needs to be. On the other hand, this could technically wind up becoming an advantage to someone trying to grow, as food requirements may actually lessen. Of course, some find that trenbolone simply wrecks appetites, so this should also be factored into the decision making process when determining if trenbolone is the right hormone for the job.

Due to the fact that trenbolone is not a substrate for either 5α reductase or aromatase, it is likely not going to shock anyone to learn that I do not feel running trenbolone-solo is a great idea. Although early trials are already being conducted to investigate trenbolone’s potential as an HRT, I just don’t believe this will ever go anywhere because males need DHT and estrogen for various important metabolic functions. If these are being suppressed long-term, it is highly likely that unwanted issues will arise. As part of this article series, I actually wanted to collect blood tests from people that had done trenbolone-solo stacks, but they were incredibly hard to find. One of the common responses I received back was that individuals just felt awful after a few weeks of trying this and gave up before blood tests could be obtained. There could be many contributing factors to why this occurred, but I do speculate suppressing downstream testosterone pathways could be a major one to consider.

Although there was nothing in the literature that specifically stated this, personal experience suggests that trenbolone is one of the more harsh AAS and should be respected as such. I do not advocate long stretches of continuous use, rather one should understand what trenbolone brings to a hormone stack and time their usage of it accordingly. This can be somewhat easier to accomplish when using the acetate (short) ester but can also be accomplished with the enanthate (long) ester. Some anecdote from message boards suggest responses to the different esters may vary, however this has not been my experience or that of folks I’ve worked with. The acetate ester has more active hormone than the enanthate ester does, so any self-experiments should keep this in mind to ensure equal doses are being used. Because enanthate will be active in the system longer, it can be wise to use the acetate ester when experimenting with trenbolone for the first time. Should unwanted symptoms arise, this will allow the hormone to clear the system much quicker.

There seems to be a potential hypertrophic synergy between androgens and β-adrenergic agonists, however I have traditionally not used the latter within any of my off-season protocols and cannot comment further than this. Hypothetically speaking, they use different anabolic pathways to induce hypertrophy but one would need to factor in the potential for decreased quality of life before deciding if this is a self-experiment to perform on themselves.

Lam DW, LeRoith D. Metabolic Syndrome. [Updated 2015 May 19]. In: De Groot LJ, Chrousos G, Dungan K, et al., editors. Endotext [Internet]. South Dartmouth (MA):, Inc.; 2000-.
Corona G, Mannucci E, Petrone L, Balercia G, Paggi F, Fisher AD, Lotti F, Chiarini V, Fedele D, Forti G, Maggi M. NCEP-ATPIII-defined metabolic syndrome, type 2 diabetes mellitus, and prevalence of hypogonadism in male patients with sexual dysfunction. J Sex Med. 2007 Jul;4(4 Pt 1):1038-45.
Mammi C, Calanchini M, Antelmi A, Cinti F, Rosano GM, Lenzi A, Caprio M, Fabbri A. Androgens and adipose tissue in males: a complex and reciprocal interplay. Int J Endocrinol. 2012;2012:789653.
BS DJHMB. Androgen Physiology, Pharmacology and Abuse. 2016 Dec 12. In: De Groot LJ, Chrousos G, Dungan K, Feingold KR, Grossman A, Hershman JM, Koch C, Korbonits M, McLachlan R, New M, Purnell J, Rebar R, Singer F, Vinik A, editors. Endotext [Internet]. South Dartmouth (MA):, Inc.; 2000-.
Laaksonen DE, Niskanen L, Punnonen K, Nyyssönen K, Tuomainen TP, Valkonen VP, Salonen JT. The metabolic syndrome and smoking in relation to hypogonadism in middle-aged men: a prospective cohort study. J Clin Endocrinol Metab. 2005 Feb;90(2):712-9.
Haring R, Ittermann T, Völzke H, Krebs A, Zygmunt M, Felix SB, Grabe HJ, Nauck M, Wallaschofski H. Prevalence, incidence and risk factors of testosterone deficiency in a population-based cohort of men: results from the study of health in Pomerania. Aging Male. 2010 Dec;13(4):247-57.
Eriksson J, Haring R, Grarup N, Vandenput L, Wallaschofski H, Lorentzen E, Hansen T, Mellström D, Pedersen O, Nauck M, Lorentzon M, Nystrup Husemoen LL, Völzke H, Karlsson M, Baumeister SE, Linneberg A, Ohlsson C. Causal relationship between obesity and serum testosterone status in men: A bi-directional mendelian randomization analysis. PLoS One. 2017 Apr 27;12(4)
Vermeulen A, Goemaere S, Kaufman JM. Testosterone, body composition and aging. J Endocrinol Invest. 1999;22(5 Suppl):110-6. Review.
Galassi A, Reynolds K, He J. Metabolic syndrome and risk of cardiovascular disease: a meta-analysis. Am J Med. 2006 Oct;119(10):812-9.
Donner DG, Beck BR, Bulmer AC, Lam AK, Du Toit EF. Improvements in body composition, cardiometabolic risk factors and insulin sensitivity with trenbolone in normogonadic rats. Steroids. 2015 Feb;94:60-9.
Donner DG, Elliott GE, Beck BR, Bulmer AC, Lam AK, Headrick JP, Du Toit EF. Trenbolone Improves Cardiometabolic Risk Factors and Myocardial Tolerance to Ischemia-Reperfusion in Male Rats With Testosterone-Deficient Metabolic Syndrome. Endocrinology. 2016 Jan;157(1):368-81.
Borst SE, Quindry JC, Yarrow JF, Conover CF, Powers SK. Testosterone administration induces protection against global myocardial ischemia. Horm Metab Res. 2010 Feb;42(2):122-9.
Rubio-Gayosso I, Ramirez-Sanchez I, Ita-Islas I, Ortiz-Vilchis P, Gutierrez-Salmean G, Meaney A, Palma I, Olivares I, Garcia R, Meaney E, Ceballos G. Testosterone metabolites mediate its effects on myocardial damage induced by ischemia/reperfusion in male Wistar rats. Steroids. 2013 Mar;78(3):362-9.
Pongkan W, Chattipakorn SC, Chattipakorn N. Chronic testosterone replacement exerts cardioprotection against cardiac ischemia-reperfusion injury by attenuating mitochondrial dysfunction in testosterone-deprived rats. PLoS One.2015 Mar 30;10(3)
Eugene F. du Toit and Daniel G. Donner (2012). Myocardial Insulin Resistance: An Overview of Its Causes, Effects, and Potential Therapy, Insulin Resistance, Dr. Sarika Arora (Ed.), InTech,
Yarrow JF, McCoy SC, Borst SE. 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. Steroids. 2010 Jun;75(6):377-89.
Yarrow JF, Conover CF, McCoy SC, Lipinska JA, Santillana CA, Hance JM, Cannady DF, VanPelt TD, Sanchez J, Conrad BP, Pingel JE, Wronski TJ, Borst SE. 17β-Hydroxyestra-4,9,11-trien-3-one (trenbolone) exhibits tissue selective anabolic activity: effects on muscle, bone, adiposity, hemoglobin, and prostate. Am J Physiol Endocrinol Metab. 2011 Apr;300(4):E650-60.
Bartle SJ, Preston RL, Brown RE, Grant RJ. Trenbolone acetate/estradiol combinations in feedlot steers: dose-response and implant carrier effects. J Anim Sci. 1992 May;70(5):1326-32.
Herschler RC, Olmsted AW, Edwards AJ, Hale RL, Montgomery T, Preston RL, Bartle SJ, Sheldon JJ. Production responses to various doses and ratios of estradiol benzoate and trenbolone acetate implants in steers and heifers. J Anim Sci. 1995 Oct;73(10):2873-81.
Foutz CP, Dolezal HG, Gardner TL, Gill DR, Hensley JL, Morgan JB. Anabolic implant effects on steer performance, carcass traits, subprimal yields, and longissimus muscle properties. J Anim Sci. 1997 May;75(5):1256-65.
Roeber DL, Cannell RC, Belk KE, Miller RK, Tatum JD, Smith GC. Implant strategies during feeding: impact on carcass grades and consumer acceptability. J Anim Sci. 2000 Jul;78(7):1867-74.
Reiling BA, Johnson DD. Effects of implant regimens (trenbolone acetate-estradiol administered alone or in combination with zeranol) and vitamin D3 on fresh beef color and quality. J Anim Sci. 2003 Jan;81(1):135-42.
Bruns KW, Pritchard RH, Boggs DL. The effect of stage of growth and implant exposure on performance and carcass composition in steers. J Anim Sci. 2005 Jan;83(1):108-16.
Johnson BJ, Anderson PT, Meiske JC, Dayton WR. Effect of a combined trenbolone acetate and estradiol implant on feedlot performance, carcass characteristics, and carcass composition of feedlot steers. J Anim Sci. 1996 Feb;74(2):363-71.
Smith KR, Duckett SK, Azain MJ, Sonon RN Jr, Pringle TD. The effect of anabolic implants on intramuscular lipid deposition in finished beef cattle. J Anim Sci. 2007 Feb;85(2):430-40
Yarrow JF, Beggs LA, Conover CF, McCoy SC, Beck DT, Borst SE. Influence of Androgens on Circulating Adiponectin in Male and Female Rodents. Lobaccaro J-MA, ed. PLoS ONE. 2012;7(10):e47315.
Ranaweera KN, Wise DR. The effects of trienbolone acetate on carcass composition, conformation and skeletal growth of turkeys. Br Poult Sci. 1981 Mar;22(2):105-14.
Istasse L, Evrard P, Van Eenaeme C, Gielen M, Maghuin-Rogister G, Bienfait JM. Trenbolone acetate in combination with 17 beta-estradiol: influence of implant supports and dose levels on animal performance and plasma metabolites. J Anim Sci. 1988 May;66(5):1212-22.
Schmidely P, Bas P, Rouzeau A, Hervieu J, Morand-Fehr P. Influence of trenbolone acetate combined with estradiol-17 beta on growth performance, body characteristics, and chemical composition of goat kids fed milk and slaughtered at different ages. J Anim Sci. 1992 Nov;70(11):3381-90.
Cranwell CD, Unruh JA, Brethour JR, Simms DD, Campbell RE. Influence of steroid implants and concentrate feeding on performance and carcass composition of cull beef cows. J Anim Sci. 1996 Aug;74(8):1770-6.
van Weerden EJ, Grandadam JA. The effect of an anabolic agent on N deposition, growth, and slaughter quality in growing castrated male pigs. Environ Qual Saf Suppl. 1976;(5):115-22.
Hermesmeyer GN, Berger LL, Nash TG, Brandt RT Jr. Effects of energy intake, implantation, and subcutaneous fat end point on feedlot steer performance and carcass composition. J Anim Sci. 2000 Apr;78(4):825-31.
Lee CY, Lee HP, Jeong JH, Baik KH, Jin SK, Lee JH, Sohnt SH. Effects of restricted feeding, low-energy diet, and implantation of trenbolone acetate plus estradiol on growth, carcass traits, and circulating concentrations of insulin-like growth factor (IGF)-I and IGF-binding protein-3 in finishing barrows. J Anim Sci. 2002 Jan;80(1):84-93.
Lee CY, Henricks DM, Skelley GC, Grimes LW. Growth and hormonal response of intact and castrate male cattle to trenbolone acetate and estradiol. J Anim Sci. 1990 Sep;68(9):2682-9.
Kellermeier JD, Tittor AW, Brooks JC, Galyean ML, Yates DA, Hutcheson JP, Nichols WT, Streeter MN, Johnson BJ, Miller MF. Effects of zilpaterol hydrochloride with or without an estrogen-trenbolone acetate terminal implant on carcass traits, retail cutout, tenderness, and muscle fiber diameter in finishing steers. J Anim Sci. 2009 Nov;87(11):3702-11.
Thompson SH, Boxhorn LK, Kong WY, Allen RE. Trenbolone alters the responsiveness of skeletal muscle satellite cells to fibroblast growth factor and insulin-like growth factor I. Endocrinology. 1989 May;124(5):2110-7.
Lough DS, Kahl S, Solomon MB, Rumsey TS. The effect of trenbolone acetate on performance, plasma lipids, and carcass characteristics of growing ram and ewe lambs. J Anim Sci. 1993 Oct;71(10):2659-65.
Dieudonne MN, Pecquery R, Boumediene A, Leneveu MC, Giudicelli Y. Androgen receptors in human preadipocytes and adipocytes: regional specificities and regulation by sex steroids. Am J Physiol. 1998 Jun;274(6 Pt 1):C1645-52.
Blouin K, Veilleux A, Luu-The V, Tchernof A. Androgen metabolism in adipose tissue: recent advances. Mol Cell Endocrinol. 2009 Mar 25;301(1-2):97-103.
Xu X, De Pergola G, Björntorp P. The effects of androgens on the regulation of lipolysis in adipose precursor cells. Endocrinology. 1990 Feb;126(2):1229-34.
De Pergola G. The adipose tissue metabolism: role of testosterone and dehydroepiandrosterone. Int J Obes Relat Metab Disord. 2000 Jun;24 Suppl 2:S59-63. Review.
James RG, Krakower GR, Kissebah AH. Influence of androgenicity on adipocytes and precursor cells in female rats. Obes Res. 1996 Sep;4(5):463-70.
Björntorp P. Neuroendocrine factors in obesity. J Endocrinol. 1997 Nov;155(2):193-5. Review.
Freedland ES. Role of a critical visceral adipose tissue threshold (CVATT) in metabolic syndrome: implications for controlling dietary carbohydrates: a review. Nutr Metab (Lond). 2004 Nov 5;1(1):12.
Sato T, Matsumoto T, Yamada T, Watanabe T, Kawano H, Kato S. Late onset of obesity in male androgen receptor-deficient (AR KO) mice. Biochem Biophys Res Commun. 2003 Jan 3;300(1):167-71.
Fan W, Yanase T, Nomura M, Okabe T, Goto K, Sato T, Kawano H, Kato S, Nawata H. Androgen receptor null male mice develop late-onset obesity caused by decreased energy expenditure and lipolytic activity but show normal insulin sensitivity with high adiponectin secretion. Diabetes. 2005 Apr;54(4):1000-8.
McInnes KJ, Smith LB, Hunger NI, Saunders PT, Andrew R, Walker BR. Deletion of the androgen receptor in adipose tissue in male mice elevates retinol binding protein 4 and reveals independent effects on visceral fat mass and on glucose homeostasis. Diabetes. 2012 May;61(5):1072-81.
Reiter M, Walf VM, Christians A, Pfaffl MW, Meyer HH. Modification of mRNA expression after treatment with anabolic agents and the usefulness for gene expression-biomarkers. Anal Chim Acta. 2007 Mar 14;586(1-2):73-81.
Joyner JM, Hutley LJ, Cameron DP. Estrogen receptors in human preadipocytes. Endocrine. 2001 Jul;15(2):225-30.
Singh R, Artaza JN, Taylor WE, Gonzalez-Cadavid NF, Bhasin S. Androgens stimulate myogenic differentiation and inhibit adipogenesis in C3H 10T1/2 pluripotent cells through an androgen receptor-mediated pathway. Endocrinology. 2003 Nov;144(11):5081-8.
Shang Y, Zhang C, Wang S, Xiong F, Zhao C, Peng F, Feng S, Yu M, Li M, Zhang Y. Activated beta-catenin induces myogenesis and inhibits adipogenesis in BM-derived mesenchymal stromal cells. Cytotherapy. 2007;9(7):667-81.
Colbert WE, Williams PD, Williams GD. Beta-adrenoceptor profile of ractopamine HCl in isolated smooth and cardiac muscle tissues of rat and guinea-pig. J Pharm Pharmacol. 1991 Dec;43(12):844-7.
Liu CY, Grant AL, Kim KH, Ji SQ, Hancock DL, Anderson DB, Mills SE. Limitations of ractopamine to affect adipose tissue metabolism in swine. J Anim Sci. 1994 Jan;72(1):62-7.
Mersmann HJ. Overview of the effects of beta-adrenergic receptor agonists on animal growth including mechanisms of action. J Anim Sci. 1998 Jan;76(1):160-72. Review.
O’Connor RM, Butler WR, Hogue DE, Beermann DH. Temporal pattern of skeletal muscle changes in lambs fed cimaterol. Domest Anim Endocrinol. 1991 Oct;8(4):549-54.
Catherine A. Ricks, R. H. Dalrymple, Pamela K. Baker, D. L. Ingle; Use of a β-Agonist to Alter Fat and Muscle Deposition in Steers, Journal of Animal Science, Volume 59, Issue 5, 1 November 1984, Pages 1247–1255,
Johnson BJ, Chung KY. Alterations in the physiology of growth of cattle with growth-enhancing compounds. Vet Clin North Am Food Anim Pract. 2007 Jul;23(2):321-32, viii. Review.
Baxa TJ, Hutcheson JP, Miller MF, Brooks JC, Nichols WT, Streeter MN, Yates DA, Johnson BJ. Additive effects of a steroidal implant and zilpaterol hydrochloride on feedlot performance, carcass characteristics, and skeletal muscle messenger ribonucleic acid abundance in finishing steers. J Anim Sci. 2010 Jan;88(1):330-7.
Braunstein GD. Aromatase and gynecomastia. Endocr Relat Cancer. 1999 Jun;6(2):315-24. Review.
Steers WD. 5alpha-reductase activity in the prostate. Urology. 2001 Dec;58(6 Suppl 1):17-24; discussion 24. Review.
Stachenfeld NS, Taylor HS. Effects of estrogen and progesterone administration on extracellular fluid. J Appl Physiol (1985). 2004 Mar;96(3):1011-8.
Carruba G. Estrogen and prostate cancer: an eclipsed truth in an androgen-dominated scenario. J Cell Biochem. 2007 Nov 1;102(4):899-911. Review.
Eckman A, Dobs A. Drug-induced gynecomastia. Expert Opin Drug Saf. 2008 Nov;7(6):691-702.
Zhou CK, Check DP, Lortet-Tieulent J, Laversanne M, Jemal A, Ferlay J, Bray F, Cook MB, Devesa SS. Prostate cancer incidence in 43 populations worldwide: An analysis of time trends overall and by age group. Int J Cancer. 2016 Mar 15;138(6):1388-400.
Calof OM, Singh AB, Lee ML, Kenny AM, Urban RJ, Tenover JL, Bhasin S. Adverse events associated with testosterone replacement in middle-aged and older men: a meta-analysis of randomized, placebo-controlled trials. J Gerontol A Biol Sci Med Sci. 2005 Nov;60(11):1451-7.
Shabsigh R, Crawford ED, Nehra A, Slawin KM. Testosterone therapy in hypogonadal men and potential prostate cancer risk: a systematic review. Int J Impot Res. 2009 Jan-Feb;21(1):9-23.
Pitts WR Jr. Validation of the Pitts unified theory of prostate cancer, late-onset hypogonadism and carcinoma: the role of steroid 5alpha-reductase and steroid aromatase. BJU Int. 2007 Aug;100(2):254-7. Epub 2007 May 17. Review.
Amory JK, Watts NB, Easley KA, Sutton PR, Anawalt BD, Matsumoto AM, Bremner WJ, Tenover JL. Exogenous testosterone or testosterone with finasteride increases bone mineral density in older men with low serum testosterone. J Clin Endocrinol Metab. 2004 Feb;89(2):503-10.
Page ST, Amory JK, Bowman FD, Anawalt BD, Matsumoto AM, Bremner WJ, Tenover JL. Exogenous testosterone (T) alone or with finasteride increases physical performance, grip strength, and lean body mass in older men with low serum T. J Clin Endocrinol Metab. 2005 Mar;90(3):1502-10.
Finkelstein JS, Yu EW, Burnett-Bowie SA. Gonadal steroids and body composition, strength, and sexual function in men. N Engl J Med. 2013 Dec 19;369(25):2457.
Dalbo VJ, Roberts MD, Mobley CB, Ballmann C, Kephart WC, Fox CD, Santucci VA, Conover CF, Beggs LA, Balaez A, Hoerr FJ, Yarrow JF, Borst SE, Beck DT. Testosterone and trenbolone enanthate increase mature myostatin protein expression despite increasing skeletal muscle hypertrophy and satellite cell number in rodent muscle. Andrologia. 2017 Apr;49(3).
Broulik PD, Kochakian CD, Dubovsky J. Influence of castration and testosterone propionate on cardiac output, renal blood flow, and blood volume in mice. Proc Soc Exp Biol Med. 1973 Nov;144(2):671-3.
Koenig H, Goldstone A, Lu CY. Testosterone-mediated sexual dimorphism of the rodent heart. Ventricular lysosomes, mitochondria, and cell growth are modulated by androgens. Circ Res. 1982 Jun;50(6):782-7.
Sebag IA, Gillis MA, Calderone A, Kasneci A, Meilleur M, Haddad R, Noiles W, Patel B, Chalifour LE. Sex hormone control of left ventricular structure/function: mechanistic insights using echocardiography, expression, and DNA methylation analyses in adult mice. Am J Physiol Heart Circ Physiol. 2011 Oct;301(4):H1706-15.
Cavasin MA, Sankey SS, Yu AL, Menon S, Yang XP. Estrogen and testosterone have opposing effects on chronic cardiac remodeling and function in mice with myocardial infarction. Am J Physiol Heart Circ Physiol. 2003 May;284(5):H1560-9.
Urhausen A, Albers T, Kindermann W. Are the cardiac effects of anabolic steroid abuse in strength athletes reversible? Heart. 2004 May;90(5):496-501.
Fanton L, Belhani D, Vaillant F, Tabib A, Gomez L, Descotes J, Dehina L, Bui-Xuan B, Malicier D, Timour Q. Heart lesions associated with anabolic steroid abuse: comparison of post-mortem findings in athletes and norethandrolone-induced lesions in rabbits. Exp Toxicol Pathol. 2009 Jul;61(4):317-23.
Vanberg P, Atar D. Androgenic anabolic steroid abuse and the cardiovascular system. Handb Exp Pharmacol. 2010;(195):411-57.
Montisci M, El Mazloum R, Cecchetto G, Terranova C, Ferrara SD, Thiene G, Basso C. Anabolic androgenic steroids abuse and cardiac death in athletes: morphological and toxicological findings in four fatal cases. Forensic Sci Int. 2012 Apr 10;217(1-3):e13-8.
Higgins JP, Heshmat A, Higgins CL. Androgen abuse and increased cardiac risk. South Med J. 2012 Dec;105(12):670-4.
Lau DH, Stiles MK, John B, Shashidhar, Young GD, Sanders P. Atrial fibrillation and anabolic steroid abuse. Int J Cardiol. 2007 Apr 25;117(2):e86-7.
Liu T, Shehata M, Li G, Wang X. Androgens and atrial fibrillation: friends or foes? Int J Cardiol. 2010 Nov 19;145(2):365-367.
Sullivan ML, Martinez CM, Gallagher EJ. Atrial fibrillation and anabolic steroids. J Emerg Med. 1999 Sep-Oct;17(5):851-7. Review.
Fineschi V, Riezzo I, Centini F, Silingardi E, Licata M, Beduschi G, Karch SB. Sudden cardiac death during anabolic steroid abuse: morphologic and toxicologic findings in two fatal cases of bodybuilders. Int J Legal Med. 2007 Jan;121(1):48-53.
Frankenfeld SP, Oliveira LP, Ortenzi VH, Rego-Monteiro IC, Chaves EA, Ferreira AC, Leitão AC, Carvalho DP, Fortunato RS. The anabolic androgenic steroid nandrolone decanoate disrupts redox homeostasis in liver, heart and kidney of male Wistar rats. PLoS One. 2014 Sep 16;9(9):e102699.
Tivesten A, Bollano E, Nyström HC, Alexanderson C, Bergström G, Holmäng A. Cardiac concentric remodelling induced by non-aromatizable (dihydro-)testosterone is antagonized by oestradiol in ovariectomized rats. J Endocrinol. 2006 Jun;189(3):485-91.
Hatanaka Y, Mukai H, Mitsuhashi K, Hojo Y, Murakami G, Komatsuzaki Y, Sato R, Kawato S. Androgen rapidly increases dendritic thorns of CA3 neurons in male rat hippocampus. Biochem Biophys Res Commun. 2009 Apr 17;381(4):728-32.
Ma F, Liu D. 17β-trenbolone, an anabolic-androgenic steroid as well as an environmental hormone, contributes to neurodegeneration. Toxicol Appl Pharmacol. 2015 Jan 1;282(1):68-76.
Tanzi RE, Bertram L. Twenty years of the Alzheimer’s disease amyloid hypothesis: a genetic perspective. Cell. 2005 Feb 25;120(4):545-55. Review.
Wojda U, Kuznicki J. Alzheimer’s disease modeling: ups, downs, and perspectives for human induced pluripotent stem cells. J Alzheimers Dis. 2013;34(3):563-88.
Blennow K. CSF biomarkers for Alzheimer’s disease: use in early diagnosis and evaluation of drug treatment. Expert Rev Mol Diagn. 2005 Sep;5(5):661-72. Review.
Mattson MP. Apoptosis in neurodegenerative disorders. Nat Rev Mol Cell Biol. 2000 Nov;1(2):120-9. Review.
Ankley GT, Defoe DL, Kahl MD, Jensen KM, Makynen EA, Miracle A, Hartig P, Gray LE, Cardon M, Wilson V. Evaluation of the model anti-androgen flutamide for assessing the mechanistic basis of responses to an androgen in the fathead minnow (Pimephales promelas). Environ Sci Technol. 2004 Dec 1;38(23):6322-7.
Sone K, Hinago M, Itamoto M, Katsu Y, Watanabe H, Urushitani H, Tooi O, Guillette LJ Jr, Iguchi T. Effects of an androgenic growth promoter 17beta-trenbolone on masculinization of Mosquitofish (Gambusia affinis affinis). Gen Comp Endocrinol. 2005 Sep 1;143(2):151-60.
Jensen KM, Ankley GT. Evaluation of a commercial kit for measuring vitellogenin in the fathead minnow (Pimephales promelas). Ecotoxicol Environ Saf. 2006 Jun;64(2):101-5. Epub 2006 Apr 17.
Orn S, Yamani S, Norrgren L. Comparison of vitellogenin induction, sex ratio, and gonad morphology between zebrafish and Japanese medaka after exposure to 17alpha-ethinylestradiol and 17beta-trenbolone. Arch Environ Contam Toxicol. 2006 Aug;51(2):237-43.
Park JW, Tompsett A, Zhang X, Newsted JL, Jones PD, Au D, Kong R, Wu RS, Giesy JP, Hecker M. Fluorescence in situ hybridization techniques (FISH) to detect changes in CYP19a gene expression of Japanese medaka (Oryzias latipes). Toxicol Appl Pharmacol. 2008 Oct 15;232(2):226-35.
Heitzman RJ, Harwood DJ, Kay RM, Little W, Mallinson CB, Reynolds IP. Effects of implanting prepuberal dairy heifers with anabolic steroids on hormonal status, puberty and parturition. J Anim Sci. 1979 Apr;48(4):859-66.
Moran C, Prendiville DJ, Quirke JF, Roche JF. Effects of oestradiol, zeranol or trenbolone acetate implants on puberty, reproduction and fertility in heifers. J Reprod Fertil. 1990 Jul;89(2):527-36.
Hotchkiss AK, Furr J, Makynen EA, Ankley GT, Gray LE Jr. In utero exposure to the environmental androgen trenbolone masculinizes female Sprague-Dawley rats. Toxicol Lett. 2007 Nov 1;174(1-3):31-41.
Peters AR. Effect of trenbolone acetate on ovarian function in culled dairy cows. Vet Rec. 1987 Apr 25;120(17):413-6.
Zhang X, Hecker M, Park JW, Tompsett AR, Newsted J, Nakayama K, Jones PD, Au D, Kong R, Wu RS, Giesy JP. Real-time PCR array to study effects of chemicals on the Hypothalamic-Pituitary-Gonadal axis of the Japanese medaka. Aquat Toxicol. 2008 Jul 7;88(3):173-82.
Zhang X, Hecker M, Park JW, Tompsett AR, Jones PD, Newsted J, Au DW, Kong R, Wu RS, Giesy JP. Time-dependent transcriptional profiles of genes of the hypothalamic-pituitary-gonadal axis in medaka (Oryzias latipes) exposed to fadrozole and 17beta-trenbolone. Environ Toxicol Chem. 2008 Dec;27(12):2504-11.
Neumann F. Pharmacological and endocrinological studies on anabolic agents. Environ Qual Saf Suppl. 1976;(5):253-64. Review.
Shahsavari Nia K, Rahmani F, Ebrahimi Bakhtavar H, Hashemi Aghdam Y, Balafar M. A Young Man with Myocardial Infarction due to Trenbolone Acetate; a Case Report. Emerg (Tehran). 2014 Winter;2(1):43-5.
Daniels JM, van Westerloo DJ, de Hon OM, Frissen PH. [Rhabdomyolysis in a bodybuilder using steroids]. Ned Tijdschr Geneeskd. 2006 May 13;150(19):1077-80.
Anand JS, Chodorowski Z, Hajduk A, Waldman W. Cholestasis induced by parabolan successfully treated with the molecular adsorbent recirculating system. ASAIO J. 2006 Jan-Feb;52(1):117-8.
Seeger, K. (1971b). R 1967: Chronische Toxizitat per oral. Unpublished report from Hoechst A.G. Submitted to WHO by Roussel Uclaf, Paris, France.
Pearson JT, Buttery PJ. Polyamine excretion by trenbolone acetate treated rats. Proc Nutr Soc. 1979 Sep;38(2):91A.
López-Bote C, Sancho G, Martínez M, Ventanas J, Gázquez A, Roncero V. Trenbolone acetate induced changes in the genital tract of male pigs. Zentralbl Veterinarmed B. 1994 Mar;41(1):42-8.
Hotchkiss AK, Nelson RJ. An environmental androgen, 17beta-trenbolone, affects delayed-type hypersensitivity and reproductive tissues in male mice. J Toxicol Environ Health A. 2007 Jan 15;70(2):138-40.

Leave a Reply

Your email address will not be published. Required fields are marked *