The Science of Trenbolone, Part 4

As we close out this article series, there are still some important aspects of trenbolone left to cover. So, in this final installment, we are going to start off discussing how androgens impact fat stores. We’ll move on from there and into the realm of side effects and finish up with my closing thoughts, including potential practical applications of what we’ve learned.

XII. LIPOLYSIS

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

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.

Heart

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.

Brain

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.

Virilization

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.

References

1. 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): MDText.com, Inc.; 2000-.
2. 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.
3. 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.
4. 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): MDText.com, Inc.; 2000-.
5. 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.
6. 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.
7. 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)
8. Vermeulen A, Goemaere S, Kaufman JM. Testosterone, body composition and aging. J Endocrinol Invest. 1999;22(5 Suppl):110-6. Review.
9. 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.
10. 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.
11. 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.
12. 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.
13. 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.
14. 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)
15. 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,
16. 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.
17. 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.
18. 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.
19. 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.
20. 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.
21. 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.
22. 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.
23. 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.
24. 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.
25. 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
26. 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.
27. 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.
28. 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.
29. 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.
30. 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.
31. 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.
32. 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.
33. 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.
34. 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.
35. 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.
36. 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.
37. 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.
38. 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.
39. 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.
40. 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.
41. 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.
42. 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.
43. Björntorp P. Neuroendocrine factors in obesity. J Endocrinol. 1997 Nov;155(2):193-5. Review.
44. 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.
45. 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.
46. 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.
47. 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.
48. 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.
49. Joyner JM, Hutley LJ, Cameron DP. Estrogen receptors in human preadipocytes. Endocrine. 2001 Jul;15(2):225-30.
50. 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.
51. 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.
52. 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.
53. 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.
54. 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.
55. 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.
56. 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,
57. 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.
58. 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.
59. Braunstein GD. Aromatase and gynecomastia. Endocr Relat Cancer. 1999 Jun;6(2):315-24. Review.
60. Steers WD. 5alpha-reductase activity in the prostate. Urology. 2001 Dec;58(6 Suppl 1):17-24; discussion 24. Review.
61. Stachenfeld NS, Taylor HS. Effects of estrogen and progesterone administration on extracellular fluid. J Appl Physiol (1985). 2004 Mar;96(3):1011-8.
62. 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.
63. Eckman A, Dobs A. Drug-induced gynecomastia. Expert Opin Drug Saf. 2008 Nov;7(6):691-702.
64. 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.
65. 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.
66. 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.
67. 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.
68. 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.
69. 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.
70. 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.
71. 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).
72. 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.
73. 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.
74. 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.
75. 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.
76. 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.
77. 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.
78. Vanberg P, Atar D. Androgenic anabolic steroid abuse and the cardiovascular system. Handb Exp Pharmacol. 2010;(195):411-57.
79. 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.
80. Higgins JP, Heshmat A, Higgins CL. Androgen abuse and increased cardiac risk. South Med J. 2012 Dec;105(12):670-4.
81. 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.
82. 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.
83. Sullivan ML, Martinez CM, Gallagher EJ. Atrial fibrillation and anabolic steroids. J Emerg Med. 1999 Sep-Oct;17(5):851-7. Review.
84. 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.
85. 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.
86. 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.
87. 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.
88. 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.
89. 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.
90. 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.
91. 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.
92. Mattson MP. Apoptosis in neurodegenerative disorders. Nat Rev Mol Cell Biol. 2000 Nov;1(2):120-9. Review.
93. 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.
94. 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.
95. 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.
96. 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.
97. 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.
98. 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.
99. 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.
100. 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.
101. Peters AR. Effect of trenbolone acetate on ovarian function in culled dairy cows. Vet Rec. 1987 Apr 25;120(17):413-6.
102. 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.
103. 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.
104. Neumann F. Pharmacological and endocrinological studies on anabolic agents. Environ Qual Saf Suppl. 1976;(5):253-64. Review.
105. 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.
106. 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.
107. 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.
108. Seeger, K. (1971b). R 1967: Chronische Toxizitat per oral. Unpublished report from Hoechst A.G. Submitted to WHO by Roussel Uclaf, Paris, France.
109. Pearson JT, Buttery PJ. Polyamine excretion by trenbolone acetate treated rats. Proc Nutr Soc. 1979 Sep;38(2):91A.
110. 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.
111. 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.
112. http://www.inchem.org/documents/jecfa/jecmono/v25je08.htm