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.
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.
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 . It can also be traditionally characterized by increased visceral adiposity, dyslipidemia (elevation of cholesterol), and insulin resistance .
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.
Another correlation has been found in males between obesity-associated metabolic syndrome and androgen deficiency . Androgen deficiency occurs in approximately 1 in 200 men  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 .
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 . 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.
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 . In castrated rats, the lipolytic effects of trenbolone have been demonstrated to be dose-dependent .
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 . 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 .
Getting back to the body of literature as a whole, trenbolone administration has been shown to reduce visceral fat , 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 . 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.
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 . 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 .
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 . The process of adipogenesis (where preadipocytes become adipocytes) is partly mediated by the estrogen receptor alpha (ERα) expressed in these preadipocytes . 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 . This was specifically seen in cell lines where activation of the Wnt/β-catenin pathway enhanced myogenesis and inhibited adipogenesis . 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.
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 . 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 . Most β-agonists used in livestock stimulate increased lipolysis, decreased lipogenesis, or stimulate protein disposition by binding to the β1- or β2-adrenergic receptors .
Steroidal implants and β-adrenergic agonists work through separate mechanisms however both ultimately act to increase protein deposition . β-adrenergic agonists are repartitioning agents that redirect absorbed nutrients away from adipose tissue, favoring protein accretion .
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 . 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].
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 . 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 . 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 . 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 . 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 . Another trial showed that the prostates of trenbolone-treated rats were not significantly different than control rats, yet significantly smaller than testosterone treated rats .
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 . 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 .
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 . 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 . 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 . 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 . 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 . A few years ago, when the infamous Ma et al study  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 . 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 . 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 . 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 .
To be blunt, trenbolone is not a female friendly androgen and I would not recommend it being used by women ever.
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 . 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 . 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 . 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 . High doses of trenbolone have been demonstrated to negatively impact male immune function in castrated mice . 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  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.
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.
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