Trenbolone Side Effects


  • Introduction
  • Metabolism, Structure, & Function
  • Anabolic Steroid Induced Hypogonadism (HPTA)
  • Liver
  • Cardiac
  • Hematology
  • Prostate
  • Pancreatitis
  • Kidney
  • Other [Neurological, Androgenization, Teratogen, Genotoxicity, and Cytotoxicity]


  • Introduction


Trenbolone is a synthetic estrane steroid a derivative of nandrolone (19-nortestosterone). It is specifically nandrolone with two additional double bonds in the steroid nucleus – addition of a cis- 9-10 double bond that inhibits aromatization and a cis- 11-12 double bond greatly enhances androgen receptor binding. Trenbolone esters, which have an ester at the C17B position, include trenbolone acetate, trenbolone enanthate, trenbolone hexahydrobenzylcarbonate, and trenbolone undecanoate. 17 –TBOH-acetate (17B-acetoxyestra-4,9,11-trien-3-one) is a potent anabolic androgenic steroid which is primarily used legally as a growth promoting agent in domestic livestock production either alone, as Finaplix or in combination with E2, as Revalor, or E2-benzoate, as Synovex. Accordingly, it has found use by sports competitors and bodybuilders. [1]

This discussion on trenbolone side effects was begun with a search of PubMed and broadened when needed. An effort was made to find studies describing the use of trenbolone and adverse/side effects. It is not exhaustive as the use of trenbolone is found in studies yet not cited in the abstract. The search strategy targeted was for all cites found with the search term ‘trenbolone’ resulting in 733 cites. Titles and abstracts resulting from the criteria were screened, and relevant information extracted from the relevant full-text articles.

The toxicity of 17B –TBOH has not been to any great extent scientifically studied in humans. The evidence regarding potential adverse events associated with 17-TBOH primarily results from studies on animals or from clinical research on other androgens (e.g., testosterone or DHT). In case reports, polypharmacy (multiple AAS as well as other drugs) makes it difficult, if not impossible, to determine the role of 17-TBOH.

Note: As the source of trenbolone is almost universally from underground labs it is of import to recognize that what one believes they are using has a good chance of being otherwise. Counterfeiting and adulteration of pharmaceuticals is a prevalent problem worldwide, with anabolic steroids being one of the main classes of drugs consumed and obtained from dubious sources. In this work, of the 40 samples analyzed, eight did not show the presence of the active principle stated on the label. Three types of adulteration were found in the analyzed samples: absence of the active ingredient, adulteration with other substances, and concentration values below those indicated on the label. [2]


  • Metabolism, Structure, & Function


In humans, ingested 6,7-3H labeled 17B –TBOH is primarily excreted intact, as 17B –TBOH, as the 17B epimer (epitrenbolone; 17B –TBOH ) or as trendione (TBO). 17 –TBOH has a greater affinity for the AR than any of its primary metabolites, suggesting that biotransformation of 17B –TBOH reduces the biological activity of this steroid. Many of the side-effects associated with supraphysiological testosterone administration appear to be primarily mediated by the more potent testosterone metabolites, DHT and E2. The metabolism of 17B –TBOH differs from that of testosterone because 17B –TBOH does not undergo 5? reduction and is reported to not be a substrate for the aromatase enzyme. In vitro bioassays and cell culture experiments demonstrate that 17B – TBOH and its metabolites have a very low binding affinity for ERs and have low estrogenic activity with approximately 20% of the efficacy of E2. Due to the reduced potency of its metabolites, 17B –TBOH appears to induce fewer systemic and tissue-specific androgenic and estrogenic side-effects than testosterone. In addition to its direct actions through ARs, 17beta-TBOH may also exert anabolic effects by altering the action of endogenous growth factors or inhibiting the action of glucocorticoids. [1, 3-12]


  • Anabolic Steroid Induced Hypogonadism (HPTA)


That trenbolone is HPTA suppressive should not be surprising at all. The evidence is clear. Disruptions of the HPG axis, including reductions in serum luteinizing hormone (LH), follicle stimulating hormone (FSH), testosterone, DHT, and E2 have been observed in a variety of species following 17B –TBOH exposure. Indirect evidence indicates disruptions of the HPG axis are present in livestock which experience reduced testicular circumference and weight and delayed puberty following administration of 17B –TBOH. While there are no comparable studies to the HPTA effects in humans of nandrolone, it would be safe and wise to expect similar suppression when looking to restore the HPTA.   [1, 13]


  • Liver


Anabolic steroids are synthetic derivatives of testosterone shown to increase muscle size and strength. Chemical substitutions on the testosterone molecule cause increased potency and duration of action. The 17-?-alkylation modification allows steroids to be taken orally, but the slower clearance in the liver makes them more hepatotoxic. The frequency and severity of side effects depends on several factors including the formulation of the drug, route of administration, dosage, duration of use, and individual sensitivity and response. Hepatotoxicity can be seen as elevated liver transaminases, acute cholestatic syndrome, chronic vascular injury, hepatic tumors, and toxicant-associated fatty liver disease, as well as significant changes in lipoproteins. Many of these changes will stabilize or reverse with cessation of steroid use, but some can be life-threatening. Case reports of liver injuries of note are cholestatic hepatitis and hepatocellular carcinoma. [14, 26-33]

Case Report: A jaundiced bodybuilder Cholestatic hepatitis as side effect of injectable anabolic-androgenic steroids. A 24-year-old male without a medical history or former cholestatic periods presented himself with loss of appetite, dark coloured urine, yellow stool and yellow sclerae since 2 weeks. The patient had finished an 8-week cycle (50 mg · day?1) of the anabolic steroid trenbolone enanthate 2 months ago. Two months after presentation, the pruritus [itching] diminished, regained his appetite, and the bilirubin levels improved. In the following weeks, he gradually recovered.

Cholestatic hepatitis is a rare side effect of AAS. After excluding other causes and performing a liver biopsy, it was the only explanation for the cholestatic hepatitis in the presented patient. Since the patient said that he only used trenbolone it may be likely as the of the cause cholestatic hepatitis. Unfortunately, it was not possible to analyse the injected AAS to confirm that it contained trenbolone and no other AAS.

Case Report: Development of hepatocellular carcinoma associated with anabolic androgenic steroid abuse in a young bodybuilder. The patient reported AAS use with different kinds of anabolic substances. For a period of at least five years he has been consuming the following AAS: Testosterone propionate, testosterone phenylpropionate, testosterone isocaproate, testosterone decanoate 250?mg, trenbolone acetate 75?mg, 5alpha-androstanediol 100?mg, boldenone and methandriol dipropionate 240?mg, 17B-Methyl-5?-androstano[3,2-c]pyrazole-17?-ol 100?mg, 17?-hydroxy-17?-methyl-2-oxa-5?-androstane-3-one ?mg, letrozole 0,065?mg, and oxymetholon ?mg or methandienone 10?mg.

The magnetic resonance imaging showed hepatomegaly, which showed features of a hepatocellular adenoma (HCA). After laparoscopic segmentectomy the histological examination revealed HCC. The clinical course was uneventful, and the patient was discharged on day 7. After a follow-up period of 27 months there was no a sign of recurrence.


  • Cardiac


The available literature on lethal cardiovascular effects of AAS consist mainly of single case reports and acute myocardial infarction due to premature atherosclerosis as the most common fatal event, although other adverse cardiovascular effects such as left ventricular hypertrophy, impaired left ventricular function, arterial thrombosis, pulmonary embolism have been also described. Interestingly, myocardial infarction without significant atherosclerotic coronary artery disease has been even reported. A lot of attention has been generated by a Swedish autopsy study where 34 male AAS users were medico-legally investigated. Chronic cardiac pathological changes were observed in 12 cases, specifically left ventricular hypertrophy, cardiac fibrosis and coronary artery disease. [14, 36-43]

The fact that AAS use employ a large number of steroid products, in various forms, singularly and in different temporal combinations and sequences, makes interpretation of pathologic findings extremely difficult. Moreover, alternative causes of myocardial hypertrophy in young athletes could have been advocated, such as in athletes exercise itself can cause left ventricular hypertrophy, regardless of the use of drugs (so-called ‘‘athlete’s heart’’). Another risk factor for hypertrophy is hypertension, either primary or associated with substance use. A number of case studies involving trenbolone have been reported. Following are those the authors cite trenbolone as contributive or causal follow.

Case Report: A Young Man with Myocardial Infarction due to Trenbolone Acetate. A 23-year-old man was referred to the emergency room with epigastric pain since the last day. Due to the absence of risk factors for heart disease, symptomatic treatment was done for him and his pain decreased so that the patient was discharged. But, after 3 days the patient presented again to ED with the same complaint. The pain radiated to the left arm accompanied by nausea. History at this time revealed use of Trenbolone Acetate for the past year. Angiography showed the stenosis of the coronary arteries.

Case Report: Anabolic Steroids Induced Cardiomyopathy. A 28-year-old male with no past medical history presented with one week of history of coughing up blood and shortness of breath. Physical exam demonstrated tachycardia, JVD, 4+ swelling in bilateral extremities and up to umbilicus. Labs were significant for elevated liver enzymes and creatinine. An electrocardiogram showed sinus tachycardia. Transthoracic and subsequently Transesophageal echocardiogram showed ejection fraction of 20%, severe mitral stenosis, severe aortic regurgitation, and left atrial mass. On further history, patient admitted to using anabolic steroids called trenbolone one week on and one week off cycle for the past 2 years. The patient had resection of left atrial mass which was biopsied revealing a thrombus and a mechanical aortic valve replacement and prosthetic mitral valve replacement.

Case Report: Steroid-induced cardiomyopathy. A 30-year-old man was admitted via the emergency department with atrial fibrillation (AF), new-onset biventricular cardiac failure, acute renal failure and elevated liver function test results. He presented with a 2-week history of dyspnoea, palpitations and epigastric discomfort. An electrocardiogram confirmed AF with a rapid ventricular response, and he was subsequently admitted to hospital. His initial heart rate varied between 120 and 140 beats/min and his blood pressure was 140/90 mmHg.

The patient was a successful bodybuilder and strongman. Over the past 12 months, he had taken testosterone 1.5 g per week, trenbolone 500 mg per week, methandrostenolone 40 mg daily, anastrozole 0.5 mg daily and naproxen 1.1 g daily in preparation for a national championship competition. He stated that he had only recently started taking trenbolone. The authors stated, “The recent addition of trenbolone to the patient’s steroid regimen potentially contributed to his presentation.”The case highlights an interesting presentation of a dilated cardiomyopathy with acute decompensated heart failure 6 weeks after cessation of anabolic steroids in a patient who had performed physically at an elite level only 2 weeks before admission. Definitive management involved cessation of the offending agents, exclusion of other reversible causes of heart failure, and initiation of conventional heart failure therapy.


  • Hematology


Erythrocytosis is one of the more prominent adverse events associated with AAS administration. Testosterone appears to be the main actor as inhibition of conversion into either E2 or DHT has had no additional effect; however E2 may have an independent effect on hepcidin suppression, and DHT has shown to independently increase hemoglobin levels. Together, these reports suggest that androgens have a direct stimulatory effect on hematopoiesis, probably through numerous mechanisms including erythropoietin stimulation, hepcidin suppression leading to higher iron availability, an increase in the expression of ferroportin and transferrin receptor, and possibly direct stimulatory effect on the bone marrow. Other mechanisms have yet to be fully elucidated. Preliminary evidence indicates that 17B –TBOH increases hemoglobin concentrations in orchiectomized male rodents in a dose-dependent manner and to a greater extent than supraphysiological testosterone. [1, 14-22]

Case Report: A 40-year-old bodybuilder presented to the Emergency Department following 2 episodes of right-sided weakness and paresthesia on the same day, each lasting 10 min. The patient admitted regular use of AAS for bodybuilding (2a-17a-dimethyl-17b-hydroxy-5a-androstan-3-one, stanozolol, testosterone and trenbolone). Past medical history was significant for steroid-induced cholestasis 6 years previously. Baseline laboratory investigations showed an elevated hematocrit of 56.9% and hemoglobin concentration of 20.6 g/dl (normal range: 13-17 g/dl). Both had been normal 6 years previously. Over the following week, the patient suffered 2 further transient ischemic events with similar clinical features. After each episode a pint of blood was removed. After venesection, his symptoms settled and the hematocrit returned to the normal range. Three months following cessation of AAS, the patient had no further symptoms and his hematocrit was normal without further venesection. [62]


  • Prostate


In a human prostate cancer cell line, 17B –TBOHincreased AR-dependent cell proliferation in a concentration dependent manner. In a rodent model, 17B –TBOH administration has been shown to reduce prostate mass in growing male rodents when compared with control animals. It should be noted cell cultures and animal models are not translatable to humans. [1, 23]

Studies and reviews suggest that little direct evidence exists to support the idea that testosterone administration increases prostate cancer risk even when administration results in supraphysiological androgen concentrations. Despite this, without evidence the risk of prostate enlargement and worsening of undiagnosed prostate cancer remains cite by practitioners. Ultimately, research examining the prevalence of androgen- and/or estrogen-mediated side effects associated with 17-TBOH administration and prostate growth is warranted. [24a-24e]


  • Pancreatitis


Case Report: According to the authors, the correlation between the timing of steroids administration and the clinical attacks, along with excluding other causes, confirms 17-TBOHas the cause of his pancreatitis by the World Health Organization (WHO) classification. In this case, his condition resolved with conservative management and withdrawal of drugs. [25]

Acute pancreatitis (AP) is the third most common inpatient gastrointestinal diagnosis and a serious medical problem that can lead to significant morbidity and mortality. Drug-induced pancreatitis (DIP) is rare, with a reported incidence of 0.1–2% of all causes of AP. The mechanism of injury is dependent on the medication-specific characteristics and not completely understood. The diagnosis of DIP, such as other medication-induced conditions, is almost always clinically based and difficult to confirm. This is particularly the case when the origin of DIP is unknown and linked to illicit drugs. Excluding all other causes of pancreatitis implies the diagnosis of DIP.

Case Report: A 24-year-old male police officer presented to the emergency room with severe epigastric and right upper quadrant abdominal pain. The past medical history included presentation to an outside hospital emergency department where his lipase was elevated to >3000 units/L (normal range 73–393 units/L). The patient denied any significant alcohol history. Known causes of AP were again excluded. Subsequently, the patient admitted to past and current anabolic steroid. Most recently and prior to his initial presentation, he self-reported starting to use 17-TBOHand reported acquiring TA from the internet. He stopped taking this drug during hospitalizations but restarted it shortly afterwards and increased the doses to 400mcg/week [sic]injection until he developed symptoms of AP once again.


  • Kidney


Case Report: A 43-year-old male with presented to the emergency department reporting 2 days of left flank pain described as severe, sudden onset, sharp, constant, and without radiation. Upon further questioning, the patient revealed that he had been using both testosterone and the injectable anabolic steroid, trenbolone acetate, intermittently over a period of 5 years, with last use 2 weeks prior to initial admission. Despite a negative thrombophilia workup, he experienced primary renal infarction while using the AAS trenbolone acetate and testosterone, as well as a subsequent renal infarction while anticoagulated with apixaban. The development of subsequent infarctions in an anticoagulated patient with discontinued recreational steroid use poses a unique situation and challenges the current understanding of a thrombophilic state associated with steroids. [34-35]


  • Other [Neurological, Androgenization, Teratogen, Genotoxicity, and Cytotoxicity]


Case studies involving trenbolone have been reported as well for acne, diabetes, subcutaneous tissue necrosis, and rhabdomyolysis. [44-47] In addition, seven hormone drugs (testosterone propionate, trenbolone acetate, estradiol, zeranol, progesterone, melengestrol acetate, and bovine somatotropin) are approved by the U.S. Food and Drug Administration for use in food animals. There is concern that these drugs or their biologically active metabolites may accumulate in edible tissues, potentially increasing the risk of exposure for consumers. From the extensive battery of data, and also taking into account published data on trenbolone, it is concluded that 17-alpha-hydroxytrenbolone and 17-beta-hydroxy-trenbolone are devoid of genotoxic, androgenization, teratogen/cancer activity. In addition, the Joint FAO/WHO Expert Committee on Food Additives has stated that 17-TBOH-acetate is an acceptable anabolic agent to use in the production of meat for human consumption based on the results of numerous studies indicating few biological effects exist following consumption of 17-TBOH residues (or metabolites thereof) in meat. [52-61]

As with so many areas the implication and inference that AAS are leading to neurological diseases is more AAS paranoia than fact. It should be duly noted that with respect to one neurological disorder, Alzheimer’s, there is a great and continuing controversy even to the cause. Four decades of intense research and development (R&D) efforts have failed to yield any effective interventions for neurodegenerative diseases. The lack of success in the search for a drug to improve the devastating symptoms of these chronic brain disorders has been one of modern medicine’s greatest frustrations with a failure rate of nearly 99.6 % as compared with about 20% success rate for cancer drugs. This situation has already precipitated the strategic decision of some pharmaceutical research companies to terminate their R&D efforts on Alzheimer’s Disease. Despite these facts, there are nonhuman studies purporting to demonstrating a connection between trenbolone and neurological disorders, particularly Alzheimer’s. Nothing seems to stop the demonization of AAS.   [48-51]

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