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 C17β
position, include trenbolone acetate, trenbolone enanthate, trenbolone
hexahydrobenzylcarbonate, and trenbolone undecanoate. 17β –TBOH-acetate (17β-
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 17β –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 17β –TBOH is primarily excreted intact, as 17β –TBOH, as the
17α epimer (epitrenbolone; 17α –TBOH ) or as trendione (TBO). 17β –TBOH has a greater affinity
for the AR than any of its primary metabolites, suggesting that biotransformation of 17β –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 17β –TBOH differs from that of
testosterone because 17β –TBOH does not undergo 5α reduction and is reported to not be a
substrate for the aromatase enzyme. In vitro bioassays and cell culture experiments demonstrate
that 17β – 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, 17β –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 17β –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 17β –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-α-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, 17α-Methyl-5α-androstano[3,2-c]pyrazole-
17β-ol 100 mg, 17β-hydroxy-17α-methyl-2-oxa-5α-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 17β –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, 17β –TBOH increased AR-dependent cell proliferation in a
concentration dependent manner. In a rodent model, 17β –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-TBOH as
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.

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-TBOH and
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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