Turinabol and the prostate: what the research says

The prostate is one of the most androgen-sensitive organs in the male body. So the question of whether Turinabol harms the prostate sounds logical. The answer is more complex than yes or no: there is almost no direct research on this specific drug, and conclusions have to be built on prostate physiology, data on testosterone and observations of anabolic steroid users. The editorial team has gathered what is known for certain and marked where the data ends.

The prostate as an androgen-dependent organ

The prostate develops and maintains its size only in the presence of androgens. In men who, for genetic reasons, lack the type 2 enzyme 5a-reductase, the prostate remains underdeveloped. This natural experiment, back in the 1970s, showed that the main androgen for the prostate is not testosterone itself but its derivative, dihydrotestosterone (DHT).

In prostate cells, testosterone is converted by 5a-reductase into DHT, which binds to the androgen receptor several times more strongly. The DHT-receptor complex activates genes responsible for the growth of glandular tissue and the synthesis of secretory proteins, in particular prostate-specific antigen (PSA).

Medical approaches are based on precisely this mechanism: 5a-reductase inhibitors (finasteride, dutasteride) reduce the volume of an enlarged prostate, and androgen deprivation is the basis for treating advanced prostate cancer. In other words, the link between androgens and the prostate is proven by clinical practice.

At the same time, it is important to understand that the prostate does not respond without limit. The androgen receptors in its tissue have a limited capacity, and this became the basis for the so-called saturation model, discussed below. So the straightforward logic of more androgens meaning more growth works only within a certain range of concentrations.

Features of Turinabol with respect to the prostate

Turinabol is a chlorinated derivative of methandienone. Its molecule has a double bond at position 1-2 and a chlorine atom at position 4. Structural features of this type generally impair interaction with enzymes that modify the steroid's A ring - aromatase and, according to pharmacological reviews, partly 5a-reductase. Because of this, Turinabol is traditionally classed among steroids with relatively low androgenic activity.

However, low androgenicity in pharmacology is an index obtained mainly from animal models (the ratio of effect on muscle versus the ventral prostate in rats). It does not mean the drug has no effect on the human prostate: Turinabol is itself an androgen receptor agonist, and receptors are present in the prostate even without the involvement of DHT.

In addition, Turinabol suppresses the body's own testosterone production. During use, endogenous testosterone and, accordingly, local DHT may decline, while the overall androgenic effect is determined by the sum of the effects of all substances present. In real practice the picture is complicated by the fact that Turinabol is rarely used in isolation.

Thus, claims like Turinabol has no effect on the prostate at all have no evidence base. It is more accurate to say that its impact profile is less pronounced compared with DHT derivatives, but there are no direct clinical data in humans to draw quantitative conclusions.

Androgens and prostate cancer: the current view

For decades it was believed that any increase in testosterone fuels prostate cancer. This idea rested on Huggins's observations in the 1940s: castration caused regression of metastatic cancer. From this arose the fear that additional androgens inevitably provoke a tumor.

A large collaborative analysis of 18 prospective studies (Roddam et al., 2008) found no link between the level of endogenous testosterone in the blood and the risk of prostate cancer. Morgentaler and Traish (2009) proposed the saturation model: the androgen receptors of the prostate become saturated at relatively low androgen concentrations, and further increases have little effect on tissue growth.

At the same time, the saturation model describes the risk of cancer developing in men with physiological hormone levels. It does not prove the safety of supraphysiological doses in people who already have an undiagnosed tumor. That is precisely why the Endocrine Society clinical guidelines (2018) consider prostate cancer a contraindication to testosterone therapy and require PSA monitoring in older men.

As for anabolic steroid users, the literature contains isolated clinical cases of prostate cancer in young bodybuilders, but such reports do not allow a cause-and-effect relationship to be established. Systematic data on the long-term incidence of prostate cancer among former AAS users, Turinabol in particular, are currently insufficient.

Benign hyperplasia and urinary symptoms

Benign prostatic hyperplasia (BPH) is an age-related enlargement of the gland that appears in most men after the age of 50. Androgens, especially DHT, are a necessary condition for its development, so in theory additional androgenic stimulation may accelerate prostate enlargement or worsen symptoms.

For young men, BPH is usually not relevant, but the age of anabolic steroid users is gradually rising: people train and experiment with drugs even after the age of 40-50. In this group the prostate question becomes practical.

• More frequent urination, especially at night.
• A weak or intermittent urine stream.
• A feeling of incomplete emptying of the bladder.
• The need to strain at the start of urination.
• Sudden strong urges that are hard to hold back.

The appearance of such symptoms is a reason to see a urologist, regardless of whether they are related to drugs. Urinary retention is an emergency. The doctor must be informed about the use of any androgens, since this affects the interpretation of PSA and the choice of treatment.

Let us mention prostatitis separately. There is no evidence-based direct link between Turinabol and inflammation of the prostate, and the symptoms of chronic pelvic pain have many causes. They should not be automatically blamed on the drug or, conversely, ignored.

Monitoring: PSA, examination and when to see a doctor

PSA is a protein produced by prostate cells; its level in the blood depends on the size of the gland, inflammation, injury and the presence of a tumor. Androgens stimulate PSA synthesis, so during anabolic steroid use the value may change independently of the presence of cancer.

In medicine, PSA monitoring is recommended for men receiving testosterone therapy, especially after the age of 40-50. The Endocrine Society advises assessing PSA before starting therapy and 3-12 months after it, and considers a significant increase a reason to consult a urologist. This approach logically extends to everyone exposed to exogenous androgens.

A digital rectal examination and prostate ultrasound complement the laboratory data. When a tumor is suspected, urologists use multiparametric MRI and biopsy. Self-diagnosis based on sensations does not work here: early prostate cancer usually has no symptoms.

Practical conclusion: a person who has used Turinabol, especially in mature age, should tell their doctor about it and undergo standard urological screening appropriate to their age. Concealing the fact of use complicates the interpretation of tests and may delay a correct diagnosis.

Editorial conclusions

The prostate is an androgen-dependent organ, and any anabolic steroid, including Turinabol, is theoretically capable of affecting its growth and secretion. The features of the Turinabol molecule probably make this effect less pronounced than with DHT derivatives, but there is no direct research in humans.

Current data do not confirm that physiological testosterone levels cause prostate cancer, yet the safety of supraphysiological doses for the prostate has not been proven. PSA, examination by a urologist and an honest conversation about the substances used remain the basis of monitoring.

We also recommend reading our materials Turinabol and male fertility, Turinabol metabolites: how the body breaks the drug down and Recovery of the body after Turinabol use.

References

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