Monitoring tests associated with metandienone use

People who use metandienone often say: "I'm taking tests, so I'm in control." The editors explain which indicators really reflect the main risks of this 17α-alkylated steroid, how to read them correctly, and why even perfect results do not mean that the drug is safe.

Why tests are important, but they do not save

Metandienone affects several body systems at once: the liver, lipid metabolism, the cardiovascular system, hormonal regulation, and hematopoiesis. Laboratory indicators allow you to see some of these changes and consult a doctor in time. In this sense, screening is a useful harm reduction tool.

However, analyzes record already existing changes, not prevent them. For example, liver tumours associated with androgens may not be accompanied by pronounced abnormalities in liver tests for a long time. Structural changes of the heart — hypertrophy of the left ventricle — are not visible at all in the blood test.

In addition, many indicators respond to exercise, diet or dehydration independently of the drug. Without understanding these factors, it is easy to either get scared of "bad" results or, on the contrary, underestimate the real problem.

Therefore, the editors consider laboratory control not as a "permission" for use, but as a way to assess the state of health and obtain a basis for consultation with a doctor. Any interpretation should be discussed with a specialist who knows your history.

Liver: ALT, AST, HGT, bilirubin

Metandienone belongs to 17α-alkylated steroids for which hepatotoxicity is a class effect. The most common type of lesion is cholestatic: the outflow of bile from liver cells is disturbed. Therefore, in addition to transaminases, important markers of cholestasis are bilirubin, gamma-glutamyltransferase (GHT) and alkaline phosphatase.

Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are enzymes that are released into the blood when cells are damaged. But they are contained not only in the liver, but also in the muscles. Intense strength training alone can increase AST and ALT several-fold, as shown in a study by Pettersson et al. (2008) in healthy men without any drugs.

To distinguish muscle-derived enzymes from liver-derived enzymes, doctors look at creatine kinase (CK), a marker of muscle damage, and HGT, which is virtually absent in muscle. If GGT and bilirubin are normal, and CK is high, the increase in transaminases is most likely related to training.

Instead, an increase in bilirubin, yellowing of the skin or sclera, itching, dark urine and light-coloured feces are signs of cholestasis that require immediate medical attention. The LiverTox database of the US National Institutes of Health describes such cases for anabolic steroids, particularly with a long and severe course.

Liver ultrasound is not a blood test, but with long-term use of 17α-alkylated drugs, it is often discussed with the doctor, because liver adenomas can be asymptomatic.

Heart and blood vessels: lipids and blood pressure

One of the most reproducible changes with oral anabolic steroids is a reduction in high-density lipoproteins (HDL, the "good" cholesterol). The mechanism is associated with an increase in liver lipase activity. At the same time, low-density lipoprotein (LDL) increases. Such a profile is considered atherogenic.

In classic studies with 17α-alkylated steroids, HDL lowering was significantly greater than with injectable testosterone. Hartgens and Kuipers, in a review of the effects of anabolic steroids in athletes, emphasized the oral route as particularly unfavourable for lipids.

Blood pressure is a simple but very informative indicator. On metandienone, it may increase due to sodium and fluid retention associated with oestrogenic activity. Regular blood pressure measurement at home gives more information than a one-time blood test.

Instrumental methods — ECG and echocardiography — allow to assess structural changes of the heart. Studies in long-term users of anabolic steroids describe reduced contractile function and accelerated atherosclerosis of the coronary arteries, so these tests are particularly important for people with a history of use.

Hormones and blood

The hormonal panel reflects the degree of inhibition of the hypothalamus–pituitary–testicular axis. Against the background of metandienone, LH and FSH are usually sharply reduced, and own testosterone falls. Standard testosterone testing does not measure metandienone itself, so a low result is an expected finding, not a "bug."

Oestradiol in men is often checked because of the risk of gynaecomastia. But, as we explained in the material about the oestrogenic activity of metandienone, its main oestrogenic metabolite — 17α-methyloestradiol — can be poorly determined by conventional immunoassays. Therefore, oestradiol values ​​should be interpreted with caution.

Sex hormone-binding globulin (GHB) significantly decreases against the background of 17α-alkylated steroids. This affects the calculation of free testosterone and is an indirect sign of the effect of the drug on the protein synthetic function of the liver.

A general blood test with haemoglobin and haematocrit shows whether erythrocytosis is developing. Androgens stimulate the formation of red blood cells, and excessive blood clotting increases the risk of thrombosis. It is also helpful to monitor fasting glucose, as anabolic steroids can affect insulin sensitivity.

• LH and FSH — degree of pituitary suppression.
• Total testosterone and SHBG — assessment of endogenous hormone production.
• Haematocrit — risk of blood clotting.
• Semen analysis is the only direct way to assess fertility.

Typical interpretation errors

The first mistake is to take liver tests the day after a heavy leg or back workout. The result will be distorted by muscle enzymes. Usually, doctors advise to refrain from intensive activities for several days before the analysis in order to get an informative picture.

The second mistake is to consider normal transaminases as evidence of a "healthy liver." Cholestasis may be manifested primarily by an increase in bilirubin, and liver tumours may not cause abnormalities in the blood at all.

The third mistake is to evaluate lipids only by total cholesterol. Against the background of oral steroids, total cholesterol may remain almost unchanged, while the ratio of LDL to HDL becomes extremely unfavourable.

The fourth mistake is to draw conclusions from one analysis. For most indicators, dynamics are important: comparison with baseline values ​​before any interventions and re-examination after withdrawal to ensure a return to normal.

And finally, independent "treatment" of abnormalities with hepatoprotectors or other drugs without a diagnosis masks the problem and postpones a visit to a doctor.

Editorial conclusions

The main risks of metandienone are reflected in liver function tests, lipid profile, haematocrit and hormone panel, as well as blood pressure. Each indicator has its own pitfalls of interpretation, especially in people who train intensively.

Analyzes help to notice problems in time, but do not make the drug safe and do not detect all possible complications.

The best strategy is an honest conversation with a doctor who sees the whole picture, rather than "adjusting" the numbers yourself.

We also recommend our materials on hepatotoxicity of metandienone, suppression of own testosterone and myths surrounding this drug.

List of used literature

1. Pettersson J, Hindorf U, Persson P, et al. Muscular exercise can cause highly pathological liver function tests in healthy men. Br J Clin Pharmacol. 2008;65(2):253–259.
2. Hartgens F, Kuipers H. Effects of androgenic-anabolic steroids in athletes. Sports Med. 2004;34(8):513–554.
3. Pope HG Jr, Wood RI, Rogol A, et al. Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement. Endocr Rev. 2014;35(3):341–375.
4. LiverTox: Clinical and Research Information on Drug-Induced Liver Injury. Androgenic Steroids. Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases.
5. Baggish AL, Weiner RB, Kanayama G, et al. Cardiovascular toxicity of illicit anabolic-androgenic steroid use. Circulation. 2017;135(21):1991–2002.
6. Rahnema CD, Lipshultz LI, Crosnoe LE, et al. Anabolic steroid-induced hypogonadism: diagnosis and treatment. Fertil Steril. 2014;101(5):1271–1279.