When it comes to the safety of stanozolol, the first thing that comes to mind is the liver. However, from the point of view of long-term health, the cardiovascular consequences may be even more important: it was on stanozolol that the first randomized study showed how strongly an oral androgen can worsen the lipid profile. The editorial examines what happens to lipids, pressure and blood and why these changes matter.
Lipid profile: a major challenge
High-density lipoprotein cholesterol (HDL) is involved in the reverse transport of cholesterol — the removal of its excess from tissues, in particular from the walls of blood vessels, to the liver. Low HDL has long been considered an independent marker of increased cardiovascular risk, although current understanding of its role is more complex than a simple "higher is better."
In 1989, Thompson et al published a classic study in JAMA. Healthy strength-trained men received either stanozolol 6 mg per day orally or testosterone enanthate 200 mg per week intramuscularly for six weeks. In the stanozolol group, HDL decreased by about a third and LDL increased; in the testosterone group, the decrease in HDL was significantly less, and LDL was not significantly changed.
The study compared oral stanozolol at 6 mg daily with testosterone enanthate at 200 mg weekly. These are different drugs and routes, so comparing their milligram totals does not establish equivalent potency. The source’s “tenfold smaller” statement was also arithmetically incorrect: 6 mg daily totals 42 mg weekly. Chemical structure and hepatic exposure help explain the different lipid effects.
A study by Kuipers et al (1991) among bodybuilders using various anabolic steroids also reported a decrease in HDL and an increase in the ratio of total cholesterol to HDL. After discontinuation of the drug, the indicators gradually returned toward baseline, but the duration of recovery varied from person to person.
Mechanism: hepatic lipase
The key to understanding the "lipid toxicity" of stanozolol is the hepatic triglyceride lipase enzyme. It hydrolyzes triglycerides and phospholipids in the composition of lipoproteins and contributes to the transformation of large HDL2 particles into smaller ones that are more quickly removed from the bloodstream.
Applebaum-Bowden, Haffner, and Hazzard (1987) showed that, in the presence of stanozolol, hepatic lipase activity increases even before HDL2 decreases. This sequence of events indicates a causal relationship: first the enzyme increases, then the HDL particles are destroyed.
In parallel, androgens reduce the synthesis of apolipoprotein A-I, the main protein of HDL. The combination of two processes — accelerated destruction and slowed formation — gives a sharp drop in the level of "good" cholesterol, which is observed in just a few weeks.
Interestingly, for lipoprotein(a) — another atherogenic marker — androgens, on the contrary, often show a decrease. However, this does not compensate for the overall adverse shift in the lipid profile, and the clinical benefit of such a reduction in the context of anabolic steroids has not been proven.
| Index | Changes during stanozolol use | Comment |
|---|---|---|
| HDL | Marked decrease | Main and fastest effect |
| LDL | Increase | More noticeable than on injectable testosterone |
| Hepatic lipase | Increased activity | Probable mechanism of HDL drop |
| Apolipoprotein A-I | Reduction | Less “building material” for HDL |
| Lipoprotein(a) | Often decreasing | Does not compensate for general risk |
Blood pressure and myocardium
Increased blood pressure has been reported in anabolic steroid users in many observational studies. For stanozolol, which does not cause pronounced fluid retention, the contribution of this mechanism is smaller than for aromatizable steroids. However, androgens affect the tone of blood vessels, the renin-angiotensin system and the function of the endothelium, so an increase in pressure is possible even without edema.
A study by Baggish et al (2017) in the journal Circulation examined the cardiovascular toxicity of illicit AAS use. Among long-term users, a reduced left ventricular ejection fraction, impaired diastolic function, and a larger volume of atherosclerotic plaques in the coronary arteries were more often detected compared to athletes who did not use steroids.
These data refer to people who mostly combined different drugs over the years, so it is impossible to isolate the "contribution of stanozolol". At the same time, the pronounced effect of stanozolol on lipids makes it one of the drugs most likely to accelerate atherogenesis in such a combination.
To assess the condition of the heart, the doctor can prescribe an ECG, echocardiography and, as indicated, daily pressure monitoring. Home pressure measurement is a simple and affordable way to detect a problem in time.
Hematocrit and blood coagulation
Androgens stimulate erythropoiesis: they increase the production of erythropoietin by the kidneys and increase the availability of iron to the bone marrow. This leads to an increase in hemoglobin and hematocrit. An excessively high hematocrit increases blood viscosity and, according to observations, is associated with the risk of thrombotic events.
Stanozolol also has a specific feature: it enhances fibrinolysis - the dissolution of blood clots. That is why it has been studied for the treatment of lipodermatosclerosis and some vascular skin conditions. At first glance, this should reduce the risk of thrombosis, but at the same time, the drug affects other coagulation factors, and the overall clinical effect in healthy people has not been clarified.
A practically important consequence of the effect on hemostasis is the interaction with anticoagulants. Anabolic steroids, in particular stanozolol, can increase the effect of warfarin, increasing the risk of bleeding. For people taking anticoagulants, any combination with androgens is possible only under the supervision of a clinician with INR monitoring.
Summarizing cardiovascular risks, it is useful to keep in mind the list of indicators that change during stanozolol:
- lipid panel: HDL, LDL, triglycerides, total cholesterol;
- blood pressure at rest, preferably measured at home at different times;
- complete blood count with hematocrit and hemoglobin;
- according to indications — ECG and echocardiography.
Editorial conclusions
The cardiovascular profile of stanozolol is determined primarily by its effect on lipids. In a randomized trial, the drug lowered HDL significantly more than injectable testosterone, despite a much lower dose.
The mechanism of this effect is related to the liver: the activity of hepatic lipase increases and the synthesis of apolipoprotein A-I decreases. This is another argument in favor of the oral form and 17α-methylation having a systemic cost.
Added to the lipid changes are the risks common to AAS — increased blood pressure, myocardial remodeling, erythrocytosis — and a specific interaction with anticoagulants.
The editors also advise you to read our materials on what tests to monitor when using stanozolol, on a complete overview of its side effects and on the mechanism of action of the drug on androgen receptors.
References
- Thompson PD, Cullinane EM, Sady SP, et al. Contrasting effects of testosterone and stanozolol on serum lipoprotein levels. JAMA. 1989;261(8):1165–1168.
- Applebaum-Bowden D, Haffner SM, Hazzard WR. The dyslipoproteinemia of anabolic steroid therapy: increase in hepatic triglyceride lipase precedes the decrease in high density lipoprotein2 cholesterol. Metabolism. 1987;36(10):949–952.
- Kuipers H, Wijnen JA, Hartgens F, Willems SM. Influence of anabolic steroids on body composition, blood pressure, lipid profile and liver functions in body builders. Int J Sports Med. 1991;12(4):413–418.
- Baggish AL, Weiner RB, Kanayama G, et al. Cardiovascular toxicity of illicit anabolic-androgenic steroid use. Circulation. 2017;135(21):1991–2002.
- 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.
- Hartgens F, Kuipers H. Effects of androgenic-anabolic steroids in athletes. Sports Med. 2004;34(8):513–554.
