We’ve long understood that high doses of testosterone can have undesirable effects on your cholesterol levels. They tend to raise LDL (bad) cholesterol, while suppressing the HDL (good) fraction. While the side effects of anabolic steroid abuse are widely overstated in the media, dyslipidemia is a tangible issue that can contribute to cardiovascular disease (CVD). Unfortunately, there is often a poor understanding of how sensitive the body actually is to high testosterone levels. Some individuals assume that it takes weeks for hormone elevations to translate into distinct cholesterol changes. This is a common justification for cycling (periodically going on and off AAS). A study just published in the journal Substance Abuse Treatment, Prevention, and Policy, makes clear this is not the case (1).
The paper discloses a recent clinical investigation involving 39 health male volunteers. Each of the men was given a single 500 mg intramuscular injection of testosterone enanthate (Testoviron Depot). The acute effects of the hormone injection on serum cholesterol levels were then charted. The researchers also looked at what effect, if any, the hormone would have on HMG-CoA reductase (HMGCR), which is an enzyme involved in the biosynthesis of cholesterol. The results were both striking and immediate. After only two days, the total cholesterol level had increased by 15%. HMGCR expression had also increased. This is the first time an alteration of lipids was observed after only a single dose of testosterone.
The results of this study may have important implications. For one, steroid abusers should be aware that the deleterious effects of AAS on cholesterol probably happen very quickly. Cycling may not avoid this harm. Instead, users may want to look at all cumulative “on time” as a period of elevated CVD risk. Furthermore, this study might even have implications in medical settings. Patients that take higher doses of testosterone less frequently (for example, 400 mg every 3-4 weeks) may be enduring some unwanted fluctuations in their lipid profile. This may be further call for clinicians to use lower doses more frequently, and drug developers to find better ways to stabilize patient testosterone levels during long-term therapy.