The relationship between steroids and cholesterol is an important part of understanding the cardiovascular effects of anabolic-androgenic steroids (AAS). Research has frequently associated non-medical AAS use with changes in blood lipids, most consistently lower high-density lipoprotein cholesterol (HDL-C) and, in many studies, higher low-density lipoprotein cholesterol (LDL-C).
These changes matter because cholesterol is transported through the bloodstream by different types of lipoproteins, and an unfavorable lipid profile can contribute to cardiovascular risk. The effect is not identical for every compound, dose, or person, and study results vary, but the overall evidence supports concern about AAS-related disruption of lipid metabolism.
This article focuses on anabolic-androgenic steroids. Corticosteroids, such as prednisone, are a different class of medication used mainly to treat inflammation, and they affect metabolism through different mechanisms.
What happens to cholesterol when steroids are used?
AAS can alter the way the body processes and transports lipids. The most consistently reported effect is a reduction in HDL cholesterol, while LDL cholesterol can increase.
An Endocrine Society scientific statement on performance-enhancing drugs notes that supraphysiological androgen exposure can markedly reduce HDL cholesterol, and that an unexplained, very low HDL level can be one clue to possible AAS exposure in an appropriate clinical context (Pope et al., 2014).
Body composition and blood lipid measurements therefore provide different information about health.
Why HDL and LDL matter
HDL and LDL are not simply “good” and “bad” cholesterol. They are lipoproteins that transport cholesterol and other lipids through the bloodstream.
HDL participates in transporting cholesterol back toward the liver, while LDL delivers cholesterol to tissues. Elevated LDL-C is an established cause of atherosclerotic cardiovascular disease. Low HDL-C is associated with higher cardiovascular risk, but evidence suggests HDL-C is better understood as a risk marker than as a direct cause, since treatments that raise HDL-C have not reliably reduced cardiovascular events.
How do steroids lower HDL cholesterol?
One of the most consistent findings in research on steroids and cholesterol is a reduction in HDL cholesterol.
A key mechanism involves hepatic lipase, a liver enzyme that helps break down HDL particles. Androgens can increase hepatic lipase activity, which accelerates HDL breakdown and lowers circulating HDL-C (Thompson et al., 1989).
The magnitude of the change varies. In a controlled study comparing an oral anabolic steroid with injected testosterone, the oral compound reduced HDL-C considerably more, consistent with the stronger effect of orally active compounds on the liver’s handling of lipids (Thompson et al., 1989).
Why a lower HDL level matters
A low HDL level is one component of an unfavorable lipid profile. However, it should not be interpreted in isolation.
Cardiovascular risk depends on multiple factors, including LDL-C, blood pressure, smoking, diabetes, age, family history, and other health characteristics. AAS-related changes in HDL therefore represent one part of a larger cardiovascular picture rather than a complete risk assessment by themselves.
Can steroids increase LDL cholesterol?
Often, yes. Many studies have associated AAS exposure with increased LDL-C.
A 2025 systematic review and meta-analysis of adverse effects in athletes and physically active individuals reported a statistically significant increase in LDL-C among AAS users compared with controls (Mingxing & Yanfei, 2025).
Not every study agrees, however. Reviews of the evidence note considerable variation between studies, with some reporting significant lipid changes and others finding smaller or no differences. This variation likely reflects differences in compounds, doses, duration of use, and study design.
The combination of higher LDL-C and lower HDL-C is particularly relevant because it represents a shift toward a less favorable cardiovascular risk profile.
Why LDL is important
LDL particles transport cholesterol through the bloodstream, and persistently elevated LDL-C contributes to the development of atherosclerotic cardiovascular disease.
AAS-related lipid changes therefore matter beyond the cholesterol number itself. They can contribute to a broader pattern of cardiovascular risk that may also include changes in blood pressure, vascular function, and other systems.
Does total cholesterol always increase?
Not necessarily. People sometimes assume that an adverse cholesterol profile must involve a large increase in total cholesterol.
AAS can substantially change the distribution of cholesterol among lipoproteins without producing an equally obvious increase in total cholesterol. Some studies have even reported relatively low total cholesterol alongside reduced HDL and altered LDL measurements.
For this reason, looking only at total cholesterol does not provide a complete picture of how AAS exposure may have affected lipid metabolism.
Why do different steroids affect cholesterol differently?
AAS are not a single chemically identical substance. As our overview of the different types of steroids and their function explains, compounds can have different androgenic, anabolic, hepatic, and metabolic effects.
Beyond the compound itself, the dose, duration of use, and use of multiple substances can all influence the size and pattern of lipid changes. This is why it would be inaccurate to claim that every anabolic steroid produces exactly the same cholesterol changes.
The safest evidence-based conclusion is that AAS exposure can adversely alter lipid profiles, while the specific magnitude and pattern can vary.
Are triglycerides affected too?
They can be. The relationship between AAS use and triglycerides is less consistent than the pattern of reduced HDL and altered LDL. Some studies have reported increased triglycerides, while others have found less pronounced or inconsistent changes.
This illustrates why a complete lipid panel is more informative than a single cholesterol measurement. A lipid assessment may include total cholesterol, LDL-C, HDL-C, and triglycerides, depending on the clinical context.
Does being fit protect against steroid-related cholesterol changes?
Physical fitness does not necessarily prevent AAS from altering lipid metabolism.
Resistance training and regular physical activity are generally associated with cardiovascular benefits, but those benefits do not cancel out the pharmacological effects of supraphysiological androgen exposure. Studies of bodybuilders have documented significant lipid changes during steroid use despite high levels of training (Hartgens et al., 2004).
This is an important distinction for people who associate a muscular appearance with cardiovascular health. Someone can be lean, strong, and highly trained while still having an unfavorable lipid profile.
What happens to cholesterol after stopping steroids?
Evidence suggests that AAS-associated lipid abnormalities often improve after cessation. Reviews report that lipid levels tend to move back toward pre-use values after stopping, although the timing varies between individuals (Achar et al., 2010; Bond et al., 2022).
What is less clear is whether periods of adverse lipid changes leave lasting effects on the arteries, particularly after long or repeated exposure.
Lipid recovery also does not necessarily follow the same timeline as testosterone recovery after steroids, which can vary considerably. Improvement in one system says little about recovery in another.
Can cholesterol changes increase cardiovascular risk?
Unfavorable lipid changes are one reason AAS exposure is associated with concern about cardiovascular health.
Lower HDL and higher LDL can contribute to an overall cardiovascular risk profile that is less favorable than it would otherwise be. Reviews of AAS-related cardiovascular effects have also identified other potential changes involving blood pressure, vascular function, cardiac structure, and thrombosis.
However, it is important not to overstate the evidence. Long-term randomized trials of non-medical supraphysiological AAS exposure are not ethically feasible, so much of the evidence comes from observational studies, clinical reports, and mechanistic research.
The lipid findings themselves are considerably more consistent than the ability to quantify an exact cardiovascular outcome for any individual.
Can a normal cholesterol test rule out steroid-related cardiovascular effects?
No. A lipid panel provides useful information about cholesterol and triglycerides, but it does not measure every cardiovascular effect potentially associated with AAS, such as changes in blood pressure, cardiac structure and function, vascular reactivity, and coagulation.
A relatively favorable lipid result therefore should not be interpreted as proof that AAS exposure has had no cardiovascular effects.
Conversely, an abnormal lipid result does not establish that steroids are the only cause. Diet, genetics, body composition, medications, and other health factors can also affect blood lipids.
Why cholesterol should be considered separately from muscle growth
The effects of AAS on muscle tissue and their effects on cardiovascular health are separate physiological questions.
AAS can increase muscle protein synthesis and contribute to skeletal muscle hypertrophy while simultaneously producing unfavorable metabolic or cardiovascular changes. This distinction is central to understanding steroids and cholesterol: a visible increase in muscle does not demonstrate that every physiological system is responding positively.
For a broader overview of how AAS affect the body, see what you need to know about steroids.
The bottom line
The evidence linking steroids and cholesterol points most consistently to lower HDL cholesterol, with increases in LDL cholesterol reported in many, though not all, studies. The magnitude of these changes varies with the specific compound, dose, duration of exposure, and individual factors.
These changes matter because LDL, HDL, and other lipid measurements contribute to the broader assessment of cardiovascular health, and a muscular, physically active person can still have an unfavorable lipid profile.
AAS-related lipid abnormalities often improve after cessation, but recovery varies and should not be assumed to occur on a fixed schedule. Cholesterol is best considered as one part of cardiovascular health rather than a single measure that determines an individual’s risk.
Anyone concerned about abnormal cholesterol results or cardiovascular health after AAS exposure should discuss those findings with a qualified healthcare professional rather than interpreting them solely through a fitness or bodybuilding lens.
References
Achar S, Rostamian A, Narayan SM. Cardiac and metabolic effects of anabolic-androgenic steroid abuse on lipids, blood pressure, left ventricular dimensions, and rhythm. American Journal of Cardiology. 2010;106(6):893–901.
Bond P, Smit DL, de Ronde W. Anabolic-androgenic steroids: how do they work and what are the risks? Frontiers in Endocrinology. 2022;13:1059473.
Hartgens F, Rietjens G, Keizer HA, Kuipers H, Wolffenbuttel BH. Effects of androgenic-anabolic steroids on apolipoproteins and lipoprotein (a). British Journal of Sports Medicine. 2004;38(3):253–259.
Mingxing L, Yanfei Y. Adverse effects of anabolic androgenic steroid abuse in athletes and physically active individuals: a systematic review and meta-analysis. Substance Use & Misuse. Published online February 13, 2025. doi:10.1080/10826084.2025.2460986.
Pope HG Jr, Wood RI, Rogol A, Nyberg F, Bowers L, Bhasin S. Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement. Endocrine Reviews. 2014;35(3):341–375.
Thompson PD, Cullinane EM, Sady SP, et al. Contrasting effects of testosterone and stanozolol on serum lipoprotein levels. JAMA. 1989;261(8):1165–1168.
