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Hypercholesterolemia in Male Power Lifters Using Anabolic-Androgenic Steroids.

J C Cohen, T D Noakes, A J Benade

    The Physician and Sportsmedicine
    |July 13, 2016
    PubMed
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    Anabolic-androgenic steroid use in powerlifters significantly elevates serum total cholesterol (TC), primarily in the low-density lipoprotein (LDL) fraction. Cholesterol levels rapidly return to normal after discontinuing steroid use.

    Area of Science:

    • Endocrinology
    • Sports Medicine
    • Cardiovascular Health

    Background:

    • Anabolic-androgenic steroids (AAS) are performance-enhancing drugs with known health risks.
    • Previous research suggests AAS can negatively impact lipid profiles.
    • Understanding the specific effects of AAS on cholesterol in athletes is crucial for risk assessment.

    Purpose of the Study:

    • To investigate the impact of anabolic-androgenic steroid (AAS) use on serum lipid profiles in male powerlifters.
    • To determine the relationship between the duration of AAS use and changes in cholesterol levels.
    • To assess the reversibility of AAS-induced lipid alterations after cessation of use.

    Main Methods:

    • Serum total cholesterol (TC), high-density lipoprotein (HDL) cholesterol, and triglyceride levels were measured.

    Related Experiment Videos

  • Three groups of male powerlifters were studied based on AAS usage duration: short-term (8 weeks), medium-term (3 years), and long-term (8 years).
  • Lipid profiles were assessed during AAS use and after cessation.

    • Main Results:

    • Mean serum total cholesterol (TC) levels increased significantly in powerlifters using AAS.
    • The increase in TC was primarily attributed to the low-density lipoprotein (LDL) fraction.
    • Following cessation of AAS use, TC levels promptly decreased to near pre-steroid concentrations.
    • Pre-steroid TC levels did not predict the magnitude of steroid-induced hypercholesterolemia.

    Conclusions:

    • Anabolic-androgenic steroid use leads to a significant, reversible increase in serum total cholesterol, mainly within the LDL fraction.
    • The duration of AAS use did not correlate with the magnitude of hypercholesterolemia in this cohort.
    • Individuals with low baseline cholesterol are not protected from developing AAS-induced hypercholesterolemia.