Key result
Anabolic steroid discontinuation is linked to a ~21 g/m² reduction in LVMI and improved LVEF.
Why the study?
Anabolic–androgenic steroid use is associated with adverse cardiac changes, but longitudinal data on myocardial effects with continued use and after discontinuation are lacking.
Does discontinuation of anabolic-androgenic steroids improve cardiac structure and function in men engaged in strength training?
Cohort (n=105)
Does discontinuation of anabolic-androgenic steroids improve cardiac structure and function in men engaged in strength training?
Mean Difference: -21
p-value: p=0.01 for LVMI; <0.001 for LVEF
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“We found that continued use of anabolic steroids among adult and middle-aged male strength athletes, even at lower dosages, was associated with a persistent thickening of the heart muscle, impaired contractions and worsening of the heart's ability to relax. As many as 17% of those who continued using AAS had severely reduced heart function. However, this could be reversed if the men stopped using anabolic steroids and continued to abstain from them over the long term.”
Discontinuation of anabolic-androgenic steroids in weightlifters is associated with partial or complete reversibility of adverse cardiac remodeling and systolic dysfunction.
Aims Anabolic–androgenic steroid (AAS) use is prevalent among men engaged in strength training and is associated with adverse structural and functional cardiac changes, but longitudinal data are lacking. This follow-up study examined myocardial effects of AAS with continued use and reversibility following discontinuation. Methods and results Participants of a previously published cohort (2017–19) of 101 AAS users and 71 non-using weightlifting controls (WLCs) were invited for a follow-up study and underwent interviews, hormonal profiling, and transthoracic echocardiography. Current AAS users at baseline were continued or discontinued users at follow-up, while former users at baseline were those with continued abstinence and those who relapsed. Among those re-enrolled, 70 were AAS users, of whom 35 continued, 15 discontinued, 14 maintained abstinence, and 6 relapsed, and 35 were WLCs. Continued AAS users had persistent indexed left ventricular mass (LVMI 119 ± 30 g/m2), reduced LV ejection fraction (LVEF 48 ± 10%), and worsened diastolic function. Continued AAS users receiving antihypertensive therapy showed improved LVEF compared with untreated users (Δ = 5 ± 8 vs. −4 ± 8%, P = 0.005). Discontinued AAS users showed reduction in LVMI (Δ = −21 g/m2, P = 0.01) and improved LVEF (Δ = 6%, P < 0.001). At follow-up, these changes were comparable with WLCs, which showed statistically but clinically insignificant differences. Conclusion Continued AAS use was associated with sustained LV hypertrophy, LV systolic dysfunction, and worsening diastolic function. Antihypertensive therapy among ongoing AAS users was associated with improved LV systolic function. Discontinuation of AAS use was associated with improvement in cardiac structure and function towards values observed in WLCs.
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Abdullah et al. (2026) conducted a cohort in Anabolic-androgenic steroid use (n=105). Anabolic-androgenic steroid (AAS) use discontinuation vs continuation vs. Weightlifting controls and ongoing AAS users was evaluated on Change in indexed left ventricular mass (LVMI) and left ventricular ejection fraction (LVEF) (ΔLVMI = -21 g/m2; ΔLVEF = 6%, p=0.01 for LVMI; <0.001 for LVEF). Discontinuation of anabolic-androgenic steroids improved cardiac parameters, including reduced left ventricular mass index (Δ=-21 g/m2, P=0.01) and increased LVEF (Δ=6%, P<0.001).
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