African Journal of Biomedical Research · Mar 25, 2026
Statin Therapy and Skeletal Muscle Homeostasis in Older Adults: Clinical Implications for Sarcopenia – A Narrative Review
By Uchacz J, Drzymała P, Kownacki JK et al.
Background: Sarcopenia is a highly prevalent geriatric syndrome, while statins are among the most widely prescribed medications in older adults. The potential impact of statin therapy on skeletal muscle homeostasis remains unclear, with conflicting mechanistic and epidemiological evidence. Methods: This narrative review synthesises current evidence on the relationship between statin therapy and skeletal muscle homeostasis in older adults, examining mechanistic pathways, observational cohort studies, and clinical implications. Results: Experimental data indicate that statins exert dual effects on skeletal muscle: deleterious effects through mevalonate pathway inhibition, mitochondrial dysfunction (primarily demonstrated in vitro and in animal models), and impaired energy metabolism; and protective effects mediated by anti-inflammatory, antioxidative and vascular benefits. Large-scale observational cohorts using consensus-based sarcopenia definitions do not demonstrate consistent increases in sarcopenia risk among community-dwelling statin users (adjusted hazard ratios typically 0.8–1.2), although susceptible subgroups likely exist. Key determinants of muscle toxicity include higher doses, lipophilic statins, comorbidities (chronic kidney disease, hypothyroidism, diabetes), polypharmacy, and genetic polymorphisms (particularly SLCO1B1 variants). Conclusion: For most older adults at elevated cardiovascular risk, the cardioprotective benefits of statins substantially outweigh average muscle-related risks. Clinicians should systematically assess muscle health using objective measures (handgrip strength, gait speed), individualise statin choice and dosing in patients with sarcopenia risk factors, and integrate resistance exercise and adequate protein intake (1.0–1.5 g/kg/day). Discontinuation based solely on age or non-specific complaints is not supported by current evidence. Future research should employ standardised sarcopenia endpoints and mechanistic biomarkers to refine risk stratification.