Is creatine bad for your heart?
Executive summary
Creatine monohydrate is not broadly “bad” for the heart in healthy adults according to the clinical and review literature: short‑term human trials report no detectable negative cardiac structural or functional effects and some trials even suggest vascular or functional benefits, particularly in heart failure where creatine stores are depleted [1] [2] [3]. However, mechanistic animal experiments that forced supranormal myocardial creatine levels produced hypertrophy and dysfunction, and human data remain limited in size and duration, so cautious optimism — not complacency — is the warranted stance [4] [2] [5].
1. What the bulk of human trials actually show about safety and function
Multiple controlled human studies find no short‑term harmful effects of creatine on cardiac structure or routine hemodynamic measures: one trial concluded short‑term creatine supplementation produced no detectable negative effect on cardiac structure or function (echocardiography, blood pressure) [1], and a randomized study in older men found improvements or neutral effects on vascular stiffness and other parameters rather than harm [6] [7]. In chronic heart‑failure cohorts, small trials and pilot studies report improved skeletal muscle performance, longer walking distance, lower perceived exertion and sometimes reduced heart‑rate response to exercise — effects compatible with better functional status rather than direct cardiac injury [8] [9] [5].
2. Why some researchers see therapeutic potential in heart disease
Reviews and mechanistic papers emphasize that creatine is central to myocardial energy buffering and that cardiac creatine content is depressed in chronic heart failure, providing a rationale to test supplementation as an adjunct to improve muscle energetics and quality of life in heart failure patients [2] [3] [8]. Preliminary human data and systematic reviews identify modest benefits for muscle strength and functional capacity in heart‑failure populations, and some studies even report vascular improvements that might lower cardiovascular risk factors [5] [6].
3. The important animal‑model caution: dosage and biology matter
A clear red flag comes from genetic and preclinical models: forcing supranormal myocardial creatine and phosphocreatine concentrations caused increased free ADP, left‑ventricular hypertrophy and dysfunction in mice, demonstrating that an overfilled creatine pool can be maladaptive for the heart’s bioenergetics [4]. Authors of clinical reviews note those harmful effects were observed at creatine levels unattainable with standard oral supplementation, yet the experiments underline that cardiac creatine homeostasis is tightly regulated and that unchecked manipulation can be detrimental [2] [4].
4. Gaps, confounders and the limits of current evidence
Most human trials are short, relatively small, focused on functional endpoints or surrogate vascular measures, and sometimes constrained to specific populations (healthy young adults, older volunteers, or selected heart‑failure patients), leaving long‑term cardiovascular safety and effects on hard endpoints (myocardial infarction, arrhythmia, mortality) unresolved [6] [5] [1]. Some pilot studies documented reversible rises in serum creatinine and transient declines in estimated GFR that normalized after stopping creatine, signaling the need to monitor renal function in at‑risk patients and to avoid extrapolating benign findings in healthy volunteers to those with chronic kidney or complex cardiovascular disease [9].
5. Bottom line and practical implication for clinicians and policy
The preponderance of evidence indicates creatine taken at conventional doses is not clearly harmful to the heart in otherwise healthy people and may have therapeutic value in heart‑failure patients with depleted myocardial creatine stores, but animal data showing harm at supraphysiologic myocardial loads and the small, short nature of human trials mandate caution: further large, long‑term randomized trials are needed to define who benefits, which doses are safe, and whether there are subgroups at risk [2] [4] [5]. Conflict‑of‑interest disclosures in some vascular studies (e.g., industry ties among authors) and the reliance on surrogate endpoints should temper overenthusiastic claims until more definitive clinical outcome data are available [7].