

Melatonin, a widely used sleep aid once regarded as harmless, has recently become the subject of scientific scrutiny.
The Heart and Stroke Statistics presented by the American Heart Association (AHA) suggested that long-term melatonin use may be associated with an increased risk of heart failure hospitalization.
This revelation has prompted renewed interest in understanding whether melatonin—a hormone integral to regulating circadian rhythm—might also influence cardiovascular health.
Melatonin is a naturally occurring hormone synthesized primarily by the pineal gland in response to darkness. Its primary role is the regulation of the sleep–wake cycle, signaling the body to prepare for rest.
In modern lifestyles, disrupted by artificial light and digital exposure, endogenous melatonin production is often suppressed. Consequently, melatonin supplements have become a popular remedy for insomnia, jet lag, and circadian rhythm disorders.
However, exogenous melatonin functions as more than a sleep regulator. It also exerts antioxidant, anti-inflammatory, and vasoregulatory effects, suggesting potential implications for cardiovascular physiology.
The recent AHA analysis observed that individuals who reported regular melatonin use over several years were approximately 3.5 times more likely to be hospitalized for heart failure compared to non-users.
While this association appears significant, it is important to interpret it cautiously. The findings indicate correlation, not causation. Melatonin use did not cause heart failure; rather, it was associated with an increased incidence among certain populations.
Potential confounding factors—such as age, pre-existing cardiovascular conditions, hypertension, diabetes, and concurrent medication use—may contribute to this observed relationship. Therefore, researchers emphasize that the results warrant further investigation rather than definitive conclusions.
Beyond its role in sleep regulation, melatonin affects vascular tone, heart rate variability, and endothelial function.
It interacts with receptors in the autonomic nervous system, which governs cardiovascular responses such as blood pressure and pulse rate.
Animal studies have shown that low-dose melatonin can protect cardiac tissue from ischemic injury and oxidative stress. However, chronic or high-dose supplementation in humans could theoretically alter these regulatory mechanisms.
Reports of heart palpitations in some melatonin users—though rare—suggest that excessive or prolonged use might disrupt normal cardiovascular rhythm, particularly in individuals with underlying heart conditions or those using interacting medications.
The safety of melatonin in cardiac patients remains an open question. Some clinical studies indicate that melatonin may reduce oxidative stress and improve nocturnal blood pressure control, offering potential cardioprotective benefits.
Conversely, the AHA study raises concerns about possible adverse outcomes with long-term, unsupervised, or high-dose use.
A key issue lies in dosage inconsistency. Over-the-counter melatonin products in the United States range from 0.3 mg to 10 mg per dose, yet the human body typically produces only 0.1–0.3 mg naturally each night.
Regular intake of supraphysiological doses—sometimes exceeding 10–30 times the body’s natural output—may alter the delicate hormonal and cardiovascular balance.
Older adults, who represent the largest demographic of melatonin users, are also at increased risk of cardiovascular disease. This overlap complicates the interpretation of study data.
Furthermore, drug interactions play a critical role. Melatonin may interact with beta-blockers, anticoagulants, antiplatelet agents, and antidepressants, potentially amplifying or mitigating their cardiovascular effects.
Such pharmacodynamic interactions underscore the need for careful medical supervision when melatonin is used by patients with hypertension, arrhythmias, or existing heart failure.
Although generally well tolerated, melatonin can produce mild adverse effects, including:
While most users experience minimal discomfort, these symptoms may become clinically relevant in individuals taking higher doses or concurrent medications that affect the cardiovascular system.
Combining melatonin and alcohol is ill-advised. Alcohol suppresses endogenous melatonin synthesis and can potentiate cardiovascular strain by increasing heart rate and dehydration.
Rather than enhancing sleep quality, this combination often leads to fragmented sleep, elevated nighttime blood pressure, and increased cardiac workload, negating any potential benefit of supplementation.
Concern should be proportionate and informed, not alarmist. For most healthy adults using low doses intermittently, there is currently no evidence of acute cardiovascular danger.
However, chronic nightly use—particularly in those with existing cardiac or metabolic disease—should prompt medical consultation. The prudent approach is to balance short-term benefit against potential long-term systemic effects.
Medical experts emphasize that melatonin’s dual identity as a hormone and supplement warrants caution.
Although marketed as a natural sleep aid, melatonin exerts endocrine-level effects that can influence the cardiovascular system.
Given its regulatory status as a dietary supplement rather than a drug, dosage variability and quality control remain significant concerns.
Thus, ongoing research is essential to clarify whether melatonin linked to heart failure reflects a direct physiological risk or a coincidental association among at-risk populations.
Evidence to date paints a complex picture.
At low doses and short durations, melatonin appears protective, mitigating oxidative damage and improving cardiac recovery after ischemic events.
However, chronic high-dose supplementation may disrupt cardiovascular regulation or signal pre-existing vulnerability among long-term users.
The most reasonable interpretation is that context, dosage, and duration determine melatonin’s cardiovascular impact—not the substance itself.
As one cardiologist summarized:
“Melatonin is neither inherently harmful nor harmless—it is biologically active. Its safety depends entirely on how, why, and for how long it is used.”
For medical students and clinicians, the emerging discourse on melatonin and heart failure underscores the importance of comprehensive patient histories, including supplement use.
For researchers, it highlights the urgent need for dose–response studies, longitudinal trials, and stratified analyses that account for age, comorbidity, and concurrent medication effects.
Ultimately, melatonin research offers a valuable reminder: in physiology, no compound is entirely benign when removed from its natural context.
In rare cases, yes. Palpitations have been reported, particularly with high-dose or long-term use, though causality remains uncertain.
Caution is recommended. Patients with cardiovascular conditions should consult a physician before using melatonin regularly.
Melatonin may lower nighttime blood pressure modestly in healthy adults but can produce unpredictable results in individuals on antihypertensive therapy.
Yes. Alcohol diminishes melatonin efficacy, and certain medications (e.g., beta-blockers, anticoagulants) may alter its cardiovascular effects.
Use the lowest effective dose (0.3–1 mg) for short durations, avoid concurrent alcohol or sedative use, and consult healthcare professionals before prolonged supplementation.
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