Melatonin, Technology, and Health: The Science Behind the Controversy

Melatonin has been recognized not only as a hormone critical for regulating the body's natural circadian rhythm but also for its potential in preventing serious health conditions like cancer and circadian dysrhythmia patterns (often seen in neurogenic decline and trauma). 

Despite its well-documented circulatory and oncostatic (cancer-suppressing) properties, a recent study presented by the American Heart Association (AHA) has raised concerns about the cardiovascular risks of melatonin use, claiming a possible link to heart failure.[1]

However, this study—based purely on epidemiological data—is being widely reported in major media without crucial context. It fails to account for the broader biological role of melatonin, particularly its relationship to metabolic repair, and the damage caused by technology-induced melatonin suppression. Furthermore, the study's core error is its reliance on a patient pool that already had pre-existing heart conditions and chronic insomnia.

This article will explore key issues with the AHA study and explain why using flawed epidemiological data to promote potentially misleading conclusions can lead to erroneous and dangerous public health advice.

Introducing Stronger Evidence: The Daliri Meta-Analysis

In contrast, another study published in March 2025, the Daliri et al. meta-analysis, examines the effects of melatonin on heart failure patients using a more reliable approach. This study pools data from Randomized Controlled Trials (RCTs), which provide more accurate insights than the AHA’s epidemiological study. The Daliri study evaluates the therapeutic potential of melatonin in clinical settings, where proper controls are in place.

Why Epidemiological Studies Are Inadequate in This Context

The primary issues in the AHA study stem from its reliance on an observational study type, which is simply not strong enough to back up the conclusion made:

Correlation Is not Causation

• Epidemiological studies can only identify correlations (two things happening at the same time) between melatonin use and heart failure; they fail to establish causal relationships (one thing causing the other).
• In this case, the study may simply show that people with existing cardiovascular disease are more likely to take melatonin, without demonstrating that melatonin causes either improvement or harm to heart health.

Pre-existing Conditions and Bias

• The AHA study compared patients who already had chronic insomnia (a known risk factor for heart disease) to other patients with the same condition. This created a highly biased, sick patient pool from the start.
• Critically, the study ignored unmeasured, high-risk conditions like trauma or PTSD. These are major drivers of severe chronic insomnia and the resulting chronic stress and inflammation are themselves a likely underlying cause of heart failure.
• The study falls into the trap of confusing the attempted symptom relief (melatonin use) with the disease progression (heart failure).

Lack of Clinical Control

• The study cannot control for dosage or quality of the supplement, making it impossible to comment definitively on true pharmacological risk.
• The use of oral melatonin means the study is practically a "sham trial," given that up to 85% or more of the dose does not make it through first-pass metabolism in the liver (low bioavailability).
• The study also failed to screen for other supplements and, most importantly, unreported toxic behaviors (like alcohol or cannabis use).
• Since self-medication is common in highly distressed patients, the elevated risk is likely a reflection of these unmeasured, toxic factors, not the melatonin itself.

Conclusion: Stop Generating Misinformation

The media narrative surrounding the AHA abstract represents a critical failure in scientific communication.

The central finding—that melatonin use is associated with heart failure risk—must be recognized as white noise, not conclusive evidence. Given that most heart patients deal with some form of metabolic dysfunction and circadian dysregulation, the decision to correlate a potentially therapeutic supplement like melatonin based on flawed epidemiological data is misguided and potentially dangerous for public health.

The following facts should guide primary care decisions:

• Association is NOT Risk: The AHA study only proves that sicker patients (those with chronic insomnia, stress, and unmeasured toxic behaviors) are more likely to seek relief via melatonin. The true risk is the underlying disease, not the supplement.
• Melatonin’s Role is Protective: Established clinical trials provide stronger evidence of melatonin’s therapeutic potential for improving heart function, quality of life, and lipid metabolism in patients who already have heart failure.
• The Misinformation Cost: When major media amplifies preliminary, flawed data, it directly discourages patients who might benefit from this supplement, undermining both the doctor-patient relationship and responsible health management.

Until proper, controlled clinical trials (RCTs) prove otherwise, the AHA abstract cannot (and should not) be used as a basis to generate misinformation or discourage the use of melatonin in patients struggling with chronic insomnia and heart-related metabolic issues.

 Furthermore, the established role of melatonin in regulating the body’s circadian rhythms and its growing evidence in supporting neuroplastic functionality underscores the urgent need for dedicated, high-quality clinical study of this essential chemical. This need, however, must be met by public health institutions, as Big Pharma's commercial incentives mean the necessary funding for a definitive RCT on a naturally occurring, non-patentable compound will likely never materialize.

References

• Daliri, A. S., Goudarzi, N., Harati, A., & Kabir, K. (2025). Melatonin as a novel drug to improve cardiac function and quality of life in heart failure patients: A systematic review and meta-analysis. Clinical Cardiology, 48(3), e70107.
• Nnadi, E., et al. (2025, November). Effect of long-term melatonin supplementation on incidence of heart failure in patients with insomnia [Abstract MP2306]. In Abstracts of the American Heart Association Scientific Sessions 2025.
• Hoseini, S. G., et al. (2022). Melatonin supplementation improves N-terminal pro-B-type natriuretic peptide levels and quality of life in patients with heart failure with reduced ejection fraction: Results from MeHR trial, a randomized clinical trial. Clinical Cardiology, 45(4), 417–426.

 

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[1] Footnote: It is essential to call out the nutraceutical industry for its deliberate misleading use of language: melatonin is not a sleep aid. It is a hormone critical for restoring and setting the body's circadian rhythm. It does not actively promote sleep in most people but rather acts as a timing signal. It does nothing to restore the crucial, deep long-wave sleep that is necessary for restorative function.