Last updated: 3 April 2020 21:00EST by Frank Cusimano

SUMMARY:

The science does not support using melatonin prophylactically. It may be useful to take after someone becomes infected. Melatonin may blunt the immune response to the virus, reduce oxidative damage in the lungs, & may be useful if one develops severe respiratory distress. The data supporting these claims are NOT robust and I consider it low quality data. One should skeptically consider it when devising a treatment plan with their doctor. Too much melatonin, may have the opposite effect.

Background:

COVID-19 is not a single-organ disease . It affects multiple organs requiring principles from pulmonology, immunology, cardiology, nephrology, virology & more.

Sadly, we can’t look towards a single drug to treat it. We have to think outside the box. COVID-19 starts as a mild undulating viral illness &, for some, may take a sudden turn towards a diffuse cytokine-induced lung injury followed by sepsis, septic shock, & acute respiratory distress syndrome .

A recent science paper proposed Melatonin (N-acetyl-5-methoxytryptamine) as an adjunct-therapeutic for COVID-19 . Melatonin is a bioactive molecule touted for its use in sleep disorders, delirium, respiratory disease & viral infections . Before I explain some of the science, it is important to note that the amount of studies for melatonin used in this context are few in comparison to the research for other therapies, like Zinc or Vitamin C, which I previously posted on. Theoretically, Melatonin may be useful, but there is a lot of theorizing, & not that many clinical studies to back up the claims. For sleep, I previously posted that melatonin works for some but not for others; according to meta-analyses, it only helps people fall asleep 7 minutes faster & remain asleep 8 minutes longer .

SCIENCE:

Below is an overview of how researchers think melatonin may work as an adjuvant therapy.

Melatonin may act in three primary ways: anti-inflammatory, anti-oxidant, anti-ALI/ARDS (acute lung injury/acute respiratory distress syndrome). First off, it is known that at the beginning of the viral infection, the amplification int he inflammatory process promotes cellular apoptosis fueling inflammation and increasing permeability of interpulmonary vessels. Melatonin may abate this response . On the inflammatory front, Melatonin may reduce inflammation via SIRT1, NF-kB, and Nrf2 . During the cytokine storm, melatonin may reduce cytokine activation; specifically: TNF-a, IL-1b, and IL-6 . Melatonin also acts as an antioxidant. It may reduce oxidative stress via superoxide dismutase, nitric oxide synthase, & TLR4 . It may prevent lung damage via NLRP3 & CD8+ T cells .

Meta-Analyses:

Although a lot of the data is somewhat arbitrary and theoretical, there was a good meta-analysis done in June of 2019 looking at clinical trials on melatonins effect on inflammation . Out of thirteen eligible studies, researchers found that Melatonin supplementation significantly decreased TNF-a and IL-6 levels. While they saw no significant change in CRP, it is interesting to see that other inflammatory cytokines were effected by melatonin supplementation.

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Disclaimer: Opinions on this site or on social media do not reflect that of my institutions. I do not provide medical advice. If you have a medical question please see your doctor or if you have a medical emergency, please go to the nearest emergency room.. I have a PhD in Nutrition and Metabolic Biology and three masters degrees including two master’s in nutrition & metabolism. I am a personal trainer & have researched nutrition for 12 years. The info I post is my interpretation of the medical and scientific literature.

References:

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Luo, J., Song, J., Zhang, H., Zhang, F., Liu, H., Li, L., Zhang, Z., Chen, L., Zhang, M., Lin, D., Lin, M., & Zhou, R. (2018). Melatonin mediated Foxp3-downregulation decreases cytokines production via the TLR2 and TLR4 pathways in H. pylori infected mice. International Immunopharmacology, 64, 116–122. https://doi.org/10.1016/j.intimp.2018.08.034
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