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Melatonin is relatively ubiquitous in nature and can be found widespread in several animal and plant foods (1,2). Regardless of its origin and the biosynthetic pathways used to manufacture it, the chemical structure of melatonin in plants and animals is similar and bioidentical to what is found in humans (3). In some cases, plants can be more concentrated sources of melatonin, perhaps because they can synthesize their tryptophan. Therefore, dietary tryptophan levels should be considered when assessing melatonin intake from food sources due to its biological conversion to melatonin. The important clinical point is that even though tryptophan levels in the diet may be substantially higher than that of melatonin, the conversion from tryptophan to serotonin and ultimately to melatonin may not be efficient in all individuals due to the enzymes involved. The enzyme that catalyzes N-acetyl-serotonin into melatonin is N-acetylserotonin methyltransferase (ASMT) (4). Because methyltransferases rely on the biochemical integrity of methylation reactions in the body to transfer a single-carbon unit, the completeness of that conversion will be determined by an individual’s gene variants related to that enzyme. Methylation inefficiencies due to single nucleotide polymorphisms (SNPs) in methylation-related enzymes like 5,10-methylenetetrahydrofolate reductase (C677T) are clinically relevant in various disease states (5–8). Unfortunately, SNPs specifically related to the ASMT enzyme have not been extensively explored in humans but would be an excellent area for translational research that could encompass clinical identification of SNPs along with nutrient modifications for therapeutic intervention (9).


Even though the amounts of melatonin in a particular serving of food may seem relatively low (on the order of an average of nanograms per gram) compared with physiological levels, there is an indication that consuming foods rich in melatonin may increase overall systemic antioxidant status. In one study with twelve healthy men (10), drinking juice extracted from one kilogram of orange or pineapple or two whole bananas resulted in significant elevations in serum melatonin and increases in antioxidant status (as measured using the FRAP and ORAC analyses). Of note, those changes in antioxidant status may be due to the melatonin content and the other vitamins and phytonutrients in the fruits. While it may not be practical to consume this quantity of juice or fruit for various reasons or due to the excessive glycemic load, it is suggestive that the diet can modify melatonin levels and, further, antioxidant status.


Research inquiries into dietary melatonin and associated health conditions have been few, perhaps due to the constraints posed by variability in melatonin content in the food supply and/or the confounding aspect of dietary tryptophan. One population-based cohort study in Japanese men (n = 13,355) and women (n = 15,724) investigated the association between dietary melatonin assessed by a food frequency questionnaire and mortality during sixteen years of follow-up between 1992–2008 (11). Higher quartiles of dietary melatonin compared with the lowest suggested a modest effect on mortality rates.

Read more about plant and animal sources of melatonin. 

Authors: Deanna Minich, Ph.D., Melanie Henning, ND, Catherine Darley, ND, Mona Fahoum, ND, Corey B. Schuler, DC, James Frame

Reviewer: Peer-review in Nutrients Journal

Last updated: September 22, 2022



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6. Mabhida SE, Muhamed B, Sharma JR, Apalata T, Nomatshila S, Mabasa L, et al. Methylenetetrahydrofolate Reductase Polymorphism (rs1801133) and the Risk of Hypertension among African Populations: A Narrative Synthesis of Literature. Genes (Basel). 2022 Apr 1;13(4):631.

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