
Takeaway
Riboflavin enables MAO enzyme function, but magnesium is the key to the conversion process - meaning riboflavin efficacy is entirely co-dependent on adequate magnesium availability.
Riboflavin to MAO is an essential pathway for brain function. The trifecta of riboflavin’s adequacy of intake, absorption, availability, and activation determines MAO availability.
Riboflavin to MAO mechanisms and processes
MAOs (Monoamine Oxidases)
MAOs are riboflavin-based enzymes located on the outer membrane of the mitochondria. They drive the breakdown of dietary amines (tyramine) and monoamine neurotransmitters to ensure normal neurotransmission and other brain functions.
Whilst increasing dopamine levels is a potential MAOI harm in mental health, it is a benefit in Parkinson’s disease management. Consequently, MAOIs (monoamine oxidase inhibitors) are gaining traction as effective interventions for depression, Parkinson’s, Alzheimer’s and other neurodegenerative diseases.
Riboflavin
Riboflavin is the basic compound that produces the FAD (flavin adenine dinucleotide) essential for MAO enzymes to be functional.
Magnesium is essential for the conversions of riboflavin to FMN and of FMN to FAD. A recent paper advised a lower acceptable limit for magnesium in adults as ≥ 0.85 mmol/L (2.06 mg/dL).
Factors that affect riboflavin and magnesium availability include –
- adequate dietary intake: Adequacy of dietary intake can be clarified with a diet history however availability of nutrients, once consumed, may not be.
- drug-based mechanisms: May compromise availability of nutrients by impairing their absorption and distribution, and by increasing their excretion. For example, an unrelated prescribed medicine may inadvertently impairing MAO functionality by inhibiting a riboflavin and/or magnesium transporter.
- diagnosis-based impacts: May increase nutrient requirements.
Very, very old evidence suggests riboflavin deficiency increases MAO susceptibility to inhibition
Riboflavin to MAO pathway
Upon entering the cell, riboflavin is converted to FMN (flavin mononucleotide) and then FAD in the cytosol. FAD then attaches to an APO-MAO (empty) enzyme that is located on the cytosol side of the mitochondrial membrane. FAD’s permanent attachment to the MAO enzyme ensures its ongoing functionality.
Effectively, inadequate riboflavin means reduced FAD production and therefore its reduced availability to create a functional MAO enzyme. Inadequate functional MAO enzymes mean increased dopamine.

Clinical Concerns
This post was meant to be part of a series on MAOI-nutrition interactions, encompassing vitamins, minerals, transporters and glycaemia. That was obviously not meant to be as the evidence is remarkably limited for those areas of potential interactions.
Seemingly there was considerable enthusiasm to resolve MAOI-nutrition interactions in the 1970s and 1980s, that then lost momentum. Consequently, much of the currently applied evidence is based on limited updates to that research from decades past.
Riboflavin status is currently not monitored, a decision based on an assumption of adequate intake. Given the risk of the “cheese effect”, that assumption requires clarification and review especially if there is increasingly brittle control.
Disease progression means other medicines will also likely be prescribed, many of which may also impair riboflavin and/or magnesium levels. Regardless of dose, should future management strategies of those prescribed MAOIs include six-monthly monitoring of riboflavin and magnesium levels?
This specific pathway demonstrates the likelihood that riboflavin +/- magnesium will impair MAO function and therefore dopamine levels. However, there does not seem to be any research addressing this specific cause and effect. This pathway highlights the constraints busy clinicians face when working with limited evidence-based data to achieve good outcomes for those in their care.
Clinical Questions
Monitoring the adequacy of intake, absorption, availability and blood levels of riboflavin and magnesium, can guide the clinical decision-making process.
If the control of any person prescribed a MAOI becomes increasingly brittle, and they are in your care, will you –
- clarify adequacy of dietary intake of riboflavin and magnesium?
- clarify whether any of their prescribed medicines are decreasing availability of riboflavin and/or magnesium?
- recommend checking that riboflavin and magnesium levels are within acceptable ranges?
Conclusions
The riboflavin to MAO pathway is vulnerable to impacts that may impair the breakdown of dietary amines and monoamine neurotransmitters.
Bibliography
Cagnin, S., Brugnaro, M., Millino, C., Pacchioni, B., Troiano, C., Di Sante, M. & Kaludercic, N. 2022. Monoamine Oxidase-Dependent Pro-Survival Signaling in Diabetic Hearts Is Mediated by miRNAs. Cells 1:2697. https://doi.org/10.3390/cells11172697
Chandra Sekar, PK., Thomas, SM. & Veerabathiran, R. 2024. An overview of the role of monoamine oxidase-B in Parkinson’s disease: implications for neurodegeneration and therapy. Exploration of Neuroprotective Therapy 4:308–18. https://doi.org/10.37349/ent.2024.00085
Gaweska H, Fitzpatrick PF. 2011. Structures and Mechanism of the Monoamine Oxidase Family. Biomolecular Concepts 2(5):365-377. https://doi.org/10.1515/BMC.2011.030. PMID: 22022344; PMCID: PMC3197729.
Han, A., Almeida, L., Anand, N., Salloum, IM., Kanaan, S., Gadad, BS. & Daher, JPL. 2025. Exploring neuropsychiatric manifestations of vitamin B complex deficiencies. Frontiers in Psychiatry 16:1569826. DOI: https://doi.org/10.3389/fpsyt.2025.1569826. PMID: 40904570; PMCID: PMC12401900.
Jiao, K., Costello, R., Gahche, J., Rosanoff, A. & Wallace, TC. 2026. Serum Magnesium Concentrations in the United States-An Updated Population Reference Interval in Children and Adults. Journal of Nutrition 156(6):101539. https://doi.org/10.1016/j.tjnut.2026.101539. Epub 2026 Apr 16. PMID: 42000046; PMCID: PMC13279296.
Leo, G., Leone, P., Ataie Kachoie, E., Tolomeo, M., Galluccio, M., Indiveri, C., Barile. M. & Capaldi, S. 2024. Structural insights into the bifunctional enzyme human FAD synthase. Structure 32(7):953-965.e5. https://doi.org/10.1016/j.str.2024.04.006. Epub 2024 Apr 29. PMID: 38688286.
Rivero, M., Boneta, S., Novo, N., Velázquez-Campoy, A., Polo, V. & Medina, M. 2023. Riboflavin kinase and pyridoxine 5'-phosphate oxidase complex formation envisages transient interactions for FMN cofactor delivery. Frontiers in Molecular Bioscience 10:1167348. https://doi.org/10.3389/fmolb.2023.1167348. PMID: 37056721; PMCID: PMC10086132.
Wiseman-Distler, MH. & Sourkes, TL. 1963. The role of riboflavin in monoamine oxidase activity. Canadian Journal of Biochemistry and Physiology, 1963. 41(1): https://doi.org/10.1139/o63-008
Yu-Yan Tan, Y-Y., Jenner, P. & Chen, S-D. 2022. Monoamine Oxidase-B Inhibitors for the Treatment of Parkinson’s Disease: Past, Present, and Future. Journal of Parkinson’s Disease 12(2):477-495. https://doi.org/10.3233/JPD-212976
Cite: Coleman, Y. 2026. The Riboflavin to MAO Pathway. MedNut Mail https://medicationsandnutrition.com/the-riboflavin-to-mao-pathway/ Accessed (date)
Professional Notice
The information in this article is designed to support healthcare professionals. It is not an exhaustive clinical protocol. Healthcare professionals are advised to maintain adequate professional supervision to ensure Duty of Care obligations with respect to safe administration of medicines is met for each individual consumer.
Core Philosophy
Whilst medications have profoundly improved global health outcomes, they typically also introduce nutritional challenges. By proactively identifying and addressing these nutritional harms, we can bridge the gap towards achieving better health outcomes.

