Nicotinamide (NAD) is a form of Vitamin B3. Nicotinamide riboside (NR), a pyridine-nucleoside form of vitamin B3 and precursor to NAD+ seems to be the most vitally beneficial form to supplement with.

Healing Properties

  • Antiaging: Helps ameliorate age-related metabolic decline and disease.[1]
    • Improves mitochondrial biogenesis and function[1]
    • Neuroprotection (neuroprotective): Prevents age-related dopaminergic neuronal loss (damage due to dopamine related activity in the brain) and motor decline.[1]
  • Heart Health:

Disease / Symptom Treatment

  • Heart Disease:
    • Heart Failure: Nicotinamide riboside supplementation attenuates the development of heart failure.[2]
      • Nicotinamide riboside efficiently rescues NAD+ synthesis in the heart and stimulates glycolysis (energy production) in cardiomyocytes (heart muscles).[2]
      • Nicotinamide riboside can help stabilize myocardial NAD+ levels in the failing heart.[2]
  • Neurodegenerative diseases:
    • Parkinsons:


  1. Title: The NAD+ Precursor Nicotinamide Riboside Rescues Mitochondrial Defects and Neuronal Loss in iPSC and Fly Models of Parkinson’s Disease
    Author(s): David C. Schöndorf, Dina Ivanyuk, Pascale Baden8, Alvaro Sanchez-Martinez, Silvia De Cicco, Cong Yu, Ivana Giunta, Lukas K. Schwarz, Gabriele Di Napoli, Vasiliki Panagiotakopoulou, Sigrun Nestel, Marcus Keatinge, Jan Pruszak, Oliver Bandmann, Bernd Heimrich, Thomas Gasser, Alexander J. Whitworth, Michela Deleidi
    Institution(s): German Center for Neurodegenerative Diseases (DZNE), Helmholtz Association, Tübingen 72076, Germany, Hertie-Institute for Clinical Brain Research, University of Tübingen, Tübingen 72076, Germany, Medical Research Council Mitochondrial Biology Unit, University of Cambridge, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK, Department of Neuroanatomy, Institute of Anatomy and Cell Biology, University of Freiburg, Freiburg 79104, Germany, Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield, Sheffield, UK,
    Publication: Cell Reports
    Date: June 2018
    Abstract: While mitochondrial dysfunction is emerging as key in Parkinson’s disease (PD), a central question remains whether mitochondria are actual disease drivers and whether boosting mitochondrial biogenesis and function ameliorates pathology. We address these questions using patient-derived induced pluripotent stem cells and Drosophila models of GBA-related PD (GBA-PD), the most common PD genetic risk. Patient neurons display stress responses, mitochondrial demise, and changes in NAD+ metabolism. NAD+ precursors have been proposed to ameliorate age-related metabolic decline and disease. We report that increasing NAD+ via the NAD+ precursor nicotinamide riboside (NR) significantly ameliorates mitochondrial function in patient neurons. Human neurons require nicotinamide phosphoribosyltransferase (NAMPT) to maintain the NAD+ pool and utilize NRK1 to synthesize NAD+ from NAD+ precursors. Remarkably, NR prevents the age-related dopaminergic neuronal loss and motor decline in fly models of GBA-PD. Our findings suggest NR as a viable clinical avenue for neuroprotection in PD and other neurodegenerative diseases.

  2. Title: Nicotinamide Riboside Preserves Cardiac Function in a Mouse Model of Dilated Cardiomyopathy
    Author(s): Nicolas Diguet, Samuel A.J. Trammell, Cynthia Tannous, Robin Deloux, Jérôme Piquereau, Nathalie Mougenot, Anne Gouge, Mélanie Gressette, Boris Manoury, Jocelyne Blanc, Marie Breton, Jean-François Decaux, Gareth G. Lavery, István Baczkó, Joffrey Zoll, Anne Garnier, Zhenlin Li, Charles Brenner, Mathias Mericskay
    Institution(s): Sorbonne Universités, Université Pierre et Marie Curie Paris 6, Department of Biology of Adaptation and Ageing, CNRS UMR8256, INSERM U1164, Institute of Biology Paris-Seine, DHU FAST, France (N.D., C.T., R.D., A. Gouge, J.B., J.-F.D., Z.L.)., Department of Biochemistry, Carver College of Medicine, University of Iowa, Iowa City (S.A.J.T., C.B.)., Signalling and Cardiovascular Pathophysiology, UMR-S 1180, University Paris-Sud, INSERM, Université Paris- Saclay, Châtenay-Malabry, France (C.T., R.D., J.P., M.G., B.M., M.B., A. Garnier, M.M.)., Institute of Metabolism and Systems Research, University of Birmingham, United Kingdom (G.G.L.)., Department of Pharmacology and Pharmacotherapy, University of Szeged, Hungary (I.B.).,
    Date: December 7 2017
    Abstract: Background: Myocardial metabolic impairment is a major feature in chronic heart failure. As the major coenzyme in fuel oxidation and oxidative phosphorylation and a substrate for enzymes signaling energy stress and oxidative stress response, nicotinamide adenine dinucleotide (NAD+) is emerging as a metabolic target in a number of diseases including heart failure. Little is known on the mechanisms regulating homeostasis of NAD+ in the failing heart. Methods: To explore possible alterations of NAD+ homeostasis in the failing heart, we quantified the expression of NAD+ biosynthetic enzymes in the human failing heart and in the heart of a mouse model of dilated cardiomyopathy (DCM) triggered by Serum Response Factor transcription factor depletion in the heart (SRFHKO) or of cardiac hypertrophy triggered by transverse aorta constriction. We studied the impact of NAD+ precursor supplementation on cardiac function in both mouse models. Results: We observed a 30% loss in levels of NAD+ in the murine failing heart of both DCM and transverse aorta constriction mice that was accompanied by a decrease in expression of the nicotinamide phosphoribosyltransferase enzyme that recycles the nicotinamide precursor, whereas the nicotinamide riboside kinase 2 (NMRK2) that phosphorylates the nicotinamide riboside precursor is increased, to a higher level in the DCM (40-fold) than in transverse aorta constriction (4-fold). This shift was also observed in human failing heart biopsies in comparison with nonfailing controls. We show that the Nmrk2 gene is an AMP-activated protein kinase and peroxisome proliferator-activated receptor α responsive gene that is activated by energy stress and NAD+ depletion in isolated rat cardiomyocytes. Nicotinamide riboside efficiently rescues NAD+ synthesis in response to FK866-mediated inhibition of nicotinamide phosphoribosyltransferase and stimulates glycolysis in cardiomyocytes. Accordingly, we show that nicotinamide riboside supplementation in food attenuates the development of heart failure in mice, more robustly in DCM, and partially after transverse aorta constriction, by stabilizing myocardial NAD+ levels in the failing heart. Nicotinamide riboside treatment also robustly increases the myocardial levels of 3 metabolites, nicotinic acid adenine dinucleotide, methylnicotinamide, and N1-methyl-4-pyridone-5-carboxamide, that can be used as validation biomarkers for the treatment. Conclusions: The data show that nicotinamide riboside, the most energy-efficient among NAD precursors, could be useful for treatment of heart failure, notably in the context of DCM, a disease with few therapeutic options.