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NMN articles and studies

NMN articles and studies

NMN Human Trial on Safety and Metabolism

Heart Health

  1. “Remarkably, NMN administered to FXN-KO mice restores cardiac function to near-normal levels.“ (Martin, 2017)
  2. “NMN significantly increased the level of NAD+ in the heart. NMN protected the heart from I/R injury” Nicotinamide mononucleotide, an intermediate of NAD+ synthesis, protects the heart from ischemia and repercussion (Yamamoto, 2014)
  3. “NMN reduces vascular oxidative stress. NMN treatment normalizes aortic stiffness in old mice. NMN represents a novel strategy for combating arterial aging” Nicotinamide mononucleotide supplementation reverses vascular dysfunction and oxidative stress with aging in mice (de Picciotto, 2016)
  4. “NMN can reduce myocardial inflammation NMN thus can cut off the initial inflammatory signal, leading to reduced myocardial inflammation.” Short-term administration of Nicotinamide Mononucleotide preserves cardiac mitochondrial homeostasis and prevents heart failure (Zhang, 2017)
  5. “Remarkably, NMN administered to FXN-KO mice restores cardiac function to near-normal levels. Restoration of cardiac function and energy metabolism upon NMN supplementation. Remarkable decrease in whole-body EE and cardiac energy wasting.” Nicotinamide mononucleotide requires SIRT3 to improve cardiac function and bioenergetics in a Friedreich’s ataxia cardiomyopathy model


  1. “NMN was able to mitigate most age-associated physiological declines in mice Treatment of old mice with NMN reversed all of these biochemical aspects of aging” Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice (mills, 2016)
  2. “Raising NAD+ levels in old mice restores mitochondrial function to that of a young mouse.”  “Restore the mitochondrial homeostasis and key biochemical markers of muscle health in a 22-month-old mouse to levels similar to a 6-month-old mouse” Declining NAD+ Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging (Gomes, Sinclair,2013)

DNA Repair

“This study showed supplementation with NMN was able to repair the DNA in cells damaged by radiation. The cells of old mice were indistinguishable from young mice after just one week of treatment.” A conserved NAD+ binding pocket that regulates protein-protein interactions during aging (Sinclair, 2017)

Weight control

  1. “NAD(+) levels were increased significantly both in muscle and liver by NMN. NMN-supplementation can induce similar reversal of the glucose intolerance. NMN intervention is likely to be increased catabolism of fats. NMN-supplementation does mimic exercise” Head to Head Comparison of Short-Term Treatment with the NAD(+) Precursor Nicotinamide Mononucleotide (NMN) and 6 Weeks of Exercise in Obese Female Mice (Uddin, 2016)
  2. “NMN was immediately utilized and converted to NAD+ within 15 min, resulting in significant increases in NAD+ levels over 60 min. Administering NMN, a key NAD+ intermediate, can be an effective intervention to treat the pathophysiology of diet- and age-induced T2D. Surprisingly, just one dose of NMN normalized impaired glucose tolerance.”  Nicotinamide Mononucleotide, a Key NAD+ Intermediate, Treats the Pathophysiology of Diet- and Age-Induced Diabetes in Mice (Yoshino, 2011)

Brain Function and Brain disease

  1. “NMN treatment reduces brain cell death and oxidative stress These results further support the neuroprotection of NMN/NAD+” Nicotinamide mononucleotide attenuates brain injury after intracerebral hemorrhage by activating Nrf2/HO-1 signaling pathway (Wei, 2017)
  2. “NMN decreased β-amyloid production, amyloid plaque burden, synaptic loss, and inflammatory responses in AD-Tg mice” (Yao, 2017)
  3. “We now demonstrate that mitochondrial respiratory function was restored” Effect of nicotinamide mononucleotide on brain mitochondrial respiratory deficits in an Alzheimer’s disease-relevant murine model (Long, 2015)
  4. “NMN could restore cognition in AD model rats.” Nicotinamide mononucleotide protects against β-amyloid oligomer-induced cognitive impairment and neuronal death (Wang, 2016)
  5. “NMN Treatment Rescues Cognitive impairments” Nicotinamide mononucleotide inhibits JNK activation to reverse Alzheimer disease (Yao, 2017)

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