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NAD, NMN & NR for Heart Health

An image titled NAD+, NMN, and NR for the heart health

Chronic heart failure is associated with a frequent consequence known as myocardial metabolic dysfunction. Because of its role as a coenzyme in fuel oxidation and oxidative phosphorylation, as well as a substrate for enzymes that communicate energy stress and oxidative stress responses, nicotinamide adenine dinucleotide (NAD+) is emerging as a metabolic target in a variety of disorders, including heart failure.

NAD+ and Heart Health

According to emerging research, derangements in the myocardial NAD pool may be directly related to metabolic remodeling and mitochondrial dysfunction in the failing heart. Stabilizing intracellular NAD+ levels is an intriguing therapeutic option for optimizing myocardial bioenergetics and function.

  • NAD+ has been shown to increase endothelial cell proliferation and provide protection against cardiovascular and cerebrovascular disorders. Increased NAD+ levels in injured hearts are required for infarct size reduction and recovery following IR injury. NAD+ precursor supplementation also prevented myocardium fibrosis or hypertrophy.
  • NAD+ also contributes to the cell’s redox stability. The ratio of NAD+ to NADH can have a significant effect on the redox balance. When this imbalance results in excessive oxidative stress, it may contribute to cardiac dysfunction, increasing the risk of heart failure and endothelial dysfunction associated with vascular aging. Improving the ratio has been found to help heart failure in mouse research.

NMN and Heart Health

NR and Heart Health

  • The effect of DNA damage on NAD+ levels and the efficiency of Nicotinamide Riboside (NR) supplementation to restore NAD+ were studied in mice. Supplementation had no effect on NAD+ levels in the hearts of either control or DNA-damaged animals. No improvement in cardiac function was noted. The researchers sought to see if a larger dose of NR was more beneficial. The increased dosage was damaging to heart health, probably due to an overabundance of Nicotinamide (NAM), a sirtuins inhibitor.
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