Best to not encounter Covid-19 at all, next best would be to somehow prevent its harmful effects. At the very least, you may want to make sure you have sufficient levels of NAD (Nicotinamide Adenine Dinucleotide) to increase your chances to survive it.
New research suggests that the method by which Covid-19 damages lung tissue includes NAD depletion, so many people ask whether Vitamin B3-based NAD precursors, like NMN (Nicotinamide Mononucleotide), which replenish NAD, might protect against the harm caused by COVID-19?
The elderly are the main risk group in the current Covid-19 pandemic. What are the actions that the most vulnerable age group can take to protect themselves from the virus? Can a NAD+ booster such as NMN (Nicotinamide Mononucleotide) be effective in fighting off infection?
Researchers have tested nicotinamide mononucleotide on aged mice to see if it can help reverse age-related cognitive decline by improving blood flow in the brain.
A new study published in Nature Metabolism finally reveals the answer to how NMN enters the cell in order to become NAD+ and that it does not need to convert into NR to do so.
In the last few years, there has been considerable interest in restoring levels of the nicotinamide adenine dinucleotide (NAD+) coenzyme to combat age-related diseases. Evidence suggests that NAD+ systemically declines with age in a variety of organisms, including rodents and humans, which contributes to the development of many age-related diseases and metabolic conditions.
Research on the biology of NAD+ has been gaining momentum, providing many critical insights into the pathogenesis of age-associated functional decline and diseases. In particular, two key NAD+ intermediates, nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN), have been extensively studied over the past several years. Supplementing these NAD+ intermediates has shown preventive and therapeutic effects, ameliorating age-associated pathophysiologies and disease conditions. Although the pharmacokinetics and metabolic fates of NMN and NR are still under intensive investigation, these NAD+ intermediates can exhibit distinct behavior, and their fates appear to depend on the tissue distribution and expression levels of NAD+ biosynthetic enzymes, nucleotidases, and presumptive transporters for each. A comprehensive concept that connects NAD+ metabolism to the control of aging and longevity in mammals has been proposed, and the stage is now set to test whether these exciting preclinical results can be translated to improve human health.
