NAD+ “eaters” in old age and consequence

In young and healthy people, the production, consumption and breakdown of NAD+ are in balance.  With increasing age, the NAD+ concentration in tissues such as skin, brain, liver, skeletal, muscle and blood decreases. On the one hand, this is probably due to the NAD+- consuming PARP1 and CD38 enzymes, which are massively activated in old age due to accumulated DNA damage and silent inflammation.  On the other hand, the amount of the enzyme NAMPT and thus NAD+ formation in skeletal muscle and blood plasma decreases, probably due to the frequently disturbed sleep-wake rhythm and inflammation in older people.

At the same time, fewer NAD+ molecules remain for the activity of useful sirtuins. Age-related NAD+ deficiency is associated with the ten hallmarks of aging, such as impaired energy metabolism, accumulation of toxins and damaged macromolecules, inadequate cellular waste removal and silent inflammation. NAD+ deficiency is also observed in premature aging due to mutations in the DNA repair system and in diseases of aging such as Alzheimer‘s, Parkinson‘s, cardiovascular disease and diabetes. Researchers suspect that the loss of NAD+ contributes to the development of these diseases:

• Neurodegenerative disease
• Metabolic diseases
• Diseases of the skeletal muscles
• Cancer
• Chronic fatigue
• Infections
• Inflammations