NAD+ is required for functioning of sirtuins – proteins that contribute to longevity by maintaining the length of critical telomeres.

Telomeres are stretches of repetitive DNA strands that cap the ends of chromosomes. Like the burning of a fuse, telomeres at the ends of our chromosomes steadily shorten every time a cell replicates itself. Once telomeres reach a critically short length, cell renewal virtually stops, leading to accelerated aging or death of the cell.

Telomere shortening is both a marker of cellular aging and a predictor of shortened lifespan.

Researchers have been searching for drugs and other interventions that might lengthen telomeres, in order to extend lifespan and/or health span. To date, exercise and weight loss have been reliably shown to be effective at telomere lengthening.

Certain other nutrients, such as resveratrol, may activate sirtuins and contribute to extending lifespan, but emerging evidence suggests sirtuins function best with an ample supply of NAD⁺.

Conclusion: The possibility of extending telomere length with NAD⁺ holds out hope for slowing the aging process and improving longevity.

Even though DNA is protected by its chromosomal shelter, it is highly vulnerable to damage.

This can lead to broken DNA strands and mutations in crucial genes. Accumulated DNA damage contributes to the aging process and can result in specific lifespan-shortening diseases like cancer and poor immune function.¹⁸

When DNA is damaged, it activates an enzyme known as PARP-1 that carries out DNA repair within cells. To carry out its function, PARP-1 consumes enormous amounts of NAD⁺. As NAD⁺ is depleted, the ability of PARP-1 to repair DNA is significantly hindered.

The good news is that replenishing NAD⁺ to cells can restore DNA repair and prevent cell death under stress. In two different animal models of neurodegenerative disease, increasing cellular NAD⁺ reduced the severity of the disorder, normalized neuromuscular function, delayed memory loss, and extended lifespan.

Conclusion: Improving DNA repair with NAD⁺ may slow cellular aging, reduce the persistence of cancer-causing mutations, and play an important role in preventing inflammatory conditions such as atherosclerosis.

As we age, our immune cells begin to lose their focus. Some become overactive, contributing to autoimmune disease, while others slow down, which increases the risk of infection. This process, called immunosenescence, is intimately related to mitochondrial function and energy balance, both of which depend on NAD⁺ activity.

Intracellular levels of NAD⁺ regulate immune and inflammatory pathways, including the cytokine TNF-alpha, a critical signaling molecule.

Conclusion: Adequate intracellular NAD⁺ is vital for youthful cellular energy, a critically important factor in fending off immunosenescence and maintaining defenses against infections and autoimmune disease.

A universal feature of aging is the loss of cellular energy, which results in diminished ATP levels and inadequate cellular fuel necessary to power your body.

One cause of this energy loss is a breakdown in the efficiency of the electron transport chain, the main pathway through which we extract energy from food (and of which NAD⁺ is an essential component). Disorders ranging from obesity and diabetes to bone loss have been associated with loss of this vital pathway.

Studies now show that restoring electron transport chain function by raising levels of NAD⁺ is a rapid and efficient means of promoting the essential enzymes involved in energy extraction and sustaining youthful cell function. This helps to reduce physiological decline and provides protection from age-related disease.

Conclusion: Improving the energy-extraction process in all cells with NAD⁺ increases their capacity to do the work they are specialized for. It also protects mitochondria from early death, a benefit that is associated with reduced cellular aging and lowered risks for cardiovascular and brain disease.

Our chromosomes are complex structures housing our DNA. Access to DNA strands for “reading out” genetic instructions requires biochemical control of those proteins to make sure each gene functions properly.

But like any complex molecular structure, chromosomes can become unstable. Eventually, this triggers errors in the ways our genes are interpreted—which ultimately contributes to deleterious changes in cell function and structure. Aging is accelerated in the presence of increased chromosome instability.

The enzymes involved in sustaining stable chromosomal structures require NAD⁺ in order to function properly.

In animal models showing that NAD⁺ contributes to longevity, a major factor has been shown to be sufficient availability of the nutrient. And studies show that when enzymes that require NAD⁺ are inactive, chromosome structure suffers and cells replicate abnormally.

Conclusion: NAD⁺ supplementation is a promising cutting edge strategy to improve chromosome stability, a treatment that may slow down cellular aging (senescence) and lower the risk of cancer.

Neurotransmitters are brain chemicals that relay signals between nerve cells. In doing so, they help regulate body-wide functions such as mood, appetite, and stress.

NAD⁺ has been found to meet all criteria for a neurotransmitter.

Evidence for NAD⁺’s neurotransmitter function has now been found in intestinal and blood vessel smooth muscles, as well as in the brain itself.

Conclusion: Ample NAD⁺ nutrition appears essential for sustaining brain health.

Proteins called sirtuins are major regulators of cellular aging because they influence fundamental functions such as DNA repair and inflammatory responses. They also influence whether cells enter a replicative cycle or instead die a programmed death (apoptosis).

Compounds that activate sirtuins are eagerly sought as chemical “fountains of youth.” Familiar supplements like resveratrol and quercetin have been evaluated as promising sirtuin activators.

NAD⁺ is required for sirtuins to function.

Conclusion: Sirtuin activation has shown great promise in fighting cardiovascular disease and preserving aging brain function, but these longevity-promoters cannot function without sufficient NAD⁺.

NAD⁺ was first discovered as an important part of the process that channels chemical energy from foods to the ATP fuel our cells require. Recent studies have revealed that NAD⁺ is itself a form of “energy currency” similar to ATP.

NAD⁺ is also a functional signaling molecule in processes related to energy production, including PARP-1 and sirtuins. When DNA damage occurs, PARP-1 consumes large quantities of NAD⁺, leading to reduced energy production. In addition, high levels of NAD⁺ can activate sirtuins, permitting them to carry out their metabolic and stress-protective responses and contributing to longevity.

Conclusion: Supporting efficient energy production and adequate ATP levels requires consistent and abundant NAD⁺. This is critical because waning energy supplies contribute to the aging process.