This, in turn, would affect adversely the rate of conversion of pregnenolone to progesterone, which requires
NAD +.
NAD + is biologically unstable, which makes it unsuitable for oral supplementation.
In other words, while a decline in
NAD + levels may negatively influence lifespan, restoring
NAD + is increasingly being viewed as a cutting - edge tool to promote longevity.
In animal models showing that
NAD + contributes to longevity, a major factor has been shown to be sufficient availability of the nutrient.46, 50,51 And studies show that when enzymes that require
NAD + are inactive, chromosome structure suffers and cells replicate abnormally.50
This process, called immunosenescence, is intimately related to mitochondrial function and energy balance, 33 both of which depend on
NAD + activity.
Studies show that supplementing with nicotinamide mononucleotide is an effective means of raising cellular
NAD + levels.6, 22,61
Published research has shown that NR is perhaps the most effective
NAD + booster, an essential metabolite found in all cells.
The authors found that «one week of treatment with a compound that boosts
NAD + levels is sufficient to 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.
Evidence for
NAD +'s neurotransmitter function has now been found in intestinal and blood vessel smooth muscles, as well as in the brain itself.52
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).23, 38 Disorders ranging from obesity and diabetes to bone loss have been associated with loss of this vital pathway.38, 39
Conclusion: The possibility of extending telomere length with
NAD + holds out hope for slowing the aging process and improving longevity.
When DNA is damaged, it activates an enzyme known as PARP - 1 that carries out DNA repair within cells.19 To carry out its function, PARP - 1 consumes enormous amounts of
NAD +.
A fascinating aspect of
NAD + is its dual role in protecting against factors that age us.
Recent studies have revealed that
NAD + is itself a form of «energy currency» similar to ATP.60
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.
NAD + levels markedly decline with age, creating an energy deficit that decreases the body's ability to retain youthful function.4
Intracellular levels of
NAD + regulate immune and inflammatory pathways, including the cytokine TNF - alpha, a critical signaling molecule.34, 35
A rigorous scientific review of
NAD + reveals that its longevity benefits arise from eight different, but interrelated, functions.
Brain tissue is highly sensitive to alterations in
NAD + levels.67 A mouse study showed that supplementation with nicotinamide mononucleotide increased
NAD + levels in the brain, slowed cognitive decline in mice with Alzheimer's, and enhanced the plasticity in neurons that underlies learning and memory.67
The good news is that replenishing
NAD + to cells can restore DNA repair and prevent cell death under stress.26, 29 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.30
When DNA damage occurs, PARP - 1 consumes large quantities of
NAD +, leading to reduced energy production.
About a decade ago, researchers discovered that the compound nicotinamide mononucleotide is rapidly converted by natural cellular enzymes into active
NAD +.
Conclusion: Supporting efficient energy production and adequate ATP levels requires consistent and abundant
NAD +.
NAD + is arguably the most important cellular cofactor for improvement of mitochondrial performance and energy metabolism.
They also showed this mitochondrial dysfunction was readily reversible by administration of
a NAD + precursor.
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.
nicotinamide mononucleotide is readily available for oral supplementation, and it is highly bioavailable.62 These benefits make nicotinamide mononucleotide the leading oral candidate to boost cellular
NAD +, and research is revealing just how effective it is.63
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.31, 32
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.
Deficiency of
NAD + predisposes us to accelerated aging and impedes our ability to fully benefit from resveratrol.
A more efficient way to increase
your NAD + levels overtime is to increase the levels of NAD +'s precursors in your body, more specifically niacinamide and niacin, found in Vitamin B3.
Since
NAD + metabolism and concentration throughout your body hold such a critical role in total cellular metabolism, it has become an attractive method for treating the negative effect aging has on not only your appearance but also your cellular function.
NAD + is a molecule that enables the transfer of energy from the food we eat to vital cell functions.
Unfortunately, many of the oral pure
NAD + supplements you see on the market today don't typically induce the benefits described above, because they are often severely under dosed and ineffective.
The April 5, 2018 issue of Life Extension Update reports findings from researcher David Sinclair and colleagues of a key role for
NAD + and the enzyme SIRT1 in maintaining youthful blood vessel and muscle function.
As you age,
your NAD + levels decline, making it more difficult for DNA mutations to be repaired, as well as decreasing your mitochondrial function and energy production.
Sirtuins are nicotinamide adenosine dinucleotide (
NAD +) dependent and known to be more active in periods of restricted calorie intake.
In a study that perhaps more serves as proof that
NAD + deficiency plays a role in diabetes researchers used high
Researchers at the Wageningen University in the Netherlands took a different approach to understand the effect of
NAD + pre-cursers and their influence
Another connection is that ALA promotes an increase in AMPk, an enzyme activated as a result of lower cellular energy levels (higher
NAD + / NADH ratio).
From plants to metazoans, an increase in intracellular levels of
NAD + directs cells to make adjustments to ensure survival, including increasing energy production and utilization, boosting cellular repair, and coordinating circadian rhythms.
High value of blood ketones could indicate issues using them as energy (type 1 diabetics,
NAD + definiciency... etc).
But only recently have scientists begun to explore the idea of supplementing with so - called «
NAD + - precursors» like NR to promote healthy aging.
Research suggests that as an evolutionary survival mechanism, the body conserves
NAD + when subjected to calorie restriction.
ANaerobic energy production is when pyruvate is turned into lactate to produce energy (in the form of
NAD +) in the absence of oxygen.
The restricted glucose metabolism lowered the so - called NADH /
NAD + ratio.
We have included Niacin as one of the ingredients, as it is very effective at raising
NAD + levels in the liver more quickly than any other precursor.
NMN is quickly metabolized into tissues throughout the body, where it bypasses the NAMPT bottleneck and restores
NAD + levels in tissues more effectively than other
NAD + precursors.
NAD + is present in many key cellular functions, from metabolic processes to circadian rhythm regulation to energy production.
Flavonoid apigenin Is an inhibitor of
the NAD + ase CD38: implications for cellular NAD + metabolism, protein acetylation, and treatment of metabolic syndrome (2013)