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NAD+ 500mg 3 pack
Original price was: $360.00.$320.00Current price is: $320.00.
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NAD+ 500mg 3 pack
Original price was: $360.00.$320.00Current price is: $320.00.
Injectable
Ingredients – 500mg NAD+ (Nicotinamide adenine dinucleotide) Peptide
Indications -Improves metabolic and muscle function, protects nervous system, anti-aging
Dosage – Use as directed
NAD+ (Nicotinamide adenine dinucleotide) was first discovered by Sir Arthur Hardin and William John Young in 1906. NAD is made up of two nucleotides, one in which is NAD+ while the other is NADH. NAD+ directly and indirectly is able to influence cellular functions. This includes metabolic pathways, DNA repair, chromatin remodelling, immune cell function, and more. All of these functions are critical for the maintenance of tissues as well as metabolic homeostasis.
NAD+ is a critical coenzyme found in your body. Unfortunately, the amount of NAD+ produced starts to decline naturally with age. Fortunately, there is a solution available in the form of NAD+. Whether you want to fight an aging complexion or find protection from age-associated diseases, NAD+ is here to help.
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NAD+
NAD+ is one of the most important molecules in the human body. It works as a shuttle, transporting electrons to different cells as both a coenzyme and as a metabolite as needed. NAD+ has a role in several important biologic and metabolic processes. It works in the mitochondria to help generate new cells, maintain cell functioning, and repair DNA responsible for maintaining a healthy metabolism, in turn slowing down the aging process.
Anti-Aging Research and NAD+
One of the primary results of the standard aging process is a decline in both the quality and activity of mitochondria. Mitochondria are the body’s power plants, producing the energy for everything from neuron firing to digestion and muscle function. A decline in mitochondrial functioning has been associated with normal aging, but is also a factor in a number of age-related disease processes. Research shows that mitochondrial aging contributes to cellular senescence, inflammation, and even changes in stem cell activity that reduce rates of healing and make it harder for the body to recover from injury in old ages (1).
Mitochondria cannot simply be viewed as bioenergetics factories, but “rather as platforms for intracellular signaling, regulators of innate immunity and modulators of stem cell activity. Mitochondria can be linked to a wide range of processes associated with aging including senescence, inflammation, as well as the more generalized age dependent decline in tissue and organ function.
Mitochondria are the crucial element of cellular aging and understanding how to protect their function is a necessary first step in understanding how to slow, stop, or even reverse the aging process.
New research suggests that at least some of the age-related decline seen in mitochondria can be reversed through dietary supplementation with NAD+. This function of NAD+ was uncovered, or at least made popular in research circles, by David Sinclair of Harvard University. Sinclair is the same researcher who uncovered the anti-aging effects of reservatrol. In 2013, Sinclair revealed that mitochondria in the muscle of mice could be restored to a more vouthful state via injection of a precursor to NAD+ (2).
Research completed in 2013 showed that declining levels of NAD+ leads to a pseudohypoxic state within cells. This, in turn, interrupts the normal signaling that takes place between the nucleus, where DNA resides, and the mitochondria. By supplementing old mice with NAD+, mitochondrial function is restored and the communication commences again (3).
At least prat of the reason that NAD+ helps to offset the effects of aging is that it activates
SIRT 1 function in the nucleus and prevents the normal age-related decline in expression of this particular gene. SIRT 1 is a gene encoding a protein known as sirtuin 1 (short for NAD-dependent deacetylase sirtuin-1). Sirtuin 1 is an enzyme that plays important roles in regulating proteins involved in cellular metabolism and processes linked to stress, longevity, and inflammation (4).
The Role of NAD+ in Muscle Function
Another link between aging and NAD+ can be seen in skeletal muscle tissue. In mouse models, age-related muscle decline occurs in two steps. In the first step, oxidative phosphorylation (the process mitochondria use to produce energy) declines because of reduced expression of mitochondrial genes (mitochondria contain their own DNA). In the second step, genes regulating oxidative phosphorylation begin to malfunction in both the mitochondria and nucleus. Phase 1 is reversible. If NAD+ is administered, mice in these studies show improved mitochondrial function and do not progress to step 2. If, however, the mice are allowed to progress to stage 2 without intervention, then NAD+ cannot rescue them (5). This evidence suggests that intervention in mitochondrial aging is possible using NAD+, but that waiting too long results in refractory dysfunction.
This is the best argument yet that early supplementation with NAD+ is critical to fighting off aging in the long term.
NAD+ and Neurodegenerative Disease
Much of what has been learned about NAD+ and the aging process is actually applicable to a number of disease conditions. In particular, changes in NAD+ appear to have far reaching effects on the central nervous system and have been linked to a number of neurodegenerative diseases such as Alzheimer’s and Huntington’s diseases. A review article published in 2019 explained the current state of the knowledge as it relates to NAD+ and the central nervous system.
In short, NAD+ is neuroprotective in a number of mouse models of human diseases such as Huntington’s disease. It appears that the cofactor is important in improving mitochondrial function, which in turn decreases the production of reactive oxygen species (ROS). ROS are known to cause damage in a number of inflammatory and disease conditions. They also acelerate the aging process (6).
Research in mouse models of Parkinson’s disease shows that NAD+ suplementation helps to protect against motor deficits and the death of dopaminergic neurons in the substantia nigra. This suggests that NAD+ may not only help ameliorate the symptoms of Parkinson’s disease, but may actually slow or even prevent the development of the disease in the first place (7).
The Role of NAD+ in Reducing Inflammation
NAD+ levels are regulated by a number of factors, one of which is NAMPT. This particular enzyme is known to be associated with inflammation and is often overexpressed by certain types of cancer. Researchers are, in fact, targeting NAMPT as a potential anti-cancer treatment. The regulator has also been linked to the development of obesity, type 2 diabetes, and nonalcoholic fatty liver disease. It is a potent activator of inflammation and its levels increase dramatically as NAD+ levels decrease. It is thought that supplementation with NAD+ can help to reduce NAMPT activation and thus modulate inflammation (8).
There is good evidence to suggest that the NAD+/NAMPT dichotomy is a primary driver of the insulin resistance that has been linked to obesity and so often leads to type 2 diabetes as well as heart disease. It appears that obesity leads to inflammation and that leads to an overall reduction in NAD+ levels, which in turn increases free fatty acid levels in the blood as a result of adiponectin down-regulation. This then causes the liver to produce more glucose even as it interferes with the insulin-mediated uptake of glucose by skeletal muscle. The result is insulin resistance, which the pancreas attempts to overcome by producing more insulin. The net result, over time, is high glucose levels and diabetes (9).
NAD+ in Addiction Treatment
It has long been known that drugs and alcohol can have a deleterious effect on NAD+ levels. This leads to nutritional deficits, but has also been linked to changes in mood and awareness. Supplementation with NAD+ to help overcome these deficits started in the 1960s, but has recently gained popularity as a result of studies showing that NAD+ in combination with specific amino acid complexes can actually boost recovery and lead to more profound and lasting results during addiction rehabilitation. Research indicates that the combination of NAD+ and certain amino acids can reduce cravings and improve stress and anxiety levels (10).
References
1. N. Sun, R. J. Youle, and T. Finkel, “The Mitochondrial Basis of Aging,” Mol. Cell, vol. 61, no. 5, pp. 654-666, Mar. 2016. [PMC]
2. D. Stipp, “Beyond Resveratrol: The Anti-Aging NAD Fad,” Scientific American Blog Network. [Online]. Available: https://blogs.scientificamerican.com/guest-blog/beyond-resveratrol-the-anti-aging-nad-fad/
3. A. P. Gomes et al., “Declining NAD+ Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging,” Cell, vol. 155, no. 7, pp 1624-1638, Dec. 2013. [PMC]
4. S. Imai and L. Guarente, “NAD+ and sirtuins in aging and disease,” Trends Cell Biol., vol. 24, no. 8, pp. 464-471, Aug. 2014. [PubMed]
5. A. R. Mendelsohn and J. W. Larrick, “Partial reversal of skeletal muscle aging by restoration of normal NAD+ levels,” Rejuvenation Res., vol. 17, no. 1, pp. 62-69, Feb. 2014. [PubMed]
6. C. Kang, E. Chung, G. Diffee, and L. L. Ji, “Exercise training attenuates aging associated mitochondrial dysfunction in rat skeletal muscle: role of PGC-1a,” Exp. Gerontol., vol. 48, no. 11, pp. 1343-1350, Nov. 2013. [PubMed]
7. S. Ringholm et al., “Effect of lifelong resveratrol supplementation and exercise training on skeletal muscle oxidative capacity in aging mice; impact of PGC-1a,” Exp. Gerontol., vol. 48, no. 11, pp. 1311-1318, Nov. 2013. [PubMed]
A. Lloret and M. F. Beal, “PGC-1a, Sirtuins and PARPs in Huntington’s Disease and Other Neurodegenerative Conditions: NAD+ to Rule Them AII,” Neurochem. Res., May 2019. [PubMed]
8. A. Lloret and M. F. Beal, “PGC-1a, Sirtuins and PARPs in Huntington’s Disease and Other Neurodegenerative Conditions: NAD+ to Rule Them All,” Neurochem. Res., May 2019. [PubMed]
9. Shan et al., “Protective effects of B- nicotinamide adenine dinucleotide against motor deficits and dopaminergic neuronal damage in a mouse model of Parkinson’s disease,” Prog. Neuropsychopharmacol. Biol. Psychiatry, vol. 94, p. 109670, Jun. 2019. [PubMed]
10. D. C. Maddison and F. Giorgini, “The kynurenine pathway and neurodegenerative disease,” Semin. Cell Dev. Biol., vol. 40, pp. 134-141, Apr. 2015. [PubMed]
11. A. Garten, S. Schuster, M. Penke, T. Gorski, T. de Giorgis, and W. Kiess, “Physiological and pathophysiological roles of NAMPT and NAD metabolism,” Nat. Rev. Endocrinol., vol. 11, no. 9, pp. 535-546, Sep. 2015. [PubMed]
12. S. Yamaguchi and J. Yoshino, “Adipose Tissue NAD+ Biology in Obesity and Insulin Resistance: From Mechanism to Therapy,” BioEssavs News Rev. Mol. Cell. Dev. Biol., vol. 39, no. 5, May 2017. [PMC]
13. J. E. Humiston, “Nicotinamide Adenine Dinucleotide,” p. 68. [FDA]
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