According to the research of David Sinclair and Lindsay Wu, co-Head of the Laboratory for Aging Research at University of New South Wales, co-Director of the Biological Mechanisms of aging at Harvard Medical School, the lack of essential metabolite called NAD+ make our cells less efficient. They have been working for five years to make NAD+ boosters into therapeutant.


NAD+is a key co-enzyme that the mitochondria in every cell of our bodies depend on to fuel all basic functions(1). Low NAD+ levels impair mitochondria function and are implicated in health problems such as cancer, diabetes, heart disease, immune problems aging(2). Scientists have now confirmed a direct link between falling NAD+ levels and aging in both animal and in human subjects.


As we age, our bodies produce less NAD+ and the communication between the Mitochondria and cell nucleus is impaired(13).
Over time, decreasing NAD+ impairs the cell’s ability to make energy, which leads to aging and disease (13) and perhaps even the key factor in why we age (1).


Researchers have found that re-upping NAD+ in older mice causes them to look and act younger, as well as live longer than expected. In a March 2017 study published in the journal Science, Sinclair and his colleagues put drops of a compound known to raise levels of NAD+ into the water for a group of mice. Within a couple hours, the NAD+ levels in the mice had risen significantly. In about a week, signs of aging in the tissue and muscles of the older mice reversed to the point that researchers could no longer tell the difference between the tissues of a 2-year-old mouse and those of a 4-month-old one.



Increase energy and metabolism

From the experiment, administration of LABELED NAD+ by IP and IV injection demonstrated that exogenous NAD+ crosses the blood brain barrier to enter the hypothalamus intact, reduces hunger and weight gain, and increases energy expenditure and fat burning in mice.

Exogenous NAD is effectively transported to the hypothalamus via a connexin 43-dependent mechanism and increases hypothalamic NAD content. Therefore, NAD supplementation is a potential therapeutic method for metabolic disorders characterized by hypothalamic NAD depletion.


Decrease Brain Damage

In the study, a rat model of transient focal ischemia has been used to test this hypothesis. We observed that intranasal NAD+ delivery significantly increased NAD+ contents in the brains. Intranasal delivery with 10 mg/kg NAD+ at 2 hours after ischemic onset profoundly decreased infarct formation when assessed either at 24 or 72 hours after ischemia. The NAD+ administration also significantly attenuated ischemia-induced neurological deficits.

These results provide the first in vivo evidence that NAD+ metabolism is a new target for treating brain ischemia, and that NAD+ administration may be a novel strategy for decreasing brain damage in cerebral ischemia and possibly other PARP-1-associated neurological diseases. It is also can be used for protecting against dementia.


Protect Against Cardiovascular Diseases

Exogenous addition of NAD was capable of maintaining intracellular levels of NAD and blocking the agonist-induced cardiac hypertrophic response via activation of the SIRT3-LKB1-AMP-activated kinase pathway.

The conducting experiment has showed that anti-hypertrophic effects of exogenous NAD are mediated through activation of SIRT3. SIRT3 deacetylates and activates LKB1, thus augmenting the activity of the LKB1-AMPK pathway. These results reveal a novel role of NAD as an inhibitor of cardiac hypertrophic signaling, and suggest that prevention of NAD depletion may be critical in the treatment of cardiac hypertrophy and heart failure.


Protect Against Age Related Diseases

NAD+ has emerged as a vital oxidoreductase cofactor that regulates metabolism, activates sirtuins and maintains mitochondrial function by enhancing oxidative metabolism to promote healthy aging, and can extend lifespan in worms through the UPRmt stress response pathway. Researches has shown that reduced NAD+/NADH ratio is strongly implicated in mitochondrial disorders and, age-related disorders including diabetes, obesity, neurodegeneration and cancer.