Anti-Aging Medicine & NAD+

There appears to be even more benefit to NAD+ therapy than simply neurotransmitter rehabilitation for neurological conditions and chemical dependence detox.

Recent research at Harvard University suggests that NAD+ decline and the resulting decline in mitochondrial function is also intimately intertwined with cross genome communication, and an increase in genetic mutation, which contributes in part to the aging process, and potentially to the physiology and development of cancer.

For reasons still unclear, as we age, levels of the initial chemical NAD decline. Without sufficient NAD, a gene referred to as SIRT1 loses its ability to keep tabs on meddlesome molecules (such as one in particular named HIF-1) that interfere with cross-genome communication which coordinates activities between the cell’s nuclear genome and the mitochondrial genome. As levels of HIF-1 escalate, such molecules begin wreaking havoc on the otherwise smooth cross-genome communication. Over time, this loss of communication reduces the cell’s ability to make energy, and signs of aging and disease become apparent.

Cells stay healthy as long as coordination between the genomes remains fluid. SIRT1’s role is intermediary, akin to a security guard; it assures that a meddlesome molecule called HIF-1 does not interfere with communication.

While the breakdown of this process causes a rapid decline in mitochondrial function, other signs of aging take longer to occur. Researchers found that by administering an endogenous compound that cells transform into NAD, they could repair the broken network and rapidly restore communication and mitochondrial function. If the compound was given early enough—prior to excessive mutation accumulation—within days, some aspects of the aging process could be reversed.

For the full story, please see:

https://hms.harvard.edu/news/genetics/new-reversible-cause-aging-12-19-13

https://newsroom.unsw.edu.au/news/health/unsw-harvard-scientists-unveil-giant-leap-anti-ageing

http://genetics.med.harvard.edu/sinclair/research.php