In this episode, David Sinclair, Ph.D., a Professor in the Department of Genetics at Harvard Medical School and co-Director of the Paul F. Glenn Center for the Biological Mechanisms of Aging, returns to the podcast to discuss the content of his new book, Lifespan: Why We Age – and Why We Don’t Have To. This conversation focuses on the biological mechanisms involved in what David terms the Information Theory of Aging which provides insights into the “clock” that determines our aging and to what degree it can be manipulated. Our discussion on aging of course leads us into interconnected topics of epigenetics, sirtuins, cellular senescence, as well as what compounds David is personally taking for his own longevity. Additionally, we discuss the most up to date information related to NAD and longevity by looking at the potential benefits (if any) of supplemental agents (NAD precursors, NR, NMR, etc.) that pose a promise of increasing NAD.

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We discuss:

SIR genes and cellular identity [8:45];

Sirtuins regulate gene expression [14:30];

DNA is methylated at the deepest layer of the epigenome [17:45];

Methylation pattern and determining cellular age [20:15];

Cellular reprogramming [33:45];

Yamanaka factors to push cells “back in time” [41:00];

Human cellular reprogramming viability [57:00];

Measuring the rate of aging [1:02:45];

Cellular reprogramming for longevity [1:14:45];

Compounds David takes for his own longevity [1:29:15]

NAD precursors (NR, NMN) and pterostilbene [1:40:00];

The current field of sirtuin activators [2:03:15];

David’s artistic work [2:05:15] and;

More.

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SIR genes and cellular identity [8:45]

The SIR gene – silent information regulator – is a gene that controls other genes

One of the roles it is most well-known for, is its implication in longevity: In a study by Matt Kaeberlin Sir2 was shown to control the aging process in yeast

The gene group’s primary roles are to: Silence other genes Repair damaged DNA



The SIR enzyme is the master regulator of this cellular survival circuit

The SIR gene cannot silence other genes and serve a cellular repair function at the same time silenced genes are temporarily “turned on” while the damage is repaired by the enzyme protein “turned on” genes help with the repair the protein then returns to its “silencing post”



Figure 1. When SIR enzyme proteins detect stress in the cell (e.g. DNA breakage) the protein leaves the silent region to go and repair the DNA. When the problem is fixed, it returns to its original post, silencing genes. Image credit: (Alves-Fernandes and Jasiulionis, 2019)

Overtime, in the back-and-forth of repair… SIR genes lose track of which genes should be silenced or not

In aging yeast, the loss of cellular identity results in a sterility phenotype

With age, our cells lose their “program” but early evidence in mice suggests that the original “hard disk program” can be recovered; restored to the original programming

“We have some early evidence from mice that we can actually find that hard disk drive and reinstall the software so that it’s pristine again and we find that we can actually improve the health quite dramatically in parts of a mouse’s body.” — David Sinclair, Ph.D

What does Claude Shannon’s Information Theory of Communication have to do with aging?…

In his 1940 paper , mathematician Claude Shannon presented his Information Theory of Communication

He presented how to encode information and make sure that information gets to the receiver

Shannon figured out how to preserve information: make a repository and reset the system

{end of show notes preview}

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