The Tyranny of NAD+, or Where'd My Dessert Go?

More evidence has just been published showing how reducing the caloric intake of cells influences their survival. Anyone want to take a guess as to what happens when a living organism (eukaryotes only, please) is subjected to noshing only on insultingly small morsels of food? Such asceticism of course is an outrage to those of us who follow the modern method of nutritional ingestion.

Again, the question: What happens when eukaryotic cells are subjected to nutrient restriction?

A. Cell survival is promoted by a reduction in apoptosis.
B. Cell survival is impaired by the genotoxic effects of fasting.
C. Cell survival is neither improved nor reduced.
D. No one knows because the post-doc fellow accidently set the lab on fire while trying to heat up his lunch.

The answer is "A." I know you got it right - you're smart, not like what everybody says.

The paper was just published by Yang and colleagues in the scientific journal Cell, in a collaboration between four different institutions. What they found is that mitochondria exposed to stress and nutrient restriction can still maintain adequate levels of the important coenzyme NAD+, and that rats fasted for 48 hours can increase production of mitochondrial NAD+ by activating the gene that can increase production of NAD+. It goes by the delightfully sesquipedalian name nicotinamide phosphoribosyltransferase, or NAMPT. It may be the most important anti-aging gene in the eukaryotic cell, not to mention us humans. But don't just take my word for it -- here's a quotation from a recent Journal of Biological Chemistry article on NAMPT:

In contrast, introducing the Nampt gene into ageing human SMCs [smooth muscle cells] delayed senescence and substantially lengthened cell lifespan, together with enhanced resistance to oxidative stress...These data indicate that Nampt is a longevity gene [my italics] that can add stress-resistant life to human SMCs...

Dr. Yang and his fellow authors summarize these very interesting findings, which are detailed with mine-eyes-glaze-over detail in their paper, as follows:

We hope that these insights into the importance of mitochondrial NAD+ will facilitate a new understanding of and the development of novel approaches to treating diseases such as cancer and neurodegeneration.

Now we're getting somewhere. Reducing the calorie intake of a mammal may delay the aging process and protect against such devastating age-related illnesses such as cancer and Alzheimer's disease. How do we report this in such a way as to not offend those Americans who are addicted to eating more than their body requires? That's easy:

"New Clue To Why Eating Fewer Calories Can Help You Live Longer"

And now, with your kind permission, may I be excused to eat my dessert? Thank you, and goodnight.

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Any inter-individual differences in expression on similar diets?

By hip hip array (not verified) on 23 Sep 2007 #permalink

Humans are programmed to take advantage of abundance to guard against want. In these times, want is, well, wanting. Abundance is ever-present. Hence, we over eat.

Couple that with the development and production of the most appealing food possible (commercial survival of the most tasty), and you have a recipe (pun not intended) for the obesity epidemic.

But the formula is susceptible to multiple attack points. Eliminate the taste of food (deny tastiness), or limit variety (the same) or reduce appetite, and weight loss will result.

Coincidently, today's web news brings word that Betahistine, an anti-vertigo drug with a long history in humans, can curb appetite. It is now being developed as a weight-loss drug.

People have a poor reputation for denying temptation.