Lifespan: Why We Age―and Why We Don’t Have To by David A. Sinclair
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Lifespan
Introduction: A Grandmother’s Prayer
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Our successes in extending life, the surgeon and doctor Atul Gawande has noted, have had the effect of “making mortality a medical experience.”
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There’s also a difference between extending life and prolonging vitality. We’re capable of both, but simply keeping people alive—decades after their lives have become defined by pain, disease, frailty, and immobility—is no virtue.
Chapter 1. ‘Viva Primordium’
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Today, analog information is more commonly referred to as the epigenome, meaning traits that are heritable that aren’t transmitted by genetic means.
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sirtuins are enzymes that remove acetyl tags from histones and other proteins and, by doing so, change the packaging of the DNA, turning genes off and on when needed.
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As we will see later, the loss of NAD as we age, and the resulting decline in sirtuin activity, is thought to be a primary reason our bodies develop diseases when we are old but not when we are young.
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If there is one paper that propelled us into the digital, wireless world in which we now live, that would be it.
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mTOR can signal cells in stress to hunker down and improve survival by boosting such activities as DNA repair, reducing inflammation caused by senescent cells, and, perhaps its most important function, digesting old proteins.27
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there are plenty of stressors that will activate longevity genes without damaging the cell, including certain types of exercise, intermittent fasting, low-protein diets, and exposure to hot and cold temperatures
Chapter 2. The Demented Pianist
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But unlike the oncogenes that were discovered in the 1970s and that have given us a good target for going to battle against cancer, we haven’t identified a singular gene that causes aging. And we won’t. Because our genes did not evolve to cause aging.
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the fundamental, upstream cause of sterility and aging in yeast was the inherent instability of the genome.
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Yet even over the course of many thousands of years, their cells do not appear to have undergone any decline in function. Scientists call this “negligible senescence.
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Studies of identical twins place the genetic influences on longevity at between 10 and 25 percent which, by any estimation, is surprisingly low.16