DELETING THE ZOMBIE SENESCENT CELLS IN OLD TISSUES. Thanks to the primordial survival circuit we've inherited from our ancestors, our cells eventuall… - David A. Sinclair

They have also evolved to require a molecule called nicotinamide adenine dinucleotide, or NAD. 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. Trading reproduction for repair, the sirtuins order our bodies to "buckle down" in times of stress and protect us against the major diseases of aging: diabetes and heart disease, Alzheimer's disease and osteoporosis, even cancer. They mute the chronic, overactive inflammation that drives diseases such as atherosclerosis, metabolic disorders, ulcerative colitis, arthritis, and asthma. They prevent cell death and boost mitochondria, the power packs of the cell. They go to battle with muscle wasting, osteoporosis, and macular degeneration. In studies on mice, activating the sirtuins can improve DNA repair, boost memory, increase exercise endurance, and help the mice stay thin, regardless of what they eat. These are not wild guesses as to their power; scientists have established all of this in peer-reviewed studies published in journals such as Nature, Cell, and Science.

the Royal Society. Founded in the 1600s during the Age of Enlightenment and formerly headed by Australia's catalyst, the botanist Sir Joseph Banks, as well as such legendary minds as Sir Isaac Newton and Thomas Henry Huxley, the society's cheeky motto is a pretty good one to live by: "Nullius in Verba," it says underneath the society's coat of arms. That's Latin for "Take nobody's word for it.

Here's the important point: 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 (I discuss this in chapter 4).