Most of my colleagues call these "longevity genes" because they have demonstrated the ability to extend both average and maximum lifespans in many organisms. But these genes don't just make life longer, they make it healthier, which is why they can also be thought of as "vitality genes."

Up until the second half of the twentieth century, it was generally accepted that organisms grow old and die “for the good of the species” — an idea that dates back to Aristotle, if not further.

Analog data are superior for this job because they can be changed back and forth with relative ease whenever the environment within or outside the cell demands it, and they can store an almost unlimited number of possible values, even in response to conditions that have never been encountered before.25 The unlimited number of possible values is why many audiophiles still prefer the rich sounds of analog storage systems. But even though analog devices have their advantages, they have a major disadvantage. In fact, it's the reason we've moved from analog to digital. Unlike digital, analog information degrades over time — falling victim to the conspiring forces of magnetic fields, gravity, cosmic rays, and oxygen. Worse still, information is lost as it's copied. No one was more acutely disturbed by the problem of information loss than Claude Shannon, an electrical engineer from the Massachusetts Institute of Technology (MIT) in Boston.

THE MAKING OF THE ICE MOUSE TO TEST IF THE CAUSE OF AGING MIGHT BE INFORMATION LOSS. A gene from a slime mold that encodes an enzyme that cuts DNA at a specific place was inserted into a stem cell and injected into an embryo to generate the ICE mouse. Turning on the slime mold gene cut the DNA and distracted the sirtuins, causing the mouse to undergo aging.

The first principle is that you must not fool yourself — and you are the easiest person to fool." R. P. Feynman,

For example, having a C instead of a T variant at position rs2764264 is associated with longer life. Two of our children, Alex and Natalie, inherited two Cs at this position, one from Sandra and one from me, so all other genes being equal, and as long as they don't live terribly negative lifestyles, they should have greater odds of reaching age 95 than I do, with my one C and one T, and substantially greater than someone with two Ts.

The way doctors treat illness today "is simple," wrote S. Jay Olshansky, a demographer at the University of Illinois. "As soon as a disease appears, attack that disease as if nothing else is present; beat the disease down, and once you succeed, push the patient out the door until he or she faces the next challenge; then beat that one down. Repeat until failure.

The longevity genes I work on are called "sirtuins," named after the yeast SIR2 gene, the first one to be discovered. There are seven sirtuins in mammals, SIRT1 to SIRT7, and they are made by almost every cell in the body. When I started my research, sirtuins were barely on the scientific radar. Now this family of genes is at the forefront of medical research and drug development. Descended from gene B in M. superstes, 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. These critical epigenetic regulators sit at the very top of cellular control systems, controlling our reproduction and our DNA repair. After a few billion years of advancement since the days of yeast, they have evolved to control our health, our fitness, and our very survival. 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.

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."

Youth → broken DNA → genome instability → disruption of DNA packaging and gene regulation (the epigenome) → loss of cell identity → cellular senescence → disease → death.

Our equivalent of the Lord's Prayer was the English author Alan Alexander Milne's poem "Now We Are Six," which ends: But now I am six, I'm as clever as clever. So I think I'll be six now for ever and ever.

Your generation, just like all the ones that came before, didn't do anything about the destruction that is being done to this planet," Alex told me that evening. "And now you want to help people live longer? So they can do even more damage to the world?
I went to bed that night troubled. Not by our firstborn's denouncement of me; of that, I admit, I was a little proud. We'll never destroy the global patriarchy if our children don't first practice on their fathers.

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If you've had your genome analyzed, you can check if you have any of the known variations of FOXO3 that are associated with a long life.40 For example, having a C instead of a T variant at position rs2764264 is associated with longer life. Two of our children, Alex and Natalie, inherited two Cs at this position, one from Sandra and one from me, so all other genes being equal, and as long as they don't live terribly negative lifestyles, they should have greater odds of reaching age 95 than I do, with my one C and one T, and substantially greater than someone with two Ts.

In 2003, Michael McBurney from the University of Ottawa in Canada discovered that mouse embryos manipulated to be unable to produce one of the seven sirtuin enzymes, SIRT1, couldn't last past the fourteenth day of development — about two-thirds of the way into a mouse's gestation period.26 Among the reasons, the team reported in the journal Cancer Cell, was an impaired ability to respond to and repair DNA damage.