Lifespan: Why We Age—and Why We Don't Have To
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Read between April 1 - April 9, 2022
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It consists of strands of DNA wrapped around spooling proteins called histones, which are bound up into bigger loops called chromatin, which are bound up into even bigger loops called chromosomes.
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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.
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Why? One of our key findings, in a study we published in 2018,42 was that when treated with an NAD-boosting molecule that activated the SIRT1 enzyme, the elderly mice’s endothelial cells, which line the blood vessels, were pushing their way into areas of the muscle that weren’t getting very much blood flow. New tiny blood vessels, capillaries, were formed, supplying badly needed oxygen, removing lactic acid and toxic metabolites from muscles, and reversing one of the most significant causes of frailty in mice and in humans. That was how these old mice suddenly became such mighty marathoners.
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one thing you can do to maximize your lifespan right now, it’s this: eat less often.
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Mayo Clinic researchers studying the effects of different types of exercise on different age groups found that although many forms of exercise have positive health effects, it’s high-intensity interval training (HIIT)—the sort that significantly raises your heart and respiration rates—that engages the greatest number of health-promoting genes, and more of them in older exercisers.36
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exposing your body to less-than-comfortable temperatures is another very effective way to turn on your longevity genes.
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“There is nothing in biology yet found that indicates the inevitability of death. This suggests to me that it is not at all inevitable and that it is only a matter of time before biologists discover what it is that is causing us the trouble.”5
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metformin the first drug to be approved to delay the most common age-related diseases by addressing their root cause: aging itself. If Barzilai and his colleagues can show metformin has measurable benefits in the ongoing Targeting Aging with Metformin (TAME) study, the US Food and Drug Administration has agreed to consider aging as a treatable condition.
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Patients with an RPE65 mutation that causes blindness, for example, can now be cured with a simple injection of a safe virus that infects the retina and delivers, forever, the functional RPE65 gene.
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Now, as we rapidly approach the era of self-driving cars—a technological and social paradigm shift that almost every expert expects will rapidly reduce car crashes—we need to confront an important question: Where will the organs come from?
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“Life is very short and anxious for those who forget the past, neglect the present, and fear the future,”
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The problem isn’t population; it is consumption.
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Skillbaticals, which might take the shape of a government-supported paid year off for every ten worked, might ultimately become cultural and even legal requisites, just as many of the labor innovations of the twentieth century have. In this way, those who are tired of “working harder” would be afforded every opportunity to “work smarter” by returning to school or a vocational training program paid for by employers or the government, a variation of the universal basic income that is being discussed in the United States and some countries in Europe.
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And that’s the world’s biggest problem: the future is seen as someone else’s concern.
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We’re no longer going to be able to wait for prejudiced people to die; we’re going to have to confront them and work to soften their hearts and change their minds.