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David Sinclair,Matthew LaPlante

Lifespan

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A paradigm-shifting book from an acclaimed Harvard Medical School scientist and one of Time's most influential people.
It's a seemingly undeniable truth that aging is inevitable. But what if everything we've been taught to believe about aging is wrong? What if we could choose our lifespan?
In this groundbreaking book, Dr. David Sinclair, leading world authority on genetics and longevity, reveals a bold new theory for why we age. As he writes: “Aging is a disease, and that disease is treatable.”
This eye-opening and provocative work takes us to the frontlines of research that is pushing the boundaries on our perceived scientific limitations, revealing incredible breakthroughs—many from Dr. David Sinclair's own lab at Harvard—that demonstrate how we can slow down, or even reverse, aging. The key is activating newly discovered vitality genes, the descendants of an ancient genetic survival circuit that is both the cause of aging and the key…
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Intryck

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Citat

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    Once you recognize that there are universal regulators of aging in everything from yeast to roundworms to mice to humans . . .

    . . . and once you understand that those regulators can be changed with a molecule such as NMN or a few hours of vigorous exercise or a few less meals . . .

    . . . and once you realize that it’s all just one disease . . .

    . . . it all becomes clear
  • aurelia anastasiahar citerati fjol
    stem cells. Yet the ICE mice were suffering from a loss of body mass, mitochondria, and muscle strength and an increase in cataracts, arthritis, dementia, bone loss, and frailty.

    All of the symptoms of aging—the conditions that push mice, like humans, farther toward the precipice of death—were being caused not by mutation but by the epigenetic changes that come as a result of DNA damage signals.

    We hadn’t given the mice all of those ailments. We had given them aging.

    And if you can give something, you can take it away.
  • aurelia anastasiahar citerati fjol
    Here’s the vital takeaway: we could age mice without affecting any of the most commonly assumed causes of aging. We hadn’t made their cells mutate. We hadn’t touched their telomeres. We hadn’t messed with their mitochondria.

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