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" "prompting the United States in 1935 to join about twenty other countries that had already instituted a social insurance program. Social Security made moral sense. It made mathematical sense, too. At that time, just over half of men who reached their 21st birthday would also reach their 65th, the year at which most could begin to collect a supplemental income. Those who reached age 65 could count on about thirteen more years of life.32 And there were a lot of younger workers paying into the system to support that short retirement; at that time only about 7 percent of Americans were over the age of 65. As the economy began to boom again in the wake of World War II, there were forty-one workers paying into the system for every beneficiary. Those are the numbers that supported the system when its first beneficiary, a legal secretary from Vermont named Ida May Fuller, began collecting her checks. Fuller had worked for three years under Social Security and paid $24.75 into the system. She lived to the age of 100 and by the time of her death in 1975 had collected $22,888.92. At that point, the poverty rate among seniors had fallen to 15 percent, and it has continued to fall ever since, owing largely to social insurance.33 Now about three-quarters of Americans who reach the age of 21 also see 65. And changes to the laws that govern the US social insurance safety net have prompted many to retire — and begin collecting — earlier than that. New benefits have been added over the years. Of course, people are living longer, too; individuals who make it to the age of 65 can count on about twenty more years of life.34 And as just about every social insurance doomsdayer can tell you, the ratio of workers to beneficiaries is an unsustainable three to one.
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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.
Like rapamycin, metformin mimics aspects of calorie restriction. But instead of inhibiting TOR, it limits the metabolic reactions in mitochondria, slowing down the process by which our cellular powerhouses convert macronutrients into energy.20 The result is the activation of AMPK, an enzyme known for its ability to respond to low energy levels and restore the function of mitochondria. It also activates SIRT1, one of my lab's favorite proteins. Among other beneficial effects, metformin inhibits cancer cell metabolism, increases mitochondrial activity, and removes misfolded proteins.21
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We also knew that many other health-promoting molecules, and chemical derivatives of them, are produced in abundance by stressed plants; we get resveratrol from grapes, aspirin from willow bark, metformin from lilacs, epigallocatechin gallate from green tea, quercetin from fruits, and allicin from garlic. This, we believe, is evidence of xenohormesis — the idea that stressed plants produce chemicals for themselves that tell their cells to hunker down and survive.