Lifespan Quotes

“Don’t be disheartened by my claim that we are the biological equivalent of an old DVD player. This is actually good news. If Szilard had turned out to be right about mutations causing aging, we would not be able to easily address it, because when information is lost without a backup, it is lost for good. Ask anyone who’s tried to play or restore content from a DVD that’s had an edge broken off: what is gone is gone. But we can usually recover information from a scratched DVD. And if I am right, the same kind of process is what it will take to reverse aging.”
― David A. Sinclair, Lifespan: The Revolutionary Science of Why We Age—and Why We Don't Have To

“After our species was almost driven to extinction 74,000 years ago, up until 1900, the human population grew at a rate amounting to a fraction of a percent each year as we expanded to all habitable regions on the planet, breeding with at least two other human species or subspecies. By 1930, thanks to sanitation and decreases in child-mother mortality, our species was increasing its numbers at 1 percent each year. And by 1970, due to immunization and improvements in food production globally, the rate was 2 percent each year. Two percent might not seem like a lot, but it added up fast. It took more than 120 years for our population to move from 1 billion to 2 billion, but after reaching that mark in 1927, it took just thirty-three more years to add another billion and then fourteen years to add another. This is how, at the end of the second decade of the twenty-first century, we came to have more than 7.7 billion people on our planet, and every year one additional person per square kilometer.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“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.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“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.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“The quantum physicist Max Planck also knew this to be true. “A new scientific truth does not triumph by convincing its opponents and making them see the light,” Planck wrote shortly before his death in 1947, “but rather because its opponents eventually die, and a new generation grows up that is familiar with it.”26”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“The problem is not just population, it’s consumption. And it’s not just consumption, it’s waste. In comes the food; out goes the effluent. In come the fossil fuels; out go the carbon emissions. In come the petrochemicals; out goes the plastic. On average, Americans consume more than three times the amount of food they need to survive and about 250 times as much water.14 In return, they produce 4.4 pounds of trash each day, recycling or composting only about of a third of it.15 Thanks to things such as cars, planes, big homes, and power-hungry clothes dryers,16 the annual carbon dioxide emissions of an average American are five times as high as the global average. Even the “floor”—below which even monks living in American monasteries typically do not go—is twice the global average.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“WE ARE ANALOG, THEREFORE WE AGE. According to the Information Theory of Aging, we become old and susceptible to diseases because our cells lose youthful information. DNA stores information digitally, a robust format, whereas the epigenome stores it in analog format, and is therefore prone to the introduction of epigenetic “noise.” An apt metaphor is a DVD player from the 1990s. The information is digital; the reader that moves around is analog. Aging is similar to the accumulation of scratches on the disc so the information can no longer be read correctly. Where’s the polish?”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“DELETING THE ZOMBIE SENESCENT CELLS IN OLD TISSUES. Thanks to the primordial survival circuit we’ve inherited from our ancestors, our cells eventually lose their identities and cease to divide, in some cases sitting in our tissues for decades. Zombie cells secrete factors that accelerate cancer, inflammation, and help turn other cells into zombies. Senescent cells are hard to reverse aging in, so the best thing to do is to kill them off. Drugs called senolytics are in development to do just that, and they could rapidly rejuvenate us.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“Small numbers of senescent cells can cause widespread havoc. Even though they stop dividing, they continue to release tiny proteins called cytokines that cause inflammation and attract immune cells called macrophages that then attack the tissue. Being chronically inflamed is unhealthy: just ask someone with multiple sclerosis, inflammatory bowel disease, or psoriasis. All these diseases are associated with excess cytokine proteins.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“one of the key hallmarks of aging is the accumulation of senescent cells. These are cells that have permanently ceased reproduction. Young human cells taken out of the body and grown in a petri dish divide about forty to sixty times until their telomeres become critically short, a point discovered by the anatomist Leonard Hayflick that we now call the Hayflick limit. Although the enzyme known as telomerase can extend telomeres—the discovery of which afforded Elizabeth Blackburn, Carol Greider, and Jack Szostak a Nobel Prize in 2009—it is switched off to protect us from cancer, except in stem cells. In 1997, it was a remarkable finding that if you put telomerase into cultured skin cells, they don’t ever senesce.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“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.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“THE THREE MAIN LONGEVITY PATHWAYS, mTOR, AMPK, AND SIRTUINS, EVOLVED TO PROTECT THE BODY DURING TIMES OF ADVERSITY BY ACTIVATING SURVIVAL MECHANISMS. When they are activated, either by low-calorie or low-amino-acid diets, or by exercise, organisms become healthier, disease resistant, and longer lived. Molecules that tweak these pathways, such as rapamycin, metformin, resveratrol, and NAD boosters, can mimic the benefits of low-calorie diets and exercise and extend the lifespan of diverse organisms.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“nicotinamide mononucleotide,”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“When sirtuins shift from their typical priorities to engage in DNA repair, their epigenetic function at home ends for a bit. Then, when the damage is fixed and they head back to home base, they get back to doing what they usually do: controlling genes and making sure the cell retains its identity and optimal function.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“But the true extent to which the survival circuit is conserved between yeast and humans wasn’t fully known until 2017, when Eva Bober’s team at the Max Planck Institute for Heart and Lung Research in Bad Nauheim, Germany, reported that sirtuins stabilize human rDNA.23 Then, in 2018, Katrin Chua at Stanford University found that, by stabilizing human rDNA, sirtuins prevent cellular senescence—essentially the same antiaging function as we had found for sirtuins in yeast twenty years earlier.24”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“Every one of our cells has the same DNA, of course, so what differentiates a nerve cell from a skin cell is the epigenome, the collective term for the control systems and cellular structures that tell the cell which genes should be turned on and which should remain off. And this, far more than our genes, is what actually controls much of our lives.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“One of these is called target of rapamycin, or TOR, a complex of proteins that regulates growth and metabolism. Like sirtuins, scientists have found TOR—called mTOR in mammals—in every organism in which they’ve looked for it. Like that of sirtuins, mTOR activity is exquisitely regulated by nutrients. And like the sirtuins, mTOR can signal cells in stress to hunker down and improve survival by boosting such activities as DNA repair, reducing inflammation caused by senescent cells, and, perhaps its most important function, digesting old proteins.27”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“The Information Theory of Aging starts with the primordial survival circuit we inherited from our distant ancestors.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“In the same way that genetic information is stored as DNA, epigenetic information is stored in a structure called chromatin.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“Yet I believe that such an answer exists—a cause of aging that exists upstream of all the hallmarks. Yes, a singular reason why we age. Aging, quite simply, is a loss of information.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“In The Structure of Scientific Revolutions, Thomas Kuhn noted that scientific discovery is never complete; it goes through predictable stages of evolution. When a theory succeeds at explaining previously unexplainable observations about the world, it becomes a tool that scientists can use to discover even more.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“There are some simple tests to determine how biologically old you probably are. The number of push-ups you can do is a good indicator. If you are over 45 and can do more than twenty, you are doing well. The other test of age is the sitting-rising test (SRT). Sit on the floor, barefooted, with legs crossed. Lean forward quickly and see if you can get up in one move. A young person can. A middle-aged person typically needs to push off with one of their hands. An elderly person often needs to get onto one knee. A study of people 51 to 80 years found that 157 out of 159 people who passed away in 75 months had received less than perfect SRT scores.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“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.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“As far back as the 1970s, though, there have been observational studies that strongly suggested long-term calorie restriction could help humans live longer and healthier lives, too.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“It needs to be pointed out that very few of the global carrying capacity models account for human ingenuity. As we have discussed, it is easier not to see things coming than to see them, so we tend to extrapolate into the future directly from the way things are now. That’s unfortunate and, in my view, scientifically wrong, for it eliminates an important factor from the equation.”
― David A. Sinclair, Lifespan: The Revolutionary Science of Why We Age—and Why We Don't Have To

“The tragedy of the commons is that humans are not very good at taking personal action to solve collective problems. The trick to revolutionary change is finding ways to make self-interest align with the common good. For people to accept widespread biometric tracking in a way that could help us get ahead of fast-moving deadly viruses, they’ll need to be offered something they have a hard time seeing themselves without.”
― David A. Sinclair, Lifespan: The Revolutionary Science of Why We Age—and Why We Don't Have To

“Hoy en día, la información analógica se conoce comúnmente como «epigenoma» y comprende los rasgos que son hereditarios, pero que no se transmiten a través de los genes.”
― David A. Sinclair, Alarga tu esperanza de vida: Cómo la ciencia nos ayuda a controlar, frenar y revertir el proceso de envejecimiento

“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.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“• I don’t smoke. I try to avoid microwaved plastic, excessive UV exposure, X-rays, and CT scans. • I try to stay on the cool side during the day and when I sleep at night. • I aim to keep my body weight or BMI in the optimal range for healthspan, which for me is 23 to 25.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“Cyteir Therapeutics, which develops novel ways to fight”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To