Lifespan Quotes

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

“As the venture capitalist and “very large yacht” owner Nick Hanauer wrote in a memo to “My Fellow Zillionaires” in 2014, “there is no example in human history where wealth accumulated like this and the pitchforks didn’t eventually come out. You show me a highly unequal society, and I will show you a police state. Or an uprising. There are no counterexamples. None. . . . We will not be able to predict when, and it will be terrible—for everybody. But especially for us.”24”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“simply keeping people alive—decades after their lives have become defined by pain, disease, frailty, and immobility—is no virtue.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“What if we didn’t have to worry that the clock was ticking? And what if I told you that soon—very soon, in fact—we won’t?”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“Aunque no es inmortal, el tiburón boreal Somniosus microcephalus sigue siendo un animal impresionante y está mucho más emparentado con nosotros. Es casi del mismo tamaño que un tiburón blanco y no alcanza la madurez sexual hasta los ciento cincuenta años. Los investigadores creen que el océano Ártico podría ser el hogar de los tiburones boreales que nacieron antes de que Colón se perdiera en el Nuevo Mundo. Según la datación por carbono 14, un ejemplar enorme podría haber vivido más de quinientos diez años, al menos hasta que los científicos lo capturaron para poder dictaminar su edad. El hecho de que las células de este tiburón envejezcan o no es un debate científico abierto; muy pocos biólogos habían estudiado al S. microcephalus hasta hace unos años. Como mínimo, este longevo vertebrado experimenta el proceso del envejecimiento muy pero que muy despacio.”
― David A. Sinclair, Alarga tu esperanza de vida: Cómo la ciencia nos ayuda a controlar, frenar y revertir el proceso de envejecimiento

“capaces de activar los genes de la longevidad sin dañar la célula, entre los que se incluyen algunos ejercicios, el ayuno intermitente, las dietas bajas en proteínas y la exposición al frío y al calor (hablaré más de esto en el capítulo 4).”
― David A. Sinclair, Alarga tu esperanza de vida: Cómo la ciencia nos ayuda a controlar, frenar y revertir el proceso de envejecimiento

“Die köstlichsten Erdbeeren wurden durch Phasen mit begrenzter Wasserzufuhr gestresst.”
― David A. Sinclair, Lifespan: Why We Age―and Why We Don't Have To

“As a species, we are living much longer than ever. But not much better. Not at all. Over the past century we have gained additional years, but not additional life—not life worth living anyway.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“take 1 gram (1,000 mg) of NMN every morning, along with 1 gram of resveratrol (shaken into my homemade yogurt) and 1 gram of metformin.7 • I take a daily dose of vitamin D, vitamin K2, and 83 mg of aspirin. • I strive to keep my sugar, bread, and pasta intake as low as possible. I gave up desserts at age 40, though I do steal tastes. • I try to skip one meal a day or at least make it really small. My busy schedule almost always means that I miss lunch most days of the week. • Every few months, a phlebotomist comes to my home to draw my blood, which I have analyzed for dozens of biomarkers. When my levels of various markers are not optimal, I moderate them with food or exercise. • I try to take a lot of steps each day and walk upstairs, and I go to the gym most weekends with my son, Ben; we lift weights, jog a bit, and hang out in the sauna before dunking in an ice-cold pool. • I eat a lot of plants and try to avoid eating other mammals, even though they do taste good. If I work out, I will eat meat. • 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. About fifty times a day I’m asked about supplements.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“to lose their identity and become cancerous. And geneticist Nir Barzilai spoke of genetic variants in long-lived humans and his belief that all aging-related diseases can be substantially prevented and human lives can be considerably extended with one relatively easy pharmaceutical intervention.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“Because this planet, our planet as it was 4 billion years ago, is a ruthlessly unforgiving place. Hot and volcanic. Electric. Tumultuous.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“To us, the second and the millimeter are short divisions of time and space, but to an enzyme about 10 nanometers across and vibrating every quadrillionth of a second, a millimeter is the size of a continent and a second is more than a year.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

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

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

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

“When the Sir2 enzyme is sitting on the mating-type genes, they remain silent and the cell continues to mate and reproduce. But when a DNA break occurs, Sir2 is recruited to the break to remove the acetyl tags from the histones at the DNA break. This bundles up the histones to prevent the frayed DNA from being chewed back and to help recruit other repair proteins. Once the DNA repair is complete, most of the Sir2 protein goes back to the mating-type genes to silence them and restore fertility. That is, unless there is another emergency, such as the massive genome instability that occurs when ERCs accumulate in the nucleoli of old yeast cells.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“How does the SIR2 gene actually turn off genes? SIR2 codes for a specialized protein called a histone deacetylase, or HDAC, that enzymatically cleaves the acetyl chemical tags from histones, which, as you’ll recall, causes the DNA to bundle up, preventing it from being transcribed into RNA.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“What I’m suggesting is that the SIR2 gene in yeast and the SIRT genes in mammals are all descendants of gene B, the original gene silencer in M. superstes.30 Its original job was to silence a gene that controlled reproduction.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“Sirtuins instruct the histone spooling proteins to bind up DNA tightly, while they leave other regions to flail around. In this way, some genes stay silent, while others can be accessed by DNA-binding transcription factors that turn genes on.12 Accessible genes are said to be in “euchromatin,” while silent genes are in “heterochromatin.” By removing chemical tags on histones, sirtuins help prevent transcription factors from binding to genes, converting euchromatin into heterochromatin.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“Up close, the epigenome is more complex and wonderful than anything we humans have invented. 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.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“Here’s the important point: there are plenty of stressors that will activate longevity genes without damaging the cell, including certain types of exercise, intermittent fasting, low-protein diets, and exposure to hot and cold temperatures (I discuss this in chapter 4).”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“The other pathway is a metabolic control enzyme known as AMPK, which evolved to respond to low energy levels. It has also been highly conserved among species and, as with sirtuins and TOR, we have learned a lot about how to control it.”
― 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.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

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

“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.”
― 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. DNA in the cell isn’t flailing around disorganized, it is wrapped around tiny balls of protein called histones. These beads on a string self-assemble to form loops, as when you tidy your garden hose on your driveway by looping it into a pile. If you were to play tug-of-war using both ends of a chromosome, you’d end up with a six foot-long string of DNA punctuated by thousands of histone proteins. If you could somehow plug one end of the DNA into a power socket and make the histones flash on and off, a few cells could do you for holiday lights. In simple species, like ancient M. superstes and fungi today, epigenetic information storage and transfer is important for survival. For complex life, it is essential. By complex life, I mean anything made up of more than a couple of cells: slime molds, jellyfish, worms, fruit flies, and of course mammals like us. Epigenetic information is what orchestrates the assembly of a human newborn made up of 26 billion cells from a single fertilized egg and what allows the genetically identical cells in our bodies to assume thousands of different modalities.24 If the genome were a computer, the epigenome would be the software. It instructs the newly divided cells on what type of cells they should be and what they should remain, sometimes for decades, as in the case of individual brain neurons and certain immune cells.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“Today, analog information is more commonly referred to as the epigenome, meaning traits that are heritable that aren’t transmitted by genetic means.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“Over fifty years, Goldman estimated, the potential economic benefits of delayed aging would add up to more than $7 trillion in the United States alone. And that’s a conservative estimate, based on modest improvements in the percentages of older people living without a disease or disability. Whatever the dollar figure, though, the benefits “would accrue rapidly,” Goldman’s team wrote, “and would extend to all future generations,”
― David A. Sinclair, Lifespan: Why We Age―and Why We Don't Have To

“Bill Gates made a convincing argument for why improving human health is money well spent, and won’t lead to overpopulation, in his 2018 video “Does Saving More Lives Lead to Overpopulation?”56 The short answer is: No.
If we were to stop all deaths—every single one around the globe—right now, we would add about 150,000 people to our planet each day. That would be 55 million people each year. That might sound like a lot, but it would be less than a single percentage point. At that rate, we would add a billion people to our ranks every eighteen years, which is still considerably slower than the rate at which the last few billion people have come along and easily countered by the global decline in family sizes.
It’s still an increase, but it’s not the sort of exponential growth many people fret about when they first encounter the idea of slowing aging.
Recall, these calculations are what we’d face if we ended all deaths right away. And although I’m very optimistic about the prospects for prolonged vitality, I’m not that optimistic. I don’t know any reputable scientist who is.”
― David A. Sinclair, Lifespan: Why We Age―and Why We Don't Have To

“Every aspect of job performance gets better as we age,” Peter Cappelli, the director of the Wharton Center for Human Resources, reported after he began to investigate the stereotypes that often surround older workers. “I thought the picture might be more mixed, but it isn’t. The juxtaposition between the superior performance of older workers and the discrimination against them in the workplace just really makes no sense.”
― David A. Sinclair, Lifespan: Why We Age―and Why We Don't Have To