Lifespan Quotes

“pregunta: «¿Qué molécula es superior: NR o NMN?». Hemos descubierto que NMN es más estable que NR y vemos algunos beneficios de salud en experimentos con ratones que no se ven cuando se usa NR. Sin embargo, es NR la que ha demostrado alargar la esperanza de vida de los ratones. NMN sigue en proceso de prueba, así que no hay una respuesta definitiva, al menos por ahora.”
― David A. Sinclair, Alarga tu esperanza de vida: Cómo la ciencia nos ayuda a controlar, frenar y revertir el proceso de envejecimiento

“A study of more than 41,000 metformin users between the ages of 68 and 81 concluded that metformin reduced the likelihood of dementia, cardiovascular disease, cancer, frailty, and depression, and not by a small amount. In one group of already frail subjects, metformin use over the course of nine years reduced dementia by 4 percent, depression by 16 percent, cardiovascular disease by 19 percent, frailty by 24 percent, and cancer by 4 percent.22 In other studies, the protective power of metformin against cancer has been far greater than that.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“but after thousands of studies, the evidence is irrefutable: if you believe climate change is a threat, you can’t say that GMOs are, because the evidence that GMOs are safe is stronger than the evidence that climate change is occurring.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“We now know that vaccines are the single most effective medical intervention in human history in terms of saving and extending lifespans.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“This is what longer life is all about—being around for your children’s important moments.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“Death by death, the world sheds ideas that need to be shed. Ipso facto, birth by birth, the world is offered an opportunity to do things better.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

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

“If the information theory is correct—that aging is caused by overworked epigenetic signalers responding to cellular insult and damage—it doesn’t so much matter where the damage occurs. What matters is that it is being damaged and that sirtuins are rushing all over the place to address that damage, leaving their typical responsibilities and sometimes returning to other places along the genome where they are silencing genes that aren’t supposed to be silenced. This is the cellular equivalent of distracting the cellular pianist.”
― David A. Sinclair, Lifespan: The Revolutionary Science of Why We Age—and Why We Don't Have To

“I had noticed that yeast cells fed with lower amounts of sugar were not just living longer, but their rDNA was exceptionally compact—significantly delaying the inevitable ERC accumulation, catastrophic numbers of DNA breaks, nucleolar explosion, sterility, and death. Why was that happening? THE”
― David A. Sinclair, Lifespan: The Revolutionary Science of Why We Age—and Why We Don't Have To

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

“One of the best ways to visualize this is to think of our genome as a grand piano.13 Each gene is a key. Each key produces a note. And from instrument to instrument, depending on the maker, the materials, and the circumstances of manufacturing, each will sound a bit different, even if played the exact same way. These are our genes. We have about 20,000 of them, give or take a few thousand.14 Each key can also be played pianissimo (soft) or forte (with force). The notes can be tenuto (held) or allegretto (played quickly). For master pianists, there are hundreds of ways to play each individual key and endless ways to play the keys together, in chords and combinations that create music we know as jazz, ragtime, rock, reggae, waltzes, whatever. The pianist that makes this happen is the epigenome.”
― David A. Sinclair, Lifespan: The Revolutionary Science of 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). That’s called hormesis.28 Hormesis is generally good for organisms, especially when it can be induced without causing any lasting damage. When hormesis happens, all is well. And, in fact, all is better than well, because the little bit of stress that occurs when the genes are activated prompts the rest of the system to hunker down, to conserve, to survive a little longer. That’s the start of longevity.”
― David A. Sinclair, Lifespan: The Revolutionary Science of Why We Age—and Why We Don't Have To

“Together, these genes form a surveillance network within our bodies, communicating with one another between cells and between organs by releasing proteins and chemicals into the bloodstream, monitoring and responding to what we eat, how much we exercise, and what time of day it is.”
― David A. Sinclair, Lifespan: The Revolutionary Science of Why We Age—and Why We Don't Have To

“Most of my colleagues call these “longevity genes” because they have demonstrated the ability to extend both average and maximum lifespans in many organisms. But these genes don’t just make life longer, they make it healthier, which is why they can also be thought of as “vitality genes.”
― David A. Sinclair, Lifespan: The Revolutionary Science of Why We Age—and Why We Don't Have To

“it. It is, in essence, a primordial survival kit that diverts energy to the area of greatest need, fixing what exists in times when the stresses of the world are conspiring to wreak havoc on the genome, while permitting reproduction only when more favorable times prevail.”
― David A. Sinclair, Lifespan: The Revolutionary Science of Why We Age—and Why We Don't Have To

“What’s the upward limit? I don’t think there is one. Many of my colleagues agree.14 There is no biological law that says we must age.15 Those who say there is don’t know what they’re talking about. We’re probably still a long way off from a world in which death is a rarity, but we’re not far from pushing it ever farther into the future.”
― David A. Sinclair, Lifespan: The Revolutionary Science of Why We Age—and Why We Don't Have To

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

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

“Therefore, we must invest in research that allows us to grow more healthy food and transport it more effectively. And please make no mistake: that includes accepting genetically modified crops, those engineered to include a trait in the plant that doesn’t occur in its wild form, such as resistance to insects, tolerance to drought, greater vitamin A production, or more efficient use of sunlight to convert CO2 to sugar—as an absolutely necessary part of our food future. With more efficient plants, we could feed up to 200 million additional people, just from plants grown in the US Midwest. 33 These crops have gotten a bad rap for being “unnatural,” although many people who hold this view don’t recognize that most of the food we think of as “natural” has already been subject to significant genetic manipulation. The ears of corn you see at the grocery store look nothing like the wild plant from which modern corn came; over the course of nine thousand years, the spindly finger-length grass known as teosinte was cultivated to evolve larger cobs and more rows of plump, soft, sugary kernels, a process of modification that significantly altered the plant’s genome.34 The apples we’ve grown accustomed to eating have a bit more resemblance to their small, wild ancestors, but good luck finding one of those ancestors; they have been nearly wiped off the planet, and that’s no great loss to our diet, since the biggest genetic contributor to modern apples, Malus sylvestris, is so tart it’s darn near inedible.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“In this more nuanced view, aging and the diseases that come with it are the result of multiple “hallmarks” of aging: • Genomic instability caused by DNA damage • Attrition of the protective chromosomal endcaps, the telomeres • Alterations to the epigenome that controls which genes are turned on and off • Loss of healthy protein maintenance, known as proteostasis • Deregulated nutrient sensing caused by metabolic changes • Mitochondrial dysfunction • Accumulation of senescent zombielike cells that inflame healthy cells • Exhaustion of stem cells • Altered intercellular communication and the production of inflammatory molecules Researchers began to cautiously agree: address these hallmarks, and you can slow down aging. Slow down aging, and you can forestall disease. Forestall disease, and you can push back death.”
― 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). That’s called hormesis.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

“Science has since demonstrated that the positive health effects attainable from an antioxidant-rich diet are more likely caused by stimulating the body’s natural defenses against aging, including boosting the production of the body’s enzymes that eliminate free radicals, not as a result of the antioxidant activity itself.”
― David A. Sinclair, Lifespan: Why We Age—and Why We Don't Have To

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

“There’s simply no way to know if the combo of NMN and metformin is the reason he’s feeling better or is simply what he started taking at the time he decided, subconsciously, that it was time for a big change in his approach to life.”
― David A. Sinclair, Lifespan: The Revolutionary Science of Why We Age—and Why We Don't Have To

“The theory is also relevant to the foods we eat; plants that are stressed have higher concentrations of xenohormetic molecules that may help us engage our own survival circuits. Look for the most highly colored ones because xenohormetic molecules are often yellow, red, orange, or blue. One added benefit: they tend to taste better. The best wines in the world are produced in dry, sun-exposed soil or from stress-sensitive varietals such as Pinot Noir; as you might guess, they also contain the most resveratrol.30 The most delectable strawberries are those that have been stressed by periods of limited water supply. And as anyone who has grown leaf vegetables can attest, the best heads of lettuce come when the plants are exposed to a one-two combo punch of heat and cold.31 Ever wonder why organic foods, which are often grown under more stressful conditions, might be better for you?”
― David A. Sinclair, Lifespan: The Revolutionary Science of Why We Age—and Why We Don't Have To

“In animal studies, the key to engaging the sirtuin program appears to be keeping things on the razor’s edge through calorie restriction—just enough food to function in healthy ways and no more. This makes sense. It engages the survival circuit, telling longevity genes to do what they have been doing since primordial times: boost cellular defenses, keep organisms alive during times of adversity, ward off disease and deterioration, minimize epigenetic change, and slow down aging.”
― David A. Sinclair, Lifespan: The Revolutionary Science of Why We Age—and Why We Don't Have To

“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: The Revolutionary Science of Why We Age—and Why We Don't Have To

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

“His name was Robert Mortimer, and if there was one adjective that seemed to come up more than any other about him after he passed away, it was “kind.” “Visionary” was another. “Brilliant,” “inquisitive,” and “hardworking,” too.”
― David A. Sinclair, Lifespan: The Revolutionary Science of Why We Age—and Why We Don't Have To

“Trading reproduction for repair, the sirtuins order our bodies to “buckle down” in times of stress and protect us against the major diseases of aging: diabetes and heart disease, Alzheimer’s disease and osteoporosis, even cancer. They mute the chronic, overactive inflammation that drives diseases such as atherosclerosis, metabolic disorders, ulcerative colitis, arthritis, and asthma. They prevent cell death and boost mitochondria, the power packs of the cell. They go to battle with muscle wasting, osteoporosis, and macular degeneration. In studies on mice, activating the sirtuins can improve DNA repair, boost memory, increase exercise endurance, and help the mice stay thin, regardless of what they eat. These are not wild guesses as to their power; scientists have established all of this in peer-reviewed studies published in journals such as Nature, Cell, and Science.”
― David A. Sinclair, Lifespan: The Revolutionary Science of Why We Age—and Why We Don't Have To