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. LOCATION: 162
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. LOCATION: 447
Cloning gives us the answer as to whether or not mutations cause aging. If old cells had indeed lost crucial genetic information and this was the cause of aging, we shouldn’t be able to clone new animals from older individuals. Clones would be born old. LOCATION: 463
Because of the fact that nuclear transfer works in cloning, we can say with a high degree of confidence that aging isn’t caused by mutations in nuclear DNA. LOCATION: 471
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. LOCATION: 520
Today, analog information is more commonly referred to as the epigenome, meaning traits that are heritable that aren’t transmitted by genetic means. LOCATION: 534
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. LOCATION: 548
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. LOCATION: 585
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. LOCATION: 591
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. LOCATION: 607
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. LOCATION: 614
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. LOCATION: 619
In the relatively short time that has come and gone since 2003, we have come to find out that within the famous double helix, there were sequences that were not just unmapped but essential to our lives. Indeed, many thousands of sequences had gone undetected because the original algorithms to detect genes were written to disregard any gene less than 300 base pairs long. In fact, genes can be as short as 21 base pairs, and today we’re discovering hundreds of them all over the genome. LOCATION: 645
Studies of identical twins place the genetic influences on longevity at between 10 and 25 percent which, by any estimation, is surprisingly low. LOCATION: 796
Youth → broken DNA → genome instability → disruption of DNA packaging and gene regulation (the epigenome) → loss of cell identity → cellular senescence → disease → death. LOCATION: 844
We demonstrated that the redistribution of Sir2 to the nucleolus is a response to numerous DNA breakages, which happen as a result of ERCs multiplying and inserting back into the genome or joining together to form superlarge ERCs. When Sir2 moves to combat DNA instability, it causes sterility in old, bloated yeast cells. That was the first step of the survival circuit, though at the time we had no idea that it was as ancient and as essential to our very existence as it turned out to be. We told the world that we could give yeast a Werner-like syndrome, causing exploded nucleoli.18 We described the ways in which mutants of SGS1, those we’d plagued with the yeast equivalent to the Werner syndrome mutation, accumulated ERCs more rapidly, leading to premature aging and a shortened lifespan.19 Crucially, by demonstrating that if you add an ERC to young cells they age prematurely, we had crucial evidence that ERCs don’t just happen during aging, they cause it. And by artificially breaking the DNA in the cell and watching the cellular response, we showed why sirtuins move—to help with DNA repair.20 That turned out to be the second step of the survival circuit.21 The DNA damage that gave rise to the ERCs was distracting Sir2 from the mating-type genes, causing them to become sterile, a hallmark of yeast aging. LOCATION: 862
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. LOCATION: 890
Our DNA is constantly under attack. On average, each of our forty-six chromosomes is broken in some way every time a cell copies its DNA, amounting to more than 2 trillion breaks in our bodies per day. And that’s just the breaks that occur during replication. Others are caused by natural radiation, chemicals in our environment, and the X-rays and CT scans that we’re subjected to. LOCATION: 893
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. In mammals, the sirtuins have since taken on a variety of new roles, not just as controllers of fertility (which they still are). They remove acetyls from hundreds of proteins in the cell: histones, yes, but also proteins that control cell division, cell survival, DNA repair, inflammation, glucose metabolism, mitochondria, and many other functions. I’ve come to think of sirtuins as the directors of a multifaceted disaster response corps, sending out a variety of specialized emergency teams to address DNA stability, DNA repair, cell survivability, metabolism, and cell-to-cell communication. LOCATION: 914
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. LOCATION: 927
Wherever epigenetic factors leave the genome to address damage, genes that should be off, switch on and vice versa. Wherever they stop on the genome, they do the same, altering the epigenome in ways that were never intended when we were born. LOCATION: 941
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. LOCATION: 1001
A couple of species of jellyfish can completely regenerate from adult body parts, earning them the nickname “immortal jellies.” Only the elegant moon jelly Aurelia aurita from the US West Coast and the centimeter-long Turritopsis dohrnii from the Mediterranean are currently known to regenerate, but I’m guessing the majority of jellies do. We just need to look. If you separate one of these amazing animals into single cells, the cells jostle around until they form clumps that then assemble back into a complete organism, like the T-1000 cyborg in Terminator 2, most likely resetting their aging clock. LOCATION: 1042
We discovered that when calories are restricted MSN2 extends yeast lifespan by turning up genes that recycle NAD, thereby giving the sirtuins a boost. LOCATION: 1083
But what about FOXO genes in humans? Certain variants called FOXO3 have been found in human communities in which people are known to enjoy both longer lifespans and healthspans, such as the people of China’s Red River Basin.39 These FOXO3 variants likely turn on the body’s defenses against diseases and aging, not just when times are tough but throughout life. 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. LOCATION: 1087
As you’ll recall, the epigenome is inherently unstable because it is analog information—based on an infinite number of possible values—and thus it’s difficult to prevent the accumulation of noise and nearly impossible to duplicate without some information loss. The earthquakes are a fact of life. The landscape is always changing. LOCATION: 1135
Regular exercise “is a commitment,” says Benjamin Levine, a professor at the University of Texas. “But I tell people to think of exercise as part of personal hygiene, like brushing their teeth. It should be something we do as a matter of course to keep ourselves healthy.” LOCATION: 1156
I also knew why: cigarette smoke contains a chemical called benzo(a)pyrene, which binds to guanine in DNA, induces double-strand breaks, and causes mutations. The repair process also causes epigenetic drift and metabolic changes that cancer cells thrive on, in a process we’ve called geroncogenesis. LOCATION: 1414
But consider this: though smoking increases the risk of getting cancer fivefold, being 50 years old increases your cancer risk a hundredfold. By the age of 70, it is a thousandfold. LOCATION: 1424
I believe that aging is a disease. I believe it is treatable. I believe we can treat it within our lifetimes. And in doing so, I believe, everything we know about human health will be fundamentally changed. LOCATION: 1445
After twenty-five years of researching aging and having read thousands of scientific papers, if there is one piece of advice I can offer, one surefire way to stay healthy longer, one thing you can do to maximize your lifespan right now, it’s this: eat less. LOCATION: 1534
But fasting—allowing our bodies to exist in a state of want, more often than most of us allow in our privileged world of plenty—is unquestionably good for our health and longevity. LOCATION: 1538
“I accustomed myself to the habit of never fully satisfying my appetite, either with eating or drinking,” Cornaro wrote in his First Discourse on the Temperate Life, “always leaving the table well able to take more.” LOCATION: 1545
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. LOCATION: 1565
Tellingly, the biochemical changes they saw in their bodies closely mirrored those Walford had seen in his long-lived calorie-restricted mice, such as decreased body mass (15 to 20 percent), blood pressure (25 percent), blood sugar level (21 percent), and cholesterol levels (30 percent), among others. LOCATION: 1586
What we’re coming to learn is that mTOR isn’t impacted only by caloric restriction.23 If you want to keep mTOR from being activated too much or too often, limiting your intake of amino acids is a good way to start, so inhibiting this particular longevity gene is really as simple as limiting your intake of meat and dairy. LOCATION: 1709
demonstrated that methionine restriction causes obese mice to shed most of their fat—and fast. Even as the mice, which Lamming called “couch potatoes,” continued to eat as much as they wanted and shun exercise, they still lost about 70 percent of their fat in a month, while also lowering their blood glucose levels. LOCATION: 1716
When researchers studied the telomeres in the blood cells of thousands of adults with all sorts of different exercise habits, they saw a striking correlation: those who exercised more had longer telomeres. LOCATION: 1749
individuals who exercise more—the equivalent of at least a half hour of jogging five days a week—have telomeres that appear to be nearly a decade younger than those who live a more sedentary life. LOCATION: 1751
Exercise, by definition, is the application of stress to our bodies. It raises NAD levels, which in turn activates the survival network, which turns up energy production and forces muscles to grow extra oxygen-carrying capillaries. The longevity regulators AMPK, mTOR, and sirtuins are all modulated in the right direction by exercise, irrespective of caloric intake, building new blood vessels, improving heart and lung health, making people stronger, and, yes, extending telomeres. SIRT1 and SIRT6, for example, help extend telomeres, then package them up so they are protected from degradation. LOCATION: 1755
One recent study found that those who ran four to five miles a week—for most people, that’s an amount of exercise that can be done in less than 15 minutes per day—reduce their chance of death from a heart attack by 40 percent and all-cause mortality by 45 percent. LOCATION: 1763
Mayo Clinic researchers studying the effects of different types of exercise on different age groups found that although many forms of exercise have positive health effects, it’s high-intensity interval training (HIIT)—the sort that significantly raises your heart and respiration rates—that engages the greatest number of health-promoting genes, and more of them in older exercisers. LOCATION: 1773
In other words: exercise turns on the genes to make us young again at a cellular level. LOCATION: 1783
When you give rats a high-calorie diet and allow them to burn off the energy, lifespan extension is minimal. Same for a CR diet. If you make food filling but not as calorific, some of the health benefits are lost. Being hungry is necessary for CR to work because hunger helps turn on genes in the brain that release longevity hormones, at least according to a recent study by Dongsheng Cai at the Albert Einstein College of Medicine. LOCATION: 1785
exposing your body to less-than-comfortable temperatures is another very effective way to turn on your longevity genes. LOCATION: 1803
As scientists have increasingly turned their attention to the impacts of reduced food intake on the human body, it has quickly become clear that calorie restriction has the effect of reducing core body temperature. LOCATION: 1809
The team inserted copies of the mouse UCP2 gene into the mice’s hypothalamus, which regulates the skin, sweat glands, and blood vessels. UCP2 short-circuited mitochondria in the hypothalamus so they produced less energy but more heat. That, in turn, caused the mice to cool down about half a degree Celsius. The result was a 20 percent longer life for female mice, the equivalent of about seven additional healthy human years, while male mice got an extension of 12 percent. LOCATION: 1814
Other studies have shown that animals with abundant brown fat or subjected to shivering cold for three hours a day have much more of the mitochondrial, UCP-boosting sirtuin, SIRT3, and experience significantly reduced rates of diabetes, obesity, and Alzheimer’s disease. LOCATION: 1836
Exercising in the cold, in particular, appears to turbocharge the creation of brown adipose tissue. LOCATION: 1866
Those who used a sauna with great frequency—up to seven times a week—enjoyed a twofold drop in heart disease, fatal hearts attacks, and all-cause mortality events over those who heat bathed once per week. LOCATION: 1893
A bit of adversity or cellular stress is good for our epigenome because it stimulates our longevity genes. It activates AMPK, turns down mTOR, boosts NAD levels, and activates the sirtuins—the disaster response teams—to keep up with the normal wear and tear that comes from living on planet Earth. LOCATION: 1902
In each cell are a total of 75,000 enzymes like catalase,4 all thrown together, jostling around in a slightly salty sea. At the nanoscale, water is gelatinous, and molecular events are more violent than a category 5 hurricane, with molecules thrown together at speeds we would perceive as a thousand miles per hour. Enzymatic reactions are one-in-a-thousand events, but at the nanoscale one-in-a-thousand events can occur thousands of times a second, enough to sustain life. LOCATION: 1982
In the dirt beneath one of the island’s famed stone heads, they discovered a new actinobacterium. That single-celled organism was Streptomyces hygroscopicus, and when it was isolated by a pharmaceutical researcher, Suren Sehgal, it soon became clear that the actinobacterium secreted an antifungal compound. LOCATION: 2014
Because in recent years it has become clear that rapamycin isn’t just an antifungal compound and it isn’t just an immune system suppressor; it’s also one of the most consistently successful compounds for extending life. LOCATION: 2030
researchers noticed a curious phenomenon: people taking metformin were living notably healthier lives—independent, it seemed, of its effect on diabetes. LOCATION: 2083
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. LOCATION: 2090
the resveratrol-fed yeast were slightly smaller and grew slightly more slowly than untreated yeast, getting to an average of thirty-four divisions before dying, as though they were calorie restricted. The human equivalent would be an extra 50 years of life. We saw increases in maximum lifespan, too—on resveratrol, they kept going past 35. We tested resveratrol in yeast cells with no SIR2 gene, and there was no effect. We tested it on calorie-restricted yeast, and saw no further increase in lifespan, suggesting that the same pathway was being activated; this was how calorie restriction was working. LOCATION: 2173
That’s because Shin-ichiro Imai and Lenny Guarente showed that NAD acts as fuel for sirtuins. Without sufficient NAD, the sirtuins don’t work efficiently: they can’t remove the acetyl groups from histones, they can’t silence genes, and they can’t extend lifespan. And we sure wouldn’t have seen the lifespan-extending impact of the activator resveratrol. LOCATION: 2239
Human studies with NAD boosters are ongoing. So far, there has been no toxicity, not even a hint of it. Studies to test its effectiveness in muscle and neurological diseases are in progress or about to begin, followed by super-NAD-boosting molecules that are a couple of years behind them in development. LOCATION: 2277
These anecdotal reports of restored menstruation and fertile horses are early but interesting indicators that NAD boosters might restore failing or failed ovaries. We also see that NMN is able to restore the fertility of old mice that have had all their eggs killed off by chemotherapy or have gone through “mousopause.” These results, by the way, even though they were done multiple times and reproduced in two different labs by different people, are so controversial that almost no one on the team voted to publish them. I was the exception. They remain unpublished, for now. LOCATION: 2316
My father’s story of reinvigoration is, of course, completely anecdotal. I won’t be publishing it in a scientific journal anytime soon—a placebo can be a powerful drug, after all. 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. Compelling evidence that the clock of aging is reversible will come when well-planned double-blind human clinical studies are completed. Until then, I remain very proud of my father, an average guy who grabbed life by the horns in his late 70s to start his life anew—a shining example of what life can be like if we don’t accept aging as “just the way it goes.” LOCATION: 2391
Aging is going to be remarkably easy to tackle. Easier than cancer. LOCATION: 2435
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. LOCATION: 2453
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. LOCATION: 2454
In 1997, it was a remarkable finding that if you put telomerase into cultured skin cells, they don’t ever senesce. LOCATION: 2456
Senescent cells are often referred to as “zombie cells,” because even though they should be dead, they refuse to die. LOCATION: 2468
Cellular senescence is a consequence of our inherited primordial survival circuits, which evolved to stop cell division and reproduction when DNA breaks were detected. LOCATION: 2490
If zombie cells are so bad for our health, why doesn’t our body just kill them off? Why are senescent cells allowed to cause trouble for decades? Back in the 1950s, the evolutionary biologist George Williams was already on the case. His work, built upon by Judith Campisi from the Buck Institute for Research on Aging in California, proposes that we evolved senescence as a rather clever trick to prevent cancer when we are in our 30s and 40s. Senescent cells, after all, don’t divide, which means that cells with mutations aren’t able to spread and form tumors. But if senescence evolved to prevent cancer, why would it eventually promote cancer in adjacent tissue, not to mention a host of other aging-related symptoms? This is where “antagonistic pleiotropy” comes into play: the idea that a survival mechanism that is good for us when we are young is kept through evolution because this far outweighs any problems it might cause when we get older. LOCATION: 2493
We’re plagued by senescent cells, which might as well be radioactive waste. If you put a tiny dab of these cells under a young mouse’s skin, it won’t be long before inflammation spreads and the entire mouse is filled with zombie cells that cause premature signs of aging. LOCATION: 2512
He needed only a quick course of two senolytic molecules—quercetin, which is found in capers, kale, and red onions, and a drug called dasatinib, which is a standard chemotherapy treatment for leukemia—to eliminate the senescent cells in lab mice and extend their lifespan by 36 percent. LOCATION: 2517
The first human trials of senolytics were started in 2018 to treat osteoarthritis and glaucoma, conditions in which senescent cells can accumulate. It will be a few more years before we know enough about the effects and safety of these drugs to provide them to everyone, but if they work, the potential is vast. LOCATION: 2524
Vaccines against senescent cells, CR mimetics, and retrotransposon suppressors are possible pathways to prolonged vitality, and work is under way already in labs and clinics around the world. LOCATION: 2590
Together, all the DNA in our body, if laid end to end, would stretch twice the diameter of the solar system. LOCATION: 2600
In Shannon’s drawing, there are three different components that have analogs in biology:
The “source” of the information is the egg and sperm, from your parents.
The “transmitter” is the epigenome, transmitting analog information through space and time.
The “receiver” is your body in the future. LOCATION: 2636
So even if a lot of the epigenetic information is lost in old age, obscured by epigenetic noise, there must be information that tells the cell how to reset. This fundamental information, laid down early in life, is able to tell the body how to be young again—the equivalent of a backup of the original data. LOCATION: 2643
To end aging as we know it, we need to find three more things that Shannon knew were essential for a signal to be restored even if it is obscured by noise:
An “observer” who records the original data
The original “correction data”
And a “correcting device” to restore the original signal LOCATION: 2650
EPIGENETIC REPROGRAMMING REGROWS OPTIC NERVES AND RESTORES EYESIGHT IN OLD MICE. The Information Theory of Aging predicts that it is a loss of epigenetic rather than genetic information in the form of mutations. By infecting mice with reprogramming genes called Oct4, Sox2, and Klf4, the age of cells is reversed by the TET enzymes, which remove just the right methyl tags on DNA, reversing the clock of aging and allowing the cells to survive and grow like a newborn’s. How the enzymes know which tags are the youthful ones is a mystery. Solving that mystery would be the equivalent of finding Claude Shannon’s “observer,” the person who holds the the original data. LOCATION: 2751
We know from our experiments that the biological information correcting device requires enzymes called ten-eleven translocation enzymes, or TETs, which clip off methyl tags from DNA, the same chemical tags that mark the passage of the Horvath aging clock. This is no coincidence, and points to the DNA methylation clock as not just an indicator of age but a controller of it. LOCATION: 2766
Yet in the United States alone, with one of the better health care systems in the world, about 5 percent of cancer patients, or 86,500 people, are misdiagnosed every year. LOCATION: 2834
Today, I can read an entire human genome of 25,000 genes in a few days for less than a hundred dollars on a candy bar–sized DNA sequencer called a MinION that I plug into my laptop. And that’s for a fairly complete readout of a human genome, plus the DNA methyl marks that tell you your biological age. LOCATION: 2895
Males don’t just differ from females at a few sites in the genome; they have a whole other chromosome. LOCATION: 2919
Treatments that work through insulin or mTOR signaling typically favor females, whereas chemical therapies typically favor males, and no one really knows why. LOCATION: 2924
Indeed, we know more about the health of our cars than we know about our own health. That’s farcical. And it’s about to change. LOCATION: 3007
Barriers fall. And they will fall again. In another generation, we’ll be well accustomed to seeing movie stars in their 60s and 70s riding motorcycles at high speeds, jumping from great heights, and delivering kung fu kicks high into the air. Because 60 will be the new 40. Then 70 will be the new 40. And on it will go. LOCATION: 3324
Today, many of my colleagues are just as optimistic as I am, even if they don’t admit it publicly. I’d wager that about a third of them take metformin or an NAD booster. A few of them even take low doses of rapamycin intermittently. LOCATION: 3374
In November 2016, the late physicist Stephen Hawking predicted that humanity had less than 1,000 years left on “our fragile planet.” A few months of contemplation later, he revised his estimate downward by 90 percent. Echoing Fenner’s warnings, Hawking believed that humanity would have 100 years to find a new place to live. “We are running out of space on Earth,” he said. LOCATION: 3490
“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.” LOCATION: 3533
Working with the world-renowned economists Andrew Scott at the University of London and Martin Ellison at Oxford University, we are developing a model to predict what the future looks like. There are quite a few variables, not all of them positive. Will people continue to work? What jobs will they be able to get in a world in which the labor market will already be being upended by automation? Will they spend a half century or more in retirement? Some economists believe that economic growth is slowed when a country ages, in part because people spend less in retirement. What will happen if people spend half of their very long lives out of work, spending only enough to get by? Will they save more? Invest more? Get bored soon after retirement and start a new career? Take long sabbaticals from work, only to return decades later when their money runs out? Spend less on health care because they are so much healthier? Spend more on health care because they are living so much longer? Invest more years and money into their educations early on? Anyone who claims to know the answer to any of these questions is a charlatan. Anyone who says these questions aren’t important is a fool. We have absolutely no idea what’s going to happen. We are flying blind into one of the most economically destabilizing events in the history of the world. LOCATION: 3619
Imagine a world of haves and have-nots unlike anything we have experienced since the dark ages: a world in which those born into a certain station in life can, by virtue of nothing more than exceptional fortune, live thirty years longer than those who were born without the means to literally buy into therapies that provide longer healthspans and enable more productive working years and greater investment returns. LOCATION: 3657
A United Nations Environment Programme report detailing sixty-five scientific estimates of global carrying capacity found that the majority—thirty-three—had pegged the maximum sustainable human population at 8 billion or fewer people. And yes, by these estimates, we have either already met or will soon meet the maximum number of human beings our planet can sustain.50 But an almost equal number of estimates—thirty-two of them—concluded that the number is somewhere above 8 billion. Eighteen of those estimates suggested that the carrying capacity is at least 16 billion. And a few estimates suggested that our planet has the potential to sustain more than 100 billion people. LOCATION: 3768
It needs to be pointed out that very few of the global carrying capacity models account for human ingenuity. LOCATION: 3789
To me, the only thing that seems unnatural—in that it has never happened in the history of our species—is to accept limitations on what we can and cannot do to improve our lives. LOCATION: 3824
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. LOCATION: 3853
Countries stagnate because they don’t innovate and don’t utilize their human capital, not because there aren’t enough jobs. This explains why countries with an earlier retirement age have a lower GDP. LOCATION: 3976
The first nations to define aging as a disease, both in custom and on paper, will change the course of the future. The first places to provide large amounts of public funding to augment the fast-growing private investments in this field will prosper in kind. It will be their citizens who benefit first. LOCATION: 4216
There is nothing wrong with skepticism, 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. LOCATION: 4478
And so, with all that on the table, what do I do? LOCATION: 4758
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.
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.